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Summarize this article:
From Ben-Gurion University of the Negev and Soroka Medical Center, Beer Sheva, Israel; Nuclear Research Center Negev, Dimona, Israel; Hadassah Hebrew University Medical Center, Jerusalem, Israel; Karolinska Institute, Solna, Sweden; University of Leipzig, Leipzig, Germany; and Brigham and Women's Hospital and Harvard School of Public Health, Boston, Massachusetts.
Acknowledgment: The authors thank the CASCADE participants for their consistent cooperation. They thank Harel Segal from Nuclear Research Center Negev; Dr. Lena Novak, Dr. Michael Friger, Dr. Arie Moran, Dr. Amos Katz, Noa Cohen, Michal Rein, Nitzan Bril, and Dana Serfaty from Ben-Gurion University of Negev; Dr. Tatiana Shuster, Sagit Saadon, Malka Kaminsky, Yasmin Asuly, Roman Tsirkin, and David Shushan from Soroka Medical Center; Eyal Goshen, Meir Aviv, Hassia Krakauer, Haim Strasler, Dr. Ziva Schwartz, Dr. Einat Sheiner, Dr. Dov Brickner, Dr. Rachel Marko, Esther Katorza, Ilanit Asulin, and Tzvika Tzur from Nuclear Research Center Negev; and Dr. Rosa M. Lamuela-Raventos, University of Barcelona.
Grant Support: By the European Foundation for the Study of Diabetes of the European Association for the Study of Diabetes.
Disclosures: The authors have no relationship with the companies that make products relevant to the manuscript. Drs. Shai and Bolotin had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis. Dr. Bluüher reports compensation as a board member of Novartis Pharmaceuticals, Boehringer Ingelheim, and Sanofi; compensation as a consultant for Novo Nordisk, Eli Lilly Pharmaceuticals, and AstraZeneca; and payment for lectures (including service on speakers bureaus) for Sanofi, Eli Lilly Pharmaceuticals, Novo Nordisk, Bayer HealthCare Pharmaceuticals, AstraZeneca, Novartis Pharmaceuticals, and Berlin-Chemie outside of the submitted work. Authors not named here have disclosed no conflicts of interest. Disclosures can also be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=M14-1650.
Editors' Disclosures: Christine Laine, MD, MPH, Editor in Chief, reports that she has no financial relationships or interests to disclose. Darren B. Taichman, MD, PhD, Executive Deputy Editor, reports that he has no financial relationships or interests to disclose. Cynthia D. Mulrow, MD, MSc, Senior Deputy Editor, reports that she has no relationships or interests to disclose. Deborah Cotton, MD, MPH, Deputy Editor, reports that she has no financial relationships or interest to disclose. Jaya K. Rao, MD, MHS, Deputy Editor, reports that she has stock holdings/options in Eli Lilly and Pfizer. Sankey V. Williams, MD, Deputy Editor, reports that he has no financial relationships or interests to disclose. Catharine B. Stack, PhD, MS, Deputy Editor for Statistics, reports that she has stock holdings in Pfizer.
Reproducible Research Statement:Study protocol: Available from Dr. Shai (e-mail, [email protected]). Statistical code and data set: Not available.
Requests for Single Reprints: Iris Shai, RD, PhD, Department of Public Health, The S. Daniel Abraham International Center for Health and Nutrition, Ben-Gurion University of the Negev, PO Box 653, Beer Sheva, 8410501, Israel; e-mail, [email protected].
Current Author Addresses: Drs. Golan, Bolotin, Rudich, and Shai; Mr. Gepner, Ms. Kovsan, Ms. Witkow, Ms. Tangi-Rosental, and Ms. Ben-Avraham: Department of Public Health, Ben-Gurion University of the Negev, PO Box 653, Beer Sheva, 8410501, Israel.
Drs. Harman-Boehm, Henkin, Shelef, Shemesh, Chassidim, and Liberty: Soroka Medical Center, Rager Boulevard, PO Box 151, Beer Sheva, 85025, Israel.
Dr. Schwarzfuchs and Mr. Sarusi: Nuclear Research Center Negev, 16th Beth Lethem Street, Dimona, 8477605, Israel.
Drs. Durst, Leitersdorf, Balag; and Ms. Spitzen: Hadassah Hebrew University Medical Center, Kiryat Hadassah, PO Box 12000, Jerusalem, 91120, Israel.
Dr. Helander: Department of Laboratory Medicine, H5, Division of Clinical Chemistry, CI:74, Karolinska Institute, Karolinska University Laboratory Hudding, Stockholm, SE-14186, Sweden.
Drs. Ceglarek, Stumvoll, Blüher, and Thiery: Department of Diagnostics, University of Leipzig, Paul List Street 13-15, 04103 Leipzig, Germany.
Dr. Stampfer: Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard School of Public Health, 181 Longwood Avenue, Boston, MA 02115.
Author Contributions: Conception and design: Y. Gepner, I. Harman-Boehm, Y. Henkin, D. Schwarzfuchs, I. Shelef, R. Durst, E. Shemesh, S. Witkow, M. Stumvoll, A. Rudich, M.J. Stampfer, I. Shai.
Analysis and interpretation of the data: Y. Gepner, R. Golan, I. Harman-Boehm, I. Shelef, R. Durst, J. Kovsan, A. Bolotin, S. Shpitzen, E. Shemesh, Y. Chassidim, A. Helander, U. Ceglarek, M. Stumvoll, M. Bluüher, A. Rudich, M.J. Stampfer, I. Shai.
Drafting of the article: Y. Gepner, R. Golan, Y. Henkin, D. Schwarzfuchs, I. Shelef, R. Durst, J. Kovsan, A. Helander, U. Ceglarek, M. Stumvoll, A. Rudich, M.J. Stampfer, I. Shai.
Critical revision of the article for important intellectual content: Y. Gepner, I. Harman-Boehm, Y. Henkin, I. Shelef, R. Durst, J. Kovsan, E. Shemesh, A. Helander, M. Stumvoll, M. Bluüher, J. Thiery, A. Rudich, I. Shai.
Final approval of the article: Y. Gepner, R. Golan, I. Harman-Boehm, Y. Henkin, D. Schwarzfuchs, I. Shelef, R. Durst, J. Kovsan, A. Bolotin, E. Leitersdorf, E. Shemesh, I.F. Liberty, B. Sarusi, A. Helander, U. Ceglarek, M. Stumvoll, M. Bluüher, J. Thiery, A. Rudich, M.J. Stampfer, I. Shai.
Provision of study materials or patients: Y. Gepner, R. Golan, I. Harman-Boehm, Y. Henkin, D. Schwarzfuchs, R. Durst, S. Witkow, O. Tangi-Rosental, I.F. Liberty, I. Shai.
Statistical expertise: R. Golan, R. Durst, A. Bolotin.
Obtaining of funding: Y. Gepner, R. Durst, M. Stumvoll, I. Shai.
Administrative, technical, or logistic support: I. Shelef, J. Kovsan, E. Leitersdorf, S. Balag, E. Shemesh, O. Tangi-Rosental, B. Sarusi, M. Stumvoll.
Collection and assembly of data: Y. Gepner, R. Golan, Y. Henkin, D. Schwarzfuchs, I. Shelef, R. Durst, J. Kovsan, E. Shemesh, S. Witkow, O. Tangi-Rosental, I.F. Liberty, B. Sarusi, S. Ben-Avraham, M. Bluüher, A. Rudich, I. Shai. ||||| TIME Health For more, visit TIME Health
Alcohol is the Goldilocks of the nutrition world. Too much can be destructive to your health, raising your blood pressure and your risk of developing several kinds of cancer. Too little may hold you back from some of the benefits that moderate drinkers enjoy, like lower incidence of cardiovascular disease, mortality and type-2 diabetes.
The amount that’s just right, according to a new study published in the Annals of Internal Medicine, might be a nightly glass of wine with dinner—for some people, anyway.
Researchers from Ben-Gurion University of the Negev in Israel wanted to look at how safe and effective it is for a specific group of people—those with well-controlled type-2 diabetes and who had a low risk for alcohol abuse—to drink moderately. People with type-2 diabetes are more likely than the general population to develop cardiovascular disease and have lower levels of heart-protective HDL cholesterol, the authors note.
They chose 224 people who fit this profile, and who didn’t drink wine currently, then assigned them to start drinking one of three things. At dinner, the people in the study were told to drink five ounces of one of the following beverages: mineral water, dry white wine or dry red wine. Under the guidance of dietitians, they also followed a Mediterranean diet without calorie restrictions—and kept it up for two years.
Intermittently, they took questionnaires and were subjected to follow-ups, including blood draws at the start of the study, six months in and at 24 months, so the scientists could look at biomarkers of glycemic control, lipids and liver function.
They found that the red wine drinkers had significantly increased their levels of good HDL cholesterol and had a more beneficial cholesterol ratio compared to the group that drank water. They were also the only group to experience a significant drop in components of metabolic syndrome. People who drank either red or white wine also reported better sleep quality than the group that drank water, and the researchers found no significant adverse effects with any group.
(It’s worth making it explicit that those who drank alcohol, drank just one glass per night, with meals.)
“This is what I’ve been telling people for years based on observational data,” says Dr. James O’Keefe, chief of preventive cardiology at Saint Luke’s Mid America Heart Institute in Kansas City, who was not involved in the study. “It seems to me that my patients who drink red wine in moderation tend to do better, and this really solid gold-standard kind of research confirms our intuitions about the beneficial effects of moderate alcohol intake.”
O’Keefe wasn’t surprised that the best results came from the group drinking red wine—which had resveratrol levels 13-fold higher than the white wine, according to the study. “Partly it’s the benefits of the alcohol, but red wine also contains a lot of unique antioxidants that are hard to get other places,” O’Keefe says. And pairing it with dinner, like they did in the study, is key.
“If you have a glass of red wine with your evening meal tonight, your peak blood sugar, if you measured it an hour later, would be about 30% lower than if you hadn’t had the wine,” O’Keefe says. The post-meal spike in sugar is one of Americans’ main sources of inflammation, which contributes to everything from diabetes to dementia to heart disease and arthritis, he adds. “It makes your system more able to sop up the sugar and the calories that you’re consuming in the meal if you have a little alcohol before,” he says.
But there’s a disclaimer, of course. Drinking every day can be a “slippery slope that a lot of people can’t safely navigate,” O’Keefe says. “If they start drinking daily and they drink a bottle or two a day, that’s a disaster.”
For those who can safely imbibe, one glass of dry red wine—like pinot noir or Cannonau—with the largest meal of the day is the very best pairing, O’Keefe says. “If you’re going to drink red wine, this study is a good reminder to do it the old fashioned way: drink it with a Mediterranean meal high in vegetables and fish and lower in meat, with fruit for dessert and using olive oil. Doing it in a social, relaxed setting also goes a long way to improving health and happiness.” ||||| A glass of red wine a day can improve cardiac health and help manage cholesterol for patients with type 2 diabetes, according to findings in a 2-year study published in the journal Annals of Internal Medicine.
Red wine can help people with type 2 diabetes to avoid heart disease. Red wine can help people with type 2 diabetes to avoid heart disease.
Moderate alcohol consumption has been linked to improved cardiovascular and total mortality rates, and a glass of red wine a day as part of a healthy diet has been considered beneficial for some time.
There is evidence that type 2 diabetes is less prevalent among moderate drinkers, yet the risk-benefit balance is controversial for such patients, due to a lack of long-term randomized studies.
Researchers from Ben-Gurion University of the Negev-Soroka Medical Center and Nuclear Research Center Negev, Israel, wondered if both red and white wine might improve glucose control, depending on alcohol metabolism and genetic profiling.
Previous research has suggested that ethanol (alcohol) is the key, meaning that alcoholic drinks other than red wine could be equally beneficial; others claim that red wine has particularly advantageous properties.
Potential benefits for people with type 2 diabetes
People with diabetes have a higher risk of developing cardiovascular disease, as well as lower levels of "good" HDL cholesterol. High levels of HDL cholesterol can reduce the risk for heart disease and stroke, as it absorbs cholesterol and carries it back to the liver, where it is flushed from the body.
Fast facts about diabetes 29.1 million people in the US probably have diabetes, or 9.3% of the population
21 million have been diagnosed
An estimated further 8.1 million have not been diagnosed. Learn more about diabetes
Should patients with type 2 diabetes be recommended to take up moderate alcohol consumption? The American Diabetes Association (ADA) leave the decision to the individual; the American Heart Association (AHA) recommend discussing alcohol with a physician.
The researchers wanted to find out what the cardiometabolic effects would be when patients with type 2 diabetes took up drinking moderate amounts of alcohol; they also wanted to assess whether the type of wine would matter.
They hypothesized that initiating moderate wine consumption would lower cardiometabolic risk, mainly because of the ethanol component. They predicted similar effects of red and white wine. Because of genetic variability in alcohol metabolism, they predicted that the effects of wine would vary according to ADH1B genotype.
The 224 participants were 40-75-year-old alcohol-abstaining men and women with well-controlled type 2 diabetes.
Among those excluded were: people already taking more than one alcoholic drink per week, anyone with a history of addiction and patients using two or more insulin injections a day.
Measurements taken at baseline included genetic markers, blood pressure, liver biomarkers, medication use and symptoms, and quality of life.
From June 2010 to May 2012, participants were randomly assigned to 150 mL of mineral water, white wine or red wine with dinner. Wines and mineral water were provided. All groups followed a Mediterranean diet without caloric restriction. At intervals, blood samples were taken, questionnaires completed and group sessions attended.
Lipid and glycemic control profiles were primarily measured. Secondary outcomes included triglyceride levels, blood pressure, waist circumference, genetic interaction, medication use, liver function tests and quality-of-life indicators.
Red wine indicates a better cardiometabolic rate
After 2 years, no material differences were identified across the groups in blood pressure, adiposity, liver function, drug therapy, symptoms or quality of life, except that sleep quality improved in both wine groups compared with the water group.
However, patients who drank wine showed decreased cardiometabolic risks compared with those drinking mineral water. The red wine drinkers experienced the most significant changes in lipid variables.
The researchers unexpectedly found that while the alcohol itself appears to aid glycemic control, red wine has a stronger effect on lipid levels and overall variables of the metabolic syndrome, suggesting that its non-alcoholic constituents also play a role.
The red wine had seven times higher levels of total phenols than the white wine. Whether the phenolic compounds increase the cardioprotectiveness is still debated. The team calls for differences between red and white wine to be further studied, with focus on the varied biodeliverability of the compounds.
The team found that genetic differences affected glycemic control and therefore suggest that genetic information could assist in identifying which patients with type 2 diabetes would benefit from moderate wine consumption.
Limitations include the participants not being blinded to treatment allocation, but the long-term nature of the study is a strength.
The authors caution that the benefits of drinking wine should be weighed against potential risks when translated into clinical practice.
Medical News Today recently reported on research suggesting that red wine can help stabilize a biomarker for Alzheimer's disease. ||||| A glass of red wine each evening with dinner may offer heart health perks to people with type 2 diabetes.
A two-year study published in the Annals of Internal Medicine is the first long-term study aimed at assessing the effects and safety of drinking moderate amounts of alcohol in people with type 2 diabetes, who are more at risk for developing cardiovascular disease than the general population. Those with type 2 diabetes also tend to have lower levels of HDL, the "good" cholesterol.
The researchers from Ben-Gurion University of the Negev reported that over two years, red wine helped improve signs of cardiac health by modestly increasing levels of HDL cholesterol and lowering overall cholesterol.
The randomized controlled intervention trial involved 224 controlled diabetes patients aged 45 to 75, who generally abstained from alcohol. The patients were randomly assigned to drink 5 ounces of red wine, white wine, or mineral water (the control group) with their dinner for two years. They were all given instructions to follow a well-balanced Mediterranean diet plan that did not have a calorie restriction.
The researchers performed genetic tests that showed how quickly the patients metabolized alcohol, as well as various lipid (cholesterol) tests. They also measured glucose control, blood pressure, liver function tests, medication use, and other symptoms at several time points during the two-year follow-up.
Compared with the group that drank water, patients in the red wine group had improvements in their lipid tests, the study showed. "Red wine was found to be superior in improving overall metabolic profiles, mainly by modestly improving the lipid profile, by increasing good HDL cholesterol and apolipoprotein A1, one of the major constituents of HDL cholesterol, while decreasing the ratio between total cholesterol and HDL cholesterol," the researchers explained.
Also, in both wine groups, patients who were "slow alcohol metabolizers" (according to the genetic tests) showed more improvements in glucose control tests than "fast alcohol metabolizers." Compared with water, wine did not increase or decrease blood pressure or liver function tests.
The study authors noted that in both red and white wine drinkers, sleep quality was significantly improved, too, compared with the water control group.
Iris Shai, principal investigator of the trial, and a member of the Department of Public Health in the Faculty of Health Sciences, said in a press statement, "The differences found between red and white wine were opposed to our original hypothesis that the beneficial effects of wine are mediated predominantly by the alcohol."
So, how much can people with type 2 diabetes sip at dinner without going over the top? "One to two glasses of red wine for men and up to one glass of red wine for women, daily, at dinner," was the amount indicated by the study, Dr. Minisha Sood, an endocrinologist at Lenox Hill Hospital, told CBS News.
Sood said researchers have known for some time that moderate amounts of alcohol are acceptable for diabetics, but the jury was out on which kind of alcohol might offer the most benefit.
Sood said of red wine's health-enhancing ingredients: "It's the non-ethanol components of the wine, which are present more so in red wine. It's the phenols, it's the resveratrol, it's the tannins. They all work together with the ethanol possibly to result in these positive changes."
While the study shows benefits, Dr. Susan Spratt, an endocrinologist and assistant professor of medicine at Duke University School of Medicine, said, "I worry about the subset of my type 2 diabetes patients who drink too much, and that this may give them more ammunition to say alcohol is good for diabetes. Over-drinking can poison the pancreas. In these patients, when they stop drinking, their diabetes gets tremendously better."
Spratt also told CBS News that in the South, where she lives, many people abstain from drinking for religious reasons. She said, "Here in the South, it would not be something I would generally recommend. I would not say, 'Now you should start drinking wine.' I wouldn't tell someone to start drinking, but if I knew a type 2 diabetes patient was a moderate drinker, I would tell them it looks like red wine is the best choice out of all alcohols to drink, rather than white wine, beer, or hard liquor."
Spratt also noted that the study did not look at cardiovascular outcomes such as heart attack and stroke.
For 51-year-old Garret Rubin, who said he has to watch out for everything -- fats, salt, sugar -- in his diet since being diagnosed with type 2 diabetes, the study is a positive note.
Rubin said diet, exercise and medication will remain his first line of defense, but he told CBS News, "Now, since I have a choice, I think red wine might be the thing."
Editor's note: In an earlier version of this article, Dr. Sood said red wine decreased development of heart disease, but that was not found in the study. The research only looked at risk factors like cholesterol levels, not whether patients actually developed heart disease. |||||
Summary: | – A glass of red wine a day might indeed keep the doctor away—at least that could be the case for those suffering from Type 2 diabetes, according to a new study. It suggests red wine in moderation helps patients manage cholesterol and improves cardiac health. Researchers set out to discover the effects of moderate alcohol consumption on people with well-controlled Type 2 diabetes, who generally have a higher risk of cardiovascular disease and lower levels of HDL cholesterol, which is good for the heart, reports Time. The 224 alcohol-abstaining participants with a low risk for alcohol abuse, aged 40 to 75, were then assigned a beverage—mineral water, dry white wine, or dry red wine—and told to drink 5 ounces with a meal each night for two years; they also followed a Mediterranean diet. At the end of the study, there were no major differences in blood pressure and liver function among the three groups, reports Medical News Today. However, red wine drinkers were the only ones to see decreased cardiometabolic risks. They also saw a significant boost in HDL cholesterol and lower cholesterol overall, while all wine drinkers reported improved sleep, reports CBS News. Though the alcohol appeared to aid glycemic control in white wine drinkers, the differences between the red wine and white wine groups suggest alcohol wasn't responsible for all the benefits. The red wine had seven times higher levels of total phenols than the white wine, and "it's the phenols, it's the resveratrol, it's the tannins" in the red wine that effect these benefits, says an expert. Genetic differences also affected glycemic control, meaning certain people are more likely to benefit from drinking wine. (Just watch out for arsenic.) | multi_news_1_0_0 |
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Article:
The mob boss had been at the federal jail in Brooklyn longer than any other inmate: four years awaiting trial and, after his conviction in 2012 on racketeering charges, nearly two more waiting to be sentenced. By the time his sentencing date arrived on Wednesday, the mobster, Thomas Gioeli, had been considered for the death penalty, convicted of conspiring to murder three mobsters and acquitted of killing a police officer; he had multiple angioplasties and, with the help of his family, even became an avid blogger and user of Twitter who taunted prosecutors and two mayors.
The measure of those six years behind bars for Mr. Gioeli — highly unusual for someone who has not yet been sentenced — were central to arguments in Federal District Court in Brooklyn on Wednesday over how much prison time Mr. Gioeli should get: the maximum 20 years, or something less.
One of Mr. Gioeli’s lawyers, Adam D. Perlmutter, said the six years had taken an especially hard toll. “He is now the senior-most person at the M.D.C.,” Mr. Perlmutter said, referring to the Metropolitan Detention Center. He named a host of medical conditions that Mr. Gioeli, 61, is living with, including diabetes, heart disease and arthritis. “People who suffer from chronic health conditions do harder time in prison than people who are healthy,” Mr. Perlmutter said. “A 20-year sentence for Thomas Gioeli is, in fact, a life sentence.”
The judge, Brian M. Cogan, said that with a 20-year sentence, credit for time served and good behavior, Mr. Gioeli would be out by his early 70s. “He’s not going to live to his early 70s?” Judge Cogan asked.
“I don’t think so,” Mr. Perlmutter answered.
A prosecutor, James Gatta, said, “Such time should not count against the sentence that the defendant should receive for his criminal conduct.”
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As the argument unfolded, Mr. Gioeli, who since his conviction last year grew a giant tuft of white hair on his chin, leaned back in his chair, twisting his white mustache, waving warmly and making baby faces at his family in the courtroom. It was odd behavior that would have been more at home at a child’s birthday party than at a sentencing for gangland murders.
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Judge Cogan knocked 16 months off the 20-year maximum and ordered Mr. Gioeli to pay $360,000 in restitution.
At the murder and racketeering trial, prosecutors said Mr. Gioeli, whom they called the former acting boss of the Colombo family, ordered the ambush and murder of an off-duty police officer, Ralph C. Dols, and ordered the killings of several other men in the 1990s. Prosecutors called admitted mob killers to testify against Mr. Gioeli (they described surprise shootings in basements, dissolving dead bodies with lye and burying them on Long Island), but the jury acquitted Mr. Gioeli of many charges, including the murder of Officer Dols. He was found guilty of one count of racketeering for conspiring to kill three mobsters.
The acts that the prosecutors described hardly meshed with Mr. Perlmutter’s portrayal of Mr. Gioeli as a family man, or “Tommy, the person,” as he called him in a long argument that roused sniffles among two or three dozen family members who showed up. “I look at their marriage and I’m jealous,” Mr. Perlmutter said of Mr. Gioeli’s relationship with his wife. It was an image that Mr. Gioeli also put forth on his blog during his years in jail, that of a family man who was wronged by zealous prosecutors.
His Twitter messages and blog posts, which family members posted after he wrote them using his prison email account, espoused a liberal vision of society, coming to the defense of the working poor, speaking out against sexism, when he was not opining on current events.
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Last month, Mr. Gioeli wrote on Twitter, “The FBI arrests old Italians for decades old robberies while allowing bankers to steal billions everyday. TSG #FBI #America #wallstreet,” signing his initials, T.S.G.
Judge Cogan, who said the evidence was overwhelming that Mr. Gioeli was a manager of the crime family and found it was more likely than not he had participated in other murders, said Mr. Gioeli was like many mobsters who are “absolutely schizophrenic in their personalities.” Judge Cogan said, “They go out there and they do things to get people murdered, and at the same time they are wonderful to their families and their communities.”
“They are vicious crimes, and they take a vicious person to do them. I recognize that’s not all there is to Mr. Gioeli.”
Judge Cogan said that Mr. Gioeli’s time served and the “wonderful” way he treated his family were mitigating factors. But he also said: “I haven’t seen any remorse. I’ve just seen self-righteousness.”
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Whether he will live to make it out after more than 18 years in prison, the judge said, “only God knows.”
A Selection of Twitter Messages From Thomas Gioeli ||||| A triple-murder suspect-turned-mob informant whose colorful stories led to the arrest of 39 underworld operators was sentenced to time served Friday — and he was even heralded by the judge for his bravery.
Thomas McLaughlin, 46, was 15 when he taken under the wing of a “bad” relative and nurtured to join the Colombo crime family, according to defense lawyer Stuart Grossman.
After getting pinched for drug trafficking and firearms possession, he went to jail for 16 years without cooperating, earning the trust of his criminal colleagues.
But in 2008 when he was released, the feds came to him and told him he would be charged with conspiracy in planning three mob hits and asked for his cooperation. Facing life in prison, he agreed to help and recorded more than 200 conversations between 2009 to 2011, leading to 39 arrests and two convictions.
He nearly put Sammy “The Bull” Gravano’s record to shame. Gravano helped jail 36 people.
‘I want to apologize for my past… I look forward to the future and continuing to be a husband and father.’ - Thomas McLaughlin
Brooklyn federal court Judge Brian M. Cohan on Friday sentenced him to the 16 years he already served and thanked him for wearing a wiretap for the government. “The number of criminal activities that were able to be prosecuted with Mr. McLaughlin’s cooperation is beyond anything I’ve ever seen… and let’s not forget the risk,” Judge Cohan said.
McLaughlin was also instrumental in the conviction of his own cousin, when he was called to testify at former Colombo boss Tommy “Tommy Shots” Gioeli 2012 trial and fingered his role in a murder.
Grossman called his client “a totally changed man,” and prosecutor Elizabeth Geddes applauded his cooperation with the government calling it “historic.”
Today McLaughlin is a family man with a “hard job. Not the kind of job you’re going to get rich on,” according to the judge, who did not say what his new employment entails.
McLaughlin addressed the court. “I want to apologize for my past, Your Honor,” he said.
“I look forward to the future and continuing to be a husband and father.”
“I’m not skeptical,” Judge Cohan said. “I’m dealing with someone who has not only gone straight but who will stay straight.” ||||| Leave the ping pong paddles, file the lawsuit.
That’s what former Colombo crime boss Thomas (Tommy Shots) Gioeli has done — suing the federal government for $10 million over injuries from a game of prison ping-pong.
The table tennis tumble happened Aug. 29, 2013, while Gioeli was being held at Metropolitan Detention Center in Brooklyn.
More than a year earlier, a Brooklyn Federal Court jury had found him guilty of racketeering conspiracy connected to murder plots.
Mob rat Thomas McLaughlin sentenced to zero jail time
Gioeli, 64, and fellow defendant Dino (Little Dino) Saracino also were accused of carrying out murders, including the killing of a police officer, but acquitted on the murder charges.
According to government court papers, Gioeli argues his slip and fall occurred because of prison officials’ negligence. They knew — or should have known — about the hazardous wet floor in recreation area, pointing to the proximity of showers and an allegedly leaky slop sink pipe.
Thomas (Tommy Shots) Gioeli, Colombo acting boss. (Jesse Ward/for New York Daily News)
The leak was reported to prison employees for days, if not weeks before the accident, Gioeli claims.
The burly Gioeli fractured his right kneecap and had to be hospitalized. The injury required surgery, physical therapy and occupational therapy, court papers obtained by the Daily News show.
Ex-Colombo hitman gets 12 years for murder of NYPD cop Dols
The government rejects any charge of negligence, saying it acted with necessary care at all times. And part of its defense is that there’s some risk that comes with playing table tennis — and Gioeli chose to take that risk.
The case has been assigned to Brooklyn Federal Court Judge Kiyo Matsumoto.
A bench trial is estimated to take about three days, though the case docket shows no trial date yet.
Gioeli is expected to make it up from his low-security North Carolina prison to testify about his spill and subsequent suffering, according to court papers.
Crime boss claims he got solitary for religious scapular
He did not take the stand at his criminal case.
The doctor who examined Gioeli is scheduled to testify about the mafioso’s mishap.
Another person who had been held at the lockup is expected to talk about the floor layout, prisoners tracking in water from the showers, and his complaints about the alleged leak.
The government said it plans to put on witnesses including a Metropolitan Detention Center general foreman.
Gioeli claims he slipped on a wet floor while playing table tennis. He's accusing prison officials of negligence. (wsantina/Getty Images/iStockphoto)
The man is expected to say he searched for records of reported water leaks or repair orders for leaks around the time of the incident, but found none.
Another planned government witness is a correction officer who says he found Gioeli on the wet floor, near the showers.
Gioeli is serving an 18-year prison sentence.
Both Gioeli’s lawyer Martin Schiowitz and the Bureau of Prisons declined comment Monday. ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. |||||
What is a summary? | – Former mob boss Thomas "Tommy Shots" Gioeli wants $10 million from the federal government over a Ping-Pong injury. Gioeli, once a high-ranking member of the Colombo crime family, is suing over an injury he suffered during a game at the Metropolitan Detention Center in Brooklyn in 2013, according to court papers seen by the New York Daily News. He says he slipped on a wet floor while playing a game and fractured a kneecap. His suit argues that the prison is negligent because employees ignored complaints about a leaky pipe that led to the slippery conditions in the recreation area. The federal government, however, says that even Ping-Pong comes with risks, and Gioeli chose to take them. Gioeli needed surgery and rehab after the fall. The 64-year-old is three years into an 18-year sentence on racketeering charges, though he was acquitted of murder charges that included the 1997 slaying of a New York City police officer. At his sentencing in 2014, his attorney argued unsuccessfully for a light sentence because his client suffered from arthritis, diabetes, and heart disease, and thus probably wouldn't live beyond his early 70s, the New York Times reported. The story also noted that Gioeli had become a colorful fan of Twitter, with tweets such as: "The FBI spends it's limited resources on terminal Italian book-makers while terrorist & cartels flourish." So how did Gioeli wind up in prison? His own cousin ratted him out, reported the New York Post. (The late Anthony Colombo had a specific influence on the Godfather films.) | multi_news_1_0_0 |
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Pat and Stanford Kipping and their dog Baby stand with their 1998 Buick Century outside their home in Red Bud, Ill. (David Carson/St. Louis Post-Dispatch)
From the beginning, Jim Ford said, he was reluctant about repossessing Pat and Stanford Kipping’s car.
Even though that was, obviously, the job.
Ford is a repo man, co-owner of Illini Recovery Inc., a company in Southern Illinois. And earlier this month, he was working a job involving the Kippings’ vehicle, a 1998 Buick, the Belleville News-Democrat reported. Instead of repo’ing the Buick, though, Ford decided to do something a little different.
He found a way to pay off the car — and return it to the couple.
“It was a miracle come true; we didn’t know what we were going to do,” Pat Kipping, 70, told the News-Democrat.
According to Ford, who spoke with The Washington Post by phone, this all unfolded after he received the order to pick up the car from a credit union.
Ford said he looked at the past due amount, which was about $350, and the payment amount, which was $95 a month.
Then, he headed out to Red Bud, Ill., where the car was. When he pulled down the street, he noticed a police officer, who told him that the vehicle was owned by an elderly couple.
“I was like, aw man,” Ford said.
He drove to the couple’s home and spotted the car but decided he wasn’t going to disturb Pat and Stanford Kipping at that hour.
The next day, he called up the couple and told them to contact their bank to try to work something out. Later, though, Pat Kipping called back and told him that she didn’t have the money, and he needed to take the car.
Ford, believing that his hands were tied, again set out for the home. When he arrived, he played with the couple’s dog, he said. The Kippings invited him in. And he tried to soften the blow, telling them that they wouldn’t have to deal with extra fees from him.
“And [Stanford Kipping] is like ‘oh Jim, you’ve been so good to us, if I ever win the lottery, I’m going to split it with you, buddy,'” Ford said. “And I’m like, aw man. Really? This is getting worse rapidly. I had to get the hell out of there.”
After seizing the car, he made it about a block before he phoned a bank official.
“I said, ‘Hey, how about if I just pay this thing current right now?'” Ford said.
That didn’t exactly work out, though — there was a process they had to follow, and a load of paperwork. The bank said they would work with the couple and see what could be done at a later date. Ford thought about it more, though, and called a business partner and discussed the matter. That man suggested an online fundraising effort.
“I was like, all right, I’ll try it. So we did that,” Ford said. “And by the time I woke up, the car was paid off.”
Donations poured in from Ford’s friends, some of whom were small-business owners. After about a day, he had raised what he needed, and had money to spare. The News-Democrat reports that Ford raised more than $3,000 — enough to pay off the car and give $1,000 to the Kippings.
Ford and his friends didn’t stop there. The car got an oil change, and they took it to get detailed. They also did some maintenance on the vehicle, replacing lightbulbs and things like that. Then, on Monday morning, one of Ford’s employees swung by the grocery store and bought the couple a turkey.
The Kippings knew the car was on its way back; they were tipped off after calling the bank, and then Ford himself.
So when the vehicle arrived, Ford said, family members were waiting, along with neighbors and a reporter from a local paper.
“I got up this morning and I looked up at the sun and I said, ‘I hope we get our car back.’ It’s just unbelievable,” Stanford Kipping, a retired dock worker, told the News-Democrat.
“They were really really happy,” Ford said. “I don’t know. I was just glad I could help somebody out.”
“Never heard of any good act of kindness like that from a repo man,” 56-year-old Grace Garris, one of Stanford Kipping’s children, told the St. Louis Post-Dispatch. “It was a beautiful, beautiful moment.”
During his discussions with the couple, Ford said, he had learned that they were behind in the payments because of health-care costs. Specially, he mentioned prescription drugs, which they told Ford had rocketed up in price.
“They were just really nice people, and they needed a break,” Ford said. “Luckily, I’m fortunate enough to be in a position that I can help somebody out like that. I really didn’t expect anyone to find out about it, ever, but apparently most of my friends are narcs.”
When people read about the gift, Ford said, he hopes it inspires more acts of generosity.
Plus, he later added: “If Trump wants to come shake my hand, that would be cool.”
“I just hope that someone goes out and does something nice for someone else,” he said. “That would be great. Just pay it forward. I’m getting so many calls from all over the country, and everyone’s so inspired by it. I’m like, oh yeah, there’s something I didn’t think I’d ever hear: Jim Ford, Mr. Inspirational.”
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‘My son is not breathing’: Harrowing video shows hero cop saving toddler in distress ||||| RED BUD • A good-hearted repo man? It’s true. Stanford and Pat Kipping can attest.
The Kippings were down on their luck, getting credit from a local grocer and pharmacist, and racking up debt. Last week, they were three months, or $350, behind in payments on their 1998 Buick Century.
Enter Jim Ford, a 20-year veteran of the car repossession business. Ford got an email last Wednesday from a bank telling him he needed to take back the car from the Red Bud couple.
Like many repo agents, Ford arrived in the dark of night. He peered into their garage and saw the Buick. But he didn’t want to knock on the door, as he normally would, to break the news then, at 1 a.m.
“I knew they were elderly, and there wasn’t a light on,” Ford said. “I didn’t want to disturb them.”
Instead, Ford called later that day to tell Pat Kipping he was hired to repossess their car. He suggested she call the bank to make payment arrangements. She called the bank but couldn’t work anything out. The couple had only $30 in their account to get them through until Social Security payments arrived, she told Ford.
Ford arrived the next day. It was cold outside, and the Kippings invited him inside.
“I got to talk to them, and they were the nicest people. They knew I had a job to do,” Ford said. “She’s telling me how their medications had already gone up in price and (her husband) couldn’t afford to get some of his medications this month. They actually owed money to the pharmacy in town and the grocery on credit.”
Stanford Kipping, 82, has been diagnosed with Alzheimer’s. He also has congestive heart failure and high blood pressure. Pat Kipping, 69, his wife of 26 years, has her own health concerns, including diabetes.
Stanford, a Navy veteran and former dock worker, is a proud man who didn’t tell his adult children about his financial woes.
“It was very, very sad,” Pat said. “Stan and I cried. We were very emotional because we need our car.”
The Kippings watched as their car was towed down the street and out of sight.
Later that day, Ford called a friend, Tom Williams. Taking the car had been gnawing at him all day. The two men talked about what they could do to help.
Without the Kippings knowing, Ford set up an account at Gofundme, a popular crowdfunding platform, to raise money. The couple owed about $2,200 on the car. By the time Ford woke the next morning, nearly enough had been raised to pay off the car. Within 12 hours, the fund had raised $3,300.
So much had poured in, from friends of Ford and Williams, that the men were able to pay off the car and have $1,000 left in cash for the Kippings. Williams got the car detailed, paid for an oil change, topped off the radiator fluid and replaced two broken lights.
When the Kippings saw their car returned home Monday, after a 3½-day absence, they both cried again.
“He’s wonderful,” Pat Kipping said of Ford. “It’s almost like a miracle. It’s unbelievable.”
Grace Garris, 56, is one of Stan Kipping’s daughters. She had seen her father’s face when he had to admit to his children that his only car had been repossessed by the bank. “He looked defeated,” Garris recalled.
Garris said the look on his face was priceless when the paid-off, cleaned-up Buick came back.
“I saw tears rolling down my dad’s face,” Garris said. “I said, ‘Papa, there are good people in this world, a lot of good people. A lot of people with heart out there.’”
Garris said a small town like Red Bud has its share of negative stories about repo men, but none like Ford.
“Never heard of any good act of kindness like that from a repo man,” she said. “It was a beautiful, beautiful moment.”
Pat was relishing the attention from reporters this week who wanted to hear her story.
“I was at my lowest end when he came and got that car. I thought, ‘This is it for me,’ I was that depressed,” she said. “I prayed to God, and God answered our prayer.”
An answer in the form of Ford, that is. A veteran repo agent who — in all his 100 repossessions a month, 100,000 cars over a career — has never been touched enough to help pay off someone’s debt.
Ford, 41, lives in O’Fallon, Ill., and his company is Illini Recovery Inc. He has some harrowing stories. People have turned their dogs on him. He’s been shot at (but never hit) in Jennings, East St. Louis and St. Louis. Once, the three shots at his face were close enough that “I could taste the gunpowder in my mouth.”
Ford says he always tries to be courteous. Ninety percent of the time, he said, he will knock on the door to let people know what’s coming and to give them time to clear their belongings out of the car.
“It’s easier than grabbing the car in the middle of the night and dragging it down the driveway at 300 mph,” Ford said. “That’s the way you do it your first year.”
But the upfront, mannerly way is easier, Ford found. “If you knock on their door and are nice to people, 90 percent of the time they’re nice back.”
But why help pay off the Kippings’ car, why this time?
Ford said Stan Kipping reminded him of his own grandfather. “He was just a nice guy,” Ford said.
“I’m there repoing his car, OK, and he tells me, ‘Jim, if I ever win the lottery I am going to split it with you because you’ve tried to work with us and been so nice to me.’” ||||| This is a set of web collections curated by Mark Graham using the Archive-IT service of the Internet Archive. They include web captures of the ISKME.org website as well as captures from sites hosted by IGC.org.These web captures are available to the general public.For more information about this collection please feel free to contact Mark via Send Mail ||||| SHARE COPY LINK More Videos 207 Two O’Fallon schools competing in Buffalo Wild Wings Spirit Bracket Challenge Pause 190 Sales tax increase could help students have normal lunch time 55 Belleville home construction to begin in April 107 Homeowner upset with demolition of her home 50 Crew demolishes Belleville home woman fought to save 104 Learn the latest on Highland’s all-abilities playground project 53 Closing Freeburg grocery store could be replaced 197 15-year-old charged in O'Fallon school threat 189 New commander at Scott AFB describes hurricane relief efforts 100 Local couple opens Shiloh pharmacy that sells local products, offers free delivery Video Link copy Embed Code copy
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Jim Ford, of Belleville, felt terrible when he had to repossess an elderly couple's car in Red Bud. He raised money to get it back for them, plus repaired it, plus filled it with Thanksgiving goodies. Here's his encounter with them. Steve Nagy [email protected]
Jim Ford, of Belleville, felt terrible when he had to repossess an elderly couple's car in Red Bud. He raised money to get it back for them, plus repaired it, plus filled it with Thanksgiving goodies. Here's his encounter with them. Steve Nagy [email protected] |||||
Summary: | – "I may be getting soft in my old age," Jim Ford tells the Belleville News-Democrat. The Illinois repo man showed up at the house of Stanford Kipping, 82, and his wife Patty, 70, at 1am to repossess their 1998 Buick for the bank but couldn't bring himself to bother the elderly couple at that hour, the St. Louis Post-Dispatch reports. He met with them to explain the situation the next day. Ford found out the Kippings were broke and sinking into debt thanks to rising medication costs. They only had $30 to get them through until their next Social Security check. Nevertheless, the Kippings understood Ford had a job to do and appreciated his concern. “[Stanford] is like, ‘Oh Jim, you’ve been so good to us, if I ever win the lottery, I’m going to split it with you,'” Ford tells the Washington Post. “And I’m like, aw man. Really? This is getting worse rapidly." Ford took their car, but it ate at him. "They are a real nice elderly couple," he tells the News-Democrat. "I can't just take their car." He and a friend ended up starting a GoFundMe page to pay off the Kippings' car and raised $3,500 in one night. Not only did they pay off the car, but they had $1,000 left over for the Kippings. Ford delivered the cash, the repaired and detailed Buick, and a Thanksgiving turkey to the Kippings. “It was a miracle come true," Patty says. "We didn’t know what we were going to do." “Never heard of any good act of kindness like that from a repo man,” the couple's daughter adds to the Post-Dispatch. But Ford remains modest: "I was just glad I could help somebody out," he tells the Post. | multi_news_1_0_0 |
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Here is a news article: TOKYO—In a country where grilled fish is a breakfast food and many think the stinkiest soybeans are the tastiest, it stands to reason Coke is now a health drink.
Once a month, Hideaki Iwaya sits at the dinner table for pizza night with his wife and two teenage daughters. They recently revised their routine to add Coca-Cola Plus, which features a government-approved laxative ingredient, hoping it would help their bodies absorb less fat from the slices.
“It’s a paradox: a cola that is healthy but my wife likes it, my daughters prefer it,” says Mr. Iwaya, 52, an automobile-insurance sales manager in Yokohama. “When I brought it home, I thought no one would drink it. I was mistaken.”
It isn’t just Coca-Cola Co. touting the healthful side of its Japan-only Plus drink. The Japanese government has given it a gold label certifying its benefits.
Japan’s life expectancy—87 years for women, 81 for men—is several years ahead of America’s, thanks in part to low obesity. Japanese ideas about good diet, such as green tea and fermented foods, have become mainstays in the West.
Now, the government thinks it can add to the dietary wisdom by certifying Coca-Cola Plus and other products as Foods for Specified Health Uses, or Foshu. The certified products, which have grown into a market of $6 billion in annual sales, according to Japan Health and Nutrition Food Association, contain compounds the government deems to have a particular benefit, such as lowering cholesterol or preventing osteoporosis.
Zero-calorie Coca-Cola Plus features a substance called indigestible dextrin. It joins two other designated “healthy” colas in Japan—Pepsi Special, made by Suntory Beverage and Food Ltd. under a licensing deal with PepsiCo, and Kirin Mets Cola from Kirin Beverage Co.
A Tokyo vending machine sells Coca-Cola Plus. Photo: Suryatapa Bhattacharya/The Wall Street Journal
Michiko Kamiyama, a lawyer with a group called Food Safety Citizens’ Watch that monitors food safety issues on behalf of consumers, wonders whether the government should be endorsing Coke and Pepsi as healthful. A vigorous 77, Ms. Kamiyama says she didn’t get that way downing lots of carbonated drinks.
“If you have a well-balanced diet and do an appropriate amount of exercise then you don’t need them,” says Ms. Kamiyama of the certified foods and drinks. “I personally think it is totally ineffective.”
Khalil Younes, an executive vice president for marketing and new business at Coca-Cola Japan, says scientists spent a decade trying to preserve the taste of Coca-Cola while including ingredients that could win the government’s gold seal.
“We were quite ballsy in how we approached the launch,” he says, “because we were supremely confident based on our data that we had a winner, both on the functionality and also on the taste.”
Tominaga Ozawa, a retired investor, says he shares doubts about health benefits but figures there is nothing to lose by adding some fibrous fizziness to his diet. Mr. Ozawa, 70, says he took to drinking Coca-Cola Plus almost immediately after it went on sale in Japan in March.
At least once a week, he plays 18 holes of golf. After nine holes, he returns to the clubhouse and buys a Coca-Cola Plus before sitting down to lunch. “I think it’s good,” he says. He prefers his cola time in solitude because “in Japan, your image can suffer if you say you drink cola.”
Miho Katori, 33, a Tokyo restaurant worker, stocks her fridge with at least two 470-milliliter bottles of Coca-Cola Plus at about $1.50 each. The government’s gold seal prompted her to switch from a diet cola, she says, in hopes the fat-absorption properties of the dextrin would help her stay slim.
She found she liked the drink. “I don’t know if it’s effective or not,” she says, “but it looks like it is good for my health because it has a Foshu stamp.”
Among the drink’s detractors is Seiji Miyata, 54, an art director at a Tokyo printing agency. He turned to artificially sweetened drinks after he discovered he had diabetes and found himself yearning for sweets. “As soon as I was diagnosed,” he says, “I started to love whisky, chocolate, everything that’s sweet.”
Seiji Miyata, 54, prefers the taste of Coke over Coca-Cola Plus. Photo: Chieko Tsuneoka
Craving a sweet cola one weekend morning, he pulled into a convenience store and found the new white-coated Coca-Cola Plus bottle. The drink tasted healthful—and, he thought, awful.
He wanted to dump it right away, but “we’re Japanese,” so he found a public ash bin into which he discreetly drained the liquid.
Others who tried Coca-Cola Plus without studying the label have been surprised by the extent of its laxative effect. Online commenters and some people interviewed in Tokyo said they ended up with upset stomachs or worse.
“There is no danger to the human body,” Coke’s Mr. Younes says. “We would never launch something that is harmful to anybody.”
Regarding side effects, he refers to the labeling: “The only caveat we have is that if you drink too much—it is in there, that you may have loose bowels from overconsumption. It depends on your condition, but what we are trying to avoid is people over-consuming in the belief that the more they drink, the more it will help.”
On the flip side, Hideo Eguchi, a 79-year-old who works as a hair stylist, says, “I like the feeling of the burps you get from drinking this.”
Coca-Cola declines to give sales figures for Plus but says it is a success. It says low-sugar or sugarless drinks—many of them teas, coffees and other noncolas—account for 62% of Coke’s sales in Japan.
In Japan’s beverage market, companies have been known to introduce as many as 100 new drinks a year. The competitiveness “is just mind-boggling,” says Coke’s Mr. Younes.
Coke ads show people drinking Plus with grilled beef—the result, he says, of careful market research.
Coke paired with sushi would be “a bridge too far,” he says. “I know that I would be crucified by my Japanese friends if they saw me do that.”
—Chieko Tsuneoka contributed to this article.
Write to Suryatapa Bhattacharya at [email protected] ||||| CLOSE Coca-Cola has a new product with fiber, called 'Coke Plus,' sold only in Japan for now. We taste test it. USA TODAY
This image provided by The Coca-Cola Company shows a bottle of Coca-Cola Plus, which adds fiber. (Photo: AP)
Coca-Cola is selling a new soda that includes fiber.
The drink, called Coca-Cola Plus, is available only in Japan. According to the company, there are no plans to bring it to the U.S. market.
In the United States, products that feature added fiber include yogurt, orange juice, white bread and artificial sweetener
The no-calorie Coca-Cola Plus boasts five grams of indigestible dextrin, a source of dietary fiber, per 470-ml bottle.
It's part of a segment of the beverage market in Japan called Food of Specified Health Use, or FOSHU, drinks.
Follow USA TODAY reporter Zlati Meyer on Twitter: @ZlatiMeyer
Read or Share this story: http://usat.ly/2pnBZH1 ||||| Coca-Cola says a new soda it just released in Japan ended up with some fiber in it — please note that this isn't another crazy recall notice, though.
In fact, the fiber was added on purpose to this beverage, which is being marketed as the company's healthiest soft drink yet, and brave soda drinkers can now find it on shelves under the product name Coke Plus.
The company gave an earlier warning about Coke Plus back in February. The official press announcement promised a no-calorie soda with "five grams of indigestible dextrin."
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It let Coke's Asia-Pacific director of product development — a certain Dr. David Machiels, who came dressed in a white lab coat to help burnish his science credentials — list the purported health pros of drinking fiber.
Among them: Consuming one Coke Plus a day (à la a multivitamin) can help "suppress fat absorption" and "moderate the levels of triglycerides in the blood."
It looks like the company has already started passing samples of fiber Coke out to reporters, so maybe soon somebody will address how putting roughage in soda affects the taste. The odds seem high that it won't improve mouthfeel, though.
In 2007, Coke actually introduced a Plus variant in several countries that was fortified with vitamins and minerals (it even carried the same name).
Japanese consumers didn't love it, but the reception in America was especially brutal.
Problem was, the FDA sent Coke a threatening letter explaining that Plus violated the Federal Food, Drug, and Cosmetic Act — any product with that word on the label must contain at least 10 percent more nutrients than comparable products.
Coke felt Plus complied with those regulations, but bottles started disappearing from stores in 2011, anyway. ||||| Coca-Cola Plus is the latest brand to join Coca-Cola Japan’s portfolio of Food of Specified Health Use (FOSHU) drinks – a large and growing segment of the country’s competitive beverage market. The first-ever Coca-Cola approved as FOSHU by the Japanese government will roll out nationwide next month in eye-catching white packaging after more than a decade of research and development.
The no-calorie beverage contains five grams of indigestible dextrin – a source of dietary fiber – per 470-ml bottle. Coca-Cola Japan is marketing Coca-Cola Plus, which features great Coca-Cola taste plus functional benefits, to health- and taste-conscious consumers 40 and older as a beverage to enjoy with food.
Drinking one Coca-Cola Plus per day with food will help suppress fat absorption and help moderate the levels of triglycerides in the blood after eating. “Coca-Cola Plus is a sugar-free and calorie-free beverage with FOSHU functions and great Coca-Cola taste, so we hope people will drink it with meals,” said Dr. David Machiels, product development director, R&D, Coca-Cola Asia Pacific.
Dr. David Machiels, product development director, R&D, Coca-Cola Asia Pacific
Japan is home to the world’s largest aging population. Older consumers are driving growth of the country’s FOSHU beverage market, led by teas, followed by cola soft drinks.
"Japanese consumers have high quality standards and are especially uncompromising when it comes to taste,” Dr. Machiels said. “And being an aging society has made it a unique market where consumers are extremely health-conscious and seek functionality.”
To help stand out in the highly competitive and crowded Japanese beverage market, where thousands of new drinks hit stores each year, Coca-Cola Plus will be sold in a white bottle with a Coca-Cola red cap, logo and description of its FOSHU benefits and other unique features.
“We chose white as the base color of the packaging so consumers will instantly recognize that it has new features never before seen in a Coca-Cola product,” Dr. Machiels added. |||||
A summary of this is? | – Those who grab a Coca-Cola Plus in Japan are definitely getting something extra: a laxative and the government's seal of approval. The Wall Street Journal reports on the unlikely sounding "health drink," which has qualified as a "Foods for Specified Health Uses" (FOSHU) product, meaning it includes an ingredient that's been determined by the government to bestow a health benefit. In this case, that ingredient is indigestible dextrin—5 grams of it per 16-ounce sugar- and calorie-free bottle. It's a source of dietary fiber, and as the company explained in a February 2017 press release touting the product's impending launch, "Drinking one Coca-Cola Plus per day with food will help suppress fat absorption and help moderate the levels of triglycerides in the blood after eating"—so long as you don't drink too much, which could cause "loose bowels," per a marketing VP for the company. He says it took researchers a decade to come up with a formulation that would fall under the FOSHU umbrella but still taste good; the Journal talks to drinkers who both love it (one line of praise: "I like the feeling of the burps you get from drinking this") and drinkers who poured it out after taking a sip. USA Today noted in May that the company doesn't intend to bring the drink to the US, though we did have Coke Plus here once. CNBC says a vitamin- and mineral-fortified "Plus" version was released in 2007, and it fell under FDA scrutiny for not complying with a regulation that stipulates a food item bearing the word "plus" contain at least 10% more of those vitamins and minerals than its counterparts. Coca-Cola made the necessary adjustments, but the product's run ended around 2011. (The company is offering $1 million for a new sugar substitute.) | multi_news_1_0_0 |
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Summarize this article:
If you've fallen asleep at your desk lately, it's no wonder. More than a third of Americans get less than seven hours of sleep each night -- a deficit that could put their health at risk, a new report says.The U.S. Centers for Disease Control and Prevention analyzed sleep surveys of 74,571 adults in 12 states and is offering up its findings in a report released Thursday. In questions about habits within the prior 30 days, almost 38% of respondents said they had fallen asleep by accident and almost 5% said they had nodded off or fallen asleep while driving.Whoa! Let's hope some of this can be attributed to dozing off late at night in front of the TV and not in the middle of the freeway. Take the test yourself with these sleep survey questions For multi-taskers pushing the envelope, it's worth noting that the National Sleep Foundation recommends seven to nine hours of sleep per day for adults and 10 to 11 hours for school-age children. (Parents can stop laughing now.)"Sleep difficulties, some of which are preventable, are associated with chronic diseases, mental disorders, health-risk behaviors, limitations of daily functioning, injury and mortality," says the report, officially named the Morbidity and Mortality Weekly Report.The news coincides (how convenient) with National Sleep Awareness Week from March 7 to 13. And let's hope no one annoyingly asks: "Got sleep?" ||||| Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: [email protected]. Type 508 Accommodation and the title of the report in the subject line of e-mail.
Unhealthy Sleep-Related Behaviors --- 12 States, 2009
An estimated 50--70 million adults in the United States have chronic sleep and wakefulness disorders (1). Sleep difficulties, some of which are preventable, are associated with chronic diseases, mental disorders, health-risk behaviors, limitations of daily functioning, injury, and mortality (1,2). The National Sleep Foundation suggests that most adults need 7--9 hours of sleep per night, although individual variations exist. To assess the prevalence and distribution of selected sleep difficulties and behaviors, CDC analyzed data from a new sleep module added to the Behavioral Risk Factor Surveillance System (BRFSS) in 2009. This report summarizes the results of that analysis, which determined that, among 74,571 adult respondents in 12 states, 35.3% reported having <7 hours of sleep on average during a 24-hour period, 48.0% reported snoring, 37.9% reported unintentionally falling asleep during the day at least 1 day in the preceding 30 days, and 4.7% reported nodding off or falling asleep while driving in the preceding 30 days. Continued public health surveillance of sleep quality, duration, behaviors, and disorders is needed to understand and address sleep difficulties and their impact on health. As a first step, a multifaceted approach that includes increased public awareness and education and training in sleep medicine for appropriate health-care professionals is needed; however, broad societal factors, including technology use and work policies, also must be considered.
BRFSS is a state-based, random-digit--dialed telephone survey of the noninstitutionalized U.S. civilian population aged ≥18 years, conducted by state health departments in collaboration with CDC (3). Based on Council of American Survey and Research Organizations (CASRO) guidelines, response rates* for 12 states† that used the optional sleep module in 2009§ ranged from 40.0% (Maryland) to 66.9% (Nebraska). Cooperation rates¶ ranged from 55.5% (California) to 83.9% (Georgia).
The following questions from the sleep module were asked: "On average, how many hours of sleep do you get in a 24-hour period? Think about the time you actually spend sleeping or napping, not just the amount of sleep you think you should get (categorized as <7 hours and ≥7 hours**)." "Do you snore? (can have been told by spouse or someone else; categorized as yes or no)?" "During the past 30 days, for about how many days did you find yourself unintentionally falling asleep during the day (categorized as none or at least 1 day reported)?" and "During the past 30 days, have you ever nodded off or fallen asleep, even just for a brief moment, while driving (categorized as yes or no)?" Age-standardized (to the projected U.S. 2000 population) prevalence estimates were calculated by state and by selected characteristics; 95% confidence intervals were calculated, and statistical significance (at p<0.05) was determined by t-test.
Among respondents, 35.3% reported sleeping <7 hours on average during a 24-hour period (Table). Adults aged ≥65 years were significantly less likely to report sleeping <7 hours (24.5%) than persons in all other age categories. Non-Hispanic blacks (48.3%) and non-Hispanic persons of other races (38.7%) were more likely to report sleeping <7 hours than non-Hispanic whites (34.9%). No significant differences were observed by sex. Compared with employed adults (37.4%), those unable to work (46.4%) were significantly more likely to report <7 hours of sleep, but retired adults (25.0%) and homemakers and students (30.8%) were less likely. Adults with at least some college education (35.8%) were significantly more likely to report <7 hours of sleep than those with less than a high school diploma (32.0%) as were divorced, widowed, or separated (39.1%) and never married adults (37.9%), compared with married adults (35.1%).
Snoring was reported by 48.0% of respondents (Table). Persons aged 18--24 years were least likely (25.6%) to report snoring. Hispanics (50.6%) were more likely to report snoring than non-Hispanic whites (46.8%), as were men (56.5%) compared with women (39.6%). Compared with employed persons (50.5%), retired adults (37.9%) and homemakers/students (37.0%) were significantly less likely to report snoring. Persons with less than a high school diploma (51.2%) and with a high school diploma or General Educational Development certificate (GED) (49.9%) were significantly more likely to report snoring than those with at least some college or a college degree (47.0%), as were married persons (49.5%) compared with never married (43.5%) persons.
An estimated 37.9% of adults reported unintentionally falling asleep during the day at least 1 day in the preceding 30 days (Table). Adults aged 18--24 years (43.7%) and ≥65 years (44.6%) were significantly more likely to report this behavior than all other age groups, as were persons from all other racial/ethnic categories compared with non-Hispanic whites (33.4%). No significant difference was observed by sex. Compared with employed persons (33.5%), those who were unemployed (44.0%), unable to work (57.3%), and homemakers/students (39.3%) were significantly more likely to report unintentionally falling asleep during the day. Persons with at least some college education (35.9%) were significantly less likely to report unintentionally falling asleep than those with a high school diploma or GED (39.6%) or less education (43.4%). Never married adults (42.9%) were significantly more likely to report unintentionally falling asleep during the day than married adults (35.9%).
Nodding off or falling asleep while driving in the preceding 30 days was reported by 4.7% of adults (Table). Persons aged ≥65 years (2.0%) were significantly less likely to report this behavior than persons aged 25--34 years (7.2%), 35--44 years (5.7%), 18--24 years (4.5%), 45--54 years (3.9%), and 55--64 years (3.1%). Hispanics (6.3%), non-Hispanic blacks (6.5%), and non-Hispanics of other races (7.2%) all were significantly more likely to report this behavior than non-Hispanic whites (3.2%). Men were more likely (5.8%) to report this behavior, compared with women (3.5%), and employed persons were more likely (5.4%), compared with homemakers and students (2.2%). No significant differences were observed by educational level or marital status.
Persons who reported sleeping <7 hours on average during a 24-hour period were more likely to report unintentionally falling asleep during the day at least 1 day in the preceding 30 days (46.2% versus 33.2%) and nodding off or falling asleep while driving in the preceding 30 days (7.3% versus 3.0%) (Figure). They also were more likely to report snoring (51.4% versus 46.0%).
Among adults in the 12 states surveyed, reports of <7 hours of sleep ranged from 27.6% in Minnesota to 44.6% in Hawaii. Snoring estimates ranged from 44.8% in California to 54.0% in Hawaii. Estimates of unintentionally falling asleep during the day in the preceding 30 days ranged from 33.0% in Wyoming to 42.8% in Hawaii. Finally, estimates of nodding off or falling asleep while driving in the preceding 30 days ranged from 3.0% in Illinois to 6.4% in Hawaii and Texas.
Reported by
LR McKnight-Eily, PhD, Y Liu, MS, MPH, AG Wheaton, PhD, JB Croft, PhD, GS Perry, DrPH, Div of Adult and Community Health, National Center for Chronic Disease Prevention and Heath Promotion; CA Okoro, MS, T Strine, PhD, Public Health Surveillance Program Office, Office of Surveillance, Epidemiology, and Laboratory Science, CDC.
Editorial Note
This report is the first to present estimates of the prevalence of unhealthy sleep-related behaviors based on responses to questions added to BRFSS in 2009. The results highlight two prevalences of self-reported sleep-related behaviors with potentially dangerous consequences: 37.9% of adults in 12 states reported unintentionally falling asleep during the day at least 1 day in the preceding 30 days, and 4.7% reported nodding off or falling asleep while driving during the same period. The sleep module, consisting of questions derived from surveillance-system and clinically validated sleep surveys, was developed by CDC and the National Sleep Awareness Roundtable†† in response to an Institute of Medicine recommendation to expand surveillance and monitoring of sleep loss and sleep disorders and to increase public awareness of unhealthy sleep behaviors (1).
Nationwide surveillance has not previously assessed the prevalence of either unintentionally falling asleep during the day or nodding off or falling asleep while driving. Drowsy driving, one of the most lethal consequences of inadequate sleep, has been responsible for an estimated 1,550 fatalities and 40,000 nonfatal injuries annually in the United States (4). In the analysis summarized in this report, the prevalence of falling asleep while driving ranged from 2.0% among persons aged ≥65 years to 7.2% among persons aged 25--34 years. Populations previously found at greatest risk included persons aged 16--29 years (particularly males), those with untreated sleep apnea syndrome or narcolepsy, and those who work shifts, particularly night shifts or extended shifts (4). Sleepiness reduces vigilance while driving, slowing reaction time, and leading to deficits in information processing, which can result in crashes (4). Differences among adults in the 12 states in the prevalence of nodding off or falling asleep while driving were substantial (range: 3.0% in Illinois to 6.4% in Hawaii and Texas) and might result from differences in the prevalence of populations at greater risk or differences in the use of safety measures, such as road rumble strips, an evidenced-based intervention that alerts inattentive drivers through vibration and sound.§§
Unintentionally falling asleep during the day can be indicative of narcolepsy or hypersomnia and has been associated with obstructive sleep apnea, which, in turn, has been associated with hypertension, cardiovascular disease, stroke, diabetes, and obesity (1). Falling asleep on the job can result in productivity losses for employers and dismissal for workers. In addition, depending on circumstances and level of responsibility, unintentionally falling asleep during the day can have dangerous consequences (e.g., while child caretaking, lifeguarding, or operating heavy equipment). To assess the potential impact of unintentionally falling asleep during the day, additional inquiry regarding the circumstances of this behavior is required.
Snoring, reported by 48.0% of participating adults, is a symptom of increased upper airway resistance during sleep and generally considered a marker for obstructive sleep apnea (1,5); pregnant women who snore can be at risk for preeclampsia (5). The finding in this report regarding average hours slept per 24-hour period is similar to findings in other reports. In this analysis, 35.3% of U.S. adults in 12 states reported having <7 hours of sleep on average during a 24-hour period, compared with approximately 29% in the 2004--2006 National Health Interview Survey (6), and compared with 37.1% in the 2005--2008 National Health and Nutrition Examination Survey who said they had <7 hours of sleep on workday and weekday nights (7).
Differences in prevalence by sociodemographic characteristics and state were observed for all four sleep-related behaviors. Adults in Hawaii had the highest prevalences for all four behaviors. The reasons for higher prevalences in Hawaii and other variations are unclear and might be subjects for further examination.
The findings in this report are subject to at least three limitations. First, the increase in the number of households with cellular telephones only and the increase in telephone number portability continue to decrease BRFSS response rates, reducing the precision of state estimates and potentially introducing bias. Although in 2009 all states conducted BRFSS surveys for cellular-only households in addition to households with landline telephones, cellular telephone data were not included for the sleep module and other optional modules. Second, institutionalized persons and persons residing in households without landline telephones are not included in the survey, nor are adults from all 50 states and U.S. territories, thereby limiting the generalizability of these findings. Finally, all estimates were based on self-report rather than physiologic measures of sleep behaviors with actigraphy (use of a movement-detection device with software that uses movement patterns to diagnose sleep disorders) (1) or polysomnography.
Substantial increases in the percentage of U.S. adults reporting an average of <7 hours of sleep per 24-hour period were observed from 1985 to 2004¶¶ and can be attributed in part to broad societal changes, including increases in technology use and shift work (1). Sleep disorders are common health concerns that can be evaluated and treated. However, many health-care professionals might have only limited training in somnology and sleep medicine, impeding their ability to recognize, diagnose, and treat sleep disorders or promote sleep health to their patients (1). The results described in this report indicate that a large percentage of adults in 12 states reported unhealthy sleep behaviors that can be related to disease comorbidity (e.g., obstructive sleep apnea and obesity), including nearly one in 20 persons who reported nodding off or falling asleep while driving in the preceding 30 days. Expanded surveillance is needed to understand and address the public health burden of sleep loss and disorders (1) and their associations with health problems and chronic diseases among adults in all 50 states and U.S. territories, which will enable further assessment of state and nationwide trends.
Healthy People 2020 includes a sleep health section, with four objectives: increase the proportion of persons with symptoms of obstructive sleep apnea who seek medical evaluation, reduce the rate of vehicular crashes per 100 million miles traveled that are caused by drowsy driving, increase the proportion of students in grades 9--12 who get sufficient sleep, and increase the proportion of adults who get sufficient sleep.*** Promoting sleep health, including optimal sleep durations, and reducing the prevalence and impact of sleep disorders will require a multifaceted approach. This approach should consider 1) sleep environments (i.e., living conditions and proximity to noise); 2) type, scheduling, and duration of work (8); 3) associated health-risk behaviors such as smoking, physical inactivity, and heavy drinking (1,9); 4) chronic conditions such as obesity and depression and other comorbid mental disorders (1,5); 5) stress and socioeconomic status (8); and 6) validation of new and existing therapeutic technologies (1). Drowsy driving also should be addressed, and additional effective interventions developed and implemented. As a first step, greater public awareness of sleep health and sleeping disorders is needed.
Acknowledgments
The findings in this report are based, in part, on contributions by BRFSS state coordinators in California, Georgia, Hawaii, Illinois, Kansas, Louisiana, Maryland, Minnesota, Nebraska, New York, Texas, and Wyoming; and DP Chapman, PhD, and LR Presley-Cantrell, PhD, Div of Adult and Community Health, National Center for Chronic Disease Prevention and Heath Promotion, CDC.
References
What is already known on this topic? An estimated 50--70 million U.S. adults have chronic sleep and wakefulness disorders, and the percentage who report <7 hours of sleep on average has increased since the 1980s to approximately one third of all U.S. adults. What is added by this report? This report provides the first prevalence estimates from nationwide (12 states) surveillance of unintentionally falling asleep during the day (37.9%) at least 1 day in the preceding 30 days, and nodding off or falling asleep while driving (4.7%) during the same period; in addition, 35.3% reported <7 hours of sleep in a typical 24-hour period. What are the implications for public health? Increased public awareness, expanded surveillance and research, training of health-care professionals, and a multifaceted approach that considers related health, employment, lifestyle, and environmental factors will be needed to improve sleep health among U.S. adults and reduce the prevalence of unhealthy sleep-related behaviors and sleep disorders.
TABLE. Age-specific and age-adjusted* percentage of adults reporting certain sleep-related behaviors, by selected characteristics --- Behavioral Risk Factor Surveillance System, 12 states, 2009 Characteristic No.† Sleeping on average <7 hrs in 24-hr period (n = 74,571) Snoring
(n = 68,462) Unintentionally fell asleep during the day at least 1 day in the preceding 30 days
(n = 74,063) Nodded off or fell asleep while driving in the preceding 30 days
(n = 71,578) % (95% CI) % (95% CI) % (95% CI) % (95% CI) Total 74,571 35.3 (34.5--36.1) 48.0 (47.2--48.8) 37.9 (37.1--38.7) 4.7 (4.2-- 5.1) Age group (yrs) 18--24 2,330 30.9 (27.8--33.9) 25.6 (22.7--28.6) 43.7 (40.4--47.1) 4.5 (3.0--5.9) 25--34 6,637 39.4 (37.3--41.6) 39.6 (37.4--41.8) 36.1 (34.0--38.2) 7.2 (5.8--8.6) 35--44 10,645 39.3 (37.7--41.0) 51.0 (49.2--52.7) 34.0 (32.3--35.6) 5.7 (4.9--6.6) 45--54 15,407 39.0 (37.6--40.5) 59.3 (57.8--60.8) 35.3 (33.8--36.7) 3.9 (3.3--4.6) 55--64 16,385 34.2 (32.7--35.7) 62.4 (60.9--63.9) 36.5 (35.0--38.0) 3.1 (2.4--3.8) ≥65 23,167 24.5 (23.4--25.6) 50.5 (49.2--51.9) 44.6 (43.4--45.9) 2.0 (1.6--2.3) Race/Ethnicity White, non-Hispanic 55,773 34.9 (33.9--35.9) 46.8 (45.9--47.8) 33.4 (32.5--34.4) 3.2 (2.8--3.6) Black, non-Hispanic 5,583 48.3 (45.7--51.0) 48.3 (45.8--50.8) 52.4 (49.7--55.1) 6.5 (5.1--7.9) Hispanic 6,198 33.0 (31.2--34.8) 50.6 (48.8--52.5) 41.9 (40.0--43.8) 6.3 (5.3--7.3) Other, non-Hispanic§ 6,484 38.7 (35.8--41.5) 48.2 (45.4--51.1) 41.0 (38.1--43.9) 7.2 (5.1--9.3) Sex Men 28,330 35.3 (34.2--36.5) 56.5 (55.3--57.8) 38.4 (37.2--39.7) 5.8 (5.1--6.5) Women 46,241 35.2 (34.2--36.2) 39.6 (38.7--40.6) 37.3 (36.3--38.4) 3.5 (3.1--3.9) Employment status Employed 38,814 37.4 (36.2--38.5) 50.5 (49.4--51.6) 33.5 (32.4--34.6) 5.4 (4.8--6.0) Unemployed 3,996 35.1 (32.2--38.0) 50.9 (47.9--54.0) 44.0 (41.0--47.0) 4.6 (3.2--6.0) Retired 20,304 25.0 (16.8--33.2) 37.9 (31.6--44.1) 27.3 (19.7--34.9) ---¶ --- Unable to work 4,001 46.4 (41.2--51.5) 55.8 (50.1--61.4) 57.3 (51.9--62.7) 9.5 (4.4--14.6) Homemaker/Student 7,134 30.8 (28.9--32.8) 37.0 (35.0--39.0) 39.3 (37.3--41.4) 2.2 (1.6-- 2.9) Education level Less than high school diploma or GED 6,393 32.0 (29.8--34.2) 51.2 (48.7--53.7) 43.4 (40.9--45.9) 5.4 (4.2--6.5) High school diploma or GED 20,504 37.0 (35.4--38.6) 49.9 (48.3--51.5) 39.6 (38.1--41.2) 4.0 (3.4--4.7) At least some college 47,426 35.8 (34.8--36.8) 47.0 (46.0--47.9) 35.9 (34.9--36.9) 4.8 (4.2-- 5.4) Marital status Married 42,965 35.1 (33.5--36.6) 49.5 (47.9--51.1) 35.9 (34.3--37.5) 4.3 (3.8--4.8) Divorced/Widowed/Separated 21,199 39.1 (36.5--41.8) 46.4 (43.0--49.9) 39.7 (35.9--43.5) 4.4 (3.3--5.5) Never married 8,590 37.9 (35.9--40.0) 43.5 (41.3--45.7) 42.9 (40.8--45.0) 4.6 (3.5--5.6) Member of unmarried couple 1,638 34.2 (30.2--38.2) 51.6 (47.4--55.8) 39.5 (35.4--43.6) 5.8 (3.5--8.1) State California 11,713 34.5 (33.3--35.8) 44.8 (43.6--46.1) 37.5 (36.3--38.8) 4.9 (4.3--5.5) Georgia 5,387 36.9 (34.5--39.2) 51.0 (48.8--53.1) 39.4 (37.1--41.8) 4.2 (3.2-- 5.2) Hawaii 6,288 44.6 (42.6--46.5) 54.0 (52.0--56.0) 42.8 (40.8--44.7) 6.4 (5.4-- 7.4) Illinois 5,549 36.1 (34.3--37.9) 49.3 (47.4--51.1) 38.6 (36.7--40.4) 3.0 (2.3-- 3.7) Kansas 8,703 30.0 (28.6--31.5) 53.9 (52.3--55.5) 35.4 (33.8--36.9) 3.3 (2.8-- 3.9) Louisiana 8,415 35.8 (34.1--37.5) 53.6 (51.9--55.4) 38.1 (36.4--39.8) 4.0 (3.3-- 4.7) Maryland 3,910 39.9 (37.4--42.4) 48.9 (46.4--51.4) 40.7 (38.1--43.3) 4.6 (3.4-- 5.7) Minnesota 5,519 27.6 (25.7--29.4) 51.6 (49.6--53.6) 33.7 (31.8--35.6) 3.1 (2.4-- 3.7) Nebraska 4,939 30.7 (27.9--33.4) 48.7 (45.6--51.7) 35.0 (32.0--38.1) 3.3 (2.3-- 4.2) New York 3,139 40.7 (38.1--43.2) 50.5 (47.8--53.1) 38.9 (36.4--41.4) 3.9 (2.8-- 5.0) Texas 5,310 34.0 (31.5--36.4) 52.1 (49.6--54.6) 38.6 (36.0--41.1) 6.4 (4.5-- 8.3) Wyoming 5,699 31.6 (29.8--33.5) 52.2 (50.4--54.1) 33.0 (31.1--34.9) 4.0 (3.1-- 4.9) |||||
Summary: | – Feeling tired? You're not alone. Some 35% of Americans average less than seven hours of sleep a night, according to a survey of nearly 75,000 adults in 12 states by the CDC. And the stats don't get rosier from there: 38% said they had fallen asleep by accident during the day in the last month, and close to 5% nodded off while driving, reports the LA Times. "Sleep difficulties, some of which are preventable, are associated with chronic diseases, mental disorders, health-risk behaviors, limitations of daily functioning, injury and mortality," says the report. "Drowsy driving, one of the most lethal consequences of inadequate sleep, has been responsible for an estimated 1,550 fatalities and 40,000 nonfatal injuries annually in the United States," wrote the report. The survey also revealed that nearly half of Americans snore; that people who are unable to work are much more likely to get less than 7 hours of sleep compared to employed people; and people who are divorced or single tend to be slightly more likely to get less sleep than their married counterparts. (Luckily, you may not need eight hours of sleep ... in a row.) | multi_news_1_0_0 |
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Article:
Legendary Chicago Cubs player and broadcaster Ron Santo died Thursday night in Arizona. He was 70.Friends of Santo's family said the North Side icon lapsed into a coma on Wednesday before dying Thursday. Santo died of complications from bladder cancer, WGN-AM 720 reported."He absolutely loved the Cubs," said Santo's broadcast partner, Pat Hughes. "The Cubs have lost their biggest fan."Hughes noted that with all the medical problems Santo had--including diabetes with resulting leg amputations, his heart and bladder cancer--"he never complained. He wanted to have fun. He wanted to talk baseball.""He considered going to games therapeutic. He enjoyed himself in the booth right to the end.""We were together for so long," said a mournful Billy Williams, who played alongside Santo for many years. "We formed a bond. It's just like losing a brother."Cubs Chairman Tom Ricketts released a statement: "My siblings and I first knew Ron Santo as fans, listening to him in the broadcast booth. We knew him for his passion, his loyalty, his great personal courage and his tremendous sense of humor. It was our great honor to get to know him personally in our first year as owners."Ronnie will forever be the heart and soul of Cubs fans."The former Cubs third baseman was best known to a younger generation for his work as an analyst on WGN, the Cubs' flagship radio station. He was expected to return for the 2011 season. He missed several road trips in 2010 but insisted he would return."What else am I going to do?" Santo said during this past season. "Doing the Cubs games is like therapy for me."Former Cubs teammate Randy Hundley, who also worked in the broadcast booth with Santo, said none of Santo's teammates realized he had diabetes until one night in St. Louis when he made a bad throw to first base and went down on one knee in pain.Later they found out Santo had had the disease for six years, Hundley said. "We kidded him about it quite a bit, made his life miserable at times," said the former catcher.Former Cubs President John McDonough compared Santo to Harry Caray, the broadcasting legend who called games for both Chicago teams, noting neither had a filter, broadcast with unvarnished emotion and were enormously entertaining.Santo mangled names, sometimes lost track of what was going on in a game and occasionally didn't realize a player had been on the roster for months, but none of that mattered because people loved it, McDonough said. "We almost thought he was doing it on purpose," he said. "It added so much entertainment value."One of the rare times he saw Santo visibly upset, McDonough recalled, was after Frank Sinatra Jr. sang during the seventh-inning stretch years ago. As Sinatra left the booth, he turned to Santo and told him he thought Santo was one of the best pitchers he had ever seen. "Ronny lost it," McDonough said.Santo was the quintessential Cubs fan and made no apologies for his on-air cheerleading or his utter frustration over a bad play.On many occasions, when Santo was upset with the way things were going for the team, a simple grunt or moan sufficed."I'm a fan," he explained last summer. "I can't plan what I do. I get embarrassed sometimes when I hear what I said, like, 'Oh, no, what's going on?' But it's an emotion."This is being a Cub fan." ||||| Legendary Chicago Cubs player and broadcaster Ron Santo died Thursday night in Arizona. He was 70.Friends of Santo's family said the North Side icon lapsed into a coma on Wednesday before dying Thursday. Santo died of complications from bladder cancer, WGN-AM 720 reported."He absolutely loved the Cubs," said Santo's broadcast partner, Pat Hughes. "The Cubs have lost their biggest fan."Hughes noted that with all the medical problems Santo had--including diabetes with resulting leg amputations, his heart and bladder cancer--"he never complained. He wanted to have fun. He wanted to talk baseball.""He considered going to games therapeutic. He enjoyed himself in the booth right to the end.""We were together for so long," said a mournful Billy Williams, who played alongside Santo for many years. "We formed a bond. It's just like losing a brother."Cubs Chairman Tom Ricketts released a statement: "My siblings and I first knew Ron Santo as fans, listening to him in the broadcast booth. We knew him for his passion, his loyalty, his great personal courage and his tremendous sense of humor. It was our great honor to get to know him personally in our first year as owners."Ronnie will forever be the heart and soul of Cubs fans."The former Cubs third baseman was best known to a younger generation for his work as an analyst on WGN, the Cubs' flagship radio station. He was expected to return for the 2011 season. He missed several road trips in 2010 but insisted he would return."What else am I going to do?" Santo said during this past season. "Doing the Cubs games is like therapy for me."Former Cubs teammate Randy Hundley, who also worked in the broadcast booth with Santo, said none of Santo's teammates realized he had diabetes until one night in St. Louis when he made a bad throw to first base and went down on one knee in pain.Later they found out Santo had had the disease for six years, Hundley said. "We kidded him about it quite a bit, made his life miserable at times," said the former catcher.Former Cubs President John McDonough compared Santo to Harry Caray, the broadcasting legend who called games for both Chicago teams, noting neither had a filter, broadcast with unvarnished emotion and were enormously entertaining.Santo mangled names, sometimes lost track of what was going on in a game and occasionally didn't realize a player had been on the roster for months, but none of that mattered because people loved it, McDonough said. "We almost thought he was doing it on purpose," he said. "It added so much entertainment value."One of the rare times he saw Santo visibly upset, McDonough recalled, was after Frank Sinatra Jr. sang during the seventh-inning stretch years ago. As Sinatra left the booth, he turned to Santo and told him he thought Santo was one of the best pitchers he had ever seen. "Ronny lost it," McDonough said.Santo was the quintessential Cubs fan and made no apologies for his on-air cheerleading or his utter frustration over a bad play.On many occasions, when Santo was upset with the way things were going for the team, a simple grunt or moan sufficed."I'm a fan," he explained last summer. "I can't plan what I do. I get embarrassed sometimes when I hear what I said, like, 'Oh, no, what's going on?' But it's an emotion."This is being a Cub fan."Santo never witnessed his longtime goal of election to the Baseball Hall of Fame despite career numbers that place him among baseball's all-time great third basemen. He finished with a .277 average over 15 major league seasons, with 342 home runs and 1,331 runs batted in.Though Santo came close to Cooperstown enshrinement in the last decade in voting by the Veterans Committee, he always fell short. In 2007, Santo received 39 of the 48 votes necessary to reach the 75 percent threshold of the living 64 Hall of Famers to cast a ballot. His 61 percent lead all candidates and no one was elected to the Hall.It was the fourth straight time the Veterans Committee had failed to elect a member, leaving Santo frustrated."I thought it was going to be harder to deal with, but it wasn't," he said that day. "I'm just kind of fed up with it. I figure, 'Hey, it's not in the cards.' But I don't want to go through this every two years. It's ridiculous."Santo was up for the Hall of Fame on 19 occasions, and first appeared on the Veterans Committee ballot in 2003. He got his hopes up on every occasion."Everybody felt this was my year," he said after the last vote in December 2008. "I felt it. I thought it was gonna happen, and when it didn't. ... What really upset me was nobody got in again."It just doesn't make sense."Santo was consistent that he did not want to make a posthumous entrance into the Hall of Fame. After being denied so many times, he was resigned to what is now the only possibility."(Induction) wasn't going to change my life," he said. "I'm OK. But I know I've earned it."Santo was beloved by many Cubs fans and players alike. When he was ill during the 2003 playoffs and couldn't travel with the team, pitcher Kerry Wood hung a No. 10 Santo jersey in the Cubs dugout in Atlanta. The Cubs won Game 5 of the division series to capture their first postseason series since 1908. Wood made an emotional call to Santo afterward, dedicating the game to him.Wood once made a case for Santo's election to the Hall of Game in an article in ESPN the Magazine, writing: "When it happens, and if the schedule lets us, I'm going to be there for the ceremony. He's the epitome of Chicago baseball. He's still part of the team. He lives and dies with it. In fact, I think we've put him in the hospital a few times. He should get in just for that."Santo got a laugh from Wood's words and denied the Cubs' play had ever put him in a hospital.Santo began his major league career with the Cubs in 1960, and spent one season with the White Sox in 1974. He earned National League Gold Glove awards five straight seasons from 1964 to 1968 and was a nine-time NL All-Star. He was one of the leaders of the 1969 team that blew the division lead to the New York Mets, a season indelibly etched in Cubs' history.Santo never forgot the hurt and hated going to New York thereafter. Before one of his final Cubs-Mets games as a WGN broadcaster in Shea Stadium in 2007, Santo told the Tribune: "I would come back here personally to blow it up. I'd pay my own way. Maybe even just to watch it."Santo joined the Cubs' radio booth in 1990 and was teamed with Hughes six years later. Santo epitomized the long-suffering Cubs fan, frequently grousing about the play on the field when things went bad.His most famous call was a simple two-word utterance -- "Oh no!" -- when outfielder Brant Brown dropped a fly ball with two outs and the bases loaded in the bottom of the ninth of a crucial game in Milwaukee in the final week of the 1998 season.He also suffered through incidents along the way that could seemingly happen only to Santo.His toupee caught fire in the Shea Stadium press box on Opening Day 2003 after he got too close to an overhead space heater. And last spring in Mesa, Ariz., Santo lost his front tooth while biting into a piece of pizza.Though Santo never made the Hall of Fame, his number was retired by the Cubs and now flies on the foul pole at Wrigley Field. He said that was equivalent to being inducted in Cooperstown. Being a Cub, and playing at their iconic stadium, meant the world to Santo."When I got here, two years after my senior year, I'm walking out of the corner clubhouse with Ernie Banks and there's nobody in the stands, and the feeling I had was unbelievable -- walking with Ernie and walking on that grass," he said. "I felt like I was walking on air. There was an electricity and an atmosphere that I'd never experienced in my life. Any ballplayer that's ever played here can tell you about that great atmosphere, and anybody who's come here to watch a game feels the exact same way." |||||Summary:
| – Renowned Chicago Cubs third-baseman and broadcaster Ron Santo died last night in Arizona of complications from bladder cancer at age 70. “Ronnie will forever be the heart and soul of Cubs fans,” said the team’s chairman. “He enjoyed himself in the booth right to the end,” said a fellow broadcaster. The Tribune recounts his career on and off the field, including the time his toupee caught fire in the press box. Santo entered the big leagues with the Cubs in 1960. A nine-time All-Star with a .277 average, 341 home runs, and 1,331 runs batted in after 15 seasons, he publicly hoped to enter the Hall of Fame, but never quite made it—despite numbers that put him among the great third-basemen of the game. In 1990, he began broadcasting on Cubs radio and was an unapologetic team booster. “He's still part of the team,” pitcher Kerry Wood once wrote of him. “He's the epitome of Chicago baseball.” | multi_news_1_0_0 |
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An Inuit village in Greenland is pictured in this September 2013 handout photo provided by Ida Moltke.
An Inuit village in Greenland is pictured in this September 2013 handout photo provided by Ida Moltke.
An Inuit village in Greenland is pictured in this September 2013 handout photo provided by Ida Moltke.
WASHINGTON The Inuit, a group of people who make the Arctic their home, have benefited from a handy set of genetic adaptations that help them survive in some of Earth's harshest conditions.
Scientists on Thursday said a study of the genomes of Inuit from Greenland revealed unique genetic variants related to fat metabolism that ward off cardiovascular disease that otherwise could be caused by a diet traditionally high in fat from blubbery seals and whales.
These genetic mutations, which the researchers said arose perhaps 20,000 years ago, help lower "bad" LDL cholesterol and fasting insulin levels, limit the height of the Inuit, keep down their weight and help them adapt to a cold environment.
"Our study is perhaps the most extreme example to date of a genetic adaptation to a specific diet," said computational biology professor Rasmus Nielsen of the University of California, Berkeley and the University of Copenhagen.
"The mutations we find seem to compensate physiologically for a large intake of animal fat and are largely an adaptation to a lifestyle in which you have a high-caloric intake of fat from marine mammals, and possibly also from other mammals."
The Inuit, formerly called Eskimos, are indigenous people in Greenland and Arctic regions of Canada and Alaska.
The researchers examined genomes of 191 Inuit, 60 Europeans and 44 Han Chinese. The genetic variants found almost universally in the Inuit were much rarer in the Europeans (2 percent) and Chinese (15 percent).
The research, published in the journal Science, is the latest to illustrate human genetic adaptation to environmental conditions.
"One of the best examples is the Tibetans' adaptation to high altitude," said University of Copenhagen computational biology professor Anders Albrechtsen, referring to a study showing that many Tibetans possess a rare variant of a gene involved in carrying oxygen in the blood, helping them in high-altitude, low-oxygen conditions.
The Inuit findings may shed light on the value of diet supplementation with omega-3 fatty acids and fish oils. Nielsen noted such supplementation was originally motivated by observations that Inuit people had a high intake of fat but low cardiovascular disease incidence, so the particular form of fat they got in their diet might be healthier than other kinds.
"Our study shows that lessons from the Inuit cannot be extrapolated to other populations. The Inuit have special genetic variants that might allow them to function better on a diet rich in omega-3s than other populations," Nielsen said.
(Reporting by Will Dunham; Editing by Eric Walsh) ||||| Greenlanders' genomes signal a fatty diet
The evolutionary consequences of inhabiting a challenging environment can be seen within the genomes of Greenland Inuit. Fumagalli et al. have found signs of selection for genetic variants in fat metabolism, not just for promoting heat-producing brown fat cells but also for coping with the large amounts of polyunsaturated fatty acids found in their seafood diet (see the Perspective by Tishkoff). Genes under selection in these populations have a strong effect on height and weight of up to 2 cm and 4 kg, respectively, as well as a protective effect on cholesterol and triglyceride levels.
Science, this issue p. 1343; see also p. 1282 ||||| The Secret To The Inuit High-Fat Diet May Be Good Genes
Enlarge this image toggle caption Uriel Sinai/Getty Images Uriel Sinai/Getty Images
We talk a lot on The Salt about the Mediterranean diet, which is rich in nuts, olive oil, fish, fruits and vegetables. Scientists believe it's one of the world's healthiest patterns of eating, and can protect against a lot of chronic diseases.
In the Arctic, the typical meal looks very different. There, a traditional plate would have some fatty marine animal like seal or whale and not much else – fruits and vegetables are hard to come by in the harsh climate.
And yet despite the fact that the high-fat Arctic diet may sound like a heart attack waiting to happen, the Inuit tend to have low rates of heart disease and diabetes.
Researchers thought maybe it was the omega-3 fatty acids in the meat and blubber that might be protective. But a new study on Inuit in Greenland suggests that Arctic peoples evolved certain genetic adaptations that allow them to consume much higher amounts of fat than most other people around the world, according a team of researchers reporting Thursday in the journal Science.
Computational biologist Rasmus Nielsen at the University of California, Berkeley lead the research, and began by looking for genetic differences between a 191 Inuit in Greenland, 60 Europeans, and 44 ethnic Chinese. "When we did that, it pointed directly to one group of genes where we had an extremely strong signal," Nielsen says. "They regulate how much of these omega-3s and omega-6s you make yourself naturally."
Nearly all of the Inuit in Nielsen's study had variances in these genes that researchers think slow down the body's natural production of omega-3 and omega-6 fats. "We saw that the Inuit have such a high diet of omega-3s, so they produce much less of it themselves," Nielsen says. And the genes seem to play a role in lowering levels of LDL cholesterol, the bad kind that's linked to heart disease. Only about 3 percent of Europeans and 15 percent of Chinese had the same genetic markers, the team writes.
Nielsen thinks these genes helped Inuit ancestors survive in the brutal cold near the North Pole and stay healthy on a diet of almost exclusively fat and protein. And he thinks the genes are mostly unique to humans living in this environment.
Enlarge this image toggle caption Malik Mifeldt/Science Malik Mifeldt/Science
But there's a lot of uncertainty about the genes. "The regulation of fats in your body is a really complex network. You turn one knob, and it just changes everything everywhere else," Nielsen says. So, he notes, the full implication of having these mutations still isn't well understood.
That's part of the reason why some researchers aren't completely blown away by the study. Whether or not these genes have helped Inuit stay slim on a high-fat diet is still unclear, says Joel Hirschhorn, a geneticist at Harvard Medical School. "They're taking a leap of faith," he says.
The genes in question seem to influence so many different processes in the body that pinpointing their effect is difficult, he says. "It's harder to go beyond the known biology of these genes and make connections to weight."
On top of that, Hirschhorn thinks there could be reasons other than diet for why Inuit have these mutations. "There are lots of things about the lifestyle in Greenland that are different and could lead to these adaptations," he says.
Even so, Hirschhorn says he's excited about the paper because "it's a clear example of human evolution." Like the genes that have allowed groups that practice dairying to tolerate lactose in milk, it's another example of human adaptations to different environments or diets, says Sarah Tishkoff, a geneticist at the University of Pennsylvania.
Nowadays, very few Greenlanders still eat a completely traditional diet. And the move away from the high-fat, high-protein diet may be leading to the rising rate of diabetes. "If they switch to a modern diet that's high in carbohydrates, particularly simple ones like glucose and sugar, then they tend to be quite unhealthy," Nielsen says.
That suggests that understanding these adaptations could eventually lead to specialized diets for each person. "We know now that the Inuit adapted to a very specific diet. That may be true for other populations as well," he says.
In other words: The answer to how harmful a high-fat diet is for you could depend on your genomics. ||||| | – One in 10 Americans take fish oil supplements thanks in part to decades-old research. The Inuit—who consumed a diet mainly of whales, seals, and fish—rarely had heart attacks, and researchers speculated in the 1970s that omega-3 fatty acids found in fish guard against them, reports the New York Times. But decades' worth of fish oil pills may have been better dumped down the drain: A new study published in Science provides what the Times calls an "intriguing new twist" to the omega-3 story. In analyzing the DNA of 191 Greenland residents of almost entirely Inuit descent, scientists found they boasted genetic variants that may help them consume high amounts of fat without negative consequences. The find suggests "lessons from the Inuit cannot be extrapolated to other populations," per study author Rasmus Nielsen. Their genetic mutations helped keep fasting insulin and LDL cholesterol levels low, reports Reuters. The Times notes that Inuit with two copies of one gene variant in particular were an average one inch shorter and weighed 10 pounds less than those without it. The genetic variants—which may have come into play 20,000 years ago—"regulate how much of these omega-3s and omega-6s you make yourself naturally," says Nielsen, per NPR. "We saw that the Inuit have such a high diet of omega-3s, so they produce much less of it themselves." This is "perhaps the most extreme example to date of a genetic adaptation to a specific diet," he adds. In speaking to NPR, a Harvard Medical School geneticist advises caution: It's tough "to go beyond the known biology of these genes and make connections to weight," says Joel Hirschhorn. "They're taking a leap of faith." (This isn't the first study to throw fish oil benefits in doubt.) | multi_news_1_0_0 |
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Article:
Using marbles instead of ballot papers, some 800,000 Gambians will vote on Thursday by dropping a clear glass ball into one of three different coloured drums representing the presidential hopefuls in this tiny nation on the west coast of Africa.
Most will land in the green drum, which represents incumbent, a close friend of Jermaine Jackson and self-proclaimed mystic who says he can cure Aids – but only on a Thursday.
Since taking power in a bloodless 1994 coup, Yahya Jammeh has swapped army fatigues for white gowns and a sceptre, holding sway through a potent mixture of state brutality and mysticism.
International rights groups have repeatedly pointed the finger at his authoritarian regime. In 2000, at least 14 people were killed during an anti-government rally, while an opposition leader was jailed in 2006 for using a microphone without official permission.
He claims powers to cure a long list of maladies including obesity and erectile dysfunction, and in 2007 hundreds of people with HIV flocked to Jammeh's Thursday-only Aids clinic in Banjul, the capital. A UN envoy who questioned it was booted out. Jermaine Jackson, brother of the late Michael and a former Jackson 5 member, said the president was a man of "truth and logic" after a 2010 visit in which he decided his ancestors had come from Gambia.
Best known for palm-fringed beaches that attract thousands of European winter sun-seekers, Africa's smallest mainland nation is also one of its most autocratic. Jammeh, whose face is used to advertise everything from food to phone credit, has cemented his 17-year reign by dishing out death sentences and gifts. He is expected to win Thursday's vote hands-down.
To deter multiple voting, electoral monitors listen closely to the sound of a bell that rings out as each marble drops, making sure there is only one. Modelled on traditional arrangements used in much of Africa, the system was introduced in 1965 for a population with illiteracy rates topping 75%. That's down to 55% thanks partly to Jammeh's efforts to improve schools.
Aminata Hydara, a beneficiary of a government scholarship in Brikama, east of Banjul, will vote for him. "He has constructed roads, hospitals … the only way for Gambians to say thank you to him is to vote massively for him." There were, she said, few signs of the two opposition candidates on the campaign trail.
In 2008 Jammeh threatened to "cut off the head" of gay people in Gambia. The following year, up to 1,000 villagers were rounded up as suspected witchdoctors behind the death of the president's aunt. They were forced to drink hallucinogens and beaten, Amnesty International said.
Gambia has the region's worst press rights. Draconian sedition rules have seen dozens of journalists routinely imprisoned and others assassinated or disappeared.
"It's a foregone conclusion Jammeh will win," said one journalist in Banjul. Speaking in hushed tones, the journalist, who has been detained in the past, added: "We have to be very tactful, anything we say can be used against us."
Senegal, which envelops Gambia, has accused it of trying to ship weapons from Iran to separatist rebels in the Casamance region. Over a dozen carts of Iranian weapons headed to Gambia were seized in a Nigerian port last year.
Jammeh retired from campaigning this week, saying God had decreed he would win. ||||| An estimated 800,000 of Gambia's two million citizens registered to vote but experts say that a climate of fear and intimidation mean that few will back anyone other than Yahya Jammeh.
Brought to power in a bloodless coup in 1994, the 46-year-old has since changed the constitution in the former British colony to removed presidential term limits, won three previous elections and recently declared that only God could remove him from power.
For added certainty, he took to the streets for a "thank you" tour last week in which he handed out biscuits, sugar, rice and farming equipment in return for pledges of support.
In a country where less than half the population can read and write, a novel polling system has been devised which sees voters pop a glass marble into a coloured drum picturing their chosen candidate. As it falls, the marble strikes a bicycle bell, enabling poll staff to detect multiple voting.
The Economic Community of West African States (ECOWAS) has already denounced the poll as unfair.
An ECOWAS fact-finding mission reported "an unacceptable level of control of the electronic media by the party in power and an opposition and electorate cowed by repression and intimidation."
Staff campaigning for Ousainou Darboe, the main opposition challenger, say they have received death threats. As he cast his vote yesterday, Mr Darboe complained about a large military presence on the streets.
"The presence of armoured vehicles all over the country, especially in Banjul (the capital), is intended to intimidate voters," he said.
Mr Jammeh, dressed in his trademark white flowing robes, brushed off criticisms of his regime as he arrived to vote.
"No Western country can tell me anything about democracy," he said. "
In this country we fear only God and I don't care what anybody says. What matters to me is the development of this country. Africa has been insulted for centuries and this is unacceptable."
The United States sees the Gambian government as an important ally against militants and drugs trafficking and Mr Jammeh has overseen strong economic growth along with the construction of roads, schools and hospitals.
But poverty remains widespread in Gambia, where thousands of European holidaymakers flock each year to lie on tropical beaches, with 67 per cent of the population living on less than $1.25 a day.
Mr Jammeh generated concern and mirth in equal measure when he claimed, in 2007, to have developed a cure for Aids that involves a green herbal paste and a diet of bananas.
His Excellency Sheikh Professor Alhaji Dr Yahya AJJ Jammeh, to give him his full title, also claims to be able to treat infertile women, asthmatics, epileptics and diabetics with his herbal remedies. |||||Summary:
| – It's election time in the Gambia, and the west African nation's 800,000 voters are dropping their marbles. With the literacy rate under 50%, the country has adopted a unique voting system in which each voter drops a marble into one of three different colored drums representing presidential hopefuls, reports the Telegraph. Election monitors listen for the sound of a bell that rings as a marble is dropped. Incumbent President Yahya Jammeh, who seized power in a 1994 coup, is widely expected to get the vast majority of the marbles, the Guardian notes. The self-proclaimed mystic, a close friend of Jermaine Jackson, has spent heavily on roads and hospitals but has also cracked down on dissent and imprisoned dozens of journalists. He retired from campaigning this week, saying God had decreed that he would win, and there have been few signs of the other two candidates on the campaign trail. | multi_news_1_0_0 |
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– If you look after your heart and educate your brain, you have a better chance of avoiding or at least delaying dementia, new research suggests. Boston University School of Medicine researchers say data from the Framingham Heart Study, which has tracked the health of thousands of people in the Massachusetts town since 1948, reveals that "since 1977, there has been a decline in the incidence of dementia of 20% per decade," NBC News reports. Heart disease rates dropped alongside dementia rates, but only among people who had at least a high school education, according to the researchers, whose study is published in the New England Journal of Medicine. "It's very good news," a National Institute on Aging epidemiologist tells USA Today. "We're seeing one generation after another where the risk is going down." The decline was steepest in cases of vascular dementia, which is caused by impaired supply of blood to the brain, though there was also a decline in Alzheimer's cases. The research suggests that dementia will not be as huge a health care problem in coming decades as earlier believed, the New York Times reports, though since people are living longer, the number of cases is still expected to go up—and rising rates of diabetes and obesity could send dementia rates back up again. Still, researchers say they hope the study will inspire people to improve heart health and keep their brains busy. "People may say, 'I don't mind getting a heart attack. It's a good way to go,'" study co-author Sudha Seshadri says. "But heart disease may not just damage your heart. It could cause dementia. And I don't know of anybody who thinks dementia is a good way to go." (A sick sense of humor could be a danger sign.)
Article: |
CLOSE Researchers have found a small piece of good news for people at high risk of some kinds of dementia: it might be possible to delay it or even prevent it. USA TODAY
Decima Assise, who has Alzheimer's disease, and Harry Lomping walk the halls on Nov. 6, 2015, at The Easton Home in Easton, Pa. (Photo: Matt Rourke, AP)
A long-running study has found that dementia rates fell steadily over the past four decades, most likely due to declining rates of heart disease.
Although the Framingham Heart Study involved just 5,200 people, its findings likely reflect a national trend, said co-author Sudha Seshadri, a professor of neurology at the Boston University School of Medicine and a senior investigator with the study. Other research also suggests that dementia rates are declining in the U.S. and other developed countries.
Rates of dementia in the new study decreased from 3.6% during the late 1970s and early 1980s to 2% during the late 2000s and early 2010s, a drop of 44%, according to the study published online Wednesday in The New England Journal of Medicine.
"It's very good news," said Dallas Anderson, an epidemiologist with the National Institute on Aging, part of the National Institutes of Health, which funded the study. "We're seeing one generation after another where the risk is going down."
Researchers found that the sharpest decline in dementia was in a type called vascular dementia, which is caused by damage to the blood vessels that carry oxygen to the brain.
Although rates of Alzheimer's disease also fell, this decline could have been due to chance, the paper said. Alzheimer's is the most common form of dementia and accounts for 60% to 80% of dementia cases. Dementia is a general term for memory loss and other intellectual abilities serious enough to interfere with daily life.
When people in the study did develop dementia, it occurred later in life, so that people were able to spend fewer years disabled, Seshadri said. The average age at which people were diagnosed with dementia increased from 80 during the early years of the study to 85 in the most recent period.
As the study progressed, fewer people in the study suffered from heart disease as well. Heart disease and strokes have long been linked to an increased risk of dementia.
The study suggests that care for people who suffered strokes also improved over the years. In the early years of the study, people who survived a stroke were nine times as likely as others to develop dementia. In the most recent period, people who had strokes were less than twice as likely.
"We’ve been preaching for years that what’s good for the heart is good for the brain," said Ronald Petersen, who directs the Mayo Clinic Alzheimer's Disease Research Center and the Mayo Clinic Study of Aging. "Maybe our efforts to watch our diet and exercise are having a spillover effect, leading to less dementia."
Dementia rates didn't fall for all participants in the study.
Dementia and heart disease rates only declined among people who had at least a high school diploma, according to the study. Research has long linked higher incomes and educational levels with better health, Seshadri said.
Education influences a person's health in countless ways, Seshadri said. People who are better educated are more likely to find good jobs with health insurance and to learn about ways to stay healthy, such as by exercising and avoiding tobacco. Better educated people may stay more mentally active in retirement.
But Seshadri notes that a person's educational level also reflects that person's childhood experiences. A person raised with poverty, crime and abuse could be less likely to graduate high school, as well as less likely to grow into a healthy adult.
The improving health seen in the new study could be fragile, said Seshadri, noting that obesity and diabetes increased over time. Both conditions harm the heart and could lead to more dementia in the future.
Even if dementia cases grow at a slower rate, the total number of people with the condition are certain to increase in incoming decades as the elderly population expands, Seshadri said.
About 5.3 million Americans have Alzheimer's today, and one in three elderly people die with dementia, according to the Alzheimer's Association. As the nation ages, the number of people over age 65 with Alzheimer's disease will increase 40% by 2025, to 7.1 million.
Seshadri said she hopes her study motivates people to keep their hearts and brains healthy for as long as possible.
"People may say, 'I don't mind getting a heart attack. It's a good way to go,'" Seshadri said. "But heart disease may not just damage your heart. It could cause dementia. And I don’t know of anybody who thinks dementia is a good way to go."
Read or Share this story: http://usat.ly/1Xjqf0Q ||||| Background The prevalence of dementia is expected to soar as the average life expectancy increases, but recent estimates suggest that the age-specific incidence of dementia is declining in high-income countries. Temporal trends are best derived through continuous monitoring of a population over a long period with the use of consistent diagnostic criteria. We describe temporal trends in the incidence of dementia over three decades among participants in the Framingham Heart Study.
Methods Participants in the Framingham Heart Study have been under surveillance for incident dementia since 1975. In this analysis, which included 5205 persons 60 years of age or older, we used Cox proportional-hazards models adjusted for age and sex to determine the 5-year incidence of dementia during each of four epochs. We also explored the interactions between epoch and age, sex, apolipoprotein E ε4 status, and educational level, and we examined the effects of these interactions, as well as the effects of vascular risk factors and cardiovascular disease, on temporal trends.
Results The 5-year age- and sex-adjusted cumulative hazard rates for dementia were 3.6 per 100 persons during the first epoch (late 1970s and early 1980s), 2.8 per 100 persons during the second epoch (late 1980s and early 1990s), 2.2 per 100 persons during the third epoch (late 1990s and early 2000s), and 2.0 per 100 persons during the fourth epoch (late 2000s and early 2010s). Relative to the incidence during the first epoch, the incidence declined by 22%, 38%, and 44% during the second, third, and fourth epochs, respectively. This risk reduction was observed only among persons who had at least a high school diploma (hazard ratio, 0.77; 95% confidence interval, 0.67 to 0.88). The prevalence of most vascular risk factors (except obesity and diabetes) and the risk of dementia associated with stroke, atrial fibrillation, or heart failure have decreased over time, but none of these trends completely explain the decrease in the incidence of dementia.
Conclusions Among participants in the Framingham Heart Study, the incidence of dementia has declined over the course of three decades. The factors contributing to this decline have not been completely identified. (Funded by the National Institutes of Health.)
Supported by the National Heart, Lung, and Blood Institute Framingham Heart Study (contract no. N01-HC-25195 and no. HHSN268201500001I) and by grants from the National Institute on Aging (AG08122 and AG033193) and the National Institute of Neurological Disorders and Stroke (NS017950). Disclosure forms provided by the authors are available with the full text of this article at NEJM.org. The content of this article is solely the responsibility of the authors and does not necessarily represent the official views of the National Institute on Aging, the National Institutes of Health, or the National Heart, Lung, and Blood Institute. We thank the study participants, as well as the study team (especially the investigators and staff of the neurology team) for their contributions to data collection over the past four decades. ||||| Researchers have found a small piece of good news for people at high risk of some kinds of dementia: it might be possible to delay it or even prevent it.
They found falling rates of vascular dementia in people who also happened to improve their heart health. The findings, published in the New England Journal of Medicine, support the idea that what’s good for the heart is good for the head.
"Our study offers cautious hope that some cases of dementia might be preventable or at least delayed," Claudia Satizabal of the Boston University Schools of Medicine and colleagues wrote in their report.
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They looked at more than 5,000 people who have been having their health tracked in minute detail as part of the Framingham Heart Study. The multi-generational study has been going on since 1948 and in 1971 children of the original volunteers signed up. Their memory has been tested since 1975.
"On average, since 1977, there has been a decline in the incidence of dementia of 20 percent per decade," the researchers wrote. The decrease in rates of vascular dementia has been 29 percent per decade.
"The decline in the incidence of Alzheimer’s disease was not significant, whereas the decline in the incidence of vascular dementia appeared to be more rapid than that of Alzheimer’s disease," they added.
“Our study offers cautious hope that some cases of dementia might be preventable or at least delayed."
Keith Fargo, director of scientific programs for the Alzheimer's Association welcomed the findings.
"The incidence rates for dementia in the Framingham heart study appear to be decreasing over the past few decades and that's good news. It's probably not everything that needs to be done, but it's good news and it points us in a couple of directions about what we might be able to do to decrease the risk for dementia as people age," Fargo told NBC News.
"We know that things like increasing your physical activity, eating a heart-healthy diet, making sure that you stay socially active, making sure that you stay cognitively engaged, if you smoke, stop smoking — all of these things are going to reduce your likelihood of cognitive decline as you age and may even delay or prevent dementia," Fargo said.
Related: Here's a Recipe for Preventing Dementia
But the news only applies to the mostly white people taking part in the study. A second study found dementia rates are highest in African Americans and lowest in Asian Americans.
And the Boston team’s findings only applied to people with a high school education or more. That supports other research that shows education can protect against dementia, probably by keeping the brain active and growing.
Vascular dementia is the second most common cause of dementia after Alzheimer’s disease.
One person who’s doing her best to stave off dementia is Cynthia Huling Hummel, a retired pastor in Elmira, New York. She was diagnosed with mild cognitive impairment, which can progress to Alzheimer’s, in 2011.
"I was preparing for my doctorate, I was preparing to defend my dissertation and I couldn't remember any of the classes I had been taking," Hummel, who is 61, told NBC News.
"I couldn’t remember the material I had read. I couldn’t remember the teachers or the students I had interfaced with so I knew there was a problem," she added.
"It’s frustrating. It’s embarrassing. By Wednesday I would forget what I had preached on Sunday," she said.
Hummel retired, but she got busy trying to do what she could to prevent the dementia from worsening.
"Getting more physically active, engaging myself more socially, challenging myself with more learning opportunities, being mindful of what I was eating, all those things," she said.
"I take classes at Elmira College. I’m now taking my 28th class in almost 4 ½ years," Hummel added.
"You want to pump that blood and stay physically active and again, what is good for the heart is good for the brain and so I swim three times a week at the Y."
“You want to pump that blood and stay physically active."
It appears to be working.
"I went to see my neurologist last month and he said, 'Whatever you’re doing continue to do it because it’s working.' And so that is good news," she said.
More than 5 million Americans have Alzheimer's disease. The Alzheimer's Association says more than 28 million baby boomers will develop the disease between now and 2050, and the cost of caring for them will consume nearly 25 percent of Medicare spending in 2040. It's worse in women.
A second study looked at just who gets dementia.
Dementia rates in African Americans are 65 percent higher than among Asian Americans, the study found.
"Our projections indicate that in every racial and ethnic group, over one in four people who survive to age 65 can expect to be diagnosed with dementia in their lifetime," said Rachel Whitmer, an epidemiologist at Kaiser Permanente Northern California, who led the study published in an Alzheimer's Association journal.
Her team’s study of 274,000 members of Kaiser Permanente found dementia incidence over the 14-year study period ranged from an average annual rate of 26.6 cases of dementia per 1,000 people for African-Americans, to 15.2 cases per 1,000 people for Asian-Americans. In between were Latinos and Pacific Islanders with an average annual rate of 19.6 cases per 1,000 people, and whites with 19.3 per 1,000.
Various studies have given people hints at what can prevent Alzheimer’s. Regular exercise and eating plenty of fruits and vegetables helps.
Others have shown that people who are socially engaged are less likely to develop memory loss. Still others have shown that keeping the brain active with puzzles or games can help, and a whole industry has arisen out of that research. ||||| | multi_news_1_0_0 |
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For three agonizing years, Sam Ou waited for justice for his little girl, murdered in her baby-sitter’s Mandarin home after being beaten with a wire fly-swatter handle.
Three years of court dates and doctors’ reports sustained by anguished memories of 2-year-old Amara’s joyful, outgoing spirit.
Tuesday finally brought the justice Ou sought with a life prison sentence handed down against Syna Lim, herself a mother of two children.
“I have relief the court part’s over,” Ou told the Times-Union afterward. “I’m very pleased.”
A jury convicted Lim, 41, of first-degree murder and aggravated child abuse last month in the October 2006 beating death of the St. Johns County girl. She died of severe head trauma three days after being rushed from Lim’s home to Wolfson Children’s Hospital.
Though the only possible sentence was life in prison, dozens of Lim’s friends and relatives — some traveling from as far as Canada — packed the courtroom to support her. None chose to speak, said Lim’s attorney, Chief Assistant Public Defender Refik Eler.
Amara’s parents also declined to testify, but issued a statement to the court through Assistant State Attorney Sam Garrison. He said the loss of their daughter was made more difficult because it came at the hands of someone they trusted.
“They will never get over this loss,” Garrison told Circuit Judge Mallory Cooper. “All the defendant had to say was she didn’t want to watch her, and this never would have happened.”
Ou said later that Amara was a friendly child who would smile and wave at everyone she saw when her parents took her out. He praised police and prosecutors for sticking with the case and ensuring justice for his daughter.
Cooper said she thought the mandatory life sentence was appropriate for Lim.
“There’s nothing the court can do to make either family feel better,” the judge said.
[email protected],
(904) 359-4107 ||||| A judge threw out the conviction and life sentence of a Mandarin baby sitter after new evidence suggesting that a 2-year-old St. Augustine child in her care was not beaten to death, but instead died from high blood sugar due to undiagnosed juvenile diabetes.
This week Circuit Judge Angela Cox ordered a new trial for Syna Lim, 48, who was convicted in 2009 for the murder of Amara Ou.
Lim will now get a new trial if outgoing State Attorney Angela Corey and State Attorney-elect Melissa Nelson choose to retry her. Prosecutors also could choose to drop the case and let Lim go free, or Cox’s ruling could be sent to the 1st District Court of Appeal in Tallahassee.
“We have advised the victim’s family of Judge Cox’s decision,” said Corey spokeswoman Jackelyn Barnard. “We are currently reviewing the order and we will be deciding in the near future whether we will appeal Judge Cox’s order or proceed to a second trial.”
Nelson will replace Corey the first week of January after defeating the incumbent in the Aug. 30 election. She has previously told the Times-Union she will not comment on any pending cases before taking office.
But a new trial could raise troubling questions about former Chief Medical Examiner Margarita Arruza, who conducted the original autopsy on Amara and did not find she was suffering from diabetes. Aruzza resigned several years later, and allegations have surfaced that she suffered from the early effects of Alzheimer’s disease while still serving as medical examiner.
The toddler’s father left her in Lim’s care at the woman’s Jacksonville residence at 6305 Devonhurst Drive in 2006.
Lim later told police the child wouldn’t wake up from a nap a few hours later, so for two hours she tried calling the mother before reaching the father.
Doctors said the 2-year-old was brain dead upon arrival at the hospital and had bruises on her head and limbs.
Lim told police she was doing laundry, and Amara must have fallen off the couch. Prosecutors charged Lim with first-degree murder and child abuse and said she hit Amara with the handle of a flyswatter and then delivered a crushing blow to the child’s skull.
Chief Assistant Public Defender Refik Eler and Assistant Public Defender Michelle Barki did not dispute that Ou had died from blunt head force trauma at the original trial but contended it wasn’t Lim who did it.
“Once blunt force trauma became accepted by all parties as the child’s cause of death, with no suggested alternate cause of death, the defendant was doomed,” wrote Lim’s current attorney, Samuel Jacobson, in court filings arguing that she deserved a new trial.
Eler has been found to be ineffective in criminal cases four times in recent years, but Cox did not find him deficient in this case.
Lim was convicted and Circuit Judge Mallory Cooper sentenced her to life in prison for the murder and an additional 30 years for child abuse.
But according to court records, years after the conviction an Orlando pathologist and a Jacksonville pediatrician re-examined the case and determined that Amara did not die from blunt force trauma at all. They testified that Amara had been suffering from diabetes and a condition called “disseminated intravascular coagulation,” or DIC, that produces uncontrolled internal bleeding.
“Uncontrolled bleeding from DIC, the physicians testified, likely caused the bruising and other discolorations on or about the child which were interpreted by the treating personnel as indications of trauma,” Jacobson said in court filings.
In other words, the medical evidence suggests Amara may have died from internal bleeding and was never the victim of blunt force trauma, Jacobson said.
He said their motions to dismiss did not involve the competence of Aruzza since the focus of their argument was that this was new evidence that justified a new trial.
“Mrs. Lim’s new evidence is her most important evidence,” Jacobson said. “With it her innocence is realistically demonstrable.”
But if prosecutors choose to go back to court, Jacobson said he intended to challenge the original autopsy and raise the issue of Aruzza’s competence.
The Orlando pathologist questioned the competence and soundness of mind of the person who did the original autopsy, Jacobson said.
Barnard said it would be inappropriate to comment on a potential second trial. Corey defended Aruzza this year after questions were raised, saying all of the cases where she performed the autopsie were re-examined by her successor Valerie Rao, or someone else in the Medical Examiner’s Office.
Other medical examiners then testified when those cases went to trial based on their own independent examinations of the evidence.
Aruzza resigned in 2010.
Larry Hannan: (904) 359-4470 ||||| JACKSONVILLE, Fla. - A woman who was convicted of murder in 2009 in the death of a 2-year-old girl she was babysitting has been granted a new trial, according to court documents.
A judge overturned the conviction of Syna Lim, who was found guilty of killing Amara Ou. According to court documents, there is newly discovered evidence as to the cause of the toddler's death.
During the October 2009 trial, prosecutors contended Lim beat the St. Augustine girl with the handle of a flyswatter, then struck the child's head with a hard object. A jury found Lim guilty of first-degree murder and she was sentenced to life in prison.
Dr. Deborah Thoni told the appeals court that the toddler had a “classical” case of diabetic ketoacidosis, which led to her death, not blunt-force trauma to the head, which was the cause of death determined at the time.
Dr. Aylin Ozdemir also told the court that medical testing done prior to Amara’s death was inadequate, especially because there was no urinalysis done before the child went into the emergency room. Post-mortem testing showed the girl had extremely high glucose levels. Ozdemir said the condition causes uncontrolled bleeding that causes internal and external bruising that could be mistaken for trauma.
Lim, now 48 years old, appealed on two claims, the new evidence and ineffective counsel. She has since withdrawn the claim of ineffective counsel.
"We have advised the victim’s family of Judge Cox’s decision," the State Attorney's Office said. "We are currently reviewing the order and we will be deciding in the near future whether we will appeal Judge Cox’s order or proceed to a second trial."
Copyright 2016 by WJXT News4Jax - All rights reserved. ||||| | – In October 2006, Amara Ou's father dropped the 2-year-old off at her babysitter's Florida home. A few hours later, after the girl wouldn't wake up from a nap, babysitter Syna Lim, now 48, tried for two hours to reach Amara's parents before getting hold of the father. When Amara finally arrived at the hospital, she was brain dead. Three years later, a jury found Lim guilty of the girl's murder, convicting her of beating the toddler with the handle of a flyswatter and hitting her on the head. She was sentenced to life in prison. But last week, the conviction was overturned and a new trial ordered, the Florida Times-Union reports. New evidence has found that Amara may not have been beaten to death after all, but may have died due to undiagnosed juvenile diabetes and another condition that causes uncontrolled internal bleeding. A pathologist and a pediatrician re-examined the case years later and testified that Amara had very high blood sugar levels at the time of her death, which caused the internal bleeding. That bleeding, in turn, would have led to the bruises found on Amara that could be mistaken as coming from a beating. The doctors told the court that not enough medical testing was done on Amara at the hospital, News 4 Jax reports. The case brings up questions about the medical examiner who performed Amara's autopsy, the Times-Union notes: She resigned in 2010, and allegations have swirled that she was experiencing early symptoms of Alzheimer's before she resigned. (Shaken baby syndrome is dividing the medical world.) | multi_news_1_0_0 |
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Here is a news article: How red wine prolongs life: Scientists uncover how 'miracle ingredient' boosts body’s cell energy
Cheers: The key ingredient in red wine resveratrol has anti-ageing powers. Posed by model
Scientists claim to have discovered the secret of how an ingredient in red wine could be the key to a longer life.
The ‘miracle ingredient’ resveratrol credited with anti-ageing powers, and the ability to work against cancer, heart disease and obesity, really does boost the body’s supply of cell energy, claim researchers.
But it is only ‘switched on’ in the presence of a gene called SIRT1 that is the key to longevity and energy.
Previous studies have shown the plant compound resveratrol improves the health of mice fed a high-fat diet and increases their lifespan.
But there has been controversy about whether it really does hold back the march of time, with conflicting results from some studies.
Now US scientists say they have solved the mystery and brought closer the prospect of a drug that would give the equivalent health benefits of 8,000 bottles of red wine.
They found the ingredient boosts the activity of mitochondria, the cell’s energy supplier, which is essential for longevity and overall health.
Lead researcher Professor David Sinclair of Harvard Medical School, Boston, said ‘The results were surprisingly clear.
‘Without the mitochondria-boosting gene SIRT1, resveratrol does not work.’ The latest study showed how resveratrol enhances the energy-generating activity of cells via a longevity gene called SIRT1.
But resveratrol only works when a gene called SIRT1 is present - but it's not known if all humans have it
Researchers are already looking at molecules that mimic the effect of resveratrol by targeting SIRT1. Such compounds could form the basis of future drugs that extend disease-free lifespan.
The effect of resveratrol on SIRT1 had been demonstrated in yeast, worms and flies before but never on higher animals.
The experiments involved a new strain of laboratory mouse whose SIRT1 gene can be successfully switched off.
When adult mice were given low doses of resveratrol with SIRT1 disabled, no effect was seen on the energy producing heart of the cells.
But mice with normal SIRT1 showed dramatic increases in energy after exposure to resveratrol.
The findings are published today in the journal Cell Metabolism (must credit).
Professor Sinclair said the new approach removed barriers to developing resveratrol for use in people, with drugs already being tested. The first could be available in three years.
He said ‘Our paper shows that SIRT1 is front and centre for any dose of resveratrol.’ Research last year suggested that such drugs allowed mice to escape the consequences of a bad diet and extended the lives of those eating junk food.
||||| How That Glass of Red Wine Might Help You Live Longer
Mouse study suggests synthetic form of compound found in grapes deserves a look
By Jenifer Goodwin
HealthDay Reporter
TUESDAY, May 1 (HealthDay News) -- Researchers have found new evidence showing that resveratrol, a compound found in red wine, may play a role in preventing cell aging.
The study in rodents found that when mice had a particular gene -- SIRT1 -- knocked out, or turned off, resveratrol had no effect on them. But tests of muscle tissue in mice with a normal SIRT1 gene that were given resveratrol found that the substance boosted mitochondrial function.
Mitochondria provide the energy that cells need to function. A decrease in mitochondrial energy production has been linked to a variety of diseases, including diabetes and Alzheimer's disease, as well as to the aging process itself, said senior study author David Sinclair, a professor of genetics at Harvard Medical School in Boston.
But don't go reaching for that Chianti yet. Yes, resveratrol is found in the skin of red grapes. But "the amounts we gave to our mice would be like drinking 100 glasses of red wine a day," Sinclair said.
Instead, the goal is to develop synthetic resveratrol compounds that activate SIRT1 and could be taken as medication. "My colleagues are in the middle of developing better molecules that we hope will be medicines that will be used to treat diseases of aging, not to extend lifespan, though that may be a side effect," Sinclair said.
The study is in the May 1 issue of Cell Metabolism.
While previous studies have also suggested that resveratrol may have anti-aging properties, the precise mechanism of resveratrol has been controversial. Several studies, including work with yeast, worms and flies, have found that resveratrol acts on a class of seven genes known as sirtuins and, in human cells, SIRT1 in particular.
But other researchers have argued that resveratrol may work by activating a separate energy pathway called AMPK, which is also related to mitochondrial energy production but does not involve sirtuin genes.
Testing the effect of resveratrol on SIRT1 in mice was difficult, Sinclair said. Mice that have their SIRT1 gene deleted are born with developmental defects and are unsuitable for experiments, he explained.
So Sinclair and two graduate students, Nathan Price and Ana Gomes, worked for years to come up with a method for knocking out SIRT1 in healthy adult mice.
"Our paper found you absolutely require the SIRT1 gene for resveratrol to improve the metabolism of the mice," Sinclair said.
The paper also showed that the AMPK pathway was activated in mice given high doses of resveratrol, yet there was no benefit to mitochondrial function. There was no effect on AMPK in mice given a lower dose of resveratrol.
Sinclair is co-founder and a consultant for Sirtris Pharmaceuticals Inc., which is developing resveratrol-like molecules for use as treatment for age-related diseases. In 2010, according to news reports, the company, which is owned by GlaxoSmithKline, halted clinical trials of resveratrol, but Sinclair said the company continues to develop improved synthetic molecules.
George Vlasuk, CEO of Sirtris, said the new findings offer the "first definitive evidence" for a direct link between SIRT1 and the metabolic benefits of resveratrol.
"The work by [first author] Price et al. strongly supports the basic rationale being pursued at Sirtris, which focuses on the development of small-molecule compounds that directly activate the enzymatic activity of SIRT1 as a new therapeutic approach to many diseases of aging," Vlasuk wrote in an email to the journal.
Philippe Marambaud, an investigator at the Litwin-Zucker Center for Research in Alzheimer's Disease and Memory Disorders at the Feinstein Institute for Medical Research in Manhasset, N.Y, said the new research adds to a body of evidence that resveratrol can potentially combat aging by boosting mitochondrial activity.
"In this study, by using an elegant adult-inducible SIRT1 knock-out mouse model, the authors now provide compelling evidence that SIRT1 is required in vivo [in the animal] for the effect of resveratrol on AMPK activation and on mitochondrial function," Marambaud said.
While studies involving animals can be useful, they frequently fail to produce similar results in humans.
"A mouse model is not a human being, especially when you are genetically manipulating this animal model, you want to be very careful," Marambaud said. "This field has been extremely controversial. We should be very careful about claiming the importance of resveratrol for medical purposes. We have to wait and see, but this study is a big step forward."
More information
The U.S. Centers for Disease Control and Prevention has more on healthy aging.
SOURCES: David Sinclair, Ph.D., professor of genetics, Harvard Medical School, Boston; Philippe Marambaud, Ph.D., investigator, Litwin-Zucker Center for Research in Alzheimer's Disease and Memory Disorders, Feinstein Institute for Medical Research, Manhasset, N.Y.; May 1, 2012, Cell Metabolism
Last Updated: May 01, 2012
Copyright © 2012 HealthDay. All rights reserved. |||||
A summary of this is? | – Scientists have unlocked the mystery of a special ingredient in red wine that could increase lifespan and promote health in humans. The organic compound resveratrol aids the body by jump-starting the activity of mitochondria—the power suppliers of cells, reports the Daily Mail. Resveratrol, which occurs naturally in red wine, is credited with combating cancer, obesity, and aging. In previous experiments, resveratrol prolonged the lifespan of mice that were fed a junk food diet. Scientists behind the current study found that the plant compound does not work without a specific gene, SIRT1, and their research could lead to drugs that mimic the effects of resveratrol. That way, people don't have to become heavy drinkers to get the benefits: "The amounts we gave to our mice would be like drinking 100 glasses of red wine a day," says one researcher, according to HealthDay. | multi_news_1_0_0 |
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Researchers at McMaster University have found that a single minute of very intense exercise produces health benefits similar to longer, traditional endurance training.
The findings put to rest the common excuse for not getting in shape: there is not enough time.
"This is a very time-efficient workout strategy," says Martin Gibala, a professor of kinesiology at McMaster and lead author on the study. "Brief bursts of intense exercise are remarkably effective."
Scientists set out to determine how sprint interval training (SIT) compared to moderate-intensity continuous training (MICT), as recommended in public health guidelines. They examined key health indicators including cardiorespiratory fitness and insulin sensitivity, a measure of how the body regulates blood sugar.
A total of 27 sedentary men were recruited and assigned to perform three weekly sessions of either intense or moderate training for 12 weeks, or to a control group that did not exercise).
The McMaster team has previously shown that the SIT protocol, which involved three 20-second 'all-out' cycle sprints, was effective for boosting fitness. The workout totalled just 10 minutes, including a 2-minute warm-up and 3-minute cool down, and two minutes of easy cycling for recovery between the hard sprints.
The new study compared the SIT protocol with a group who performed 45 minutes of continuous cycling at a moderate pace, plus the same warm-up and cool down. After 12 weeks of training, the results were remarkably similar, even though the MICT protocol involved five times as much exercise and a five-fold greater time commitment.
"Most people cite 'lack of time' as the main reason for not being active," according to Gibala. "Our study shows that an interval-based approach can be more efficient -- you can get health and fitness benefits comparable to the traditional approach, in less time."
Gibala, who has studied has been studying interval training for more than a decade. O, was the first researcher to show that a few minutes per week of intense exercise produced benefits similar to longer, continuous workouts. Over time, his team has experimented with different protocols in an effort to identify the most time-efficient exercise strategies.
"The basic principles apply to many forms of exercise," he says. "Climbing a few flights of stairs on your lunch hour can provide a quick and effective workout. The health benefits are significant."
The findings are published online in the journal PLOS ONE. ||||| Peak oxygen uptake increased after training by 19% in both groups (SIT: 32±7 to 38±8; MICT: 34±6 to 40±8ml/kg/min; p<0.001 for both). Insulin sensitivity index (CS I ), determined by intravenous glucose tolerance tests performed before and 72 hours after training, increased similarly after SIT (4.9±2.5 to 7.5±4.7, p = 0.002) and MICT (5.0±3.3 to 6.7±5.0 x 10 �?�4 min -1 [μU/mL] -1 , p = 0.013) (p<0.05). Skeletal muscle mitochondrial content also increased similarly after SIT and MICT, as primarily reflected by the maximal activity of citrate synthase (CS; P<0.001). The corresponding changes in the control group were small for VO 2 peak (p = 0.99), CS I (p = 0.63) and CS (p = 0.97).
The purpose of the present study was to compare the effects of 12 weeks of SIT or MICT on insulin sensitivity and other indices of cardiometabolic health including cardiorespiratory fitness and skeletal muscle mitochondrial content in sedentary men. The two protocols differed markedly with respect to total exercise volume and time commitment: SIT involved 1 minute of intense intermittent exercise within a 10-minute session, whereas MICT consisted of 50 minutes of moderate-intensity continuous exercise. We hypothesized that compared to a non-training control group (CTL), SIT and MICT would similarly increase insulin sensitivity based on the intravenous glucose tolerance test method, cardiorespiratory fitness as determined by a peak oxygen uptake (VO 2peak ) test and mitochondrial content as reflected by the maximal activity of citrate synthase.
Given that Wingate-based SIT involves ~20–30 minutes per session, not including warm-up or cool-down, the purported “time efficiency” of this type of training has been questioned [ 14 ]. Recent studies have shown that very brief SIT protocols involving ≤10 min per session elicit adaptations similar to longer SIT protocols and MICT [ 15 – 17 ]. For example, a cycling protocol involving three, 20-second �?all-out’ sprints, within a 10 minute training session including warm-up and cool-down, improved cardiorespiratory fitness and reduced 24-hour average blood glucose concentration in overweight adults when performed three times per week for 6 weeks [ 17 ]. No study has directly compared this type of very brief SIT protocol to traditional endurance training, nor measured changes in glycemic control using a robust measure of insulin sensitivity.
In contrast to traditional endurance training, sprint interval training (SIT) is characterized by brief intermittent bursts of relatively intense exercise separated by periods of low-intensity exercise for recovery [ 9 ]. A commonly studied SIT model is repeated Wingate Tests; typically, four to six 30-second “all-out” cycling efforts are performed per session, interspersed by 4 minutes of recovery. Studies that have directly compared several weeks of Wingate-based SIT to moderate-intensity continuous training (MICT) have reported similar improvements in cardiorespiratory fitness [ 10 ], skeletal muscle oxidative capacity [ 10 , 11 ] and insulin sensitivity based on oral glucose tolerance tests [ 12 , 13 ].
Regular exercise training is well accepted as an effective therapeutic intervention for the prevention and treatment of many chronic diseases, including type 2 diabetes [ 1 , 2 ]. Endurance exercise training enhances cardiorespiratory fitness [ 3 ], induces skeletal muscle remodelling towards a more oxidative phenotype [ 4 ] and promotes favourable changes in insulin sensitivity [ 1 ]. These well-established health benefits provide support for current physical activity guidelines that recommend 150 minutes of moderate-intensity or 75 minutes of vigorous-intensity aerobic physical activity per week [ 5 – 7 ]. Despite the association between low amounts of physical activity and increased risk of many chronic diseases, the prevalence of physical inactivity is higher than that of all other modifiable risk factors [ 2 ]. The reasons for not engaging in regular physical activity are numerous and complex, but “lack of time” remains one of the most commonly cited barriers [ 8 ]. Therefore, developing more time-efficient, yet equally effective exercise strategies are urgently needed.
Baseline characteristics ( Table 1 ) were analyzed using a one-way (group) analysis of variance (ANOVA). Muscle, blood, VO 2 peak and body composition data were analyzed using a two-way ANOVA with the between factor, group (levels: SIT, MICT, CTL) and the within factor, time (levels: pre- and post-training for all variables except for VO 2 peak which also included a mid-training time point). Significant group x time interactions (p<0.05) were analyzed using a Tukey’s honestly significant difference post hoc test. All analyses were conducted using SPSS software, and significance was set at p<0.05. Data are presented as means±S.D. for n = 10 (MICT), n = 9 (SIT) and n = 6 (CTL). Due to difficulties during data collection, we report n = 9 (MICT) and n = 5 (CTL) for body composition data and n = 8 (SIT) for blood analyses.
For western blotting, a piece of muscle (~30mg) was homogenized in RIPA buffer as previously described [ 17 ] and western blot analysis was conducted using established techniques [ 17 , 24 ]. ImageJ software was used to quantify the optical density of protein bands. α-tubulin (Cell Signaling Technology, #2125), which did not change following training (p = 0.85), was used as a loading control. The following primary antibodies from Mitosciences were used: NDUFA9 (MS111), CII-70 kDa subunit (MS204), CIII-Core protein 2 (MS304), CIV subunit IV (MS408), ATP synthase α-subunit (MS507) and GLUT4 (Millipore, AB1345).
For enzyme activity, one piece of muscle (~25mg) was homogenized as described previously [ 17 ]. The maximal activities of citrate synthase (CS) and 3-β-hydroxyacyl CoA dehydrogenase (β-HAD) were determined using established techniques [ 23 ]. Samples were run in duplicate and the intra-assay coefficient of variation for CS and β-HAD were 3.0 and 6.5%, respectively. Protein concentration was determined (BCA Protein Assay, Pierce, USA) and enzyme activity is expressed as mmol/kg protein/h.
Plasma glucose was analyzed (Pointe Scientific, USA), and serum insulin was measured with ELISA (ALPCO Immunoassays, USA). The insulin sensitivity index (CS I ) from the 50-minute IVGTT was calculated as proposed by Tura et al. [ 19 ]. CS I is highly correlated with the Minimal Model insulin sensitivity index (S I ) obtained from a 3-hour IVGTT, as well as the glucose infusion rate during a hyperinsulinemic-euglycemic clamp [ 19 ]. This method has also been used to assess insulin sensitivity in response to acute exercise [ 20 , 21 ], and has greater reproducibility than the Matsuda composite index (M ISI ) derived from an OGTT [ 20 ]. Briefly, CS I was calculated as follows: where α is a scaling factor (0.604), K G is the glucose disappearance rate (mmol/L; calculated as the slope of log [glucose]), ΔAUC INS is the insulin area under the curve above basal (uIU/ml) and T is the time between 10 and 50 minutes (40 minutes) from which K G and ΔAUC INS were calculated [ 19 ].
Training involved a lead-in phase, in which one session was completed in week 1, and two sessions in week 2. Exercise was performed three times per week thereafter, with the exception of week 7 where two sessions were replaced with a “mid-training assessment” for VO 2 peak and arterial ultrasound imaging (a collaborative measure not reported in the present manuscript). During training, a HR monitor recorded HR every 5 seconds, from which average HR during each session was determined. The SIT protocol consisted of 3x20-second �?all-out’ cycling efforts against 0.05kg/kg body mass, separated by 2 minutes of low-intensity cycling (50W). The MICT protocol consisted of 45 minutes of continuous cycling at ~70% HR max . A 2-minute warm-up and 3-minute cool-down at 50W were included, resulting in 10- and 50-minute sessions for SIT and MICT, respectively. To accommodate progression, training loads were adjusted to maintain the desired relative exercise intensity. Ratings of perceived exertion (RPE; Borg 6–20 scale) were recorded at the end of each sprint (SIT) or at 15, 30 and 45 minutes of exercise (MICT), on the 1 st , 15 th and 30 th sessions. Participants in CTL did not report to the laboratory during the 12-week intervention, with the exception of week 7 for mid-assessment.
At least 5 days following the muscle biopsy, exercise familiarization took place. Participants in SIT performed two 20-second �?all-out’ sprints on an electronically-braked ergometer (Veletron, RacerMate, USA). Participants in MICT were fitted with a heart rate (HR) monitor (Polar A3, Lake Success, USA) and cycled on an ergometer (Kettler, Ergo Race I, Germany) for ~20 minutes to determine the workload that elicited 64–76% of maximal heart rate (HR max ). The target HR for MICT was based on the classification for “moderate-intensity” put forth by the American College of Sports Medicine [ 6 ].
Approximately 2 days later, a resting muscle biopsy from the vastus lateralis (~100mg) was obtained using the Bergström needle adapted with suction, as described previously [ 18 ]. Briefly, a single muscle sample (~100 mg) was obtained from the vastus lateralis under local anesthesia (1% lidocaine) using a Bergström needle adapted with suction. Samples were sectioned into several pieces, snap frozen in liquid nitrogen and stored at -80°C for later analysis.
Approximately 5 days later and following a 10-hour overnight fast, participants underwent a body composition test and a 50-minute intravenous glucose tolerance test (IVGTT). Participants consumed a standardized meal the evening before the visit consisting of 561±99kcal (47±2% carbohydrate, 31±3% fat and 22±4% protein). Fat mass was determined through air-displacement plethysmography (BodPod®,COSMED). Subsequently, a trained nurse inserted two indwelling catheters into forearm veins (one in each arm). A fasting blood sample (12ml) was obtained from the “sampling arm”, and glucose (0.5g/kg up to 35g) was manually delivered to the contralateral “infusion arm” over 3 minutes. A 38±2% glucose solution (Hospira LifeCare) was used in a total volume of 90ml. Blood samples (8ml) were obtained from the “sampling arm” every 10 minutes for 50 minutes post-infusion. Plasma and serum were separated by centrifugation and stored at -80°C.
Participants performed an incremental VO 2 peak test on an electronically-braked cycle ergometer (Lode Excalibur Sport V 2.0, The Netherlands), as described previously [ 17 ]. Briefly, following a 1-minute warm-up at 50 W, the resistance was increased by 1 W every 2 seconds until exhaustion or when pedal cadence fell below 50 rpm. For all tests an RER >1.1 was achieved. Oxygen consumption and carbon dioxide production data were acquired through a metabolic cart with an online gas collection system (Moxus, AEI Technologies, PA), and VO 2 peak was defined as the highest average oxygen consumption over 30 seconds.
Twenty-seven sedentary men took part in the study. Participants were generally deemed inactive based on an International Physical Activity Questionnaire score of less than 600 MET-minutes per week. Participants were matched for age, BMI and VO 2 peak, and assigned to SIT, MICT or CTL. One subject in each of the two training groups dropped out for reasons unrelated to the study, resulting in n = 9, 10 and 6 in SIT, MICT and CTL, respectively ( Table 1 ). The experimental protocol was approved by the Hamilton Integrated Research Ethics Board. All participants provided written informed consent.
Measured in muscle biopsy samples obtained from the vastus lateralis before (PRE) and 96 h after (POST) the 12-week intervention in MICT, SIT and CTL. Maximal activity of citrate synthase (A), individual changes in maximal activity of citrate synthase (B) and protein content of various subunits from complexes in the electron transport chain (C). Representative western blots are shown. Values are means ± S.D. * p<0.05, vs. same group at PRE; † p<0.05, vs. CTL at POST.
The maximal activity of CS increased by 48 and 27% after 12 weeks of SIT (p<0.0001) and MICT (p = 0.004), respectively, and was higher than CTL post-training (p = 0.03 for both; Fig 3 ). Training also increased the protein of Complex II-70kDa (SIT: p<0.001; MICT: p = 0.02) Complex III-Core protein 2 (SIT: p<0.001; MICT: p = 0.003), COX subunit IV (SIT: p<0.001; MICT: p = 0.001) and ATP Synthase α-subunit (SIT: p = 0.001; MICT: p = 0.004), all of which were higher than CTL post-training (p<0.05; Fig 3 ). The absolute increase in β-HAD maximal activity was 28% and 17% in SIT and MICT, respectively, compared to a change of -2% in CTL, but a time by group interaction was not observed (p = 0.16). GLUT4 protein content increased by ~50% after SIT (p = 0.001) and MICT (p-0.002), whereas there was little change in CTL (p = 0.50; Table 2 ).
CS I increased by 53 and 34% after 12 weeks of SIT (p = 0.002) and MICT (p = 0.013; Fig 2 ) whereas the change was small in CON (p = 0.64). Glucose AUC during the 50-minute IVGTT was reduced to a greater extent after SIT (p<0.001) and MICT (p = 0.001) compared to CON (p = 0.32). These data and other fasting indices of glycemic control are summarized in Table 2 .
VO 2 peak increased compared to pre-training by ~12% after 6 weeks of both SIT and MICT (p<0.001 for both). VO 2 peak increased further after 12 weeks compared to 6 weeks (p = 0.007 and p = 0.005 for SIT and MICT, respectively), resulting in a 19% overall increase versus pre-training (p<0.001 for both; Fig 1 ). The CTL group showed only small changes from baseline when measured at both 6 (p = 0.43) and 12 (p = 0.99) weeks.
A total of 31±1 and 32±2 sessions were completed in SIT and MICT, respectively. Mean HR, averaged over all training sessions, was 79±4% and 71±5% of HR max for SIT and MICT, respectively. Mean RPE, measured during the 1 st , 15 th and 30 th exercise sessions, was 16±1 for SIT and 13±1 for MICT. Mean total work was ~60 and ~310kJ per session for SIT and MICT, respectively. Body mass remained similar over the course of the study in all groups. Percent body fat decreased after SIT (p = 0.011) and MICT (p = 0.011) whereas there was little change in CON (p = 0.12) ( Table 2 ). Change scores with 95% confidence intervals are available in a supplemental file for all training-induced outcomes summarized in Table 2 ( S1 Fig ).
Discussion
The major novel finding from the present study was that 12 weeks of SIT in previously inactive men improved insulin sensitivity, cardiorespiratory fitness, and skeletal muscle mitochondrial content to the same extent as MICT, despite a five-fold lower exercise volume and training time commitment. SIT involved 1 minute of intense intermittent exercise, within a time commitment of 10 minutes per session, whereas MICT consisted of 50 minutes of continuous exercise at a moderate pace. A few previous studies have reported similar improvements in skeletal muscle remodeling and markers of health status after SIT and MICT lasting up to 6 weeks [10,11,13]. The present work was intended to be more ambitious in scope as compared to previous studies that compared SIT versus MICT. Specifically, it involved a SIT protocol that required less total time commitment than in previous studies (i.e., 10 vs ~25 min), a training program that was twice as long (i.e., 12 vs 6 wk), a more robust measure of insulin sensitivity (i.e., an IVGTT vs OGTT and fasting blood measures of insulin sensitivity), and inclusion of a non-training control group.
Cardiorespiratory fitness Low cardiorespiratory fitness is a strong independent risk factor for cardiovascular disease and all-cause mortality [25,26]. It has been known for decades that interval training involving brief hard efforts is a potent stimulus to improve cardiorespiratory fitness [27,28]. Recent studies have shown that protocols involving as little as one minute of sprint interval training per session can be very effective in this regard [15–17]. Prior to the present work, no study had directly compared this type of SIT protocol with traditional endurance training as reflected in public health guidelines. We found a strikingly similar 19% improvement in VO 2 peak after 12 weeks of SIT and MICT, which compares favorably with the typical change reported after several months of traditional endurance training [29,30]. Exercise intensity is generally regarded to be the more critical factor in the trainability of VO 2 peak, with higher intensity exercise conferring larger improvements in cardiorespiratory fitness when exercise is matched for total energy expenditure [31–34]. This message was recently reinforced by Ross et al. [35], who found that low-intensity exercise (50% VO 2 peak) performed for about 150 minutes per week, over 24 weeks, may not be sufficient to improve cardiorespiratory fitness for a substantive proportion of adults. In contrast, the present data show it is possible for previously sedentary individuals to markedly improve VO 2 peak by performing a total of 3 minutes per week of short intense bursts of exercise, within a 30-minute time commitment, over 12 weeks. The absolute change in relative VO 2 peak was ~6 ml/kg/min in both SIT and MICT, which corresponds to ~1.7 metabolic equivalents (METs). These findings are noteworthy given that a 1-MET increase in cardiorespiratory is comparable to a 7 cm decrease in waist circumference, a 5 mmHg lowering of systolic blood pressure or a 1 mmol/L reduction in fasting plasma glucose, in terms of relative risk reduction in all-cause and cardiovascular disease mortality [25]. Unfit individuals also have twice the risk of death regardless of BMI, while fit and overweight/obese adults have similar mortality risk as their normal weight counterparts [26]. The precise mechanisms responsible for the improved cardiorespiratory fitness observed after SIT and MICT in the present study are unknown. The increase in VO 2 peak after traditional endurance training is generally attributed to an enhanced cardiac output owing to a greater stroke volume, although numerous factors may contribute to this adaptive response [3]. A limited number of studies have assessed cardiovascular adaptations to SIT and these have yielded equivocal results, likely due in part to differences in experimental design as well as the specific analytical procedures employed [36,37]. Increases in resting stroke volume have been observed after 7 weeks of SIT using cardiac MRI [38], as has stroke volume during submaximal exercise based on the CO 2 -rebreathing technique following 4 weeks of SIT [36]. Conversely, MacPherson et al. [37] reported no changes in maximal cardiac output based on the acetylene non-rebreathing technique after 6 weeks of run-based SIT. It has also been suggested that peripheral factors that enhance oxygen extraction may contribute to SIT-induced improvements in VO 2 peak, at least over the short-term [39]. Additional studies are warranted to clarify both the time course and precise mechanisms responsible for the improved cardiorespiratory fitness after SIT compared to MICT.
Insulin sensitivity Perhaps the most striking and novel finding form the present work was the similar increase in insulin sensitivity after SIT and MICT. It has previously been shown that SIT improves indices of glycemic control, as determined by the hyperinsulinemic-euglycemic clamp method [40], continuous glucose monitoring [17] and oral glucose tolerance tests [13,41]. In the present investigation, we employed a 50-minute IVGTT (CS I ), which was recently validated by Tura and colleagues as a robust marker of insulin sensitivity [19]. The technique was shown to be highly correlated with the gold standard glucose infusion rate obtained during a hyperinsulinemic-euglycemic clamp [19], and have greater reproducibility than M ISI derived from OGTTs [20]. Houmard et al. [42], using the IVGTT method, previously reported that a continuous training protocol involving 170 minutes of exercise per week improved insulin sensitivity to a greater extent than 115 minutes per week, regardless of exercise intensity and volume. Several recent reports, however, suggest that when exercise is matched for total volume or energy expenditure, higher-intensity exercise training confers larger improvements in insulin sensitivity in individuals with obesity [43], metabolic syndrome [33] and type 2 diabetes [31,34]. Our findings support this general concept and demonstrate that a surprisingly small amount of high-intensity exercise can be as effective as a large volume of moderate-intensity continuous exercise for improving insulin sensitivity. The potential mechanisms that mediate exercise training-induced increases in whole-body insulin sensitivity are obviously complex [1]. With respect to potential changes in skeletal muscle that might in part explain the improved insulin sensitivity, we found similar increases in GLUT4 protein content after the two training protocols despite large differences in exercise volume. SIT and MICT have also been shown to similarly increase skeletal muscle microvascular density [44], which is associated with improved glucose transport and insulin sensitivity [44,45]. It is also possible that the improvement in mitochondrial content [1] or an increased capacity for intramuscular triglyceride utilization [12] could be involved.
Mitochondrial content Reduced skeletal muscle mitochondrial content is associated with aberrant lipid handling, poor insulin sensitivity and an impaired metabolic health profile [46]. Physical activity increases mitochondrial content and insulin sensitivity, but it remains unclear whether these effects are directly linked [1,46]. The maximal activity of citrate synthase is a commonly measured marker that is strongly associated with mitochondrial content in human skeletal muscle [47]. A novel finding from the present work was the similar increase in citrate synthase maximal activity after 12 weeks of SIT and MICT, despite the large difference in total exercise volume. We also observed similar increases in the protein content of various subunits from complexes in the electron transport chain, highlighting similar mitochondrial adaptation in both groups. We did not examine the time course of skeletal muscle remodeling, but the mean increase in CS maximal activity after training was similar to the 30–40% increase that we previously observed after 2 [48] and 6 weeks [10,17] of both SIT and MICT. Consistent with the recent observations by Egan et al. [49], who examined the time course of increased mitochondrial content in response to 14 sessions of endurance training, these data seem to imply that much of the increase in mitochondrial content occurs relatively early in response to training. Given the much lower exercise volume involved with SIT, these data also seemingly suggest that training intensity, rather than volume, may be the more critical determinant of the improvement in mitochondrial content. As recently reviewed by Bishop et al. [50], a surprisingly small number of studies have investigated the impact of varying training intensity and volume on changes in mitochondrial function and content in human skeletal muscle, and additional work in this regard is warranted. ||||| Photo
Phys Ed Gretchen Reynolds on the science of fitness.
For many of us, the most pressing question about exercise is: How little can I get away with? The answer, according to a sophisticated new study of interval training, may be very, very little. In this new experiment, in fact, 60 seconds of strenuous exertion proved to be as successful at improving health and fitness as three-quarters of an hour of moderate exercise.
Let me repeat that finding: One minute of arduous exercise was comparable in its physiological effects to 45 minutes of gentler sweating.
I have been writing for some time about the potential benefits of high-intensity interval training, a type of workout that consists of an extremely draining but brief burst of exercise — essentially, a sprint — followed by light exercise such as jogging or resting, then another sprint, more rest, and so on.
Athletes rely on intervals to improve their speed and power, but generally as part of a broader, weekly training program that also includes prolonged, less-intense workouts, such as long runs.
But in the past few years, exercise scientists and many of the rest of us have become intrigued by the idea of exercising exclusively with intervals, ditching long workouts altogether.
The allure of this approach is obvious. Interval sessions can be short, making them a boon for anyone who feels that he or she never has enough time to exercise.
Previously, I have written about a number of different interval programs, involving anywhere from 10 minutes of exhausting intervals in a single session to seven minutes, six, four and even fewer. Each program had scientific backing. But because of time and funding constraints, most studies of interval training have had limits, such as not including a control group, being of short duration or studying only health or fitness results, not both.
Consequently, fundamental questions have remained unanswered about just how well these very short, very intense workouts really stack up against traditional, endurance-style training.
So scientists at McMaster University in Hamilton, Ontario, who had themselves conducted many of those earlier studies of interval training, decided recently to mount probably the most scientifically rigorous comparison to date of super-short and more-standard workouts.
They began by recruiting 25 out-of-shape young men and measuring their current aerobic fitness and, as a marker of general health, their body’s ability to use insulin properly to regulate blood sugar levels. The scientists also biopsied the men’s muscles to examine how well their muscles functioned at a cellular level.
Then the researchers randomly divided the men into three groups. (The scientists plan to study women in subsequent experiments.) One group was asked to change nothing about their current, virtually nonexistent exercise routines; they would be the controls.
A second group began a typical endurance-workout routine, consisting of riding at a moderate pace on a stationary bicycle at the lab for 45 minutes, with a two-minute warm-up and three-minute cool down.
The final group was assigned to interval training, using the most abbreviated workout yet to have shown benefits. Specifically, the volunteers warmed up for two minutes on stationary bicycles, then pedaled as hard as possible for 20 seconds; rode at a very slow pace for two minutes, sprinted all-out again for 20 seconds; recovered with slow riding for another two minutes; pedaled all-out for a final 20 seconds; then cooled down for three minutes. The entire workout lasted 10 minutes, with only one minute of that time being strenuous.
Both groups of exercising volunteers completed three sessions each week for 12 weeks, a period of time that is about twice as long as in most past studies of interval training.
By the end of the study, published in PLOS One, the endurance group had ridden for 27 hours, while the interval group had ridden for six hours, with only 36 minutes of that time being strenuous.
But when the scientists retested the men’s aerobic fitness, muscles and blood-sugar control now, they found that the exercisers showed virtually identical gains, whether they had completed the long endurance workouts or the short, grueling intervals. In both groups, endurance had increased by nearly 20 percent, insulin resistance likewise had improved significantly, and there were significant increases in the number and function of certain microscopic structures in the men’s muscles that are related to energy production and oxygen consumption.
There were no changes in health or fitness evident in the control group.
The upshot of these results is that three months of concerted endurance or interval exercise can notably — and almost identically — improve someone’s fitness and health.
Neither approach to exercise was, however, superior to the other, except that one was shorter — much, much shorter.
Is that reason enough for people who currently exercise moderately or not at all to begin interval training as their only workout?
“It depends on who you are and why you exercise,” said Martin Gibala, a professor of kinesiology at McMaster University who oversaw the new study.
“If you are an elite athlete, then obviously incorporating both endurance and interval training into an overall program maximizes performance. But if you are someone, like me, who just wants to boost health and fitness and you don’t have 45 minutes or an hour to work out, our data show that you can get big benefits from even a single minute of intense exercise.”
Related:
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What is a one-paragraph summary of the above article? | – "Most people cite 'lack of time' as the main reason for not being active," professor of kinesiology Martin Gibala says in a press release. But that's no longer a valid excuse for not getting in better shape. According to a study published Tuesday in PLOS One, Gibala and fellow researchers have shown that just one minute of go-for-broke exercising is as beneficial as a 45-minute moderate workout. "If you are someone, like me, who just wants to boost health and fitness and you don’t have 45 minutes or an hour to work out, our data show that you can get big benefits from even a single minute of intense exercise,” Gibala tells the New York Times. Researchers split 27 "sedentary men" into three groups. The first group continued not working out as usual, the second group did 45 minutes of moderate pedaling on a stationary bike plus five minutes of warm-up/cool-down, and the final group did 10 minutes of sprint interval training. That training included just the aforementioned one minute of intense exercise: three 20-second intervals of pedaling as hard as possible, which alternated with two two-minute recovery periods of very slow pedaling and five total minutes of warm-up/cool-down. Both exercising groups worked out three times a week for 12 weeks and showed nearly identical improvements in their health and fitness. (This man lost 70 pounds eating nothing but potatoes.) | multi_news_1_0_0 |
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Article:
Close Fitness tracker for pets keeps cats and dogs healthy
There is a new wearable that is bringing new meaning to having a personal trainer at users' fingertips.
If a consumer is into health and fitness, then there is a really good chance they own a wrist-worn wearable of some sort. However, not everyone chooses to wear their device all day, especially when at work or on a date — no matter how fashionable. That means that the user can't get a really clear overview of their daily health metrics in order to improve or reach their goals. Plus, there are so many options out there, it may be hard to tell which is the best and what really sets them all apart.
Forget the watch-like wearables that all feel like slightly different versions of each other and go for this new health tracker that is worn like a ring.
BioRing is not only a more comfortable solution as far as wearables go, but it also has impressive tracking capabilities that make it even more attractive to consumers.
"Having a small ring around your finger gives you more flexibility in your daily life," Michael Johnson, co-founder of BioRing, told Tech Times. "Many wrist-worn wearables are big and feel unnatural to wear. Our vision was to create something that works with any outfit and in any situation."
The device is equipped with three sensors that enable BioRing to measure more than just the standard calories and steps taken — although it does measure distance and steps with its 3-axis accelerometer.
BioRing also has a bioimpedance sensor that is able to give insights into nutrition such as calorie, carb, fat and protein intake. The sensor does so by measuring the changes of fluid levels in the user's cells, which happens when carbs are broken down into glucose.
This data is then sent to the wearable's app, where the Sweden-based company has developed an algorithm to calculate caloric intake as well as a macro-nutrients breakdown. Since everyone's body is different, BioRing will learn each specific user's metabolic rhythm in just one week to give accurate data to that user and personalized health plans.
"Other fitness trackers only measure your calorie burn. BioRing measures both your calorie burn and your calorie intake automatically, giving you your calorie balance. If you are eating more calories that you are burning, you are gaining weight," Johnson said. "Our app is very user-friendly and works as your personal coach and helps you reach your weight goals unlike any other device."
The wearable also features an optical HR sensor to be able to measure heart rate, heart health and activity intensity. Other data measured includes sleep level, water level and stress level.
This makes BioRing a viable option for those who are looking to shed a few pounds, maintain a healthy lifestyle, improve their sleep patterns and stay hydrated. BioRing will alert the user to drink more water and tell them when they should relax to reduce their stress. Users will know the best time for them to wake up in the morning based on their sleep cycle and be nudged to get up and start moving.
The device has a vibration motor for alerts, is waterproof and syncs to its smartphone app via Bluetooth Smart, where all data is encrypted for users' privacy. It features a lithium polymer 35 mAh battery, with battery life lasting up to seven days on a single charge and needs only one hour of charging to get to 80 percent battery using the wireless charging station.
The ring is scratch-proof, made of ceramic zirconium, and it feels natural to wear since it contains no metals and comes in black and white color options.
"The trend is that people are demanding wearables that look good and work in their day to day lives," Johnson said.
BioRing is currently available via a crowdfunding campaign on Indiegogo. Backers can get the wearable, charging station, a start guide and a one-year warranty for the early bird price of $199 or two for $249, with estimated shipping for this November.
BioRing has already reached its $50,000 goal, raising more than $77,000 with a month still to go.
Source: Indiegogo
© 2017 Tech Times, All rights reserved. Do not reproduce without permission. ||||| When Telly Lau saw the ad for BioRing on her Facebook timeline, it seemed like exactly what she was looking for: a waterproof, wearable fitness tracker with a heart rate monitor that she could wear on her finger. It also said it could detect her calorie intake using technology that even medical researchers had yet to perfect. And Lau could get all this for just $219. She wouldn’t even have to pay for shipping from the company’s Stockholm headquarters.
If that sounds too good to be true, well, perhaps you can guess how this all turns out.
“Everything I was reading seemed to check out,” says Lau, a graphic designer in New York City. So, she bought the ring. Later, BioRing offered an extended warranty and 14-day full refund for $35. She bought that, too. She had never backed a crowdfunded product before and admits she was wary of backing a product with no reviews that she’d have to wait until November to receive. But she did think she would receive something.
BioRing started raising money through the crowdfunding site Indiegogo last June, and went on to raise nearly three-quarters of a million dollars before the campaign was mysteriously and suddenly closed by Indiegogo at the end of October. Over a month later and now past the promised delivery date, the product still hasn’t materialized and most of that money has disappeared — leaving thousands of backers like Lau in the lurch.
“I thought, worst case scenario: even if the movement tracking was off or the calorie intake capabilities were inaccurate, I could still benefit from having a compact waterproof heart rate sensor,” Lau says.
The worst case scenario is that Lau won’t get a ring at all. And around the time she gave BioRing her money, it began seeming that scenario is also the most likely.
Crowdfunded projects are always a bit of a tricky proposition — often, they are started by would-be entrepreneurs with good intentions but no track record or business experience, raising money for a dream idea. And they’ve failed before. The Coolest cooler raised more than ten million dollars on Kickstarter, but still hasn’t shipped all of its orders several years later. In 2014, Indiegogo ran another campaign for a fitness tracker called Healbe Gobe that made claims similar to BioRing’s, including that it could determine the wearer’s calorie intake. It raised over a million dollars before being released to reviews that said it didn’t do much of what it promised.
But BioRing looks like something entirely different. What if instead of a product that over-promised or hit some hurdles in the production process, the product never existed at all?
“It started off really, really well,” says Corey Herscu, the president of Herscu & Goldsilver, a marketing firm based in Toronto. H&G is part of a burgeoning cottage industry of companies that help crowdfunding campaigns get off the ground in exchange for a portion of the money those campaigns then raise. Indiegogo says H&G has helped raise nearly $3 million for seven other campaigns. When BioRing expressed interest in some marketing help, Indiegogo connected the two.
“It seemed too good to be true,” Herscu admits. But he spoke with a few people in the wearables industry who told him that what BioRing was proposing wasn’t impossible and decided the concept could do well on Indiegogo’s platform. H&G agreed to work on BioRing’s campaign in return for 10 percent of the money raised.
Meanwhile, Funded Today, which has helped raise nearly $35 million for 62 Indiegogo campaigns, also entered into an agreement with BioRing, for 25 percent of the money raised. That’s more than most PR firms ask for, but Funded Today pays out of pocket to place digital ads like the one Lau saw on her Facebook timeline. This allows cash-strapped campaigns to afford ads, which in turn helps them raise more money. (A third Indiegogo partner, Command Partners, was also in the mix, according to both H&G and Funded Today, but it did not respond to request for comment.)
As the campaign went live, BioRing’s PR companies went about pitching the product to the press, building BioRing’s social media presence, creating and placing digital ads, and making slick YouTube videos to show off the product and simulate how it would work. The campaign met its initial $50,000 goal very quickly, and it looked like everyone involved had a winner on their hands.
But not everyone was convinced the product was legit. Guy Lev Raz, a mechanical engineer and self-professed “compulsive crowdfunder,” came across BioRing’s campaign and was suspicious.
“After about five minutes of skimming it, my head exploded because I thought immediately this was an impossible product,” Raz says. The 3-D rendering of the inside of the BioRing, in his experience, “looked like someone who’d maybe seen a circuit and tried to copy it from memory and put wires all over the place where they shouldn’t be.” Not only that, but, Raz says, some of the components BioRing claimed it could pack in just 3.55 millimeters of space don’t exist in such small scales.
John Lewis, a freelance writer and editor, came across the BioRing campaign in July and wrote a blog post on LinkedIn warning that BioRing was promising a lot with no evidence that it could deliver on any of it. Raz saw Lewis’s post and invited him to co-moderate a Facebook group he runs dedicated to exposing possible crowdfunding scams. They tried to get the word out about BioRing. Raz even gave the campaign one dollar so he could post warnings in the comments section. (He says his dollar was promptly refunded, restricting his access.)
They found some more red flags: BioRing’s updates were frequent but usually offered more ways for backers to spend more money on product upgrades, rather than saying much about the progress of actually manufacturing the ring. The press write-ups featured prominently the campaign page that helped give the product legitimacy in the eyes of people like Lau simply recapped the company’s promises without questioning them. A Forbes article — perhaps the most recognizable name that wrote about BioRing — was posted on its contributor blogging platform, which means it wasn’t written by Forbes’ staff.
More This Crowdfunding Campaign Is Either A Scam Or A Massive Troll
And then there was BioRing’s most incredible claim: that it could detect how many calories its wearer consumed, and even which of those calories came from fat, protein, or carbohydrates. It said it could do all of this by detecting glucose levels in the wearer’s cells — a feat diabetes researchers have been trying to perfect for years, even decades. How had BioRing figured it out sooner? One co-founder, Michael Johnson, seemed to have some kind of medical technology experience, saying he worked was an “algorithm developer” at Elekta, which creates medical devices and software for cancer treatments. (This claim is dubious: Elekta tells Vocativ that it has no record of Johnson’s employment.) When Vocativ asked BioRing in September how it beat diabetes researchers to the punch, the response was brief and jargon-filled.
“BioRing doesn’t measure you [sic] blood glucose levels directly,” Johnson said. “It is equipped with a bio-impedance sensor that measures the flow of liquids in and out of your cells and our algorithms analyze the data to measure your glucose curve. We analyze your glucose curve and its properties to determine your calorie intake automatically. We don’t measure you [sic] blood glucose, we measure the dynamics of the changing fluid levels in your cells.”
The initial campaign ended in August. As per Indiegogo’s policies, the money raised was disbursed to BioRing two weeks later, around the beginning of September. But BioRing continued to raise money through Indiegogo’s “InDemand” program, which allows campaigners to keep getting contributions even after the campaign successfully concludes.
This would also have been the time to pay the marketing companies the tens of thousands of dollars they were owed. But H&G and Funded Today say that when they asked Johnson for the money (there are two other men named as BioRing’s co-founders, one of whom— James Lee — appeared in a video to describe how the ring worked, but Johnson appears to be the only person anyone had contact with), he kept putting them off. Funded Today’s co-founder, chairman, and in-house attorney, Thomas Alvord, says that when they got more aggressive in their attempts to collect and accused Johnson of fraud, he let loose with a profane screed on Skype that said they would never get the money, could never trace him to try to collect it or sue him, and that it was all being held in offshore accounts anyway. Johnson, who was now calling himself “Big Mike,” also threatened physical violence. “We had a great launch at your expense, you son of a bitch,” Big Mike concluded.
“He obviously has some serious issues going on,” Alvord says.
Soon after, Funded Today filed for arbitration, as per the terms of their agreement with BioRing, and Johnson exited the Skype chatroom. This was in mid-September. They haven’t heard from him since.
“No point in proceeding and getting an [arbitration] award if you don’t even know where the other party is so you can collect,” Alvord says. If anyone ever does manage to find Johnson, Alvord says Funded Today will sue both him and BioRing. In the meantime, he suggests that backers who were scammed report it to the Federal Trade Commission. The more who do, he says, the better the chances are that the FTC will launch an investigation.
As for H&G, Herscu says they gave up on ever getting paid by BioRing once they heard what Johnson said to Funded Today. They appealed to Indiegogo for help or at least to pause BioRing’s campaign. They say Indiegogo said there was nothing it could or would do. Indiegogo confirmed that it was alerted that BioRing was refusing to pay these third parties, but says that it does not act as a go-between between campaigns and backers or vendors.
In the meantime, the campaign stayed open. With little recourse, H&G turned to the one part of BioRing’s campaign it still had some control over: the social media accounts. Lewis and Raz had been a constant thorn in H&G’s side with their attempts to let the world know BioRing was a scam. Now, H&G turned BioRing’s official Facebook page over to them.
In mid-October, BioRing’s Facebook page, now under Lewis and Raz’s command, started warning backers that it was a scam and giving them instructions on how to get their money back. Lewis and Raz also set up an Indiegogo campaign of their own: “BioRing Scam — Get A Refund NOW!” It isn’t trying to raise any money; it basically just serves as another source of information for frustrated BioRing backers.
More Repairs To The Great Wall Of China Are Being Crowdfunded
At the end of October, Indiegogo finally closed the campaign for violating its terms of service. More than $200,000 was immediately refunded to backers — money raised that hadn’t been given to BioRing yet, Indiegogo says. The crowdfunding site refuses to say exactly which terms BioRing violated, just that whatever BioRing did wrong has nothing to do with the product itself.
Indiegogo maintains BioRing has a working prototype that it verified in video chats and emails, but the company said it wouldn’t speculate on whether the ring will ever see the light of day. BioRing said on its campaign page that rings would start being shipped in November. So far, no one reports having received one.
Most surprisingly, Indiegogo says it is still in contact with BioRing. If true, it may be the only one. Backers have been complaining for weeks that their comments and emails to BioRing have not been responded to. Funded Today and H&G haven’t heard from them in over a month. Other than the initial email sent months ago, BioRing has not responded to multiple requests for comment.
When Lau, one of the ring’s purchasers, saw BioRing’s Facebook page’s new posts claiming that it is a scam, she assumed it had been hacked. When BioRing didn’t take its page back after several days, she got suspicious.
“For a new company to sit idly by as their flagship product was being defamed on social media would mean they don’t care about their product,” Lau says. “Which, in turn, means there may not be a product at all.”
But by the time Lau realized something was wrong, the time Indiegogo gives to request a refund — 10 days for product purchased through InDemand — had long since expired. She is currently disputing the charges with her credit card company.
“If it works out for me, great,” she says. “Dodged a bullet. My money lives to see another day. If it’s gone, I just have to suck it up as stupid tax and know not to buy things that don’t exist (yet) ever again.”
The PR companies’ lesson has been much more expensive. They expected to be paid tens of thousands of dollars, and Funded Today spent its own money on the campaign. While Funded Today has the resources to absorb the cost, H&G is a much smaller operation. Herscu says BioRing nearly put it out of business.
“If it wasn’t for a project coming through with a check that helped us pay our rent, we would have had to close our doors,” Herscu says. He’s not sure he wants to work on a crowdfunded campaign ever again.
Indiegogo did tell Vocativ it will continue to improve its protocols for how it evaluates campaigns, though not exactly how. One way it could do this is to follow its rival Kickstarter’s lead. In 2012, Kickstarter announced that campaigns had to have a working, physical product before they are allowed to begin. Renderings and simulations were not enough.
“Indiegogo is basically fertile ground for every scammer who can fake a campaign,” Raz alleges. “And they take no legal responsibility for it.”
Raz and Lewis believe there are more Indiegogo scams out there, and they will continue as long anyone who can talk a good enough game can start a campaign on that platform for a product that can do something revolutionary and looks cool to boot.
“These [scam campaigns] are based on either pseudoscience or … pseudotechnology,” Raz says. “It’s enough to fool laypeople and technologically illiterate people and people who love buying tech but don’t understand how it works.”
At the end of the day, Indiegogo — which kept BioRing’s campaign open for several weeks after its partners expressed concerns — made five cents off every dollar pledged to BioRing’s product. As of press time, BioRing has raised about $460,000, netting Indiegogo $23,000.
Lau may well get her money back through her credit card company, but she says her crowdfunding days are over.
“It was my first Indiegogo crowdfunding purchase and I felt good about investing in an idea from ‘the little guy,'” she says. She doesn’t have such warm feelings about those “little guys” now: “I want to punch them in the face.”
She’ll have to find them first. ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. ||||| The Rise Of Deep Learning
Imagine if you could track everything from your calorie intake to your vital signs through a device no wider than your ring finger? If a recent crowdfunding campaign is any indication, this may soon become a reality, one that will reshape the wearable world.
In a market that is all but dominated by FitBit and other such wrist-worn devices, the “BioRing” hopes to point fingers in its direction. According to its Indiegogo page, the ring contains several tiny sensors that measure not only caloric and fat intake, but also the wearer’s own personal heart, stress, water, and sleep levels, as well as distance and steps measurements. Effective while the wearer is both awake and asleep, the “Personal Trainer on Your Finger” has enough onboard memory for a week’s work of statistics that can be communicated to an iOS or Android app.
So far, BioRing’s Indiegogo campaign has raised close to half a million dollars, well over its initial goal. If all goes as planned, the first units will start to ship out to early backers by November.
It is only a matter of time before wearable tech comes out with, say, an earring that also reads your vitals PLUS tells your horoscope and the day’s weather. |||||
What is a summary? | – A ring that seemed too good to be true is apparently too good to exist at all. So reports Vocativ in an exposé about a product that may have never been in the works—and the marketing teams and fundraisers who were seemingly duped by a shiny gadget. The object at hand is the BioRing, a waterproof heart rate monitor and fitness tracker that claimed it would be able to do something medical researchers have not yet achieved: count the calories its wearer consumes, and even differentiate between calories from fat, protein, and carbs. It's something of a holy grail for diet and fitness tracking, and hundreds of people chipped in more than $450,000 to the product's Indiegogo campaign, which launched last June. Forbes thought it might be "the next evolution in wearable tech," while Tech Times likened it to having a "personal trainer at users' fingertips." But the campaign has ended, with an Indiegogo message explaining only that it "violated our Terms of Use." Only about $200,000 has been returned to backers, and no ring is in sight. It all looks dubious in hindsight. Michael Johnson, a co-founder, claimed to have experience as an "algorithm developer" at cancer treatment firm Elekta, which tells Vocativ it has no record of the man's employment. A separate Indiegogo page created by scientists and consumer advocates (it's not selling anything) flat out calls the BioRing a "scam" and picks apart the claims one by one. It also accuses Indiegogo of being too lax on vetting such products. "If it seems too good to be true, it probably is," they caution. By Vocativ's calculations, Indiegogo made about $23,000 on the elusive ring. (Beware your online holiday shopping.) | multi_news_1_0_0 |
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Possible Risks and Side Effects
Side effects Possible signs of a serious problem
Risks of NuvaRing
Blood clots
The hormones in NuvaRing may cause changes in your blood clotting system which may allow your blood to clot more easily. If blood clots form in your legs, they can travel to the lungs and cause a sudden blockage of a vessel carrying blood to the lungs. Rarely, clots occur in the blood vessels of the eye and may cause blindness, double vision, or other vision problems. The risk of getting blood clots may be greater with the type of progestin in NuvaRing than with some other progestins in certain low-dose birth control pills. It is unknown if the risk of blood clots is different with NuvaRing use than with the use of certain birth control pills.
If you take hormonal contraceptives and need elective surgery, need to stay in bed for a prolonged illness or have recently delivered a baby, you may be at risk of developing blood clots. You should consult your doctor or health care professional about stopping hormonal contraceptives 3 to 4 weeks before surgery and not taking hormonal contraceptives for 2 weeks after surgery or during bed rest. You should also not take hormonal contraceptives soon after delivery of a baby. It is advisable to wait for at least 4 weeks after delivery if you are not breastfeeding. If you are breastfeeding, you should wait until you have weaned your child before using the pill or NuvaRing (see PRECAUTIONS, NURSING MOTHERS in the Prescribing Information.
Strokes and heart attacks
Hormonal contraceptives may increase your risk of strokes (blockage of blood flow to the brain) or heart attacks (blockage of blood flow to the heart). Any of these conditions can cause death or serious disability. Smoking greatly increases the risk of having strokes and heart attacks. Furthermore, smoking and the use of combination hormonal contraceptives, like NuvaRing, greatly increases the chances of developing and dying of heart disease. If you use combination hormonal contraceptives, including NuvaRing, you should not smoke.
High blood pressure and heart disease
Combination hormonal contraceptives, including NuvaRing, can worsen conditions like high blood pressure, diabetes, and problems with cholesterol and triglycerides.
Cancer of the reproductive organs and breast
Breast cancer has been diagnosed slightly more often in women who use the Pill than in women of the same age who do not use the Pill. This small increase in the number of breast cancer diagnoses gradually disappears during the 10 years after stopping use of the Pill. It is not known whether the difference is caused by the Pill. It may be that women taking the Pill are examined more often, so that breast cancer is more likely to be detected. You should have regular breast examinations by a health care professional and examine your own breasts monthly. Tell your health care professional if you have a family history of breast cancer or if you have had breast nodules or an abnormal mammogram.
Women who currently have or have had breast cancer should not use hormonal contraceptives, including NuvaRing, because breast cancer is usually a hormone-sensitive tumor.
Some studies have found an increase in the incidence of cancer of the cervix in women who use oral contraceptives. However, this finding may be related to factors other than the use of oral contraceptives. There is insufficient evidence to rule out the possibility that Pills may cause such cancers.
Gallbladder disease
Combination hormonal contraceptive users may have a higher chance of having gallbladder disease.
Liver tumors
In rare cases, combination hormonal contraceptives, like NuvaRing, can cause noncancerous (benign) but dangerous liver tumors. These benign liver tumors can break and cause fatal internal bleeding. In addition, it is possible that women who use combination hormonal contraceptives, like NuvaRing, have a higher chance of getting liver cancer. However, liver cancers are extremely rare.
Lipid metabolism and inflammation of the pancreas
In women with inherited defects of lipid metabolism, there have been reports of significant elevations of plasma triglycerides during estrogen therapy. This has led to pancreatitis in some cases.
Possible side effects of NuvaRing
Common side effects
The most common side effects reported by NuvaRing users are:
Vaginal infections and irritation
Vaginal secretion
Headache
Weight gain
Nausea
Additional side effects
In addition to the risks and side effects listed above, users of combination hormonal birth control methods have also reported the following side effects:
Vomiting
Change in appetite
Abdominal cramps and bloating
Breast tenderness or enlargement
Irregular vaginal bleeding or spotting
Changes in menstrual cycle
Temporary infertility after treatment
Fluid retention (edema)
Spotty darkening of the skin, particularly on the face
Rash
Weight changes
Depression
Intolerance to contact lenses
Nervousness
Dizziness
Loss of scalp hair
Possible signs of a serious problem
Call your doctor right away if you get any of the symptoms listed below. They may be signs of a serious problem:
Sharp chest pain, coughing blood, or sudden shortness of breath (possible clot in the lung)
Pain in the calf (back of lower leg; possible clot in the leg)
Crushing chest pain or heaviness in the chest (possible heart attack)
Sudden severe headache or vomiting, dizziness or fainting, problems with vision or speech, weakness, or numbness in an arm or leg (possible stroke)
Sudden partial or complete loss of vision (possible clot in the eye)
Yellowing of the skin or whites of the eyes (jaundice), especially with fever, tiredness, loss of appetite, dark-colored urine, or light-colored bowel movements (possible liver problems)
Severe pain, swelling, or tenderness in the abdomen (gallbladder or liver problems)
Sudden fever (usually 102°F or more), vomiting, diarrhea, dizziness, fainting, or a sunburn-like rash on the face or body (very rarely, toxic shock syndrome)
Breast lumps (possible breast cancer or benign breast disease)
Irregular vaginal bleeding or spotting that happens in more than 1 menstrual cycle or lasts for more than a few days
Urgent, frequent, burning and/or painful urination, and cannot locate the ring in the vagina (rarely, accidental placement of NuvaRing into the urinary bladder)
Swelling (edema) of your fingers or ankles
Difficulty in sleeping, weakness, lack of energy, fatigue, or a change in mood (possible severe depression) ||||| Brenner also speaks to Megan Henry, coincidentally a college classmate of Erika’s and a member of World Class Athletes, the army’s elite team of soldier-athletes. Ten days after she had started using NuvaRing, Megan, like Erika, found herself gasping for breath. “One doctor I went to told me I was under stress, or maybe I had asthma,” she tells Brenner. “He gave me an inhaler.” On a flight to Florida for more training, she almost collapsed. “At Urgent Care, I was given an X-ray—it was clear. I said, ‘Could this be the NuvaRing?’ ‘Absolutely not,’ the doctor said.” Megan’s mother, Barbara, told her, “Megan, you need to come home now, and I will get you an appointment with a pulmonologist.” After a second flight—she later learned that that alone could have killed her—Megan told her history to a Connecticut doctor, who ordered a CT scan. It revealed dozens of blood clots in her lungs. Rushed to the hospital, she was put on blood thinners in the E.R., and she remained hospitalized for a week. “I was told, ‘Your career as an athlete is over,’ ” she said. “If you weren’t in the shape you are, you would be dead,” her doctor informed her. Though Megan tells Brenner that she is almost back to normal and training again, she will have a much higher risk of blood clots for the rest of her life, she said, and if she gets pregnant, she will likely have to go on a painful regimen of injections of Lovenox to prevent clots.
Brenner interviews Hunter Shkolnik, a lawyer bringing lawsuits against Merck. Shkolnik tells Brenner that Organon (the Dutch pharmaceutical company that created the device) launched into NuvaRing’s marketing with a scientist’s research study that had examined only 16 women using NuvaRing. That study, No. 34218, on the release of hormones in different birth-control delivery systems, was so outrageous, Shkolnik tells Brenner, that he felt it justified focusing his entire legal career on drug cases. Shkolnik tells Brenner that the summary prepared by Organon for the F.D.A. was attached to thousands of pages of backup, in which were buried the risks associated with blood clots. “This is a standard subterfuge used by Pharma,” he says. “You bury your bad news in one of 500 studies you have done on ease of use or lipid disorder. Then when the F.D.A. comes back to the drug company, the drug company can say, ‘You had it in your documents.’ If it isn’t in the 30-page summary, the F.D.A. is so understaffed it will never be noticed.”
Brenner investigates the way Merck has dealt with the F.D.A., talking to Shkolnik about a study that recently came out of Denmark, led by scientist Dr. Øjvind Lidegaard, who, after examining the health records of more than a million women, concluded that women using NuvaRing were more than six times as likely to develop blood clots as those who did not use hormonal contraceptives. Brenner reports that, while Merck Canada has changed its label to include the warnings from Lidegaard’s study, the U.S.-based Merck has failed to do so in the U.S.
In response to Brenner’s request for an interview with Merck chairman Ken Frazier or one of the company lawyers, Merck responded, “Ken Frazier and our other colleagues are not available to participate in this opportunity.” The e-mail also included Merck’s official statement: “Blood clots have long been known as a risk associated with combined hormonal contraceptives. The FDA-approved patient information and physician package labeling for NuvaRing include this information….We remain confident in the safety and efficacy profile of NuvaRing—which is supported by extensive scientific research—and we will continue to always act in the best interest of patients.”
Langhart recalls the day her daughter first told her about NuvaRing: “Erika came home that day and said, ‘Mom, my doctor said that this is a product that will be so easy. I only have to change it once a month. And he gave me samples.’ ” Langhart, weeping, tells Brenner, “I will never forgive myself for not checking it out on the Web. It didn’t occur to me. Erika was always so meticulous about everything she did.” |||||
Write a summary. | – A potentially deadly contraceptive called NuvaRing is still on the US market—but why? That's what Marie Brenner aimed to find out in Vanity Fair. She learned that NuvaRing maker Merck made $623 million selling NuvaRing last year, despite users who developed terrifying blood clots and filed roughly 3,500 lawsuits. Saddest of all is the story of Erika Langhart, who was found writhing on the floor on the Monday before Thanksgiving. "Was your daughter using birth control?" asked a doctor when she was admitted to ER. "I thought so, because she's having a pulmonary embolism." Langhart died, and the program at her memorial service reads, "Cause of Passing: Massive, Double Pulmonary Embolism—a direct result of the NuvaRing." A Danish study only heightened concerns by analyzing health records of over a million women, and concluding that NuvaRing users were far more likely to get blood clots than women who didn't use hormonal contraceptives. Even NuvaRing admits to a blood-clot problem. So how did NuvaRing get past the FDA? By burying the bad news in one of 500 studies, according to a lawyer who is suing Merck. "When the FDA comes back to the drug company, the drug company can say, 'You had it in your documents,'" he said. "If it isn’t in the 30-page summary, the FDA is so understaffed it will never be noticed." Click for Brenner's full piece. | multi_news_1_0_0 |
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Here is a news article: Number 120, April 2013
PDF Version (770 KB)
Marian F. MacDorman, Ph.D.; Donna L. Hoyert, Ph.D.; and T.J. Mathews, M.S.
Key findings
Following a plateau from 2000 through 2005, the U.S. infant mortality rate declined 12% from 2005 through 2011. Declines for neonatal and postneonatal mortality were similar.
From 2005 through 2011, infant mortality declined 16% for non-Hispanic black women and 12% for non-Hispanic white women.
Infant mortality declined for four of the five leading causes of death during the 2005–2011 period.
Infant mortality rates declined most rapidly among some, but not all, Southern states from 2005 through 2010. Despite these declines, states in the South still had among the highest rates in 2010. Rates were also high in 2010 in some states in the Midwest.
Infant mortality is an important indicator of the health of a nation (1,2). This report describes the recent decline in the U.S. infant mortality rate from 2005 through 2011. Changes in infant mortality rates over time are examined by age at death, maternal race and ethnicity, cause of death, and state. The linked birth/infant death data set (linked file) is generally the preferred source for infant mortality rates by race and ethnicity (3,4). This is particularly important for racial and ethnic groups other than non-Hispanic white, non-Hispanic black, and Hispanic. For these three groups, rates calculated from the mortality and linked files have been very similar for many years, and trends are unlikely to differ (3–5). Thus, data from the mortality file are used for this analysis because of their greater timeliness (3,6). Data for 2011 are preliminary (6). Because preliminary data are not available by state, data for the 2005–2010 period were used for the geographic analysis.
Keywords: infant death, trends, geographic differences, National Vital Statistics System
U.S. infant, neonatal, and postneonatal mortality rates declined from 2005 through 2011.
Figure 1. Infant, neonatal, and postneonatal mortality rates: United States, 2000 and 2005–2011
NOTE: Data for 2011 are preliminary.
SOURCE: CDC/NCHS, National Vital Statistics System, mortality data set.
After significant declines throughout the 20th century, the U.S. infant mortality rate plateaued from 2000 through 2005 (7). In 2005, the infant mortality rate was 6.87 infant deaths per 1,000 live births, not significantly different from the rate of 6.91 in 2000 (Figure 1).
Subsequently, the U.S. infant mortality rate declined significantly from 2005 to 2006, did not change significantly from 2006 to 2007, and then declined significantly each year from 2007 through 2010.
In 2011, the U.S. infant mortality rate was 6.05 infant deaths per 1,000 live births (based on preliminary data), 12% lower than the rate of 6.87 in 2005, but not significantly lower than 6.15 in 2010.
From 2005 through 2011, the neonatal mortality rate (deaths under age 28 days per 1,000 live births) declined 11%, and the postneonatal mortality rate (deaths at ages 28 days to under 1 year per 1,000 live births) declined 14%.
From 2005 through 2011, the U.S. infant mortality rate declined most rapidly for non-Hispanic black women.
The U.S. infant mortality rate declined 12% for both the total population and non-Hispanic white women from 2005 through 2011 (Figure 2).
The infant mortality rate declined the most for non-Hispanic black women (16%), and the least for Hispanic women (9%).
Historically, infant mortality rates for non-Hispanic black women have been more than twice those for non-Hispanic white women, while rates for Hispanic women have been similar to those for non-Hispanic white women (3).
Figure 2. Percent change in infant mortality rates, by race and ethnicity: United States, 2005–2011
NOTE: Data for 2011 are preliminary.
SOURCE: CDC/NCHS, National Vital Statistics System, mortality data set.
The infant mortality rate declined for four of the five leading causes of infant death from 2005 through 2011.
The leading cause of infant death in 2011 was congenital malformations, followed by short gestation/low birthweight, Sudden infant death syndrome (SIDS), maternal complications, and unintentional injuries (Figure 3). Together, these five leading causes accounted for 56% of all infant deaths in the United States in 2011 (6).
During 2005–2011, the infant mortality rate declined 6% for congenital malformations.
The infant mortality rate declined 9% for short gestation/low birthweight and 7% for maternal complications, both causes that occur primarily among preterm infants (8).
The SIDS rate declined 20% from 2005 through 2011, although this decline may be due in part to changes in the way SIDS is diagnosed and reported (9). The rate for unintentional injuries did not change significantly from 2005 to 2011.
Figure 3. Infant mortality rates for the five leading causes of infant death in 2011: United States, 2005 and 2011
NOTE: Data for 2011 are preliminary. SIDS is Sudden infant death syndrome.
SOURCE: CDC/NCHS, National Vital Statistics System, mortality data set.
From 2005 through 2010, infant mortality declined most rapidly for selected Southern states.
Sixteen states and the District of Columbia had statistically significant declines in their infant mortality rates from 2005 through 2010 (Figure 4).
Four states (Georgia, Louisiana, North Carolina, and South Carolina) and the District of Columbia had a decline of 20% or more in their infant mortality rate from 2005 through 2010. These areas have had persistently high infant mortality rates for many years (1,2).
Several other Midwestern and Southern states with higher-than-average infant mortality rates (1,6) also experienced significant declines: Florida, Illinois, Kansas, Michigan, Mississippi, Missouri, Tennessee, and Texas. States with the largest declines tended to be states with the highest rates.
No states had a statistically significant increase in infant mortality during this period.
Figure 4. Decline in infant mortality rates, by state: United States, 2005–2010
NOTE: Access data table for Figure 4 [PDF - 165 KB].
SOURCE: CDC/NCHS, National Vital Statistics System, mortality data set.
In 2010, the U.S. infant mortality rate was highest among selected states in the South and Midwest regions.
In 2010, 13 states and the District of Columbia had infant mortality rates of 7.00–7.99, and two additional states (Mississippi and Alabama) had infant mortality rates of 8.00 or higher. In contrast, 12 states had infant mortality rates below 5.00 (Figure 5).
Although infant mortality rates declined most rapidly among selected Southern states, selected states in the South and Midwest regions still had the highest infant mortality rates in 2010. Pennsylvania and Rhode Island also had high infant mortality rates (7.00 or above) in 2010.
Differences by state reflect, in part, differences in the population composition of states by race and ethnicity.
Figure 5. Infant mortality rates, by state: United States, 2010
NOTE: Access data table for Figure 5 [PDF - 165 KB].
SOURCE: CDC/NCHS, National Vital Statistics System, mortality data set.
Summary
After a plateau from 2000 through 2005, the U.S. infant mortality rate declined by 12% to a rate of 6.05 in 2011. Provisional infant mortality counts for the first half of 2012 suggest a continued downward trend (10). Infant mortality declined from 2005 through 2011 for all major racial and ethnic groups, with the most rapid decline among non-Hispanic black women. Among leading causes of death, infant mortality declined for four of the five leading causes. Infant mortality rates declined most rapidly from 2005 through 2010 for selected Southern states; still, rates in 2010 remained higher in the South and Midwest than in other regions.
In 2008, the United States ranked 27th in infant mortality rate among Organization for Economic Cooperation and Development countries (11), and a previous report linked the United States' relatively unfavorable infant mortality ranking to its higher percentage of preterm births (12). Despite the recent infant mortality decline, comparing the 2011 U.S. infant mortality rate with the 2008 international rankings would still have the United States ranked 27th.
Definitions
Infant death: Death of an infant before his or her first birthday.
Infant mortality rate: Number of infant deaths per 1,000 live births.
Neonatal mortality rate: Number of deaths before age 28 days per 1,000 live births.
Postneonatal mortality rate: Number of deaths from age 28 days to under 1 year per 1,000 live births.
Preterm birth: Birth before 37 completed weeks of gestation.
Data source and methods
Data presented in this report were based on information from death certificates filed in state vital statistics offices, and subsequently compiled into national data by the National Center for Health Statistics. Data for 2011 are preliminary (6). Causes of death are classified according to the 10th revision of the International Statistical Classification of Diseases and Related Health Problems (13). Causes of death are sorted into rank order according to the number of deaths, beginning with the largest number; see the Technical Notes section of National Vital Statistics Reports on annual final deaths data for more detail (5). Text statements were tested for statistical significance using methods described elsewhere (3), and a statement that a given infant mortality rate is higher or lower than another rate indicates that differences in the rates are statistically significant.
About the authors
Marian F. MacDorman, Donna L. Hoyert, and T.J. Mathews are with the Centers for Disease Control and Prevention's National Center for Health Statistics, Division of Vital Statistics.
References
Suggested citation
MacDorman MF, Hoyert DL, Mathews TJ. Recent declines in infant mortality in the United States, 2005–2011. NCHS data brief, no 120. Hyattsville, MD: National Center for Health Statistics. 2013.
Copyright information
All material appearing in this report is in the public domain and may be reproduced or copied without permission; citation as to source, however, is appreciated.
National Center for Health Statistics
Charles J. Rothwell, M.S., Acting Director
Jennifer H. Madans, Ph.D., Associate Director for Science
Division of Vital Statistics
Delton Atkinson, M.P.H., M.P.H., P.M.P., Acting Director ||||| The states with the steepest declines in infant deaths — Georgia, Louisiana, North Carolina and South Carolina — have long been plagued with some of the nation’s highest infant mortality rates, Dr. MacDorman added. In all four states the rate dropped by more than 20 percent from 2005 to 2010, the latest year for which state data are available. The District of Columbia, which has expanded a home-visit program for poor pregnant women and stepped up other efforts to keep mothers and their babies healthy, saw the biggest drop: from 14.05 deaths per 1,000 births in 2005 to 7.86 in 2010.
The states with the highest infant mortality rates are Mississippi and Alabama, according to the report. But even Mississippi saw its rate drop by 15 percent from 2005 to 2010.
Dr. MacDorman said the nation’s rate of premature births — babies born before 37 weeks of gestation — peaked at 12.8 percent in 2006 and had dropped every year since then. That is a likely factor in the decline of the infant mortality rate, she said. In 2009, the latest year for which C.D.C. data is available, two-thirds of all infant deaths in the United States were among preterm babies.
Another possible factor is a recent emphasis on preventing planned early deliveries. A growing number of hospitals are not allowing mothers to schedule births before 39 weeks without a medical reason. In 2011, the March of Dimes started a public education campaign, Healthy Babies are Worth the Wait, to reduce medically unnecessary deliveries before 39 weeks of gestation. The Department of Health and Human Services began a similar effort, Strong Start, last year.
“It’s been going on for a few years now and I think it has had an impact,” Dr. MacDorman said of concerted efforts to discourage early deliveries. “It’s maybe leading to just a little change in the culture.”
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Infant mortality dropped in four of the five leading causes of death from 2005 to 2011: congenital malformations, short gestation/low birth weight, sudden infant death syndrome and maternal complications. The death rate from unintentional injuries rose slightly.
The decline in deaths attributed to sudden infant death syndrome was particularly striking — the rate went down by 20 percent — but that could have resulted from changes in the way SIDS is diagnosed and reported, Dr. MacDorman said.
While improving, the nation’s infant mortality rate is still high compared with the rates in a number of other developed countries. In 2008, the United States ranked 27th in infant mortality among the 30 countries in the Organization for Economic Cooperation and Development, according to the National Center for Health Statistics.
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Janice A. Freedman, executive director of the North Carolina Healthy Start Foundation, a nonprofit group focused on reducing infant death and illness, said that it was difficult to pinpoint reasons for the 20 percent drop in her state’s infant mortality rate from 2005 to 2010, but that better education about preventing SIDS was probably one factor.
At the same time, Ms. Freedman said she was concerned that state budget constraints would hamper continuing efforts to curb infant deaths.
“We are cutting budgets and so we are concerned that babies don’t get lost in the politics,” she said. “Numbers can bump up and down, and there are still racial disparities. So there’s still a lot of work to be done.”
Dr. Kevin Ryan, chief of the women’s and children’s health section of the North Carolina Division of Public Health, said a particularly important goal was to improve the health of women before they become pregnant, focusing on diet, exercise and prevention of chronic diseases like diabetes.
“In years past, the key was access to early, high-quality prenatal care,” Dr. Ryan said. “We’re looking more and more at addressing the whole life cycle of girls and young women, not just focusing on the period of pregnancy. That’s going to be critical to our success in continuing to improve birth outcomes.” |||||
A summary of this is? | – After holding steady from 2000 through 2005, the US infant mortality rate dropped 12% from 2005 through 2011, according to a new CDC report. In 2011, the rate was 6.05 deaths of babies less than a year old for every 1,000 births, down from 6.87 in 2000. Premature births also have been dropping since 2006, and many hospitals and other organizations have been working to prevent mothers from scheduling deliveries before 39 weeks without a valid medical reason. Researchers say both those factors likely contributed to the drop in the infant mortality rate, the New York Times reports. Southern states, which have some of the highest infant mortality rates in the country, saw some of the biggest improvements. In Georgia, Louisiana, North Carolina, and South Carolina, the rate declined by more than 20%. Black women, who have also typically seen higher infant mortality rates than white women, experienced a decline of 16%. One report author calls it "encouraging," but says the gap is still too large. The biggest drop was in the District of Columbia, which went from 14.05 deaths per 1,000 births in 2005 to 7.86 by 2010. It has been improving services to moms, babies, and poor pregnant women. The highest infant mortality rates are in Mississippi and Alabama. | multi_news_1_0_0 |
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Summarize this article:
Mayor Menino Issues Order to End Sugary Drink Sales on City Property
Aims to curb obesity, make the healthier choice the easier choice
Citing a link between the consumption of sugary beverages and rising obesity rates and healthcare costs, Mayor Thomas M. Menino today issued an executive order requiring City departments to take steps in the next six months to phase out the sale, advertising, and promotion of sugary beverages on City-owned property.
“Now is the time to expand our efforts that began in our public schools and set an example for the city as a whole,” Mayor Menino said, referring to the 2004 ban on soda and junk food in vending machines in Boston Public Schools. “I want to create a civic environment that makes the healthier choice the easier choice in people’s lives, whether it’s schools, worksites, or other places in the community.”
Mayor Menino announced the executive order at a City Hall press conference where he was joined by Boston Public Health Commission officials and leading health and nutrition experts, including Dr. Walter Willett, chairman of the Department of Nutrition at Harvard School of Public Health and Bill Walczak, president of Carney Hospital in Dorchester.
Soda and other sugar-sweetened beverages account for up to 10 percent of total calories consumed in the U.S. diet, and are known to be major contributors to obesity. According to the Boston Public Health Commission, about 63 percent of black adults, 51 percent of Latino adults, and 49 percent of while adult residents in Boston are considered overweight or obese. Nearly 30 percent of preventable diseases, such as type 2 diabetes and certain cancers, arthritis, heart attacks and strokes, are linked to obesity in adults.
Mayor Menino’s executive order sets science-based standards for what’s considered a healthy beverage and what can be sold or served on City property. The policy applies to cafeterias, vending machines, concession stands, and beverages served at meetings, City-run programs, and events where food is purchased with City dollars.
City buildings and departments have a six-month grace period before they’ll be required to phase out the sale of so-called “red” beverages, or those loaded with sugar, such as non-diet sodas, pre-sweetened ice teas, refrigerated coffee drinks, energy drinks, juice drinks with added sugar and sports drinks. The order allows for the sale of “yellow” beverages such as diet sodas, diet iced teas, 100 percent juices, low-calorie sports drinks, low-sugar sweetened beverages, sweetened soymilk and flavored, sweetened milk. “Green” beverages, such as bottled water, flavored and unflavored seltzer water, low-fat milk, and unsweetened soymilk can continue to be sold. The promotion of “red” beverages on City property through sponsorship agreements with City departments, including banners and advertising panels on vending machines, will be prohibited.
The Boston Public Health Commission has developed signage and a brochure to help City workers and visitors navigate the labyrinth of beverages to find the healthy choice. Posters featuring a traffic light symbol are being placed near vending machines and the healthiest beverage choices get a green light, the less healthy drinks get a yellow light, and those that are most loaded with sugar get a red light. The poster says “Stop. Rethink Your Drink. Go on Green.”
Public health employees will conduct educational workshops for City employees and also will be responsible for working with City departments to ensure that the executive order is fully implemented.
Dr. Barbara Ferrer, executive director of the Boston Public Health Commission, said, in the long term, the policy will decrease healthcare costs for the City and cut into lost productivity. “Economists estimate that medical costs for an obese patient are about 42 percent higher a year than for a patient with a healthy weight,” Dr. Ferrer said.
Other cities and states - including San Francisco, San Antonio, Los Angeles County, and New York City -have taken steps to create nutritional standards that limit or prohibit the sale or distribution of unhealthy foods, including sugar-sweetened beverages.
Two years after the Boston Public Schools removed soda and unhealthy snacks from vending machines, BPS’ youth surveillance data showed that overall consumption of sugary drinks by BPS high school students decreased significantly. Since that time, Boston has taken additional steps such as expanding neighborhood walking groups, subsidizing gym memberships, supporting backyard gardens, and investing City dollars in the Bounty Bucks program so that more families can afford to buy fresh fruits and vegetables at Farmers’ Markets. This summer, Boston will launch New England’s first bike share program, which will put 600 bikes on the streets for residents and visitors to use in the city.
Along the way, the City has found no shortage of supportive partners. Yesterday, Bill Walczak of Carney Hospital in the Steward Health Care System said he’d implemented on Monday a ban on sugar-sweetened beverages sold or provided on hospital grounds. The ban has begun in cafeterias, retail, and patient service areas. Carney is the first hospital in Boston to implement such a policy.
“I applaud Mayor Menino and Bill Walczak for their leadership in creating healthier civic, workplace, school and healthcare environments by eliminating soda and other sugary drinks wherever possible,” said Dr. Willett of the Harvard School of Public Health and a leading expert internationally on obesity. “There is abundant evidence that the huge increase in soda consumption in the past 40 years is the most important single factor behind America’s obesity epidemic. These steps will greatly assist in creating a new social norm, in which healthier beverages are the preferred choice.”
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Boston's long-time mayor, Thomas M. Menino just made quenching the thirst of city-workers that much harder. According to The Boston Globe , Menino issued an executive order to phase out sugary drinks from all city property in an effort to curb rising obesity rates. So long non-diet sodas. Adios sweet tea. Arrivederci you sexy sports drinks, you.City departments have six months to phase out the sinister sugary beverages in cafeterias, vending machines, concession stands and during city-run meetings. And just in case parched public workers aren't quite sure what constitutes a healthy beverage, the Boston Public Health Commission is applying the familiar red, yellow and green labels to drinks, and reinforced by nearby posters that say, "Stop. Rethink Your Drink. Go On Green." According to a release from the Mayor's office, "red" beverages include non-diet sodas, sweetened ice teas, sports drinks, etc. Diet sodas and diet iced teas, 100 percent fruit juices and low calorie sports drinks qualify as "yellow" beverages, while "green" drinks mean bottled water, low fat milk or unsweetened soy milk. Mmmm. Unsweetened soy milk -- yum.Boston's not alone in trying to combat obesity through mandated choices. Cities like San Francisco Los Angeles County and New York City have also set standards to limit or prohibit the sale or distribution of unhealthy food -- including sugary drinks.There's some proof this type of food policing works. Two years after the Boston Public Schools removed soda and unhealthy snacks from vending machines, data showed that overall consumption of sugary drinks decreased significantly.Dr. Barbara Ferrer, executive director of the Boston Public Health Commission, said in the long term, the policy will decrease healthcare costs for Boston and will positively impact productivity.Soda and other sugar-sweetened beverages account for up to 10 percent of total calories consumed in the U.S. diet, and are known to be major contributors to obesity. According to Ferrer's office, about 63 percent of black adults, 51 percent of Latino adults and 49 percent of white adult Boston residents are considered overweight or obese. What it boils down to is health care costs."Economists estimate that medical costs for an obese patient are about 42 percent higher a year than for a patient with a healthy weight," said Dr. Ferrer in the city's press release.Which makes us wonder what's next? A ban on smokeless tobacco at Fenway? Doh! Wait... ||||| | – No more soda on Boston city property, or sports drinks or sweetened ice teas, for that matter. In an effort to reduce the city's rising obesity rates—and the soaring health costs associated with obesity—Slashfood reports that Mayor Thomas Menino has banned all sugary beverages from vending machines, cafeterias, and concession stands. “I want to create a civic environment that makes the healthier choice the easier choice in people’s lives, whether it’s schools, worksites, or other places in the community," said Menino in a press release. | multi_news_1_0_0 |
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Here is a news article: These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. ||||| More than 60 percent of Americans drink one or more cups of coffee daily, according to the National Coffee Association USA. (Photo: Volker Möhrke/Corbis)
Go ahead, indulge your love affair with steaming hot Joe. In addition to having the superpower of transforming cranky morning-monsters into pleasant, friendly monsters that vaguely resemble well-functioning human beings, coffee has some pretty amazing science-backed health benefits.
In fact, a government advisory committee recently said that three to five daily cups can be part of a healthy diet, citing evidence that java is linked to a reduced risk for heart disease and type 2 diabetes.
Related: 6 Foods That People Think Are Healthy But Aren’t
Some of the research findings outlined below are well established, while others are less understood or may lead to breakthroughs in years to come. But they all have one thing in common: They’ll give you plenty of good excuses to enjoy a second (or third) mug of liquid heaven. So fill that filter, flip the brew switch, and settle in to learn some new facts about this beloved morning ritual.
1. Coffee may help prevent multiple sclerosis
In a new study presented Thursday at the annual meeting of the American Academy of Neurology, researchers from Johns Hopkins School of Medicine found that coffee drinking may help decrease the likelihood of developing multiple sclerosis. When the researchers compared people with MS to people without the disease, they found that java abstainers were about 1.5 times more likely to develop MS, compared to people who drank four or more cups daily.
"There are many compounds in coffee that could be contributing [to the findings]," study researcher Ellen Mowry, MD, of Johns Hopkins Medicine, tells Yahoo Health. “Caffeine is a compelling connection given it may be protective against Parkinson’s disease and Alzheimer’s disease. Interestingly, it does affect the functioning of immune cells in the brain but has impacts on other potentially relevant processes too.” Mowry says that if the results from this study are confirmed, the findings could lead to new treatment approaches for MS.
2. Coffee might reduce the risk of developing a dangerous type of skin cancer
Researched released in January 2015 found that people who drank four cups of coffee a day had a 20 percent lower risk for melanoma, the deadliest form of skin cancer. The study, which was published online in the Journal of the National Cancer Institute, followed approximately 500,000 older adults for 11 years. The study authors write that coffee might prevent cancer growth by guarding against DNA damage.
Hopefully obvious disclaimer: Preventing excessive exposure to ultraviolet rays by slathering on a high-SPF broad-spectrum sunscreen, avoiding too much direct sun exposure, and shunning indoor tanning is the best way to prevent skin cancer. We’re not suggesting that sipping an iced coffee while baking under the sun will protect you from skin cancer.
Related: What Former Miss Maryland Brittany Cicala Wishes She Had Done To Prevent Skin Cancer
3. Coffee is associated with a lower risk for breast cancer
Although the research is mixed, “the bulk of previous studies suggest that high coffee consumption is associated with a modest reduction of breast cancer risk,” Swedish researchers write in a study published in Breast Cancer Research. That study found that older women who drank more than five cups of coffee daily had a significantly lower risk for a certain type of breast cancer — although lifestyle factors may also partly explain the association.
Some studies have also found a decreased risk for mouth and throat cancers and endometrial cancer among heavy coffee drinkers.
4. Coffee can prevent death
OK, coffee can’t ward off death forever — as one astute researcher pointed out in this journalist’s early career, the risk of death is always (eventually) 100 percent. But in a large study of 400,000 Americans ages 50 and older published in the New England Journal of Medicine, coffee drinkers were significantly less likely to die during the 13-year study period. And the more coffee consumed, the lower the risk of death. (Again, during the study period. Even miracle beverages have their limits.) An earlier study in the Annals of Internal Medicine, which followed people for either 18 or 24 years, found similar associations.
Read More ||||| Drinking upward of four cups of coffee a day may lower the risk of developing multiple sclerosis (MS), a debilitating disease that affects the nervous system, researchers say.
The finding isn't without its caveats, and the scientists said they do not recommend that anyone at risk for developing MS go out and start guzzling coffee.
However, the study of nearly 7,000 people in the United States and Sweden does support observations previously made in mice, and it provides the most compelling evidence to date that caffeine offers protection against numerous neurological disorders. The researchers will present the findings in April at the annual meeting of the American Academy of Neurology.
In people with MS, the body's immune system inexplicably attacks the protective covering around nerve fibers, called myelin. The damage interrupts proper communication between the brain and the rest of the body, resulting in muscle weakness, poor coordination, blurred vision and pain, among other symptoms.
There is no cure for the disorder, and medications reduce symptoms only partially and temporarily. MS is more common in people living at very northern and southern latitudes, suggesting an association with sun exposure and vitamin D levels in certain ethnic groups, but the condition's cause remains unknown.
More than 400,000 Americans and 2.4 million people worldwide have MS, according to the National Multiple Sclerosis Society. Most people experience their first symptoms, often blurred or double vision, between ages 20 and 40.
In 2008, scientists led by Margaret Bynoe at Cornell University reported that mice that were bred to develop an MS-like disease failed to develop the condition when fed high amounts of caffeine. (The mice consumed the equivalent caffeine of four to six cups of coffee.) The researchers' study was published in the Proceedings of the National Academy of Sciences (PNAS).
The scientists hypothesized that caffeine blocked a chemical in the body called adenosine, which would otherwise enable immune cells to enter the central nervous system and destroy myelin. [10 Interesting Facts About Coffee]
In experiments, the mice that were fed caffeine "had reduced numbers of inflammatory immune cells in their central nervous system and, therefore, did not develop MS-like symptoms," said Linda Thompson of the Oklahoma Medical Research Foundation, a co-author on the 2008 PNAS report.
Thompson said a similar biological mechanism might occur in humans to protect against MS.
In the new study, researchers examined two datasets that each included healthy people and MS patients; one of the datasets came from Sweden, and the other came from the United States.
Analysis of both datasets revealed that the people who did not drink coffee had about a 1.5-times increased risk of developing MS compared with those who drank more than 30 ounces, or about four cups, daily.
The scientists could not discern, however, whether coffee helps reduce the severity of symptoms or postpones the relapse of symptoms in people who already have MS.
In MS patient forums, people have discussed the topic of coffee drinking for several years, with some patients reporting benefits, such as clearer thinking, while others report a worsening of their symptoms, such as poor sleep and jittery nerves.
"I think from the MS perspective, there are too few data to support changing coffee intake at this time," said Dr. Ellen Mowry, who led the new study and is an assistant professor of neurology at Johns Hopkins University School of Medicine in Baltimore. "Further research should be done to evaluate the role of coffee, including caffeine, in MS, as it may lead to identifying new targets for treatment."
One limitation of the study is that coffee habits were self-reported and retrospective, with participants asked to recall their coffee drinking patterns from as far back as 10 years, Mowry told Live Science. Yet the fact that the results of the Swedish and U.S. studies were so similar is particularly compelling, she added.
Coffee, most likely due to the caffeine it delivers, has been shown to reduce the risk and severity of other neurological disorders, such as Parkinson's and Alzheimer's diseases, as well as non-neurological conditions like heart disease, type 2 diabetes, liver disease and some cancers.
On the flip side, coffee can cause gastrointestinal problems and increase the intensity and frequency of migraines for many people. Unfiltered coffee can increase your levels of "bad" LDL cholesterol. And the science remains unclear on whether more than a daily cup of coffee increases the risk of miscarriage among pregnant women.
But more to the bottom line, ongoing studies at Harvard School of Public Health following more than 130,000 volunteers have found no increased risk of death from drinking as much as six cups, or 48 ounces, of coffee daily.
So depending on one's personal disposition, there may be far more reasons to increase your coffee drinking instead of kicking the habit.
Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science. |||||
A summary of this is? | – Rejoice yet again, coffee lovers: A new study says that four or more cups a day may reduce your chance of getting multiple sclerosis, LiveScience reports. An international group of researchers looked at two datasets—one Swedish and one American—and found that people who didn't drink coffee were 1.5 times more likely to develop MS than those who downed about four cups daily. The analysis of nearly 7,000 people echoes earlier research that mice, raised to get an MS-like illness, never developed it when given hefty doses of caffeine. Why caffeine? Well, with MS, the immune system strikes nerve fibers by attacking a protective covering called myelin. And scientists believe that caffeine blocks a body chemical that allows immune cells into the central nervous system to crush myelin. Now, the caveats: The new study finds no causal link between caffeine and reducing the chances of MS, the LA Times notes. Further, it's based on self-reported coffee habits that date back 10 years and may be sketchy. "I think from the MS perspective, there are too few data to support changing coffee intake at this time," says study leader Ellen Mowry. "Further research should be done ... as it may lead to identifying new targets for [MS] treatment." On the bright side, she says, the two data sets came up with very similar results. Coffee has also been found to reduce the chance of skin cancer and breast cancer, Yahoo reports, and a Harvard study of over 130,000 volunteers found that even six cups daily led to no greater chance of dying. (But toddlers may be drinking more coffee than we realize.) | multi_news_1_0_0 |
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Here is a news article: Life expectancy is rising globally thanks to disease prevention and medical advancements. In which countries are lives being cut short? WSJ’s Jason Bellini has #TheShortAnswer.
Global life expectancy for men and women has increased by about six years over the past two decades, according to one of the most comprehensive studies of global health done so far.
The rise in global life expectancy is mainly the result of dramatic advances in health care. In richer countries longer lifespans are spurred by a big drop in deaths related to heart disease, while poorer countries have seen big declines in the death of... ||||| Between 1990 and 2013, global life expectancy increased by nearly 5.8 years in men and 6.6 years in women, according to a new analysis of the Global Burden of Disease Study 2013 published in The Lancet.
Life expectancies in high-income regions have been increased due to falling death rates from most cancers and cardiovascular diseases. Life expectancies in high-income regions have been increased due to falling death rates from most cancers and cardiovascular diseases.
"The progress we are seeing against a variety of illnesses and injuries is good, even remarkable, but we can and must do even better," says lead author Dr. Christopher Murray, professor of Global Health at the University of Washington.
"The huge increase in collective action and funding given to the major infectious diseases such as diarrhea, measles, tuberculosis, HIV/AIDS and malaria has had a real impact," he says.
"However, this study shows that some major chronic diseases have been largely neglected but are rising in importance, particularly drug disorders, liver cirrhosis, diabetes and chronic kidney disease."
The analysis suggests that life expectancies in high-income regions have been increased due to falling death rates from most cancers - which are down by 15% - and cardiovascular diseases - which are down by 22%.
In low-income countries, rapidly declining death rates for diarrhea, lower respiratory tract infections and neonatal disorders have boosted life expectancy.
Despite the increases in global life expectancy by nearly 5.8 years in men and 6.6 years in women, some causes of death have seen increased rates of death since 1990.
These increased causes of death include:
Liver cancer caused by hepatitis C (up by 125%)
Atrial fibrillation and flutter (serious disorders of heart rhythm; up by 100%)
Drug use disorders (up by 63%)
Chronic kidney disease (up by 37%)
Sickle cell disorders (up by 29%)
Diabetes (up by 9%)
Pancreatic cancer (up by 7%).
HIV/AIDS has 'erased years of life expectancy' in sub-Saharan Africa
The report also points to one notable global region where life expectancy is not increasing. Deaths from HIV/AIDS have erased more than 5 years of life expectancy in sub-Saharan Africa, say the authors. HIV/AIDS remains the greatest cause of premature death in 20 of the 48 sub-Saharan countries.
Since 1990, years of life worldwide lost due to HIV/AIDS is reported as having increased by 334%.
In Syria, war is the leading cause of premature death - the conflict caused an estimated 29,947 deaths in 2013, and up to 54,903 and 21,422 deaths in each of the preceding 2 years.
Countries that the authors consider to have made "exceptional gains in life expectancy" over the past 23 years include Nepal, Rwanda, Ethiopia, Niger, Maldives, Timor-Leste and Iran - where, for both sexes, life expectancy has increased by more than 12 years.
Life expectancy at birth in India increased from 57.3 years for men and 58.2 years for women in 1990 to 64.2 years and 68.5 years, respectively, in 2013. The authors say that India has made "remarkable progress" in reducing deaths, with the death rates for children dropping 1.3% per year for adults and 3.7% per year for children.
The report also welcomes dramatic drops in child deaths worldwide over the study period. In 1990, 7.6 million children aged 1-59 months died, but this death rate was down to 3.7 million by 2013.
Igor Rudan and Kit Yee Chan, from the Centre for Population Health Sciences and Global Health Academy at the University of Edinburgh Medical School in the UK, write in a linked comment: |||||
A summary of this is? | – The average life is stretching longer. A new study in the Lancet—which analyzed 240 causes of death in 188 countries, the Wall Street Journal reports—finds humans today are living 71.5 years on average, an increase of about six years since 1990. Men are living an average 5.8 years longer, while women gained 6.6 years. Experts credit the change to more medical funding for infectious diseases and a 15% decline in deaths from most cancers (pancreatic cancer is the exception here, notes Medical News Today, up by 7%), as well as those from cardiovascular disease, in high-income countries. A decline in deaths from diarrhea and neonatal complications also helped in low-income countries, Time reports. But on the flip side, deaths from HIV/AIDS increased to the point that sub-Saharan Africa actually saw a drop in life expectancy. And chronic diseases shot up, with one researcher calling "largely neglected" conditions, "particularly drug disorders, liver cirrhosis , diabetes, and chronic kidney disease." Of particular note: Liver cancer caused by hepatitis C jumped by 125%, and drug use disorders were up by 63%. | multi_news_1_0_0 |
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– The FDA today put severe restrictions on Avandia, GlaxoSmithKline’s embattled diabetes drug, but stopped short of banning it outright. The once-popular drug will now only be available only as a last resort to type 2 diabetes patients who can’t control their glucose levels with any other medication, the AFP reports. Avandia has come under fire because data suggests it carries, in the FDA’s words, “an elevated risk of cardiovascular events” like heart attacks and strokes. Regulators in Europe, meanwhile, pulled the drug off the market altogether, Bloomberg reports. "We struggled with it, and colleagues in other jurisdictions struggled as well," said the European Medicines Agency's top medical officer. "There’s no single perfect tool to study this risk." GlaxoSmithKline sent out an email saying it would stop promoting the drug. But it also issued a statement saying it "continues to believe that Avandia is an important treatment." For more on the controversy over the drug, click here.
Article: |
Glaxo’s Avandia to Be Pulled in EU, Restricted in U.S.
By Kristen Hallam and Catherine Larkin
(Updates with close of trading in second, eighth paragraphs.)
Sept. 23 (Bloomberg) -- GlaxoSmithKline Plc’s Avandia, once the world’s best-selling diabetes drug, will be withdrawn in Europe and restricted in the U.S. after a three-year review of the medicine’s heart risks.
Glaxo said it will stop promoting the drug in all countries after the decisions announced today by the European Medicines Agency and the U.S. Food and Drug Administration. Regulators disagreed on the reliability of the data and whether potential risks could be contained. Glaxo’s American depository receipts fell the most in a month in New York trading.
Avandia’s sales have fallen by two-thirds since an analysis released in May 2007 tied it to a 43 percent increased risk in heart attacks. Glaxo said sales will be minimal after this year. The financial impact on Glaxo will also be limited because Avandia’s patent expires in 2012, said Eric Le Berrigaud, an analyst at Raymond James in Paris.
“We struggled with it, and colleagues in other jurisdictions struggled as well,” Hans-Georg Eichler, the EMA’s senior medical officer, said on a conference call with reporters. “There’s no single perfect tool to study this risk.”
In the U.S., the medicine will carry new warnings after a three-year battle that divided staff at the FDA. London-based Glaxo must add new cautions to Avandia’s prescribing information, the agency said today. The decision to allow continued sales of the treatment follows the recommendations of an FDA advisory panel in July.
Heart Attack Risk
The FDA advisers called for stronger warnings on the label after re-examining a 2007 decision to keep the medicine on the market. Glaxo has said “extensive clinical data” have shown the treatment to be safe.
“Ninety-nine percent of drug use should go away,” Steven Nissen, chairman of the Cleveland Clinic’s department of cardiovascular medicine and author of the 2007 analysis, said in a telephone interview. “The drug will essentially disappear from use in the U.S. and will disappear in Europe.”
Glaxo’s ADRs fell 72 cents, or 1.8 percent, to $39.43 at 4:01 p.m. in New York Stock Exchange composite trading, their biggest percentage decline since Aug. 24. Each receipt represents two ordinary shares.
‘Important Treatment’
“The company continues to believe that Avandia is an important treatment for patients with Type 2 diabetes and is now working with the FDA and EMA to implement the required actions,” according to Glaxo’s statement.
“Our primary concern continues to be patients with Type 2 diabetes and we are making every effort to ensure that physicians in Europe and the U.S. have all the information they need to help them understand how these regulatory decisions affect them and their patients,” Ellen Strahlman, Glaxo’s chief medical officer, said in an e-mailed statement.
Avandia and Avandamet, which both contain the active ingredient rosiglitazone, last year garnered revenue of 771 million pounds ($1.2 billion), down from 1.6 billion pounds in 2006. Actos, from Takeda Pharmaceutical Co., is the world’s best-selling diabetes medicine, generating 387 billion yen ($4.6 billion) in the year ended March 31, according to the Osaka, Japan-based company’s annual report.
‘Minimal’ Revenue Ahead
Glaxo said it expects Avandia sales of 100 million pounds to 150 million pounds in the second half, and “minimal” revenue from the drug after that. The drugmaker said it will have one-time costs of 100 million pounds this year to write off Avandia and inventories of the medicine.
Le Berrigaud, the analyst at Raymond James, will cut his revenue estimates by 300 million pounds to 400 million pounds for the next couple of years, he said.
“That’s not very meaningful when you have annual sales of 30 billion pounds and as the drug will go off patent in 2012 anyway,” Le Berrigaud said.
Avandia already had restrictions in Europe, limiting use to patients that had failed to respond to another treatment, the EMA said. The regulators said they couldn’t identify another way to limit the risk to patients other than suspending sales. The drug will stop being available in Europe in a few months, the agency said.
“I am not happy with this decision,” said Gregor M. Hess, a physician from Worms, Germany, who specializes in diabetes. Pulling the medicine from the market doesn’t make sense “because it could always be an option for some patients,” he said in Stockholm, where he was attending the European Association for the Study of Diabetes annual meeting.
A Decade to Decide
The EMA’s Eichler said it took the agency a decade to be sure that the heart risk seen in studies was linked to the drug and not merely a result of diabetes.
“Are we happy with the fact it took 10 years? Of course not,” Eichler said on the conference call. “Could there have been a better way to handle this? I don’t think there would have been many other opportunities to handle this faster.”
Glaxo conducted a study of Avandia, dubbed Record, at the request of European regulators. The 4,447-person, five-year trial found that Avandia more than doubled the risk of heart failure without increasing the rate of hospitalization or death from cardiovascular causes, compared with older diabetes medicines. The data, presented in June 2009, are limited because more people in the group receiving Avandia were taking cholesterol medications and patients and doctors knew which diabetes drug was prescribed.
Increased Danger
“Data from clinical trials, observational studies and meta-analyses of existing studies that have become available over the last three years have suggested a possibly increased risk of ischaemic heart disease associated with the use of rosiglitazone,” the EMA said today.
A study published last month found that Actos, which is the same type of treatment as Avandia, causes as many heart problems as the Glaxo medicine. Takeda says the drug is safe. Eric Abadie, the chairman of the EMA’s Committee for Medicinal Products for Human Use, said on a conference call that Actos doesn’t appear to have the same risks as Avandia.
FDA reviewers were divided about the Record study, according to documents released on July 9. Thomas A. Marciniak, a medical team leader at the agency, said Record “was inadequately designed and conducted,” while Ellis Unger, deputy director of the FDA’s Office of Drug Evaluation, called the results of the study “reassuring.”
Considerable Uncertainty
“We are not withdrawing the drug at this time because there is considerable uncertainty about this signal and whether it is valid,” said Janet Woodcock, head of the FDA’s Center for Drug Evaluation and Research, on a conference call today with reporters. The next step is for independent doctors to review Glaxo’s Record study.
The FDA ordered Glaxo to develop a program where doctors will register patients who are prescribed Avandia and document why they need the drug. Patients will have to review statements describing the cardiovascular safety findings and acknowledge that they understand the risks. Physicians will have to prove that people prescribed Avandia for the first time haven’t been helped by other diabetes drugs and choose not to take Actos because of medical reasons.
The new risk-management program will take “several months” to implement, the FDA said.
Warring Factions
“This is clearly a compromise between warring factions in the FDA,” said Diana Zuckerman, director of the National Research Center for Women & Families in Washington, whose father had taken Avandia. “For FDA to say they can manage this restriction seems overly optimistic, not evidence-based.”
European regulators may reconsider their decision if new data emerges on Avandia, said FDA Commissioner Margaret Hamburg. The agencies came to different conclusions on how best to protect patients because the U.S. is comfortable relying on restricted access programs to manage risks, Hamburg said.
Patients should consult their doctors before they stop taking any treatment for diabetes, said Ulf Smith, president of the European diabetes group.
“Physicians have an array of drugs that they can replace rosiglitazone with,” Smith said in an interview in Stockholm.
Earlier this year, Glaxo agreed to settle about 10,000 lawsuits alleging the drugmaker hid Avandia’s heart-attack risk for about $460 million, or an average of $46,000 a case, people familiar with the settlements said. Those people sought anonymity because the accords are private.
The company still faces about 3,000 suits over Avandia, analysts say. Those cases are consolidated in federal and state courts in Pennsylvania.
--With reporting by Dermot Doherty in Geneva, Jef Feeley in Wilmington and Albertina Torsoli in Stockholm. Editors: Bruce Rule, Donna Alvarado
To contact the reporter on this story: Kristen Hallam in London at [email protected]; Catherine Larkin in Washington at [email protected].
To contact the editors responsible for this story: Phil Serafino at [email protected]; Reg Gale at [email protected]. ||||| Diabetes drug Avandia banned in Europe, restricted in US
LONDON — The diabetes drug Avandia will no longer be available to patients in Europe and will be restricted in the US over fears it increases the risk of heart attack and strokes, regulators said Thursday.
The controversial drug made by British company GlaxoSmithKline would be pulled in Europe within the next few months, said the European Medicines Agency.
In the United States, the Food and Drug Administration decided to severely limit the availability of Avandia but stopped short of an outright ban.
It cited data that suggested "an elevated risk of cardiovascular events, such as heart attack and stroke, in patients treated" with the drug, which has long been associated with such health problems.
GlaxoSmithKline said it believed Avandia -- which generated some 1.2 billion dollars in 2009 for the firm -- remained an "important treatment" and was working with the regulators to resolve the concerns.
The European watchdog said it had taken the decision to pull the drug due to concerns over its active substance rosiglitazone.
It decided also to halt the sale of Glaxo's other diabetes drugs, Avandamet and Avaglim, since they too contained rosiglitazone.
"The European Medicines Agency today recommended the suspension of the marketing authorisations for the rosiglitazone-containing anti-diabetes medicines Avandia, Avandamet and Avaglim," said a statement from the EMA.
"These medicines will stop being available in Europe within the next few months. Patients who are currently taking these medicines should make an appointment with their doctor to discuss suitable alternative treatments."
The EMA said the Europe-wide suspension would remain unless there was "convincing data to identify a group of patients in whom the benefits of the medicines outweigh their risks".
US regulator the FDA had already slapped a health warning on the drug after a study in 2007 linking the medication to serious health concerns.
Under the FDA's restrictions announced Thursday, Avandia will be available to new US patients with type 2 diabetes only if they are unable to control their glucose levels through other medications.
Existing diabetes sufferers taking Avandia will be allowed to continue to take the medicine if they so choose, the FDA statement said.
Doctors will now have to attest that their patients are eligible to be prescribed Avandia, and the patients will have to acknowledge that they are aware of the risks.
"The FDA is taking this action today to protect patients, after a careful effort to weigh benefits and risks," said FDA commissioner Margaret Hamburg.
"We are seeking to strike the right balance to support clinical care."
The FDA said it would require Glaxo to develop a restricted access program for Avandia under a risk evaluation and mitigation strategy.
Copyright © 2013 AFP. All rights reserved. More » ||||| | multi_news_1_0_0 |
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Rennes — More research on camel milk is needed to develop potentially valuable dairy products for marginalised communities in desert regions, experts have said.
A staple in the diets of many nomads in Africa and Asia, camel milk has been "neglected" by Western research, resulting in the under-development of one of the few foods that can be produced in harsh, desert conditions, according to Bernard Faye, a camel milk expert with the French agricultural research institute CIRAD.
He was speaking at a meeting on milk's development potential, held in France last month (21-23 May).
Of the 10,000 studies published on milk each year, only about ten are devoted to camel milk, estimated Faye. He added that little is known about the proteins in camel milk - which are structurally different from those in other milks - and consequently methods to preserve it.
Unlike cow milk, whose shelf life is extended from weeks to months by sterilising it using ultra-high temperature (UHT) treatment, a similar process has yet to be found for camel milk, said Faye.
The lack of UHT camel milk means that camel herders in the Sahel region of Africa have milk surpluses during the wet season and shortages during the dry season, said Nancy Abeiderrahmane, whose Mauritania-based dairy Tiviski sources milk from local nomadic groups.
In a research partnership with CIRAD and the UN Food and Agriculture Organization (FAO), Abeiderrahmane initially attempted to deal with milk surpluses by developing the first cheese from camel milk, a process complicated by the lack of coagulating proteins in the milk.
But the product has proved unpopular in Mauritania, where cheese is not traditionally eaten, she said.
Instead, she added, UHT milk would be the ideal way to deal with seasonal "gluts".
"UHT milk would enable processing plants to accept all the milk that herders can supply," Abeiderrahmane said. "The milk would fill market gaps during leaner periods and the surplus could be exported, allowing for expanded production."
While UHT camel milk would be an "important economic asset for the Sahel", it is impossible for a medium-sized dairy such as hers to undertake research without support from larger funding institutions, she said. She called on the FAO to spearhead research efforts.
But Anthony Bennett, the FAO's livestock industry officer, said firms should take the lead in developing new technologies when there is "market potential".
"We see our role as identifying the potential for these different kinds of milk and then working with our R&D partners to encourage investments in those areas," he said.
National research institutes should also play more of a role, added Faye, noting that research could be advanced through greater coordination between the "very atomised" existing research initiatives on camel milk.
Such research would ultimately help highlight nomadic people's importance to regional food chains, said Abeiderrahmane.
"There are resources in deserts. You can make meat and milk, but the only way to do it is by moving around," she said. "Economically, nomads make sense, but it's a very tough lifestyle and they should be supported. Countries should acknowledge their importance in producing wealth." ||||| It seems like every other week someone gets ill from raw milk. The most recent incident occurred last month in West Michigan, when a 31-year-old woman and a six-year-old girl from different counties fell ill after drinking raw milk from a farm called Green Pastures. The Centers for Disease Control have released updated information on the link between raw milk and outbreaks of E. Coli infections, warning that a record number of such outbreaks were reported between 2010 and 2012.
We have a fraught relationship with raw milk in the US, but elsewhere the routine consumption of raw milk is far more normalized. Raw milk vending machines, for example, have recently been installed all over Europe, allowing unpasteurized dairy fiends to get a fix on the regular. The Middle East is long accustomed to drinking raw milk, and we're not talking about cows or goats here. There, the milk of the humble dromedary—the camel—is so prized that camel owners often forego drinking the milk themselves, saving it for special occasions or when guests drop by. The Bedouins believe it to have curative powers, and anecdotal evidence seems to support such assertions: some parents of autistic children claim the milk improves sociability and mood in their kids.
Walid Abdul-Wahab believes that raw camel milk packs a double-whammy of good health. The Saudi Arabian native is the founder of Desert Farms, a California-based company that sources raw camel milk from a network of Amish farms in the Midwest (the Amish have a history with raw milk—in 2011, a Pennsylvania farm was raided and its owner accused of smuggling the dairy into Washington, D.C., where its sale was illegal). We caught up with Abdul-Wahab to find out about what's going on his product.
Desert Farms camel milk. Photo courtesy of Desert Farms.
MUNCHIES: So, why camel milk? Why did you decide to start selling it in the US? Walid Abdul-Wahab: I grew up in Saudi Arabia, where camel milk was ingrained in our culture. In the Middle East it's used to honor your guests. Then I realized, by reading religious texts, that people felt that it could actually benefit the ill, people with diabetes, with autism. They didn't mention these diseases by name, but they described their symptoms and all these prophets were recommending camels' milk. I wanted to try to bring something positive from my home country to the US, when there's often a barrier of communication between the two countries, and a lot of misconceptions about the Middle East. I also wanted to sell camel milk because of its health benefits—it's been helping a lot of children with autism.
Yeah, I've read about that. How does it help? There is no scientific research behind this yet so we don't make any of those kinds of claims. But I can tell you what I've heard from people who have tried it. The anti-inflammatory properties are the major factor that helps improve brain function. Anything you consume that's anti-inflammatory reduces the amount of toxins in found in your gut, and reducing those toxins has a clear effect on the brain. It improves function. That's why all these autistic children are on very strict diets, particularly gluten-free. Any food that has gluten in creates inflammation, and that's exactly what you want to avoid.
What does the milk taste like? Camels seem like pretty funky animals. The milk tastes sweeter than cow's milk, sometimes quite earthy. It isn't repulsive at all. It's a very clean taste, closer to cow's milk than any other.
Where are these camels that you're getting the milk from? All our farms are run by the Amish community, in places like Ohio and Pennsylvania. The camels on these farms actually come from Australia. Camels run wild over there—they're an invasive species—so a couple of years ago these Amish farmers imported them by the thousands.
Why does the Amish community have a monopoly over these camel farms? The Amish knew about camels' milk a while before anyone else did. The first farmer in the US to milk a camel, that I know of, was one of our farmers in Missouri. He told the Amish community that it could be a really good source of income, and, if it doesn't work out, then we'll have camels for camel rides at Christmas for the living Nativity scenes. It was a win-win situation for them.
So why do you offer raw camels' milk in addition to pasteurized? Are you concerned about reports linking serious illnesses to the consumption of raw milk? I believe that raw milk is more nutritious. It all depends on how much you trust the source of the milk—if I were in the middle of the desert and someone offered me camels' milk and I didn't know where it came from, I'd rather have pasteurized. But if I trusted the source of the milk and knew exactly where it was coming from, knew how healthy the animal was, and what it was eating, then I'll drink the raw milk right away. People seem to tolerate the raw milk a lot better than the pasteurized. It makes sense that if you're heating up milk to the point where you're killing bacteria, you're also killing beneficial bacteria. The way most dairy processors are heating their milk is at a ridiculously high temperature. They heat it at 275 degrees Fahrenheit for two to three seconds. But you can heat the milk slowly at a moderate temperature, as we do, which keeps the flavor and the nutrition inside. The way we look at it is that these reports state illnesses in their hundreds within a year, which I see as insignificant when you compare it to something like smoking. It really depends on the treatment of the farm. A lot of these breakouts are because these farms are not inspected. If the government had a system in place for inspecting raw milk farms in the way it does pasteurized milk farms, I don't think we'd have the same problem.
Given the restrictions that some states have on the sale of raw milk, how does that work for you? We are not allowed to sell in every state, but what we do offer is a herd share. You basically buy into being a member of the farm, so you're a part-owner of the camels. If you own the livestock then you can drink it wherever you are. That's a very common practice in the raw dairy industry. But most of our customers live in states that allow raw milk. California is our biggest state. There, raw milk is legal and we sell in nine locations of the store Lassenes Market. Right now we're also finalizing a deal with Whole Foods—they're going to be carrying our pasteurized camel milk at 40 of their stores in northern California.
What's the deal with the "colostrum" I saw on your website? It sounds intense. Colostrum is basically the first milk that comes out of the female camel when her baby is born. It's extra-nutritious, helping to get the new baby healthy and strong as fast as possible. Colostrum has been known for hundreds of years, regardless of the mammal. It's the ultimate superfood. For us it's very popular—whenever we get a baby calf we always notify our customers, and within a couple of hours it sells out. It's our fastest-selling item, and is also very rare—we only get, like, four or five bottles at a time, and that's reflected in the price—half a bottle costs $40. It's just milk, so it tastes basically the same as the milk that the mother produces later—a little thicker and more sour—but it's much darker in color, like a dark yellow.
Wow. Thanks for talking to me, Walid. ||||| | – Could camel's milk be the health drink of the future? Dr. Frank King hopes so. He currently has 23 camels on his farm near Asheville, NC, a mix of humped dromedaries and double-humped Bactrians that are milked by hand—no crouching or seat needed. The creatures' milk has less cholesterol than cow's milk, and it's got more protein, vitamin C, and iron, per scientific studies, the Citizen-Times reports. And "the milk is tasty," says King, who describes the dromedaries' milk as the saltier and creamier of the two. What's more, the milk is also expensive, potentially at least $18 a pint. It's often raw as well; King says he's still testing pasteurization methods. King's camels are just a handful of the estimated 5,000 now in the US, with camel-milking outfits established in seven states (including Pennsylvania, Michigan, and Ohio) and on deck in seven more. Last month Vice spoke with the owner of California-based Desert Farms, which relies on Amish farmers to supply its milk. Walid Abdul-Wahab extols the drink's health benefits, too, which are said to include an unproven one: that it helps kids with autism. "There is no scientific research behind this yet so we don't make any of those kinds of claims. But I can tell you what I've heard from people who have tried it": that its anti-inflammatory properties have beneficial effects on the brain. As far as camel-milk studies go, one expert last month argued there aren't enough. By his count, only about 10 of the 10,000 milk-related studies published annually focus on camel milk, reports allAfrica. (As far as healthy eats go, watercress has been named the No. 1 "powerhouse" vegetable.) | multi_news_1_0_0 |
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– If taking a pill that tricks your body into feeling full isn't appealing, how about some quick zaps instead? The FDA has approved a device that uses electrodes implanted in the abdomen to fool the brain, reports Bloomberg. The electrodes stimulate the hunger-controlling vagus nerve, which in turn tells the brain that the stomach is full, explains HealthDay News. The Maestro Rechargeable System will be available only to obese adults who have one other related condition, such as Type 2 diabetes, says an FDA release. The Wall Street Journal likens it to a "pacemaker for the stomach" and quotes a gastrointestinal surgeon who predicts the cost will be between $30,000 and $40,000, on par with gastric bypass surgery. The device's maker, EnteroMedics of Minnesota, must keep track of at least 100 patients for five years after surgery for a follow-up study. (Click to read why people tend to weigh less on Fridays.)
Expand this summary. | EnteroMedics Inc.'s weight-loss device uses implantable electrodes to trick the brain into thinking the stomach is full.
EnteroMedics Inc.'s weight-loss device uses implantable electrodes to trick the brain... Read More
EnteroMedics Inc.'s weight-loss device uses implantable electrodes to trick the brain into thinking the stomach is full. Close
A first-of-its-kind weight-loss device from EnteroMedics Inc. (ETRM), which uses implantable electrodes to trick the brain into thinking the stomach is full, was approved in the U.S.
The Food and Drug Administration cleared the Maestro Rechargeable System today, the first weight-loss device that targets the pathway between the brain and the stomach that controls feelings of hunger and fullness.
The system, approved for obese patients 18 and older who have at least one other weight-related condition such as Type 2 diabetes, is also the first obesity device approved in the U.S. since 2007, the FDA said in a statement.
EnteroMedics, which has been publicly traded since 2007, rose 21 percent to $1.42 at 12:30 p.m. in New York, bringing its market value to almost $100 million. The shares had declined 50 percent in the past year through yesterday.
Products to help Americans lose weight have been a hot category in the last few years, though one that has had some trouble producing major revenue. The FDA has approved four weight-loss drugs since 2012, three pills and one injection.
St. Paul, Minnesota-based EnteroMedics’ system uses electrodes implanted in the abdomen to send electrical pulses to nerves, the FDA said. Patients use external controllers to charge the device and allow doctors to adjust its settings.
Source: EnteroMedics Inc. via Bloomberg EnteroMedics’ system uses electrodes implanted in the abdomen to send electrical pulses to nerves, the FDA said. Close EnteroMedics’ system uses electrodes implanted in the abdomen to send electrical pulses... Read More Close Open Source: EnteroMedics Inc. via Bloomberg EnteroMedics’ system uses electrodes implanted in the abdomen to send electrical pulses to nerves, the FDA said.
How exactly the system helps people lose weight is unknown, the FDA said.
“Obesity and its related medical conditions are major public health problems,” William Maisel, deputy director for science and chief scientist in the FDA’s Center for Devices and Radiological Health, said in the statement. “Medical devices can help physicians and patients to develop comprehensive obesity treatment plans.”
Adverse Events
Serious adverse events for EnteroMedics’ system included nausea, pain at the neuroregulator site, vomiting and surgical complications. Other side effects included heartburn, problems swallowing, belching and chest pain.
A clinical trial of the Maestro didn’t achieve its primary objective of getting patients to lose 10 percent more excess weight than the control group, the FDA said. Still, an agency advisory panel found that data from the trial provided evidence of sustained weight loss and that the device’s benefits outweighed its risks for some patients.
Even with the FDA ruling, the Maestro faces a tough road for wide adoption. Many insurers and government health programs have refused to cover weight-loss treatments since Belviq, from Arena Pharmaceuticals Inc. and Eisai Co. (4523), and Qsymia, by Vivus Inc. (VVUS), were approved in 2012.
To contact the reporter on this story: Anna Edney in Washington at [email protected]
To contact the editors responsible for this story: Crayton Harrison at [email protected] Andrew Pollack ||||| Federal regulators on Wednesday approved a novel dieting device that acts like a pacemaker for the stomach by manipulating the nerve pathway that makes people feel hungry or full.
The device, made by EnteroMedics Inc. of St. Paul, Minn., is the first of its kind to treat obesity by targeting nerves that link the stomach and the brain. The Maestro Rechargeable System would block electrical signals in the abdominal vagus nerve by... ||||| By Scott Roberts, HealthDay Reporter
WEDNESDAY, Jan. 14, 2015 (HealthDay News) -- A new electrical stimulation device designed to control obesity by targeting the nerve pathways between the brain and stomach that regulate hunger and fullness has been approved by the U.S. Food and Drug Administration.
The Maestro Rechargeable System is the first FDA-approved obesity device since 2007, the agency said Wednesday in a news release. The system is sanctioned for adults with a body-mass index (BMI) of between 35 and 45, with another obesity-related condition such as type 2 diabetes, who haven't been able to lose enough weight with an approved weight loss program.
"Obesity and its related medical conditions are major public health problems," said Dr. William Maisel, deputy director for science and chief scientist in the FDA's Center for Devices and Radiological Health. "Medical devices can help physicians and patients to develop comprehensive obesity treatment plans."
The Maestro system includes a rechargeable pulse generator and wire electrodes that are implanted in the abdomen. The electrodes stimulate the vagus nerve, which carries signals to the brain that the stomach feels empty or full, the FDA said.
The device's safety and effectiveness were evaluated in studies involving 233 people with a BMI of 35 or greater, a height-to-weight measurement that indicates clinical obesity. People who used the device for 12 months lost about 8.5 percent more excess weight than people who didn't use the device, the FDA said.
The most serious side effects included nausea, device-site pain, vomiting and surgical complications. More common but less serious side effects included heartburn, problems swallowing, belching, mild nausea and chest pain.
As a condition of approval, device maker EnteroMedics must conduct a five-year, follow-up study involving at least 100 users, the FDA said.
EnteroMedics is based in St. Paul, Minn.
More information
Visit the FDA to learn more.
Copyright © 2015 HealthDay. All rights reserved.
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The U.S. Food and Drug Administration today approved the Maestro Rechargeable System for certain obese adults, the first weight loss treatment device that targets the nerve pathway between the brain and the stomach that controls feelings of hunger and fullness.
The Maestro Rechargeable System, the first FDA-approved obesity device since 2007, is approved to treat patients aged 18 and older who have not been able to lose weight with a weight loss program, and who have a body mass index of 35 to 45 with at least one other obesity-related condition, such as type 2 diabetes.
BMI, which measures body fat based on an individual’s weight and height, is used to define the obesity categories. According to the Centers for Disease Control and Prevention, more than one-third of all U.S. adults are obese, and people with obesity are at increased risk of heart disease, stroke, type 2 diabetes and certain kinds of cancer.
“Obesity and its related medical conditions are major public health problems,” said William Maisel, M.D., M.P.H., deputy director for science and chief scientist in the FDA’s Center for Devices and Radiological Health. “Medical devices can help physicians and patients to develop comprehensive obesity treatment plans.”
The Maestro Rechargeable System consists of a rechargeable electrical pulse generator, wire leads and electrodes implanted surgically into the abdomen. It works by sending intermittent electrical pulses to the trunks in the abdominal vagus nerve, which is involved in regulating stomach emptying and signaling to the brain that the stomach feels empty or full. Although it is known that the electric stimulation blocks nerve activity between the brain and the stomach, the specific mechanisms for weight loss due to use of the device are unknown.
External controllers allow the patient to charge the device and allow health care professionals to adjust the device’s settings in order to provide optimal therapy with minimal side effects.
The safety and effectiveness of the Maestro Rechargeable System were evaluated in a clinical trial that included 233 patients with a BMI of 35 or greater. The weight loss and adverse events of 157 patients who received the active Maestro device (the experimental group) were compared to 76 patients in the control group who received a Maestro electrical pulse generator that was not activated. The study found that after 12 months, the experimental group lost 8.5 percent more of its excess weight than the control group. About half (52.5 percent) of the patients in the experimental group lost at least 20 percent of their excess weight, and 38.3 percent of patients in the experimental group lost at least 25 percent of their excess weight.
The clinical study did not meet its original endpoint, which was that the experimental group lose at least 10 percent more excess weight than the control group. However, an FDA Advisory Committee (the Gastroenterology and Urology Devices Panel) found the 18-month data supportive of sustained weight loss, and agreed that the benefits of the device outweighed the risks for use in patients who met the criteria in the device’s proposed indication.
In considering the benefits and risks of the device in its review of the Maestro Rechargeable System, the FDA considered the clinical study and the Panel’s recommendations. Additionally, the Agency looked at an FDA-sponsored survey relating to patient preferences of obesity devices that showed a group of patients would accept risks associated with this surgically implanted device for the amounts of weight loss expected to be provided by the device.
As part of the approval, the manufacturer must conduct a five year post approval study that will follow at least 100 patients and collect additional safety and effectiveness data including weight loss, adverse events, surgical revisions and explants and changes in obesity-related conditions.
Serious adverse events reported in the clinical study included nausea, pain at the neuroregulator site, vomiting, as well as surgical complications. Other adverse events included pain, heartburn, problems swallowing, belching, mild nausea and chest pain.
The Maestro Rechargeable System is manufactured by EnteroMedics of St. Paul, Minnesota.
The FDA, an agency within the U.S. Department of Health and Human Services, protects the public health by assuring the safety, effectiveness, and security of human and veterinary drugs, vaccines and other biological products for human use, and medical devices. The agency also is responsible for the safety and security of our nation’s food supply, cosmetics, dietary supplements, products that give off electronic radiation, and for regulating tobacco products.
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Summarize this article:
The web archive for cms.gov, the Agency website of the Centers for Medicare & Medicaid Services in the US department of Health & Human Services. ||||| WASHINGTON—President Donald Trump unveiled dozens of initiatives aimed at curbing high drug prices Friday, a raft of modest moves that left the pharmaceutical industry relieved and buoyed their stocks.
“We’re going to take on one of the biggest obstacles to affordable medicine: the tangled web of special interests,” Mr. Trump said from the White House Rose Garden. “The drug lobby is making an absolute fortune at the expense of American consumers.”
... ||||| Secretary of Health and Human Services Alex Azar looks on as President Donald Trump speaks during an event about prescription drug prices in the Rose Garden of the White House, Friday, May 11, 2018, in... (Associated Press)
WASHINGTON (AP) — President Donald Trump's long-awaited plan to bring down drug prices, unveiled Friday, will mostly spare the pharmaceutical industry he previously accused of "getting away with murder" and instead focus on increasing private competition and requiring more openness about costs.
In Rose Garden remarks at the White House, Trump called his plan the "most sweeping action in history to lower the price of prescription drugs for the American people." But it does not include his campaign pledge to use the massive buying power of the government's Medicare program to directly negotiate lower prices for seniors.
That idea has long been supported by Democrats but is a non-starter for drugmakers and most Republicans in Congress.
Instead, the administration will pursue a raft of old and new measures intended to improve competition and transparency in the notoriously complex drug pricing system. Those include a proposal requiring drugmakers to disclose the cost of their medicines in their television advertisements. Health Secretary Alex Azar said the Food and Drug Administration would immediately examine requiring that information in TV ads.
The proposals also include banning the pharmacist "gag rule," which Trump said prevents druggists from telling customers about lower-cost options so they can save money, and speeding up the approval process for over-the-counter medications so patients can buy more drugs without prescriptions.
It's an approach that avoids a direct confrontation with the powerful pharmaceutical lobby, but it could also underwhelm Americans seeking relief from escalating prescription costs.
Perhaps the most threatening idea under consideration is to give the private health insurers who run Medicare plans more negotiating power with drugmakers. But administration officials offered few specifics on how that might work.
"Consumers are ultimately going to be the judge of this announcement," said Dan Mendelson, a health care consultant. "If they don't address the cost that patients see at the pharmacy counter it's not going to be seen as responsive."
A majority of Americans say passing laws to bring down prescription drug prices should be a "top priority" for Trump and Congress, according to recent polling by the Kaiser Family Foundation.
As a candidate, Trump railed against the pharmaceutical industry. But as president he has shied away from major reforms and staffed his administration with appointees who have deep ties to the industry. That includes Azar, a former top executive at Eli Lilly.
Azar and other Trump officials have described the pricing problem in stark terms and promised bold action.
"Every incentive is toward higher list prices because everyone in the system gets a cut off that list price except the patient," said Azar, speaking on "Fox and Friends" on Friday morning.
He said one new proposal would allow senior citizens enrolled in Medicare who hit the catastrophic period to pay nothing out of pocket, "so really relieve a huge burden on our senior citizens."
Parts of the plan were previously released in the president's budget proposal and would require action by Congress. Those steps include: requiring insurers to share rebates from drug companies with Medicare patients and changing the way Medicare pays for high-priced drugs administered at doctors' offices.
Trump staffers said the new steps coming Friday could be taken immediately without action by lawmakers, who are mainly focused on November elections. The measures aim to increase competition, create incentives for drugmakers to lower initial prices and stop foreign governments from "freeloading" off U.S. pharmaceutical research. But the officials gave few specifics.
Public outrage over drug costs has been growing for years as Americans face pricing pressure from multiple sources: New medicines for life-threatening diseases often launch with prices exceeding $100,000 per year. And older drugs for common ailments like diabetes and asthma routinely see price hikes around 10 percent annually. Meanwhile Americans are paying more at the pharmacy counter due to health insurance plans that require them to shoulder more of their prescription costs.
Trump officials have hinted for weeks that the plan, in part, will untangle the convoluted system of discounts and rebates between drugmakers and insurers, pharmacy benefit managers and other health care middlemen. FDA Commissioner Scott Gottlieb — another Trump official with industry ties — says this lack of transparency creates perverse incentives in which drugmakers and other health care companies all benefit from rising prices.
"Right now, we don't have a truly free market when it comes to drug pricing, and in too many cases, that's driving prices to unaffordable levels for some patients," Gottlieb said in a speech last week.
Experts who study drug pricing are encouraged that the discussion has moved on from outrage to more sophisticated proposals.
"This is progress and I think there's no question that opening up the machine to make it more clear how it works will lead to change — hopefully to constructive change," said Dr. Peter Bach, director of Memorial Sloan Kettering's Center for Health Policy and Outcomes.
But others warn there is no guarantee that unraveling the current pricing-setting bureaucracy will lead to lower prices, because it all starts with drugmakers' initial prices.
Drugmakers generally can charge as much as the market will bear because the U.S. government doesn't regulate medicine prices, unlike most other countries.
The result, in part, is the highest drug prices in the world.
The U.S. spent $1,162 per person on prescription drugs in 2015, according to the Organization for Economic Cooperation and Development. That's more than twice the $497 per person spent in the United Kingdom, which has a nationalized health care system.
Medicare is the largest purchaser of prescription drugs in the nation, covering 60 million seniors and Americans with disabilities, but it is barred by law from directly negotiating lower prices with drugmakers. Democrats have long favored giving Medicare that power, but Republicans traditionally oppose the idea.
Allowing Medicare to negotiate prices is unacceptable to the powerful drug lobby, which has spent tens of millions of dollars since Trump's inauguration to influence the Washington conversation around drug prices, including a high-profile TV advertising campaign portraying its scientists as medical trailblazers.
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Associated Press writers Ken Thomas and Catherine Lucey contributed to this report.
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Matthew Perrone can be followed on Twitter: @AP_FDAwriter |||||
Summary: | – President Trump's long-awaited plan to bring down drug prices will mostly spare the pharmaceutical industry he previously accused of "getting away with murder" and instead focus on increasing private competition and requiring more openness about costs, per the AP. In Rose Garden remarks at the White House, Trump called his plan the "most sweeping action in history to lower the price of prescription drugs for the American people." (The plan is here.) But it does not include his campaign pledge to use the massive buying power of the government's Medicare program to directly negotiate lower prices for seniors. The Washington Post notes that the idea was the one feared most within the industry. The Wall Street Journal reports that drugmakers and pharmacy-benefit managers "suggested privately they were relieved to avoid harder blows from the plan." Instead, the administration will pursue a raft of old and new measures intended to improve competition and transparency in the drug-pricing system. Those include a proposal requiring drugmakers to disclose the cost of their medicines in their TV advertisements. Health Secretary Alex Azar said the Food and Drug Administration would immediately examine requiring that information in TV ads. The proposals also include banning the pharmacist "gag rule," which Trump said prevents druggists from telling customers about lower-cost options so they can save money, and speeding up the approval process for over-the-counter medications so patients can buy more drugs without prescriptions. It's an approach that avoids a direct confrontation with the powerful pharmaceutical lobby, but it could also underwhelm Americans seeking relief from escalating prescription costs. | multi_news_1_0_0 |
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PRAGUE (AFP) -
Czech President Milos Zeman, known for showing hostility towards journalists, taunted them on Thursday, saying he regretted making them look like "little idiots" during a bizarre event in which he set a huge pair of red underpants on fire.
The visibly frail 73-year-old Zeman abruptly announced a press conference on Thursday afternoon, raising speculation about his possible resignation.
"I apologise to the journalists whose intelligence I tested, unsuccessfully as always," Zeman told reporters gathered for the briefing the gardens of Prague Castle where he was flanked by his spokesman, assistants and several firemen.
To their amazement, Zeman then proceeded to burn a huge pair of red underpants in a fire pit, assisted by two firemen dressed in full gear.
"The time of underwear in politics is over," Zeman declared. "I'm sorry to make you look like little idiots, you really don't deserve it," he told reporters before leaving in his car.
The red underpants, measuring roughly one square metre, resembled a pair that Czech pranksters had flown from a flag pole atop the presidential palace in 2015 in protest against Zeman.
The pranksters said that the red colour of their boxer-short style protest flag symbolised the unhealthily close link they believed Zeman, a former communist, had with China and Russia.
Staunchly pro-Russian and pro-Chinese, Zeman once dubbed journalists "manure" and "superficial" before telling Russian President Vladimir Putin in China in May 2017 that "journalists should be liquidated".
He also showed up at a press conference in October 2017 with a toy Kalashnikov in his hand labelled "for journalists".
Zeman narrowly won a second consecutive term in January elections, beating his pro-European liberal rival Jiri Drahos in a knife-edge run-off that underscored deep divisions in the EU and NATO state.
Zeman's stunt drew a barrage of criticism on Thursday, with Jiri Pospisil, leader of the right-wing TOP 09 party, exclaiming "let us wake up from this nightmare!"
Zeman's health has come under heavy scrutiny in recent months.
He walks with a cane, is diabetic and is a former heavy drinker and smoker.
© 2018 AFP ||||| PRAGUE (AP) — A fiery stunt by the Czech president has really stunned journalists this time.
Milos Zeman announced a press conference for Thursday, but instead of briefing reporters, he had two firefighters in protective gear burn a huge pair of red underpants in front of them.
Czech media said the boxer shorts in question had been hoisted by activists in 2015, replacing the official presidential flag on Prague Castle. The red underwear was meant to symbolize Zeman's close relationships with Russia and China and has since become a symbol for criticism of his presidency.
After the incineration, Zeman told reporters: "I'm sorry to make you look like little idiots, you really don't deserve it."
Zeman, 72, has often clashed with the press, even waving a fake machine gun at reporters last year. |||||
Write a summary. | – A fiery stunt by the Czech president has really stunned journalists this time. Milos Zeman announced a press conference for Thursday, but instead of briefing reporters, he had two firefighters in protective gear help him burn a huge pair of red underpants in front of them, the AP reports. Per AFP, a "visibly frail" Zeman did the deed on a 10-foot-by-10-foot pair of boxer shorts, and he had some words after the incineration. "The time of underwear in politics is over," he declared to reporters. "I'm sorry to make you look like little idiots, you really don't deserve it." Czech media said the boxer shorts in question resembled a pair that had been hoisted by activists in 2015, replacing the official presidential flag on Prague Castle. The red underwear was meant to symbolize Zeman's close relationships with Russia and China and has since become a symbol for criticism of his presidency. Zeman, 73, has often clashed with the press, even waving a fake machine gun at reporters last year. | multi_news_1_0_0 |
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Article:
By Robert Preidt, HealthDay Reporter
(HealthDay)
THURSDAY, March 31, 2016 (HealthDay News) -- More people worldwide are obese than underweight, a new study found.
The researchers added that about one-fifth of adults could be obese by 2025.
The number of obese people in the world rose from 105 million in 1975 to 641 million in 2014, with obesity rates rising from 3 percent to 11 percent among men and from 6 percent to 15 percent among women, the study found.
Over the same time, the proportion of underweight people fell from 14 percent to 9 percent of men and from 15 percent to 10 percent of women, according to the study.
More than one-quarter of severely obese men and nearly one-fifth of severely obese women in the world live in the United States, the researchers said.
On average, people worldwide have become an average of 1.5 kilograms (3.3 pounds) heavier each decade. At the current pace, about 18 percent of men and 21 percent of women will be obese, and more than 6 percent of men and 9 percent of women will be severely obese by 2025, the study found.
The findings were released online on March 31 in The Lancet.
"Over the past 40 years, we have changed from a world in which underweight prevalence was more than double that of obesity, to one in which more people are obese than underweight," said study senior author Majid Ezzati, a professor at Imperial College London's School of Public Health, in England.
"If present trends continue, not only will the world not meet the obesity target of halting the rise in the prevalence of obesity at its 2010 level by 2025, but more women will be severely obese than underweight by 2025," he said in a journal news release.
"To avoid an epidemic of severe obesity, new policies that can slow down and stop the worldwide increase in body weight must be implemented quickly and rigorously evaluated, including smart food policies and improved health care training," Ezzati said.
Despite the findings, extremely low weight remains a serious public health problem in the poorest parts of the world, the researchers noted. For example, nearly one-quarter of people in south Asia are underweight, as are 15 percent of men and 12 percent of women in central and east Africa.
The study findings reflect "a fatter, healthier but more unequal world," wrote George Davey Smith in an accompanying journal editorial. He is a professor of clinical epidemiology at the University of Bristol, in England.
"A focus on obesity at the expense of recognition of the substantial remaining burden of undernutrition threatens to divert resources away from disorders that affect the poor to those that are more likely to affect the wealthier in low-income countries," he noted.
More information
The U.S. National Institute of Diabetes and Digestive and Kidney Diseases outlines the health risks of being overweight. ||||| More than one in ten men and one in seven women across the globe are now obese, according to the world's biggest obesity study.
The research, which was led by scientists from Imperial College London, involved the World Health Organization and over 700 researchers across the globe, incorporated measurements of weight and height from nearly 20 million adults in most of the world’s countries. The research team has also created interactive maps and other visuals - available here - that show the data for each country, and how they compare to each other.
The number of people across the globe whose weight poses a serious threat to their health is greater than ever before – Professor Majid Ezzati Study author
The study, published in the journal The Lancet, calculated and compared BMI among adult men and women from 1975 to 2014. BMI is a measure of a person’s weight for their height, and indicates whether their weight is healthy.
The data revealed that in four decades global obesity among men has tripled - from 3.2% in 1975 to 10.8%. Obesity among women meanwhile has more than doubled, from 6.4 % in 1975 to 14.9% in 2014.
This translates as 266 million obese men and 375 million obese women in the world in 2014. It also means the world’s population has become heavier by around 1.5kg in each subsequent decade since 1975.
In addition, 2.3% of the world’s men, and 5% of the world’s women are now classed as severely obese, which is defined as having a BMI of over 35 kg/m2. This places an individual at significantly increased risk of conditions such as diabetes, heart disease and cancer.
Analysis of the findings showed more obese men and women now live in China and the USA than in any other country. However the USA still has the highest number of severely obese men and women in the world.
The team predicted if these global trends continue, by 2025 18% of the world’s men and 21% of women will be obese. Furthermore, the probability of reaching the World Health Organization global obesity target (which aims for no rise in obesity above 2010 levels by 2025) will be close to zero.
Professor Majid Ezzati, the senior author of the study from the School of Public Health at Imperial, said: “The number of people across the globe whose weight poses a serious threat to their health is greater than ever before. And this epidemic of severe obesity is too extensive to be tackled with medications such as blood pressure lowering drugs or diabetes treatments alone, or with a few extra bike lanes. We need coordinated global initiatives – such as looking at the price of healthy food compared to unhealthy food, or taxing high sugar and highly processed foods - to tackle this crisis.”
The team also examined the number of people who are underweight in different countries. The results revealed levels have decreased from 14% to 9% in men, and 15% to 10% in women. The percentage of underweight individuals was nonetheless still quite high in countries such as India and Bangladesh, where nearly a quarter of adults are underweight.
Professor Ezzati added: “Our research has shown that over 40 years we have transitioned from a world in which underweight prevalence was more than double that of obesity, to one in which more people are obese than underweight. Although it is reassuring that the number of underweight individuals has decreased over the last four decades, global obesity has reached crisis point.
“We hope these findings create an imperative to shift responsibility from the individual to Governments, and to develop and implement policies to address obesity. For instance, unless we make healthy food options like fresh fruits and vegetables affordable for everyone, and increase the price of unhealthy processed foods, the situation is unlikely to change.”
The findings also showed that:
• Japanese men and women had the lowest BMI in the high-income world. Average BMI was higher in English-speaking high-income countries than in non-English speaking high-income countries, with American men and women having the highest BMI of any high-income country.
• The lowest BMIs in Europe were among Swiss women and Bosnian men. Men in the UK had the 10th highest BMI in Europe and women the 3rd highest in Europe. Globally, the UK ranked with the 42nd highest BMI for men and 67th highest for women.
• The country with the highest average BMI was American Samoa (average BMI of 35 kg/m2 for women and 32 kg/m2 for men), where the average individual is classed as obese.
• Morbid obesity, where a person’s weight interferes with basic physical functions such as breathing and walking, now affects around 1 % of men in the world, and 2% of women. In total, 55 million adults are morbidly obese.
The study was funded by The Wellcome Trust, and Grand Challenges Canada. |||||Summary:
| – It's a big world after all: Researchers say that over the last 40 years, the number of obese people worldwide has ballooned and the obese now outnumber the underweight, HealthDay reports. The proportion of obese people worldwide now stands at 11% among men and 15% among women, while 9% of men and 10% of women are underweight, according to researchers who analyzed data on 20 million people in 186 countries for a study in the Lancet medical journal. The researchers warn that if current trends continue, there's no chance of meeting the global target of keeping obesity at 2010 levels in 2025. Instead, they predict that around a fifth of adults worldwide will be obese by 2025. "Although it is reassuring that the number of underweight individuals has decreased over the last four decades, global obesity has reached crisis point," warns lead researcher Majid Ezzati of Imperial College London. To tackle the crisis, he says, there should be global initiatives to ensure that healthy food isn't more expensive than unhealthy, highly processed food. In a Lancet editorial, George Davey Smith from the University of Bristol says we are living in "a fatter, healthier, but more unequal world." He warns that focusing on obesity in wealthy countries could divert resources away from regions like East Africa and South Asia, where a high proportion of people are still underweight. (Another study found that millions of Americans considered to be obese are actually "quite healthy.") | multi_news_1_0_0 |
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Summarize this article:
An article by a woman who is "fighting" her 7-year-old daughter's "childhood obesity" at home—published in the April issue of Vogue—is causing a big backlash online among readers critical of the magazine and its author.
Dara-Lynn Weiss, the author, wrote about her response to a pediatrician who suggested that her daughter, Bea, should be put on a diet because—at 4 feet 4 inches and 93 pounds—she was clinically obese and could be at risk for high blood pressure, cholesterol and diabetes.
It wasn't the diagnosis that readers railed against, but Weiss' management of Bea's subsequent yearlong diet.
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"Sometimes Bea's after-school snack was a slice of pizza or a gyro from the snack vendor," Weiss wrote. "Other days I forced her to choose a low fat vegetable soup or a single hard-boiled egg. Occasionally I'd give in to her pleas for a square of coffee cake, mainly because I wanted to eat half of it. When she was given access to cupcakes at a party, I alternated between saying, 'Let's not eat that, it's not good for you'; 'Okay, fine, go ahead, but just one'; and 'Bea, you have to stop eating crap like that, you're getting too heavy,' depending on my mood. Then I'd secretly eat two when she wasn't looking."
Weiss continued:
I once reproachfully deprived Bea of her dinner after learning that her observation of French Heritage Day at school involved nearly 800 calories of Brie, filet mignon, baguette, and chocolate. I stopped letting her enjoy Pizza Fridays when she admitted to adding a corn salad as a side dish one week. I dressed down a Starbucks barista when he professed ignorance of the nutrition content of the kids' hot chocolate whose calories are listed as "120-210" on the menu board: Well, which is it? When he couldn't provide an answer, I dramatically grabbed the drink out of my daughter's hands, poured it into the garbage, and stormed out.
After Bea lost 16 pounds—meeting her mom's weight-loss goal for her before a Vogue photoshoot—Weiss wrote about her daughter's reaction:
"That's still me," she says of her former self. "I'm not a different person just because I lost 16 pounds." I protest that indeed she is different. At this moment, that fat girl is a thing of the past. A tear rolls down her beautiful cheek, past the glued-in feather. "Just because it's in the past," she says, "doesn't mean it didn't happen."
"I have not ingested any food, looked at a restaurant menu, or been sick to the point of vomiting without silently launching a complicated mental algorithm about how it will affect my weight," Weiss admitted. "Who was I to teach a little girl how to maintain a healthy weight and body image?"
"The socialites who write personal essays for Vogue aren't known for their kindness and humility," Katie Baker wrote on Jezebel.com. But Weiss "has to go down in history as the one of the most f---ed up, selfish women to ever grace the magazine's pages."
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Weiss "comes across as obsessive and the fact that she made such an issue of her daughter's weight, both in public and in Vogue—seems wrong," Dhani Mau wrote on Fashionista.com.
An anonymous blogger for New York magazine added: "I'm pretty sure Weiss just handed her daughter the road map to all her future eating disorders."
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• Erin Burnett 'annoyed' she was used in RNC's 'War on Women' ad ||||| Vogue published kind of a tricky article in their April issue about a woman putting her seven-year-old daughter on a diet. The larger issue of child obesity is, as Weiss makes sure to point out, a real one, and Weiss' daughter was clinically obese and needed to lose weight for health reasons. The article's author, Dara-Lyn Weiss is faced with the complicated task of helping her daughter lose weight without giving her long-term body image issues. Any article on the subject--especially one written in Vogue by a socialite-y upper-class Manhattanite--is going to raise some eyebrows. This one in particular has inspired serious outrage.
For example, Jezebel calls it "the worst Vogue article ever" and Weiss "one of the most fucked up, selfish women to ever grace the magazine's pages." Indeed, some of the things Weiss did to keep her kid from breaking her diet are a little nuts. For example, the article began with the following interaction:
I stepped between my daughter and a bowl of salad nicoise my friend was handing her, raising my palm like a traffic cop. "Thanks," I said, "but she already ate dinner." "But she said she's still hungry," my friend replied, bewildered. I forced a smile. "Yeah, but it's got a lot of dressing on it and we're trying--" "Just olive oil!" my friend interrupted. "It's superhealthy!" My smile faded and my voice grew tense. "I know. She can't." My friend's eyes moved to my daughter, whose gaze held the dish in the crosshairs: a Frisbee-size bowl bursting with oil, tuna, eggs, potatoes, olives.
This may have not been the best way to set up the article if she wanted the reader to believe her to be a sane, reasonable person. Some other not-so-sane things she admitted to doing:
• Angrily throwing an untouched kid's sized hot chocolate in the trash and stormed out of a Starbucks because a barista didn't know exactly how many calories were in it. • Not letting Bea partake in "Pizza Fridays" at school • Making Bea go without dinner because she ate "nearly 800 calories of brie, filet mignon, baguette and chocolate" at school for French Heritage Day (I wish I went to that school)
Also a red flag: Weiss admits to having had issues with food her whole life, including obsessive dieting, fasting, using laxatives, etc. The thing is, she fully acknowledges that, stating, "Who was I to teach a little girl how to maintain a healthy weight and body image?"
Overall, Weiss comes across as obsessive and the fact that she made such an issue of her daughter's weight, both in public and in Vogue--seems wrong. Jezebel contacted Dr. Dolgoff, the founder of "Red Light, Green Light, Eat Right," the which is what Bea's diet was based on, who said she "wasn't thrilled" with the way Weiss interpreted her book. "The parents aren't supposed to react in public," she said. "They're supposed to be on their child's team. Another parent in [Weiss'] situation may have seen that, while weight loss was progressing, there were some emotional issues. But she chose to continue dieting in her own way. I believe that if she had continued coming, the end result would have been more than just weight loss: she'd have weight loss and a happy child."
To me, it's a tricky situation that's hard to criticize if you haven't been in it yourself. Most moms aren't perfect and don't a lot of them end up screwing their kids up one way or another?
What do you think? Was it irresponsible of Vogue to publish that article? ||||| weighty issues A Mom’s Reaction to Vogue’s Story About a ‘Fat’ 7-Year-Old Girl
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I've never known Vogue's annual "Shape" issue to have a firm grasp on reality, but this month's article by Dara-Lynn Weiss on her struggle to cure her "obese" 7-year-old daughter, Bea, reached new levels of pathos. The heartbreaking chronicle of little Bea, subjected to public humiliation and the Red Light, Green Light, Eat Right diet (sort of a "kid-oriented" version of Weight Watchers), begins thus: As Bea grew I was relieved to cross several items off my mental checklist of possible issues she might develop. She was not colicky. She was not autistic. She was not dyslexic. No, it was far, far worse than any of those things: She was fat. And Weiss admits that she felt particularly ill-equipped to confront the problem because of her own struggle to control her weight over the years, which included subjecting herself to Weight Watchers, Atkins, juice fasts, laxatives, and even deadly appetite suppressants. So for several years, Weiss ignored her child's overeating, anxiously hoping it would just go away, even after Bea's 6-year-old check-up when the pediatrician suggested they address Bea's weight. But then it got serious.
One day Bea came home from school in tears, confessing that a boy at school had called her fat. The incident crushed me, but it was a wake-up call. Being overweight is not a private struggle. Everyone can see it.
A boy called her fat. Well, that certainly can't happen in a home ruled by the sort of social striving found in the pages of Vogue! We all know that the reasons we eat or deprive ourselves of food don't always coincide with appetite. But rather than identifying the cause of the overeating (maybe a mom so wrapped up in her own social standing that she was willing to put her daughter's well-being at stake?), Weiss chose to project her own self-loathing onto her daughter.
Full disclosure: I have three children, including a 7-year-old girl. I can attest to the ways in which children are a mirror for our worst fears about ourselves. I am sure I've made mistakes by voicing (however inadvertently) my own dissatisfactions with myself. And yet, I feel so fiercely protective of my children's future physical and mental well-being that I won't even use my real name for this piece. If my own daughter were to encounter a weight problem, I'd like to think I would approach it like Janell Hoffman did in her honest take "'Mom, I'm Fat:' One Mother's Inspired Response to Her 7 Year Old." If that wasn't enough, we would seek the help of professionals in a rational, loving manner. And if I were the root cause, I'd seek my own help too. Which is, of course, the opposite of Weiss's approach:
Sometimes Bea's after-school snack was a slice of pizza or a gyro from the snack vendor. Other days I forced her to choose a low fat vegetable soup or a single hard-boiled egg. Occasionally I'd give in to her pleas for a square of coffee cake, mainly because I wanted to eat half of it. When she was given access to cupcakes at a party, I alternated between saying, "Let's not eat that, it's not good for you"; "Okay, fine, go ahead, but just one"; "and "Bea, you have to stop eating crap like that, you're getting too heavy," depending on my mood. Then I'd secretly eat two when she wasn't looking.
But perhaps the most poignant part of the article comes at the end, when Bea meets her mother's deadline for Vogue's "Shape" issue and loses a total of sixteen pounds in time for them to be photographed together. For enduring her mother's obsessive narcissism, she receives many beautiful dresses and a feather hair extension as a reward. Seems like a fair trade-off for being in Vogue before second grade, right? But if Bea thought she could finally eat her coffee cake without being tormented, she'd better think again:
The struggle is obviously not over. I don't think it will ever be for either of us. Bea understands that, just as some kids have asthma, her weight is something she may always have to think about, unfair as it seems.
Unfair indeed. Weiss continues:
She will probably always want to eat more than she is supposed to. She will be tempted to make bad choices. But now she has the foundation to make these choices in an educated and conscious way. Only time will tell whether my early intervention saved her from a life of preoccupation with her weight, or drove her to it.
Um, really? I'm pretty sure Weiss just handed her daughter the road map to all her future eating disorders. But it gets even more tragic with Bea's tearful reproach:
"That's still me," she says of her former self. "I'm not a different person just because I lost sixteen pounds." I protest that indeed she is different. At this moment, that fat girl is a thing of the past. A tear rolls down her beautiful cheek, past the glued-in feather. "Just because it's in the past," she says, "doesn't mean it didn't happen." |||||
Summary: | – When Dara-Lynn Weiss wrote in Vogue about her yearlong struggle to help her clinically obese 7-year-old daughter lose 16 pounds, she probably wasn't expecting quite the level of backlash that has ensued. Yahoo has highlights from Weiss's article, including her admission that she herself has struggled with eating and body image issues her entire life. Among the tactics Weiss used with daughter Bea: depriving her of dinner because she ate 800 calories at school during "French Heritage Day," refusing to allow her to participate in "Pizza Fridays" because she once added a corn salad on the side, and angrily dumping out her Starbucks hot chocolate when the barista couldn't tell her exactly how many calories it contained. Yahoo rounds up some reactions: Katie Baker pulls no punches on Jezebel, writing that Weiss "has to go down in history as the one of the most fucked up, selfish women to ever grace the magazine's pages." Yes, Weiss found herself in a complicated and difficult situation, but "the obvious fact that Weiss was projecting her hatred of her own body onto her child throughout her yearlong diet" is "truly disgusting." On Fashionista.com, Dhani Mau notes an incident in which Weiss steps between her daughter and a salad nicoise, physically preventing her from eating it. "This may have not been the best way to set up the article if she wanted the reader to believe her to be a sane, reasonable person," Mau writes. "Weiss comes across as obsessive and the fact that she made such an issue of her daughter’s weight, both in public and in Vogue—seems wrong." "Rather than identifying the cause of the overeating … Weiss chose to project her own self-loathing onto her daughter," writes an anonymous blogger and mom in New York. "I'm pretty sure Weiss just handed her daughter the road map to all her future eating disorders." | multi_news_1_0_0 |
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– A conservative Utah senator has apologized to "my family, my Idaho constituents, and any others who have put their trust in me," after being arrested in Virginia in the wee hours of yesterday morning with a blood-alcohol level of .11, reports Politico. Mike Crapo was arrested after police spotted his car run a red light around 12:45am. CBS News reports that the senator, a member of the "Gang of Six," failed "several" field sobriety tests. In his statement, the 61-year-old professed, "I am deeply sorry ... I made a mistake. I accept total responsibility and will deal with whatever penalty comes my way in this matter." That penalty may become more clear following his Jan. 4 court date. A first-time DUI conviction in the state carries a mandatory minimum $250 fine and license revocation for one year. The AP adds that Crapo has explained in past interviews that, as a Mormon, he does not drink.
Let's expand this into a news article: Updated Dec. 24, 1:10 p.m. ET
Sen. Michael Crapo, R.-Idaho, was arrested in Virginia early Sunday morning and charged with driving under the influence, Alexandria, Va., police say.
Police spokesman Craig T. Fifer said an officer was on routine patrol when he saw Crapo's vehicle run a red light. It was stopped at Hume Avenue and Mount Vernon at 12:45 a.m. and he was alone at the time.
Sen. Michael Crapo, R-Idaho, following his arrest for DUI, December 23, 2012 / Alexandria Police Department
Crapo then underwent several field sobriety tests, which he failed, Fifer said in a statement. He was then taken into custody without incident. According to the Alexandria police, his blood alcohol level was 0.11; 0.08 is the legal limit in Virginia.
Police took Crapo to the Alexandria jail and he was released on $1,000 bond at about 5 a.m., Crapo's office said. He has a January 4 court date.
"I am deeply sorry for the actions that resulted in this circumstance," Crapo said Sunday night. "I made a mistake for which I apologize to my family, my Idaho constituents and any others who have put their trust in me. I accept total responsibility and will deal with whatever penalty comes my way in this matter. I will also undertake measures to ensure that this circumstance is never repeated."
Crapo, a Mormon who has been a bishop in the church for decades, has said before in interviews that he doesn't drink alcohol, consistent with his church's doctrine. ||||| Sen. Mike Crapo (R-Idaho) issued a public apology after being arrested for drunken driving in Alexandria, Va., early Sunday morning.
Jody Donaldson, a spokesperson for the Alexandria Police Department, said in an e-mail that Crapo was arrested at 12:45 a.m. Sunday. An Alexandria police officer noticed Crapo’s vehicle run through a red traffic light, and after the vehicle was stopped, the officer conducted field sobriety tests, which Crapo failed, Donaldson said. Crapo was arrested for driving under the influence, and taken into custody without incident, Donaldson said.
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In a statement, Crapo apologized for his actions.
“I am deeply sorry for the actions that resulted in this circumstance,” Crapo said. “I made a mistake for which I apologize to my family, my Idaho constituents and any others who have put their trust in me. I accept total responsibility and will deal with whatever penalty comes my way in this matter.
“I will also undertake measures to ensure that this circumstance is never repeated.”
Police said the senator’s blood-alcohol level was .110. In Virginia, drivers at .08 or higher are considered intoxicated.
He was released on $1,000 bond, and has a court date scheduled for Jan. 4.
The 61-year-old Republican is serving his third term in the U.S. Senate. Crapo is Mormon, and has said publicly that he abstains from alcohol. |||||
– If you're worried about diabetes, you might want to stock up on blueberries and ditch the fruit juice. That's the upshot of a new study in the British Medical Journal that tracked the eating habits of 180,000 subjects over nearly 30 years. The simplified findings: Those who ate five servings of whole blueberries a week had a 26% lower risk of contracting type 2 diabetes, reports the New York Times. Grapes and apples also did well, followed by prunes, pears, bananas, and grapefruit. Other fruits didn't seem to have much of an effect in terms of diabetes. One striking part of the study is that fruit juice might actually raise the risk for the disease, notes National Geographic. That's probably in part because dietary fiber and nutrients are lost in the juicing process, explains Bloomberg. So are blueberries a silver bullet? Not even close. “We don’t want to leave the impression that there’s any magical fruit,” says a co-author of the study, per the Boston Globe. And, he adds, no amount of blueberries in the world will compensate for things like a lack of exercise, an otherwise lousy diet, or a pack of smokes. (A previous study suggested blueberries also helped ward off dementia.)
| Let's expand this into a news article: We excluded participants who reported a diagnosis of diabetes (including types 1 and 2 and gestational diabetes), cardiovascular disease, or cancer at baseline (n=10 134 for the Nurses’ Health Study, 6155 for the Nurses’ Health Study II, and 6707 for the Health Professionals Follow-up Study), those who had missing data for individual fruits and fruit juice or an unusual level of total energy intake (<500 or >3500 kcal/day for the Nurses’ Health Study and the Nurses’ Health Study II and <800 or >4200 kcal/day for the Health Professionals Follow-up Study) (n=4765 for the Nurses’ Health Study, 5647 for the Nurses’ Health Study II, and 5750 for the Health Professionals Follow-up Study), those whose diagnosis date of type 2 diabetes was unclear (n=200 for Health Professionals Follow-up Study), and those who completed only the baseline questionnaire (n=719 for the Nurses’ Health Study, 699 for the Nurses’ Health Study II, and 1103 for the Health Professionals Follow-up Study). After excluding these participants, 66 105 women in the Nurses’ Health Study, 85 104 women in the Nurses’ Health Study II, and 36 173 men in the Health Professionals Follow-up Study were available for the analysis.
We used data from the Nurses’ Health Study (established in 1976; n=121 700), the Nurses’ Health Study II (established in 1989; n=116 671), and the Health Professionals Follow-up Study (established in 1986; n=51 529). These cohort studies are discussed in detail elsewhere. 14 15 16 Every two years since baseline, follow-up questionnaires have been mailed to the participants to collect and update information on lifestyle practices and occurrence of chronic diseases. In all three cohorts the follow-up rates are approximately 90%.
In 1984 a 118 item food frequency questionnaire was sent to the participants of the Nurses’ Health Study to assess their habitual diet in the past year. In 1986 and every four years thereafter, a similar but expanded questionnaire was sent to the participants to update their dietary information. The expanded questionnaire was also administered every four years to assess diet among the participants in the Health Professionals Follow-up Study since 1986 and those in the Nurses’ Health Study II since 1991. In all food frequency questionnaires we asked the participants how often, on average, they consumed each food in a standard portion size. Participants could choose from nine possible responses, ranging from “never, or less than once per month” to “six or more times per day.” We consistently asked about 10 individual fruits since baseline: grapes or raisins; peaches, plums, or apricots; prunes; bananas; cantaloupe; apples or pears; oranges; grapefruit; strawberries; and blueberries. We calculated total whole fruit consumption by summing the consumption levels of the 10 individual fruits and watermelon, which we inquired about sporadically during follow-up. Fruit juice included apple, orange, grapefruit, and other juices. The food frequency questionnaires were validated against diet records among 173 participants in the Nurses’ Health Study in 1980 and 127 participants in the Health Professionals Follow-up Study in 1986. 17 18 19 Corrected correlation coefficients between food frequency questionnaire and diet record assessments of individual fruit consumption were 0.80 for apples, 0.79 for bananas, and 0.74 for oranges in women, 17 and 0.67 for total whole fruits, 0.76 for fruit juice, 0.95 for bananas, 0.84 for grapefruit, 0.76 for oranges, 0.70 for apples and pears, 0.59 for raisins and grapes, and 0.38 for strawberries in men. 18 19 For some individual fruits, the corrected correlation coefficients were not available owing to large within person variability in the comparison methods.
In the follow-up questionnaires administered every two years, we inquired and updated information on anthropometric and lifestyle factors for chronic diseases, including body height and weight, cigarette smoking, physical activity, multivitamin use, and family history of diabetes. Among participants in the Nurses’ Health Study and Nurses’ Health Study II, we ascertained menopausal status, post-menopausal hormone use, and oral contraceptive use (Nurses’ Health Study II only). Estimates of total physical activity levels were calculated by multiplying the energy expenditure in metabolic equivalent tasks (METs) measured in hours per week of each activity by hours spent on the activity and summing the values of all activities. Each MET hour is the caloric need per kilogram of body weight per hour of an activity, divided by the caloric need per kilogram of weight per hour at rest. Based on the food frequency questionnaire, we derived a score of the alternate healthy eating index, an indicator of adherence to healthy eating behavior, described in detail elsewhere. 20 In brief, the alternate healthy eating index score summarizes the consumption of 11 foods or nutrients (including consumption of vegetables, fruits, whole grains, sugar sweetened beverages and fruit juice, nuts and legumes, red and processed meat, trans fat, long chain n-3 fat, polyunsaturated fat, sodium, and alcohol). Each component was scored on a scale of 0 to 10. In the current analysis, we excluded fruits and fruit juice when calculating the alternate healthy eating index score.
In all three cohorts, to inquire about symptoms, diagnostic tests, and diabetes drug use we mailed a supplementary questionnaire to participants who reported physician diagnosed diabetes in the follow-up questionnaires. A type 2 diabetes diagnosis was confirmed if participants met at least one of the following National Diabetes Data Group criteria 21 : one or more classic symptoms (excessive thirst, polyuria, weight loss, and hunger) plus raised blood glucose levels (fasting levels ≥140 mg/dL (7.8 mmol/L), random blood levels ≥200 mg/dL (11.1 mmol/L), and/or two hour blood glucose levels ≥200 mg/dL during oral glucose tolerance testing), raised blood glucose levels on two different occasions in the absence of symptoms, or treatment with antidiabetic drugs (insulin or oral antidiabetic agent). The diagnostic criteria changed in June 1998 and a fasting blood glucose level of 126 mg/dL (7.0 mmol/L) instead of 140 mg/dL was considered the threshold for the diagnosis of diabetes. 22 The validity of the supplementary questionnaire for the diagnosis of diabetes has been examined in validation studies. 23 24 Of 62 self reported cases of type 2 diabetes randomly selected in the Nurses’ Health Study, 61 (98%) were confirmed after an endocrinologist reviewed the medical records without the information from the supplementary questionnaire 23 ; and in the Health Professionals Follow-up Study, 57 of 59 self reported cases of type 2 diabetes (97%) were confirmed by a review of medical records. 24
Statistical analysis
We calculated each participant’s person years from the return date of the baseline food frequency questionnaire to the date of the type 2 diabetes diagnosis, date of death, last return of a valid follow-up questionnaire, or end of follow-up (2008 for the Nurses’ Health Study and Health Professionals Follow-up Study, or 2009 for the Nurses’ Health Study II), whichever came first. To represent long term dietary intake and minimize within person variation, we calculated and used the cumulative average of dietary intake based on valid assessments from baseline to the end of follow-up.26 To minimize the effects of chronic diseases diagnosed during follow-up on subsequent diet, we stopped updating dietary information after self reported diagnosis of hypertension, hypercholesterolemia, gestational diabetes, cardiovascular disease, or cancer, since these chronic diseases may lead to changes of fruit consumption levels in the cohorts.27 To reduce the effect of potential outliers and to pool the results from the three cohorts, we used the same cut-off points to categorize consumption levels in these studies. The highest two consumption levels were combined for prunes, cantaloupe, and blueberries owing to the small number of participants with high consumption levels of these fruits.
To minimize missing covariates, we replaced missing data on body mass index and physical activity with the last valid values. For missing data on body mass index and physical activity at baseline, we created a dummy variable when making categories for these two continuous covariates. Similarly, we also used missing indicator variables to include participants with missing categorical variables, including cigarette smoking, oral contraceptive use (Nurses’ Health Study II only), menopausal status, and post-menopausal hormone use. The overall percentages of missing data for body mass index and physical activity were, respectively, 6.8% and 9.5% in the Nurses’ Health Study, 6.7% and 8.5% in the Nurses’ Health Study II, and 12.8% and 14.0% in the Health Professionals Follow-up Study. The overall percentages of missing values during follow-up ranged from 0.6% (for cigarette smoking) to 5.1% (for menopausal status and post-menopausal hormone use) in the Nurses’ Health Study, from 0.3% (for cigarette smoking) to 4.7% (for menopausal status and post-menopausal hormone use) in the Nurses’ Health Study II, and from 0.1% (for physical activity) to 12.2% (for cigarette smoking) in the Health Professionals Follow-up Study.
Using Cox proportional hazard regression, we estimated the hazard ratios and 95% confidence intervals of type 2 diabetes for fruit consumption. We tested the proportional hazard assumption by including interaction terms between individual fruit consumption and duration of follow-up, and the assumption was unlikely violated (P>0.05 for all tests). We examined linear trend by modelling the median values for fruit consumption categories as a continuous variable. Using a fixed effects model, we pooled multivariable adjusted hazard ratios from three cohorts, and we used the Cochrane Q statistic and the I2 statistic to examine the heterogeneity of associations among the cohorts.
To examine whether the associations with risk of type 2 diabetes were heterogeneous among individual fruits, we fitted two fully adjusted models: one with total fruit consumption and the other with total fruit consumption plus consumption of individual fruits excluding oranges (which had the most similar association as the total fruit consumption) to avoid over-fitting. Then we used the likelihood ratio test to examine whether the model including individual fruits had better fit than that including total fruit consumption only.
We also estimated potential effects of substituting specific fruit consumption for fruit juice consumption by examining the median values for consumption categories of individual fruits and fruit juice in the same multivariate model; the hazard ratios and 95% confidence intervals for substitution effects were calculated based on the differences in point estimates, and the variance and covariance for the regression coefficients of specific fruits and fruit juice.28 To examine the robustness of our findings, we also conducted four sensitivity analyses: evaluating the influence of adjustment for major dietary variables including polyunsaturated to saturated fat ratio, and intakes of trans fat, red meat, fish, whole grains, sugar sweetened beverages, coffee, and nuts (all in fifths) instead of the modified alternate healthy eating index score; adjusting for baseline body mass index instead of updated body mass index to estimate the impact of potential over-adjustment; using baseline consumption levels as an exposure instead of cumulative average of intake levels; and stopping updating diet after diagnosis of gestational diabetes, cardiovascular disease, or cancer only when calculating the cumulative averages.
We further examined whether the associations of individual fruit consumption with risk of type 2 diabetes depended on the glycemic index/glycemic load values of fruits. We calculated the glycemic load values per serving for individual fruits based on the glycemic index values from the international glycemic index database13 and the amount of carbohydrate in fruits from the USDA nutritional database11 (see supplementary table 1). We categorized individual fruits into three groups based on their glycemic load values per serving: prunes, bananas, grapes, raisins, apples, and pears for high glycemic load fruits (glycemic load 8.1-19.2); cantaloupe, blueberries, and oranges for moderate glycemic load fruits (5.7-8.0); and peaches, plums, apricots, strawberries, and grapefruit for low glycemic load fruits (1.3-5.6). In terms of the categorization of fruits by the glycemic index values, high glycemic index fruits included cantaloupe, bananas, grapes, raisins (glycemic index 60-70); moderate glycemic index fruits included prunes, blueberries, and grapefruit (47-59); and low glycemic index fruits included apples, pears, oranges, peaches, plums, apricots, and strawberries (34-46). Moreover, to estimate the degree to which the observed associations were explained by flavonoid intake, in a secondary analysis we further adjusted for intake of flavonoid subtypes (flavonols, flavones, flavanones, flavan-3-ols, and anthocyanins).
The analysis was stratified jointly by age and calendar year and adjusted for body mass index (kg/m2; <23, 23.0-24.9, 25.0-26.9, 27.0-28.9, 29.0-30.9, 31.0-32.9, 33.0-34.9, 35.0-36.9, 37.0-38.9, 39.0-40.9, 41.0-42.9, 43.0-44.9, ≥45.0, or missing), ethnicity (white, African-American, Hispanic, or Asian), physical activity (MET hours/week; <3, 3.0-8.9, 9.0-17.9, 18.0-26.9, ≥27.0, or missing), cigarette smoking (never, former, currently smoke 1-14 cigarettes/day, currently smoke 15-24 cigarettes/day, or currently smoke ≥25 cigarettes/day, or missing), multivitamin use (yes or no), family history of diabetes (yes or no), menopausal status and post-menopausal hormone use (premenopause, post-menopause (never, former, or current hormone use), or missing) (for women), oral contraceptive use (yes, no, or missing) (Nurses’ Health Study II only), total energy intake (kcal/day), fruit juice consumption (fifths), and the modified alternate healthy eating index score (fifths).20 When examining the association for total whole fruit, we included total fruit consumption in the multivariate model without further adjusting for individual fruits. Likewise, when examining the associations for individual fruits or fruit groups based on their glycemic index/glycemic load values, we included consumption levels of all other individual fruits or fruit groups instead of total fruit consumption in the final model.
Statistical analyses were performed with SAS 9.2. All P values were two sided, and statistical significance was defined as P<0.05. ||||| View Images Blueberries on the Charlotte Berry Farm in Charlotte, Vermont
Photograph by Robert Nickelsberg, Getty Images
Science is finding more health benefits from blueberries—but raising more concerns about fruit juice. According to a new study by Harvard University researchers, eating whole fruits helps ward off diabetes, while drinking juice can actually raise the risk of developing the disease.
In a study published in the British Medical Journal, nutrition experts report that consumption of certain fruits—especially blueberries—cut people’s risk of type 2 diabetes by as much as 26 percent in a survey of more than 180,000 subjects over two and a half decades.
Study participants were asked about their consumption of grapes or raisins, prunes, bananas, cantaloupe, apples or pears, oranges, grapefruit, blueberries, strawberries, and stone fruits (peaches, plums, or apricots).
Blueberries had the strongest effect on cutting diabetes risk, followed by grapes and apples, especially when three or more servings a week were eaten. A standard serving of blueberries was half a cup.
Prunes, pears, bananas, and grapefruit also helped lower diabetes risk, while the other fruits did not.
The difference is something called polyphenols, said study co-author Qi Sun, an assistant professor of nutrition at Brigham and Women’s Hospital and Harvard School of Public Health. Some of these plant-based chemical compounds—including anthocyanins, chlorogenic acid, and resveratrol, all powerful antioxidants—may help the body process glucose. Blueberries, grapes, and apples are all rich in these beneficial polyphenols.
Sun and his collaborators based their research on data from 151,209 female participants in the long-running Nurses' Health Studies, which have tracked the lifestyles and health of participating nurses since 1976 through questionnaires and medical testing. They also included a cohort of 36,173 men from a similar survey of male medical health professionals, the Health Professionals Follow-Up Study, conducted from 1986 to 2008.
Juicy Details
The study also revealed an interesting twist. Consumption of fruit juices—including apple, orange, and grapefruit—not only failed to deliver the same benefits as whole fruit but even appeared to raise the risk of diabetes. People who drank at least one serving a day of juice had a 21 percent higher risk of developing diabetes than those who did not.
There are a few possible reasons, said Sun.
"During juicing processes, some phytochemicals and dietary fiber are lost,” said Sun. And since fluids are more rapidly absorbed than solids, drinking juice brings on a “more rapid and more dramatic glucose and insulin response” than eating whole fruits.
The questionnaires did not specifically ask whether the juice people were consuming was pasteurized or sweetened, although many store-bought juices are.
It’s hard to get that kind of specific data from large epidemiological studies, said Sun: “Participants often are not aware of how much sugar is added to the juices that they typically drink.” But, he added, “One can reasonably assume that juices with added sugar may be more strongly associated with diabetes risk.” ||||| 3 fruits that lower your risk of type 2 diabetes, at least a little
For years, nutritionists have debated whether fruit—rich in natural sugars—has a net positive or net negative impact on type 2 diabetes risk. Now a Harvard School of Public Health finding suggests that overall, eating several servings of fruit a week offers slight protection against type 2 diabetes. But certain fruits—blueberries, grapes, and apples—offer greater benefits.
In the study, published online Wednesday in the British Medical Journal, the Harvard researchers examined the dietary habits of more than 187,000 participants involved in three long-term studies and found that people who ate fruit at least three times a week had a 2 percent lower risk of developing type 2 diabetes compared with those who ate less fruit.
Nearly 7 percent of the participants developed type 2 diabetes during the studies, which followed volunteers for more than two decades.
But those who ate three servings a week of blueberries had more than a 25 percent lower risk, while grapes were associated with an 11 percent reduced risk and apples with a 5 percent lower risk.
Drinking fruit juice, on the other hand, slightly raised a person’s risk of developing the disease, and so did eating cantaloupes. Other fruits such as blackberries and raspberries weren’t included in the dietary questionnaire.
Should these results lead us to change our eating habits, choosing, say, blueberries over melon?
No, said study co-author Qi Sun, an epidemiologist. “We don’t want to leave the impression that there’s any magical fruit,” he said, since the study doesn’t prove that eating blueberries actually helps people avoid diabetes.
But the study does point to the need for more research to gain a better understanding of how fruit alters blood sugar levels. For example, it’s long been known that fruit high in fiber is digested more slowly, leading to a slower rise in blood sugar—which is thought to help protect against diabetes. But fruits also contain an array of plant chemicals that can play a role in blood sugar levels.
Blueberries, in particular, are rich in anthocyanins, which have been shown to play a role in how the body metabolizes the blood sugar glucose. ||||| If you want to reduce your chances of becoming a diabetic, you’re better off munching apples or blueberries instead of sipping fruit juice, researchers found.
Eating more blueberries, apples and grapes was shown to lower the risk of developing Type 2 diabetes, while increased consumption of fruit juice was linked to a higher risk, according to a study published in The BMJ.
People should “replace fruit juice with solid fruits, maintaining the same energy level” while substituting a less healthy option with a healthier one, Qi Sun, the senior author of the study, said in a telephone interview. He’s an assistant professor of medicine at Brigham and Women’s Hospital in Boston and Harvard Medical School.
This adds to a growing body of evidence that eating fruit is beneficial for health, and is the strongest confirmation to date that it can also lower Type 2 diabetes risk.
Previous studies showed links between increased fruit consumption and a lower risk of cardiovascular disease, metabolic syndrome and hypertension. According to one published last year in the Annals of Neurology, berries are good for the brain and can help fend off the mental decline of aging.
For the study published today, researchers from the U.K., the U.S. and Singapore set out to examine the relations between consumption of different kinds of fruits and diabetes, analyzing data from three groups of U.S. nurses and health workers who were surveyed about their eating habits and physical activity over the course of about two decades. The participants included 151,209 women and 36,173 men.
Three Groups
The results are convincing as they are consistent among the three groups, said Sun, also an assistant professor in the Department of Nutrition at the Harvard School of Public Health.
Among study participants who had three servings a week of blueberries, grapes, raisins, apples and pears rather than juice, the risk of diabetes was reduced by 7 percent, the study showed.
The study is part of a body of evidence showing benefits from fruit. Eating at least 2 1/2 cups of vegetables and fruits a day is associated with lower risk of cardiovascular disease, according to U.S. government dietary guidelines, which encourage the increased consumption of fruit. Most Americans don’t eat enough fruit, according to the guidelines, which were last updated in 2010.
Fruit juices are probably less healthy for a number of reasons, Sun said. In the juicing processes, some beneficial nutrients, for example flavonoids and dietary fibers, are lost, he said. Juices also pass through the gastrointestinal tract more quickly, leading to more rapid and more dramatic changes in blood sugar and insulin levels after eating, he said.
Eating Habits
Researchers asked about consumption of grapes or raisins, peaches, plums or apricots, prunes, bananas, cantaloupe, apples or pears, oranges, grapefruit, strawberries and blueberries. The juices used included orange, apple and grapefruit. Participants were submitted a questionnaire every four years to assess their eating habits, and were asked how often they consumed each food in a standard portion size.
Greater consumption of fruit juice was associated with an increased risk of Type 2 diabetes, the most common form of the disease, the study showed. Substitution of juices with fruits was linked with a lower risk, with the exception of strawberries and cantaloupe, the researchers said.
“Some fruits are more beneficial than others, in terms of diabetes prevention,” Sun said. “Based on our data, blueberries, apples, grapes and raisins are preferred.”
Future Studies
Such results will have to be corroborated in future studies, he added.
Diabetes is caused by a lack of insulin the body needs to convert blood sugar into energy. Lifestyle changes around the globe have kindled a surge in cases. The number of sufferers worldwide will reach an estimated 552 million by 2030, according to the International Diabetes Federation.
Some diabetics, suffering from Type 1 diabetes, have a lifelong inability to produce insulin. The Type 2 variant tends to strike later in life, brought on by obesity and sedentary lifestyles, as people become resistant to the insulin their own body produces.
The study was funded by research grants from the National Institutes of Health. Professor Sun also was supported by a career development award from the National Heart, Lung, and Blood Institute.
For Related News and Information: Eating More Berries May Delay Memory Decline, Research Shows
To contact the reporter on this story: Albertina Torsoli in Geneva at [email protected]
To contact the editor responsible for this story: Phil Serafino at [email protected] ||||| | multi_news_1_0_0 |
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– Studies on a wide range of species have found that calorie restriction almost always extends lifespan—and this is true in yeast, worms, flies, mice, and more. But whether this applies to primates has been the subject of considerable debate since studies by two highly reputable organizations have reported such different results, reports New Scientist. Now, however, those two organizations—the University of Wisconsin and the National Institute on Aging—have come together to dissect the differences, and they conclude in the journal Nature Communications that calorie restriction does in fact improve both the health and longevity of rhesus monkeys. It turns out the NIA's preliminary results, which found no difference in survival rates between the groups, were marred by flaws in study design, including that calorie restriction began in some of the monkeys when they were juveniles, which actually reduces primate lifespan. The trials have been going since the late 1980s, and four of the NIA monkeys that began dieting as adults lived past 40 (typical lifespan tops out at 30), breaking any known record for the species. In Wisconsin, meanwhile, the calorie-restricted males typically lived two years longer than controls eating whatever they wanted, while calorie-restricted females lived six years longer. Another finding: the University of Wisconsin reports that females are less susceptible to the negative effects of excess fat than males. (People tend to snack less after looking at this.)
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Put down the cake. Going on a permanent diet could make you live longer, if findings from monkeys hold true for people.
A long-running trial in macaques has found that calorie restriction makes them live about three years longer than normal, which would translate to about nine years in people.
Such a strict diet might not be for everyone, but understanding the mechanisms behind any benefits of calorie restriction may one day lead to anti-ageing medicines, says Julie Mattison at the National Institute on Aging (NIA) in Baltimore, Maryland. “The goal is to improve human health,” she says.
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Many studies have shown that calorie restriction extends lifespan for lab organisms, from yeast through to worms, flies and mice. This has prompted a few thousand people to choose to restrict their calories to between 1500 to 1800 kcal a day (women and men are usually advised to consume 2000 and 2500 kcal, respectively). Their hope is it will give them longer and healthier lives, and there’s some evidence that such people have better blood cholesterol and glucose levels.
Age record breakers
But it’s unclear if the approach can really lengthen the lives of long-lived animals like us. Two trials of calorie restriction in macaques, which live around 26 years in captivity, have until now produced conflicting results.
The trials were set up in the late 1980s, and not all the monkeys have died yet. But an interim report from one group, based at the University of Wisconsin, previously found that the monkeys on a restricted diet were indeed living longer than the control group. However, the second study, run by the NIA, found there was no difference in the survival rates of their animals, which cast doubt on the entire premise.
Now the teams have compared their most recent results and their analysis backs the earlier trial that had positive findings. The NIA study, on the other hand, had several problems, including issues with some of the control monkeys eating fewer calories than expected, and some of the animals beginning their restricted diet as juveniles – which reduces lifespan.
Even so, in the NIA trial, four of the monkeys that began the diet as adults lived to be over 40, breaking all known records for macaques – an observation which may cheer those who practise calorie restriction. However, picking out single results like this from a larger study isn’t good evidence, says Mattison.
Side effects
In the Wisconsin trial, animals did live significantly longer than controls – calorie-restricted males lived about two years longer, while calorie-restricted females lived about six years longer. There were also lower rates of heart disease and cancer in these monkeys. These are the major causes of death in people, lending support to the idea that the results apply to humans, says Luigi Fontana of the University of Brescia in Italy.
However, Brian Delaney, who is president of the Calorie Restriction Society, an organisation that supports the practice in people, says some who follow this diet are disappointed by the relatively modest benefits in monkeys compared with mice, which have lived up to 50 per cent longer than normal.
“Is it worth it?” asks Delaney. “My choice is to do it. But I’m so used to the diet that it really isn’t very difficult for me anymore.”
Delaney has been practising calorie restriction for 24 years. Until someone is used to it, the diet involves planning every meal with precision, and side effects can include feeling cold and reduced libido.
Journal reference: Nature Communications, DOI: 10.1038/ncomms14063
Read more: Eat less, live longer?
We have clarified the relationship between the studies and the issues with the NIA work. ||||| Intrinsic differences in study design
Most of the early rodent CR studies involved very young onset life-long CR initiated post-weaning, usually in inbred genetic backgrounds. In the 1980s it became clear that adult onset CR (12-month-old mice) was also effective in delaying ageing and extending lifespan in rodents, albeit to a lesser extent than the young onset model22. Many rodent CR studies opt to feed control animals ad libitum amounts of food while others provide less than ad libitum amounts arguing that this strategy avoids the confounding effects of obesity and reduces variability in food intake among individuals. With the launch of the NIA rhesus monkey study in 1987, the implementation of CR was such that the control monkeys were not free-fed. Food allotments were determined in accordance with data published by the National Research Council to provide approximate ad libitum intake based on their age and bodyweight for the maturing control monkeys without overfeeding23. Rations were increased to maintain growth and development until full stature was attained. CR monkeys received 30% less food than height-, age- and sex-matched control monkeys. The intervention was initiated as young-onset and old-onset groups of males, and young, adult, and old-onset groups of females24 (Table 1). Launched in 1989, the UW study initiated the CR diet in adult animals only, after full stature was achieved (∼8 years of age for rhesus monkeys)25. Food was provided at levels approximating ad libitum to control animals. To accommodate heterogeneity in the feeding behaviours within the cohort, the ad libitum reference for each individual was established using baseline food intake measured over 3–6 months, and CR was implemented on a per-individual basis. The rationale for these design features at UW was to implement a study as it might have been conducted in humans.
Table 1: Study design. Full size table
The source of the monkeys in each cohort and the population type represented is also a point of difference for the two studies. The UW monkeys were born and raised at the Wisconsin National Primate Research Center and were all of Indian origin. The NIA monkeys were sourced from several locations and included monkeys of both Indian and Chinese origin. Chinese male rhesus monkeys are generally heavier and longer than their Indian counter parts with the reverse being the case for females, and Chinese rhesus monkeys are also thought to exhibit greater sexual dimorphism26. Monkeys of different origin are sufficiently genetically different that they can be distinguished using a panel of single nucleotide polymorphisms27. Apart from population differences, rhesus monkeys share a similar degree of inter-individual genetic variation as humans28. In this way, the contribution of population type to differences in outcomes of the two studies as opposed to the contribution of individual genetic heterogeneity is difficult to ascertain.
The diet compositions were another important difference between the two studies. First, the source of diet components was different. A naturally sourced diet was employed at the NIA facility to ensure that micronutrients such as phytochemicals and trace minerals were provided, acknowledging that there was potential for seasonal variation. In contrast, a semi-purified diet was employed at UW to ensure that intake could be fully defined and consistent throughout the course of the study. Second, although diets at both locations had a similar caloric density, the relative macronutrient composition of the diets was not equivalent (Table 2). Compared to the UW diet, the NIA diet was lower in fat, higher in protein and higher in fibre. Finally, the nutrient content of the diets was also different. At both locations diets contained∼60% carbohydrates by weight, but sucrose comprised less than 7% of total carbohydrates at NIA and 45% of total carbohydrates at UW. Diets at both locations were replete for vitamins that were provided at or above the recommended daily allowance.
Table 2: Diet composition at each location. Full size table
Feeding practices also differed between studies. At NIA, the monkeys were fed two meals at ∼6:30 and 13:00 each day. Any food remaining after the morning meal was removed after about 3 h, and a low calorie treat was provided, typically in the form of a small piece of fruit. The afternoon meal was not removed so that monkeys had access to food at night. At UW, all monkeys were fed in the morning at∼8:00 and any remaining food was removed at ∼16:00 when a treat of fresh fruit or vegetable, which was quickly and completely eaten, was provided. Food allotment for control animals was adjusted to ensure that there was always some uneaten food to be removed at the end of the day. In this way UW animals were ad libitum fed during the day but food deprived overnight. While there were considerable differences in study design as outlined above, it should be noted that animal housing and routine animal care were equivalent at NIA and UW primate facilities. This included identical housing conditions, temperature and humidity range, light cycles, and the use of tap water, which was continuously available. Both studies included animal monitoring several times per day, and a designated veterinary staff that inspected the animals routinely and provided outstanding care as needed.
Impact of CR on survival
The initial goal of both NIA and UW studies was to determine the impact of CR on the health of rhesus monkeys, as it was not a foregone conclusion that CR would be an appropriate intervention in long-lived species. The investigation of the impact of CR on longevity was not considered a primary outcome at either study location. Even though 121 monkeys were enrolled in the NIA study, the differences in age of onset (from 1 to 23 years) precluded the animals from being grouped together for data analyses. Although the age range for time of onset is smaller for the UW study (ages 7–15), with only 38 outbred genetically distinct monkeys per group (including both sexes), it seemed unlikely that the study would have the statistical power required to test CR’s effect on longevity. While neither study reports longevity data, both studies have yielded survival data. For rhesus monkeys in captivity, the previously reported median survival was ∼26 years of age, 10% survival was ∼35 years of age and maximal survival was ∼40 years of age29. Mortality curves were generated separately for UW and NIA (Fig. 1). Survival estimates for monkeys at both sites were calculated based on data captured up to July 2015 using the three most common statistical methods: Kaplan-Meier product-limit method; Cox proportional hazard regression and parametric survival analysis assuming a Weibull distribution (Table 3). Because the Weibull distribution is a special case of the generalized extreme value distribution, it can accommodate estimation of the upper quantiles of a survival distribution and maximal lifespan, especially when there are censored data due to animals that remain alive30.
Figure 1: Mortality curves for monkeys at UW and at NIA. These curves depict data for male and female monkeys on the UW study and on the NIA study. Animals are grouped by age where male J/A include juvenile and adolescent onset animals, female J/A include juvenile and adult onset animals, and old include the advanced age onset animals. Inset boxes indicate animals still alive, dashed line marks 50% mortality. Statistics related to this figure are provided in Supplementary Information, Supplementary Table 1. Full size image
Table 3: Survival estimates. Full size table
In the UW adult-onset study, the estimated survival of UW control animals was close to that of the average recorded for monkeys in captivity (∼26 years of age). Considering both males and females together, a statistically significant effect of CR in increasing survival was observed (Cox regression P=0.017; Supplementary Table 1). The hazard ratio (HR) of 1.865 (95% confidence interval (CI): 1.119–3.108) indicated that at any time-point the control monkeys had almost twice the rate of death when compared to CR animals. The effect of sex on the response to CR was not statistically significant. Kaplan-Meier analysis showed that median survival estimates were greater for CR animals for both males and females (Table 3). In the NIA study large differences in ages of monkeys at time of recruitment to the study (Table 1) prompted a separation of data from the early and late onset groups. Here and throughout this report, NIA male juveniles and adolescents (J/A) were grouped and female juveniles and adults were grouped (J/A). The Kaplan-Meier median estimated survival was not different between NIA control and CR animals for the J/A onset groups of males or females (Fig. 1). Although Cox proportional hazard regression indicated that the differences in survival between J/A control and CR were not statistically significant (Supplementary Table 1), CR monkeys reached 80% mortality before the controls for both sexes. With 38% of the NIA J/A cohort still alive, the survival curves are incomplete and the impact on survival remains to be determined; however, the early mortality suggests that for some individuals implementation of CR in the very young may confer a survival risk. For old-onset CR, Kaplan-Meier estimated survival was not different between control and CR groups for either males or females (Table 3), but survival estimates were higher than those of J/A monkeys and UW controls. For both males and females, survival estimates for the NIA old-onset cohort were comparable to or exceeded those for UW CR.
Although there were slight discrepancies in the estimated median survival between the non-parametric Kaplan-Meier and parametric Weibull estimation methods, the survival comparisons between study sites using either analysis were consistent. A certain degree of sexual dimorphism was observed in survival outcomes where incidence of early death appeared to be greater for females. This observation might be explained in part by endometriosis, which is the proliferation of endometrial tissue outside of the uterus. Endometriosis can occur at relative high incidence in monkeys in captivity (∼25%), and risk is considerably greater for nulliparous females31,32. Incidence of endometriosis was equivalent for control and CR groups. For the J/A cohorts in the NIA study, 12 of the 44 females died of complications due to endometriosis, and of these the juvenile onset females were confirmed nulliparous. Females recruited to the UW study, in contrast, had at least one but no more than three healthy infants33, and only 2 of 30 females died of complications due to endometriosis. A further contributing factor relates to the policy on treatment of clinical conditions. At UW the policy to treat clinical conditions was implemented from the outset. At NIA, although acute pain and suffering were always treated, chronic medical conditions, including endometriosis, were monitored but not medically treated. A policy change was implemented in 2010 due to the high incidence of endometriosis. The power to assess the impact of CR on survival for NIA J/A females has been compromised somewhat by this one condition.
Biometric and food intake measures from both studies
For over a quarter of a century during these studies, bodyweight, body composition and food intake were measured for all 197 monkeys. Bodyweight was determined in fasted and anesthetized monkeys 2–4 times per year during routine procedures. Longitudinal data for all monkeys were averaged by age of the animal (Fig. 2a). As is the case for humans, monkeys often experience cachexia or end-of-life rapid weight loss. To avoid confounding effects of weight change that is not related to food intake or diet, data from the last year of life for each monkey were excluded. To facilitate comparisons among the cohorts, data were grouped into three age categories representing young adult (11–13 years of age), late mid-age (18–20 years of age) and advanced age (25–27 years of age) (Supplementary Tables 2 and 3).
Figure 2: Bodyweight data for monkeys at NIA and UW. (a) Bodyweight (kg) for male and female monkeys at UW and at NIA grouped by age where male J/A include juvenile and adolescent onset animals, female J/A include juvenile and adult onset animals, and old include the advanced age onset animals. Digits shown in white within the boxes are the numbers of individual animals contributing to each data point, data are shown as mean±s.e. of the mean. (b) Comparison of bodyweight averages for monkeys from UW and NIA studies with records of the internet Primate Aging Database (iPAD). Average bodyweight for control and CR monkeys at both study locations were determined by age category including adult (11–13 years of age), late mid-age (18–20 years of age) and advanced age (25–27 years of age). Data are expressed as percent deviation from the iPAD average for females and males from each age category. Statistics related to this figure are provided in Supplementary Information, Supplementary Tables 2 and 3. Full size image
Considering first the female monkeys, bodyweight for the NIA J/A was not significantly different between control and CR monkeys for any age categories. UW CR females weighed significantly less (17–26%) than controls throughout the study period, and UW female controls weighed significantly more than NIA J/A female controls throughout (Supplementary Table 2). For NIA old-onset females, bodyweight was not significantly different between controls and CR, and was significantly lower than bodyweight of UW female controls. In summary, for NIA J/A and old-onset female cohorts, bodyweight for control and CR monkeys was not different from each other and all were significantly lower than the UW controls. Considering next the male monkeys, NIA J/A CR males weighed significantly less (19–22%) than their control counterparts throughout the study. The difference between UW control and CR was slightly greater (24–35%), with CR males weighing significantly less than controls. The average peak weight for NIA J/A control males was ∼15% lower than that of UW control males, but differences in bodyweight were significant for the young age category only (Supplementary Table 3). Bodyweight of the old-onset NIA control and CR males were not significantly different at either mid-age or advanced ages, and old-onset NIA male controls weighed significantly less than UW controls. In summary, NIA J/A and UW male cohorts showed a clear bodyweight response to CR, but old-onset NIA control and CR males were not different from each other and were significantly lower than the UW controls.
The internet Primate Aging Database (iPAD; http://ipad.primate.wisc.edu) is a repository of clinical and biometric data from healthy, non-experimental, captive nonhuman primates housed at research facilities across the USA. Using data from over 1,200 individual rhesus monkeys of Indian origin, mean bodyweights were calculated for the above age categories for males (11.6, 12.1, 11.5 kg respectively) and females (7.4, 8.4, 7.8 kg respectively). UW control and CR monkeys fell on either side of these averages; control monkeys were heavier than the iPAD average (∼18% for males; ∼19% for females), and CR monkeys had lower bodyweight than the iPAD average (∼12% for males; ∼11% for females) (Fig. 2b). For NIA J/A, control males were the same to slightly heavier (5–10%) than the iPAD average and CR weighed less than the iPAD average (∼20%), while control and CR female monkeys both weighed less than the iPAD average throughout the study (∼10% and ∼20% respectively). All NIA old-onset monkeys weighed less than the iPAD average for both control (∼15% for females; ∼10% for males) and CR (∼22% for females; ∼21% for males) monkeys. In summary, bodyweights of UW and NIA control monkeys were not equivalent to each other, and apart from J/A males, were respectively higher and lower of the iPAD average.
To gain insight into differences in the effect of age and diet on body composition, dual X-ray absorptiometry measures were conducted at intervals throughout the course of the two studies (Fig. 3). Since each animal had multiple measures taken over time, estimates of the average percent adiposity (fat/bodyweight expressed as percent) were adjusted for age (Supplementary Fig. 1). Within groups a main effect of age on adiposity was detected for NIA J/A and UW cohorts. A main effect of diet was detected for NIA J/A males and for both males and females from the UW study, where CR was associated with significantly lower adiposity. The NIA J/A control and CR females did not differ from each other in adiposity and neither of the NIA old-onset monkey groups had a main effect of CR on adiposity. Combining the data from NIA J/A and UW, a difference in adiposity was detected between controls on the two studies for both males and females, where NIA monkeys had significantly lower percent body fat. Control monkeys from NIA J/A were not statistically different from UW CR in percent body fat for both sexes. These data show an impact of age on adiposity in all three groups and reveal that the impact of CR on adiposity was observed for both groups of UW monkeys and at NIA for J/A males only.
Figure 3: Adiposity data for female and male monkeys at NIA and UW. Percent adiposity (fat (g)/total bodyweight (g)) calculated from DXA (dual energy X-ray absorptiometry) measures conducted during the course of the studies for male and female monkeys at UW and at NIA grouped by age where male J/A include juvenile and adolescent onset animals, female J/A include juvenile and adult onset animals, and old include the advanced age onset animals. Digits shown in white within the boxes are the numbers of individual animals contributing to each data point, data are shown as mean±s.e. of the mean. Full size image
Food intake was monitored daily at both sites. At UW daily measures of food intake were used to calculate means. At NIA food intake means were calculated based on measures conducted during a single week per year as representative of typical intake. Longitudinal data for all monkeys were averaged by age of the animal (Fig. 4). Data from the last year of life of each monkey were excluded to avoid confounding effects of end-of-life feeding behaviours that usually include loss of appetite. Considering first the females and using the age categories defined above for both UW and NIA J/A, the controls consumed significantly more calories than CR at both young and mid-age, but the difference persisted only for UW female monkeys at advanced age. For the old-onset NIA, caloric intake was not different between control and CR. Among control monkeys, UW females consumed significantly more calories than NIA J/A at mid-age and advanced age and more than old-onset at advanced age. Considering next the males, the NIA J/A controls consumed significantly more calories than CR at young and mid-age and the difference between control and CR was significant for UW at mid-age only. Old-onset males at NIA differed significantly in their caloric intake between control and CR only at advanced age. Among controls, caloric intake was not different for NIA J/A and UW males at any point in the study, but old-onset males consumed significantly less than UW males and NIA J/A males at mid-age. In summary, significant differences in caloric intake were identified between control and CR monkeys for male and female NIA J/A and UW cohorts, but not for old-onset cohorts until advanced age and then for males only. Comparing between sites, caloric intake for NIA female controls of both J/A and old-onset was lower than that of UW controls, and for males, caloric intake of NIA J/A and UW controls were not different from each other but old-onset NIA controls were lower than both.
Figure 4: Food intake data for monkeys at NIA and UW. Food intake (daily values in Kcalories) for male and female monkeys at UW and at NIA grouped by age where male J/A include juvenile and adolescent onset animals, female J/A include juvenile and adult onset animals, and old include the advanced age onset animals. Digits shown in white within the boxes are the numbers of individual animals contributing to each data point, data are shown as mean±s.e. of the mean. Full size image
Impact of CR on incidence of disease
The concept of healthspan is a fairly recent development in ageing research, where a distinction is drawn between chronological age and health status34. Traditionally, an increase in both median and maximum lifespan was considered the hallmark of delayed ageing, and improvements in health were deemed to be a necessary and obvious component of longevity. The perspective has shifted somewhat towards greater emphasis on health and morbidity, so an intervention that imparts improved health even in the absence of increased longevity, is viewed as a highly favourable and legitimate example of an ageing intervention. With advancing age, rhesus monkeys are vulnerable to many of the same conditions observed in humans. Among the most prevalent are cancer, cardiac disease, and conditions related to immune dysfunction and inflammation, and examples of each were identified in monkeys on the ageing and CR studies at both NIA and UW (Supplementary Table 4).
Fasting glucose measures were common to both studies and the longitudinal data are shown (Fig. 5). In healthy adult rhesus monkeys fasting glucose levels are 64–68 mg dl−1 (refs 18, 35). For NIA J/A, fasting glucose levels were equivalent for controls and CR up to ∼23 years of age, after which the control and CR males, but not females, began to diverge. Both control and CR females showed an age-related increase in fasting glucose levels after ∼21 years of age. For UW monkeys, the control males had higher fasting glucose levels than CR from 15 years of age with a further divergence of the curves after ∼23 years of age, while a noticeable difference between control and CR females emerged after only ∼21 years. For the NIA old-onset cohorts, fasting glucose was consistently low for the duration of the study period. These data point to an age-related increase in fasting glucose for rhesus monkeys and single out the UW control males as being predisposed to elevated circulating glucose in the fasted state. Using multilevel modelling to investigate the relationship between adiposity and fasting glucose levels a significant relationship was identified for UW males only (P=0.005). A significant age by diet interaction was also detected (P=0.014), suggesting that the impact of age on the relationship between adiposity and glucoregulatory parameters is distinct for control and CR monkeys.
Figure 5: Fasting glucose values for monkeys at NIA and UW. Circulating levels of glucose (mg dl−1) are shown for male and female monkeys at UW and at NIA grouped by age where male J/A include juvenile and adolescent onset animals, female J/A include juvenile and adult onset animals, and old include the advanced age onset animals. Digits shown in white within the boxes are the numbers of observations contributing to each data point, data are shown as mean±s.e. of the mean. Full size image
Veterinarians documented body condition and overall health of monkeys biannually at both study locations and indicators of diseases or disorders identified. The age at which a monkey was first diagnosed with an age-related condition was used to generate morbidity curves (Fig. 6). Age-related conditions included sarcopenia, osteoporosis, arthritis, diverticulosis, cataracts and persistent heart murmurs, in addition to age-related diseases including cancer, diabetes and cardiovascular disease. Cox proportional hazard regression modelling indicated that age-related conditions occurred at ∼2.7 times the rate in control animals compared to CR for UW monkeys (HR: 2.665; CI: 1.527–4.653; P=0.0006). In the NIA J/A cohort, age-related conditions occurred at twice the rate in control monkeys compared to CR (HR: 2.091; CI: 1.169–3.641; P=0.0125) (Supplementary Table 5; Supplementary Fig. 2). The advanced age of the old-onset NIA monkeys precluded detection of the first occurrence of an age-related condition.
Figure 6: Morbidity curves for monkeys at NIA and UW shown. (a) Graphs represent the first occurrence of any age-related disease, disorder or condition for combined males and females from UW (top) and NIA J/A (bottom). Statistics related to this figure are provided in Supplementary Information, Supplementary Table 4. (b) Incidence of prevalent age-related conditions in nonhuman primates for control and CR animals from UW and NIA (J/A and old-onset combined). To compare studies, cancer and cardiovascular disorders are reported as incidence upon necropsy and are expressed as a percentage of the animals that are deceased. Full size image ||||| Settling a persistent scientific controversy, a long-awaited report shows that restricting calories does indeed help rhesus monkeys live longer, healthier lives.
A remarkable collaboration between two competing research teams — one from the University of Wisconsin–Madison and one from the National Institute on Aging — is the first time the groups worked together to resolve one of the most controversial stories in aging research.
The findings by the collaboration — including Senior Scientist Ricki Colman of the Wisconsin National Primate Research Center and UW–Madison Associate Professor of Medicine Rozalyn Anderson; and NIA Staff Scientist and Nonhuman Primate Core Facility Head Julie Mattison and Senior Investigator and Chief of the Translational Gerontology Branch Rafael de Cabo — were published today (Jan. 17, 2017) in the journal Nature Communications.
In 2009, the UW–Madison study team reported significant benefits in survival and reductions in cancer, cardiovascular disease, and insulin resistance for monkeys that ate less than their peers. In 2012, however, the NIA study team reported no significant improvement in survival, but did find a trend toward improved health.
“These conflicting outcomes had cast a shadow of doubt on the translatability of the caloric-restriction paradigm as a means to understand aging and what creates age-related disease vulnerability,” says Anderson, one of the report’s corresponding authors. Working together, the competing laboratories analyzed data gathered over many years and including data from almost 200 monkeys from both studies. Now, scientists think they know why the studies showed different results.
The upshot of the report is that caloric restriction does indeed seem to be a means to affect aging. However, for primates, age, diet and sex must all be factored in to realize the full benefits of lower caloric intake.
First, the animals in the two studies had their diets restricted at different ages. Comparative analysis reveals that eating less is beneficial in adult and older primates but is not beneficial for younger animals. This is a major departure from prior studies in rodents, where starting at an earlier age is better in achieving the benefits of a low-calorie diet.
Second, in the old-onset group of monkeys at NIA, the control monkeys ate less than the Wisconsin control group. This lower food intake was associated with improved survival compared to the Wisconsin controls. The previously reported lack of difference in survival between control and restricted groups for older-onset monkeys within NIA emerges as beneficial differences when compared to the UW–Madison data. In this way, it seems that small differences in food intake in primates could meaningfully affect aging and health.
Third, diet composition was substantially different between studies. The NIA monkeys ate naturally sourced foods and the UW–Madison monkeys, part of the colony at the Wisconsin National Primate Research Center, ate processed food with higher sugar content. The UW–Madison control animals were fatter than the control monkeys at NIA, indicating that at nonrestricted levels of food intake, what is eaten can make a big difference for fat mass and body composition.
Finally, the team identified key sex differences in the relationship between diet, adiposity (fat), and insulin sensitivity, where females seem to be less vulnerable to adverse effects of adiposity than males. This new insight appears to be particularly important in primates and likely is translatable to humans.
The upshot of the report is that caloric restriction does indeed seem to be a means to affect aging. However, for primates, age, diet and sex must all be factored in to realize the full benefits of lower caloric intake. ||||| | multi_news_1_0_0 |
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Question:
Here is a news article: Taylor Swift has taught a generation of kids to appreciate country music over the last five years. Now she's donating $4 million to the Country Music Hall of Fame and Museum to make sure that education continues.
This artist's rendering by Tuck-Hinton Architects provided by the Country Music Hall of Fame and Museum shows the Taylor Swift Education Center in Nashville, Tenn. The country music superstar is donating... (Associated Press)
In this Nov. 20, 2012 photo, Taylor Swift arrives at the 39th Annual American Music Awards in Los Angeles. Swift is donating $4 million to the Country Music Hall of Fame and Museum to fund the 7,500 square... (Associated Press)
The gift is the largest given to the museum by an artist, officials said. It will fund the Taylor Swift Education Center, an exhibit and classroom space scheduled to open in 2014.
The new education center is part of the museum's $75 million expansion project that will include a new concert theater and more room for exhibits and archives.
The 22-year-old singer-songwriter is country music's top-selling artist. The six-time Grammy winner has taken the genre to Asia, Europe and Australia as well as the top of the U.S. pop charts.
One of her first public performances was on the museum's plaza. She also signed her record contract there. ||||| Who says celebrities only blow their millions on mansions and cars?
A-listers like Sandra Bullock, Angelina Jolie and Brad Pitt have all pitched in and contributed time and money to charitable causes over the years. Lately, Oscar-nominee George Clooney has been making waves with his activism -- even getting arrested with the CEO of Jewish World Watch after protesting at the Sudanese embassy on March 16, 2012.
Who else has been using their fame to help the world? Click through the gallery to find out!
Now more than ever, celebs are rolling up their sleeves and speaking out for a great cause. Along with Lisa Edelstein and How I Met Your Mother's Josh Radnor, Hotel Rwanda star Don Cheadle is continuing his work against injustice in Darfur by partaking in the Walk to End Genocide happening this May.
Celebuzz Single Player No Autoplay (CORE) No changes are to be made to this player |||||
A summary of this is?
Answer:
– Taylor Swift is donating a sizable $4 million to the Country Music Hall of Fame and Museum, the largest gift ever donated to the museum by an artist. It will fund the Taylor Swift Education Center, a new classroom and exhibit space opening in 2014, the AP reports. Swift proves that not all celebrities spend their dough on things like $12,000 Chanel bicycles and $18,500 olive trees, and Celebuzz rounds up 14 more who give freely of their money and/or their time. And while some are obvious (hello, George Clooney) many might surprise: Sandra Bullock: Has donated $1 million to relief organizations that give aid to those affected by 9/11, the 2004 Indian Ocean earthquake, and the recent earthquakes in Haiti and Japan. Ellen DeGeneres: Her pet cause is, ahem, animal rights and rescue organizations, and her pet food line benefits charity. Alicia Keys: This ambassador for Keep A Child Alive, an organization focused on families affected by AIDS, does everything from hosting fundraisers to traveling to Africa. Nick Jonas: He has diabetes, and acts as an ambassador for Bayer Diabetes Care, promoting research funding. Eva Longoria: She’s a spokesperson for PADRES Contra El Cancer and supports many other Latino causes and community organizations. Click for the complete list, which includes one celeb who has raised more than $125 million for the AIDS Foundation.
Question:
Here is a news article: FILE - In this July 13, 2018, file photo, first lady Melania Trump takes a seat during a visit to The Royal Hospital Chelsea in central London. Trump is visiting Philadelphia on Wednesday, Oct. 17, to... (Associated Press)
FILE - In this July 13, 2018, file photo, first lady Melania Trump takes a seat during a visit to The Royal Hospital Chelsea in central London. Trump is visiting Philadelphia on Wednesday, Oct. 17, to meet with families of children who were affected by exposure to opioids while in the womb. (AP Photo/Luca... (Associated Press)
FILE - In this July 13, 2018, file photo, first lady Melania Trump takes a seat during a visit to The Royal Hospital Chelsea in central London. Trump is visiting Philadelphia on Wednesday, Oct. 17, to meet with families of children who were affected by exposure to opioids while in the womb. (AP Photo/Luca... (Associated Press) FILE - In this July 13, 2018, file photo, first lady Melania Trump takes a seat during a visit to The Royal Hospital Chelsea in central London. Trump is visiting Philadelphia on Wednesday, Oct. 17, to... (Associated Press)
WASHINGTON (AP) — First lady Melania Trump's plane was forced to return to a Washington area military base on Wednesday because of smoke in the cabin.
Her spokeswoman, Stephanie Grisham, said "everyone is fine and everyone is safe" after the plane returned to Joint Base Andrews.
Mrs. Trump had been scheduled to visit a Philadelphia hospital and meet with families of children affected by exposure to opioids while in the womb.
Grisham said the first lady's team was "evaluating" whether to make other arrangements to travel to the event.
According to TV reporters traveling with the first lady, the flight was in the air about 10 minutes when smoke filled the cabin, and then Secret Service agents rushed to the front of the plane.
It was not immediately clear what caused the problem.
The event was planned for Thomas Jefferson University Hospital, where Health and Human Services Secretary Alex Azar was to join the first lady. The hospital has provided care to mothers with opioid use disorder and their newborn children for more than 45 years.
Mrs. Trump was to tour a neonatal intensive care nursery and speak at an HHS conference on a new system that tracks infants suffering from opiate withdrawal.
The first lady's intended visit was to be one of stops as she promotes her "Be Best" campaign, which focuses on issues affecting children, including the importance of healthy pregnancies. ||||| Evan Vucci/AP photo white house Melania Trump's plane makes unplanned landing after smoke issue
First lady Melania Trump’s plane made an unplanned landing at Joint Base Andrews after the aircraft experienced a “minor mechanical issue.”
“Everything is fine, and everyone is safe,” Trump's spokeswoman, Stephanie Grisham, said in a statement.
Story Continued Below
The first lady was on her way to an event with Health and Human Services Secretary Alex Azar at Thomas Jefferson University Hospital in Philadelphia. Grisham said they are “evaluating travel plans” in regards to the event.
Melania Trump and Azar were both on the flight.
Smoke could be seen inside the plane, and there was a burning smell, according to a pool report. Damp washcloths were passed out to passengers to hold over their faces because of the smell.
The aircraft was a Boeing C-32A identified as “Bright Star.”
Trump’s motorcade departed the White House for Joint Base Andrews at 8:01 a.m. The plane returned to the base for the unplanned landing at 9 a.m.
Trump and her party then boarded a second plane at 9:55 a.m. |||||
A summary of this is?
Answer:
| – First lady Melania Trump's plane was forced to return to a Washington area military base on Wednesday because of smoke in the cabin, the AP reports. Her spokeswoman, Stephanie Grisham, said "everyone is fine and everyone is safe" after the plane returned to Joint Base Andrews. Trump had been scheduled to visit a Philadelphia hospital and meet with families of children affected by exposure to opioids while in the womb. Grisham said the first lady's team was "evaluating" whether to make other arrangements to travel to the event. According to TV reporters traveling with the first lady, the flight was in the air about 10 minutes when smoke filled the cabin and there was a burning smell, and then Secret Service agents rushed to the front of the plane. It wasn't immediately clear what caused the problem, which Grisham called a "minor mechanical issue." The event was planned for Thomas Jefferson University Hospital, where Health and Human Services Secretary Alex Azar was to join the first lady; he was also on the plane, per Politico. The hospital has provided care to mothers with opioid use disorder and their newborn children for more than 45 years. Mrs. Trump was to tour a neonatal intensive-care nursery and speak at an HHS conference on a new system that tracks infants suffering from opiate withdrawal. The first lady's intended visit is part of stops to promote her "Be Best" campaign, which focuses on issues affecting children, including the importance of healthy pregnancies. (Melania is getting it from all corners lately.) | multi_news_1_0_0 |
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Write a summary based on this article:
Red onions aren’t just an essential cooking ingredient, they could also be a vital tool in the battle against cancer. University of Guelph scientists carried out a study which looked to discover which onions had the best cancer-fighting properties and discovered one in particular packed a powerful punch.
nailiaschwarz via Getty Images
The Ruby Ring, in particular the Ontario-grown variety, was shown to have the highest levels of a particular type of flavonoid. To test how effective the onions were the research team placed colon cancer cells in direct contact with quercetin extracted from the Ruby Ring variety. “We found onions are excellent at killing cancer cells,” said study author PhD student Abdulmonem Murayyan. “Onions activate pathways that encourage cancer cells to undergo cell death. They promote an unfavourable environment for cancer cells and they disrupt communication between cancer cells, which inhibits growth.” The researchers also found the onion cells were also just as capable of killing breast cancer cells. ||||| TIME Health For more, visit TIME Health
The next time you’re shopping for burger toppings or salad ingredients, opt for red onions over white. Both types of veggies contain potent antioxidant properties, but a new study suggests that the red variety may be especially powerful at fighting cancer.
When researchers exposed human cancer cells to extracts from five different varieties of onions, they found that the red-onion extract killed three to four times the number of cells compared to extracts of lighter-colored onions, says co-author Suresh Neethirajan, PhD, associate professor of bioengineering. His team’s findings are published in Food Research International.
RELATED: 6 Surprising Superfoods
The study looked specifically at onions grown in Ontario, which have been shown to have higher concentrations of the flavanoid compound quercetin than other varieties around the world. The authors can’t say for sure that their findings would apply to onions grown elsewhere, but they say it’s likely.
To test different Ontario-grown varieties head-to-head, the researchers used a newly developed technique to extract quercetin and other compounds from five onion species. Then they placed those extracts in direct contact with human colorectal cancer cells. All five species were “excellent at killing cancer cells,” says Neethirajan, but the red variety, Ruby Ring, tested highest for total phenolic content. (Phenols are compounds produced by plants.)
The authors say that red onions not only have high levels of quercetin, but that they’re also rich in anthocyanin—a plant pigment that enhances the ability of quercetin molecules to “scavenge,” or hunt down and destroy, dangerous free radicals that can lead not only to cancer but also to heart disease, diabetes and other inflammation-related conditions.
Anthocyanins are also what provide the red, blue, purple, and black hues of many fruits and vegetables. Nutrition experts have long recommended choosing richly colored fruits and vegetables, and it’s not surprising that red onions would have more cancer-fighting power than white, the authors say. Still, this is the first time the hypothesis has been confirmed in this type of laboratory setting.
The researchers recently found that onions are effective at killing breast cancer cells, as well. They say that onions appear to disrupt communication between cancer cells and promote an unfavorable environment for their growth, encouraging them to die. The next step, they add, will be testing these theories in human trials.
RELATED: 8 Things That Happen to Your Body When You Eat Beets
They also hope that the extraction technique tested in their study—which uses heated water in a pressurized container—will allow the quercetin in onions to one day be added to variety of fortified foods and even medicines. Unlike other extraction methods, this one does not use toxic solvents or chemicals.
For now, the best way to get those valuable nutrients is to eat onions themselves; for the biggest nutritional punch, choose red and eat them raw, since cooking destroys some of their antioxidant properties.
The study was funded by the Natural Science and Engineering Research Council of Canada and the Ontario Ministry of Agriculture, Food and Rural Affairs, and the onions were provided by the Holland Marsh Growers Association.
The findings are important not just to onion consumers, says Neethirajan, but also to onion growers, as well. “There are many types of onion varieties, and farmers need to know which is the best to invest in a crop,” he says. Planting more red varieties could give these growers an edge, not just in the food industry but perhaps in the functional food industry, as well.
This article originally appeared on Health.com ||||| | – Have an appetite for onions? Your body could be benefitting in ways scientists are just beginning to understand. In the latest study on what may well be a superfood, scientists at the University of Guelph in Ontario, Canada, report in the journal Food Research International that red onions in particular boast an ability to disrupt cancer cell communication and promote a generally poor environment for cancer cells, "which inhibits growth." The team was looking specifically at colon cancer, but they found that the onion cells are just as good at killing breast cancer cells. The trick, reports Huffpost, will be to extract the key ingredient, dose it just right, and use it medicinally. That key ingredient is quercetin, a flavonoid already known for its cancer-fighting properties. This study finds that onions in general have unusually high levels of quercetin compared to other foods, and that Ontario onions in particular have high levels of the compound compared to onions grown elsewhere. But red onions also boast high levels of anthocyanin, a plant pigment that help make quercetin molecules better scavengers. (Because anthocyanin helps make foods colorful, it makes sense to the researchers that red onions, which are so dark, have the greatest cancer-fighting potential.) It's unclear whether red onions from outside of Ontario will be as effective, but Time reports the researchers think it's likely, and plan to start clinical trials. (Onions also help reduce the risk of heart disease.) | multi_news_1_0_0 |
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News article:
When most people think of the Justice Department, they are likely to imagine the most visible parts of our job – the law enforcement agents who investigate crimes or the lawyers who prosecute them. But the department’s core responsibilities go beyond investigation and prosecution. Unlike most states, the federal government puts its law enforcement agents, criminal prosecutors, and correctional officers all in a single department. We handle every step from the start of an investigation to the end of a prison sentence. Our work to house and rehabilitate individuals incarcerated in the Federal Bureau of Prisons is an important part of our responsibility and operations, accounting for 25 percent of the department’s budget every year.
The federal prison population increased by almost 800 percent between 1980 and 2013, often at a far faster rate than the Bureau of Prisons could accommodate in their own facilities. In an effort to manage the rising prison population, about a decade ago, the bureau began contracting with privately operated correctional institutions to confine some federal inmates. By 2013, as both the federal prison population and the proportion of federal prisoners in private facilities reached their peak, the bureau was housing approximately 15 percent of its population, or nearly 30,000 inmates, in privately operated prisons.
2013 was also the year that the Department of Justice launched its Smart on Crime Initiative after identifying reforms that would ensure more proportional sentences and effective use of federal resources. Today, in part as a result of that initiative, we are experiencing declining numbers in our prison population. We now have approximately 195,000 inmates in bureau or private contract facilities down from a high in 2013 of approximately 220,000. This decline in the prison population means that we can better allocate our resources to ensure that inmates are in the safest facilities and receiving the best rehabilitative services – services that increase their chances of becoming contributing members of their communities when they return from prison.
Today, I sent a memo to the Acting Director of the Bureau of Prisons directing that, as each private prison contract reaches the end of its term, the bureau should either decline to renew that contract or substantially reduce its scope in a manner consistent with law and the overall decline of the bureau’s inmate population. This is the first step in the process of reducing—and ultimately ending—our use of privately operated prisons. While an unexpected need may arise in the future, the goal of the Justice Department is to ensure consistency in safety, security and rehabilitation services by operating its own prison facilities.
Today’s memo reflects important steps that the bureau has already taken to reduce our reliance on private prisons, including a decision three weeks ago to end a private prison contract for approximately 1,200 beds. Taken together, these steps will reduce the private prison population by more than half from its peak in 2013 and puts the Department of Justice on a path to ensure that all federal inmates are ultimately housed at bureau facilities. |||||
"The DOJ plan notes that there are 13 private prisons run by companies like GEO and CXW. It does not impact state contracts, ICE contracts or US Marshall contracts," Meliker said in the note, which pointed out that GEO has 11 percent exposure to the federally contracted private prisons and CXW has 9 percent exposure.
SunTrust Robinson Humphrey analysts also said in a Thursday note that the sell-off was "overdone" and that contracts with the DOJ will likely be reviewed individually over time, spreading out the risk of revenue loss. The firm has a "neutral" rating on CXW and a "buy" on GEO.
To be sure, states' use of private prisons has been under protest.
Exposure to those state operations is declining. Corrections Corp said in a 10-K filing last year that state customer business constituted 42 percent of total revenue in 2015, down from 49 percent in 2013.
The news was initially reported by The Washington Post, which cited a memo from Deputy Attorney General Sally Yates instructing officials to either not renew private prison contracts or "substantially reduce" their scope.
The goal is to ultimately end the Justice Department's use of the privately operated prisons as they provide lower quality services and are less cost efficient, the report said.
Ending federal use of private prisons is part of Democratic Presidential Nominee Hillary Clinton's justice reform platform. ||||| Looking for news you can trust?
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Chapter 1: “Inmates Run This Bitch”
Have you ever had a riot?” I ask a recruiter from a prison run by the Corrections Corporation of America (CCA).
“The last riot we had was two years ago,” he says over the phone.
“Yeah, but that was with the Puerto Ricans!” says a woman’s voice, cutting in. “We got rid of them.”
“When can you start?” the man asks.
I tell him I need to think it over.
I take a breath. Am I really going to become a prison guard? Now that it might actually happen, it feels scary and a bit extreme.
I started applying for jobs in private prisons because I wanted to see the inner workings of an industry that holds 131,000 of the nation’s 1.6 million prisoners. As a journalist, it’s nearly impossible to get an unconstrained look inside our penal system. When prisons do let reporters in, it’s usually for carefully managed tours and monitored interviews with inmates. Private prisons are especially secretive. Their records often aren’t subject to public access laws; CCA has fought to defeat legislation that would make private prisons subject to the same disclosure rules as their public counterparts. And even if I could get uncensored information from private prison inmates, how would I verify their claims? I keep coming back to this question: Is there any other way to see what really happens inside a private prison?
CCA certainly seemed eager to give me a chance to join its team. Within two weeks of filling out its online application, using my real name and personal information, several CCA prisons contacted me, some multiple times.
They weren’t interested in the details of my résumé. They didn’t ask about my job history, my current employment with the Foundation for National Progress, the publisher of Mother Jones, or why someone who writes about criminal justice in California would want to move across the country to work in a prison. They didn’t even ask about the time I was arrested for shoplifting when I was 19.
When I call Winn Correctional Center in Winnfield, Louisiana, the HR lady who answers is chipper and has a smoky Southern voice. “I should tell you upfront that the job only pays $9 an hour, but the prison is in the middle of a national forest. Do you like to hunt and fish?”
“I like fishing.”
“Well, there is plenty of fishing, and people around here like to hunt squirrels. You ever squirrel hunt?”
“No.”
“Well, I think you’ll like Louisiana. I know it’s not a lot of money, but they say you can go from a CO to a warden in just seven years! The CEO of the company started out as a CO”—a corrections officer.
Ultimately, I choose Winn. Not only does Louisiana have the highest incarceration rate in the world—more than 800 prisoners per 100,000 residents—but Winn is the oldest privately operated medium-security prison in the country.
I phone HR and tell her I’ll take the job.
“Well, poop can stick!” she says.
I pass the background check within 24 hours.
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Two weeks later, in November 2014, having grown a goatee, pulled the plugs from my earlobes, and bought a beat-up Dodge Ram pickup, I pull into Winnfield, a hardscrabble town of 4,600 people three hours north of Baton Rouge. I drive past the former Mexican restaurant that now serves drive-thru daiquiris to people heading home from work, and down a street of collapsed wooden houses, empty except for a tethered dog. About 38 percent of households here live below the poverty line; the median household income is $25,000. Residents are proud of the fact that three governors came from Winnfield. They are less proud that the last sheriff was locked up for dealing meth.
Thirteen miles away, Winn Correctional Center lies in the middle of the Kisatchie National Forest, 600,000 acres of Southern yellow pines crosshatched with dirt roads. As I drive through the thick forest, the prison emerges from the fog. You might mistake the dull expanse of cement buildings and corrugated metal sheds for an oddly placed factory were it not for the office-park-style sign displaying CCA’s corporate logo, with the head of a bald eagle inside the “A.”
At the entrance, a guard who looks about 60, a gun on her hip, asks me to turn off my truck, open the doors, and step out. A tall, stern-faced man leads a German shepherd into the cab of my truck. My heart hammers. I tell the woman I’m a new cadet, here to start my four weeks of training. She directs me to a building just outside the prison fence.
“Have a good one, baby,” she says as I pull through the gate. I exhale.
I park, find the classroom, and sit down with five other students.
“You nervous?” a 19-year-old black guy asks me. I’ll call him Reynolds. (I’ve changed the names and nicknames of the people I met in prison unless noted otherwise.)
“A little,” I say. “You?”
CCA RUNS 61 FACILITIES ACROSS THE UNITED STATES: These include 34 state prisons, 14 federal prisons, 9 immigration detention centers, and 4 jails.
state prisons, federal prisons, immigration detention centers, and jails. It owns 50 of these sites.
of these sites. 38 hold men, 2 hold women, 20 hold both sexes, and 1 holds women and children.**
hold men, hold women, hold both sexes, and holds women and children.** 17 are in Texas, 7 are in Tennessee, and 6 are in Arizona.
“Nah, I been around,” he says. “I seen killin’. My uncle killed three people. My brother been in jail, and my cousin.” He has scars on his arms. One, he says, is from a shootout in Baton Rouge. The other is from a street fight in Winnfield. He elbowed someone in the face, and the next thing he knew he got knifed from behind. “It was some gang shit.” He says he just needs a job until he starts college in a few months. He has a baby to feed. He also wants to put speakers in his truck. They told him he could work on his days off, so he’ll probably come in every day. “That will be a fat paycheck.” He puts his head down on the table and falls asleep.
The human resources director comes in and scolds Reynolds for napping. He perks up when she tells us that if we recruit a friend to work here, we’ll get 500 bucks. She gives us an assortment of other tips: Don’t eat the food given to inmates; don’t have sex with them or you could be fined $10,000 or get 10 years at hard labor; try not to get sick because we don’t get paid sick time. If we have friends or relatives incarcerated here, we need to report it. She hands out fridge magnets with the number of a hotline to use if we feel suicidal or start fighting with our families. We get three counseling sessions for free.
I studiously jot down notes as the HR director fires up a video of the company’s CEO, Damon Hininger, who tells us what a great opportunity it is to be a corrections officer at CCA. Once a guard himself, he made $3.4 million in 2015, nearly 19 times the salary of the director of the Federal Bureau of Prisons. “You may be brand new to CCA,” Hininger says, “but we need you. We need your enthusiasm. We need your bright ideas. During the academy, I felt camaraderie. I felt a little anxiety too. That is completely normal. The other thing I felt was tremendous excitement.”
I look around the room. Not one person—not the recent high school graduate, not the former Walmart manager, not the nurse, not the mother of twins who’s come back to Winn after 10 years of McDonald’s and a stint in the military—looks excited.
“I don’t think this is for me,” a postal worker says.
“Do not run!”
The next day, I wake up at 6 a.m. in my apartment in the nearby town where I decided to live to minimize my chances of running into off-duty guards. I feel a shaky, electric nervousness as I put a pen that doubles as an audio recorder into my shirt pocket.
In class that day, we learn about the use of force. A middle-aged black instructor I’ll call Mr. Tucker comes into the classroom, his black fatigues tucked into shiny black boots. He’s the head of Winn’s Special Operations Response Team, or SORT, the prison’s SWAT-like tactical unit. “If an inmate was to spit in your face, what would you do?” he asks. Some cadets say they would write him up. One woman, who has worked here for 13 years and is doing her annual retraining, says, “I would want to hit him. Depending on where the camera is, he might would get hit.”
Mr. Tucker pauses to see if anyone else has a response. “If your personality if somebody spit on you is to knock the fuck out of him, you gonna knock the fuck out of him,” he says, pacing slowly. “If a inmate hit me, I’m go’ hit his ass right back. I don’t care if the camera’s rolling. If a inmate spit on me, he’s gonna have a very bad day.” Mr. Tucker says we should call for backup in any confrontation. “If a midget spit on you, guess what? You still supposed to call for backup. You don’t supposed to ever get into a one-on-one encounter with anybody. Period. Whether you can take him or not. Hell, if you got a problem with a midget, call me. I’ll help you. Me and you can whup the hell out of him.”
“If a inmate hit me, I’m go’ hit his ass right back. I don’t care if the camera’s rolling.”
He asks us what we should do if we see two inmates stabbing each other.
“I’d probably call somebody,” a cadet offers.
“I’d sit there and holler ‘stop,'” says a veteran guard.
Mr. Tucker points at her. “Damn right. That’s it. If they don’t pay attention to you, hey, there ain’t nothing else you can do.”
He cups his hands around his mouth. “Stop fighting,” he says to some invisible prisoners. “I said, ‘Stop fighting.'” His voice is nonchalant. “Y’all ain’t go’ to stop, huh?” He makes like he’s backing out of a door and slams it shut. “Leave your ass in there!”
“Somebody’s go’ win. Somebody’s go’ lose. They both might lose, but hey, did you do your job? Hell yeah!” The classroom erupts in laughter.
We could try to break up a fight if we wanted, he says, but since we won’t have pepper spray or a nightstick, he wouldn’t recommend it. “We are not going to pay you that much,” he says emphatically. “The next raise you get is not going to be much more than the one you got last time. The only thing that’s important to us is that we go home at the end of the day. Period. So if them fools want to cut each other, well, happy cutting.”
When we return from break, Mr. Tucker sets a tear gas launcher and canisters on the table. “On any given day, they can take this facility,” he says. “At chow time, there are 800 inmates and just two COs. But with just this class, we could take it back.” He passes out sheets for us to sign, stating that we volunteer to be tear-gassed. If we do not sign, he says, our training is over, which means our jobs end right here. (When I later ask CCA if its staff members are required to be exposed to tear gas, spokesman Steven Owen says no.) “Anybody have asthma?” Mr. Tucker says. “Two people had asthma in the last class and I said, ‘Okay, well, I’ma spray ’em anyway.’ Can we spray an inmate? The answer is yes.”
Five of us walk outside and stand in a row, arms linked. Mr. Tucker tests the wind with a finger and drops a tear gas cartridge. A white cloud of gas washes over us. The object is to avoid panicking, staying in the same place until the gas dissipates. My throat is suddenly on fire and my eyes seal shut. I try desperately to breathe, but I can only choke. “Do not run!” Mr. Tucker shouts at a cadet who is stumbling off blindly. I double over. I want to throw up. I hear a woman crying. My upper lip is thick with snot. When our breath starts coming back, the two women linked to me hug each other. I want to hug them too. The three of us laugh a little as tears keep pouring down our cheeks.
“Don’t ever say thank you”
Our instructors advise us to carry a notebook to keep track of everything prisoners will ask us for. I keep one in my breast pocket and jet into the bathroom periodically to jot things down. They also encourage us to invest in a watch because when we document rule infractions it is important that we record the time precisely. A few days into training, a wristwatch arrives in the mail. One of the little knobs on its side activates a recorder. On its face there is a tiny camera lens.
On the eighth day, we are pulled from CPR class and sent inside the compound to Elm—one of five single-story brick buildings where the prison’s roughly 1,500 inmates live. When we go through security, we are told to empty our pockets and remove our shoes and belts. This is intensely nerve-wracking: I send my watch, pen, employee ID, and pocket change through the X-ray machine. I walk through the metal detector and a CO runs a wand up and down my body and pats down my chest, back, arms, and legs.
The other cadets and I gather at a barred gate and an officer, looking at us through thick glass, turns a switch that opens it slowly. We pass through, and after the gate closes behind us, another opens ahead. On the other side, the CCA logo is emblazoned on the wall along with the words “Respect” and “Integrity” and a mural of two anchors inexplicably floating at sea. Another gate clangs open and our small group steps onto the main outdoor artery of the prison: “the walk.”
From above, the walk is shaped like a “T.” It is fenced in with chain-link and covered with corrugated steel. Yellow lines divide the pavement into three lanes. Clustered and nervous, we cadets travel up the middle lane from the administration building as prisoners move down their designated side lanes. I greet inmates as they pass, trying hard to appear loose and unafraid. Some say good morning. Others stop in their tracks and make a point of looking the female cadets up and down.
We walk past the squat, dull buildings that house visitation, programming, the infirmary, and a church with a wrought-iron gate shaped into the words “Freedom Chapel.” Beyond it there is a mural of a fighter jet dropping a bomb into a mountain lake, water blasting skyward, and a giant bald eagle soaring overhead, backgrounded by an American flag. At the top of the T we take a left, past the chow hall and the canteen, where inmates can buy snacks, toiletries, tobacco, music players, and batteries.
There are almost never more than two floor officers in a general population unit. That’s one per 176 inmates.
The units sit along the top of the walk. Each is shaped like an “X” and connected to the main walk by its own short, covered walk. Every unit is named after a type of tree. Most are general population units, where inmates mingle in dorm-style halls and can leave for programs and chow. Cypress is the high-security segregation unit, the only one where inmates are confined to cells.
In Dogwood, reserved for the best-behaved inmates, prisoners get special privileges like extra television time, and many work outside the unit in places like the metal shop, the garment factory, or the chow hall. Some “trusties” even get to work in the front office, or beyond the fence washing employees’ personal cars. Birch holds most of the elderly, infirm, and mentally ill inmates, though it doesn’t offer any special services. Then there are Ash and Elm, which inmates call “the projects.” The more troublesome prisoners live here.
WINN CORRECTIONAL CENTER Medium-security prison for inmates serving 50 years or less Inmate population: About 1,500
75% black, 25% white or other
black, white or other Average inmate age: 36
Average sentence: 19 years
Average time served: 5.7 years
Daily rate charged to state per inmate (2015): $34 INMATE OFFENSES Violent crimes: 55%
Drug crimes: 19%
Property crimes: 13%
Other: 13%
We enter Elm and walk onto an open, shiny cement floor. The air is slightly sweet and musty, like the clothes of a heavy smoker. Elm can house up to 352 inmates. At the center is an enclosed octagonal control room called “the key.” Inside, a “key officer,” invariably a woman, watches the feeds of the unit’s 27-odd surveillance cameras, keeps a log of significant occurrences, and writes passes that give inmates permission to go to locations outside the unit, like school or the gym. Also in the key is the office of the unit manager, the “mini-warden” of the unit.
The key stands in the middle of “the floor.” Branching out from the floor are the four legs of the X; two tiers run down the length of each leg. Separated from the floor by a locked gate, every tier is an open dormitory that houses up to 44 men, each with his own narrow bed, thin mattress, and metal locker.
Toward the front of each tier, there are two toilets, a trough-style urinal, and two sinks. There are two showers, open except for a three-foot wall separating them from the common area. Nearby are a microwave, a telephone, and a Jpay machine, where inmates pay to download songs onto their portable players and send short, monitored emails for about 30 cents each. Each tier also has a TV room, which fills up every weekday at 12:30 p.m. for the prison’s most popular show, The Young and the Restless.
At Winn, staff and inmates alike refer to guards as “free people.” Like the prisoners, the majority of the COs at Winn are African American. More than half are women, many of them single moms. But in Ash and Elm, the floor officers—who more than anyone else deal with the inmates face-to-face—are exclusively men. Floor officers are both enforcers and a prisoner’s first point of contact if he needs something. It is their job to conduct security checks every 30 minutes, walking up and down each tier to make sure nothing is awry. Three times per 12-hour shift, all movement in the prison stops and the floor officers count the inmates. There are almost never more than two floor officers per general population unit. That’s one per 176 inmates. (CCA later tells me that the Louisiana Department of Corrections, or DOC, considered the “staffing pattern” at Winn “appropriate.”)
In Elm, a tall white CO named Christian is waiting for us with a leashed German shepherd. He tells the female cadets to go to the key and the male cadets to line up along the showers and toilets at the front of the tier. We put on latex gloves. The inmates are sitting on their beds. Two ceiling fans turn slowly. The room is filled with fluorescent light. Almost every prisoner is black.
A small group of inmates get up from their beds and file into the shower area. One, his body covered with tattoos, gets in the shower in front of me, pulls off his shirt and shorts, and hands them to me to inspect. “Do a one-finger lift, turn around, bend, squat, cough,” Christian orders. In one fluid motion, the man lifts his penis, opens his mouth, lifts his tongue, spins around with his ass facing me, squats, and coughs. He hands me his sandals and shows me the soles of his feet. I hand him his clothes and he puts his shorts on, walks past me, and nods respectfully.
Like a human assembly line, the inmates file in. “Beyend, squawt, cough,” Christian drawls. He tells one inmate to open his hand. The inmate uncurls his finger and reveals a SIM card. Christian takes it but does nothing.
Staff and inmates alike refer to guards as “free people.” More than half are women, many of them single moms.
Eventually, the TV room is full of prisoners. A guard looks at them and smiles. “Tear ’em up!” he says, gesturing down the tier. Each of us, women included, stops at a bed. Christian tells one cadet to “shake down bed eight real good—just because he pissed me off.” He tells us to search everything. I follow the other guards’ lead, opening bottles of toothpaste and lotion. Inside a container of Vaseline, I find a one-hitter pipe made out of a pen and ask Christian what to do with it. He takes it from me, mutters “eh,” and tosses it on the floor. I go through the mattress, pillow, dirty socks, and underwear. I flip through photos of kids, and of women posing seductively. I move on to new lockers: ramen, chips, dentures, hygiene products, peanut butter, cocoa powder, cookies, candy, salt, moldy bread, a dirty coffee cup. I find the draft of a novel, dedicated to “all the hustlers, bastards, strugglers, and hoodlum childs who are chasing their dreams.”
One instructor notices that I am carefully putting each object back where I found it and tells me to pull everything out of the lockers and leave it on the beds. I look down the tier and see mattresses lying on the floor, papers and food dumped across beds. The middle of the floor is strewn with contraband: USB cables refashioned as phone chargers, tubs of butter, slices of cheese, and pills. I find some hamburger patties taken from the cafeteria. A guard tells me to throw them into the pile.
Inmates are glued up against the TV room window, watching a young white cadet named Miss Stirling pick through their stuff. She’s pretty and petite, with long, jet-black hair. The attention makes her uncomfortable; she thinks the inmates are gross. Earlier this week, she said she would refuse to give an inmate CPR and won’t try the cafeteria food because she doesn’t want to “eat AIDS.” The more she is around prisoners, though, the more I notice her grapple with an inner conflict. “I don’t want to treat everyone like a criminal because I’ve done things myself,” she says.
Miss Stirling says she sometimes wonders if her baby’s dad will end up here. She doesn’t like doing chokehold escapes in class because they bring back memories of him. He cooked meth in their toolshed and once beat her so badly he dislocated her shoulder and knee. “You know that bone at the bottom of your neck? He pushed it up into my head,” she says.
Senior Reporter Shane Bauer can be reached by email at [email protected]. Have a scoop for Mother Jones? Send it here.
If he ends up in this prison, another cadet assures her, “we could make his life hell.”
As we shake down the tier, a prisoner comes out of the TV room to get a better look at Miss Stirling, and she yells at him to go back in. He does.
“Thank you,” she says.
“Did she just say thank you?” Christian asks. A bunch of COs scoff.
“Don’t ever say thank you,” a woman CO tells her. “That takes the power away from it.”
“Ain’t no order here”
Most of our training is uneventful. Some days there are no more than two hours of classes, and then we have to sit and run the clock to 4:15 p.m. We pass the time discussing each other’s lives. I try mostly to stay quiet, but when I slip into describing a backpacking trip I recently took in California, a cadet throws her arms in the air and shouts, “Why are you here?!” I am careful to never lie, instead backing out with generalities like, “I came here for work,” or “You never know where life will take you,” and no one pries further.
Few of my fellow cadets have traveled farther than nearby Oklahoma. They compare towns by debating the size and quality of their Walmarts. Most are young. They eat candy during break time, write their names on the whiteboard in cutesy lettering, and talk about different ways to get high.
Miss Doucet, a stocky redheaded cadet in her late 50s, thinks that if kids were made to read the Bible in school, fewer would be in prison, but she also sticks pins in a voodoo doll to mete out vengeance. “I swing both ways,” she says. She lives in a camper with her daughter and grandkids. With this job, she’s hoping to save up for a double-wide trailer.
The shoulders of a young cadet are slumping. He says his check was for $577, after they took $121 in taxes.
She worked at the lumber mill in Winnfield for years, but worsening asthma put an end to that. She’s been hospitalized several times this year and says she almost died once. “They don’t even want me to bring this in,” she whispers, leaning in, pulling her inhaler out of her pocket. “I’m not supposed to, but I do. They ain’t takin’ it away from me.” She takes a long drag from her cigarette.
Miss Doucet and others from the class ahead of mine go to the front office to get their paychecks for their first two weeks of work. When they return, the shoulders of a young cadet are slumping. He says his check was for $577, after they took $121 in taxes.
“Dang. That hurts,” he says.
Miss Doucet says they withheld $114 from her check.
“They held less for you?!” the young cadet says.
“I’m may-ried!” she says in a singsong voice. “I got a chi-ild!”
Outwardly, Miss Doucet is jovial and cocky, but she is already making mental adjustments to her dreams. The double-wide trailer she imagines her grandkids spreading out in becomes a single-wide. She figures she can get $5,000 for the RV.
CCA Facilities
At the end of one morning of doing nothing, the training coordinator tells us we can go to the gym to watch inmates graduate from trade classes. Prisoners and their families are milling around with plates of cake and cups of fruit punch. An inmate offers a piece of red velvet to Miss Stirling.
I stand around with Collinsworth, an 18-year-old cadet with a chubby white baby face hidden behind a brown beard and a wisp of bangs. Before CCA, Collinsworth worked at a Starbucks. When he came to Winnfield to help out with family, this was the first job he could get. Once, Collinsworth was nearly kicked out of class after he jokingly threatened to stab Mr. Tucker with a plastic training knife. He’s boasted to me about inmate management tactics he’s learned from seasoned officers. “You just pit ’em against each other and that’s the easiest way to get your job done,” he tells me. He says one guard told him that inmates should tell troublemakers, “‘I’m gonna rape you if you try that shit again.’ Or something; whatever it takes.”
As Collinsworth and I stand around, inmates gather to look at our watches. One, wearing a cocked gray beanie, asks to buy them. I refuse outright. Collinsworth dithers. “How old you is?” the inmate asks him.
“You never know,” Collinsworth says.
“Man, all these fake-ass signals,” the inmate says. “The best thing you could do is get to know people in the place.”
“I understand it’s your home,” Collinsworth says. “But I’m at work right now.”
“It’s your home for 12 hours a day! You trippin’. You ’bout to do half my time with me. You straight with that?”
“It’s probably true.”
“It ain’t no ‘probably true.’ If you go’ be at this bitch, you go’ do 12 hours a day.” He tells Collinsworth not to bother writing up inmates for infractions: “They ain’t payin’ you enough for that.” Seeming torn between whether to impress me or the inmate, Collinsworth says he will only write up serious offenses, like hiding drugs.
“Drugs?! Don’t worry ’bout the drugs.” The inmate says he was caught recently with two ounces of “mojo,” or synthetic marijuana, which is the drug of choice at Winn. The inmate says guards turn a blind eye to it. They “ain’t trippin’ on that shit,” he says. “I’m telling you, it ain’t that type of camp. You can’t come change things by yourself. You might as well go with the flow. Get this free-ass, easy-ass money, and go home.”
“I’m just here to do my job and take care of my family,” Collinsworth says. “I’m not gonna bring stuff in ‘cuz even if I don’t get caught, there’s always the chance that I will.”
“They ain’t got shit for us here. What you think gonna happen when a man got nuttin’ to do?
“Nah. Ain’t no chance,” the inmate says. “I ain’t never heard of nobody movin’ good and low-key gettin’ caught. Nah. I know a dude still rolling. He been doin’ it six years.” He looks at Collinsworth. “Easy.”
The inmates’ families file out the side entrance. A couple of minutes after the last visitors leave, the coach shouts, “All inmates on the bleachers!” A prisoner tosses his graduation certificate dramatically into the trash. Another lifts the podium over his head and runs with it across the gym. The coach shouts, exasperated, as prisoners scramble around.
“You see this chaos?” the inmate in the beanie says to Collinsworth. “If you’d been to other camps, you’d see the order they got. Ain’t no order here. Inmates run this bitch, son.”
A week later, Mr. Tucker tells us to come in early to do shakedowns. The sky is barely lit as I stand on the walk at 6:30 with the other cadets. Collinsworth tells us another prisoner offered to buy his watch. He said he’d sell it for $600. The inmate declined.
“Don’t sell it to him anyway,” Miss Stirling admonishes him. “You might get $600, but if they find out, you ain’t go’ get no more paychecks.”
“Nah, I wouldn’t actually do it. I just said $600 because I know they don’t got $600 to give me.”
“Shit,” a heavyset black cadet named Willis says. He’s our main authority on prison life. He says he served seven and a half years in the Texas State Penitentiary; he won’t say what for. (CCA hires former felons whom it deems not to be a security risk; it says all Winn guards’ background checks were also reviewed by the DOC.) “Dudes was showing me pictures,” says Willis. “They got money in here. One dude in here, don’t say nothin’, but he got like six to eight thousand dollars. They got it on cards. Little money cards and shit.”
Collinsworth jumps up and down. “Dude, I’ma find me one of them damn cards! Hell yeah. And I will not report it.”
Officially, inmates are only allowed to keep money in special prison-operated accounts that can be used at the canteen. In these accounts, prisoners with jobs receive their wages, which may be as little as 2 cents an hour for a dishwasher and as much as 20 cents for a sewing-machine operator at Winn’s garment factory. Their families can also deposit money in the accounts.
The prepaid cash cards Willis is referring to are called Green Dots, and they are the currency of the illicit prison economy. Connections on the outside buy them online, then pass on the account numbers in encoded messages through the mail or during visits. Inmates with contraband cellphones can do all these transactions themselves, buying the cards and handing out strips of paper as payments for drugs or phones or whatever else.
Miss Stirling divulges that an inmate gave her the digits of a money card as a Christmas gift. “I’m like, damn! I need a new MK watch. I need a new purse. I need some new jeans.”
“There was this one dude in Dogwood,” she continues. “He came up to the bars and showed me a stack of hundred-dollar bills folded up, and it was like this—” She makes like she’s holding a wad of cash four inches thick. “And I was like, ‘I’m not go’ say anything.'”
“Dude! I’ma shake him the fuck down!” Collinsworth says. “I don’t care if he’s cool.”
“He had a phone,” Miss Stirling says, “and he’s like, ‘I don’t have the time of day to hide it. I just keep it in the open. I really don’t give a fuck.'”
Mr. Tucker tells us to follow him. We shake down tiers all morning. By the time we finish at 11, everyone is exhausted. “I’m not mad we had to do shakedowns. I’m just mad we didn’t find anything,” Collinsworth says. Christian pulls a piece of paper out of his pocket and reads off a string of numbers in a show-offy way. “A Green Dot,” he says. Christian hands the slip of paper to one of the cadets, a middle-aged white woman. “You can have this one,” he says. “I have plenty already.” She smiles coyly.
“We are going to win this unit back”
“Welcome to the hellhole,” a female CO greeted me the first time I visited the segregation unit. A few days later I’m back at Cypress with Collinsworth and Reynolds to shadow some guards. The metal door clicks open and we enter to a cacophony of shouting and pounding on metal. An alarm is sounding and the air smells strongly of smoke.
On one wall is a mural of a prison nestled among dark mountains and shrouded in storm clouds, lightning striking the guard towers and an enormous, screeching bald eagle descending with a giant pair of handcuffs in its talons. Toward the end of a long hall of cells, an officer in a black SWAT-style uniform stands ready with a pepper-ball gun. Another man in black is pulling burnt parts of a mattress out of a cell. Cypress can hold up to 200 inmates; most of the eight-by-eight-foot cells have two prisoners in them. The cells look like tombs; men lie in their bunks, wrapped in blankets, staring at the walls. Many are lit only by the light from the hallway. In one, an inmate is washing his clothes in his toilet.
“How are you doing?” says a smiling white man dressed business casual. He grips my hand. “Thank you for being here.” Assistant Warden Parker is new to CCA, but he was once the associate warden of a federal prison. “I know it seems crazy back here now, but you’ll learn the ropes,” he assures me. “We are going to win this unit back. It’s not going to happen in an hour. It’s gonna take time, but it will happen.” Apparently the segregation unit has been in a state of upheaval for a while, so corporate headquarters has sent in SORT officers from out of state to bring it back under control. SORT teams are trained to suppress riots, rescue hostages, extract inmates from their cells, and neutralize violent prisoners. They deploy an array of “less lethal” weapons like plastic buckshot, electrified shields, and chili-pepper-filled projectiles that burst on contact.
I get a whiff of feces that quickly becomes overpowering. On one of the tiers, a brown liquid oozes out of a bottle on the floor. Food, wads of paper, and garbage are all over the ground. I spot a Coke can, charred black, with a piece of cloth sticking out of it like a fuse. “I use my political voice!” an inmate shouts. “I stand up for my rights. Hahaha! Ain’t nowhere like this camp. Shit, y’all’s disorganized as fuck up in here.”
“That’s why we are here,” a SORT member says. “We are going to change all that.”
The cells look like tombs. Men lie in their bunks, wrapped in blankets, staring at the walls.
“Y’all can’t change shit,” the prisoner yells back. “They ain’t got shit for us here. We ain’t got no jobs. No rec time. We just sit in our cells all day. What you think gonna happen when a man got nuttin’ to do? That’s why we throw shit out on the tier. What else are we going to do? You know how we get these officers to respect us? We throw piss on ’em. That’s the only way. Either that or throw them to the floor. Then they respect us.”
I ask one of the regular white-shirted COs what an average day in seg looks like. “To be honest with you, normally we just sit here at this table all day long,” he tells me. They are supposed to walk up and down the eight tiers every 30 minutes to check on the inmates, but he says they never do that. (CCA says it had no knowledge of guards at Winn skipping security checks before I inquired about it.)
Collinsworth is walking around with a big smile on his face. He’s learning how to take inmates out of their cells for disciplinary court, which is inside Cypress. He’s supposed to cuff them through the slot in the bars, then tell the CO at the end of the tier to open the gate remotely. “Fuck nah, I ain’t coming out of this cell!” an inmate shouts at him. “You go’ have to get SORT to bring me up out of here. That’s how we do early in the morning. I’ll fuck y’all up.” The prisoner climbs up on the bars and pounds on the metal above the cell door. The sound explodes down the cement hallway.
Collinsworth and the CO he is shadowing move another inmate from his cell. The inmate tries to walk ahead as the CO holds him. “If that motherfucker starts pulling away from me like that again, I’m gonna make him eat concrete,” the CO says to Collinsworth.
“I kind of hope he does mess around again,” Collinsworth says, beaming. “That would be fun!”
I take a few inmates out of their cells, too, walking each one a hundred feet or so to disciplinary court with my hand around one of his elbows. One pulls against my grip. “Why you pulling on me, man?” he shouts, spinning around to stand face-to-face with me. A SORT officer rushes over and grabs him. My heart races.
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One of the white-shirted officers takes me aside. “Hey, don’t let these guys push you around,” he says. “If he is pulling away from you, you tell him, ‘Stop resisting.’ If he doesn’t, you stop. If he keeps going, we are authorized to knee him in the back of the leg and drop him to the concrete.”
Inmates shout at me as I walk back down the tier. “He has a little twist in his walk. I like them holes in your ears, CO. Come in here with me. Give me that booty!”
At lunchtime, Collinsworth, Reynolds, and I go back to the training room. “I love it here,” Collinsworth says dreamily. “It’s like a community.”
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Chapter 2: Prison Experiments
People say a lot of negative things about CCA,” the head of training, Miss Blanchard, tells us. “That we’ll hire anybody. That we are scraping the bottom of the barrel. Which is not really true, but if you come here and you breathing and you got a valid driver’s license and you willing to work, then we’re willing to hire you.” She warns us repeatedly, however, that to become corrections officers, we’ll need to pass a test at the end of our four weeks of training. We will need to know the name of the CEO, the names of the company’s founders, and their reason for establishing the first private prison more than 30 years ago. (Correct answer: “to alleviate the overcrowding in the world market.”)
To prepare us, Miss Blanchard shows a video in which CCA founders T. Don Hutto and Thomas Beasley playfully tell their company’s origin story. In 1983, they recount, they won “the first contract ever to design, build, finance, and operate a secure correctional facility in the world.” The Immigration and Naturalization Service gave them just 90 days to do it. Hutto recalls how the pair quickly converted a Houston motel into a detention center: “We opened the facility on Super Bowl Sunday the end of that January. So about 10 o’clock that night we start receiving inmates. I actually took their pictures and fingerprinted them. Several other people walked them to their ‘rooms,’ if you will, and we got our first day’s pay for 87 undocumented aliens.” Both men chuckle.
There is much about the history of CCA the video does not teach. The idea of privatizing prisons originated in the early 1980s with Beasley and fellow businessman Doctor Robert Crants. The two had no experience in corrections, so they recruited Hutto, who had been the head of Virginia’s and Arkansas’ prisons. In a 1978 ruling, the Supreme Court had found that a succession of Arkansas prison administrations, including Hutto’s, “tried to operate their prisons at a profit.” Guards on horseback herded the inmates, who sometimes did not have shoes, to the fields. The year after Hutto joined CCA, he became the head of the American Correctional Association, the largest prison association in the world.
To Beasley, the former chairman of the Tennessee Republican Party, the business of private prisons was simple: “You just sell it like you were selling cars, or real estate, or hamburgers,” he told Inc. magazine in 1988. Beasley and Crants ran the business a lot like a hotel chain, charging the government a daily rate for each inmate. Early investors included Sodexho-Marriott and the venture capitalist Jack Massey, who helped build Kentucky Fried Chicken, Wendy’s, and the Hospital Corporation of America.
The 1980s were a good time to get into the incarceration business. The prison population was skyrocketing, the drug war was heating up, the length of sentences was increasing, and states were starting to mandate that prisoners serve at least 85 percent of their terms. Between 1980 and 1990, state spending on prisons quadrupled, but it wasn’t enough. Prisons in many states were filled beyond capacity. When a federal court declared in 1985 that Tennessee’s overcrowded prisons violated the Eighth Amendment’s ban on cruel and unusual punishment, CCA made an audacious proposal to take over the state’s entire prison system. The bid was unsuccessful, but it planted an idea in the minds of politicians across the country: They could outsource prison management and save money in the process. Privatization also gave states a way to quickly expand their prison systems without taking on new debt. In the perfect marriage of fiscal and tough-on-crime conservatism, the companies would fund and construct new lockups while the courts would keep them full.
Private and public prison populations, 1990-2014
When CCA shares appeared on the NASDAQ stock exchange in 1986, the company was operating two juvenile detention centers and two immigrant detention centers. Today, it runs more than 60 facilities, from state prisons and jails to federal immigration detention centers. All together, CCA houses at least 66,000 inmates at any given time. Its main competitor, the GEO Group, holds more than 70,000 inmates in the United States. Currently, private prisons oversee about 8 percent of the country’s total prison population.
Whatever taxpayer money CCA receives has to cover the cost of housing, feeding, and rehabilitating inmates. While I work at Winn, CCA receives about $34 per inmate per day. In comparison, the average daily cost per inmate at the state’s publicly run prisons is about $52. Some states pay CCA as much as $80 per prisoner per day. In 2015, CCA reported $1.9 billion in revenue; it made more than $221 million in net income—more than $3,300 for each prisoner in its care. CCA and other prison companies have written “occupancy guarantees” into their contracts, requiring states to pay a fee if they cannot provide a certain number of inmates. Two-thirds of the private-prison contracts recently reviewed by the anti-privatization group In the Public Interest had these prisoner quotas. Under CCA’s contract, Winn was guaranteed to be 96 percent full.
“If you come here and you breathing and you got a valid driver’s license and you willing to work, then we’re willing to hire you.”
The main argument in favor of private prisons—that they save taxpayers money—remains controversial. One study estimated that private prisons cost 15 percent less than public ones; another found that public prisons were 14 percent cheaper. After reviewing these competing claims, researchers concluded that the savings “appear minimal.” CCA directed me to a 2013 report—funded in part by the company and GEO—that claimed private prisons could save states as much as 59 percent over public prisons without sacrificing quality.
Private prisons’ cost savings are “modest,” according to one Justice Department study, and are achieved mostly through “moderate reductions in staffing patterns, fringe benefits, and other labor-related costs.” Wages and benefits account for 59 percent of CCA’s operating expenses. When I start at Winn, nonranking guards make $9 an hour, no matter how long they’ve worked there. The starting pay for guards at public state prisons comes out to $12.50 an hour. CCA told me that it “set[s] salaries based on the prevailing wages in local markets,” adding that “the wages we provided in Winn Parish were competitive for that area.”
Based on data from Louisiana’s budget office, the cost per prisoner at Winn, adjusted for inflation, dropped nearly 20 percent between the late ’90s and 2014. The pressure to squeeze the most out of every penny at Winn seems evident not only in our paychecks, but in decisions that keep staffing and staff-intensive programming for inmates at the barest of levels. When I asked CCA about the frequent criticism I heard from both staff and inmates about its relentless focus on the bottom line, its spokesman dismissed the assertion as “a cookie-cutter complaint,” adding that it would be false “to claim that CCA prioritizes its own economic gain over the needs of its customers” or the safety of its inmates.
The escape
Two weeks after I start training, Chase Cortez (his real name) decides he has had enough of Winn. It’s been nearly three years since he was locked up for theft, and he has only three months to go. But in the middle of a cool, sunny December day, he climbs onto the roof of Birch unit. He lies down and waits for the patrol vehicle to pass along the perimeter. He is in view of the guard towers, but they’ve been unmanned since at least 2010. Now, a single CO watches the video feeds from at least 30 cameras.
Cortez sees the patrol van pass, jumps down from the back side of the building, climbs the razor-wire perimeter fence, and then makes a run for the forest. He fumbles through the dense foliage until he spots a white pickup truck left by a hunter. Lucky for him, it is unlocked, with the key in the ignition.
In the control room, an alarm sounds, indicating that someone has touched the outer fence, a possible sign of a perimeter breach. The officer reaches over, switches the alarm off, and goes back to whatever she was doing. She notices nothing on the video screen, and she does not review the footage. Hours pass before the staff realizes someone is missing. Some guards tell me it was an inmate who finally brought the escape to their attention. Cortez is caught that evening after the sheriff chases him and he crashes the truck into a fence.
The prison is on lockdown. Staff are worried CCA is going to lose its contract.
When I come in the next morning, the prison is on lockdown. Staff are worried CCA is going to lose its contract with Louisiana. “We were already in the red, and this just added to it,” the assistant training director tells me. “It’s a lot of tension right now.”
CCA said nothing publicly about the escape; I heard about it from guards who had investigated the incident or been briefed by the warden. (The company later told me it conducted a “full review” of the incident and fired a staff member “for lack of proper response to the alarm.” When I asked CCA about its decision to remove guards from Winn’s watchtowers, its spokesman replied that “newer technologies…are making guard towers largely obsolete.”)
Later that day, Reynolds and I bring food to Cypress, the segregation unit. It is dinnertime, but inmates haven’t had lunch yet. A naked man is shouting frantically for food, mercilessly slapping the plexiglass at the front of his cell. In the cell next to him, a small, wiry man is squatting on the floor in his underwear. His arms and face are scraped with little cuts. A guard tells me to watch him.
It is Cortez. I offer him a packet of Kool-Aid in a foam cup. He says thank you, then asks if I will put water in it. There is no water in his cell.
When inmates are written up for breaking the rules, they are sent to inmate court, which is held in a room in the corner of Cypress unit. One day, our class files into the small room to watch the hearings. Miss Lawson, the assistant chief of security, is acting as the judge, sitting at a desk in front of a mural of the scales of justice. “Even though we treat every inmate like they are guilty until proven innocent, they are…?” She pauses for someone to fill in the answer.
“Innocent?” a cadet offers.
“That’s right. Innocent until proven guilty.”
This is not a court of law, although it issues punishments for felonies such as assault and attempted murder. An inmate who stabs another may end up facing new criminal charges. He may be transferred, yet prisoners and guards say inmates who stab others typically are not shipped to a higher-security prison. The consequences for less serious offenses are usually stints in seg or a loss of “good time,” sentence reduction for good behavior. According to the DOC, Winn inmates charged with serious rule violations are found guilty at least 96 percent of the time.
“Inmate counsel, has your defendant appeared before the court?” Miss Lawson asks a prisoner standing at the podium.
“No, ma’am, he has not,” he replies. The inmate counsel represents other inmates in the internal disciplinary process. Every year, he is taken to a state-run prison for intensive training. Miss Lawson later tells me that inmate counsel never really influences her decisions.
For removing a broom from a closet at the wrong time, this inmate will stay in prison an extra 30 days.
The absent inmate is accused of coming too close to the main entrance. “Would the counsel like to offer a defense?”
“No, ma’am.”
“How does he plead?”
“Not guilty.”
“Mr. Trahan is found guilty.” The entire “trial” lasts less than two minutes.
The next defendant is called.
He is being considered for release from segregation. “Do you know your Bible?” Miss Lawson asks.
“Yes, ma’am.”
“Do you remember in the Gospel of John when the adulteress was brought before Jesus? What did he say?”
“I don’t remember that, ma’am.”
“He says, ‘Sin no more.'” She points for him to leave the room.
The next inmate, an orderly in Cypress, enters. He is charged with being in an unauthorized area because he took a broom to sweep the tier during rec time, which is not the authorized time to sweep the tier. He starts to explain that a CO gave him permission. Miss Lawson cuts him off. “How would you like to plead?”
“Guilty, I guess.”
“You are found guilty and sentenced to 30 days’ loss of good time.”
“Man! Y’all—this is fucked up, man. Y’all gonna take my good time!?” He runs out of the room. “They done took my good time!” he screams in the hall. “They took my good time! Fuck them!” For removing a broom from a closet at the wrong time, this inmate will stay in prison an extra 30 days, for which CCA will be paid more than $1,000.
True colors
One day in class we take a personality test called True Colors that’s supposed to help CCA decide how to place us. Impulsive “orange” people can be useful in hostage negotiations because they don’t waste time deliberating. Rule-oriented “gold” people are chosen for the daily management of inmates. The majority of the staff, Miss Blanchard says, are gold—dutiful, punctual people who value rules. My results show that green is my dominant color (analytical, curious) and orange is my secondary (free and spontaneous). Green is a rare personality type at Winn. Miss Blanchard doesn’t offer any examples of how greens can be useful in a prison.
The company that markets the test claims that people who retake it get the same results 94 percent of the time. But Miss Blanchard says that after working here awhile, people often find their colors have shifted. Gold traits tend to become more dominant.
Studies have shown that personalities can change dramatically when people find themselves in prison environments. In 1971, psychologist Philip Zimbardo conducted the now-famous Stanford Prison Experiment, in which he randomly assigned college students to the roles of prisoners and guards in a makeshift basement “prison.” The experiment was intended to study how people respond to authority, but it quickly became clear that some of the most profound changes were happening to the guards. Some became sadistic, forcing the prisoners to sleep on concrete, sing and dance, defecate into buckets, and strip naked. The situation became so extreme that the two-week study was cut short after just six days. When it was over, many “guards” were ashamed at what they had done and some “prisoners” were traumatized for years. “We all want to believe in our inner power, our sense of personal agency, to resist external situational forces of the kinds operating in this Stanford Prison Experiment,” Zimbardo reflected. “For many, that belief of personal power to resist powerful situational and systemic forces is little more than a reassuring illusion of invulnerability.”
Personalities can change dramatically when people find themselves in prison environments.
The question the study posed still lingers: Are the soldiers of Abu Ghraib, or even Auschwitz guards and ISIS hostage-takers, inherently different from you and me? We take comfort in the notion of an unbridgeable gulf between good and evil, but maybe we should understand, as Zimbardo’s work suggested, that evil is incremental—something we are all capable of, given the right circumstances.
One day during our third week of training I am assigned to work in the chow hall. My job is to tell the inmates where to sit, filling up one row of tables at a time. I don’t understand why we do this. “When you fill up this side, start clearing them out,” the captain tells me. “They get 10 minutes to eat.” CCA policy is 20 minutes. We just learned that in class.
Inmates file through the chow line and I point them to their tables. One man sits at the table next to the one I directed him to. “Right here,” I say, pointing to the table again. He doesn’t move. The supervisor is watching. Hundreds of inmates can see me.
“Hey. Move back to this table.”
“Hell nah,” he says. “I ain’t movin’.”
“Yes, you are,” I say. “Move.” He doesn’t.
I get the muscle-bound captain, who comes and tells the inmate to do what I say. The inmate gets up and sits at a third table. He’s playing with me. “I told you to move to that table,” I say sternly.
“Man, the fuck is this?” he says, sitting at the table I point to. I’m shaky with fear. Project confidence. Project power. I stand tall, broaden my shoulders, and stride up and down the floor, making enough eye contact with people to show I’m not intimidated, but not holding it long enough to threaten them. I tell inmates to take off their hats as they enter. They listen to me, and a part of me likes that.
For the first time, for just a moment, I forget that I am a journalist. I watch for guys sitting with their friends rather than where they are told to. I scan the room for people sneaking back in line for more food. I tell inmates to get up and leave while they are still eating. I look closely to make sure no one has an extra cup of Kool-Aid.
“Hey, man, why you gotta be a cop like that?” asks the inmate whom I moved. “They don’t pay you enough to be no cop.”
“Hey Bauer, go tell that guy to take his hat off,” Collinsworth says, pointing to another inmate. “I told him and he didn’t listen to me.”
“You tell him,” I say. “If you’re going to start something, you got to finish it.” A CO looks at me approvingly.
The dog team
Out in the back of the prison, not far from where Chase Cortez hopped the fence, there is a barn. Miss Blanchard, another cadet, and I step inside the barn office. Country music is playing on the radio. Halters, leashes, and horseshoes hang on the walls. Three heavyset white COs are inside. They do not like surprise visits. One spits into a garbage can.
The men and their inmate trusties take care of a small herd of horses and three packs of bloodhounds. The horses don’t do much these days. The COs used to mount them with shotguns and oversee hundreds of inmates who left the compound every day to tend the grounds. The shotguns had to be put to use when, occasionally, an inmate tried to run for it. “You don’t actually shoot to kill; you shoot to stop,” a longtime staff member told me one day. “Oops! I killed him,” she said sarcastically. “I told him to stop! We can always get another inmate, though.”
Prisoners and officers alike talk nostalgically about the time when the men spent their days working outside, coming back to their dorms drained of restless energy and aggression. CCA’s contract requires that Winn inmates are assigned to “productive full time activity” five days a week, but few are. The work program was dropped around the same time that guards were taken out of the towers. Many vocational programs at Winn have been axed. The hobby shops have become storage units; access to the law library is limited. The big recreation yard sits empty most of the time: There aren’t enough guards to watch over it. (Asked about the lack of classes, recreation, and other activities at Winn, CCA insisted “these resources and programs were largely available to inmates.” It said the work program was cut during contract negotiations with the DOC, and it acknowledged some gaps in programming due to “brief periods of staffing vacancies.”)
Prisoners and officers talk nostalgically about when the men worked outside, coming back to dorms drained of aggression.
“Things ain’t like they used to be,” Chris, the officer who runs the dog team, tells us. “It’s a frickin’ mess.”
“Can’t whup people’s ass like we used to,” another officer named Gary says.
“Yeah you can! We did!” Chris says. He then sulks a little: “You got to know how to do it, I guess.”
“You got to know where to do it also,” Miss Blanchard says, referring, I assume, to the areas of the prison the cameras don’t see.
“We got one in the infirmary,” Chris says. “Haha! Gary gassed him.”
“You always using the gas, man,” the third officer says.
“If one causes me to do three or four hours of paperwork, I’m go’ put somethin’ on his ass,” Gary says. “He’s go’ get some gas. He’s go’ get the full load. I ain’t go’ do just a light use of force on him; I’m go’ handle my business with him. Of course, y’all the new class. I’m sitting here telling y’all wrong. Do it the right way. But sometimes, you just can’t do it the right way.”
With no work program to oversee, the men’s main job is to take the horses and the packs of bloodhounds anywhere across 13 nearby parishes to help the police chase down suspects or prison escapees. They’ve apprehended armed robbers and murder suspects.
When we step inside the kennel, the bloodhounds bay and howl. Gary kicks the door of one cage and a dog lunges at his foot. “If they can get to him, they go’ to bite him,” he says. “They deal with ’em pretty bad.”
Back in the barn office, Gary pulls a binder off the shelf and shows us a photo of a man’s face. There is a red hole under his chin and a gash down his throat. “I turn inmates loose every day and go catch ’em,” Chris says, rubbing the stubble on his neck. “And that was the result to one of ’em.”
“A dog, when he got too close to him, bit him in the throat,” Gary says.
“That’s an inmate?” I ask.
“Yeah. What we’ll do is we’ll take a trusty and we’ll put him in them woods right out there.” He points out the window. The trusty wears a “bite suit” to protect him from the dogs. “We’ll tell him where to go. He might walk back here two miles. We’ll tell him what tree to go up, and he goes up a tree.” Then, after some time passes, they “turn the dogs loose.”
He holds up the picture of the guy with the throat bite. “This guy here, he got too close to ’em.” Christian walks in the door.
“That looks nasty,” I say.
“Eh, it wasn’t that bad,” Christian cuts in. “I took him to the hospital. It wasn’t that bad.” (CCA says the inmate’s injuries were “minor.”)
Gary, still holding out the picture, says, “He was a character.”
“He was a piece of crap,” Christian says. “Instigator.”
“I gave him his gear and he didn’t put it on correctly. That’s on him,” Chris says with a shrug.
“Part of the bid’ness”
“I would kill an inmate if I had to,” Collinsworth says to me during a break one day. We are standing around outside; most cadets are smoking cigarettes. “I wouldn’t feel bad about it, not if they were attacking me.”
“You got to feel some kinda remorse if you a human being,” Willis says.
“I can’t see why you’d need to kill anyone,” Miss Stirling says.
“You might have to,” says Collinsworth.
“I do what needs to get done,” says a fortysomething, chubby-faced white officer. He wears a baseball cap low over his eyes. “I just had a use of force on an inmate who just got out of open-heart surgery. It’s all part a the bid’ness.” (CCA says it cannot confirm this incident.)
The officer’s name is Kenny. He’s been working here for 12 years, and he views inmates as “customers.” While teaching class, he lectures us on CCA’s principle of “cost-effectiveness,” which requires us to “provide honest and fair, competitive pricing to our partner and deliver value to our shareholders.” A part of being cost-effective is not getting sued too often. “One thing the Department of Corrections does is they give us a certain amount of money to manage this facility,” Kenny explains. “They set a portion of money back for lawsuits, but if we go over budget, it’s kind of like any other job. We got 60-something-plus facilities. If they not making no money at Winn Correctional Center, guess what? We not go’ be employed.”
“I just had a use of force on an inmate who just got out of open-heart surgery. It’s all part a the bid’ness.”
Kenny is detached and cool. He says he used to have a temper but he’s learned to control it. He doesn’t sit in bed at night writing up disciplinary reports while his wife sleeps, like he did years ago. Now, if an inmate gives him a smart mouth or doesn’t keep a tidy bed, he’ll throw him in seg to set an example. There are rules, and they are meant to be followed. This goes both ways: When he has any say, he makes sure inmates get what they are entitled to. He prides himself on his fairness. “All them inmates ain’t bad,” he reminds us. Everyone deserves a chance at redemption.
Still, we must never let inmates forget their place. “When you a inmate and you talk too much and you think you free, it’s time for you to go,” he says. “You got some of these guys, they smart. They real educated. I know one and I be talkin’ to him and he smarter than me. Now he might have more book sense, but he ain’t got more common sense. He go’ talk to me at a inmate level, not at no staff level. You got to put ’em in check sometimes.”
Kenny makes me nervous. He notices that I am the only one in class who takes notes. One day, he tells us that he sits on the hiring committee. “We don’t know what you here for,” he says to the class. He then glances at me. “There might be somebody in this room here hooked up wit’ a inmate.” Throughout the day, he asks my name on several occasions. “My job is to monitor inmates; it’s also to monitor staff. I’m a sneaky junker.” He turns and looks me directly in the eyes. “I come up here and tell you I don’t know what your name is? I know what your name is. That’s just a game I’m playing with you.” I feel my face flush. I chuckle nervously. He has to know. “I play games just like they play games. I test my staff to test their loyalty. I report to the warden about what I see. It’s a game, but it’s also a part of the bid’ness.”
Mail call
Over Christmas week, I am stationed in the mail room with a couple of other cadets to process the deluge of holiday letters. The woman in charge, Miss Roberts, demonstrates our task: Slice the top of each envelope, cut the back off and throw it in the trash, cut the postage off the front, staple what remains to the letter, and stamp it: Inspected.
Miss Roberts opens a letter with several pages of colorful child’s drawings. “Now, see like this one, it’s not allowed because they’re not allowed to get anything that’s crayon,” she says. I presume this is for the same reason we remove stamps; crayon could be a vehicle for drugs. There are so many letters from children—little hands outlined, little stockings glued to the inside of cards—that we rip out and throw in the trash.
One reads:
I love you and miss you so much daddy, but we are doing good. Rick Jr. is bad now. He gets into everything. I have not forgot you daddy. I love you.
Around the mail room, there are bulletins posted of things to look out for: an anti-imperialist newsletter called Under Lock and Key, an issue of Forbes that comes with a miniature wireless internet router, a CD from a Chicano gangster rapper with a track titled “Death on a CO.” I find a list of books and periodicals that aren’t allowed inside Louisiana prisons. It includes Fifty Shades of Grey; Lady Gaga Extreme Style; Surrealism and the Occult; Tai Chi Fa Jin: Advanced Techniques for Discharging Chi Energy; The Complete Book of Zen; Socialism vs Anarchism: a Debate; and Native American Crafts & Skills. On Miss Roberts’ desk is a confiscated book: Robert Greene’s 48 Laws of Power, a self-help book favored by 50 Cent and Donald Trump. Other than holy books, this is the most common text I see in inmates’ lockers, usually tattered and hidden under piles of clothes. She says this book is banned because it’s considered “mind-bending material,” though she did enjoy it herself. There are also titles on the list about black history and culture, like Huey: Spirit of the Panther; Faces of Africa; Message to the Blackman in America, by Elijah Muhammad; and an anthology of news articles called 100 Years of Lynchings.
“That’s the craziest girl I ever seen,” Miss Roberts says of the woman who wrote the letter she holds in her hand. She is familiar with many of the correspondents from reading about the intimate details of their lives. “She’s got his whole name tattooed across her back, all the way down to her hip bone. When his ass gets out—whenever he gets out, ‘cuz he’s got 30 or 40 years—if he ever gets out, he ain’t going to her.”
There are so many letters from children that we throw in the trash.
I feel like a voyeur, but the letters draw me in. I am surprised at how many are from former inmates with lovers still at Winn. I read one from a man currently incarcerated in Angola, Louisiana’s infamous maximum-security prison:
Our anniversary is in 13 more days on Christmas and we could have been married for 2 years why can’t you see that I want this to work between us?…Bae, [remember] the tattoo on my left tittie close to my heart that won’t never get covered up as long as I have a breath in my body and I‘m about to get your name again on my ass cheek.
Another is from a recently released inmate to his lover:
Hope everything is going well with you. Very deeply in love with you… I won’t be able to spend x-mass with my family either. Baby my heart is broken and I am so unhappy. I always had a great fear of being homeless…And even if I did find a job and had to work nights or work the evening shift, then I wouldn’t have anywhere to sleep because the shelter won’t let you in to sleep after hours. In order to get my bed every night I have to check in before 4pm. After that you lose your bed so the program is designed to keep you homeless. It don’t make sense… I bet that this is a sad letter. I wish that I had good news. This will be a short letter because I don’t have a lot of paper left. Merry Christmas baby. Very deeply in love with you.
The front of one card reads, “Although your situation may seem impossible…” and continues on the inside, “through Christ, all things are Him-possible!” It contains a letter from the wife of an inmate:
Here I am once again w/ thoughts of you. I hate it here everything reminds me of you. I miss u dammit! It’s weird this connection we have its as if I carry you in my soul. It terrifies me the thought of ever losing you. I pray you haven’t replaced me. I know I haven’t been the most supporting but baby seriously you don’t know the hell I’ve been through since we got torn apart And I guess my family got fed up w/ seeing me kill myself slowly I attempted twice 90 phenobarb 2 roxy 3 subs. I lived. 2nd after I hung up w/ you 60 Doxepin 90 propananol i lived WTF? God has a sense of humor i don’t have anyone but u, u see no one cares whether I live die hurt am hungry, well, or safe…So I’ve been alone left to struggle to survive on my income in and out mental wards and running from the pain of you bein there… Your my everything always will be Love your wife.
This note and its list of pills haunt me all weekend. What if no one else knows this woman tried to commit suicide? I decide I need to tell Miss Roberts, but when I return to work, I sit in the parking lot and have a hard time summoning the courage. What if word gets out that I’m soft, not cut out for this work?
After I pass through the scanner, I see her. “Hey, Miss Roberts?” I say, walking up behind her.
“Yes,” she says sweetly.
“I wanted to check with you about something. I meant to do it on Friday, but, uh…” She stops and gives me her full attention, looking me in the eyes. “When we had a class by the mental health director, she told us to report if there was any kind of suicidal—”
She cuts me off, waving her hand dismissively, and starts walking away.
“No, but it was like a letter thing—”
“Yeah, don’t even worry about that,” she says, still walking toward her door.
“Really?”
“Mmmhmmm. That’s if you see something going on down there,” she says, pointing toward the units. “Yeah, don’t worry about it. All right.” She enters the mail room.
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After Christmas, we take our final test. It is intimidating. The test was created by CCA; we never take the qualification exam given to the state’s guards. Ninety-two questions ask us about the chain of command, the use-of-force policy, what to do if we are taken hostage, how to spot a suicidal inmate, the proper way to put on leg irons, the color designation for various chemical agents. We went through most of these topics so cursorily there’s no way I could answer half of them. Luckily, I don’t need to worry. The head of training’s assistant tells us we can go over the test together to make sure we get everything right.
“I bet no one ever doesn’t get the job because they fail the test,” I say.
“No,” she says. “We make sure your file looks good.” (CCA says this was not consistent with its practices.)
About a third of the trainees I started with have already quit. Reynolds is gone. Miss Doucet decides she can’t risk an asthma attack, so she quits too. Collinsworth goes to Ash on the night shift. Willis works the night shift too; he will be fired after he leaves the prison suddenly one day and a bunch of cellphones are found at his post. Miss Stirling gets stationed in Birch on the day shift. She won’t last either. Two and a half months from now, she will be escorted from the prison for smuggling contraband and writing love letters to an inmate.
Chapter 3: “The CCA Way”
It’s the end of December, and I come in at 6 a.m. for my first of three days of on-the-job training, the final step before I become a full-fledged CO. The captain tells an officer to take me to Elm. We move slowly down the walk. “One word of advice I would give you is never take this job home with you,” he says. He spits some tobacco through the fence. “Leave it at the front gate. If you don’t drink, it’ll drive you to drinking.”
Research shows that corrections officers experience above-average rates of job-related stress and burnout. Thirty-four percent of prison guards suffer from post-traumatic stress disorder, according to a study by a nonprofit that researches “corrections fatigue.” That’s a higher rate than reported by soldiers returning from Iraq and Afghanistan. COs commit suicide two and a half times more often than the population at large. They also have shorter life spans. A recent study of Florida prison guards and law enforcement officers found that they die 12 years earlier than the general population; one suggested cause was job-related stress.
The walk is eerily quiet. Crows caw, fog hangs low over the basketball courts. The prison is locked down. Programs have been canceled. With the exception of kitchen workers, none of the inmates can leave their dorms. Usually, lockdowns occur when there are major disturbances, but today, with some officers out for the holidays, guards say there just aren’t enough people to run the prison. (CCA says Winn was never put on lockdown due to staffing shortages.) The unit manager tells me to shadow one of the two floor officers, a burly white Marine veteran. His name is Jefferson, and as we walk the floor an inmate asks him what the lockdown is about. “You know half of the fucking people don’t want to work here,” Jefferson tells him. “We so short-staffed and shit, so most of the gates ain’t got officers.” He sighs dramatically. (CCA claims to have “no knowledge” of gates going unmanned at Winn.)
“We so short-staffed and shit, so most of the gates ain’t got officers.”
“It’s messed up,” the prisoner says.
“Man, it’s so fucked up it’s pitiful,” Jefferson replies. “The first thing the warden asked me [was] what would boost morale around here. The first two words out of my mouth: pay raise.” He takes a gulp of coffee from his travel mug.
“They do need to give y’all a pay raise,” the prisoner says.
“When gas is damn near $4 a gallon, what the fuck is $9 an hour?” Jefferson says. “That’s half yo’ check fillin’ up your gas!”
Another inmate, whom Jefferson calls “the unit politician,” demands an Administrative Remedy Procedure form. He wants to file a grievance about the lockdown—why are inmates being punished for the prison’s mismanagement?
“What happens to those ARPs?” I ask Jefferson.
“If they feel their rights have been violated in some way, they are allowed to file a grievance,” he says. If the captain rejects it, they can appeal to the warden. If the warden rejects it, they can appeal to the Department of Corrections. “It’ll take about a year,” he says. “Once it gets to DOC down in Baton Rouge, they throw it over in a pile and forget about it. I’ve been to DOC headquarters. I know what them sonsabitches do down there: nothin’.” (Miss Lawson, the assistant chief of security, later tells me that during the 15 years she worked at Winn, she saw only one grievance result in consequences for staff. )
I do a couple of laps around the unit floor and then see Jefferson leaning against the threshold of an open tier door, chatting with a prisoner. I walk over to them. “This your first day?” the prisoner asks me, leaning up against the bars.
“Yeah.”
“Welcome to CCA, boy. You seen what the sign say when you first come in the gate? It says, ‘The CCA Way.’ Know what that is?” he asks me. There is a pause. “Whatever way you make it, my boy.”
Jefferson titters. “Some of them down here are good,” he says. “I will say dat. Some of ’em are jackasses. Some of ’em just flat-out ain’t worth a fuck.”
“Just know at the end of the day, how y’all conduct y’all selves determines how we conduct ourselves,” the prisoner says to me. “You come wit’ a shit attitude, we go’ have a shit attitude.”
“I have three rules and they know it,” Jefferson says as he grips the bars with one hand. “No fightin’. No fuckin’. No jackin’ off. But! What they do after the lights are out? I don’t give a fuck, ‘cuz I’m at the house.”
The next day, I’m stationed in Ash, a general population unit. The unit manager is a black woman who is so large she has trouble walking. She is brought in every morning in a wheelchair pushed by an inmate. Her name is Miss Price, but inmates call her The Dragon. It’s unclear whether her jowls, her roar, or her stern reputation earned her that name. Prisoners relate to her like an overbearing mother, afraid to anger her and eager to win her affection. She’s worked here since the prison opened in 1991, and one CO says that in her younger days, she was known to break up fights without backup. Another CO says that last week an inmate “whipped his thing out and was playing with himself right in front of her. She got out of her wheelchair, grabbed him by the neck, threw him up against the wall. She said, ‘Don’t you ever fucking do that to me again!'”
In the middle of the morning, Miss Price tells us to shake down the common areas. I follow one of the two COs into a tier and we do perfunctory searches of the TV room and tables, feeling under the ledges, flipping through a few books. I bend over and feel around under a water fountain. My hand lands on something loose. I get on my knees to look. It’s a smartphone. I don’t know what to do—do I take it or leave it? My job, of course, is to take it, but by now I know that being a guard is only partially about enforcing the rules. Mostly, it’s about learning how to get through the day safely, which requires decisions like these to be weighed carefully.
A prisoner is watching me. If I leave the phone, everyone on the tier will know. I will win inmates’ respect. But if I take it, I will show my superiors I am doing my job. I will alleviate some of the suspicion they have of every new hire. “Those ones who gets along with ’em—those ones are the ones I really have to watch,” SORT commander Tucker told us in class. “There is five of y’all. Two and a half are gonna be dirty.”
I take the phone.
Miss Price is thrilled. The captain calls the unit to congratulate me. The other COs couldn’t care less. When I do count later, each inmate on that tier stares at me with his meanest look. Some step toward me threateningly as I pass.
Later, at a bar near my apartment, I see a man in a CCA jacket and ask him if he works at Winn. “Used to,” he says.
“I just started there,” I say.
He smiles. “Let me tell you this: You ain’t go’ like it. When you start working those 12-hour shifts, you will see.” He takes a drag from his cigarette. “The job is way too fucking dangerous.” I tell him about the phone. “Oh, they won’t forget your face,” he says. “I just want you to know you made a lot of enemies. If you work in Ash, you gonna have a big-ass problem because now they go’ know, he’s gonna be the guy who busts us all the time.”
He racks the balls on the pool table and tells me about a nurse who gave a penicillin shot to an inmate who was allergic to the medicine and died. The prisoner’s friends thought the nurse did it intentionally. “When he came down the walk, they beat the shit out of him. They had to airlift him out of there.” (CCA says it has no knowledge of this incident.) He breaks and sinks a stripe.
Suicide watch
On my first official day as a CO, I am stationed on suicide watch in Cypress. In the entire prison of more than 1,500 inmates, there are no full-time psychiatrists and just one full-time social worker: Miss Carter. In class, she told us that a third of the inmates have mental health problems, 10 percent have severe mental health issues, and roughly a quarter have IQs under 70. She said most prison mental health departments in Louisiana have at least three full-time social workers. Angola has at least 11. Here, there are few options for inmates with mental health needs. They can meet with Miss Carter, but with her caseload of 450 prisoners, that isn’t likely to happen more than once a month. They can try to get an appointment with the part-time psychiatrist or the part-time psychologist, who are spread even thinner. Another option is to ask for suicide watch.
A CO sits across from the two official suicide watch cells, which are small and dimly lit and have plexiglass over the front. My job is to sit across from two regular segregation cells being used for suicide watch overflow, observe the two inmates inside, and log their behavior every 15 minutes. “We never document anything around here on the money,” Miss Carter taught us a month ago. “Nothing should be 9:00, 9:15, 9:30, because the auditors say you’re pencil-whipping it. And truth be known, we do pencil-whip it. We can’t add by 15 because that really puts you in a bind. Add by 14. That looks pretty come audit time.” One guard told me he just filled in the suicide watch log every couple of hours and didn’t bother to watch the prisoners. (CCA’s spokesman says the company is “committed to the accuracy of our record keeping.”)
One guard told me he just filled in the log every couple of hours and didn’t bother to watch the prisoners.
For one inmate, Skeen, I jot down the codes for “sitting” and “quiet.” For the other, Damien Coestly (his real name), the number for “using toilet.” He is sitting on the commode, underneath his suicide blanket, a tear-proof garment that doubles as a smock. “Ah hell nah, you can’t sit here, man!” he shouts at me. Other than the blanket, he is naked, his bare feet on the concrete. There is nothing else allowed in his cell other than some toilet paper. No books. Nothing to occupy his mind.
The sparse conditions are intended to be “a deterrent as well as protection,” Miss Carter said. Some inmates claim to be suicidal because, for one reason or another, they want out of their dorms and don’t want to go to protective custody, where they would be labeled as snitches. Inmates on suicide watch don’t get a mattress; they have to sleep on a steel bunk. They also get worse food. The official ration is one “mystery meat” sandwich, one peanut butter sandwich, six carrot sticks, six celery sticks, and six apple slices per meal. Assuming this meal contains no nutritional supplements, I calculate that eating it three times a day provides at least 250 calories less than the US Department of Agriculture’s daily recommendation for sedentary adult men younger than 41 years old. (CCA says suicide watch meals are of “equivalent nutritional value” to general-population meals. It also says suicide watch “is designed for the safety of the inmate and nothing else.”)
Nowhere else does a single guard oversee one or two inmates. If more than two inmates are on constant watch for more than 48 hours, the prison has to ask the regional corporate office for permission to continue, Miss Carter tells us. (CCA says this is inaccurate.) Sometimes the regional office says no, she says, and the prisoners are put back on the tiers or in seg.
“Come on, man, get the fuck out of here,” shouts Coestly. “You know what I’m about to do is, get up on top of this bed and jump straight onto my motherfucking neck if y’all don’t get the fuck out from the front of my cell.”
I look over to the cell to the right and see Skeen sitting on his metal bed, staring at me and masturbating under his suicide blanket.
I tell him to stop.
“I’m having some mental health issues, man.” He has a wild look in his eyes and he speaks intensely, but quietly.
“Move your chair, then. I’m just doing my thing.” He keeps going.
I get up and grab a pink slip to write him up, my first disciplinary report.
“You making a mistake,” he says. “You fuck with me like that, I’m gonna go all night.”
“All right,” I say.
“Write that bitch. I don’t give a fuck. I’m on extended lockdown.” He tells me he’s been in Cypress for three years. He starts singing and dancing in his cell. “All night, all niiiiiight.” Prisoners down the tier laugh. “I’ll add that to my collection. I have about a hundred write-ups. I don’t give a fuck!”
Someone down the tier calls for me. He’s not on suicide watch, just regular segregation. “I’m having some mental health issues, man,” he says. He has a wild look in his eyes and he speaks intensely, but quietly. “I’m not suicidal or homicidal necessarily, but it’s hard for me to be around people.” There is another man in his cell with him, sitting on the top bunk, shaving his face. “And, and, and the voices, demons, whatever you want to call them, want me to wait till y’all come down here and throw defecation or urine or something. I don’t want to do that, okay?” He says he wants to go on suicide watch as a preventive measure. “Until I figure out what’s going on here”—he taps the sides of his head with his index fingers—”then that’s where I need to be.” His request is denied by the unit manager. With four inmates on suicide watch, we are already over capacity.
“We are gonna have a Mexican standoff,” Coestly says. “Ever seen one of those? I get off the bed, jump off that mothafucker headfirst.” He says he’s having a mental health emergency, which I am required to report. When I tell the key officer, she rolls her eyes. In class, Miss Carter told us that “unless he’s psychotic and needs a shot to keep him from doing the behavior, then I just let them get it out of their system.” It takes six hours for a psychiatrist to show up.
One of the other inmates on suicide watch, who’s been silent until now, starts yelling through his food slot. “World war!” he shouts. “I got some niggas who need to tell the CIA something, since they already got their eye in the sky, the satellite orbiting in space processing global information.” His voice has a demonic quality to it and he occasionally hits the plexiglass to punctuate his sentences. The CO sitting directly across from him twiddles his thumbs and gazes ahead blankly.
In the neighboring cell, Skeen is staring at me, completely naked, masturbating vigorously. I tell him to stop. He gets up, comes to the bars, and strokes himself five feet in front of me. I leave and come back with the pink sheet and he shouts, “Stop looking like that ‘cuz you making my dick hard!” I don’t respond. “Stop looking like that ‘cuz you making my dick hard! Stop looking like that ‘cuz you making my dick hard!” The seemingly schizophrenic man next to him hits the plexiglass over and over. “That’s what the devil’s doing to you, in the invisible world—sticking his invisible dick in your white or black ass and fucking you with it.” My heart is pounding. For an hour, I stare at a cup on the floor and study the blotches in the concrete.
A few hours later, a SORT officer walks a cuffed man onto the tier. The man’s eyes are tightly closed and snot is dripping off his upper lip. He was pepper-sprayed after punching my old instructor Kenny in the face as Kenny sat in his office doing paperwork. Kenny’s in the hospital now—after he confiscated another inmate’s cellphone, the prisoner put a paid hit out on him.
Building rapport
Kenny is gone for days, recovering from his busted nose. The message his assailant sent was clear: Keep your hands off our phones. Meanwhile, the fact that I took the phone in Ash showed Miss Price that I’m a strong officer who plays by the rules, so she asked the warden if I could be posted there permanently. Now I work there, on the floor, almost every day. I immediately try to smooth over the phone thing with the inmates. I tell a few of them that I took it because I didn’t have a choice and suggest they should try to hide their contraband better. “You ain’t no police?” one asks me. “Nah. I ain’t here to be police,” I reply. “If people ain’t fucking with me, I ain’t got a problem with them.”
Don’t be like your partner Bacle, they tell me. In some units and on some shifts, the pairing of floor officers changes day to day, but for whatever reason Bacle and I become a regular pair. (He has allowed me to use his real name.) I tell the inmates I’ll never be like him, all that shouting and hollering.
The truth is, Bacle’s temper tantrums make us laugh. One inmate asks him for his Social Security number every day just to set him off. If he were not a squat, hobbling 63-year-old, Bacle’s occasional fantasies about putting shock collars on inmates or shoving his keys down their throats might not seem so harmless. But he hates the company too. “All you are is a fucking body to ’em. That’s the way I feel,” he says. He counts the days until his Social Security kicks in and he no longer needs to work here to supplement his retirement checks from the Coast Guard.
Every day, I come to know him more and more. He is a reader of old westerns and an aficionado of Civil War reenactments. He uses words like “gadzooks” and phrases like “useful as tits on a boar hog.” Back before the hobby shops closed, he liked to buy his wife gifts made by prisoners. Once, he bought her a handmade saddle for her toy unicorns. “When she seen it, she was tickled pink. We are still fat, dumb, and happy over it!” His breath smells perpetually of menthol chewing tobacco, a fleck of which is always stuck in the corner of his mouth.
Bacle becomes a teacher of sorts. “You got to have what I call a rapport with some of the inmates,” he says. Mostly, he is referring to the orderlies, the prisoners selected for special roles inside each unit. When an orderly passes out toothpaste, Bacle tells me to follow the inmate’s lead. “I just kind of modify it from when I was in the service. I might have rank over someone, but I don’t want to step on their toes.”
Without the orderlies, the prison would not function. Each unit has a key orderly, whose job is to keep the key clean and pack up the property of any prisoner sent to seg. Count room orderlies deliver the tallies from each unit to the room where they’re tabulated. Tier orderlies, floor orderlies, yard orderlies, walk orderlies, and gym orderlies keep the prison clean. Orderlies typically maintain a friendly relationship with the guards but take every opportunity to make it clear to other inmates they are not snitches. And they rarely are. It is much more likely for them to be movers of contraband. They cozy up to guards who will bring it in, and their freedom of movement allows them to distribute the goods. I will see some of the most trusted orderlies get busted while I’m here.
Bacle regularly gives his lunch to the muscular key orderly. We are not allowed to do this, so he does it discreetly. “It’s a habit I got into when I started,” he says. Bacle isn’t afraid to bend the rules to keep things under control. When one inmate starts marching around angrily, saying “fuck white people” and we’re too afraid to try to get him into his tier, Bacle buys cigarettes from another inmate, gives them to the agitated prisoner, and says, “Why don’t you go have a smoke on your bed to calm your nerves?” And it works. When Miss Price isn’t watching, Bacle lets a guy called Corner Store off his tier so he can run deodorant and chewing tobacco and sugar and coffee between inmates on different tiers. They aren’t allowed to trade commissary items, but they do anyway, so when we let Corner Store handle it, they stop pestering us with ploys to get off the tier, like faking medical emergencies.
Corner Store is a 37-year-old black man who looks 55. His hair is scraggly, his uniform tattered, his face puffy. He walks with the clipped gait of a stiff-legged old man who is late for a meeting he doesn’t really want to attend. He’s been in prison for half his life, though I don’t know what for. I rarely know what anyone is in for. I do know that he used to sell crack, that he saw his friend get shot to death when he was eight, and that he once had a firefight with some white men in Mississippi who called him a “nigger.” At least that’s what he tells me. Fourteen of his 18 years behind bars have been at Winn.
Corner Store has to hustle because he has no family support. He learned early that little comes without strings in prison.
Corner Store does not inspire fear, yet he is confident. He tells COs to open the tier door for him; he does not ask. On his pluckier days, he flaunts his status by sitting in the guards’ chairs and smoking. He talks to us as if we are office colleagues from different departments. And unlike the floor orderly who protects his reputation by loudly proclaiming that rats deserve to get stabbed, Corner Store doesn’t need to make a show of his loyalty to inmates, yet it is unwavering. When I ask him to teach me some prison lingo, he refuses gently.
The first time I meet Corner Store, he walks through the metal detector at the entrance of the unit. It beeps, but neither Bacle nor I do anything; its sound is one of the many we tune out. The device was installed not long before I started working here, in an effort to cut down on the number of inmates carrying shanks, but functionally it is a piece of furniture. We never use it since it takes at least two officers to get inmates to line up, walk through it, and get patted down whenever they enter or exit the unit, which leaves no one to let inmates into their tiers. When Corner Store makes it beep, he calls over to me: “Hey, watch this here! I’m going to go back through this thing and it won’t go off.” He jumps through it sideways, and it doesn’t make a sound. I laugh. “This is something my granddaddy taught me years ago,” he says. “Anything that a man makes can always be altered. Always.”
He had to learn to hustle because he has no money and no support from his family. For his courier services, inmates kick him cigarettes, coffee, and soup. He doesn’t take charity; he learned early that little comes without strings in prison. Sexual predators prey on needy inmates, giving them commissary or drugs, seemingly as gifts, but eventually recalling the debt. If you don’t have money, the only way to pay is with your body. “When I first come to prison, I had to fight about five times for my ass,” Corner Store says. “This is how it starts: You’re scared of being in prison because of the violence or whatever. You go to people for protection. But this is the No. 1 thing you don’t do. You have to be a man on your own.” He tries to discourage vulnerable inmates from seeking help and says he’s gotten into fights to stop new prisoners from being sexually assaulted. “It just hurts me to see it happen. A kid who really don’t even understand life yet, you turn and fuck his life up even more?”
He says there have been periods when he’s had to pack a shank. “Sometimes it’s best, because you got some bullheaded people in prison who don’t understand nothin’ but violence. When you show them you can get on the same level they gettin’ on, they leave you the fuck alone.”
“They always talking about how prison rehabilitates you,” he says. “Prison don’t rehabilitate you. You have to rehabilitate yourself.” When Miss Price is around, Bacle and I are careful not to make it obvious we are letting Corner Store out, and he makes sure to stay out of her sight.
Instructors like Kenny preached against giving concessions to inmates, but in reality most guards think you have to cooperate with them. Frankly, there just aren’t enough staff members to do otherwise. Bacle and I don’t have time, for example, to keep watch over the corrections counselor when she is in her office, where there are no security cameras, so she uses two inmates as her bodyguards. (CCA says this went against its policy.) COs are always under pressure to impress on the supervisors that everything is under control. We rely on inmates for this, too, letting some stand out in front of the unit to warn us when a ranking officer is coming so we can make sure everything is in order.
It can be a slippery slope. In 2007, a Tennessee inmate, Gary Thompson, sued CCA, claiming that guards, including a captain, periodically ordered him to beat up other inmates to punish them, giving him the best jobs and privileges as a reward. On one occasion, he claimed, guards called him the “largest nigger,” put him with a mentally ill inmate who’d cut a swastika into his arm, and ordered Thompson to “rough [him] up.” When Thompson filed a complaint, he was put in the hole. CCA denied his allegations but settled the case.
In Idaho, CCA was accused of ceding control to prison gangs to save money on wages. A lawsuit filed in 2012 by eight inmates at the Idaho Correctional Center alleged there was effectively “a partnership between CCA and certain prison gangs,” in which gang members were used to discipline inmates. A subsequent FBI investigation found that employees had falsified records and understaffed mandatory positions.* A confidential Idaho Department of Correction memo shared with CCA that was disclosed in the case showed that by August 2008, inmate-on-inmate assaults and other incidents of violence had “steadily increased to the point that there are four incidents for every one that occurs in the rest of the Idaho state operated facilities combined.” (CCA points to a later analysis by an independent monitor that concluded that the rate of violence at ICC over the entire first eight months of 2008 was not disproportionate to that of other facilities.) No charges were brought against CCA, nor were any sanctions levied against it. But the state ended automatic renewal of its contract, and reopened it to bidders. CCA did not bid.† “It was a lot better than this place,” an out-of-state guard who worked in Idaho at the time told me.
In a prison that is 75 percent black, people of different races sit together in the chow hall.
There are no gangs at Winn, but that has more to do with Louisiana prison culture than the management of the prison. In most prisons around the country, the racial divide is stark and internal politics are determined by racialized prison gangs like the Aryan Brotherhood and the Mexican Mafia. But Louisiana is an anomaly. Here, there are no prison gangs. In a prison that is 75 percent black and less than 25 percent white, people of different races sit together in the chow hall, hang out on the yard, and sleep in the same dorms.
Throughout my time at Winn, I meet guards from CCA prisons around the country who talk up the benefits of gangs. Two SORT members filling in from Oklahoma speak to each other in Sureño sign language that they learned from prisoners transferred from California. The influx of gang members is a “good thing,” one of the SORT guys tells me, because gang culture is highly disciplined. “With their politics, they have to clean their cells. They have to maintain cleanliness. If they don’t, they get stabbed. If they acted the way these guys act, they’d get stabbed.”
I quickly learn it’s no longer possible to be the silent observer I was in training, so I try to find the middle ground between appearing soft and being draconian. When I write up one inmate after he runs off the tier against my orders, I think about it all weekend, wondering if he will get sent to Cypress. I feel guilty and decide I will only write up inmates for two things: threatening me and refusing to get on their tier after they enter the unit. The floor is where most assaults happen, and if a lot of inmates are out there, things can get out of hand. That’s not why I choose to write them up for it, though. I write them up because my main job is to keep inmates off the floor, and if I don’t establish authority, I end up having to negotiate with each prisoner over how long he can wander the unit, which is exhausting.
I spend free moments leaning up against the bars, making chitchat with prisoners about their lives. I tell one, Brick, that I am from Minnesota. He says he has friends there. “We got to hook up!” he says. I cultivate these relationships; having gray-haired, charming inmates like him in my good graces helps me because younger, harder prisoners follow their lead. I do favors for others—I let a cop killer outside when it’s not yard time because he seems to have influence over some of the inmates. Guys like him and Corner Store teach me how to win inmates’ respect. They teach me how to make it in here.
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I try to address every request and respond to every inmate who yells “Minnesota,” my new nickname. The microwaves on some tiers are broken, so I help out by carrying cups of water for soup or coffee to Brick’s tier, where he heats them up. When Corner Store isn’t working and people ask if I can let them off the tier for a minute so they can run and exchange a honey bun for a few cigarettes, I unlock the door. “You’re cool,” one inmate says to me. “Real laid-back.” I let people out to see the corrections counselor when they need a mattress or need to call their lawyers, even when she tells me she doesn’t want to field these requests, which is most of the time.
Brick can see that I get tired striking across the unit from one place to the next for 12 hours a day. He sees that by the end of the day my feet and back hurt and I start to ignore the inmates. He knows that two people aren’t enough to run this floor. “This shit don’t work,” he says to me. We bump fists.
Chapter 4: “You Got to Survive”
There is a looming sense of crisis at Winn. Shortly after Cortez escaped, the warden decreed that the security staff should meet at the start of every shift. So at 6 a.m. each day, everyone is shepherded into a conference room, where they brood over coffee and Monster Energy drinks. “I apologize if it seems as though we’re coming down on y’all all the time,” says Assistant Warden Parker, who introduced himself to me in Cypress four weeks ago. He’s sitting on a table, the picture of a guy-next-door, we’re-in-this-together type of boss. “Unfortunately, due to a series of events that took place over 2014, culminating with that escape, there is a high, high level of scrutiny on how you do your job.”
He doesn’t get into specifics, but guards tell me there was a rash of stabbings over the summer that CCA didn’t report to the Louisiana DOC. (The company’s spokesman says it reported all assaults.) “Someone said this place has slid downhill for a long time,” the assistant warden says to us. “Here’s what we have before us: We have to climb up that hill extremely fast.”
PRIVATE PRISONS HOLD 7% of state inmates
of state inmates 19% of federal inmates
of federal inmates 62% of immigration detainees
of immigration detainees 31% of juvenile detainees.
The DOC, which has ultimate authority over all prisons in the state, has been taking a closer look at Winn’s day-to-day operations. (According to DOC documents I later obtained, the department had just written to CCA about “contract compliance” and areas where Winn’s “basic correctional practices” needed improvement.) Wardens from publicly run state prisons have appeared out of nowhere, watching over COs as they work, asking them questions. The newer guards fret about losing their jobs. Old-timers shrug it off—they say they’ve seen Winn weather tough times before.
At each morning meeting, we are given a new “game plan”: keep inmates off the bars of the tiers, move them quicker out to chow, keep them off the floor, finish count faster. We never discuss the problem that both guards and inmates complain about most: There aren’t enough employees. Corporate has tried to mitigate the problem by bringing officers in from out of state. The economics of this are never clear to me—it seems far more expensive to pay for their transportation and lodging than to hire more locals or raise wages. In addition to the SORT members, there are an average of five guards filling in for a month or so at a time from places like Arizona and Tennessee.
According to CCA’s contract with Louisiana, 36 guards are expected to show up for work at 6 a.m. every day. Twenty-nine of them fill mandatory 12-hour positions that require a body in them at all times—these include unit floor officers, front-gate officers, perimeter patrol, supervisors, and infirmary officers. I make a habit of counting the number of security staff at the meetings. Some days there are 28, some days 24, but there are almost always fewer than 29.
It’s possible that employees working overtime from the night shift aren’t there or that others trickle in late. But it still appears there are often fewer people on the shift than contractually required to keep the prison open, let alone running smoothly. CCA’s spokesman later tells me I was too low on the totem pole to have an accurate understanding of staffing at Winn. (He adds that “security is everyone’s job” and a “team effort” involving even employees who are not guards.) Correspondence between CCA and the DOC shows that in early 2015 Winn had 42 vacancies for regular guards and 9 vacancies for ranking officers. Miss Lawson, the assistant chief of security, says that when officials from the DOC were scheduled to visit, “we would be tripping over each other, but it was just because we were paying people overtime to come in and work extra.”
Wardens from state prisons have appeared out of nowhere, watching over guards as they work.
Often, the only guards in a 352-inmate unit are the two floor officers and the key officer. There is supposed to be an officer controlling the gate that connects each unit walk to the main walk, but often there isn’t. From 9 a.m. to 5 p.m. on weekdays, every unit should have two case managers, who manage rehabilitation and reentry programs, two corrections counselors, who are in charge of resolving inmates’ daily issues, and a unit manager, who supervises everything. Not once do I see all these positions filled in a unit.
During my time at Winn, I witness corners cut daily. Key officers, who are charged with documenting activities in the units, routinely record security checks that do not occur. I hear that these logbooks are audited by the state and are the only evidence of whether guards walk up and down the tiers every half-hour. I almost never see anyone do such a security check unless DOC officials are around. Collinsworth tells me that when he worked in the key he was told repeatedly to record security checks every 15 to 30 minutes, even though they weren’t being done. Miss Lawson later says she was once reprimanded by a warden for refusing to log checks that did not occur. “I’m just going to write down that you are doing your security checks every 30 minutes,” a ranking officer once told me. “That’s just how it’s been done, so until someone up top tells me different, that’s how we’ll do it.” (CCA’s spokesman says the company had no knowledge of security checks being skipped or logbooks being falsified.)
Even with the guards filling in from out of state, we are required to work extra days, which means that for up to five days in a row, I have just enough time to drive home, eat, sleep, and come back to the prison. Sometimes I have to stay longer than 12 hours because there is no one to take over for me. A guard I relieve one morning is ending a four-day stretch; in a 48-hour period he worked 42 hours at the warden’s insistence, he says. He didn’t sleep the whole time. (CCA says no such incident occurred.)
Assistant Warden Parker tells us the DOC has required CCA’s corporate office in Nashville, Tennessee, to report what CCA is doing to fix the mess at Winn. An obvious remedy would be to raise the pay of nonranking officers to the level of DOC officers—which starts at $12.50 per hour, $3.50 more than ours—and reinstate rehabilitative and recreational programs for inmates. Miss Lawson says such requests hit a roadblock at the corporate level. “There were years that the wardens would beg for more money, and it was like, ‘Okay, on to the next subject,'” she tells me.
“If inmates want to act stupid, then we’ll give them some pain to help increase their intelligence level.”
Instead, corporate takes a different approach to show it means business: A few days after I worked suicide watch, it removed the local officers from Cypress and turned the unit entirely over to members of the company’s national SORT team. These are guys who “use force constantly,” Assistant Warden Parker says at a morning meeting. “I believe that pain increases the intelligence of the stupid, and if inmates want to act stupid, then we’ll give them some pain to help increase their intelligence level.” DOC data shows that during the first 10 months of 2015, which includes part of the time I worked there, Winn reported twice as many “immediate” uses of force as the eight other Louisiana prisons combined. (“CCA expressly forbids retaliatory force,” its spokesman tells me.)
Over the next four months, Winn will report using chemical agents 79 times, a rate seven times higher than that reported by Angola. Collinsworth recalls an inmate who insulted a SORT officer’s mother. The officer cuffed him, stood him in his underwear out of view of the cameras, and covered his whole body with pepper spray for “about eight seconds or so.” When Collinsworth filed a report, standard procedure following a use of force, he says he was ridiculed by members of the SORT team, who told him “that I should have said I didn’t see anything.” He says an assistant supervisor admonished him for “tattling.” (CCA says the officer who sprayed the inmate was fired.)
I enter Cypress briefly after SORT takes over. At 6:30 in the morning, the air is so saturated with pepper spray that tears stream down my face. The key officer is doing paperwork in a gas mask. A man screams and flails naked in a shower, his body drenched with pepper spray. Cockroaches run around frantically to escape the burning.
Sex and violence
One day, as prisoners go to chow, Bacle runs past me shouting, “Code Blue outside!” I dash out the front door of Ash, through a crowd of inmates. A couple of prisoners are pinning each other up against the fence, and a frail-looking, young white guy is rolling around on the ground.
I run to him. He rolls from side to side, whimpering and heaving in panic, grasping at small cuts and lumps on his arms. They are not deep like stab wounds; they are shallow and there are many. Under them there is a multitude of tiny scars, cut crosswise—the trademark self-mutilation of the sexually abused.
Assaults behind bars 19% of all male inmates in US prisons say they’ve been physically assaulted by other inmates.
of all male inmates in US prisons say they’ve been physically assaulted by other inmates. 21% say they’ve been assaulted by prison staff.
say they’ve been assaulted by prison staff. Officials reported fewer than 8,800 incidents of rape and other sexual victimization in all American prisons and jails in 2011.
incidents of rape and other sexual victimization in all American prisons and jails in 2011. Yet between 3 percent and 9 percent of male inmates say they have been sexually assaulted behind bars, which suggests more than 180,000 current prisoners may have been victimized.
of male inmates say they have been sexually assaulted behind bars, which suggests more than 180,000 current prisoners may have been victimized. Former inmates of private state prisons are half as likely to say they have been sexually victimized by another inmate as those who were in public state prisons. However, they are nearly twice as likely to report being sexually victimized by staff.
to say they have been sexually victimized by another inmate as those who were in public state prisons. However, they are nearly to report being sexually victimized by staff. 66% of incidents of sexual misconduct by prison staff involve sexual relationships with inmates who “appeared to be willing,” according to authorities.
WOMEN ARE:
of incidents of sexual misconduct by prison staff involve sexual relationships with inmates who “appeared to be willing,” according to authorities. 7% of the total prison population
of the total prison population 22% of all victims of inmate-on-inmate sexual victimization
of all victims of inmate-on-inmate sexual victimization 33% of all victims of staff-on-inmate sexual victimization
“Calm down, man,” I say, leaning over him. “We are going to take care of you. Just calm down.” He keeps rolling and crying.
“He didn’t get nothing he ain’t deserve!” someone shouts from down the walk.
A sergeant and the captain come and cuff the inmate who’s been pinned to the fence. When the crowd around him clears, I am shocked. It’s Brick. The guy on the ground is probably about 25 years old. As Brick is taken off to Cypress, he calls the man a “bitch.”
A couple of officers look down at the young man disdainfully, pull him off the ground, and take him away. Brick beat him with a lock in a sock. He was angry because the young man had stayed in Cypress for seven months, partly by his own choice. He was supposed to come back to Brick. He is Brick’s punk.
There are many things about this incident that I don’t know—intimacy and rape in prison are complex issues. Did the young man stay in Cypress to escape Brick? Does he belong to Brick like a sex slave? Or would he say the relationship is consensual in the way a battered woman might say she stays with her husband because she loves him? Did he agree to exchange sex for protection? Did he understand that once he crossed that bridge, there would be no going back?
Once a punk, always a punk. Miss Carter, the mental health director, told us she’s seen just two inmates reverse their punk status in the eight years she’s been here, and both cases involved stabbing a lot of people. Guards here do not turn a blind eye to overt rape, but the more subtle abuse of punks is accepted. Inmates and COs know a punk when they see one. He will do menial tasks when someone demands it. He is expected to keep his face clean-shaven at all times. He has to pee sitting down or by backing up to the urinal with his penis tucked between his legs. He must shower facing the wall.
Since 2003, the federal Prison Rape Elimination Act (PREA) has required prisons to take measures to prevent sexual assaults. At Winn, this includes teaching new cadets about the law. “Why is the law so important?” our instructor Kenny asked us during training. “Liability.” It was never fully clear whether the goal was to eliminate rape or to suppress homosexuality in the prison. Even consensual sex could lead to time in seg. “Don’t even go there and entertain nicknames,” Kenny said. “There’s homosexuals down here got nicknames: Princess, Malibu, Tiki, Coco, Nicki. By calling them nicknames, that’s entertainment. They think they got you goin’ along with what they got goin’ on. We can’t stop 100 percent of the homosexuality that goes on down there, but we try to prevent and slow it down as much as possible.”
Nationwide, as many as 9 percent of male inmates report being sexually assaulted behind bars, but given the anti-snitch culture of prison, the real number might be higher. According to the Louisiana budget office, Winn reported 546 sex offenses in the 2014 fiscal year, a rate 69 percent higher than that of Avoyelles Correctional Center, a publicly operated prison of comparable size and security level.
A survey by the federal Bureau of Justice Statistics (BJS) showed that in 2011 the rate of substantiated rapes and other “nonconsensual sexual acts” between inmates in a sampling of CCA prisons was similar to that of public prisons. CCA prisons reported less serious incidents of “abusive sexual contact” at more than twice the rate of public prisons. CCA says this data may be inaccurate because it predates the final implementation of the PREA standards. The company states it has “a zero-tolerance policy with regard to sexual abuse.”
Prison has a reputation as a place of homosexual predation, but it’s not that simple. Inmates like Brick rarely see themselves as gay and typically go back to pursuing women once they get out. Self-identified gay or transgender prisoners are, however, often on the receiving end of abuse: Federal data shows that 39 percent of gay ex-prisoners reported being sexually assaulted by another inmate. One study found that 59 percent of transgender women in California’s prisons for men reported being assaulted.
But not all sex in prison is violent; many of the letters from male lovers I read in the mail room were full of tenderness and longing. Take, for example, this one from a man in Angola, written to one of the most flamboyant men at Winn:
You are the only same sex person in my life. So you have to never worry about anyone taking your place, not even a female…Sweetie, you are a good wife. I don’t give a damn what anybody said because I saw the good in you; the true you. That’s why when we had sex I’d always look you in the eyes. To truly understand you was my hardest goal but when I did our relationship got so good.
An hour after the young man who was attacked went to the infirmary, he walks into Ash, his arms still bleeding. It’s not clear whether Brick’s absence is good or bad for him. Now, he has no protection. A couple of well-muscled inmates stand at the bars and look at him lustfully, telling him to try to get placed on their tier. He speaks with Miss Price and she abruptly tells me to put him on B1—Brick’s dorm. Inmates have complained to me about this sort of thing; even people who have stabbed each other are sometimes put back in the same dorm. I open the gate and watch him walk down the tier.
Minutes later, he asks me to let him out. I do. He talks to Miss Price, telling her that he is in danger. People think he’s a rat. Maybe they think he snitched on Brick to get away from him. Miss Price doesn’t give it a moment of consideration, telling him to get back on the tier. When I open the door, a large, bearded man inside pushes him back out onto the floor. “You was asking her to put you on another tier?” he says. “If you think you can’t live in here, you can’t live in here. We don’t need that kind of shit on the tier anyway.” He slams the bars behind him.
The young man has two options: Go back on the tier or go to the count room, where they will assign him to another unit.
Miss Price tells me to take him out.
“You gotta go,” I tell him halfheartedly.
“I don’t want to go on no PC, man,” he says to me. He thinks they are going to put him in protective custody.
“I don’t know what to tell you,” I say. I really don’t.
Consider the options swirling in his mind: He could go back to his tier, where a man twice his size has made it very clear he is not welcome. There, he would risk nights as a punk without a protector. He might get robbed. He might get raped. He might get stabbed.
Then there is the alternative, the only one that Winn, like many other prisons, offers to inmates like this: the protective custody wing in Cypress. He would be put in a cell, maybe alone, maybe with another man, for 23 hours a day. He would be branded a snitch just for going there, which means that when he eventually left, the odds of getting stabbed would be high.
He storms past me, back to the key. “I ain’t going on no PC, man,” he shouts at Miss Price. “I just came from Cypress!” He paces back and forth, working himself up. “Y’all go’ have to drag me out this bitch, man. Real talk. I ain’t trippin’ on what the fuck y’all fixing to do to me,” he says, pointing at Bacle and me. “Real talk! ‘Cuz I ain’t going on no PC.” Miss Price screams for him to get out.
“Man, I can live on any fucking tier you put me on!” he shouts. I escort him out of the unit; he’s eventually placed in another one.
During our training, Kenny warned us how easy it was to be manipulated into sex by inmates. Even male guards “fall victim to bein’ involved in a relationship wit’ a inmate,” he said. “We got some folks come in here with relationships on the outside, and it just blows my mind how these inmates get in that ear and they wind up falling victim. That’s just the way it is. They don’t call ’em cons for no reason.” He warned us to be vigilant because even in a consensual relationship, the guard could be classified as a sex offender. He told us about one captain at Winn, Charlie Roberts (his real name), who got “involved wit’ a inmate. Havin’ oral sex wit’ him. So guess where he is sittin’ at? A federal institution.”
This story came up several times as an example of a guard who had to face the consequences of his weak will. Nothing was ever said about the inmate who gave Roberts blow jobs. When I looked at the files from Roberts’ case, I learned the inmate was a transgender woman who went by the name China. She had identified as a girl from age 11. Her father beat her repeatedly, and by the time she turned 13 she had left home and begun stripping on Bourbon Street in New Orleans. In 2000, she was sentenced to four years in prison for a “crime against nature”—oral sex for pay—and sent to Winn. During her first year, she was serving a stint in seg for a dirty urine test when, she later testified, Roberts shackled her, brought her to an office, and told her to give him a blow job. If she didn’t, he said he would put her in a cell with an inmate who would “handle” things. When she later told two administrators what had happened, one allegedly told her that if she ever lied about one of his guards again, he would “plant [her] ass under Cypress.”
Over the next two years, China said, she was raped several times by inmates, but she kept it to herself. “I was ridiculed and picked on by the staff, and that made it to where I couldn’t go to the staff for help at all,” she said in a deposition. “If an inmate did want to rape me…who could I turn to?” She became another inmate’s punk. One day in 2003, Miss Price sent her to the count room for having an “outrageous” feminine haircut. There, an officer ordered her to take another urine test by peeing in a cup while standing. China had been through this with him before—she’d told him she couldn’t pee standing up. After a long standoff, Roberts showed up and told her she could sit on the toilet. The other guards left. As she peed, Roberts entered the bathroom and closed the door behind him. He told her that if she didn’t give him oral sex again, he would taint her urine test and send her back to Cypress.
Over the next two years, China said, she was raped several times by inmates, but she kept it to herself.
“Stop playing,” China said. Roberts slapped her in the face. She dropped to her knees and did what he asked. When she finished, he said, “Bitch, you better swallow.”
“I would die before I ever fucking swallowed anything he put in my mouth,” she later recalled. She held the semen in her mouth and spit it out onto her shirt. After she filed a grievance and contacted the American Civil Liberties Union, she called the FBI. An agent came to the prison, took the shirt, and interviewed Roberts. The next day, CCA shipped China off to a publicly operated state prison, where she was held in a solitary cell “no bigger than a broom closet” and never let out for exercise. She was released from prison 11 months later.
“If I knew that the prison was going to shave me bald and send me to another prison and put me on maximum- security lockdown,” she later testified, “I would have swallowed.” Even harder than the solitary was knowing that, had she swallowed, she would have been able to finish her auto body class, which might have kept her from having to live on the streets and going back to sex work when she got out. “I would have swallowed and I would have kept on swallowing until I got that piece of paper.”
CCA denied all of China’s allegations, but it settled the case out of court for an undisclosed amount. Roberts also denied her allegations when the FBI interviewed him, but the bureau found that the semen on her shirt was his. Roberts ultimately pleaded guilty to sexually assaulting China and making false statements to the FBI, and he was sentenced to six years in federal prison and a $5,000 fine. I have not been able to track down China. Roberts served his sentence and was released in 2012.
Nearly half of all allegations of sexual victimization in prisons involve staff. In the 2011 BJS survey, CCA prisons reported a rate of substantiated staff-on-inmate sexual assault similar to that of public facilities. However, CCA prisons’ rate of reported staff-on-inmate sexual harassment was five times higher. Another federal report found that former inmates of private state prisons are twice as likely to report being sexually victimized by staff members as inmates who were in public prisons.
Prisoners also sexually harass and abuse officers. A recurring issue is inmates standing at the bars and masturbating at women guards sitting in the key. I see some women’s reports of sexual abuse by prisoners handled swiftly, but I hear other female guards complain that their sexual-harassment charges have gone nowhere. (CCA says it “takes any allegation of sexual harassment very seriously and has strong policies and practices in place for investigating such claims.”) I once write up an inmate for masturbating in front of a nurse, a violation that should cause him to be moved to Cypress, but he isn’t. I regularly see the macho culture of prison transcend the division between guards and inmates—male officers routinely ignore the harassment of their female colleagues. “Some of them staff, they’ll wear clothes so tight you can see everything they got,” Kenny lectured in class. “They’ll walk down there and they just struttin’ they stuff. We got one, shoot, trying to sue the company ‘cuz an inmate touched her on the butt. Man, you was down here every day shaking your stuff! If you do all this trying to draw attention to yourself, you go’ get some, and if you ain’t mindful, you’ll get more than what you asked for.”
In a class on “inmate manipulation,” Kenny told us that when he was a unit manager, there was a female officer he didn’t like. Many prisoners didn’t like her either, and one in particular was “bound and determined to get this girl fired.” One night, the woman fell asleep in a chair on a unit floor, he said. She had also left the inmate’s tier door open. The inmate crept out of his tier, pulled his penis out, and “went to town wit’ it” inches from her head. Not long afterward, the inmate was released, and he sent a letter to the prison, telling them to look at the surveillance footage from that night. CCA fired the guard for sleeping on the job and for leaving the tier door open, Kenny recalled.
“Ain’t nuttin’ we could do to him,” Kenny said of the inmate. “That’s over wit’. He gone home.” (CCA says it is unaware of such an incident and that it would have reported the inmate to law enforcement.) “I laughed, but it’s also kind of scary. I don’t want nothing bad to happen to nobody.” But, he added, “We was lookin’ to get her too. He got her for us. It worked out on both ends.”
Cracking down
In the morning meeting, the supervisor and Assistant Warden Parker admonish us about the topic they’ve been lecturing about all week—cracking down on sagging pants and homemade clothing. They are frustrated because no one is doing it. In private, the officers grumble that if the supervisors don’t want inmates to wear bleach-stained jeans instead of their “CCA blues,” they should confiscate the pants themselves. Why should the guards put themselves on the line? Parker seems to be aware of this, and he’s keen to show he’s not a front-office kind of guy. His personal goal is to become “lord of the do-rags,” taking the prohibited head coverings whenever he sees them.
“Does anybody know why we don’t want them to individualize their uniform?” Parker asks us. “We want them institutionalized. You guys ever heard that term? We want them institutionalized, not individualized. Is that sort of a mind game? Yup. But you know what? It’s worked over the couple hundred years that we’ve had prisons in this country. So that’s why we do it. We do not want them to feel as though they are individuals. We want them, for lack of a better term, to feel like a herd of cattle. We’re just moving ’em from point A to point B, letting them graze in the dining hall and then go back to the barn. Okay?”
“We do not want them to feel as though they are individuals. We want them to feel like a herd of cattle.”
Parker says the DOC wardens have been pestering him. “Are they scared, Mr. Parker?” he mimics. “Are you not providing the adequate training that your staff members need, Mr. Parker, to be strong enough to take clothing away from an inmate? Are they that scared, Mr. Parker?”
His tone softens. “I don’t know when it last dawned on me in the last couple weeks—I actually care about this institution and I care about all of you. I’m tired of people telling me that people at Winn aren’t doing their jobs. A term that was used a couple of weeks ago that was very embarrassing to me was: They don’t even understand basic prison management at Winn.” Some of the guards shake their heads. “Anybody feel good about that one? I know I sure as hell don’t.”
After the meeting, everyone moves slowly down the walk. Edison, a big white CO with a bull neck, says he’s tired of this “‘Kumbaya’ bullshit.” He was removed from his post in Cypress when the SORT team took it over. Suggesting he can’t handle his own is about the worst insult you could give him. “I’m sick and tired of doin’ this shit,” he says. “The security in this place is pathetic. They need to tighten up on the tier doors, re-man the towers, and reinstitute the inmate work out in the field and the inmate programs, and give these fools something to do besides sit in their beds, eat, watch TV, and figure out how to fuck with us.” He blames the “ivory tower” in Nashville—CCA’s corporate headquarters—for Winn’s problems. “Those fools ain’t got nothing in their mind but the bottom line.”
Today, the supervisor tells Edison to join Bacle and me in Ash. Having a new guard come to Ash is like having a visitor to our twisted household. This morning, standing around, waiting for the day to begin, Bacle complains about the most mundane of issues: Some inmates don’t sit on their bunks during count like they are supposed to.
“How’s your fighting skills, Bauer?” Edison asks. The question makes me nervous. This is the opposite of the approach I’m trying to take in here.
“All right,” I say.
“They need to give these fools something to do besides eat, watch TV, and figure out how to fuck with us.”
“You’re with me,” he says. “We’re going to give these motherfuckers an eye-opener today. I don’t play that bullshit. You get your ass on the bunk.”
“You’re not into this playing shit,” Bacle says sympathetically.
“That’s right,” Edison says.
“You’re a grade A1 asshole when it needs to be,” Bacle says.
“I’m a grade A1 drill instructor when I have to be.”
“That’s what this place needs!”
“I know it does,” Edison says. “It needs to go back to about 1960. Give a goddamn PR-24″—a police baton—”and hand a can of gas to everybody. You get stupid, you get beat down. You get big and stupid, you get gassed and beat down. Either way, you learn your fucking place.”
Edison has been here for a year and a half. “With my skill set, and with where I moved to, it was the only fuckin’ thing open,” he says. He is an Army Rangers veteran and was once a small-town police chief. He says he retired when “the city council got afraid of me.” “When I was a cop, I knew damn well that I would shoot your ass. I didn’t carry two extra clips, I carried four. When I went to work, I went to war. When I got off, I still went to war. I carried two clips on me regardless of what I was wearing. I carried at least my Glock 40 underneath my arm, and usually I had a Glock .45 on my ankle. Go ahead, play with me.”
We walk the floor. He stops. We stop. “You know what is stupid?” he says. “I see murderers. I see rapists. I see robbers. And then I see, the vast majority is in here for bein’ stupid enough to smoke a joint too close to a school. Twenty-five years, federal mandatory. Then you got somebody that slaughtered a whole fucking family gets 25 to life and he’s out in six to eight.” (About one-fifth of Winn inmates are in for drug-related crimes. Getting busted with a joint near a school will typically land you about six years, not 25.) Edison’s indignation about drug criminalization surprises me. “Now, where’s the fucking justice in that? And we’re paying how much per inmate per day?”
“Count time!” the woman in the key yells. I unlock the door of B1 tier and Edison walks in. An inmate is standing at the sink, brushing his teeth. “Get on your bunk,” Edison barks. The inmate keeps his back turned to Edison. “Or would you like to do it in Cypress?” Edison steps in toward him. “Step out!” Edison shouts, pointing to the door. He’s seriously sending a prisoner to seg for this?
The inmate walks out, still brushing his teeth. “This man is going on about some bullshit,” he says, waving his toothbrush around. A spot of toothpaste lands on Edison’s jacket, which is hanging on a nearby chair.
“Go ahead! Be dumb! Let’s go!” Edison yells, turning his hat backward. “Please be stupid enough to touch me. I’m already taking your ass to Cypress.” The inmate continues to brush his teeth.
I walk down the tier and do count. “That Crip boy go’ to tear his ass up,” one inmate says as I pass. “Your work partner going to get stabbed.”
I can’t keep count straight in my head. I just want to get off the tier.
When we leave the tier everyone comes up to the bars and yells at Edison. “You want to go next?” he shouts. “Behind the wall!” They don’t budge. “Every one of y’all is going to Cypress.”
“Suck my dick!”
The captain and a sergeant enter the unit. The captain tells Edison to step aside so he can talk to the inmates and try to ease the tension. “This pacification bullshit,” Edison mutters to me. “Yeah, we knew how to pacify ’em in Vietnam. We dropped a fuckin’ 500-pounder on ’em. That pacifies.” The captain tells Edison to come with him. “It’s not warm and fuzzy enough,” Edison says to me as he leaves.
The sergeant, whose name is King, pulls me aside. “I’m here for you, bro,” he says. In the past, I’ve heard him complain that the supervisors don’t back the line officers enough. “Don’t ever think I’m against you. ‘Cuz I’m gonna knock one of ’em out if I have to. And we go’ to write that report like he was trying to kill me and it was self-defense. Hahahaha!”
King has only been working at Winn for five months, but he’s been in corrections for eight years. As a kid, he spent time in juvenile hall. Like Edison, he is an Army vet, and he credits the military for correcting his delinquent ways. After 22 years in the service, he got a job in a juvenile correctional facility in Texas. One day, he told a boy to get off the basketball court and the kid grabbed his throat and tried to strangle him. “I damn near beat the piss out of him. Sixteen years old, 6 foot 3. As soon as you put your hands on me, you’re not a teenager, you’re a man. I put that uppercut on his ass and the superintendent said, ‘I strongly suggest that you resign, sarge.’ I fucked him up pretty good.”
“Oh well!” Bacle says.
“All of this I shattered,” he says, pointing to his jaw and mouth.
“Oh well!”
Pink Shades
During count, I tally bodies, not faces. If I look at faces, it means I have to keep the numbers straight while constantly calibrating sternness and friendliness in my eyes for each individual. When I go down the tier, I make a point to walk in a fast, long stride with a slight pop in my left step, trying to look tough. I practiced this in the mirror because inmates comment every day on a twist in my walk that I never knew existed. Sometimes prisoners whistle at me as I pass. In my normal life, I try to diffuse any macho tendencies. Now, I try to annihilate anything remotely feminine about me. As I walk and count, I tighten my core to keep my hips from moving.
I steel myself for A1 tier. For some reason, inmates on this tier are always testing me, and as I walk down one side, someone makes a comment about my “panties” as I pass. “You like that dick. You like that dick,” someone sings as I go by. I ignore it. Another comments that I look like a model. I pretend I don’t hear him. On my way back toward the front, I hear again, “You like that dick. You like that dick.”
This has been going on for weeks, but this time something snaps. I stop count and march back to the guy calling out to me, a thirtysomething black man with pink sunglasses and tattoos crawling up his neck. “What did you say to me?” I shout.
“I ain’t said nothin’.”
“Why are you always saying shit like that? You are always focusing so much on me, maybe you like the dick! Bitch ass!”
“Say that again?”
“Maybe you like the dick!” I shout. I am completely livid.
“He doesn’t know how big a mistake he just made,” another inmate says as I storm out.
“I ain’t got nothing against any of y’all officers. I understand that you gotta live. You got to survive.”
When we finish count, I go back to Pink Shades’ tier. “Give me your ID,” I say to him. He refuses. “Give me your ID! Now!” I shout at the top of my lungs. He doesn’t. I get his name from another officer and write him up for making sexual comments. He says he’s going to file a PREA grievance on me.
I try to cool down. My heart is still hammering 10 minutes later. “Are you all right, sarge?” a prisoner asks me. Slowly, my rage turns to shame and I go into the bathroom and sit on the floor. Where did those words come from? I rarely ever shout. I am not homophobic. Or am I? I feel utterly defeated. I go back to A1 and call Pink Shades to the bars.
“Look, I just want you to understand I don’t have a problem with any of y’all,” I tell him. “I think a lot of you are in here for sentences that are too long. I’m not like these other guys, all right?”
“All right,” he says.
“But, you know, when people disrespect me like that for no reason, I can’t just take that—you know what I mean?”
He tries to deny taunting me, but I won’t back down. “Look, you going to have inmates talkin’ crazy,” he says.
“But you don’t want me talking crazy to you, right?” There are inmates staring at us in astonishment.
“I feel you,” he says. “You came here and talked to me like a man. And I apologize. I ain’t got nothing against any of y’all officers. You feel me? I understand that you gotta live. You got to survive. Those words hurt you. I feel you. I mean I was singing a song, but you probably took it the wrong way. It triggered something in you.” He’s right. Something about being here reminds me of being in junior high, getting picked on for my size and the fact that I read books, getting called a faggot.
I tear up his disciplinary report and throw it in the trash. When I walk back down the tier for the next count, no one pays any attention to me.
Man down
One day in Ash, a few inmates shout, “Man down! Man down!” A large man, Mason, is lying on his bed in C2, his right hand over his bare chest. His eyes are closed and his left leg is moving back and forth slowly.
“We just put him on his bed. He had fell off this side of his fucking bed just now, bro,” an inmate says to me. “He’s fucked up.” I radio for a stretcher.
Mason starts to cry. His left hand is a fist. His back arches. “I’m scared,” he mouths. Someone puts a hand on his arm for the briefest moment: “I know, son. They finna come see you now.”
A stretcher finally arrives. The nurses and their orderlies move slowly. “They weren’t supposed to send that man back down here,” an inmate says to me. Earlier today Mason was playing basketball and fell to the ground in pain, he explains. He went to the infirmary, where they told him that he had fluid in his lungs.
Three inmates pick up Mason in his sheet and put him on the stretcher. His hands are crossed over his chest like a mummy as two prisoners wheel him away.
Within a few hours he is sent back to the tier.
“They told me I got fluid on my lungs and they won’t send me to the hospital.”
Days later, I see Mason dragging his feet, his arms around his chest. I tell him to take my chair. He sits and hunches over, putting his head in his lap. It feels like a “throbbing pain in my chest,” he says. We call for a wheelchair. “They told me I got fluid on my lungs and they won’t send me to the hospital,” he says. “That shit crazy.”
A nurse happens to be in the unit, passing out pills. I tell her they keep sending Mason to the infirmary but won’t take him to the hospital. She insists “nothing serious” is wrong with him.
“When I saw him last week, he was almost passed out,” I say. “He was in a lot of pain.”
She looks at me sidelong. “But the doctor still ain’t going to send him to the hospital just ’cause of that.”
If he were sent to the hospital, CCA would be contractually obligated to pay for his stay. For a for-profit company, this presents a dilemma. Even a short hospital stay is a major expense for an inmate who brings the company about $34 per day. And that’s aside from the cost of having two guards keep watch over him. Medical care within the prison is expensive, too. CCA does not disclose its medical expenses, but in a typical prison, health care costs are the second-biggest expense after staff. On average, a Louisiana prison puts 9 percent of its budget toward health care. In some states it can be much higher; health care is 31 percent of a California prison’s budget. Nearly 40 percent of Winn inmates have a chronic disease such as diabetes, heart disease, or asthma, according to Louisiana’s budget office. About 6 percent have a communicable disease such as HIV or hepatitis C.
One day, I meet a man with no legs in a wheelchair. His name is Robert Scott. (He consented to having his real name used.) He’s been at Winn 12 years. “I was walking when I got here,” he tells me. “I was walking, had all my fingers.” I notice he is wearing fingerless gloves with nothing poking out of them. “They took my legs off in January and my fingers in June. Gangrene don’t play. I kept going to the infirmary, saying, ‘My feet hurt. My feet hurt.’ They said, ‘Ain’t nothin’ wrong wicha. I don’t see nothin’ wrong wicha.’ They didn’t believe me, or they talk bad to me—’I can’t believe you comin’ up here!'”
His medical records show that in the space of four months he made at least nine requests to see a doctor. He complained of sore spots on his feet, swelling, oozing pus, and pain so severe he couldn’t sleep. When he visited the infirmary, medical staff offered him sole pads, corn removal strips, and Motrin. He says he once showed his swollen foot, dripping with pus, to the warden. On one of these occasions, Scott alleges in a federal lawsuit against CCA, a nurse told him, “Ain’t nothing wrong with you. If you make another medical emergency you will receive a disciplinary write-up for malingering.” He filed a written request to be taken to a hospital for a second opinion, but it was denied.
His fingertips and toes turned black and wept pus. Inmates began to fear his condition was contagious.
Eventually, numbness spread to his hands, but the infirmary refused to treat him. His fingertips and toes turned black and wept pus. Inmates began to fear his condition was contagious. When Scott’s sleeplessness kept another inmate awake, the inmate threatened to kill him if he was not moved to another tier. A resulting altercation drew the attention of staff, who finally sent him to the local hospital.
“But when I got my legs cut off they didn’t come back and say, ‘Robert, I’m sorry.’ I done taked my lickin’. Part of being locked up.” He is now suing CCA for neglect, claiming that inmates are denied medical care because the company operates the prison “on a ‘skeleton crew’ for profitable gain.”
“Where do you think is one of the No. 1 areas that we get hit on as a confinement business?” Assistant Warden Parker asks us at a staff meeting. “Medical! Inmates have this thing that if they have a sniffle they are supposed to be flown to a specialist somewhere and be treated immediately for that sniffle.” His tone becomes incredulous. “Believe it or not, we are required by law to take care of them.”
It’s true: Under Supreme Court rulings citing the Eighth Amendment, prisons are required to provide inmates with adequate health care. Yet CCA has found ways to minimize its obligations. At the out-of-state prisons where California ships some of its inmates, CCA will not accept prisoners who are over 65 years old, have mental health issues, or have serious conditions like HIV. The company’s Idaho prison contract specified that the “primary criteria” for screening incoming offenders was “no chronic mental health or health care issues.” The contracts of some CCA prisons in Tennessee and Hawaii stipulate that the states will bear the cost of HIV treatment. Such exemptions allow CCA to tout its cost-efficiency while taxpayers assume the medical expenses for the inmates the company won’t take or treat.
In 2010, the company and Immigration and Customs Enforcement settled a federal lawsuit brought by the ACLU that asserted immigration detainees at a CCA-run facility in California were routinely denied prescribed medical treatment. (CCA admitted no wrongdoing.) In a rare case that made its way to trial in 2001, the company was found to have violated the 8th and 14th Amendments and ordered to pay $235,000 to an inmate whose broken jaw was left wired shut for 10 weeks. (He removed the wires himself with nail clippers while guards watched.) The jury wrote they hoped the message sent by the ruling would “echo throughout the halls of your corporate offices as well as your corporate housing facilities.” (CCA appealed and settled for an undisclosed amount.)
Subjects of lawsuits filed against CCA
CCA has also been the subject of medical malpractice cases involving pregnant inmates. In 2014, it settled a case for $690,000 over the death of a prisoner’s baby at a county jail in Chattanooga, Tennessee. When the inmate went into labor, she was put in a cell with no mattress and left there for three hours as she bled heavily onto the floor. CCA employees did not call an ambulance until approximately five hours after the prisoner asked for help. Her newborn baby died shortly thereafter. In court proceedings, the warden testified that surveillance footage showed no signs of an emergency. But before the footage could be reviewed, CCA claimed it had been accidentally erased. The court sanctioned the company for destroying evidence.
CCA settled another case for $250,000 after a pregnant woman being held in a jail in Nashville complained of vaginal bleeding and severe abdominal pain. She said medical staff demanded “proof,” so they put her in solitary and turned off the water so her blood loss could be “monitored.” She claimed they did nothing to alleviate her pain as she endured contractions, filling the toilet with blood. The next morning, the inmate was shackled and taken to a hospital, where doctors found that she was already dilated. While prison guards watched, she gave birth and was immediately sedated. When she woke up, medical staff brought her the dead baby. She said she was not allowed to call her family and was given no information about the disposal of her son’s body.
At least 15 doctors at Winn have been sued for delivering poor medical care. The prison hired several of them even after the state had disciplined them for misconduct. One, Aris Cox, was hired in the ’90s, after his license was temporarily suspended for writing prescriptions to support his tranquilizer addiction. While Mark Singleton was at Winn, the Louisiana board of medical examiners discovered that he had failed “to meet the standard of care” at his previous position in New Mexico. He was put on probation, but CCA kept him on. Winn hired Stephen Kuplesky after his license had been temporarily suspended for prescribing painkillers to a family member with no medical condition. Robert Cleveland was working at Winn when he was put on medical probation for his involvement in a kickback scheme with a wheelchair company. He was later disciplined for prescribing narcotics from his home and vehicle. (It’s not clear if he was working at Winn at the time. CCA says all doctors at Winn had “appropriate credentials.”)
Data collected by Prison Legal News on more than 1,200 state and federal suits against CCA shows that 15 percent of them were related to medical care. (This sample is not a complete list of complaints against the company; in 2010 alone, CCA faced more than 600 pending cases. Between 1998 and 2008, the company settled another 600 cases.) Since most inmates can’t afford legal counsel, it’s nearly impossible for them to prevail in court. When I made public-records requests in a couple of states for a more recent accounting of lawsuits settled by CCA, the company intervened, arguing that a list of settlements involving claims of medical malpractice, wrongful deaths, assaults, and the use of force “constitutes trade secrets.”
My reconciliation with Pink Shades encouraged me. Every time I have a problem with a prisoner, I try the same approach and eventually we tap knuckles to show each other respect. Still, these breakthroughs are fleeting. In the moment, they feel like a glimmer of a possibility that we can appreciate each other’s humanity, but I come to understand that our positions make this virtually impossible. We can chat and laugh through the bars, but inevitably I need to flex my authority. My job will always be to deny them the most basic of human impulses—to push for more freedom. Day by day, the number of inmates who are friendly with me grows smaller.
There are exceptions, like Corner Store, but were I to take away the privileges Bacle and I have granted him, I know that he, too, would become an enemy.
My priorities change. Striving to treat everyone as human takes too much energy. More and more, I focus on proving I won’t back down. I am vigilant; I come to work ready for people to catcall me or run up on me and threaten to punch me in the face. I show neither fear nor compunction. Sometimes prisoners call me racist, and it stings, but I try as hard as I can not to flinch because to do so would be to show a pressure point, a button that can be pressed when they want to make me bend.
Striving to treat everyone as human takes too much energy. More and more, I focus on proving I won’t back down.
Nearly every day the unit reaches a crescendo of frustration because inmates are supposed to be going somewhere like the law library, GED classes, vocational training, or a substance abuse group, but their programs are canceled or they are let out of the unit late. Inmates tell me that at other prisons, the schedule is firm. “That door would be opening up and everybody would be on the move,” an inmate who’s been incarcerated throughout the state says. Here, there is no schedule. We wait for the call over the radio; then we let the inmates go. They could eat at 11:30 a.m. They could eat at 3 p.m. School might happen, or maybe not. It’s been years since Winn has had the staff to run the big yard. Sometimes we let the inmates onto the small yard attached to the unit. Often we don’t. Canteen and law library hours are canceled regularly. There just aren’t enough officers to keep everything going.
Guards bond with prisoners over their frustrations. Prisoners tell us they understand we are powerless to change these high-level management problems. Yet the two groups remain locked in battle like soldiers in a war they don’t believe in.
Whenever I open a tier door, I demand that everyone shows me his pass, and I use my body to stop the flood of people from pouring out. Some just push through.
I catch one. “Get back in!” I shout. “I’m writing you up right now if you don’t get back in there right now. You hear me?”
He walks back in, staring me down. “White dude all on a nigga’s trail, man,” he says. I shut the door, ignoring him. “You better get the fuck from down here before I end up hurtin’ one of y’all,” he shouts at me. “You green as a motherfucker!”
I’m tired.
An inmate comes around the key. Bacle is following him and calls for me to stop him. I stand in the inmate’s path. I know him, the one with the mini-dreads. I feel threatened, frankly, whenever I see him. “This way,” I say, pointing back to where he came from. He tries to walk past me. I lock eyes with him. “This way!” I command. He turns back and walks slowly away. I walk behind him. He stops, spins around, throws his hands in the air, and shouts, “Get the fuck off my trail, dog!” I know he’s testing me. I open his tier door. He walks in, stands just inside, and stares me down hard. I grab the door and slam it shut—bang!—in his face.
I turn and step back into the throng of inmates milling around the floor. “Motherfucker’s going to end up dead!” he shouts after me. I stop and turn around. He just stares. I grab the radio on my shoulder, then pause. Was I ever taught what to do when something like this happens? I know how to press the button and speak into the radio, but whom do I call? I think of King, the officer who smashed the kid’s jaw. “Sergeant King, could you come down to Ash?” I say into my shoulder.
“En route.”
When he arrives, I take him into B1 tier. I find Mini-Dreads.
“He needs to get locked up,” I say, looking him in the eyes.
King cuffs him. I tell King he threatened my life. He needs to go to seg.
“What happened?! I ain’t said nuttin’!” the inmate shouts. I walk away.
I go back to chasing the others into their tiers. “What you lock that dude up for?” an inmate asks me. “Dude was ’bout to go home,” another says. “He ain’t go’ go home now.” I walk away, unyielding. In the back of my mind, however, there is a voice: Did you see him say anything? Wasn’t your back turned? Are you sure what you heard? It doesn’t matter, really. He wanted to intimidate me and it was about time I threw someone in the hole. They need to know I am not weak.
One morning, Ash smells like feces. On D2, liquid shit is oozing out of the shower drain and running down the tier. “It’s been here over 12 hours,” one inmate says.
“Man, you got worms and everything on the floor. Real talk.”
“This is a health and safety violation!”
“Man, this is cruel and unusual punishment!”
We let inmates out to go to the small yard. As they flow out of the tiers, I see a large group run to A1 tier. Bacle pushes the tier door shut and calls a Code Blue over the radio. Inside the tier, two prisoners are grappling, their bodies pressed up against the bars. Each is gripping a shank in one hand while holding the other’s arm to keep him from swinging. Drops of blood spatter the floor. The surrounding scene is oddly calm. Inmates stand around and watch, not saying anything.
“Break it up,” Bacle says indifferently. “Break it up.”
The two combatants are speaking to each other quietly, almost at a whisper.
One man breaks his hand free, swings it up, and jams his shank into the side of the other man’s neck.
“Come on,” one says. “Come on with it, big dog.”
“I’ma do you like you did me.”
They grapple some more.
“Break it up!” Bacle yells.
“Come on!” I shout, feeling utterly impotent.
Bacle, Miss Price, a CCA employee from out of state, and I stand just two feet from them, separated by the bars, and watch the two try to press their knives into each other.
One man breaks his hand free, swings it up, and jams his shank into the side of the other man’s neck. My breath stops for a moment, and I utter a gagging sound. “It ain’t sharp enough, big dog,” says the guy who was just stabbed. “Let me show you where the sharp one is.”
Bacle reaches through the bars and grabs the stabber by his hood as the other inmate struggles to break loose. For the first time, the other prisoners make noise. “Hey, man, you’re gonna get him killed like that!” one shouts at Bacle. Bacle lets go, and the two men tumble across the floor, landing in a heap by the toilet, blocked from our view by a short wall. They keep scuffling. An arm swings up and jabs down. One prisoner walks over to the urinal two feet from them and pees as they keep stabbing.
The fight lasts nearly four minutes, until a SORT member comes in with a can of pepper spray. “Don’t fucking move,” he barks. “Everybody lay the fuck down.” He sprays the men as they try to stab each other. One, who’s had a bit of his ear sliced off, is taken to the hospital. The other goes to seg.
The smell of pepper spray fades, but the smell of shit does not. It’s not until the afternoon that someone comes in to fix the toilets and finds a shank stuck in the plumbing.
Later, I recount to a sergeant how one of the inmates was poking the knife into the other guy’s neck. “Did you learn something from that?” he asks me.
“Not really.”
The inmate could have slit the other guy’s throat if he wanted to, he says. But he didn’t. “Both of ’em scared. That’s the reason for having’ them shanks in the first place, ‘cuz they are scared.”
The audit
At the end of my shift, I stride briskly down the dark walk. I am relieved to be going home, but after two weeks on the job as a full-time CO, I’m afraid in a way I wasn’t at first. The longer I work here, the more people have grudges against me. As I head down the walk, inmates are coming and going from various parts of the prison and I can’t see any other guards around. I don’t have a radio—I am required to give it to the officer who relieves me. I’ve seen the surveillance footage, and I doubt it would be clear enough to identify anyone who might jump me in this darkness.
The gate before the exit is locked and I am routed through the visitation area. There, 20 or so officers from my shift are sitting at the tables, frowning. Two inmates are serving pizza. We’ve been trapped in a company meeting. Assistant Warden Parker is there. The chief of security. HR. I grab some pizza and sit down, frustrated.
“How many people here got less than a year in?” Parker asks. I raise my hand. “You’ve probably seen a lot of bad days, okay? We’re gonna change that. And it takes all of us working together. It really, really does. As long as we stay as a decent team and we remember that the bad guys are the guys who stay here 24/7 and don’t get to leave.”
On the wall is a painting of a black kid and a white kid lying on their bellies on a grassy hillside, looking at a rainbow. Next to it is another mural of a lion and a tiger tearing through an American flag with a bald eagle flying overhead. “The CCA Way” is written above it.
“The company took a look at things and they realized that we need to do a little bit better for the staff here at Winn. I’m not going to say that we’ve waved a magic wand and everybody’s walking out of here, gonna go buy new cars, but the hourly wage for a correctional officer is going to go up to $10 an hour. So congratulations to everybody sitting inside this room.” He starts clapping and a few people join unenthusiastically. “This is going to be one of those proud moments,” he says.
“‘ACA’s coming. We gotta panic! Hit the panic button!'”
“Does anybody know what the ACA is?” Parker asks. “Have you been hearing about ‘We got ACA coming up. Ooooh! ACA’s coming. We gotta panic! Hit the panic button!'”
“The American Correctional Association,” someone volunteers.
“Okay, why do we care about ACA?” Parker asks.
“We need our jobs. We need to pass.”
“That’s a theme that goes with it. Years and years and years ago, I think it was 1870, there was a governor upset with what he thought was cruel and unusual punishment,” he lectures. “So he started drafting up a little group of people that would go around and they would check on prisons and prison conditions to ensure that the people who were confined were not being treated cruelly. After time they started developing a sophisticated auditing process. So, a third-party person who has no dog in the fight, so to speak, comes in and they take a look at how are we treating our inmates. And they give us a stamp of, ‘You’re treating them with proper care.’
“That way when we go to court and the inmate says, ‘Oh, they made me eat Pizza Hut pizza! That’s cruel and unusual punishment! It should have been Domino’s!’—when it goes to court, we pull up our ACA files and say, ‘Hey, look, here’s how we prepare our food in the kitchen. We prepare the food in our kitchen under these standards.'”
The ACA is a trade association, but it’s also the closest thing we have to a national regulatory body for prisons. More than 900 public and private correctional facilities and detention centers are accredited under its standards. Winn was the first prison to be accredited in Louisiana. Shortly after T. Don Hutto co-founded CCA, he became the president of ACA.
Over the next few weeks, inmates repaint every unit in preparation for the ACA audit. The maintenance man is run ragged as he tries to fix busted vents, plumbing, and cell and tier doors. (“We didn’t own the facility,” CCA’s spokesman told me, noting that major maintenance issues at Winn were the DOC’s responsibility. CCA’s contract states that it was responsible for routine and preventive maintenance.)
In anticipation of the audit, I read the ACA standards. How will the auditors deal with the fact that the cells in segregation are at least 20 square feet smaller than required? Or that inmates only get 10 minutes to eat, not the mandated 20? There are many other ACA standards and recommendations Winn does not appear to meet: We rarely have the required number of positions staffed; guards’ pay is not comparable to the pay of state corrections officers; guards rarely ever use the metal detectors at the entrances to the housing units; prisoners often don’t get one hour of daily access to exercise space; suicide watch meals are below caloric requirements; there aren’t enough toilets in the dorms. (The ACA did not respond to a request for comment.)
Then again, Winn passed its last ACA audit, in 2012, with a near-perfect score of 99 percent, the same score it received in its previous audit three years earlier. In fact, CCA’s average score across all its accredited prisons is also 99 percent.
On the morning of the audit, we wake everyone up and tell them to make their beds and take any pictures of women off their lockers. Two well-dressed white men enter Ash unit and do a slow lap around the floor. The only questions they ask Bacle and me are what our names are and how we’re doing. They do not examine our logbook, nor do they check our entries against the camera footage. If they did, they would find that some of the cameras don’t work. They do not check the doors. If they did, they would see they need to be yanked open by hand because most of the switches don’t work. They don’t check the fire alarm, which automatically closes smoke doors over the tiers, some of which must be jimmied back open by two guards. They do not ask to go on a tier. They do not interview any inmates. They do a single loop and they leave.
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After nearly two decades, Corner Store is about to be free. He has just six weeks to go before he qualifies for early release with the “good time” he’s earned. How does someone reenter the world after two decades behind bars, with no friends on the outside and no money to his name? His first step, he says, will be to stay in a shelter until he can get on his feet. He doesn’t know where he will go yet. He tells me he doesn’t want to count the days. “It stresses me out. Anxiety sets in. Your mind goes, working and thinking about stuff. How am I going to do this? How am I going to do that? It causes a panic attack. When I walk, I walk.”
But fantasies creep into his mind. “I’ma get me a big bottle of Kaopectate, a big German chocolate cake, five-gallon thing of milk,” he says. “Just get out the way, that’s all I’ma tell you.” We are outside, talking through the fence; he’s on the small yard and I’m on the Ash walk. “After that, I want me a seafood platter, a real seafood platter about the size of the kitchen table, just for me and Mom. It’s all about Mom when I go home.”
He puts his hand on the fence and leans in. “What I’m sayin’ is this here, man: I just wanna go have fun, boy. And fun does not mean me-gettin’-in-trouble fun. Fun means just enjoying life. I wanna be able to take my mothafuckin’ shoes off and socks off and walk in the sand. I wanna be able to just go outside in my shorts and just my house slippers and stand in the rain and just—” he spreads his arms, points his face to the sky, and opens his mouth. “Them thangs I miss. You can’t do that in here. Alls I’m sayin’ is this here: When I get out, I don’t want to have to poke my chest out any longer. It hurts to poke my chest out. It’s a weight on my shoulders I’ve been toting for the last 20-somethin’ years, and I’m ready to drop that weight because the load is heavy.”
Chapter 5: Lockdown
On my fifth week on the job, I’m asked to train a new cadet. He is a short white man in his 40s with peppered black hair. He says he worked as a security contractor in Iraq and Afghanistan for Triple Canopy and Blackwater. He is hoping to go back to Afghanistan soon. “I had terrorists who blew up schools and shit that I had to take care of. It wasn’t all PC like it is here.” Prisoners here, he says, get treated with kid gloves. “They got rights and all this crap. Fuck that.”
I show him how to open the doors and do callouts, and I tell him we are going to start letting people out for chow soon. “What do you mean?” he says, suddenly looking frightened. “You are just going to open the doors and let them out? I can’t believe that!”
He doesn’t think they should go out at all. “Fuck ’em. Not unless you have absolutely an emergency. Or you’re on a work plan or some shit like that. I’d make prison so bad that you would never want to come back. When I was growing up, my mom used to live in Mississippi. They had all the work gangs and they were all in orange and all chained up. Chain gangs and shit like that. That’s how it should be. Make it so bad, you’d never want to come back.”
“It’s pretty bad in here,” I tell him. “People get stabbed here all the time.” At least seven inmates have been stabbed in the last six weeks. As people come in from chow, I hear on the radio, “Code Blue in Elm! Code Blue in Elm!” A CO is frantically calling for a stretcher. Several inmates are stabbing each other; they can’t count how many.
Several people were injured, and I hear one was stabbed about 30 times. Miraculously, no one dies.
“Everyone on the tier!” Bacle shouts to the prisoners milling about. “Fuck all that,” one says. “We’ll have another Code motherfucking Blue.” Bacle blows his whistle. We get everyone in and I head out onto the Ash walk to see what is happening.
A minute later, a bleeding man is wheeled by on a work cart and I return inside. Several people were injured, and I hear one was stabbed about 30 times. Miraculously, no one dies.
Three days later, I see two inmates stab each other in Ash.
A week after that, another inmate is stabbed and beaten by multiple people in Elm. People say he was cut more than 40 times. During this time, Miss Price quits after nearly 25 years of service. She says she’s tired of this work. (We will go without a unit manager in Ash for weeks.) Not long after she leaves, someone is beaten unconscious and stabbed through the cheek in Birch and another inmate is stabbed in Cypress.
It is difficult to imagine how someone gets stabbed in segregation. How do shanks get in? How do inmates get to each other? The morning after the stabbing in Cypress, I hear Assistant Warden Parker call over the radio for maintenance to come and fix the cell doors there. A month ago, he told us that inmates in the unit could pull some cell doors off their tracks. A month before that, Mr. Tucker, the SORT commander, told us something similar. Apparently this problem still hasn’t been fixed.
Miss Calahan (her real name), the Ash key officer, tells me they had the same problem in the unit before I started. She points at D1 tier and says that for two months, she and Bacle told the higher-ups to fix the door. At least one inmate filed a grievance about it. “I popped it several times using my foot,” Bacle says. He even showed the warden how it was done. Then, one evening, two inmates shook the tier door open from the outside, apparently unnoticed by the floor officers. One was carrying an eight-inch knife, the other an ice pick. According to a legal complaint, the two inmates found another inmate who lived on the tier and stabbed him 12 times in the head, mouth, eye, and body. One of the attackers warned that he would kill anyone who alerted the guards, so the victim lay bleeding, waiting for a CO to come through for the mandatory half-hour security check. Unsurprisingly, no one did. He bled for an hour and a half until a guard came by for count. He spent nine days in the infirmary.
“Child, next day they was out here fixing that door!” Miss Calahan says.
Bacle says he wishes an investigative reporter would come and look into this place. He complains about how, in other prisons, inmates get new charges for stabbing someone. Here, they are put in seg, but they rarely get shipped to another prison with tighter security. “CCA wants that fucking dollar!” Bacle says through clenched teeth. “That’s the reason why we play hell on getting a damn raise, because all they want is that dollar in their pocket.”
High levels of violence have been documented at several CCA prisons. At Ohio’s Lake Erie Correctional Institution, which CCA bought in 2011, inmate-on-inmate assaults increased 188 percent and inmate-on-staff assaults went up more than 300 percent between 2010 and 2012, according to a state report. (A 2015 report by the state prison inspector, provided by CCA, noted that Lake Erie had “drastically improved” and said the facility was “outperforming some of the state institutions.”)† In 2009, Kentucky declined to raise CCA’s per diem rate at one facility because the company’s prison was twice as violent as its state-run counterpart and because a suicidal employee smuggled in a gun and shot herself in the warden’s office. There is no current data on how violence in public prisons compares with violence in private ones. The last study released by the Department of Justice was in 2001, and it found that the rate of inmate-on-inmate assaults was 38 percent higher at private prisons than at public prisons.
The stabbings start to happen so frequently that the prison goes on indefinite lockdown. No inmates leave their tiers.
But are any of these numbers accurate? If I were not working at Winn and were reporting on the prison through more traditional means, I would never know how violent it is. While I work here, I keep track of every stabbing that I see or hear about from supervisors or eyewitnesses. During the first two months of 2015, at least 12 people are shanked. The company is required to report all serious assaults to the DOC. But DOC records show that for the first 10 months of 2015, CCA reported only five stabbings. (CCA says it reports all assaults and that the DOC may have classified incidents differently.)
Reported or not, by my seventh week as a guard the violence is getting out of control. The stabbings start to happen so frequently that, on February 16, the prison goes on indefinite lockdown. No inmates leave their tiers. The walk is empty. Crows gather and puddles of water form on the rec yards. More men in black are sent in by corporate. They march around the prison in military formation. Some wear face masks.
The new SORT team, composed of officers from around the country, shakes down the prison bit by bit. The wardens from the DOC continue to wander around, and CCA also sends in wardens of its own from out of state. Tension is high. No inmates except kitchen workers can leave the tiers. Passing out food trays becomes a daily battle. Prisoners rush the food cart and take everything.
“CCA is not qualified to run this place,” an inmate shouts to me a day into the lockdown. “You always got to shut the place down. You can’t function. You can’t run school or nothing because you got everybody on lockdown.”
Another inmate cuts in. “Since I been here, there’s been nothing but stabbings,” he says. “It don’t happen like this at other prisons because they got power. They got control. Ain’t no control here, so it’s gonna always be something happening. You got to start from the top to the bottom, you feel me? If [the warden] really want to control this prison—goddamn!—why ain’t you go’ call and get some workers? But you know what it’s all about? It’s about the money. ‘Let them kill theyselves.’ They don’t give a fuck.”
One day, a former public jail warden visits Ash. “I don’t know what’s going on down here, but it’s not good,” he says to me. “There’s something fucked up, I can tell you that.”
“I been doing this for 16 years. This is a free jail to me. Too much shit going on down here.”
I ask if Winn seems different from publicly operated prisons. “Oh, hell yeah,” he says. “Too lax.” If this were his prison, he says, there would be four officers on the floor, not two. At his public facility, officers start at $12.50 an hour. When they go to police academy, they get another $500 a month. Every time they pass a quarterly fitness test, they get $300. The initial training is 90 days. I tell him it was 30 days here. “This is a joke,” he says. “I been doing this for 16 years. This is a free jail to me. Too much shit going on down here. Not no consequences.” He says CCA could lose its contract.
One day, the visiting SORT team comes to Ash. One masked officer keeps watch over everyone with a pepper-ball gun. Other SORT members stand around, eating Twinkies and Oatmeal Creme Pies and drinking Mountain Dew. They tear up the tiers, throwing things out, slicing up mattresses. They find drugs and cellphones. Bacle tries to stop them from taking inmates’ coffee or destroying their matchstick crafts. Their overzealousness riles him. “Some people here think just because they’re locked up they’re a bunch of shitheads. I look at it, they fucked up and they’re doing their damn time.”
As soon as SORT leaves, inmates scream over each other to tell me what was taken, cursing me for not standing up for them.
During the lockdown, Corner Store asks me to let him out of his tier. With the canteen closed, his services are badly needed. Everyone’s commissary is getting low; many inmates are in search of cigarettes. They ask me to ferry things from one tier to the next, but I refuse, mostly because I know that once I do, the requests will never stop. I don’t let Corner Store out. I tell him it’s too risky with all these eyes around. For days, he just lies on his bed, staring at the ceiling.
His release date is five days away, but he still doesn’t know where he’s going when he gets out.
“Isn’t it Tuesday you are getting out?”
“Supposedly,” he says. Louisiana law doesn’t allow early release unless the inmate has an address to go to. New parolees have to stay in the state, and his mother doesn’t live in Louisiana. With no one outside to assist him, he has to rely on CCA to make arrangements with a shelter. The prison’s coach was trying to help, but Corner Store says he got “roadblocked” by the administration.
“So they just keep you here?” I say, incredulous.
“Yeah, basically. I’m not even angry, man. I just know my day is coming. I’ve waited years for this. I’m not mad.”
I ask Corner Store’s case manager what is happening with him. “He might be supposed to be getting out,” he says, but “as long as he don’t have that [address], his feet will not hit outside that gate. It ain’t nothin’ I can do for him.”
“They don’t want nobody to leave,” Corner Store tells me. “The longer they keep you, the more money they make. You understand that?”
One of the SORT members tells me they’ll be at Winn for months. Yesterday, they found 51 shanks in Elm, roughly one for every seven men. DOC records show that during the first four months of 2015, CCA reported finding nearly 200 weapons at Winn. That made it the state’s most heavily armed prison, with more than five times more confiscated weapons per inmate than GEO’s similarly sized Allen Correctional Center, and 23 times more than Angola. “They getting ready to start a war,” one officer says in a morning meeting.
Sergeant King stops by Ash. As he makes to leave, people start shouting from their tiers. “What’s up with the fuckin’ store?” It’s been three weeks since anyone here went to canteen. Inmates are up at the bars, looking angry. “You ’bout to start a whole riot,” one says to King.
Bacle seems nervous. “If they start throwing shit, you step right up here where they can’t gitcha,” he tells me, pointing toward the entrance. Less than a week ago, inmates rioted in a privately operated immigrant detention center in Texas. I saw prisoners here watching it on the news.
I walk over to one of the tiers.
“There ain’t go’ be no count or no nothing!” one shouts at me.
“Ain’t no COs coming in this bitch until we go to canteen.”
“That’s what’s up. We all standing behind that.”
“If this shit don’t get handled, y’all going to have a fuckin’ riot on y’all hands.”
“We gonna put this bitch on the channel eight news.”
“Y’all risking your fucking life around here playing these fucking games!”
“Fuck the count! Bring the warden down here.”
King comes over to one of the tiers. “Y’all gotta give me an opportunity. Before y’all start bucking. Before y’all start refusing. Because here’s what’s going to happen: They’re gonna bring the SORT force down here.”
“We don’t give a fuck!”
“I ain’t got no fucking soap! No nothing! No deodorant! No fucking cigarettes! This place is shit!”
I don’t want to give the impression we are afraid, so I walk the floor. Everyone, everywhere, is pissed. I feel an explosion coming and I want to flee. “I’m surprised ain’t nobody got you yet,” a white inmate with a shaved head says to me, his eyes cold and focused. “They go’ get you.”
A few years ago, a riot erupted in a low-security CCA prison in Mississippi over what inmates saw as inadequate health care and poor food. A guard was beaten to death. When Alex Friedmann, a former CCA inmate and a company shareholder, asked for a moment of silence for the guard at a corporate meeting in 2013, the board chair refused to honor the request. (At the time, CCA said it had “honored his memory a number of ways.”)
King calls Bacle and me to the door. “Listen, it’s a lot of tension down here,” he says.
“No shit,” Bacle says.
“They found 75 shanks in two days. These sonsabitches is dangerous, y’all. I don’t want y’all goin’ in them tiers. I don’t want y’all lettin’ nobody out. As of right now, if this shit don’t get handled, y’all going to have a fuckin’ riot on y’all hands. All the black suits ain’t going to do nothin’ but pepper-ball and gas all of they asses.” He leaves.
A while later, a CCA warden from Tennessee comes and talks to the inmates. “Y’all saying that y’all are being mistreated. I got plenty of people here. If we want to act like refugees and animals, then we can do it that way.” The prisoners don’t back down.
A couple of hours later, SORT comes and escorts the inmates to the canteen.
A drastic change
The lockdown lasts a total of 11 days. When it ends, Corner Store stands at the bars, waiting for me to let him out to work the floor. I ignore him. He pleads, but I am unbending. I have become convinced that he thinks he has influence over me, though I can’t articulate why. I become suspicious of his friendliness and wonder if he is manipulating me. I start to talk to him like every other inmate and he looks at me with confusion. When he lingers too long as I hold the gate open for chow, I slam it shut and let him stew. He calls my name as I walk away. I feel a twinge of guilt, but it lasts only momentarily.
His release date comes and goes. When I do count, I see him lying on his bunk. Eventually, he stops making eye contact as I pass.
An inmate orderly corners me. “Listen, what’s the problem?” he says, leaning against his broom.
“What problem?” I say curtly.
“Listen, be cool. Be cool. We talking. Relax. Why you so aggressive when I talk to you? You’re too snappy.”
“I’m not aggressive, man!”
“No, no, no. There’s been a drastic change in you. What the fuck went wrong?”
Things I used to view as harmless transgressions I now view as personal attacks.
I tell him we are under pressure from management to tighten up. This is true, but there is more. I see conspiracies brewing. Things I used to view as harmless transgressions I now view as personal attacks. When a physically disabled man doesn’t leave the shower in time for count, I am certain he is testing me, trying to break me down, to dominate me. The same is true when I see prisoners lying under their blankets during the daytime or standing at the bars. I don’t care about the rules, per se; many of them seem arbitrary. But I become obsessed with the notion that people are breaking them in front of me to whittle away at my will. I write inmates up all day long. One paper after another, I stack them, sometimes more than 25 disciplinaries in a day. Some inmates are clever; they know how to get under my skin without breaking the rules. So I shake down their beds and look for a reason to punish them.
I carry all this with me. Some days, when I stop for gas on the way home from work I notice myself, for a split second, casing the black men who enter the gas station. When I shoot pool at the local bar, I imagine—I hope—that the white man in hunting camouflage who’s playing against me will do something to spark a fight.
One day, the key officer tells me to go to the captain’s office. I am nervous; this has never happened before. He is sitting alone at his desk. “I think you are a very strong officer,” he says. I relax—it’s my employee evaluation. “I think you are a very detailed officer. You got a knack for this. You got a ‘it’ factor for this. It’s just who you are as a person. So, like you went down there to Ash and you just took the bull by the horns and just ran with it. It seems like them guys are starting to understand now—this is how this unit is go’ run. This is how CO Bauer go’ run it.”
The computer screen in front of him reads, “He is an outstanding officer. He has a take-charge attitude. He is dependable and stern. He would be an excellent candidate for promotion.”
“That’s how we feel about you. I just think that you need to stay consistent with what you are doing. Don’t break.” Despite myself, I crack a smile.
Even after the lockdown ends, SORT does not leave. They patrol the walk, frisking random inmates, and shake down tiers relentlessly. One morning, I spot white buses parked outside the prison as I pull in for work. At the morning meeting, there are about 15 wardens and COs from public prisons across the state. The Winn warden steps up to the podium. “Our friends here from the Louisiana Department of Corrections have come to help us out,” he says. This is the moment everyone has feared. Are they taking over? Will we lose our jobs?
A warden and a couple of officers from Angola follow Bacle and me to Ash. One tells us they are taking inmates who are too friendly with staff and shipping them to other prisons. He also says they’ve been administering lie detector tests to officers. Several have already refused to take one and walked off the job. When he says this, I get nervous. I go into the bathroom and flip through my notebook. I rip out my notes. I throw them in the toilet and hold the handle down for a good 10 seconds.
When it’s count time, the COs from Angola blow a whistle and bark for everyone to sit up straight on their bunks. We’ve never done this. They tell us that if we get used to counting people sleeping under their blankets, we might eventually count someone who is dead. All the inmates sit up without hesitation. As long as the DOC officers are here, everything is quiet and smooth. They make inmates walk through the metal detector as they enter the unit, and Bacle and I put them in their tiers. I feel less worried about getting attacked, and some inmates tell me things are better for them, too. But others say that as soon as the DOC is gone, things will go back to the way they were. “It’s like Mommy and Daddy back home,” one prisoner says. “But when they go back on vacation, the kids is back out.”
The Winn COs are deferential to the DOC officers, but in private they describe them as elitist pricks. It feels like incompetence has been replaced with overzealousness. The DOC officers chide us for letting inmates smoke inside, and when they spot someone smoking on camera, they find him and strip-search him in front of everyone. When I sit on a chair to take a break, a DOC officer, staring at the monitor inside the key, tells me to go into the TV room in one of the tiers. There is an inmate in there whose pants are sagging. He orders me to tell the man to pull them up.
“It gets in your blood”
Three days later, the DOC officers leave, and the order they imposed vanishes with them. COs slide back into their old routines and prisoners resist more than usual. Assistant Warden Parker, however, is jubilant: CCA has hung onto the prison. “The great state of Louisiana came in with both guns a-blazing,” he tells us during a morning meeting. “They were ready to tear Winn apart.” In interviews with staff, the DOC learned that staff members had been “bringing in mountains and mountains of mojo”—synthetic marijuana—and having sex with inmates. “One person actually said that they trusted the inmates more than they trusted me, the warden. One staff member said, ‘The inmate made me feel pretty. Why wouldn’t I love him? Why wouldn’t I bring him things he needs because you all won’t let him have it?'”
Later that morning, I clench up when my old instructor Kenny enters the unit and approaches me. “The warden told me to find somebody that’s knowledgeable and ready for leadership,” he says, smiling slightly. “Out of all y’all’s crew down here, I’m gonna handpick you. If you are interested in moving on up, I’m go’ make it happen. I’m going to train you for the next level.” I’ve been on the job for two months.
In the following days, I walk up and down the tiers at count time, barking at inmates to sit up on their bunks. If they are asleep, I kick their beds. Some refuse to obey, so I write them up.
“Someone asked me if we were pretty picky about who we hire. I said, ‘Well, I’d love to tell you yes, but we take ’em six-legged and lazy.’”
At the end of a long day, I head down the walk. On my way out, I meet Miss Carter, the mental health director.
“How do you like it so far?” she asks.
“It’s okay. It can be exciting,” I say.
“It gets in your blood, doesn’t it? Someone asked me if we were pretty picky about who we hire,” Miss Carter continues as we pass through the front gate. “I said, ‘Well, I’d love to tell you yes, but we take ’em six-legged and lazy.’ We take whatever we can get!” she says with a laugh. “When you get down like this, you’ll take whatever. But then we come across a few good people like yourself. That’s not the norm.”
Outside, there is a chorus of frogs and crickets. The air is sweet and balmy. Like I do every night when I get off work, I take a breath and try to remember who I am. Miss Carter is right. It is getting in my blood. The boundary between pleasure and anger is blurring. To shout makes me feel alive. I take pleasure in saying “no” to prisoners. I like to hear them complain about my write-ups. I like to ignore them when they ask me to cut them a break. When they hang their clothes to dry in the TV room, an unauthorized area, I confiscate the laundry and get a thrill when they shout from down the tier as I take it away. During the lockdown, when Ash threatened to riot, I hoped the SORT team would come in and gas the whole unit. Everyone would be coughing and gasping, including me, and it would be good because it would be action. All that matters anymore is action.
Until I leave. When I drive home, I wonder who I am becoming. I feel ashamed of my lack of self-control, my growing thirst for punishment and vengeance. I’m getting afraid of the expanding distance between the person I am at home and the one behind the wire. My glass of wine with dinner regularly becomes three. I hear the sounds of Ash unit as I fall asleep. I dream of monsters and men behind bars.
Late one night in the middle of March, my wife wakes me. James West, my Mother Jones colleague who’s recently come to Louisiana to shoot video for my story, has not returned from trying to get a nighttime shot of the outside of Winn. Something is wrong. The sheriff of Winn Parish answers James’ phone. James, he says, will be in jail for a while. I feel the blood drain from my face. Then I wonder, “Will they come for me?” We scramble to pack up everything that has anything to do with my reporting and check into a hotel at 2 a.m. A few hours later, I call in sick.
The same morning, James tells the sheriff he needs to make a call. “You can tell them we didn’t shoot you at dawn!” the sheriff says. James is later taken in leg irons into a room for questioning. “We don’t care if you are doing an exposé on CCA,” a deputy tells him. “We have nothing to do with them. They have given us trouble in the past.” A state trooper adds, “I don’t care if that guy works in the prison.” James assumes he is referring to me but says nothing.
James is charged with trespassing. By evening, a $10,000 bond is posted and he is released. “Send me a copy of the article when it’s done,” one of the cops tells him.
We pick up James at a gas station at the edge of Winnfield and drive out of town. The next morning, as I get coffee in the hotel lobby, I see a SORT officer standing outside in a black uniform, flex-cuffs hanging from his belt. Are they looking for me? We exit through a side door, and as I pull my truck out I see another man I recognize from the prison. We go back to the apartment, hurriedly throw everything in plastic bags, and leave. We drive across the border to Texas. I feel, oddly, sad.
A couple of days later, I call HR at Winn. “This is CO Bauer. I’m calling because I’ve decided to resign.”
“Oh! Mr. Bauer, I hate to hear that!” the HR woman says. “I hate to lose you. Your evaluation looked good and it looked like you were willing to hang in there and hopefully promote. Well, I hate it, Mr. Bauer. I truly do. In the future, if you decide to change your mind, you know the process.”
EPILOGUE
When Bacle pulled into Winn’s front gate after I left town, the guard told him the assistant warden wanted to see him. “What the hell did I do?” he thought. In his office, Assistant Warden Parker asked Bacle what he knew about me. “He was a good partner,” Bacle told him. “I enjoyed working with the dude. He has no problem writing ’em up.” He asked what was wrong, but Parker wouldn’t say. On his way out, Bacle asked the officer at the front gate, “What’s going on with Bauer?”
“You ain’t heard?” the officer said. “He was an undercover reporter!”
Bacle recounted this to me on the phone 10 months later. “Oh, I laughed,” he said. “I don’t know if you remember, but I told you once that it would be nice to have an investigative reporter out there.”
Word about me got out quick. The day after I quit, the Winnfield newspaper reported that I had been working at the prison. National media picked up the story and CCA issued a statement saying my approach “raises serious questions about his journalistic standards.” A couple of guards I worked with reached out to me right away. Miss Calahan, who’d quit before me because she thought the job was getting too dangerous, wrote to me on Facebook: “Hey boy you got they ass lol.” Another sent me an email: “Wow, Bauer! I’m honored. I don’t even know what to say.”
One concern raised by the Department of Corrections was a bonus paid to Winn’s warden that “causes neglect of basic needs.”
I attempted to contact everyone who’s mentioned in this story to ask them about their experiences at Winn. Some refused outright. Others didn’t respond to my phone calls and letters, and a few I could not track down. A surprising number, however, were eager to talk. Corner Store insisted he and other inmates knew something was up all along. “I just don’t know no CO to pull out his pad every five minutes,” he told me. “Everybody’s like, ‘Oh man, I knew it, I knew it, I knew it.'” Collinsworth said that when he found out I was a reporter, he “thought it was cool.” Christian thought “pretty much what most people thought: Can’t wait to read the story!”
Some people whom I would never have expected spoke to me. One was Miss Lawson, who’d been the assistant chief of security. “They were scared to death of who you were,” she told me. “After they found out you were a reporter, it was like, ‘Oh my God. Oh my God.'” The DOC quickly required the staff to undergo fresh background checks. CCA’s corporate office sent people to Winn to open what she described as an “extensive” investigation on me. They gathered “everything that had your name on it,” Miss Lawson said. Ironically, the investigation narrowed in on the item that, in my mind, had symbolized my transformation from an observer into a real prison guard: the cellphone I had confiscated in Ash. “I got called like four or five times for that one phone from corporate,” Miss Lawson said. “It was like they were insinuating that you brought the phone in or there was some information in the phone. I’m like, ‘No, he found it in a water fountain.'”
After I’d filled out the paperwork about the phone and handed it off to Miss Price, it had disappeared somewhere in the chain of command. The mystery of the missing cellphone grew into a broader probe in which Christian and Miss Lawson were fired for allegedly selling phones to inmates. Both deny it, and CCA did not pursue legal action against them.
Miss Lawson also told me that Assistant Warden Parker texted her a photo of me, asking if she knew who I was. After she identified me, Miss Lawson says, Parker told her to delete the photo and “forget I sent it to you.” She kept it, however, and emailed it to me. The image was a shot of a laptop screen on which a video of me was playing. I recognized the footage immediately: James had filmed it on the afternoon before he was arrested.
When James was detained, he was careful to protect his camera and the footage on it, even as he was surrounded by SORT officers from the prison and Winn Parish deputies. Police body-cam footage that I later obtained shows one deputy grabbing James’ camera as James struggles to hang on to it, telling the officer that searching his camera and memory cards would be illegal. After James was cuffed and put in a police cruiser, two officers left their body cameras on. The video shows a SORT member scrolling through the images on James’ camera. The sheriff never obtained a search warrant for my colleague’s belongings, but someone apparently searched them anyway. Geolocation data on the photo Miss Lawson sent me points to the sheriff’s office. (The Winn Parish sheriff says he was “not aware” of anyone searching James’ things.)
In April 2015, about two weeks after I left Winn, CCA notified the DOC that it planned to void its contract for the prison, which had been set to expire in 2020. According to documents that the DOC later sent me, in late 2014 the department had reviewed CCA’s compliance with its contract and asked it to make immediate changes at Winn. Several security issues were identified, including broken doors and cameras, and unused metal detectors. The DOC also asked CCA to increase inmate recreation and activities, improve training, hire more guards, hire more medical and mental health employees, and address a “total lack of maintenance.” Another concern raised by the DOC, CCA’s chief corrections officer acknowledged, was a bonus paid to Winn’s warden that “causes neglect of basic needs.” The DOC also noted that CCA had charged inmates for state-supplied toilet paper and toothpaste and made them pay to clip their nails. In a message to its shareholders, the company gave no hint of any problems at Winn; it only said the prison wasn’t making enough money. LaSalle Corrections, a Louisiana-based company, took over in September.
The Department of Corrections also noted that CCA had charged inmates for state-supplied toilet paper and toothpaste.
Some guards stayed on with the new company, but many left. Bacle got a job at a lumber mill. Miss Calahan became a CO at a local jail. One went on to Army basic training. Another took a security guard job in Texas. Some are still unemployed. Assistant Warden Parker took a similar position at another CCA prison. Some Winn prisoners have been transferred across the state and some have been released. Robert Scott is still suing over his amputated legs. I still don’t know what most of them were in for, but I was shocked to find out that Corner Store was in for armed robbery and forcible rape.
One inmate’s mother read about me in the news and asked an attorney to connect us. When the lawyer told me her son’s name—Damien Coestly—it took me back to my first day on the job, when I was working suicide watch. It had been a year since I’d pulled my chair across from him as he sat on the toilet, his entire body hidden under his suicide blanket. He had told me to “get the fuck out of here” and threatened that if I didn’t he would “get up on top of this bed and jump straight onto [his] motherfucking neck.” He had gone on hunger strike repeatedly to protest the limited dietary options and inadequate mental health services. In June 2015, he hanged himself. His autopsy said he weighed 71 pounds.
Five months after I left Winn, Mother Jones received a letter from a law firm representing CCA. The letter dropped hints that the company had been monitoring my recent communications with inmates and was keeping an eye on my social-media presence. CCA’s counsel claimed I was bound by the company’s code of conduct, which states, “All employees must safeguard the company’s trade secrets and confidential information.” Since guards are not privy to confidential business information, the implication is that what I experienced and observed inside Winn should remain secret.
CCA insisted on receiving a “meaningful opportunity to respond” to this story prior to its publication. Yet when I asked for an in-person interview, the company refused. CCA did eventually reply to the more than 150 questions I sent; its responses are included throughout this article. In one letter to me, CCA’s spokesman scolded me 13 times for my “fundamental misunderstanding” of the company’s business and “corrections in general.” He also suggested that my reporting methods were “better suited for celebrity and entertainment reporting.”
In March 2016, Corner Store walked free. He stayed in prison a full year while CCA was supposed to help him find a place to go. A lawyer eventually tracked down his father’s address and arranged for him to stay there. He rode a Greyhound bus to Baton Rouge. His mother drove from Texas to see him. He got his seafood platter. He walked in the rain. He got a job detailing cars. Sometimes he would hop on a bus, any bus, and ride the entire route just to see the city.
Two weeks after he gets out, James and I visit him at his house on a quiet street near the airport. His father invites us in.
“You all taking [him] somewhere?” his father asks us as we sit on the couch waiting for Corner Store to get ready.
“Yeah, we were going to see if he wants to go anywhere,” I say.
“You all ain’t come here to arrest him?”
Corner Store comes out of his room and walks directly outside. He tells us to get straight in the car—no talking in the street. He’s tense.
“Hey, this no names involved, huh?”
“What are you worried about?” I ask.
“Let’s just say something happens and I go back.”
“Who would you be worried about?”
“The free people.” He means the guards.
“Do you think you might go back?”
“Anything is possible,” he says. The smallest parole violation could land him back in prison. “If they were ever to see me again, they wouldn’t have too much of a liking for me. They feel like you shouldn’t even be talking about this.”
When we pick up Corner Store the next day, he tells me he hasn’t seen the Mississippi yet. He used to fish in it, growing up. We head to the river. After we sit and talk awhile, he stops scoping out everyone who passes by, and he stares out at the glistening surface. A tugboat chugs past. He walks down to the bank, scoops up some water, brings it to his nose, and breathes in deep.
Story by Shane Bauer Shane Bauer is a senior reporter at Mother Jones. He has previously reported on solitary confinement, police militarization, and the Middle East. He is the co-author, with Sarah Shourd and Joshua Fattal, of A Sliver of Light, an account of his two years as a prisoner in Iran. Videos by James West Edited by Dave Gilson Researchers: Becca Andrews, Gregory Barber, Brandon Ellington Patterson, and Madison Pauly Senior Research Editor: Maddie Oatman Creative Director: Ivylise Simones; Art Director: Carolyn Perot Photo Editor: Mark Murrmann Developer: Ben Breedlove Web Editor: Jahna Berry Funding for this project has been provided in part by the Puffin Foundation, the Jacob and Valeria Langeloth Foundation, the Glaser Progress Foundation, and the ongoing support of Mother Jones readers like you.
*This sentence has been revised for accuracy.
**Correction: A production error that caused an incorrect figure has been fixed.
†These sentences have been clarified. ||||| Opinion: Private prisons are a public shame
A new law signed by Gov. Rauner would promote more mentally ill people being transferred from jails and prisons to treatment facilities. | AP file photo
Why have private prisons at all?
That is the question to ask in the wake of a new U.S. Department of Justice report that has revealed elevated safety and security incidents at privatized federal prisons. The 80-page report by the DOJ’s inspector general confirms what has long been suspected: Private prisons are often less safe than publicly operated prisons.
The private prison industry has expanded exponentially in the past quarter-century. The number of inmates in private prisons increased by roughly 1,600 percent between 1990 and 2009. Today, some 130,000 men and women live in for-profit prisons in the United States — and that number doesn’t include those locked up in private local jails and immigration prisons. As incarceration skyrocketed due to the war on drugs, three strikes laws and mandatory minimum sentences, the private prison industry reaped lucrative rewards. The more people for-profit prisons lock away, the more money they make.
OPINION
From a human rights standpoint, privatized incarceration presents a serious threat. A private prison in Idaho was dubbed the “Gladiator School” due to extreme levels of violence. A private juvenile prison in Mississippi was once described by a federal judge as “a picture of such horror as should be unrealized anywhere in the civilized world.”
Some of the safety concerns at private prisons may reflect the higher rate of staff turnover, which can result in inexperienced guards walking the tiers. After an infamous escape from an Arizona private prison in 2010, for example, the Arizona Department of Corrections reported that at the prison, staff were “green,” not proficient with weapons and had a rather dangerous habit: ignoring sounding alarms.
While the for-profit prison industry claims that governments can save money through privatization, private prisons often fail to deliver demonstrable fiscal benefits and can even cost taxpayers more than publicly operated institutions. Numerous studies by researchers, state governments and federal agencies contradict the supposed economic benefits touted by industry supporters.
Although Illinois bans private prisons, the sheer scale of the industry and the masses of people locked up in private prisons make it unrealistic to think that these institutions will vanish from the national scene anytime soon. But there is much that can be done to curtail prison privatization—including the enactment of federal legislation banning new private prison construction across the country. With new evidence of private prison dysfunction coming from the Justice Department report, there is no time like the present to enact this important reform.
The DOJ inspector general’s report recommended improved monitoring and oversight of federal contract prisons. That’s the least DOJ should do. The more appropriate response would be to phase out private prisons and limit incarceration to publicly operated jails and prisons directly accountable to local, state and federal elected leaders.
David M. Shapiro is director of appellate litigation at the Roderick and Solange MacArthur Justice Center at Northwestern Pritzker School of Law where he is a clinical assistant professor of law.
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What is a shorter version of the above article? | – Shares for two big corrections companies took a deep dive Thursday after a report that the Justice Department is moving away from using private prisons, with the eventual goal of no private prisons under its umbrella at all, CNBC reports. Prison companies GEO and Corrections Corporation of America saw more than 40% drops in their share prices after a memo issued by Deputy AG Sally Yates was reported by the Washington Post, with instructions for prison officials to not renew contracts with private operators or to "substantially reduce" what the contracts cover. The end goal: "reducing—and ultimately ending—our use of privately operated prisons," upon which the federal Bureau of Prisons spent $639 million in fiscal 2014, per an Office of the Inspector General report issued this month. Yates' memo notes the 13 private prisons under the bureau's watch, holding about 12% of the bureau's total prison population, aren't as safe as those run by the feds, don't offer notable cost-savings, and don't have the "same level of correctional services, programs, and resources" as government-run facilities. An in-depth report by Mother Jones in its July/August issue by a journalist who went undercover to work in a private Louisiana prison highlighted some of those issues. The three private companies that run the contracts for the private prisons, which David Shapiro calls a "public shame" in the Chicago Sun-Times, are already expressing discontent with the IG's report, with the president of Management and Training Corporation writing in response that comparing private prisons to federally run ones is like "comparing apples and oranges." (Bernie Sanders is against private prisons.) | multi_news_1_0_0 |
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About 100,000 bats dead after heatwave in southern Queensland
Updated
About 100,000 bats may have died as a result of last weekend's heatwave in southern Queensland, the RSPCA says.
Mass deaths at about 25 separate colonies have been reported since the weekend, including at Mt Ommaney, Redbank, Boonah, Palmwoods, Laidley and Gatton.
RSPCA spokesman Michael Beatty says the heatwave was a significant hit to the population of bats across the state.
"The heatwave was basically a catastrophe for all the bat colonies in south-east Queensland," he said.
"That's obviously going to have a pretty disturbing impact on those colonies and those colonies are vital to our ecosystem."
The smell of bat carcasses has caused problems for locals.
The Scenic Rim Regional Council, west of Brisbane, has organised rubbish collectors to clear up the carcasses of about 2,000 bats.
Residents near Boonah's Athol Terrace lookout say they have been putting up with the stench of the dead animals for four days.
Hundreds of bats also lie dead in trees and nearby bushes, and are being eaten by maggots.
The council today advised local residents it will not send workers into nearby bushland to collect the remaining bat carcasses, as it could cause further disruption to the nearby colony.
One resident has told the ABC she is receiving anti-viral treatment after being scratched by a baby bat while clearing the dead animals out of her tree with a rake.
Further north, Lockyer Valley Regional Council says it also faces a massive task of cleaning up thousands of dead bats from around Laidley and Gatton.
Sunshine Coast Regional Council has sent workers out to collect thousands more dead bats near Palmwoods.
At least 16 people across south-east Queensland are receiving anti-viral treatment after coming into close contact with a bat.
Queensland Health is advising people not to touch the animals and to call authorities for help in clearing them away.
Sammy Ringer from Bat Rescue echoed those concerns, saying it was best to call a wildlife volunteer or a vet.
"Don't touch them, they're stressed," she said.
"If they do bite or scratch you and break the skin you can get a vaccination, you can get a shot for the lyssavirus."
Topics: local-government, phenomena, environmental-impact, boonah-4310, southport-4215, maroochydore-4558
First posted ||||| Queensland heatwave: Brisbane set to roast as weekend temperatures soar
Updated
The scorching heatwave gripping much of Queensland is being felt in Brisbane today, with residents set to roast in temperatures of up to 41 degrees Celsius.
At 9:25am, the mercury had already hit 35.1C, with the apparent temperature hovering at 37.4C, according to the Bureau of Meteorology website.
By 1:00pm, the temperature had risen to 38C, although the apparent temperature was 41C.
Queensland's interior has been sweltering through record-breaking heat in recent days, along with parts of Central Australia and north-western New South Wales.
The heatwave continued as a Bureau of Meteorology report revealed 2013 was the hottest year on record in Australia.
The mass of hot air causing the extreme weather again led to searing temperatures in central and western Queensland on Friday.
St George topped the temperature list with 47.2C, while Winton and Longreach also had scorchers at 46.4C and 46.3C respectively.
Charleville followed on 46.1C, while Blackall, Roma and Thargomindah all recorded temperatures just above 45C.
Brisbane's top for Friday was 34.3C, but the mercury is predicted to reach 41C today as northerly winds push the heatwave south.
Further evacuations not expected
Firefighters are confident no further evacuations will be needed as they battle a large bushfire on Stradbroke Island.
Firefighters are confident no further evacuations will be needed as they battle a large bushfire on Stradbroke Island.
The Gold Coast's beaches have been packed with people keen to beat the heat, and that is sure to be the case over the weekend.
Queenslanders have also been urged to put their health first during the current heatwave.
Last summer, paramedics responded to more than 350 cases of heat-related illness across the state.
Steven Clarke from Queensland Ambulance says drinking plenty of water is the key.
Mr Clarke says families should ensure loved ones are coping with the heat, with the elderly particularly vulnerable.
"For the elderly and people with chronic illnesses, especially with kidney problems, diabetic problems, obese people, they need to take extra care," he said.
"Probably a critical point to make is family need to check their loved ones - grandad and grandma living on their own - they need to ring them up, they need to go around and visit them and make sure they are doing the right thing.
Live heatwave tracker
Track the heatwave rolling over inland Australia with Track the heatwave rolling over inland Australia with our animated visualisation
"Especially with the elderly. They'll lock their windows to make themselves feel safe; they live on their own. Family need to spend the time and go visit them."
Meanwhile, cooler weather has arrived in South Australia's outback, after two days of scorching heat and a catastrophic fire danger rating.
It reached 49.3C at Moomba in the state's far-north-east on Thursday, but conditions are set to ease to 32C today.
The state's fire danger rating has been reduced by two levels to severe.
In New South Wales, Walgett recorded 49.1C on Friday, which is the highest temperature recorded in NSW since 1939, according to the Bureau of Meteorology.
Former tropical cyclone Christine has further weakened as it passes into northern New South Wales, and the system can now barely be seen on satellite images.
2013 was hottest year on record
The weather bureau's Annual Climate Statement shows that in 2013, average temperatures were 1.20C above the long-term average of 21.8C, breaking the previous record set in 2005 by 0.17C,
All states and territories recorded above average temperatures in 2013, with Western Australia, Northern Territory and South Australia all breaking annual average temperature records.
Every month of 2013 had national average temperatures at least 0.5C above normal, according to the statement.
The country recorded its hottest day on January 7 - a month which also saw the hottest week and hottest month since records began in 1910.
A new record was set for the number of consecutive days the national average temperature exceeded 39C – seven days between January 2 and 8, 2013, almost doubling the previous record of four consecutive days in 1973.
The highest temperature recorded during 2013 was 49.6C at Moomba in South Australia on January 12, which was the highest temperature in Australia since 1998.
Australia has experienced just one cooler-than-average year in the last decade - 2011.
Australian temperatures have warmed approximately 1C since 1950, consistent with global climate trends
Topics: weather, phenomena, brisbane-4000, qld, australia, st-george-4487, roma-4455, winton-4735, longreach-4730, charleville-4470
First posted ||||| About 100,000 bats have fallen from the sky and died during a heatwave in Australia that has left the trees and earth littered with dead creatures.
In scenes likened to "an Alfred Hitchock thought bubble", a heatwave across the north-east state of Queensland in recent days caused mass deaths of flying foxes from an estimated 25 colonies.
"It's a horrible, cruel way to die," a conservation worker, Louise Saunders, told The Courier Mail .
"Anything over 43 degrees [Celsius, 109F] and they just fall. We're just picking up those that are just not coping and are humanely euthanising what we can."
Health experts have warned residents not to touch the dead creatures amid concerns about the spread of virus or bites and scratches from bats that may still be alive. At least 16 people have been are receiving antiviral treatment after coming into close contact with a bat.
"If you find a bat it is very important not to touch it because of the risk of infection with Australian bat lyssavirus," the state's chief health officer, Dr Jeannette Young, told APN.
"Some bats may appear dead but they are not and when people have attempted to remove them they have been bitten or scratched. Bats also have a claw on their wings which is a frequent cause of injury."
The stench from the rotting carcasses has begun to disturb residents of Brisbane and large towns. Authorities have dispatched rubbish collectors to pick up thousands of carcasses from populated areas.
The RSPCA said the heatwave could have a devastating effect on the state's wildlife.
"The heatwave was basically a catastrophe for all the bat colonies in south-east Queensland," a spokesman, Michael Beatty, told ABC News.
"That's obviously going to have a pretty disturbing impact on those colonies and those colonies are vital to our ecosystem." |||||
Write a summary. | – As the US emerged from that whole "polar vortex," Australia saw an intense heatwave last weekend—leading to the deaths of 100,000 bats, many of which reportedly dropped from the sky. In one video that went viral, a man filmed what he estimated to be more than 1,000 bat carcasses in his backyard, the Guardian reports. "The heatwave was basically a catastrophe for all the bat colonies in southeast Queensland," a rep for the RSPCA tells Australia's ABC News, noting that mass deaths were reported at 25 colonies. Bats are fragile and can't withstand temperatures above 109 degrees, a conservation worker explains. (Queensland's Brisbane got as hot as 106 on Saturday, notes ABC News.) "They just fall," she says. "It's a horrible, cruel way to die." Another problem: The stench from the bodies is bothering locals. In one area, residents say they've had to live with the smell for days; in others, teams of trash collectors have been put together by regional councils to clean up the carcasses. In addition to those that fell to the ground, hundreds of bodies are still in trees and bushes, and maggots have already set in. As if all that isn't enough, at least 16 people have had to undergo anti-viral treatment after getting scratched or otherwise coming into close contact with a bat. | multi_news_1_0_0 |
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News article:
President says it will be ‘every bit as good’ as Obamacare
President Donald Trump said Monday the Republican health-care bill being negotiated in Congress ultimately will protect Americans with pre-existing conditions as well as Obamacare does.
“I want it to be good for sick people. It’s not in its final form right now," he said during an Oval Office interview Monday with Bloomberg News. "It will be every bit as good on pre-existing conditions as Obamacare."
The latest version of the House GOP bill, which Republican leaders are trying to figure out whether they have the votes to pass this week, wouldn’t live up to that promise and would weaken those protections.
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A new amendment aimed at winning over conservative holdouts would allow states to apply for waivers from Obamacare’s requirements to provide certain essential health benefits if they are able to show that the modifications would cut prices. It also would allow states to sidestep the requirement that all consumers in a certain area must be charged the same rate for insurance, which would make plans significantly more expensive for those with pre-existing conditions.
The Republican bill would hurt protections for people with pre-existing conditions like a history of cancer, said Kirsten Sloan, senior director of policy analysis and legislative support at the American Cancer Society’s Cancer Action Network.
Obamacare “allowed a person with cancer to both get and keep insurance because of the insurance market protections; it made sure the insurance the kind of person with cancer was purchasing was meaningful,” Sloan said in an interview. The Republican proposal “begins to erode those protections.”
If states are allowed to use waivers for some protections, Sloan said, “you really are not guaranteeing that a cancer patient could get and afford coverage.” Her group supported the Affordable Care Act and has opposed the GOP bill.
‘Continuously Covered’
House Speaker Paul Ryan’s office defended the GOP health bill on Monday, saying the measure does protect people with pre-existing conditions.
“States can’t opt out without a high-risk pool to take care of them. And waivers never apply to anyone who has been continuously covered,” said AshLee Strong, Ryan’s press secretary. “We believe there is more than one way to address this problem.”
Trump repeated in the interview his contention that the Affordable Care Act is already disintegrating.
“And Obamacare just so you know, Obamacare’s terrible on preexisting conditions, you know why? Cause you’re not going to have it,” he said. “It’s folding. It’s gone.”
Reconsidering Floor Vote
The GOP bill to repeal and replace Obamacare has stalled ever since leaders scrapped a planned floor vote in late March.
After several embarrassing setbacks, Republican leaders, under pressure from the White House, spent much of last week weighing whether to hold a vote on the measure that included the new amendment, which was negotiated by New Jersey Representative Tom MacArthur and North Carolina Representative Mark Meadows, who chairs the House Freedom Caucus.
Conservative holdouts endorsed the revised bill but a number of moderate Republicans remained opposed to the measure, making it unclear whether it had enough votes to pass.
Vice President Mike Pence said in an interview Sunday on NBC’s “Meet the Press” that he hopes the House might act on a health-care bill soon. But he also said a final version from Congress might not be ready “before the end of the year" for Trump to sign.
Two of Trump’s top aides, Chief of Staff Reince Priebus and National Economic Council director Gary Cohn, in interviews with CBS, both projected confidence Monday that it would. "This is going to be a great week – we’re going to get health care down to the floor of the House. We’re convinced we’ve got the votes," Cohn said.
House Republicans are far less certain. There is no vote scheduled yet for this week and there are still not enough votes to pass a bill, a congressional aide said after Priebus’s and Cohn’s comments. While the new language won over some conservative holdouts, a number of moderate Republicans remain opposed.
Leaders are continuing to work to get more votes on board and will schedule a vote for this week if they believe they have enough to pass a bill, the aide added. ||||| House Speaker Paul Ryan, Majority Whip Steve Scalise and House Majority Leader Kevin McCarthy spent the weekend calling reluctant moderates. | Getty GOP suffers surprise defection on Obamacare repeal The scramble for votes is still very much on.
President Donald Trump dialed up his campaign-trail ally Rep. Billy Long on Monday, after the Missouri Republican announced his decision to vote against the Republican plan to replace Obamacare. The goal was straightforward: Persuade Long to change his mind.
It didn't work. Though Long hails from a deeply conservative district that overwhelmingly backed Trump over Hillary Clinton in November, and Long supported earlier versions of the legislation, the president's entreaties fell short, GOP insiders said.
Story Continued Below
It was an unexpected blow for House GOP leaders and the White House, who were bullish over the weekend that they were on the cusp of clinching the votes to pass the legislation. Instead, the scramble for support is still very much on.
“I have always stated that one of the few good things about Obamacare is that people with pre-existing conditions would be covered," Long said in a statement. "The MacArthur amendment strips away any guarantee that pre-existing conditions would be covered and affordable,” he added, referring to the last-ditch compromise between conservatives and House moderate Rep. Tom MacArthur (R-N.J.).
And the task was made even harder by an unforced error from Trump. The president told Bloomberg News in an interview Monday morning that the bill might change to provide more protections to people with preexisting conditions. “It’s not in its final form right now,” he said. Trump's comments frustrated the House whip effort, as some members interpreted them to mean the president was reopening negotiations.
“I don’t know if there are going to be any kinds of changes,” said Rep. Patrick Meehan (R-Pa.), who opposes the AHCA, as he exited a meeting of Ryan’s whip team.
By late evening Monday, Trump was calling lawmakers to walk back his comments.
Even after Trump’s failed attempt to persuade Long, House leaders said they hoped to convince the Missouri lawmaker to change his mind. “I think we just need to sit down with Billy,” said House Majority Leader Kevin McCarthy. “I’d like to see Billy on the bill.” Trump, too, has begun calling around to other members as he and House leaders attempt to shore up enough support for the bill.
Other House leaders downplayed the significance of Long’s defection, which came as Vice President Mike Pence headed to the Capitol to discuss health care with Republican lawmakers, and members of the GOP whip team met to gauge support for the bill.
“Billy’s been outside the ‘yes’ column for a while now, [he] just hadn’t been public,” said House Majority Whip Steve Scalise. Asked whether Long’s rejection portended additional defections, Scalise said, “There’s others that have questions that we’re getting them answered on. The work still goes on.”
Scalise’s assessment follows a similar attempt by the White House to lower expectations after a weekend of making lofty pronouncements of imminent success.
“We’re not there yet,” White House press secretary Sean Spicer said at a press briefing Monday afternoon, hours after other top White House officials all but predicted an imminent legislative victory for Trump.
“I think the president has made it clear that he’s not instituting a timeline,” Spicer added. “We have a good whip count, I think we feel good about where we are and where it's headed. But ultimately [Speaker Paul Ryan] and House leadership determine when to call a vote. I think that we know when the vote gets called, we’ll feel confident it will be able to pass.”
Spicer’s measured tone was markedly more subdued than comments just hours earlier by White House chief economic adviser Gary Cohn and chief of staff Reince Priebus. In separate interviews on “CBS This Morning,” the two senior White House hands drove expectations for House action on health care.
"Do we have the votes for health care? I think we do," said Cohn.
Priebus said he expected the vote “this week” and said it would be “one of the fastest pieces of signature legislation to go through for a president since [Franklin] Roosevelt." Trump himself seemed to suggest over the weekend that the House already had enough votes to pass the measure last week.
"I think they could have voted on Friday," he said in an interview that aired Sunday on CBS’ “Face the Nation.”
But on Monday, Trump told Bloomberg News that the bill is "not in its final form right now," and said, "It will be every bit as good on pre-existing conditions as Obamacare." That potentially off-the-cuff comment seemed to undercut GOP leaders on the Hill, who have insisted the bill is in its final form.
Lawmakers return to the Capitol Monday evening where House leaders and vote-counters will once again test the level of support they have for the AHCA. Though the White House has signaled its desire for a vote on the measure by Wednesday, House leaders have insisted they’ll only move the bill when they can guarantee it will garner the 216-vote bare majority it needs to pass. GOP leaders have insisted they’re closer than ever to passing the bill, but wavering support from moderate Republicans and other scattered defections have left little margin for error.
Underscoring the difficulty House leaders are having securing the votes, a slew of lawmakers tasked by leadership with corralling support for the AHCA say they’re not yet sure how they intend to vote.
While walking into a vote-counting meeting in the basement of the Capitol Monday evening, half a dozen whips — including Reps. Erik Paulsen (R-Minn.), David Valadao (R-Calif.) and Kevin Yoder (R-Kan.) — said they remained undecided.
Meanwhile, House Appropriations Chairman Rodney Frelinghuysen, another whip, rushed out of the meeting to avoid reporters. The New Jersey Republican previously opposed the bill, but GOP insiders said leadership and other senior House Republicans had changed his mind. Frelinghuysen refused to say how he intends to vote.
Rep. Billy Long, left, an ally of President Donald trump, told reporters he opposed the GOP health care bill, known as the American Health Care Act. | Getty
Ryan, McCarthy, Scalise and Chief Deputy Whip Patrick McHenry spent the weekend calling reluctant moderates and connecting some with Trump’s Health and Human Services secretary, former Rep. Tom Price. Vulnerable Republicans are concerned that the bill would harm people with pre-existing conditions or eliminate insurance coverage for millions on Medicaid.
Privately, Republicans on the Hill and in the White House realize this week may be their last, best shot to pass the AHCA. That’s because of renewed momentum for the bill after the endorsement of the hard-line House Freedom Caucus as well as procedural constraints.
GOP lawmakers are relying on arcane Senate budget rules in an attempt to pass their health care plan with a 51-vote majority in the Senate, rather than the typical 60-vote threshold required for most legislation.
But Republicans can’t move on to their next big priority — tax reform — without launching a new budget process and canceling out their existing authority to pass health reform at the lower threshold. That would effectively kill the measure as Democrats would certainly block any Obamacare repeal bill that requires 60 votes. ||||| Washington (CNN) The White House and congressional Republicans are in serious danger of not having enough votes to pass their health care bill.
Several Republicans have come out Monday against the current measure to repeal and replace Obamacare, bringing CNN's whip count to 21 Republicans -- mostly moderates -- opposed to the bill with at least 17 lawmakers still undecided.
There is no vote scheduled and it's unclear if there will be one before the House leaves for a week-long break Friday. There is a lot of talk and significant pressure from the Trump administration to act -- Vice President Mike Pence, who has been working with congressional leaders from the start on the health care effort, headed to Capitol Hill as well to lobby lawmakers.
Pence will spend much of Tuesday on Capitol Hill as well. He will meet with Senate Republicans for lunch, then meet with lawmakers during the afternoon.
Yet, President Donald Trump, whose White House was optimistic the House could pass a bill Wednesday, once again muddied the waters by suggesting the measure may still be changed.
"I want it to be good for sick people. It's not in its final form right now," he said during an Oval Office interview Monday with Bloomberg News . "It will be every bit as good on pre-existing conditions as Obamacare."
The Republican Party can only afford to lose 22 votes assuming all of the Republicans are able to attend the vote and no Democrats cross over. As they count votes, GOP Rep. Jason Chaffetz, who was expected to be out for three to four weeks after surgery, is returning Monday from Utah and will back the bill, his office said.
Most notably Monday, Rep. Billy Long, a Republican from Missouri who serves on the Energy and Commerce Committee, announced he was opposed to the legislation. Reps. Brian Fitzpatrick of Pennsylvania, Daniel Webster of Florida and Chris Smith of New Jersey will also vote against the current bill, making their decisions public in succession Monday afternoon.
Heading into a Republican whip meeting Monday afternoon, some of the members going in still didn't know how they would personally vote for the health care bill: Reps. Kevin Yoder, David Valadao, Erik Paulson, Elise Stefanik, and Adam Kinzinger all were undecided.
Rep. Patrick McHenry, chief GOP deputy whip, told reporters that he had no predictions on when and if a bill would come up this week.
But asked how close they were, he said "very."
The hope is that leadership can sell moderates on the fact that this bill is going over to the Senate where it might be significantly reworked. Rep. Peter King, R-New York, he was already talking to members in the Senate about changes he'd like to see.
Pushing forward
As hard as it is, Republican congressional leaders know they can't simply abandon their effort now.
"I hope we keep going. I don't think we can stop," said Rep. Brett Guthrie, a Republican who serves on the House's Energy and Commerce Committee told CNN last week.
White House chief economic adviser Gary Cohn sounded optimistic Monday morning when asked if he thought Republicans' plans for health care had enough votes.
"I think we do," Cohn told CBS. "This is going be a great week. We're going to get health care down to the floor of the House. We're convinced we've got the votes and we're going to keep moving on with our agenda."
Pre-existing conditions
The fight over how pre-existing conditions are covered is at the center of the fight.
Trump said Sunday the White House is pushing forward, and that the GOP plan "guarantees" coverage for Americans with pre-existing conditions.
"Pre-existing conditions are in the bill. And I mandate it. I said, 'Has to be,'" Trump said on CBS's "Face the Nation" Sunday.
Pressed further, Trump said that "we actually have a clause that guarantees" coverage for those with pre-existing conditions. Trump also said the health care legislation is "changing."
Unlike the mandate under Obamacare, however, under the GOP bill insurers could charge them higher rates than others in the plan if they allow their coverage to lapse.
Republicans might seem stuck in a never ending cycle of trying to please the moderate and conservative wings of their party but pressure from the White House to deliver a legislative win for Trump is real. Also real: the repeated pledges to their constituents over the past seven years to repeal and replace Obamacare if given the chance.
MacArthur amendment not enough?
Last week, Republicans seemed to reach a major breakthrough.
A new amendment sponsored by moderate leader Rep. Tom MacArthur of New Jersey gave states the ability to opt out of more Obamacare regulations. The amendment was also enough to finally bring the conservative House Freedom Caucus on board.
But the amendment, which experts noted could drive up the cost of insurance for older Americans and those with pre-existing conditions, spooked moderates and left some -- who had been supportive of the legislation before -- scrambling to publicly voice their discontentment. All of a sudden, it was moderates in the hot seat.
It seemed that even though leadership may have gained upwards of 30 new votes from the Freedom Caucus, they were suffering significant enough losses from the other side of the party that they still couldn't bring a bill up to the floor for a vote in order to mark Trump's first 100 days in office.
This week, leadership's focus remains trying to help those moderates get comfortable with the new MacArthur amendment. Over the weekend, House leaders, as well as Pence and Health and Human Services Secretary Tom Price, spoke with members hoping to flip enough votes to move the bill forward. Leadership aides emphasize that there isn't much room to change the proposal at this point, but many deputy whips are trying to get members to keep the process in perspective.
"You remind them there is a United States Senate, and it will change things. What we send over there isn't going over there on stone tablets," said Rep. Tom Cole, R-Oklahoma.
"Going back to the drawing board would be death to repeal and replace," one aide said.
After last week, though, many moderates are frustrated with the process. Some say they see their party making the same kind of mistakes Republicans criticized Democrats for making back in 2010.
"We didn't learn anything from their mistakes," said Rep. Mark Amodei, a moderate Republican from Nevada told CNN. "We learned nothing from their mistakes."
As to promises the bill will be changed once it's in the Senate?
"Seriously, you want me to go back and tell the people in my fourth of Nevada 'the Senate will make it better?'" Amodei said. "What the hell?" ||||| This week is witnessing what must count as at least the third round of the House GOP’s peculiar, staccato legislative process on health care. In some ways, it resembles the prior rounds: An idea has emerged that seems like it could address the daunting political problems that bedevil any significant Republican health reform advanced through reconciliation, and so it is being held up as the end-all proposal. There is a rush to vote. The overall bill remains unfinished in key respects. And a great deal of incoherence and dysfunction has been driven by the House Republican moderates yet blamed on the conservatives.
All of that we have seen for two or three months. But this round does feel different, and to me at least it seems reasonably likely to end in the passage of a bill through the House.
For one thing, the substantive idea itself—embodied in the MacArthur Amendment—is a real step in the right direction. As I suggested around here a few weeks ago, state waivers from federal insurance regulations are (unlike much of what Republicans have tried so far this year) an idea native to the actual circumstances Republicans now face: the uneven (at best) commitment of some Republican members to actually doing anything about Obamacare, the constraints of the budget reconciliation process, and the sheer multiplicity of problems now confronting the individual insurance market in different parts of the country.
It is also responsive to what House Republicans have learned about the priorities of different factions within their coalition in the course of the prior rounds of this internal debate. The Freedom Caucus prioritizes deregulation of the individual insurance market to lower costs and constrain the federal role. The moderates prioritize coverage levels and protection for people with pre-existing conditions. These are both very worthwhile sets of causes to prioritize, and they are in some important respects compatible. But rather than try to arrive at a single overall balance between them, the approach House Republicans are now pursuing says to state governments that they can have relief from the rules that drive up costs and make their insurance markets unsustainable if they themselves propose alternative rules that would still protect people with pre-existing conditions and make coverage accessible. This course recognizes that different states will approach the tense balance between these priorities differently, and allows them to do that—thereby perhaps also enabling congressional Republicans to achieve the precarious political balance they require.
The extent of the waivers is constrained, in light of the political pressures involved, though it would allow for some meaningful variation and experimentation with insurance rules. If they show that their proposed alternative rules would reduce premiums, increase coverage, or otherwise strengthen insurance markets, states can request to waive the age bands on premiums starting next year. They can set their own essential health benefits (and therefore can recover the right to define insurance coverage in their jurisdictions to a significant degree) starting in 2020. And, if a state has established a high-risk pool or similar mechanism for covering people with pre-existing conditions, it can allow insurers to consider health status when pricing coverage for people who have not been continuously insured.
The waivers approach may also help the bill survive the reconciliation process in the Senate. Because it explicitly connects state regulatory waivers to effects on premiums and other factors that would influence the cost of a federal insurance subsidy, it creates a link between insurance-rule changes and federal spending that might not otherwise be clear. This at least is the theory behind the argument that this approach could make it through reconciliation in the Senate. I see no reason to consider that any more than a theory, but it’s probably a better theory than Republicans have had so far.
The practical implications of this amendment would depend heavily on how many states actually seek waivers, and of what sort. It’s possible that few states will want to play ball. But given the very real problems states are seeing in their individual insurance markets, there is reason to think that different states—both red and blue—would seek and find different ways to maximize their options under the waiver regime given their particular circumstances. They could well be under pressure from insurers and providers to find such ways, and they would have help too: I’d expect that a fair amount of model waiver language would be out there next year if something like this passes—language from insurers, providers, and activists on the left and right intended to help states pick up the pieces of their individual markets and put them back together in different arrangements to suit different needs, interests, and preferences. This would be a good thing. And the political pressures involved would likely drive states to prioritize coverage—even in the reddest states, the constituencies governors face are much more diverse and complicated than those of most Republican House members.
There are certainly some peculiarities in the amendment. For instance, allowing some waivers to take effect in the 2018 plan year seems to introduce some needless complications into an already horribly complicated transitional challenge for insurers. It also seems to me (as it has to others) that on its face section (a)(5)(A)(ii) of the amendment exempts members of Congress from the amendment’s effects, which would be truly just insane and inexcusable. Word is that this provision will now be removed (through a separate amendment), but that it was ever there is pretty staggering.
There is also no question that this bill, even with the MacArthur Amendment, is no one’s idea of an ideal solution. It retains Obamacare’s regulatory architecture as a default from which states can opt out, and only in restricted ways. But as a compromise that takes account of the fact that a full replacement is beyond Republicans’ reach given their numbers and the rules of the Senate, it does look like a meaningful step.
This would be an amendment to the broader AHCA that has, and would still have, some significant further problems. But with this amendment, the bill would reach the Senate in a form that could be made into a workable partial repeal and replacement of Obamacare, and might be reasonably close to the most that congressional Republicans can do about Obamacare at this point that would also be worth doing.
There would be some significant work for the Senate to do if this passes the House, and we should hope there is a real legislative process in the Senate and not a rushed vote on the House product as it is. The premium tax credit in the bill will need to be rethought so as to be more useful to more of the uninsured, and this could be done in ways that also make the bill more likely to survive reconciliation rules. That could involve something like Avik Roy’s very constructive proposals or it might even involve a move away from a tax credit toward a benefit more suitable for a state-waiver approach (which might also assuage concerns about reconciliation and the Hyde Amendment that otherwise could easily still kill the whole process in the Senate). Some ideas on how to proceed are out there, and Senators and staff are already chewing them over. And of course some fundamental questions about spending levels will need to be resolved, and ought to be resolved in ways that prioritize protecting the vulnerable. Essentially punting these questions to the Senate offers some hope that this could happen, but it will not be a simple matter.
Still, it does now look as though the rough, frustrating, unruly process House Republicans have been going through, with its multiple near-death experiences, has actually enabled some learning about their own priorities, the nature of the substantive policy challenges they face, and the difficulties involved with bringing their conference together. In the end, if this is the end of this stage of the process, what has worked best on the latter front has been direct negotiation between the different factions of the House Republicans, rather than leadership efforts at preventive mediation to assuage them all while keeping their substantive differences below the surface. There is surely a lesson in that for everything else Republicans imagine they can achieve this year. Republicans are divided, this president is not likely to play the role presidents usually play in overcoming internal divisions in their parties, and that means differences will need to get worked out through frank bargaining. Face to face discussions between different flavors of Republicans—not finished products from above, let alone “now or never” dictates and cheap twitter bravado from down the street—is how reconciliation bills might work in this Congress. And for other bills, some frank bargaining with actual human Democrats might be required too.
Even if the House does pass this amended bill, much work and time will remain before they get near any final product on health care. That is as it should be. It makes no sense to rush this effort, especially now that Republicans are exploring a relatively novel set of approaches—rooted in federalism and responsive to the distinct political and substantive constraints they face. There are lots of needles left to thread. But progress is something, and this looks like progress. ||||| A number of states would likely pursue waivers in the House Republican health plan enabling them to charge higher premiums to people with pre-existing conditions who let their coverage lapse, health analysts said.
The waivers are the latest twist to the House GOP proposal that would topple most of the Affordable Care Act and replace it with a new plan that would bring steep Medicaid cuts and refundable tax credits to help people... ||||| Jimmy Kimmel.
After weeks of negotiations, last week House Republicans reached a compromise that they said could finally allow them to repeal and replace Obamacare. It involves letting states opt out of certain Obamacare provisions, which would allow insurers to once again charge people with preexisting conditions exorbitant fees.
Protecting people with preexisting conditions may be Obamcare’s most popular provision. A recent Kaiser poll found that even among the 26 percent of Americans who want Obamacare repealed, 38 percent changed their mind when told that would hurt people with preexisting conditions.
The original vote on the American Health Care Act in March was canceled, in part, because opponents of the bill — which only had the support of 17 percent of Americans — called their representatives and protested at town hall meetings. Now Republicans say they may vote this week on a version of the bill that’s even worse for the sick, the elderly, and the poor — yet there’s been less organized resistance to the latest health-care push.
Two possible reasons: It’s been hard to keep track of GOP efforts to revive Zombie Trumpcare, and Republicans aren’t advertising that the latest version would weaken protections for people with preexisting conditions. President Trump added to the confusion in recent days when he appeared to offer false information about the contents and status of the GOP health plan.
“I want it to be good for sick people. It’s not in its final form right now,” he told Bloomberg News on Monday. “It will be every bit as good on pre-existing conditions as Obamacare.”
In Trump’s defense, the Republican plan to get AHCA passed by making it crueler doesn’t make any sense — unless your real aim is to shift the blame for the GOP’s failure to make good on seven years’ of promises to replace Obamacare with something better. The Post reported on Monday that House GOP leaders are now focused on one political goal: “Pass a bill they can say repeals Obamacare — even if it has no hope of survival in the Senate — to shield their members in next year’s elections.”
This time around, the House Freedom Caucus would prefer not to take the brunt of the blame for AHCA’s failure, and they’ve successfully pushed the legislation to the right. They frame reducing Obamacare’s protections for people with preexisting conditions as cutting costs and making the U.S. health system freer.
But GOP Representative Mo Brooks slipped on Monday, admitting that he doesn’t think we should punish healthy people for being “good” by forcing them to pay for people who don’t take care of themselves.
“It will allow insurance companies to require people who have higher health care costs to contribute more to the insurance pool that helps offset all these costs, thereby reducing the cost to those people who lead good lives, they’re healthy, they’ve done the things to keep their bodies healthy,” explained Brooks. “And right now, those are the people who have done things the right way that are seeing their costs skyrocketing.”
Watch Alabama Rep. Mo Brooks make the case for Trumpcare on CNN.
Twitter quickly filled up with people asking Brooks what moral failing gave them thyroid cancer, or how their poor choices at age 3 ended in a car accident. But the most vivid counterpoint to the GOP’s entire health-care push came later on Monday night from, of all people, a late-night comedian.
In a heart-wrenching 13-minute monologue, Jimmy Kimmel opened up about his son’s heart condition, which was discovered just hours after his birth ten days ago. With tears in his eyes, the host described the harrowing ordeal, which started with a nurse noticing baby William John Kimmel’s color was off and ended with him being rushed into open-heart surgery.
Baby Billy is doing well, though he’ll need several more surgeries. Kimmel closed with a plea for politicians to make sure others have a similarly happy outcome, even if they aren’t born to wealthy parents.
We were brought up to believe that we live in the greatest country in the world, but until a few years ago, millions and millions of us had no access to health insurance at all. You know, before 2014, if you were born with congenital heart disease, like my son was, there’s a good chance you’d never be able to get health insurance, because you had a pre-existing condition. You were born with a preexisting condition. And if your parents didn’t have insurance, you may not even live long enough to get denied because of a preexisting condition.
If your baby is going to die and it doesn’t have to, it shouldn’t matter how much money you make. I think that’s something that whether you’re a Republican or a Democrat or something else, we all agree on that, right?
Kimmel said that regardless of party, “We need to make sure that the people who are supposed to represent us, people who are meeting about this right now in Washington, understand that very clearly.”
The GOP’s Obamacare repeal effort appeared to be hanging by a thread before Kimmel’s monologue aired. Republicans reportedly see this week as their last opportunity to pass a version of AHCA, and on Monday several Trump officials claimed they’re close to the 216 votes needed to pass the bill. However, by the Wall Street Journal’s count, they can only afford a few defections:
At least 19 House Republicans are currently opposed to the bill, with at least 17 undecided, according to a Wall Street Journal survey of the lawmakers. The GOP can only afford to lose about 22 votes, depending on absences.
On Monday afternoon, Representative Billy Long, a Trump ally who supported a previous version of the bill, said he’ll vote against the current measure, citing its lack of protections for people with preexisting conditions.
“I have always stated that one of the few good things about Obamacare is that people with preexisting conditions would be covered,” Long said. “The MacArthur amendment strips away any guarantee that preexisting conditions would be covered and affordable.”
Around 2 million people watch Kimmel’s show each night, and his name was trending on Twitter following his moving monologue about his son. Kimmel succinctly explained what tinkering with protections for preexisting conditions could do to an innocent baby, and pointed out that’s what the GOP is trying to do this week. What wavering House Republican is going to decide now is the time to come out in favor of the bill? ||||| Says of the GOP health care proposal, "pre-existing conditions are in the bill."
President Donald Trump remains hopeful that he can deliver on his promise to repeal the Affordable Care Act and replace it with a plan from the Republican Party.
In an interview with CBS’ Face the Nation, Trump argued that the GOP’s health care plan covers pre-existing conditions, despite what news reports have said.
"Pre-existing conditions are in the bill," Trump said April 30. "And I just watched another network than yours, and they were saying, ‘Pre-existing is not covered.’ Pre-existing conditions are in the bill. And I mandate it. I said, ‘Has to be.’ "
Trump was more than likely referring to the most recent version of the GOP health care overhaul, an amendment by U.S. Rep. Tom MacArthur, R-N.J., introduced in late April.
"This bill is much different than it was a little while ago, okay? This bill has evolved," Trump said. "But we have now pre-existing conditions in the bill. We've set up a pool for the pre-existing conditions so that the premiums can be allowed to fall."
When CBS’ John Dickerson pressed Trump on whether everyone with pre-existing conditions would be covered, Trump said, "We actually have a clause that guarantees."
White House spokesman Sean Spicer said at the May 1 news briefing that Trump was referring to the MacArthur amendment and that Trump is ensuring that "coverage of pre-existing conditions is at the core" of the legislation.
But the reality of how the bill addresses pre-existing conditions -- which are health problems patients have before new insurance kicks in -- is much more complicated than Trump makes it sound.
What the amendment says on pre-existing conditions
In March, the Republican’s American Health Care Act died without a vote when Republicans couldn’t agree on the bill designed to replace the Affordable Care Act. Under the new bill, called ACHA, insurers had to cover pre-existing conditions, but they could have charged more for people who are recently uninsured.
The MacArthur amendment would allow states to obtain waivers to some requirements of the Affordable Care Act, including the "essential health benefits" provision that requires maternity care or mental health services.
The amendment has language that appears to protect those with pre-existing conditions stating that "nothing in this Act shall be construed as permitting insurers to limit access to health coverage for individuals with pre-existing conditions."
But experts say other parts of the amendment suggest that those with pre-existing conditions could struggle to maintain affordable health insurance.
The amendment permits insurers to set premiums based on the "health status" of an individual by looking at their current and past health status and make predictions about how much an individual will use medical care in the future, said Linda Blumberg, senior fellow in the Health Policy Center at the Urban Institute.
That’s where pre-existing conditions could come into play, because it would mean that the costs rise for consumers who are sicker, said Timothy Jost, Washington and Lee University School of Law emeritus professor.
"Health status underwriting is literally charging a higher (possibly much, unaffordably, higher) premium to people with pre-existing conditions," Jost said. "Under the MacArthur amendment, they could not be refused coverage, but insurers could impose high enough premiums that coverage would be unaffordable."
The amendment says that the waiver would allow states to set up a high-risk pool or participate in a new federal invisible risk-sharing program to help states reimburse insurers for covering high-risk consumers.
"No state may obtain a waiver for health status unless it has taken these efforts to protect those who might be affected," stated a MacArthur press release. "In states with a waiver, individuals who maintain continuous coverage could not be rated based on health status."
That means people who stay insured without any lapses can’t be charged more by insurance companies if they get sick.
But experts said that many low-income people aren’t able to stay covered without breaks, and that questions remain about the effectiveness of the high-risk pools.
The American Medical Association, which opposes the amendment, said in a statement that it "could make coverage unaffordable for people with pre-existing conditions." The AMA raised questions about whether the high-risk pool would be "sufficient to provide for affordable health insurance or prevent discrimination against individuals with certain high-cost medical conditions."
Our ruling
Trump said of the GOP health care amendment, "Pre-existing conditions are in the bill."
The amendment says that health insurers can’t limit access to coverage for people with pre-existing conditions, but that insurers can charge people more if states agree. In some states, health insurers would be able to charge sicker people more. And experts warn that high-risk pools -- the mechanisms meant to keep premiums lower for sick people -- might not be effective.
Overall, the latest proposal seems to weaken existing protections for people with pre-existing conditions, not strengthen them.
We rate the statement Mostly False. ||||| President Trump says the revised House GOP health care bill would protect people with pre-existing conditions, but a multitude of experts and advocates beg to differ.
The latest change to the bill, called the MacArthur amendment after its author, Republican House member Tom MacArthur, would allow states to opt out of several key Obamacare insurance regulations. Two of these are critical for protecting those with health care issues obtain policies that are affordable and cover their treatments.
Related: Trump: GOP health care bill 'guarantees' coverage for pre-existing conditions
Obamacare revolutionized health insurance for people with pre-existing conditions who buy policies on the individual market. Prior to the health reform law, consumers with a medical issue -- even if it were years earlier and completely resolved -- could be denied coverage or charged much more in premiums.
The MacArthur amendment keeps Obamacare's guaranteed access clause, which requires insurers to provide policies to those with pre-existing conditions. MacArthur and other politicians cite this part of the bill to say that the sick and formerly sick would continue to be protected.
But the bill would allow states to apply for waivers that could greatly change the cost and quality of their coverage.
States could opt out of the law's essential health benefits measure, which requires insurers to cover 10 main benefits, including hospitalization, prescription drugs and other services.
Insurers in those states would likely offer skimpier policies that don't cover all the treatments and medications that those with medical issues need. Carriers would be hesitant to offer more comprehensive policies because they would attract consumers with costly conditions.
Related: First 100 Days: What Trump has done to Obamacare
The amendment would also allow states to change Obamacare's community rating provision, which bans insurers from charging enrollees more based on their medical history. Under the revised bill, insurers could charge higher premiums to those with pre-existing conditions who let their coverage lapse.
States that apply for this waiver would have to set up high-risk pools or other programs aimed at minimizing insurers' exposure to costly policyholders. This could offset some of the price hikes carriers would levy on those with pre-existing conditions.
But experts say the $130 billion that Republicans would set aside to fund these programs through 2026 is woefully inadequate. High risk pools existed before Obamacare, but most were underfunded, charged policyholders high premiums and had waiting lists.
Health policy experts, consumer advocates, provider groups and even some Republican lawmakers have voiced concerns about how the amendment would affect those with medical issues. Several have come out strongly opposing the revised bill.
Related: Republicans continue to work on health care. They can't afford not to.
"The individuals and families we represent cannot go back to a time when people with pre-existing conditions could be denied coverage or forced to choose between purchasing basic necessities and affording their health care coverage," said a coalition of 10 patient advocacy groups, including the American Diabetes Association, the American Cancer Society and the National MS Society.
Also, many lower-income people could get caught by this amendment if the bill becomes law, noted Sabrina Corlette, research professor at Georgetown University's Health Policy Institute. A Congressional Budget Office analysis of an earlier version of the bill found 24 million more people would be uninsured under the GOP legislation, and experts say that number could grow as a result of the recent changes.
Related: AMA, AARP oppose latest Obamacare repeal effort
These uninsured folks could encounter higher premiums when they try to return because insurers would be allowed to set rates based on their health backgrounds.
"If they try to go back in, they will face insurers that could price them out of the market if they have a pre-existing condition," she said. |||||
What is a shorter version of the above article? | – The Republicans' new attempt to repeal and replace ObamaCare is suddenly in serious trouble, reports CNN, with the White House engaging in a furious push to win over wavering lawmakers. One sticking point is coverage of pre-existing conditions, with one blogger arguing that Jimmy Kimmel's emotional plea on Monday night's show may have effectively killed the GOP bill. Here's what's happening, much of which revolves around an amendment offered by Republican Tom MacArthur of New Jersey: President Trump insists the GOP bill will cover people with pre-existing conditions in its final form. In fact, "it will be every bit as good on pre-existing conditions as ObamaCare," he told Bloomberg, echoing comments he made over the weekend. He's basing that on the MacArthur amendment, which states explicitly that "nothing in this act shall be construed as permitting health insurance issuers to limit access to health coverage for individuals with pre-existing conditions.” (The full amendment is here.) But that's not true, say critics, because the amendment allows states to grant waivers to insurers to set rates based on people's "health status." The New York Times explains it this way: "Rates for a person with cancer, diabetes or multiple sclerosis could be far higher than the standard rate, effectively pricing the sick out of the market without technically blocking coverage, critics say." The American Medical Association says that "health status underwriting could effectively make coverage completely unaffordable to people with pre-existing conditions." PolitiFact digs into the nuances and concludes that Trump's statement is "mostly false." (CNN has more particulars on the waivers.) Politico takes note of a key GOP defector, Rep. Billy Long of Missouri. He's voting no, explaining that he thinks coverage of pre-existing conditions is one of the few things ObamaCare got right. "The MacArthur amendment strips away any guarantee that pre-existing conditions would be covered and affordable." Defenders of the waivers say they give states necessary flexibility that will result in lower rates. "People with pre-existing conditions today can’t access health care because the premiums and deductibles are so high," says Rep. Richard Hudson of North Carolina, per the Wall Street Journal. A National Review columnist also backs them. The vote count is razor-thin at the moment, and Margaret Hartmann at New York suggests that Kimmel's monologue may have doomed the GOP bill. Kimmel spoke of his infant's heart condition and the need for insurance to be available to people with pre-existing conditions, and he urged people to make sure lawmakers know that. He's got an audience of 2 million, and the clip is going viral. "What wavering House Republican is going to decide now is the time to come out in favor of the bill?" she writes. | multi_news_1_0_0 |
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Summarize this article:
As Mahmoud Ahmadinejad prepares to speak to the United Nations General Assembly in New York on Wednesday, an electronic billboard in Times Square and subway placards around the city will remind the Iranian president and U.N. delegates of an American who has been missing in Iran for more than five years.
"I'm trying to make the public realize that my husband is the second-longest held hostage in American history," said Christine Levinson, husband of former FBI agent Robert Levinson. "It's been five and a half years since he disappeared on Kish Island and two years since we received a video from his captors . . . and we still have no information about Bob since the day he disappeared."
"This week, with the UN General Assembly in New York," Christine Levinson told ABC News, "we are trying to get the whole world's attention. I am hoping we will finally be able to get him home."
Robert Levinson, a father of seven and grandfather of two, began working as a private detective after leaving the FBI. He disappeared in March 9, 2007 while on a business trip to the Iranian resort island of Kish. U.S. officials believe he is being held by unknown captors in Southwest Asia.
Five months after his disappearance, against the advice of the U.S. government, Christine Levinson and her son traveled to Tehran to conduct their own investigation, but the trip yielded no results.
The Levinson family received a so-called "proof of life" video in late 2010 showing Levinson, who suffers from diabetes and high blood pressure, in deteriorating health. Levinson, who was 62 at the time, addressed Christine as "my beautiful, my loving, my loyal wife" and referred to his 33 years of service to the federal government before pleading for help from U.S. authorities.
Christine Levinson is now appealing directly to Ahmadinejad, who is under the international spotlight as he prefers to give his final speech to the U.N. as Iranian president. He leaves office next year. "In the past he has said that he will investigate and he will have his people investigate," Levinson told CNN. "He has promised to help us. So we need to get him in touch with whoever can help us get the job done and get Bob home."
Pictures of Levinson began appearing on subway placards in Midtown Manhattan last week. The signs, and a Times Square billboard, feature a picture of Levinson next to the word "Missing" and ask United Nations delegates to "encourage the Islamic Republic of Iran to work with the U.S. to bring Bob home."
This year the FBI offered a $1 million reward for information. The case has frustrated investigators, whose diplomatic strategies have failed.
"We ask ourselves how is it possible that someone -- especially someone 6'4? and (then) 225 pounds -- disappears without a trace," reads a statement from the Levinsons on the family's website.
Iranian representatives did not respond immediately to a request for comment.
Click Here for the Blotter Homepage. ||||| Story highlights Ahmadinejad sits down for an interview with CNN's Piers Morgan
During the sometimes contentious conversation, he talks about the Holocaust, Syria
Ahmadinejad also discusses an anti-Islam film and Osama bin Laden
Iran's president is to address the U.N. General Assembly on Wednesday
Iranian President Mahmoud Ahmadinejad made clear what he meant when he said Israel should be "wiped off" the map and touched on everything from the Holocaust to homosexuality in a wide-ranging interview that aired Monday on CNN's "Piers Morgan Tonight."
The president, speaking through a translator, also said what his country would do if attacked by Israel, and he slammed an anti-Islam film that has triggered protests in the Muslim world.
"If a group comes and occupies the United States of America, destroys homes while women and children are in those homes, incarcerate the youth of America, impose five different wars on many neighbors, and always threaten others, what would you do? What would you say? Would you help it? ... Or would you help the people of the United States?" Ahmadinejad asked in response to whether Israel should be "wiped off" the face of the map, as he once said.
"So when we say 'to be wiped,' we say for occupation to be wiped off from this world. For war-seeking to (be) wiped off and eradicated, the killing of women and children to be eradicated. And we propose the way. We propose the path. The path is to recognize the right of the Palestinians to self-governance."
When asked whether he believes in a two-state solution to the Israeli-Palestinian conflict, Ahmadinejad declined to comment.
JUST WATCHED Ahmadinejad: Iran has right to defend itself Replay More Videos ... MUST WATCH Ahmadinejad: Iran has right to defend itself 01:39
JUST WATCHED Ahmadinejad: 'Very close' with Iran Jews Replay More Videos ... MUST WATCH Ahmadinejad: 'Very close' with Iran Jews 01:10
"I cannot express an opinion. That is their prerogative," Ahmadinejad said. "But the people of Palestine must be allowed by everyone, and helped by everyone, to allow them, to give them the right to choose for themselves."
In New York this week to visit the United Nations, Ahmadinejad spoke at a meeting on the rule of law Monday and is scheduled to address the U.N. General Assembly on Wednesday.
U.N. Secretary-General Ban Ki-moon met with the Iranian president over the weekend and warned him of the "potentially harmful consequences of inflammatory rhetoric," according to a U.N. statement.
During his speech Monday, Ahmadinejad accused "some members of the Security Council with veto rights" of having "chosen silence with regard to the nuclear warheads of a fake regime, while at the same time they impede scientific progress of other nations."
Though he didn't name the countries, he was clearly talking about the United States, Israel and his own country.
Some world powers, particularly Western nations, suspect that Iran is seeking to build nuclear weapons. Tehran insists its nuclear program is for peaceful purposes.
When asked by CNN's Morgan what Iran would do if Israel were to attack it, Ahmadinejad said, "Any nation has the right and will indeed defend herself."
"But my question is this: Why should the world be managed in such a way that an individual can allow himself to threaten a rich and deeply rooted historical, ancient country such as Iran? A great country, such as Iran, based on an excuse of his own fabrication. ... Another country can say, 'I am guessing that country B is doing activity X, therefore I will attack that country' ... can this be ... a successful formula for the management of the world?"
Again there, the president was likely referring to Iran's disputed nuclear program.
Asked whether he feared a war or military conflict with Israel was imminent, Ahmadinejad said: "The Zionists are very much, very adventuresome, very much seeking to fabricate things, and I think they see themselves at the end of the line and I do firmly believe that they seek to create new opportunities for themselves and their adventurous behaviors."
Among other topics the president touched on in the interview taped in New York over the weekend were:
Anti-Islam film
Ahmadinejad denounced the film, "Innocence of Muslims," that portrays the Prophet Mohammed as a womanizer, child molester and killer. The online video has led to a wave of global unrest.
"Fundamentally, first of all, any action that is provocative, offends the religious thoughts and feelings of any people, we condemn," he said.
"Likewise, we condemn any type of extremism. Of course, what took place was ugly. Offending the Holy Prophet is quite ugly. This has very little or nothing to do with freedom and freedom of speech. This is the weakness of and the abuse of freedom, and in many places it is a crime. It shouldn't take place, and I do hope the day will come in which politicians will not seek to offend those whom others hold holy," Ahmadinejad said.
"We also believe that this must also be resolved in a humane atmosphere, in a participatory environment, and we do not like anyone losing their lives or being killed for any reason, anywhere in the world."
The privately produced film sparked protests against the United States, where it was made. While most of the demonstrations have been peaceful, some were marred by violence that has left more than two dozen people dead -- among them U.S. Ambassador to Libya Chris Stevens and three other Americans killed in an attack on the consulate in Benghazi, Libya, that reportedly followed a demonstration against the film.
When asked by Morgan whether he thought protesters should stop threatening U.S. staff abroad, Ahmadinejad said he cannot say what other people or nations should do, but that he believes "extremism gives birth to following and subsequent extremists."
Syria
A long-time supporter of embattled Syrian President Bashar al-Assad, Ahmadinejad told CNN's Morgan the crisis in Syria must be resolved through dialogue, and without outside interference.
He condemned the violence, which has left more than 26,000 people dead since March 2011, according to opposition activists.
"We must all say enough of this violence, right now," Ahmadinejad said, adding that he is working to organize a group to bring the two sides together.
"We do believe that freedom, the right to choose, the right to vote, respect and justice is the fundamental right of all people. All people must obtain these rights. No one has the right to restrict a people and nation, but we believe as a friend of nations, we must help the nations around the world to obtain these rights through peaceful paths, though peaceful actions."
The Holocaust
The conversation was contentious at times, particularly when the topic turned to the Nazi Germany extermination of the Jews last century. Ahmadinejad has long questioned the existence of the Holocaust.
"I pass no judgment about historic events. I defend the human freedoms. Whatever event has taken place throughout history, or hasn't taken place, I cannot judge that. Why should I judge that? I say researchers and scholars must be free to conduct research and analysis about any historical event," the Iranian president said.
Homosexuality
"I'm sorry. Let me ask you this. Do you believe that anyone is giving birth through homosexuality? Homosexuality ceases procreation. Who has said that if you like or believe in doing something ugly, and others do not accept your behavior, that they're denying your freedom?" he asked Morgan.
"Proper education must be given ... the education system must be revamped. The political system must be revamped. And these must be also reformed, revamped along the way. But if you, if a group recognizes an ugly behavior or ugly deed as legitimate, you must not expect other countries or other groups to give it the same recognition."
Jews
When asked how he would feel if one of his children dated a Jew, Ahmadinejad replied, "I would have to see who that Jewish man or woman would be. I see love amongst people as completely acceptable. There are many Jews living in Iran with whom we are very close. There are ... some Muslims that marry into Jewish families or marry Christians."
"I -- we have no such problems," he added.
"Of course, I think none of us should represent the whole population of the United States, but we believe that color, religion, native tongue, ethnic background shouldn't create differences or distances between people, nor should it be the sole reason to bring people closer together. It has always been like this."
Osama bin Laden
Ahmadinejad also discussed his reaction to Osama bin Laden's death last year by American Navy Seals under President Barack Obama.
"I would have been happier to see a transparent trial, a formal trial, and find out the root causes of all of the events of the last few years," the Iranian president said. ||||| | – Mahmoud Ahmadinejad is in town, and the wife of a former FBI agent taken hostage in Iran in 2007 is taking advantage of that fact. The Iranian president "has said that he will investigate and he will have his people investigate," says Christine Levinson, whose husband, Robert, is believed to be held in Southwest Asia. "So we need to get him in touch with whoever can help us get the job done and get Bob home." With the UN General Assembly meeting in New York, Levinson has put up a billboard and subway signs to remind Ahmadinejad and UN delegates of her husband, ABC News reports. "I'm trying to make the public realize that my husband is the second-longest held hostage in American history," she says. Meanwhile, Ahmadinejad—who will address the General Assembly tomorrow—used his visit as an opportunity to sit down with Piers Morgan on CNN last night and revisit his favorite topics, including bashing Israel, denouncing homosexuality, and questioning the existence of the Holocaust, among other things. On the topic of homosexuality: "I'm sorry. Let me ask you this. Do you believe that anyone is giving birth through homosexuality? Homosexuality ceases procreation. Who has said that if you like or believe in doing something ugly, and others do not accept your behavior, that they're denying your freedom?" Ahmadinejad said. "If you, if a group recognizes an ugly behavior or ugly deed as legitimate, you must not expect other countries or other groups to give it the same recognition." Click for more from the interview. | multi_news_1_0_0 |
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FILE - In this file photo dated Tuesday, Oct. 3, 2017, Zimbabwe's President Robert Mugabe, during his meeting with South African President Jacob Zuma, at the Presidential Guesthouse in Pretoria, South... (Associated Press)
FILE - In this file photo dated Tuesday, Oct. 3, 2017, Zimbabwe's President Robert Mugabe, during his meeting with South African President Jacob Zuma, at the Presidential Guesthouse in Pretoria, South Africa. Zimbabwe President Robert Mugabe has long faced United States sanctions over his government's... (Associated Press)
FILE - In this file photo dated Tuesday, Oct. 3, 2017, Zimbabwe's President Robert Mugabe, during his meeting with South African President Jacob Zuma, at the Presidential Guesthouse in Pretoria, South Africa. Zimbabwe President Robert Mugabe has long faced United States sanctions over his government's... (Associated Press) FILE - In this file photo dated Tuesday, Oct. 3, 2017, Zimbabwe's President Robert Mugabe, during his meeting with South African President Jacob Zuma, at the Presidential Guesthouse in Pretoria, South... (Associated Press)
GENEVA (AP) — Shock and condemnation continued Saturday after Zimbabwe President Robert Mugabe was named a "goodwill ambassador" for the World Health Organization by the agency's first African leader.
The 93-year-old Mugabe, the world's oldest head of state, has long been criticized at home for going overseas for medical treatment as Zimbabwe's once-prosperous economy falls apart. Mugabe also faces United States sanctions over his government's human rights abuses.
"The decision to appoint Robert Mugabe as a WHO goodwill ambassador is deeply disappointing and wrong," said Dr. Jeremy Farrar, director of the Wellcome Trust, a major British charitable foundation. "Robert Mugabe fails in every way to represent the values WHO should stand for."
Ireland's health minister, Simon Harris, called the appointment "offensive, bizarre." ''Not the Onion," tweeted the head of Human Rights Watch, Kenneth Roth, in a reference to the satirical news site.
With Mugabe on hand, WHO director-general Tedros Ghebreyesus of Ethiopia announced the appointment at a conference in Uruguay this week on non-communicable diseases.
Tedros, who became WHO's first African director-general this year, said Mugabe could use the role "to influence his peers in his region" on the issue. He described Zimbabwe as "a country that places universal health coverage and health promotion at the center of its policies." A WHO spokeswoman confirmed the comments to The Associated Press.
Two dozen organizations — including the World Heart Federation, Action Against Smoking and Cancer Research U.K. — released a statement slamming the appointment, saying health officials were "shocked and deeply concerned" and citing his "long track record of human rights violations."
The groups said they had raised their concerns with Tedros on the sidelines of the conference, to no avail. U.N. agencies typically choose celebrities as ambassadors to draw attention to issues of concern, but they hold little actual power.
Zimbabwe's government has not commented, but the state-run Zimbabwe Herald newspaper called the appointment a "new feather in president's cap."
The southern African nation once was known as the region's prosperous breadbasket. But in 2008, the charity Physicians for Human Rights released a report documenting failures in Zimbabwe's health system, saying Mugabe's policies had led to a man-made crisis.
"The government of Robert Mugabe presided over the dramatic reversal of its population's access to food, clean water, basic sanitation and health care," the group concluded. Mugabe's policies led directly to "the shuttering of hospitals and clinics, the closing of its medical school and the beatings of health workers."
The 93-year-old Mugabe, who has led Zimbabwe since independence in 1980, has come under criticism at home for his frequent overseas travels that have cost impoverished Zimbabwe millions of dollars. His repeated visits to Singapore have heightened concerns over his health, even as he pursues re-election next year.
The U.S. in 2003 imposed targeted sanctions, a travel ban and an asset freeze against Mugabe and close associates, citing his government's rights abuses and evidence of electoral fraud. ||||| Image copyright AFP/Getty Image caption Critics say health services have collapsed under Mr Mugabe's rule
The choice of Zimbabwe President Robert Mugabe as a World Health Organization (WHO) goodwill ambassador has been criticised by several organisations including the British government.
It described his selection as "surprising and disappointing" given his country's rights record, and warned it could overshadow the WHO's work.
The opposition in Zimbabwe and campaign groups also criticised the move.
The WHO head said he was "rethinking his approach in light of WHO values".
Dr Tedros Adhanom Ghebreyesus had previously praised Zimbabwe for its commitment to public health.
He said it was a country that "places universal health coverage and health promotion at the centre of its policies to provide health care to all".
Mr Mugabe's appointment as a "goodwill ambassador" to help tackle non-communicable diseases has attracted a chorus of criticism.
Image copyright Getty Images Image caption Critics have long argued that Zimbabwe's health service is not meeting the needs of patients
The British government said it was all the more surprising given US and EU sanctions against him.
"We have registered our concerns" with the director general, a spokesman said.
"Although Mugabe will not have an executive role, his appointment risks overshadowing the work undertaken globally by the WHO on non-communicable diseases."
Zimbabwe's leader has been frequently taken to task over human rights abuses by the European Union and the US.
Critics say Zimbabwe's health care system has collapsed, with staff often going without pay while medicines are in short supply.
Dr Tedros, who is Ethiopian, is the first African to lead the WHO. He was elected in May with a mandate to tackle perceived politicisation in the organisation.
'Basic necessities lacking'
US-based campaign group Human Rights Watch (HRW) said it was an embarrassment to give the ambassador role to Mr Mugabe, because his "utter mismanagement of the economy has devastated health services".
Image copyright Getty Images Image caption Critics of the president say that Zimbabwe's health care system is in a shambolic state
HRW's Kenneth Roth said Mr Mugabe's appointment was a cause for concern because the president and some of his officials travel abroad for treatment.
"When you go to Zimbabwean hospitals, they lack the most basic necessities," he said.
Zimbabwe's main MDC opposition party also denounced the WHO move.
"The Zimbabwe health delivery system is in a shambolic state, it is an insult," spokesman Obert Gutu told AFP.
"Mugabe trashed our health delivery system... he allowed our public hospitals to collapse."
Other groups who have criticised Mr Mugabe's appointment include the Wellcome Trust, the NCD Alliance, UN Watch, the World Heart Federation and Action Against Smoking.
President Mugabe heard about his appointment while attending a conference held by the WHO, a UN agency, on non-communicable diseases (NCDs) in Montevideo, Uruguay.
He told delegates his country had adopted several strategies to combat the challenges presented by such diseases, which the WHO says kill about 40 million people a year and include cancers, respiratory diseases and diabetes.
"Zimbabwe has developed a national NCD policy, a palliative care policy, and has engaged United Nations agencies working in the country, to assist in the development of a cervical cancer prevention and control strategy," Mr Mugabe was reported by the state-run Zimbabwe Herald newspaper as saying.
But the president admitted that Zimbabwe was similar to other developing countries in that it was "hamstrung by a lack of adequate resources for executing programmes aimed at reducing NCDs and other health conditions afflicting the people".
Image copyright AFP Image caption Medicine is often in short supply at Zimbabwe's hospitals, critics say
Stardust lacking
Imogen Foulkes, BBC News, Geneva
The UN has a bit of thing for goodwill ambassadors, especially famous ones.
Angelina Jolie, as ambassador for the UN Refugee Agency, was regularly pictured comforting displaced families in over-crowded camps.
Swiss tennis star Roger Federer visits aid projects in Africa for Unicef and plays charity matches to raise money.
Further back in time, film star and Unicef goodwill ambassador Audrey Hepburn visited disaster zones and graced gala dinners where her glittering presence was an encouragement to donors.
The publicity does attract support for relief efforts.
But it is hard to imagine 93-year-old Robert Mugabe fulfilling a similar remit.
Will he provide comfort in WHO field clinics in conflict zones? Would one of his suit jackets fetch a high price at auction? Would the presence of a man who is widely accused of human rights abuses encourage more $10,000-a-plate attendees at a gala ball?
Somehow it just does not seem likely, which begs the question, what exactly is Mr Mugabe going to do in his new role? The World Health Organization has not made this at all clear. ||||| This article is over 1 year old
Decision will be re-evaluated after appointment of Zimbabwean despot provokes global anger
The head of the World Health Organization has said he is rethinking his decision to name Zimbabwe’s president, Robert Mugabe, as a goodwill ambassador after the move provoked global outrage.
Tedros Adhanom Ghebreyesus, the director general of the UN health agency, had this week asked Zimbabwe’s 93-year-old authoritarian leader to serve in the role to help tackle non-communicable diseases such as heart attacks, strokes and asthma across Africa.
The decision triggered confusion and anger among WHO member states and activists who noted that Zimbabwe’s health care system, like many of its public services, has collapsed under Mugabe’s regime.
“I’m listening. I hear your concerns. Rethinking the approach in light of WHO values. I will issue a statement as soon as possible,” Tedros, a former Ethiopian health minister, tweeted on Saturday night.
Earlier in the day the UK government criticised the WHO’s decision as “surprising and disappointing”. A Downing Street spokesman said British diplomats had raised serious concerns with Tedros.
A UK government spokesman said the WHO decision was at odds with US and EU sanctions against Mugabe. “Although Mugabe will not have an executive role, his appointment risks overshadowing the work undertaken globally by the WHO on non-communicable diseases,” he said.
The US state department said: “This appointment clearly contradicts the United Nations ideals of respect for human rights and human dignity.”
And the Canadian prime minister, Justin Trudeau, said he thought Mugabe’s appointment “was a bad April Fool’s joke”.
'The president sleeps with one eye open': Mugabe reshuffles as power games begin Read more
Mugabe was in Uruguay for the announcement by Tedros, the former Ethiopian health minister who was elected as the WHO’s first director general from Africa this year after defeating the British candidate, David Nabarro, in three close rounds of voting.
Tedros said he was “honoured” to announce that Mugabe had agreed to serve as a goodwill ambassador on non-communicable diseases for Africa. He hailed Zimbabwe as “a country that places universal health coverage and health promotion at the centre of its policies to provide healthcare to all”.
The choice of Mugabe for the role has also angered opposition parties in Zimbabwe and human rights campaigners who accuse the leader of violent repression, election rigging and presiding over the country’s economic ruin.
Iain Levine, a programme director at Human Rights Watch, tweeted:
Iain Levine (@iainlevine) Given Mugabe's appalling human rights record, calling him a Goodwill Ambassador for anything embarrasses @WHO and @DrTedros https://t.co/fsqDSraWc9
The main opposition party in Zimbabwe, MDC, described the appointment as “laughable”. “The Zimbabwe health delivery system is in a shambolic state. It is an insult,” the spokesman Obert Gutu said.
“Mugabe trashed our health delivery system. He and his family go outside of the country for treatment in Singapore after he allowed our public hospitals to collapse.”
Grace Mugabe denies plotting to poison rival for Zimbabwe presidency Read more
Mugabe is in increasingly fragile health and makes regular trips abroad for medical treatment.
Zimbabwe’s state-run Herald newspaper reported the appointment under the headline “New feather in President’s cap”. It said Mugabe had told the WHO conference in Montevideo on Wednesday that Zimbabwe had developed a national policy on non-communicable diseases, and that he had called for more funds for developing nations.
According to the WHO, non-communicable diseases are by far the world’s leading cause of death, killing more than 36 million people a year.
UN agencies such as the WHO, UNHCR and Unesco all appoint goodwill ambassadors to highlight specific causes and often to draw publicity.
Unicef ambassadors include the singer Katy Perry and the tennis player Serena Williams. |||||
What is a one-paragraph summary of the above article? | – The World Health Organization has chosen a new "goodwill ambassador" whose human rights abuses have left him with very little goodwill internationally: Robert Mugabe. The 93-year-old president of Zimbabwe was chosen by new WHO chief Tedros Adhanom Ghebreyesus to help fight non-communicable diseases like strokes and asthma across Africa, the BBC reports. The Guardian reports that the appointment was condemned by multiple governments and human rights groups, which pointed out that health care in Zimbabwe has collapsed under Mugabe's regime—and that Mugabe has been regularly leaving the country to seek medical treatment elsewhere. "The decision to appoint Robert Mugabe as a WHO goodwill ambassador is deeply disappointing and wrong," says Dr. Jeremy Farrar of the Wellcome Trust, a British charitable foundation, per the AP. "Robert Mugabe fails in every way to represent the values WHO should stand for." A group of around two dozen other health organizations said they were "shocked and deeply concerned" by the appointment. A spokesman for Zimbabwean opposition party MDC described the appointment as "laughable." "Mugabe trashed our health delivery system," he said. | multi_news_1_0_0 |
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Article:
Boy, 5, accidentally shoots brother, 7, in northeast Houston
HOUSTON -- A 7-year-old boy was accidentally shot in the back by his younger brother in northeast Houston Tuesday evening.
Officials said they were called to a house in the 5600 block of Lyons around 9 p.m. Tuesday.
Police said after the mother had given her five and seven-year-old sons a bath, they started to play. That’s when the 5-year-old managed to find a .22-caliber rifle and accidentally shoot his brother.
Officials said the bullet went straight through the boy’s back. He was taken to the hospital with non-life threatening injuries. He is expected to be OK.
Police said the gun appeared to look old, almost as if it did not work.
Officers are now investigating whether the gun was properly secured.
At this time no charges have been filed. ||||| Page 1 of 1
The shooting took place at a home along Lyons and Sam Wilson on Tuesday evening. (Mike Glenn/Chronicle)
An east Houston boy is expected to recover after his younger brother shot him inside their home, Houston police said.
The boy, 7, was shot with a .22 rifle about 9 p.m. on Tuesday at the family's home along Lyons and Sam Wilson. He was taken to Memorial Hermann Hospital. Police at the scene said the child's wounds did not appear to be life-threatening.
HPD officials said the 7-year-old and his brother were in the bathtub when their mother stepped away for a moment. The younger boy then got out of the tub and found the rifle — an old and rusty bolt-action .22.
The younger boy was apparently playing with the rifle when it fired, striking his brother in the lower back area, police said.
Their father returned home after the shooting and is being questioned. Depending on the investigation, both parents may face charges for leaving the rifle unsecured, police said. |||||
In short:
– Another case of a young child shooting a young sibling: Police say an east Houston mother left her 5- and 7-year-old sons alone either during or after giving them a bath last night (reports conflict). The younger child apparently retrieved a .22 rifle in her absence and began playing with it. The gun went off, sending a bullet through the 7-year-old's back; the injuries are not life-threatening. Police told KHOU that the gun appeared so old that one might think it was inoperable; the Houston Chronicle echos that, calling it an "old and rusty bolt-action .22." No charges have been filed, but the Chronicle reports that charges could come if the gun was not properly secured. Two similar shootings have happened in the last 10 days; click for those stories.
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"American Teens Are Exercising More, Watching Less TV, And Eating More Vegetables" Share:
CREDIT: Shutterstock
American teenagers are eating more vegetables, getting more exercise, watching less television, and eating fewer portions of junk food that’s high in sugar, according to a new study by the University of Massachusetts in Boston.
Researchers collected data on 35,000 children aged 11 to 16 from 2001 to 2009. They found that average Body Mass Index (BMI) for the teens dropped between 2005 and 2009, and that over the course of the total decade, consumption of fruits and vegetables nearly doubled from two to four days per week to five or six days per week. Younger Americans also ate breakfast more times per week over this period, while their weekly sugary drink consumption fell by 20 percent. The number of days they exercised for at least 60 minutes went up significantly from 4.33 days per week to 4.53 days per week.
The study is the latest in a series of encouraging reports suggesting that Americans are beginning to take better care of their physical health. “It’s only recently, in the past decade, that some studies have begun to see some leveling off [in behavior that causes obesity],” said lead study author Ronald Iannotti.
In June, the Centers for Disease Control (CDC) found that adult obesity rates had risen by a mere 0.2 percent between 2011 and 2012 — a significant decrease from previous years. Other surveys suggest parents may be promoting similar behaviors in their children. For instance, the obesity rate for low-income U.S. children fell significantly for the first time in history between 2008 and 2011.
These lifestyle changes may be a consequence of changing attitudes about personal health and obesity. But the available data suggests that regulatory changes in nutrition and physical education programs may be driving the positive trend, too. According to the CDC, almost half of all public school districts had banned junk food in vending machines as of last month — a trend that will only continue as new rules go into effect limiting the amount of salt, sugar, and fat that can be used in school cafeterias and vending machines beginning in the 2014-2015 school year. ||||| Photo
Teenagers are exercising more, consuming less sugar and eating more fruits and vegetables, a trend that may be contributing to a leveling off of obesity rates, a new study shows.
The findings suggest that aggressive anti-obesity messages aimed at children may be starting to make a difference, albeit a small one. The study was published in the journal Pediatrics on Monday.
Still, most teenagers were falling short of federal recommendations, which call for children to get at least an hour of physical activity daily, a central message of Michelle Obama’s signature “Let’s Move” campaign. The new data showed that most children engaged in an hour of exercise fewer than five days a week and spent more than two hours a day watching television, chatting online and playing video games.
The numbers also revealed something of an age and racial divide. Younger children had the highest levels of physical activity and fruit and vegetable consumption. But as children got older, the frequency of eating junk foods and engaging in sedentary behaviors crept up, along with average body mass index, a crude measure of obesity.
Black and Hispanic adolescents lagged behind whites on almost every measure of progress, even after the researchers tried to take into account the influence of socioeconomic factors.
“In some ways you can interpret what we found positively by saying we’re beginning to bend the curve, and hopefully we’ll start seeing a downward trend in obesity,” said Dr. Ronald J. Iannotti, a study author and chair of the department of exercise and health sciences at the University of Massachusetts Boston. “But there’s large room for improvement.”
The study analyzed data from a national survey of tens of thousands of schoolchildren in grades 6 through 10, which was carried out once every four years from roughly 2001 to 2010.
Childhood obesity rates, which have more than doubled since 1980, rose slightly between 2001 and 2006, then leveled off by 2010, at roughly 13 percent. The proportion of those who were overweight also plateaued at around 17 percent.
Obesity tends to follow children into adulthood, raising the risk of heart disease and cancer as well as Type 2 diabetes, a disease that has also risen sharply among children.
In the past year, other studies have hinted at improvements in the obesity rate among younger children, with some even showing a decline in some cities. But little was known about the extent to which physical and dietary behaviors might have played a role.
The new study found that at the same time obesity and overweight appeared to level off, there were, on average, very slight increases in physical activity, fruit and vegetable consumption and the eating of breakfast, another habit public health officials consider a marker of healthy behavior.
The opposite trend was seen for behaviors that are widely discouraged. The amount of time teenagers spent watching television fell from about three hours a day in 2001 to less than two-and-a-half hours by 2010. Teenagers also reported drinking slightly fewer soft drinks and eating less candy.
Boys overall reported more physical activity than girls, but they also watched more television and played more video games and ate fewer fruits and vegetables.
One expert who was not involved in the study, David B. Allison, the director of the Nutrition Obesity Research Center at the University of Alabama at Birmingham, said it was impossible from the data to deduce a cause and effect, since any number of factors that could influence obesity rates may have changed over time.
“We should be very cautious about drawing any attributions about causes based on time trend data,” Dr. Allison said.
But Dr. Iannotti said the findings seemed to suggest a pattern. “I think the public health message is beginning to be accepted,” he said. |||||
Summary:
| – American teenagers may not be the junk food-scarfing, video game-addicted balls of lard the media likes to make them out to be—or at least, they may not be anymore. A new study has found teens in 2010 were eating more vegetables, getting more exercise, drinking less soda, and watching less TV than they were in 2001, the New York Times reports. The study of 35,000 young people aged 11 to 16 found they were eating fruits and vegetables nearly twice as often, drinking 20% fewer sugary beverages, and the number of times they exercised for an hour or more had gone up from 4.33 days per week to 4.53 days per week, Think Progress reports. And between 2005 and 2009, the teens' average BMI went down. So that's the good news. The bad news is that the teens still weren't meeting the federal recommendations for an hour of exercise a day, while they did manage to fit in at least two hours a day watching TV, chatting online, and playing video games, the Times reports. The study also found younger teens tended to get more exercise and eat more healthfully, with their habits growing unhealthier as they got older. And black and Hispanic teens were behind white teens in almost every category, even after adjusting for socioeconomic factors. | multi_news_1_0_0 |
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The active ingredient in magic mushrooms helps decrease mental health problems in cancer patients, say researchers. A single dose of the hallucinogenic component found in magic mushrooms – psilocybin – reduces anxiety and depression in the patients for a long period of time.
The study was presented on 10 December at the annual meeting of the American College of Neuropsychopharmacology. The researchers say that study participants showed significantly greater attitudes towards themselves, life, and even showed positive effects on social behaviour. All 51 participants in the study had been diagnosed with life-threatening cancer, and had symptoms of anxiety or depression.
The research, led by Roland Griffiths at the Johns Hopkins University School of Medicine, compared the effects of psilocybin with different doses:
25 participants received a very low dose – between 1mg and 3mg per 70kg; and
26 were given a moderately high dosage of between 22mg and 30mg per 70kg.
After five weeks, the higher dosage group showed signs of much lower mental health problems compared to the low dose group. The results were also recorded six months after the initial chemical compound, psilocybin, was given.
Scientists also noted that on days that the chemical was given, the participants receiving the higher dosage showed "substantially greater effects, including perceptual changes [and] mystical-type subjective experiences."
This study follows research carried out in 2011 which showed psilocybin effectively decreased anxiety and depression in 12 cancer patients. Results from that study showed depression had declined by 30% after six months.
"We were pleased with results," said Charles Grob, lead author of the 2011 study. "They're not substances that should be used recreationally or casually, but nonetheless it appears that we can conduct research with these compounds safely."
Psilocybin is a chemical compound found in around 200 species of mushrooms. The effects of the compound are subjective, and include changes in perception, a distorted sense of time, hallucinations, and even nausea. ||||| A single dose of psilocybin, the major hallucinogenic component in magic mushrooms, induces long-lasting decreases in anxiety and depression in patients diagnosed with life-threatening cancer according to a new study presented today at the annual meeting of the American College of Neuropsychopharmacology.
Patients who receive a cancer diagnosis often develop debilitating symptoms of anxiety and depression. Reports from the 1960s and 1970s suggest that hallucinogenic drugs such as LSD may alleviate such symptoms in cancer patients, but the clinical value of hallucinogenic drugs for the treatment of mood disturbances in cancer patients remains unclear. In this new study, Roland Griffiths and colleagues from the Johns Hopkins University School of Medicine investigated the effects of psilocybin on symptoms of anxiety and depression in individuals diagnosed with life-threatening cancer. Five weeks after receiving a dose of psilocybin sufficiently high to induce changes in perception and mystical-type experiences, patients reported significantly lower levels of anxiety and depression compared with patients that received a low dose of the drug. The positive effects on mood persisted in the patients at 6 month follow-up.
The authors suggest that a single dose of psilocybin may be sufficient to produce enduring decreases in negative mood in patients with a life-threatening cancer.
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Presenter: Roland Griffiths, Ph.D. Professor of Psychiatry and Biobehavioral Sciences, and Neuroscience Johns Hopkins Bayview Medical Campus [email protected]
Media contact: David Echols
Email: [email protected]
ACNP, founded in 1961, is a professional organization of more than 1000 leading scientists, including four Nobel Laureates. The mission of ACNP is to further research and education in neuropsychopharmacology and related fields in the following ways: promoting the interaction of a broad range of scientific disciplines of brain and behavior in order to advance the understanding of prevention and treatment of disease of the nervous system including psychiatric, neurological, behavioral and addictive disorders; encouraging scientists to enter research careers in fields related to these disorders and their treatment; and ensuring the dissemination of relevant scientific advances. ||||| Neuropsychopharmacology (2015) 40, S1–S105; doi:10.1038/npp.2015.324
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1. The Molecular Pathology and Dynamics of Spine Loss in Schizophrenia
Top of page 1.1 Selective Loss of Small Spines in the Auditory Cortex of Schizophrenia Matthew MacDonald University of Pittsburgh Medical Center / Western Psychiatric Institute & Clinic, Pittsburgh, Pennsylvania, United States Background: Dendritic structural features, such as spine density and volume, are dynamically regulated by glutamate signaling to the actin cytoskeleton. Spine growth and retraction result from enhanced polymerization and depolymerization of F-actin. Decreased spine density has been observed in layer 3 of multiple cortical areas in schizophrenia while genetic and pharmacological studies support a role for glutamate signaling to F-actin in disease pathology. However, the mechanics by which spine signaling is impaired and the effect this impairment has on homeostasis of spine formation and retraction is currently unknown. To begin to address this question in human postmortem brain tissue we have utilized orthogonal approaches of confocal microscopy and targeted mass spectrometry to investigate spine density, volume, and protein expression. Methods: Primary auditory cortex tissue from 20 pairs of SCZ and matched control subjects, in which we have previously evaluated the expression of 155 synaptic proteins, were utilized. Dendritic spines were identified by co-localization of spinophilin and F-actin (defined by binding of phalloidin). This approach is innovative as it allows for an estimate of spine F-actin content and volume in human postmortem tissue. Results: In line with previous reports we observed a 20% decrease in auditory cortex deep layer 3 spine density (p = 0.009). Total F-actin per spine object was increased in disease (p = 0.03), but mean F-actin per spine was unchanged, indicating that the assay’s ability to measure F-actin signal was unaltered between disease and controls. To gain a more detailed picture of spine alterations in schizophrenia we used F-actin as a measure of spine volume and then calculated the density of spines of different volumes, as defined by bins with 0.15 μm3 increments. Significant decreases in spine density were limited to spines with the smallest volumes (p = 0.01). We recently reported the altered expression of glutamate signaling proteins including the AMPA receptor subunits GRIA3 and GIRA4 as well as GNAQ, a modulator of mGLUR5 signaling, in the primary auditory cortex of schizophrenia subjects. Interestingly, only the expression of GRIA3 was correlated with spine density (r = 0.4, p = 0.029). Conclusions: We have identified a specific sub-population of spines that are lost in schizophrenia. Two-photon in vivo imaging studies reveal that smaller spines are often transient, emerging from and retreating into the dendritic shaft over a period of a few hours if a new synaptic connection is not formed. Thus, this constantly churning population of young spines serves as the substrate for new learning and memory. Our findings show that the density of small, presumptive transient spines is decreased in schizophrenia and that affected cortical areas may be less capable of forming new synaptic connections, impairing cognitive function. However, the dynamics and molecular pathology of this loss is still unknown. A decrease in either the rate at which small/new spines emerge or the duration of their existence could both lead to a decreased total number. Future studies using time lapse and in vivo imaging in genetic model culture and mouse systems will likely shed light on this question. These findings further implicate glutamate signaling in spine pathology and support the continuing investigation of compounds that act on glutamate receptors, such as mGLUR5 positive allosteric modulators. Disclosures: Nothing to Disclose.
Top of page 1.2 Cellular Functions of Schizophrenia-Enriched Kalirin Mutations Peter Penzes Northwestern University, Chicago, Illinois, United States Background: Our laboratory has been investigating the signal transduction pathways that regulate actin cytoskeletal remodeling in dendritic spines and their impact on spine structure and function. One of the major regulators of spine plasticity is the protein kalirin, encoded by the KALRN gene. Several rare point mutations in human KALRN have recently been found to be enriched in subjects with schizophrenia versus controls. In addition, kalirin mRNA and protein levels are altered in several cortical regions in subjects with schizophrenia, as compared to controls. Methods: We have employed primary neuronal and heterologous cell cultures, molecular and biochemical approaches, as well as advanced imaging methods including structured illumination microscopy (SIM), a recently-developed superresolution imaging method. Results: In this symposium, I will present recent and unpublished data from our laboratory on the functional impact of such schizophrenia-enriched rare mutations in KALRN. We examined the effect of such mutation, in content of several kalirin isoforms, on actin regulation, dendrite and spine morphology, and glutamate receptor trafficking. Using SIM imaging, we find that different kalirin isoforms are localized to distinct microcompartments of the dendritic spine. Schizophrenia-enriched point mutations affect the molecular function and localization of individual kalirin isoforms. Conclusions: These studies shed new light on the roles of protein isoforms and their schizophrenia-enriched mutations in the regulation of dendritic spine structure and plasticity. Disclosures: Nothing to Disclose.
Top of page 1.3 Morphological Brain Abnormalities in Serine Racemase Knockout Mice: A Genetic Model of NMDA Receptor Hypofunction Darrick Balu Harvard University / McLean Hospital, Belmont, Massachusetts, United States Background: There are morphological brain changes in schizophrenia, including reductions in cortico-hippocampal gray matter and enlarged ventricles. As there is no neuronal loss in schizophrenia, the volumetric changes are believed to be due in part to reductions in neuronal dendritic complexity and spine density. There is substantial evidence that N-methyl-D-aspartate receptor (NMDAR) hypofunction is a core pathophysiological mechanism underlying schizophrenia, especially the cognitive impairments and negative symptoms. The largest schizophrenia GWAS to date recently identified genes involved in glutamatergic neurotransmission and the postsynaptic density with increased risk for schizophrenia, including serine racemase (SR), the enzyme that produces the NMDAR co-agonist D-serine. SR and D-serine are concentrated in corticolimbic regions of the brain. Genetic and biochemical findings suggest that serine racemase (SR) and D-serine are reduced in schizophrenia. Thus, our laboratory has used SR deficient (SR-/-) mice as a model to elucidate the molecular mechanisms responsible for dendritic atrophy as result of NMDAR hypofunction. Methods: Adult (3-4 months old) male wild type (WT) and SR-/- mice were used for all studies. Golgi impregnation was used to examine the neuronal architecture and spine density of pyramidal neurons in the medial prefrontal cortex (mPFC) and primary somatosensory cortex (S1), as well as spine density of granule cells in the dentate gyrus (DG) of the hippocampus. Cortical and hippocampal brain volumes from WT and SR-/- were estimated from Nissl stained tissue sections. In vivo ventricular volumes of anesthetized WT and SR-/- mice were quantified using 9.4T magnetic resonance imaging. Molecular and biochemical approaches were used to quantify mRNA levels, protein levels, and promoter occupancy. For drug reversal studies, WT and SR-/- mice were systemically administered either vehicle or drug. Results: In the mPFC and S1, pyramidal neurons of SR-/- mice displayed significant reductions in dendritic complexity and total dendritic length, as well as reduced spine density. Spine atrophy was also observed on granule cells in the DG of SR-/- mice. All of these neuropil changes in SR-/- mice were associated with reduced cortico-hippocampal volumes and increased ventricular volume. The dendritic abnormalities in SR-/- mice were paralleled by diminished occupancy of the transcription factor CREB to the promoter regions of BDNF, miR-132, and Arc, and therefore reduced expression. SR-/- mice also had reduced Akt/GS3K/mTOR signaling, all of which are regulated by NMDAR activity. Chronic administration of D-serine or a metabotropic glutamate receptor 5 (mGlu5) positive allosteric modulator (PAM) to adult SR-/- mice was able to rescue the structural, neurochemical, and cognitive deficits. Conclusions: These data demonstrate that SR-/- mice recapitulate the morphological and neurochemical brain abnormalities observed in schizophrenia, which can be rescued by pharmacologic treatment. Furthermore, they provide a mechanism by which NMDAR hypofunction impairs spine formation through BDNF and Akt signaling. Future studies could utilize proteomics to allow for more detailed comparison of this model with schizophrenia, while in vivo imaging studies would provide information on the course and dynamics of spine pathology in these mice. Disclosures: Nothing to Disclose.
Top of page 1.4 Astrocytic Contributions in Synaptic and Behavioral Abnormalities of Fragile X Syndrome Yi Zuo University of California Santa Cruz, Santa Cruz, California, United States Background: Fragile X syndrome (FXS), the most common inherited form of human intellectual disability, is caused by mutations in the FMR1 gene. Like schizophrenia, FXS is a developmental disorder in which patients suffer from cognitive impairments and postmortem studies have identified alterations in spine density. Fmr1 global knock out (KO) mice share many behavioral phenotypes with human FXS patients: they exhibit deficiency in learning and memory, sensory processing, and social behaviors. They also exhibit an abnormally high number of morphologically immature spines along dendrites of neocortical neurons. Despite the prevailing neuron-centric view of brain function, many lines of evidence suggest that astrocytes are important contributors to developmental and degenerative neurological diseases. Methods: To investigate the contributions of astrocytes to the progression of synaptic abnormalities and learning impairments associated with FXS, we generated astrocyte-specific Fmr1 KO mice. In this study, we used two-photon in vivo imaging to follow individual spines along dendrites of neurons in the motor cortex over time, and compared spine morphology and dynamics of WT, global and astrocyte-specific Fmr1 KOs. We also tested the motor-cortex associated skill learning in all these mice. Results: We found that astrocyte-specific Fmr1 KO mice display impaired motor-skill learning during adulthood, which correlates with the lack of enhanced spine dynamics in the motor cortex that normally occurs in response to the acquisition of a fine motor skill. Live imaging also revealed increased spine formation in adolescent astrocyte-specific Fmr1 KO mice, which preceded the elevated spine density found in adulthood. Furthermore, the behavioral and synaptic phenotypes in astrocyte-specific Fmr1 KO mice recapitulated those observed in the global Fmr1 KO mice. Conclusions: Our work reveals a significant contribution of astrocytes in FXS etiology. We are currently investigating other behavioral defects of astrocyte-specific Fmr1 KO mice. We are also exploring the possibility of Fmr1 rescue in astrocytes in vivo. Finally, these findings demonstrate the utility of two-photon in vivo imaging to investigate the dynamics of pathological spine activity in a mouse model of a developmental neuropsychiatric disease with cognitive impairments. Disclosures: Nothing to Disclose.
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2. A Multi-Modality Imaging Approach for the Identification of Brain Biomarkers of Clinical Outcomes in Human Addiction
Top of page 2.1 Using a Multi-Modal Neuroimaging Approach to Track Longitudinal Changes in Brain Function and Structure, and Associated Self-Control and Reward Valuation Functions in Cocaine Addiction Rita Goldstein Mount Sinai School of Medicine, New York, New York, United States Background: Persistent deficits in self-control and reward valuation characterize drug addiction, marked by abnormalities in functional and structural integrity of the prefrontal cortex (PFC). In a series of imaging studies, and using a multimodal approach, we aimed to ascertain the impact on brain function and structure of a 6-month follow-up in initially treatment-seeking abstinent individuals with cocaine use disorders (iCUD). We explored functions that are commonly impacted in drug addiction, inclusive of drug-related inhibitory control and attention-bias towards drug-related stimuli as compared to other salient affective cues. Methods: Initially abstinent treatment-seeking iCUD participated in a magnetic resonance imaging (MRI) study complemented by recordings of event-related potentials (ERPs). The MRI study acquired functional MRI (fMRI) blood-oxygen level dependent (BOLD) activations during performance of a salient drug Stroop-like task and structural T1-weighted images used for quantification of grey matter volumes in select regions. The ERPs were acquired separately while participants passively viewed pleasant, unpleasant, neutral and cocaine-related pictures. The late positive potentials (LPP) component of the ERP was scored to index motivated attention to these pictures. Procedures were performed at baseline and then again after 6-months; iCUD showed substantially reduced drug use during this period, with 57% maintaining complete abstinence. Results: Compared to healthy controls, in iCUD at follow-up as compared to baseline we report: 1) higher (and more positively correlated) task fMRI BOLD responses in the dopaminergic midbrain and the mediodorsal nucleus of the thalamus; increases in the midbrain correlated with reduced simulated cocaine choice, indicating that heightened (and normalized) midbrain activations may be marking lower approach motivation for cocaine in this context. Enhanced self-control was suggested by a trend for the commonly hypoactive dorsal anterior cingulate cortex to increase response during the drug trials. 2) increased LPPs to the pleasant (vs. neutral) pictures and decreased LPPs to the drug (vs. pleasant) pictures. And 3) increased grey matter volumes in the left inferior frontal gyrus and the ventromedial PFC. Conclusions: Results show that reduction of drug use (up to and including full abstinence) over a 6-months period is associated with normalization of function (subcortical and cortical responses to a salient cognitive task, and enhancements in scalp-recorded markers of salience of pleasant relative to that of drug stimuli) and structure (PFC grey matter volume). In addition to providing hope to abstaining drug addicted individuals, these results, which highlight brain plasticity, suggest that neuroimaging could be useful in sensitively tracking follow-up outcomes in drug addiction. By focusing on the utility of both MRI and ERP measures as biomarkers of important end-points (e.g., drug-mediated attention-bias and self-control), these studies also set the stage for a comparative effort to identify the best biomarkers to longitudinally track treatment course or efficacy in drug addiction and related conditions. Disclosures: Nothing to Disclose.
Top of page 2.2 Pet Imaging of the Kappa Opioid Receptor / Dynorphin System in Cocaine Abuse Diana Martinez Columbia University, New York, New York, United States Background: Animal studies have shown that the kappa receptor/dynorphin opioid receptor system plays a crucial role in addiction, particularly stress-induced relapse. Human postmortem studies have shown that cocaine dependence is associated with an upregulation of kappa opioid receptors (KOR) and dynorphin, but these are limited with respect to correlating neurochemistry with behavior. Our goal in this study was to investigate changes in the KOR/dynorphin system in cocaine abuse using Positron Emission Tomography (PET) and the KOR-selective radiotracer [11C]GR103545 and a laboratory model of relapse. Our hypotheses was that cocaine exposure would increase endogenous signaling of dynorphin at the KOR, and that KOR availability would increase the vulnerability to stress-induced relapse. Methods: Cocaine abusers were admitted to a research unit for a 28 days. They underwent a baseline scan with the KOR selective agonist radiotracer [11C]GR103545 after 7-8 days of inpatient monitored abstinence. Following this baseline scan, subjects performed cocaine self-administration sessions. These sessions began with a modified cold pressor test, which resulted in 3 minutes of pain/stress, followed by nine opportunities to choose cocaine versus an alternative reinforcer (money). A group of matched healthy controls underwent one set of PET scans to compare between group differences in KOR availability. Subjects were given a 2 day break, followed by 3 days of binge smoked cocaine (300 mg/day, total of 900 mg) in the laboratory. Then the [11C]GR103545 PET scan was repeated following the cocaine binge to investigate the effect of endogenous dynorphin upregulation on [11C]GR103545 binding. The outcome measure for the PET scans was the volume of distribution (VT) in the regions of interest, which included the striatum and its subdivisions, cortical regions including prefrontal cortex, and medial temporal structures. Between condition comparisons were made with a repeated measures ANOVA and the correlation were investigated with Spearman's rank-order correlation. Results: The cocaine abusers were heavy, chronic users of smoked cocaine. There was a positive correlation between KOR binding in the striatum and stress-induced cocaine self-administration: higher values of VT were associated with more choices for cocaine following the cold pressor test (Spearman correlation coefficient = 0.53, p = 0.03). A significant decrease in [11C]GR103545 VT was detected in the striatum (-17.7% ± 2.3%) when comparing the baseline and post-binge scans, with similar decreases in other brain regions (-12.9% ± 5.1%). No difference in baseline VT in any of the regions of interest between the cocaine abusers and controls. Conclusions: These results demonstrate that binge cocaine administration significantly upregulates endogenous dynorphin in the human brain, measured as displacement of the PET radiotracer [11C]GR103545. Additionally, high KOR availability correlates with greater choices to self-administer cocaine in the setting of pain/stress. Taken together, these findings indicate that KOR/dynorphin signaling is amplified in the setting of cocaine abuse, and plays a role in a laboratory model of relapse. Disclosures: Nothing to Disclose.
Top of page 2.3 Chronic Alcohol-related Brain Homeostatic and Stress Alterations and the Development of Biomarkers of Treatment and Relapse in Alcoholism Rajita Sinha Yale University, New Haven, Connecticut, United States Background: Growing evidence indicates that chronic alcohol abuse results in multilevel peripheral and brain adaptations in stress and homeostatic pathways that significantly impact cognitive, affective, alcohol craving and reward processes. However, identification of such measures as biomarkers of alcohol relapse and treatment outcome has rarely been assessed. Methods: Data from multimodal neuroimaging and human laboratory experiments combined with a prospective clinical outcomes design will be presented. Participants included treatment seeking alcohol dependent (AD) individuals who were abstinent for 4 weeks and engaged in inpatient treatment during separate laboratory and neuroimaging experiments. Healthy social drinking volunteers were included as control subjects. Multimodal neuroimaging using structural and functional magnetic resonance imaging (MRI and fMRI) assessing structural gray matter volume and functional neural responses to brief script-driven guided imagery of stress, alcohol cues and neutral relaxing states, and a laboratory experiment assessing autonomic and hypothalamic pituitary adrenal (HPA axis) basal states and responses to stress, alcohol cue and neutral states were conducted in both AD and controls. AD subjects were followed prospectively after inpatient discharge with repeated assessment of alcohol use outcomes over a 90 day period. Results: Findings indicate hyperactive basal and neutral state autonomic and HPA axis measures (heart rate, cortisol, cortisol/ACT ratio), lower medial frontal brain volume and hyperactive neutral state ventromedial prefrontal (VmPFC) and blunted VmPFC response to stress and alcohol cue, with each predicting future relapse and treatment outcome. Remarkably, there was a significant association between the cortisol/ACTH ratio and VmPFC disruption with VmPFC changes accounting for 33% of the HPA axis disruption in abstinent patients. Using receiver operating characteristics (ROC) to assess future relapse versus abstinence outcome prediction accuracy, we found that VmPFC hyperactivity in neutral state showed the most optimal prediction characteristics across measures in sensitivity and specificity for alcohol relapse and outcome prediction. Conclusions: These findings support both multimodal neuroimaging to assess addiction-related neuroadaptations in clinical samples and also further biomarker development to validate optimal biomarkers of alcohol relapse so as to improve treatment outcomes. Disclosures: Supported by UL1-DE019586, R01-AA013892; PL1-DA24859
Top of page 2.4 Neurophysiological and HPA Axis Measures of Systemic Dysregulation as Biomarkers of Treatment Outcome in Prescription Opiate Dependence Scott C. Bunce Penn State University College of Medicine, Hershey, Pennsylvania, United States Background: There is growing evidence for a model of addiction positing that neuroadaptations of the central nervous system (CNS) reward and stress response systems resulting from long-term opiate use render opioid-dependent patients at high risk for relapse. Theoretically, new set-points are established in the HPA axis and brain reward systems that may persist following withdrawal from habitual opiate use. These include: 1) heightened responses to drug-related stimuli; 2) dampened responses to natural rewards (e.g., food, sex); 3) disturbances in the normal homeostasis of the HPA axis; and 4) increased anhedonia and sleep disturbance. This model has not been well characterized in humans, however, and the temporal dynamics of dysregulation following opiate withdrawal are unknown. The current study is evaluating clinical measures hypothesized to mirror elements of allostatic dysregulation in patients who are dependent on prescription opioids with the following goals: 1) to examine the timecourse of re-regulation, and 2) to evaluate the prognostic value of these variables in the prediction of treatment outcomes. Methods: Recently withdrawn prescription opiate-dependent patients in an upscale, supervised, drug-free, residential care facility are assessed on 1) prefrontal cortical and psychophysiological responses to images depicting a) drug cues and b) natural rewards; 2) diurnal cortisol, and 3) 12 days of sleep actigraphy and subjective measures of sleep, as well as self-reported mood, stress and craving. Neuroimaging data were collected using functional near-infrared spectroscopy. All patients are assessed 2-3 weeks following initial withdrawal; and a subset of patients who stay in residential treatment for an additional 60-90 days are evaluated again 30 and 60 days after the initial assessment battery. All patients are followed a minimum of 90 days following discharge to ascertain abstinence/relapse using self-report and objective indices of relapse. Results: Results will be presented linking neurophysiological, sleep and HPA axis measures to treatment outcome. Preliminary results from the cue reactivity paradigm among patients in 30-day residential treatment (n=33) indicate heightened brain responses to prescription opiate pill cues among patients who relapsed to opiates (n=5) relative to those who maintained abstinence (n=28; t=2.34, p = 0.026). Neural responses were in right prefrontal cortical areas identified in previous cross-sectional pilot studies to differentiate patients in early versus extended sobriety. Impaired response to natural reward cues, hedonic responses to drug cues, HPA axis dysregulation and sleep disturbances are being analyzed for their contribution to the heightened risk of relapse in the early, drug-free period following withdrawal. Conclusions: Preliminary results suggest prefrontal cortical response to drug cues may indicate relative vulnerability to relapse in prescription opiate dependent patients. Further analyses will be used to identify the prognostic significance of these measures in combination, leading to more effective individualized treatment strategies. The assessments employed in this study may readily be adapted to a clinical environment, and could be explored as possible biomarkers in clinical efficacy trials. Disclosures: Part 1: Owns stock in FNIR Devices, LLC. A company that manufactures and sells fNIR devices for research.
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3. Functional Neurogenomics in Schizophrenia: Recent Accomplishments and Future Perspectives
Top of page 3.1 Exploring 3-Dimensional Genome Architectures and Function in Normal and Diseased Human Brain Schahram Akbarian Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: 3-dimensional chromosomal conformations regulate transcription by moving enhancers and regulatory elements into spatial proximity with target genes. However, there is very little information on ‘chromosomal loopings', including promoter-enhancer physical interactions, in normal and diseased human brain. This is surprising given that genome-scale mappings of promoter-distal regulatory regions for a large variety of cell lines and tissues, including brain, have suggested that each transcription start site (TSS) could be targeted on average by five different enhancers. Methods: We undertook deep and integrative analyses of spatial genome architectures across 100Kb-1Mb of sequence surrounding multiple neuronal genes implicated in the neurobiology and genetic risk architecture of schizophrenia. Chromosome conformation capture assays were conducted in postmortem prefrontal cortex, in neuronal cultures in the context of differentiation and activity-dependent regulation, and in the animal models for cognitive disease. Gene expression regulation by loop-bound sequences was assessed with TALE- and CRISPR/CAS based sequence-specific transcriptional activators and repressors. Results: We identify activity-regulated long-range loopings bypassing up to hundreds of kilobases of linear sequence in the neuronal genome. Neuronal gene expression was altered when loop-bound intergenic and distal intronic cis-regulatory elements were targeted by designer transcription factors. 3D genome organization is partially conserved between human and mouse brain. A subset of loop-bound sequences matched to non-coding risk polymorphisms implicated in psychiatric GWAS. Conclusions: Our integrative approach provides a roadmap to assign neurological function for a subset of the vast but largely unexplored non-coding sequences in the human genome. The study of 3-dimensional genome architecture and function, including chromosome conformation capture assays in normal and diseased postmortem brain tissue, are likely to provide important insights into the genetic risk architecture and 'genome pathophysiology' of schizophrenia and related disease. Disclosures: Nothing to Disclose.
Top of page 3.2 Searching for Potential Mechanisms of Schizophrenia Risk in the Human Brain Andrew Jaffe Lieber Institute for Brain Development, Baltimore, Maryland, United States Background: Genetic risk for schizophrenia and related brain disorders has begun to emerge through large genome-wide association studies (GWAS) in hundreds of thousands of unrelated individuals. However, the exact gene(s) and/or transcript(s) that are being regulated by these risk SNPs are largely uncharacterized due to the difficulty in obtaining expression and genotype data in large samples of postmortem human tissue. Advances in RNA sequencing (RNA-seq) have further permitted flexible and largely unbiased characterization of high-resolution transcriptomes, but the incomplete annotation of the human brain transcriptome can potentially affect the ability to use existing tools that rely on complete gene structure information. Methods: We have sequenced the transcriptomes of the dorsolateral prefrontal cortex (DLPFC) from 320 non-psychiatric controls across the lifespan at deep coverage, including 50 second trimester fetal samples, and 175 samples from patients with schizophrenia, and completely characterized their expression profiles across five complementary summarizations that capture elements of transcription – genes, exons, junctions, transcripts, and expressed regions. These samples have been further genotyped and imputed to the latest 1000 Genomes reference panel, defining genetic variation across the genome. Results: Using expression changes across development and simulated data, we show that annotation-agnostic approaches like junction and expressed-region analysis may outperform gene-, exon- and transcript-based approaches when the annotation is incomplete. We further conducted global expression quantitative trait loci (eQTL) analyses across the five expression summarizations in the adult control samples (age > 13, N=237), and identify hundreds of thousands of expression features that associate with local genetic variation, including extensive genetic regulation of previously unannotated sequence. The eQTLs in junction-level data (N= 53,497 unique junctions annotated to 16,481 genes at FDR < 0.01) showed the largest effect sizes (fold change per allele copy) and identified SNPs as eQTLs with the lowest minor allele frequencies (18.1% versus 23.1-24.2%). We lastly identified eQTLs to specific transcript elements in individual genes in over half of the genome-significant genetic variants for schizophrenia identified genome-wide association studies (GWAS), with a large subset directionally consistent in the brains of patients with schizophrenia, illuminating potential mechanisms of risk for many of these genetic variants. Conclusions: Leveraging human postmortem brain data can fine map the functional effects of genetic risk variation for schizophrenia identified in large GWAS, and can identify novel targets for drug discovery and more focused biological assays. Disclosures: Nothing to Disclose.
Top of page 3.3 Differential Expression and Functional Analysis of MicroRNAs in Schizophrenia: Focus on miR-132 Claes Wahlestedt Miller School of Medicine at University of Miami, Miami, Florida, United States Background: Epigenetic mechanisms, which encompass DNA methylation, histone modifications, and non-coding regulatory RNAs, coordinate transcriptomic programs in the brain. Recent research has shown that epigenetic mechanisms can contribute to gene expression changes that underlie neuronal connectivity and behavior. However, relatively little is known regarding the potential role of epigenetic mechanisms in psychiatric disorders. We hypothesize that dysregulation of epigenetic signaling pathways in schizophrenia could underlie gene expression changes in the brain, ultimately leading to synaptic plasticity deficits and behavioral abnormalities. Methods: We used microarrays and Nanostring nCounter analysis to identify microRNAs and epigenetic enzymes that are dysregulated in the dorsolateral prefrontal cortex (dlPFC) of subjects with schizophrenia compared to matched controls. MicroRNAs and epigenetic enzymes of interest were further characterized by determining their expression patterns during neuronal development in mice. Viral-mediated overexpression of microRNAs was used to validate potential epigenetic enzyme targets in vitro. Results: By large scale profiling of miRNAs in the dlPFC of multiple cohorts of human schizophrenic subjects, stringent analysis revealed that miR-132 is selectively downregulated. We found that miR-132 expression inversely correlates with that of its DNA methyltransferase target DNMT3a during development and in schizophrenia. MiR-132 has at least 34 additional bioinformatically predicted epigenetic enzyme targets. In fact, a previous study found that among 78 conserved microRNAs, miR-132 is statistically enriched for target genes with functional roles in chromatin remodeling. Expression analysis of predicted miR-132 epigenetic enzyme targets revealed that a histone methyltransferase EZH1 is upregulated in the dlPFC of two cohorts of schizophrenic subjects known to have miR-132 downregulation. Both DNMT3a and EZH1 are regulated by miR-132 in vitro. Furthermore, miR-132 and EZH1 are discordantly dysregulated by early life stress, an environmental risk factor for schizophrenia. Conclusions: Our findings show that miR-132 dysregulation in schizophrenia could contribute to changes in epigenetic regulatory networks, particularly though DNMT1 and EZH1. Ongoing studies aim to identify the functional consequences of DNMT1 and EZH1 dysregulation in the dlPFC, including identification of target genes, synaptic plasticity changes, and behavioral deficits. Exploring the identity and consequences of such micoRNA-epigenetic signaling pathways in schizophrenia may help to elucidate the etiology of this complex psychiatric disease, and potentially identify novel therapeutic targets. Disclosures: Nothing to Disclose.
Top of page 3.4 Transcriptome Alterations in DLPFC and Genetic Liability Contribute to Risk for Schizophrenia Panos Roussos Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: The most recent Psychiatric Genomic Consortium GWAS in schizophrenia (SCZ) reported more than a hundred susceptibility loci, which are predominantly found in non-coding regions. Functional understanding of non-coding disease-associated loci is an important next step towards the development of testable hypotheses regarding biological processes that may be involved in the pathogenesis of SCZ. We have developed the CommonMind consortium to generate and analyze molecular data from human post-mortem brain samples including RNA sequencing and epigenome data. In this study, we combined a diversity of informative data (e.g. genomic; expression quantitative trait loci (eQTLs), cis-regulatory elements (CREs) annotations) to study the distribution of risk variants in gene coexpression networks. Methods: High density eQTLs, differential expression and coexpression network analysis was conducted in 537 human post-mortem samples (258 SCZ samples and 279 controls) from the dorsolateral prefrontal cortex (DLPFC, BA9/46) as part of the CommonMind Consortium (CMC, http://commonmind.org). A variety of publicly available CRE annotations for promoters, enhancers or open chromatin (DNase hypersensitivity regions) were used. Furthermore, in a subset of cases and controls, we obtained cell type-specific (neuronal and glial) annotations for open chromatin. Results: Differential expression was detected with 199 upregulated transcripts and 267 down-regulated transcripts in the DLPFC at an FDR of 5%. Prior SCZ genetic findings were significantly enriched among differentially expressed genes (P = 0.01). Gene coexpression analysis identified a neuronal subnetwork of ~1400 genes subserving functions related to synaptic transmission in the DLPFC that is significantly perturbed in SCZ and is highly enriched for SCZ genetic signal (P = 1.37 x 10-04). Certain SCZ risk loci are positioned within cis regulatory sequences and affect gene expression. Conclusions: The analysis presented here has two fundamental goals, to describe differences in gene expression and the mechanisms that underlie genetic risk. Our findings point to a functional link between SCZ susceptibility loci and regulation of gene expression affecting transcripts clustered in specific subnetworks. Disclosures: Nothing to Disclose.
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4. Opportunities and Challenges for Buprenorphine in Treating Depression
Top of page 4.1 Pharmacological Mechanisms Underlying the Antidepressant and Anxiolytic Effects of Buprenorphine Irwin Lucki University of Pennsylvania, Philadelphia, Pennsylvania, United States Background: Buprenorphine (BPN) may be effective in alleviating symptoms in treatment-resistant depressed patients. Buprenorphine has mixed pharmacological effects at opioid receptors, acting as a partial agonist at mu (μ-ORs) and nociceptin receptors and an antagonist at kappa (κ-ORs) and delta receptors. Preclinical studies have shown that BPN produces behavioral effects on rodent tests that are also responsive to clinically effective antidepressant and anxiolytic drugs. Using the forced swim test (FST) and novelty-induced hypophagia (NIH) test, two behavioral tests sensitive to conventional antidepressant drugs, we probed the pharmacological mechanisms associated with the antidepressant and anxiolytic behavioral effects of BPN, respectively. In addition, chronic administration of buprenorphine was evaluated in two models of depressive behavior, chronic unpredictable mild stress and chronic social defeat. Methods: C57BL/6J mice were tested in the FST and NIH test as described previously. The effects of buprenorphine were evaluated after pretreatment with opioid receptor antagonists or in mice with genetic deletion of opioid receptors. The effects of chronic buprenorphine (0.25 mg/kg for 7-10 days) were examined on deficits of sucrose preference and increased anxiety produced in mice exposed to unpredictable chronic mild stress (UCMS) for 21 days. The effect of chronic buprenorphine (0.25 mg/kg for 1-7 days) was also examined on deficits of social approach behavior induced by chronic social defeat, as previous described. Results: BPN reduced immobility in the FST in C57BL/6J, similar to effects produced by selective κ-OR antagonists, such as nor-BNI (10 mg/kg). BPN did not reduced immobility in mice pretreated with nor-BNI or with genetic deletion of κ-ORs (Oprk1-/-), but was effective in mice with genetic deletion of either μ-ORs (Oprm1-/-) or delta opioid receptors. In the NIH test, BPN reduced approach latencies for peanut butter chips provided in a novel arena in wild-type mice. Oprm1-/- mice took twice as long to train to eat the chips in their home cage as Oprk1-/- and wild-type mice. The response to BPN in the novel arena of the NIH test was blocked in Oprm1-/- mice, but not altered in Oprk1-/- mice. Using UCMS to induce anhedonia and increased anxiety in mice, chronic administration of buprenorphine reversed deficits in sucrose preference and anxiety behavior induced by chronic stress. The behavioral response of stressed animals was associated with changes of κ-OR gene expression rather than μ-ORs. Chronic buprenorphine also reversed deficits in social approach and interaction induced in susceptible mice by exposure to chronic social defeat. Conclusions: The pharmacological mechanisms associated with the behavioral effects of BPN in measures of affective behavior were test-dependent and involved both μ-ORs and κ-ORs. The reversal of anhedonia and anxiety behavior after chronic stress was associated with κ-ORs. Disclosures: Nothing to Disclose.
Top of page 4.2 Effects of Buprenorphine on Negative Affective Stimuli in Healthy Adults Harriet de Wit The University of Chicago, Chicago, Illinois, United States Background: The opioid system has been implicated in both physical pain and psychological distress. Preclinical studies suggest that low doses of opioid drugs reduce isolation distress and increase play behavior, and clinically, opioid abusers report that these drugs reduce social stress and negative affect. The effects of opioid analgesic drugs on responses to negative affective stimuli have not been thoroughly studied in humans. Here we examined the effects of the μ-opioid partial agonist buprenorphine on three measures of social distress: 1) response to a public speaking task; 2) response to simulated social rejection, 3) attention to negative emotional facial expressions. Methods: Healthy young adults attended laboratory sessions during which they received either placebo or 0.2mg sublingual buprenorphine, under double-blind conditions. Ninety minutes after drug administration, they completed a standardized public speaking stress task, a social exclusion task (Cyberball) or a task measuring attention to facial emotions using electrooculography. Results: During the stress task, buprenorphine dampened the increase in cortisol during the task and reduced subjects’ appraisal of how threatening the task was. During the Cyberball task, buprenorphine reduced participants’ negative mood responses to rejection, and decreased their perception of the degree to which they were excluded. During the attention task, the drug reduced initial attention to fearful facial expressions, without influencing attention to angry, happy, and sad faces. Buprenorphine produced these behavioral effects at doses that did not increase ratings of ‘high’ or ‘like’ drug. Conclusions: These results suggest that low doses of buprenorphine may have stress-reducing effects in healthy adults. This provides further support for the role of the opioid system in mediating responses to social rejection and stress, and suggests a possible therapeutic role for this type of drug, at very low doses. Disclosures: Nothing to Disclose.
Top of page 4.3 Abuse Potential of Buprenorphine (BPN) in Humans under Varying Conditions Sandra Comer Columbia University, New York, New York, United States Background: BPN is approved by the Food and Drug Administration for treating pain and opioid use disorders. Although it is effective in treating both disorders and is generally considered to be safe and well tolerated, several studies have demonstrated that BPN has abuse potential. The conditions under which BPN may be abused are complicated, however, and depend on a number of variables including whether or not the user is physically dependent on opioids, the opioid(s) upon which the user is dependent, and the dose and route of BPN administration. In order to mitigate this risk, a formulation of BPN has been developed that contains the opioid antagonist naloxone. This presentation will describe the various parameters under which BPN may be abused. Methods: Opioid-dependent participants lived in the hospital for the duration of the studies and were either detoxified from opioids or maintained on an opioid (morphine, hydromorphone or BPN). After a stabilization period (~1 week), behavioral testing began. Primary dependent measures included drug taking behavior, subjective effects (to assess euphoria (drug liking, high), side effects (sedated, itchy), and opioid withdrawal (nausea, anxiety)) and physiological effects. Results: In recently detoxified participants, intravenous (IV) BPN was self-administered significantly above placebo levels and produced positive subjective effects that were comparable to those of IV methadone, a full mu agonist. However, when participants were maintained on the short-acting opioid morphine, IV BPN was not self-administered at any dose tested, even though it significantly increased positive subjective effects. In comparison, morphine, heroin, oxycodone, and fentanyl self-administration increased in a dose-related manner in these same participants. In BPN-maintained subjects, IV BPN was self-administered and produced positive subjective effects that were comparable to heroin. Intranasal (IN) BPN, however, was not well liked and was self-administered less than heroin. The addition of naloxone dose dependently reduced abuse potential indicators of both IV and IN BPN among a BPN-maintained sample. Conclusions: The results of these studies suggest that the abuse liability of BPN is complex and depends on a number of different factors including state of dependence, BPN dose, and route of BPN administration. The data also indicate that the combination of BPN and naloxone has lower abuse potential than BPN alone under all of the conditions tested. These results are important to consider for the use of BPN in other patient populations. Disclosures: Part 1: AstraZeneca, Camarus, Janssen, Mallinkcrodt, Medicinova, Omeros, Pfizer, Reckitt Benckiser, Salix, Shire, Part 2: Reckitt Benckiser, Part 4: Reckitt Benckiser (investigator-initiated research grant).
Top of page 4.4 Low-dose Buprenorphine for Late-Life Treatment Resistant Depression: Assessing Effect and Probing Mechanisms Jordan Karp University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States Background: Over 50% of mid-life and older adults with depression fail to respond to traditional antidepressants. When monoaminergic antidepressants are ineffective at eliciting a full response for patients with treatment resistant depression (TRD), augmentation pharmacotherapy using medications with a unique mechanism of action and rapid onset may offer relief. Modulation of the opiate system may be a novel treatment approach for TRD. Buprenorphine is a partial agonist at mu opiate receptors and antagonist of kappa opiate receptors (KOR). It has a favorable safety profile with low risk of respiratory depression, and the pharmacokinetics are not affected by advanced age or renal dysfunction, supporting its use in late-life. These qualities make buprenorphine an intriguing molecule to test for clinical effect in older adults with TRD and to probe the opiate system in the depressed aging brain. Methods: Two studies will be presented. In the first unblinded project, fifteen midlife and older adults with TRD received 8 weeks of primarily augmentation pharmacotherapy with buprenorphine (average daily dose = 0.40 mg/day). In the second ongoing multisite project, 80 older patients with TRD receive 8 weeks of augmentation pharmacotherapy with buprenorphine dosed at 0.2-1.2 mg/day. The unique methodology of this project, in which different tools of modern neuroscience are used to probe target engagement of buprenorphine will be presented. Mechanism of action (MOA) study methods unique to each site are: 1) Neuroreceptor PET study of KOR before and after exposure to BPN to demonstrate pharmacodynamic MOA (i.e., target engagement, defined as appreciable CNS receptor occupancy) at our dosing range (St. Louis); 2) fMRI study comparing activation in the limbic system and reward circuits before and after exposure to examine neurocircuitry-level MOA (Pittsburgh); and 3) transcranial magnetic stimulation (TMS) study of cortical inhibition deficits (a neurophysiological proxy for dysfunctional GABA-ergic neurotransmission) before and after exposure to examine neurophysiological MOA (Toronto). Results: In the open-label project, the average depression score (MADRS) at baseline was 27.0 (SD=7.3), and at week 8 was 9.5 (SD=9.5). Depression severity sharply declined during the first 3 weeks of exposure (mean delta = -15.0). The trajectories for the two depression-specific items (low mood and anhedonia) matched the trajectory for the total MADRS score, representing depression-specific clinical improvements. Response, defined as MADRS < 10 at any week, was observed for 10/15 participants (66.7%). Response at the end of 8 weeks was observed for 8/13 participants (61.54%). During discontinuation of buprenorphine, no subjects experienced withdrawal symptoms. After withdrawing the buprenorphine, the average MADRS score increased to 17.8 (SD=12.9), indicating a relapse of depression. Conclusions: Low-dose buprenorphine may be a novel mechanism medication that provides rapid and sustained improvement for older adults with TRD. Clinical trials provide a unique infrastructure to both assess target engagement and promote understanding of an intervention’s MOA. Disclosures: Part 4: Provision of medication supplies for investigator initiated trials from Pfizer and Reckitt Benckiser.
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5. Going with your Gut: Appetitive Hormones and the Regulation of Substance Use
Top of page 5.1 A Novel Microendoscopy System for Functional Imaging of Circuits that Drive Feeding-Reward Behaviors Yeka Aponte National Institute on Drug Abuse, Baltimore, Maryland, United States Background: Beginning with early lesion and electrical stimulation studies, the hypothalamus has long been considered essential in regulating feeding. Furthermore, it has been hypothesized that the hypothalamus may regulate food reward through its connections to brain regions associated with reward and goal-directed behaviors, such as the nucleus accumbens and the ventral tegmental area. However, in these experiments, it is not clear which cell types and relevant projections are important for regulating feeding behaviors. Moreover, experiments to date have been unable to measure the activity of specific cell types to provide quantitative relationships between neuronal activity and behavior. To address these questions, we are measuring and manipulating the activity of genetically-defined hypothalamic neurons in awake, behaving mice using a combination of optogenetics, electrophysiology, two-photon fluorescence endomicroscopy, and behavioral assays. Methods: We implemented two-photon fluorescence endomicroscopy to measure the activity of genetically-identified hypothalamic neurons in head-fixed Cre-expressing transgenic mice during behavior. First, we designed a thin-walled polyimide guide cannula which allows for a minimally invasive implantation of the gradient refractive index (GRIN) lenses. Once mice were acclimated to head restraint, endomicroscopic imaging was performed during anesthetized and awake states in mice expressing the genetically encoded calcium indicator GCaMP6 in specific hypothalamic cell types. Results: During our preliminary experiments in anesthetized and awake head-fixed mice, we were able to a) acquire high quality three-dimensional images of hypothalamic neurons with little brain motion across days, b) resolve neuronal processes such as dendrites and axons, c) image and record calcium transients indicative of action potential firing from lateral hypothalamic neurons that expressed the genetically encoded calcium indicator GCaMP6. Conclusions: Having established imaging and surgical approaches, we are currently measuring the activity of genetically-identified cell types in the lateral hypothalamus of cre-expressing transgenic mice during different behavioral states, such as hunger, satiety, and feeding. By imaging neuronal activity, rather than using stimulation or inactivation experiments, we will be able to develop a better quantitative understanding of the specific role each cell type plays in controlling feeding behavior. Disclosures: Nothing to Disclose.
Top of page 5.2 New Roles for GLP-1 Receptors in Mediating Reward and Drug Abuse Gregg Stanwood Florida State University, Tallahassee, Florida, United States Background: Glucagon-like peptide-1 (GLP-1) is both a peripherally expressed incretin and a centrally active neuropeptide that is released in response to food intake. GLP-1 regulates energy homeostasis and metabolism by interacting with its receptors expressed on neurons in the gut and in the brain, and several GLP-1 analogs are approved for clinical use in type 2 diabetes to improve glycemic control and support weight loss. Recent studies have begun to elucidate the central pathways that mediate GLP-1 effects on food intake and reward, including the mesolimbic dopamine system. This presentation will discuss how forebrain GLP-1 receptors can coordinate inter-dependent food and drug reward circuits with central stress circuitry, at least in part through modulation of brain dopamine homeostasis. Methods: Animals: Mice were purchased from Jackson Laboratories or bred internally. All experiments were in accordance with the directives of the “Principles of Laboratory Animal Care” and local institutional animal care and use committees. Reporter mice were created by the Vanderbilt Transgenic and Embryonic Stem Cell Core using a BAC clone containing the Glp1r gene. Behavioral Studies: Some mice were subjected to a 5 day cocaine behavioral sensitization protocol, whereby they were injected with cocaine ± Ex-4 (or vehicle). Mice were then tested for locomotor activity following a ten day abstinence period. For conditioned place preference, mice were tested for initial bias, randomly assigned a drug treatment, and received four pairings of cocaine or saline vehicle (±Ex-4). Mice were re-assessed for preference on day 10. Cocaine self-administration was conducted in the laboratory of Dr. A. Fink-Jensen, using nose-poke responses that result in tail vein injection of cocaine. Biochemistry and Neuroanatomy: DA uptake assays, slice biotinylation and immunoblotting were all conducted using standard protocols. Glp1r transcript was measured using fluorescent in situ hybridization and RNAScope. GLP-1 receptor expressing cells were mapped in BAC transgenic mice using antibody-mediated amplification of mApple. Results: We have demonstrated that systemic administration of a GLP-1 analog, Ex-4, reduces cocaine reward, as measured both by conditioned place preference and self-administration. GLP-1 receptor activation also alters central DA homeostasis, at least in part through altering DAT expression and function within the lateral septum. In contrast, cocaine-induced locomotor activity and sensitization were not altered by Ex-4. Ongoing circuit mapping studies in a Glp1r-mApple reporter mouse is allowing us to delineate the sites of GLP-1 receptors and GLP-1 responsive pathways. Conclusions: We have demonstrated new roles for the peptide hormone and satiety signal GLP-1 in cocaine reward and in the regulation of DA signaling. Our studies expose GLP-1 receptors as a potential target for the treatment of drug abuse, and point to mechanisms in which the autonomic and behavioral processes that regulate energy balance may also be recruited in drug addiction. Disclosures: Nothing to Disclose.
Top of page 5.3 On the Role of Feeding Peptides in Alcoholism: Recent Clinical Findings Carolina Haass-Koffler Brown University Center for Alcohol and Addiction Studies, Providence, Rhode Island, United States Background: Increasing evidence supports the role of appetite-regulating pathways, including ghrelin and leptin, in alcoholism. Consistent with the opposite orexigenic and anorectic effects of ghrelin and leptin this set of studies tested the hypothesis that intravenous (IV) exogenous ghrelin administration acutely decreases endogenous serum leptin levels, and changes in leptin levels negatively correlate with alcohol craving. Methods: This was a double-blind, placebo-controlled human laboratory study. Non-treatment-seeking, alcohol-dependent, heavy-drinkers (n = 45) were randomized to receive IV ghrelin or placebo, followed by a cue-reactivity procedure, during which participants were exposed to neutral (juice) and alcohol trial cues. To determine the change in hormone levels, blood samples were collected at baseline and during the entire cue-reactivity experiment. Results: There was a main effect for IV ghrelin administration, compared to placebo, in reducing serum leptin levels (p<0.05). Post hoc analysis showed significant differences in serum leptin levels at the alcohol trial (p<0.05) that persisted at the end of the experiment (p<0.05). By contrast, there were no significant differences in serum leptin levels at the juice trial (p=n.s.). Serum ghrelin level was correlated with the increase in alcohol urge at alcohol trial (p<0.01). By contrast, urge to drink juice craving questionnaire was not significantly correlated with serum ghrelin levels. The reduction of serum leptin level at the alcohol trial negatively correlated with the increase in alcohol urge (p<0.05), while urge to drink juice was not correlated with the leptin change at the juice trial (p=n.s.). This effect was specific for leptin, since there were no significant effects for IV ghrelin on resistin or visfatin serum level. Conclusions: These novel findings provide preliminary evidence of ghrelin – leptin cross-talk in alcoholic individuals and suggest that their relationship may play a role in alcohol craving. Disclosures: Nothing to Disclose.
Top of page 5.4 Nicotine and the Endocrine Modulation of Appetitive Responses Nils Kroemer Technische Universität Dresden, Dresden, Germany Background: In animals, nicotine administration has been demonstrated to reduce body weight by attenuating food intake. Moreover, effects of endocrine signals reflecting metabolic status such as leptin and ghrelin are partly modulated by nicotinic acetylcholine receptors. These molecular interactions point to potential interactions in the modulation of appetitive responses via mesolimbic dopaminergic projections, but little is known about potential interactions in humans. Methods: We investigated food-cue reactivity and cue-induced appetite using functional magnetic resonance imaging during a fasting state and following the administration of an oral glucose tolerance test (OGTT; ~300 kcal). In a sample of healthy normal-weight never-smokers (N=26), we administered either nicotine (2 mg) or placebo gums following a double-blinded randomized cross-over design on separate days. In a second sample, we investigated quitting smokers before smoking cessation and at least two weeks after successful abstinence and matched never-smoking controls (N=31). Results: In the sample of healthy never-smokers, we have shown that a) fasting levels of ghrelin correlate with cue-induced appetite and the mesolimbic response to food pictures, b) nicotine administration reduces the hypothalamic response to food pictures during the fasting state and decreases the functional coupling with the ventral striatum, and c) nicotine enhances the modulatory effects of leptin and ghrelin on food-cue reactivity in the amygdala and the ventromedial prefrontal cortex. In the sample of quitting smokers, we found that the reduction in hypothalamic food-cue reactivity after being fed was significantly greater in smokers than non-smokers. Critically, reduced food-cue reactivity in the hypothalamus in smokers was correlated with reduced subjective appetite after the caloric load indicating a link to satiation. Conclusions: Our findings indicate that nicotine may increase the impact of metabolic state on appetitive behavior and brain responses in homeostatic and hedonic circuits. Taken together, this modulation of endocrine signals might hint at a mechanism contributing to nicotine’s anorexic potential. Disclosures: Nothing to Disclose.
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6. Extinction: New Directions from Basic Science to Clinical Interventions
Top of page 6.1 Persistent Avoidance Depends on Prefrontal-Striatal Interactions Gregory Quirk University of Puerto Rico School of Medicine, San Juan, Puerto Rico Background: Anxiety and related disorders are characterized by persistent avoidance of stimuli containing aversive associations. Persistent avoidance often fails to respond to extinction-based therapies. We investigated extinction of active avoidance using pharmacological and immunohistochemical techniques in rats, in a platform-mediated avoidance task (Bravo-Rivera et al, 2014). Methods: Rats were trained to avoid a tone paired with footshock by stepping onto a platform. While protective, the platform also prevented rats’ access to sucrose pellets. After 10 days of conditioning, avoidance responses were extinguished over two sessions. Some rats were infused with a BDNF-neutralizing antibody in the infralimbic (IL) prefrontal cortex prior to extinction training, while others were analyzed for cFos or BDNF two hours after extinction training. Results: Persistent avoidance following extinction training was associated with elevated activity in prelimbic (PL) cortex, ventral striatum (VS), and basolateral amygdala (BLA), and reduced activity in IL. Combining cFos with a retrograde tracer implicated direct projections from IL to VS. Blocking extracellular BDNF in IL had no effect on the acquisition of extinction (p=0.609) but impaired the recall of avoidance extinction the following day (p< 0.001). Extinction training increased neuronal BDNF in ventral hippocampus (vHPC), but unlike fear extinction, BDNF was also increased in mediodorsal thalamus but not BLA. Conclusions: These findings suggest that extinction of active avoidance involves inhibition of striatal avoidance circuits by IL. The plasticity necessary for avoidance likely depends on BDNFergic inputs to IL from vHPC or MD, but not BLA. Persistent avoidance could result from deficient BDNF in MD-IL or vHPC-IL projections, limiting extinction plasticity in prefrontal-striatal circuits. Disclosures: Nothing to Disclose.
Top of page 6.2 Fear Network Reactivity and Communication in Response to Conditioned Threat Across Anxiety Disorders and PTSD Mohammed Milad Massachusetts General Hospital / Harvard Medical School, Charlestown, Massachusetts, United States Background: A network of brain regions including the amygdala, hippocampus, insular cortex, and regions of the medial prefrontal cortex have been implicated in the pathophysiology of anxiety and fear-based disorders. It remains unclear as to what is shared and what is different in terms of the dysfunctional activation or functional connectivity between those nodes, especially within the context of responding to threat-conditioning. Methods: The sample studied (110 subjects) was composed of patients diagnosed with panic disorder (PD), social anxiety disorder (SAD), generalized anxiety disorder (GAD), and posttraumatic stress disorder (PTSD), along with subjects not diagnosed with any fear or anxiety disorders. All subjects underwent the same 2-day threat conditioning and extinction paradigm while in an fMRI scanner. BOLD signal was compared across disorders, and psychophysiological interactions analyses will be conducted across all studies. In addition, dynamic causal modeling (DCM) will also be conducted to test information flow across the different nodes of the network. Results: Deficits in extinction of conditioned threat responses were only noted in the PTSD cohort; the remaining disorders showed what appeared to be intact threat extinction, at least as indexed by SCR. Distinct functional activations were noted to each of the disorders within the ventromedial prefrontal cortex, dorsal anterior cingulate cortex, amygdala, insular cortex as well as somatosensory cortex. The hyper and hypo-activation signature per disorder was noted across the different phases of the experiment (i.e. conditioning, extinction, and extinction recall). DCM analysis on over 100 healthy subjects revealed distinct pattern of information flow between the areas noted above; a patter that was found to be impaired in PTSD. DCM and PPI analyses across the remainder of the disorders is currently being analyzed and will be presented during the talk. Conclusions: The work to be presented will help us continue to shape our thinking of what is similar and what is different across the fear- and anxiety-based disorders. Disclosures: Nothing to Disclose.
Top of page 6.3 Translating Fear Extinction Phenotypes: From the Rodent Chamber to the Clinic Seth Norrholm Emory University / Atlanta VA Medical Center, Atlanta, Georgia, United States Background: Psychophysiological measures of fear expression provide observable intermediate phenotypes of fear-related symptoms. Negative Valence Systems in the Research Domains Criteria (RDoC) matrix include the construct of acute threat, which can be measured using psychophysiological indices. Extinction impairments have been observed in traumatized individuals who express maladaptive fear-related behaviors. Genomic factors, such as those associated with FK506 binding protein 5 (FKBP5), have been shown to underlie diverse post-traumatic behavioral patterns. As an example, the role of FKBP5 has only been examined in relation to a priori diagnostic categories or in relation to aggregate behaviors. Methods: Our current program of study has employed the use of translational fear conditioning, extinction, and inhibition paradigms that are well-suited to advance the study of the non-pharmacological (e.g., retrieval+extinction) and pharmacological (e.g., losartan, dexamethasone, d-cycloserine) manipulations that may facilitate extinction learning. Outcome measures include freezing in rodents and fear-potentiated startle in humans. With these translational tools in hand, we empirically identified heterogeneous trajectories of fear extinction learning in mice (n=122) and humans (n=723) using Latent Growth Mixture Modeling. In humans, we determined if risk variants of FKBP5 were associated with abnormal fear extinction trajectories. In mice, we determined: (1) if FKBP5 mRNA expression in the amygdala following extinction learning was associated with abnormal extinction trajectories of freezing behavior and (2) if high dose dexamethasone altered expression and altered trajectory membership. Results: In humans, three distinct trajectories were identified: a normative trajectory of moderate increase in fear acquisition and complete extinction, a high fear reactive but extinguishing trajectory, and a high fear reactive non-extinguishing trajectory. Risk alleles associated with FKBP5 were significantly associated with the high fear reactivity trajectory. In mice, three trajectories including a trajectory of rapid and complete extinction, a trajectory of slow but complete extinction, and a non-extinguishing trajectory were identified. High dose dexamethasone significantly increased the probability of extinction and altered FKBP5 expression in the amygdala. Conclusions: Genetic variation in FKBP5 is associated with abnormal phenotypes of extinction learning. High dose dexamethasone temporally alters FKBP5 mRNA expression in the amygdala but permanently alters behavioral responses to the conditioned threat cue. Findings indicate that FKBP5 confers risk for abnormal fear extinction but also represents a target for treatment. These results will be discussed in terms of rescuing impaired extinction learning (ie., changing trajectory "class" membership) using non-pharmacological and pharmacological manipulations. Disclosures: Nothing to Disclose.
Top of page 6.4 The Prevention of PTSD with Early Extinction Training Barbara Rothbaum Emory University School of Medicine, Atlanta, Georgia, United States Background: Unlike other psychiatric disorders, the precipitant for adult posttraumatic stress disorder (PTSD) is a known event, allowing for immediate intervention, presenting the potential to prevent, and ultimately eliminate for many, the occurrence of this most serious condition. The evidence from animal studies suggests that immediate extinction training (10 min after conditioning) was more effective on spontaneous recovery, renewal, and reinstatement than later extinction training (72 hours). This knowledge of the precipitant combined with excellent animal models of fear memory consolidation and the ability to interrupt this consolidation in the early post-trauma-exposure period, has led to the exciting possibility that interventions in the immediate aftermath of trauma could potentially prevent the development of PTSD. Methods: Patients (N=137) were randomly assigned to receive 3 sessions of an early intervention beginning in the emergency department (ED) compared to an assessment only control group. PTSD symptoms were assessed at 4 and 12 weeks post-injury and depression at baseline and week 4. The intervention consisted of modified prolonged exposure including imaginal exposure to the trauma memory, processing of traumatic material, and in vivo and imaginal exposure homework. Results: In our completed pilot work, an early exposure-based intervention begun within hours of trauma exposure significantly decreased PTSD and depression 1- and 3-months post-trauma compared to those who did not receive the intervention and seemed to mitigate a genetic risk for PTSD. Conclusions: Evidence supports that this early extinction training/exposure therapy in the immediate aftermath of trauma can reduce indices of fear and PTSD and depression symptoms. Disclosures: Nothing to Disclose.
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7. As Good as It Gets? New Insights from Genetic and Circuitry-Based Models of OCD and Tourette Syndrome
Top of page 7.1 Identifying Neural Activity Changes Underlying OCD-Like Behaviors Using In Vivo Microscopy Susanne Ahmari University of Pittsburgh, Pittsburgh, Pennsylvania, United States Background: Obsessive Compulsive Disorder (OCD) is a chronic, severe mental illness that affects 2-3% of people worldwide, yet the pathophysiology remains unclear. However, multiple lines of evidence indicate that dysregulation within cortico-striato-thalamo-cortical (CSTC) circuits is correlated with OCD. Specifically, in previous work we demonstrated that brief but repeated optogenetic hyperstimulation of projections from orbitofrontal cortex (OFC) to ventromedial striatum (VMS) leads to long-lasting perseverative grooming, a mouse behavior linked to OCD. However, the changes in cortical and striatal cellular activity that occur during the development of perseverative grooming are unknown. We therefore examined changes in cellular activity in both orbitofrontal cortex (OFC) and ventromedial striatum (VMS) during the evolution of perseverative grooming behavior using miniaturized head-mounted microscopes and calcium imaging. Methods: We injected EMX-Cre or C57/Bl6 mice with the genetically encoded calcium indicator AAV5.syn.GCaMP6f and implanted microendoscopes (6.1mm x 0.5mm GRIN lens) in either OFC or VMS. 2 weeks after virus injection, mice were fitted with a microscope baseplate. After recovery, behavioral experiments were performed. Using a cross-over within subjects’ experimental design, mice were treated with either the D1 agonist, SKF38393 to induce perseverative grooming, or vehicle. Both behavior and calcium signaling was monitored for 30 minutes post injection, using 5 minute imaging blocks every 10 minutes. Calcium transient data was extracted from processed videos to analyze event frequency and time locked activity. In a separate set of experiments, mice were injected with the red-shifted channelrhodopsin, AAV-ReaChR, and implanted with custom combined microendscopes and fiberoptic probes. Data were analyzed using repeated-measures ANOVAs and post-hoc tests (α = 0.05). Results: Perseverative grooming increased after systemic D1 agonist injection in both OFC and VMS implanted mice compared to saline controls (p<0.05). Although average firing rates over the 5 minute imaging blocks in both regions were not significantly different, patterns of firing during individual grooming events were altered by administration of the D1 agonist. Specifically, grooming events were negatively correlated with activity in striatal neurons. Ongoing analysis is delineating the precise relationship between changes in neural activity and bouts of perseverative grooming in OFC. We have also demonstrated effective combined stimulation of ReaChR with 593nm laser light and visualization of GCaMP6f with blue LED light. Conclusions: As expected, we demonstrated an increase in perseverative grooming following D1-agonist stimulation; however, we did not observe increased striatal firing rates in response to induction of perseverative behavior. Surprisingly, time-locking of neuronal firing with calcium events showed that striatal neurons were less likely to fire during episodes of perseverative grooming, which may provide insights into novel mechanisms underlying perseveration. Analysis of firing patterns in the OFC during grooming induction is ongoing. Combining in vivo optogenetics and in vivo microscopy as demonstrated here will provide a new powerful approach for the investigation of plasticity mechanisms underlying the development of perseverative thoughts and actions. Disclosures: Nothing to Disclose.
Top of page 7.2 Histamine Modulation of Basal Ganglia in a Pathophysiologically Grounded Model of Tourette Syndrome Maximiliano Rapanelli Yale University Medical School, New Haven, Connecticut, United States Background: Tourette syndrome (TS) represents the most severe end of the continuum of tic disorders. TS is substantially genetic, but causative have been elusive; this has impeded the development of well-validated animal models in which to study pathophysiology. Methods: We used two approaches to specifically manipulate histaminergic neurons in the posterior hypothalamus in otherwise normal mice. First, we ablated these cells, using a combination transgenic-viral strategy. Second, we introduced an inhibitory designer receptor (M4 DREADD) into these cells, allowing them to be chemogenetically silenced. To probe the effects of HA in the basal ganglia we pharmacologically manipulated the H3 receptor and examined behavioral and molecular consequences in wild-type and Hdc-KO mice, using transgenic reporter animals to isolate molecular abnormalities in D1- and D2-positive medium spiny neurons (MSNs) in the striatum by immunohistochemistry. Results: Both ablation and chemogenetic silencing of histaminergic neurons produced a dramatic increase in grooming; mice in which these neurons were ablated developed bald patches from excessive grooming. H3 agonist treatment produced a range of molecular effects, activating the MAP kinase pathway in D1-positive MSNs and the Akt-Gsk3 pathway in D2-positive MSNs, and inhibiting the Akt-Gsk3 pathway in D1-MSNs. Interactive effects with D1 activation using SKF were reflected in alterations in exploratory behavior. These signaling pathways are altered both in Hdc-KO mice and after ablation or silencing of histaminergic neurons. Conclusions: The fact that ablation or silencing of histaminergic neurons in an otherwise normal adult mouse can recapitulate TS-relevant behavioral phenomenology implies that the relevant pathophysiological consequences of HA deficiency occur in the adult brain, not during development or in the periphery. Behavioral abnormalities are more marked after adult silencing of these neurons, suggesting compensatory affects in the knockout animal. Histaminergic regulation of the basal ganglia is complex but suggests possible nodes for pharmacological intervention. Authors: Maximaliano Rapanelli, Christopher Pittenger, Yale University. Disclosures: Nothing to Disclose.
Top of page 7.3 Characterization of the Putative OCD Risk Gene BTBD3 Using Mouse Models Stephanie Dulawa University of Chicago, Chicago, Illinois, United States Background: Obsessive-compulsive disorder (OCD) is a severe anxiety disorder characterized by unwanted and intrusive thoughts, images, or impulses and/or repetitive compulsive behaviors. The first genome-wide association study (GWAS) of OCD identified the gene BTBD3 as genome-wide significant (p=3.8E-8) in the trio portion of the sample. BTBD3 is a transcription factor that regulates dendritic orientation towards active axons; however, no work has examined the role of BTBD3 in modulating phenotypes relevant to OCD. Methods: We assessed the role of BTBD3 in modulating OCD-relevant phenotypes using male and female BTBD3 wild-type (WT), heterozygous (HT) and knockout (KO) mice. Mice were pair-housed mice by genotype and gender, and assessed barbering behavior over 14 weeks. Barbering refers to the plucking of hair or whiskers using the teeth. In addition, mice were also assessed in the open field, the dig test, the splash-induced grooming test, and in the prepulse inhibition (PPI) paradigm. In another cohort, we assessed the effects of chronic fluoxetine (10 mg/kg/day) or desipramine (20 mg/kg/day) treatment on observed phenotypes. Barbering was assessed each week during the fourteen weeks of drug treatment, while all other phenotypes were evaluated after four weeks of drug treatment. Finally, we compared neuronal activation using Fos mRNA expression in the orbitofrontal cortex, dorsal striatum, dorsal thalamus, and anterior cingulate gyrus of the genotypes. Results: We found that KO and HT mice barbered their cagemates significantly more than WT mice. In the open field, BTBD3 KO mice showed increased locomotion compared to WT and HT mice, and HT and KO mice exhibited robust reductions in rearing behavior. BTBD3 HT and KO mice also showed less digging behavior. In the splash-induced grooming test, HT and KO mice exhibited more frequent, but shorter grooming bouts than WT mice. BTBD3 genotype did not affect PPI or startle reactivity. Chronic fluoxetine treatment reduced barbering beginning at four weeks of treatment, whereas desipramine had no effect at any time point. Within genotype, fluoxetine significantly reduced barbering in WT and HT but not KO mice, indicating an interplay between BTBD3 expression and fluoxetine-specific reversal of barbering. No other behavioral phenotypes were altered by chronic drug treatment. Fos mRNA expression did not differ between genotypes in any brain region examined. Conclusions: In summary, decreased BTBD3 expression reduces exploratory behaviors including digging and rearing, and increases perseverative behaviors such as barbering. The reduction of barbering in BTBD3 WT and HT mice by chronic fluoxetine, but not desipramine, suggests that this phenotype may be relevant to OCD. In sum, BTBD3 expression modulates some OCD-relevant behaviors in mice. We are currently assessing the mechanisms by which BTBD3 regulates these behaviors. Disclosures: Nothing to Disclose.
Top of page 7.4 Investigation of EAAT3 Reduction as a Therapeutic Target for Obsessive Compulsive Disorder Jeremy Veenstra-VanderWeele Columbia University / New York State Psychiatric Institute, New York, New York, United States Background: Emerging structural, neurochemical, and behavioral findings point to a significant role for cortico-striatal-thalamic (CST) circuits in Obsessive Compulsive Disorder (OCD). Despite this, our understanding of the molecular pathophysiology of OCD remains inadequate, and our treatment options leave most patients with continued impairment. Cerebrospinal fluid levels and magnetic resonance spectroscopy implicate the glutamate system in OCD, including in CST circuits. Genetic linkage and association studies in OCD point to SLC1A1, encoding the neuronal glutamate/asparate/cysteine transporter EAAT3/EAAC1. No previous studies have investigated EAAT3 in CST circuits or in relation to OCD-related behavior. The most commonly associated SLC1A1 allele leads to increased expression, leading to our hypotheses that 1) increased EAAT3 contributes to OCD susceptibility, and 2) decreasing EAAT3 activity may alleviate OCD-related behavior by modulating CST signaling. Methods: To test this hypothesis, we developed a STOP-TetO knock-in mouse line that allows us to flexibly manipulate Slc1a1 expression. Initial validation of the model used quantitative RT-PCR and Western blot to examine expression. Functional validation approaches included both glutamate and cysteine uptake in striatal synaptosomes. Amphetamine (AMPH)-induced hyperactivity and stereotypic movements were used as a probe of CST circuitry-dependent behavior. To build upon AMPH-dependent behavioral changes, stereotyped repetitive grooming behavior was assessed following dopamine D1 agonist SKF-38393 administration. Immediate early gene expression (cFos immunohistochemistry) was used to evaluate the regional specificity of these findings. Dopamine receptor D1 and D2 membrane binding were measured in striatum. Dopamine and metabolite levels were used to assess presynaptic effects of EAAT3 ablation within dopaminergic neurons. Results: Slc1a1-STOP animals show a successful ablation of both mRNA and protein levels, leading to loss of cysteine uptake. Using amphetamine as a probe, we found that EAAT3 loss decreases CST circuitry-mediated hyperactivity and stereotypic behavior. Further, EAAT3 ablation diminishes response to a dopamine receptor D1 agonist, a pharmacologic model of OCD-like grooming behavior. Diminished immediate early gene response to AMPH was observed in the dorsal striatum of Slc1a1-STOP animals compared to wildtype littermate controls. Further, dopamine receptor D1 membrane binding was decreased in the dorsal striatum, with a trend for decreased D2 membrane binding as well. In wildtype animals, dopamine levels in the ventral tegmental area were decreased following AMPH administration, but no such change was observed in Slc1a1-STOP mice. Conclusions: These are the first findings implicating the most consistently associated OCD candidate gene, Slc1a1, in striatal-dependent repetitive behavior. The constellation of molecular data points to diminished dopamine receptor expression and immediate early gene response in medium spiny neurons within the dorsal striatum. Ongoing experiments are focused on understanding the regional specificity of EAAT3 ablation within CST circuits, as well as the mechanisms underlying these findings. Overall, these data suggest EAAT3 as a potential target for OCD treatment. Disclosures: Part 1: Consulting: Roche, Novartis, SynapDx, Seaside Therapeutics. Research funding: Roche, Novartis, SynapDx, Seaside Therapeutics, Forest, Sunovion. Editorial funding/support: Springer, Wiley, Part 4 Research funding: Roche, Novartis, SynapDx, Seaside Therapeutics, Forest, Sunovion. Editorial funding/support: Springer, Wiley.
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8. Reproducibility and Robustness of Experimental Data in the Neurosciences - Opportunities for Improvements Raquel Gur * , Thomas Steckler, George Koob, Patricio O’Donnell, Anton Bespalov, Robert Freedman, Stephan Heckers, Mark Geyer, Malcolm Macleod, Elena Koustova, Magali Haas University of Pennsylvania, Philadelphia, Pennsylvania, United States Reproducibility and robustness of research data are the pillars of the scientific method. However, reproducibility and robustness of published data in research, including neuroscience, is considered low, which has raised major concerns amongst industrial and academic scientists, editors, publishers and funding organizations. As a scientific community, there is a shared responsibility to address and resolve this issue. This study group will discuss the factors underlying the lack of reproducibility, but in particular will aim to address ways to improve data reproducibility, robustness and data quality in the neuroscience field using a forward-looking approach. Participants will highlight examples from various areas, including in vivo animal studies, the area of –omics, biomarkers and small explorative clinical studies, provide the different academic, industrial, editorial and funding organization perspectives, give an overview of ongoing initiatives to tackle the problem in the US and Europe, propose possible solutions and provide recommendations for future neuroscience research. Disclosures: Part 1: Served on Advisory Board for Otsuka 2013/14.
Top of page Tuesday, December 8, 2015
Top of page Study Group
9. The Future of Sex Difference Research in Neuropsychopharmacology Debra Bangasser * , Rebecca Shansky, Mohammed Milad, Tracy Bale, David Rubinow, Margret McCarthy, Janine Clayton, Jill Becker Temple University, Philadelphia, Pennsylvania, United States A goal of modern pharmacology is personalized medicine, where treatments are tailored to the specific biology of individual patients. Thus, there is an effort to identify factors that explain why patients respond differently to the same treatment. Surprisingly, the sex of the patient is often ignored as a moderating factor in treatment response. This inattention to sex differences begins at the preclinical stage of the pipeline, where the majority of pharmacology studies—from molecular mechanisms up to behavioral outcomes—are conducted only in males. However, the importance of considering sex is becoming increasingly recognized by the scientific community, and the National Institutes of Health (NIH) are promoting efforts to enhance and stimulate research examining the role of sex in health and disease. Yet it is unclear to many new to sex difference research how best to economically and efficiently include both males and females in their research programs. This study group will help address this issue and generate a discussion of the future of sex difference research in the field of Neuropsychopharmacology among the College membership. Disclosures: Nothing to Disclose.
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10. Behavioral Implications of Adult Neurogenesis and Its Potential as Treatment Target
Top of page 10.1 Tuning Lineage Homeostasis to Rejuvenate Memory Circuits and Constrain Fear Generalization in Adulthood and Aging Amar Sahay Massachusetts General Hospital / Harvard Medical School, Boston, Massachusetts, United States Background: The generation of adaptive fear responses to ambiguous threats in the environment is critically dependent on how contexts and cue-contingency relationships are encoded. Inefficient encoding of ambiguous threats results in inappropriate retrieval of aversive memories and activation of fear circuits to produce heightened avoidance behavior, overgeneralization of fear, hyper vigilance and arousal, symptoms that characterize anxiety disorders such as post-traumatic stress disorder. Recent studies by us and others has found that adult-born neurons generated from neural stem cells in the hippocampus play a critical role in discrimination of ambiguous threats and modulating generalization of fear. One neural mechanism by which this is accomplished is pattern separation, a process by which interference between similar memories is minimized. We recently hypothesized that impaired pattern separation may result in the re-activation of previously stored aversive memories and aberrant activation of circuits subserving fear and stress responses to produce fear overgeneralization, a hallmark of PTSD. Methods: Here, we employ a novel inducible genetic system by which we modulate competition for perforant path inputs between adult-born and mature dentate granule neurons. We generated mice in which we reversibly overexpress a negative transcriptional regulator of dendritic spines in mature dentate granule neurons but not young adult-born neurons. Using genetic reporters, immediate-early gene based analysis of population coding, rabies virus based mono-synaptic synaptic tracing, imaging and behavior, we analyzed the neural stem cell and progenitor compartment, connectivity of mature and adult-born dentate granule neurons and network level pattern separation following rejuvenation of the DG with an expanded population of young adult-born dentate granule neurons. We examined the behavioral impact of rejuvenating the DG with an expanded population of young adult-born neurons in adulthood, middle age and aging on contextual discrimination, reversal learning, remote memory precision and pattern separation. Results: Partial elimination of dendritic spines of mature dentate granule neurons results in a robust increase in stable long-term integration of adult-born dentate granule neurons and activation of neural stem cells without affecting olfactory bulb neurogenesis. Remarkably, complete reversal of elimination of dendritic spines in mature dentate granule neurons restores neuronal competition- and lineage-homeostasis to steady state levels. Genetic expansion of population of age-matched adult-born neurons does not affect anxiety or depression-like behaviors, but enhances contextual fear discrimination, reversal learning and precision of remote fear memories in adulthood. Furthermore, enhancements in contextual fear discrimination and precision of remote fear memories were also seen in middle-age and aging. At a network level, enhancing the population of adult-born dentate granule neurons increases pattern separation through global remapping in the DG in both adulthood and in middle-age. Conclusions: Our studies suggest that rejuvenation of the DG with adult-born neurons decreases interference as assessed behaviourally and at a network level through increased pattern separation in the DG in adulthood and middle-age. Stimulation of adult hippocampal neurogenesis may represent a novel therapeutic strategy to constrain the overgeneralization of fear in adulthood, middle-age or aging. Disclosures: Nothing to Disclose.
Top of page 10.2 Stress, Unpredictability, and the Role of Adult Neurogenesis in Response to Threat Heather Cameron National Institute of Mental Health, Bethesda, Maryland, United States Background: New neurons are born in the dentate gyrus throughout life, but their normal function and potential role in depressive illness are unclear. Stress is an important factor in depression and also interacts with adult neurogenesis, strongly inhibiting production of the new neurons. New neurons, in turn, modulate endocrine and behavioral stress responses, though it is not known how this occurs. Unpredictability is a key feature of stress, so we asked whether adult-born neurons affect behavior differently in response to predictable and ambiguous threats. Methods: Mice expressing herpes simplex virus thymidine kinase under the control of the GFAP promoter (GFAP-TK mice) and wild type littermate controls were given valganciclovir during adulthood to selectively ablate adult-born neurons in the transgenic mice. Mice with and without new neurons were trained on cued fear conditioning using either a reliable cue or an ambiguous cue, which terminated with a shock in only 50% of trials. Behavioral responses to the cues and to novel situations were tested following conditioning. Results: Mice lacking new neurons had normal freezing responses to reliable cues but showed diminished response to ambiguous cues. This same pattern was reflected in activation of mature granule cells and CA3 pyramidal cells as measured by immediate early gene expression. In the novelty-suppressed feeding test of anxiodepressive-like behavior, reliable cue conditioning had no effect on normal mice, while ambiguous cue conditioning dramatically increased latency to eat in these mice. Mice lacking neurogenesis showed intermediate increases in latency following both reliable and ambiguous cue conditioning, and their response did not differ according to the predictability of previous conditioning. Conclusions: These experiments demonstrate that new neurons are important for behavioral responses to ambiguous threat. New neurons enhance hippocampal activation and protective stress-related behaviors toward an ambiguous threat cue. Days after an aversive experience, new neurons enable differential responding in novel situations according to the predictability of previous threats. These changes could bias behavior in ambiguous situations to optimally adapt to safe and stressful environments. Disclosures: Nothing to Disclose.
Top of page 10.3 Modes of Division and Differentiation of Adult Neural Stem Cells may Define Long Term Consequences of Therapies Grigori Enikolopov Stony Brook University, Stony Brook, New York, United States Background: Production of new neurons in the adult brain is important for behavior, pathophysiology, aging, and neural tissue repair in humans and animals. New hippocampal neurons may mediate the action of antidepressants and other drugs and therapies. New neurons are born from neural stem cells which are maintained at specific locations in the adult brain. Neural stem cells are the only source of new neurons in the adult brain. Therefore, our understanding of the features and the role of new neurons depends on the ability to identify adult stem cells and reveal basic mechanisms governing their maintenance, division, differentiation, and death. Methods: Our main approach is generating animal models that enable visualization of stem cells and their environment and monitoring of their signaling landscape. These animal models are complemented by new methods that we developed to determine parameters of division and differentiation of neural stem cells. Results: The use of our reporter mouse lines allowed us to develop a new model for the quiescence, maintenance, and division of the hippocampal stem cells. Our results indicate that adult neural stem cells may remain quiescent for their entire postnatal life, but, when activated, rapidly divide several times in quick succession to bud off daughter cells that eventually yield neurons, while the remaining stem cell differentiates into a mature astrocyte, thus leaving the stem cell pool. We found that decrease in the number of new neurons that accompanies aging is driven by the disappearance of stem cells via their division-coupled astrocytic differentiation. This continuous loss of stem cells underlies age-dependent diminished production of new neurons and may contribute to age-related cognitive impairment. We next applied our approach to determine the classes of stem and progenitor cells that are affected by various pro- and anti-neurogenic factors. We found that stem cell output can be increased in different ways and that each mode of augmented production of new neurons may have different effect on the pool of stem cells, with important implications. For instance, while some antidepressant treatments (e.g., fluoxetine or deep brain stimulation) do not affect stem cells, but instead target rapidly amplifying progenitor population, other antidepressant therapies increase the number of asymmetric divisions of stem cells without recruiting additional stem cells (and therefore leading to an increased number of new neurons without additional loss of stem cells). In contrast, some clinically used compounds increase recruitment of normally quiescent stem cells in division, potentially leading to an increase in new neurons at the expense of premature exhaustion of the stem cell pool. Conclusions: Our findings highlight the potential clinical relevance of studies of adult neural stem cells and may have direct implications for human therapy. Our results warn that any drug or therapeutic treatment that involves changes in neurogenesis should be investigated for the precise mechanisms of those changes, since seemingly identical outcomes may be induced by different mechanisms and with different long-term consequences. Disclosures: Nothing to Disclose.
Top of page 10.4 Molecular Regulation of Hippocampal Neurogenesis in Neuropsychiatric Disease and Treatment Maura Boldrini Columbia University / New York State Psychiatric Institute, New York, New York, United States Background: Major depressive disorder (MDD) presents with inability to disengage from negatively valenced material and biased memory recall, and depression score is negatively correlated to pattern separation performance. Adult hippocampal neurogenesis is required for pattern separation and adaptations to stress in rodents. Increasing adult hippocampal neurogenesis is sufficient to improve pattern separation in mice. We reported fewer dentate gyrus (DG) mature granule neurons (GNs) in unmedicated MDD, compared with psychiatrically healthy controls. We published that subjects with earlier onset of MDD have fewer GNs in anterior DG vs. subjects with later MDD onset. Although age-related decline of adult neurogenesis is less pronounced in human than in mice, it may still mediate age-related changes in cognitive processing. Selective serotonin repute inhibitors (SSRIs) treatment increase adult neurogenesis in mice and we found that in MDD is associated with more neural progenitor cells (NPCs), GNs, mitotic cells, and angiogenesis. It is unclear if the neurogenesis cascade in MDD is compromised at the level of cell proliferation, maturation or survival, and which are the mechanism by which SSRIs increase adult neurogenesis. Proliferation of NPCs is affected by growth factors, including brain derived neurotrophic factor (BDNF), but fluoxetine-mediated increase in cell survival is BDNF-independent. Vascular endothelial growth factor (VEGF), through the Flk-1 receptor (VEGFR2), is required for fluoxetine-induced cell proliferation. Serotonin receptors and trophic factors act on kinases modulating downstream intracellular molecules that regulate cell maturation and survival. These include cyclic-AMP response element binding (CREB), a leucine zipper transcription factor increased by antidepressants and expressed during cell maturation, and poly [ADP-ribose] polymerase (PARP), a DNA-binding protein activated by DNA strand breaks that protects survival via enzymatic DNA repair. PARP ribosylation also regulates chromatin histone ribosylation in the hippocampus after memory acquisition, regulating the epigenetic mechanism involved in reprogramming neuronal gene expression in memory consolidation. We aimed to assess molecular pathways involved in the regulation of human DG cell proliferation, maturation and survival in MDD, with SSRI treatment, and aging. Methods: We performed immunohistochemistry and stereology to quantify DG neurons and glia expressing VEGFR2, CREB and PARP in 22 psychiatrically healthy controls, 22 unmedicated subjects with MDD and 11 MDD subjects treated with SSRIs for at least 3 months before death. Subject age ranged from 19 to 84 years. All subjects received DSM-IV-validated psychological autopsy for diagnosis, brain and blood toxicology, and neuropathology. All subjects died from sudden death and time between demise and autopsy was within 24 hours. Results: Uncleaved PARP and non-phosphorylated CREB are expressed in more DG cells in untreated MDD than in SSRI-treated MDD and controls. VEGFR2 expression in DG cells correlated with more NPCs and GNs in anterior DG. More lifetime depressive episodes and more severe Global Assessment Scale (GAS) score correlated with fewer GNs in untreated MDD. We did not detect fewer NPCs or GNs with aging, but angiogenesis was decreased. Conclusions: Findings support the hypothesis that PARP and CREB have a role in regulating GN maturation and survival and that VEGF action may result in more adult neurogenesis in human DG. MDD is a major cause of global burden and its severity shows a relationship with GN number. Intracellular pathways that regulate brain structural plasticity may be drug targets for new classes of antidepressants or cognitive-enhancing treatments. Disclosures: Nothing to Disclose.
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11. The Role of Epigenetic Mechanisms in the Transition into Alcohol Addiction
Top of page 11.1 The Role of Epigenetic Mechanisms in the Medial Prefrontal Cortex in the Transition to Alcohol Dependence Markus Heilig National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland, United States Background: In rodent models, a prolonged history of alcohol dependence is associated with persistent escalation of alcohol seeking and intake. We have previously shown that this is in part driven by coordinated and persistent dysregulations of gene expression networks in the medial prefrontal cortex (mPFC). Recent work in our laboratory has identified contributions to these processes from microRNA (Tapocik et al, J Neurosci 2014) and DNA-methyl transferase activity (Barbier et al, J Neurosci 2015), but little is known about a potential role of other epigenetic enzymes in reprogramming the mPFC transcriptome. Methods: Alcohol dependence was induced using chronic intermittent alcohol vapor exposure. Following recovery, RNA-sequencing was used to screen the transcriptome of the mPFC for persistent differential expression of epigenetic enzymes. PRDM2 was identified as a differentially expressed candidate, and the molecular consequences of its repression were assessed by measuring H3K9 mono-methylation. Functional consequences at the behavioral level were then assessed by knocking down PRMD2 expression in the mPFC of non-dependent rats using a lenti-viral shRNA vector. Chip-Seq was used to identify PRDM2 regulated target genes as downstream mediators. Functional consequences on addiction-like traits were evaluated by assessing operant self-administration, stress-induced reinstatement of alcohol seeking, and aversion-resistant alcohol seeking. Results: In rats with a history of dependence, both the RNA-seq screen and a focused confirmatory qPCR analysis showed decreased expression of PRDM2. Immunohistochemical analysis indicated that this occurred in neurons. Alcohol-induced PRDM2 repression was reversed by the DNA methyltransferase inhibitor RG108, suggesting that it is driven by DNA methylation. Conversely, PRDM2 knockdown in non-dependent rats induced a set of gene expression changes that overlapped with those found following alcohol dependence. These expression changes were associated with behavioral consequences otherwise seen following a history of dependence. These consequences included escalated alcohol intake, increased resistance to quinine adulteration, and enhanced stress-induced reinstatement. Several genes that exhibited a significant decrease in H3K9me1 enrichment following dependence were identified in the ChIP-seq study, including synaptotagmin 1 (Syt1). Since neurosynaptic communication was heavily implicated in the gene ontology analysis, we confirmed H3K9me1 enrichment in controls compared to post-dependent rats using ChIP-PCR. Conclusions: We demonstrate for the first time a role of PRDM2 for behaviors that are critical in alcoholism. Specifically, our findings indicate that DNA-methylation mediated repression of PRDM2 is involved in multiple aspects of alcohol dependence, specifically stress-induced relapse, compulsivity-like behavior and escalation in alcohol intake) and therefore provide a rationale for exploring the potential of targeting PRDM2 for treatment. Disclosures: Nothing to Disclose.
Top of page 11.2 A Novel Role for the Histone Demethylase KDM6B in Alcohol Dependence Andrea Johnstone Miller School of Medicine at University of Miami, Miami, Florida, United States Background: Epigenetic signaling pathways oversee DNA methylation and post-translational histone modifications to encode transcriptomic changes in response to environmental cues. Enzymes that catalyze these modifications are increasingly recognized to mediate behaviors associated with drug and alcohol dependence. We hypothesize that alcohol exposure influences long-term gene expression and behavioral abnormalities through changes in epigenetic enzyme activity. Methods: We used a rat model of alcohol dependence to identify epigenetic enzyme expression changes in the brain that are induced by alcohol exposure. In this model, rats are chronically and intermittently exposed to intoxicating concentrations of ethanol vapors. These rats exhibit behavioral and molecular changes reminiscent of human alcoholics, including long-term voluntary increases in alcohol consumption. Three weeks after ethanol exposure, Nanostring nCounter analysis was used to quantify mRNA expression levels of over 100 epigenetic enzymes in the nucleus accumbens (NAc) of alcohol dependent rats compared to controls. Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) was used to validate significantly altered genes. Several enzymes of interest were also quantified using qRT-PCR in prefrontal cortex (PFC) tissue from alcohol dependent rats and human alcoholics. Western blot analysis was used to quantify the protein levels and signaling pathways associated with KDM6B, a histone demethylase implicated in the RNA expression analyses. To identify the genes regulated by this epigenetic enzyme, we used chromatin immunoprecipitation to isolate the DNA associated with trimethylated histone H3 lysine 27 (H3K27me3), the histone site regulated by KDM6B. DNA associated with H3K27me3 in the NAc of control and alcohol dependent rats was then subjected to DNA sequencing (ChIP-seq). Results: RNA levels of a histone demethylase, KDM6B, are dysregulated in both the PFC and NAc of alcohol dependent rats and human alcoholics. KDM6B protein is increased in the NAc of alcohol dependent rats. Upregulation of KDM6B protein is paralleled by downregulation of H3K27me3, consistent with the known demethylase activity of KDM6B. Preliminary analysis of ChIP-seq data implicated H3K27me3-mediated disruption of inflammatory signaling pathways in response to alcohol exposure. Conclusions: KDM6B is dysregulated in key brain regions involved in reward perception in a relevant rat model of alcoholism as well as in human alcoholics. KDM6B dysregulation is associated with alcohol induced epigenetic changes in inflammatory signaling pathways. Ongoing experiments aim to determine whether genes implicated in the ChIP-seq study are functionally dysregulated by KDM6B. We also aim to study alcohol-seeking behavior in response to in vivo viral-mediated manipulation of KDM6B expression. These studies may elucidate how an epigenetic mechanism translates alcohol exposure into the chronic transcriptional and behavioral changes that underlie alcohol dependence. Disclosures: Nothing to Disclose.
Top of page 11.3 Breakdown in the Corticostriatal BDNF Pathway Drives the Transition from Social to Compulsive Drinking for Alcohol Dorit Ron University of California at San Francisco, San Francisco, California, United States Background: Previously we found that the brain-derived neurotrophic factor (BDNF) in the dorsal striatum and specifically in the dorsolateral striatum (DLS) is part of a homeostatic signaling pathway that keeps alcohol drinking of rodents in moderation1-3. Methods: We used mouse paradigms that model moderate and excessive alcohol drinking, in combination with molecular methods, viral-mediated gene delivery, pharmacology and a transgenic mouse line. Results: We found that moderate drinking of alcohol leads to an increase in BDNF expression in the DLS, which is abolished in response to repeated cycles of binge drinking and withdrawal. The same excessive drinking paradigm produces a robust reduction of BDNF expression in the prefrontal cortex (mPFC) and the orbital frontal cortex (OFC). We obtained data suggesting that epigenetic modifications as well as microRNAs expression are the mechanisms underlying the breakdown of corticostriatal BDNF expression that in turn drives excessive drinking. Using a transgenic mouse model, we discovered that a single point mutation within the BDNF gene produces compulsive alcohol drinking despite negative consequences. Finally, we found that restoring the normal function of the corticostrial BDNF signaling pathway brings alcohol drinking back to moderate levels. Conclusions: Malfunction of the corticostriatal BDNF signaling drives the transition from moderate consumption to excessive, compulsive intake. Restoring the function of the BDNF signaling in the corticostriatal pathway shifts alcohol consumption from excessive to moderate levels. Disclosures: This work was supported by NIH-NIAAA R01 AA016848 (D.R.), NIH-NIAAA P50 AA017072 (D.R.) and by the State of California for medical research on alcohol and substance abuse through the University of California, San Francisco (D.R.). References: 1. McGough, N.N. et al. J Neurosci 24, 10542-52 (2004). 2. Jeanblanc, J. et al. J Neurosci 29, 13494-502 (2009). 3. Jeanblanc, J. et al. Eur J Neurosci 37, 607-12 (2013).
Top of page 11.4 Transcriptome Sequencing Reveals Novel Splice Variants in Human Alcoholic Brain Dayne Mayfield The University of Texas, Austin, Texas, United States Background: Long-term alcohol abuse and dependence (Alcohol Use Disorder; AUD) alters brain function and is linked to lasting changes in gene expression. AUD is a chronic, relapsing condition that imposes a significant socioeconomic burden by adversely affecting the health of millions of individuals worldwide. Similar to other complex trait disorders, the development and continuance of AUD is influenced by the interaction of multiple genetic and environmental factors that may be distinctly regulated across multiple brain regions. Methods: To identify novel transcripts that are differentially expressed in brain regions involved in substance abuse, we conducted whole transcriptome sequencing (RNA-Seq) of the central nucleus of amygdala, basolateral amygdala, and superior prefrontal cortex from postmortem brain tissue of alcoholics (N=30) and matched control (N=30) subjects. Results: RNA-Seq analysis permits an unbiased deeply sequenced assessment of the transcriptional profile altered in disease. For example, over 1 million potentially novel exons that neighbor known genes were identified. In addition, transcriptome profiling revealed global effects on gene co-expression networks altered by chronic alcohol abuse in these brain regions. We identified alterations in complex gene networks that may involve multiple splice variants relevant for the neurobiology of AUD. Gene specific sequencing of GABBR1 from postmortem cortex revealed a number of novel transcripts altered in relation to AUD. Conclusions: The expression of alternatively spliced transcripts uncovered human-specific isoforms that are not present in animal models, underscoring the importance of human postmortem brain analyses. Disclosures: Nothing to Disclose.
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12. From Animals to Humans: The Role of Neuroinflammation in Psychosis and Psychosis Risk
Top of page 12.1 Neuroinflammation and Oxidative Stress Precede the Onset of Schizophrenia-Relevant Behavioral Dysfunctions in Mouse Models of Prenatal Infection Urs Meyer University of Zurich - Vetsuisse, Zurich, Switzerland Background: Neuroinflammation and oxidative stress have been widely implicated in schizophrenia and related psychotic disorders. It remains a matter of debate, however, whether these pathophysiological processes develop before or subsequently to the onset of full-blown psychotic disease. Methods: We used infection-based neurodevelopmental mouse models of schizophrenia and related disorders to study the temporal association of neuroinflammation, oxidative stress, and behavioral dysfunctions. In addition, we explored the functional contribution of neuroinflammation and oxidative stress to the behavioral abnormalities by anti-inflammatory and anti-oxidant pharmacological interventions. Results: Using a two-hit model of combined exposure to mild prenatal viral-like immune activation (polyI:C, 1 mg/kg; on embryonic day 9) and sub-chronic peri-adolescent stress, we found marked microglia activation, pro-inflammatory cytokine expression, and cellular signs of oxidative stress in the hippocampus and prefrontal cortex of adolescent but not adult animals. On the contrary, multiple schizophrenia-related behavioral abnormalities emerged with a delayed onset in adulthood but not adolescence. Treatment with the anti-inflammatory agent minocycline (MINO) or the anti-oxidant N-acetyl-cysteine (NAC) during peri-adolescent stress exposure prevented the subsequent emergence of behavioral deficits in this environmental two-hit model. Similar findings were obtained in a mouse model of intense prenatal viral-like immune activation (polyI:C, 5 mg/kg; on embryonic day 9), which demonstrated a temporal dissociation between the emergence of neuroinflammation (in early adolescence) and schizophrenia-related behavioral dysfunctions (in adulthood). Conclusions: Our novel preclinical data suggest that neuroinflammation and oxidative stress are manifest before and contribute to the adult onset of schizophrenia-relevant behavioral dysfunctions following infection-mediated neurodevelopmental disruption. Disclosures: Nothing to Disclose.
Top of page 12.2 Study of Altered Markers of Oxidative Stress in Patients with Early Stage Schizophrenia Jennifer Coughlin Johns Hopkins University School of Medicine, Baltimore, Maryland, United States Background: Aberrant glutamatergic pathways and oxidative stress may underlie the pathophysiology of schizophrenia. The molecular mechanisms underlying aberrant reduction-oxidation (redox) cascades in the pathophysiology of psychosis remain elusive. N-Acetylaspartate (NAA) levels are high in neurons, sensitive to change in mitochondrial function, and metabolically linked to both redox and glutamatergic pathways. Therefore alterations in the homeostatic relationship between NAA and glutamate in the brains of patients may reflect changes in oxidative stress pathways. We hypothesize that early stage schizophrenia involves an underlying noxious cycle with imbalance of key antioxidants, namely superoxide-dimutase-1 (SOD1) and glutathione (GSH), resulting oxidative stress and decoupling of the homeostatic relationship between NAA and glutamate. Methods: We collected cerebrospinal fluid (CSF) samples from patients with recent-onset schizophrenia (SZ), antipsychotic-naïve patients with first episode of psychosis (FEP), those at high risk for SZ, and matched healthy controls (HC). The CSF concentrations of several key inflammatory and oxidative markers were compared between cases and controls. We also examined the levels of NAA and Glx (the sum of glutamate and glutamine) measured using proton spectroscopy ([1H]MRS), relative to the level of creatine (Cr) as an internal control. The dorsolateral prefrontal cortex (DLPFC) and anterior cingulate cortex (ACC) in 25 patients with schizophrenia and 17 matched healthy controls were studied. Results: We report greatly changed levels of several markers of oxidative processes in CSF from patients with recent-onset SZ, medication-naïve patients with FEP, and those at risk for SZ. Ratios of NAA/Cr and Glx/Cr did not differ significantly between the patient and control groups in either the DLPFC or ACC. The NAA/Cr and Glx/Cr ratios correlated positively (r= 0.63, p=0.017) after controlling for age and smoking in healthy controls, but not in persons with schizophrenia (r= -0.33, p=0.124). No significant correlation between NAA/Cr and Glx/Cr ratios was observed in the ACC in either group. Conclusions: Our findings of diminished levels of SOD1, IL6, and other markers of redox imbalance support our proposed oxidative stress model of schizophrenia. Furthermore, decoupling of NAA and Glx in the DLPFC may reflect the interconnection of glutamatergic pathways and oxidative stress in the pathology of schizophrenia, and may prove a biomarker of the disease. Disclosures: Nothing to Disclose.
Top of page 12.3 PET Imaging of Microglia in Drug Naive Patients at High Risk of Psychosis and the Effects of Antipsychotics on Microglia Oliver Howes King's College London / Institute of Psychiatry, London, United Kingdom Background: Converging lines of epidemiological, genetic and biological indicate that altered inflammatory processes play a role in schizophrenia. Evidence from post-mortem and PET imaging studies in patients with schizophrenia indicates microglia activation plays a role in this. However, it is not known when microglial changes occur in the development of the disorder or what the effect of antipsychotic treatment is on microglia. Methods: To test this people at ultra-high risk of psychosis (n=14) who were all antipsychotic naive and patients diagnosed with schizophrenia (n=14) were studied using a second generation PET tracer that shows high affinity for a marker express on activated microglia and compared to age matched controls (n=28). PET imaging data were acquired using [11C]-PBR28 and controlling for genotypes that may affect binding. To investigate the effect of antipsychotics on microglia, rats were treated with antipsychotics or vehicle after receiving an inflammatory stimulus (lipopolysaccharide) or vehicle. Results: Relative [11C]-PBR28 binding was elevated in grey matter throughout the brain in subjects at ultra-high risk of psychosis with a large effect size (d=0.9, p<0.05). Greater elevation in relative [11C]-PBR28 binding was positively associated with greater symptom severity (r>0.4, p<0.05) and negatively with total grey matter volume (r>0.4, p<0.05). [11C]-PBR28 relative binding was also elevated in the patients with schizophrenia with a large effect size (d=1.1, p<0.05). Antipsychotic treatment reduced absolute density of microglia, and reduced morphological changes associated with activation in the LPS treated rats. Conclusions: These data suggest that i) microglia activation is present prior to the onset of psychosis and linked to the severity of prodromal symptoms; ii) antipsychotic treatment is not responsible for microglial activation in rat models; and iii) microglial activation persists despite antipsychotic treatment in patients with schizophrenia. Disclosures: Part 1: Dr. Howes has received investigator-initiated research funding from and/or participated in advisory/ speaker meetings organised by Astra-Zeneca, BMS, Eli Lilly, Jansenn, Lundbeck, Lyden-Delta, Otsuka, Servier, and Roche. Neither Dr. Howes nor his family have been employed by or have holdings/ a financial stake in any biomedical company, Part 4: Dr. Howes has received investigator-initiated research funding from and/or participated in advisory/ speaker meetings organised by Astra-Zeneca, BMS, Eli Lilly, Jansenn, Lundbeck, Lyden-Delta, Otsuka, Servier, and Roche. Neither Dr. Howes nor his family have been employed by or have holdings/ a financial stake in any biomedical company.
Top of page 12.4 Imaging Neuroinflammation in Clinical High Risk and First Episode Antipsychotic Free Psychosis: An in-Vivo Pet Study with [ (18)F ] -FEPPA Romina Mizrahi University of Toronto, Toronto, Canada Background: Neuroinflammation and abnormal immune responses have been implicated in schizophrenia. Past studies using positron emission tomography (PET) that examined neuroinflammation in patients with schizophrenia in-vivo using the translocator protein 18kDa (TSPO) target were limited by radioligand use, resolution of scanners used, and the potential confounding effect of antipsychotic medications. No previous report investigated the state of the clinical high risk for schizophrenia. Methods: A cross-sectional study was performed using [(18)F]-FEPPA and a high-resolution research tomograph (HRRT). PET data were analyzed to obtain [(18)F]-FEPPA total volume of distribution (VT) using a 2-tissue compartment model with an arterial plasma input function, as previously validated. All subjects were classified as high-, medium- or low-affinity [(18)F]-FEPPA binders on the basis of rs6971 polymorphism, and genotype information was incorporated into the analyses of imaging outcomes. Results: 8 (mean age = 23.25, SD = 4.43) CHR and 17 patients with untreated first episode psychosis (FEP) (mean age = 26.53, SD = 7.32), and 15 healthy volunteers (HV) (mean age = 25.07, SD = 4.96) underwent [(18)F]-FEPPA PET and magnetic resonance imaging. We found a trend for a significant effect in medial prefrontal cortex (F=2.62 p=0.08) with CHR participants having 30.5 % increased [(18)F]-FEPPA binding relative to HV, with no difference with FEP (7.14%). No other significant effects were found, although several regions (temporal, DLPFC and PFC) show >20% increase in CHR. Explorative association analyses found a significant negative association between PANSS total and general scores and [(18)F]-FEPPA binding in hippocampus (r = -0.573, p = 0.026; r = -0.637, p = 0.011), and total gray matter (r = -0.522, p = 0.046; r = -0.628, p = 0.012). Further analyses with cognitive measures will be presented, together with analyses with pseudo-reference regions (cerebellum/total gray matter) and comparison data in Alzheimer's disease with the same radioligand. Conclusions: This study addresses a relevant question in schizophrenia research; the role of neuroinflammation in the pathophysiology of the disease, without the confound of antipsychotic medications, using state of the art imaging technology and a second generation TSPO radioligand while controlling for genotype. Understanding the neurobiological changes associated with microglial activation has the potential to identify novel treatment targets (i.e. decrease neuroinflammation) in schizophrenia and in those at clinical high risk for the disease. Disclosures: Nothing to Disclose.
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13. Genetic Approaches to Delay Discounting: Human and Non-Human Animal Approaches
Top of page 13.1 Genetic Basis of Impulsive Behavior in Humans Project: Initial Delay Discounting James MacKillop McMaster University / St. Joseph's Hospital, Hamilton, Canada Background: Delay discounting is a behavioral economic index of impulsivity that is robustly associated with addictive behavior and hypothesized to be an endophenotype for addiction. A small number of molecular genetic studies have reported significant associations between loci associated with dopaminergic signaling and DD, but have had a number of limitations. These studies have used relatively small numbers of participants and clinical samples within which genetic and disorder-induced influences on impulsivity cannot be disentangled. Furthermore, the studies to date have largely focused on polymorphisms that are the “usual suspects” within candidate genes. This presentation will report on the initial findings pertaining to delay discounting within the Genetics of Impulsive Behavior project, a study of genetic associations with diverse impulsivity phenotypes that employs candidate genes, candidate systems, and genomewide approaches in a large sample of healthy young adults. The focus is on the latent phenotypic structure of the impulsivity phenotypes and, specifically, the hypothesis that the phenotypes would conform to an orthongonal tripartite model, the three factors being delay discounting, behavioral inhibition, and impulsive personality traits. Methods: A sample of 1262 healthy young adults (18-25) with limited substance abuse was ascertained from two sites and all participants were evaluated for delay discounting, motor inhibition, and personality indices of impulsivity using multiple measures (15 total phenotypes). A comprehensive assessment of control variables (e.g., income, education) was also conducted. A urine drug screen confirmed no recent drug use. DNA was collected via saliva sample and genotyping using the Illimina Infinium PsychArray BeadChip, developed by the Psychiatric Genomics Consortium to augment coverage of loci associated with psychiatric disorders (515,000 loci). Confirmatory factor analysis (CFA) was used for hypothesis testing. Results: Preliminary analyses revealed significant site differences in impulsivity, but these were eliminated when other control variables (e.g., education, age) were included and site was not included in subsequent models. The primary CFA provided strong support for the three-factor structure (CFI=0.948, TLI=0.936, RMSEA=0.06, SRMR=0.041). The four indices of delay discounting were highly intercorrelated (rs>0.75) and all substantially loaded on the latent delay discounting factor. Similar patterns were present for behavioral inhibition and impulsive personality traits, although the trait of Sensation Seeking did not substantially load on the personality traits factor. The delay discounting factor exhibited low magnitude associations with the other factors, suggesting it is an independent trait. Conclusions: Using an a priori hypothesis-testing approach for the first time, these findings reveal the multidimensional nature of impulsivity as a trait. Specifically, the results indicate that the latent phenotypic structure of impulsivity is tripartite in nature and, within that structure, delay discounting is one independent factor. Based on these findings, the individual’s latent impulsivity phenotypes will be the focus of genomic dissection. Disclosures: Nothing to Disclose.
Top of page 13.2 Genetics of Delay Discounting in Humans: Heritability and Preliminary Evidence for Genetic Association Andrey Anokhin Washington University School of Medicine, St. Louis, Missouri, United States Background: Delay discounting (DD), preference for smaller immediate rewards over larger but delayed rewards, is an established behavioral model of impulsive choice, a key component of a broader impulsivity construct. Elevated DD has been implicated as a potential intermediate phenotype (endophenotype) for a range of psychopathologies characterized by impulsive decision making, most notably, addictions and psychopathology. DD has been extensively studied in animal models of impulsive behavior, including genetic studies. However, few studies examined genetic influences on DD in humans. Methods: Adolescent twins participating in a prospective longitudinal study of (n=602, 52% females, ages 16-20) completed a computerized DD test. DD was quantified using both parametric and non-parametric methods (the k-coefficient of a hyperbolic function and area under the discounting curve, respectively). We investigated age-related changes in DD, long-term stability of individual differences, heritability (i.e. the proportion of inter-individual variability that can be attributed to genetic factors), and examined the role of genetic variation in the 5HT system in the determination of DD. Results: DD rate showed a modest but significant decrease with age, suggesting a reduction in overall impulsivity from middle to late adolescence. Significant test-retest correlations were observed in the age range from 16 to 20 years (r=0.64 to 0.75, p<0.001) indicating longitudinal stability of individual differences in decision-making behavior during middle and late adolescence. The genetic analysis using the twin design revealed significant heritability of both DD measures, with genetic factors accounting for 45%-64% of inter-individual variability in DD. Furthermore, DD showed significant associations with 5HT receptor genes (HTR1B, HTR2B) and tryptophan hydroxylase gene (THP2), providing preliminary support for possible contribution of genetic variation in the serotonergic system to individual differences in DD and warranting further association studies in larger samples. Conclusions: In conclusion, converging evidence suggests that DD is a stable and heritable trait in adolescents and emerging adults that can serve as an intermediate phenotype in genetic studies of addictive and impulsive disorders. Disclosures: Nothing to Disclose.
Top of page 13.3 Strategies and Results: When using Mouse Models to Identify Commonalities Between a Delay Discounting Endophenotype and Endophenotypes Associated with Alcohol Use Disorder Suzanne Mitchell School of Medicine Oregon Health & Science University, Portland, Oregon, United States Background: High levels of impulsivity (delay discounting [DD], relative preference for smaller but immediate rewards over larger but delayed rewards) are associated with various psychopathologies including alcohol use disorder. Data indicate that there are genetic influences on DD and on the development of alcohol use disorder, but the genetic relationships amongst DD and alcohol consumption and other heritable features of alcohol response are unclear. Methods: In all studies, male mice were exposed to the adjusting amount procedure (Richards et al. 1997, J Exp Anal Behav, 67, 353-366). This method allows mice to choose between a small, immediate sucrose-solution reward and a larger sucrose-solution reward that is delayed 0, 2, 4, 8 or 12 s on different sessions. An initial within-subject study compared behavior on this procedure and a variant in which delays were presented in within sessions blocks. However, little discounting was seen in the latter procedure, causing behavior on the two task variants to be uncorrelated, and its use was discontinued. In Study 1, behavior for 11 inbred strains was assessed, and genetic correlations with ethanol-associated endophenotypes derived. In other studies, we assessed DD in lines selected for differing levels of ethanol withdrawal symptomatology or ethanol consumption, and on-going studies are examining correlations between DD and responses to passively administered ethanol in a heterogeneous mouse stock to identify novel phenotypic targets. Results: In Study 1, our data indicated significant strain differences in DD and substantial heritability for DD as a behavioral trait (h2=0.39), as well as heritability for side bias away from the “delayed” alternative when the delay was absent (h2=0.31). Further, there were significant genetic correlations between DD and ethanol preference (10%, n=10: r=0.72), though not with other indices of response to ethanol (e.g., chronic withdrawal, n=7: r=-0.65; sedation, n=10: r=0.11), nor with sucrose consumption or preference (n=11: r=-0.04 and 0.19 respectively). In selected line studies, heightened chronic withdrawal tended to be associated with steeper DD (p=0.07) but short term selection for high and low ethanol drinking was not (p=0.12). Preliminary data from on-going studies suggest that, for heterogeneous stock mice, there are positive correlations amongst DD and various chronic withdrawal measures, including social approach, and chronic exposure measures, including behavioral sensitization. Conclusions: These data suggest that DD has a heritable component in mice, and is genetically associated with chronic withdrawal and consumption, but that effect sizes are small. Reasons for this, including differences in amount and delay sensitivity that contribute to heightened delay discounting, as well as pleiotropic genetic contributions to these complex behaviors, warrant additional investigation. Further, heterogeneous stock studies suggest addition ethanol-associated behaviors which could be examined for shared genetic contribution in future studies. Disclosures: Nothing to Disclose.
Top of page 13.4 Identification of Individual Differences in Delay Discounting by Heterogeneous Stock Rats Jerry Richards Research Institute on Addictions, Buffalo, New York, United States Background: In the natural environment important reinforcers such as food or water are often distributed in patches. Staying in a patch may deplete the density of available reinforcers to low levels so that it is better to travel to a new patch. The decision about when to leave a depleting patch in order to maximize overall reinforcement rate depends upon the time required to travel to a new patch. Longer travel delays mean that it is better to stay in the patch longer and deplete the patch to lower densities before leaving. Decisions made in the patch foraging situation are similar to those made in delay discounting (DD) procedures. In each case, choices are made between a delayed larger reinforcers and more immediate smaller reinforcers. Optimal foraging theory predicts that the animal will discount by delay to a degree that maximizes over all reinforcement. Patch foraging differs from laboratory based “self-control” procedures typically used to study DD in non-human animals because repeated choice of the more immediate alternative can lead to greater reinforcer rates, whereas in “self-control” procedures choice of the delayed alternative always produces greater reinforcement due to experimenter imposed inter-trial intervals. It is arguable that the contingencies of reinforcement imposed by laboratory based “self-control” procedures are unlikely to be encountered in the natural environment. Methods: A large number of heterogeneous stock rats (n >100) with highly variable genotypes were tested on a sequential choice DD procedure that simulates contingencies of reinforcement that are intended to be similar to those encountered by animals foraging in patchy environments. Delays of 0, 6, 12, 18, 24 s were tested. Lococotor activity in a novel environment was tested prior to DD testing. Results: Rats were sorted according to how much they discounted by delay. Comparison of the twenty of rats that discounted the most (high discounters) with the 20 rats that discounted the least (low discounters) showed that high DD yielded the greater reinforcement rates. We also observed marked differences in switching between the two water feeders at the 0 s delay with some rats switching after every reinforcer while others stayed at the depleting water feeders for much longer periods before switching. There was no correlation between DD and the tendency to switch patches. Switchers and stayers were equally sensitive to the effects of delay. We found no correlation between loco motor activity and either switching or discounting, indicating that the observed differences were not due to general differences in activity. Conclusions: These results demonstrate that DD can be advantageous by increasing overall consumption rate. Two behavioral phenotypes, high & low discounters and switchers & stayers were observed. Research is currently underway to identify genotypes that may underlie these patterns. This research may contribute to the identification of genetically determined biases in decision making underlying personality differences related to impulsivity. Disclosures: Nothing to Disclose.
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14. The Road to Recovery: Delineating the Neural Circuits of Compulsive Drug Use
Top of page 14.1 The ‘Ins’ and ‘Outs’ of the Striatum: Mapping Addiction Circuits Susan Ferguson University of Washington / Seattle Children's Research Institute, Seattle, Washington, United States Background: Addiction is a chronic relapsing disorder characterized by the loss of control over drug intake, high motivation to obtain drug, and a persistent craving for the drug. Accumulating evidence implicates cellular and molecular alterations within cortico-basal ganglia-thalamic circuitry in the development and persistence of this disease. The striatum is a heterogeneous structure that sits at the interface of this circuit, receiving input from a variety of brain regions (e.g., prefrontal cortex, ventral tegmental area) to guide behavioral output, including motor planning, decision-making, and motivation. However, the vast interconnectivity of this circuit has made it difficult to isolate how individual projections and cellular subtypes within this circuit modulate each of the facets of addiction. Methods: To begin to address these issues, we used novel viral vector targeting approaches to express inhibitory Gi/o-coupled DREADDs (Designer Receptors Exclusively Activated by Designer Drugs) selectively in striatal cells of the indirect or the direct pathways or in prefrontal cortical afferents to the striatum. Activation of DREADDs by the otherwise inert ligand clozapine-n-oxide produces transient decreases in neuronal activity and allowed us to examine the effect of these targeted cellular manipulations on behaviors associated with addiction (drug self-administration, psychomotor sensitization). In addition, we have expressed the genetically encoded calcium indicator GCaMP6m into the striatum to exam calcium signaling following different patterns of cocaine administration (drug self-administration under continuous or spiking access as well as following extended access, acute and repeated experimenter administered) using two-photon imaging in a slice preparation. Results: We found that decreasing activity of the indirect pathway enhanced the development of psychomotor sensitization whereas decreasing activity of the direct pathway blocked the persistence of this phenomenon. Although decreasing activity of cortical afferents to the striatum had no effect on drug-taking in a self-administration paradigm it did impair the development of sensitization. Interestingly, inhibiting corticostriatal afferent activity during drug use enhanced conditioned responding to the drug-associated context as well as produced slower rates of extinction and increased responding during drug prime-induced reinstatement – an effect that was normalized by inhibiting these corticostriatal afferents immediately prior to the drug prime. Finally, we found that different patterns of drug administration lead to distinct alterations in calcium signaling in the striatum, both at baseline and following drug exposure. Conclusions: These studies use cell-specific targeting and novel molecular tools to begin to isolate the contributions of specific striatal afferent and efferent projections in behaviors related to addiction as well as to map changes in the activity of striatal neurons following different patterns of drug use. The findings from these studies support the hypothesis that an imbalance between direct and indirect striatal pathway activity may mediate a transition to addiction, and that activity of these pathways is regulated by top-down control from the cortex. However, they also demonstrate that the cortico-basal ganglia-thalamic circuitry is more complex and dynamic than has been revealed previously. Disclosures: Nothing to Disclose.
Top of page 14.2 Corticostriatal Mechanisms of Compulsive Cocaine Seeking in Rats Barry Everitt University of Cambridge, Cambridge, United Kingdom Background: Compulsive drug use is defined as the maladaptive propensity to repeat, or perseverate, in drug seeking or consumption in the face of significant aversive or disadvantageous consequences. But not all individuals that initially take drugs develop compulsive drug seeking and this individual vulnerability has been modeled in procedure that requires drug seeking to be performed under the threat or actual receipt of punishment, enabling investigation of the neural mechanisms underlying compulsive drug seeking. Methods: Rats were trained in a seeking-taking chained procedure in which responding on one lever (the ‘seeking’ lever) results in access to a second, ‘taking’ lever, responding on which results in a cocaine infusion. Randomly on 50% of trials, seeking responses result not in access to the taking lever, but in mild punishment, thereby capturing the conflict between opponent motivational states that has been suggested to characterize addictive behavior. We have investigated the neurochemical correlates and neural substrates of compulsive cocaine seeking using pharmacological manipulations of the brain. Results: A discrete domain of the anterior dorsolateral striatum was shown to be involved specifically in punished, but not unpunished, cocaine seeking. We also identified reduced levels of 5-HT utilization across prefrontal cortical areas (as well as decreased DA utilization in the dorsal striatum) selectively in compulsive, but not non-compulsive rats, despite a very similar history of cocaine exposure. Forebrain 5-HT depletion, or systemic treatment with a 5-HT2C receptor antagonist after a short cocaine history (no rats are compulsive), resulted in increased levels of seeking under punishment. A serotonin-selective 5-HT reuptake inhibitor, citalopram, dose-dependently reduced compulsive seeking. Conclusions: The results show that the great majority of a population of rats with an escalated, or long history of, cocaine intake are able to withhold their cocaine seeking responses — effectively achieving abstinence — when there is the intermittent risk of punishment. However, 20% of rats continued to seek cocaine compulsively. A discrete zone of the anterior dorsolateral striatum exerts a strong influence on compulsive drug seeking by mediating the influence of the threat of intermittent and unpredictable contingent punishment on cocaine seeking responses. Reductions in cortical 5-HT and striatal DA utilizatisation clearly differentiated compulsive and punishment-sensitive groups despite their common drug history. This indicates both the possible causal involvement of reduced 5-HT transmission in the compulsive cocaine seeking phenotype and the therapeutic potential of reversing this deficit and thereby the propensity to seek cocaine. Disclosures: Nothing to Disclose.
Top of page 14.3 Dynamic Changes in Phasic Dopamine Release to Drug-associated Cues Following Chronic Use and Withdrawal Paul Phillips University of Washington, Seattle, Washington, United States Background: When drug-related cues are presented to drug abusers in a non-contingent manner (i.e., not dependent on their own actions), they often illicit drug craving and promote drug seeking. This type of cue exposure is considered to be one of the most robust stimuli to elicit relapse of drug use following periods of abstinence. In fact the potency of drug cues increases over periods of time without exposure to drugs, a phenomenon known as ‘incubation of craving'. Prominent theories of drug addiction hypothesize that the amount of mesolimbic dopamine elicited by drug-related cues increases following chronic drug and this change accounts for hyper-responsiveness to these cues. However, there are no previous empirical reports that directly measured how phasic dopamine elicited by non-contingent drug cue presentation changes over chronic drug use and following periods of withdrawal. Methods: Male Wistar rats underwent intravenous cocaine self-administration in one-hour or six-hour sessions followed by periods of drug withdrawal (one, seven or thirty days). Prior to and following some self-administrations (early and late training) and following withdrawal, animals were subjected to short cue (non-contingent) exposure sessions. Also following withdrawal rats underwent extinction sessions (self-administration sessions without cocaine or cue delivery) followed by cue presentation to elicit reinstatement of drug seeking, and test the degree of 'incubation of craving'. During self-administration, cue-exposure and extinction/reinstatement sessions, dopamine release was recorded in the nucleus accumbens using fast-scan voltammetry. Results: Dopamine release to non-contingent drug cues increases following chronic drug use. This effect was more marked following six-hour cocaine self-administration sessions versus one-hour sessions, and in individuals that escalated their drug intake compared to those with stable drug use. This increase in phasic dopamine release to drug cues correlated with increased motivation to obtain the drug as assessed in behavioral sessions using progressive ratio of reinforcement. We also observed incubation of drug craving that progressed from one to seven to thirty days of withdrawal and was more pronounced following six-hour self-administration sessions compared to two-hour sessions. Conclusions: Phasic dopamine release elicited by non-contingent drug-cue exposure increases during chronic drug use and withdrawal and enhances cue elicited drug-seeking behavior. These findings are in stark contrast to phasic dopamine transmission to response-contingent presentation of drug cues during drug taking which decrease following chronic drug use promoting escalation of drug taking. We conclude that while decreased phasic dopamine release during drug taking promotes escalation, increased phasic dopamine release contributes to craving and relapse, consistent with incentive sensitization theories. Disclosures: Part 1: My spouse is an employee of Amgen Inc. and we own stock in that company, Part 2: My spouse is an employee of Amgen Inc. and we own stock in that company, Part 3: My spouse is an employee of Amgen Inc. and we own stock in that company, Part 5: My spouse is an employee of Amgen Inc. and we own stock in that company.
Top of page 14.4 Functional Network Connectivity Between Rostral ACC and Insula Predicts Response to Varenicline for Tobacco Dependence (TD) Claire Wilcox University of New Mexico, Placitas, New Mexico, United States Background: More than 95% of smoking cessation efforts fail. Clarifying the neural circuitry underlying relapse can improve treatment research. Resting state functional connectivity (rsFC) and functional network connectivity (FNC) analyses provide information about coherence between brain regions and networks. Previous work has shown that the nicotine withdrawal state is associated with greater rsFC between rACC and insula (Huang 2014) or less negative rsFC between networks comprised of rACC (DMN) and insula (salience) (Lerman 2014). Insula-rACC connectivity decreases with varenicline (Sutherland 2013b). We explored whether insula-rACC FNC predicted later smoking behavior in individuals enrolled in a clinical trial of varenicline for TD. Methods: Participants were 145 treatment-seeking cigarette smokers between the ages of 18 and 55 enrolled in a double-blind, placebo-controlled trial of varenicline, and who underwent a 6 minute resting state scan before treatment initiation. Individuals were randomized to active medication or placebo for a period of 12 wks, titrated as tolerated to 1 mg twice daily by day 8, with a target quit date of day 8. The time-line follow-back procedure was used to record tobacco use. Binary point prevalence data were not analyzed due to low numbers of quitters in the placebo group. Missing data were imputed to screen visit values. Resting state data was preprocessed using a standard pipeline. Group independent components analysis was utilized to extract individual subject time series from 2 intrinsic connectivity networks (which fell within insula and rACC) previously identified from a large sample of controls (Allen 2011). Time series were filtered and motion was regressed out. Functional network connectivity (FNC) between insula and rACC components was calculated. Two linear regressions were performed with number of cigarettes (NumCig) at screen, treatment group assignment (RxGrp), rACC-insula FNC, and an interaction term (FNC X RxGrp) as predictors. Outcome variables were NumCig smoked over the past 4 wks at 6 wk and 12 wk. Results: There was a significant RxGrp X FNC interaction for insula-rACC FNC predicting both 6 (p=.03) and 12 wk (p=.02) NumCig. In the varenicline group, but not the placebo group, FNC predicted overall NumCig at 6 (p=.035, b=-.23) and 12 wk (p=.05; b=-.21) such that greater FNC at baseline predicted less smoking, correcting for baseline smoking. It was not a significant predictor in the placebo group (6 wk NumCig, p=.47, b = .08; 12 wk NumCig, p=.33, b = .10). When baseline smoking was removed from the model, the RxGrp X FNC interaction term was still significant at 6 wk and 12 wk (ps=.02), and there was a positive association between insula-rACC FNC and greater smoking at a trend level at 12 wk (b=.22, p=.09). Conclusions: In individuals on varenicline, higher insula-rACC connectivity predicted better smoking outcomes. Greater FNC did not significantly predict outcomes when varenicline and placebo participants were combined, although there was a positive association between FNC and smoking at week 12, at a trend level. Consistent with data that excessive insula-rACC rsFC occurs during withdrawal, and evidence that varenicline decreases withdrawal, our data indicate that rsFC or FNC between rACC and insula may be an important treatment target and predictor of response to varenicline. Disclosures: Nothing to Disclose.
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15. Sharing is Caring: An Overview of the Data Sharing Landscape
Top of page 15.1 Data Sharing at NIMH Bruce Cuthbert National Institute of Mental Health, Bethesda, Maryland, United States Background: Data sharing has become an issue for several reasons. There are broad public concerns about the reproducibility of both clinical and preclinical research. Congress worries about redundancy of research investments. NIH wants to improve the efficiency of research, noting the value of secondary data analyses. Data sharing is also one aspect of increasing transparency of the entire research process. Methods: Beginning with the Autism Centers of Excellence, NIMH required the sharing of individual level clinical data into the National Database for Autism Research (NDAR). A similar deposition and sharing policy was deployed for genomic data. Last year, NIMH extended this policy to all clinical trials, requiring individual level data to be deposited to the National Database for Clinical Trials (NDCT). Descriptive/raw data are expected to be submitted to NDCT on a semi-annual basis (beginning six months after the award budget period has begun). Analyzed data are expected to be submitted prior to publication/public dissemination (whether the findings are positive or negative). Data access and sharing of de-identified data are worked out on an individual basis but the goal is release to qualified investigators at the time of publication. Results: The NIMH Limited Access Datasets project, including data from 23 large NIMH-supported clinical trials, recently sent out its 300th dataset. The datasets are referred to as "limited access" because, for the protection of the human study participants from whom the data were obtained, only qualified researchers may obtain access to the datasets, and only upon the approval of a Data Use Certification (DUC), which stipulates specific terms and conditions under which the data may be used, including terms for data security and confidentiality, and acknowledgement of the original data submitters in publications. The datasets have provided the raw material for at least 160 published scientific papers, an example of how data sharing provides an avenue for multiplying the return on investment and benefit from clinical research. Conclusions: Standardization, integration, and sharing are the principles underlying a new culture of clinical research. The transition to this new culture will not be easy for everyone, but transparency is ultimately essential for public trust and data sharing is a critical aspect of transparency. Note that data sharing introduces its own set of problems: issues of privacy, access, and data provenance will need to be addressed in this new world of open science. Disclosures: Nothing to Disclose.
Top of page 15.2 Perspectives on Responsible Clinical Trial Data Sharing Timothy Coetzee National Multiple Sclerosis Society, New York, New York, United States Background: The Institute of Medicine (IOM) recently released a report entitled “Sharing Clinical Trial Data: Maximizing Benefits, Minimizing Risk” (http://www.iom.edu/Reports/2015/Sharing-Clinical-Trial-Data.aspx). The report, which was sponsored by a diverse group of stakeholders including government funding agencies, regulators, foundations, and pharmaceutical and medical device manufacturers, was produced by an expert committee with the goal of fostering emergence of a culture of clinical trial data sharing that will increase scientific knowledge and ultimately improve therapies for patients. Methods: The committee recognized that there are several stages in the clinical trial cycle at which data can be shared and made four main recommendations for responsible sharing of clinical trial data. Results: Stakeholders in clinical trials should foster a culture in which data sharing is the expected norm. Sponsors and investigators should share the various types of clinical trial data at appropriate times in the clinical trial life cycle: at trial registration, 12-18 months after study completion, no later than 6 months after publication, 30 days after regulatory approval, or 18 months after abandonment. Holders of clinical trial data should employ publicly available data use agreements that reduce risks, enhance secondary analysis, and protect public health. The public should be involved in reviewing data requests. Stakeholders should work together to address key challenges and foster a culture toward a vision of data sharing. Conclusions: Clinical trial data sharing has many potential benefits to the scientific community and to patients. However, risks and concerns remain, and the infrastructure and culture to support data sharing are currently only in the infancy stages. Nevertheless, finding solutions for disease demands increased data sharing. To change the culture, data sharing must be rewarded, required, and enforced. Protections of all interested parties must be in place, and user-friendly infrastructure to support data deposition must be developed and standardized. The challenge is significant, but worthy of our collective effort. Disclosures: Nothing to Disclose.
Top of page 15.3 Current Practices for Sharing Data: The Landscape in the Private Sector Lisa Gold Merck & Co., Inc., North Wales, Pennsylvania, United States Background: According to Wikipedia “Data sharing is the practice of making data used for scholarly research available to other investigators. Replication has a long history in science. Many funding agencies, institutions, and publication venues have policies regarding data sharing because transparency and openness are considered by many to be part of the scientific method.” Shifts in the research ecosystem including big data opportunities, electronic health records and data transparency policies are converging to inspire new thinking and action around the sharing of research data to drive novel research queries and innovation. In July 2013 PhRMA joined with the EFPIA in adopting Principles for Responsible Clinical Trial Data Sharing, reflecting the biopharmaceutical sector’s strong support for responsible data sharing that recognizes the importance of protecting patient privacy, respects the integrity of national regulatory systems, and maintains incentives for continued investment in biopharmaceutical research. This initiative further encourages all medical researchers to promote medical and scientific advancement by adopting 5 commitments related to enhanced data sharing with Researchers, public access to clinical Study Information, sharing results with patients who participate in clinical trials, certifying procedures for sharing clinical trial Information and reaffirming commitments to publish clinical trial results. Recent focus in the regulatory arena is exemplified by the European Medicines Agency new standards for clinical trial data transparency. In January, the Institute of Medicine issued a global report concluding that a multi-stakeholder effort is needed to develop a culture, infrastructure, and policies that will foster responsible sharing—now and in the future. Methods: In response to this changing landscape pharmaceutical companies have committed to principles on data sharing and invested in supportive policies and systems. Merck has had a data sharing policy since 2008 that has generated at least 40 manuscripts and 8 presentations to date. A revised policy in 2014 introduced a website, guidelines for submission of research proposals for data and a charter for governance of an external review board. Multi-company initiatives are helping to drive unified approaches. A GSK launched website has evolved into a multi-sponsor site involving 13 companies, where researchers request access to anonymized patient level data and supporting documents from clinical studies to conduct further research. Other stakeholder groups such as the Harvard Multi Regional Clinical Trials Center include a focus on return of results, providing clinical trial participants with plain language summaries of the trial results and information about the outcome of the study. Non-competitive consortia are harnessing the power of collaboration across research sectors. The Innovative Medicines Initiative (IMI) does this by facilitating collaboration between key players involved in healthcare research, including universities, pharmaceutical and other industries, patient organizations, and medicines regulators. An integrated basic and clinical approach within IMI is the NEWMEDS program, Novel Methods leading to New Medications in Depression and Schizophrenia. This international consortium of scientists comprises one of the largest ever academic-industry collaboration projects. Results: The NEWMEDS collaborative has assembled a dataset of individual patient level information from randomized placebo-controlled trials of second-generation antipsychotics by 5 pharmaceutical companies. Examination of patient and trial-design-related determinants of outcome has revealed new insights into optimal trial duration and patient attributes that will result in reducing patient exposure to placebo and experimental treatments in future trials. Additional examples of such high impact results from data sharing activities will be presented. Conclusions: For all its promise, data-sharing entails significant risks, burdens and challenges that must be addressed in order to fulfill its potential. These include infrastructure, patient privacy, sponsor responsibility and respect for the data. Despite these concerns, there are now enough results with positive impact to provide a strong rationale for continuing. Momentum continues to build and these efforts have the potential to transform research and improve health by speeding up the development of, and patient access to, innovative medicines. Disclosures: Part 1: Full time employee of Merck & Co, Part 2: Full time employee of Merck and Co, Part 3: Full time employee of Merck & Co, Part 5 Merck & Co.
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16. Brain-wide 'Glymphatic' Pathway: Visualization and Function
Top of page 16.1 Evidence for the Impairment of Glymphatic Pathway Function in the Aging Brain Jeffrey Iliff Oregon Health & Sciences University, Portland, Oregon, United States Background: Alzheimer’s disease (AD), like other neurodegenerative conditions characterized by the mis-aggregation of different proteins, is primarily a disease of the aging brain. Yet the changes in the aging brain that render it vulnerable to protein mis-aggregation and neurodegeneration remain unknown. The glymphatic system is a brain-wide paravascular pathway along which CSF from the subarachnoid space recirculates through the brain parenchyma, clearing interstitial solutes such as amyloid β (Aβ) and tau, from the brain interstitium. Paravascular CSF recirculation and Aβ clearance are dependent on the astroglial water channel, which is expressed along perivascular endfeet that ensheath the cerebral vasculature. Methods: Glymphatic pathway function was evaluated in the young by ex vivo whole slice fluorescence microscopy and radiolabeled Aβ clearance assay. Perivascular aquaporin-4 (AQP4) localization was evaluated by immunofluorescence. AQP4 localization was assessed in the post-mortem human frontal cortex by immunofluorescence. Results: In the aging mouse cortex, perivascular localization of AQP4 was impaired, and this AQP4 mis-localization was associated with slowed glymphatic CSF recirculation and Aβ clearance in the aging brain. In α-syntrophin knockout mice, which express normal AQP4 levels, but lack perivascular AQP4 polarization, CSF recirculation was similarly impaired, suggesting that loss of perivascular AQP4 localization is sufficient to impair glymphatic pathway function. In studies carried out in human autopsy tissue, perivascular AQP4 localization in the frontal cortex declined with increasing age. Strikingly, among a cohort of so-called ‘super-agers’ that survived cognitively intact beyond 85 years of age, perivascular AQP4 localization was maintained at levels observed in the young cortex. Impairment of perivascular AQP4 localization was significantly associated with worsening Aβ plaque burden, more advanced Braak stage, and worsening cognitive decline. Conclusions: These findings demonstrate that glymphatic pathway function is impaired in the aging rodent brain, and suggest that age-related impairment of glymphatic pathway function may be one factor making the aging human brain vulnerable to Aβ aggregation and the development of AD. Disclosures: Nothing to Disclose.
Top of page 16.2 Metabolic Aspects of Cerebral Capillary Water Efflux William Rooney Oregon Health & Science University, Portland, Oregon, United States Background: The cerebral capillary endothelium provides extensive surface area for water exchange between the plasma and brain parenchyma. Cerebral capillary endothelial cells are in intimate contact with astroglial and pericytes which are thought to be important in control of local blood flow and ultimately drive gylmphatic flow. Combinations of neurons, glia, and microvessels have been termed “neurogliovascular units,” because of their fundamental symbiotic metabolic and energetic interactions. Methods: A 7T whole-body MRI instrument, with quadrature transmission and 24-channel phased-array receive head RF coils, was used. Dynamic contrast measurements employed a single-slice inversion recovery (IR) turboflash technique, sampling magnetization eight post-inversion times across a 0.05 mmol/kg gadoteridol injection. Data were processed using a pharmacokinetic model that incorporated two-site exchange formalism. Results: As an example, areas of the brain damaged by multiple sclerosis (MS) disease activity have impaired energy metabolism leading to abnormal capillary mean water lifetimes; in chronic lesions we find a nearly 2-fold decrease in trans-capillary water flux and normal appearing brain tissue (NABT) shows ~20% decrease; consistent with positron emission tomography estimates of reduced cerebral metabolism in MS. Conclusions: Results from our work suggest that tight metabolic coupling between neurons, glia, and endothelia, the “neurogliovascular unit”, produces a phenomenon that allows assessment of metabolic activity using dynamic contrast MRI techniques. Water flux across the capillary endothelium is driven by the local tissue homeostatic sodium-potassium ATPase (NKA) turnover which in turn is responsive to metabolic activity behind the blood-brain barrier. The slower the metabolic activity, the slower the NKA turnover and accompanying water flux. The capillary blood water efflux is a sensitive measure of this metabolic activity, and can be mapped with dynamic contrast enhanced MRI techniques. Regional cerebral metabolic activities vary significantly across the sleep-wake cycle which is expected to result in regional differences in capillary water efflux and may be an important component of glymphatic system function. Disclosures: Nothing to Disclose.
Top of page 16.3 Brain-Wide Glymphatic Transport in the Unconscious State: Influence of Body Position Helene Benveniste The State University of New York, Stony Brook School of Medicine, Stony Brook, New York, United States Background: We recently discovered a brain-wide waste removal pathway which shares many features with the classical lymphatic drainage system in other body organs. We named this system the ‘glymphatic’ pathway because it is dependent on aquaporin 4 water channels expressed on perivascular astrocytic endfeet. Importantly, our studies also show that soluble amyloid-beta and tau proteins are cleared from the brain along this newly discovered glymphatic pathway. Transport through this pathway is controlled by the brain’s arousal level because during sleep or anesthesia the brain’s interstitial space volume expands (compared to wakefulness) resulting in faster waste removal. Humans, as well as animals, exhibit different body postures during sleep, which may also affect waste removal. The objective of this study was to evaluate the influence of body position on CSF-ISF exchange rates in the unconscious state. Methods: Dynamic contrast enhanced MRI and kinetic modeling was used to quantify CSF-ISF exchange rates in anesthetized rodents’ brains in supine, prone or lateral positions. To validate the MRI data and to specifically assess the effect of body posture on clearance of amyloid beta we used a mouse model in combination fluorescence microscopy and radioactive tracers, respectively. Results: Glymphatic transport in the anesthetized, unconscious rat and mouse was most efficient in the lateral position when compared to supine or prone positions. In the prone position, where the rat’s head was in the most upright position (mimicking posture during the awake state), transport was characterized by ‘retention’ of the tracer, slower clearance and more CSF efflux along larger caliber cervical vessels. The optical imaging and radiotracer studies confirmed that glymphatic transport and amyloid-beta clearance was superior in the lateral and supine positions. Conclusions: In rats, the MRI analysis showed that the reduced uptake of Gd-DTPA in the brain of PRONE rats was paralleled by increased efflux of CSF along the cervical vasculature. Imaging of fluorescently tagged CSF tracers in mice revealed that the PRONE position also was linked to reduced CSF influx in brain, while the influx of fluorescent tracers into spinal cord was increased. We suspect that the head position affect the activity of the glymphatic system similarly in rat and mice, but the difference in approach (MRI vs optical imaging) did not allow a formal species comparison. However, both sets of observations suggest that the lateral position during sleep has a clear advantage with regard to glymphatic removal of beta amyloid and other metabolic waste products of neural activity. While this is speculative and awaits testing in human subjects, other clinical studies have shown that beta amyloid content in CSF is lower in sleep than wakefulness, consistent with increased clearance. We propose that the most popular sleep posture (lateral) has evolved to optimize waste removal during sleep and that posture must be considered in diagnostic imaging procedures developed in the future to assess CSF-ISF transport in humans. Disclosures: Nothing to Disclose.
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17. rt-fMRI Neurofeedback: Are We There Yet? Steven Grant * , Vani Pariyadath, Pearl Chiu, Anna Rose Childress, Hans Breiter, Anne Evins, Mark George, Sean Mackey, Jon-Kar Zubieta National Institute on Drug Abuse, Bethesda, Maryland, United States Over a decade ago, studies that human subjects are able to modulate fMRI signals from specific brain regions in real-time (real-time fMRI neurofeedback / modulation, or rt-fMRI). rt-fMRI has been used not only for experimental research, but has been proposed as a means for non-invasively treating brain dysfunctions by having patients can learn to control activity in brain regions that mediate specific symptomology. Neuromodulation using rt-fMRI has been demonstrated recently in several contexts. For example, some studies have shown that subjects can modulate behavioral and emotional responses to pain and emotionally-valenced photographs, motor response cues, lexical stimuli and reward-related stimuli by selectively manipulating fMRI BOLD signal in anterior cingulate cortex, amygdala, insula, precentral gyrus, and Broca’s area and ventral striatum. However, rt-fMRI remains controversial as a number of issues remain unresolved. Such issues include, individual difference in people's ability to modulate rt-fMRI signals, optimal subject instructions, relation of regional brain activation to specific symptoms, and whether the proper control conditions involve rt-fMRI originating irrelevant brain circuitry, non-contingent feedback, or signals from another subject. In particular, the question of the proper control condition raises difficult ethical and policy issues that could affect the course of future research and potential clinical applications. In 2008 NIDA issued a Request for Applications entitled “Facilitating Self-Control of Substance Abuse Related Brain Activity Through Real-Time Monitoring of fMRI Signals”. In this study group, the investigators supported by this RFA will discuss the advances and challenges encountered during their studies, with an emphasis on implementation, ethical and policy issues relevant to having fMRI neurofeedback progress to being a robust research procedure and a potential treatment modality. Disclosures: Nothing to Disclose.
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18. Signals from the 4th Dimension: How the Extracellular Matrix Regulates Synaptic Plasticity and Neuropsychiatric Disease
Top of page 18.1 Mechanisms Through which Extracellular Proteolysis Shapes Neuronal Structure and Function George Huntley Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: Synaptic structural and functional plasticity underlies many forms of enduring behavioral experience, including learning and memory, and is critical for proper formation of circuits during early postnatal development. The molecular mechanisms that drive coordinated remodeling of both synaptic form and function have been enigmatic, but there is an emerging recognition that matrix metalloproteinases (MMPs) are critically involved in the rapid remodeling of the synaptic microenvironment associated with synaptic, cellular and behavioral plasticity, both in adulthood and during development. MMPs are a large family of extracellularly-acting, mostly secreted proteases whose targets include extracellular matrix (ECM), adhesion proteins and other cell-surface molecules that are important for maintaining and modifying synaptic architecture. The focus of this talk is on the mechanistic underpinnings of these varied roles of MMPs and their canonical targets in shaping circuit structure and function. Methods: Gain- and loss-of-function approaches (i.e. mouse genetics, exogenous inhibitors and recombinant-active MMPs) are applied to both acute hippocampal slices and adult mice and rats in vivo in combination with synaptic electrophysiology, live-cell imaging, novel and standard localization methods and behavioral assays in order to understand MMP control of synaptic morphology, circuit connectivity and brain function. Results: MMP-9 is rapidly upregulated and becomes proteolytically active in hippocampus by stimuli that induce LTP as well as by a single-trial, inhibitory-avoidance learning experience. Such regulation of MMP-9 is specific MMP-9 is not regulated during LTD, nor is the closely related MMP-2 regulated by experimentally- or behaviorally-induced plasticity. Once proteolytically active, MMP-9 signals though integrin receptors both to potentiate synapses and concomitantly to enlarge the spine-heads in which they sit. These processes require dynamic actin and modification of certain actin-binding proteins. When MMP function is abrogated, stable functional and structural synaptic plasticity as well as hippocampal-dependent memory are significantly impaired. Developmentally, the effects of manipulating a canonical target of extracellular proteolysis on establishment of functional cortical circuitry was investigated in mouse somatosensory barrel cortex. Sema7A, an atypical member of the semaphorin family of guidance cues, is normally cleaved and deposited at high levels within barrel centers during early postnatal development when thalamocortical axons grow in and establish the characteristic isomorphic map of the contralateral whisker pad. We found that ablation of Sema7A disrupts barrel cytoarchitecture, reduces the polarized orientation of spiny cell dendrites, and impairs thalamocortical evoked synaptic responses. Conclusions: Together these data provide compelling support for the idea that MMPs and other extracellularly-acting proteases function in normal synaptic physiology, coordinating both synaptic structural and functional plasticity appropriate for establishing circuit structure/function developmentally as well as enabling memory later in life. Disclosures: Nothing to Disclose.
Top of page 18.2 Role of Perineuronal Nets in Cocaine-Induced Plasticity Barbara Sorg Washington State University, Vancouver, Washington, United States Background: Specialized aggregations of extracellular matrix called perineuronal nets (PNNs) appear during juvenile stages of development and surround primarily fast-spiking, parvalbumin-containing GABAergic interneurons in the central nervous system. Several studies have shown that removal of PNNs re-establishes juvenile-like states of plasticity. However, only a single study has examined a role for PNNs in plasticity induced by drugs of abuse. Here we determined 1) whether PNN removal in the medial prefrontal cortex (mPFC) prevented cocaine-induced plasticity; and 2) whether cocaine altered PNN intensity in the mPFC. Methods: In the first experiment, male Sprague-Dawley rats were trained for cocaine-induced conditioned place preference (CPP). PNNs were removed by the enzyme chondroitinase-ABC (Ch-ABC) prior to training for CPP, prior to extinction of CPP, or prior to cocaine memory reactivation. In the second experiment, PNNs were removed by Ch-ABC prior to training for cocaine self-administration. In the third experiment, cocaine was given non-contingently for 1 or 5 days and PNN staining intensity was analyzed 2 hr later. Results: Removal of PNNs within the prelimbic region of the medial prefrontal cortex (mPFC) impaired both the acquisition/consolidation and reconsolidation of cocaine-associated memories in the CPP task. Preliminary studies also indicate that PNN removal impaired the acquisition of cocaine self-administration. Consistent with reduced cocaine-induced plasticity when PNNs were removed, 1 day of cocaine decreased PNN intensity while 5 days of repeated cocaine treatment increased the intensity of PNNs, and this intensity was positively correlated with increased cocaine-induced behavioral sensitization. Conclusions: Our studies indicate that PNNs within the mPFC impair cocaine-induced plasticity. Consistent with our findings, decreased PNN intensity is generally associated with enhanced plasticity and learning while increased PNN intensity is associated with diminished plasticity and establishment of strong memories. Our studies have implications for understanding how these extracellular matrix structures may be manipulated during the formation and maintenance of cocaine-associated memories to reduce relapse. Disclosures: Nothing to Disclose.
Top of page 18.3 Matrix Metalloproteinases and Cell Surface-Associated Substrates Katherine Conant Georgetown University Medical Center, Washington, District of Columbia, United States Background: Matrix metalloproteinases (MMPs) are zinc-dependent endopeptidases that were named for their ability to remodel extracellular matrix. A subset of MMPs may be released from brain-derived cells including neurons and glia. Release is increased in a neuronal activity dependent manner and plays a role in specific types of learning and memory. Because MMP activity is concentrated at the cell surface, the processing of specific cell surface molecules could be critical to MMP-dependent effects on neurotransmission. Work is focused on the processing of synaptic cell adhesion molecules (CAMs) and G protein coupled receptors. Methods: We utilize striatal slices from mice that express the calcium indicator GCaMP3 specifically in D2 dopamine receptor-bearing neurons. Slices are pretreated with vehicle, dopamine, or the D1 receptor agonist SKF81297 and subsequent NMDA stimulated calcium flux is recorded and analyzed. In complementary studies, we measure proliferation and neuronal differentiation of progenitor cells derived from the hippocampal dentate gyrus of adult mice that over express a glial-derived MMP. Results: Dopamine and the D1 receptor agonist SKF81297 enhance NMDA-stimulated calcium flux in striatopallidal neurons. Potentiation is diminished by pretreatment with a broad-spectrum antagonist of MMP activity or by an inhibitor of integrin-dependent signaling, and may thus involve the generation of soluble CAM fragments that contain integrin-binding domains. In complementary studies, increased expression of MMP-1 enhances proliferation and neuronal differentiation of progenitor cells from the adult hippocampal dentate gyrus. Both effects are reduced by an inhibitor of protease activated receptor-1, a G protein coupled receptor that is engaged following cleavage in its N-terminal domain. Conclusions: Findings suggest that processing of specific cell surface molecules may contribute to MMP-associated plasticity. Specific findings may be relevant to addiction, as well as to anti-depressant associated neurogenesis. Disclosures: Nothing to Disclose.
Top of page 18.4 Nitric Oxide Signaling in the Accumbens Core Drives Relapse to Cocaine Seeking Alexander Smith Medical University of South Carolina, New York, New York, United States Background: Matrix metalloproteinases (MMPs) are pro-plasticity enzymes that degrade the extracellular matrix to promote synaptic growth and reorganization. Both MMP-2 and MMP-9 are required for cue-induced reinstatement of cocaine seeking and the associated transient synaptic potentiation of corticostriatal synapses. Following extinction of cocaine self-administration (SA) there is a constitutive upregulation of MMP-2 in the nucleus accumbens core (NAcore), and cue-induced reinstatement causes a transient induction of MMP-9 activity. However, it is unknown how either of these two enzymatic inductions occurs. One mechanism by which MMPs are activated is S-nitrosylation by nitric oxide (NO). NO is produced in the NAcore by neuronal nitric oxide synthase (nNOS) inside a subpopulation of interneurons that is approximately 1% of neurons in the striatum. We hypothesized that cocaine SA induces nNOS activity that in turn increases activity of MMP-2/9, and that stimulation of NO production in the NAcore would stimulate MMP activity, synaptic potentiation, and reinstatement of cocaine seeking. Methods: Male NOS1-Cre transgenic mice were used to selectively chemogenetically target nNOS-expressing interneurons in the NAcore with a Gq-DREADD virus (AAV2-hSyn-DIO-HM3Dq). In the first experiment, we tested the ability of stimulation of these cells to stimulate MMP activity. To do this, mice were implanted with intra-NAcore guide cannula, and either CNO or vehicle was microinjected 15 minutes prior to measuring MMP activity via in vivo zymography. A second experiment examined the dependence of MMP activity on nNOS activity, using either a cocktail of CNO and the nNOS inhibitor NPLA, or CNO and vehicle prior to zymography. In order to determine whether nNOS activity was able to potentiate synapses on medium spiny neurons (MSNs), patch-clamp electrophysiology examined AMPA/NMDA ratios (A/N). Animals received systemic CNO or vehicle prior to being sacrificed for electrophysiological recording. In the final experiment, mice were trained in cocaine SA with conditioning light and tone cues for 10 days, and then extinguished for 10 days, then either CNO or vehicle was injected i.p. 15 minutes before either an extinction or cue-induced reinstatement session. Results: We show that stimulating nNOS-expressing interneurons via Gq-DREADD increased MMP activity, and this effect was completely abolished by pre-treatment with the nNOS inhibitor NPLA. Furthermore, Gq-stimulation of nNOS-expressing interneurons was able to potentiate A/N on MSNs, the major cell type that constitutes 95% of the accumbens. Finally, stimulation of these interneurons was not only able to potentiate cue-induced reinstatement, but also drove reinstatement in the absence of cues. Conclusions: We conclude that nNOS activity is not only necessary, but also sufficient to drive drug seeking behavior and the associated pathophysiology. Although nNOS-expressing interneurons constitute only approximately 1% of the NAcore, activation of these cells stimulated MMP activity globally, potentiated synapses on MSNs, and induced drug-seeking behavior. Thus, this small cell population may represent a ‘master-switch’ by which cocaine seeking is initiated, and may be an important pharmacotherapeutic target for the treatment of relapsing behavioral disorders. Disclosures: Nothing to Disclose.
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19. Neuroimaging, Addiction and Big Data: Opportunities and Challenges
Top of page 19.1 Prediction of Substance Misuse Initiation (Alcohol, Nicotine and Cannabis): Insights from the Imagen Project Robert Whelan University College Dublin, Dublin, Ireland Background: It has been demonstrated repeatedly that early substance use is a strong risk factor for adult substance dependence and, therefore, identifying predictors of substance use in adolescence would be undeniably advantageous. Longitudinal population neuroscience studies, though logistically challenging, offer a promising approach to detecting the predictors of substance misuse as they potentially enable the causes and effects of substance misuse to be separated. Methods: Brain data from a large number of regions of interest, encompassing the entire brain, were extracted for the following: structural gray matter (corrected for total gray matter volume), successful and unsuccessful inhibitory responses from the Stop Signal Task, reward anticipation and outcomes from the Monetary Incentive Delay Task, and responses to angry faces in a test of emotional reactivity. For all analyses (alcohol, nicotine & cannabis), participants were non-users at the time of data acquisition (age 14 years-old). At age 16, 150 non-drinkers were compared with 121 binge drinkers, 916 non-smokers were compared with 178 regular smokers, and 1216 non-cannabis users were compared to 173 cannabis users with a median of 20 lifetime uses of cannabis. A machine-learning approach was employed, utilizing forward feature selection and regularized regression via the Elastic Net. Total gray matter volume (GMV), total gray: white matter ratio (GWR), scanner location (8 sites), pubertal development status, sex, and handedness were also included as features. Results are reported with respect to performance on novel test data, using 10-fold cross validation. Results: For all analyses, brain data were moderate predictors of future substance misuse, with area under the curve of the receiver operating characteristic (AROC) ranging from .6 (nicotine) to .63 (alcohol) to .64 (cannabis). Nicotine was primarily characterized by differences in GMV and GMR rather than by specific regional differences; alcohol by increased activity for future binge drinkers in the pre- and post-central gyri and smaller gray matter volume in the ventromedial prefrontal cortex; and cannabis by structural and functional differences (all tasks) in the temporal lobes, with smaller volumes and less activity for future cannabis users. Conclusions: The use of a prospective, longitudinal design, in combination with a machine-learning approach to interrogate a high-dimensional data set has demonstrated that it is possible to predict, to a certain extent, future substance misuse using structural and functional brain data. Notably, no participants had engaged in substance misuse at the time of data collection. In general, these findings, such as the differences such as those found temporal lobe for future cannabis users, are consistent with previous research in this area. However, other results, such as a lack of differences in the orbitofrontal cortex, are discrepant with previous studies. Disclosures: Nothing to Disclose.
Top of page 19.2 A Selective Drug and Alcohol Prevention Programme that Targets Neurocognitive Correlates of Sensation Seeking: Focus on Reward Sensitivity Patricia Conrod Université de Montréal, Montreal, Canada Background: Sensation seeking (SS) has been identified as a risk factor for substance misuse, yet very few clinical interventions have been developed to target SS in treatment or prevention. Our research demonstrates that SS is associated with a motivational sensitivity to reward which mediates the relationship between SS and early onset alcohol misuse (Castellanos-Ryan et al., 2011). We also developed a brief intervention designed to help youth better manage their SS (Conrod et al., 2006). Multiple, large prevention trials investigating the impact of this intervention approach (Conrod et al., 2010; 2013) provide unique opportunities to conduct research on personality-specific trajectories of substance misuse risk within an experimental design. With the recognition that SS is also a specific risk factor for cannabis misuse, we turn to the data in our previous and ongoing prevention trials to 1) examine if interventions targeting SS and reward sensitivity are specifically effective in reducing cannabis use; and 2) test whether reward sensitivity longitudinally mediates the relationship between SS and cannabis use, as previously shown for alcohol misuse (Castellanos-Ryan et al., 2011; 2014). Methods: Secondary analysis of the cluster-randomised Adventure Trial (Conrod et al., 2013) examined the impact of SS interventions on cannabis use and frequency of use within a subset of SS high school students. 2) The Coventure Trial is a large (n=3641) cluster-randomised trial of a school-based drug and alcohol prevention programme targeting 4 personality risk factors, of which one is SS. Neurocognitive factors such as response inhibition, reward sensitivity, are assessed at baseline and annually for 4 years following the brief intervention. Analyses focused on the 435 year 7 students who scored one standard deviation above the school mean on the Substance Use Risk Profile Scale - SS subscale (SURPS-SS; Woicik, et al., 2009). Reward sensitivity was measured using a passive-avoidance learning go-nogo task (Castellanos-Ryan et al., 2011), in which we contrast task performance on conditions involving reward and punishment-avoidance as incentives. Results: Results indicate that 1) Subgroup analyses (both logistic and two-part models) reveal that the SS intervention delayed the onset of cannabis use among SS students (OR: .25, ß=-0.833, SE=0.342, p=.015) in the Adventure Trial. 2) Mediation analyses suggest that reward sensitivity only partially explains risk for cannabis use within this personality group. Conclusions: Targeting SS in school-based drug and alcohol interventions appears to be a promising approach to preventing risk for substance misuse in this high risk group. However, more research is needed to understand how reward sensitivity is implicated in SS and enhancement drug use motives. We suggest that the relationship between SS and addiction vulnerability is explained through a u-shaped relationship with arousal, whereby both under-arousal and over-arousal are motivational triggers for substance misuse in SS youth. Disclosures: Nothing to Disclose.
Top of page 19.3 ENIGMA Addiction Working Group: Initial Findings Scott Mackey University of Vermont, Burlington, Vermont, United States Background: An unbiased search across the whole genome for unknown associations between phenotypic traits of interest and single nucleotide polymorphisms (SNP) typically involves testing the significance of hundreds of thousands to millions of SNP-trait associations and requires a strict multiple comparisons correction threshold, conventionally p 5x10-8, to avoid reporting spurious findings. Since the sample size of a typical neuroimaging study lacks sufficient statistical power to explore unknown genomic associations with brain phenotypes, several international genetic imaging consortia, such as the ENIGMA project, have been organized in recent years to pool data across sites. This presentation will describe the formation and initial results of a large international working group that has leveraged the structure of the ENIGMA project, a template for multisite genetic imaging consortia, to study the genetic and neurobiological basis of addiction. Methods: The Addiction working group used the genetic neuroimaging protocols developed by the Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) project (http://enigma.ini.usc.edu/) to harmonize data across multiple sites. The working group consists of 22 labs on 4 continents and possesses case/control and cohort datasets that collectively contain multimodal neuroimaging (e.g. task-related and resting state functional MRI, structural MRI, DTI) and genomic data on over 10,000 subjects. The first analysis examined brain volume correlates of addiction in case/controls datasets. All data were processed with freesurfer to ensure comparability of neuroimaging results across sites and the quality of data was assessed by standardized imaging protocols (http://enigma.ini.usc.edu/protocols/imaging-protocols/). Results: Brain volumetric data relating to the use of five substances (i.e. alcohol, nicotine, cocaine, methamphetamine and cannabis) were combined to identify neural substrates of core addiction processes. This included brain scans from 3012 individuals. Total intracranial volume as well as right and left volumes of the thalamus, caudate, putamen, ventral pallidum, hippocampus, amygdala, and nucleus accumbens were compared between individuals with heavy or dependent patterns of substance use and those with little or no exposure. While the volumes of all structures were smaller in the heavy users than in the controls, after controlling for site, age, sex, and intracranial volume, two structures were significantly smaller bilaterally in heavy users: the putamen and nucleus accumbens, p < 0.01. Conclusions: An initial analysis found lower grey matter volume in two subcortical brain regions was associated with heavy use or dependence on one of several addictive substances. The nucleus accumbens encodes reward value. Less grey matter volume in this brain region may alter the perception of the rewarding properties of drugs and alcohol. The putamen is involved in habitual instrumental behaviors that are not affected by devaluation of the expected outcome and which may be related to persistent drug taking despite negative consequences in addiction. The high dimensionality of follow-up genetic imaging analyses performed by the working group will be reduced by limiting the search for associations to a small set of brain regions. Disclosures: Nothing to Disclose.
Top of page 19.4 Bayesian Neural Adjustment of Inhibitory Control Predicts Emergence of Problem Stimulant Use Martin Paulus Laureate Institute for Brain Research, Tulsa, Oklahoma, United States Background: Bayesian ideal observer models quantify individuals’ context- and experience-dependent beliefs and expectations about their environment, which provides a powerful approach (a) to link basic behavioral mechanisms to neural processing and (b) to generate clinical predictors for patient populations. Here, we focus on (b) and determine whether individual differences in the neural representation of the need to stop in an inhibitory task can predict the development of problem use (i.e., abuse or dependence) in individuals experimenting with stimulants. Methods: One-hundred fifty-seven non-dependent occasional stimulant users (OSU), aged 18-24, completed a stop-signal task while undergoing functional magnetic resonance imaging. These individuals were prospectively followed for three years and evaluated for stimulant use and abuse/dependence symptoms. At follow-up, thirty-eight OSU met criteria for a stimulant use disorder (problem stimulant users/PSU), while fifty had discontinued use (desisted stimulant users/DSU). Results: We found that those individuals who showed greater neural responses associated with Bayesian prediction errors, i.e. the difference between actual and expected need to stop on a given trial, in right mPFC/ACC, caudate, anterior insula, and thalamus were more likely to be diagnosed with problem use three years later. Importantly, these computationally based neural predictors outperformed clinical measures and non-model based neural variables in predicting clinical status. Conclusions: In conclusion, young adults who show exaggerated brain processing underlying whether to “stop” or to “go” are more likely to develop stimulant abuse. Disclosures: Nothing to Disclose.
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20. Schizophrenia as a "Dysplasticity" Disorder
Top of page 20.1 Experience-Dependent Dysregulation of Plasticity in the Aging and Younger "Noisy" Brain Etienne de Villers-Sidani McGill University / Montreal Neurological Institute, Montreal, Canada Background: Brain maturation is associated with a radical shift in the rules of regulation of neuroplasticity. During early sensitive periods of development, mere exposure to passive sensory stimuli can drive enduring changes in the structure and function of cortical circuits. In the adult mature brain, however, several cortical mechanisms powerfully restrict similar plasticity to the context of behavior. This tight control of plasticity in adults stabilizes the brain's response to experience (i.e., to learning) and ensures the reliability of established sensori-motor representations. Cortical GABAergic tone and several brain neuromodulators such as acetylcholine play a central role in this regulation of adult plasticity. Recent basic science evidence acquired in the sensory system demonstrates that several of these regulators of plasticity become significantly down-regulated with natural aging. The emerging data suggest that similar processes are likely to be operating in neuropsychiatric conditions associated with de-correlated or “noisy” brain activity, such as schizophrenia. In the animal experiments presented here, we investigate the consequences of a reduction in plasticity regulation on auditory learning and processing. We also investigate how chronic “noise” in brain circuits leads to altered plasticity mechanisms and destabilization of auditory processing. Methods: Experiments were conducted in the auditory cortical fields and associated brain areas of young and older (3-30 months old) Brown Norway rats (n=56) using a combination of dense intra-cortical electrophysiology, custom signal analyses, behavior and immunohistochemistry. Rats from different groups were exposed to synthetic noise stimuli with varying degree of structure for periods of a few days to a few weeks and presented at an intensity sufficient to mask ambient auditory patterns but not sufficient to cause hearing loss. The impact of these exposures on indexes of plasticity in the auditory cortex and its overall functional and structural organization was then assessed. Results: We find that the chronic cortical disinhibition and cortical desynchronization associated with normal aging causes a short and long-term instability of sensory representations in the auditory cortex, which in turn causes slower and more rapidly decaying learning. We also find that desynchronizing the activity of auditory cortical neurons for several days in younger rats is sufficient to induce a similar state of dysregulated plasticity, abnormal sensory processing, and poor learning. Conclusions: Our data demonstrate that a chronic desynchronization of cortical activity-- whether due to endogenous factors (aging) or through exogenous abnormal sensory inputs (auditory noise exposure)-- was sufficient to de-regulate plasticity in the auditory cortex. Such dysplasticity resulted in negative downstream impacts on local and distributed auditory processing circuitry and learning. Our findings suggest that similar dysplastic changes induced by developmental pathophysiology that results in de-synchronized or "noisy" cortical activity may be implicated in schizophrenia. Disclosures: Nothing to Disclose.
Top of page 20.2 Dysplasticity, Metaplasticity and Schizophrenia: Implications for Risk, Illness Progression, and Novel Preventive Interventions Matcheri Keshavan Harvard University, Boston, Massachusetts, United States Background: The brain maintains plasticity throughout life in response to learning and to injury, though in varying degrees at the different epochs of age. This remarkable ability of the brain is orchestrated by the inherent networking properties of neurons, synapses and glia, as dynamically modified through neurotransmitter systems such as glutamate, GABA and neurotrophic factors. The extent to which the brain can remodel itself in response to learning events and exogenous exposures is thus determined by genetic, epigenetic and environmental influences. It is increasingly recognized that these plastic changes can be adaptive--resulting in greater levels of neural efficiency and/or increasingly fine-tuned and appropriate behavioral outputs-- or can result in maladaptive cascades secondary to inherent genetic constraints, neurodevelopmental anomalies, behaviors, and environmental inputs. It is highly plausible that such maladaptive cascades underlie many of the neurobehavioral features of psychiatric illness, but such a model has only rarely been explored in schizophrenia. Methods: We will systematically review current evidence supporting a developmental model of aberrant neuroplasticity and metaplasticity (the plasticity of synaptic plasticity) associated with schizophrenia, as well as the risk for developing the illness. We will present examples from the recent literature and our unpublished structural and functional imaging data and sleep EEG data in genetic high risk subjects and in first-episode schizophrenia. Results: Several lines of recent evidence point to diminished neuroplasticity in widespread brain regions in schizophrenia. These include reductions in dendritic and glial density, altered function of glutamatergic, GABAergic and neurotrophic function, and in vivo evidence of diminished LTP and LTD-like plasticity. We will present our findings in genetic high risk and first-episode subjects that demonstrate brain structural and functional alterations, altered BDNF levels, and reduced sleep spindles as additional examples of developmental abnormalities in normal neuroplastic mechanisms. Such abnormalities may account for the core deficit symptoms of schizophrenia, while positive symptoms might result from excessive or maladaptive neuroplasticity associated with aberrant reorganization in prefrontal-limbic circuits. Conclusions: The dysplasticity model, in conjunction with the notion of sensitive periods as they relate to the premorbid and onset periods of psychosis, allow for a parsimonious explanation of how risk states may evolve through aberrant plastic reorganization of neural circuits. Genetic, epigenetic, behavioral, and environmental factors undoubtedly influence the nature, extent, timing and persistence of such abnormalities. Preventive and therapeutic interventions with medications, neuromodulation, and behavioral/psychosocial treatments may be directed both at reversing aberrant circuitry as well as harnessing compensatory neuroplasticity in more adaptive channels. An increased understanding of brain mechanisms underlying dysplasticity in schizophrenia may thus suggest new ways of detecting preclinical disease, better biomarkers to guide treatment selection, and novel therapeutic targets. Disclosures: Nothing to Disclose.
Top of page 20.3 Developmental Trajectory of Brain Bioenergetics and Oxidative Stress Measures in Schizophrenia: Implications for “Dysplasticity” Dost Ongur McLean Hospital, Belmont, Massachusetts, United States Background: The brain requires a large amount of energy to support healthy neural functioning and plasticity operations. Much of this energy appears to support neurotransmission, with a 1:1 stoichiometry observed between glutamate release into the synaptic cleft and glucose oxidation for ATP generation. Several lines of evidence indicate that the generation and utilization of high energy phosphate (HEP) molecules and related processes, together termed bioenergetics, is abnormal in schizophrenia-- suggesting a fundamental alteration in metabolic processes supporting neuronal functioning. These processes can be probed using noninvasive 31P magnetic resonance spectroscopy (MRS) techniques in vivo. Recent developments in these techniques now make it possible to examine enzyme reaction rates as well as oxidative stress markers in patient groups; however, little work has been done examining how these measures evolve from early to chronic phases of schizophrenia. Methods: All studies were carried out at the 4 Tesla Varian MRI scanner at McLean Hospital using a custom-built surface coil tuned to the 31P frequency. We collected data from a 4x5x5cm voxel in the prefrontal cortex. T1-weighted images were also collected for grey and white matter segmentation. In the 31P MRS scan procedures, we use outer volume suppression for localization, and magnetization transfer (MT) approach for metabolite quantification and enzyme reaction rate calculation. MT relies on the fact that the creatine kinase (CK) enzyme reversibly transfers HEP moieties from ATP to creatine to generate ADP and phosphocreatine (PCr). When the signal from ATP in the 31P MRS spectrum is suppressed using a radiofrequency pulse, this leads to reduction of the PCr signal over time (due to exchange of HEP between the two). The rate of loss of the PCr signal is the rate of the CK enzyme reaction rate. pH can also be calculated from 31P MRS data based on the distance between the PCr and inorganic phosphate resonances. Measures of oxidative stress derived from 31P MRS data have also been developed. Results: In 22 chronic schizophrenia patients, we found a 22% reduction (p=0.001) in the CK reaction rate as compared with 22 matched healthy controls. pH was also significantly reduced in the patient cohort. In 11 first episode schizophrenia patients, the CK reaction rate was reduced at a similar magnitude, but pH was less acidic and was not significantly different from a group of 8 age-matched healthy controls. We also found evidence of elevated oxidative stress in chronic patients, with even greater oxidative stress observed in first episode patients. Conclusions: Both chronic and first episode schizophrenia patients show evidence for bioenergetic compromise in 31P MRS studies in vivo. First episode patients show some abnormalities similar in magnitude to that seen in chronic patients (CK reaction rate), while some abnormalities have not yet emerged (pH). Finally, abnormalities in oxidative stress measures are even more pronounced in first episode patients than in chronic patients. This pattern indicates that there are multiple active pathophysiologic processes in the early phases of schizophrenia with a nonlinear progression. We do not see evidence of monotonic emergence of abnormalities that get more severe over time; rather a period of increased oxidative stress emerges and then weakens while reduced bioenergetics are constant in earlier and later phases of illness. Recent basic science work shows that oxidative stress in fast-spiking inhibitory interneurons induces abnormal plasticity and destabilization of cortical networks. The increased oxidative stress measures we observe in first-episode schizophrenia is consistent with the model that early psychosis represents a pathologic “sensitive period” characterized by dysplasticity. Disclosures: Nothing to Disclose.
Top of page 20.4 Abnormal Cortical Activation Patterns in People with Schizophrenia may Represent Compensatory Plasticity Sophia Vinogradov University of California at San Francisco, San Francisco, California, United States Background: Basic science research unequivocally shows that, after brain injury, extensive neuroplastic compensation and re-organization occurs throughout neural circuits, particularly when the injury occurs early in development. Concurrently, the individual animal's behaviors and experiences also impact these same neural circuits, such that there is a reverberating interaction between degenerative and regenerative cascades that ultimately determines neural reorganization and functional outcome. A well-known example is the cortical plasticity that results from compensatory reliance on the “good” forelimb in rats given unilateral cortical infarcts-- compensatory plasticity that further reduces the potential for gains in the injured hemisphere. Thus, the interaction between injury-induced plasticity and plasticity induced by experience and “learning” can have both behaviorally beneficial and detrimental effects. Although increasing attention is now being given to these processes in schizophrenia, we still know very little about cross-modality and other compensatory appropriation of cortical resources in this illness and what it might imply for plasticity-based treatment approaches. At the same time, our field has abundant evidence of aberrant neural network activation patterns and dysconnectivity across broad brain regions in individuals with the illness. Methods: We examined abnormal activation patterns in cortical sectors during an auditory working memory task and a reward anticipation task, and we investigated their possible compensatory role in support of behavior. These two processes are known to be aberrant in individuals with schizophrenia, who typically show impaired auditory working memory task performance, as well as abnormal reward representation in experimental and real-world settings. During numerous functional imaging studies of these processes, patients also show evidence of abnormal neural activity patterns and abnormal connectivity. MEG was performed on 36 schizophrenia and 15 healthy subjects during a speech-sound reproduction task that taxes auditory working memory for human speech stimuli. fMRI was performed on 37 schizophrenia and 20 healthy subjects during the Monetary Incentive Delay (MID) task, with a focus on the reward anticipation period after the presentation of a monetary cue. Measures of task performance were obtained, along with standard symptom ratings, cognitive and functional capacity measures, and self-ratings of anticipatory and consummatory pleasure. Results: During auditory working memory as assessed via MEG, schizophrenia subjects failed to show the normal correlation between posterior planum temporale (PTp) high gamma power (HGP) and working memory task performance observed in controls. Instead, they activated the visual word form area (VWFA) during both stimulus encoding and response preparation, and VWFA HGP correlated with the severity of hallucinations. In patients with severe hallucinations, VWFA activity correlated with performance accuracy on the auditory working memory task, as well as an independent neuropsychological measure of verbal working memory (Letter-Number Sequencing). During reward anticipation as assessed via fMRI, schizophrenia subjects showed hypoactivity in ventral striatum as compared to healthy controls; they also failed to show the normal correlation between striatal activation and self-ratings of consummatory pleasure in everyday life observed in controls. Instead, they activated the right inferior parietal lobule (IPL), and right IPL activity correlated with self-ratings of consummatory pleasure and a measure of functional capacity (UPSA-B). Conclusions: Individuals with schizophrenia may harness compensatory plasticity in cortical sectors to support basic cognitive operations. During the auditory working memory task, cross-modality compensation is observed, with the ventral visual word processing network apparently “co-opted” to support auditory working memory in patients with high hallucinations. During the reward anticipation task, compensation for ventral striatal hypoactivation appears to be subserved by the right IPL, a node in the fronto-parietal network important for “own-body” perception. These compensatory activation patterns show a significant association with cognitive, subjective, and functional capacity measures. It is likely that they arise as the result of interactions between schizophrenia-induced “dysplasticity” and experience-dependent re-organization of distributed neural circuits. There is also no doubt that these interactions are complex, influenced by development, and affected by endogenous and exogenous factors. A better understanding of these interactions is needed to understand how to optimize treatments that focus on brain remodeling and functional outcome. For example, it is entirely unknown whether strategies should be developed that make explicit use of compensatory mechanisms, or conversely, that mitigate or disallow them. Indeed, a fundamental question will be to determine the developmental time course of this process and to develop interventions to pre-empt the negative consequences of dysplasticity before maladaptive neural circuit remodeling has progressed beyond a point of “no return.” Disclosures: Part 1: Site PI on an SBIR grant to Positscience Inc.; scientific advisory board to Forum Pharmaceuticals; consultant to Takeda Pharmaceuticals, Part 4: Site PI on an SBIR grant to PositScience, Inc.
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21. Inflammation-Induced Modulation of Motivation: Impact on Neurotransmitters and Neurocircuits
Top of page 21.1 Preclinical Characterization of Inflammation-Induced Motivational Deficits Elisabeth Vichaya University of Texas MD Anderson Cancer Center, Houston, Texas, United States Background: Inflammation induces sickness that can transition to depression in response to activation of the kynurenine metabolism pathway. Dimensional analysis of inflammation-induced depression indicates a possible predominance of neurovegetative over psychological and affective symptoms. However, this possibility has not yet been tested. Reduced sucrose preference and motivation for food rewards are observed in animal models of inflammation. Although these results are usually interpreted to suggest that inflammation induces anhedonia, the exact dimension of anhedonia that is associated with inflammation (i.e., the liking or the wanting) is still uncertain. In the context of the Research Domain Criteria initiative, our current studies aim at specifying the basic neurobehavioral units that are induced by inflammation and the possible role of neurotoxic kynurenine metabolites. Methods: In our basic paradigm, mice treated with lipopolysaccharide (LPS) experience an episode of sickness that peaks within a few hours followed by depression-like behavior (reduced sucrose preference and increased immobility in forced swim and tail suspension tests) concomitant with activation of the tryptophan metabolizing enzyme indoleamine 2,3 dioxygenase (IDO). Motivational deficits were characterized during the late stage of the LPS response by measuring behavioral and physiological arousal to conditioned cues associated with food delivery to food restricted mice receiving food during their subjective night. The amount of effort mice were willing to invest to gain a food reward was assessed in a concurrent performance task in which mice had the choice between a high effort high reward (10 nose pokes for 1 chocolate pellet) and a low effort low reward (1 nose poke for 1 grain pellet) response modality. Spontaneous preference for chocolate over grain was assessed at the completion of the task. Results: Food anticipatory activity and pituitary-adrenal activation, as measured by plasma levels of corticosterone, were suppressed following treatment with LPS. This suppression of food anticipatory activity was associated with reduced expression of Per1 and Per2 clock genes in the liver. LPS treated mice still displayed a preference for chocolate over grain pellets. In the concurrent choice task, mice showed a global decrease in performance, but this decrease affected the low effort low reward response modality more than the high effort high reward. Ongoing work is evaluating whether activation of IDO mediates the effects of LPS. Conclusions: The reduced behavioral and physiological arousal evoked by expectation of food delivery indicates a decreased motivation in LPS-treated mice. Further, these results indicate that inflammation-induced motivational deficits are not caused by decreased sensitivity to reward since the spontaneous preference for chocolate versus grain pellets is not altered. Reduced performance in the concurrent performance task confirms that the main effect of LPS is to attenuate incentive motivation. Disclosures: Nothing to Disclose.
Top of page 21.2 A Neuro-Computational Account of how Inflammation Diminishes Sensitivity to Reward and Simultaneously Promotes Avoidance Behavior Neil Harrison Brighton & Sussex Medical School: University of Sussex, Brighton, United Kingdom Background: Inflammation rapidly impairs mood and cognition and, when severe, can appear indistinguishable from major depression. These sickness responses are characterized by an acute reorientation of motivational state; pleasurable activities are avoided and sensitivity to negative stimuli is enhanced. However it remains unclear how these rapid shifts in behavior are mediated in the brain. Methods: Here, we combined computational modeling of choice behavior, experimentally-induced inflammation and functional brain imaging (fMRI) to describe these mechanisms. Using a double-blind, randomized crossover study design, 24 healthy volunteers completed a probabilistic instrumental learning task on two separate occasions, once three hours after typhoid vaccination and once three hours after saline (placebo) injection. Participants learned to select high probability reward (win £1) and avoid high probability punishment (lose £1) stimuli. An action-value learning algorithm was fit to the observed behavior, then used within fMRI analyses to identify neural coding of prediction error signals driving motivational learning. Results: Inflammation acutely biased behavior; reducing sensitivity to reward yet heightening sensitivity to punishment through distinct actions on neural representations of reward and punishment prediction errors within ventral striatum and anterior insula. Consequently, choice options leading to potential rewards were less behaviorally attractive, and those leading to punishments more aversive. Conclusions: Our findings demonstrate the neural mediation of a rapid, state-dependent reorientation of reward versus punishment sensitivity during inflammation. This mechanism may aid the adaptive reallocation of metabolic resources during acute sickness, but might also account for maladaptive, motivational changes that underpin the association between chronic inflammation and depression. Disclosures: Nothing to Disclose.
Top of page 21.3 Inflammatory Responses to Stress are Associated with Altered Prediction Error Signaling During Reinforcement Learning Michael Treadway Emory University, Atlanta, Georgia, United States Background: Psychiatric symptoms related to impaired reinforcement, anhedonia and low-motivation are common across many disorders. In both humans and animals, such symptoms have been shown to reflect alterations in a dopamine-rich corticostriatal network. Importantly, these studies have also suggested that exposure to stress may precipitate functional changes in this circuitry, thereby creating a plausible link between stress exposure and subsequent disorder onset. To date, however, the factors underlying the deleterious effects of stress are unknown. One candidate mechanism is inflammation; inflammatory signaling is both increased following stress exposure and has been found to disrupt dopamine signaling pathways. Here, we examine changes in interleukin-6 (IL-6) expression following acute stress, and its association with reinforcement learning signals in the human nucleus accumbens. Methods: Data from 75 healthy female participants were collected in a dual-session experimental paradigm. During session 1, plasma levels of Il-6 were collected at three time points before and after participants were exposed to a cold-pressor stress challenge. In session 2, participants returned to complete a task-based BOLD fMRI scanning session. The task involved instrumental conditioning of abstract stimuli that were probabilistically associated with either monetary wins or losses. A standard Q-learning model was fit to behavioral choice data, and model-based prediction-errors were regressed against neural activity using spm8. Participants were also exposed to a social-stressor during the scan session, and completed runs of the reinforcement learning task before, during and after the social stress manipulation. An anatomical mask of the nucleus accumbens drawn from the Harvard-Oxford probabilistic atlas was used to examine associations between activity in this region during prediction-error feedback, and inflammatory responses to stress. Results: In a sub-set of participants with available IL-6 data at the time of submission (n = 21), we observed a significant increase in plasma IL-6 levels following administration of the cold-pressor task during session 1 (F(2,19) = 6.56, p = 0.007). For prediction error modeling during session 2, we observed an overall main effect of prediction-error signaling in nucleus accumbens (p <0.05, whole-brain cluster-corrected), though this effect was not modulated by stress. Importantly, however, PE signaling in this area was inversely associated with percent increase of stress-induced Il-6 levels (r = -0.54, p < 0.05). Conclusions: These results suggest a critical link between inflammatory responses to stress and reinforcement learning signals in the human nucleus accumbens. Importantly, they extend prior empirical and theoretical work positing that increased risk for depression following stress may partly result from the effects of stress-induced immunoreactivity on basal-ganglia function and associated reinforcement learning behavior. Disclosures: Nothing to Disclose.
Top of page 21.4 Inflammation-Related Decreases in Dopamine and Effects on Corticostriatal Reward Circuitry: Evidence from Humans and Non-Human Primates Jennifer Felger Emory University School of Medicine, Atlanta, Georgia, United States Background: Administration of inflammatory cytokines or cytokine inducers to humans and laboratory animals leads to depressive symptoms, and especially anhedonia, which is believed to involve cytokine effects on mesolimbic dopamine. Neuroimaging studies in humans have shown that cytokines decrease neural activation of the ventral striatum to hedonic reward. Moreover, our non-human primate (NHP) work has revealed inflammatory cytokine-induced decreases in striatal dopamine release in a back-translational model of cytokine-induced depression. Herein, we present data from both humans and NHPs indicating that inflammatory cytokines affect synthesis and subsequent release of dopamine to affect reward circuitry in association with symptoms of reduced motivation and anhedonia. Methods: A NHP model of cytokine-induced depressive behavior was used to examine inflammatory cytokine effects on striatal dopamine release and potential for its reversal by the dopamine precursor, levodopa (L-DOPA), administered via reverse in vivo microdialysis in monkeys chronically administered the cytokine interferon (IFN)-alpha. Effort-based sucrose consumption from a puzzle feeder was also assessed. Plasma and cerebrospinal fluid (CSF) biomarkers of decreased dopamine synthesis were also examined in patients administered IFN-alpha for chronic hepatitis C virus. Finally, patients with major depression exhibiting a range of inflammation from high to low, as measured by plasma C-reactive protein (CRP), underwent resting-state fMRI to assess relationships between functional connectivity within reward-related brain regions and symptoms of anhedonia and psychomotor retardation. Results: Cytokine-induced decreases in striatal dopamine release were correlated with reduced effort-based sucrose consumption, and reversed by administration of L-DOPA, in NHPs administered chronic IFN-alpha. Patients receiving IFN-alpha exhibited decreased ventral striatal activation to hedonic reward, and deceased biomarkers relevant to dopamine synthesis in the periphery that correlated with decreased CSF dopamine and dopamine metabolites, all of which were associated with depressive symptoms including reduced motivation. In patients with major depression, increased plasma CRP was associated with decreased functional connectivity between both ventral and dorsal striatum and the ventromedial prefrontal cortex, which correlated with symptoms of anhedonia and psychomotor slowing. Moreover, preliminary data suggest that a single dose of L-DOPA can reverse inflammation-related disruptions in reward-related corticostriatal connectivity in patients with high CRP. Conclusions: These data in humans and NHPs indicate that inflammation-related decreases in dopamine synthesis and release have functional consequences on reward circuitry in depression that are associated with fundamental alterations in motivation and motor function. This work supports development of novel therapeutic strategies to increase dopamine availability in depressed patients with increased inflammation and anhedonia, thus personalizing care. Disclosures: Nothing to Disclose.
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22. Molecular Mechanisms Underlying Psychopathology and Treatments in OCD
Top of page 22.1 Role of SLITRK5 and PTPRD in BDNF-Dependent Synapse Remodeling Francis Lee Weill Cornell Medical College, New York, New York, United States Background: Slit- and NTRK-like family (Slitrks) are transmembrane proteins that localize to and function at central nervous system synapses where they mediate synapse formation through trans-synaptic interactions of their ectodomains with a presynaptic binding partner, protein tyrosine phosphatase, receptor type, D (PTPRD), a recently identified candidate risk gene for obsessive compulsive disorder (OCD). Recent studies in a genetic knock-out mouse model have also provided compelling links between Slitrk5 to OCD. Slitrk5-null mice displayed repetitive and excessive self-grooming behaviors. Treatment with chronic fluoxetine, a selective serotonin reuptake inhibitor (SSRI), alleviated the excessive grooming behavior. These mice also showed selective overactivation of the orbitofrontal cortex. In this context, overactivation of orbitofrontal-subcortical circuits has been observed in functional imaging studies of human subjects with OCD. Thus, the Slitrk5-null mouse recapitulates important aspects of the human disease. However, the molecular mechanisms underlying Slitrk5 function are not known. We hypothesized that, based on structural similarities that Slitrk5, interacts with the neurotrophin system, in particular, with the BDNF receptor, TrkB, to mediate biological responses in key cortico-striatal circuitry. Methods: Super-resolution structured illumination microscopy (SIM) was utilized to assess localization of Slitrk5 with its interacting synaptic proteins (PTPRD, TrkB receptors) in cultured striatal neurons, as well as its impact on synapse formation. Results: Our cell biological studies in cultured striatal neurons demonstrate that Slitrk5, a postsynaptic plasma membrane protein containing extracellular LRR domains, interacts under basal conditions with the presynaptic adhesion molecule PTPRD in trans, but in the presence of BDNF, shifts to a cis-interaction with TrkB receptor that mediates its postendocytic recycling, leading to functional resensitization of neurotrophic signaling. Our current studies elucidate a new aspect of Slitrk5 function in which Slitrk5 has a cis interaction with activated TrkB receptors on the surface of postsynaptic sites via extracellular interactions involving their respective LRR domains. Intriguingly, the cis interactions of Slitrk5 with TrkB receptors compete with trans interactions with its presynaptic partner, PTPRD, and the competition was modulated by BDNF stimulation. Conclusions: In summary, the present studies identify an unanticipated role for Slitrk5, a cell surface transmembrane protein in mediating a balance between functioning as a synapse adhesion molecule by interacting with PTPRD, as well as a facilitator of trophic responses by interacting with TrkB receptors. By engaging with both presynaptic PTPRD and postsynaptic TrkB receptors, Slitrk5, plays a key role in striatal function that may underlie the OCD-like behaviors observed in the Slitrk5-null mice. In addition, these findings provide a potential molecular framework to understand for how PTPRD may be implicated in OCD. Disclosures: Nothing to Disclose.
Top of page 22.2 Rare Functional Mutations in SLITRK5 are Associated with OCD Carol Mathews University of Florida, Gainesville, Florida, United States Background: Obsessive compulsive disorder (OCD) affects approximately 2% of the population, and is a leading cause of morbidity worldwide. Despite having a substantial heritable component, few specific genetic risk factors for OCD have been identified. Genome-wide association studies (GWAS) of OCD have found associations to common polymorphisms at near genome-wide significance (e.g., PTPRD) but the majority of the genetic risk for OCD remains unidentified. Knockout mice lacking Sapap3 and Slitrk5 display OCD-like phenotypes, including altered cortico-striatal circuitry and pathologic grooming behavior that is responsive to serotonin transporter targeting drugs. Rare missense variants in human SAPAP3 are statistically overrepresented in OCD cases versus controls, implicating them in risk for OCD. We screened the complete protein-coding sequence of SLITRK5 in OCD subjects to identify rare mutations that may contribute to OCD. Methods: We re-sequenced the complete protein sequence of SLITRK5 in three hundred and seventy seven individuals with DSM-IV OCD. Rare, non-synonymous mutations (RNMs) (prevalence < 0.01) identified in the OCD sample were compared with data from the 1000 Genomes database. Putative functional effects of OCD and control RNMs were assessed in silico. To test for functional effects of SLITRK5 RNM’s mutant proteins were introduced into COS7 cells and co-cultured with primary hippocampal neurons. We analyzed all OCD mutations and a subset of pseudo-matched mutations from the 1000 Genomes database sample for synaptogenic activity of hippocampal neurons onto Slitrk5-expressing COS7 cells. Results: We identified four RNMs in the 377 OCD participants (0.011). There were 15 RNMs in the 1000 Genomes database (0.014). All of the OCD mutations were singletons, while 7 of the 15 control mutations were singletons. There was no association between OCD with either the number of SLITRK5 RNM’s or the prevalence of chromosomes containing those mutations. There were no differences in the bioinformatically predicted effects of RNM’s using Combined Annotation Dependent Depletion (CADD). However, all Slitrk5 alleles containing OCD-associated mutations significantly impaired synapse formation relative to wild type Slitrk5 when expressed in COS7 cells whereas none of the pseudo-matched controls did (Fisher’s exact P<0.03. Impaired synaptogenesis for one OCD mutation was explained by impaired surface expression and the other three displayed impaired interaction with PTP-δ, a highly associated gene in a recent OCD GWAS. Conclusions: RNM’s in SLITRK5 that impair synaptogenesis are associated with OCD. These results implicate SLITRK5 in the genetic risk for OCD and highlight the importance of biological characterization to identify genotype-phenotype relationships. They also add the growing role of corticostriatal synaptic function in the pathophysiology of OCD. Disclosures: Nothing to Disclose.
Top of page 22.3 From Good Habit to Bad: Corticostriatal Synaptic and Circuit Mechanisms in Habit and Compulsion Nicole Calakos Duke University Medical Center, Durham, North Carolina, United States Background: Compulsivity drives maladaptive behavioral responses in many contexts, ranging from the prototypical, Obsessive Compulsive Disorder (OCD), to addiction, autism-related behaviors, and eating disorders. Although compulsive behavior has been widely hypothesized to derive from habit learning mechanisms, direct testing of how the synaptic and circuit mechanisms that give rise to these behaviors relate is largely lacking. Here we examine the relationship between corticostriatal plasticity and behavior in habit and compulsion using mouse models. Methods: Corticostriatal plasticity was examined at the local circuit level by imaging action potential firing of striatal projection neurons (SPN) in response to defined cortical stimuli delivered in the acute brain slice preparation. Such a measurement integrates the effects of synaptic, intrinsic and homeostatic plasticity throughout the local microcircuitry and reveals the net effect on striatal output. SPN firing was imaged using two-photon, calcium imaging of genetically defined SPNs. The two types of projection neurons, direct and indirect pathway-projecting SPNs, were simultaneously evaluated to enable measurement of the balance of activity between these two mutually antagonistic pathways. Habitual behavior was induced through training in a lever-press paradigm (Dickinson et al., Quar. J. Exp. Psych., 1983). Compulsive behavior was modeled by SAPAP3 knockout (KO) mice which display persistent self-injurious grooming and anxiety-like behaviors that respond to chronic fluoxetine treatment or gene rescue in striatum (Welch et al., Nature 2007). Results: We found that mice with persistent OCD-like behaviors and those with habitual responding share increases in striatal output excitability and pathway imbalances that favor activity in the action-promoting “direct” pathway. However, the specific features of striatal excitability affected differ between the two behavioral states. Additionally, we show that the efficacy of a novel drug treatment in normalizing circuit defects in the SAPAP3 KO model corresponds with behavioral efficacy against the OCD-like behaviors. Conclusions: These findings reveal both common and distinguishing features of striatal circuitry in habit and compulsion. The behaviorally predictive hypotheses generated by analysis of plasticity at the level of pathway-defined striatal output can be used to direct future mechanistic investigations as well as assist in the development of novel drug and circuit therapies. Disclosures: Nothing to Disclose.
Top of page 22.4 Pilot Trial of a Brief Course of Exposure-Based CBT in Extending IV Ketamine’s Effects in OCD Carolyn Rodriguez Stanford University, Stanford, California, United States Background: A single subanesthetic intravenous (IV) dose of ketamine leads to rapid anti-obsessional effects in OCD patients with near-constant intrusive obsessions, but these effects usually do not persist. We tested whether a brief course of exposure-based cognitive behavioral therapy (CBT) could extend ketamine’s effects in a 2 week pilot open trial and if this effect was maintained (without additional treatment) 2 weeks later. Our rationale was: 1) in rodents, ketamine is reported to enhance plasticity and extinction learning (and this effect is maintained for at least 14 days), and 2) enhanced extinction learning may facilitate CBT gains, as reported in prior trials combined trials of CBT with agents that facilitate extinction learning. CBT was abbreviated (i.e. 10 one-hour exposure sessions) but delivered during the putative time interval when ketamine facilitates extinction learning. Methods: Ten unmedicated OCD outpatients (aged 18-55) with near-constant intrusive obsessions (>8 hours/day) were recruited (3/2014-3/2015) and provided informed consent. Participants met DSM-IV/5 criteria for OCD with at least moderate symptoms (YBOCS score 16). Exclusion criteria included severe depression or current CBT. In an open-label design, participants received a single 40-minute IV infusion of ketamine (0.5 mg/kg), followed by 10 one-hour exposure sessions delivered over two weeks. The CBT treatment was planned in a 90-minute session prior to the ketamine infusion. At baseline, during, and up to 230 minutes post-infusion, patients rated their obsessional severity using the OCD-VAS. We focused on obsessions because the patients were supine and connected to stationary monitoring equipment during the infusion. At baseline and weekly for four weeks post-ketamine, an independent evaluator, blind to study design, evaluated patients using the Y-BOCS. Treatment response was defined a priori as 35% Y-BOCS reduction at week 2. Y-BOCS outcomes were analyzed using mixed-effects regression to model symptoms as a function of time. Results: Of 10 patients who started ketamine, nine completed the infusion. Eight reported a rapid reduction in obsessive severity as measured by the OCD-VAS, which persisted up to 230 minutes post-infusion in seven. Eight completed the 10 hours of exposure and the two week follow-up and were included in the Y-BOCS analyses. From baseline to 4-weeks post-infusion, OCD severity as measured by the YBOCS was significantly decreased over time (F=14.36, df=4,28, p<.0001). Compared to baseline, the mean estimated Y-BOCS score was significantly lower at week 2 (difference= -10.75 points, SE=1.44, p<.0001) and at week 4 (difference=-6.88, SE=2.61,p=0.01); there was a trend-level increase between week 2 and 4 (difference=3.63, SE=1.97, p=0.07). At the end of CBT (week 2) response rate was 63%. Conclusions: These results corroborate prior findings that ketamine can rapidly relieve symptoms in unmedicated OCD patients and suggest that a brief course of CBT can extend these effects for at least two weeks in 63% of OCD patients with constant intrusive thoughts. Disclosures: Nothing to Disclose.
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23. Research Paradigms and Non-Pharmacological Interventions aimed to Prevent the Onset and Progression of Bipolar Disorder in Children
Top of page 23.1 White Matter Structure of Major White Matter Tracts in Youth Offspring of Bipolar and Non-Bipolar Patents Amelia Versace University of Pittsburgh, Pittsburgh, Pennsylvania, United States Background: Bipolar Disorder (BD) is a highly heritable mental illness, placing offspring of parents with BD at highest risk for this disorder. (Craney and Geller 2003; Faraone, Glatt et al. 2003; McGuffin, Rijsdijk et al. 2003; Rende, Birmaher et al. 2007; Birmaher, Axelson et al. 2009) Yet, offspring of parents with other psychiatric disorders, such as depression or ADHD are at higher risk to develop BD. Whether or not they develop the illness, these children can present ongoing emotional and/or behavioral dysregulation, associated with functional impairment.(Carlson and Weintraub 1993; Birmaher, Axelson et al. 2006; Luby and Navsaria 2010) In addition, developmental differences in the presentation of the disorder in youth (e.g., symptoms of inattention, irritability, impulsivity, etc.) can often be misinterpreted as the onset of other psychiatric conditions (e.g., ADHD, ODD), and lead to inappropriate or less efficient treatment. The identification of early neuroimaging markers of risk for BD may help shed light on the pathophysiologic mechanisms of BD, regardless of whether vulnerable children will go on to develop full syndromal BD. Yet, a limited number of studies have examined white matter structure in offspring of BD.(Frazier, Breeze et al. 2007; Versace, Ladouceur et al. 2010; Roybal, Barnea-Goraly et al. 2015) Methods: Global probabilistic tractography of 10 major white matter tracts was performed in eighty-seven youth including age- and gender-matched offspring of BD parents (OBP: N=27; mean[SD] age=13.6[2.2]; M/F=14/13), offspring of non-BD (i.e., depression, anxiety or ADHD/ODD) parents (OCP: N=24; mean[SD] age=13.9[2.5]; M/F=15/9), and offspring of healthy parents (OHP: N=36; mean[SD] age=13.2[2.4]; M/F=21/15). A multivariate multiple regression model was used to test putative age by genetic risk (OBP, OCP, OHC) interaction upon fractional anisotropy (FA) of 9 tracts (1. forceps major, 2. forceps minor, 3. anterior thalamic radiation, 4. cingulum, 5. angular bundle, 6. inferior and 7. superior longitudinal fasciculus, 8. arcuate and 9. uncinate fasciculus). In this tract of interest approach, the corticospinal tract was examined as a control tract. At scan time, 13 youth had a diagnosis of emotional dysregulation disorder (6 OBP and 7 OCP) and 7 youth had a diagnosis of behavioral dysregulation disorder (2 OBP and 5 OCP). Results: After controlling for diagnosis (offspring with emotional dysregulation disorder, offspring with behavioral dysregulation disorder, healthy offspring) and gender, there was an age by genetic risk interaction across all white matter tracts (Pillai’s=.4; F[20,144]=1.8; p=0.033). Further analyses revealed that this interaction was significant in the forceps major (F[20,144]=10.2; p<0.001), in the angular bundle of the cingulum (F[2,86]=4.6; p=0.013), and in the inferior longitudinal fasciculus (F[2,86]=3.0; p=0.056). Conclusions: Our findings suggest that the at-risk youth (both, OCP and OBP) show lower FA when compared to OHP in the forceps major (OCP, p<0.001), in the angular bundle of the cingulum (OCP to a greater extent than OBP; p=0.006 and p=0.020) and in the inferior longitudinal fasciculus (OBP; p=0.021), as previously shown11. However, while there is a decrease of FA (inverted U shape) in the OHP as they get older, such an effect is not present in the at-risk offspring of non-BD parents. Interestingly in the at-risk offspring of BD parents, FA values are lower in the angular bundle of the cingulum and in the inferior longitudinal fasciculus in younger offspring, but normalize as they get older. A steeper decline of FA might be present later in OBP. Further studies in adult OBP are needed. Disclosures: Nothing to Disclose.
Top of page 23.2 Neurofunctional Characteristics of Risk and Resilience in Youth Offspring of Bipolar Parents Manpreet Singh Stanford University School of Medicine, Stanford, California, United States Background: Bipolar Disorder (BD) in parents is a significant source of stress for children and families. We previously demonstrated that youth offspring of bipolar parents have dysfunctional prefrontal-subcortical connectivity that correlates with chaotic family environments even before children experience frank mood symptoms (Singh et al., 2014). It is not known whether aberrant functional connectivity is associated with daily stress exposure that predisposes youth to developing mood disorders (Ellenbogen et al., 2006) or if youth are demonstrating adaptive neural functioning amidst family chaos. We used a combination of endocrine (salivary assessment of levels of diurnal cortisol production), resting state and task based functional magnetic resonance imaging (fMRI) assessments to compare healthy offspring living with parents with BD (high-risk) and healthy comparison youth without any personal or family history of psychopathology (low-risk). We hypothesized that high-risk youth would differ from low-risk youth in functional disruptions in prefrontal and subcortical regions involved in emotion regulation. We further predicted that a subset of vulnerable youth with elevated diurnal cortisol production would demonstrate disconnectivity between the prefrontal cortex and subcortical regions. Methods: 8–17 year old healthy children of parents with bipolar I or II disorder (“high-risk,” n=25) and age comparable control children of parents without any psychopathology were recruited (“low-risk,” n=25). High-risk and low-risk youth were scanned using a 3 Tesla Signa MRI system with a standard whole head coil at rest and during an emotion face processing task (Garrett et al., 2012). We used hypothesis-driven region-of-interest (ROI)-based intrinsic connectivity to analyze the fMRI data, investigating connectivity in the following ROIs selected a priori and created from the Harvard-Oxford atlas: left and right amygdala and the left and right ventrolateral prefrontal cortex (VLPFC). We conducted partial correlations between connectivity estimates and cumulative neurofunctional, endocrine, and family chaos measures within each group. We then conducted Fisher’s r-to-z transformations to determine whether the high- and low-risk groups differed significantly with respect to these within-group correlations. Results: High-risk youth had greater levels of family chaos than low-risk youth. High-risk youth had greater resting state functional connectivity in the VLPFC (t(48) = 6.01, p < .001) and greater total diurnal cortisol production than did the low-risk group (t(48) = 5.73, p < .001). The high-risk group had greater resting state functional connectivity than did the low-risk group between the left VLPFC and left superior parietal lobule (t(48)=1.69, p=0.048) and greater functional connectivity between the VLPFC and amygdala while viewing happy versus neutral facial expressions (t(48)=2.41, p=0.039). Connectivity estimates between the VLPFC and amygdala within the high-risk group both at rest and during face emotion processing were negatively correlated with level of family chaos in high-risk (r=-.707, p=0.005) and total diurnal cortisol production (r=-.586, p=0.008) but not low-risk youth (r=0.079, p=0.788; z;s=2.90-3.15, p’s<0.001). Conclusions: Our results provide new evidence that in the context of high levels of family chaos and elevated total diurnal cortisol production, healthy offspring of parents with BD have increased VLPFC connectivity compared to healthy offspring with no family history of psychopathology, This increase in prefrontal connectivity may represent an early marker of resilience from developing mood disorders that can only be verified by longitudinal follow-up. Improved methods for identifying children with certain neural vulnerabilities may inform preventive and early intervention strategies prior to the onset of fully syndromal BD. Disclosures: Nothing to Disclose.
Top of page 23.3 Neural Correlates of Symptom Improvement Following Family Focused Therapy for Youth at High-Risk for Bipolar Disorder Kiki Chang Stanford University, Stanford, California, United States Background: Family focused therapy (FFT) is a well-tolerated nonpharmacological intervention that has demonstrated efficacy in reducing depressive symptoms, anxiety, and stress and in improving function and diagnostic outcome in adults and teens with bipolar disorder (BD). A modified version of FFT for youth at high-risk for BD (FFT-HR) was shown to be effective in reducing depressive symptoms and functioning in these youth, all with a first-degree relative with BD. Understanding task-independent neural mediators of clinical improvement by FFT may suggest mechanisms underlying risk for BD and targets for treatments. This study investigates changes in intrinsic functional connectivity during rest associated with FTT –HR. Methods: 25 youth (ages 9-18 years) with a current non-bipolar I or II mood disorder and a biological first- or second-degree relative with bipolar I disorder were recruited from an academic Bipolar Disorders Program and from the community. Subjects received either FFT (n=13) or enhanced care (EC) (n=12), a control condition consisting of 3-6 general and crisis intervention sessions. FFT consisted of 12 weekly hourly sessions, attended by youth, parents, and siblings. The goals of treatment included educating the family about mood disorders, managing mood symptoms, preventing adverse mood episodes, enhancing communication, and solving problems. At baseline and endpoint after treatment, subjects were scanned using a 3 Tesla GE Signa MRI system with a standard whole head coil at rest for 7 minutes. Participants were instructed to rest quietly with their eyes closed but not sleep. An implicit facial emotion task was also administered, consisting of fearful, calm, and neutral faces. Mood and anxiety symptom ratings were obtained at baseline and endpoint. Results: Both treatment groups exhibited similar significant baseline-endpoint reductions in depression and anxiety severity scores. Baseline-endpoint intrinsic connectivity between the posterior cingulate gyrus and the bilateral medial prefrontal cortex increased after FFT (p=.001 height and k=20 extent). Baseline-endpoint intrinsic connectivity between the precuneus and the subgenual anterior cingulate cortex decreased following FFT (p=.005 height and k=20 extent). Increased posterior cingulate connectivity after FFT was inversely correlated with a decrease in depressive symptoms from baseline to endpoint. Furthermore, during a fearful versus calm face contrast task, greater right DLPFC activation increase from baseline to follow-up was correlated with greater decrease in depressive symptoms. Conclusions: Reductions in depressive symptoms in bipolar offspring following FFT are associated with changes in intrinsic functional connectivity between posterior subregions of the default mode network and regions critical for emotion regulation. Furthermore, prefrontal activation increase appears to be correlated with symptom improvement, which could reflect greater prefrontal control over limbic areas in order to regulate mood. These changes in connectivity and activation may represent desired neural change following interventions to prevent the development of BD. Longitudinal assessment of these patients through the risk period of BD development is necessary to extrapolate these results toward the concept of prevention. Disclosures: Part 1: Consultant for Sunovion, Actavis, Merck, GSK, Part 4: GSK, Merck.
Top of page 23.4 Neurofunctional Changes Associated with Mindfulness-Based Cognitive Therapy in Youth at Risk for Bipolar Disorder Melissa DelBello University of Cincinnati, Cincinnati, Ohio, United States Background: Child and adolescent offspring of parents with bipolar disorder have a greater risk for developing anxiety disorders and emotional dysregulation than those without bipolar parents. Antidepressants, which are typically used to treat these symptoms, may increase the risk for developing mania. Therefore, studies evaluating non-pharmacological interventions for anxiety and mood dysregulation in youth with a bipolar parent are needed. Preliminary studies from our group and others suggest that mindfulness-based cognitive therapy (MBCT) is effective for reducing symptoms of anxiety and mood dysregulation. The aim of this study was to evaluate the neurofunctional effects of mindfulness-based cognitive therapy (MBCT) in youth at risk for bipolar disorder. We hypothesized that MBCT will reduce symptoms of anxiety and mood dysregulation and that reduction in these symptoms will be associated with changes in amygdala, insula, anterior cingulate, and ventral prefrontal cortical function. Methods: Ten youth (mean age: 13±2 years) with an anxiety disorder and a bipolar parent completed an fMRI session while performing a continuous performance task with emotional and neutral distractors (CPT-END) and a facial affect task of viewing fearful faces prior to and following 12 weeks of group MBCT. In a separate cohort, 10 youth (mean age: 14.0 +1 years) with significant mood dysregulation and a bipolar parent completed an fMRI session while performing the same facial affect tas prior to and following 12 weeks of group MBCT. Anxiety and mood dysregulation were measured using rating scales prior to and during the group MBCT. Results: MBCT was associated with improvement in anxiety and mood dysregulation in both cohorts of at-risk youth. MBCT was associated with increases in activation of the bilateral insula, lentiform nucleus, and thalamus as well as the left anterior cingulate while viewing emotional stimuli during the CPT-END, and decreases in anxiety were correlated with change in activation in the bilateral insula and anterior cingulate bilaterally. In the facial-affect driven analysis (fear vs. neutral) of amygdala activity, MBCT was associated with a significant decrease in right amygdala activity (p=0.01) in the anxious youth. In contrast, during the facial affect task (fear vs. neutral) mood dysregulated at-risk youth exhibited increases in right amygdala (p=0.04), right and left anterior cingulate (p< 0.04), and right insula (p<0.03) activity following MBCT. Conclusions: MBCT treatment in anxious and mood dysregulated youth with a familial history of bipolar disorder reduces anxiety and mood symptoms and is associated with increased activation of brain structures that subserve interoception and the processing of internal stimuli, functions presumably improved by this treatment. However, the impact of MBCT on amygdala function during fear processing is distinct in anxious vs. mood dysregulated youth, suggesting that the underlying alterations in amygdala function may be distinct in each of these cohorts and the primary neural impact of MBCT may be on modulatory (prefrontal and insular) regions rather than directly on the amygdala. Disclosures: Part 1: Pfizer, Lundbeck, Sunovion, Otsuka, Supernus, Forest, Actavis, Part 4: Eli Lilly, Otsuka, GlaxoSmithKline, Merck, Martek, Novartis, Lundbeck, Shire, Purdue, Amylin, Sunovion, Pfizer.
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24. Social (Cognitive) Functioning in Schizophrenia: Course, Mechanisms, and Treatment
Top of page 24.1 The 20-Year Longitudinal Trajectories of Social Functioning in Psychotic Disorders Eva Velthorst Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: Social deficits are a core feature of schizophrenia and common in other psychotic disorders. Nevertheless, only a few studies have systematically investigated the course of social impairment in psychotic disorders, yielding mixed findings. We will present new data on the differential longitudinal trajectories of social functioning in patients diagnosed with psychotic major depressive disorder, psychotic bipolar disorder and schizophrenia. Methods: We used data from the Suffolk County Mental Health Project (New York, US), which is an epidemiological cohort of first admission psychotic patients (n=485) followed over a 20-year period and Never Psychotic comparison subjects (n=262). Social functioning was assessed at 6 months, 2, 4, 10 and 20 years after first admission. Latent Class Growth curve modeling was applied to establish latent trajectories of social functioning across diagnoses. Regression analyses were used to examine how these latent trajectories were associated with premorbid functioning scores in childhood, early- and late adolescence. Regression analyses were also used to examine whether the latent classes were related to other clinical outcome measures. Results: Four latent classes with stable life-course trajectories of ‘Preserved’, ‘Mildly Impaired’, ‘Severely Impaired’, and ‘Profoundly Impaired’ social functioning were identified. Differences in social functioning among the groups were already evident in childhood. Specifically, those with the lowest social functioning during childhood also showed the lowest social functioning after illness onset. In addition, they had significantly more cognitive deficits and positive and negative symptoms over the course of 20 years. Overall, social functioning was poorest in schizophrenia, best in psychotic bipolar disorder and intermediate in psychotic major depressive participants. Social functioning at 20-year follow-up was still significantly worse in those with a psychotic illness (all P<.001) compared to Never Psychotic individuals. Conclusions: The current results demonstrate four stable functional trajectories that differ quantitatively in severity across psychotic disorders. However, social functioning also varied widely within disorders, which suggests a need for continuous representation of social outcomes. Our findings indicate that a large group of individuals admitted to hospital with psychotic disorders have lifelong, stable social impairment. These findings highlight the importance of a detailed assessment of social functioning and emphasize the need for targeted, transdiagnostic treatment interventions aiming to preserve and improve social functioning. Disclosures: Nothing to Disclose.
Top of page 24.2 Levels of Empathy in Schizophrenia Michael Green University of California Los Angeles Neuropsychiatric Institute, Los Angeles, California, United States Background: The social cognitive neuroscience of empathy is a growing topic in schizophrenia research. Current models define empathy as the ability to understand and share the feelings of others. Empathy includes: affective empathy, which refers to relatively automatic processes that trigger a shared emotion response, and cognitive empathy which refers to reflective processes. We will review 3 studies of affective and cognitive empathy that compared patients with schizophrenia (SZ) and healthy controls (HC) on: 1) self-reported empathy, 2) fMRI of pain empathy, and 3) empathic accuracy. Methods: For self-reported empathy, we compared 145 SZ, and 45 HC on The Questionnaire of Cognitive and Affective Empathy (QCAE) that assesses cognitive and affective components of empathy. Pain empathy, a type of affective empathy, typically involves examination of neural responses during first-hand experience of pain, and when watching stimuli depicting other people in pain. In this fMRI study, 21 SZ and 21 HC watched videos of people described as medical patients who were in pain and made judgments about these people. Empathic accuracy refers to the ability to accurately infer emotional states of another person, and involves both affective and cognitive empathy. Participants were asked to judge changes in emotional states of another person shown in a video clip while he/she describes an autobiographical event. In this psychometric study, 82 SZ and 59 HC were assessed on empathic accuracy at baseline, and SZ retested at 4-weeks. Results: For self-reported empathy, factor analyses provided consistent support for a two-factor solution (affective versus cognitive) in SZ. Patients showed significantly lower cognitive (p < .01) but higher affective empathy (p < .05) than controls. Cognitive empathy showed significant correlations with negative symptoms and functional outcome. For pain empathy, both groups showed similar overall levels of anterior cingulate cortex and anterior insula activation while observing others in pain. In one experimental condition the HC showed more activation when they imagined themselves versus others in pain, whereas patients showed the opposite pattern. In the psychometric study, empathic accuracy discriminated between patients and HC (effect size = .79), showed adequate test-retest reliability (.72), had no practice effect, and was well-tolerated. The task had significant relationships with functional capacity. Conclusions: Across studies, we found clear support for differences in SZ and HC on self-reported cognitive empathy and empathic accuracy. These measures showed correlations with functionally meaningful external variables. In contrast, findings of affective empathy and pain empathy did not show consistent impairment. Patients self-reported normal emotional responses to close personal contacts and elevated emotional response to others in their social environment. This findings across studies suggest that affective empathy might be relatively preserved and a social cognitive strength in schizophrenia. Disclosures: Part 1: I have consulted for AbbVie, DSP, Forum, Mnemosyne (scientific board) and Takeda, Part 4: I have received grants from Forum and Amgen.
Top of page 24.3 Oxytocin for Schizophrenia: A Randomized Controlled Trial Mark Weiser Sheba Medical Center, Ramat Gan, Israel Background: Both human and animal studies have found that the neuropeptide oxytocin (OXT) is involved in regulating affiliative behaviors, including sexual behavior, mother–infant and adult–adult pair-bond formation. Social dysfunction is among the most disruptive outcomes of schizophrenia. Intranasal OXT administration has been reported to have pro-social effects in patients with autism spectrum disorders and with schizophrenia. The aim of this study was to examine the effectiveness of intranasal administration of OXT alone, and of OXT combined with social skills training in the treatment of social dysfunction in patients with schizophrenia. Methods: Using a 2X2 design, we conducted a randomized, double blind, placebo-controlled, 3 week trial testing the effect of intranasal OXT (24IU X3/d) or placebo in combination with social skills training or supportive psychotherapy. Subjects were 51 patients with schizophrenia or schizoaffective disorder with significant impairment of their social abilities, stabilized on anti-psychotics. The primary outcome measure was a structured assessment of social interaction, done by video-taping interviews with subjects, and then having raters blinded to treatment status assessing the quality of the social interactions, specifically focusing on gaze to experimenter's face, vocalization (patient’s vocal output, positive/negative tone, and fluent speech), affect, body tone, movements, and other non-verbal signals. Secondary outcome measures included PANSS and the PENN Emotion recognition tasks. Results: Of the 51 patients randomized, 48 completed the study (23 in the oxytocin and 25 in the placebo group). Analysis of the primary outcome measure did not show significant effects of oxytocin in any of the variables rated (all p values > 0.05). However, the following variables did show non-significant improvement in patients receiving drug compared to placebo during the social interaction: positive affect, effect size (ES)= 0.20, negative affect ES= 0.53, fluency of conversation ES =0.35, decreased constriction ES= 0.378 and decreased tension ES= 0.44. No improvement was found in the PENN-CNP emotion battery tasks, nor in the PANSS scales (all p values > 0.05). Conclusions: Although changes were not statistically significant, oxytocin improved affect, reduced tension and improved fluency of social interactions at effect sizes of mild-moderate amplitude, and it is conceivable that larger sample sizes will yield statistically significant findings. These variables might reflect subtleties of social interaction not reflected in PANSS scores. The results of the published studies of add-on oxytocin vs placebo for schizophrenia are heterogeneous, with both positive and negative findings. We conclude that before further studies are performed, individual patient meta-analysis of all add-on oxytocin studies in schizophrenia should be performed. Disclosures: Nothing to Disclose.
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25. Neuropsychiatric Disorders in Isolated Populations
Top of page 25.1 Clustering of Mendelian Disease Loci and Bipolar Disorder Risk Alleles in a Large Multigenerational Old Order Amish Pedigree Maja Bucan Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States Background: Bipolar affective disorder (BP) is a common, highly heritable psychiatric disorder characterized by periods of depression and mania. The Old Order Amish are a genetic isolate of European ancestry currently residing in several states in North America, with a concentration in Pennsylvania and Ohio. Bipolar disorder type I (BPI) and bipolar disorder type II (BPII) in the Amish occur with similar prevalence, pattern of symptoms, clinical course and response to mood-stabilizing medicines as observed in the general North American population. Alcohol and drug abuse, which often complicate psychiatric diagnoses, are rare among the Amish. Their lifestyle provides a remarkably uniform environment in which behavioral changes can be readily and longitudinally ascertained. Methods: To identify the genetic basis of bipolar disorder in the Amish, our research returned to the expanded multigenerational Old Order Amish pedigree available as the Amish Study of Major Affective Disorders at the Coriell Institute for Medical Research and applied contemporary genomic and statistical methodology by integrating genotype and whole-genome sequence data. Using dense SNP genotype data, we characterized copy number variants (CNVs) in 388 members of an Old Order Amish Pedigree with bipolar disorder. We identified CNV regions arising from common ancestral mutations by utilizing the pedigree information. Results: Our findings reveal multiple linkage regions that each harbor a considerable number of sequence and CNV variants, supporting initially reported locus heterogeneity. Dissection of exonic and intronic variants that reside in these linkage peaks has identified credible candidate genes that will be further examined in large-scale population- and family-based studies (Bipolar Sequencing Consortium). We identified 541 inherited CNV regions, of which 268 are rare in a control population of European origin but present in a large number of Amish individuals. We report a trend towards a higher burden of CNVs in known Mendelian disease loci in bipolar individuals (BPI and BPII, p = 0.06). Also, we identified a set of CNVs found at higher frequencies in BP individuals, including a set of deletions (encompassing PWRN2 on 15q11.2 and PARK2 on 6q26) and duplications (ANKMY1 on 2q37.3, TMEM-AS1 on 10q11.2, SALL3 and NFATC1 on 18q23) detected in an overlapping Anabaptist (Amish and Mennonite) population (see ABSTRACT by McMahon). Conclusions: Our results suggest that both SNPs and CNVs contribute to the phenotypic presentation of mood disorders and co-morbid medical conditions in this extended pedigree. These results reinforce the hypothesis of a complex genetic architecture underlying BP disorder, and suggest that the role of CNVs should be investigated in BP and co-morbid conditions. Disclosures: Nothing to Disclose.
Top of page 25.2 Heritable White Matter Diffusion Endophenotypes and Traits in Population Isolate Elliot Hong Maryland Psychiatric Research Center, Baltimore, Maryland, United States Background: Diffusion weighted imaging methods have been proposed to non-invasively decipher cerebral microstructure by examining the behavior of diffusion signals. We calculated heritability for diffusion weighted imaging parameters for cerebral white and gray matter to study the genetic contribution to the diffusion signals. Our approach is to identify diffusion weighted imaging models with the highest heritability using a family study design, here in a population isolate with large pedigree and favorable environmental homogeneity. The Old Order Amish are Caucasians with large family structure that enable heritability analyses with modest sample size. Methods: Using a large pedigree from an Old Order Amish population isolate, we compared the heritability among three representative diffusion weighted imaging methods targeting corpus callosum white matter and cingulate gyrus gray matter: diffusion tensor imaging (DTI), the permeability-diffusivity (PD) model, and the neurite orientation dispersion and density imaging (NODDI) model. The models represent mono-, bi-, and tri-compartmental modeling of diffusion signal, respectively. We compared the heritability of these three models in 137 members (59M/78F, average age=51.2±15.1; range=18-80 years) of Amish families from Lancaster County, PA. The participants were from a total of 17 nuclear families although they were connected into a single large pedigree within 8 generations. Results: We replicated the high heritability (h2) of the DTI-based fractional anisotropy (h2=0.67) and radial diffusivity (h2=0.72) in white matter. High heritability in both white matter and gray matter tissues were observed for the permeability-diffusivity index from the PD model (h2=0.64 and 0.84), and the neurite density from the NODDI model (h2=0.70 and 0.55), respectively. Orientation dispersion index from NODDI model was only significantly heritable in gray matter (h2=0.68). Phenotypic correlation analyses further suggest convergence vs. divergence across these diffusion measures with tissue specificity. Conclusions: Diffusion weighted imaging parameters measured from multi-compartmental models were heritable in both white matter and gray matter with robust heritability values. Our results posit diffusion weighted imaging parameters as important phenotypes for gene search; and genes thus identified may lead to better understand on causes of mental and neurological disorders that have been extensively associated with abnormal diffusion imaging findings. Overall, the study took advantage of a large, multigenerational family design with known pedigree structure that permits genetic dissections and comparisons of the diffusion weighted imaging models with good statistical power using only modest sample size. The relative environmental homogeneity in the cohort further increased the confidence on the calculated heritability. The strong additive genetic load thus identified, particularly regardless of whether measured in white matter or gray matter, supports the use of advanced diffusion weighted imaging models to derive diffusion-based endophenotypes for genetic studies on the cerebral microstructure under normal and neuropsychiatric conditions. Disclosures: I (or my spouse/partner) do have relevant financial interests to disclose. Part 1 Dr. Hong has been a Consultant/Advisor to Pfizer Part 4 Dr. Hong has received research grants from Mitsubishi Pharma, Pfizer, and Your Energy Systems, LLC.
Top of page 25.3 Genome Sequencing of Anabaptist Patients with Bipolar Disorder Reveals Enrichment of Rare, Functional Variants Within Genes Involved in GTPase Signaling Francis McMahon National Institute of Mental Health, Bethesda, Maryland, United States Background: Bipolar disorder is a highly heritable but genetically complex disorder afflicting about 1% of the population. Genome-wide association studies have identified a number of genetic markers, but each confers only a small increased risk of bipolar disorder. Exome sequencing studies in founder populations, such as the Anabaptists, may facilitate the identification of higher risk alleles, owing to decreased genetic heterogeneity and enrichment of otherwise rare alleles. Methods: We have ascertained over 150 individuals with bipolar disorder within Anabaptist (Amish or Mennonite) communities in North America. All individuals were directly interviewed with the Diagnostic Interview for Genetic Studies and diagnosed by a Best Estimate Final Diagnosis procedure. Blood samples were collected from cases and all available parents. Exome sequencing was completed on an Illumina platform, followed by extensive quality control using GATK Best Practices. Here we report initial results of annotation, filtering, and gene set enrichment analyses from 57 cases with bipolar disorder and their 30 available parents. Results: After filtering out common variants with a minor allele frequency >1% in any of several reference data sets, 706 functional variants (defined as non-synonymous, splicing, frame-shift, stop gain/loss by ENSEMBL) in 642 genes were found to be shared by 2 or more cases. Among the non-synonymous variants, 2 were found in ANK3 and one in SYNE1 - both genes have been implicated by previous genome wide association studies of bipolar disorder. We also found 21 non-synonymous variants and two frame-shift deletions that mapped to genes within copy number variants known to be associated with schizophrenia, autism, epilepsy, or bipolar disorder. Gene set enrichment analysis indicated that genes involved with GTPase signaling were enriched for rare functional variants shared by cases (Fold enrichment = 2.49, FDR = 0.0015). In order to replicate these results, we applied the same filtering strategy to an independent, whole genome-sequencing data set drawn from an overlapping Anabaptist population (Georgi et al 2014). We identified 804 rare functional variants in 771 genes that were shared by 2 or more cases in that sample. The same 40 variants were shared by cases in both samples. In addition, 88 genes carried different variants shared cases in each sample. Enrichment of rare functional variants was again found among genes involved in GTPase signaling (Fold enrichment = 2.13, FDR = 0.019), replicating the initial results in an independent sample. Conclusions: These results suggest that a number of different variants in many genes contribute to bipolar disorder even within an isolated population. Despite this genetic heterogeneity, we observed substantial overlap at the variant, gene, and gene-set levels between two independent samples ascertained from within the same broad isolated population. If confirmed in larger samples, these findings could point to novel drug targets for bipolar disorder. Disclosures: Nothing to Disclose.
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26. Training Aspects of International Research Collaborations: Experiences from Multinational Initiatives in Biological Psychiatry Between the USA, Europe, Asia, and Africa Thomas Schulze * , Raquel Gur, Akira Sawa, Frank Schneider, George Koob, Tobias Halene, Chao Chen, Chunyu Liu, Susan Weiss, Bruce Cuthbert, Triptish Bhatia, Ibtihal Ibrahim, Vishwajit Nimgaonkar, Ruben Gur, Isabella Schneider, Yoichiro Takayanagi Institute of Psychiatric Phenomics and Genomics Ludwig-Maximilans-University, Munich, Germany International collaborative efforts are a hallmark of 21st research in biological psychiatry. They have provided samples sizes needed for statistically robust results and have propelled the harmonization of research tools and analytical strategies. Moreover, they bring together both experienced and early career researchers from around the globe to share their knowledge and innovative ideas. They also foster the exchange of doctoral students or post-doctoral fellows for extended research stays. While the North American research community has benefited from high numbers of international early career investigators for many decades already, recent multinational collaborative endeavors are catalyzing and accelerating these developments even further. On the other hand, one can also witness a more balanced flow of young researchers between North America and the rest of the world, whereas until a few years the scientific migration was typically unidirectional, i.e. from Europe or Asia to the United States or Canada. This is in part also explained by increasingly better funding opportunities outside North America. Funding bodies across the globe have adapted to these developments, allowing consortia to apply for funds specifically geared towards early career investigators planning on an extended research stay abroad. Highly structured programs have been set up to make the training aspect the key element in international collaborations. The International Research Training Group “Brain-behavior relationship of emotion and social cognition in schizophrenia and autism” between the University of Aachen (and affiliates) in Germany and the University of Pennsylvania in the USA, funded by the Deutsche Forschungsgemeinschaft perfectly illustrates this development. The Tri National Training Program in Psychiatric Genetics between the University of Pittsburgh and institutions in India and Egypt, funded by NIH’s Fogarty International Center is another example. This study group will bring together PIs and early career investigators from such and other training programs. Participants hail from the USA, Germany, Japan, China, India, and Egypt. The early career researchers participating in this panel have diverse educational backgrounds and are at different stages in their career. The PIs and (former) trainees can offer a unique first-hand perspective of the challenges and opportunities of multinational research training programs. They will discuss the impact on their respective labs, personal career development, funding opportunities. The audience will hear about typical pitfalls, administrative snags and creative and pragmatic ways around. Leaders and policy makers of the relevant NIH institutes, i.e. NIMH, NIDA, and NIAAA, will join the discussion and present their positions on the future development of multinational training programs for research in neuroscience and psychiatry. With formal presentations limited to an absolute necessary minimum, the panel will be interactive, engaging the audience in sharing their own experiences. At the end of the session, the audience will have a first overview of international training programs in neuropsychopharmacological research and a basic knowledge of how to devise such programs at their respective institutions. By design, the panel is quite diverse, including male and female early career scientists at various stages, PIs, and NIH institute directors. Disclosures: Nothing to Disclose.
Top of page Wednesday, December 9, 2015
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27. Complimentary and Integrative Treatment for Mood and Anxiety Disorders
Top of page 27.1 Molecular Loci for Antidepressant Effects of n-3 Polyunsaturated Fatty Acids Mark Rasenick University of Illinois College of Medicine, Chicago, Illinois, United States Background: Chronic antidepressant treatment increases physical coupling between the G-protein, Gαs and adenylyl cyclase (AC), increasing cAMP signaling. Biochemical and imaging studies demonstrated this is due, at least in part, to the translocation of Gαs from lipid-rafts into non-raft membrane fractions where it is more effectively coupled to AC. While perturbation of lipid rafts translocates many species of Galpha, antidepressant treatment is specific to Gαs. This effect requires sustained drug treatment and is not seen with antipsychotics or mood stabilizers. Methods: A monomeric variant of our previously developed GFP-Gαs fusion protein was used to generate stable, clonal cell lines (C6 glioma) containing this fluorescent Gsα. GFP- Gαs not only translocates from lipid-rafts similar to endogenous Gαs in response to antidepressant treatment, but can be used to study individual cells under physiologic conditions. To do these studies, we used Fluorescence Recovery After Photobleaching measured in a Zeiss 710Meta microscope. Cells were treated with drug (at concentrations from 50 nM to 10 μM) for 1-3 days in the presence or absence of n-3 PUFA (EPA or DHA). Cells were also treated with n-3 PUFA alone. The acylation status of Gαs was also determined by mass spectrometry. Results: Chronic treatment with antidepressants increases fluorescence recovery time. This appears due to immobility of AC as AC/ GFP-Gαs complexes are much less mobile than GFP-Gαs alone. Other G protein alpha subunits are not altered by antidepressant treatment. Mutations to Gαs that render it cytosolic shorten recovery time, and mutations that augment membrane association due to an additional acylation site retard recovery further. n-3 PUFA treatment both translocates Gαs and facilitates antidepressants in doing so. Acylation status of Gαs is modified by sustained antidepressant treatment. Conclusions: It is suggested that both rafts and AC anchor Gαs, and removal from the former increases the latter. It is also suggested that n-3 PUFA might modify the lipid microenvironment and might also modify Gαs directly at its acylation site. We also suggest that FRAP of GFP-Gαs provides a platform that can be used for the development of antidepressant compounds and, perhaps, a prognostic indicator for drug selection in patients. Disclosures: Part 1: Eli Lilly, Pfizer, Part 2: Pax Neuroscience, Part 4: Eli Lilly, Lundbeck.
Top of page 27.2 Depression, Inflammation, and Omega-3 Fatty Acids David Mischoulon Harvard Medical School / Massachusetts General Hospital, Boston, Massachusetts, United States Background: Omega-3 (n-3) fatty acids have been studied as a possible treatment for major depressive disorder (MDD). While the literature is generally supportive of their efficacy and safety, studies as a whole have produced mixed or contradictory results. There is evidence that n-3 fatty acids may exert at least some of their clinical effect via anti-inflammatory mechanisms of action. This suggests that individuals with MDD who have elevations in inflammatory biomarkers may be better candidates for n-3 therapy. We sought to compare the efficacy of two n-3 fatty acids, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) in a sample of patients with MDD, and determine whether inflammatory biomarkers act as moderators of clinical response. Methods: 196 adults (53% female; age 44.7 ± 13.4 years) with DSM-IV MDD and a baseline 17-item Hamilton Depression Rating Scale (HAM-D-17) score 15, were randomized to 8 weeks of double-blind treatment with eicosapentaenoic acid (EPA)-enriched n-3 1060 mg/day, docosahexaenoic acid (DHA)-enriched n-3 900 mg/day, or placebo. Outcomes were determined using mixed model repeated measures (MMRM) analysis for the entire sample and for “high” and “low” inflammation groups based on individual and combined biomarkers. Results: Modified Intent-to-Treat (MITT) analysis examined 177 subjects (59.3% female, age 45.8 ± 12.5 years) with 1 post-baseline visit. All 3 groups demonstrated statistically significant improvement in the HAM-D-17, Quick Inventory of Depressive Symptomatology (QIDS-SR), and Clinical Global Improvement-Severity Scale (CGI-S) (P < 0.05), but neither n-3 preparation separated from placebo (P > 0.05). Response and remission rates were in the range of 40-50% and 30% respectively, for all treatments, with no significant differences between groups. 155 subjects had baseline biomarker data (IL-1ra, IL-6, hs-CRP, leptin, adiponectin) available for analysis. For the “inflammation-based” subgroups, we determined standardized treatment effect size (ES) for change in HAM-D-17 from baseline to week 8. While overall treatment group differences were negligible (ES=-0.13 to +0.04), subjects with any “high” inflammation improved more on EPA than placebo (ES=-0.39) or DHA (ES=-0.60) and less on DHA than placebo (ES=+0.21). Furthermore, EPA-placebo separation increased with increasing numbers of markers of high inflammation. Subjects randomized to EPA with “high” IL-1ra or hs-CRP or low adiponectin (“high” inflammation) had medium ES decreases in HAM-D-17 scores versus subjects “low” on these biomarkers. Subjects with “high” hs-CRP, IL-6 or leptin were less placebo-responsive than subjects with low levels of these biomarkers (medium to large ES differences). Conclusions: Neither EPA-enriched nor DHA-enriched n-3 was superior to placebo for the treatment of MDD in our sample as a whole. However, employing multiple markers of inflammation facilitated identification of a more homogeneous cohort of subjects with MDD responding to EPA versus placebo. These results may have implications for personalized medicine in that selection of a specific cohort of depressed patients may result in better outcomes with n-3. Studies are needed to replicate and extend these preliminary findings. Disclosures: Part 1: Dr. Mischoulon has received royalties from Lippincott Williams & Wilkins for published book “Natural Medications for Psychiatric Disorders: Considering the Alternatives, Part 4: Dr. Mischoulon has received research support through grants from the Bowman Family Foundation, FisherWallace, Nordic Naturals, Methylation Sciences, Inc. (MSI), and PharmoRx Therapeutics.
Top of page 27.3 Massage Therapy for GAD: Lessons Learned about Outcomes, Hormones, and Immune Function Mark Rapaport Emory University School of Medicine, Atlanta, Georgia, United States Background: Epidemiology studies indicate that a significant of patients in the US would prefer to seek treatment from integrative medicine healers than from traditional medical practitioners. In fact, stress, anxiety and depression are some of the most common reasons for individuals to seek massage therapy. Yet, little is known about the efficacy of massage for the treatment of GAD nor about the potential biological under-pinnings of massage therapy. Methods: Data from 2 NCCIH- funded pilot projects will be presented and synthesized. The first study is a 40 subject 12-session, single-masked, study comparing and contrasting Swedish Massage Therapy (SMT) vs. a light touch control condition (LT) on measures of efficacy, cortisol, oxytocin (OT), AVP, and immune parameters. The second study is a 44 subject pilot study in healthy volunteers investigating the acute and longer-term effects of SMT vs. LT on hormone levels and immune function. Results: After 12 sessions (end of week 6), clinician-rated HAM-A scores decreased 11.67 points (SE=1.09) for the SMT group, compared to 8.41 (SE=1.01) points for the LT group (t= -2.19; df=106; p=0.030), for a standardized treatment effect size (ES) -0.69 (95% CI= -1.330 to -0.051). Differences in improvement on the HAM-A total score were accompanied by non-significant but moderate effect size differences favoring SMT on both the Psychic Anxiety and the Somatic Anxiety subscales (ES=-0.429 and -0.552, respectively). We did not see differences in immune parameters between SMT and LT. the OT and AVP data are pending. So far, these findings are in agreement with our data from healthy controls where we found that twice-weekly SMT had much greater effect on hormone levels and less effect on immune function than weekly SMT. Conclusions: SMT was an effective treatment for subjects with GAD, it was well-tolerated and the advantage over LT could not be explained merely by differences in expectancy and credibility. This effect was not immune-mediated and was the result of improvement in both somatic and psychic anxiety. These findings with respect to twice-weekly SMT are consistent with our published data about the effects of SMT “dosage on biological measures in healthy controls. This work highlights the challenges and some new strategies that can be used to investigate a manual therapy in psychiatric subjects. Disclosures: Nothing to Disclose.
Top of page 27.4 Complementary and Integrative Health Approaches for Mental Health Conditions Emmeline Edwards National Center for Complementary and Integrative Health / National Institutes of Health, Bethesda, Maryland, United States Background: The National Center for Complementary and Integrative Health (NCCIH) is the Federal Government’s lead agency for scientific research on complementary and integrative health strategies. Methods: Our research portfolios include a group of diverse medical and health care interventions, practices, products, or disciplines that are not generally considered part of conventional medicine but are increasingly incorporated into integrative medicine practices and are most often used by the general public as a complement or adjunct to conventional medical care. There has been increasing interest from the psychiatry community in understanding the efficacy, safety and patterns of use of complementary and integrative health approaches for mental health conditions. In managing symptoms of mental health disorders, the most commonly used complementary and integrative approaches fall into the categories of mind and body approaches (massage, meditation, yoga) and natural products ( St John Wort, omega-3 fatty acids, chamomile). Results: N/A Conclusions: This presentation will highlight pre-clinical and clinical work with a strong emphasis on basic mechanism-oriented research that has the potential to yield mechanistic insights, and to identify biological signals of physiological effects. Disclosures: Nothing to Disclose.
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28. Synaptic Addiction: New Insights into the Cellular Mechanisms of Drug Action and Substance Use Disorders
Top of page 28.1 From Optogenetics to rTMS: A Clinical Trials on Cocaine Craving Antonello Bonci National Institute on Drug Abuse, Baltimore, Maryland, United States Background: Human studies have shown that dysfunction of subregions of the prefrontal cortex (PFC) is strongly correlated with compulsive drug use. Importantly, recent optogenetic studies in rodents demonstrated that compulsive cocaine seeking strongly reduces prelimbic cortex activity, while optogenetic stimulation of this brain area significantly inhibits compulsive cocaine seeking, providing both a causal link between cocaine abuse and hypoactivity of the PFC, and a strong rationale for using brain stimulation techniques to reduce cocaine consumption. Methods: 32 cocaine-addicted patients were enrolled in a 29-day outpatient study (Phase 1) and randomly assigned to either the experimental group receiving rTMS on the left Dorsolateral PFC (DLPFC), or to a control group treated with pharmacological agents (dopaminergic medications and benzodiazepines). Phase 1 was followed by a 63-day follow-up (Phase 2), during which completers in the control group were offered to switch to rTMS treatment and completers in the experimental group continued receiving rTMS. Results: In the rTMS group, no serious or unexpected adverse events were observed. During Phase 1, there was a significantly higher number of cocaine-free urine drug tests in the rTMS group compared to control. Craving for cocaine was also significantly lower in the rTMS group compared to the controls. Out of 13 patients who completed Phase 1 in the control group, 10 patients received rTMS treatment during Phase 2 and showed significant improvement with favorable outcomes becoming comparable to those of the rTMS group. Conclusions: The present study, albeit very preliminary, provides data supporting the safety of rTMS in cocaine-addicted patients and suggest its potential therapeutic role for rTMS-driven PFC stimulation in reducing cocaine use. Disclosures: Nothing to Disclose.
Top of page 28.2 Strengthening Accumbal Indirect Pathway Promotes Resilience to Compulsive Cocaine Use Veronica Alvarez National Institute of Mental Health, Bethesda, Maryland, United States Background: Substance use disorders are highly prevalent and comorbid with all major mental illnesses including depression, posttraumatic stress disorders, bipolar disorder, and schizophrenia. Over the past decade, rapid technological advances have spurred unprecedented advancement in the synaptic, cellular, and circuit mechanisms underlying compulsive behaviors including addiction. A key goal of the session will be to present advances in the synaptic mechanisms subserving compulsive behaviors and addiction in a manner accessible to clinicians and non-specialists, and to highlight translational potential of research findings made at the synaptic level to higher levels of analysis at the circuit, behavioral, and ultimately clinical level. Methods: Operant intravenous cocaine self-administration in mice combined with ex vivi electrophysiological analysis of glutamatergic synaptic transmission and two-photon laser scanning imaging. Results: Dr. Alvarez will present results that identify a synaptic mechanism that confers resilience against the development of compulsive cocaine use in mice. Her group found that recruitment of indirect-pathway neurons in the NAc functions to restrain cocaine self-administration and suggests that individuals with robust indirect-pathway are resilience to developing addictive behaviors. Conclusions: These findings suggest that the activity state of the accumbal-pallidum indirect-pathway strongly influences cocaine taking behavior and the motivation to seek cocaine and that strengthening of accumbal-pallidum indirect-pathway can serve as a natural protective mechanism towards the development of compulsive seeking. Disclosures: Nothing to Disclose.
Top of page 28.3 Neuroplasticity in Fronto-Cortical Circuits Associated with Compulsive Eating Stephanie Borgland Hotchkiss Brain Institute / University of Calgary, Calgary, Canada Background: In an environment rich in easily accessible palatable foods, the ability to withhold food consumption is of key importance for maintaining a healthy body weight. The orbitofrontal cortex (OFC) encodes the current incentive value of food cues and is implicated in cognitive flexibility. Dysfunction of the OFC leads to perseverative behaviours including compulsive eating. Most studies have used lesions to assess the function of the OFC. However, these studies provide little information on the underlying cellular mechanisms as lesions destroy both the pyramidal neurons and the GABAergic interneurons that tightly control the firing and output of the pyramidal projection neurons. Furthermore, it is unknown if and how neurons in the OFC adapt to a pathological insult, such as compulsive behavior. Therefore, we used a model of compulsive feeding to determine if diet can induce neuroplasticity of the OFC. We hypothesized that extended access to a cafeteria diet can induces neuroadaptations in the OFC. Methods: We used whole cell patch clamp in coronal OFC brain slices to measure basal excitability and synaptic transmission of lateral OFC pyramidal neurons from rats that had extended or restricted access to a cafeteria diet as well as chow-fed controls. We also tested for compulsive behavior using a conditioned suppression model where rats were presented with the cafeteria diet in the presence of footshock predicting cues. Results: After 6-7 weeks of extended access to a cafeteria diet, obese rats did not suppress feeding in response to foot-shock predicting cues, in contrast to rats restricted to one hour a day of the cafeteria diet or chow-fed rats. OFC pyramidal neurons from extended access rats had greater excitability. This was accompanied by a reduction of inhibitory synaptic transmission to these neurons. Although restricted access rats binge eat their caloric intake during the 1 h exposure to the cafeteria diet, there were no significant changes of OFC pyramidal neurons from these rats compared to chow fed rats. Conclusions: Taken together, extended access to a cafeteria diet can induce neuroplasticity of OFC that may alter the animal’s ability to withhold feeding responses during aversive situations. Disclosures: Nothing to Disclose.
Top of page 28.4 Nucleus Accumbens Parvalbumin Expressing Interneurons Regulate Synaptic and Behavioral Plasticity Brad Grueter Vanderbilt University Medical Center, Nashville, Tennessee, United States Background: Maladaptive circuit function within the reward system is likely a key component to susceptibility to drug addiction. The nucleus accumbens (NAc) is a key brain region involved in mediating aspects of addiction-related behaviors and is comprised of parallel output loops (D1 and D2 dopamine receptor expressing medium spiny neurons (MSNs)) whose activity is governed by excitatory drive and by often overlooked inhibitory interneuronal microcircuitry. Parvalbumin (PV) expressing fast spiking interneurons (FSIs) are GABAergic cells that regulate the activity of networks through inhibition of local projection neurons. Activity of PV-FSIs is thought to gate excitatory drive within the NAc to correctly process goal-directed behaviors. Endocannabinoid (eCB) signaling is an on-demand synapse-specific negative feed-back signal that regulates emotional and motivational states. A major established role of eCBs is regulation of excitatory and inhibitory synaptic transmission. ECB signaling via cannabinoid 1 receptors (CB1Rs) and transient receptor potential vanilloid 1 (TRPV1) inhibits D2 MSN excitatory synapses within the NAc. We hypothesize that NAc PV-FSIs differentially regulate D1 and D2 MSNs under physiological and pathophysiological conditions in an eCB dependent manner. The rationale is that, NAc MSN subtypes dynamically integrate inhibitory signaling from PV-FSIs via eCB signaling to selectively filter excitatory drive and thus propagate information through the reward circuit leading to behavioral outcomes. Methods: We identified NAc core D1 or D2 MSNs in acute slices from transgenic mice and use targeted whole-cell patch-clamp recordings to investigate synaptic and membrane properties of NAc D1 and D2 MSNs. These mice consist of combinations of D1-tdTomato bacterial artificial chromosome (BAC) transgenic mice, parvalbumin (PV)-Cre mice, conditional ChR2 mice (B6;129S-Gt(ROSA)26Sortm32(CAG-COP4*H134R/EYFP)Hze/J), and homozygous Cnr1floxed mice generated by Dr. Eric Delpire (INIA). 470 nm blue light stimulation activates ChR2 expressed on PV-FSIs and elicit light-evoked inhibitory post synaptic currents (oIPSCs) in cells being recorded from. Behavioral analysis consists of locomotor responding and conditioned place preference to psychostimulants and exocannabinoids. Real time place preference is performed by implanting fiber optics into the NAc of PV-cre/cChR2 mice. Results: Our results show CB1R activation can inhibit IPSCs from PV-FSIs to D1 and D2 MSNs while TRPV1 activation inhibits GABAergic neurotransmission preferentially at D1 MSN synapses. LFS of PV-FSI to MSNs results in a state dependent depression of synaptic transmission. Long term depression of IPSCs (iLTD) from PV-FSI to D1 but not D2 MSN synapses is expressed at hyperpolarized membrane state. Conversely, while at depolarized state, iLTD is elicited at PV-FSI to D2 but not D1 MSN synapses. Preliminary studies suggest this iLTD is CB1R dependent. Further work analyzing excitatory/inhibitory (E/I) synaptic function at synapses onto D1 and D2 MSNs suggests the E/I balance is sensitive to CB1R expression on PV-FSIs. This E/I balance is also sensitive to prior cocaine experience. Conditional knockout of CB1Rs in PV-FSIs results in have a shift in CB1R agonist dependent learning and attenuated cocaine-induced learning. Finally, behavioral analysis suggests that this LFS stimulation pattern investigated in the slice elicits conditioned place aversion in PV-ChR2 mice. Conclusions: PV-FSIs, although limited in number, make vast inhibitory connections to MSNs thereby greatly influencing NAc output. Thus, PV-FSI synaptic activity is a putative mediator of NAc circuit adaptations by influencing NAc synaptic and membrane properties. Changes in NAc circuit dynamics likely underlie addiction behaviors. Indeed, we find that manipulation of these PV-FSIs in the NAc and CB1R signaling on PV-FSIs bi-directionally modulate drug-related behaviors. Disclosures: Nothing to Disclose.
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29. Normalizing Cognitive Impairments in Schizophrenia: New Leads from Novel Glutamatergic Manipulations
Top of page 29.1 Cognitive Enhancement Through Inhibition of Kynurenic Acid Synthesis Robert Schwarcz Maryland Psychiatric Research Center, Baltimore, Maryland, United States Background: The levels of the tryptophan metabolite kynurenic acid (KYNA) are elevated in the brain and cerebrospinal fluid of persons with schizophrenia (SZ) and may be causally involved in pathophysiology. This view is based on the ability of KYNA to antagonize the function of α7 nicotinic and NMDA receptors, both of which are critical to normal brain development and cognitive processes, and are impaired in schizophrenia. In experimental animals, even relatively moderate increases in brain KYNA result in a spectrum of biochemical and cognitive abnormalities reminiscent of SZ. Interventions leading to a reduction of KYNA synthesis in the brain therefore provide a novel approach to achieve pro-cognitive effects. We tested this hypothesis using a new, systemically active inhibitor of the key KYNA-synthesizing enzyme kynurenine aminotransferase II (KAT II). Methods: Using biochemical and behavioral outcome measures, we tested the effects of the specific KAT II inhibitor BFF-816 (Wu et al., Schiz. Bull., 2014) in adult rats. Microdialysis was performed in awake animals, and extracellular levels of KYNA (all regions), glutamate (dorsal hippocampus, medial prefrontal cortex) and dopamine (striatum) were determined by established HPLC methods. The Morris water maze was used to study spatial navigation and reference memory in normal animals. BFF-816 or vehicle was administered 90 min prior to the first trial of behavioral testing on each day. Finally, using an established passive avoidance paradigm, we tested the acute effects of KAT II inhibition in adult rats that show deficits in contextual memory following chronic prenatal KYNA elevation (Pocivavsek et al., Psychopharmacology, 2014). In all experiments, BFF-816 was given orally at 30 mg/kg. Results: Compared to respective baseline levels, BFF-816 consistently reduced extracellular KYNA and increased extracellular glutamate and dopamine levels in the brain areas studied. Maximal effects (~25% decrease in KYNA and ~60% elevation in glutamate and dopamine, respectively) were seen between 90 and 150 min after BFF-816, and the levels of all analytes returned to control values after approximately 4 h. No tolerance was seen when animals were treated daily for five consecutive days. Behaviorally, daily injections of BFF-816 significantly decreased escape latency in the Morris water maze, indicating improved performance in spatial and contextual memory in normal animals. In developmentally challenged adult rats, BFF-816 restored the memory deficit when administered prior to training on Day 1, but not when given prior to testing avoidance latency on Day 2 of the contextual memory task. Conclusions: Systemically applied BFF-816 is an excellent tool for studying the neurobiology of KYNA and, in particular, for investigating the mechanisms linking KAT II inhibition to changes in glutamatergic and dopaminergic function in brain physiology and pathology. Disclosures: Part 1: Vistagen, Part 2: Vistagen, Part 4: Mitsubishi-Tanabe, Lundbeck.
Top of page 29.2 Calcium-Permeable Ampa Receptor and Asc-1 Transporter Regulate the Cortical Extracellular D-Serine Concentration: Potential Targets for Development of Novel Pharmacotherapy for NMDA Receptor Dysfunction in Schizophrenia Toru Nishikawa Tokyo Medical and Dental University, Tokyo, Japan Background: In mammalian brains, D-serine has been shown to act as an endogenous co-agonist for NMDA type glutamate receptors (NMDARs) that are presumed to be hypofunctional in schizophrenia (SZ). This pivotal role of D-serine indicates that the control systems of the extracellular D-serine in the brain could be potential targets for analysis of the pathophysiology of and creation of new treatment for SZ. However, the molecular and cellular mechanisms underlying the D-serine signaling are largely unknown. To gain a cue to clarify this important issue, we have studied the effects of agents acting at AMPA type glutamate receptors (AMPARs) and Asc-1 neutral amino acid transporter on the extracellular D-serine concentrations in the medial frontal cortex (mFC). Methods: The cortical extracellular concentrations of D-serine and other amino acids were measured in freely moving rats by an in vivo microdialysis technique in combination with high-performance liquid chromatography with fluorometric detection, because the in vivo conditions are needed to avoid the influence of anesthesia and to maintain integration of neuron-neuron and/or neuron-glia interaction, in which D-serine has been found to participate. Results: The intra-mFC infusion of (S)-AMPA, an active enantiomer at the AMPAR, via the dialysis probing causes a significant reduction in the extracellular contents of D-serine in the cortical portion in a concentration-dependent, an AMPA/kainate receptor antagonist NBQX- and a calcium permeable AMPA receptor antagonist 1-naphthyl acetyl spermine-reversible manner. The reducing effects of (S)-AMPA are augmented by co-infusion of cyclothiazide that prevents AMPA receptor desensitization. Moreover, attenuation of glial activity by toxin fluorocitrate, but not cessation of nerve impulse traffic by tetrodotoxin blocked the AMPAR-D-serine interaction. The local infusion of a system A and Asc-1 amino acid transporter inhibitor, S-methyl-L-cysteine, into the mFC produces an increase in the cortical dialysate contents of D-serine in a concentration-related manner. Conclusions: Our data support the views that a calcium permeable AMPAR subtype may exert a phasic inhibitory regulation of the extracellular D-serine release in the mammalian frontal cortex and that the liberated D-serine in the cortical glutamate synapse may be taken up into certain cells, at least in part, via the Asc-1 neutral amino acid transporter. Therefore, development of pharmacotherapy enhancing the extracellular D-serine levels by blockade of either of the two molecules could facilitate NMDAR functions and improve current treatment-resistant cognitive deficits and negative symptoms of SZ that are related to reduced NMDAR activity. It is also possible that dysfunction of these molecules might be involved in the pathophysiology of SZ. Disclosures: Part 1: The authors declare no conflict of interest related to the subject of this presentation. Dr. Nishikawa was recently compensated for his lectures by Astllas, MSD, Eli Lilly, GSK and Otsuka pharmaceutical industries and for his consultancy by Mochida Pharmaceutical Co., Ltd. He also received grants for scientific research, but not for clinical drug assessment, from Tanabe-Mitsubishi, MSD, Pfizer, Astllas, Otsuka and Shionogi directly or indirectly through a foundation, Part 4: As shown in a part of the above “Disclosure Part 1", Dr. Toru Nishikawa received grants for scientific research, but not for clinical drug assessment, from Tanabe-Mitsubishi, MSD, Pfizer, Astllas, Otsuka and Shionogi pharmaceutical industries directly or indirectly through a foundation.
Top of page 29.3 Endogenous D-Serine Maintains the Level of NMDA Receptor Activation Required for LTP Induction at Hippocampal Synapses Vadim Bolshakov Harvard Medical School McLean Hospital, Belmont, Massachusetts, United States Background: Activation of NMDA receptors (NMDAR) at central synapses leads to the intraneuronal calcium influx required for the induction of synaptic and developmental plasticity. In addition to binding glutamate, NMDAR activation requires occupation of the glycine binding site on the NR1 subunit by endogenous co-agonists, glycine or D-serine. The NMDAR glycine site is not saturated at central synapses in vivo, and, therefore NMDAR function could be regulated through changes in the glycine site occupancy. Genetic, pharmacologic and post-mortem studies have implicated hypofunction of NMDARs in the pathophysiology of schizophrenia. Focusing on the analysis of mice with the expression of serine racemase (SR) conditionally or constitutively suppressed to inhibit D-serine synthesis, we explored whether the hypofunction of NMDARs due to the lack of D-serine may be translated into the functional deficits in the hippocampus, a brain region severely affected in schizophrenic patients. Methods: Electrophysiological recordings were performed in slices from SR-/- mice and their control littermates. Thin hippocampal slices were cut with a vibratome and transferred to an incubation chamber filled with ACSF. Whole-cell patch-clamp recordings were obtained from visualized (with DIC/infrared optics) neurons. Extracellular fEPSPs were recorded with glass pipettes filled with the extracellular solution. Results: We found that long term potentiation (LTP) at the Schaffer collateral-CA1 neuron synapses was markedly reduced in slices from mice in which SR was specifically inactivated in neurons (but not in astrocytes). The observed effect on LTP was associated with significant reductions in the amplitude of NMDAR-mediated synaptic currents in CA1 neurons in these mice. Similarly, the amplitude of NMDAR-mediated synaptic currents was diminished in the dentate gyrus (DG) of SR-/- mice. The hypofunction of NMDARs, detected in SR-/- mice did not affect basal synaptic transmission but resulted in reduced LTP at the medial perforant pathway to DG synapses in the hippocampus. Chronic D-serine treatment normalized the electrophysiological deficits observed in SR-/- mice. Notably, the metabotropic glutamate receptor 5 (mGluR5) positive allosteric modulator, VU0409551, enhanced NMDAR responses and rescued LTP in hippocampal slices obtained from SR-/- mice. The alterations in LTP and its pharmacologic rescue paralleled performance in a trace conditioning memory task. Conclusions: Our findings indicate that D-serine is required for optimal activation of postsynaptic NMDA receptors and induction of long-term synaptic plasticity in the hippocampus needed for certain cognitive functions of the brain. Disclosures: Nothing to Disclose.
Top of page 29.4 Oxidative Stress in Interaction with Nmda Receptor Hypofunction as a Core Mechanism in Schizophrenia Pathophysiology: Spatial-temporal Development and Potential Protection with Antioxidants Kim Do Lausanne University Hospital, Prilly-Lausanne, Switzerland Background: Excitatory-inhibitory (E/I) balance, as set by parvalbumin interneurons (PVI) GABAergic circuitry, is critical for high-frequency neuronal synchrony, sensory gating and cognition. PVI alterations constitute a hallmark in schizophrenia (SZ). Their fast-spiking activity implies enhanced oxidative metabolism and generation of reactive oxygen species (ROS), in tight link with inflammatory processes. If the redox regulation is deficient, as described in patients, it will lead to oxidative stress (OX) in PVI. In addition, most developmental environmental insults such as infection or psycho-social trauma induce ROS production. NMDAR hypofunction also leads to PVI impairment through OX (Hardingham): Synaptic NMDAR activation boosts intrinsic antioxidant defenses, through direct transcriptional control of glutathione (GSH), promoting its synthesis, recycling and utilization. Inversely, NMDAR hypoactivity during development leads to deleterious loss of this control. We studied the regional distribution and the developmental timing of OX induced PVI impairment and the convergence of various SZ models on OX. Methods: Spatiotemporal distribution of OX was assessed by 8-oxo-DG and PVI integrity by PV and perineuronal net (PNN) immunohistochemistry (Cabungcal &al, 2014). Various SZ models have been investigated: One model concerns directly the redox dysregulation (gclm-/-, knock-out of the key GSH synthesizing enzyme), while the others do not: ventral hippocampal neonatal lesion (NVHL) rats, D-serine-racemase knock-out (SR-/-) mice, LgDel 22q11 deletion syndrome mice and methylazoxy-methanol acetate (MAM) rats. Results: During development of gclm-/-, the spatio-temporal sequence of OX and PVI deficit show that they appear first in thalamic reticular nucleus (from D10 on), then in amygdala, ventral hippocampus, globus pallidus and the latest in anterior cingulate cortex. This suggests a staging of OX sensitivity and of its consequences for PVIs in various telencephalic regions, potentially affecting their respective functions. Interestingly, various models studied also converge on OX. The NVHL that does not entail direct manipulation of redox pathways, presents OX and PVI impairment. Treatment with antioxidants such as N-acetyl-cysteine (NAC) or Ebselen prevents both, as well as their physiological and behavioral deficits, suggesting that they are secondary to OX. These reversal effects of NAC are also present when applied during adolescence. The OX induced impairment of PVI is also observed in other SZ models including SR-/-, LgDel22q11 and MAM models. Conclusions: Combined with evidence of OX and PVI impairment both in patients and in other genetic models (DISC1, PROD, G72, NRG), our results suggest that vulnerability to OX of PVI/PNN appears as a final common pathway for various genetic and environmental risk factors and places them at the core of SZ pathophysiology. This opens perspectives for early prevention with antioxidants/redox modulators. Disclosures: Nothing to Disclose.
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30. The Research Domain Criteria (RDoC) Initiative: New Data Across Psychiatric Conditions and Age Groups
Top of page 30.1 A Multi-modal Assessment of Positive Valence Systems Across Unipolar and Bipolar Depression Diego Pizzagalli Harvard Medical School, Belmont, Massachusetts, United States Background: Current diagnostic criteria often fail to differentiate bipolar disorder from unipolar depression when a person presents in a depressed state. Consequently, for someone with bipolar disorder the average length of time from symptom onset to correct diagnosis is over ten years. This indicates an urgent need to move beyond our current diagnostic system and identify neurobiological markers that better predict bipolarity. The current study aims to address this need by identifying biomarkers that predict (hypo)mania in a transdiagnostic sample of individuals seeking treatment for mood disorders, focusing on the key domain of Reward Learning within the RDoC Positive Valence Systems matrix. Methods: We evaluated predictors of (hypo)mania across three units of analysis that assess distinct yet complementary aspects of reward processing. First, we examined the acquisition of a behavioral response bias during a probabilistic reward task (PRT). Second, we measured the amplitude of the feedback-related positivity (FRP) during the PRT. This is an event-related potential component elicited by positive prediction errors, thought to arise from dopaminergic burst-firing within the anterior cingulate cortex (ACC) and striatum during reward learning. Third, we measured levels of glutamate (Glu) within the ACC using magnetic resonance spectroscopy. Glu is an excitatory neurotransmitter that has been associated with motivation for rewards. To date, 25 mood disorder patients, and 9 psychiatrically healthy subjects have been recruited. Results: Across the entire sample, levels of ACC Glu positively correlated with severity of (hypo)mania (r=.68, p=.046). Although more severe (hypo)mania was associated with greater depressive illness severity, the correlation between Glu and (hypo)mania remained significant after controlling for depressive symptoms. This indicates that elevated Glu was specifically associated with (hypo)mania rather than illness severity. In contrast, reduced FRP to rewards was associated with more severe anhedonia (r=-.53, p=.02). Conclusions: Findings indicate that increased ACC Glu is associated with an increased risk for (hypo)mania. The results also corroborate prior evidence of an association between blunted FRP (putatively indexing reduced dopaminergic firing during reward learning) and anhedonia. The potential for these markers to improve diagnosis of depressive disorders will be discussed. Disclosures: Part 1: Consulting/honorarium from Pfizer, Otsuka.
Top of page 30.2 The Neuroimmunology of Anhedonia and Related Positive Valence System Deficits in Adolescents Vilma Gabbay Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: Adolescence represents a critical developmental stage, during which many psychiatric disorders first emerge. This phenomenon has been attributed, in part, to maturational disturbances within the neuronal reward circuitry. Clinically, such alterations can manifest as anhedonia, the reduce capacity to experience pleasure, a core symptom of major depression and a salient feature across psychiatric conditions. Utilizing a dimensional investigative approach, we have examined the role of peripheral inflammatory processes and brain chemicals in anhedonia among depressed adolescents as well as across psychiatric conditions. Further, to delineate the specific deficits of reward processes associated with peripheral inflammation and neurometabolites abnormalities, we have developed the reward flanker task to examine brain function during reward expectancy and attainment. Methods: Subjects are adolescents ages 12-18 of Tanner 4, all medically healthy. All are diagnosed by the K-SADS-PL. Anhedonia, fatigue, sleep, and anxiety are assessed quantitatively. Immune assessment: Blood samples are collected between 8-9AM after an overnight fast ( 12h), before and after the Trier Social Stress Test. PBMC are being exposed for 24 to LPS to examine response to biological stresses. Kynurenine pathway metabolite, cytokines, and composition of innate and adaptive immune system are examined. Within an hour after the blood draw participants have an imaging session including: a) 1H MRS assessing striatal and cortical glutathione (antioxidant), ACC GABA, N-acetylaspartate (neuronal/mitochondrial marker) and total choline (lipid peroxidation); b) FMRI includes resting state and the Reward Flanker Task (RFT), a combination of the incentive flanker and monetary incentive tasks, that examines brain function during reward expectancy (motivation) and immediate attainment. Results: Adolescents with moderate to severe MDD as well as with diverse psychiatric symptoms exhibited a full range of anhedonia severity. We have reported positive relationships between inflammatory neurotoxins and anhedonia severity. We also documented that decreased ACC GABA levels in depressed adolescents were driven by the anhedonic subgroup and reported a negative relationship between anhedonia severity and ACC GABA levels in the whole sample. Using striatal based intrinsic functional connectivity, we identified specific network associated with anhedonia severity while controlled for other depressive symptomatology. Using the RFT, anhedonia severity was associated with specific brain regions during reward anticipation and attainment. Conclusions: Peripheral inflammatory processes and neurochemical alterations implicated across psychiatric conditions may play a role in the neurobiology of anhedonia and be associated with specific deficits of reward processes. Such investigative approach can facilitate the early identification of alterations within specific neurocircuits. Disclosures: Nothing to Disclose.
Top of page 30.3 Do the Neural Mechanisms Mediating Irritability Differ Across Diagnoses? Ellen Leibenluft National Institute of Mental Health, Bethesda, Maryland, United States Background: The RDoC framework makes an implicit assumption that the neural mechanisms mediating a psychological trait or symptom (e.g., irritability) do not vary across DSM-5 diagnoses. We tested this assumption in youth with disruptive mood dysregulation disorder (DMDD) and bipolar disorder (BP). Severe, chronic irritability is the hallmark of DMDD, and is also common in pediatric bipolar disorder (BP) during euthymia; however, the two phenotypes differ in that only those with BP have distinct manic episodes. Both BP and DMDD show deficits in face emotion labeling. In this study we used fMRI and a face emotion labeling paradigm to test whether the neural mechanisms mediating irritability differ between BP and DMDD. Methods: During fMRI, 71 youths (24 DMDD, 25 BD, 22 HV) performed an event-related face emotion labeling task with happy, fearful, and angry faces of varying intensity. In all subjects, trait irritability was characterized dimensionally on the Affective Reactivity Index (ARI). We tested, not only main effects of diagnosis (BP, DMDD, HV) and ARI on neural activity, but also diagnosis x ARI interactions in a whole-brain corrected analysis. Results: ARI scores did not differ between DMDD and BD, and there were no behavioral differences among groups in the scanner. We found a trait x diagnosis interaction in the amygdala, where irritability correlated with neural activity for all emotions in DMDD, but only for fearful faces in BD. Moreover, higher irritability was associated with greater amygdala activity in response to subtle fearful faces in BD, but less amygdala activity in DMDD. Other temporal, parietal, and occipital regions showed positive correlations between irritability and BOLD response to subtle negative emotion faces in DMDD, but not BD. Conclusions: Although irritability severity did not differ between DMDD and BD, the neural mechanisms mediating irritability did differ significantly between the two patient groups. These data challenge the RDoC assumption that, across diagnoses, neural mechanisms mediating a specific trait are necessarily the same. Clearly, this assumption needs to be tested for other traits and across other diagnoses. Additionally, the current findings add to existing longitudinal, familial, and neuroimaging data suggesting that DMDD (characterized by chronic irritability, without manic episodes) and BP (characterized by episodic mania with or without chronic irritability between episodes) are distinct phenotypes. Disclosures: Nothing to Disclose.
Top of page 30.4 A Common Functional Topography Across the Major Psychiatric Disorders Sophia Frangou Ichan School of Medicine at Mount Sinai, New York, New York, United States Background: Epidemiological, phenomenological, family and molecular genetic studies suggest that psychiatric disorders have overlapping aetiology and pathophysiology. Meta-analyses of the brain magnetic resonance imaging (MRI) literature have identified brain structural alterations shared across multiple disorders. The aims of the present study were (1) to identify a ‘disorder-general’ functional map of schizophrenia (SZ), bipolar disorder (BD), major depressive disorder (MDD), obsessive compulsive disorder (OCD), and anxiety disorders (ADs) (2) quantify the effect of functional MRI (fMRI) task paradigm, as classified by Research Domain Criteria (RDoC), on the pattern of neural engagement observed across disorders. Methods: Following extensive search of databases available through the National Center for Biotechnology Information up to December 2013, we extracted brain coordinates from 541 task-related fMRI case-control studies in SZ, BD, MDD, OCD and ADs comprising observations from 25,626 participants. We used quantitative meta-analytic and meta-regression techniques to identify the common neural functional architecture implicated in all five disorders and define the contribution RDoC constructs while controlling for other important variables (neuroimaging parameters of the primary studies, age, sex, medication status). Results: We identified a ‘disorder-general’ meta-analytic map of shared transdiagnostic functional alterations (regardless of direction) in three clusters encompassing bilaterally the amygdala, hippocampus, thalamus, striatum, insula perigenual anterior cingulate cortex, posterior cingulate cortex, ventromedial prefrontal and the entire lateral prefrontal cortex. Within these regions, patients were more likely to show increased activation in limbic and medial temporal regions and decreased activation in the thalamus and the lateral prefrontal cortex. The effect of RDoC domains was significant for subcortical regions (amygdala, hippocampus, putamen, nucleus accumbens) but not in cortical regions with the exception of the medial prefrontal cortex and frontal operculum. Conclusions: These results provide evidence in support of a common functional topography across multiple psychiatric disorders. A model assuming disorder-specific pathogenesis would have resulted in minimal or no transdiagnostic overlap in functional architecture. Instead, the disorder-general map identified suggests that some brain regions are relatively more vulnerable and thus likely to be affected by a range of pathogenetic mechanisms. Disclosures: Nothing to Disclose.
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31. Caffeine Interactions with Dopamine in Adolescence: An Unappreciated Risk for Obesity and Addiction?
Top of page 31.1 Addiction Vulnerability Characteristics Following Adolescent Caffeine Consumption Ryan Bachtell University of Colorado, Boulder, Colorado, United States Background: Caffeine is the most commonly used psychoactive substance worldwide, and consumption by children and adolescents has risen dramatically in recent years. Previous studies have found that caffeine intake in adults is positively correlated with substance use disorders, increased illicit drug use and increases in anxiety. We have recently demonstrated that adolescent caffeine consumption enhances acute cocaine sensitivity in adulthood suggesting that adolescent exposure may render individuals vulnerable to the development of addiction. These experiments extend our previous work by exploring the effects of adolescent caffeine consumption on cocaine intake and vulnerability traits that are associated with the development of drug addiction. Methods: Sprague-Dawley rats consumed 0.3 g/L of caffeine for 14-28 days during the adolescent period (postnatal days 28-55). Age-matched control rats continued to receive water. Caffeine and water consumption were monitored throughout the procedure, and animals consumed approximately 30 mg/kg/day without producing significant changes in body weight gain during this developmental period. Following caffeine consumption, the caffeine solution was replaced with water for the remainder of the experiment. Behavioral testing and tissue collection occurred during adulthood (postnatal days 62-82). To evaluate how caffeine exposure influences the reinforcing properties of cocaine, rats were trained to self-administer cocaine and tested on fixed-ratio and progressive ratio schedules. We also evaluated how adolescent caffeine consumption influences incentive salience to reward-related cues in a Pavlovian learning procedure, which has been shown to correlate with a greater propensity to self-administer drugs. We also assessed how adolescent caffeine consumption alters impulsivity using a delayed-discounting procedure. Finally, we determined how adolescent caffeine exposure alters dopamine-related protein expression and dopamine levels in the prefrontal cortex using immunoblotting and in vivo microdialysis, respectively. Results: Adolescent caffeine consumption increased the acquisition of cocaine self-administration on a fixed-ratio 1 schedule and increased performance on a progressive ratio schedule of reinforcement. Adolescent caffeine consumption also increased measures of incentive salience for reward-related cues and impulsivity. Consumption of caffeine during adolescence also enhanced cocaine-induced extracellular dopamine in the nucleus accumbens and prefrontal cortex. We also observed altered protein expression of a variety of dopamine-related proteins in the nucleus accumbens and prefrontal cortex that may relate to the behavioral changes. Conclusions: Together these findings suggest that caffeine consumption during adolescence produces changes in the mesocorticolimbic dopamine system that persist into adulthood. These neurobiological changes are thought to contribute to the behavioral changes resulting from adolescent caffeine consumption that associate with increased addiction vulnerability and enhanced cocaine intake. Disclosures: Nothing to Disclose.
Top of page 31.2 Changing Classical Pharmacology by Exploring the Allosteric Mechanisms of Caffeine Within the Adenosine A2A-Dopamine D2 Receptor Heterotetramer Sergi Ferre National Institute on Drug Abuse, Baltimore, Maryland, United States Background: Heteromerization of the adenosine A2A receptor (A2AR) with dopamine D2 receptor (D2R) takes place in a specific population of striatal neuron, the striatopallidal neuron. Previous studies suggested that the psychostimulant effects of caffeine depend largely on its ability to target the A2AR-D2R heteromer, by blocking an allosteric interaction by which adenosine decreases the affinity and intrinsic efficacy of dopamine. But in a recent human PET study using the D2R antagonist [11C]raclopride, we found that caffeine increases D2R availability in the dorsal and ventral striatum. Since the agonist-agonist interaction within the A2AR-D2R heteromer would predict the opposite effect we revisited all possible allosteric interactions between orthostheric agonists and antagonists within the heteromer with extensive experiments in transfected cells and human and sheep striatal tissue. Methods: Allosteric effects of caffeine and other selective A2AR antagonists and the A2AR agonist CGS 21680, alone and in combination, were studied with radioligand binding experiments with [3H]raclopride or the D2R agonist [3H]quinpirole in transfected cells and sheep and human striatal tissue. Parallel MAPK signaling experiments were performed in transfected cells and sheep striatum. Bimolecular Sensor Complementation (BiSC) was used to determine the ability of synthetic peptides with amino acid sequences of transmembrane domains of A2AR and D2R (TM peptides) to disrupt A2AR-D2R heteromers in transfected cells. BRET with double BiSC was used to determine the possible tetrameric structure of the A2AR-D2R heteromer. Proximity Ligation Assay (PLA) was used to visualize A2AR-D2R heteromers in sheep striatal tissue. Patch clamp in rat striatal D2R agonist-responsive neurons and locomotor activity recording in rats were used to establish functional correlates of the allosteric effects of A2AR ligands demonstrated in vitro and in situ. Results: Not only CGS 21680, but also caffeine and selective A2AR antagonists decreased the affinity and intrinsic efficacy of D2R agonist and the affinity of D2R antagonist. These allosteric modulations disappeared upon A2AR agonist and antagonist co-administration. This could be explained by a model that considers A2AR-D2R heteromers as heterotetramers, with A2AR and D2R homodimers, which was supported by experiments with BRET with double BiSC. TM peptides corresponding to the amino acid sequences of TM5, but not TM7, of both A2AR and D2R, disrupted A2AR-D2R heteromerization in transfected cells (BiSC) and in sheep striatal tissue (PLA). Importantly, the same disruptive peptides disrupted the ability of caffeine to modulate [3H]raclopride binding in sheep striatal tissue. As predicted by the model, high concentrations of A2AR antagonists behaved as A2AR agonists and decreased D2R function in the brain (patch-clamp and locomotor activity experiments). Conclusions: The heterotetrameric model assumes that occupancy of the A2AR homodimer with either an agonist or an antagonist, but not with both, conduces the same allosteric modulation to the D2R homodimer. The model explains the effects of caffeine on locomotor activity under doses typically consumed and the PET imaging results with [11C]raclopride. Disclosures: Nothing to Disclose.
Top of page 31.3 Adenosine Regulation of Dopamine Release and Behavior in Adolescent Rats Cynthia Kuhn Duke University Medical Center, Durham, North Carolina, United States Background: Caffeine is the most widely consumed psychoactive drug in the world. Caffeine consumption by children and adolescents is significant: 75% of children and adolescents consume caffeine daily, in various forms including soda, energy drinks, tea and coffee-based beverages. While caffeine itself exerts modest reinforcing/rewarding effect, like nicotine it enhances the effects of other reinforcers, including the sugar present in the caffeine-containing beverages that young people consume. The purpose of this study was to test the hypothesis that caffeine has exaggerated effects in adolescents, perhaps due to presynaptic effects on DA release that decline with age. Methods: Male Sprague Dawley rats (postnatal day 28, 42 or 65) from Charles River laboratories (Raleigh NC) were used in all experiments. In the first experiment, all rats received caffeine, 25 mg/kg ip, and locomotor activity was assessed in an automated device. In the next set of experiments, PN 28 or PN 65 animals were habituated to the locomotor box for 60 minutes, then lights were turned off suddenly, and locomotor activation assessed for 15 minutes. Some animals were pretreated 30 minutes before lights off with saline, quinpirole (0.1 mg/kg ip) or the adenosine A1 agonist N6-cyclopentyladenosine (CPA, 0.3 mg/kg) to test the ability of presynaptic inhibition of DA release to suppress locomotion. Finally, PN 28 or PN 65 animals were anesthetized with urethane, and phasic dopamine release events monitored by fast-scan cyclic voltammetry at carbon fiber electrodes after saline, caffeine (25 mg/kg), caffeine followed by cocaine (15 mg/kg), the D2 antagonist raclopride (2 mg/kg) or raclopride + cocaine. Frequency, amplitude, and duration of phasic release events were quantitated. Statistics on all results were analyzed by 3 way ANOVA (age x time x treatment) using NCSS. All experiments were approved by the Duke University IACUC. Results: Caffeine elicited an age-related increase in spontaneous locomotion, with greater locomotion observed in adolescent than adult animals. Sudden darkness triggered a surge of locomotion that was suppressed slightly by a presynaptically-active dose of quinpirole and substantially by CPA in adults. Comparison of quinpirole and CPA effects on adolescents and adults showed that CPA was more effective than quinpirole in adults, but the opposite was the case in adolescents: quinpirole was more effective than CPA. In adults, raclopride enhanced spontaneous DA release events and exaggerated the changes after cocaine, while caffeine did not affect DA release. In contrast, caffeine but not raclopride enhanced baseline and cocaine-induced DA release events in adolescents. Conclusions: These data show that the adenosine antagonist caffeine exerts age-specific effects on dopaminergically-mediated behaviors and on dopamine release in rats. These findings as consistent with the interpretation that adenosine acting via presynaptic heteroreceptors tonically inhibits DA release and suppresses behavior in adolescents more than in adults, while presynaptic D2 autoreceptors assume greater control over DA release as animals become adult. These developmental differences in adenosine regulation of DA function suggest that caffeine might act at multiple sites to enhance the effects of reinforcers like dietary sugar more in children and adolescents than adults. Disclosures: Nothing to Disclose.
Top of page 31.4 Motivational Effects of Caffeine in Adult and Adolescent Rats Matthew Palmatier East Tennessee State University, Johnson City, Tennessee, United States Background: Caffeine is the most widely used psychoactive drug in the world. Caffeine is commonly self-administered in salient vehicles such as coffee and energy drinks and initiation of caffeine use usually occurs during adolescence. Despite the widespread human consumption of caffeinated beverages, no previously published research has demonstrated reliable and repeatable caffeine self-administration in non-human subjects. We have shown previously that caffeine, like nicotine, increases the reinforcing effects of non-drug gustatory stimuli (e.g., sucrose). We hypothesized that robust, reliable, and repeatable increases in operant behavior would be observed in adolescent and adult rats if caffeine were self-administered in conjunction with a reinforcing non-drug stimulus (e.g., saccharin). Methods: Adult and adolescent rats were used for these experiments. Adult rats began experiments between post-natal days 60 and 90 (P60-90). Adolescent rats began experiments on P32. In Experiment 1, adult and adolescent rats were initially shaped to press a nose-response key for an oral sucrose reward (20% w/v, 0.1 ml/reinforcer) under a progressive ratio (PR) reinforcement schedule. After shaping, all rats were pretreated with caffeine (12 mg/kg) 15 min before testing sessions. In Experiment 2 adult rats were shaped to press a lever for oral saccharin (0.2% w/v) under the PR schedule. Following shaping, all rats were instrumented for intravenous (IV) self-administration and randomly assigned to one of three groups (SACC, CAFF, or CAFF+SACC). IV caffeine infusions and oral saccharin were earned by the CAFF+SACC group in subsequent sessions. There was no change in the operant contingency for the SACC group. IV caffeine infusions (0.5 mg/kg/infusion) replaced saccharin as the reinforcer in the CAFF group. In Experiment 3, adult rats were allowed to respond under the PR schedule for a complex vehicle containing decaffeinated coffee (0.5% w/v) and saccharin (0.2% w/v), oral caffeine (0.5-5 mg/ml; 0.1 ml/reinforcer) was added in a subset of these rats. Results: In Experiment 1 caffeine significantly increased responding in both adult and adolescent rats (main effect of Drug, p<0.05). Caffeine maximally increased responding in adult rats on the first day of treatment, but responding in adolescent rats increased more gradually (Drug x Age interaction, p<0.05). In Experiment 2, the CAFF+SACC groups responded significantly more than both control groups across 5 days of testing (p<0.05), confirming that caffeine self-administration is reliable and repeatable when it is administered in conjunction with a gustatory reinforcer. In Experiment 3 caffeine dose-dependently increased the motivation to obtain the coffee/saccharin vehicle (p<0.05), with peak concentrations between 1.5 and 2.5 mg/ml. Conclusions: Caffeine potently enhances the motivation to obtain gustatory non-drug stimuli and this effect may involve different neurobiological processes (e.g., sensitization) when initial exposure to caffeine occurs in adolescence. Inclusion of non-drug stimuli increases the reliability of self-administration in non-human subjects and suggests that the ‘reinforcing’ effects of caffeine in humans may be difficult to separate from the salient vehicles in which the drug is consumed. Disclosures: Nothing to Disclose.
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32. Mining a Genomic Hotspot for Psychosis: Mechanistic Insights from 22q11.2 Microdeletions
Top of page 32.1 From Genes to Cognition in a Mouse Model of the 22q11.2 Microdeletion Joshua Gordon Columbia University, New York, New York, United States Background: The 22q11.2 microdeletion results in a syndrome of partially-penetrant phenotypes including psychosis and cognitive deficits. To explore the neurobiological mechanisms underlying cognitive deficits, we study Df(16)A+/- mice, which carry a deletion of the syntenic region in the mouse genome. We have previously shown that these mice have deficits in hippocampal-prefrontal synchrony that correlate with deficits in spatial working memory. Here we set out to determine the cellular and circuit bases of these deficits using a combination of molecular and circuit-based approaches. Methods: We have used a combination of multi-site awake, behaving neural recordings, single gene knockout mice, optogenetic terminal inhibition, and pharmacological and viral rescue to examine the neurobiological consequences of the microdeletion that may underlie spatial working memory deficits. We recorded both local field potential and multiple single unit activity from the hippocampus (HPC) and prefrontal cortex (PFC) of Df(16)+/- mice, as well as mice hemizygous for Dgcr8 and Zdhhc8, two genes within the microdeletion region in both humans and mice. We used viral overexpression and pharmacological manipulations to attempt to rescue these phenotypes, and optogenetic inhibition of HPC terminals in the PFC to mimic the phenotype. Results: We demonstrate that hemizygous deletion of Dgcr8 or Zdhhc8, as well optogenetic inhibition of HPC terminals in the PFC, impair HPC-PFC synchrony and disrupt working memory performance. Moreover, pharmacological rescue of a downstream consequence of Zdhhc8 deficiency, and viral genetic rescue of Dgcr8, reverse the physiological and behavioral phenotypes in the single gene models. Conclusions: These results, coupled with earlier findings demonstrating axonal and synaptic deficits in Df(16)A+/-, Dgcr8 and Zdhhc8 mice, permit us to construct a model by which deficiency of these two genes results in altered anatomical and functional connectivity within the HPC-PFC circuit, resulting in impaired spatial working memory performance. This model incorporates effects of these genes at the level of cellular, circuit and system function that explains the behavioral phenotype seen in mice. Furthermore, we demonstrate successful rescue of the behavioral phenotype by intervening in this pathway, suggesting the possibility that this understanding may lead to novel treatments. Disclosures: Nothing to Disclose.
Top of page 32.2 Thalamic MicroRNA Controls Antipsychotic Sensitivity of Thalamocortical Projections in the Auditory Cortex of Mouse Models of 22q11 Deletion Syndrome Stanislav Zakharenko St. Jude Children's Research Hospital, Memphis, Tennessee, United States Background: Auditory hallucinations and other positive symptoms of schizophrenia (SCZ) typically appear during adolescence or early adulthood, and in most patients, these symptoms are alleviated by antipsychotics that inhibit dopamine receptors D2 (DRD2s). The mechanisms of SCZ symptom onset and the underlying neuronal circuits, however, remain unknown. A leading risk factor for the development of SCZ is 22q11 deletion syndrome (22q11DS), which is caused by hemizygous deletion of multiple genes in the q arm of chromosome 22. In mouse models of 22q11DS, thalamocortical (TC) projections to the auditory cortex (ACx) have emerged as candidates for mediating positive symptoms because they have disrupted synaptic transmission and aberrant sensitivity to antipsychotics. Deletion of a microRNA (miRNA)-processing gene Dgcr8, leads to increased expression of Drd2 in the auditory thalamus, abnormal sensitivity of TC projections to antipsychotics, reduced TC transmission, and deficits in acoustic-startle response, which is characteristic of patients with SCZ. The miRNA(s) that mediates this mechanism in the auditory thalamus is unknown. Methods: To identify the culprit miRNA, we performed miRNA microarray analysis in the auditory thalamus and verified those results by using quantitative RT-PCR (qPCR). To test synaptic transmission at TC projections, we used single-cell electrophysiological recordings in TC slices containing portions of the auditory thalamus and ACx. To visualize activity of neurons in the auditory cortex, we used in vivo 2-photon calcium imaging. To overexpress miRNAs, we used adeno-associated viruses (AAVs) encoding miRNAs, and to knock them down, we used miRNA sponges. We also generated mutant mice lacking the miRNAs of interest. To test behavioral changes, we measured acoustic-startle response and prepulse inhibition (PPI) of startle response in mice. Results: We identified 5 miRNAs that target Drd2 in the thalamus and are depleted 22q11DS mice and Dgcr8+/– mice. Of the 5 miRNAs, only miR-338 is enriched in the thalamus. Overexpression of only this miRNA rescued TC disruption and abnormal sensitivity to antipsychotics in 22q11DS mice. Knocking down or deleting miR-338 was sufficient to elevate Drd2 levels in the thalamus and render TC connections sensitive to antipsychotics in wild-type mice. Similar to Dgcr8+/– mice and the mouse models of 22q11DS, miR-338+/– mice were deficient in the acoustic startle response and PPI and have abnormal neuronal activity in the auditory cortex. Conclusions: These data suggest that depletion of miR-338 is a crucial mediator of the Dgcr8–miRNA–Drd2 pathogenic disruption of TC pathways in the ACx and thus mediates the positive symptoms of 22q11DS-associated SCZ. Disclosures: Nothing to Disclose.
Top of page 32.3 Cortico-Thalamic Circuits and Psychosis Risk in 22q11.2 Deletion Carriers Carrie Bearden University of California at Los Angeles, Los Angeles, California, United States Background: Copy number variants (CNVs) that are highly penetrant for developmental neuropsychiatric disorders -like the 22q11.2 deletion - offer incredible translational potential, as the same genetic defect observed in human patients can be modeled in animals and in culture. Here we present novel data from a prospective study of a large cohort of youth with 22q11.2 deletions (22q11DS), in which we investigated a candidate neural system implicated in schizophrenia (i.e., functional connectivity within thalamo-cortical circuits) in relation to gene expression profiles and the development of psychotic symptoms over time. Methods: We acquired structured clinical interviews, high-resolution T1-weighted structural magnetic resonance imaging (MRI) scans and resting-state functional MRI scans in 65 youth with 22q11.2 deletions and 60 demographically matched typically developing controls. A seed-based approach was used to assess resting thalamo-cortical connectivity. We conducted whole-genome transcriptional profiling and used systems biology methods (Weighted Gene Coexpression Network Analysis; WGCNA) to identify networks of co-expressed genes associated with these neuroanatomic traits at baseline. To test for significance of over-representation of brain-expressed genes within identified modules, we conducted hypergeometric probability tests. Gene ontology (GO) annotation was performed using DAVID (http://david.abcc.ncifcrf.gov). A subset of the sample was followed longitudinally for one year. Results: Resting state functional connectivity (FC) analyses revealed that 22q11DS patients showed thalamic hyper-connectivity with auditory cortex, but under-connectivity with striatal and cerebellar regions, consistent with patterns recently observed in idiopathic schizophrenia and in clinical high risk youth who subsequently developed overt psychosis. Findings also parallel those observed in a 22q11DS mouse model. Further, longitudinal data indicated that changes in thalamo-cortical connectivity over time predicted the development of prodromal psychotic symptoms in 22q11DS patients. We identified a particular gene module (Orange module) in which up-regulation of gene expression was associated with increased psychotic symptom severity (p=.009), increased thalamo-cortical dysconnectivity (p=.01), as well as reduced surface area in the left temporal pole (p=.04) in 22q11DS. GO analyses revealed that genes in the Orange module were primarily related to immunological processes. Hypergeometric tests revealed: 1) significant enrichment of brain-expressed genes in this module, and 2) significant overlap with genes implicated in idiopathic psychosis. This module was not associated with age, gender, antipsychotic use, scanner location, or batch. Conclusions: Disruption of thalamo-cortical circuits is a neural phenotype characteristic of idiopathic psychosis which also predicts symptom development in 22q11DS. Further, dysregulation of peripheral gene expression in 22q11DS is significantly related to thalamo-cortical connectivity, temporal lobe structure, and to psychotic symptomatology. While 22q11DS may account for only a small proportion of risk for psychosis overall, dysregulated genes within this locus may converge on biological pathways and neural systems relevant to broader psychosis susceptibility. Disclosures: Nothing to Disclose.
Top of page 32.4 Using Patient-Derived Neurons to Gain Novel Insights into the Neuronal Basis of 22q11 Deletion Syndrome Sergiu Pasca Stanford University, Palo Alto, California, United States Background: Development of disease-modifying drugs for psychiatric disorders such as autism and schizophrenia has been difficult despite sustained efforts over the last few decades. This is partly due to the complex pathophysiology and clinical heterogeneity of these disorders, as well as restricted access to neuronal cells from patients. The advent of induced pluripotent stem cells (iPSCs) provides an opportunity to generate and directly study neurons from patients with psychiatric disease. The highly penetrant 22q11.2 deletion syndrome provides a unique opportunity to mitigate the challenges raised by the high degree of genetic heterogeneity underlying complex neuropsychiatric disorders and to enable the study of cellular neuronal phenotypes in these patients. Methods: We generated induced pluripotent stem cells (iPSC) from a cohort of subjects carrying a 3 megabase 22q11.2 deletion and from unaffected healthy subjects, and differentiated these cells in vitro into cortical neural progenitors cells (NPCs) and cortical excitatory neurons. Results: Using transcriptional profiling at multiple in vitro developmental stages, as well as live imaging and electrophysiological methods, we identified a series of robust cellular phenotypes in patient-derived neurons when compared to neurons derived from healthy controls. Conclusions: These results provide novel insights into the underlying cellular defects that lead to psychiatric diseases in 22q11DS and open new therapeutic possibilities. Disclosures: Nothing to Disclose.
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33. Prenatal Maternal Environment, Immune Mechanisms, and Neurodevelopment Relevant to Psychiatric Disorders and Preventive Mechanisms
Top of page 33.1 Maternal High Fat Diet Alters Long-Term Metabolic, Monoamine, Neuroimmune, and Behavioral Outcomes in Mouse Offspring: A Role for Placental Inflammation? Staci Bilbo Duke University, Durham, North Carolina, United States Background: Maternal obesity during pregnancy and lactation can “program” offspring long-term for increased obesity themselves, along with increased vulnerability to neuropsychiatric disorders. Emerging evidence suggests that this programming by maternal diet is propagated via inflammatory mechanisms, which impact both placental and fetal brain development. Methods: To explore the mechanisms by which inflammatory responses within the placenta impact fetal brain development and thus long-term behavioral and biochemical outcomes in offspring, we placed female mice on either a low-fat diet (LFD) or high-fat diet (HFD) for 6 weeks prior to breeding, and throughout gestation and lactation. Placenta, fetal brain, and newborn brain were assessed for monoamine and neuroimmune endpoints, along with adult offspring immune, metabolic, brain, and behavioral outcomes. Results: PCR array analysis of 84 immune genes in mid-gestation placentas revealed that HFD altered the expression of multiple inflammatory genes in a sex-specific manner, and HPLC revealed disrupted placental serotonin synthesis in males—a critical function for embryonic brain development. One week after birth, qPCR analysis of offspring brains revealed that HFD altered expression of both serotonergic and immune genes, as in the placenta. Despite placement on a LFD at weaning, adult male and female offspring of HFD dams had decreased insulin sensitivity and visceral fat, respectively, along with changes in leptin receptor expression within the hypothalamus and hippocampus. Adult male and female HFD offspring also exhibited increased microglial activation within the hippocampus, whereas only HFD males showed increased inflammatory IL-1β responses in serum and brain, along with evidence of inflammatory monocyte infiltration into the hypothalamus, assessed using flow cytometry. Finally, male and female HFD offspring exhibited increased anxiety-like and depressive-like behavior in adulthood, in conjunction with increased serotonin turnover in prefrontal cortex. Moreover, the male, but not female, offspring of this group were hyperactive and had altered dopaminergic metabolism, suggesting that the long-term effects of maternal nutrition are also sex-specific. Conclusions: Perinatal diet can profoundly modulate placental and fetal monoamine and immune responses, as well as program brain development and behavior of offspring in a sex-specific manner. Disclosures: Nothing to Disclose.
Top of page 33.2 Interaction Between Serotonin Transporter Genotype and Prenatal Stress on Neurodevelopment with Implications for Autism Spectrum Disorder David Beversdorf University of Missouri, Columbia, Missouri, United States Background: Stress exposure during gestation is implicated in several neuropsychiatric conditions, including autism spectrum disorder (ASD). Previous research showed that prenatal stress increases risk for ASD with peak exposure during the end of the second and the beginning of the third trimester. However, exposures to prenatal stress do not always result in ASD, suggesting that other factors may interact with environmental stressors and increase ASD risk. Also, previous research in a mouse model revealed that a maternal heterozygous knockout of the serotonin transporter gene, known to affect stress reactivity, combined with maternal chronic variable stress late in pregnancy, resulted in altered social behavior in the offspring. This gene is well known to impact stress reactivity in clinical populations. The present study examined a maternal genetic variation in the promoter region of the serotonin transporter gene (5-HTTLPR) affecting stress tolerance and its interaction with the effect of environmental stressors on risk for ASD. Furthermore, as GABAergic changes are frequently observed in ASD, we wished to examine the effects of prenatal stress combined with this genetic variation on GABAergic migration in the rodent model. Finally, stress and the serotonergic system have significant effects on immunity, which will be of particular interest in this setting, as a range of atypical immune markers are observed in ASD patients and in mothers of patients with ASD. Methods: Two independent cohorts of mothers of ASD children recruited by the University of Missouri and Queen’s University were surveyed regarding the prenatal environment and genotyping on 5-HTTLPR was performed to explore this relationship. For the rodent model, a 2x2 design was implemented (Heterozygous serotonin transporter KO vs. wild type dams, exposed to restraint stress vs no stress during late pregnancy), and brains of the offspring were collected at E13.5, E15.5, and E18.5, and immunofluorescent calbindin labeling was performed. Results: In both clinical samples, mothers of children with ASD carrying the stress susceptible short allele variant of 5-HTTLPR experienced a greater number of stressors and greater stress severity when compared to mothers carrying the long allele variant. The temporal peak of stressors during gestation in these mothers was consistent with previous findings. Additionally, increased exposure to prenatal stress was not reported in the pregnancies of typically developing siblings from the same mothers, regardless of maternal genotype, suggesting against the possibility that the short allele might increase the recall of stress during pregnancy. In the mouse study, at each time point tested, the offspring of the heterozygous, maternally stressed mice had significantly delayed GABAergic migration as compared to all other groups. Ongoing work is examining immune mediators of these effects. Conclusions: The present study provides further evidence of a specific maternal polymorphism that may affect the risk for ASD with exposure to prenatal stress, and animal model studies suggest that it may occur by affecting GABAergic migration. Current work will explore potential epigenetic and immune factors that may mediate this effect. Disclosures: Nothing to Disclose.
Top of page 33.3 Inflammatory Mediators of Prenatal Stress Effects on Neurodevelopment Hanna Stevens University of Iowa Carver College of Medicine, Iowa City, Iowa, United States Background: Prenatal stress (PS) is a risk factor for altered cognitive and emotional development in children and adolescence. In animal models, prenatal stress persistently changes behavior and the brain. The mechanisms by which stress during embryonic development can induce long-term effects may shed light on preventive strategies for childhood psychiatric disease. Our lab has shown that prenatal restraint stress influences the development of GABAergic cells in offspring, with unclear maternal factors influencing the embryonic brain. Multiple different mediators in maternal stress physiology have been implicated in prenatal stress. Here, we investigated which mechanisms involved in prenatal stress influence the brain development and behavioral outcomes seen in offspring. Methods: We examined embryonic brain following prenatal restraint stress and repetitive maternal prenatal exposure to corticosterone, interleukin-6 (IL-6), and interleukin-1beta (IL-1beta). We assessed cellular and molecular markers of GABAergic cell embryonic development. To test involvement of inflammatory mechanisms, Iba1+, embyronic microglia morphology was assessed. Blockade of the pro-inflammatory mediator, IL-6, was tested with repetitive maternal exposure to neutralizing IL-6antibody and examination of offspring brain development and adult anxiety-like behavior. Results: The distribution of inhibitory neuron progenitors was initially restricted after one day of exposure by prenatal stress, corticosterone and both cytokines; however, this effect persisted after 2 days only in prenatally-stressed and IL-6-exposed offspring. Corticosterone-exposed embryos showed other distinct differences from prenatal stress in the development of GABAergic progenitors: GABAergic progenitor proliferation was reduced early, and expression of transcription factors involved in inhibitory neuron migration (dlx2, nkx2.1) was increased not decreased. Cytokine-exposed embryos showed some similar effects on GABAergic progenitor gene expression as found with prenatal stress. Inflammatory mediation of the effects of prenatal stress was further tested by evaluation of Iba1+ microglia in the embryonic cortical plate. Prenatal stress exposure resulted in a higher density of Iba1+ cells that appeared to be actively phagocytosing apoptotic cells. This was also found in IL-6 exposed embryonic brain. Blockade of IL-6 signaling by anti-IL-6 antibody injection during prenatal stress normalized the morphology of Iba1+ cells in embryonic cortical plate. However, migration deficits of GABAergic progenitors with prenatal stress were not normalized. Similarly, behavioral changes in adult animals after prenatal stress were not rescued by anti-IL-6 antibody. Conclusions: In sum, exposure to glucocorticoids did not replicate the effect of prenatal stress on GABAergic cells, but cytokine exposure showed very similar trajectories in the development of these precursors and of microglia. Blockade of IL-6 in the maternal stress response did not rescue effects of prenatal stress on GABAergic progenitor development or behavior. This work demonstrates that inflammatory systems, including microglia and cytokines, which have an increasingly recognized role in brain development, are among the mechanisms by which prenatal stress may influence childhood functioning. Disclosures: Part 1: Research Fellowship from APIRE/Wyeth (2010-2015), Part 4: Research Fellowship from APIRE/Wyeth (2010-2015).
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34. Harnessing Sex-Differences as Biological Clues in Neurodevelopmental Psychiatry
Top of page 34.1 The Female Protective Effect in Autism Spectrum Disorder Stephan Sanders University of California San Fransico, San Francisco, California, United States Background: The 4:1 male to female sex bias is one of the most consistent and striking observations in autism spectrum disorder (ASD). One explanation for this sex bias is the existence of a female protective effect (FPE), in which a greater burden of ASD risk factors are required for a diagnosis of ASD in females than in males. Direct observation of de novo ASD risk factors in genomic analysis supports this hypothesis, however indirect assessment of sibling ASD recurrence risk in epidemiological studies finds little supporting evidence for the FPE. Should the FPE exist, understanding the nature and mechanism of this protection may hold great potential for therapeutic strategies. Methods: To explain the discordant genomic and epidemiological evidence for the FPE we developed a simulation of ASD risk in families to estimate the power to detect a difference in the burden of de novo mutations vs. sibling recurrence risk. Should the FPE exist, it must act through sexually dimorphic processes, including gene expression. We therefore compared gene expression data from male and female brain samples in the BrainSpan dataset ranging from mid-fetal to adult developmental stages. Results: Under a quantitative model of ASD risk, in which 50% of ASD risk in the population comes from unique environmental exposure, 47% comes from common inherited genetic variants and 3% comes from rare de novo mutations (Gaugler et al., Nature Genetics 2014), we estimated the power to detect the FPE. Considering de novo mutations we achieve 80% power at about 500 ASD families, consistent with genomic literature. Furthermore, by combining the exome and CNV data for over 5,500 ASD cases we show that the increased burden of ASD risk factors is observed consistently to a similar extent as predicted by the simulation. In contrast, the power to detect a significant difference in sibling recurrence rate in 10,000 ASD remains below 30%. The FPE hypothesis is therefore consistent with the epidemiologic literature too. To explore the nature of the FPE, we assessed the differential gene expression using RNA-Seq from over 1,200 region and time specific samples from males and females. We find similar developmental trajectories of gene expression in both sexes, with the exception of genes specific to microglia that appear earlier in males. Overall we find about 200 coding and non-coding transcripts with robust sexually dimorphic gene expression (FDR 0.01) and a further 1,000 sexually dimorphic genes with weaker evidence (FDR 0.1). Of note, these transcripts are not enriched for known ASD risk genes, suggesting that the protective effect occurs downstream of specific genetic risk factors. Conclusions: The FPE is the leading hypothesis of the underlying mechanism of ASD sex bias, with strong supporting evidence from genomic studies. The existing large-scale epidemiological analyses remain under-powered to corroborate this finding. There is little evidence for differing rates of neurodevelopment between the sexes at the level of gene expression, with the possible exception of microglia. Finally, the ASD risk genes discovered to date do not appear to be sexually dimorphic in their expression in the human brain. Disclosures: Nothing to Disclose.
Top of page 34.2 Sex Differences in the Infant Brain: Mechanistic Considerations and Relevance to Neurodevelopmental Disorders Rebecca Knickmeyer University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States Background: Many early-onset neurodevelopmental disorders (NDDs) show a striking male-bias, including autism spectrum disorders (ASD), attention-deficit hyperactivity disorder (ADHD), early onset persistent antisocial behavior, and early-onset schizophrenia. These patterns are likely related to sex differences in typical brain development, and ASD in particular has been described by some researchers as an ‘extreme male brain’. However, there is currently a major gap in research relevant to this hypothesis: data on sex differences in brain development during infancy and toddlerhood, the period of time most relevant to NDDs, are extremely limited. In addition, the mechanisms underlying sex differences in human brain development remain poorly understood, though gonadal steroid and sex chromosome effects are strong candidates for a causal role. Methods: My research group addresses this critical research gap by integrating pediatric neuroimaging with genomics and analytical chemistry. We are characterizing sex differences in brain development in an extraordinary cohort of over 800 typically developing neonates. We test whether variation in salivary testosterone, anthropometric proxies of prenatal testosterone, and genes involved in sex steroid synthesis, transport, signaling, and metabolism, predict individual variation in sexually dimorphic outcomes. In addition, we study whether brain development is altered in infants with Turner syndrome (TS), a well-defined genetic disorder resulting from the partial or complete loss of one of the sex chromosomes. Results: Although global brain volumes are larger in male neonates, females have relatively larger gray matter volumes around the temporal-parietal junction, a key region in the sense of agency, reorienting attention to salient stimuli, and higher level social processes. This may explain why female infants show better social interactive capacities than male infants and are less likely to be diagnosed with ASD. Studies of infants with TS suggest some of these effects are mediated by the sex chromosomes. In contrast, androgen exposure and sensitivity do not appear to be primary determinants of sexual dimorphism at this age. Sex and X-chromosome loss exert minimal effects on diffusion tensor imaging parameters. Conclusions: Sex effects on brain development show tremendous spatio-temporal complexity. It is likely that sexual dimorphism of the brain reflects the dynamic interplay of multiple mechanisms both biological (prenatal hormone production, neonatal hormone production, pubertal hormone production, direct sex chromosome effects) and experiential (e.g. parental expectations and interactive behavior, exposure to physical hazards, culturally influenced lifestyle differences). Ultimately, a better understanding of the pathways leading to sexually dimorphic brain development and the emergence of psychiatric illness will improve diagnosis and open up possibilities for sex tailored interventions and therapeutics aimed at normalizing adverse developmental trajectories. Disclosures: Part 1: I am co-investigator on a grant supported by Pfizer, Part 4: I am co-investigator on a grant supported by Pfizer. I do not receive any salary support.
Top of page 34.3 Studying the where and how of Sexually Dimorphic Brain Development Through Cross-Species Neuroimaging and Genomics Armin Raznahan National Institute of Mental Health, Bethesda, Maryland, United States Background: Epidemiological studies clearly establish that male sex robustly increases risk for several common early onset neurodevelopmental disorders (NDDs) including Autism Spectrum Disorder (ASD), and Attention Deficit Hyperactivity Disorder (ADHD). Studying the basis for this sex-bias could potentially advance the prevention, early detection and treatment of multiple disorders. Consequently, our laboratory uses several complementary research approaches to (i) localize brain systems that show sexually dimorphic brain development in health, (ii) test the hypothesis that sex differences in X- and Y-chromosome dosage contribute to sexually-dimorphic brain development and risk for NDD. Methods: We map normative sex-differences in brain development at high spatio-temporal resolution using a large, longitudinal structural neuroimaging study of human brain development which spans ages 3-35 years, and includes ~1200 MRI scans from 700 individuals. We assess sex-chromosome dosage effects on brain anatomy and NDD-related phenotypes through a translational research program that integrates neuroimaging and transcriptomic methodologies in humans and mice with a range of sex chromosome complements (e.g XX, XY, XXX, XXY, XYY karyotypes). Results: Global brain volumes are larger in males than females throughout typical development, but this well-replicated observation is underpinned by highly localized neuroanatomical sex-differences that shift their spatial distribution over development. Several such “hotspots” of sexually dimorphic brain development in health also show structural and functional abnormalities in independent clinical samples of youth with sex-biased NDDs. Our analyses of sex chromosome aneuploidy suggest they male-female differences in sex-liked gene dosage may shape normative sex differences in overall brain size. However, X- and Y-chromosome dosage changes exert convergent effects on local brain anatomy in humans, which preferentially strike regions linked to normative and NDD-related differences in social behavior. We also identify sex-chromosome dosage effects on anatomy of social brain systems in mice, which often encompass foci of normative sexual dimorphism. To identify candidate genomic mediators of these sex and sex-chromosome dosage effects on brain development we (i) clarify transcriptomic consequences of varying X and Y chromosome dosage in humans, and (ii) specify the gene-expression signatures that distinguish murine brain regions with contrasting anatomical sensitivity to gonadal profile and sex chromosome dosage. Conclusions: By specifying spatiotemporal patterns of brain development that differ between males and females in health, our findings prioritize candidate brain systems that might mediate sex-differences in the incidence and/or resilience to NDD risk factors. Our complementary imaging and genomic studies of sex chromosome dosage effects help to (i) mechanistically dissect biological contributions to sexually dimorphic brain development and NDD risk, and (ii) identify molecular pathways that might mediate these contributions. Disclosures: Nothing to Disclose.
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36. Sex Hormones, the Medial Prefrontal Cortex and Their Role on Eating Disorder Behavior in Basic Science and Human Brain Imaging Studies
Top of page 36.1 An Individual Differences Animal Model of Binge Eating Reveals Sex Differences in Binge Eating-proneness and Enhanced Activation of the Neural Reward Circuit by Palatable Food in Binge Eating-Prone Rats Cheryl Sisk Michigan State University, East Lansing, Michigan, United States Background: Eating disorders emerge during puberty and disproportionately affect girls. Most theories of sex differences in eating disorders focus on sociocultural factors, however recent evidence indicates that biological factors contribute to sex differences as well. The most prevalent forms of eating disorders are characterized by binge eating. The neurobiological underpinnings of binge eating in either sex are poorly understood, but recent research points to dysregulation of food reward circuits as one component of binge eating. The purpose of this research is to examine between- and within-sex differences in binge eating using an established laboratory animal model of binge eating proneness. Methods: Male and female rats were given intermittent access (24 hr period, 3x/wk) to palatable food (PF; Betty Crocker Frosting) for 2-3 wk, with ad lib access to standard lab chow and water. PF consumption was measured 4 and 24 hr after introduction of PF on feeding test days; chow consumption and body weights were measured daily. Binge eating prone (BEP) and binge eating resistant (BER) rats were identified on the basis of the pattern of PF consumption across the feeding tests. Rats met criteria for BEP if they ate in the highest tertile of PF intake on at least half of the feeding tests, and never ate in the lowest tertile on any feeding test. Rats met criteria for BER if they ate in the lowest tertile of PF intake on at least half of the feeding tests, and never ate in the highest tertile on any feeding test. Study 1: a sample of 30 female and 30 male adult rats was studied to determine whether there are sex differences in the proportion of rats that meet criteria for BEP or BER. Study 2: BEP and BER rats were identified in a sample of 40 adult female rats. One week after completion of the feeding tests, rats were given a PF 90 min prior to being anesthetized and perfused. Brains were removed and processed for immunohistochemical identification of fos, a nuclear transcription factor used as an index of neuronal activation. The number of fos expressing cells was microscopically quantified in subregions of the prefrontal cortex (PFC) and nucleus accumbens (NA), two primary components of the mesocorticolimbic reward circuit. Results: Study 1: Overall, female rats consumed higher quantities of PF than male rats. Within the sample of female rats, 47% met criteria for BEP and 3% met criteria for BER. Within the sample of male rats, 3% met criteria for BEP and 37% met criteria for BER. Two-proportion z test revealed a significant sex difference in binge eating proneness. Study 2: BEP rats consumed more PF than BER rats on feeding test days, whereas 24 hr chow intake on feeding test days was higher in BER rats than in BEP rats. BEP and BER rats did not differ in body weight. BEP rats had higher PF-induced fos expression than BER rats within the NA core (pairwise comparison p<0.1; Hedge’s g=1.02, large effect size), NA shell (p<0.1; g=0.82, large effect size), prelimbic PFC (p<0.01; g=2.59, large effect size), infralimbic PFC (p<0.05; g=1.55, large effect size), and cingulate PFC (p<0.01; g=1.64, large effect size). Conclusions: Using an individual differences animal model to identify extreme binge eating phenotypes, a greater proportion of female rats are BEP compared to males, providing evidence for a sex difference in binge eating that is biologically, rather than socioculturally based. Furthermore, the BEP phenotype is associated with enhanced responsiveness to PF within the neural reward circuit, suggesting that heightened food reward may underlie binge eating proneness. Disclosures: Nothing to Disclose.
Top of page 36.2 Disruption of ESRRA-HDAC4 Activity in Prefrontal Cortex Induces Eating Disorder-Related Behaviors in Mice Michael Lutter University of Iowa, Iowa City, Iowa, United States Background: Eating disorders (EDs), such as anorexia nervosa and bulimia nervosa, are characterized by marked disturbances in eating patterns, social interactions, and behavioral compulsivity. While the neurobiological basis of EDs is incompletely understood, recent research has highlighted a potential role for frontostriatal circuits in the development of ED-related behaviors. We used a family-based approach to identify rare missense mutations in the estrogen-related receptor alpha (ESRRA) and histone deacetylase 4 (HDAC4) genes that are associated with the development of eating disorders. Here we use mice as a model system to dissect the functional role of ESRRA and HDAC4 activity in the medial prefrontal cortex (mPFC) in ED-related behavioral deficits. Methods: Knock-in mice were generated with the A778T mutation in the Hdac4 gene (corresponding to the human A786T mutation). Floxed-Esrra mice were obtained and used to conditionally deleted Esrra expression from mPFC neurons. Mice expressing Cre-recombinase under control of the Esrra promoter were generated to allow for optogenetic studies. Results: Loss of Esrra in the mPFC disrupts food intake in female mice. HDAC4A778T knock-in mice display hyperphagia in response to high-fat diet in female, but not male mice. Furthermore, AAV-mediated overexpression of HDAC4A778T, but not wild-type HDAC4 or control GFP, in mPFC recapitulates high-fat diet hyperphagia. Stimulation of mPFC-Esrra neurons by channel rhodopsin 2 induces consumption of high-fat diet in female, but not male mice. Conclusions: Our results demonstrate that the mPFC-Esrra neurons modulate intake of high-fat diet. Furthermore, genetic manipulation of the Esrra-Hdac4 pathway, which was originally identified in human patients with EDs, in the prefrontal cortex of mice causes a bi-directional modulation in the consumption of high-fat diet (both hypophagia and hyperphagia) and that these effects are primarily observed in female mice. These findings offer new insights in the cellular and molecular basis of ED-related behaviors. Disclosures: Nothing to Disclose.
Top of page 36.3 Medial Prefrontal Cortex is Integral to Altered Social and Self Perception in Anorexia Nervosa Carrie McAdams University of Texas Southwestern Medical Center, Dallas, Texas, United States Background: Anorexia nervosa (AN) is a complex psychiatric illness that includes a failure to maintain one’s body weight in concert with cognitive distortions related to body size and shape. Both psychological and neural differences in social and self-perception have previously been demonstrated in AN. Here, we evaluated the function of medial prefrontal cortex (MPFC) in both currently ill as well as patients with long-term weight recovery following AN, to assess its relevance in the pathogenesis of AN. Methods: Three groups of adult subjects, healthy comparison women (HC, n = 19), women currently with anorexia nervosa (AN-C, n = 22), and women in long-term weight recovery following anorexia nervosa (AN-WR, n = 18, 2 years with BMI > 19.0) performed a social self-appraisal task during 3t magnetic resonance imaging (MRI). The task involved considering social adjectives presented in three different conditions: Self (“I believe I am nice”), Friend (“I believe my friend is selfish”), and Reflected (“My friend believes I am polite”). Neural activations were analyzed using ANOVAs comparing whole-brain activations in contrasts of the three conditions with the statistical criterion set to thresholding at an initial voxel p unc < 0.005 and cluster p FWE corr < 0.05. Results: Differences in activation of the MPFC (232 vox, Z = 4.34, MNI -8, 48, 0) were found in the Self – Friend contrast, a comparison designed to isolate self-relevant neural processing. Both patient groups had elevated mPFC activity in contrast to the healthy subjects (mPFC beta values, HC -1.3, AN-C -0.3, AN-WR 1.23; p< 0.001). Furthermore, in the Reflected – Self contrast, a comparison designed to evaluate social cognitive neural processes, differences in activation of the bilateral inferior frontal gyri and anterior insula (RIFG, 79 voxels, Z = 4.29, MNI x=36, y=32, z=8; LIFG, 51 vox, Z = 3.54, MNI -44, -16, 8), caudate (41 vox, Z = 4.12, MNI x=-16, y=12, z=12), and cingulate (78 voxels, Z = 4.07, MNI x=4, y=32, z=32) were observed. Severity of the eating disorder (Eating Attitudes Test) amongst the patient groups correlated with less self-related activation of the MPFC (r = 0.64, p < 0.003) and R Insula (MNI x=36, y=28, z=16, r = 0.64, p<0.0001). Conclusions: All the regional differences identified were in frontostriatal circuits typically engaged during reward tasks, suggesting that biological differences related to motivation may underlie altered social and self-perception in AN. Importantly, the AN-WR group showed the largest differences in MPFC compared to the HC group, suggesting that differences in social and self-perception do not resolve even after long-term weight-recovery. In sum, AN may be associated with a biological predisposition to engage the MPFC for self-evaluation, connecting environmental pressures related to appearance with psychological symptoms related to impaired self-knowledge and social perceptions. Disclosures: Nothing to Disclose.
Top of page 36.4 Brain Structure and Function Implicate the Medial Prefrontal Cortex in Anorexia Nervosa Pathophysiology Guido Frank University of Colorado Anschutz Medical Campus / Children's Hospital, Aurora, Colorado, United States Background: Anorexia nervosa (AN) is a severe psychiatric disorder with high mortality that typically starts in adolescence and is characterized by a complex interaction of biological, psychological and social factors. The predominantly female gender of affected individuals suggests that gonadal hormones play an important role. Here we present data from two studies that suggest that the medial prefrontal cortex may have an important role in AN and maybe in eating disorders in general. Methods: In study 1, we compared adolescents with AN (n=19, mean age 16±2 years) with age matched healthy controls (n=16, age M 15±3 years) on brain response during a dopamine associated reward-conditioning task that tests brain response to unexpected receipt or omission of monetary reward. Adolescents with AN performed the task twice, before weight gain and 5 weeks later after weight normalization. Controls performed the task also twice, 5 weeks apart. In study 2, we compared brain white matter connectivity (estimation of fiber connections) in healthy young adults (n=26, age M 23±5 years) with individuals with AN (n=26, age M 24±3 years) or bulimia nervosa (BN, n=26, age M 25±4 years). Diffusion weighed imaging was acquired for tractography of white matter connection between taste-reward circuitry relevant brain regions. In both studies AN subjects were at low gonadal hormone state as evidenced by lack of menstrual cycle. Comorbid conditions and medication use were controlled for in the analyses. Results: Study 1: Adolescents with AN showed greater brain response to unexpected win-omission compared to controls in bilateral ventral striatum and medial prefrontal cortex (p<0.05, FEW corrected). On follow up after weight restoration, right ventral striatal activation had normalized, while medial prefrontal cortex activation had not. Study 2: White matter tractography indicated reduced fiber path connectivity between the ventro-medial prefrontal cortex and the hypothalamus in both AN and BN compared to controls (p<0.01, Bonferroni corrected). Conclusions: The results of those studies indicate that the medial prefrontal cortex may have an important role in the pathophysiology of anorexia nervosa and maybe in eating disorders in general. Study 1 suggests that the heightened functional response in adolescent anorexia nervosa recovers less with weight restoration in the medial prefrontal cortex compared to the ventral striatum and could be a risk factor for early relapse. Study 2 indicates that lower white matter connectivity between medial prefrontal cortex and hypothalamus could be a common finding across eating disorders and interfere with normal feeding stimulation. The medial prefrontal cortex, which receives sensory input and is strongly connected to limbic areas, is important in decision-making, fear processing and social cue processing. Disruptions in this area due to trait alterations or hormonal effects such as low estrogen during starvation could lead to disturbances in eating regulation, social interaction and emotion regulation. Importantly, the medial prefrontal cortex contributes to reward valuation and the connection to the hypothalamus may be particularly important for taste-cue dependent feeding stimulation (Holland & Petrovich, 2005). Weak fiber connectivity in this pathway in eating disorder could interfere with normal taste conditioning and impair normal food intake. Disclosures: Nothing to Disclose.
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37. A Fresh Perspective on Neuregulin in Schizophrenia
Top of page 37.1 Schizophrenia-Relevant, Endophenotypes in Transgenic Mouse Models of NRG1 / ErbB4 Hyperstimulation Markus Schwab Max-Planck-Institute of Experimental Medicine, Goettingen, Germany Background: The neuregulin 1 (NRG1) gene encodes a family of growth and differentiation factors with an epidermal growth factor (EGF)-like signaling domain that serve as ligands for receptor tyrosine kinases of the ErbB family. ErbB4 is the most prominent neuronal NRG1 receptor in the brain. NRG1/ErbB4 signaling regulates multiple aspects of nervous system development and synaptic plasticity in the mature brain. Variants of the human NRG1 and ErbB4 genes are possible risk factors for schizophrenia. Increased NRG1 expression and ErbB4 hyperphosphorylation were found in postmortem brains of schizophrenia patients, suggesting a working hypothesis according to which chronic NRG1/ErbB4 hyperstimulation represents a pathomechanisms in schizophrenia. Methods: To test our working hypothesis, we examined transgenic mice with pan-neuronal’ NRG1 type III overexpression. In addition, to study NRG1/ErbB4 hyperstimulation in a more specific in vivo model, we have generated a ,conditional’ transgenic mouse line, which permits Cre recombinase-mediated NRG1 type III overexpression in the brain. These transgenic mice are currently being studied using biochemical, histological, and behavioral approaches. Results: To address our working hypothesis, we first validated that chronic NRG1 type III overexpression in the brain causes permanent ErbB4 hyperphosphorylation. NRG1/ErbB4 hyperstimulation in ,pan-neuronal’ transgenic mice was associated with synaptic dysfunctions, altered dendritic spine growth, ventricular enlargement, and deficits in sensorimotor gating. Cortex-restricted NRG1 type III overexpression was not associated with ventricular enlargement and sensorimotor gating deficits, but caused hyperactivity. Overexpressed NRG1 type III was present in synaptosomal fractions and pilot studies suggest a recruitment of the LIM kinase1/cofilin signaling pathway by hyperstimulated NRG1/ErbB4 signaling. Conclusions: NRG1 type III transgenic mouse lines model chronic ErbB4 hyperstimulation in the brain. The spectrum of ,endophenotypes’ in ,pan-neuronal’ transgenic mice suggests that human NRG1 risk haplotypes exert a gain-of-function effect. Findings in ,cortex-restricted’ transgenic mice indicate brain area-specific NRG1 functions, including a role of NRG1 type III signaling in subcortical networks. Recruitment of LIM kinase1/cofilin by hyperstimulated NRG1/ErbB4 signaling provides a potential mechanism for altered dendritic spine growth. These studies could provide novel targets for future treatment strategies of schizophrenia. Disclosures: Nothing to Disclose.
Top of page 37.2 Evaluating the Validity of a Novel Transgenic Mouse Model for Neuregulin 1 Type III for Schizophrenia Tim Karl Neuroscience Research Australia, Randwick, Australia Background: Neuregulin 1 (NRG1) is a well-characterized risk gene for schizophrenia (SZ). Elevations in NRG1 protein and transcripts have been found in SZ with a recent study showing that the transcript for the NRG1 type III isoform (NRG1-III) is overexpressed in the forebrain of SZ patients that carry a risk haplotype for NRG1. In light of this, a mouse overexpressing Nrg1-III specifically in the forebrain was created in order to assess how Nrg1-III overexpression might cause or contribute to SZ-related deficits thereby considering construct and face validity of this novel mouse model. Methods: Adult Nrg1-III transgenic and wild type-like control littermates of both sexes were characterized comprehensively for behaviours relevant to SZ including social and cognitive domains. Once behavioural testing was completed, brains were collected to analyse mRNA expression levels of Nrg1 type III as well as for three housekeeper genes in the prefrontal cortex (PFC) using qPCR. Results: Nrg1-III transgenic mice were healthy and showed normal sensory abilities and neurological reflexes. Nrg1-III overexpression resulted in impaired learning of a fear-eliciting context and reduced social interaction times with a novel mouse. Furthermore, transgenic mice were characterised by deficient prepulse inhibition, one of the hallmarks of SZ mouse models. Importantly, these mice also displayed an increase in normalized Nrg1-III mRNA expression in the PFC. Conclusions: These findings confirm that the Nrg1-III transgenic mouse has a robust overexpression of Nrg1-III mRNA in forebrain (similar to that found in the disease state of a subset of SZ patients) and that this overexpression causes behavioural deficits, which are highly relevant to SZ. These data will be discussed in relation to recently published findings on Nrg1-III knockout mice and compared to the phenotype of one of the best characterised genetic mouse models for Nrg1, the transmembrane domain Nrg1 mutant mouse. In conclusion, our results provide evidence that an overexpression of Nrg1-III may contribute to the symptomatology of SZ and that a newly developed mouse model for Nrg1-III overexpression possesses both face as well as construct validity for SZ research. Disclosures: Nothing to Disclose.
Top of page 37.3 Structural Brain Morphometry and NRG1 Gene Variants in First-episode Nonaffective Psychosis: Cross-sectional and Longitudinal Analyses Benedicto Crespo-Facorro University of Cantabria / HU Marques de Valdecilla, Santander, Spain Background: Structural brain abnormalities are already present at early phases of psychosis and might be the consequence of neurodevelopmental deviance. Nonetheless, brain anomalies progression is still under debate and no clear profile of progression can be identified. The study of certain genetic susceptibility factors with neurodevelopmental implications, such as neuregulin 1 (NRG1), can be key tools to understand brain morphology anomalies in schizophrenia. We examined in first-episode schizophrenia subjects whether variations in NRG1 polymorphisms influence brain volumes at illness onset or volume changes during a 3-year follow-up. Methods: Ninety-five minimally medicated patients experiencing their first episode of schizophrenia underwent genotyping of three SNPs within the NRG1 gene and structural brain magnetic resonance imaging. A comparison of volumes of lobar GM, lateral ventricles, and cortical CSF was made between the groups according to their genotype after controlling for total intracranial volume. In addition, 3-year follow-up magnetic resonance imaging (MRI) study on 59 minimally medicated patients who were experiencing FEP and 14 healthy control individuals underwent genotyping and structural brain MRI at baseline and at 1- and 3-year follow-up. A comparison of brain volumes, GM, WM, LV, cortical cerebrospinal fluid, and thalamus and caudate was made between the groups according to their genotype. Three NRG1 polymorphisms have been studied: SNP8NRG243177, SNP8NRG221533 and SNP8NRG221132. The possible interactive effects of NRG1 and DISC1 on brain volumes have also been investigated. Results: The cross-sectional study reveals that the SNP8NRG243177 risk T allele was significantly associated, in an allele copy number-dependent fashion, with increased lateral ventricle volume. Genotype explained 7% of the variance of lateral ventricle volume at illness onset. Strikingly, those patients with the “at risk” allelic combinations in NRG1 and DISC1 had LV volumes which were 48% greater than those with none of the allelic combinations. In the longitudinal study, patients with the SNP8NRG6221533 risk C allele showed increased LV volume across time. C allele carriers had significantly less WM compared with subjects homozygous for the T allele after the follow-up. No significant changes according to the genotypes were found in healthy individuals. Conclusions: Genetic variations of the NRG1 gene can contribute to the enlargement of the lateral ventricles described in early phases of schizophrenia and also can contribute to brain abnormalities described in early phases of schizophrenia and progressive changes during the initial years of the illness. Additive effect of NRG1 and DISC1 genes on lateral ventricle enlargement has been observed. Disclosures: Nothing to Disclose.
Top of page 37.4 Neurobiological Consequences of Neuregulin-1 Loci Associated with Psychosis Onset Chad Bousman University of Melbourne, Carlton South, Australia Background: Recent evidence suggests the schizophrenia associated Icelandic haplotype (HapICE) region may harbor single nucleotide polymorphisms (SNPs) that could assist in differentiating high-risk individuals who will or will not transition to psychosis. Two such SNPs (rs4281084 and rs12155594) were recently shown to independently predict psychosis transition in a large ultra-high risk cohort in Australia and for every additional rs4281084-A allele and/or rs12155594-T allele (allelic load range 0 – 4) the relative risk of psychosis onset increased 1.56 (95% CI = 1.20 – 2.04) (Bousman et al., Translational Psychiatry, 2013, 3, e251). However, the neurobiological consequences and mechanism by which these two newly associated polymorphisms might confer risk for transition to psychosis is not clear. The aim of this study was to utilize bioinformatic tools as well as human post-mortem brain and neuroimaging data from individuals with and without a psychotic disorder to elucidate what effect, if any, these SNPs have on NRG1 function, regulation, gene expression, and brain structure. Methods: To examine the neurobiological consequences of the candidate SNPs and their combined allelic load a three-pronged approach was employed. First, each SNP was analyzed in silico to predict effects on transcription and splicing factor expression and publicly available GWAS data was used to identify epistatic effects with SNPs within genes that interact with NRG1. Second, three independent human postmortem brain cohorts from Sydney, Australia (37 cases, 37 controls), Melbourne, Australia (50 cases, 18 controls), and the UK Brain Expression Consortium (134 controls) were used to determine the presence of putative cis-regulatory effects on NRG1 gene expression. Third, structural magnetic resonance imaging and diffusion tensor imaging data from 333 (156 controls, 177 cases) individuals were used to identify associations with human brain structure. Results: In silico analysis predicted variation at the rs4281084 locus would be associated with both transcription factor (glucocorticoid receptor) and splicing factor (SC35) expression. Epistasis analyses showed both rs4281084 and rs12155594 had multiple nominally significant interactions with SNPs in ERBB4, NRG1's main receptor. In healthy human postmortem brain, an increase in the number of rs4281084-A allele and rs12155594-T allele was associated with a decrease in pan-NRGI expression, particularly in the occipital cortex. Whereas, an increase in the combined allelic load of rs4281084 and rs12155594 was associated with an increase in right and left lateral ventricle volume as well as lower fractional anisotropy in a middle frontal cluster. Conclusions: These results represent the first attempt to functionally characterize the impact of two recently identified NRG1 loci associated with psychosis onset. They build on a growing body of research supporting the functional importance of genetic variation within the HapICE region of the NRG1 gene. In concordance with previous studies our findings suggest that the functional effects conveyed by sequence variation within NRG1 are likely not driven by one SNP but rather, a diverse accumulation of nucleotide changes particularly in upstream regions capable of regulating gene expression. Disclosures: Nothing to Disclose.
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38. Real-Life Proxies of Social Context in Affective Problems Across the Lifespan: Evidence from Human and Rodent Studies
Top of page 38.1 Reward and Social Circuitry: A Link Between Adolescents' Depression and Real-Life Social Experiences? Erika Forbes University of Pittsburgh, Pittsburgh, Pennsylvania, United States Background: Peer social reward becomes increasingly salient during adolescence, when reward circuitry continues to develop and reward-driven behavior increases. This vulnerable developmental point is also the time of emergence of depression, a form of psychopathology postulated to involve disrupted social functioning, reward response, and positive affect. Personally relevant reward stimuli might be particularly effective at eliciting individual differences in reward circuitry that are relevant both to depression and to affective experiences in social contexts. We investigated whether a personally relevant neuroimaging task--watching videos of a best friend from a recent conversation about a shared experience--would reveal mechanisms of adolescents’ depressive symptoms and their real-world social experiences. Furthermore, because depression involves altered circadian mood patterns, with particularly low positive affect early in the day, we tested whether regions sensitive to peer social reward and depression would also predict differences in mood and social behavior at different times of day. Methods: Community adolescents (N =36, age 14-18, 11 male, 73% European American) varying in depressive symptom severity completed functional magnetic resonance imaging (fMRI) in Siemens Tim TRIO 3T scanner using an ecologically valid social reward paradigm. The paradigm involved viewing video clips of the participant's same-sex best friend or an unfamiliar same-sex adolescent (stranger) expressing positive and neutral affect, with best-friend video clips selected from a lab interaction between the participant and best friend. At 20 time points across two 5-day periods, participants completed experience sampling of mood and behavior during daily life. Preprocessing of fMRI data and analyses were conducted in SPM8. Results: Participants with higher depressive symptoms exhibited less response to best-friend positive affect vs. stranger positive affect in a set of regions implicated in reward and social processing. Regions negatively associated with depressive symptoms included the precuneus, temporoparietal junction (TPJ), and ventromedial prefrontal cortex (PFC). Conjunction analyses indicated that a region of the vmPFC that responded to peer social reward was related to both higher depressive symptoms and lower emotional closeness to companions in real life. Additionally, conjunction analyses with morning vs. evening real-life data indicated circadian modulation of depression-brain-behavior associations in 2 regions: the dorsomedial PFC, which was related to lower levels of morning positive affect, and the TPJ, which was related to greater time with peers in the evening. Conclusions: Common associations of neural response to reward with depressive symptoms and social experience suggest a mechanism for disrupted social functioning in depression. Findings with time of day indicate possible circadian modulation of this mechanism. Disclosures: Nothing to Disclose.
Top of page 38.2 Long-Term Neurobiological Consequences of Physical Versus Emotional Stress During Adolescence in Male Mice Carlos Bolanos-Guzman Florida State University, Tallahassee, Florida, United States Background: Individuals with a history of childhood maltreatment commonly suffer from a variety of adult-onset psychiatric disorders, including major depressive disorder and post-traumatic stress disorder. While much has been learned from models of early-life stress, current paradigms emphasize physical stressors, while models of emotional stress focus on parental neglect and social isolation. Thus, it is critical to develop animal models that allow for independent assessment of the neurobiological consequences of emotional stress (ES). Here we introduce a novel social stressor that is insulated from the effects of physical stress. Methods: In this study, adolescent male C57/BL6J mice were forced to witness the social defeat of another mouse. The home cage of a male CD-1 retired breeder mouse was divided by a Plexiglas divider into two adjacent compartments, and an adolescent male (postnatal day 35) mouse was then introduced into the compartment territorialized by the CD-1 where it was repeatedly attacked (PS) and demonstrated escape-like behaviors, vocalizations, and submissive posturing, while a second mouse witnessed (ES) this interaction from the adjacent compartment. Results: Acute and chronic ES and PS exposure increased serum corticosterone, and these mice also lost more weight than controls. ES and PS exposure increased anxiety- and depression-like behaviors: ES and PS exposure induced social avoidance, while decreasing exploratory behavior in the elevated plus-maze and open field, along with increased novelty-induced hypophagia and depression-like behavior in the forced swim test. Molecular analyses yielded reduced expression of the scaffolding protein Shank3 within the ventral tegmental area (VTA), a brain region implicated in responses to stress. Overexpressing shank3 within the VTA in adulthood was sufficient to restore control levels of social interaction in both ES- and PS-exposed mice. Conclusions: Together, these data indicate that witnessing traumatic stress early in life stress is a potent stressor capable of inducing life-long biological and behavioral dysregulation, and changes in shank3 expression within the VTA mediate these effects. Disclosures: Nothing to Disclose.
Top of page 38.3 Endogenous Opioid Release and BOLD Activation During Romantic Rejection and Acceptance: Implications for Impaired Social Functioning in Major Depressive Disorder David Hsu Stony Brook University, Stony Brook, New York, United States Background: Seeking out romantic relationships is a significant part of adolescent and adult life. However this process often involves rejection by desired partners, which can strongly elicit negative moods. In animal models, the endogenous opioid peptides acting at μ-opioid receptors (MORs) have been shown to be critical for both behavioral recovery during social distress and promoting social motivation during social reward. In humans it is not known if the MOR system plays a similar role. In this talk I will present studies using both positron emission tomography (PET) and functional magnetic resonance imaging (fMRI) to support the hypothesis that abnormal MOR functioning and neural activity contribute to poor social functioning in major depressive disorder (MDD). Methods: PET STUDIES: Subjects were 18 HCs (13 women; 32 ± 12 years) and 17 medication-free adult patients with current MDD (13 women; 30 ± 10 years). Prior to PET scanning, subjects rated online profiles of preferred-sex individuals with whom they would most like to form a close relationship. A few days later they were given feedback that they were not liked (rejection) or liked (acceptance) by their highest-rated profiles during PET with intravenous administration of the selective MOR radiotracer [11C]carfentanil. MOR activation (i.e., increased endogenous opioid release) was measured as acute reductions in receptor availability during rejection or acceptance compared to baseline blocks, which did not contain feedback. FMRI STUDIES: Subjects were 19 female HCs (31 ± 12 years) and 18 medication-free female patients with current MDD (30 ± 11 years). An identical profile-rating procedure was used as described above. During fMRI scanning, subjects experienced blocks of rejection, acceptance, and neutral trials. Results: PET STUDIES: Both HCs and MDDs showed sustained negative affect in response to rejection, although only HCs showed broad MOR activation, which was found in the nucleus accumbens, amygdala, midline thalamus, and periaqueductal gray. In contrast, MDDs showed MOR deactivation in the amygdala and persistent negative affect after rejection trials had ended. During acceptance, HCs but not MDDs showed a positive correlation with MOR activation in the nucleus accumbens (a structure involved in reward and motivation) and an increased desire for social interaction. FMRI STUDIES: Preliminary analyses show that during rejection, MDDs have greater BOLD activation in the right anterior insula compared to HCs, indicating that rejection may be more salient and/or unpleasant in MDDs. Conclusions: In HCs, rejection and acceptance activated the endogenous opioid system, potentially dampening negative emotions and increasing social motivation, respectively. In MDD, altered opioid and neural function may be a mechanism for slower/incomplete recovery from rejection and poorly sustained engagement during positive social interactions. Together, these alterations may contribute to difficulties in seeking and maintaining relationships. Disclosures: Nothing to Disclose.
Top of page 38.4 How does the Brain Understand the Death of a Loved One? Neural Correlates of Complicated Grief in Older Adults Mary-Frances O’Connor The University of Arizona, Tucson, Arizona, United States Background: Complicated Grief (CG) is marked by a persistent and intrusive grief lasting beyond the expected period of adaptation. Hypothesized neural mechanisms distinguishing CG from Noncomplicated Grief (NCG) include deficits in updating reward-related processes related to attachment behavior, and emotion regulation deficits. Methods: In Study 1, 23 bereaved women (11 CG, 12 NCG) participated in an event-related functional magnetic resonance imaging (fMRI) scan, during grief elicitation with photos of their deceased loved one and a stranger. In Study 2, 28 older adults (CG=8, NCG=9 and Nonbereaved, married controls =11) completed the emotional-counting Stroop task with self-relevant grief and neutral words. Results: Analyses of Study 1 revealed that whereas both CG and NCG participants showed pain-related neural activity in response to photos of the deceased (compared to a stranger), only those with CG showed reward-related activity in the nucleus accumbens (NA). This NA cluster was positively correlated with self-reported yearning, but not with time since death, participant age, or positive/negative affect. For Study 2, behavioral Stroop data showed that the CG group had slower reaction times to grief-related words compared to NCG and Nonbereaved groups. FMRI studies investigating the neural networks associated with Stroop performance consistently implicate the rostral anterior cingulate cortex (rACC). Those with CG showed an absence of rACC recruitment. Activity in the medial prefrontal cortex was significantly elevated in the NCG group compared to Nonbereaved controls, consistent with this as an emotion regulation region. Conclusions: For those with CG, reminders of the deceased may still activate neural reward activity, which may interfere with adapting to the reality of the loss. In addition, those with CG show a relative inability to recruit the regions necessary for successful grief-related emotion regulation when processing reminders of their loss. In addition to learning about distinct regions of activation during expected grief, neuroimaging of CG provides insights into the neuroanatomical correlates of behaviors seen in this disorder. Disclosures: Nothing to Disclose.
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39. Advances from Three Hallmark Genetic Consortia on Endophenotypes in Schizophrenia to Four Collaborations Operating at the Exciting Frontiers of Genomic Science
Top of page 39.1 De Novo Mutations in Schizophrenia Map to Prefrontal Cortical Network Jon McClellan University of Washington, Seattle, Washington, United States Background: Schizophrenia is characterized by extreme genetic heterogeneity. Rare damaging mutations, many of which are de novo, or arose in recent generations, appear to play an important role in the illness. Given that most affected persons may have different genetic causal events, strategies are needed to identify shared pathways or neurobiological processes that, when disrupted, lead to schizophrenia. Methods: Using quads and trios from COGS and PAARTNERS, we previously found that persons with sporadic schizophrenia are more likely to harbor damaging de novo mutations that disrupt genes in developing fetal brain, as compared to healthy siblings (Gulsuner et al., 2013). We have constructed expanded gene networks, using seed genes harboring damaging de novo events in affected persons, to identify genes that operate in related neurobiological processes predicted to be relevant to schizophrenia. Results: Genes in the expanded network cluster into modules with distinct patterns of brain expression, based on RNAseq data, and operate in pathways important to early brain development. The next step is to determine whether the disruption of different genes, and their related neurobiological functions, predicts patterns of endophenotypic profiles in affected persons and families. Conclusions: Each candidate gene implicates mechanisms and pathways potentially important to disease. Well-characterized family-based cohorts can be exploited to define genomic and neurodevelopmental aspects of schizophrenia, and to guide the next generation of intervention research. Disclosures: Nothing to Disclose.
Top of page 39.2 Associations of Gene Expression with Schizophrenia and Related Neurocognitive Endophenotypes Laura Almasy University of Texas Health Science Center at San Antonio, San Antonio, Texas, United States Background: There is strong evidence for a genetic contribution to risk of schizophrenia. It is likely that some variants contributing to genetic risk are regulatory and act through alterations in the amount, timing or location of gene expression rather than through changing protein structure. We are using RNA expression levels as a means of scanning the genome for potential schizophrenia risk loci by assessing correlations between gene expression and established neurocognitive risk factors for schizophrenia in the Consortium on the Genetics of Schizophrenia (COGS), Multiplex Multigenerational Investigation of Schizophrenia (MGI), and Project among African Americans to Explore Risk for Schizophrenia (PAARTNERS) studies. Methods: RNA transcription levels were assayed using Illumina HT-12 Expression BeadChips in 4,369 lymphoblastoid cell lines from COGS, MGI, and PAARTNERS. Variance component methods implemented in SOLAR were used to assess correlations between gene expression and seven measures of cognition, assessed using the PENN computerized neurocognitive battery. These include measures of abstraction and mental flexibility, emotion processing, face memory, sensorimotor dexterity, spatial memory, spatial processing, and verbal memory. Age, sex, self-reported ethnicity (African-American versus European-American), and study were included as covariates. Results: Measures of gene expression are available for 1,029 individuals with schizophrenia, 2,729 unaffected family members, and 611 healthy community controls. Analyses of the first half of these data showed 828 probes associated with risk of schizophrenia and 55 associated with neurocognitive endophenotypes at p < 5x10-5. Permutation analysis comparing these results to 1,000 sets of randomly selected probes, indicated overrepresentation of genes associated with a variety of KEGG pathways, including calcium signaling, MAPK signaling, circadian rhythm, peroxisome proliferator-activated receptor signaling, and tyrosine metabolism. However, in these analyses many genes showed differing mean mRNA levels between African- and European-Americans and between the COGS, MGI and PAARTNERS samples, even after controlling for ethnicity. Conclusions: Correlations of mRNA levels with schizophrenia and neurocognitive endophenotypes show promise as a means of scanning for loci harboring potential non-coding, regulatory variants affecting schizophrenia risk. However, evidence for differences in gene expression by ethnicity and study raise concern. To address these issues, analyses in the full sample are being run separately by study and using principal components-derived covariates to control for ethnicity and for other unmeasured, systematic sources of variance. Disclosures: Nothing to Disclose.
Top of page 39.3 Linking Clinical Outcome and Genotype to Schizophrenia Predisposition using Stem Cells Kristen Brennand Mount Sinai School of Medicine, New York, New York, United States Background: Schizophrenia (SZ) is a debilitating neurological disorder. Though postmortem studies have revealed reduced neuron size and spine density in SZ brain tissue, the molecular mechanisms underlying the disease state remain unclear. Methods: We directly reprogrammed fibroblasts from SZ patients into human induced pluripotent stem cells (hiPSCs) and subsequently differentiated these disorder-specific hiPSCs into neural progenitor cells (NPCs) and neurons. We and others have found that SZ hiPSC NPCs show evidence of aberrant migration, increased oxidative stress, perturbed responses to environmental stressors; while SZ hiPSC neurons exhibit diminished neuronal connectivity, decreased neurite number, reduced synaptic maturation and reduced synaptic activity. Now, we wish to test if rare mutations, identified in COGS, PGC and/or NIH genetic studies, are causal contributors to SZ. Results: First, we are investigating the link between genotype and gene expression. From two related individuals with large (289kb) heterozygous deletions in CNTNAP2 and discordant clinical outcomes, we generated hiPSC neural cells, observing exon-specific changes in CNTNAP2 expression in both carriers as well as allele-biased expression in CNTNAP2 that was consistent with both clinical outcome and neural migration in vitro. Second, we intend to explore the relationship between genotype and neuronal function by restoring defined mutations in SZ hiPSC neurons and recapitulating them in controls, in order to assess whether they are necessary and sufficient for disease across a range of genetic backgrounds. Conclusions: Taken together, we believe these studies will inform the relationship between genotype, neuronal phenotype and clinical outcome. Disclosures: Nothing to Disclose.
Top of page 39.4 Epigenetics of Schizophrenia Andrew Feinberg Johns Hopkins University School of Medicine, Baltimore, Maryland, United States Background: Our group, working with COGS, PAARTNERS, and MGI, have been investigating epigenetics changes in schizophrenia in a large case-control study, as well as genetic and epigenetic mediators of neurocognitive epigenetic transmission. Methods: We have used a combination of assays, including CHARM, Illumina 450K, and integration of epigenetic data with GWAS to search for differences in a large case control series, as well as, with Laura Almasy, familial transmission of neurocognitive traits linked to epigenetic modification. In the case control set, we measured the methylation levels of 456,513 CpG autosomal loci using the Infinium HumanMethylation450 BeadChip assay in independent case-control discovery and replication sets of blood and brain tissue. We implemented linear regression analysis for disease outcome, adjusting for age, gender, race, smoking, batch and cell heterogeneity. The discovery sample set included samples of 689 SZ cases and 645 controls. Replication samples were from the Genomic Psychiatry Cohort, frequency matched with respect to smoking status, age, and sex (Janet Sobell collaborating). Results: We identified SZ-associated methylation differences which were replicated in controls, and included genes likely to play a role in SZ either by known genetic association or neurodevelopmental phenotype. We also noted that at least some previous epigenetic studies are affected by cell type confounding, and by confounding with smoking, which we went to great lengths to avoid. However, it remains to be determined whether the changes we observe occur before or after disease onset. Conclusions: Purely genetic analysis of schizophrenia can miss disease associations that become apparent through a combined approach. Disclosures: Nothing to Disclose.
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40. The Role of Neuroinflammation in Depression: Pet Imaging and Clinical Implications
Top of page 40.1 Positron Emission Tomographic Imaging of Translocator Protein (TSPO) as a Biomarker of Neuroinflammation in Alzheimer's Disease Robert Innis National Institute of Mental Health, Bethesda, Maryland, United States Background: In addition to reviewing the use PET imaging of translocator protein (TSPO) as a biomarker of neuroinflammation, Dr. Innis will provide novel results on TSPO imaging in Alzheimer’s disease. His laboratory found that this marker of neuroinflammation is increased in patients with AD compared to subjects with mild cognitive impairment (MCI, a precursor syndrome) and to control subjects (Kreisl et al., Brain, 136: 2228, 2013). Furthermore and unlike amyloid, the amount of inflammation, indirectly measured as TSPO binding, was correlated with the severity of cognitive impairment. The results of this between-group comparison have been confirmed in a larger groups of subjects (unpublished) and, more importantly, have been extended with repeated PET scans in patients over a two to three year follow-up period (unique data to be presented in this talk). Methods: Eleven patients with either AD or mild cognitive impairment (Mini Mental State Exam score = 21.6 ± 5.2) and 8 cognitively-normal age-matched controls underwent 11C-PBR28 PET at baseline and after median follow up of 2.7 years. Patients were amyloid-positive and controls were amyloid-negative on 11C-PIB PET. Dynamic PET images were corrected for partial volume effects. Relative 11C-PBR28 binding was calculated 60-90 min post-injection using cerebellar gray matter as a pseudo-reference region. Results: For patients, 11C-PBR28 binding in target regions was 2.5 – 17% greater at follow up than baseline, with greatest increase in entorhinal cortex. For controls, regional binding at follow up was within ±5% of baseline values. Corrected for baseline values, patients had greater 11C-PBR28 binding at follow up than controls in superior and inferior parietal lobule, occipital cortex, superior and middle temporal cortex, and entorhinal cortex (P < 0.03). Change in Clinical Dementia Rating scale score correlated with change in 11C-PBR28 binding in prefrontal cortex, inferior parietal lobule, precuneus, and superior and middle temporal cortex (r > 0.66, P < 0.023). Conclusions: TSPO binding increases with progression of AD but not in healthy aging. Furthermore, the increased TSPO binding was significantly correlated with the increase of cognitive impairment during the follow-up period. Overall, these results suggest that neuroinflammation is a marker of the conversion from MCI to AD and that neuroinflammation correlates with disease severity both between groups and within subjects during progression of the disease. Of relevance to this panel, this study in AD shows that TSPO imaging can visualize and quantify neuroinflammation in a disorder, whose pathology is known to include significant neuroinflammation at the time of death. Thus, TSPO imaging can now be used as a validated tool to explore the role on neuroinflammation in Major Depression Disorder, whose neuropathology if far less clear than that in AD. Disclosures: Part 1: Research collaboration and financial support from Eli Lilly, Part 4: Research collaboration and financial support from Eli Lilly.
Top of page 40.2 New Evidence that Microglial Activation, an Important Component of Neuroinflammation, Is found Throughout Grey Matter Regions in the Brain During Major Depressive Episodes Jeffrey Meyer Center for Addiction and Mental Health, Toronto, Canada Background: The neuroinflammatory model of major depressive disorder (MDD) is supported by the several main findings including commonality of sickness behaviors with symptoms of major depressive episodes (MDE), the association of elevated peripheral inflammatory markers with MDD, and high rates of MDE in neuroinflammatory illnesses. However, a key limitation has been the lack of brain inflammation studies in reasonably large samples of MDE secondary to MDD. Recent advances in positron emission tomography (PET) enable measurement of TSPO VT, an index of translocator protein levels which elevate when microglia are activated. The aim of the study was to determine whether TSPO VT, is elevated in the prefrontal cortex (PFC), anterior cingulate cortex (ACC) and insula in MDE secondary to MDD. Methods: 20 subjects with MDE secondary to MDD and 20 healthy controls, underwent an [18F]FEPPA PET scan. TSPO VT was measured in the PFC, ACC, and insula. MDE subjects were medication-free for at least 6 weeks. All participants were otherwise healthy, and non-smoking. Results: In MDE, TSPO VT was significantly elevated in the PFC, ACC, and insula (average 30%, multivariate analysis of variance, F(3,35)=4.73, P<0.001). A similar increase was observed in other brain regions. In MDE, greater TSPO VT in the ACC and insula correlated with greater depression severity and lower body mass index (BMI), respectively (ACC: r=0.628, P=0.005; insula: r=-0.605, P=0.006). Conclusions: This finding provides strong evidence for brain inflammation, and more specifically, microglial activation, in MDE, implying that novel therapeutics which either modulate or reduce microglial activation may be promising for MDE. The correlation between higher ACC TSPO VT and the severity of MDE is consistent with the perspective that neuroinflammation in specific regions may contribute to sickness behaviors that overlap with symptoms of MDE. Disclosures: Part 1: Drs. Meyer has received operating grant funds for other studies from Janssen, Eli-Lilly, GlaxoSmithKline, Bristol Myers Squibb, Lundbeck, and SK Life Sciences in the past 5 years. Dr. Meyer has consulted to several of these companies, as well as Takeda, Sepracor, Trius, Mylan, and Teva, Part 2 It is possible that the total amount from Trius or Teva could have reached $10000, Part 4: Janssen, Part 5: not applicable. I have several patents (submitted/completed) related to use of MAO-A markers and inflammatory markers as biomarkers in mood disorders as well as one for a dietary supplement to prevent mood disorders. These have potential to generate income in the future.
Top of page 40.3 Using PET Imaging of Translocator Protein (TSPO) to Investigate the Link Between Inflammation and Depression Erica Richards National Institute of Mental Health, Bethesda, Maryland, United States Background: Neuroinflammation may be a predisposing factor for major depressive disorder (MDD). Translocator protein 18 kDa (TSPO) is a highly expressed protein in glial cells of the brain and, therefore, a potential biomarker of neuroinflammation. TSPO can be accurately quantified using positron emission tomography (PET) and [11C]PBR28, a TSPO tracer developed in our laboratory. During this panel, in an earlier presentation, Dr. Jeffrey Meyer will report findings from his group showing increased TSPO binding in multiple brain regions of unmedicated MDD patients currently experiencing a major depressive episode. Our current study has three aims. The first aim is to replicate the findings presented by the Meyer group. The second aim is to investigate antidepressant effects on TSPO binding in patients with MDD. The third aim is to determine the relationship of peripheral and central inflammatory markers to TSPO binding. Methods: Unmedicated MDD (n = 13), medicated MDD (n = 10) and healthy control (n = 12) subjects underwent PET imaging using [11C]PBR28. We measured total distribution volume (VT, proportional to Bmax/Kd) using arterial input function and corrected for TSPO genotype. Based on previous post-mortem findings, we chose the subgenual prefrontal cortex and anterior cingulum as regions of interest and compared VT values obtained in medicated and unmedicated MDD subjects and healthy controls. We also obtained peripheral blood samples and cerebrospinal fluid, for later analysis, to investigate the relationship between peripheral and central inflammatory markers and TSPO binding. Results: The interim results of this ongoing study show no significant differences in TSPO binding in depressed patients compared to healthy subjects in any of the predetermined brain regions. In the anterior cingulate, VT was 12.5% higher in unmedicated MDD patients compared to healthy controls (p=0.25, Cohen’s d=0.49) and 10.3 % higher in medicated patients compared to healthy controls (p=0.45, Cohen’s d = 0.31). In the subgenual cortex, VT was 11.1% higher in both the unmedicated (p=0.30, Cohen’s d = 0.43) and medicated patients (p=0.44, Cohen’s d = 0.32) compared to healthy controls. TSPO binding did not correlate to peripheral blood C-reactive protein levels. Conclusions: With about 50% recruitment completed for this study, we have not replicated the previous findings of Meyer’s group showing increased TSPO binding in brain regions of depressed patients compared to healthy controls. However, based on the Cohen’s d effect sizes reported, there is a moderate effect showing increased TSPO binding in the anterior cingulate and subgenual cortex of unmedicated patients. The moderate effect sizes noted indicate that increasing the sample size may result in significant differences, specifically with increased TSPO binding in unmedicated depressed patients. Effect size decreases when medicated patients are compared to healthy controls. For future analysis, there may be some utility in polling the data of these two similar studies to look for greater significance and to subgroup the patient populations given the heterogeneous nature of major depressive disorder. These findings are important because they may help further elucidate pathways involved in the development of MDD as well as identify potential novel treatments and pharmacological targets. Disclosures: Nothing to Disclose.
Top of page 40.4 Efficacy of the Anti-Inflammatory Agents Minocycline and Aspirin in Bipolar Depression Wayne Drevets Janssen Pharmaceuticals of Johnson & Johnson, Inc., Titusville, New Jersey, United States Background: The literature suggests a subgroup of individuals with mood disorders manifests elevated release of pro-inflammatory cytokines in the peripheral blood and cerebrospinal fluid (CSF), and activation of microglia in the brain. The latter finding has been informed by post mortem assessment of microglial activation in the cingulate cortex of suicide victims with mood disorders, and appears consistent with the results of in vivo PET-TSPO binding in some, but not all studies, of major depressive disorder. Studies in rodents show that suppressing microglial activity using minocycline or drugs targeting microglia-based receptors reduce depression-like behaviors in chronic stress models. To examine whether anti-inflammatory treatments improve depressive symptoms in bipolar disorder (BD) we evaluated the efficacy of minocycline, which selectively inhibits the microglia polarization to a pro-inflammatory state, and aspirin, at a dose expected to relatively selectively inhibit cyclooxygenase 1 (COX-1). Both minocycline and COX-1 inhibition exert neuroprotective effects in preclinical models. The rationale and study design appears in Savitz et al (BMJ Open 2012; 2:e000643; Clinical Trials.gov: NCT01429272. LI-Jonathan Savitz; PI-Sheldon Preskorn). The study completes enrollment in summer, 2015, and final results will be presented. Methods: Outpatients 18 to 65 years of age, who met DSM-IV-TR criteria for BD (types I, II, or NOS) in a current depressive episode were recruited to participate in a randomized, double-blind, placebo-controlled, parallel-group, clinical trial following a 2 × 2 design. The total enrollment target was n=120. The study was conducted at three sites: Laureate Institute for Brain Research, Tulsa, OK, Kansas University School of Medicine, Wichita, KS and University of Oklahoma School of Community Medicine, Tulsa, OK. As adjuncts to existing treatment, subjects were randomized to receive one of four treatment combinations: placebo-minocycline plus placebo-aspirin, active-minocycline plus placebo-aspirin, placebo-minocycline plus active-aspirin or active-minocycline plus active-aspirin. The dose of minocycline and aspirin is 100 mg twice daily and 81 mg twice daily, respectively. Antidepressant response was assessed by changes in the MADRS score between baseline and the end of the 6-week trial. As secondary outcome measures, the anti-inflammatory effects of minocycline and aspirin was tested by measuring pre-treatment and post-treatment serum levels of C reactive protein and inflammatory cytokines. Results: Using an adaptive trial design during this study, a blinded interim analysis was conducted once 60 individuals had been randomized to determine whether any of the cells were separating from the others. Two cells appeared to be separating. A power calculation was performed based on the mean difference between cells in relationship to the variance. That calculation determined that 30 subjects in each of the two cells would produce power > 80% for alpha = 0.05. An unblinded investigator not involved in the study conduct then evaluated the two cells to determine whether a reduction to just these two cells going forward was reasonable from a scientific perspective. That decision allowed for a reduction of the total enrollment goal from n=120 (i.e., 30 subjects in 4 cells) to n=100 (30 subjects in each of the two critical cells plus 40 individuals already enrolled in the two intermediate cells). The last patient in is anticipated in July, 2015. Conclusions: The final study results will be presented and will address the therapeutic potential of anti-inflammatory agents in bipolar depression. Relationships between the clinical outcome measures and the pre- and post-treatment serum biomarkers will be assessed to explore whether patients manifesting evidence of a pro-inflammatory process may particularly benefit from anti-inflammatory treatment. Disclosures: Part 1: Johnson & Johnson, Inc., Use Patent filed “Composition and Method for Treating Bipolar Disorder", Use Patent awarded, “Scopolamine in the Treatment of Depression” (no financial proceeds to date), Part 2: Johnson & Johnson, Inc., Equity and Salary, Part 3: Johnson & Johnson, Inc., Part 5: Johnson & Johnson, Inc.
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41. Fear Generalization: Neurobiological and Behavioral Mechanisms Across the Pre-clinical and Clinical Spectrum
Top of page 41.1 Fear Learning Circuitry is Biased Toward Generalization of Fear Associations in Posttraumatic Stress Disorder Rajendra Morey Duke University, Durham, North Carolina, United States Background: Fear conditioning is an established model for investigating posttraumatic stress disorder (PTSD). However, symptom triggers may only vaguely resemble the initial traumatic event, differing on a variety of sensory and affective dimensions. We extended the fear-conditioning model to assess generalization of the conditioned-fear response on fear processing neurocircuitry in PTSD. Methods: Military veterans (n=67) consisting of PTSD (n=32) and trauma-exposed comparison (n=35) groups underwent functional MRI during fear-conditioning to a low fear-expressing face while a neutral face was explicitly unreinforced. Baseline responses before, and generalization responses after, fear conditioning used stimuli that varied along a neutral-to-fearful continuum. Results: Compared to trauma-exposed controls, PTSD patients exhibited more severe post-study memory distortion of the fear-conditioned stimulus toward the stimulus expressing the highest fear intensity. PTSD patients exhibited biased neural activation toward high-intensity stimuli in fusiform gyrus (p<.02), insula (p<.001), primary visual cortex (p<.05), locus coeruleus (p<.04), thalamus (p<.01), and at the trend-level effect in inferior frontal gyrus (p=.07). All regions except fusiform were moderated by childhood trauma. Amygdala-calcarine (p=.01) and amygdala-thalamus (p=.06) functional connectivity selectively increased in PTSD patients for high-intensity stimuli during generalization. In contrast, amygdala-vmPFC (p=.04) connectivity selectively increased in trauma-exposed controls compared to PTSD patients for low-intensity stimuli during generalization, representing a safety-learning response. Conclusions: Fear generalization in PTSD is biased toward stimuli with higher emotional intensity than the original conditioned-fear stimulus. The functional brain differences provide a putative neurobiological model for fear generalization where PTSD symptoms are triggered by threat cues that merely resemble the index trauma. Disclosures: Nothing to Disclose.
Top of page 41.2 Erring on the Side of Caution: One Cell at a Time Sumantra Chattarji Institute for Stem Cell Biology and Regenerative Medicine, Bangalore, India Background: The early stages of fear memory formation involve strengthening of sensory afferents from the thalamus to the amygdala. As useful as this simple behavioral model has been in studying basic cellular mechanisms of associative learning, it does not capture some of the essential features of learning in the “real world”. What makes learning a challenging problem is that it requires that animals generalize appropriately from experience. There are costs associated with both too little and too much generalization: If an animal under-generalizes it may overlook future signs of danger, whereas if it overgeneralizes it may fail to explore and thereby miss opportunities for feeding, mating, etc. Methods: I will present recent findings obtained using a combination of in vivo unit recordings and optogenetics in awake behaving rodents, on the cellular mechanisms in the amygdala mediating generalization during fear learning. Results: We identified distinct neuronal populations in the lateral amygdala (LA) of rats that signaled generalized versus cue-specific associations and determined how their distributions switched during fear generalization. Notably, the same LA neurons that were cue-specific before the behavioral shift to generalized fear lost their specificity afterwards, thereby tilting the balance of activity toward a greater proportion of generalizing neurons (Fig. 1). Neuronal activity in the LA, but not the auditory cortex, was necessary for fear generalization. Furthermore, targeted activation of cAMP/PKA signaling in the LA increased neuronal excitability of LA neurons and led to generalized fear. Conclusions: These results provide a cellular basis in the amygdala for the alteration of emotional states from normal to pathological fear. Disclosures: Nothing to Disclose.
Top of page 41.3 Aversive Learning and Generalization Predict Sub-Clinical Anxiety Symptoms Six Months Later Bram Vervliet Massachusetts General Hospital / Harvard Medical School, Charlestown, Massachusetts, United States Background: The identification of premorbid markers of risk for psychopathology is one of the most important challenges for present-day psychiatric research. There is a pressing need for efficient, low-cost, low-effort screening tools in order to deliver targeted prevention and cure. This study focuses on deviant generalization as a key behavioral vulnerability factor, and uses simple behavioral tasks to assess the level of generalization. The first experiment examines the predictive value of aversive learning and generalization for the development of sub-clinical anxiety. The second and third experiment focus on the diagnostic value of non-aversive learning and generalization in panic disorder and autism, respectively. Methods: The behavioral task involved two rings of different size, with one ring (CS+) consistently followed by an aversive picture (Experiment 1) or a neutral picture (Experiments 2 and 3), whereas the other ring not (CS-). Learning was tracked by asking participants during each ring to rate the probability that the (aversive) picture would follow. Subsequent generalization testing comprised repeated presentations of rings of varying sizes. In Experiment 1, 375 college students completed the task, while levels of anxiety were assessed by questionnaires (DASS and STAI) at that moment and after a six-month follow-up. In Experiment 2, learning and generalization were compared between 22 panic disorder patients, 27 other anxiety patients, and 29 healthy controls. In Experiment 3, learning and generalization were compared between 18 high-functioning autistic patients and 19 matched controls. Results: Experiment 1 showed that both discrimination learning and generalization added significantly to the explained variance in anxiety symptomatology at 6 months follow-up. Experiment 2 showed weaker discrimination learning in panic disorder patients, due to heightened expectancies during the non-associated control stimulus (CS-). Experiment 3 showed weaker discrimination learning in high-functioning autistic patients, due to lowered expectancies during the associated stimulus (CS+) as well as heightened expectancies during the non-associated stimulus (CS-). Conclusions: Simple behavioral tasks that probe discrimination learning and generalization can be used as efficient, low-cost, low-effort screening tools for the prediction and diagnosis of various forms of psychopathology. The behavioral and neural processes underlying explicit expectancy learning have relevance for the study of psychopathology and should be studied in more detail. Disclosures: Nothing to Disclose.
Top of page 41.4 The Effect of Generalized Fear Learning on Episodic Memory Joseph Dunsmoor New York University, New York, New York, United States Background: Pavlovian fear conditioning has been used successfully to investigate fear learning in humans and nonhuman animals for stimuli in the environment that signal aversive events. Beyond understanding how fear is acquired and expressed, fear learning can also provide insights into other memory systems involved in remembering episodic details of a fearful event. Little research has been conducted in the effects of fear conditioning on episodic memory for neutral details associated with aversive experiences because most experimental protocols in humans utilize only one or two conditioned stimuli repeatedly paired with the aversive event. Methods: Here, we used a novel trial-unique form of fear conditioning in which 119 healthy subjects learned to fear an entire category of objects (either animals or tools). This procedure enabled us to test memory for items from a conceptual category viewed prior, during, and after Pavlovian fear conditioning of semantic categories of stimuli. Results: We demonstrated that memory for pictures from a category paired with an electric shock (animals or tools) was greater than for an unpaired control category (tools or animals, respectively). At 24 hour (N = 30) and 6 hour (N = 30) retrieval tests, enhanced episodic memory was observed for items from the feared category viewed before fear conditioning, suggesting a retroactive enhancement in episodic memory for items related to a future threat. The latter finding is in accord with recent animal studies on “behavioral tagging” in which weak learning is enhanced through subsequent activation that engages common neural pathways minutes to hours later. Conclusions: These results provide new evidence for a generalized tagging process during memory encoding, whereby seemingly inconsequential information can be retroactively credited as relevant, and therefore selectively remembered, if conceptually similar information acquires salience in the future. Disclosures: Nothing to Disclose.
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42. Probing the Perinatal Expression of Risk for Mental Disorder: Basic Molecular, Neurobiological, Neuroimaging and Clinical Intervention Studies in Pregnancy and Fetal Development
Top of page 42.1 Neurexin 1 (NRXN1) Gene Expression Across the Normal Human Lifespan: Implications for Normal and Abnormal Neurodevelopment Amanda Law University of Colorado School of Medicine, Aurora, Colorado, United States Background: Genetic studies have identified neurexin-1 (NRXN1; 2p16.3) as a risk gene for several neurodevelopmental disorders, including autism spectrum disorder, schizophrenia, developmental delay and mental retardation, implicating a pleotropic role for NRXN1 in human cortical development. NRXN1, a presynaptic cell adhesion molecule and receptor that plays critical roles in synaptogenesis, encodes two major isoforms, NRXN1-α and NRXN1-β. To gain insight into NRXN1’s involvement in human cortical development we used quantitative real time PCR to examine the expression trajectories of NRXN1, and its predominant isoforms NRXN1-α and NRXN1-β in prefrontal cortex (PFC) from fetal stages to aging and in patients with schizophrenia or bipolar disorder. Methods: Postmortem human brains from the Clinical Brain Disorders Branch were obtained at autopsy from the Washington, D.C. and Northern Virginia medical examiners’ offices (protocol 90-M-0142 approved by the NIMH/NIH IRB). Additional postmortem fetal, infant, child, and adolescent brain tissue samples were provided by the National Institute of Child Health. Dorsal lateral prefrontal cortex (DLPFC) was available from 245 normal individuals (0-85 years), 110 patients with schizophrenia and 34 patients with bipolar disorder. Fetal PFC was derived from 39 individuals (14-39 weeks). NRXN1 and its predominant splice isoforms NRXN1-α and NRXN1-β, were measured using Taqman Gene Expression Assays by real time RT-PCR using an ABI Prism 7900 sequence detection system with 384-well format (Applied Biosystems) and quantified via the standard curve method. Results: Linear Regression revealed that in the human fetal brain, NRXN1-α (P=0.01) and NRXN1-β (P=1.38E−5) increased significantly with gestational age. Highly significant effects of age on NRXN1-α (β= -0.57; P=2.1E−18) and NRXN1-β (β= -0.49; P=6.28E−15) expression were also observed during postnatal development, whereby NRXN1 expression was highest at birth until 3 years of age, after which expression declined and remained steady throughout childhood, adolescence and aging. Expression levels of NRXN1-α were significantly elevated in patients with bipolar disorder compared to age matched healthy controls (p=0.01). Conversely, expression levels of NRXN1-β were significantly higher in the DLPFC of patients with schizophrenia compared to age matched controls (p=0.01). Conclusions: Our data provide novel insight into NRXN1 splice isoform expression profiles during normal human neocortical development and demonstrate that expression is highest during critical periods of plasticity in pre- and early postnatal development, consistent with the association of NRXN1 with a broad spectrum of neurodevelopmental disorders. Our data also demonstrate abnormal patterns of NRXN1 expression in psychiatric disorders, suggestive of an immature molecular phenotype. These data will be discussed together and in the context of emerging animal studies and the roles of NRXN1 in early pre-and perinatal brain development. Disclosures: Part 1: Dr. Law has served as a paid consultant for Astra Zeneca Pharmaceuticals.
Top of page 42.2 Genetic Neuropathology in Human Brain Development and Schizophrenia Joel Kleinman Lieber Institute for Brain Development, Baltimore, Maryland, United States Background: Recent advances in genome-wide association studies have led to the identification of 108 regions of genetic variation, single nucleotide polymorphisms (SNPs), associated with increased risk for schizophrenia (p<1.0e-8) (PGC2, Nature 511, 2014). Although these genetic variants each increase risk to a relatively small degree, understanding their mechanisms has the potential to have a large impact with regard to diagnosis and treatment. The molecular biology mechanisms by which genetic variation increases risk for schizophrenia involve expression of specific alternative transcripts thought to be critical for early brain development. Many of these transcripts may be brain and/or primate specific and several are preferentially expressed in fetal human brain. Methods: We have generated qRT-PCR and RNA sequencing data on over 604 -701 postmortem prefrontal cortical (PFC) specimens that have been genotyped for over 650,000 SNPs (Illumina Bead chips). We have used this data to look for mechanisms involving genetic variants that increase risk for schizophrenia from the PGC2 data including ZNF804A and the locus at 10q24.32 as well as other genes of interest including CHRNA7 and CHRFAM7A. Comparisons in expression of these genes have been made across the human lifespan in normals ranging in age from week 14 in the fetus to 80 years of age (n= 313) as well as between patients and controls (schizophrenia (n=169), bipolar disorder (n=57), major depression (n=133) and normal controls (n =198)). N’s are for the ZNF804A study (Tao R et al, JAMA Psychiatry 71, 2014). Comparable sample sizes were used for CHRNA7/CHRFAM7A and the 10 q24.32 locus study). Results: ZNF804: The risk allele is associated with decreased expression of a novel truncated transcript in ZNF8O4A specifically in PFC of fetal human brain (p<.05). This transcript is preferentially expressed in fetal human PFC relative to postnatal specimens. Moreover, this same transcript is underexpressed in PFC of patients with schizophrenia and overexpressed in patients with affective disorders (p= 1.8e-19). CHRNA7/ CHRFAM7A: CHRFAM7A is preferentially expressed in fetal PFC while CHRNA7 is relatively unchanged across the lifespan. CHRFAM7A is expressed more in PFC of all patient groups relative to normals (p=1.3e-7), while CHRNA7 is decreased in PFC of patients with schizophrenia (p=2.8e-5) and increased in major depression (p= 1.0e-17). Gene expression for transcripts of these genes are not associated with any known risk alleles. 10q24.32 locus: rs7085104 is associated with increased expression of a novel truncated transcript in AS3MT (n=604, p=1.99e-30). Although the transcript is expressed in fetal PFC it is not preferentially expressed in fetal human brain. The expression of this transcript is increased in PFC of patients with schizophrenia relative to controls (p=7.2e-4). Conclusions: Postmortem human brain is critical for elucidating the mechanisms by which genetic variation increases risk for schizophrenia. In so far as the transcripts may be brain and primate specific and are developmentally regulated, fetal human brain may also be important for fully understanding the genetic neuropathology of schizophrenia. Genetic variations that increase risk for schizophrenia in ZNF804A and AS3MTare associated with expression in normal PFC that is in the same direction as that seen between patients with schizophrenia and controls. The differences in expression in CHRNA7 and CHRFAM7A in PFC remain to be determined. Disclosures: Nothing to Disclose.
Top of page 42.3 Altered Amygdala Functional Connectivity in Neonates at Risk for Schizophrenia or Bipolar Disorder John Gilmore University of North Carolina School of Medicine, Chapel Hill, North Carolina, United States Background: Emotional processing deficits are common in schizophrenia and appear to be related to abnormal functional connectivity of the amygdala with the prefrontal cortex and other regions. Amygdala dysconnectivity has been observed in adolescents at risk for psychosis, indicating that functional networks associated with emotional processing and the amygdala may predate and potentially contribute to the onset of psychosis. Methods: Neonates of mothers with schizophrenia (SCZ), bipolar disorder (BD), and Mood Disorder not otherwise specified (MD-NOS) underwent resting state functional magnetic resonance imaging (rsfMRI) shortly after birth. Neonates were scanned unsedated in a natural sleep. Twenty SCZ-risk, 26 BD-risk, 23 MD-NOS-risk neonates, and 20 matched control subjects (CONTROL) were scanned. Seed-based functional connectivity analyses of the amygdala were conducted. Nine brain areas that show gray matter deficits in adult schizophrenia patients were also studied to test the specificity of amygdala-based findings and explore if additional functional connections are altered as well. Results: The left amygdala demonstrated hyper-connectivity with the right dorsal lateral prefrontal cortex while the right amygdala demonstrated common hyper-connectivity with the thalamus for both SCZ-risk and BD-risk groups. The exploration analysis revealed that two of nine brain areas, including the thalamus and ventral anterior cingulate cortex, demonstrated additional schizophrenia-specific functional connectivity alterations. The levels of thalamic connectivity detected predicted cognitive development scores at 1 year of age. Conclusions: This is the first study of functional connectivity in neonates at risk for schizophrenia and suggests that functional connectivity abnormalities of the amygdala associated with schizophrenia and bipolar illness arise during prenatal brain development. We found both common and disorder-specific abnormal profiles of functional connectivity in neonates at genetic risk for schizophrenia, bipolar illness, and mood disorder NOS. It may be possible to develop imaging-based biomarkers for the early identification of risks for later psychiatric illness. Disclosures: Nothing to Disclose.
Top of page 42.4 Human Perinatal Choline Supplementation Decreases Preschool Parent-Reported Attentional and Social Withdrawal Symptoms via an alpha7 Nicotinic Cholingergic Receptor Mediated Effect on Infant Developmental of Sensory Gating Randal Ross University of Colorado School of Medicine, Aurora, Colorado, United States Background: Most neuropsychiatric illnesses—including ADHD, anxiety disorders, autism, bipolar, and schizophrenia—are neurodevelopmental disorders, where onset illness is the end result of brain developments changes which begin prenatally. Thus, one potential window for primary prevention is the perinatal period. In animal models, prenatal stimulation of the alpha7 nicotinic cholinergic receptor with dietary choline supplementation leads to improved development of sensory gating, improved memory, and decreased anxiety. Previously published work has supported perinatal choline supplementation’s positive impact on human infant sensory gating development at 1 month of age. This report is a follow-up of these same children to 30 months of age. Methods: Randomized controlled trial of perinatal choline supplementation in 100 healthy mothers (phosphatidylcholine 6300 mg QD) and infants (phosphatidylcholine 700 mg QD). Outcomes of P50 sensory gating (1 months of age) and parent-reported behavior utilizing the Child Behavior Checklist (CBCL; 40 months of age). All infants were genotyped for a schizophrenia-associated SNP in CHRNA7, rs3087454. Results: Infant sensory gating predicted the 40-month CBCL total problems score. Homozygosity for a schizophrenia risk allele in either CHRNA7 is associated with delayed development of infant cerebral inhibition and increased CBCL total problems at 40 months of age. Both genetic effects are reversed by perinatal choline supplementation, with a particular benefit of perinatal choline supplementation on 40-month-old attention and social withdrawal. Conclusions: Prenatal choline supplementation compensates for genetic vulnerability’s impact on the infant development of sensory gating and the 3-year-old development of behavior. The effect of choline is moderated by CHRNA7 genotype supporting perinatal stimulation of the alpha7 nicotinic receptor as the mechanism of action. Universal prevention strategies have a role in preventing major mental illnesses. Disclosures: Nothing to Disclose.
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43. Neurocircuit-based Interventions in Addictions: When and How? David Goldman * , Primavera Spagnolo, Antonelle Bonci, Gary Aston-Jones, Trevor Robbins, Meaghan Creed, DAmiaan Denys, Alan Green, Paul Holtzheimer, Osama Abulseoud, Ali Rezai, Helen Mayberg National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland, United States This Study Group will discuss opportunities and challenges in developing neurocircuit-based interventions for the treatment of addictive disorders. The group will draw from experience of the use of deep brain stimulation (DBS) and other interventions for neuropsychiatric disorders, as well as basic science experience in modulating addictive behaviors in model organisms. The development and growing application of neurocircuit interventions for the treatment of addictions has been stimulated by a confluence of clinical epidemiologic facts and relevant neuroscience observations. High rates of relapse, disability and mortality suggest that more effective interventions are needed. Preclinical studies as well as human neuroimaging studies have demonstrated that addictions are mediated and maintained by circuits rather than a single brain region or neurotransmitter system. Addictions are systems-level disorders affecting integrated cortical, subcortical, and limbic neural circuits, and maintained by allostatic alterations in expression of their related neurotransmitter and molecular mediators. Within this framework, successful treatments for addiction should be capable of modulating limbic and executive control circuits implicated in craving and relapse. Multiple neuromodulation techniques are FDA-approved for clinical and investigational use in humans. Three of the most promising include deep brain stimulation (DBS), repetitive transcranial magnetic stimulation (rTMS), and brain lesioning by focused ultrasound. Beyond direct electrical stimulation, encouraging preclinical studies suggest that a number of focused chemogenic approaches may be possible, including optogenetic stimulation, DREADDS, and genetic transfection (e.g., with dopamine receptor genes). Each is potentially feasible, but safety data have to be developed in each instance, requiring a substantial institutional commitment, in addition to confirming efficacy in preclinical models. Therefore, a question equally as contentious as when, is how. Potentially, many methods may be used against a multiplicity of targets. A unifying theme across different methodologies and neural targets could include some commonalities of assessment and enrollment, including assessment of neuropsychological changes associated with addiction and neuroimaging of brain connectivity and responses. This study group will address, or debate: 1) Which regions, neurocircuits or molecules are the most appropriate target for neurocircuit-based intervention in addictions? (2) Where treatment can be calibrated, for example stimulation parameters, how should this be done, and most importantly, standardized across studies? (3) Who should be eligible? (4) What are the clinical outcomes providing the most realistic and consistent measures of efficacy (5) Can we design human neurocircuit intervention studies so that they can back to model organisms to unravel mechanisms of addiction and understand how the human interventions are working, or why they are not? This study group will bring together investigators with experience in neurocircuit-based interventions to discuss the challenges, strategies, and solutions applied to date. A major goal will be to identify common elements of concern and, through audience interaction, raise awareness of the obstacles and potential future approaches. Disclosures: Nothing to Disclose.
Top of page Thursday, December 10, 2015
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44. The Role of Impulsivity vs. Impulse Control on the Developmental Trajectories of SUD - New Insights from Neuroimaging Research
Top of page 44.1 A Longitudinal fMRI Study of Reward and Inhibitory Control in Youth at Risk for Substance Use Disorder Mary Heitzeg University of Michigan, Ann Arbor, Michigan, United States Background: Evidence suggests that the relatively early maturation of subcortical incentive-responding systems compared with prefrontal inhibitory systems may bias adolescents toward seeking out reward. This bias is proposed to underlie the impulsive, risky decision-making and related escalation of substance use that occurs during adolescence. The longitudinal work reported here aims to investigate inhibitory control and reward system functioning as both prospective predictors of early problem substance use and, in a separate sample, as markers of substance use disorder (SUD) in young adults. Methods: The Michigan Longitudinal Study (MLS) is an ongoing prospective study of youth at high-risk for SUD based on parent history. Longitudinal fMRI is being conducted in two cohorts recruited from the MLS. The child cohort had a baseline scan prior to substance use initiation (n=125; average age=10). The young adult cohort had a baseline scan during the age where normative peaks in SUD are observed (age 18-21; n=160; average age=20). Scans were collected during inhibitory control (go/no-go) and reward (monetary incentive delay; MID) tasks. Participants completed annual questionnaires regarding substance use and behavior problems as part of the MLS assessment. For the child cohort, prospective predictors of the initiation of problem substance use by age 13-16 were investigated using baseline scans. For the young adult cohort, differences between participants with and without SUD were investigated. Results: Activation to successful inhibition did not predict initiation of problem substance use in the child sample whereas blunted activation of left middle frontal gyrus (LMFG) during failed inhibition was a significant predictor of later problem substance use. Blunted LMFG activation was also observed in the young adults with an SUD compared with controls. In both cohorts, less LMFG activation was associated with increased externalizing behavior problems. During the MID, nucleus accumbens (NAcc) activation to reward anticipation did not predict problem substance use involvement in the child sample; however, activation in those who went on to problem use was increased compared with controls after problem substance use initiation. Higher NAcc activation was also observed in older adolescents with an SUD compared with controls. NAcc activation was not associated with externalizing behavior problems in either cohort. In the older cohort, NAcc activation was positively correlated with past year drinking volume. Conclusions: Blunted activation during performance errors in childhood may underlie problems with adapting behavior appropriately, leading to undercontrolled behavior generally and problem alcohol and drug use specifically. The replication in an older sample with SUD suggests it may be a persistent, stable marker of risk for SUD identifiable in childhood. In contrast, hyper-activation of the reward system in childhood is not an early predictor of the initiation of problem substance use. Ongoing analyses of the longitudinal data are investigating whether heightened activation of the reward system is a later-emerging risk factor or a result of substance use. Disclosures: Nothing to Disclose.
Top of page 44.2 Neural Activation to Response Inhibition Predicts Subsequent Substance Use Initiation and Escalation in Adolescence Susan Tapert University of California at San Diego, San Diego, California, United States Background: Response inhibition and cognitive control have been recently appreciated as risk factors for substance use and related disorders. Our early work suggested that poor scores on cognitive tests of attention predicted greater substance use and dependence symptoms 8 years later, even in youth without ADHD, conduct disorder, or learning disorders (Tapert et al, 2002). Here, we sought neurocognitive and neuroimaging markers of response inhibition and cognitive control systems during early adolescence in predicting substance use in mid- to late- adolescence. Methods: We recruited 295 substance-naïve 12-14 year-olds from community schools, and followed them into early adulthood. At each time point, participants were given a comprehensive neuroimaging session and neuropsychological test battery, plus quarterly interviews on substance use. Brain activation to response inhibition (i.e., a go/no-go task) and performance on a test of inhibiting prepotent responses (i.e., a Stroop task) was assessed prior to the onset of substance use. Annual follow-up interviews assessed substance use and mental health symptoms. Results: Poorer baseline performance on tests of cognitive inhibition interference predicted higher follow-up peak drinks on an occasion, more days of drinking, and more marijuana use days (p<.001) by ages 17 to 18, above and beyond covariates. Prior to the onset of substance use, youth who later transitioned into heavy drinking showed significantly less activation during response inhibition than those who went on to remain non to minimal users throughout adolescence, in right inferior frontal gyrus, left dorsal and medial frontal areas, bilateral motor cortex, cingulate gyrus, left putamen, bilateral middle temporal gyri, and bilateral inferior parietal lobules (corrected p<.01/cluster 32 contiguous voxels). In mid-adolescent substance users, less ventromedial prefrontal activation during response inhibition predicted increased substance use and dependence symptoms at follow-up (p<05). These variables will be examined as predicts of substance use outcomes in a single model. Conclusions: Blunted activation during response inhibition and poorer performance on tasks of inhibition may be linked to behavioral undercontrol and propensity to substance use and use disorder. Ongoing analyses will incorporate additional neuroimaging markers to examine the degree to which substance use can be predicted prior to the onset of substance use. Disclosures: Nothing to Disclose.
Top of page 44.3 A Longitudinal Investigation of Reward and Control Brain Systems as Predictors of Adolescent Drug Use Hugh Garavan University of Vermont, Burlington, Vermont, United States Background: Individual differences in neurodevelopment during adolescence may explain why some youth are more inclined to use and abuse alcohol and other drugs. The IMAGEN study, a multi-site, longitudinal study of 2,000 European adolescents, was designed to investigate this possibility. Extensive assessments at age 14 included genetics, structural and functional imaging and numerous phenotypic measures (e.g., personality, cognition, IQ, mental health, drug use, family histories of drug use). The fMRI tasks included an assessment of inhibitory control (the STOP task) and reward processing (the Monetary Incentive Delay task). Subjects were assessed two years later on their drug use and mental health. The longitudinal design allows us to search for baseline predictors of drug use. Moreover, the large sample size allows us (a) to identify youth who were drug-naïve at baseline enabling us to rule out confounding influences of exposure and (b) allows us to quantify the generalizability of our findings using cross-validation techniques. Methods: The STOP task requires motor response inhibition yielding activation associated with successful inhibitions as well as failures to inhibit. The MID task assesses both the anticipation and the receipt of rewards. These brain measures were included with numerous phenotypic measures to develop regression models predicting future use and assessed using ten-fold cross-validation. We report the models from two separate analyses that predict future binge drinkers (n=121 16 year olds with just 1-2 lifetime drinks at baseline) and future cannabis users (n=170 16 year olds who were cannabis naïve at baseline). Future users were compared to subjects who did not increase their alcohol use (Binge Drinking analysis) or remained cannabis-naïve (Cannabis analysis). Results: We were able to predict future drug use with relatively high accuracy (Binge Drinking: area under the ROC = .75; Cannabis use: area under the ROC = .80). The best predictors of future binge drinking and future cannabis use were personality factors, a family history of drug use, and a history of stressful life events. Brain structure (total and regional grey matter volumes) and brain activation associated with both inhibitory control and reward processing were shown to predict future drug use. The best predictors included medial prefrontal and premotor areas (Binge Drinking) and parietal cortex and premotor cortex (Cannabis). Conclusions: The analyses reveal that individual differences at age 14 in brain function associated with reward and control predicted binge drinking and cannabis use two years later. Although the cannabis group analyses are ongoing, the initial sets of results suggest that of the two brain systems, individual differences in control systems are better predictors than individual differences in reward systems. This conclusion would be consistent with the critical role that prefrontal maturation is thought to play in adolescence in regulating impulsive and risky behaviors. Disclosures: Nothing to Disclose.
Top of page 44.4 Impulsivity and Reward Processing in Drug Naïve Youth at Risk for Substance Use Disorders Iliyan Ivanov Mount Sinai School of Medicine, New York, New York, United States Background: Extensive evidence has shown that impulsivity in childhood is associated with elevated risk for the development of substance use disorders (SUD). Impulsivity, however, is not a unitary contract and does interact with other behavioral traits (e.g. reward sensitivity) that also contribute to the development of SUDs. These interactions are purportedly linked to the activity of distinct brain systems. This presentation will report on studies investigating reward processing and impulsivity in typically developing youth and youth at various clinical risks for SUD (i.e. childhood disruptive behavior disorders and familial SUD) before exposure to abusable substances. Methods: We examined the interaction between reward processing and impulsivity in 2 cohorts: 1) 47 drug naïve pre-adolescents aged 8-13 divided in a) low risk group (LR, N=14) - participants with ADHD only; b) high risk group (HR, N=18) - participants with ADHD and familial SUD, and c) controls (N=15). All participants performed a novel Anticipation, Conflict, Reward (ACR) imaging task; 2) 472 drug-naïve youth aged 13-14 selected from a larger cohort of typically developing youth (e.g. IMAGEN study). These youth were further characterized by measures of impulsivity (IMP) and sensation seeking (SS) in 4 groups: High IMP/High SS (N= 205), High IMP/Low SS (N=59), Low IMP/High SS (N=149) and Low IMP/Low SS (N= 60). All subjects performed the Monetary Incentive Delay (MID) imaging task. Results: Higher activation in the brain reward system (e.g. insula, OFC, VS) during reward outcomes of the ACR task was documented in the HR group vs. LR and control groups whereas controls showed higher activation in the behavioral control system (inferior frontal gyrus, caudate, and anterior cingulate gyrus) compared to both LR and HR groups during the ACR flanker trials. For the typically developing sample ANOVA analyses showed significant main effect for IMP and significant IMP by SS interaction in the left VS during the cue component of the MID so that High IMP/Low SS group showed the lowest activation vs. the other 3 groups. Further analyses will examine if differences in brain activation at baseline may be linked to drug experimentation at age 16. Conclusions: These preliminary results suggest that the activation in the brain reward system varies among drug-naive youth in relation to impulsivity, sensation seeking as well as clinical risk factors for SUD (e.g. childhood ADHD and familial SUD). Possible clinical implications are related to identification of biological predictors of drug experimentation/use in typically developing youth and selecting optimal pharmacological treatments for children with ADHD with and without familial predisposition for SUD. Disclosures: Part 1: DSMB member for Lundbeck- honoraria.
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45. Ontogeny of Autism: Identification of very Early Signs of Autism Spectrum Disorder in Humans and Mice
Top of page 45.1 Onset of ASD and Behavioral Signs in the First Year of Life Sally Ozonoff University of California at Davis, Sacramento, California, United States Background: Autism Spectrum Disorder (ASD) is diagnosed at a mean age of 4 years in the United States, but studies demonstrate that behavioral signs of ASD can be detected reliably by the first birthday. Some of the earliest indicators of ASD documented in infants who are later diagnosed with the disorder include reduced interest in faces, increased interest in objects and atypical looking patterns at objects, reduced vocalizations and babbling, and limited shared affect. Methods: Participants were 25 infant siblings of children with ASD, all of whom were later diagnosed with ASD themselves, and 25 gender-matched younger siblings of children with typical development. A prospective longitudinal design was used and participants were evaluated at 6, 12, 18, 24, and 36 months of age. Infants were video-recorded during an object-based interaction with an examiner. Frequencies of gaze to faces, social smiles, and directed vocalizations were coded by researchers unaware of risk or outcome group. Results: A Generalized Estimating Equations approach was used to analyze developmental trajectories for the dependent variables. The frequency of gaze to faces, shared smiles, and vocalizations to others were highly comparable between groups at 6 months of age, but significantly declining trajectories over time were apparent in the group later diagnosed with ASD, while the trajectories of the control group significantly increased with age. Group differences were significant by 12 months of age and widened over time. Conclusions: This work demonstrates that atypical signs of development, particularly in the realms of social engagement and vocalization frequency, are present prior to the first birthday in infants later diagnosed with ASD. These findings may lead to the development of more sensitive methods for diagnosis in infancy, which may in turn permit the application of preventive therapies and earliest intervention to lessen the symptoms of ASD or even prevent onset of the full syndrome. Disclosures: Nothing to Disclose.
Top of page 45.2 Vocal Development in Infants and Children with ASD D. Kimbrough Oller The University of Memphis, Memphis, Tennessee, United States Background: Kanner himself posited vocalization anomalies in autism. Yet descriptions of ASD speech often seem contradictory—pitch is said to be too high and on other occasions too low, with pitch too variable or too monotonous. At Univ. of Memphis, and in collaboration with other universities and the LENA Research Foundation (LRF), we have developed descriptions of vocalizations of infants/children with ASD designed to clarify the diverse vocal patterns in ASD as well as providing a basis, especially an automatic basis, for differentiating children with ASD from typically developing (TD) or language delayed (LD) infants and children. Methods: We use home movies, laboratory audio-video, and all-day audio recordings with a battery-powered, wearable recorder. The materials come from our own laboratories, and from collaborations with individuals at other universities and with the LRF, which maintains a database of 100,000 hours of all-day recordings. In many instances we observe recordings and code the vocalizations within an infraphonological framework. In other cases we use automated tools, some from the LRF, some developed by us or our collaborators. Results: Young ASD children showed high proportions of vocalizations with non-normal phonation. Some were high in pitch and some low. Variability of phonation then was the key to differentiation. The finding also suggested that vocalizations of the ASD children were less mature than those of TD children, because younger TD children also show high variability in phonation. A subsequent study with over 230 children at 8-48 months included over 20,000 hours of recording conducted in homes, and over 3 million automatically identified child utterances. Automated analysis showed that 12 acoustic parameters could differentiate ASD from TD with 86% accuracy, and could predict age in the TD group accounting for >50% of variance. Principal components analysis revealed that the primary factors predicting age and group classification were related to well-formed syllabification: production of syllables within a duration range found in mature speech, phonation as occurs in speech, well-timed, rapid transitions between consonant-like elements and vowel-like elements, and speech-like spectral entropy within syllables. We then confirmed that ASD children show late onset of well-formed syllables in a study of home movies with 9-12 month olds later diagnosed with ASD. In most recent results we are attempting to develop a workable clinical assessment based on the automated procedures, an approach that focuses on prediction of language development rather than age. Results suggest much better performance within TD, ASD and LD groups than in prior age-based modeling. Conclusions: Research is rapidly developing new perspectives on vocalization in ASD. Based on the results, we anticipate within the next decade that diagnostic vocal markers will become practical for infants within the first year. Disclosures: Nothing to Disclose.
Top of page 45.3 Modeling Social Communication Deficits in Mouse Models of Autism Maria Luisa Scattoni Istituto Superiore di Sanità, Rome, Italy Background: Autism Spectrum Disorder can include impaired abilities to express emotions or respond to the emotions of others. Speech provides a mechanism for expressing emotions, by both what words are spoken and by the melody or intonation of speech (prosody). Some aspects of autistic speech incorporate both features of the diagnosis: repetitive behaviors, deficits in the ability to express emotions and in communication. For instance, some children with autism repeat the use of certain sounds, syllables or words, more than typically developing children, or fail to use appropriate patterns of intonation to communicate. Prosodic features of mouse ultrasonic vocalizations (USVs), indicated by changes in frequency and amplitude, also convey social and emotional information. Dams retrieve pups that emit separation calls, females approach males emitting solicitous calls, and mice can become fearful of a cue associated with the vocalizations of a distressed conspecific. Because acoustic features of mouse USVs respond to drugs and genetic manipulations that influence reward circuits, USV analysis can be employed to examine how genes influence social motivation, affect regulation, and communication. This talk will focus primarily on a detailed spectrographic evaluation of ultrasonic vocalizations emitted during infant social isolation and dyadic interactions in inbred, outbred mice and three synapsin mutant lines. Methods: At postnatal days 2, 4, 6, 8 and 12, spontaneous movements and ultrasonic vocalizations were recorded (3-min) in response to social separation (from mother and siblings). At three months of age, male mice were socially isolated for one hour before the test and social behaviors and ultrasonic vocalizations were recorded (3-min-session) during an interaction between a male mouse and a female in estrous (C57BL/6J). Results: Each mouse strain emits distinct pattern of vocalizations associated with different levels of social investigation throughout lifespan. In the same social contexts, deficits in spontaneous behaviors and ultrasonic vocalizations measured during the first two postnatal weeks of age and at adulthood were detected in SynI, SynII mutant mice. By contrast, SynIII mice did not show deficits at either infancy or adulthood. Conclusions: Overall, motor and social communication deficits observed in SynI and Syn II mutant mice support the view that these genes are involved in the expression of autistic-like behavioral traits and identify these mutant lines as useful experimental models of ASD and epilepsy. These data support the role of vocalizations as a valuable tool for identifying alterations in several mouse models of human neurodevelopmental disorders, starting from those in which deficits in social communication are a primary core symptom e.g. autism spectrum disorders. Disclosures: Nothing to Disclose.
Top of page 45.4 Structure and Function of Neonatal Social Communication in a Genetic Mouse Model of Autism Noboru Hiroi Albert Einstein College of Medicine, Bronx, New York, United States Background: Babies with incipient autism spectrum disorder (ASD) and pups of genetic mouse models of ASD exhibit atypical vocalizations. However, the precise sequence structure of and functional impacts of such atypicalities on social communication between babies and mothers have not been isolated and determined. Methods: We used vocal call data from a genetic mouse model of ASD to test the hypothesis that call type sequences have functional impacts on maternal approach. Calls were recorded from Tbx1 heterozygous and wild-type littermates at postnatal fay (P) 8 or P12 during 5-min maternal separation. The sequence structure of vocal calls was analyzed by Shannon entropy analysis, Markov model, and Sparse Partial Least Square Discriminant Analysis (sPLS-DA). The functional impact of call sequences on maternal approach was examined by playing back wild-type, heterozygous and randomized wild-type calls to C57BL/6J mothers. Results: Tbx1 heterozygous pups emitted significantly fewer complicated call types, compared to wild-type pups at P8; vocal calls considerably declined thereafter for wild-type pups so that the two groups were indistinguishable for any call type by P12. Wild-type pups emitted longer complicated call types than heterozygous pups at P8. Wild-type pups exhibited decreased lengths of these calls by P12 so that the two genotypes no longer differed at that time. Wild-type and heterozygous pups did not differ in the pitch or peak amplitude of vocal calls. Shannon entropy analysis showed that pups non-randomly chose call types to emit two, three and four successive calls. A sequence structure of calls exists in normal mouse pups and Tbx1 heterozygous pups have a higher degree of non-random sequence. Markov modeling determined the predominant sequences of calls of wild-type and heterozygous pups. Wild-type pups more frequently connected complicated call types than heterozygous pups. In contrast, heterozygous pups more frequently formed connections among simple call types than wild-type pups. A Sparse Partial Least Square Discriminant Analysis (sPLS-DA) showed that wild-type pup call sequences were more individually variable along the two identified components, compared to call sequences of heterozygous pups. Finally, C57BL/6J mothers stayed longer in the tube from which wild-type calls were presented compared to that from which no call was presented; heterozygous calls did not induce such a preference. When a randomized wild-type sequence was presented, mothers did not show a preference for the sound tube compared to the no-sound tube. Conclusions: Our data suggest that an ASD risk gene has a negative impact on social communication with mothers due to atypical sequence structures of vocalizations during the neonatal period. Disclosures: Nothing to Disclose.
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46. Using Neural Connectivity Biomarkers in Major Depressive Disorder (MDD) to Identify Subtypes and Predict Treatment Response
Top of page 46.1 Abnormal Resting State Functional Connectivity as a Biomarker for Major Depressive Disorder (MDD) and Clinical Subtypes Roselinde Kaiser Harvard Medical School / McLean Hospital, Belmont, Massachusetts, United States Background: Major depressive disorder (MDD) is a chronic, serious psychiatric illness that has been linked to abnormal communication among distributed brain systems, as assessed via resting state functional connectivity (RSFC). However, differences between studies in methods and analytic approach have made it difficult to unify this research. In addition, heterogeneity in the presentation of MDD suggests the presence of clinical subtypes with distinct neurobiological profiles, which have rarely been targeted by previous RSFC studies. Unifying the evidence for abnormal RSFC in MDD through meta-analysis and extending this research to identify potential biomarkers of MDD subtypes may help to clarify the nature of depression and inform more precise delivery of treatment. Methods: First, a coordinate-based spatial meta-analysis was conducted of functional magnetic resonance imaging (fMRI) studies comparing seed-based RSFC of 556 individuals with MDD to 518 healthy controls. Second, in a new and independent sample, voxelwise RSFC of seed regions in the amygdala and nucleus accumbens (NACC) was compared between 103 individuals with MDD and 109 healthy controls. Third, in a subset of the above sample, potential biomarkers of the anhedonic subtype of depression were investigated by testing the association between anhedonic symptoms of depression and voxelwise RSFC of amygdala or NACC within the MDD group. Results: The meta-analysis revealed abnormal RSFC in MDD between frontoparietal and limbic brain systems. Results of empirical analyses comparing MDD with healthy controls were consistent with the meta-analysis, showing weakened RSFC between frontoparietal systems and both NACC and amygdala. Within the MDD group, increased severity of anhedonia predicted weakened RSFC between NACC and temporoparietal and insular regions, and increased RSFC between amygdala and medial prefrontal regions. Conclusions: Meta-analytic results and new empirical evidence both suggest that MDD is characterized by abnormal RSFC among brain systems involved in processing and regulating emotion. Critically, additional patterns of abnormal RSFC were detected as a function of anhedonia between brain regions implicated in processing reward and positive emotion and those involved in processing salience; or between regions implicated in processing fear and negative emotion and those involved in self-referential processing. Together, these results suggest that anhedonia may be distinguished by particular patterns of imbalanced RSFC, and RSFC may be a useful tool for identifying biomarkers of MDD subtypes. Disclosures: Nothing to Disclose.
Top of page 46.2 Cognitive Control Performance and Salience Network to Cognitive Control Hyperconnectivity Predict Depression Relapse in Early Adulthood Scott Langenecker University of Illinois at Chicago, Chicago, Illinois, United States Background: A practical gap exists in our understanding of major Depressive Disorder. While the neuroimaging, affective, and cognitive markers associated with acute state of illness are well known, and emerging work on prediction of treatment response is present, there is limited work that is directed toward understanding early course risk features using the neuroimaging milieu. There are significant advantages to determining and refining neuroimaging, performance, and psychosocial markers and features that are predictive of risk for illness recurrence. Identifying those at high risk is a way to direct limited resources toward secondary prevention that is aimed at reversing or mitigating these risk features. Methods: This is a two-site study of young adults between ages 18 and 23 who report 1-3 previous episodes of MDD and are currently remitted from MDD. Resting state functional connectivity and functional MRI during completion of a Parametric Go/No-go test were used to predict relapse of illness between the index assessment and one year follow-up, conducted with the Longitudinal Interview Follow-Up Evaluation (LIFE). Performance on the PGNG, activation during correct rejections (fMRI), and seed-based connectivity from the left amygdala, subgenual cingulate, and dorsolateral prefrontal cortex were used to evaluate differences at the baseline measurement that might predict risk for recurrence in the subsequent year. Recurrence was defined as experiencing a MDE episode (n = 19) and/or reinitiaton of treatment (n=2), and resilience was the absence of these (n = 29). 29 Healthy comparison (HC) with no emergence of illness were used for comparison/reference. Results: There were a number of significant predictors of relapse from baseline to the naturalistic follow-up point 1 year later. Reaction Time on the PGNG (with age) predicted 26% of the variance in relapse, (X = 9.34, p = .009). Decreased activation during correct rejections in the relapse group relative to both the HC and resilient groups were present in right inferior frontal gyrus (predicted 42% of variance, X = 14.33, p = .001). Increased connectivity from the left subgenual cingulate to bilateral anterior middle frontal gyrus (MFG) and left anterior nucleus (AntNuc) of the thalamus was higher in the relapse group relative to both the resilient and HC groups (F = 14.98, p = .000006) accounting for 71% of relapse status (X = 26.0, p = .00001, LMFG Wald = 5.16, p = .023, LAntNuc Wald = 1.78, p = .182, RMFG Wald = 3.87, p = .049; 84% prediction accuracy for resilient, 80% prediction accuracy for relapse). An omnibus model with all significant predictors resulted in two predictors, activation during rejections, and left subgenual cingulate to rMFG connectivity (X = 25.0, p = 0.000004, 73% R2, 100% prediction in both groups). Conclusions: Multimodal imaging and performance markers can enhance predictive capacity for longitudinal illness course in MDD. These techniques can aid in identifying higher risk groups and may lead to earlier and more targeted prevention trials in the area of secondary prevention. Secondary prevention strategies have the distinct advantage over primary prevention in that the risk ratio is 50% for recurrence. Identifying the high risk group can focus limited resources and can also define primary domains (cognitive control) and inter network relationships (salience network-cognitive control). Disclosures: Nothing to Disclose.
Top of page 46.3 Functional Connectivity Predictors of Response to Behavioral Activation Therapy for Depression Gabriel Dichter University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States Background: Despite the heterogeneous symptom presentation and complex etiology of Major Depressive Disorder (MDD), functional neuroimaging studies have shown with remarkable consistency that dysfunction in mesocorticolimbic brain systems are central to the disorder. Relatively less research has focused on the identification of biological markers of response to antidepressant treatment that would serve to improve the personalized delivery of empirically-supported antidepressant interventions. To this end, the purpose of the current study was to evaluate functional connectivity predictors of response to Behavioral Activation Therapy for Depression (BATD), an empirically validated psychotherapy modality designed to increase engagement with rewarding stimuli and reduce avoidance behaviors. Methods: Thirty-eight outpatients with MDD and twenty matched controls completed functional MRI scans after which the MDD group received an average of 12 sessions of BATD, and the average decline in BDI scores was 11, a statistically significant (p<.0001) and clinically meaningful response. The scan session included a resting-state scan (five minutes with eyes open) as well as task-based scans using the Monetary Incentive Delay (MID) task and a positive emotion regulation task. Heart rate and respiration were collected during scanning to regress out these sources of physiologic noise. Hierarchical linear modeling analyses were used to evaluate the predictive effects of pre-treatment functional connectivity on response to BATD measured by BDI scores collected every two weeks during treatment. Results: Resting-state connectivity revealed that response to treatment was predicted by pre-treatment connectivity of the right insula with the right middle temporal gyrus. Task-based connectivity using Psychophysiological Interaction Analyses (PPI) revealed that response to treatment was predicted by increased endurance of nucleus accumbens connectivity with a number of cortical regions during the MID task, whereas response to treatment was predicted by increased connectivity between the anterior insula with clusters in the thalamus and left caudate during the emotion regulation task. Conclusions: Findings highlight the critical role of mesocorticolimbic connectivity in predicting which patients with MDD respond to a given treatment modality. Future research will evaluate the capacity of these metrics to predict response to different antidepressant modalities to inform prospectively treatment decisions for individual patients with MDD. Additionally, future research will likely need to include genetic, epigenetic, or neuroendocrine markers to improve algorithms that predict patient-specific response to different antidepressant modalities. Disclosures: Nothing to Disclose.
Top of page 46.4 Differences in Resting State Functional Connectivity Between Patients with Treatment-Resistant Versus Treatment-Responsive Depression Paul Holtzheimer Dartmouth Medical School, Lebanon, New Hampshire, United States Background: Treatment-resistant depression (TRD) is a significant public health concern. The medial prefrontal cortex (BA10) has been implicated in the neurobiology of depression and antidepressant treatment response. We hypothesized that BA10 functional connectivity would differ between treatment-responsive (RESP) and TRD patients actively taking antidepressant medications. Methods: Resting state functional MRI (rs-fMRI) was performed in 22 TRD and 22 matched RESP patients, aged 22-70 years. All patients were taking adequate doses of at least one antidepressant medication and had no other clinically significant psychiatric or neurological comorbidities. The CONN toolbox and SPM12 were used to perform univariate, seed-to-voxel functional connectivity analyses. Results: Compared to the RESP group, TRD patients showed decreased functional connectivity of left BA10 with premotor, dorsal anterior cingulate, and dorsal frontal cortices (FDR 0.05). Secondary analyses identified additional differences in connectivity of the right dorsal anterior cingulate and right putamen between the groups. Conclusions: In TRD patients, despite adequately dosed antidepressant treatment, BA10 functional connectivity with several regions involved in the neurobiology of depression was weaker compared to connectivity in treatment responders. This may represent an imaging biomarker of TRD or an “uncorrected” abnormality in TRD patients. Either way, this difference may indicate a potential target for further treatment development (e.g., altering BA10 FC directly via focal brain stimulation). Disclosures: Part 1: St. Jude Medical Neuromodulation (consultant), Part 4: Cervel Neurotech; Otsuka Pharmaceuticals.
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47. Combining Imaging Modalities in Understanding and Treating Stress-related Disorders
Top of page 47.1 Disrupted Neural Synchrony During Social Interaction in Borderline Personality Disorder Edda Bilek University of Heidelberg, Mannheim, Germany Background: Recent developments in social neuroscience provided first linked neuroimaging data sets from subjects interacting live using a two-person fMRI environment (hyperscanning), which enables synchronized data acquisition and interaction-based fMRI tasks. While previous research mostly emulated social interaction (using photographs, recorded videos or computerized partners), these new data give insight into the coupling of two brains working together. Our work examining healthy subjects during cooperation revealed a coupling of specific neural systems, indicative of the flow of information between brains, that is unique to subjects interacting live, only present during the interaction, and based on right temporo-parietal junction (rTPJ) function of both subjects. We investigate this pair marker of neural coupling in a Borderline Personality Disorder (BPD) sample performing identical social-interactive tasks, since difficulties in social contexts, interaction, and associated emotions describe the core of BPD diagnosis. Methods: Subjects were examined in pairs either formed from one patient with BPD and one healthy subject, or from two healthy subjects. Pairs completed a cooperative Joint Attention task during hyperscanning, which allowed for simultaneous fMRI scan and task presentation, as well as live video streaming of task partner and interaction-based paradigms. Recently, we reported a data analysis routine fit to identify unique properties of truly interacting subjects, which is now applied to the current data set. The analysis included a group independent component analysis of fMRI data, followed by calculation of neural coupling indices as a measure cross-brain information flow within interacting pairs of subjects. True interaction is assessed by means of permutation-based tests of coupling indices against permutated data sets from non-interacting (i.e., sequentially scanned) data pairs. Finally, group differences are assessed. Results: Neural coupling differs significantly depending on health status, and is higher in healthy pairs than in the patient subsample (HC > BPD). Only healthy pairs exhibit increasing neural coupling through familiarity with a task partner, i.e. learn from experience. Coupling of non-interacting (sequentially scanned) individuals is the same across subsamples. Conclusions: Neural coupling represents a neural marker that is sensitive for health status in BPD even during basal social interaction. Pairs involving BPD exhibit considerably less synchronization of relevant brain systems than healthy pairs, indicating impaired flow of social information. This is not due to generally lower brain activation in this region or missing engagement in the task. While this study confirms prior conclusions regarding synchronization of interacting brains, and expands validation evidence to clinical subgroups, future studies need to investigate the causal status of the described indices. For example, stability and treatment factors are of high interest in BPD; similarly generalizability to other psychiatric disorders involving social impairment as well as validity in varying social-behavioral contexts need further focus in research. However, online second-person approaches such as fMRI hyperscanning are mandatory. Disclosures: Nothing to Disclose.
Top of page 47.2 Amygdala Neurofeedback Modulates Amygdala-VMPFC Connectivity in Healthy Participants and Borderline Patients Christian Schmahl Central Institute of Mental Health, Mannheim, Germany Background: Neurofeedback training by functional magnetic resonance (fMRI) signals has the potential of enabling voluntary control over brain processes and treating impaired brain circuits in a directed closed-loop intervention. Providing patients with neurofeedback from the amygdala might be a way to normalize affected prefrontal-limbic brain circuits in mental disorders of emotion dysregulation, such as borderline personality disorder (BPD). Methods: Healthy females (N = 32) were randomized in two age-matched groups with same group size and eight female BPD inpatients were recruited. Participants viewed aversive pictures while receiving fMRI. One group of healthy subjects and BPD patients received amygdala feedback, the second healthy group was provided with feedback from a control region. Healthy participants completed a single session and BPD patients participated in four sessions. Psychophysiological interaction (PPI) analysis was used to investigate functional connectivity. Subjects rated stimulus arousal after the session outside the MRI suite. Ratings on dissociation (DSS-4) and difficulties in emotion regulation (DERS) were collected from BPD patients on during each session. Results: Voluntary amygdala down-regulation by amygdala neurofeedback was associated with increased connectivity of the right amygdala to the ventromedial prefrontal cortex (vmPFC) in healthy subjects, as evidenced by a significant group interaction. Furthermore, BPD patients were able to alter functional amygdala-vmPFC connectivity towards the healthy pattern with repeated sessions. Consistent with a transfer of emotional information, picture-associated arousal was positively correlated with increases in amygdala-vmPFC connectivity. Neurofeedback training was associated with improvements in self-assessments of dissociation and emotional awareness in patients. Conclusions: These results show demonstrate that key neural networks of emotion regulation can be changed with amygdala neurofeedback down-regulation. This is initial evidence for a potential benefit of amygdala neurofeedback for the therapy of BPD patients. A randomized controlled trial study with BPD patients is needed. Disclosures: Nothing to Disclose.
Top of page 47.3 Real-time fMRI Emotion Regulation Training in PTSD: Altered Amygdala Activity and Connectivity as a Function of Depersonalization Ruth Lanius University of Western Ontario, London, Canada Background: Real time fMRI (rtfMRI) neurofeedback has increasingly been used as a noninvasive tool to better understand the neurobiological correlates of psychiatric disorders, as it allows for precisely localized brain regions to be self-regulated through signal feedback. Emerging evidence points towards unique amygdala activity and resting state functional connectivity among dissociative subtype and non-dissociative PTSD patients. The objective of the present study was to examine amygdala activity an amygdala-medial prefrontal cortex connectivity during real-time fMRI emotion regulation training in PTSD patients with various levels of dissociative (depersonalization/derealization) symptomatology. Methods: BOLD signal from the amygdala was displayed to PTSD patients (n=10) while viewing words associated with their past traumatic experiences. Participants were asked to regulate their emotional state by decreasing their amygdala activity. Functional scans were acquired, and regions-of-interest (ROIs) processed in real-time via Turbo-Brain Voyager. Brain activity was then relayed back to the participant in the scanner as a simple thermometer during three runs. Subsequently, patients were asked to regulate their amygdala activity in the absence of neurofeedback during a transfer run. Patients’ ability to self-regulate was also evaluated as a function of state dissociation, as previous evidence has suggested that amygdala activity would be attenuated and amygdala-medial prefrontal cortex connectivity would be altered in the trials in which state dissociation occurs. Results: Within PTSD patients, we observed initial increased amygdala activation in response to the trauma-related words, when conducting offline analyses. Over trials of rtfMRI emotion regulation training, we found decreased amygdala activation, which was sustained during the transfer run. Critically, correlational analyses revealed a significant relationship between self-reported state dissociation and activity in the amygdala, within dissociative subtype PTSD patients. Moreover, altered amygdala connectivity patterns and emotion regulation capacities as a function of dissociative symptomatology were observed. Conclusions: This study has the potential to develop promising non-invasive treatments for different PTSD phenotypes. Disclosures: Nothing to Disclose.
Top of page 47.4 Identification of a Causal Pathway for Amygdala Control in Humans and Abnormalities in PTSD Amit Etkin Stanford University, Stanford, California, United States Background: Anatomical tracing in non-human primates has revealed largely uni-directional pathway from the ventrolateral PFC (vlPFC) to amygdala. These areas often co-activate in human neuroimaging studies of emotion regulation but, to date, no causal evidence of communication between these brain areas has been established in humans. Thus, we do not know whether and how the vlPFC and amygdala causally interact. Methods: To determine the directional causal influence of vlPFC activation on the amygdala and to investigate possible abnormalities in this pathway in PTSD, we stimulated the right vlPFC (or a control site in the superior frontal gyrus; SFG) first in healthy participants (N=24) and then in patients with PTSD (N=22, DSM-IV-TR, CAPS). Stimuli were delivered as single transcranial magnetic stimulation pulses (spTMS) using MRI-based neuronavigation, concurrent with interleaved acquisition of fMRI BOLD. Results: Among healthy participants, vlPFC stimulation resulted in deactivation (ie inhibition) of the right amygdala (FWE p<.05), while stimulation of the SFG did not affect amygdala activity. Similarly, vlPFC stimulation resulted in greater amygdala inhibition in healthy participants than patients with PTSD (FWE p<.05 for group and group x stimulation site interaction). We found no evidence that vlPFC stimulation resulted in medial prefrontal activation, suggesting that amygdala inhibition occurred through a direct vlPFC-amygdala pathway. The vlPFC and amygdala were also disconnected in patients during a resting-state scan, relative to healthy participants. Patients' failure to inhibit the amygdala correlated as well with PTSD severity, with a greater failure in the most severe patients. Finally, failure in patients of vlPFC stimulation to inhibit the amygdala correlated with their failure to do so in a reappraisal-based emotion regulation task in the absence of stimulation. Conclusions: We provide the first evidence for a causal and inhibitory pathway for amygdala control in humans, and demonstrate its disruption in PTSD -- disruption that correlates with both their clinical severity and deficits in emotion regulation. These data have implications for understanding normal mechanisms in the human brain by which amygdala activity is regulated and identify an important, and never previously examined, brain pathway for potential treatment of emotion regulatory abnormalities in PTSD. Disclosures: Nothing to Disclose.
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48. Genomes and Cells: New Models for Target Discovery and Validation
Top of page 48.1 Probing Neural Phenotype in Macrocephalic Autism Maria Marchetto Salk Institute for Biological Studies, La Jolla, California, United States Background: Autism spectrum disorders (ASD) comprise a group of complex neurodevelopmental disorders that affect more than 1% of children in the United States. ASD is characterized by impaired social interaction and limited and repetitive interests and behavior at its core. Family history and twin studies suggest that, at least in some cases, these disorders share genetic roots (Piven et al., 1997; Ronald et al., 2006). Mounting evidence proposes that heritable and de novo genetic variation plays a significant role, but these studies also demonstrate striking genetic heterogeneity (Garber, 2007; Marchetto et al., 2010; Sanders et al., 2012). Neuropathological imaging and gene expression studies of postmortem brains from ASD patients have revealed disruption of developmental and proliferation gene networks (Chow et al., 2012; Voineagu et al., 2011). One relevant observation in ASD pathophysiology has been the occurrence of macrocephaly and altered growth trajectory with early overgrowth and later normalization in a subset of affected individuals. (Courchesne et al., 2011a; Courchesne et al., 2003; Courchesne et al., 2001; Courchesne et al., 2005; Hazlett et al., 2011; Shen et al., 2013). The major impediment to testing ASD hypotheses is the lack of relevant animal and cell models. Methods: We reprogrammed fibroblasts to generate induced pluripotent stem cells (iPSCs), neural progenitor cells (NPCs) and neurons from 8 ASD Individuals with early brain overgrowth and 5 non-ASD gender and age-matched controls with normal brain size. Results: ASD-derived NPCs display increased cell proliferation due to dysregulation of a β-catenin/BRN2 transcriptional cascade. ASD-derived neurons display premature differentiation, reduced synaptogenesis and altered levels of excitatory and inhibitory neurotransmitters, leading to functional defects in neuronal networks. RNA expression analysis revealed that ASD-derived NPCs displayed significant enrichment for genes involved in brain development, whereas ASD-derived neurons displayed up- and down-regulation of genes related to extracellular matrix and cilium/axoneme, consistent with the observed synaptic dysregulation. Conclusions: This work demonstrates that, in heterogeneous conditions such as ASD, the selection of subjects based on endophenotypes improves the power to detect biologically relevant pathway disruption that may help the development of novel therapies. Disclosures: Nothing to Disclose.
Top of page 48.2 Using IPSC Models to Identify Cellular Phenotypes Associated with Autism and Schizophrenia Ricardo Dolmetsch Novartis Institutes for Biomedical Research, Cambridge, Massachusetts, United States Background: Human neurons derived from Induced Pluripotent Stem Cells (IPSCs), can provide important clues about the underlying cellular and molecular basis of complex psychiatric disorders like autism and schizophrenia. IPSCs can be developed from patients with penetrant mutations that lead to syndromes that include autism and schizophrenia. Cells can also be developed from patients with less penetrant mutations that are associated with idiopathic disease though these are presently difficult to analyze. In addition, IPSCs can be engineered to express mutant alleles that are associated with disease. These tools are helping us identify cellular and molecular phenotypes associated with psychiatric disease. Methods: We have developed automated methods of generating a neurons from iPSCs to model human neuropathologies in vitro. Our industrial approach is allowing us to generate cells from many patients in parallel with the quality and reliability that is required to identify new drug targets and develop new drugs. We have automated the process of making a subset of neurons and brain organoids. Results: We have identified both biochemical and molecular phenotypes associated with monogenic forms of autism like Timothy Syndrome, Phelan-McDermid Syndrome and 22q11 deletion syndrome. We are using these phenotypes to identify new drug targets as well as to screen for new drugs and have identified some candidate molecules that may be helpful for developing future treatments. We have also embarked on a project to study gene expression and identify phenotypes associated with less penetrant disease risk alleles. Conclusions: IPSC-derived neurons are an important new tool for identifying cellular phenotypes. They can be useful for identifying cellular phenotypes that may provide insights into the underlying basis of psychiatric diseases. We have improved many of the methods for making and analyzing iPSC derived neurons making them a more reliable method for identifying new targets and developing new drugs. However there are still many limitations associated with IPSC based drug discovery including the slow maturation of the cells, the difficulty of identifying cellular phenotypes that are important clinically and the lack of reliability of the assays. Disclosures: Part 1: Novartis Institutes for Biomedical Research, Part 5: Novartis.
Top of page 48.3 Ectopic Expression of Peripheral Ion Channel Genes in the Central Nervous System Underlies an Autism Spectrum Disorder Brady Maher Lieber Institute for Brain Development, Baltimore, Maryland, United States Background: Genome-wide association studies (GWAS) have identified a number of loci associated with risk for SZ and several of these risk variants are located within introns of Transcription Factor 4 (TCF4; E2-2, ITF2). In addition, autosomal dominant mutations in TCF4 result in Pitt-Hopkins Syndrome (PTHS), a rare neurodevelopmental disorder characterized by a spectrum of symptoms including hyperventilation, seizures, autistic behaviors, and intellectual disability. Currently, the molecular mechanisms and underlying pathophysiology responsible for these two disorders are not understood. Our goal is identify and validate therapeutic targets identified by modeling PTHS in a cell-autonomous rodent model. Methods: To model PTHS we altered the in utero expression of TCF4 by transfecting neuroprogenitor cells that give rise to layer 2/3 pyramidal cells in the rat medial prefrontal cortex by in utero electroporation (IUE). We knockdown TCF4 expression using shRNA and Crispr/Cas9 constructs that target independent sequences within the TCF4 transcript or gene, respectively. Resulting physiological phenotypes were assayed using whole-cell electrophysiology. A novel molecular profiling technique that combines IUE with translating ribosome affinity purification (iTRAP) was used to identify candidate ion channels underlying cellular phenotypes. Molecular phenocopy and pharmacological rescue were used to validate candidate target genes. Results: Knockdown of TCF4 produced a severe and consistent reduction of action potential (AP) output (p<0.0001) and an increase in the resting membrane potential (p<0.0001) compared to control cells. Crispr/Cas9 mutation of TCF4 resulted in a similar deficit in AP output compared to cells expressing an empty Crispr/Cas9 vector (p<0.0016). The decrease in AP output was attributed to a significant increase in the afterhyperpolarization (AHP, p<0.0003). Using iTRAP, ribosomes from transfected layer 2/3 neurons were affinity purified and the associated RNA was processed for expression analysis on prefabricated 384-well plates that contained primers for all known ion channels in the rat genome. Knockdown of TCF4 resulted in a significant increase (>2-fold) in the expression of KCNQ1 (p<0.005) and SCN10a (p<0.01) compared to control transfected cells. Application of antagonists to KCNQ1 (UCL2077 p=0.0002; JNJ303 p=0.0084) or SCN10a (A-803367; p<0.04) significantly rescued AP output in TCF4 knockdown cells but had no effect on control cell firing. Furthermore, molecular phenocopy of reduced AP output and increased RMP was observed when recombinant SCN10a was expressed in control cells (p<0.0006). Conclusions: Our results describe a novel approach to model psychiatric risk at the cellular level. We model an autism spectrum disorder in cortical neurons and identify physiological phenotypes associated with deficits of intrinsic excitability. Using a novel molecular profiling technique (iTRAP) we identify two candidate genes that are associated with the observed phenotypes. These target genes were validated using pharmacological rescue and molecular phenocopy. We propose that ectopic expression of peripheral ion channel genes in the central nervous system may underlie cognitive deficits observed PTHS patients. Disclosures: Nothing to Disclose.
Top of page 48.4 Modeling Major Mental Disorders Using Patient-derived iPSC and Humanized Mouse Models Hongjun Song John Hopkins University School of Medicine, Baltimore, Maryland, United States Background: Psychiatric disorders, such as schizophrenia, are disabling brain disorders and development of rational therapeutics based on knowledge of the etiology and pathogenesis is critically needed. Patient-derived induced pluripotent stem cell (iPSC) has been proposed as a promising model for understanding disease mechanism and for drug discovery. However, there are major gaps in our knowledge on whether disease modeling and drug testing using iPSC-derived developing immature cell types in dish would provide predictive validity for in vivo pathophysiology and drug efficacy in adulthood. Methods: We used iPSCs derived from psychiatric patients with a mutation in Disrupted-in-Schizophrenia 1 (DISC1) as an example for mechanism-based drug discovery to correct pathophysiology-relevant cellular phenotypes in vitro, followed with in vivo testing using a humanized animal model carrying the same mutation in adulthood. Results: Our previous study using isogenic iPSC lines has revealed that mutant DISC1 causes defects in the presynaptic synaptic function and gene expression. We found that multiple phosphodiesterases (PDEs) were elevated in forebrain neurons with the DISC1 mutation, and rolipram, a PDE4 inhibitor, rescued the presynaptic deficit of mutant neurons with little effect on isogenic normal neurons. Similar to iPSC-derived developing cortical neurons in vitro, adult DISC1-KI mice exhibit aberrant gene expression, including elevated expression of some PDEs, in both cortex and hippocampus, as well as increased pair-pulse facilitation, indicating reduced presynaptic release probability. Furthermore, DISC1-KI mice exhibited behavioral deficits, some of which can be rescued by rolipram treatment. Conclusions: Our study provides a proof-of-principle example for drug discovery-in-dish with predictive validity for efficacy in the animal model at the adult stage and has significant implications for application of patient-derived iPSCs for personalized medicine. Disclosures: Nothing to Disclose.
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49. Studies of Stress Identify Novel Signal Transduction and Epigenetic Antidepressant Targets
Top of page 49.1 REDD1 / mTORC1 / S6K1 Signaling and Synapse Formation in the Pathophysiology and Treatment of Depression Ronald Duman Yale University School of Medicine, New Haven, Connecticut, United States Background: Major Depressive Disorder (MDD) affects nearly one fifth of the population and is the second leading cause of disability worldwide. Although the precise molecular mechanisms underlying MDD remain largely unknown, our lab has recently demonstrated an important role for the mechanistic target of rapamycin complex 1 (mTORC1)/S6 Kinase 1 pathway in mediating stress-related behavior and rapid antidepressant responses. The mTORC1/S6K1 pathway is a critical regulator of protein synthesis, cell growth and cytoskeletal rearrangement, and inhibition of this pathway could contribute to the atrophy of neurons seen in cortical and limbic structures in depressed patients and in rodent stress models. Our recent studies have extended this work in two important areas. Methods: We use a combination of molecular, cellular and behavioral approaches to examine the role of REDD1 and S6K1 in the regulation of mTORC1 and antidepressant synaptic and behavioral responses. Results: First, we have identified an up-stream negative regulator of mTORC1, referred to as REDD1 (regulated in development and DNA damage responses 1) that is induced by chronic stress and is increased in postmortem dlPFC of depressed subjects. Viral expression of REDD1 in the mPFC is sufficient to cause atrophy of neurons and depressive behaviors in rodent models. Conversely, mice with a deletion of REDD1 display a resilient phenotype in that chronic stress exposure does not cause atrophy of pyramidal neurons in the mPFC or anhedonic behaviors. Second we have investigated whether direct modulation of a key downstream element of the mTORC1 pathway, S6K1 is sufficient to control depressive behavior. S6K1 is decreased in postmortem PFC of depressed subjects and we have found that chronic stress decreases the phosphorylated and active form of S6K1 in the mPFC. Importantly, we show that infusion of a constitutively active S6K1 in the mPFC produces an antidepressant response, while infusion with a kinase-inactive S6K1 form demonstrated results in pro-depressive behavior. We have also found expression of S6K1 in primary cortical cultures increases neuronal complexity. Together, these data suggest that up-regulation of REDD1 in response to stress or aberrant protein synthesis through S6K1 contributes to the pathology of MDD. Conclusions: The results also raise the possibility of developing drugs that inhibit REDD1 or that active mTORC1-S6K1 signaling as novel therapeutic targets for the treatment of depression. Disclosures: Nothing to Disclose.
Top of page 49.2 RGS4 Plays a Key Role in the Efficacy of Classical and Fast-Acting Antidepressants Venetia Zachariou Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: Most major depression patients undergo treatment with monoamine targeting antidepressant drugs. As 30-40% of treated patients fail to show remission, there is a great need for development of more efficacious medications. Understanding the cellular adaptations induced by chronic stress may provide important information for the development of new drug targets or adjunct medications. Recent research efforts have been directed towards the development of fast acting antidepressants (ketamine-like drugs) that target glutamatergic transmission. We recently demonstrated that the GPCR modulator RGS4 plays a key role in adaptations to stress and antidepressant drug efficacy. RGS4 controls the function of monoamine, opiate and other GPCRs via interactions with Galpha subunits, and it is expressed in several brain regions involved in mood, motivation and cognition. Using conditional knockout models, or viral mediated gene transfer, we manipulated RGS4 expression in the Nucleus Accumbens (NAc) and in the medial prefrontal cortex (mPFC) and demonstrated that in the NAc, RGS4 acts as a positive modulator of monoamine-directed antidepressants. Interestingly, in the mPFC, RGS4 acts a negative modulator of the actions of the NMDA receptor antagonist ketamine. We also investigated the key protein interactions and signal transduction events underlying these phenotypes. Methods: Advanced genetic mouse models for brain region specific manipulations of RGS4 activity in the NAc and mPFC have been used along with the chronic unpredictable stress paradigm. For targeted RGS4 overexpression, we generated Adenoassociated Viruses (AAV) expressing RGS4. To knockdown RGS4 in the NAc and mPFC we used a line of floxed RGS4 mice, and stereotaxically infused AAV-Cre and AAV-CamkII-Cre (or AAV-EGFP) vectors in the targeted region. qPCR and western blot analysis have been used to monitor RGS4 expression following chronic stress or drug treatment. Finally, protein interactions in the mPFC were monitored using co-immunoprecipitation assays. Results: RGS4 in the NAc plays a potent positive modulatory role in the actions of TCAs, SSRIs and SNRIs, and promoting RGS4 activity in this brain region improves antidepressant efficacy. On the other hand, RGS4 in the mPFC acts as a negative modulator of ketamine actions. Our work also reveals that adaptations in RGS4 expression in the mPFC (but not in the NAc) modulate responses to chronic stress. Using western blot analysis and co-immunoprecipitation assays we show that RGS4 is dynamically regulated in the mPFC by chronic unpredictable stress, whereas this molecule is also playing a negative modulatory role in the antidepressant effects of ketamine by forming complexes with components of the mTOR pathway as well as with metabotropic glutamate receptors. Conclusions: The study demonstrates that the signal transduction modulator RGS4 plays a potent role in chronic stress vulnerability and modulates the actions of monoamine and fast acting antidepressants via distinct mechanisms. Interventions in the activity of RGS4 complexes may provide a new pharmacological target for the treatment of depression. Disclosures: Nothing to Disclose.
Top of page 49.3 Cell Type-Specific Epigenetic Reprogramming of the Fosb Gene Controls Depression-Related Behaviors Elizabeth Heller Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: Genome-wide histone posttranslational modifications have been shown to underlie the pathophysiology of stress exposure, leading to the characterization of many highly relevant genes. We have found that Fosb gene expression is repressed in the nucleus accumbens of depressed human subjects and that this repression is associated with increased histone methylation at the Fosb promoter. To test the hypothesis that increased Fosb methylation is a causal mechanism underlying depression, it is necessary to manipulate the epigenome solely at this locus. While stress represses deltaFosB protein in total NAc, recent findings have demonstrated an increase in deltaFosB expression in the Drd2-expressing medium spiny neuron subtype following chronic social defeat stress. We found that this cell-type and locus-specific epigenetic manipulation of FosB expression is sufficient to regulate depressive behaviors. The role of engineered transcription factors are a novel tool to study the function of epigenetic reprogramming at a single gene in a single brain region in vivo, for the study of neuropsychiatric disease and beyond. Methods: We have targeted the Fosb gene promoter in NAc using a HSV-mediated expression engineered zinc-finger protein (ZFP) fused to the transcriptional activator, p65, which promotes histone acetylation or the transcriptional repressor, G9a, a histone methyltransferase. qRT-PCR and immunohistochemistry were used to measure Fosb expression. Quantitative chromatin immunoprecipitation (qChIP) was used to measure the chromatin modifications. To achieve cell-type specific expression, we generated Cre-depended HSV constructs into the NAc of transgenic mice expressing Cre recobinase under control of either the Drd1- or Drd2- promoter, which specify each of the two medium spiny neuron cell types. For behavioral studies, mice were subject to social defeat stress following NAc infection with the HSV-ZFP constructs. Results: FosB-ZFP-p65 efficiently and robustly activate FosB/ΔFosB expression in NAc neurons, while FosB-ZFP-G9a represses expression. HSV-G9a deposits H3K9me2 specifically at the FosB gene in vivo, while FosB-ZFP-p65 activates FosB via H3K9/14 acetylation. In addition, we found epigenetic remodeling at the FosB promoter, including enrichment of histone protein 1a and depletion of H3K9me3. Repression of Fosb in total NAc by Fosb-ZFP-G9a sensitizes animals to subthreshold defeat stress, as does activation of Fosb expression by Cre-dependent Fosb-ZFP-p65 in Drd1+ NAc medium spiny neurons. Conclusions: Using engineered transcription factors, we have identified a direct molecular mechanism for stress-mediated repression of the Fosb gene, and have efficiently manipulated behavioral responses to social defeat stress. This approach allows a functional analysis of chromatin modifications that underlie affective disorders. Disclosures: Nothing to Disclose.
Top of page 49.4 Maternal Stress Epigenetic Programming Through Maternal and Fetal Exosomes Tracy Bale University of Pennsylvania, Philadelphia, Pennsylvania, United States Background: Perturbations during gestation, including maternal stress, are associated with an increased risk for neurodevelopmental disorders. Therefore, understanding the mechanisms by which stress affects the maternal and fetal milieu is important for identifying factors involved in dysregulation of neurodevelopment. In our well-established mouse model, male offspring exposed to early prenatal stress (EPS) have altered HPA axis programming and increased behavioral stress sensitivity, similar to endophenotypes identified in autism and schizophrenia. Previously, we established in this model that gene sets important for endo- and exosomal cellular processes were significantly down-regulated in male placentas in response to EPS, suggesting that stress was imparting a programming effect on maternal and fetal exosome signaling. Exosomes are small lipid vesicles secreted locally and into the circulation by most tissues, and through the transfer of proteins, microRNAs (miRNAs), and other signaling factors between cells and tissues, are able to communicate unique information regarding the environment. Importantly, exosomes can cross the blood-brain barrier to impact neural gene expression, and potentially alter brain development. Less is known regarding their ability to cross the maternal:fetal barrier and directly impact fetal development. Methods: To examine the impact of EPS on exosome signaling, maternal and fetal serum and tissue samples are collected on embryonic day 18.5 from control and stressed pregnant dams. Exosomes are first isolated from the serum samples, and then protein and RNA are extracted for further proteomics and small RNA-Seq analyses. Bioinformatics analyses will determine the impact of stress on total exosome production, and exosomal protein and miRNA content. Comparisons between maternal and fetal tissues and the exosomal content will identify stress effects on exosome secretion and the target tissues involved. Results: In these studies, we have found that maternal stress during the first week of pregnancy produced lasting and significant effects on exosome signaling, as well as intriguing sex differences in the overall exosomal production in fetal and neonate circulation. Our proteomics data suggest that stress induces long-term changes in exosome production and cargo from a variety of maternal sources, including maternal immune cells and the placenta. Conclusions: These studies provide exciting insights into a novel mechanism by which cellular communication from maternal and fetal tissues can carry information regarding dynamic changes in the environment. Exosomal cargo, proteins and miRNAs, are especially important in this signaling, and maternal stress can impart significant and lasting changes in exosomal production that may directly be altering the course of neurodevelopment. Understanding placental and maternal serum exosomal changes with stress can be developed as a potential biomarker of perturbations during pregnancy related to neurodevelopmental disease risk. Disclosures: Nothing to Disclose.
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50. Orphan GPCRs and Psychiatric Disorders
Top of page 50.1 Orphan GPCRs in Psychiatry Olivier Civelli University of California at Irvine, Irvine, California, United States Background: The GPCRs bind all the known neurotransmitters, neuropeptides and peptide hormones and are the omnipresent modulators of brain function. Many bind ligands that have not been thus far described. These are the orphan GPCRs. We will present our results on the deorphanization of the melanin-concentrating hormone (MCH) receptor. MCH is a neuropeptide that is mainly produced in the lateral hypothalamus. Its receptor is highly expressed along the mesocorticolimbic dopamine pathway. The MCH receptor is present in the circuitry in which dopamine system overactivity is thought to lead to schizophrenia. We examined whether the MCH system activity modulates the prepulse inhibition (PPI) of the startle reflex, directly or when disrupted by dopamine-related drugs, which serves as an animal model that is relevant to schizophrenia symptoms. Methods: Startle reactivity was measured using startle chambers. One week before drug testing, animals underwent a brief baseline session to create matched treatment groups. PPI session consisted of startle, prepulse and no-stimulus trials and these were presented in a pseudorandom order. The amount of PPI was calculated as a percentage score for each acoustic prepulse trial type: % PPI= 100-{[(startle response for prepulse+pulse)/(startle response for pulse-alone)]x100}. Results: Regarding the prepulse inhibition (PPI) of startle, we found that there is no significant effect of central MCH injection on either startle or PPI level, although there was significant main effect of prepulse intensity on PPI. Because the mixed D1/D2 agonist apomorphine is known to disrupt PPI, we then tested whether MCH could affect apomorphine-induced PPI disruption and found that MCH dose dependently increased PPI deficit upon low doses of apomorphine. In contrast, central MCH injection did not affect stereotyped behaviors. We then used an animal model of schizophrenia, apomorphine-susceptible (APO-SUS) and apomorphine-unsceptible (APO-UNSUS) rats to test whether modulating the MCH system activity affects PPI and stereotyped behaviors. Conclusions: We found that the MCH system can modulate dopamine-related responses. In sensorimotor gating, MCH is able to increases the disruptions induced by low doses of apomorphine. Because the MCH1R is expressed at a very low level in the striatum, these data position the MCH system as a unique target for therapies directed at modulating the dopamine tone selectively in the nucleus accumbens. Disclosures: Nothing to Disclose.
Top of page 50.2 An Orphan GPCR Highly Enriched in the Medial Habenula and Lateral Septum Detects L-Tryptophan and L-Phenylalanine and May Represent a Novel Sensor that Modulates Behavior Timothy Lovenberg Janssen Pharmaceutical R&D, LLC, San Diego, California, United States Background: L-Tryptophan (TRP) and L-phenylalanine (PHE) are essential amino acids required for protein synthesis as well as biogenic amine neurotransmitter synthesis. In susceptible humans and some animal models, reduced TRP and PHE intake has been shown to be depressogenic, whereas anecdotal reports of TRP and PHE loading are reported to be mood elevating. The effects of altered TRP and PHE levels on behavior has been hypothesized to be mediated by downstream conversion to serotonin or dopamine. GPR139 is a highly conserved orphan G-Protein Coupled Receptor that is expressed in the Medial Habenula and Lateral Septum. The Medial Habenula is a relatively understudied but conserved region in the brain implicated as a key part of the limbic circuits that may mediate mood and stress. Methods: HEK293 cells transfected with GPR139 were subjected to various orphan ligands and tissue extracts and the effects on GTPgS activity was measured. In situ hybridization of GPR139 antisense riboprobes and immunohistochemistry of anti-GPR139 antibodies were evaluated on rat and mouse brain sections. Rats implanted with EEG electrodes were injected with GPR139 agonists and monitored for behavior and sleep EEG parameters. A high throughput screen was run to identify lead agonists and antagonists and these compounds were optimized for potency and drug-like properties. Results: Random screening of amino acids, orphan ligands, and tissue extracts revealed that, compared to untransfected cells, HEK293 cells transfected with GPR139 responded only to TRP and PHE. Neither serotonin nor dopamine nor any other known neurotransmitters had any effect on GPR139-transfected cells. Chromatographed extracts of rat brain, rat plasma, and human plasma revealed two peaks of activity which corresponded to the elution peaks of TRP and PHE. A selective small molecule agonist (JNJ-63533054) with low nM affinity and potency, when radiolabelled, bound to GPR139-transfected cells and showed specific displacement by TRP and PHE. mRNA for GPR139 was mapped to habenula and lateral septum. Anti-GPR139 antibodies detected reactivity in medial habenula and lateral septum. Animals injected with GPR139 agonists exhibited decreased locomotor activity and increased sleep. Conclusions: Using multiple biochemical and cell-based assays we demonstrated that the two essential amino acids, L-tryptophan and L-phenylalanine activate a G protein coupled receptor GPR139 with an EC50 in the 20-200 uM range, consistent with the physiological concentrations of TRP and PHE in human blood. Our findings suggest that TRP and PHE are likely physiological ligands for GPR139 and might explain the biological and behavioral effects of these substances without relying on their conversion to biogenic amines. It is tempting to speculate that the brain has system to detect levels of these essential amino acids and that changes in the availability of these amino acids may elicit behavioral responses. GPR139 could respond to dynamic changes of TRP and PHE under physiological conditions and thus represent a potential new drug target for CNS diseases. Disclosures: Part 1: I am an employee of a pharmaceutical company, Part 5: Janssen Pharmaceutical R&D. LLC.
Top of page 50.3 GPR88: An Orphan GPCR for the Potential Treatment of CNS Disorders Carolyn Dzierba Bristol-Myers Squibb Company, Wallingford, Connecticut, United States Background: GPR88 is an orphan G-protein coupled receptor (GPCR) of the rhodopsin family, expressed in striatum, caudate putamen, nucleus accumbens and olfactory tubercle. Its CNS expression is particularly robust in striatum, paralleling that of the dopamine D2 receptor, suggesting the receptor may play a role in regulating dopaminergic activity. GPR88 knock-out (KO) animals display increased locomotor activity in response to treatment with dopaminergic compounds, demonstrating a role for GPR88 in dopaminergic signaling. Additional studies with GPR88 knock-out mice showed increased glutamatergic excitation and reduced GABAergic inhibition in medium spiny neurons, thereby enhancing neuronal firing rates in vivo and resulting in hyperactivity, poor motor coordination and impaired cue-based learning. In addition, transcriptional profiling studies have revealed that GPR88 expression is altered in a number of CNS related diseases, providing additional evidence that GPR88 is an essential modulator of CNS signaling pathways related to psychiatric disease. Methods: To develop an understanding of the in vivo phenotype, GPR88 knock-out mice were generated and examined in a battery of in vivo tests. Localization studies were carried out to determine the expression pattern of GPR88 in the CNS. Additionally, small molecule agonists of GPR88 identified from a high throughput screening campaign were characterized in vitro. Results: The GPR88 KO mice were shown to potentiate the locomotor effects of the dopamine D2 agonist quinpirole. Additionally, GPR88 KO mice were shown to have impaired prepulse inhibition (PPI) as well as enhanced quinpirole sensitivity in the PPI model, suggesting that GPR88 is a negative regulator of dopaminergic (D2 receptor) signaling. GPR88 mRNA was found to be most abundantly expressed in the nervous system and prominently expressed in striatum paralleling that of Dopamine D2. Finally, a series of small molecule agonists of GPR88 were identified and shown to have excellent potency in a cAMP assay as well as in a GTP□S binding assay. The compounds were examined in GRP88 KO and wild type (WT) tissue showing the activity to be GPR88 dependent. Conclusions: Our preclinical findings with the GPR88 KO mouse phenotype and CNS tissue distribution add further evidence to support the hypothesis that modulators of GPR88 activity may have the potential to treat CNS related diseases. Disclosures: Nothing to Disclose.
Top of page 50.4 Neural Functions of SREB - The Most Evolutionarily Conserved G-Protein Coupled Receptor Family Associated with Psychiatric Disorders Mickey Matsumoto Astellas Phrama Inc., Tsukuba, Japan Background: The SREB (Super-conserved Receptor Expressed in Brain) family of SREB1/GPR27, SREB2/GPR85 and SREB3/GPR173 is a unique subfamily of G protein-coupled receptor (GPCR) expressed in the CNS. SREB2 is virtually the most conserved GPCR in vertebrate evolution, i.e. the primary amino acid sequence is 100% identical between humans and rodents. Conservation rates of SREB1 (97%) and SREB3 (99%) are also very high and equivalent to glutamate and GABA receptors, suggesting the existence of undiscovered fundamental neural systems involving SREB family members. Human genetic studies have indicated a possible link between SREB2 and schizophrenia and autism spectrum disorder. Studies using SREB2 transgenic (over-expression) and knockout (KO) mice revealed that SREB2 is implicated in determining brain size and regulating hippocampal adult neurogenesis and its related cognitive functions. Although the highest conservation rate of SREB2 indicates its critical roles in the CNS, clear-cut neural functions of SREB2 have not been revealed yet by studies of single SREB2 KO mice presumably due to compensational mechanisms involving SREB1 and SREB3. Methods: To investigate neuronal functions of SREB family, we have generated all single SREB gene knockout mice (SREB1 KO, SREB2 KO and SREB3 KO mice) and double SREB genes knockout mice by intercrossing of single SREB KO lines. To avoid compensational mechanisms and elucidate clear-cut neural functions of SREB family, triple knockdown/knockout of all SREB genes in neurons has been attempted. We have applied RNAi approach to knockdown the third SREB gene expression in neurons established from double SREB genes KO mice. Results: SREB2 transgenic (over-expression) mice showed 20% brain weight reduction compared to wild-type littermates (WT). Reciprocally, increased brain weight (~ 15%) was observed in SREB2 KO mice. Single SREB1 KO mice (~ 10%) and SREB3 KO mice (~ 5%) showed a significant brain weight increase compared to WT. In addition, macroscopic analysis using Nissl staining in coronal brain section of single SREB1 and SREB3 KO mice demonstrated no gross structural abnormalities in laminar formation of cerebral cortices or position of major brain nuclei, which is consistent with previous data from single SREB2 KO mice. By intercrossing of single SREB1 KO and SREB2 KO lines, SREB1/2 double KO mice have been generated and turned out to be viable. Primary cultured neurons established from SREB1/2 double KO mice were treated with SREB3 shRNA. RT-qPCR assays confirmed null mutation of SREB1 and SREB2 genes and knockdown of SREB3 gene expression in the cultured neurons. Conclusions: Single SREB1 KO and SREB3 KO mice showed similar brain phenotypes with single SREB2 KO mice. Our results indicate that SREB family members presumably share the same downstream pathway to regulate brain development and function. Molecular analyses of neurons with triple knockdown/knockout of all SREB members will reveal clear-cut neural functions of the SREB family, which addresses two questions existing: why SREB family has been so conserved in vertebrate evolution and how SREB family is involved in psychiatric disorders. Disclosures: Part 1: I am a full-time employee of Astellas Pharma Inc., Part 5: Astellas Pharma Inc.
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51. Addictions Neuroclinical Assessment: The Search Continues David Goldman * , Laura Kwako, Harriet de Wit, Vijay Ramchandani, Melanie Schwandt, Barbara Mason, Valerie Voon National Institute on Alcohol Abuse and Alcoholism, Rockville, Maryland, United States The focus of the proposed study group is on a new clinical framework for understanding addictive disorders, which we call Addictions Neuroclinical Assessment (ANA). The need for this new framework is apparent in the relatively static nosology for addictive disorders, which has clinical reliability but significant within-diagnosis heterogeneity. This heterogeneity limits our ability to understand, treat, and prevent addictive disorders, which comprise significant public health problems. ANA builds on advances in our understanding of the neurobiologic underpinnings of addictive disorders and emphasizes the assessment of three neurofunctional domains: Cognitive Control, Reward, and Negative Emotionality. Each domain may be associated with various aspects of the addiction cycle, including binge-intoxication (Reward), withdrawal (Negative Emotionality), and preoccupation-anticipation (Cognitive Control). There is significant overlap between these three functional domains and those included in the National Institute of Mental Health’s major initiative to redefine the research framework for varied psychiatric disorders, the Research Domain Criteria (RDoC) initiative. RDoC includes five functional domains (Cognitive Systems, Negative Valence Systems, Positive Valence Systems, Systems for Social Processes, and Arousal and Regulatory Systems). The primary differences between ANA and RDoC are that RDoC focuses on multiple psychiatric disorders, while ANA emphasizes addictions, and that RDoC is a research tool, while ANA is clinical in nature. Proposed assessments to be incorporated within ANA include specific magnetic resonance imaging (MRI)-based measures of each functional domain, along with MRI assessments of brain structure, volume, and connectivity. These neuroimaging measures will be supplemented by collection of blood for genomic analysis and a battery of ancillary instruments, including assessments of specific drug use patterns, psychiatric disorders, and psychosocial functioning. Thus, the neuroimaging and ancillary instruments will comprise a deep phenotyping of addicted individuals, to be analyzed in conjunction with the genomic data. This assessment package will be piloted within the National Institute on Alcohol Abuse and Alcoholism’s (NIAAA) intramural research program, which includes inpatient and outpatient treatment facilities. ANA will further be expanded on and disseminated through collaboration with universities, health providers and organizations, and other research and treatment facilities. This study group would describe ANA in further detail and allow for a discussion of how best to maximize this opportunity to better understand the heterogeneity of addictive disorders, reconceptualize the nosology, and, ultimately, improve efforts at prevention and intervention. Disclosures: Nothing to Disclose.
Top of page 52.1 Regulation of 5-HT2A Receptor-induced Behavioral Responses by mGlu2 / 3 and mGlu5 Receptors Adam Halberstadt University of California at San Diego, La Jolla, California, United States Background: Metabotropic glutamate (mGlu) receptors have been suggested to play a role in schizophrenia and depression. Because serotonergic hallucinogens increase glutamate release and mGlu receptors modulate the response to serotonin (5-HT)2A activation, the interactions between serotonin 5-HT2A receptors and mGlu receptors may prove to be important for our understanding of these disease states, and may help to unravel the mechanisms underlying the potential therapeutic effects of hallucinogens. Methods: One series of experiments assessed whether the head twitch response (HTR) induced by the highly selective 5-HT2A agonist 25CN-NBOH in C57BL/6J mice is modulated by acute or chronic treatment with the mGlu2/3 agonist LY379268. In the acute experiment, mice were treated with LY379268 (0.1-10 mg/kg SC) 30 min prior to administration of 25CN-NBOH. In the chronic experiment, mice were treated with vehicle or LY379268 (10 mg/kg/day SC) for 21 days, and then challenged with 25CN-NBOH after a 48-h washout period. We also tested whether deletion of the mGlu5 gene in mice alters the locomotor hyperactivity induced by the 5-HT2A agonists DOM (0.5 mg/kg IP) and TCB-2 (0.3 mg/kg IP). Results: 25CN-NBOH induced the HTR (ED50 = 0.40 (95% CI 0.20-0.81) mg/kg) in C57BL/6J mice. The response to 25CN-NBOH (1 mg/kg SC) was significantly attenuated (52.5% reduction) by acute treatment with 10 mg/kg LY379268 (F(3,20)=5.00, p<0.01). When mice were treated with LY379268 for 21 days and then challenged 48-h later with 25CN-NBOH, the HTR was attenuated 26.7% relative to mice treated chronically with vehicle (F(1,54)=30.91, p<0.001). The locomotor hyperactivity induced by DOM (gene x drug: F(1,28)=12.83, p<0.002) and TCB-2 (gene x drug x time: F(5,125)=3.30, p<0.008) was potentiated in mGlu5 knockout mice relative to their wild-type littermates. Conclusions: These studies demonstrate that mGlu2/3 and mGlu5 receptors modulate the behavioral responses induced by 5-HT2A activation. Additionally, these findings show that repeated activation of mGlu2/3 receptors can reduce the response to a 5-HT2A agonist. These studies provide additional support for the link between the serotonergic and glutamatergic systems. Additional studies are necessary to understand why 5-HT2A responses are altered by chronic mGlu2/3 activation and by the loss of mGlu5 signaling. Disclosures: Part 1: L-3 Communications; Roche, Part 4: Roche.
Top of page 52.2 Mood, Craving, and Self-efficacy in Psilocybin-Assisted Treatment of Alcoholism Michael Bogenschutz New York University, Albuquerque, New Mexico, United States Background: Evidence suggests that classic hallucinogens have clinically relevant effects in alcohol and drug addiction. It is hypothesized that acute pharmacological and psychological effects trigger longer-term changes in psychological variables such as mood, craving, and self-efficacy, and that these changes in turn lead to persisting improvement in substance use behavior. This report explores the effects of psilocybin administration on changes in mood, alcohol craving, and self-efficacy, and the relationship of these changes to short-term drinking outcomes that were previously reported. Methods: Ten patients with DSM-IV alcohol dependence received psilocybin 0.3 mg/kg PO in a supervised 8-hour session after 4 weeks of outpatient psychotherapy. Nine of these participants remained in the study for at least 4 additional weeks, during which no psilocybin was administered. Measures of acute medication effects included the total score from the Mystical Experience Scale, the General scale from the Altered States of Consciousness Scale (5D-ASC), and the Intensity subscale of the Hallucinogen Rating Scale. Measures of mood (the Profile of Mood States), self-efficacy (the Alcohol Abstinence Self-Efficacy Scale, Confidence sub-scale), craving (the Penn. Alcohol Craving Scale), and drinking were obtained at baseline and at intervals during and following treatment. Drinking outcomes were percent drinking days and percent heavy drinking days. Results: Mean Profile of Mood States subscale scores did not change significantly in the week following psilocybin administration (week 5) relative to the week before (week 4). However, individual changes in tension, depression, vigor, and confusion were significantly (p < .05) correlated with one or more of the three measures of the subjective experience during the first psilocybin session (r = .680 to .920). In all cases, more favorable mood outcomes were observed in participants who had stronger subjective experiences. Changes in mood symptoms at week 5 were significantly correlated with changes in drinking during the month following the first psilocybin session (weeks 5-8) relative to the month before (weeks 1-4). Similarly, craving was not significantly decreased at week 5, but change in craving was strongly correlated (r > .8, p < .01) with two of three measures of subjective experience intensity, and this change in craving was correlated with subsequent changes drinking outcomes in weeks 5-8 (r > .7, p < .05). Significant correlations were observed between change in craving and change in depression, vigor, fatigue, and confusion. An increase in self-efficacy was also observed at week 5, and this change too was significantly correlated (r > .7, p < .05) with two of the three measures of subjective experience. However, change in self-efficacy was not significantly correlated with subsequent change in drinking, or with measures of mood and craving. Conclusions: In this proof-of concept trial, stronger experiences with psilocybin produced more positive change in mood, craving, and self-efficacy, and changes in mood and craving were in turn predictive of short-term improvement in drinking. Controlled trials are necessary to test whether the causal mechanisms suggested here can be reproduced prospectively. Disclosures: Part 4: Research grant for a non-pharmacologic treatment study from the Lundbeck, Foundation, through the University of Southern Denmark.
Top of page 52.3 A Single Dose of Psilocybin Produces Substantial and Enduring Decreases in Anxiety and Depression in Patients with a Life-Threatening Cancer Diagnosis: A Randomized Double-blind Trial Roland Griffiths Johns Hopkins University School of Medicine, Baltimore, Maryland, United States Background: Patients with cancer often develop chronic, clinically significant symptoms of anxiety and depression that have a significant negative impact on the quality of their life. Existing pharmacological and psychological treatments are very limited. Several trials in the 1960s and 1970s with the classic hallucinogens LSD and DPT in cancer patients showed clinically significant improvement in ratings of depression and anxiety. These trials involved 236 cancer patients. Recently, Grob and colleagues (2011) reported a pilot study with a moderate dose of the classic hallucinogen psilocybin (about 14 mg/70 kg) showing decreases in anxiety and depression in 12 cancer patients. Methods: The study used a randomized, double-blind, cross-over design to investigate the acute and sustained effects of a very low psilocybin dose (1 or 3 mg/70 kg) vs. a moderate-high dose (22 or 30 mg/70 kg). Instructions to participants and staff minimized expectancy effects. 51 patients with a life-threatening cancer diagnosis who had symptoms of anxiety or depression received a low or high dose of psilocybin in counterbalanced order with about 5 weeks between sessions and a final follow up at 6 months. For this preliminary analysis, results between the low (n=25) and high (n=26) dose groups on the first session were compared. Enduring effects were assessed at a 6 month follow-up. Results: On session days, the high dose group showed substantially greater effects including perceptual changes, mystical-type subjective experiences, and labile mood. At the 5-week follow-up the high dose group showed significantly lower anxiety (STAI Trait Anxiety, HAM-A) and depression (BDI, HAM-D) compared to the low dose group (effect size mean and range 0.98, 0.60-1.30). The participants attributed significantly greater positive changes in attitudes about life/self, positive social effects, and positive behavior changes to the experience, and a higher percentage reported the experience to be among the 5 most personally meaningful of their lives (54% vs. 16%). Total mystical experience scores at the end of the session showed significant negative correlations with the above measures of anxiety and depression at 5 weeks. Partial correlation analysis showed this relationship remained significant after controlling for ratings of intensity of drug effect. The decreases in anxiety and depression were sustained at 6 month follow-up. Conclusions: A single moderate-high dose of psilocybin, when administered under supportive conditions to carefully screened and prepared participants, can produce substantial and enduring decreases in anxiety and depression in patients with a life-threatening cancer diagnosis. Disclosures: Part 1: I am a consultant to Merck and Co and Jazz Pharmaceuticals. I am on the Board of Directors of the Heffter Research Institute, Part 4: Heftier Research Institute has provided grant funding of some of my research.
Top of page 52.4 Results: Of a Multi-Modal Neuroimaging Study of LSD and a Psilocybin for Treatment-Resistant Depression Clinical Trial Robin Carhart-Harris Imperial College London, London, United Kingdom Background: Our research team have conducted a series of MRI and MEG studies with the 5HT2A receptor agonist psilocybin in comparison with MDMA, an entactogen that releases 5HT. The MRI studies of psilocybin (both ASL and fMRI) revealed unexpected reduction in brain blood flow and a decrease in BOLD signal (Carhart-Harris et al 2013 PNAS) in high-level cortical regions and the thalamus, with post-hoc analysis showing large increases in brain connectivity between, rather than within, the usual resting state networks (Petri et al J Roy Soc 2014). The cortical psilocybin MRI findings were confirmed by a later MEG study that revealed a major loss of power in all measured frequency bands (1-100Hz) after psilocybin with decreases in alpha power in the posterior cingulate cortex correlating with ego-dissolution measures (Carhart-Harris & Muthukumaraswamy et al 2013 J Neurosci). Results from the fMRI and MEG work suggested psilocybin has antidepressant properties and from these we are now conducting the first study of psilocybin in resistant depression. Data from a pilot phase will be ready for the ACNP meeting. MDMA also decreased blood flow and BOLD signal but the effects were largely subcortical, particularly in the amygdala, and no psychedelic effects were seen (Carhart-Harris et al 2014 Biol Psych). Negative memories were attenuated and positive ones enhanced by MDMA and these effects were associated with fMRI-measured changes in brain activity (Carhart-Harris et al 2013 Int Neuropychopharm). LSD is the prototypical hallucinogen, with much greater use than the others in psychiatric and research settings, with over 1000 papers published before it was banned in 1967. Since then, and only in the past year, there have been 3 research reports, but none using modern brain imaging methods. Methods: Over the course of 6 hours, 20 healthy volunteers were scanned sequentially with ASL/BOLD-fMRI/ and MEG following 75 microgm LSD iv or saline placebo in a cross-over design at least 2 weeks apart. Subjective ratings of psychedelic experiences were then correlated with the imaging data. Twelve patients with resistant depression were treated with two sessions of psilocybin. Significant improvements in symptom severity were observed for up to 5 weeks post-treatment, with a far greater before and (1 week) after treatment effect size (Cohen's d = 3.4) than seen with currently available anti-depressant interventions. Results: LSD decreased integrity and segregation of brain networks and this effect correlated with subjective ratings of changes in consciousness, including ego-dissolution. Increased functional connectivity between the visual cortex and high-level cortical regions correlated strongly with ratings of visual hallucinations. Patients treated with psilocybin for resistant depression have shown marked improvements in the symptom severity post-treatment. Conclusions: The LSD data and our three prior psilocybin studies show that 5HT2A agonist hallucinogens provoke profound changes in consciousness due to decreased integrity of brain networks and a decrease in between-network segregation found in resting state measures, leading to a more chaotic or “entropic” brain state. These effects may also explain the utility of these drugs in addiction and mood disorders. The psilocybin for depression findings suggest that psilocybin is a safe and effective treatment for severe depression. This work was led by R Carhart-Harris and supported by D Nutt, M Kaelen, L Roseman, S Muthukumaraswamy and A Feilding as part of the Beckley-Imperial College psychedelic research program. Disclosures: Nothing to Disclose.
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53. Beta Arrestin Signaling: An Avenue to Novel Psychopharmacology
Top of page 53.1 Physiological Responses to Mu Opioid Receptor Agonists Promoting Bias Toward G Protein Signaling Pathways Laura Bohn The Scripps Research Institute, Jupiter, Florida, United States Background: Mu opioid receptors (MOR), the cognate targets for endorphins, endomorphins and enkephalins, are pharmaceutical targets for pain treatment, depression disorders and addiction therapies. As a G protein-coupled receptor, MOR signals through G proteins to dampen pain responses. These receptors also recruit βarrestins, which are intracellular regulatory proteins. Studies in βarrestin2-knockout mice suggest that preventing βarrestin2 interactions with MOR may lead to better analgesics with fewer side effects. Methods: A series of novel MOR agonists were generated and analyzed for their ability to promote G protein signaling over βarrestin2 recruitment. Mathematical application of the operational model of nonlinear regression analysis was used to rank the degree of bias for G protein signaling over βarrestin2 recruitment. Compounds with high G-preferring bias factors were analyzed in mouse for their ability to induce a wide array of behavioral responses. Pharmacokinetic evaluations were also performed. Results: We demonstrate that antinociceptive properties of these drugs are maintained, with potencies and efficacies comparable to conventional agonists. However, we find that agonists biased for G protein signaling lead to a loss of some of the behavioral effects induced by balanced agonists, such as morphine. In further comparison to morphine, the MOR biased agonists produce less tolerance, constipation, respiratory suppression and locomotor activity. Pharmacokinetic analysis reveals that the compounds are long lasting in plasma and they are brain penetrant. Conclusions: Biased agonists identified in vitro are shown to display diverse physiological responses in vivo when compared to morphine. While the direct demonstration of βarrestin2 activation in vivo is still forthcoming, the current findings support the earlier observations made in the βarrestin2-KO mice: reduction of the MOR-βarrestin2 interaction may lead to preserving antinociception with reduced side effects. Disclosures: Part 1: A patent has been filed by TSRI on this work, Part 4: Funding from Eli Lilly in Company, not on the work presented here. (Funded by NIH DA033073, DA031927, DA038964).
Top of page 53.2 A Unique Dual Cortico-Striatal Action of a Beta-arrestin Biased Dopamine D2 Receptor Ligand Nikhil Urs Duke University, Durham, North Carolina, United States Background: β-arrestin2 (βarr2) signaling at D2 receptors (D2Rs) plays an important role in antipsychotic responses, allowing development of signaling biased therapies. In preclinical studies βarr2 biased D2R ligands behave as efficacious antipsychotic compounds. The dopamine (DA) hypothesis of schizophrenia postulates hypodopaminergia in the prefrontal cortex (PFC) and hyperdopaminergia in the striatum. Current antipsychotics effectively reverse excess striatal activity, but do not fully reverse cortical deficits. Using cell-specific βarr2KO mice and β-arrestin biased ligands we address this problem here. Methods: To achieve cell type-specific deletion of βarr2 we crossed βarr2 floxed mice to D1R, D2R or A2aR CRE mice. We then tested the ability of clinically effective antipsychotics haloperidol (HAL), clozapine (CLOZ), aripiprazole (ARI) and the β-arrestin-biased D2R ligands UNC9994A (94A) and UNC9975A (75A) to inhibit psychostimulant-induced hyperlocomotion in these neuron-specific βarr2KO mice. We employed in vitro GPCR signaling assays to test ARI, 94A and 75A for their antagonist/partial agonist activity at D2Rs. Results: Deletion of βarr2 in striatal D2R+ (A2aCRE) or all D2R+ (D2CRE) but not D1R+ (D1CRE) neurons causes β-arrestin-biased D2R ligand 94A but not 75A to lose its antipsychotic activity against amphetamine. However other antipsychotics tested (HAL, CLOZ and ARI) were still effective in all βarr2KO mouse lines. Interestingly, unlike AMPH, when tested against phencyclidine (PCP), 94A lost its antipsychotic activity only in D2R+ (D2CRE) but not striatal D2R+ (A2aCRE) or D1R+ (D1CRE) βarr2KO mice suggesting a role for cortical βarr2 in this effect. Upon western blot analyses we observed higher expression of βarr2 and GRK2 in the PFC compared to the striatum. In vitro signaling assays revealed that upon over-expression of GPCR Kinase2 (GRK2) - ARI and 94A but not 75A have partial agonist activity at βarr2 recruitment at the D2R. However, with endogenous expression levels of GRK2 - ARI, 75A and 94A antagonize βarr2 recruitment to the D2R but that only ARI and 75A antagonize Gi mediated D2R signaling. Conclusions: Using neuron-specific βarr2KO mice and the β-arrestin-biased D2R ligand 94A, we show that βarr2 antagonism in striatal D2R+ neurons is sufficient for antipsychotic activity against amphetamine. However, for antipsychotic activity against phencyclidine, 94A displayed a unique regional selectivity, suggesting a role for PFC D2R/βarr2 agonism. The switch of 94A from antagonism to agonism is due to higher PFC expression of βarr2 and GRK2 compared to striatum. Therefore, unlike current antipsychotics, β-arrestin-biased D2R ligands that behave as agonists in the cortex but antagonists in the striatum may be sufficient for clinical antipsychotic efficacy, with a superior ability to correct cortical hypodopaminergia. Such a mechanism would allow for the amelioration of not only psychosis but also cognitive and negative symptoms observed in schizophrenia. Disclosures: Nothing to Disclose.
Top of page 53.3 D2 Beta Arrestin-Signaling Enhances Prefrontal Cortical Interneuron Activity Patricio O'Donnell Pfizer, Cambridge, Massachusetts, United States Background: Fast spiking interneurons (FSI) in the prefrontal cortex exhibit a protracted developmental trajectory with the acquisition of their adult profile of dopamine modulation during adolescence. In juvenile animals FSI can be activated by D1 and inhibited by D2 agonist, while in adult animals D2 activation becomes excitatory. We tested the hypothesis that such excitatory effect, unlikely driven by Gi activation, is dependent on signaling through beta arrestin 2 (bARR). Methods: We conducted whole-cell recordings in FSI from wildtype and bARR KO mice testing the effects of the unbiased agonist quinpirone, the unbiased partial agonist aripiprazole and the bARR biased ligand UNC9994A (94A). Results: All compounds increase excitability and firing in prefrontal FSI, but 94A had a much stronger effect on FSI than the other compounds, and did not exert an excitatory effect on pyramidal neurons. The excitatory effect of 94A was abolished in bARR KO mice. Conclusions: In conclusion, the data suggest that biased signaling could have significant impact on dopamine modulation of FSI in the prefrontal cortex, an effect that could provide cognitive improvement by bARR biased D2 agonists. Disclosures: Part 1: Employee and stockholder at Pfizer, Part 5: Pfizer.
Top of page 53.4 Novel Cellular Mechanisms Underlying Actions of Dopamine D2 Receptors on Prefrontal Pyramidal Neurons Vikaas Sohal University of California at San Francisco, San Francisco, California, United States Background: Dopaminergic modulation of prefrontal function has been implicated in a wide variety of normal and pathological processes. Recently our laboratory described a novel action of dopamine D2 receptors (D2Rs) on a specific subtype of subcortically projecting (SC) pyramidal neurons in layer 5 of the prefrontal cortex (PFC). Specifically, when D2Rs are activated in the presence of synaptic NMDAR activation, these neurons produce prolonged afterdepolarizations (ADPs) that can drive spiking for several seconds in the absence of further input. Thus, this phenomenon may powerfully regulate top-down output from the prefrontal cortex to subcortical structures. Several key questions about this phenomenon remain. Does this phenomenon influence the excitability of SC neurons in other ways, besides producing ADPs? How exactly do NMDARs contribute? Does this phenomenon reflect canonical or non-canonical D2R signaling? And finally, how does this phenomenon contribute to normal or pathological behaviors? Methods: We made whole cell patch clamp recordings from visually identified L5 pyramidal neurons in the medial PFC in acute brain slices from 8-10 week old mice. To activate D2Rs, we used 10-20 micromolar quinpirole. To activate synaptic NMDARs, we optogenetically stimulated callosal fibers, or bath applied 4 micromolar NMDA. To knockout the NR2B subunit, we used NR2B conditional knockout mice injected with a virus to drive expression of Cre in the mPFC. For behavioral experiments, we used TH-Cre mice to optogenetically stimulate TH-positive projections from the VTA to mPFC. Results: First, we confirmed that interactions between D2Rs and NMDARs can modulate prefrontal SC neuron excitability in other ways, besides simply eliciting ADPs. Activating D2Rs in the presence of synaptic stimulation (to recruit NMDARs) increases the sensitivity of SC neurons to brief inputs. Next, we explored mechanistic aspects of this phenomenon. The ability of synaptic stimulation to facilitate D2R-induced increases in excitability is suppressed when hyperpolarizing current is delivered concurrent with synaptic stimulation, suggesting that it requires Ca2+ influx via NMDARs. Surprisingly, knocking out the NR2B subunit increases D2R-induced afterdepolarizations, suggesting that NR2A and NR2B-containing NMDARs differentially contribute to this phenomenon. Antagonists for cAMP-PKA mediated signaling consistently block the D2R-induced afterdepolarization, suggesting that it is not mediated through canonical Gi signaling pathways. Finally, we have been exploring the effects of stimulating TH-positive VTA to mPFC projections during a rule switching task. We paired phasic stimulation of these fibers with either correct or incorrect choices and found that both pairings disrupted learning of a new rule, while also suppressing perseverative behavior. Thus dopaminergic signaling in the mPFC does not simply transmit feedback about recent choices and reinforces specific behaviors, but rather can nonspecifically destabilize behavioral strategies in a way that could facilitate exploratory behavior. Conclusions: Our results confirm that D2Rs can powerfully regulate PFC output in ways that may guide flexible behaviors. This appears to reflect non-canonical signaling through D2Rs, as well as novel D2R-NMDAR interactions. Disclosures: Part 1: Research support from Roche.
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54. Novel Molecular Targets in Cocaine Addiction
Top of page 54.1 Acid Sensing Ion Channel: A New Player in Addiction-Related Behavior John Wemmie University of Iowa College of Medicine, Iowa City, Iowa, United States Background: Synaptic physiology and structure in the nucleus accumbens (NAc) is known to be altered as a consequence of chronic exposure to drugs of abuse, and these changes are believed to be critical components in the pathology of drug addiction. A potential regulator of these changes in the NAc are acid-sensing ion channels (ASICs). In particular, acid-sensing ion channel 1A (ASIC1A) is abundant in the nucleus accumbens (NAc), and previous evidence from our laboratory has suggested that ASIC1A influences learning and memory mechanisms dependent on other brain regions. However, the function of ASIC1A in the accumbens in regulating NAc-dependent behavior and functioning within the NAc is unknown. Therefore, we hypothesized that manipulating ASIC1A in the NAc would alter addiction-related behavior, including drug-seeking behavior, in rodents. Methods: To address this issue, we conducted studies in both mice and rats, utilizing the strengths and capabilities of each approach to understand the role of ASIC1A in the NAc. In mice, we explored our hypothesis by: 1) examining the effects of manipulating ASIC1A in the mouse on cocaine conditioned place preference, 2) investigating the effects ASIC1A disruption on synaptic transmission and dendritic spine morphology in the NAc, and 3) determining how alterations in ASIC1A affect cocaine-evoked synaptic plasticity. Based on the results from our mouse studies, we then examined the function of ASIC1A in the NAc of rats using self-administration models. Specifically, we expressed ASIC1A in the NAc in the rat and examined cocaine self-administration, post-withdrawal cocaine-seeking behavior, and synaptic transmission. Results: We found that disrupting ASIC1A in the mouse NAc increased cocaine-conditioned place preference and overexpressing ASIC1A in the rat NAc reduced cocaine self-administration. Investigating the underlying mechanisms, we identified a previously unknown postsynaptic current during neurotransmission that was mediated by ASIC1A and ASIC2 subunits and thus well positioned to regulate synapse structure and function. Additional studies of ASIC1A in the rat NAc further suggest significant effects of ASIC1A on cocaine craving following cocaine withdrawal, as ASIC1A overexpression in the NAc of rats produced a significant increase in cocaine-seeking behavior following a withdrawal period. In contrast, such overexpression had no effect on food-seeking behavior. Conclusions: Together, these findings suggest that ASIC1A contributes to excitatory synaptic transmission in the NAc and, moreover, that altering ASIC1A in the NAc had profound influences on synaptic functioning and addiction-related behaviors. In particular, the evidence that manipulating ASIC1A selectively influences measures of relapse to cocaine-seeking, but not food-seeking, behavior suggests an interaction between chronic cocaine use and ASIC1A functioning. As a result, our work raises the possibility of developing therapies for drug addiction by targeting ASIC-dependent neurotransmission. Disclosures: Nothing to Disclose.
Top of page 54.2 Regulation of Protein Translation in the Nucleus Accumbens Marina Wolf Rosalind Franklin University of Medicine and Science, North Chicago, Illinois, United States Background: Cue-induced cocaine craving progressively intensifies ("incubates") during withdrawal from extended access cocaine self-administration. After prolonged withdrawal, expression of incubated craving is mediated by calcium-permeable (CP)-AMPARs that accumulate in NAc synapses. Group I mGluR plasticity is also altered. Our recent results suggest that ongoing dendritic protein translation is required to maintain these adaptations. Thus, when NAc slices were prepared from “incubated rats” (rats subjected to extended-access cocaine self-administration followed by >40 days of withdrawal) and then exposed for ~1 h to inhibitors of protein translation, synaptic transmission was normalized (Scheyer et al., 2014). Is protein translation globally upregulated after incubation? Or, is there dysregulated translation of a few critical proteins that are required to maintain cocaine-induced plasticity? Information about regulation of protein translation in neurons comes mainly from studies of hippocampus. For example, group I mGluR stimulation increases translation, while NMDAR transmission can exert a suppressive effect. Our goals are: 1) determine if the same pathways regulate translation in the NAc and if this is altered after incubation of cocaine craving, and 2) identify specific proteins that are differently translated in the NAc of “incubated rats”. Methods: Metabolic labeling was used to tag newly synthesized proteins in freshly dissected NAc tissue from drug-naive rats or rats killed >40 days after discontinuing extended access saline or cocaine SA. Tissue was incubated with 35S-Met/Cys in the presence of vehicle (control) or antagonists of mGluR5, mGluR1 or NMDARs, and then processed for SDS-PAGE/autoradiography to quantify incorporation of radiolabel into newly synthesized proteins. This method is useful to measure overall rates of translation but not translation rates of individual proteins. Therefore, parallel studies are underway using bioorthogonal noncanonical amino acid tagging (BONCAT) combined with immunoprecipitation and mass spectrometry. Results: The mGluR5 antagonist MTEP increased 35S-Met/Cys incorporation into newly translated proteins in the NAc of drug-naive rats and cocaine-exposed rats. The mGluR1 antagonist LY367385 had no effect in any group. The NMDAR antagonist APV increased translation in drug-naive but not cocaine-exposed rats. Conclusions: Our results show that tonic mGluR5 signaling suppresses protein translation in the NAc of drug-naive rats, opposite to what has been found in hippocampus, and that this effect is not altered after incubation of craving. In contrast, mGluR1 blockade did not affect translation in any experimental group, despite emergence of mGluR1-LTD in the NAc after incubation. Finally, we found that NMDARs suppress translation in the NAc of drug-naive rats, as in hippocampus, but this braking influence is lost in the cocaine group. This may explain, at least in part, the abnormal translation that maintains neuroadaptations in NAc synapses of “incubated rats”. Using BONCAT, we will test the hypothesis that loss of NMDAR-mediated inhibitory tone permits excessive translation of proteins that regulate AMPAR transmission. Disclosures: Nothing to Disclose.
Top of page 54.3 Cocaine-Induced Adaptations in Astrocyte-neuron Communication Mediate Cocaine Seeking Kathryn Reissner University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States Background: Recent studies indicate that cocaine use alters astrocytes and neuron-astrocyte communication within the brain’s reward circuitry. In particular, downregulation of astroglial glutamate transporter GLT-1 is a hallmark feature observed after extended withdrawal from multiple drugs of abuse. A growing list of compounds known to affect glial physiology and restore glutamate uptake, including N-acetylcysteine (NAC), ceftriaxone, and propentofylline, impair reinstatement of cocaine seeking. Given this, it is of great interest to determine specifically how cocaine experience affects astrocytes and contributes to maladaptive cellular dynamics that underlie relapse. Methods: Prior to behavioral training, astrocytes in the nucleus accumbens were transduced with an AAV2/5 expressing membrane-tagged Lck-GFP under the control of an astrocyte-specific promoter. Rats then either underwent cocaine self-administration or served as yoked-saline controls. Following two weeks of extinction training, properties of fluorescent accumbens core astrocytes were measured, including surface area and volume. Slices were also immunostained for synapsin I, to allow for colocalization of synaptic puncta with GFP-positive pixels containing peripheral astrocyte processes. Astrocytes were imaged at 63x on a Zeiss confocal microscope, and analyzed using Imaris software. For behavioral studies, rats were treated with riluzole (1 or 4 mg/kg, i.p.) thirty min prior to each extinction session and reinstatement test. For electrophysiology, rats were overdosed with pentobarbital and nucleus accumbens slices were taken for whole-cell patch-clamp recording. Results: Following cocaine self-administration and extinction, nucleus accumbens astrocytes are significantly smaller and make fewer presynaptic contacts than following saline experience. Moreover, the decrease in synaptic colocalization is reversed by administration of the glial modulator ceftriaxone during extinction training. Thus, a model is emerging in which retraction of astrocytes from neurons exacerbates decreased glutamate uptake caused by decreased GLT-1 expression, leading to glutamate spillover and stimulation of accumbens neurons which drive reinstatement. Based on this model, we should expect other compounds known to enhance GLT-1 to also impair cocaine reinstatement. In fact, we have found that in addition to NAC, ceftriaxone, and propentofylline, the GLT-1 regulator riluzole also impairs both cue- and cocaine-primed reinstatement. Interestingly, we find that riluzole also normalizes excitability of prelimbic (PL) prefrontal cortical neurons, which is increased by cocaine self-administration and extinction. Thus, we hypothesize that the mechanism of action of riluzole against cocaine seeking includes decreased PL neuron excitability paired with enhanced glutamate uptake by astrocytes in the nucleus accumbens. Conclusions: These studies collectively demonstrate that nucleus accumbens astrocytes are retracted from synapses in the nucleus accumbens following cocaine self-administration and extinction, an effect that is ameliorated by administration of ceftriaxone during extinction. Moreover, a growing list of compounds that restore GLT-1 expression also impede cocaine seeking, including NAC, ceftriaxone, propentofylline, and riluzole. We propose that reduced astrocyte contact with neurons in the nucleus accumbens represents an important functional adaptation to chronic cocaine use and an amenable target for pharmacological intervention. Ongoing studies are designed to more fully understand the functional consequences of this phenomenon, as well as the mechanism by which GLT-1 is downregulated. Disclosures: Nothing to Disclose.
Top of page 54.4 Corticosterone Potentiates Cocaine-induced Reinstatement of Drug Seeking by Inhibiting OCT3-mediated Dopamine Clearance in the Nucleus Accumbens Paul Gasser Marquette University, Milwaukee, Wisconsin, United States Background: Cocaine addicts report that craving responses to drug-associated stimuli are intensified during periods of stress, resulting in heightened susceptibility to relapse of drug use. These studies suggest that stress may act as a “stage-setter”, inducing state-dependent changes in the sensitivity of brain reward circuits to the reinforcing properties of drugs, and enhancing the potency of drugs of abuse or drug-associated cues to induce relapse. We recently demonstrated that the stress hormone corticosterone acutely blocks dopamine clearance in the nucleus accumbens (NAc) via a dopamine transporter-independent mechanism likely mediated by organic cation transporter 3 (OCT3). We provided evidence that, through this mechanism, corticosterone potentiates the actions of low-dose cocaine on dopamine signaling and reinstatement of drug-seeking behavior in rats. We have hypothesized that decreased clearance of dopamine in the NAc, due to inhibition of OCT3 by corticosterone, enhances dopaminergic neurotransmission, resulting in increased sensitivity to cocaine, and heightened vulnerability to relapse of cocaine-seeking behavior. The present studies test this hypothesis by examining: 1) corticosterone effects on the reinstatement of drug-seeking behavior in OCT3-deficient mice; 2) the effects of corticosterone and cocaine treatment, alone and in combination, on sub-second dopamine dynamics in the nucleus accumbens; and 3) the subcellular distribution of OCT3 in the mouse brain. Methods: 1.) We examined the effects of corticosterone and normetanephrine, two inhibitors of OCT3-mediated transport, on low-dose cocaine-induced reinstatement of conditioned place preference in wild type and OCT3 knockout mice. 2.) Using fast scan-cyclic voltammetry, we measured naturally-occurring transient dopamine release events during a baseline period, after a systemic injection of corticosterone (2 mg/kg) or vehicle, and after a subsequent systemic injection of low-dose cocaine (2.5 mg/kg). 3.) Coronal sections of aldehyde-fixed mouse brains were incubated with OCT3 antiserum and processed for avidin-biotin-peroxidase labeling. Ultrathin sections were examined with an electron microscope. Results: 1.) OCT3-knockout mice were both: a) more sensitive to low-dose cocaine-induced reinstatement of conditioned place preference, and b) insensitive to corticosterone-induced potentiation of reinstatement. 2.) Low-dose cocaine injection did not lead to increases in time-averaged dopamine concentrations in the nucleus accumbens unless it was preceded by corticosterone injection. Corticosterone injection alone tended to increase extracellular dopamine concentration. 3.) OCT3 immunostaining was observed on plasma membranes of dendritic spines adjacent to putative monoamine release sites, as well as in glial processes. Conclusions: These data indicate that OCT3 represents an important post- or peri-synaptic clearance mechanism, and that inhibition of OCT3 by corticosterone potentiates the effects of low-dose cocaine on both dopamine signaling in the nucleus accumbens and drug-seeking behavior. As OCT3 is capable of transporting norepinephrine, serotonin and histamine in addition to dopamine, its presence in the brain has profound implications for the regulation of monoaminergic neurotransmission under basal and stress conditions. Disclosures: Nothing to Disclose.
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55. Visualizing Neurocircuit Dynamics in Rodent Models of Addiction and Anxiety
Top of page 55.1 Neural Activity in Processing Positive and Negative Valence Kay Tye Massachusetts Institute of Technology, Cambridge, Massachusetts, United States Background: Dopamine in the medial prefrontal cortex (mPFC) has been implicated in aversion, yet the circuits mediating avoidance have yet to be identified. Our goal is to understand how mPFC neuronal subpopulations encode the positive or negative valence of discrete stimuli and where this information is communicated downstream to instigate adaptive behavioral responses, such as approach or avoidance. We also seek to understand how dopamine may signal aversion in mPFC circuitry. Methods: We use freely-moving deep-brain endoscopic calcium imaging to visualize the dynamics of mPFC neurons in behaving mice across a number of behavioral tasks. We also use in vivo optogenetics to manipulate circuit components and fast-scan cyclic voltammetry to measure dopamine transients related to the optogenetic manipulations. Results: We show that an aversive stimulus causes dopamine release in the mPFC, as the increase in catecholamine content is unaffected by locus coeruleus inactivation but is blocked by ventral tegmental area inactivation. We have found that the mPFC neurons have diverse response profiles. Approximately 50% of neurons (n=273) responded similarly, perhaps encoding general salience. ~26% showed selective responding to only one of the stimuli. Another subset of mPFC neurons (~19%) showed opposing responses, characterized by increased activity to one stimulus and decreased activity to the other. mPFC neurons encoding positive or negative valence likely have distinct downstream targets. The periaqueductal gray (PAG) is has been linked to aversive behaviors and we have found that optogenetic activation of mPFC terminals in the PAG produces avoidance [n = 6 ChR2, p = 0.01] and anxiety-related behaviors [p = 0.04]. Further, stimulation of this pathway evokes defensive [p = 0.03] and escape [p = 0.01] behaviors in the marble burying assay, suggesting that stimulation of the mPFC:PAG circuit triggers active avoidance behaviors. These effects were not observed in control animals [n = 6 eYFP; p > 0.05]. The paraventricular nucleus of the thalamus (PVT) has been implicated in reward, and receives dense input from the mPFC. To selectively manipulate mPFC neurons terminating in PVT, we used an anterogradely traveling viral vector carrying ChR2 in a double inverted open reading frame in the mPFC and a retrogradely traveling viral vector carrying cre-recombinase in the PVT. In animals expressing ChR2 only in neurons originating in the mPFC and terminating in the PVT, we show that activation of the PVT-projecting mPFC neurons is positively reinforcing [n = 3 ChR2, p = 0.04]; an effect not observed in controls [n = 3 eYFP; p > 0.05]. Conclusions: Together, these data suggest that dopamine is released in the mPFC with an aversive stimulus and the mPFC controls avoidance and approach behaviors through its projections to the PAG and PVT, respectively. Our results advance us towards a circuit-level explanation for how the mPFC can exert control over valence-defined motivated behaviors. Disclosures: Nothing to Disclose.
Top of page 55.2 Visualization of a Feeding Authorization Mechanism Christian Luscher University of Geneva, Geneva, Switzerland Background: Feeding satisfies metabolic need but is also powerfully controlled by external stimuli, like palatability or predator threat. Nucleus accumbens shell (NAcSh) projections to the lateral hypothalamus (LH) are implicated in such feeding control, but the neurons involved and their mechanism of action remains elusive. Methods: To address these questions, we established a paradigm in which food consumption can be monitored on a moment-to-moment basis in genetically modified mice, permitting the observation and control of identified cell types. We monitor neuroal exctivity with in vivo electrophysiology (tetrode recordings in freely moving animals) and by visualizing calcium transients with genetically encoded calcium indicators. We then establish links of causality with bidirectional optogenetic control of neural activity while observing the effect on feeding. Results: We show that dopamine D1 receptor expressing NAcSh neurons (D1R-MSNs) provide the dominant source of accumbal inhibition to LH and control food consumption via LH GABA neurons. In freely feeding mice, D1R-MSN activity reduced during consumption, while their optogenetic inhibition prolonged feeding, even in the face of distracting stimuli. Conversely, activation of D1R-MSN terminals in LH was sufficient to abruptly stop ongoing consumption, even during hunger. Direct inhibition of LH GABA neurons, which receive strong accumbal inhibition, suppressed feeding, while their activation generated unrestrained consummatory behavior. Conclusions: Our study identifies a permissive feeding circuit that overrides immediate metabolic need to enable rapid consumption control in response to changing external stimuli. Disclosures: Nothing to Disclose.
Top of page 55.3 Neural Substrates of Anxiety-Like Behavior in the Prefrontal Cortex Ilana Witten Princeton University, Princeton, New Jersey, United States Background: The medial prefrontal cortex subserves a staggering range of behaviors, and accordingly, its dysfunction is implicated in many neuropsychiatric conditions, including addiction and anxiety disorders. Subsets of prefrontal cortical neurons send descending projections to various subcortical areas, including the nucleus accumbens, the ventral tegmental area, the raphe and the amygdala. This “top-down” control is thought to play an important role in anxiety and addiction, in part because the targeted subcortical areas are also implicated in the same conditions. However, due to technological limitations and the complexity of the underlying circuitry, it has been difficult to ascertain what information is being encoded by each of these top-down projections. We believe that characterizing the top-down regulation of subcortical structures will play a crucial role in the generation of novel and valid hypotheses about the etiology and possible therapies for these conditions. Methods: In order to image cellular resolution activity from neurons that project from the prefrontal cortex to the nucleus accumbens, a Cre-dependent gCaMP6f virus was injected into the medial prefrontal cortex of mice, and a retrograde virus expression Cre-recombinase was injected into the nucleus accumbens. Subsequently, a GRIN lens was implanted above the dorsal region of the prefrontal cortex (prelimbic cortex). Mice explored anxiety assays (elevated plus maze, open field test) while neural activity was imaged using a head-mounted microscope (Inscopix). Results: Over 400 neurons were imaged from 6 mice. Activity of many neurons within this population encodes the mouse's location while it explored the elevated plus maze (an anxiety assay), with some neurons responding more strongly in the non-preferred, unprotected region (open arm), and other others responding more strongly in the preferred, protected location (closed arm). In addition, several analyses revealed consistent differences in the population-level encoding of the open versus the closed arms. For example, the average activity across the population of neurons was stronger in the open arms rather than the closed arms. In addition, neural activity was correlated across the closed arms within the population of neurons, while it was anti-correlated across the open arms. Conclusions: Neurons that project from prefrontal cortex to the nucleus accumbens encode an animal's location while exploring an anxiety assay, with distinct coding schemes in the protected and unprotected locations in an environment. These data provide an important step in characterizing the role of top-down signals from the prefrontal cortex in rodent models of anxiety. Disclosures: Nothing to Disclose.
Top of page 55.4 Imaging Network Dynamics to Rewards and Predictive Stimuli in VTA and PFC Circuits Garret Stuber University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States Background: Accurate neuronal encoding and representation of reward availability is critical to survival, and this adaptive function of the brain becomes highly disruptive in addiction and other neuropsychiatric conditions. While midbrain dopamine neurons are hypothesized to encode a reward prediction error signal, it is unclear whether individual neurons in the VTA or in upstream targets such as the lateral hypothalamus (LH) or medial prefrontal cortex (mPFC) develop learned signals in response over many repeated cue-reward pairings. Methods: To address this, we have developed in vivo imaging approaches to record neural activity dynamics of 100’s of genetically or circuit defined neurons in awake and behaving mice. We have selectively expressed the genetically-encoded calcium indicator in select subsets of neurons in the VTA, LH, or mPFC based on their molecular phenotype or projection targets. Following expression of the calcium indicator in targeted cells, micro-endoscopic GRIN lenses or optical cannula are implanted directly above the VTA, LH, or mPFC. We then use single photon or two-photon imaging approaches to resolve neural activity dynamics in these structures in response to primary rewards (sucrose) or reward-predictive stimuli (CS+). Results: By imaging activity in the LH, we have demonstrated that individual LH GABAergic neurons, many of which project to the VTA, encode appetitive stimuli or primary reward consumption, but rarely both. Appetitive and consummatory encoding LH neurons are largely intermixed within the LH, suggesting the encoding of these processes occurs on a cell by cell basis and may be dictated based on the project targets of individual LH GABAergic neurons, or their afferent inputs. In addition, We show that using imaging approaches, we can reliably track the activity dynamics of individual neurons throughout repeated behavioral sessions, thus demonstrating that changes in the neuronal representation of rewards or predictive cues can now be resolved over many days. The experiments investigating VTA and mPFC neuronal encoding are still ongoing, but we will present our unpublished results of these experiments in this session. Conclusions: By imaging neuronal activity in the LH our data demonstrate that individual LH GABAergic neurons can encode select behavioral aspects critical for motivated behavior. In addition, by establishing methods to resolve neural activity from the same neurons over many repeated behavioral sessions, we demonstrate the feasibility of studying how neuronal representations of behavior are altered following learning, or throughout the progression of a maladaptive behavioral state such as addiction. Disclosures: Nothing to Disclose.
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56. Translational Neural Network Approaches for Identifying Individualized Targets for Neurostimulation in Mood Disorders and OCD
Top of page 56.1 Cortical Nodes in the Ventrolateral Prefrontal and Anterior Cingulate Cortex and the Functional Segmentation of the Internal Capsule: Implications for Potential Treatment Targets for Psychiatric Disease Suzanne Haber University of Rochester School of Medicine & Dentistry, Rochester, New York, United States Background: The dorsal anterior cingulate cortex (dACC), ventrolateral prefrontal cortex (vlPFC), along with the orbital prefrontal cortex (OFC), dorsolateral prefrontal cortex (dlPFC), and amygdala are associated with several psychiatric diseases. Non-invasive stimulation methods, including transcranial direct current stimulation (tDCS) and the invasive method, deep brain stimulation (DBS), are currently being explored as treatment options for several diseases including obsessive-compulsive disorder (OCD) and depression. In the noninvasive approaches stimulation is placed over specific cortical regions. Our hypothesis is that there exist ‘critical nodes’ within cortical areas that receive converging inputs from several functionally diverse areas (i.e. a combination of different emotion and cognitive control areas). These nodes are potentially an important focus for treatment targets that are designed to modulate the balance between top-down and bottom-up control. Here we show the location and composition of 2 nodes, one in the vlPFC and one in the dACC. In contrast to tDSC, DBS targets white matter, with one major target, the anterior limb of the internal capsule (ALIC). We sought to delineate where, within the ALIC, fibers from the vlPFC and dACC travel. We tested these fiber trajectories in humans using diffusion MRI (dMRI) and determined which fibers are likely to be involved at different DBS sites in DBS treated-patients. Methods: Using animal tracing experiments, we analyzed the specific cortical and amygdala inputs that converge in the vlPFC and dACC and the location of these critical nodes. We identified a similar region in the human brain using resting state functional MRI that could be used as a tDCS target. We also determined where fibers from the vlPFC, dACC, and dlPFC traveled through the ALIC in animals, combining the analysis with previous data of OFC fiber location in the ALIC. We used this data to guide dMRI identified fiber locations in the human ALIC and the likely pathways stimulated at different DBS sites within the capsule. Results: We found critical nodes located in specific dACC and vlPFC regions. The dACC region receives convergent inputs from the amygdala, OFC, dlPFC, vlPFC. The vlPFC node receives inputs from the amygdala, OFC, dlPFC, dACC, and pSMA. Regions adjacent to the nodes do not receive these inputs. These data guided specific seed placements for a resting state analysis in humans. The results show a functional connectivity map that was consistent with the anatomical connections. Fibers from these cortical nodes travel within specific parts of the ALIC. In particular, DBS of the central ALIC involves dACC and vlPFC fibers, but not OFC fibers. Conclusions: Specific areas of the dACC and vlPFC receive inputs from the amygdala and OFC that converge with those from cognitive control areas (dlPFC, dACC, and vlPFC). We found that each DBS electrode captures a specific combination of fibers depending on the electrode location. Disclosures: Nothing to Disclose.
Top of page 56.2 Associations Between Distinct Patterns of Reward Circuitry Function and Impulsive Sensation Seeking Provide Novel Neural Targets for Transcranial Direct Current Stimulation as an Intervention to Reduce Risk-Taking Behaviors Mary Phillips University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, United States Background: Neuroimaging studies of mood disordered individuals highlight relationships among measures of function and structure in ventrolateral prefrontal (vlPFC)-striatal-amygdala neural circuitry and reward-related behaviors, e.g., risk-seeking and impulsive sensation seeking. This dimensional approach is elucidating neural mechanisms associated with dysfunctional behaviors in psychiatric disorders, and can identify key nodes in neural circuitries implicated in underlying psychopathological processes in these disorders that can serve as targets for interventions with novel neurostimulation techniques. Methods: In a large, ongoing study of neural mechanisms underlying dysfunctional reward-related behaviors in distressed, treatment-seeking 18-25 year-olds, we have, to date, scanned over 40 such individuals during performance of different tasks, including a number-guessing reward task. Each trial of the reward task includes an expectancy period, when participants anticipate uncertain reward or loss future outcome, and the outcome phase itself. In a pilot study in healthy volunteers, cathodal (inhibitory) and sham transcranial direct current stimulation (tDCS) were implemented in a randomized, single-blind, within-subjects study design, during neuroimaging. The goal of this pilot study was to determine the extent to which this neurostimulation technique could perturb functioning within reward circuitry during performance of the above reward task. Results: We show significant positive relationships between a measure of trait impulsive sensation seeking and activity during uncertain outcome expectancy in distributed reward circuitry, including bilateral visual cortices (cuneus; p<0.05, FWE) and left vlPFC (p<0.005). These data replicate our previous findings in independent studies of a significant positive relationship between fun-seeking and activity in left vlPFC across individuals with bipolar disorder and healthy volunteers, and abnormally elevated left vlPFC activity in individuals across the bipolar disorder spectrum, during uncertain reward and outcome expectancy. Pilot study findings in healthy volunteers show that cathodal (vs. sham) tDCS applied to the left vlPFC results in decreased positive functional connectivity between this region and ventral striatum during reward task performance. Conclusions: The vlPFC links specific stimulus and specific reward outcome representations. Our new and previous findings suggest that abnormally elevated visual cortical and left vlPFC activation to uncertain outcome expectancy may reflect heightened representation of visual stimulus-reward outcome relationships that, in turn, may be a neural mechanism for impulsive sensation seeking. Our pilot findings suggest that left vlPFC cathodal tDCS may help reduce vulnerability to risk-taking behaviors, especially in individuals with higher trait impulsive sensation seeking. Disclosures: Part 1: I am a consultant for Roche Pharmaceuticals.
Top of page 56.3 Mapping Functional Connectivity Networks in the Individual Hesheng Liu Harvard Medical School / Massachusetts General Hospital, Charlestown, Massachusetts, United States Background: The capacity to identify the unique functional architecture of an individual subject’s brain is a critical step towards personalized medicine and understanding the neural basis of variations in human cognition and behavior. Clinical and imaging studies have demonstrated marked inter-individual variability in the organization of different functional systems of the brain, particularly in higher order association areas. Localizing specific functional circuitries in a particular subject is therefore a fundamental requirement in clinical procedures such as surgical planning or non-invasive brain stimulation therapies. However, functional imaging techniques are generally limited in accuracy and reliability at the single-subject level. Methods: Here we developed a novel brain parcellation approach to accurately map functional organization at the individual level using resting-state fMRI. A population-based functional atlas and a map of inter-individual variability were employed to guide the iterative search for functional networks in individual subjects. This strategy allows the idiosyncratic functional organization of the individual to drive the network solution. Reliability and accuracy of the resulting functional maps were tested in several independent datasets. Results: Functional networks mapped by this approach were highly reproducible within subjects and effectively captured the variability across subjects, including individual differences in brain lateralization. The algorithm performed well across different subject populations and data types including task fMRI data. The resulting parcellation networks were significantly more reliable than networks localized by traditional task-evoked response. This novel technology can also reliably identify the ventrolateral prefrontal (vlPFC)-striatal circuitry at the single subject level, a potential neurostimulation treatment target for OCD. Conclusions: Functional connectivity variability has a specific topographic distribution with heteromodal association cortex being most variable therefore within-subject functional mapping is particularly important in psychiatric research. The novel functional mapping technique developed in this study can provide an individual-level functional atlas which may help the identification of personalized therapeutic targets for various diseases including OCD. Disclosures: Nothing to Disclose.
Top of page 56.4 DBS Electrode Position and Clinical Outcomes in the Context of Tractography Benjamin Greenberg Brown University / Butler Hospital, Providence, Rhode Island, United States Background: Deep brain stimulation (DBS) for intractable OCD, which has regulatory approvals in the U.S. and E.U., remains the subject of ongoing research. Similar to its uses in movement disorders, the method requires time-consuming programming to select the individual electrode contacts, or groups of contacts, where stimulation is associated with the best clinical responses, and the greatest tolerability, over time. Our DBS target, the VC/VS or ventral capsule-ventral striatum, spans the ventral anterior limb of the internal capsule (ALIC) and the adjacent ventral striatum (VS). Previous work by ourselves and others has provided hints of systematic relationships between activation of DBS contacts in certain locations within the target region and both therapeutic and adverse effects. In general, enhanced positive affect (and later OCD improvement) has been somewhat more likely with use of contacts at or dorsal to the anterior commissure, a landmark along the trajectory of the DBS leads. Conversely, adverse affective and autonomic effects may be more likely when more ventral contacts are stimulated. However, both kinds of effects differ notably across individual cases, even with electrode placements which appear comparable when visualized with high-resolution structural MRI. It is likely that this variability in outcomes, which adds complexity and patient burden to programming, can be explained by relationships between electrodes and specific fiber tracts connecting the ventral prefrontal cortex to thalamic and brainstem nuclei which course through the DBS target. Methods: Our multicenter NIMH-supported controlled trial of DBS for OCD has enrolled 27 patients, the last of whom will exit the masked phase by July 2015. In contrast to earlier open-label studies of VC/VS DBS in intractable OCD, using a lead covering a relatively large territory (contacts spanned 24mm, each electrode 3mm in length), in this trial we selected a device which was more than twice as compact (10.5mm electrode span, electrodes 1.5mm long). This choice was based on prior clinical outcomes and 3D modeling of fiber tracts hypothesized to be most relevant which were based on nonhuman primate tracer experiments informed by human DTI tractography (S. Haber et al.). Among the baseline pre-surgical measures obtained in this trial is diffusion-weighted MRI. These were obtained on the same research magnet for patients from three of the nine study centers participating in the trial. Results: Open-label data suggest that there is wide case-by-case variability in the DBS electrode contacts associated with the greatest improvements in YBOCS OCD severity. The most optimal responses are seen with cathodal stimulation at contact 0 (most ventral) in some individuals, and with activation of contact 3 (most dorsal) in others, and in others when the middle two contacts 1 and 2 are used for chronic stimulation. The same pattern obtains for symptoms of comorbid depression and nonspecific anxiety. Localization of clinically-identified contacts will be confirmed using data from the study masked phase. The contact sites will then be placed within ventral PFC-thalamic and ventral PFC-brainstem pathways using DTI-based tractography. Conclusions: Open-label data suggest substantial variability in locations of DBS electrodes associated with the greatest benefit and lowest burden of adverse effects, even when using a stimulating lead with less than half the anatomical extent of that in prior studies. Our hypothesis that clinical outcomes is explained by specific relationships between electrodes and fiber tracts connecting the ventral prefrontal cortex to subcortical nuclei will be tested using tractography. Disclosures: Nothing to Disclose.
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57. New Twists on Transmembrane Transporter Function in Psychiatric and Neurodegenerative Disorders
Top of page 57.1 Missense Mutations in the Dopamine Transporter Gene: Commonality Between Neuropsychiatric and Neurodegenerative Diseases? Ulrik Gether University of Copenhagen, Copenhagen, Denmark Background: Dopamine dysfunction is of central importance in neuropsychiatric diseases, such as schizophrenia, affective disorder, ADHD and autism, as well as in neurodegenerative parkinsonism. The presynaptic dopamine transporter (DAT) mediates reuptake of dopamine and thereby plays a key role in regulating dopamine homeostasis by terminating dopamine signaling and ensuring maintenance of reusable pools of transmitter. There is accumulating evidence that rare genetic variants in the DAT gene, including de novo mutations, can play a hitherto unknown key role in the pathophysiology of both neuropsychiatric and neurodegenerative disorders. Methods: Patient cohorts are screened for genetic variants in the DAT gene. This includes patients with atypical movement disorder and large cohorts of patients (>10,000) with psychiatric disease (schizophrenia, bipolar disorder, ADHD and autism). Missense variants in the coding region are phenotypically characterized in vitro to assess alterations in uptake, pharmacology, trafficking and electrophysiological properties. Knock-in mice of selected mutations are generated to study causality and disease mechanisms. Results: We recently identified two novel DAT coding variants in an adult male diagnosed with both neuropsychiatric disorder and early-onset neurodegenerative parkinsonism. The variants included Ile312Phe in transmembrane segment 6 and a presumed de novo mutant Asp421Asn in the second sodium site. In heterologous cells, both mutants exhibited markedly reduced dopamine uptake capacity but preserved membrane targeting, consistent with impaired catalytic activity. For Asp421Asn, substrate efflux experiments revealed a constitutive, anomalous efflux of dopamine, and electrophysiological analyses identified a cation leak that might contribute to perturbed dopaminergic neurotransmission. To assess causality and investigate disease mechanisms, knock-in mice expressing Asp421Asn and/or Ile312Phe have been generated. Importantly, our genetic screening has led to identification of yet other DAT variants. This includes a variant, located in the C-terminal PDZ binding sequence, which is also associated with neuropsychiatric disorder and early-onset neurodegenerative parkinsonism. Preliminary data suggest impaired surface targeting and an interesting dominant negative effect on the wild type transporter. Moreover, sequencing of 155 patients with severe affective disorder has revealed new variants that currently are subject to phenotypic characterization in vitro. Conclusions: Our data provide strong evidence that missense mutations in DAT can cause or contribute to both neuropsychiatric diseases and movement disorders, and that the resulting disease phenotype depends on the nature of the functional perturbations caused by the mutations. Moreover, the results suggest a yet unappreciated commonality between neurodegenerative and neuropsychiatric diseases and accordingly that the study of DAT missense variants can lead to novel understanding that pertain to dopamine pathologies in general. Disclosures: Nothing to Disclose.
Top of page 57.2 An Inside Job: Endosomal Na + / H + Exchangers in Autism and Neurological Disorders Rajini Rao Johns Hopkins School of Medicine, Baltimore, Maryland, United States Background: A subset of Na+/H+ exchangers (eNHE) localize to endosomal compartments where they mediate proton leak, countering the action of proton pumps. This important safety valve precisely sets the pH of the lumen to control the trafficking and turnover of cargo critical for neurological function. Dysregulation of eNHE has been implicated in both neurodevelopmental and neurodegenerative disorders, including autism, ADHD, intellectual disability and Alzheimer disease. Rare variants in SLC9A9, the gene encoding NHE9, may underlie autism whereas significant depression in gene expression links to the APOE4 variant associated with Alzheimer and other neurodegenerative disorders. Although genetic approaches are important in candidate gene identification, functional analysis of transporter activity is essential to predict clinical outcome and for personalized therapy. Methods: We use homology models based on evolutionary conservation to distant bacterial orthologs of known structure to predict functional consequences of rare variants in NHE9. This structure-driven assessment is followed by sequential phenotype screening in the yeast model organism and primary astrocytes to distinguish harmless polymorphisms from disease-causing mutations. Lentiviral mediated knockdown and overexpression strategies in astrocytes and genotyped patient fibroblasts allow us to correlate changes in endosomal pH to delivery, removal and activity of cell membrane receptors and transporters that mediate specific cellular phenotypes, including glutamate uptake, growth factor signaling and amyloid beta peptide clearance. Results: Functional assessment of autism-associated NHE9 variants revealed that changes in conserved residues led to loss of transporter phenotypes in both yeast and astrocyte model systems. Unexpectedly, substitution of a variable side chain caused functional deficiency in astrocytes but failed to show differences from wild type protein in yeast. Loss of eNHE associated proton leak in NHE9 mutants resulted in endosomal hyperacidification and reduction in uptake of the neurotransmitter glutamate, consistent with elevated levels of brain glutamate and predisposition to seizures in patients. Similarly, decreased NHE9 expression in patients with Alzheimer disease correlated with reduced clearance of the amyloid peptide Abeta and missorting of endosomal cargo, both pathological hallmarks of neurodegeneration. Conclusions: Endosomal dysfunction is central to several neurological disorders, ranging from autism to Alzheimer disease. A mechanistic understanding of the role of Na+/H+ exchanger NHE9 could lead to potential therapeutic intervention. Several FDA-approved drugs have been reported to mildly alkalinize endosomal pH and could be repurposed to counter loss of eNHE function in the treatment of these neurological disorders. With the advent of personal genomics on the horizon, our phenotype screening approach offers a rapid, inexpensive and accurate evaluation of human variants, distinguishing disease-causing mutations from harmless polymorphisms. Disclosures: Nothing to Disclose.
Top of page 57.3 Unraveling Mechanisms Contributing to Lack of Antidepressant Efficacy in Juveniles and Adolescents: are Organic Cation Transporters to Blame? Lynette Daws University of Texas Health Center at San Antonio, San Antonio, Texas, United States Background: Depression is a major public health problem for which most patients are not effectively treated. This problem is further compounded in children and adolescents where only two antidepressant drugs are currently approved for clinical use. Both belong to the selective serotonin (5-HT) reuptake inhibitor (SSRI) class of antidepressant, and act by blocking the high-affinity uptake of 5-HT from extracellular fluid via the serotonin transporter (SERT). The therapeutic utility of SSRIs is thought to be triggered by downstream events that occur in response to their ability to increase extracellular levels of 5-HT. However, in juveniles and adolescents, little is known about mechanisms contributing to 5-HT uptake. Essentially nothing is known about expression and function of SERT during this period, and nothing is known about expression and function of organic cation transporters (OCTs) and the plasma membrane monoamine transporter (PMAT), low-affinity, high-capacity transporters for 5-HT. Here we present data that PMAT is a promising new target for the treatment of pediatric depression. Methods: All studies were carried out in male mice (C57BL/6 background). Chronoamperometry was used to measure clearance of 5-HT from extracellular fluid in hippocampus. Radioligand binding together with western blot was used to quantify expression of SERT, OCT3 and PMAT. The tail suspension test was used to assay for antidepressant-like effects of drugs. Results: During juvenile and adolescent periods, we found that PMAT expression is increased and SERT function is decreased, relative to adults. The increase in PMAT was magnified in SERT+/- and SERT-/- mice suggesting that during adolescence PMAT upregulates to compensate for a constitutive reduction in, or loss of SERT expression/function. In contrast, in adults OCT3 expression is increased in SERT+/- and SERT-/- mice. Functionally, we found that clearance of 5-HT from extracellular fluid in hippocampus was equally efficient among adolescent SERT+/+, SERT+/- and SERT-/- mice, indicating contributions to 5-HT clearance by a mechanism(s) other than SERT, putatively PMAT. In contrast, in adult mice, the same concentration of 5-HT was cleared with lower efficiency in SERT+/- and SERT-/- mice than in SERT+/+ mice, suggesting that OCT3 is not as effective in clearing 5-HT as PMAT. Importantly, we found that D22 (an inhibitor of OCTs and PMAT) produced antidepressant-like effects in wild-type juvenile mice, whereas in adult mice, antidepressant-like effects of D22 were only apparent when SERT was pharmacologically or genetically inactivated. In adult mice the potency of D22 to produce antidepressant-like effects was reduced in OCT3 knockout mice. Studies using juvenile and adolescent PMAT and OCT3 knockout mice are ongoing. Conclusions: Here we show that during juvenile and adolescent periods, PMAT plays a previously unsuspected role in 5-HT uptake, whereas in adults, OCT3 contributes to 5-HT clearance. The antidepressant-like activity of D22 suggests that activity of these transporters likely limits the therapeutic utility of SSRIs. Moreover, the role of PMAT and OCT3 in 5-HT clearance increases when SERT function is genetically compromised. This is of particular interest given the link between low expressing and/or functioning variants of the SERT gene and psychiatric disorders. Our findings point to PMAT and OCT3 as promising targets for the development of new antidepressants with improved therapeutic potential. Disclosures: Nothing to Disclose.
Top of page 57.4 Towards Chemical Screening of Antidepressant Efficacy via Voltammetric Characterization of In Vivo Serotonin Clearance Parastoo Hashemi University of South Carolina, Columbia, South Carolina, United States Background: Antidepressants treat the symptoms of depression, a debilitating neurological disorder, and are among the most widely prescribed medications. Unfortunately, most antidepressants have limited therapeutic benefits. Resources for antidepressant drug discovery are declining primarily because of the unavailability of pre-clinical tests that predict clinical efficacy. Behavioral tests, such as the forced swim and the tail suspension tests, in rodents are not always reliable predictors of antidepressant efficacy. Most antidepressants influence serotonin neurotransmission either by blocking the serotonin transporter, or by targeting dopamine and norepinephrine systems to indirectly modulate serotonin neurotransmission. Here we describe using in vivo fast scan cyclic voltammetry (FSCV) at carbon fiber microelectrodes (CFMs) for measuring hippocampal serotonin clearance kinetics in mice treated with different antidepressants. We outline how different antidepressants create unique voltammetric serotonin profiles which correlate to clinical efficacy, finally discussing the potential of FSCV for chemical screening of antidepressant efficacy. Methods: A single carbon fiber was aspirated into a glass capillary, pulled apart under heat and cut to 150 μM. The resulting CFM was electroplated with Nafion. Adult, male C57BL/6 mice weighing 20-25g were anesthetized with urethane. Mouse procedures were in compliance with WSU’s Guide for the Care and Use of Laboratory Animals, approved by the Institutional Animal Care and Use Committee (IACUC). Stereotaxic surgery was performed to implant the CFM into the CA2 region of the hippocampus, a stimulating electrode into the medial forebrain bundle (MFB) and a reference electrode into the contralateral brain hemisphere. Electrical pulses were delivered via a linear constant current stimulus isolator. Results: We tested the effects of a large, acute antidepressant dose on stimulated serotonin release and reuptake. Escitalopram increased serotonin release amplitude rapidly (~5 minutes) after administration. Additionally, and surprisingly, escitalopram caused an increase in the rate of serotonin reuptake: an effect which persisted for over 2 hours. This effect may be associated with transporter up-regulation and/or shift to high efficiency state. Importantly, when we tested the effects of other different antidepressants on serotonin, we found a similar increase in the rate of serotonin reuptake. Most interestingly, we found that antidepressants with a greater ability to increase serotonin reuptake (independent of class) are reported to be the most efficacious in the clinical literature. We therefore present the potential power of FSCV measurements for chemical screening of antidepressant efficacy. Conclusions: Antidepressants continue to carry limited therapeutic benefit. Elucidating techniques to more powerfully predict clinical efficacy of novel antidepressants would greatly facilitate drug discovery. In this study, we found that in vivo FSCV of serotonin provides important, novel insights into antidepressant mechanisms. Furthermore, different antidepressant’s effects on serotonin uptake correlate to clinical efficacy, giving rise to the potential of FSCV as a chemical screen for antidepressant efficacy. Disclosures: Nothing to Disclose.
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58. Revisiting the Mu Opiate Receptor for the Treatment of Depression
Top of page 58.1 Opioid Receptors and Mood Brigitte Kieffer McGill University, Montreal, Canada Background: The roles of opioid receptors in pain and addiction have been extensively studied, but their function in mood disorders has received less attention. Accumulating evidence from animal research reveals that the three receptors (mu, delta and kappa) exert highly distinct controls over mood-related processes, and the potential of each receptor for the treatment of major depressive disorders is being actively investigated. Methods: In this presentation, we will first summarize data from genetic mouse models by our group and others, which have allowed positioning each opioid receptor in the control of hedonic homeostasis and mood control. Those studies have used behavioral models of anxiety and depression, as well as a recent model for emotional deficits in protracted abstinence from drugs of abuse from our laboratory, which involves serotonergic neurotransmission. We will then focus on the mu opioid receptor and present two new genetic mouse models that (i) allow deciphering the neuroanatomy of mu opioid receptor expression in vivo with subcellular resolution and (ii) produce conditional ablation of the mu opioid receptor gene in targeted neuron populations within reward and aversion pathways. Results: Data indicate that mu opioid receptors mediate rewarding properties of both drugs of abuse and natural rewards, with implication for autism spectrum disorders. Delta receptors show anxiolytic and antidepressant activities, which have now translated to clinical trials, and the kappa/dynorphin system contributes to dysphoric states induced by drug abuse or chronic stress. Further, delta and kappa receptors oppositely influence susceptibility to develop depressive-like behavior and social withdrawal upon prolonged abstinence to chronic heroin. Finally, knock-in mice expressing a functional fluorescently-tagged mu opioid receptor (mcherry) show highest receptor expression in cholinergic and substance P neurons of the medial habenula, and we currently identify afferent and efferent pathways within and outside the habenular complex using tracing experiments. We also currently develop mice with a conditional deletion of mu receptors in targeted neurons of this intriguing, yet poorly investigated brain microstructure structure to test the hypothesis that this receptor regulates negative affect states at the level of the medial habenular-interpeduncular pathway. Conclusions: Our current knowledge of opioid receptor function in mood control clearly posits delta receptor activation and kappa receptor blockade as promising therapeutic approaches to improve mood states. The role of mu receptors in mediating reward is well-established, but basic knowledge of its role in depression-related behaviors is still missing. This new area of investigation hold promises for treatment, should the addictive liability of mu opiates be circumvented. Disclosures: Nothing to Disclose.
Top of page 58.2 The Antidepressant-Like Effects of Tianeptine are Mediated by the Mu Opiate Receptor Rene Hen Columbia University / New York State Psychiatric Institute, New York, New York, United States Background: Tianeptine is an antidepressant used in Europe for the treatment of Major Depressive Disorder and Anxiety Disorders. In preclinical studies tianeptine was shown to decrease depression and anxiety-related behaviors and to prevent stress-induced decreases in neuronal dendrites in the hippocampus. Despite earlier suggestions that tianeptine influenced the serotonergic and glutamatergic systems, its mechanism of action has remained elusive. Methods: We have used a combination of pharmacology, cell-based assays and gene knockouts in mice to study the mechanisms underlying the physiological and behavioral effects of tianeptine. Results: Using radioligand binding and cell-based functional assays, including bioluminescence resonance energy transfer (BRET)-based assays for G-protein activation and cAMP accumulation, we identified tianeptine as an efficacious mu-opioid receptor (MOR) agonist (Ki-Human of 383±183 nM and EC50-Human of 194±70 nM for G-protein activation). Tianeptine was also a full delta-opioid receptor (DOR) agonist, although with much lower potency (EC50-Human of 37.4±11.2 μM for G-protein activation). In contrast, tianeptine was inactive at the kappa-opioid receptor (KOR). We have also shown that the behavioral and analgesic effects of tianeptine in a mouse model of depression are blocked by the opioid antagonist naltrexone and are absent in MOR knockout mice. Conclusions: On the basis of these pharmacological and behavioral data, we propose that activation of MOR (or dual activation of MOR and DOR) could be responsible for the antidepressant and anxiolytic effects of tianeptine in humans. Targeting the MOR may therefore represent a novel approach in the treatment of depressed patients who do not respond to classic antidepressants. Disclosures: Nothing to Disclose.
Top of page 58.3 Evaluation of Agonist-Antagonist Opioid Modulation with ALKS-5461 in Major Depressive Disorder Elliot Ehrich Alkermes, Inc., Waltham, Massachusetts, United States Background: An accumulating body of evidence derived from animal models, human PET imaging investigations and human autopsy studies indicate that major depressive disorder (MDD) is associated with significant dysregulation of the endogenous opioid system. The contemporary use of opioids to treat MDD and related mood disorders, however, is very limited due to their potential for abuse and addiction. In an effort to therapeutically address endogenous opioid dysregulation in MDD while avoiding the potential for abuse and addiction, we studied a combination of buprenorphine (BUP), a μ-opioid partial agonist and κ-opioid partial agonist with low intrinsic activity, and samidorphan (SAM), a potent μ-opioid antagonist. Methods: Fixed ratios of BUP and SAM were co-formulated in a single sublingual tablet (ALKS 5461). Pupilometry and subjective pharmacodynamic effects of ALKS 5461 were evaluated in N=16 non-addicted opioid experienced subjects. Safety and antidepressant effects were evaluated as adjunctive treatment in subjects with MDD and an inadequate response to SSRI or SNRI therapy in two trials; a 1-week pilot study (N=32) and a follow-up 2-stage phase 2 study (N=142). The clinical studies were double-blind, randomized and placebo-controlled and utilized the Montgomery–Åsberg and Hamilton Depression Rating Scales (MADRS and HAM-D17). The phase 2 MDD study employed sequential parallel comparison design (SPCD) to minimize placebo effect. Nonclinical in vivo microdialysis studies in Wistar rats measured regional changes in extracellular concentrations of brain neurotransmitters following subcutaneous administration of BUP and SAM individually and in combination. Results: In the study of non-addicted, opioid experienced subjects, maximal blockade of pupilary and opioid subjective and physiologic effects was observed with a 1:1 ratio of BUP:SAM. In both the pilot and the follow-up phase 2 MDD studies, adjunctive treatment with the 1:1 ratio demonstrated statistically significant and clinically important antidepressant efficacy vs placebo (pilot study: MADRS p=0.032, HAMD-17 p=0.054; phase 2 study MADRS p=0.004, HAMD-17 p=0.026). Comparison of the individual stages of the phase 2 MDD study demonstrated that the SPCD design successfully attenuated placebo response. ALKS 5461 was generally well tolerated. The most common AEs were nausea, vomiting, and dizziness. There was no evidence of opioid withdrawal post-treatment. Microdialysis studies in rats showed that combined BUP/SAM resulted in sustained low-level, ceiling-limited increases in extracellular dopamine, serotonin, and/or metabolites in the nucleus accumbens (NAc) shell, medial prefrontal cortex (mPFC) and other brain regions. A small reproducible increase in mPFC glutamate with delayed (2-3 hr) onset was also observed. Conclusions: A “balanced” agonist-antagonist opioid modulation with ALKS 5461 is a novel treatment approach for patients with MDD. Microdialysis studies in rats suggest that the observed clinical response may be mediated via modulation of the release of multiple neurotransmitters in key brain regions including the NAc and mPFC. Large phase 3 studies to confirm and extend the results of the current work are ongoing. Disclosures: Part 1: Full-time employee of Alkermes, Inc., Part 5: Alkermes, Inc.
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59. DBS and the Identification of Circuits Mediating Depression
Top of page 59.1 Using DBS to Define Circuits Mediating Depression Wayne Goodman Icahn School of Medicine at Mount Sinai, New York, New York, United States Background: Recently several targets have been identified as potential sites for DBS to treat treatment resistant depression (TRD). Defining the circuits activated in successful responses following DBS may provide detailed information on the circuits that are central to depression. It is now more than 10 years since the first subcallosal cingulate DBS implant for TRD. The research has made steady progress with emerging clues as to which patients are most likely to benefit and the technique has now been refined to optimize surgical targeting using diffusion tractography with improved outcomes. As testing of DBS for TRD evolves, imaging will continue to play a crucial role, with recent work now focused on refinement and optimization of the procedure using combined structural, function and diffusion MRI data combined with real-time behavioral and electrophysiological metrics, providing a more precise method to identify the optimal target location for the individual patient. In an animal models combining new studies combining optogenetic activation of a circuit with fMRI is allowing a detailed investigation of downstream effects of stimulation. Using these methods in animal models and subjects is leading to a clear analysis of the circuit changes necessary to lead to remission of TRD. Data on the ongoing MT. Sinai DBS study involving l.habenular stimulation for treatment resistant depression will be presented with a discussion of new targeting methods. Methods: In this presentation using animal studies involving optogenetics, fMRI, proteomics and histological staining, circuits will be defined that appear to mediate depression. Using data from patient DBS studies involving DTI, activation volume, probabilistic tractography and 7T segmentation activated tracts will be identified and correlated with clinical outcome. Results: The discussion will formulate an approach to defining in situ measures from successful DBS targeting. This will include an analysis of the activation of medial frontal cortex, uncinate fasciculus and rostral and cingulate cortex as well as sub cortical nuclei such as VTA, DRN and inhibition of the l. habenula. Of interest is the examination of targets for change in one procedure, such a l. habenula inhibition or cingulate cortex stimulation, in procedures targeting another area. Patient characteristics that predict successful DBS, such as previous remission with ECT, will also be examined. These results suggest a common final pathway mediating depression through changes in cortical and monoaminergic pathways and a patient profile that better predicts response to DBS. Conclusions: There are extensive networks involving input from an anxiety and fear circuit involving hippocampus, amygdala, BNST, mPFC and l. habenula, a circuit involving reward and the control of monoaminergic nuclei and feedback to the mPFC. A proposed methodology for identifying candidates with a high probability of positive outcomes to DBS using the above methods will be presented. Disclosures: Part 4: Medtronic donated devices for study of Lateral Habenula DBS in TRD.
Top of page 59.2 Delineating Alterations of Brain Circuitry Due to Lateral Habenula DBS in TRD Alexander Sartorius University of Heidelberg, Mannheim, Germany Background: The Lateral Habenula (LHb) has received growing attention as a key player in the pathophysiology of major depression. Down-regulation of LHb activity by (unspecific electrical) deep brain stimulation has been successfully demonstrated in two patients by our group. An animal model of treatment-resistant depression (congenital Learned Helplessness, cLH) exhibits altered habenula activity as well as increased functional connectivity between, among others, the cingulate gyrus and retrosplenial cortex. This finding is homologous to the midline resting-state network, which has repeatedly been reported to be over-active in human depression. Methods: Using the novel combination of opto-genetics and high-field functional Magnetic Resonance Imaging (og-fMRI), we sought to reduce habenula activity in cLH animals. This approach unifies a highly specific perturbation of brain circuitry while still observing whole brain connectivity changes. Three weeks after ArchT-containing adenovirus injection in cLH animals (a control group received an empty viral cassette) optic fibers were implanted at the same site (n=19 in total). Laser stimulation was performed during resting-state image acquisition in a high-field 9.4 Tesla animal scanner. Additionally, resting state data (without laser stimulation) were acquired before and after stimulation. Virus expression was assessed histologically after sacrifice. Results: In our hypothesis-driven analyses we found laser-dependent specific reductions in the connectivity between retrosplenial cortex and cingulate cortex. This difference was present both when comparing connectivity during laser stimulation versus baseline condition (i.e. before laser application), and after laser stimulation vs. baseline. The changes were significant when compared to the control group. Conclusions: Midline resting state hyperconnectivity is a well-described depression-related intermediate endophenotype that can be studied in a translational manner. Our results further support the lateral habenula as a promising target for treatment of (especially treatment-resistant) depression. Disclosures: Nothing to Disclose.
Top of page 59.3 Refined Methods: for Subcallosal Cingulate DBS Targeting using Network-Specific Structural Connectivity Maps Helen Mayberg Emory University School of Medicine, Atlanta, Georgia, United States Background: The first studies of subcallosal cingulate deep brain stimulation (SCC DBS) for treatment resistant depression (TRD) were initiated in 2003 [1] with follow-up now exceeding 7-10 years [2-3]. While a 6-mo response rate of 40-60% is reported, there is variability in onset of initial effects and the rate of symptom improvement. Mechanisms mediating antidepressant effects have generally focused on regional change patterns evoked by chronic stimulation; new studies are additionally examining acute as well as chronic changes in network dynamics using electrophysiological recordings, with precise delineation of essential network ‘nodes’ an emerging priority [4]. Based on post-hoc analyses of the structural connectivity pattern differences in 6-mo responders and non-responders to SCC DBS using DTI-based probabilistic tractography (sc-DTI) [5], we hypothesized that pre-surgical delineation and individualized targeting of this specific combination of white matter tracts would improve response over standard methods using solely SCC anatomy and trial and error testing of individual lead contacts. Methods: Eleven patients with TRD scheduled for SCC DBS had pre-operative MRI, including DTI. A software tool employing deterministic tractography was used to visualize the surgical target--namely the intersection of four well-defined white matter bundles converging at the SCC: bilateral uncinate fasciculus, cingulum bundle, forceps minor and cingulo-subcortical fibers. Intra-operative, blinded testing of behavioral and physiological effects with stimulation of each of the 8 contacts along the DBS lead was performed to test the specificity of the predetermined optimal site. Chronic stimulation at this ‘optimal’ location was initiated 1 mo post implantation with both location and stimulation parameters held stable for 6 mo (130Hz, 60usec, 6-8mA). Symptom improvement was monitored using the Hamilton Depression Rating Scale (HDRS). Results: 11/11 patients showed maximal behavioral effects during blinded testing in the predefined optimal target location in each hemisphere. The 6-mo response rate (>50% HDRS decrease) improved from 41% (7/17 pts in the original cohort) where lead placement and contact selection was based on structural anatomy alone, to 73% (8/11) in the new group using pre-surgical sc-DTI guidance. Group-wise probabilistic sc-DTI maps of the active contacts used for chronic DBS (location verified by post-op CT scans) confirmed that the pre-defined 4- bundle template was impacted in all subjects. Conclusions: Individualized, pre-operative DTI targeting of a 4-bundle SCC-network improves DBS outcomes over the previous approach based on local SCC anatomy. Further, ‘effective’ versus ‘ineffective’ contacts were confirmed using a combination of behavioral, autonomic and electrophysiological changes elicited during intra-operative testing. These findings have implications for refining and standardizing targeting methods for future trials of this potential intervention. Disclosures: Part 1: Consultant, licensing of IP to St Jude Medical, Inc., Part 2: licensing of IP to St Jude Medical, Inc. (neuromodulation), Part 4: Medtronic Inc. and St Jude Medical Inc. (Donation of unapproved devices). Support: Dana Foundation, Hope for Depression Research Foundation. Devices donated by St. Jude Medical Inc.and Medtronic, Inc. Co-authors: P Riva Posse, K Choi, O Smart, V Tiruvadi, S Garlow, A Crowell, P Holtzheimer, R Gross. References: 1. Mayberg, et al. Neuron 45, 651-60, 2005. 2. Kennedy, et al. Am J Psych 168:502-10, 2011. 3. Holtzheimer, et al. Arch Gen Psych 69, 150-58, 2011. 4. Smart, et al. Biol Psych epub Jan 28, 2015. 5. Riva-Pose, Choi, et al. Biol Psych 76:963-9, 2014. ||||| | – People who receive life-threatening cancer diagnoses and find themselves battling depression and anxiety might consider munching on magic mushrooms, and that's not coming from a snake oil salesman. Scientists at the Johns Hopkins University School of Medicine announced last week at the annual meeting of the American College of Neuropsychopharmacology that a single dose of the hallucinogenic ingredient, called psilocybin, appears to have a protective effect that lasts for an astonishing six months, per a press release. Found in some 200 mushroom species, psilocybin can give users hallucinations, nausea, and a distorted sense of time, reports the International Business Times. To study its effects on cancer patients, Roland Griffiths and colleagues compared low and moderately high doses of psilocybin in 51 patients. On the day the drug was administered, those with the higher dosage exhibited "substantially greater effects, including perceptual changes [and] mystical-type subjective experiences," the researchers write. When the patients were checked five weeks and six months later, the higher-dose group continued to experience reduced mental health problems compared to the low-dose group. Further, the researchers write "a higher percentage [of the higher-dose group] reported the experience to be among the 5 most personally meaningful of their lives (54% vs. 16%)." The findings piggyback on a 2011 study showing similar effects on 12 cancer patients. (Magic mushrooms were last year found growing in this famous person's gardens.) | multi_news_1_0_0 |
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Abstract Bisphenol A (BPA) is an endocrine disrupting environmental contaminant used in a wide variety of products, and BPA metabolites are found in almost everyone’s urine, suggesting widespread exposure from multiple sources. Regulatory agencies estimate that virtually all BPA exposure is from food and beverage packaging. However, free BPA is applied to the outer layer of thermal receipt paper present in very high (~20 mg BPA/g paper) quantities as a print developer. Not taken into account when considering thermal paper as a source of BPA exposure is that some commonly used hand sanitizers, as well as other skin care products, contain mixtures of dermal penetration enhancing chemicals that can increase by up to 100 fold the dermal absorption of lipophilic compounds such as BPA. We found that when men and women held thermal receipt paper immediately after using a hand sanitizer with penetration enhancing chemicals, significant free BPA was transferred to their hands and then to French fries that were eaten, and the combination of dermal and oral BPA absorption led to a rapid and dramatic average maximum increase (Cmax) in unconjugated (bioactive) BPA of ~7 ng/mL in serum and ~20 µg total BPA/g creatinine in urine within 90 min. The default method used by regulatory agencies to test for hazards posed by chemicals is intra-gastric gavage. For BPA this approach results in less than 1% of the administered dose being bioavailable in blood. It also ignores dermal absorption as well as sublingual absorption in the mouth that both bypass first-pass liver metabolism. The elevated levels of BPA that we observed due to holding thermal paper after using a product containing dermal penetration enhancing chemicals have been related to an increased risk for a wide range of developmental abnormalities as well as diseases in adults.
Citation: Hormann AM, vom Saal FS, Nagel SC, Stahlhut RW, Moyer CL, et al. (2014) Holding Thermal Receipt Paper and Eating Food after Using Hand Sanitizer Results in High Serum Bioactive and Urine Total Levels of Bisphenol A (BPA). PLoS ONE 9(10): e110509. doi:10.1371/journal.pone.0110509 Editor: David O. Carpenter, Institute for Health & the Environment, United States of America Received: August 13, 2014; Accepted: September 23, 2014; Published: October 22, 2014 Copyright: © 2014 Hormann et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Data Availability: The authors confirm that all data underlying the findings are fully available without restriction. All relevant data are within the paper and its Supporting Information files. Funding: This work was supported by a grant from The Passport Foundation (no URL available) and by NIEHS grant ES018764 to FvS (NIEHS website http://www.niehs.nih.gov). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Competing interests: The authors have declared that no competing interests exist.
Introduction Bisphenol A [BPA; bis(4-hydroxyphenyl)propane; CAS #80-05-7] is one of the highest volume chemicals in commerce with 15-billion pounds produced per year [1], and based on the presence of BPA metabolites in urine, it can be concluded that virtually everyone is exposed [2], [3]. BPA has estrogenic and other endocrine disrupting activities [4], [5]. BPA molecules are polymerized to make polycarbonate plastic used for food and beverage containers, epoxy resins used to line cans, and dental composites and sealants, but free (unpolymerized) BPA is also used as an additive (plasticizer), such as in polyvinyl chloride (PVC) products. Our interest is in the use of BPA in thermal paper, which is used for airline ticket, gas, ATM, cash register and other types of receipts (Figure 1). The print surface of thermal paper is coated with milligrams of free BPA per gram paper as a heat-activated print developer [6], and it appears that free BPA is readily transferred to other materials that the thermal paper contacts [7]. PPT PowerPoint slide
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larger image ( ) TIFF original image ( ) Download: Figure 1. Schematic diagram of thermal receipt paper identifying the thermal reactive layer that contains BPA as a developer and a leuco dye, as well as stabilizers and binders (not shown). doi:10.1371/journal.pone.0110509.g001 While small lipophilic compounds such as BPA (logP = 3.4; molecular weight 228 Da) can pass through skin [8], [9], regulatory agencies have assumed that this route of human BPA exposure should not be significant in spite of the lack of data and acknowledged “significant uncertainties” around the issue of human exposure to BPA from thermal paper [10]. However, a factor that has not been considered in estimating transdermal exposure to BPA from thermal paper is that hand sanitizers are now commonly used, particularly in fast-food restaurants where people may handle thermal receipts before eating or ordering food. Hand sanitizer and other skin care products may also be used by cashiers while working. Exposure to BPA from thermal paper goes beyond just transdermal exposure and consumption of food that is picked up and eaten with a BPA-contaminated hand. The transfer of a chemical directly from hand-to-mouth (mouthing behavior) has been proposed to be an important variable for estimating total chemical exposure in humans [11], particularly in young children [12]. The use of hand sanitizers and other skin-care products, including soaps, lotions and sunscreens, is significant because some contain mixtures of chemicals that are also used as dermal penetration enhancers to increase the transdermal delivery of drugs. Drugs and chemicals that are suitable for transdermal delivery and are impacted by dermal penetration enhancers have a LogP>1.5 and a molecular weight <500 Da [9]. There are many factors that impact the ability of compounds to pass through skin in addition to molecular weight and lipophilicity, including differences arising from the location of skin on the body, gender and age [13]. Mixtures of dermal penetration enhancing chemicals can act synergistically to increase by up to 100 fold the dermal penetration of small lipophilic molecules such as estradiol [8], [9], with which BPA shares physical-chemical and biological properties [4]. For example, Purell hand sanitizer (Gojo Industries), which we used in the current study, contains a number of dermal penetration enhancers, such as isopropyl myristate and propylene glycol, and is (63% w/w) ethanol. The use of hand sanitizers has increased in recent years and is now about a 200 million dollar a year industry just in the USA [14]. The impact of the use of personal care products such as moisturizing lotions that contain dermal penetration enhancing chemicals on exposure to environmental chemicals has been identified as a concern [15]. To assess the relevance of this research to real-world behavior, we conducted a preliminary observational study in fast-food restaurants, food courts and shopping malls in Columbia Missouri. Receipt contact time varied widely, but was sometimes substantial. In one restaurant, we found that receipt contact time ranged up to 65 sec for people purchasing food that was eaten in the restaurant; the 75th percentile for time holding the receipt was >12 sec, and the 90th percentile >32 sec. In a fast-food restaurant that is part of an international chain, take-out food was placed into a bag and the top of the bag was folded, then the thermal receipt was stapled to the top of the bag; the result was that the print surface of the receipt (coated with BPA) was grabbed when the bag was picked up. The contact time between the hand and thermal receipt was thus considerably longer than would be the case for food eaten in the restaurant. In a food court we observed that some fast-food restaurants had hand sanitizer dispensers available for use by customers next to the cash register, and customers were observed using the hand sanitizer before handling the thermal receipt. The estimate is that 50 million people eat in a fast-food establishment every day in the USA [16]. Finally, our experiments here are also relevant to occupational exposures, because we observed in a national chain big-box store that all cash registers had a hand sanitizer dispenser next to them for use by the cashiers. Our objectives were to examine the impact of having dry hands vs. wet hands due to using a popular hand sanitizer that contains dermal penetration enhancing chemicals on extraction of BPA from the surface of thermal receipt paper coated with BPA. We also measured (using a LC/MSMS assay) unconjugated, bioactive BPA (uBPA) and its conjugated metabolites, BPA-glucuronide (BPA-G) and BPA-monosulfate (BPA-S), in serum and urine in adult male and female subjects after holding a thermal receipt. To determine the proportion of thermal receipts that contained BPA, we examined receipt papers for the presence and amount of BPA. We also examined receipts for the most commonly used BPA replacement chemical, bisphenol S [bis(4-hydroxyphenyl)sulfone; BPS; CAS #80-09-1].
Methods Ethics statement The University of Missouri School of Medicine Institutional Review Board approved all procedures involving human subjects, and sample collection was conducted by licensed personnel in the Clinical Research Center (CRC) within the University of Missouri School of Medicine. Subjects were informed of the procedures, and provided written consent. The signed consent forms were retained. The University IRB approved the consent procedure. Subjects Participants for the different experiments in this study were recruited through a weekly University of Missouri campus-wide email newsletter. Candidates (men and women) were pre-screened by age, height, weight, and health status. Participants selected were 20–40 years old (average 27.0 yrs), and an attempt was made to select those with average height, weight and normal-range body-mass index. Participants selected were not taking any prescription or non-prescription medication other than oral contraceptives; the type of oral contraceptive used was recorded. To ensure that pregnant women were excluded from the study, all women were administered a pregnancy test when they arrived at the CRC. For all studies participants were asked to refrain from touching thermal paper receipts, consuming food or beverages stored in polycarbonate or other types of plastic containers as well as canned food and beverages during the 48 hr prior to participating in the study, in order to reduce background BPA levels in body fluids as much as possible. The participants also filled out a questionnaire concerning their activities during the prior 48 hr (see Section S3 in File S1 for questionnaire). For experiments in which there was hand contact with thermal receipt paper, subjects were required to wash their hands with soap and water, rinse thoroughly, and then dry using Kimwipes (Kimberly-Clark, Irving, TX). A number of soaps were screened for BPA content and/or chromatographic interference prior to the start of the study, and the soap chosen was Softsoap “Aquarium series” (Colgate Palmolive Company, Manhattan, NY), which showed no detectable BPA or chromatographic interference with the assay of BPA. Standard brown laboratory paper towels were tested and found to contain BPA at around 6 µg/towel. Because of this, Kimwipes, which tested negative for BPA, were used throughout for drying hands. Water from faucets used in the CRC was tested and found to be below the limit of detection (LOD) for BPA content (detection limit was 10 pg/mL by HPLC with CoulArray detection based on C-18 extraction of 250 ml of water). Sample analysis Analysis of BPA in extracted samples occurred within an accredited facility (Veterinary Medicine Diagnostic Laboratory) within the College of Veterinary Medicine at the University of Missouri. Reagents. Solvents (methanol, acetonitrile) and water were HPLC grade, and were obtained from Fisher Scientific. BPA, bisphenol S (BPS), and BPA monosulfate (BPA-S) were obtained from Sigma-Aldrich (St. Louis MO; purity >99%, 98% and 95% respectively). C13-BPA was obtained from Cambridge Isotope Laboratories Inc. (Andover, MA; purity 99%), and both BPA-G (purity 98%) and BPA D-glucuronide (BPA-DG; purity >99%) were provided by the National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC. Ethanol (200 proof) used for hand swipes was obtained from Decon Labs, Inc. (King of Prussia, PA). Total receipt BPA and BPS content. Weighed samples of each receipt (3×3 cm) were incubated overnight in methanol at room temperature. The methanol extracts were diluted in methanol, typically to a final dilution of 1/10,000, and BPA content was analyzed by HPLC with CoulArray detection (see Section S1 in File S1 for details). We also analyzed the same receipt sample extracts for BPS using LC/MSMS (see Section S1 in File S1 for details). BPA levels in Kimwipe hand swipes. Kimwipe swipes were incubated in methanol at room temperature overnight, and aliquots were taken from the methanol extract for analysis. BPA in the methanol extract was determined by HPLC with CoulArray detection. BPA levels in French fries. French fries were incubated individually in methanol overnight. The fries were then removed, and the samples centrifuged briefly to separate any solid and/or oily matter, and a sample of the clear methanol extract was assayed. Equal volumes from the 10 extracts from the 10 French fries touched by each participant were pooled, and a single measurement was made for each participant. Quantitation was made by HPLC with CoulArray detection. Serum sample collection and extraction. Multiple-point blood samples were collected via IV catheter into 10 mL syringes, and the syringes were emptied into the same uncoated vacutainer tubes (for details and catalog numbers of collection materials Section S1 in File S1). Single point blood samples were collected by venipuncture into uncoated glass vacutainer tubes (Becton Dickinson, Franklin Lakes, NJ). All blood samples were allowed to clot at room temperature for 15–30 min and then refrigerated until centrifugation at 4°C for 15 min. The serum was transferred with glass Pasteur pipets into 15 mL centrifuge tubes and then frozen at −20°C. Samples were extracted using C18 SPE as previously described [17]; see Section S1 in File S1. Procedural blanks were also run alongside the samples to monitor for reagent contamination or interference. Serum extracts were analyzed by LC/MSMS. Urine sample collection and extraction. All urine samples were collected directly into Samco polypropylene specimen cups (Fisher Scientific, Waltham, MA) and were immediately refrigerated (4°C for 2–5 hours) until they could be transferred to the research laboratory, at which point they were frozen at −20°C. The total BPA concentration (representing a combined measure of unconjugated and conjugated BPA) was measured by LC/MSMS (see Section S1 in File S1). Assay of creatinine in urine. To calculate creatinine-corrected urine BPA concentrations, urine creatinine was measured using an ELISA kit (R&D Systems Inc., Minneapolis, MN), according to manufacturer’s instructions. Sensitivity of this assay is 0.02 mg/dL. Field blanks. The possibility of BPA leaching from each piece of equipment used in the collection or processing of samples identified above was determined by passing BPA-free water through all collection equipment, which was then handled and assayed for BPA as described below for the actual samples. All equipment and sample handling was determined to not leach detectable BPA before any sample collections occurred. Statistical methods and calculation of pharmacokinetic parameters For both uBPA and BPA-G, the area under the concentration-time curve (AUC) up to the last measured serum concentration above the LOQ, i.e. AUC (0–90 min), was calculated by using the linear trapezoidal rule. The average AUC (0–90 min) (ng/mL) was calculated by dividing AUC (0–90 min ng/mL)/90 min. Time (Tmax) of maximal plasma BPA concentration (Cmax) was directly obtained from the raw data. Comparisons of men and women were conducted using the Mann-Whitney U test or ANOVA. Statistical significance was set a P<0.05, two-tailed test. All data are presented as mean±SEM. Experiment 1: Measurement of BPA and BPS in 50 used thermal receipt papers The objective of this experiment was to determine the amount of BPA and BPS in thermal receipt paper and to determine the proportion of receipts that contained BPA or BPS, which is the most commonly used BPA replacement chemical. Thermal paper sales receipts were obtained by purchasing items from 41 different vendors in Columbia, MO and from a further 9 vendors in Southern Missouri (50 receipts total). Weighed portions of each paper were extracted and assayed for BPA by HPLC with CoulArray detection and for BPS by LC/MSMS. After screening, an unused roll was obtained from a vendor from which a BPA-positive receipt had been identified. The BPA content of paper from this roll was confirmed prior to being used for testing with human subjects in Experiments 2, 3 and 4. Experiment 2: BPA transferred to a hand with and without using hand sanitizer due to holding a thermal receipt for different lengths of time The objective of this experiment was to determine the amount of BPA extracted by a hand from a standard piece of thermal receipt paper immediately after using Purell hand sanitizer (Experiment 2-A) or with dry hands (Experiment 2-B). Subjects in both experiments cleaned and dried their hands prior to the experiment and between each trial. For Experiment 2-A the subjects (2 men and one woman) each held the thermal paper for different lengths of time: 2, 15, 30, 45, 60 or 240 sec (in 6 separate trials for each subject). Both hands were wetted by applying three “squirts” of Purell to each hand, and the hands were then briefly rubbed together to distribute the hand sanitizer evenly across both palms and fingers, but the sanitizer was not allowed to dry prior to holding the receipt paper. In experiment 2-B the subjects (2 men and 2 women) held the receipt with dry hands for 60 or 240 sec (2 separate trials for each subject). In both experiments an 8×12 cm portion of thermal paper cut from an unused receipt roll that was obtained from a local merchant (previously identified as containing 27.2 mg BPA/g paper) was placed BPA-coated (print surface) side down into the right hand. The hand was swiped 3 times each with 3 ethanol-soaked Kimwipes, and BPA was extracted from the Kimwipes with methanol and measured by HPLC with CoulArray detection. Experiment 3: Serum and urine BPA in men and women before and after transdermal and oral exposure to BPA from thermal receipt paper after using hand sanitizer The objective of this experiment was to measure the transfer of BPA from thermal paper receipts to hands, and the amount of BPA remaining on the surface of a hand 90-min later, after using Purell hand sanitizer (as described in the prior experiment) in 5 male and 5 female subjects. In addition, we measured the amount of BPA transferred from a BPA-contaminated hand to 10 French fries, and measured blood and urine concentrations of uBPA, BPA-G and BPA-S before and after ingestion of the French fries and BPA absorption through skin. The design of the study is shown in Figure 2. PPT PowerPoint slide
PowerPoint slide PNG larger image ( )
larger image ( ) TIFF original image ( ) Download: Figure 2. Schematic diagram of the protocol for Experiment 3 in which thermal receipt paper containing BPA was held with a hand wet from using Purell hand sanitizer, after which the subjects picked up 10 French fries and ate them, resulting in both oral and transdermal routes of exposure. Of the 5 male and 5 female subjects, 7 subjects had serum collected from the cubital vein in the arm with a contaminated hand that contained the BPA from holding thermal paper. Three subjects had blood collected from the cubital vein in the unexposed arm that did not have BPA on the hand throughout the 90-min test period during which blood was collected. Urine samples were obtained before and at the end of the test period. doi:10.1371/journal.pone.0110509.g002 The background level of BPA on the dominant hand was determined when the subjects first arrived at the CRC. The dominant hand was swiped 3 times with 3 separate Kimwipes soaked with ethanol, from which we extracted BPA for analysis by HPLC with CoulArray detection, and the hands were then cleaned. The subjects’ weight and height were determined, after which they provided a baseline urine specimen, an IV port was inserted into the cubital vein, and a baseline blood sample was collected. Purell hand sanitizer was applied to the hands as described in Experiment 2. An 8×12 cm piece of thermal paper cut from an unused receipt roll (used in Experiment 2) was then placed BPA-coated side down into each hand with the hands still wet. The subjects held the receipt papers for 4 min in each hand. The dominant arm of each subject was determined based on whether the person was right or left handed, and in this experiment the non-dominant hand remained contaminated with BPA for the duration of the experiment. Blood was collected from the cubital vein in the contaminated arm of one set of subjects (N = 7) and from the cubital vein in the non-contaminated arm of other subjects (N = 3). We note that the phlebotomist did not handle the thermal paper for either Experiment 3 or Experiment 4. The study coordinator who did handle the paper wore gloves to do so and did not touch the blood tubes of other equipment. A separate person swiped the subjects’ hands after thermal paper exposure and wore fresh gloves for each swipe session and discarded them immediately afterwards. French fries that had been purchased from a local fast food restaurant and had been found to not contain detectable BPA were briefly warmed in a toaster oven. Immediately after holding the thermal receipts in each hand, the subjects picked up a French fry in each hand, and held both fries for 10 sec. The fry held in the dominant hand was placed into a labeled glass tube, and the fry that was held in the non-dominant hand was eaten. A total of 10 French fries was handled by each hand and either placed in a test tube or eaten using this same procedure. Approximately 4 min elapsed between removal of the receipt paper from the hand and consumption of the last French fry. Thus, it took about 8 min from the time that the thermal receipt paper was first touched and consumption of the last French fry. After the last French fry was consumed, the subject’s dominant hand was swiped with 3 ethanol-soaked Kimwipes to clean BPA off the hand and for determination (by extracting BPA from the Kimwipes) of the amount of BPA remaining on the hand immediately after holding the 10 French fries that were placed into test tubes. The non-dominant hand was not cleaned after holding the receipt paper and eating French fries, and thus was a continuing source of transdermal BPA exposure over the following 90-min period of blood collection. Blood samples were collected from the cubital vein from the still contaminated arm of 7 subjects, 4 males and 3 females, and from the uncontaminated arm of 3 subjects, one male and 2 females. The blood collected from the BPA-contaminated arm provided direct information about BPA absorbed from the hand on which BPA remained for 90 min, since the cubital vein is one of the major veins draining the hand; this blood is not subject to first-pass liver metabolism prior to going to the heart and being transported in the arterial circulation to tissues. The blood collected from the uncontaminated arm provided information about BPA in the systemic (mixed) circulation. Blood was collected from the IV port before holding the thermal paper (baseline) and at 15, 30, 60 and 90 min after consumption of the last French fry. The non-dominant contaminated hand (from which the French fries were eaten) was not allowed to touch anything during the 90-min after holding the receipt paper and then picking up the 10 French fries; this hand was swiped with 3 ethanol-soaked Kimwipes after the final 90-min blood collection at the end of the study. After these swipes were obtained, both hands were thoroughly cleaned and a second urine sample was collected. Experiment 4: Serum and urine BPA in men and women before and after transdermal exposure to BPA from thermal receipt paper with dry hands The objective of this study was to examine the amount of BPA transferred to a clean dry hand and then present in serum and urine without using hand sanitizer. In this study we examined 12 adult men and 12 adult women subjects. The subjects washed and dried their hands and provided a baseline blood and urine sample as described in Experiment 3. The non-dominant hand was swiped 3 times each with 3 ethanol-soaked Kimwipes to obtain a baseline measure of BPA on the hand prior to holding a thermal receipt. After the hand was dry, subjects held an 8×12 cm piece of thermal receipt paper (from the roll used in Experiment 1) with the non-dominant dry hand for 4 min. Thirty minutes later a second blood sample was collected from the contaminated arm, after which the BPA was swiped from the contaminated hand with ethanol-soaked Kimwipes as described previously. As above, the contaminated hand was not allowed to touch anything during the 30-min period prior to the second blood collection. The hands were washed, and a second urine sample was collected 60 min after holding the receipt paper.
Conclusions Thermal paper requires a chemical in the surface coating as a print developer. The current preferred developers, BPA and BPS, have both been shown to have estrogenic activity [45], [46]. This is leading to widespread exposure to both of these endocrine-disrupting chemicals [7], [47], and BPS is more persistent in the environment relative to BPA and is thus an unacceptable replacement for BPA [18], [48]. A recent EPA report examined 19 alternative chemicals, including BPS, that could potentially replace BPA as a developer in thermal paper and concluded that “No clearly safer alternatives to BPA were identified in this report; most alternatives have Moderate or High hazard designations for human health or aquatic toxicity endpoints” [18]. The report identified that “decision makers may wish to consider alternative printing systems”. Two of the papers screened for our current study employed a developer other than BPA or BPS that was not estrogenic in a MCF-7 human breast cancer cell proliferation assay (data not shown), but lack of estrogenic activity does not imply safety, as indicated in the EPA report. Thermal paper is a major source of BPA contamination in recycled paper, and its use results in the widespread contamination of other products and the environment [49] due to the presence of large amounts of free, unpolymerized BPA in the surface coating of thermal paper (Figure 1). Further, our findings are consistent with other data reporting that BPA can be transferred from the surface of thermal paper to items it contacts. Because no safe alternatives to the use of BPA or its primary replacement chemical BPS in thermal paper have been identified, our findings provide support for the EPA’s recommendation that thermal paper should be replaced with other safer technologies [18]. Our study provides the first data that thermal paper may be a significant factor in accounting for high levels of bioactive BPA in human serum and total BPA in urine that have been associated with diseases that are increasing in frequency in human populations [21], [34]. Our findings also suggest that the impact of the use of dermal penetration enhancing chemicals in skin care products on transdermal absorption of environmental contaminants should be taken into consideration in risk assessments and should be a priority for future research.
Supporting Information File S1. Section S1: Sample handling, extraction and assay methods. Section S2: Table of individual BPA and BPS values for 50 thermal receipt papers. Section S3: List of questions asked each subject. doi:10.1371/journal.pone.0110509.s001 (DOCX) ||||| Bisphenol A (BPA) is used to manufacture polycarbonate plastics. This type of plastic is used to make some types of beverage containers, compact disks, plastic dinnerware, impact-resistant safety equipment, automobile parts, and toys. BPA epoxy resins are used in the protective linings of food cans, in dental sealants, and in other products.
How People Are Exposed to BPA
General exposure to BPA at low levels comes from eating food or drinking water stored in containers that have BPA. Small children may be exposed by hand-to-mouth and direct oral (mouth) contact with materials containing BPA. Dental treatment with BPA-containing sealants also results in short-term exposure. In addition, workers who manufacture products that contain BPA can be exposed.
How BPA Affects People’s Health
Human health effects from BPA at low environmental exposures are unknown. BPA has been shown to affect the reproductive systems of laboratory animals. More research is needed to understand the human health effects of exposure to BPA.
Levels of BPA in the U.S. Population
In the Fourth National Report on Human Exposure to Environmental Chemicals (Fourth Report), CDC scientists measured BPA in the urine of 2,517 participants aged six years and older who took part in CDC’s National Health and Nutrition Examination Survey (NHANES) during 2003–2004. By measuring BPA in urine, scientists can estimate the amount of BPA that has entered peoples’ bodies.
CDC scientists found BPA in the urine of nearly all of the people tested, which indicates widespread exposure to BPA in the U.S. population.
Finding a measurable amount of BPA in the urine does not imply that the levels of BPA cause an adverse health effect. Biomonitoring studies on levels of BPA provide physicians and public health officials with reference values so that they can determine whether people have been exposed to higher levels of BPA than are found in the general population. Biomonitoring data can also help scientists plan and conduct research on exposure and health effects.
Additional Resources
Department of Health and Human Services
Bisphenol A (BPA) Information for Parents
https://www.hhs.gov/safety/bpa/
Food and Drug Administration
Food Ingredients & Packaging | Bisphenol A
https://www.fda.gov/Food/FoodIngredientsPackaging/ucm166145.htm
https://www.fda.gov/Food/FoodIngredientsPackaging/ucm166145.htm Bisphenol A (BPA): Use in Food Contact Application
https://www.fda.gov/NewsEvents/PublicHealthFocus/ucm064437.htm
National Toxicology Program ||||| The Facts About Bisphenol A
In 2008, the possible health risks of Bisphenol A (BPA) -- a common chemical in plastic -- made headlines. Parents were alarmed, pediatricians flooded with questions, and stores quickly sold-out of BPA-free bottles and sippy cups.
Where do things stand now? Have plastic manufacturers changed their practices? How careful does a parent need to be when it comes to plastics and BPA? Here's the latest information we have about possible BPA risks.
BPA Basics
BPA is a chemical that has been used to harden plastics for more than 40 years. It's everywhere. It's in medical devices, compact discs, dental sealants, water bottles, the lining of canned foods and drinks, and many other products.
More than 90% of us have BPA in our bodies right now. We get most of it by eating foods that have been in containers made with BPA. It's also possible to pick up BPA through air, dust, and water.
BPA was common in baby bottles, sippy cups, baby formula cans, and other products for babies and young children. Controversy changed that. Now, the six major companies that make baby bottles and cups for infants have stopped using BPA in the products they sell in the U.S. Many manufacturers of infant formula have stopped using BPA in their cans, as well.
According to the U.S. Department of Health, toys generally don't contain BPA. While the hard outer shields of some pacifiers do have BPA, the nipple that the baby sucks on does not.
BPA Risks
What does BPA do to us? We still don't really know, since we don't have definitive studies of its effects in people yet. The U.S. Food and Drug Administration used to say that BPA was safe. But in 2010 the agency altered its position. The FDA maintains that studies using standardized toxicity tests have shown BPA to be safe at the current low levels of human exposure. But based on other evidence -- largely from animal studies -- the FDA expressed "some concern" about the potential effects of BPA on the brain, behavior, and prostate glands in fetuses, infants, and young children. |||||
Write a summary. | – Thought you'd cut your risk of BPA exposure by ditching plastic water bottles? You might have to add "stop asking for receipts at the store" to the list. Scientists tested the skin, blood, and urine of people before and after they handled receipts and other thermal papers that use bisphenol A as a print developer—and found that levels of the chemical rose, Forbes reports. Although the CDC won't definitively acknowledge BPA's risks—"More research is needed" is the official hedge on its fact sheet—WebMD points to various studies that have linked BPA to a variety of health issues, including a higher risk of cancer, heart problems, and brain and behavioral issues in babies and young children. Researchers who conducted the new study in PLoS One had participants handle receipt paper, then asked some of them to eat French fries using their hands. BPA levels in the skin spiked to 581 micrograms of BPA within 45 seconds (and 40% of that was absorbed in just two seconds). Urine and blood BPA levels were also strikingly higher 90 minutes after holding the receipts—and numbers here were on par with those from previous studies that were linked to Type 2 diabetes and heart disease, Forbes notes. Levels were even higher for subjects who had used hand sanitizer before handling the receipts; scientists attribute this to sanitizers (and toiletries like sunscreen and lotion) making hands more absorbent. Forbes notes the study was "quite small and more research will be needed," while a spokesman for the American Chemistry Council notes the study's "unrealistic experimental conditions" and that "much of the data presented in this new study has very limited relevance to the potential for human exposure to BPA from handling thermal receipt paper." (Your BPA-free water bottle may still not be safe.) | multi_news_1_0_0 |
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Image caption Heart experts say men who have lost their hair 'should not be alarmed'
Men going thin on top may be more likely to have heart problems than their friends with a full head of hair, according to researchers in Japan.
Their study of nearly 37,000 people, published in the online journal BMJ Open, said balding men were 32% more likely to have coronary heart disease.
However, the researchers said the risks were less than for smoking or obesity.
The British Heart Foundation said men should focus on their waistline, not their hairline.
A shifting hairline is a fact of life for many men. Half have thinning hair by their 50s and 80% have some hair loss by the age of 70.
Researchers at the University of Tokyo sifted through years of previous research into links between hair loss and heart problems.
It's more important to pay attention to your waistline than your hairline Doireann Maddock, British Heart Foundation
They showed that hair that went thin on the crown was associated with coronary heart disease. This was after adjusting for other risk factors such as age and family history.
However, a receding hairline did not seem to affect the risk.
Focus on lifestyle
Dr Tomohide Yamada, of the University of Tokyo, told the BBC: "We found a significant, though modest, link between baldness, at least on the top of the head, and risk for coronary heart disease.
"We thought this is a link, but not as strong as many other known links such as smoking, obesity, cholesterol levels and blood pressure."
He said younger men losing hair on the top of their head should focus on improving their lifestyle to ensure they keep their heart healthy.
However, he said there was not enough evidence to suggest screening bald men for heart problems.
Deadly disease Coronary heart disease is the biggest killer in the UK. One in five men and one in eight women dies of the disease. It is caused by blood vessels that nourish the heart becoming blocked.
Any explanation for the link is uncertain.
There are ideas about increased sensitivity to male hormones, insulin resistance and inflammation in blood vessels affecting both the heart and the hair.
Doireann Maddock, a cardiac nurse with the British Heart Foundation, said: "Although these findings are interesting, men who've lost their hair should not be alarmed by this analysis.
"Much more research is needed to confirm any link between male pattern baldness and an increased risk of coronary heart disease. In the meantime, it's more important to pay attention to your waistline than your hairline.
"Hereditary hair loss may be out of your control, but many of the risk factors for coronary heart disease are not. Stopping smoking, maintaining a healthy weight and being as active as possible are all things that you can do to help protect your heart."
Patrick Wolfe, a professor of statistics at University College London, said: "Right now the link that is seemingly responsible for this relative risk increase is not well understood, and so in future we might look forward to a day when understanding more about the various mechanisms underlying heart disease will tell us more about those underlying male pattern baldness, and vice versa.
"In the meantime it's a case of focusing on the things that we can control - our diet, exercise regimens and other risk factors - to lower our overall risk for heart disease." ||||| Baldness may be a sign of increased resistance to insulin, a precursor to diabetes; a state of chronic inflammation; or increased sensitivity to the male sex hormone testosterone, and those conditions may lead to the development of cardiovascular disease, the researchers said.
Baldness may be a sign of increased resistance to insulin, a precursor to diabetes; a... Read More
Baldness may be a sign of increased resistance to insulin, a precursor to diabetes; a state of chronic inflammation; or increased sensitivity to the male sex hormone testosterone, and those conditions may lead to the development of cardiovascular disease, the researchers said. Close
Losing hair at the crown of the head may signal an increased risk of heart disease in men.
The strength of the association depends on the degree of baldness, researchers at the University of Tokyo’s department of diabetes and metabolic diseases found by reviewing past studies. No link to heart disease was found for men with a receding hairline, said the scientists, who reviewed six studies with a total of almost 37,000 participants. Their findings were published today in the BMJ Open medical journal.
Hair loss has been associated with the risk of developing prostate cancer in previous research. Baldness may be a sign of increased resistance to insulin, a precursor to diabetes; a state of chronic inflammation; or increased sensitivity to the male sex hormone testosterone, and those conditions may lead to the development of cardiovascular disease, the researchers said.
“The present meta-analysis provided useful evidence regarding the potential influence of baldness on coronary heart disease,” the authors said in the published paper. “Patients and physicians should consider the possibility that baldness is associated with an increased risk.”
Three of six studies analyzed tracked the participants’ health for at least 11 years. They suggested that men who had lost most of their hair were a third more likely to develop heart disease than peers who retained a full head of hair.
Relative Risk
The other three studies showed that balding men were 70 percent more likely to have heart disease, the researchers found. The more extensive the baldness, the higher the risk, they said. The scientists got no specific grant to fund the study, they said.
“It is important to remember that the study reports an increase in relative risk,” said Patrick Wolfe, a professor of statistics at University College London.
Comparing two non-smoking males in good physical condition, one of of whom is bald and the other not, their absolute risks for heart disease are likely to be very small, even if their relative risks may be different, Wolfe said.
“In the meantime, it’s a case of focusing on the things that we can control -- our diet, exercise regimes and other risks factors -- to lower our overall risk for heart disease,” he said.
To contact the reporter on this story: Makiko Kitamura in London at [email protected]
To contact the editor responsible for this story: Phil Serafino at [email protected] |||||
Summary: | – Bald men seem to be at higher risk of heart disease, say Japanese researchers after poring over old studies. Their finding applies only to those who have lost hair on top, at the crown, as opposed to those with receding hairlines, reports Bloomberg. The greater the baldness, the greater the risk. "We thought this is a link, but not as strong as many other known links such as smoking, obesity, cholesterol levels, and blood pressure," one of the University of Tokyo researchers tells the BBC. Why? That part is unclear, but one theory is that some of the same factors associated with baldness—such as heightened sensitivity to testosterone and resistance to insulin—are also linked to cardiovascular trouble. The baldness, then, could be a visible sign of trouble within. One analysis found that bald men were about 30% more likely to have heart trouble, while another put the figure at 70%. It may sound alarming, but "much more research is needed to confirm any link between male pattern baldness and an increased risk of coronary heart disease," says a cardiac expert with the British Heart Foundation. "In the meantime, it's more important to pay attention to your waistline than your hairline." | multi_news_1_0_0 |
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– If you hate spending time at the mechanic, you'll need a Porsche. Or at least a Kia. JD Power and Associates is out with its annual rankings on new-vehicle quality, and those brands are at the top of the list, reports AP. The results factor in problems reported by owners in the first 90 days. Forbes says the biggest surprise on the overall list is that Japanese cars now fall below the industry average for the first time in 30 years. Here is the top 10, with the number of problems reported per 100 vehicles, and the number of spots the brand rose or fell from last year: Porsche (80, same) Kia (86, +5) Jaguar (93, -1) Hyundai (95, same) Infiniti (97, +18) BMW (99, +2) Chevrolet (101, -1) Lincoln (103, +2) Lexus (104, -6) Toyota (104, -4)
Let's expand this into a news article: This will appear next to all of your comments
This will NOT appear anywhere on Newser ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. |||||
– Animal experts believe a dog in Oregon was only trying to be helpful when he chewed off three of his diabetic owner's toes as the man slept. The dog, a Shiba Inu called Cosmo, was acting on instinct to help remove diseased flesh and doesn't seem to be dangerous, according to a county official. Its owner, who suffers from numbness in his hands and feet caused by diabetes, called 911 after waking up to find himself short a few toes. He has put the dog up for adoption, AP reports. The dog has to remain quarantined for 10 days after eating human flesh but the animal adoption center hopes to find a home for him afterward. Cosmo, who was healthy but anxious when he arrived at the center, "is a bit aloof, but overall he's a friendly dog, I suppose," the director of the center tells Seattle Weekly. Bizarrely enough, this has happened before...
| Let's expand this into a news article: Do you need some added companionship around the house? Are you an animal lover? And most important, do you have or plan to have an abundance of dead tissue on your body, like, say, a few dead and infected toes? Well, the Saving Grace Pet Adoption Center in Roseburg, Ore., has just the dog for you!
His name is Cosmo. He's a Shiba Inu. And, as we told you about last week, he recently ate half his owner's foot.
Now, for some reason, the owner, James Little, no longer wants the dog.
Seattle Weekly talked with Saving Grace Pet Adoption Center Director Wendy Kang, who said the rambunctious pup isn't quite available yet, since he has to remain quarantined for 10 days after eating human flesh. But by this time next week, he could be munching the toes off all your gangrenous friends.
Kang has nothing but the most glowing endorsements for little Cosmo. "[He] is a bit aloof, but overall he's a friendly dog, I suppose," she says.
According to the American Kennel Club, the Shiba Inu ranges from 17 to 23 pounds and was originally bred for hunting small game, boar, and bear in Japanese forests (no, really, it says they hunted freaking bears).
Little, a diabetic man who has no feeling in his feet, didn't even realize that little Cosmo was feasting on his phalanges until he woke up sans three toes and half his foot. The phenomenon isn't unique to Cosmo--several other cases of dogs eating infected or dead tissue from their masters have been reported.
In one case, a dog's eating of his drunk and passed-out owner's toe is credited with saving the man's life, because the eaten toe alerted doctors to the man having deadly type-II diabetes.
So little Cosmo isn't necessarily a bloodthirsty zombie dog--he just cares a lot about his master's hygiene.
Follow The Daily Weekly on Facebook and Twitter. ||||| A dog ate three of his owner's toes as the diabetic man slept, most likely out of instinct to help remove diseased flesh, animal experts say.
James Little, 61, made an emergency call on Tuesday to say his dog had eaten the body parts while he was sleeping. He told The Associated Press on Friday that he is "doing fine."
Little suffers from diabetes, of which one symptom is numbness in the hands or feet.
The dog, a Shiba Inu, was acting on its instinct to remove diseased flesh and does not appear to be dangerous, said Douglas County Animal Control Deputy Lee Bartholomew.
Dogs have been known to eat dead or diseased human flesh. A family's dog in Illinois ate the toes off a 10-year-old girl's left foot while she slept last December. She had a sore on her foot.
In August, a dog in Michigan bit off most of its owner's infected big toe after the man passed out from alcohol. The man had diabetes, and the animal was apparently attracted to a festering wound.
Little has given up ownership of his dog, putting it up for adoption pending an examination and a standard 10-day quarantine to determine it does not have rabies, Bartholomew said.
The dog was taken to Roseburg's Saving Grace Pet Adoption Center, where executive director Wendy Kang said the animal is healthy but appears anxious.
Little was in fair condition at a hospital and expected to be released later Friday. ||||| | multi_news_1_0_0 |
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– When it comes to sugar, Americans need to be a lot more careful, a study finds. Even two cans of soda a day can significantly boost the risk of death from heart disease. If a quarter of your daily caloric intake comes from added sugar—in processed foods, for instance—your risk of death from heart disease could be triple the risk faced by someone who gets less than 10% of her calories from sugar. What could get you to the 25% level? The AP give this example: a breakfast cinnamon roll, a super-sized soda at lunch, and ice cream after dinner. About 10% of adults hit that level; between 2005 and 2010, Americans got an average 15% of their calories from added sugar, Bloomberg notes. Researchers led by a CDC expert found that the dangers from sugar weren't just due to obesity: The threat exists for people of normal weight. The study reviewed national health surveys between 1988 and 2010; the researchers investigated data on some 30,000 people. Soda and other sugary drinks are the main problem, accounting for some 37% of the added sugar in an American diet. Desserts and fruit drinks make up much of the rest. (Sugars found naturally in fruits and vegetables weren't classified as "added sugar.") Says an expert who write an editorial accompanying the study in JAMA Internal Medicine, "Too much sugar does not just make us fat; it can also make us sick." | Special Sections
JAMA Internal Medicine has several sections devoted to contemporary issues confronting internists.
Case studies of patients with challenging electrocardiograms.
Articles about how overuse of medical care may result in harm and how less intervention may lead to better health.
JAMA Internal Medicine publishes a subsection of Perspectives, Teachable Moments, to bring attention to the harms that can result from medical overuse and from underuse of needed medical interventions. The format for submitting an entry is described here; manuscripts should be submitted here as usual. Note we need written permission from patients to include their story. Read all Teachable Moments here.
Articles addressing health care reform in JAMA Internal Medicine's Health Care Reform feature.
Firearm Violence
Articles from the JAMA Network ||||| High sugar consumption may double the chance of dying from heart disease, according to a study that adds to evidence that high levels of the sweetener in processed foods and drink is bad for a person’s health.
People whose sugar intake is about a quarter or more of their total daily calories had twice the risk of dying from heart disease than those who whose intake was 7 percent, according to the research today in JAMA Internal Medicine. For those whose intake of added sugar was about 19 percent, their risk of dying from heart disease was about 38 percent higher.
Today’s study is the first to link on a national level the amount of sugar American adults eat to their risk of dying from heart disease after taking into account weight, age, health, exercise and diet, said lead study author Quanhe Yang, an epidemiologist at the U.S. Centers for Disease Control and Prevention. Research has already linked sugar consumption to diabetes, weight gain and obesity.
“Too much sugar can make you fat; it can also make you sick, sick from diseases like cardiovascular disease, which is the No. 1 killer in America,” said Laura Schmidt, a school of medicine professor at the University of California at San Francisco, in a telephone interview. “Small amounts of sugar are fine. It’s consuming massive amounts of sugar that’s a growing problem in America.”
The study also found that regular consumption of sugar-sweetened beverages, seven servings or more each week, was linked to an increased risk of dying from heart disease.
600,000 Deaths
Heart disease, which can cause heart attack, chest pain and heart failure, is the leading cause of death worldwide for both men and women and kills more than 600,000 Americans each year, according to the Atlanta-based CDC.
There is no specific national guideline for sugar consumption. The Institute of Medicine recommends sugar be less than 25 percent of total calories, the World Health Organization recommends less than 10 percent, while the American Heart Association suggests limiting sugar to less than 150 calories a day for men and less than 100 calories a day for women, the authors wrote.
‘The majority of us are consuming more added sugar than the recommendations,’’ Yang said in a telephone interview.
About 37 percent of added sugar in U.S. diets comes from sugar-sweetened beverages, while the rest comes from grain-based desserts, fruit drinks, dairy desserts and candy, the authors said. Sugar from fresh fruits and vegetables isn’t considered added sugar.
Better food labels would help people identify their sugar intake, said Schmidt, who wrote an editorial accompanying the study.
Sugar Effects
Scientists don’t have a clear understanding why sugar may raise the risk of dying from heart disease, Yang said. Sugar may increase blood pressure and weight gain, both risk factors for heart disease, or it may raise bad cholesterol and triglycerides and lower good cholesterol. Sugar may also increase insulin resistance, a factor in diabetes, or increase fat accumulation in the liver, he said.
Researchers in the study looked at data from several National Health and Nutrition Examination Surveys, which provides nationally representative information on U.S. adults.
They found that U.S. adults consumed about 14.9 percent of daily calories from added sugar in 2005-2010, down from 16.8 percent in 1999-2004. For most U.S. adults, added sugar made up 10 percent or more of their daily calories during 2005-2010 and for 10 percent of people, sugar made up 25 percent or more of their daily calories.
Today’s findings support recommendations to limit intake of sugar-added foods and drinks, Yang said.
“We are in the midst of a paradigm shift in research on the health effects of sugar, one fueled by extremely high rates of added sugar overconsumption in the American public,” Schmidt said in an editorial accompanying the study.
To contact the reporter on this story: Nicole Ostrow in New York at [email protected]
To contact the editor responsible for this story: Reg Gale at [email protected] ||||| | multi_news_1_0_0 |
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Taylor Swift has taught a generation of kids to appreciate country music over the last five years. Now she's donating $4 million to the Country Music Hall of Fame and Museum to make sure that education continues.
This artist's rendering by Tuck-Hinton Architects provided by the Country Music Hall of Fame and Museum shows the Taylor Swift Education Center in Nashville, Tenn. The country music superstar is donating... (Associated Press)
In this Nov. 20, 2012 photo, Taylor Swift arrives at the 39th Annual American Music Awards in Los Angeles. Swift is donating $4 million to the Country Music Hall of Fame and Museum to fund the 7,500 square... (Associated Press)
The gift is the largest given to the museum by an artist, officials said. It will fund the Taylor Swift Education Center, an exhibit and classroom space scheduled to open in 2014.
The new education center is part of the museum's $75 million expansion project that will include a new concert theater and more room for exhibits and archives.
The 22-year-old singer-songwriter is country music's top-selling artist. The six-time Grammy winner has taken the genre to Asia, Europe and Australia as well as the top of the U.S. pop charts.
One of her first public performances was on the museum's plaza. She also signed her record contract there. ||||| Who says celebrities only blow their millions on mansions and cars?
A-listers like Sandra Bullock, Angelina Jolie and Brad Pitt have all pitched in and contributed time and money to charitable causes over the years. Lately, Oscar-nominee George Clooney has been making waves with his activism -- even getting arrested with the CEO of Jewish World Watch after protesting at the Sudanese embassy on March 16, 2012.
Who else has been using their fame to help the world? Click through the gallery to find out!
Now more than ever, celebs are rolling up their sleeves and speaking out for a great cause. Along with Lisa Edelstein and How I Met Your Mother's Josh Radnor, Hotel Rwanda star Don Cheadle is continuing his work against injustice in Darfur by partaking in the Walk to End Genocide happening this May.
Celebuzz Single Player No Autoplay (CORE) No changes are to be made to this player |||||
What is a one-paragraph summary of the above article? | – Taylor Swift is donating a sizable $4 million to the Country Music Hall of Fame and Museum, the largest gift ever donated to the museum by an artist. It will fund the Taylor Swift Education Center, a new classroom and exhibit space opening in 2014, the AP reports. Swift proves that not all celebrities spend their dough on things like $12,000 Chanel bicycles and $18,500 olive trees, and Celebuzz rounds up 14 more who give freely of their money and/or their time. And while some are obvious (hello, George Clooney) many might surprise: Sandra Bullock: Has donated $1 million to relief organizations that give aid to those affected by 9/11, the 2004 Indian Ocean earthquake, and the recent earthquakes in Haiti and Japan. Ellen DeGeneres: Her pet cause is, ahem, animal rights and rescue organizations, and her pet food line benefits charity. Alicia Keys: This ambassador for Keep A Child Alive, an organization focused on families affected by AIDS, does everything from hosting fundraisers to traveling to Africa. Nick Jonas: He has diabetes, and acts as an ambassador for Bayer Diabetes Care, promoting research funding. Eva Longoria: She’s a spokesperson for PADRES Contra El Cancer and supports many other Latino causes and community organizations. Click for the complete list, which includes one celeb who has raised more than $125 million for the AIDS Foundation. | multi_news_1_0_0 |
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News article:
Robert A Levinson vanished in the Persian Gulf in 2007, though the US has claimed it has evidence he is still alive
The FBI has offered an award of up to $1m for information leading to the location of a former special agent who disappeared in Iran five years ago.
Robert A Levinson vanished on Kish Island, a Persian Gulf resort, in March 2007. He was 59 at the time. Formerly an FBI agent, Levinson was working as a private investigator when he disappeared. His family and US officials say he was investigating cigarette smuggling for a private client at the time of his disappearance.
In December, a video of Levinson surfaced showing him alive, if gaunt, a year earlier. Levinson addresses the camera from inside a concrete cell, where he claims to have been held for three years. He said he had been treated well, but implored US authorities to co-operate with his unidentified captors.
A screenshot from the video released in December
"I need the help of the United States government to answer the requests of the group that has held me," Levinson said at the time.
"Please help me get home. Thirty-three years of service to the United States deserves something," he added.
Levinison's wife and seven children received an email last year containing photographs of him wearing what appears to be an orange prison uniform and with a full beard. While federal agents were able to trace the emails back to Afghanistan or Pakistan, they were unable to pinpoint their exact source.
On Tuesday, the FBI issued a statement reading: "The Federal Bureau of Investigation will hold a press conference to announce a reward of up to $1,000,000 for information leading directly to the safe location, recovery and return of Robert A Levinson. Robert A Levinson is a US citizen and former FBI Special Agent who disappeared from Kish Island, Iran, five years ago on March 9, 2007."
The agency announced the reward at a press conference at the FBI's field office in Washington, DC.
Officials in Iran have denied any knowledge of Levinson's disappearance. President Mahmoud Ahmadinejad, during a 2010 trip to the US, said his government was willing to co-operate in the investigation.
Last year, the secretary of state, Hilary Clinton, indirectly referred to the case, saying the US had evidence Levinson was alive. ||||| FBI Director Robert Mueller has made a personal plea for the safe return of a former FBI agent who disappeared in Iran five years ago. NBC's Pete Williams reports.
U.S. investigators believe the captors of retired FBI agent Robert Levinson, missing since 2007, are in the border region that Iran shares with Pakistan and Afghanistan.
That detail, one of the most specific ever offered by the FBI in the long search for Levinson, emerged Tuesday as FBI Director Robert Mueller announced the offer of a $1 million reward for information that leads to Levinson’s safe return.
A 22-year veteran of the FBI, he disappeared five years ago from the resort island of Kish in Iran, after meeting a contact while working as a private investigator looking into cigarette smuggling. Very little has been learned about his whereabouts since then, despite an intensive investigation and the release of a video last fall in which he pleaded for help.
"There have been some indications that a group has him" and that they are located in the border regions of Afghanistan, Iran, and Pakistan, said James McJunkin, the FBI assistant director in charge of the Washington field office.
Over 100 current and former agents stood on the front steps of the FBI's Washington, D.C., office Tuesday in a show of solidarity with their former colleague and his family. Levinson's wife of 37 years, Christine, choked up as she discussed her ordeal.
"There are no words to describe the nightmare my family and I have been living every day. I never imagined that we would still be waiting for Bob to come home five years later," she said.
Secretary of State Hillary Clinton said the Levinson case “remains a priority for the United States.”
Manuel Balce Ceneta / AP An FBI poster shows a composite image of former FBI agent Robert Levinson, right, indicating how he would look now after five years in captivity, an image, center, taken from the video released by his kidnappers, and a picture before he was kidnapped, left, displayed during a news conference.
“We welcome the assistance of our international partners in this investigation. We also call on the Government of Iran to uphold its promise of assistance and help safely return Mr. Levinson to the United States,” she said in a written statement.
The FBI is spreading the word of the reward offer through billboards, fliers, and radio announcements overseas. "Help Robert get back to his family by contacting your nearest American embassy or US consulate," the messages say, printed and broadcast in the languages of the border regions.
The billboards and fliers include photos to show how Levinson appeared in the recent video and how he might look now, with longer hair and a graying beard. They also include local telephone numbers to receive confidential tips. Information can be sent over the Internet to an FBI tips link.
"We hope that this reward will encourage anyone with information about Bob or his captors, no matter how insignificant it seems, to contact the FBI," McJunkin said.
Levinson, whose 64th birthday is March 10, is diabetic with high blood pressure, and his family is concerned for his health. Agents say they have no hard evidence to indicate where he may have been taken the day he disappeared.
More content from msnbc.com and NBC News |||||
What is a shorter version of the above article? | – The FBI is offering up to $1 million for information leading to the return of former special agent Robert Levinson, a 63-year-old who vanished in Iran five years ago while working as a private investigator probing cigarette smuggling, the Guardian reports. A video of Levinson pleading for help from the US government, in which he says a group has been holding him for years, surfaced late last year. An FBI assistant director says investigators believe Levinson is being held in the border region Iran shares with Afghanistan and Pakistan. Emails sent to the former agent's wife and seven children containing photos of him in an orange prison uniform are believed to have been sent from Afghanistan or Pakistan. More than 100 current and former FBI agents stood on the steps of the agency's Washington, DC, office yesterday in a show of support for Levinson, reports MSNBC. | multi_news_1_0_0 |
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Bedtime procrastination: introducing a new area of procrastination
Department of Clinical and Health Psychology, Utrecht University, Utrecht, Netherlands
Background: Procrastination is a prevalent and problematic phenomenon that has mostly been studied in the domain of academic behavior. The current study shows that procrastination may also lead to harmful outcomes in the area of health behavior, introducing bedtime procrastination as an important factor related to getting insufficient sleep and consequently affecting individual well-being. Bedtime procrastination is defined as failing to go to bed at the intended time, while no external circumstances prevent a person from doing so.
Methods: To empirically support the conceptual introduction of bedtime procrastination, an online survey study was conducted among a community sample (N = 177). The relationship between bedtime procrastination and individual difference variables related to self-regulation and general procrastination was assessed. Moreover, it was investigated whether bedtime procrastination was a predictor of self-reported sleep outcomes (experienced insufficient sleep, hours of sleep, fatigue during the day).
Results: Bedtime procrastination was negatively associated with self-regulation: people who scored lower on self-regulation variables reported more bedtime procrastination. Moreover, self-reported bedtime procrastination was related to general reports of insufficient sleep above and beyond demographics and self-regulation.
Conclusions: Introducing a novel domain in which procrastinators experience problems, bedtime procrastination appears to be a prevalent and relevant issue that is associated with getting insufficient sleep. ||||| In 2008, a nameless commenter at Procrastinator's Anonymous asked a question that garnered significant response:
"I often find myself delaying my bedtime hour, even when I have nothing important that keeps me from going to bed. It's an odd feeling, because I feel sleepy. Can we even call this 'procrastination'? I'm not sure."
Six years later, researchers from Utrecht University have an answer: Yes.
The Centers for Disease control labels insufficient sleep a "public health epidemic." Thirty percent of adults report sleeping fewer than six hours per night. That's not healthy. According to the CDC, "Persons experiencing sleep insufficiency are... more likely to suffer from chronic diseases such as hypertension, diabetes, depression, and obesity, as well as from cancer, increased mortality, and reduced quality of life and productivity." Even more startling, a 2009 survey found that one in twenty individuals admitted to dozing off behind the wheel in the previous month.
Clearly, we need more sleep. So why aren't we getting it? Some of the more popular reasons include artificial lighting, stress, and restrictive work hours. Now, in a new study published to Frontiers in Psychology, Floor Kroese, an assistant professor in psychology at Utrecht University, and a team of researchers put forward the notion that we don't get enough sleep because... meh.
In other words, we procrastinate.
The textbook definition of procrastination is a “voluntary delay of an intended course of action despite expecting to be worse off for the delay." At least half of college students do it on academics and a tenth of the general population procrastinates chronically.
In her study, Kroese surveyed 177 individuals via Amazon's Mechanical Turk on all sorts of lifestyle and demographic factors, sleep and inclination to procrastinate among them. Bedtime procrastination was gauged by assessing subjects' level of agreement with statements like "I go to bed later than I had intended" and "I easily get distracted by things when I actually would like to go to bed." Digging into the data, Kroese found moderate levels of bedtime procrastination among the survey population. She also found that it was negatively correlated with reported hours of sleep and positively correlated with fatigue and insufficient sleep.
But the results prompt some obvious skepticism. It's not like sleep is a chore, so why would people procrastinate on it?
"We speculate that it is not so much a matter of not wanting to sleep, but rather of not wanting to quit other activities," Kroese explains. Instead of going to sleep, it's "one more episode" on Netflix or "one more quest" on that video game.
"Bedtime procrastination may be a relatively modern phenomenon," she adds.
For those bedtime procrastinators out there, fixing their problem could be a tall task. Sleep is nice, but watching people get beheaded on Game of Thrones, well, that's hard to contend with.
Source: Kroese F, De Ridder D, Evers C and Adriaanse M (2014). Bedtime Procrastination: Introducing a New Area of Procrastination. Front. Psychol. 5:611. doi: 10.3389/fpsyg.2014.00611 ||||| People who plan on getting an early night but instead spend their evenings binging on their Netflix favourites may be succumbing to the ‘modern phenomenon’ of bedtime procrastination.
Researchers at the University of Utrecht found people who regularly failed to get to sleep at the time they intended to were often still awake because they were struggling to quit other activities, such as watching Netflix, despite feeling tired.
The authors defined procrastination as the: "voluntary delay of an intended course of action despite expecting to be worse off for the delay”.
Procrastination usually involves wasting time to avoid un-enjoyable tasks, but sleep is not an activity that falls into this category, the authors noted.
Floor Kroese, who led the study, looked at how procrastinating affected not only people's ability to sleep, but also how it affected their general health and well-being.
A team asked questions about the lifestyle and demographic factors of 177 individuals, as well as their sleep patterns and tendency to procrastinate via an online survey.
Participants were asked to state their level of agreement with statements such as "I go to bed later than I had intended" and "I easily get distracted by things when I actually would like to go to bed" in order to measure bedtime procrastination.
The study found people who did not go straight to bed found it harder to self-regulate and stick to a workable routine.
“Bedtime procrastination may be a relatively modern phenomenon,” Kroese explained. “We speculate that it is not so much a matter of not wanting to sleep, but rather of not wanting to quit other activities.
“With the development of electrical devices and the 24/7 entertainment industry, people may be facing many more distractions now compared to several decades ago.”
The study Bedtime procrastination: introducing a new era of procrastination” was published in the journal Frontiers. ||||| By eleven-ish o’clock on weeknights, I know that I probably should be at least considering getting ready for bed. But getting up off the couch in order to brush my teeth, wash my face, and change into pajamas — sometimes it all just seems so hard. And so I avoid it for a little while and end up going to sleep far too late, all for the sake of watching one more episode of Orange Is the New Black or screwing around on social media.
It’s not quite insomnia, because it isn’t that I can’t sleep; I’m just putting it off. Recently, researchers in the Netherlands put a name to this phenomenon: “bedtime procrastination,” which they define as “failing to go to bed at the intended time, while no external circumstances prevent a person from doing so.”
Jordan Gaines Lewis is studying sleep at Penn State College of Medicine, and while she wasn’t involved in this new research, she offers some practical tips on overcoming the urge to procrastinate your bedtime:
I think it’s most important to realize how crappy you feel and how much your work suffers after an OitNB nighttime binge. … A simple fix is to keep a schedule for yourself and stick to it. If you can’t fit in all of your fun daytime activities in before your scheduled bedtime, then take comfort in knowing you’ll be alert and well-rested the next day to experience them.
This isn’t, of course, a brand-new phenomenon. But it is newly named, and naming a thing is the first step toward beating it. |||||
Write a summary. | – After a sleepy start to the week, you swore you'd be in bed last night by 10—but when the clock struck midnight, you were still catching up on Game of Thrones. You're not the only one struggling to get to bed despite wanting to sleep: Researchers are describing "bedtime procrastination," which "may be a relatively modern phenomenon." The definition, per Science of Us, is "failing to go to bed at the intended time, while no external circumstances prevent a person from doing so." Working in the Netherlands, the experts asked 177 people to respond to questions like "I go to bed later than I had intended" and "I easily get distracted by things when I actually would like to go to bed," the Independent reports. They found that bedtime procrastination was fairly common and associated with less sleep and more tiredness, Real Clear Science notes. An expert tip: "Keep a schedule for yourself and stick to it. If you can't fit in all of your fun daytime activities before your scheduled bedtime, then take comfort in knowing you'll be alert and well-rested the next day to experience them." | multi_news_1_0_0 |
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Summarize this article:
Calories from "ultraprocessed" foods make up more than half of all calories in the average American diet and account for nearly 90 percent of all added sugars, a new study finds.
Ultraprocessed foods are defined by the researchers as "formulations of several ingredients" which, besides sugar, salt, oils and fats, include additives such as flavors, colors, sweeteners and emulsifiers.
This ultraprocessed classification includes foods such as breads; soft drinks, fruit drinks and milk-based drinks; cakes, cookies and pies; salty snacks; frozen foods; and pizza and breakfast cereals, according to the study, which was published today (March 9) in the journal BMJ Open.
The researchers also found that the more ultraprocessed foods a person eats, the more likely he or she is to exceed the recommended daily limit for added sugars in the diet, according to the study. (The new Dietary Guidelines for Americans recommend that calories from sugars should account for no more than 10 percent of a person's daily calories. For someone who eats 2,000 calories a day, this would mean no more than 200 calories should be from added sugars.) [Diet and Weight Loss: The Best Ways to Eat]
"Limiting the consumption of ultraprocessed foods may be a highly effective way to decrease added sugars," the researchers, led by Euridice Martinez Steele, a researcher at the University of São Paulo in Brazil, wrote in the study. Consuming too much added sugar is "most likely contributing" to growing levels of obesity, Type 2 diabetes and heart disease, they added.
In the study, the researchers used data from the 2009-2010 National Health and Nutrition Examination Survey (NHANES). Specifically, they looked at the survey responses of more than 9,300 participants who had provided data on the foods they had eaten in a 24-hour period. (One limitation of the study, the researchers noted, is that people may not accurately report the foods they consumed in the 24-hour period.)
In addition to ultraprocessed foods, the researchers also looked at the amounts of unprocessed or minimally processed foods, processed culinary ingredients and processed foods in the average American's diet.
Unprocessed or minimally processed foods include meat, fruits, vegetables, fish and grains; and processed culinary ingredients include table sugar, plant oils and animal fats. Processed foods (which were defined as unprocessed or minimally processed foods manufactured with added salt, sugar or other culinary substances) include such foods as cheese, canned foods and salted meats.
The researchers found that unprocessed or minimally processed foods contributed to, on average, 29.6 percent of a person's total daily calories; processed culinary ingredients contributed to, on average, 2.9 percent of a person's total daily calories; and processed foods contributed to, on average, 9.4 percent of a person's total daily calories, according to the study.
Ultraprocessed foods, on the other hand, accounted for, on average, 57.9 percent of a person's total daily calories, or nearly 3 out of every 5 calories consumed, the researchers wrote in the study.
In addition, only those who reported eating the least amount of ultraprocessed foods (accounting for, on average, 28.9 percent of their daily calories) were found to meet the recommended limit of getting less than 10 percent of their daily calories from added sugar, according to the study.
The researchers recommend that Americans reduce their intake of ultraprocessed foods — doing so, they argue, would increase the intake of more healthful, minimally processed foods such as milk, fruits and nuts, as well as freshly prepared dishes with whole grains and vegetables, which would produce health benefits beyond cutting out added sugar.
Follow Sara G. Miller on Twitter @SaraGMiller. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science. ||||| To design and implement effective measures to reduce added sugars, their dietary sources must be clearly identified. Added sugars can be consumed either as ingredients of dishes or drinks prepared from scratch by consumers or a cook, or as ingredients of food products manufactured by the food industry. According to market disappearance data from 2014, more than three-quarters of the sugar and high fructose corn syrup available for human consumption in the USA were used by the food industry. 12 This suggests that food products manufactured by the industry could have an important role in the excess added sugars consumption in the USA. However, to assess this role, it is essential to consider the contribution of manufactured food products to both total energy intake and the energy intake from added sugars, and, more relevantly, to quantify the relationship between their consumption and the total dietary content of added sugars. To address these questions, we performed an investigation utilising the 2009–2010 National Health and Nutrition Examination Survey (NHANES).
All reports recommended limiting intake of added sugars. 1 , 3–5 In the USA, the USDGAC recommended limiting added sugars to no more than 10% of total calories. This is a challenge, as recent consumption of added sugars in the USA amounted to almost 15% of total calories in 2005–2010. 10 , 11
These reports concluded that a high intake of added sugars increases the risk of weight gain, 1 , 4 , 5 excess body weight 5 and obesity; 3 , 5 type 2 diabetes mellitus; 3 , 5 higher serum triglycerides 5 and high blood cholesterol; 3 higher blood pressure 5 and hypertension; 5 stroke; 3 , 5 coronary heart disease; 3 , 5 cancer; 3 and dental caries. 1 , 3 , 5 Moreover, foods higher in added sugars are often a source of empty calories with minimum essential nutrients or dietary fibre, 6–8 which displace more nutrient-dense foods 9 and lead, in turn, to simultaneously overfed and undernourished individuals.
The NHANES sample weights were used in all analyses to account for differential probabilities of selection for the individual domains, non-response to survey instruments, and differences between the final sample and the total US population. The Taylor series linearisation variance approximation procedure was used for variance estimation in all analysis in order to account for the complex sample design and the sample weights. 14
All regression models were adjusted for age (1–5, 6–11, 12–19, 20–39, 40–59, 60+ years), sex, race/ethnicity (Mexican-American, Other Hispanic, Non-Hispanic white, Non-Hispanic black, Other race including Multi-racial), ratio of family income to poverty (categorised on the basis of Supplemental Nutrition Assistance Program (SNAP) eligibility as 0.00–1.30, >1.30–3.50 and >3.50 and above) 14 and educational attainment of respondents, for participants aged 20+ years, and of household reference persons otherwise (<12, 12 and >12 years). Since 908 participants had missing values on family income and/or educational attainment, multivariable-adjusted analysis included 8409 individuals. The analysis which also adjusted for the added sugar content of all non-ultra-processed foods grouped together included 8335 individuals.
The average content of added sugars in the overall diet was compared across quintiles of the dietary contribution of ultra-processed foods. Poisson regression was used to assess whether the percentage of diets with more than 10% or 20% of total energy from added sugars increased across quintiles. This increase was also evaluated across demographic subgroups in stratified analysis. Tests of linear trend were performed in order to evaluate the effect of quintiles as a single continuous variable.
We used Gaussian regression to estimate the association between the dietary contribution of ultra-processed foods and the dietary content of added sugars, each expressed as proportions of total energy. This association was also explored after adjusting for the proportion of added sugars in non-ultra-processed energy intake. The dietary contribution of ultra-processed foods was transformed using restricted cubic spline functions to allow for non-linearity.
We utilised all available day 1 dietary data for each participant. Food items were sorted into mutually exclusive food subgroups within unprocessed or minimally processed foods (n=11), processed culinary ingredients (n=4), processed foods (n=4) and ultra-processed foods (n=18), as shown in table 1 . First, we evaluated the contributions of each of the NOVA food groups and subgroups to total energy and to the energy from added sugars. Next, we calculated the average content of added sugars in the overall US diet and in fractions of this diet composed by each of the NOVA food groups and subgroups. We also calculated the dietary content of added sugars in the group of unprocessed or minimally processed foods combined with the group of processed culinary ingredients, as foods belonging to these two groups are usually combined together in culinary preparations and therefore consumed together.
Data on added sugars per Food Code and per SR Code were obtained by merging the Food Patterns Equivalents Database (FPED) 2009–2010 and the Food Patterns Equivalents Ingredients Database (FPID) 2009–2010. 32 Added sugars are defined in these databases as “sugars that are added to foods as an ingredient during preparation, processing, or at the table. Added sugars do not include naturally occurring sugars (eg, lactose in milk, fructose in fruits). Examples of added sugars include brown sugar, cane sugar, confectioners’ sugar, granulated sugar, dextrose, white sugar, corn syrup and corn syrup solids, molasses, honey, and all types of syrups such as maple syrup, table syrups, and pancake syrup.” 32 These two databases express the content of added sugars in teaspoons per 100 g. Teaspoons were converted into grams using the factor 4.2 g/teaspoon and into kcal using the factor 3.87 kcal/g.
We classified all recorded food items (N=280 132 Food Codes for both recall days) according to NOVA, a food classification based on the extent and purpose of industrial food processing. 23–25 This classification includes four groups: ‘unprocessed or minimally processed foods’ (such as fresh, dry or frozen fruits or vegetables, grains, legumes, meat, fish and milk); ‘processed culinary ingredients’ (including table sugar, oils, fats, salt, and other substances extracted from foods or from nature, and used in kitchens to make culinary preparations); ‘processed foods’ (foods manufactured with the addition of salt or sugar or other substances of culinary use to unprocessed or minimally processed foods, such as canned food and simple breads and cheese) and ‘ultra-processed foods’ (formulations of several ingredients which, besides salt, sugar, oils and fats, include food substances not used in culinary preparations, in particular, flavours, colours, sweeteners, emulsifiers and other additives used to imitate sensorial qualities of unprocessed or minimally processed foods and their culinary preparations or to disguise undesirable qualities of the final product). A detailed definition of each food group and examples of food items classified in each group are shown in online supplementary table S1. The rationale underlying the classification is described elsewhere. 26–29
We evaluated 9317 survey participants aged 1 year and above who had 1 day 24 h dietary recall data and had not been breast fed on either of the 2 days. These individuals had similar sociodemographic characteristics (gender, age, race/ethnicity, family income and educational attainment) to the full sample of 10 109 interviewed participants aged 1 year and above.
The survey included an interview conducted in the home and a subsequent health examination performed at a mobile examination centre (MEC). All NHANES examinees were eligible for two 24 h dietary recall interviews. The first dietary recall interview was collected in-person in the MEC 15 while the second was collected by telephone 3–10 days later but never on the same day of the week as the MEC interview. 16 Dietary interviews were conducted by trained interviewers using the validated 17–19 US Department of Agriculture Automated Multiple-Pass Method (AMPM). 20 For children under 9 years of age, the interview was conducted with a proxy; for children between 6 and 8 years of age, in the presence of the child. Children aged 9–11 years provided their own data assisted by an adult household member (assistant). The preferred proxy/assistant was the most knowledgeable person about the child's consumption on the day before the interview. If the child had more than one caregiver, several individuals could contribute to the intake data. 15 , 16
NHANES is a continuous, nationally representative, cross-sectional survey of the non-institutionalised, civilian US residents. 14 The NHANES sample was obtained by using a complex, stratified, multistage probability cluster sampling design based on the selection of counties, blocks, households and the number of people within households. 14 In order to improve the estimate precision and reliability, NHANES 2009–2010 oversampled the following subgroups: Hispanic, Non-Hispanic black, Non-Hispanic white and Other persons at or below 130% of the federal poverty level and Non-Hispanic white and Other persons aged 80+ years. 14
Across quintiles of energy-adjusted ultra-processed food consumption, the intake of added sugars increased substantially and monotonically from 7.5% of total calories in the lowest quintile to 19.5% in the highest quintile. Across the same quintiles, the proportion of individuals consuming more than 10% of total energy from added sugars (59.6% in the total population) increased from 26.4% to 82.1%, respectively. An even more pronounced increase was seen in the proportion of individuals consuming more than 20% of their total energy from added sugars: from 4.7% in the lowest quintile to 41.2% in the highest quintile ( table 2 ). Similar increases were seen in stratified analysis by major demographic subgroups ( see online supplementary table S2 ) . The magnitude and the statistical significance of the association between the dietary contribution of ultra-processed foods and the dietary content in added sugars did not change with adjustment for sex, age, race/ethnicity, family income and educational attainment.
There was little evidence of non-linearity in the restricted cubic spline model (Wald test for linear term p<0.0001; Wald test for all non-linear terms p=0.27). The strength of the association remained fairly the same after adjusting for age, sex, race/ethnicity, family income, educational attainment and proportion of added sugars in non-ultra-processed energy intake (coefficient for linear term=0.19, 95% CI 0.17 to 0.22). Overall, each increase in 5 percentage points of energy in consumption of ultra-processed foods was associated with 1 higher percentage point of energy in the consumption of added sugars.
The dietary content in added sugars regressed on the dietary contribution of ultra-processed foods evaluated by restricted cubic splines. US population aged 1+ years (National Health and Nutrition Examination Survey 2009–2010) (N=9317). The values shown on the x-axis correspond to the 5th, 27.5th, 50th, 72.5th, and 95th centiles for percentage of total energy from ultra-processed foods (knots). Coefficient for linear term=0.20 (95% CI 0.17 to 0.23). There was little evidence of non-linearity in the restricted cubic spline model (Wald test for linear term p<0.0001; Wald test for all non-linear terms p=0.27).
The average US daily intake of added sugars was 292.2 kcal ( table 1 ). Notably, almost 90% of this (89.7%) came from ultra-processed foods. The main sources of added sugars among ultra-processed foods were: soft drinks (17.1% of US intake of added sugars); fruit drinks (13.9%); milk-based drinks (4.6%); cakes, cookies and pies (11.2%); breads (7.6%); desserts (7.3%); sweet snacks (7.1%); breakfast cereals (6.4%); and ice creams and ice pops (5.9%). In contrast, only 8.7% of the added sugars in the US diet came from processed culinary ingredients (table sugar consumed as part of dishes or drinks prepared from scratch by consumers or a cook), and only 1.6% from processed foods.
Unprocessed or minimally processed foods contributed 29.6% of total calories, processed foods an additional 9.4%, and processed culinary ingredients the remaining 2.9%. The most common ultra-processed foods in terms of energy contribution were breads; soft drinks, fruit drinks and milk-based drinks; cakes, cookies and pies; salty snacks; frozen and shelf-stable plates; pizza and breakfast cereals. Meat, fruit and milk provided the most calories among unprocessed or minimally processed foods; ham and cheese, the most calories among processed foods; and table sugar and plant oils, the most calories among processed culinary ingredients.
Discussion
In this analysis of nationally representative data, we confirmed the excessive consumption of added sugars in the USA.10 ,11 We also provide new evidence that ultra-processed foods represent more than half of all calories in the US diet, and contribute nearly 90% of all added sugars. Added sugars represented 1 of every 5 calories in the average ultra-processed food (21.1%), far higher than the content of added sugars in processed foods (2.4%) and in unprocessed or minimally processed foods, and processed culinary ingredients grouped together (3.7%). A strong linear relationship was found between the dietary contribution of ultra-processed foods and the dietary content of added sugars. Moreover, the risk of exceeding the recommended upper limit of 10% energy from added sugars was far higher when ultra-processed food consumption was high, and risk differences were even more pronounced for exceeding a limit of 20% energy. Notably, only those Americans in the lowest quintile of ultra-processed food consumption met the recommended limit of <10% energy from added sugars. To the best of our knowledge, this is the first study to assess the consumption of ultra-processed foods and establish its relationship with excessive added sugar intake in the USA.
The high consumption of added sugars in the USA is most likely contributing to excess obesity, type 2 diabetes, dyslipidaemia, hypertension and coronary heart disease.1 ,3–5 Consequently, most dietary guidelines now recommend limiting added sugar consumption. However, such guidelines are not always clear on how to put this recommendation into practice. Our study suggests that in the USA, limiting the consumption of ultra-processed foods may be a highly effective way to decrease added sugars. A reduction in ultra-processed foods should also increase the intake of more healthful, minimally processed foods such as milk, fruits and nuts, and freshly prepared dishes based on whole grains and vegetables, which would produce additional health benefits beyond the reduction in added sugar. Consistent with this approach, in Brazil, where the consumption of added sugars is as high as in the USA,33 the new dietary guidelines launched in 2014 emphasise the importance of not replacing unprocessed or minimally processed foods and freshly prepared dishes by ultra-processed foods.34
Few studies have assessed the impact of levels of food processing on the nutrient profile of the US diet. One analysis using data from NHANES 2003–200835 used a food classification system36 including ‘Mixtures of combined Ingredients’ and ‘Ready-to-eat’, which are mostly ultra-processed foods, and together contributed to about half of the total energy intake and three-quarters of energy intake from added sugars. Another study evaluated household barcoded purchasing data from 2000 to 2012 using a classification system guided by the one used in our study.37 In 2012, the mean per capita purchase of ‘highly processed foods’, a category similar to ultra-processed foods, corresponded to 61.0% of all calories and had higher adjusted median total sugar content than ‘less processed foods’. This report did not evaluate added sugars nor the contribution of processed foods to sugar intake. It also did not capture non-barcoded items such as unpackaged fresh fruit, vegetables and meat, or highly processed foods such as ready-to-eat store-prepared items. An investigation in Canada, using 2001 household purchasing data, found that ultra-processed foods are high in free sugars and that only households in the lowest quintile of ultra-processed food purchasing might have met the recommended limit of <10% energy from free sugars (9.2%).38 Being based on household purchasing data, these two prior studies and others based on the NOVA classification system23 ,39–42 could not evaluate the fraction of wasted food nor purchases at restaurants, which represent a substantial proportion of US calories. Our findings build on and considerably extend these prior reports by evaluating food processing and added sugar intake using contemporary, nationally representative dietary intake data in the USA.
Our study has several strengths. We studied a large, nationally representative sample of the US population, increasing generalisability. Use of data on added sugars, rather than total sugars or sugar-sweetened beverages, corresponds to the relevant area of prioritisation of recent national and international guidelines. Our investigation was based on individual consumption data, rather than market disappearance or household purchasing data which cannot account for differences between amounts purchased and amounts actually consumed.
Potential limitations should be considered. As with most population measures, dietary data obtained by 24 h recalls are imperfect. However, the standardised methods and approach of NHANES minimise potential error and bias, particularly for assessing population averages as focused on in the present study. Previous studies suggest that people with obesity may under-report consumption of foods with caloric sweeteners43 such as desserts and sweet baked goods.44 ,45 If so, these biases may lead to an underestimation of the dietary contribution of ultra-processed foods and the overall intake of added sugars, but should have much less effect on the association between these. Although NHANES collects some information indicative of food processing (ie, place of meals, product brands), these data are not consistently determined for all food items, which could lead to modest overestimation or underestimation of the consumption of ultra-processed foods.
In conclusion, we found that ultra-processed foods contribute almost 60% of calories and 90% of added sugars consumed in the USA. Only Americans in the lowest quintile of ultra-processed food consumption met the recommended guidelines for intake of added sugars. Decreasing the consumption of ultra-processed foods could be an effective way of reducing the excessive intake of added sugars in the USA. |||||
Summary: | – Lots of people talk a good game about eating more natural foods, but a new study suggests that the convenience of "ultra-processed" meals is just too hard to resist. Researchers found that nearly three in five of our calories come from this category, reports the Los Angeles Times. That raises a host of health concerns, given that these foods are loaded with sugar, preservatives, artificial flavors, colors—generally speaking, the unpronounceable stuff in ingredient lists. So what qualifies as "ultra-processed"? Think breakfast cereals, frozen pizzas, soda, cookies, salty snacks, etc. The study in the journal BMJ Open looked at what more than 9,000 participants ate over a 24-hour period and found that 58% of the average 2,070 calories consumed qualified for the "ultra-processed" label. As for the rest, 28% came from foods with zero or minimal processing—eggs, fish, vegetables, essentially food "you've just ripped ... out of the ground or off a tree and shoved ... in your mouth," explains the Atlantic. Another 10% came from foods with a higher degree of processing (but not at the "ultra" level), such as cheese, canned vegetables, bread, and cured meat. The remainder of the calories came from cooking ingredients such as olive oil. The researchers were particularly concerned that the ultra-processed foods delivered 90% of the added sugar in participants' diets, writing that limiting their consumption "may be a highly effective way" to keep sugar intake under control, notes Live Science. (If you're trying to cut down on not-so-healthy snacking, one key might involve your sleep.) | multi_news_1_0_0 |
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Here is a news article: You've heard the term "hangry," right? People who are hungry often report being unreasonably angry until they're fed.
"Hangry" is a relatively new buzz word, but science is backing it up. A new study published in the journal PNAS suggests married couples are more aggressive when they have low blood sugar levels.
Background
Everyone gets upset at their spouse or significant other sometimes. But self-control hopefully prevents you from taking that anger out on them in a physical manner.
Yet scientists know that self-control is a limited resource. You have a tank of it, so to speak, in your brain. Each time you use self-control to avoid telling off your boss or to skip the dessert bar, that tank becomes less full.
And "aggression often starts when self-control stops," says Brad Bushman, a psychologist at Ohio State University who's studied aggression for 25 years.
What refills your self-control tank? Energy, which comes in part from the food you eat.
The study
Researchers recruited 107 married couples to participate in the study. The husbands and wives measured their glucose (or blood sugar) levels every morning and night for 21 days.
Each night they were asked to stick up to 51 pins in a voodoo doll, depending on how angry they were at their spouse. The researchers compared this aggression level to the participants' average glucose levels over the study period.
At the end of the 21 days, researchers had the couples come into the lab for another test. They asked each husband and wife to compete against their significant other in a virtual game. The couples were told the winner got to blast the loser with a loud, obnoxious noise. (In reality, their partner was not on the receiving end.)
Researchers measured how long and how intense the winner chose to blast the noise, and compared that aggression level to their average blood sugar level.
The results
Study participants with lower nightly blood sugar levels were more aggressive - both in "pinning" their voodoo doll and in blasting their partner with a louder noise for longer. These findings remained true even after researchers controlled the data for relationship satisfaction.
More evidence
This study supports previous research done by Bushman's lab at Ohio State University. In an earlier study, Bushman and his colleagues found participants who drank a sugar-sweetened beverage behaved less aggressively than those who drank a beverage sweetened with a sugar substitute.
Another study linked diabetes to more aggressive behavior. Because glucose increases self-control, people who have difficulty metabolizing glucose should have less self-control, the researchers theorized.
In a separate series of studies, Bushman showed diabetics were less inclined to forgive others. "These findings provide the first evidence that forgiveness depends on how efficiently the body uses glucose," the study authors wrote.
Takeaway
The study authors say giving people more access to food could reduce aggression in certain settings, such as prisons or psychiatric hospitals. As for the rest of us:
"I would recommend couples discuss sensitive issues over dinner," Bushman said. "Or better yet, after dinner." ||||| New study finds that spouses are more likely to get angry with each other if they're dealing with low blood sugar levels. So have a snack, and chill out.
Brad Bushman, professor of communication and psychology at Ohio State University, holds one of the voodoo dolls used in the study. (Photo: Jo McCulty, Ohio State University)
The next time you get annoyed at your spouse, you might want to grab something to eat. That's the take-home message from a new study that found marital hostility is at its highest when blood sugar is at its lowest.
Spouses of both genders jabbed more pins into a voodoo doll on evenings when their blood sugar was the lowest, according to the new study, published online Monday in the Proceedings of the National Academy of Sciences.
Lead researcher Brad Bushman of Ohio State University said his own marriage has improved since he took his study's advice: "When you discuss a sensitive topic with your spouse, you should do so over dinner, or better yet after dinner – but you should definitely not do it on an empty stomach."
Bushman and his colleagues paid $100 each to 107 married couples, found through public advertisements, to participate in the study.
This is one of the voodoo dolls used in the study to measure participants' anger with their spouses. (Photo: Jo McCulty, Ohio State University)
To measure aggressiveness, each husband and wife was given a voodoo doll and 51 pins. They were told to check their blood glucose level before bed each night for three weeks, and to stick any number of pins into the doll, depending on how angry they were with their spouse that day. They didn't see each other's dolls.
After three weeks, the couples were invited back to the lab, placed in separate rooms and told to compete against each other to see who could press a computer button faster after a given command. The winner could blast the loser with a loud, ugly sound.
The spouses who stabbed their voodoo doll more freely also were more likely to turn up the volume on the punishing sounds, the study found. The results did not differ between couples who said their marriages were weak or strong, he said.
Angry people are more impulsive, more likely to lash out, both verbally and physically, said Bushman, adding that anger is the leading cause of homicide.
Ann Goebel-Fabbri, a psychologist with the Joslin Diabetes Institute in Boston, praised the creativity of the study but said she thinks the researchers went too far in suggesting that low blood sugar could lead to violence.
People with diabetes – who are prone to large swings in blood glucose – do complain about being moody, she said. But they are certainly not any more likely to be violent than the general population.
"There is no connection between diabetes and aggression," said Goebel-Fabbri, also an assistant professor at Harvard Medical School.
"I think the translation from voodoo doll and loud noise to domestic violence, I think is way overstating it," she said. "It would be lovely if we could solve the domestic violence problem by feeding people better, but…there's no data that would support that."
Read or Share this story: http://usat.ly/1kqc5Jm ||||| Husbands and wives reported being most unhappy with their spouses when their blood-sugar levels were lowest, usually at night, according to research released today in the Proceedings of the National Academy of Sciences.
Husbands and wives reported being most unhappy with their spouses when their... Read More
Husbands and wives reported being most unhappy with their spouses when their blood-sugar levels were lowest, usually at night, according to research released today in the Proceedings of the National Academy of Sciences. Close
Serious discussions between spouses shouldn’t take place on an empty stomach, a study suggests.
Husbands and wives reported being most unhappy with their spouses when their blood-sugar levels were lowest, usually at night, according to research released today in the Proceedings of the National Academy of Sciences. Missing a meal, dieting or just being hungry may be the reason, researchers said.
Sugar, or glucose, is used by the brain as fuel to help regulate self-control. Without the fuel, it is more difficult for people to control emotions like anger and aggression, researchers said. Today’s findings are among the first to show how low sugar levels in the body may play a part in marital arguments, confrontations and even domestic violence, said Brad Bushman, the lead study author.
“Self-control comes in part from the fuel we give our brains. This is one of the few physiological aspects we can control,” said Bushman, a professor of communication and psychology at Ohio State University in Columbus, in a telephone interview today. “People who are hungry are often very cranky.”
Researchers in the study included 107 married couples who for 21 days had to test their blood-sugar levels before breakfast in the morning and before bed in evening. They were also given voodoo dolls representing their spouses and told to insert as many as 51 pins daily depending on how angry they were with their partner. The researchers were testing aggressive impulses.
Measuring Aggression
Those with the lowest nighttime blood-sugar levels inserted the most pins, while those with the highest glucose levels inserted the least, the study found. Women tended to stick more pins into their husband voodoo doll, but the finding wasn’t significant. The authors only found the association for nighttime blood glucose levels as the amount of sugar in the body drops throughout the day, Bushman said.
After 21 days, the couples went into a laboratory where they were told they would compete with their spouse to see who could press a button the fastest to test aggressive behavior. The winners could blast their spouse with a loud noise through headphones. The spouses in reality were playing against a computer, not each other.
The researchers found that those with the lowest average nighttime blood-sugar levels sent louder and longer noises to their spouse no matter how good their relationship was or whether they were male or female.
Timing Important
“If couples have a sensitive topic to discuss, it would be really smart to do it over dinner or better yet after dinner,” Bushman said. “They should definitely not do it on an empty stomach.”
Low blood sugar can trigger hormones that activate the body’s “fight or flight” system and cause people to become more aggressive, anxious and irritable, said Timothy Graham, who wasn’t an author of today’s study.
For families with someone who has diabetes, where swings between highs and lows can occur more often, he suggests counseling. For others, regular, small meals throughout the day may help keep blood sugar levels consistent and help prevent dips that can cause aggression.
“Probably more regular and healthy meals could improve the dynamics of a relationship,” Graham, an assistant professor of medicine at the University of Utah in Salt Lake City, said in a telephone interview.
To contact the reporter on this story: Nicole Ostrow in New York at [email protected]
To contact the editors responsible for this story: Reg Gale at [email protected] Andrew Pollack, Angela Zimm |||||
A summary of this is? | – "If couples have a sensitive topic to discuss, it would be really smart to do it over dinner or better yet after dinner," say researchers who have linked low blood sugar to marital hostility. "They should definitely not do it on an empty stomach." Researchers tracked the blood sugar levels—and, using voodoo dolls, the aggression levels—of 107 married couples and found that those with the lowest nighttime blood sugar were the most likely to stick pins in the doll representing their partner, CNN reports. In laboratory tests, people with low blood sugar were also the most willing to blast their partner with a loud, obnoxious noise in what they were told was a game, USA Today reports. The results were similar no matter how strong a couple said their marriage was. Low blood sugar can trigger hormones that cause people to become aggressive and irritable, a professor of medicine explains to Bloomberg. "Probably more regular and healthy meals could improve the dynamics of a relationship," he says, adding that counseling should be considered when diabetes is involved. | multi_news_1_0_0 |
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Here is a news article: — Gen. Ahmed al Berri, the top officer of the Western-backed Syrian rebels in Hama province, was driving up Syrias main north-south highway in mid-December when he slowed at a checkpoint, expecting a friendly wave-through by the radical Islamists who were manning it.
The fighters of the Islamic State of Iraq and Syria, most of them non-Syrians, had something else in mind, however.
They wanted the car, and I refused to give it, he recounted to McClatchy. They showed their weapons, and we showed ours. But there were 30 of them and only four of us, so he agreed to go with his two bodyguards and a second officer for what the Islamists said would be an appearance before a Shariah court judge.
Instead, Berri and his companions were arrested, blindfolded and bound.
For the next 18 days, Berri said, he was held in a makeshift prison inside a house in the village of Killi, about five miles south of the Turkish border. For Berri, it was a surprising introduction to a radical group that in the space of a few months had come to dominate much of northern and eastern Syria, lording it over more moderate rebels and installing a reign of terror the extent of which is only now becoming clear.
They were professionals, Berri said of the men who regularly interrogated him in two-hour sessions. Each of his questioners two were Syrians and the others were from Egypt and Tunisia focused on a different topic. One would ask when he defected from the Syrian army, a second would ask what weapons hed brought with him and a third questioned him about his contacts. They grilled him about his relationships with Americans, Turks, Qataris and Saudis all countries that have provided aid to rebel groups.
Their aim was to know what the rebels were doing, what weapons they are using, how theyre distributing forces, who theyre in contact with outside the country and what their goals are, Berri said. And they sought to identify fighters in his militia, the sort of information that an ostensible ally could obtain by much simpler means.
It was like Syrian intelligence, he said, concentrating on minor details. He added, It indicates they know their business very well.
Berri said the entire compound in Killi appeared to have been organized around the prison and interrogation process, rather than war-fighting. He estimated that at least 100 armed personnel were deployed to run and guard it, including his team of professional interrogators.
How the Islamic State of Iraq and Syria became a dominant force in Syrias rebellion against the government of President Bashar Assad in just a few months after it announced its formation last April is a mystery. It was considered an ally by most other rebels until well into the summer; the U.S.-backed Free Syrian Army even praised its role in the August capture of the Mannagh air base north of Aleppo, which other rebel groups had been besieging for more than a year, unsuccessfully, until two ISIS suicide bombers blew themselves up and destroyed the bases command center.
But its enmity toward much of the rebel movement had been growing. In July, it kidnapped the leader of a rival rebel group in Raqqa, who hasnt been seen since. In August, it bombed that groups Raqqa headquarters, killing many of its commanders. In September, it seized the town of Azaz from the Free Syrian Army, and it took control of several major crossing points along the border with Turkey, cutting other rebels from their supply routes.
The consequences for Syrias opposition movement could be many, and severe: As extemists have co-opted the revolution, the U.S. and other countries have hesitated to help or have even suspended aid to Syrias rebels, fearing the spread of radical Islam.
Last month, moderate and Islamist rebel militias combined forces to attack ISIS throughout northern Syria, forcing it to abandon Killi and roughly half its bases, and releasing hundreds from ISIS jails. But ISIS remains the dominant rebel force in Raqqa province and in much of eastern Syria, where it controls the countrys oil fields and its transit routes to Iraq, where ISIS traces its origin.
ISISs stated aim is to restore a medieval Islamic caliphate in the area now occupied by Syria and Iraq. But moderate Syrian activists wonder now whether it doesnt serve some other purpose. They note that its primary mode of reaching its goal has been through the abduction primarily of Assad opponents, the torture and interrogation of its detainees and massive theft. Rebel leaders dont hesitate to link ISIS to the Assad regime, though the evidence they cite is largely circumstantial. Its claim to al Qaida lineage has been rejected by that groups head, Ayman al Zawahiri, who last week pronounced that not only had al Qaida opposed ISISs move into Syria, but al Qaida also hadnt been consulted on it.
On the eve of last months uprising, the newly elected overall rebel commander, Jamal Maarouf, said his forces were attacking ISIS because it behaves like the Assad regime, according to an interview in Syrias Second Front, a documentary to be shown Tuesday on the PBS news program Frontline.
At its peak, a McClatchy investigation shows, ISIS had at least 60 bases in northern Syria. Opposition activists say that almost every one of them had a prison. About half of those remain under ISIS control.
Interviews with others whove been freed from ISIS prisons show the extent to which the group mixed professionalism with terrorism and torture.
Bunyamin Aygun, a Turkish photojournalist who was held for 40 days, said he was questioned for 17 days at Killi by interrogators who took precautions in verifying his statements that he was journalist. They were very professional in the way they did background checks, he told McClatchy.
They asked him for the dates of his photographs, rather than looking him up under his name, fearing that Turkish authorities would track down a routine Web search for him coming from Syria. And they took his credit card and PIN number to a bank in Reyhanli, inside Turkey on the border, to search his bank account and see whether his earnings were that of a journalist and not a spy.
What wasnt so professional was the supposed court that decided his case. I was never actually put on trial, he said. They just told me my case was going before the qaid (judge) and he would decide. One day later he was told hed been sentenced to death by beheading. His captors told him he should repent and read the Quran, and his execution would take place the next day.
At that point, Turkish news outlets began to write about his disappearance. His jailers told him that he was more important than we thought and decided not to kill him. Aygun was rescued when rebel forces seized Killi on Jan. 5.
Other prisoners told similar tales that rebel authorities memorialized in statements McClatchy reviewed. They reveal not only torture and abuse, but also an ISIS fixation on property and cash that provides insight into the groups finances. Well-informed humanitarian aid officials say ISIS relied in part on ransoms paid by foreign news organizations and aid organizations for the release of kidnapped workers. Expropriation of private property appears to be another method.
Rae Shaabo an Naser, a 35-year-old taxi driver from Sarmande, near the city of Idlib, told his rescuers that hed been beaten, tied to the ceiling and doused with water and forced to sit naked out of doors. Throughout it all, his interrogators asked him about the property of his brother, whod emigrated to Hungary. They asked me to give them the keys to his farmhouse, he said in his statement.
That, too, was a theme in another of ISISs prisons, this one at the former eye hospital in Aleppo, Syrias largest city, where ISIS became a force in August.
Khalid A., 25, a media activist whos worked for the anti-Assad opposition and who asked not to be identified by his full name because of security concerns, said he was held there after he was stopped in mid-August by a black four-wheel-drive car that blocked the road. Masked gunmen seized him and took him to the recently captured Mannagh air base. On the way into a building four men beat him with cables, and after he was taken to his room, a non-Syrian, possibly an Iraqi, interrogated him about his job and his contacts.
The beatings after his transfer to the eye hospital were worse, he said. For most of his 34 days there, he was held in a makeshift underground dungeon with 10 other people. For five days, he had no food at all and later only a half-pound of bread a day. He lost 66 pounds in prison.
People were in a tragic state, he told McClatchy of the others in his cell. One had bones broken. Another couldnt walk. Another couldnt use his hands, after being hanged from the ceiling for 22 days. And there was Abu Tony, an elderly Christian whod been held for 60 days, and was given no medicine for his diabetes.
Everyone was there for a reason. There were no random abductions, he said. Everyone had been captured by name, many of them arrested at their houses. Abu Tony was accused of converting to Islam and then trying to re-convert to Christianity, charges Khalid said were almost certainly specious. The real reason for holding him, Khalid suspected, was that he owned a metalworking factory in Aleppo that ISIS wanted to expropriate.
There were two brothers, aged 25 and 28, who owned a flour mill and farm near the air base. Khalid said they told him theyd donated weapons to the Free Syrian Army to help in the siege of the base but that ISIS had accused them of supporting Assads military.
But the real reason they were arrested, Khalid said, was probably their wealth. The brothers said ISIS had taken their cars, 200,000 euros - about $270,000 - and more than 37 pounds of gold, worth about $750,000 at todays prices.
One day, Khalid said, the guards removed them from the room, and they never returned.
Many of the guards and interrogators, Khalid said, had been on death row at Abu Ghraib, the Iraqi maximum-security prison west of Baghdad, and had escaped during an al Qaida-organized breakout in mid-July. Other guards were volunteers from Tunisia, Afghanistan, France, Denmark and Chechnya. One of the Iraqis concealed a tattoo forbidden in Islam beneath his shirtsleeve. The Chechen escorted prisoners for their once-daily excursion to the toilet. He only had two words of Arabic, Khalid said.
Khalids first interrogation in Aleppo occurred seven days after his abduction. The investigation room smelled of diesel fuel, and he could smell blood on the floor. Hooded, he couldnt see who was attaching electrodes to his back and neck. They tied my hands behind my back, sat me on the ground and asked me how I was, he recalled. Then they turned on the power. No one said anything. They just used electricity for 40-50 minutes. They paused for about a minute between jolts; the longest, he said, lasted about 10 seconds.
At the end, I couldnt see or hear anything for 10 minutes. My system was completely confused. I couldnt stand up.
His captors then hanged him by the handcuffs in what is called a ghost torture. He dislocated his shoulder and was later diagnosed as having a herniated disk. After another hour, two men with electrical cables beat him he calculated 400 to 500 times. My body was purple from the pelvis to the neck, he recalled. I was shouting and yelling. I dont remember what I said. I remember the pain. He lost consciousness. I couldnt handle the pain.
He showed a reporter large welts on his upper left back, where he said the electrode had been attached.
On the second day, his captors brought him in for interrogation about opposition forces, the Free Syrian Army, his job, his bosses and his co-workers.
Finally, a man described as a judge came in. You must be killed, Khalid recalled him saying. Do you prefer a rope or a knife? Khalid said he replied, Maybe a bullet in the head would be better. The judge responded that hed decided to slaughter him with a knife. One of the guards came, grabbed Khalid by the hair and put a knife to his throat.
Get ready to face your God, the judge said. I said, Im ready. I dont want to face another interrogation, he said. I felt the angel of death pass in front of me, Khalid told McClatchy.
But the knife stroke never came. Ten days later he was released.
Hundreds of prisoners werent so lucky. The Frontline special includes video of masked gunmen executing seven Free Syrian Army soldiers in al Atarib in late November, shooting them in the back of the head.
In a Dec. 19 report, Amnesty International quotes detainees who reported on two ISIS executions in or near Raqqa in eastern Syria in mid-October. Four members of other armed militias were condemned to death after purported trials. Take him away for retribution. Let his head fly, the prisoner quoted the unnamed emir as decreeing for each of the four. That night, guards called out the names of the prisoners and they were taken away, never to reappear. Three others were sentenced to death for alleged adultery.
As described by freed detainees, ISIS devoted enormous resources to find, seize, hold and interrogate its prisoners. But even as it set up a state within a state, the Assad regime left ISIS untouched.
Khalid recalled that in the 34 days he was held in Aleppo, the regime never attacked the ISIS base. But the base of Liwa al Tawhid, an Islamist militia, just 50 yards away, was bombed many times.
Berri recalled that during his time at the house in Killi, Syrian government forces never attacked the camp.
Berri eventually was released, thanks to influential friends. A brigade of Hama fighters mounted a siege of an ISIS base near Saraqeb and threatened to attack it if anything happened to him. And a delegation of Islamic clerics went to the Shariah court in Ad Dana, the ISIS headquarters, and warned that 10,000 militants were ready to attack if anything happened to Berri, he said. To prevent him from being abducted, the clerics arrived Dec. 23 in a convoy of seven vehicles, mounted with heavy machine guns. It still took eight days before he was freed.
Even then, Berris captors refused to release the second officer and the bodyguards. So Berri returned to the prison until the judge whod ordered his release freed them.
When Berri left, they kept his car and his personal effects: my wallet, my money, my ring, everything.
Five days later, Syrian rebels stormed the Killi camp and freed it.
This story is part of a collaboration between McClatchy and Frontline, whose documentary Syrias Second Front will air Tuesday, Feb. 11. Check your local listings for the time. You can also join a live Web chat below on Wednesday at 1 p.m. ET with FRONTLINE correspondent Muhammad Ali and McClatchy's Roy Gutman.
Syria's Second Front
Email: [email protected]; Twitter: @roygutmanmcc ||||| BAGHDAD — A series of daring but little noticed breakouts from Iraqi prisons has freed hundreds of hardened militants who are now among the leaders and foot soldiers of the radical Sunni groups operating in neighboring Syria and, increasingly, in Iraq itself.
The role of the former inmates in fueling a new wave of Sunni jihad across the region is an unfortunate reminder of the breakdown of authority in Iraq since the United States departed in 2011, of the security vacuum that has spread around the region and of the continuing threat of Sunni-led terrorist groups that the United States said it was fighting during its occupation of Iraq.
The prison breaks also reflect the surging demand for experienced fighters, which led to a concerted effort by militant groups, particularly the Islamic State of Iraq and Syria, or ISIS, to seek them in the one place where they were held en masse — Iraq’s prison cells.
That group even had a name for its prison strategy, “Operation Breaking the Walls,” which unfolded during a 12-month campaign from July 2012 until a major break at Abu Ghraib, the main Iraqi prison, on the western outskirts of the capital, in July 2013. In all, American officials estimate, a few hundred of the escapees have joined the Islamic State of Iraq and Syria, several in senior leadership roles.
While the group was already gaining strength in this period, an American counterterrorism official said, “The influx of these terrorists, who collectively have decades of battlefield experience, probably has strengthened the group and deepened its leadership bench.”
One such escapee was Abu Aisha, who declined to be identified by his full name and is now leading a group of Qaeda fighters on the western edge of Falluja, his hometown, which for nearly six weeks has been held by antigovernment Sunni fighters. With Falluja under siege, the American government has been rushing guns, ammunition and missiles to help the Shiite-dominated Iraqi security forces and allied tribal fighters retake the city, where so many American Marines once fought — and died — nearly 10 years ago.
Abu Aisha was a car mechanic before 2003 but found new purpose in fighting the Americans. Many detainees, himself included, he said, spent their time in prison learning the ways of militant Islam, studying the Quran and Shariah law and preparing to return to waging jihad once free.
Abu Aisha was originally arrested by the Americans and then released from Camp Bucca, the infamous American prison in southern Iraq, in 2008. He was rearrested by the Iraqis in 2010.
“Finally, they put me in Abu Ghraib, and I again met some of the leaders and fighters I knew, including princes from Al Qaeda — Iraqis, Arabs and other nationalities,” he said. “Most of them had been at Bucca as well.”
One night last summer, as Abu Aisha sat in his cell waiting, as he did each day, for his date with the executioner, explosions and gunfire erupted and a familiar prison guard opened the doors to his cell and told him to leave immediately. With hundreds of others, Abu Aisha ran through the prison’s corridors until he escaped through a hole that had been blasted through a wall. He hopped into a waiting Kia truck that took him to freedom — and back to the battlefield.
Abu Aisha said leaders of the Islamic State of Iraq and Syria gave him a choice: leave and fight with them in Syria, or stay and fight in Iraq.
“Many of the leaders that I know went to Syria and the jihad there once they fled from Abu Ghraib,” he said in a recent interview. “Other fighters went there after a while because they felt they would be freer in Syria. I decided to stay with my group.”
The prison breaks, and the mayhem they helped fuel in Syria, also had the effect of altering the calculus of many Western officials toward the war there. In the beginning, they saw the conflict in the terms of a dictator — President Bashar al-Assad — brutally oppressing his largely peaceful opponents.
But after the Islamic State of Iraq and Syria took on an increasingly important role in the fighting there — often battling with more moderate insurgent groups, to the dismay of Al Qaeda, which broke ties with ISIS over the issue — Western powers were even more reluctant to intervene.
Osama al-Nujaifi, the speaker of Iraq’s Parliament and the country’s most important Sunni politician, said that the escaped fighters “went to Syria to lead large fighting groups there.”
“So, people started thinking, Is Bashar better, or is Qaeda better?” he said.
Many Western experts have blamed Turkey’s open-door policy along its southern border with Syria for fostering the growth of the Islamic State of Iraq and Syria and other extremist groups. But Turkish officials have pushed back, citing intelligence reports that trace the growth of the group to the Iraqi prison breaks.
More than 600 prisoners are believed to have escaped in the largest of these sophisticated attacks, facilitated by corrupt prison guards who were easily bought, the officials said.
Two prison breaks in particular — the one at Abu Ghraib and the other, in September 2012, in the northern city of Tikrit — have had a significant impact on the group’s overall capacity to undermine Iraqi security and contributed to its expansion in Syria, the officials said.
In the Tikrit break, for instance, 47 death row detainees escaped, and they appear to have been instrumental in facilitating the group’s re-energizing and escalation of operations throughout 2013, according to Charles Lister, a visiting scholar at the Brookings Doha Center in Qatar.
American officials said more than 500 prisoners escaped in the Abu Ghraib operation alone. They also say that “the majority” of the escapees had been originally detained by Iraqi forces, but acknowledged that large numbers — perhaps scores — had been captured during American operations in Iraq before the United States military left the country at the end of 2011.
Shaker Waheeb, perhaps the most dangerous Al Qaeda figure to emerge here recently, was one of those captured. Mr. Waheeb was studying computer science at a university in Anbar when the American invasion of Iraq led him to quickly change paths and fight the Americans. He was detained and held in Camp Bucca before being turned over to the Iraqis. He escaped from the prison in Tikrit in late 2012.
In Iraq, Mr. Waheeb has become something of a cult figure for up-and-coming jihadis — he has been referred to as the heir apparent to Abu Musab al-Zarqawi, the brutal Qaeda leader who was killed by American forces in 2006 — and public enemy No. 1 to the broader public. Iraqi officials have claimed more than once to have killed him, but today he is a key figure leading the fighting within Falluja. Last summer, he was seen on a grisly video executing three Shiite truck drivers on the side of a highway in the deserts of Anbar Province and was linked to an attack in which 14 Shiite truck drivers in Iraq were found beheaded.
Among the more moderate fighting groups within Syria, the prison breaks have helped stoke conspiracy theories that the Islamic State of Iraq and Syria, which has been fighting recently with the groups, is a pawn of the Assad government. While there is no evidence to back that up, some said they believed that the Syrian government — with assistance from the Iraqi government of Prime Minister Nuri Kamal al-Maliki, which has largely sided with Mr. Assad — helped orchestrate the escapes.
“By doing this, exporting more foreign fighters to Syrian territory, the Maliki government did Assad’s regime a favor by supporting his claim of fighting terrorism inside Syria,” said Abduljabbar Osso, a rebel leader in Aleppo who has been fighting with the Islamic State of Iraq and Syria.
Another rebel commander, Lt. Col. Ahmad al-Aboud, said that the moment his people heard about the prison escapes in Iraq, “We knew we would face more trouble after that.”
“We have always faced difficulties smuggling light weapons from Iraq to Syria through the Iraq border,” he said, “but it was very easy for ISIS to get full patrols of vehicles, weapons and fighters across to Syria.”
The Iraqi government has done little to explain how the prison breaks happened, although most agree that the inmates had help from the inside. Parliament members said that when they tried to investigate the Abu Ghraib break, they were stymied by security forces and top government officials.
“Unfortunately, the government did not allow us to even get close to the prison for a week,” said Shwan Muhammed, a member of Parliament and one of the investigators.
Not all of the escaped prisoners returned to the fight.
Ahmed al-Dulaymi, 31, who fled from Abu Ghraib, is working as a farmer in Diyala Province, another Qaeda stronghold, using fake identification. Like many Sunnis in Iraq, he explains the recent resurgence of Sunni extremism as a reaction to the policies of the Shiite-dominated government, including broad security sweeps that have landed many innocent Sunni men in prison.
“Many of my friends were good people, but because of the government’s actions, my friends have become dangerous people and leaders in Al Qaeda,” he said. “Injustice is what gives birth to Al Qaeda.” |||||
A summary of this is? | – The most extreme faction in Syria didn't just spring up naturally—it was purposely built through a series of daring Iraqi prison breaks, the New York Times reports. With demand for fighters high, and the US recently departed, the group now known as the Islamic State of Iraq and Syria filled its ranks with a series of prison breaks, beginning in July 2012 and culminating in a massive raid on Abu Ghraib a year later. They called the strategy "Operation Breaking the Walls." One inmate freed in the Abu Ghraib raid explained that like many he'd been radicalized in prison, and was freed by a corrupt guard. Once freed, ISIS gave him a choice: Stay and fight in Iraq, or go to Syria. Many leaders chose the latter. "They felt they would be freer" there, he says. The prison break story has fueled the rebel conspiracy theory that ISIS is a pawn of Bashar al-Assad's regime, and that Iraq's Assad-friendly government helped free its fighters. There's no evidence supporting this, and many freed ISIS fighters are fighting Iraq's government, too. But McClatchy has an in-depth piece on moderate rebels' animosity toward ISIS that notes some circumstantial evidence: Assad's forces have largely left ISIS alone, it notes, and ISIS has mostly abducted and tortured Assad opponents. "It was like Syrian intelligence," says one rebel chief who fell into the group's hands. | multi_news_1_0_0 |
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– Five city and state officials were charged Wednesday with involuntary manslaughter over the water crisis in Flint, Michigan, the Detroit Free Press reports. They are Michigan Department of Health and Human Services Director Nick Lyon—the highest-ranking official to be charged in the water crisis so far, per the Detroit News—former Flint Emergency Manager Darnell Earley, former City of Flint Water Department Manager Howard Croft, plus Michigan Department of Environmental Quality’s Drinking Water Chief Liane Shekter-Smith and Water Supervisor Stephen Busch. Twelve people died after the city's water supply was changed to the Flint River in April 2014 and there was an outbreak of Legionnaires' disease. Prosecutors allege that Lyon knew about the outbreak by at least Jan. 28, 2015, yet did not make the news public until a year later; he is charged with causing the Dec. 13, 2015, death of Robert Skidmore. All of the involuntary manslaughter charges are linked to Skidmore's death; the 85-year-old died after many cases of Legionnaires' disease had been diagnosed, but the public still had not been notified of the outbreak. Lyon is also charged with misconduct in office for allegedly telling an official to halt an analysis that would have helped figure out what caused the outbreak, the Detroit Free Press reports. Also Wednesday, Chief Medical Executive Dr. Eden Wells was charged with obstruction of justice and lying to a police officer; she is accused of giving false testimony to a special agent, lying to a peace officer about when she knew of the outbreak, and threatening to withhold funding for the Flint Area Community Health and Environment Partnership if it did not stop investigating the outbreak. Flint residents are still advised to use a filter if they plan to drink the city's tap water, and many use bottled water instead, which is distributed for free in the city. | CLOSE The ongoing Flint water crisis has taken a toll on residents of this iconic Michigan city, who have been living with lead-tainted tap water for over two years. One Flint resident describes the experience as, “like being in war, but without violence.”
Buy Photo Attorney General Bill Schuette takes questions after announcing new charges against two high-ranking state health officials in the Flint drinking water crisis on Wednesday June 14, 2017. (Photo: Ryan Garza, Detroit Free Press)Buy Photo
Michigan Attorney General Bill Schuette today filed new, more serious charges in the Flint Water Crisis investigation, but also said the case is shifting to a new phase.
"We will turn to the prosecution of this investigation," Schuette said at a news conference in Flint this morning. "We are confident that the charges that we have filed will be upheld in the courts."
Schuette's statement came after he announced involuntary manslaughter charges against Nick Lyon, director of the Michigan Department of Health, as well as Darnell Earley, Flint's former emergency manager; Howard Croft, the city's former director of public works; Liane Shekter-Smith, the state's former top drinking water official and water supervisor Stephen Busch of the Department of Environmental Quality.
Those charges, felonies punishable by up to 15 years in prison, stem from the death of 85-year-old Robert Skidmore, who December 2015 death is tied to the Legionnaire's Disease outbreak in Flint.
State officials, they said, knew about the outbreak but refused to sound a public alarm that could have saved lives. At least 12 people died from complications related to the outbreak.
In all, 15 people have been charged with 51 counts. Two have plead no contest to lesser charges and agreed to help with the investigation, but none of the cases have gone to court yet.
Todd Flood, a former Wayne County Prosecutor who is serving as special counsel in the investigation, said today's charges stem from the deadly inaction of government officials.
"There are two types of people: those who give a damn and those who don't," Flood said. "I have run across many public servants who do care, but this is a case where there is willful disregard."
Andrew Arena, a former head of the Detroit FBI branch who is serving as lead investigator, said he began the probe thinking perhaps people just made mistakes, but concluded otherwise as the investigation continued.
"Many people attempted to do what is right," Arena said. "People didn't just make mistakes, they willfully and intentionally failed to do what they were supposed to do."
And Schuette said that while no charges currently are planned against Gov. Rick Snyder, his investigation continues, and "we have attempted to interview the governor," but "we were not successful."
More Flint water crisis coverage:
Michigan health director Nick Lyon, 4 others charged with involuntary manslaughter over Flint water
Flint water crisis: 5 officials face manslaughter charges
Criminal charges against top Michigan officials extremely rare
Watch: Manslaughter charges announced in Flint water crisis probe
Buy Photo Attorney General Bill Schuette announces new charges against two high-ranking state health officials in the fourth round of criminal charges in the Flint drinking water crisis on Wednesday June 14, 2017 during a press conference at Riverfront Banquet Center in downtown Flint. (Photo: Ryan Garza, Detroit Free Press)
Here are the list of additional charges announced today:
Michigan Health and Human Services Director Nick Lyon is charged with involuntary manslaughter and misconduct in office, both felonies.
Chief Medical Executive Eden Wells is charged with obstruction of justice and lying to a police officer.
Four defendants charged earlier -- former Flint emergency manager Darnell Earley, former Michigan Department of Environmental Quality drinking water chief Liane Shekter-Smith; DEQ drinking water official Stephen Busch; and former City of Flint Water Department manager Howard Croft -- were each charged with involuntary manslaughter.
All of the new charges are in connection with the Legionnaires' disease outbreak in the Flint area that led to 12 deaths after the city's water supply was switched to the Flint River in April 2014.
Read more Free Press coverage of the Legionnaires' disease outbreak:
Read the Free Press investigation from April 2016: Why were officials silent on Legionnaires' in Flint?
Here are all the victims of the Legionnaires' disease outbreak in Flint
Database: Search all of the Legionnaires' disease cases by county
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EDITOR'S NOTE: Here is the full news release sent by Michigan Attorney General Bill Schuette this morning regarding five people charged with involuntary manslaughter in the Flint water crisis.
FLINT – Michigan Attorney General Bill Schuette today announced that he has charged Michigan Department of Health and Human Services Director Nick Lyon, former Flint Emergency Manager Darnell Earley, former City of Flint Water Department Manager Howard Croft, as well as Michigan Department of Environmental Quality’s Drinking Water Chief Liane Shekter-Smith and Water Supervisor Stephen Busch with involuntary manslaughter related to their alleged failure to act in the Flint Water Crisis. Involuntary manslaughter is punishable by up to 15 years in prison, and/or a $7,500 fine. In addition to the involuntary manslaughter charges, Schuette also charged Lyon with Misconduct in Office, a felony, subject to 5 years in prison and/or a $10,000 fine. MDHHS Chief Medical Executive Eden Wells has also been charged with lying to a peace officer and obstruction of justice related to an alleged attempt to stop an investigation into the health crisis in Flint and later misleading investigators as to her actions. Schuette was joined at the announcement by Genesee County Prosecutor David Leyton, Flint Water Investigation Special Prosecutor Todd Flood, and Chief Investigator Andrew Arena. INVESTIGATION INTERIM REPORT
With more than a dozen people now having been charged, and pre-trial hearings and other legal proceedings occurring, Schuette released the initial results of the more than yearlong investigation. Included in the report is a comprehensive look at today’s and past charges made, as well as a review of the facts and evidence in the case. NOTE: The report is attached to this press release. DEFENDANTS
Multiple Flint-area residents died of Legionnaires’ disease in the time immediately following the switch from Detroit Water and Sewer Department to the Flint River. All defendants charged with involuntary manslaughter are charged in relation to the death of Robert Skidmore, 85, of Mt. Morris, Michigan. Skidmore died of Legionnaires’ disease after many others had been diagnosed with the illness, yet no public outbreak notice had been issued. The charges allege failure to notify and lack of action to stop the outbreak allowed the disease to continue its spread through Flint’s water system. NICK LYON
As the Director of the Michigan Department of Health and Human Services, a position whose duties are outlined in the Michigan Constitution, Lyon has a duty to protect public health. The investigation has shown that Lyon allegedly received notice of a deadly Legionnaires’ Disease outbreak in Genesee County nearly one year before he informed the public. After being informed about a potentially fatal health risk, Lyon allegedly deliberately failed to inform the public of a deadly Legionnaires’ Disease outbreak, which resulted in the death of Robert Skidmore. Furthermore, Lyon allegedly participated in covering up the source of Genesee County’s Legionnaires’ Disease outbreak by repeatedly attempting to prevent an independent researcher from looking into the cause of the outbreak. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. COUNT 2 – MISCONDUCT IN OFFICE Did between February 2015 and May 2017, commit misconduct in office, an indictable offense at common law, in violation of his duty to protect the health of the citizens of the County of Genesee, State of Michigan and to protect the public health enjoined upon him by the Michigan Public Health Code, MCL 333.5111(1); MCL 333.5111(2)(f);MCL 333.2251(1): MCL 333.2251(3); and MCL 333.20531 and the Critical Health Problems Reporting Act; contrary to MCL 750.505. [750.505] FELONY: 5 Years and/or $10,000.00. EDEN WELLS
As the Chief Medical Executive of the Michigan Department of Health and Human Services, Dr. Eden Wells has a responsibility to protect the health and welfare of Michigan residents. During the course of the investigation of the Flint Water Crisis, it is alleged that Wells attempted to withhold funding for programs designed to help the victims of the crisis, and then lied to an investigator about material facts related to the investigation. Charges:
COUNT 1 – OBSTRUCTION OF JUSTICE Did commit the common law offense of obstruction of justice by knowingly providing false testimony to a Special Agent and by threatening to withhold funding for the Flint Area Community Health and Environment Partnership if the partnership did not cease its investigation into the source of the Legionnaires’ Disease outbreak in Flint, Michigan; contrary to MCL 750.505. FELONY: 5 Years or $10,000. DNA to be taken upon arrest. COUNT 2 – LYING TO A PEACE OFFICER – 4 YEAR OR MORE CRIME INVESTIGATION After being informed by Special Counsel Todd Flood, in the presence of Special Agent Arthur Wimmer, that they were conducting a criminal investigation, did knowingly and willfully make a statement or statements to the officer that he or she knew was false or misleading regarding the following material fact or facts relating to the investigation: the date she knew of the Legionnaires’ Disease outbreak in Flint, Michigan, and the officer was conducting a criminal investigation regarding involuntary manslaughter; contrary to MCL 750.479c(2)(c). [750.470C2C]. HIGH COURT MISDEMEANOR: 2 Years and/or $5,000.00. STEPHEN BUSCH
Stephen Busch served as the Michigan Department of Environmental Quality District 8 Water Supervisor, a position which would have allowed him to order the Flint Water Treatment Plant be shut down because it was not producing safe water. In January of 2015, Busch was made aware of the Legionnaires’ Disease outbreak, yet he allegedly represented to the public that Flint’s drinking water was safe. Busch was previously charged with felony Misconduct in Office, Tampering with Evidence, Conspiracy to Tamper with Evidence, and two misdemeanor counts for both a treatment and monitoring violation of the Michigan Safe Water Drinking Act. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. LIANE SHEKTER-SMITH
As the Chief of the Office of Drinking Water and Municipal Assistance at the Department of Environmental Quality, Shekter-Smith had the ability to order the Flint Water Treatment Plant shut down for failure to produce safe water. Shekter-Smith was previously charged with a felony of Misconduct in Office and a misdemeanor charge of Willful Neglect of Duty. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. HOWARD CROFT
As Director of Public Works for the City of Flint, Croft had the ability to mandate changes to the treatment processes at the WTP to ensure proper disinfection was occurring, or switch back to DWSD. Mike Glasgow, former Flint Water Treatment Plant Operator, was allegedly pressured by Croft to start using the Flint Water Treatment Plant. Croft’s alleged failure to treat the water properly contributed to the bacterial outbreaks found in Flint, including the legionella in the spring of 2015. Croft was previously charged with felony False Pretenses and Conspiracy to Commit False Pretenses. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. DARNELL EARLEY
As an appointed Emergency Manager for the City of Flint, Earley was tasked with ensuring the health and welfare of the City. During his terms as Emergency Manager, Earley contributed to the decisions that allegedly caused the death of Robert Skidmore by keeping the City on the water source even as it became obvious the source should be switched back to Detroit Water & Sewer. Earley was previously charged with felony False Pretenses, Conspiracy to Commit False Pretenses, Misconduct in Office and a misdemeanor charge of Willful Neglect of Duty. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. Acriminal charge is merely an accusation and the defendants are presumed innocent until proven guilty.
Read or Share this story: http://on.freep.com/2t1Kvv3 ||||| Buy Photo Clockwise from upper left, Dr. Eden Wells, Nick Lyon, Darnell Earley and Howard Croft (Photo: Detroit Free Press, Michigan Attorney General)Buy Photo
FLINT — Attorney General Bill Schuette charged two high-ranking state health officials today in the fourth round of criminal charges in the Flint drinking water crisis.
He also said he will be adding new, serious felony charges against four defendants who were charged earlier in the investigation.
And Schuette said that while no charges currently are planned against Gov. Rick Snyder, his investigation continues, and "we have attempted to interview the governor," but "we were not successful."
Michigan Health and Human Services Director Nick Lyon is charged with involuntary manslaughter and misconduct in office, both felonies.
More Flint water crisis coverage:
Michigan health director Nick Lyon, 4 others charged with involuntary manslaughter over Flint water
Flint water crisis: 5 officials face manslaughter charges
Criminal charges against top Michigan officials extremely rare
Watch: Manslaughter charges announced in Flint water crisis probe
Chief Medical Executive Dr. Eden Wells is charged with obstruction of justice and lying to a police officer.
Buy Photo Michigan Health and Human Services Director Nick Lyon is charged with involuntary manslaughter and misconduct in office, both felonies. (Photo: Ryan Garza, Detroit Free Press)
And four defendants charged earlier -- former Flint emergency manager Darnell Earley, former Michigan Department of Environmental Quality drinking water chief Liane Shekter-Smith, DEQ drinking water official Stephen Busch, and former City of Flint Water Department manager Howard Croft -- each will faced additional charges of involuntary manslaughter. Schuette said.
All of the new charges are in connection with the Legionnaires' disease outbreak in the Flint area that led to 12 deaths after the city's water supply was switched to the Flint River in April 2014.
Read more Free Press coverage of the Legionnaires' disease outbreak:
Read the Free Press investigation from April 2016: Why were officials silent on Legionnaires' in Flint?
Here are all the victims of the Legionnaires' disease outbreak in Flint
Database: Search all of the Legionnaires' disease cases by county
Health department officials released a statement from Gov. Rick Snyder saying he stands behind Lyon and Wells, and that they would remain in their jobs pending trial.
Lyon, 49, of Marshall is accused of causing the death of Robert Skidmore on Dec. 13, 2015 by failing to alert the public about a foreseeable outbreak of Legionnaires' disease. It's a 15-year felony.
All of the other involuntary manslaughter charges also relate to the death of Skidmore, who was 85 at the time of his death.
Buy Photo Chief Medical Executive Eden Wells is charged with obstruction of justice and lying to a police officer. (Photo: Ryan Garza, Detroit Free Press)
"Defendant Lyon was aware of Genesee County's Legionnaires' disease outbreak at least by Jan. 28, 2015, and did not notify the public until a year later," the charging documents allege.
Lyon "exhibited gross negligence when he failed to alert the public about the deadly outbreak and by taking steps to suppress information illustrating obvious and apparent harms that were likely to result in serious injury."
According to the charging documents, Lyon "willfully disregarded the deadly nature of the Legionnaires' disease outbreak," later saying he "can't save everyone," and "everyone has to die of something."
Chip Chamberlain and Larry Williey, Lyon's Grand Rapids attorneys, sai: "We are confident in our defense of Nick Lyon," and "the true facts simply do not support the prosecution’s claims." they said the case "appears to be a misguided theory looking for facts that do not exist," and Schuette's news conferences are prejudical and include false statements.
"We absolutely and vehemently dispute the charges," the attorneys said. "They are baseless. We intend to provide a vigorous defense of Nick Lyon and we expect the court system to vindicate him entirely."
Schuette said that he's heard from many people frustrated and angry that he has not brought charges against Snyder, the state's Republican governor since 2011. But he said he's also heard from those who feel he's been too hard on the Snyder administration, and charges are only being filed when the evidence warrants them.
Tuesday's charges, while they do not end the investigation, mark the end of one phase of the investigation and "a significant milestone," he said.
Buy Photo Former Flint emergency manager Darnell Earley will face additional charges of involuntary manslaughter. (Photo: Jessica J. Trevino, Detroit Free Press)
Andrew Arena, Schuette's chief criminal investigator and the former FBI director in Detroit, said what he has found most shocking is that "people had information in their possession" about the Legionnaires' disease outbreak, "and just failed to act."
Charges were authorized Wednesday morning by 67th District Court Judge G. David Guinn, in Flint.
On the misconduct in office charge, a five-year felony, Lyon is accused of instructing an official to discontinue an analysis that would help determine the cause of the outbreak.
Related:
Wells, 54, of Ann Arbor is accused in connection with the obstruction of justice charge of providing false testimony to a special agent and threatening to withhold funding for the Flint Area Community Health and Environment Partnership if the partnership did not cease its investigation into the source of the outbreak. That's a five-year felony.
Wells also is charged with lying to a peace officer about the date she knew of the outbreak of Legionnaires' disease. That's a two-year misdemeanor.
"Dr. Wells vehemently denied the charges and the charges will be vigorously defended," Wells' lawyer, Jerold Lax told the Free Press in a statement.
Buy Photo Former City of Flint Water Department manager Howard Croft will face additional charges of involuntary manslaughter. (Photo: Ryan Garza, Detroit Free Press)
According to the charging documents, Wells gave a statement to Schuette's investigators on April 12, 2016, pursuant to an agreement under which she would not be charged, provided she made no false statements.
Wells allegedly lied by saying she had no knowledge of the Legionnaires' disease outbreak until late September or early October of 2015, when in fact she knew about the outbreak in March 2015.
Watch our mini-documentary on the Flint water crisis, winner of a Michigan Emmy:
CLOSE The ongoing Flint water crisis has taken a toll on residents of this iconic Michigan city, who have been living with lead-tainted tap water for over two years. One Flint resident describes the experience as, “like being in war, but without violence.”
Wells was appointed chief medical executive in May 2015. She previously served as medical consultant to the department's Bureau of Epidemiology from 2004 to 2011.
There were 12 deaths linked to Legionnaires' disease during a 17-month period in 2014 and 2015 in the Flint area. Dozens more were sickened by the disease, a severe type of pneumonia.
In previous years, six to 13 cases were typically confirmed annually in the county.
So far, 15 current or former state or City of Flint officials have been charged, including two emergency managers who were appointed by the governor and reported to the state treasurer.
Flint Mayor Karen Weaver issued a statement that said "manslaughter is a serious charge," and "it’s good to see that state Attorney General Schuette and his team are taking this matter seriously by bringing such serious charges against those who they believe didn’t do enough to address this public health threat, or to alert the Flint community about it."
Flint's drinking water became contaminated with lead in April 2014 after the city switched from treated Lake Huron water supplied from Detroit to raw water from the Flint River, which was treated at the Flint Water Treatment Plant.
Michigan Department of Environmental Quality officials have acknowledged a mistake in failing to require corrosion-control chemicals be added to the more corrosive water. As a result, lead leached from pipes, joints and fixtures into Flint households.
Though lead levels in the water have come down significantly since the state acknowledged the contamination around Oct. 1, 2015, residents are still advised not to drink tap water without a filter. Many still rely on bottled water, which can be picked up free at distribution centers in Flint.
Five of the current or former state employees charged previously are from the DEQ. Three are from the Department of Health and Human Services (DHHS).
DEQ drinking water official Stephen Busch will face additional charges of involuntary manslaughter. (Photo: Michigan Attorney General)
Outbreaks of Legionnaires' disease in the Flint area following the water switch were tied to the deaths. Officials haven't definitely linked the water switch to the disease, but Schuette and his investigators have come close to doing so in public statements and documents related to the criminal charges.
Lyon was told in September by state investigators that he was a focus of the investigation, Lyon's lawyer Willey of the Grand Rapids criminal defense firm Willey & Chamberlain told the Free Press in October.
"We haven't heard from them for months," Willey said late Tuesday. "I've received no notification ... that anything is in the offing."
Snyder named Lyon director of DHHS in April 2015 when he created a new agency that merged the former departments of community health and human services.
Previously, Lyon had served as health director beginning in September 2014, Before that, he was the agency's chief deputy director beginning in 2011.
Contact Paul Egan: 517-372-8660 or [email protected]. Follow him on Twitter @paulegan4.
Read or Share this story: http://on.freep.com/2t1qdlv ||||| Buy Photo Attorney Bill Schuette, at podium, announces Wednesday he's charging five officials with involuntary manslaughter in connection with the Flint water scandal. Behind him are, from left, Special Counsel Todd Flood, Genesee County Prosecutor David Leyton and lead investigator Andy Arena. (Photo: Dale G. Young, The Detroit News)Buy Photo
Flint — Michigan’s health department director and four other officials involved with Flint’s lead-contaminated water were charged Wednesday with involuntary manslaughter, the most serious charges to date in the criminal investigation.
Nick Lyon was accused of misconduct in office and involuntary manslaughter, becoming the highest-ranking member of Gov. Rick Snyder’s administration to be targeted in the criminal probe. The manslaughter charges carries a penalty of up to 15 years in prison and a $7,500 fine, while the misconduct charge carries a prison sentence of up to five years and a $10,000 fine.
Lyon, former Flint Emergency Manager Darnell Earley, former Michigan Department of Environmental Quality Drinking Water Chief Liane Shekter-Smith, state Water Supervisor Stephen Busch and former Flint Water Department Manager Howard Croft are accused of failing to alert the public about an outbreak of Legionnaires’ disease in the Flint area. Earley, Shekter-Smith, Busch and Croft already have been charged with less-serious crimes.
There were 12 deaths and 79 other people sickened by Legionnaires’ disease in 2014-15, which some experts have linked to the contaminated water after the city switched to Flint River water in April 2014.
One legal expert said the “aggressive” manslaughter charges will be challenging to prove to juries.
But Michigan Attorney General Bill Schuette remained undeterred and indicated during a Wednesday press conference that he is continuing not to rule out possible charges against Snyder. When asked why Snyder has not been charged, Schuette said no “crime has been established,” and “we’re not filing charges at this time.”
Lyon and four others failed to protect the residents of Flint, said Schuette, who was joined by Genesee County Prosecutor David Leyton, Special Prosecutor Todd Flood and investigator Andy Arena. Lyon’s failure to act resulted in the death of at least one person, 85-year-old Robert Skidmore of Genesee Township, the attorney general said.
Skidmore’s death certificate shows that he died Dec. 13, 2015, from “end stage congestive heart failure.” Only diabetes is listed as a contributing cause to the death of Skidmore, according to the certificate.
But the charging document indicates that a McLaren Flint Hospital doctor on June 2, 2015, collected a sample from Skidmore that tested positive for Legionella and that the Genesee County medical examiner will “not refute the medical doctor’s findings that Legionnaires’ Disease was a cause of Robert Skidmore’s death.”
The state’s chief medical officer, Dr. Eden Wells, was charged Wednesday with obstruction of justice and lying to a police officer. The obstruction charge carries a prison term of up to two years. Wells’ lawyer was not immediately known.
“People have died because of the decisions people made,” Schuette said.
“There are two types of people in the world: Those who give a damn and those who don’t. This is a case where there has been willful disregard” for the health and safety of others, Flood said.
Lyon attorneys Chip Chamberlain and Larry Willey fired back that the case “appears to be a misguided theory looking for facts that do not exist.”
“To that point, we’ve witnessed numerous press conferences by the prosecution that have been intentionally prejudicial to the process and unfair to those targeted. Worse yet, they have made many statements that are completely false. ... We expect the court system to vindicate him entirely.”
Michigan’s health department director and four other individuals involved with Flint’s lead-contaminated water were charged Wednesday with involuntary manslaughter (Photo: Detroit News file photos)
Snyder fires back
Email records released by Snyder’s administration show Lyon was aware of a spike in Legionella — bacteria that causes Legionnaires’ disease, a form of pneumonia — as early as January 2015 but didn’t put out a public alert. Snyder informed the public about the Legionnaires’ outbreak in January 2016.
Lyon has said he knew about Legionnaires’ for months but wanted to wait until investigators in the Health and Human Services Department finished their own probe.
Snyder fired back at Schuette’s office while keeping Lyon and Wells on the job, telling Health and Human Services employees in an email that “I am standing behind Nick and Eden.”
“Director Lyon and Dr. Eden Wells, like every other person who has been charged with a crime by Bill Schuette, are presumed innocent unless and until proven guilty beyond a reasonable doubt,” Snyder said in a statement.
“Some state employees were charged over a year ago and have been suspended from work since that time. They still have not had their day in court. That is not justice for Flint nor for those who have been charged. Director Lyon and Dr. Wells have been and continue to be instrumental in Flint’s recovery.”
Senate Minority Leader Jim Ananich, D-Flint, called Snyder’s response to the charges “tone deaf” and argued the governor should be focused on the harm done to Flint residents rather than state employees.
Ananich questioned if Lyon can continue leading the state health department “if he has not been protecting the public and not been informing his superiors” about real or potential threats.
“I think it’s very troubling, and I think he probably should step down,” he said about Lyon. “I think the question needs to be why the governor doesn’t think so.”
Schuette charges face hurdles
Wayne State University law professor Peter Henning said the attorney general’s office will have to prove that any public warning he may have made about Legionnaires’ disease could have prevented deaths.
“For any homicide charge, you have to prove causation and that there is a direct linkage for what he did or failed to do and the death,” said Henning, a former federal prosecutor. “That will certainly be a hurdle for the attorney general’s office.”
Prosecutors may also have to prove a link between Flint water and the Legionnaires’ disease outbreak, Henning added. Experts and the state have debated whether the water itself is to blame or a local hospital where many of the cases originated.
“This case is going to turn very much on expert testimony,” Henning said. “It’s not a whodunit. It’s: Did he do anything that caused the death? The death occurred; now it’s a matter of tracing it back, and there’s a challenge there.”
But in a Wednesday interview, Leyton said he and Schuette had a “duty to bring those charges.”
“Every single case you bring to court as a prosecuting attorney is a challenge because of so many factors,” he said. “But our job is provide justice for the people of Michigan and, in this specific instance, the city of Flint.”
About 15 state and Flint officials have been charged in what Schuette called “the most comprehensive investigation in Michigan history.” The longtime Republican elected official has been considering a run for governor in 2018.
“I am duty bound to uphold the laws in the state of Michigan,” Schuette said.
Flint official, residents react
Flint Mayor Karen Weaver was watching the press conference on a livestream from her chief of staff and said “wow” when the involuntary manslaughter charges were announced.
“It’s terrible what has occurred but it’s a good day for the people of the city of Flint,” Weaver later said. “We’ve had people die as a result of this water crisis. And for justice to be had is wonderful.”
The charges are “a measure of justice,” said U.S. Rep. Dan Kildee, a Flint Township Democrat who has gained national attention speaking out on the crisis. He told MSNBC host Rachel Maddow on Wednesday. “… It’s somewhat comforting to know that the system works, that when you see a state government do something as bad as they did to the city of Flint, that individuals will be held accountable for it. But we need more. We need other forms of justice, we need people to make it right. We need the state government to step up and make it right.”
Flint resident Shelby Offord, 28, said the charges filed Wednesday are “a good start,” but wishes officials would do more.
“I feel there should be more charges coming because the ones who have been affected and got the lead poisoning, that’s something they’ve got to deal with the rest of their lives,” Offord said as she walked in downtown Flint with her two 10-year-old girls, both of who had some form of lead in their system because of the water.
Doug McGruder, 75, of Flint Township, said Earley is the “scapegoat” and that others such as the governor need to be held accountable by Schuette. But he said he is not holding his breath.
“Earley shouldn’t have been charged because like me, on my job, I have a boss,” McGruder said. “The person that’s in charge of me should be charged. And that’s the governor.”
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A power generator tips in front of Texas' CHRISTUS Spohn Hospital in Corpus Christi, Texas, as Hurricane Harvey hits Friday, Aug. 25, 2017. (Courtney Sacco /Corpus Christi Caller-Times via AP) (Associated Press)
CORPUS CHRISTI, Texas (AP) — The Latest on Tropical Storm Harvey (all times local):
8:25 a.m.
President Donald Trump says he will be traveling to Texas "as soon as that trip can be made without causing disruption" in the wake of Hurricane Harvey.
Trump tweeted that the "focus must be life and safety."
At least two people are dead and more than a dozen injured due to the storm that has battered the region, including the cities of Corpus Christi and Houston.
Trump has been complimenting the response to the storm on his Twitter feed, commending "Great coordination between agencies at all levels of government."
Trump adds that: "Many people are now saying that this is the worst storm/hurricane they have ever seen. Good news is that we have great talent on the ground."
The storm could linger for days in the region and could unload as much as 40 inches of rain on cities including Houston.
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8:15 a.m.
The U.S. Coast Guard says it's received more than 300 requests for urban search and rescue in the Houston area.
The Coast Guard has five helicopters working the emergency calls and is asking for additional helicopters from New Orleans to help.
Officials are advising people in dire straits to get to the roofs of their homes and mark them somehow to be seen from the air. They're suggesting people wave sheets or towels.
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7:45 a.m.
Flooding in some parts of the county that includes the city of Houston is so bad that residents are being urged to seek refuge on their roofs.
Harris County Flood Control District official Jeff Lindner says people inundated by rising waters shouldn't crawl into attics of their homes but should get on top of them.
He says rainfall of more than 4 inches per hour has sent water higher than in recent Houston floods side and are exceeding levels seen in Tropical Storm Allison in June 2001.
Lindner says areas south of the city appear hard-hit and some flooding is reported in downtown Houston and in the Texas Medical Center, which was devastated in Allison.
He calls Harvey "a different animal" from Allison and a "historic situation."
He says he's most amazed that he's getting reports "of water into second-story of apartments and homes." Considering Houston's flat terrain, "it's very rare to get that depth of water."
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6:20 a.m.
Authorities say rescue attempts continue in Houston for those stranded inside flooded homes and submerged vehicles in the wake of Harvey.
The Houston Chronicle reports that hundreds of calls have been fielded for water rescues as of early Sunday, including Houston police officials who evacuated two apartment complexes and rescued more than 50 children.
Meanwhile, Harris County Sheriff Ed Gonzalez and Houston Mayor Sylvester Turner on Sunday continued urging residents via Twitter to "shelter in place" and stay off rain-swollen roadways.
Gonzalez actively used Twitter overnight to field assistance for those trapped inside water-soaked homes, attics and vehicles. Those appealing for assistance or being steered to help via Gonzalez's Twitter feed included a person suffering "cardiac-arrest," and a woman who posted: "I have 2 children with me and the water is swallowing us up. Please send help."
Gonzalez at one point appealed for calm and patience, saying officials were "trying to make it to everyone as best we can."
Turner's official Twitter account said "911 services at capacity. If u can shelter in place do so, a few inches in your home is not imminent danger. Only call if in imminent danger."
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4:03 a.m.
The National Hurricane Center says Harvey continues to cause "catastrophic flooding in southeastern Texas."
The hurricane center says in its 4 a.m. Sunday update that the tropical storm has maximum sustained winds of 45 mph (72.42 kph) and remains stationary about 45 miles (72.42 kilometers) northwest of Victoria, Texas.
A storm surge warning and a tropical storm warning also are both in effect for Port O'Connor to Sargent. The hurricane center says a storm surge warning means there is a danger of life-threatening inundation from rising water moving inland from the coastline.
The center says Harvey is likely to weaken to a tropical depression later Sunday. Harvey made landfall Friday night as a Category 4 hurricane.
Meanwhile, the National Weather Service says a Flash Flood Emergency over west and central Harris County, where Houston is located, as well as for eastern Fort Bend and northern Brazoria counties remains in effect until 6:15 a.m. Sunday, calling it a "Particularly Dangerous Situation."
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2:11 a.m.
Jersey Village, Texas, officials are recommending that people who live along the White Oak Bayou, about 17 miles northwest of Houston, consider whether they need to evacuate their homes.
Jersey Village City Manager Austin Bleess says the city issued a notice to residents about 1:30 a.m. saying the bayou looked like it would be out of its banks before long. He says city officials worried that streets may soon become impassable and wanted those residents to have time to make arrangements.
"Certainly if people can stay in their homes, they can do that," Bleess said. "It's quite possible that the streets could get impassable so we wanted to get that recommendation out."
Bleess says the city is in the process of opening a storm shelter at the Champion Forest Baptist Church, Jersey Village chapter.
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1:20 a.m.
The National Hurricane Center says Harvey continues to weaken at a slow pace as it produces torrential rains across parts of Southeast Texas.
In its early Sunday update, the hurricane center said the tropical storm has maximum sustained winds of 45 mph (72.42 kph) and it is practically stationary about 45 miles (72.42 kilometers) northwest of Victoria, Texas.
The airport in Austin, about 165 miles (265.53 kilometers) west of Houston, reported sustained winds of 38 mph.
The center says Harvey is likely to weaken to a tropical depression later Sunday. Harvey made landfall Friday night as a Category 4 hurricane.
Meanwhile, the National Weather Service extended a Flash Flood Emergency over west and central Harris County, where Houston is located, as well as for eastern Fort Bend and northern Brazoria counties until 6:15 a.m. Sunday, calling it a "Particularly Dangerous Situation."
___
12:30 a.m.
At least two people have died as Tropical Storm Harvey continues to dump rain on Southeast Texas.
The Harris County medical examiner's office confirmed the death of one person late Saturday in Harris County, but the office did not identify the cause of death.
Gary Norman, a spokesman for the Houston emergency operations center, says the woman appeared to have gotten out of her vehicle in high water. She was found by neighbors about 30 yards away from the vehicle. Norman says she was pronounced dead at the scene by a doctor who was in the area.
Earlier Saturday, Aransas County Judge C.H. "Burt" Mills Jr. said the storm left one person dead in the county.
Harvey came ashore Friday night as a Category 4 hurricane, but has since been downgraded to a tropical storm. ||||| JP Morgan Chase Bank, N.A. Houston, TX ABA # 021000021 For credit to: Greater Houston Community Foundation A/C#: 849170287 For further credit to: Hurricane Harvey Relief Fund
Online Credit Card Donations: Visit www.ghcf.org . Online credit card donations will be assessed a small fee, typically 3 percent, by the credit card companies. Donors have the option of increasing their credit card donations to cover this fee. Checks/Money Orders: Mail to Greater Houston Community Foundation, 5120 Woodway Drive, Suite 6000, Houston, TX 77056. Transfer Cash by Wire: Wire To:
"We are getting calls from across the country and right here in our hometown, and the generosity of people who understand this disaster is truly amazing," Mayor Turner said. "Together we can make a difference to those who will need extensive help to get back on their feet once this storm is over."
Earlier Sunday, Abbott said the state activated 3,000 National Guard and State Guard members as a result of the storm damage. He also said 500 vehicles and 14 aircraft had been put into service.
Texas Gov. Greg Abbott says another 1,000 National Guard members will be sent to Houston on Monday as flooding from Harvey continues to ravage the area. The governor announced the move late Sunday on his personal Twitter account.
Meanwhile, officials in Fort Bend County, Houston's southwestern suburbs, late Sunday issued widespread mandatory evacuation orders along the Brazos River levee districts. County officials were preparing for the river to reach major flood stages late Sunday. County Judge Robert Herbert said at a news conference that National Weather Service officials were predicting that the water could rise to 59 feet, three feet above 2016 records and what Herbert called an "800-year flood level." Herbert said that amount of water would top the levees and carries a threat of levee failure.
Thousands of homes could be affected by the releases, CBS Houston affiliate KHOU-TV reports .
Harris and Fort Bend county officials said Sunday that residents around certain areas should be prepared for the influx of water that was scheduled to happen at Addicks around 2 a.m. local time Monday and a day later at Barker. Officials warned residents they should pack their cars Sunday night and wait for daylight Monday to leave.
Residents living around the Addicks and Barker reservoirs designed to help prevent flooding in downtown Houston, were warned Sunday that a controlled release from both reservoirs would cause additional street flooding and could spill into homes. Rising water levels and continuing rain was putting pressure on the dams that could cause a failure without the release.
he American Red Cross was expanding the shelter by the hour. Volunteers initially set out around 1,300 cots and quickly assembled more in anticipation of other evacuees arriving through the night. They have enough space and cots to house 5,000 people.
Hundreds of people affected by devastating flooding in Houston have flocked to a downtown showcase convention center-turned-emergency shelter. Many arrived Sunday carrying little more than what was in their pockets. Most are preparing for a stay of several days, as water rises inside their homes and roads remain impassable.
Some 269,000 homes and businesses were in the dark in Southest Texas early Monday due to Harvey, utilities reported.
Smith says the city's 911 emergency response system has been challenged by sharply increased call volumes since the tropical storm made landfall late Friday.
Public Information Officer Keith Smith also says Sunday that rescue efforts continue and now are focused on those who feel trapped inside a home or building.
Houston officials continue to urge people to shelter in place and stay off flooded roadways as Harvey continues to batter the nation's fourth-largest city.
The center says people in the upper Texas coast and in southwestern Louisiana should continue to monitor Harvey's progress.
The hurricane center says Harvey's center was expected to drift off the middle Texas coast Monday and meander offshore through Tuesday before beginning "a slow northeastward motion."
That means it remains virtually stalled near the coast and continues to drop heavy rain on the Houston and Galveston areas. In the past 48 hours, numerous spots in the region have measured more than 25 inches of rain.
The National Hurricane Center said in its 4 a.m. CDT update that the tropical storm still has sustained winds of up to 40 mph and is centered 20 miles east of Victoria, Texas, about 120 miles southwest of Houston. It continues to creep to the southeast at 3 mph.
Harvey continues to head back toward the Gulf of Mexico at a slow pace.
Edwards said life-saving efforts such as search and rescue and shelters will be needed, especially in southwest Louisiana where forecasters say 10 to 20 inches of rain could fall.
Gov. John Bel Edwards said he sent a letter to the White House requesting the initial disaster declaration for five parishes in southwest Louisiana, and could add more areas to the request later.
Louisiana's governor is asking President Trump for a federal emergency declaration for Louisiana since forecasters expect Harvey to cause significant damage in the state.
Those in need of assistance should visit www.disasaterassistance.gov if they have internet access or call 1-800-621-FEMA.
Long encouraged Americans who want to help storm victims to go to the website www.NVOAD.org to connect with National Voluntary Organizations Active in Disaster, which is coordinating donations and volunteers.
According to the latest forecast from the National Weather Service, the storm is expected to dump another 15 to 20 inches of additional rainfall on the region before it's over.
Duke said she will accompany President Trump as he visits Houston on Tuesday.
For now, she urged local residents to avoid calling 911 unless they were in need of urgent, immediate medical assistance.
Duke said emergency officials are currently focused on rescue efforts and plan to move into recovery mode later this week.
"We are not out of the woods yet," said Elaine Duke, Acting Secretary of the Department of Homeland Security. "Harvey is still a dangerous and historic storm."
"All disasters begin and end at the local level," he added. "All evacuation decisions are made at the local level in Texas."
When it comes to the emergency response and evacuations, Long said he believes local, state and federal agencies thus far have operated with the "best information that they had at the time." More widespread evacuations would have been "difficult" given the time frame, putting people at risk of becoming trapped in long lines of vehicles trying to escape rising floodwaters, which would have been worse than the shelter-in-place scenario playing out now.
Calling Harvey a "landmark event," Long said "you could not dream this forecast up."
In a Monday morning briefing, FEMA Administrator Brock Long said officials are expecting 30,000 people in emergency shelters. As many as 50 counties are feeling the impact of the storm.
The statement said the Department of Homeland Security and FEMA would coordinate disaster relief efforts "to save lives and to protect property and public health and safety, and to lessen or avert the threat of a catastrophe in the parishes of Beauregard, Calcasieu, Cameron, Jefferson Davis, and Vermillion."
A statement from the White House Monday said President Donald Trump has declared an emergency in Louisiana, authorizing federal assistance for Harvey relief efforts in the state.
Follow along below for live updates on the storm. All times are Eastern unless otherwise noted.
The director of the Federal Emergency Management Agency (FEMA), Brock Long, predicted that the aftermath of the storm would require FEMA's involvement for years. "This disaster's going to be a landmark event," Long said.
"The breadth and intensity of this rainfall is beyond anything experienced before," the National Weather Service said in a statement.
As the water rose, the National Weather Service issued another ominous forecast: Before the storm is gone, some parts of Houston and its suburbs could get as much as 50 inches of rain. That would be the highest amount ever recorded in Texas.
Judging from federal disaster declarations, the storm has so far affected about a quarter of the Texas population, or 6.8 million people in 18 counties. It was blamed for at least two deaths.
Rescuers had to give top priority to life-and-death situations, leaving many affected families to fend for themselves. And several hospitals in the Houston area were evacuated due to the rising waters.
Volunteers joined emergency teams to pull people from their homes or from the water, which was high enough in places to gush into second floors. The flooding from Harvey, which made landfall late Friday as a Category 4 hurricane and has lingered dropping heavy rain as a tropical storm, was so widespread that authorities had trouble pinpointing the worst areas. They urged people to get on top of their houses to avoid becoming trapped in attics and to wave sheets or towels to draw attention to their location.
The incessant rain covered much of Houston in gray-green floodwaters and turned streets into rivers navigable only by boat. In a rescue effort that recalled the aftermath of Hurricane Katrina, helicopters landed near flooded freeways, airboats buzzed across submerged neighborhoods and high-water vehicles plowed through water-logged intersections. Some people managed with kayaks or canoes or swam.
"We are not out of the woods yet," Elaine Duke, Acting Secretary of the Department of Homeland Security, said at a Monday morning briefing. "Harvey is still a dangerous and historic storm."
The National Weather Service says flooding isn't expected to peak until Wednesday or Thursday.
HOUSTON -- The remnants of Hurricane Harvey continued dumping historic levels of rainfall on the Houston area Monday morning as devastating floods swamped the nation's fourth-largest city. Rising water chased thousands of people to rooftops or higher ground and overwhelmed rescuers who could not keep up with the constant calls for help.
About 300,000 customers were without power statewide. Gov. Greg Abbott said it would probably be several days before electricity is restored.
One person was killed in Aransas County when in a fire at home during the storm, county Judge C.H. "Burt" Mills Jr. said. A second person died in flooding in Harris County, where Houston is located.
Harvey continues to cause "catastrophic flooding in southeastern Texas," the National Hurricane Center says.
The National Weather Service said catastrophic flooding in the Houston metropolitan area "is expected to worsen and could become historic in association with Harvey."
EMERGENCY MANAGEMENT HAS REQUESTED: IF HIGHEST FLOOR OF YOUR HOME BECOMES DANGEROUS...GET ON THE ROOF. #houwx #glswx #txwx #Harvey pic.twitter.com/rG3dsdQUxu
The National Weather Service Houston/Galveston said Emergency Management officials are requesting that people get on the roof of their home if the highest floor becomes dangerous.
In Houston, authorities were pleading with people not to leave their homes as a flood emergency was declared.
The U.S. Coast Guard says it has received more than 300 requests for urban search and rescue in the Houston area amid flooding from Harvey. The Coast Guard has five helicopters working the emergency calls and is asking for additional helicopters from New Orleans to help.
Great coordination between agencies at all levels of government. Continuing rains and flash floods are being dealt with. Thousands rescued.
"Great coordination between agencies at all levels of government," he tweeted Sunday morning. "Continuing rains and flash floods are being dealt with. Thousands rescued."
Mr. Trump has sent a flurry of tweets about the powerful storm, and has complimented the government's response to it so far.
I will be going to Texas as soon as that trip can be made without causing disruption. The focus must be life and safety.
President Donald Trump said in a tweet he will travel to Texas "as soon as that trip can be made without causing disruption." He added: "The focus must be life and safety."
"We're very appreciative of our fellow states as well as what the federal government has done," Abbott said. "I gotta tell you the Trump administration has provided us everything that we need ."
Abbott also applauded the efforts of the Trump administration.
"And so we are working on as many water rescues as we possibly can and trying to find ways to get people out of harm's way," Abbott said on "Face the Nation" Sunday, as catastrophic flooding hit Houston.
Texas Gov. Greg Abbott said "our first and foremost focus at this particular time is saving lives."
Houston Assistant Police Chief Larry Satterwhite said there has been an increase in calls from residents with flooded homes in the city's northeast, southeast and southwest sections.
Pena said his agency has made more than 250 water rescues, all of them people in vehicles, during a three-hour period overnight.
Houston Fire Chief Samuel Pena said that since midnight his agency has responded to more than 2,500 emergency calls and another 1,000 calls were waiting to be serviced.
All commercial operations at Hobby Airport have ceased until further notice. No flights in/out and roadways in/out are closed.
Commercial operations have ceased at both George Bush Intercontinental Airport (IAH) and William P. Hobby Airport (HOU) in Houston until further notice "due to severe weather," an alert said Sunday. "No inbound or outbound flights from either airport at this time. For flight details, rescheduling and waivers, please contact your air carrier."
This event is unprecedented & all impacts are unknown & beyond anything experienced. Follow orders from officials to ensure safety. #Harvey pic.twitter.com/IjpWLey1h8
"This event is unprecedented & all impacts are unknown & beyond anything experienced," the National Weather Service tweeted Sunday. "Follow orders from officials to ensure safety."
Rainfall totals since Thursday evening have reached about 25 inches in south Houston. In Dayton, located 38 miles northeast of Houston, rainfall has already reached 27 inches.
The NWS says in a statement that "the breadth and intensity of this rainfall is beyond anything experienced before and is resulting in catastrophic flooding."
"We're in kind of unprecedented territory with this storm," Burke said.
NWS meteorologist Patrick Burke said rainfall totals will end up around 40 inches or more for Houston on average, but some isolated spots will see 50 inches or more.
The National Weather Service said some parts of Houston and areas just west of the city could get 50 inches of rain as Tropical Storm Harvey stalls over the state. It would be the highest ever recorded in Texas.
A tornado watch has been issued for parts of Louisiana and Texas until 2 AM CDT pic.twitter.com/U07kpmb05G
The agency has also been tweeting a series of tornado warnings for locations in Texas, including Humble, Moonshine Hill and Kingwood, among other areas.
The National Weather Service in Houston issued a tornado watch for parts of Texas and Louisiana. It said the watch is valid until 2 a.m. CT Monday. The alert warned of possible tornadoes, marble-sized hail and isolated winds up to 60 mph.
Do you have a HIGH WATER VEHICLE or BOAT and helping rescue in your community? Call us to coordinate: 713-881-3100. Ask for Fire Marshal. pic.twitter.com/D3SfSYWgxr
"Do you have a HIGH WATER VEHICLE or BOAT and helping rescue in your community? Call us to coordinate: 713-881-3100. Ask for Fire Marshal," officials wrote on Twitter.
Harris County officials are asking the public to volunteer high-water vehicles and boats to help rescue efforts in the area.
Regional distribution centers would be set up Monday for food distribution purposes in Rockport, Port Aransas, Aransas Pass, Ingleside and Portland.
Abbott said that helicopters and additional resources have been provided by Nebraska, Tennessee, Utah, California, Missouri, Ohio, Arizona and New York, in addition to the federal government.
Texas Gov. Greg Abbott said in a news conference Sunday that 3,000 national and state guard members were activated as a result of Tropical Storm Harvey. He said there are now 250 highway closures across the state.
Been sleeping after being up all nite but here's some more perspective on #HoustonFlooding problem. This is near galleria. #khou11 #Harvey pic.twitter.com/JyhRWnLVdf
Videos posted online Sunday showed flooding that resulted from Harvey after it dumped massive amounts of rain on southeast Texas.
Houston needs our prayers! Our TV station is evacuated. Headed back out in the field to help us get back on the air #Harvey #KHOU11 🙏 pic.twitter.com/roq8Q6xlZN
Rainfall totals climbed by the hour. Since Thursday, South Houston had received nearly 25 inches and the suburbs of Santa Fe and Dayton got 27 inches.
Staff at CBS affiliate KHOU-TV, broadcasting live coverage of the floods, had to evacuate after water started to gush into the building. The anchors and news operations at the station moved first to a second floor before finally abandoning the station.
"We are coordinating logistics with state and local officials, and once details are finalized, we will let you know. We continue to keep all of those affected in our thoughts and prayers," Sanders said in a statement.
White House press secretary Sarah Huckabee Sanders said President Trump will travel to Texas on Tuesday.
It warned that flying drones without authorization may violate federal, state, or local laws and ordinances. "Allow first responders to save lives and property without interference," the FAA said in a statement.
#Harvey Info: The #FAA does not want you to fly #drones in the aftermath of #Harvey . Allow 1st responders to work. https://t.co/rN9b6GgxhX pic.twitter.com/DFOq1R1Hio
"The FAA warns unauthorized drone operators that they may be subject to significant fines if they interfere with emergency response operations," the FAA said in a statement .
The Federal Aviation Administration is asking people not to fly drones over areas affected by Tropical Storm Harvey.
Rosenberg police did not immediately provide additional details on the sinkhole, other than urging drivers to avoid the area.
Water could be seen filling the sinkhole as pieces of highway asphalt hung from the edge of the damaged roadway.
The 3900 block of FM 762 (in front of 24 HR fitness) has just collapsed. There is a massive sinkhole in the roadway. AVOID THE AREA! #Harvey pic.twitter.com/BJreUS1D9C
Rosenberg police on Sunday tweeted a photo of the gaping hole that spread across more than half of a two-lane highway -- Farm-to-Market 762.
Police say a sinkhole has opened on a Texas highway about 25 miles southwest of Houston as Tropical Storm Harvey dumps more rain on the region.
McLeod says the evacuations won't start until the water recedes from around the facility and will likely take several days. The hospital is part of the Texas Medical Center, and has 350 patients.
McLeod says the flooding resulted in only a small amount of water in the basement and did not affect the hospital's power supply. But shutting down the kitchen leaves the hospital with a limited supply of dry food for patients.
Bryan McLeod, a spokesman for Harris Health System, said Sunday that minor flooding in the basement of Ben Taub Hospital and a busted sewer pipe forced officials to close the kitchen.
The evacuation of Houston's main public hospital hasn't begun yet because it is surrounded by waist-deep water as a result of Tropical Storm Harvey.
"Many in our HISD family will be dealing with the task of cleaning up the damage Harvey left behind. As a result, all HISD schools and district administrative offices will be closed all week."
The Houston Independent School District announced Sunday that all schools will be closed from Monday, August 28 through Friday, September 1, due to damage from Tropical Storm Harvey. The district said in a statement that schools and offices are expected to reopen on Tuesday, Sept. 5.
The State has requested we prepare to open our Mega Shelter to receive coastal guests. The City plans to open it by Tuesday morning.
The city opened a third smaller shelter about 4:30 p.m. Sunday. About 415 evacuees are staying at the two other shelters, where they will remain for the time being.
The city, Red Cross, Dallas County, Parkland Hospital, the Salvation Army, Children's Hospital and other volunteer groups are coordinating the logistics of getting the shelter ready.
City Office of Emergency Management Director Rocky Vaz says the state made a formal request to open the convention center, which should be ready by early Tuesday morning.
Officials say the Kay Bailey Hutchinson Convention Center will open to evacuees on Tuesday morning. Dallas has three shelters currently open for evacuees, but the convention center will serve as a "mega shelter."
Dallas officials say they'll open the city's convention center to about 5,000 people who are fleeing the southern part of the state.
The city of Houston opened the convention center Sunday to people fleeing the flooding from Tropical Storm Harvey.
Asked if he wishes he'd have evacuated, Cain laughed and walked away. He said: "That's a no-brainer, brother."
William Cain says the water outside their home was in some spots several feet high. He says, "I live in a lake where there was once dry land." Water had started to come into their apartment, and they had already lost power.
She suffers from congestive heart failure - when the heart's pumping power is weaker than normal - and other illnesses. Her son, William, and 9-year-old grandson were waiting for her inside. Both were barefoot as well.
Patricia Cain entered the George R. Brown Convention Center barefoot and carrying two oxygen tanks. The first was empty. The second was given to her by the Houston Fire Department after the U.S. Coast Guard rescued her from her home.
The NFL's Houston Texans flew to Dallas after their preseason game Saturday in New Orleans instead of returning home and have said they'll stay there until conditions improve enough for them to come back to Houston. They'll practice at the suburban practice facility of the Cowboys on Monday and said they will provide details on their schedule for the rest of the week later.
The Rangers had been scheduled to head to Houston after playing Oakland to await the start of a three-game series with the Astros beginning Tuesday. Instead, they'll return to Dallas to await word on its status. The Astros are in Anaheim and also will fly to Dallas while a decision is made on when and where the series will be played.
The Houston Astros and Texas Rangers won't travel to Houston as planned after their games Sunday in California because of torrential floodwaters that have engulfed the city.
Thank you to all the first responders and people helping each other out. That's what we do as Americans. Here's one way you can help now. https://t.co/iGfE8rAoAu
Former President Barack Obama thanked first responders in Houston as the city was slammed with flood water Sunday. Mr. Obama tweeted a link to the American Red Cross, saying, "Here's one way you can help now."
"We were airlifting grandmothers and grandfathers," David Popoff of Dickinson County Emergency Management told The Daily News, who showed him the viral image. "These people have been evacuated."
Eighteen people were rescued, including 15 seniors, from the La Vita Bella living facility, a city official told The Galveston County Daily News .
Residents of a nursing home in Dickinson, Texas, were evacuated Sunday after a viral image showed them sitting in waist-deep flood waters .
Henry is appealing for volunteers to help staff rescue shelters and see to the needs of the 2,000 to 10,000 people that have sheltered in them. He says he appealed for state and federal help mid-morning Sunday, adding "we have gotten some help, but we still need more."
Henry says about 90 percent of the county's rescue calls have come from Dickinson. An appeal had been made through social media for assistance by private boat owners and their vessels, and 25 to 35 owners responded.
The area hardest-hit by floods has been Dickinson, a low-lying city of about 20,000 residents along Dickinson Bayou, where crews had to lead to safety 19 residents and five staff members from an assisted-living center flooded with waist-deep water.
Galveston County Judge Mark Henry said Sunday that about 22 inches of rain has fallen on the coastal county so far with another 10 to 15 inches still expected.
A Galveston County official says Harvey has caused unprecedented flooding and 800 to 1,200 residents have had to be rescued.
Zetterstrom says the dams will impound water for one to three months as water is gradually released. He adds that some neighborhoods on the fringes of the reservoir are likely to see some floods.
Zetterstrom says the water contained by the dams is "unparalleled in the dams' history." The waters are rising about 4 inches per hour.
Downtown Houston is 17 miles downstream from the dams, which were built during the 1940s in response to a 1935 flood that inundated much of downtown area.
Col. Lars Zetterstrom is commander of the Galveston District of the Corps of Engineers. He says water will be released from the Barker Reservoir and Addicks Reservoir very slowly on Monday morning to prevent uncontrollable flooding of downtown Houston and the Houston Ship Channel.
The U.S. Army Corps of Engineers plans to begin releasing water into Buffalo Bayou from two flood-control dams on the western outskirts of the city.
"The decision that we made was a smart one. It was in the best interest of Houstonians. It was the right decision in terms of their safety... absolutely no regrets. We did what was the right thing to do," Turner said.
The mayor also defended his decision not to order an evacuation.
In addition, 35 boats and 93 dump trucks were being used by the city for high water rescues.
Turner said 22 aircrafts were working to help identify people stranded on roofs. Sixteen of those aircrafts are from U.S. Coast Guard.
Turner said that so far only one fatality has been confirmed -- a woman who died Saturday evening after getting out of her car when it drove into a flooded street.
Houston Mayor Sylvester Turner said that as of 5 p.m. on Sunday, Houston police and fire departments had received nearly 6,000 calls for rescues and had rescued more than 1,000 people. Many of these rescues were of people trapped on their roofs or in their attics.
On Sunday, videos emerged showing dramatic rescues by the coast guard. A number of rescues by boat took place, but Morgan reports there are still many people unaccounted for.
CBS News' DeMarco Morgan is in Dickinson, Texas, where he met one family who was rescued by boat. They live in a two-story home and one of the homeowners said the water level was up to her chest. She said all the furniture was just floating on the first floor as the family took refuge in the second story.
More video from the U.S. Coast Guard has been released showing rescues from their helicopter. A Coast Guard MH-60 Jayhawk helicopter crew from Air Station Houston rescued five people from floodwaters in a southeastern Houston neighborhood Sunday:
Dramatic video from @USCG shows some of the many rescue efforts underway in Texas https://t.co/WZP2arvuWh pic.twitter.com/Ex1D23BzvK
The clip shows a Coast Guard member airlifting various people (including a dog) into one of their aircraft.
The United States Coast Guard posted video online that showed various rescues Sunday from the aftermath of Hurricane Harvey.
The Coast Guard says they assess each call of distress and that those in medical need take priority, according to Adm. Karl Schultz during a late Sunday press update.
They say that rescues have been done from bridges, rooftops, attics and they will continue to respond to calls.
Officials from the Coast Guard said that 19 helicopters have been deployed, 250 people have been rescued.
Officials say to call 911 if there is an immediate threat or 311 if you need help relocating from your home, but not in immediate danger.
If you see this do not share, KENS-TV writes. The number belongs to an insurance group and not the National Guard. If you are in danger and call this number you will not be rescued.
The station adds that the post reads, "The National Guard is being deployed to our Texas area. If you find yourself in a state of emergency. Call 1-800-527-3907. Please copy, paste or share!!!!!!!!!"
Despicable! Please share this story so no one affected by #Harvey who needs help/support/rescue is taken in by this scam https://t.co/c50wbWVGJn
A scam targeting victims of Tropical Storm Harvey posted on various social media sites has gone viral, CBS affiliate KENS-TV reports .
The hurricane center says Harvey's center was expected to drift off the middle Texas coast on Monday and meander offshore through Tuesday before beginning "a slow northeastward motion."
That means it remains virtually stalled near the coast and continues to drop heavy rain on the Houston and Galveston areas. In the past 48 hours, numerous spots in the region have measured more than 25 inches of rainfall.
In its 10 p.m. CDT advisory, the National Hurricane Center reports the storm still has sustained winds of up to 40 mph and is centered 20 miles east of Victoria, Texas, about 120 miles southwest of Houston. It continues to creep to the east-southeast at 3 mph.
Tropical Storm Harvey continues to head back toward the Gulf of Mexico at a slow pace.
3:35 a.m.: Houston rainfall totals eclipse 500-year rain level mark
Harris County Sheriff Ed Gonzalez tweeted that the rainfall totals in three hours had eclipsed the 500-year rain level mark.
Rainfall totals over the last 3 hours have eclipsed the 500 year rain level mark. #Harvey — Ed Gonzalez (@SheriffEd_HCSO) August 27, 2017
Harris County Flood Control District meteorologist Jeff Linder tweeted there have been calls of people climbing into their attics due to floodwaters. According to Linder, 13-14 inches of rain fell in three hours.
Calls to HCFCD of people climbing into their attics. Flooding in SE Harris County is equal to or greater than TS Allison #houwx — Jeff Lindner (@JeffLindner1) August 27, 2017
Life threatening flash flooding across the Harris County. 13-14 inches in 3 hrs — Jeff Lindner (@JeffLindner1) August 27, 2017
The National Weather Service said Houston is in a catastrophic, life-threatening flash flood emergency. The flash flood emergency will last until 7 a.m.
1:50 a.m.: Fatality is confirmed from flooding in Houston
A motorist died Saturday after being stranded in the floodwaters from Harvey, County Judge Ed Emmett told CBS affiliate KHOU.
KHOU reports the woman tried to get out of her car but didn't make it. A neighbor found her body.
Cars sit abandoned at a flooded gas station after Hurricane Harvey made landfall on the Texas Gulf coast and brought heavy rain to the region, in Houston, Texas, U.S. August 26, 2017. NICK OXFORD / REUTERS
Several major Houston roadways are underwater.
Houston mayor Sylvester Turner said the streets are "treacherous."
11:35 p.m.: Flash flood emergency declared in Houston's Harris County
A flash flood emergency is in effect for Harris County, meaning life-threatening flooding is possible, CBS affiliate KHOU reports.
"We're seeing just incredible rainfall rights right now in the heart of Houston," said Jeff Lindner with the Harris County Flood Control District.
The Harris County Sheriff's office tweeted that a man had been rescued from his car in three feet of rushing water.
HCSO deputies rescued one male driver in 3 feet of rushing water in west Harris County — Saums Rd. & Park View Dr. pic.twitter.com/i51U6jcT42 — HCSOTexas (@HCSOTexas) August 27, 2017
Most areas have seen more than 2 inches in the last hour, according to KHOU.
They've had more than 4 inches in the last hour in the Meyerland area and there is a threat of water in homes there, Lindner said.
The Houston Office of Emergency Management tweeted that the Red Cross shelter is closing due to high water. The METRO Houston has suspended all bus and rail service.
The Fort Bend County Sheriff's Office is also reporting tornado sightings in Stafford, Missouri City and near US 90 and the Texas Parkway.
Tornados have already caused damage in Cypress, Sienna Plantation, Katy, Richmond and Atascocita.
9:40 p.m.: Coast Guard launches helicopter rescue
The Coast Guard said Saturday that it was responding to a call of seven distressed people in Aransas Pass, Texas.
The Coast Guard said it received the call at about 7 p.m. central time of seven people, one of which is reportedly on oxygen and had run out, in need of assistance.
The Coast Guard said its Air Station Corpus Christi aircrews rescued in total 20 people and a dog after they received reports from watchstanders at Coast Guard Sector Corpus Christi Saturday morning and afternoon.
7:50 p.m.: "Biggest concern" is the 20-30 inches of rain, Texas Gov. says
More than a foot-and-a-half of rain fell in just 24 hours in Victoria, Texas -- and by the time the storm is over, the city could get in only days the amount of rain it sees in one year, CBS News' Manuel Bojorquez reports.
Rain from Harvey not nearly finished
"Our biggest concern is the possibility of between 20 and 30 inches of rain in areas ranging from Corpus Christi over to Houston," said Texas Gov. Greg Abbott. "Because of the flooding, one of the top focal points that we are concerned about is ongoing rescue and recovery."
Angela and Mario Manzano are checking on the home they recently purchased.
"It's devastating because like I said, we're barely purchasing the home, we're still paying it off, to lose it now, it's going to be hard," Angela said.
Their home is in a low-lying area prone to flooding.
"If it was just the two of us, it would be different, but having our kids, that why we took, we just took the most important things -- our important documents and pictures that can't be replaced and that stuff," Angela said.
7:30 p.m.: Inside Rockport, the city in the eye of Harvey
Inside the city directly hit by Harvey
Ferocious winds and floodwater have left this quaint city on the gulf a disaster zone, CBS News' David Begnaud reports. Parts of the high school were torn to shreds. Harvey showed no mercy on the local First Baptist church. Some homes have collapsed into the water.
"We went upstairs and looked out the window and down the road here it was a sheer wall of water, like 100 mph it was crazy," said Tim Freiburger. His garage was lifted up and jammed against the side of the house.
"It was insane all you could do was just feel stuff pounding the house," he said.
Residents of this senior living complex were stranded when portions of its roof torn away and emergency workers were unable to respond at the height of the storm.
Nearly every police car in town has been damaged, but still officers were out Saturday, banging on doors, making sure no one was trapped.
When the hurricane made landfall here late Friday night, the city was under a mandatory evacuation.
"I'll take a while to get it all straightened backup," said Randy Bonnett, who has been through Texas hurricanes before but he says he will not forget Harvey.
"You got three hours of hell and then an hour lull and then three hours hell," Bonnett said.
7:10 p.m.: Millions in danger of potentially catastrophic flooding
Harvey churns over southeast Texas
Harvey is still going and it's not going anywhere for awhile, CBS News' DeMarco Morgan reports. There are over 1,000 people assigned to search and rescue operations. Near Corpus Christi on Saturday, the Coast Guard rescued 17 people whose vessels were in distress. The governor of Texas has issued a disaster declaration for 50 counties. Saturday morning, Galveston got pounded.
With the storm stalling out, now millions are in danger of potentially catastrophic flooding. More than three feet of rain could fall in some places.
"We are just getting into this so people need to understand that the longevity of this is gonna go thru the weekend and even into the early part of next week," said Jeff Linder with the Harris County Flood Control in Houston.
Nearly 300,000 power outages have been reported and Corpus Christi is under a boil water order. Incredibly, no fatalities have been reported yet. In Rockport, where the storm took a direct hit, ten people were injured when the roof of a senior housing complex collapsed, according to local media reports. Hundreds of people were evacuated from a hotel there last night.
5:34 p.m.: White House releases photos of President Trump on teleconference call earlier Saturday
The White House said President Trump was briefed on the response to Harvey at Camp David, where he's spending the weekend.
President Trump hosts a teleconference on Hurricane Harvey, Saturday, Aug. 26, 2017. Official White House Photo by Shealah Craighead
President Trump hosts a teleconference on Hurricane Harvey, Saturday, Aug. 26, 2017. Official White House Photo by Shealah Craighead
4:11 p.m.: Coast Guard rescues 17 people
Coast Guard rescues 17 in Texas
The Coast Guard says it has rescued 15 people onboard vessels near Port Aransas, Texas. Two Coast Guard helicopters were dispatched to help the ships earlier Saturday after receiving distress calls.
The Coast Guard said in a release that seven people were rescued from the tugboat Sabine; four people from the Signet Enterprise; and four from the vessel Sandy Point.
A man and a woman were also rescued in Houston, along with their dog. Read the full story here.
3:47 p.m.: President Trump thanks volunteers
THANK YOU to all of the great volunteers helping out with #HurricaneHarvey relief in Texas! https://t.co/Ds95oSgo8f — Donald J. Trump (@realDonaldTrump) August 26, 2017
3:31 p.m.: Harvey shuts down one-fifth of U.S. oil production
About one-third of the America's refining capacity reside in low-lying areas on the coast from Corpus Christi, Texas, to Lake Charles, Louisiana, the Associated Press reports.
The Bureau of Safety and Environmental Enforcement said Friday that workers were evacuated from 86 of 737 manned oil production platforms where oil and gas are pumped from the Gulf of Mexico.
The agency estimated that approximately 21.55 percent of oil production had been shut down along with 23.24 percent of natural gas production.
The AP reports, citing FlightAware, that nearly 1,200 flights were cancelled on Friday and Saturday, and an additional 485 flights for Sunday were cancelled.
2:27 p.m. President Trump receives update from cabinet officials
President Trump and Vice President Mike Pence met with cabinet members and senior administration officials via video teleconference Saturday about the hurricane, according to a White House readout of the meeting. Mr. Trump expressed that all departments and agencies involved should stay focused on saving lives, the White House said.
Mr. Trump, who had been receiving updates from his chief of staff John Kelly Friday night and Saturday morning, directed his team to support the governors of Texas and Louisiana. Mr. Trump on Friday night signed a disaster declaration for the state of Texas at Gov. Greg Abbott's request. The declaration frees up federal resources to alleviate affected localities.
2:18 p.m.: Texas governor: No confirmation of fatalities; 338,000 without power
Texas Gov. Greg Abbott said he could not confirm any fatalities from now-Tropical Storm Harvey. He says 338,000 customers are without power and service might not be restored for several days.
Gov. Greg Abbott speaks at a news conference about Hurricane Harvey at the State Operations Center in Austin, Texas, on Fri., Aug. 25, 2017. AP
2:15 p.m.: Hotel taxes suspended for evacuees
Evacuees from areas affected by Harvey as well as first responders will be able to stay in hotels tax-free, Abbott says. He said he has waived the state's surcharge in a proclamation.
Abbott said about 1,500 evacuees are currently staying at Texas state park facilities. Nearly 1,500 more are staying in 21 Red Cross shelters and 42 more shelters are standing by to accept more evacuees. More than 200 buses have been deployed to transport residents, Abbott said.
2:13 p.m. 1,000 people involved in search and rescue operations
Abbott says 1,000 workers are focused on search and rescue operations, which he said "will be one of the foremost tasks that we take in the coming days."
Search and rescue "will be one of the foremost tasks that we take in the coming days," Gov. Abbott says https://t.co/8YHzAJZ5CQ pic.twitter.com/xh7822hmG8 — CBS News (@CBSNews) August 26, 2017
2:10 p.m.: 1,800 service members to assist in recovery in Texas
Abbott says 1,300 Texas service members are already assisting in recovery and search and rescue efforts, with another 500 to be activated soon.
2:06 p.m.: Abbott says state concerned about 20 to 30 more inches of rain
"Turn around. Don't drown," the governor said. He says flooding is still a major concern.
"Now that the hurricane has come on shore our primary concern remains dramatic flooding," Abbott said. Abbott said about 20 inches of rain has already fallen in Corpus Christi and about 16 inches in Houston.
2:05 p.m.: Texas governor gives update on Harvey
Texas Gov. Greg Abbott is providing an update on Harvey from Austin, Texas. You can watch on CBSN at the top of this post.
1:50 p.m. Harvey downgraded to tropical storm
Harvey is now a tropical storm, the National Hurricane Center (NHC) says in its latest release.
Winds have slowed to 70 mph, down from a peak of 130 mph when Harvey made landfall late Friday. The storm is now located 45 miles north-northwest of Victoria, Texas, and moving at 2 mph.
But Texas isn't out of the woods yet. The NHC adds that an "extremely serious flooding event is unfolding" as the storm continues to drench the area in rain. Some areas have seen rainfall of up to 3 inches per hour at times. The threat of storm surge continues to threaten low-lying areas, as well.
1:39 p.m.: Texas attorney general warns against price gouging
Texas attorney general says Harvey is "probably the biggest storm in [Texas] history"
Texas Attorney General Ken Paxton joined CBSN to discuss Harvey, and warned potential price gougers from taking advantage of residents as flooding continues.
"Under Texas law, you're not allowed to massively increase your prices by more than 10 percent, [that's] the approximate number, when there's some type of crisis or catastrophe," Paxton said. "There's significant fines for that, up to $20,000 per incident. If you're doing that to somebody over 65, it could be up to $250,000."
Paxton said his office has received over 200 calls about potential price gouging. He said investigators have looked into instances of alleged price gougers charging nearly $100 for a case of water.
12:45 p.m.: Texas evacuates prisoners threatened by flooding
The Texas Department of Criminal Justice announced Saturday three prisons would be evacuated in Brazoria County, just south of Houston, as rainfall from Hurricane Harvey slams the area.
In a news release, the department said approximately 4,500 inmates will be evacuated beginning Saturday morning.
"These evacuated offenders will not be available for visits at the designated receiving units, but will have the ability to use the offender telephone system," the statement said. "Additional food and water has been delivered to the prisons receiving the displaced inmates."11:59 a.m.: Texas Gov. Greg Abbott warns of "ongoing danger" from flooding.
Texas Gov. Greg Abbott on the state's response to Hurricane Harvey
Texas Gov. Greg Abbott on Saturday said ongoing flooding in the wake of Harvey poses the greatest danger in the days ahead, as rescue efforts are already underway in the southeast part of the state.
The Republican governor told CBSN that the hurricane, which made landfall late Friday night as a Category 4 storm but has since been downgraded to Category 1, has caused "great devastation." As it moves slowly and unleashes devastating amounts of rain on the Texas coastline, Abbott says flooding is the greatest concern. Read the full story here.
11:32 a.m.: Mayor of Rockport, Texas, details "widespread damage"
Rockport, Texas, suffers "widespread damage" from Harvey, mayor says
The mayor of Rockport, Texas, says the town has suffered "widespread damage" from Hurricane Harvey as the storm continues to dump rain across southeast Texas. Mayor Charlie Wax joined CBSN to discuss the situation in Rockport, one of the towns hardest hit by the storm.
"Our high school is damaged. One of our learning centers is also damaged. We have businesses that are destroyed, we have homes that have been destroyed, and at the very least lives are disrupted," Wax said.
The mayor said, as of Saturday morning, there were no confirmation of any deaths, but said it was likely because the response teams haven't been able to survey the town completely.
He also warned residents to "stay in place," adding that it wasn't safe to return home.
"Stay in place, protect yourself. If you did evacuate, do not even attempt to go back," he said. "Stay away, let the first responders do their job."
10:55 a.m.: Harvey expected to weaken to tropical storm this afternoon
Catastrophic flooding predicted over the coming days
The National Hurricane Center says Harvey remains a Category 1 hurricane as wind speeds remain at 75 mph. The threat for serious flooding will continue for several days as the storm continues to move slowly over inland Texas.
In its latest advisory, the NHC says "torrential rains will continue for a few more days." The center says Harvey should become a tropical storm sometime Saturday afternoon.
Harvey made landfall late Friday night as a Category 4 hurricane with sustained wind speeds of 130 mph. It has slowed overnight but will continue to pull in moisture from the Gulf of Mexico, and could still move back out over water.
10:28 a.m.: NASA animation of satellite data shows rainfall upon making land
@NASA's GPM satellite analyzed Hurricane Harvey's rainfall as it made landfall in Texas: https://t.co/OGW4LLZvd5 pic.twitter.com/eWF3cHVL1N — CBS News (@CBSNews) August 26, 2017
10:25 a.m.: Houston airport lifts ground stop on incoming flights
Flights are beginning to land again at Houston's George Bush Intercontinental Airport following an earlier ground stop on incoming flights. The airport said 225 flights have been canceled so far.
IB ground stop has been lifted, and aircraft are now beginning to land. Get the latest at https://t.co/9gZJSkXIjn #fly2houston — Houston Bush Airport (@iah) August 26, 2017
10:11 a.m.: Coast Guard responds to mayday calls
The Coast Guard says it is responding to tugboats in distress near Port Aransas, Texas.
In a statement, the Coast Guard says its Corpus Christi sector received mayday calls from the boats Belle Chase, Sandy Point and Sabine Pass near the Lydia Ann Channel. It has dispatched two MH-65 Dolphin helicopter crews to the scene.
10:05 a.m.: Wind speeds slow to 75 mph
The National Hurricane Center says in an advisory that sustained wind speeds have decreased slightly to 75 mph. The storm remains a Category 1 hurricane.
Harvey's center is now about 25 miles west of Victoria, Texas, moving at 6 mph.
9:20 a.m.: More than 16 inches of rain have fallen in Victoria, Texas
Hurricane Harvey slams the Gulf Coast
CBS News correspondent Manuel Bojorquez joined CBSN from Victoria, Texas, with an update from the heart of the storm. Speaking from his hotel as Harvey's eyewall whipped palm trees in the background, Bojorquez reports Victoria has received more than 16 inches of rain in the past 24 hours.
His hotel began swaying in the wind early Saturday morning. The roof of a car dealership behind the hotel began flapping in the heavy winds, indicating the likelihood of extensive structural damage as Harvey swirls over Texas.
"The big concern is not only all this wind, but of course all of this rain," Bojorquez reports. "They're not expecting just inches of rain here. They are expecting to get up to 2.5 feet. And so the major flooding that will happen as a result of this hurricane is something that they will deal with for days to come here."
9:12 a.m.: Michio Kaku says "agony has just begun"
Michio Kaku on Hurricane Harvey: "Agony has just begun"
CBS News science contributor Michio Kaku joined "CBS This Morning: Saturday" to discuss the science behind Harvey and why it will continue to cause damage for days.
"First of all, if it lingers over the land, it could cause massive flooding. And then, watch out," he said. "If it goes back into the Gulf, it could get reenergized and create a second, even a third landfall. And so the agony has just begun with this hurricane of the decade."
8:55 a.m.: Power outages now affect more than 255,000 customers in Texas
More than a quarter-million customers are without power in Texas early Saturday after Hurricane Harvey made landfall. Utilities are reporting outages affecting more than 255,000 customers.
AEP reported more than 192,000 customers without power as of early Saturday. CenterPoint Energy reported nearly 58,000 customers without power.
Outages were also reported by Austin Energy, CPS, Entergy and Oncor. Read the full story here.
8:35 a.m.: Latest forecast as Harvey settles over Texas
Hurricane Harvey forecast: Weakening winds, days of rain to come
Texans are facing days of rain as Hurricane Harvey settles in. Meteorologist Megan Glaros joined "CBS This Morning: Saturday" with the latest forecast at the top of the hour.
The system continues to weaken in terms of wind speed, but it continues to pull in moisture from warm waters in the Gulf of Mexico. Winds have decreased to 80 mph and the storm continues to move at a sluggish 6 mph, which will continue for the next few days.
In Victoria, Texas, more than 16 inches of rain has fallen. McFaddin and Austwell have received just under 12 inches, and Edna and Sugar Land about 9 inches. Total rainfall could total more than 40 inches in places over the coming days.
7:25 a.m.: President Trump says he is "closely monitoring" storm, FEMA director doing "great job"
Closely monitoring #HurricaneHarvey from Camp David. We are leaving nothing to chance. City, State and Federal Govs. working great together! — Donald J. Trump (@realDonaldTrump) August 26, 2017
You are doing a great job - the world is watching! Be safe. https://t.co/PJLdxy3hD9 — Donald J. Trump (@realDonaldTrump) August 26, 2017
6:15 a.m.: Category 1, with maximum winds near 90 mph
Hurricane Harvey became a Category 1 storm with top wind speeds near 90 mph, the National Hurricane Center reported. Tide gauges near Port Lavaca, Texas, recorded water levels more than 6.5 feet higher than normal.
Craig "Cajun" Uggen, 57, nearly floods his truck as Hurricane Harvey comes ashore in Corpus Christi, Texas, on Fri., Aug. 25, 2017. Minutes later, high winds blew off the camper carrying all of his belongings. Reuters
5 a.m.: From Category 3 to Category 2
The National Hurricane Center downgraded Hurricane Harvey to a Category 2 storm, with maximum sustained winds near 100 mph. Harvey is likely to become a tropical storm later today as it moves further inland, predicted NHC forecasters who also warned of "catastrophic flooding over the next few days due to heavy rainfall."
4:30 a.m.: Emergency crews in limbo
Many emergency crews were unable to make rescues early Saturday because of Harvey's strong winds. Melissa Munguia, the deputy emergency management coordinator in Nueces County, which includes Corpus Christi, said early Saturday that it could be several more hours before crews could fully assess the damage in coastal communities.
Corpus Christi, Texas. Reuters
3:40 a.m.: More than 211,000 homes and businesses lose power
More than 211,000 customers were without power on the Texas Gulf Coast due to effects from Hurricane Harvey, the Electric Reliability Council of Texas reported. The storm was downgraded to a Category 3 hurricane early Saturday morning, as Harvey's maximum sustained winds decreased to nearly 125 mph. Additional weakening is forecast during the next 48 hours while the center of Harvey is over southeastern Texas.
2:30 a.m.: Homeowner shoots intruder, cops say
A homeowner shot an alleged intruder in Corpus Christi just as Hurricane Harvey was making landfall late Friday night, Corpus Christi police said. Read the full story here on CBSNews.com.
The victim was taken to a local hospital, and was coherent when police arrived on scene, Corpus Christi police tweeted. According to the Corpus Christi Caller-Times, the victim was shot in the head.
Update on shooting @ 7100 Ficus Ct. homeowner shot intruder. Victim @ Hosp. with gunshot wound was coherent when medics took him. PIO Pace — Corpus Christi PD (@CorpusChristiPD) August 26, 2017
1:45 a.m.: "Boil water," Corpus Christi residents told
In Corpus Christi, the major city closest to the center of the storm, wind whipped palm trees and stinging sheets of horizontal rain slapped against hotels and office buildings along the city's seawall as the storm made landfall. Boats bobbed violently in the marina. It was too dark to tell whether any boats had broken their moorings.
City officials notified residents to "boil their water prior to consumption (e.g., washing hands/face, brushing teeth, drinking, etc)" to kill all potentially harmful bacteria and other microbes. "Water for drinking, cooking and ice making should be boiled and cooled prior to use for drinking water or human consumption purposes. The water should be brought to a vigorous rolling boil and then boiled for two minutes."
1:15 a.m.: Early details emerge from Rockport
Rockport, Texas, a coastal city of about 10,000 people some 30 miles northeast of Corpus Christi, was directly in the path of Harvey when it came ashore. The city had peak wind surges of more than 125 mph, according to the National Weather Service.
Volunteer Fire Department Chief Steve Sims said there were about 15 firefighters at the city's fire station waiting for conditions to improve enough for their vehicles to safely respond to pleas for help. "There's nothing we can do at this moment. We are anxious to get out there and make assessments, but we're hunkered down for now," Sims said, according to an Associated Press report.
Fire Department spokeswoman Gillian Cox told the Corpus Christi Caller-Times that the roof of Rockport's high school has partially caved in. But Cox says social media posts that the school has "disappeared" are inaccurate.
Rockport City Manager Kevin Carruth told the newspaper that the courthouse also sustained major damage. Carruth said a cargo trailer was halfway in the building.
Earlier Friday, Rockport Mayor Pro Tem Patrick Rios offered ominous advice, telling a local TV station that those who chose to stay put "should make some type of preparation to mark their arm with a Sharpie pen," implying doing so would make it easier for rescuers to identify them.
When I reported people in Rockport, TX were being told to write their social security # on their arms, people tweeted me it was ridiculous. https://t.co/BkVhUJsGz6 — David Begnaud (@DavidBegnaud) August 26, 2017
12:30 a.m.: Facebook activates "Safety Check" feature
Facebook has activated its Safety Check feature for Hurricane Harvey, allowing Facebook users to inform friends and family of their whereabouts during the weather emergency.
Facebook users can also find the feature on their smartphone apps. As CBSNews.com sibling site CNET explains: "Safety Check is now integrated into the mobile apps, meaning you can manually notify friends of your status as well as follow crises worldwide and even offer support. The only trick is finding it. When Facebook does a server-side activation, you'll usually see a notification right at the top of the app. But if you want to access the feature yourself, it requires a bit of menu-diving."
Here's a primer from CNET on how to find the feature on Android devices and iPhones.
12:00 a.m.: Roof collapses at senior housing complex
Several residents are trapped inside a senior housing complex in Rockport, Texas, where a roof collapsed, a city manager confirmed to CBS News.
City manager in Rockport, TX tells CBS News people trapped inside of senior housing complex where roof collapsed; rescuers unable to get in — David Begnaud (@DavidBegnaud) August 26, 2017
A couple is trapped in a mobile home in Rockport after a tree fell on it, according to Rockport City Manager Kevin Carruth.
More than 32,000 homes and businesses have lost power in Corpus Christi, CBS affiliate KZTV reports. The city of Corpus Christi has issued a precautionary water boil advisory.
The City of Corpus Christi.. yeah, I'd say we lost some power. #hurricaneharvey 🙏🏻 pic.twitter.com/CAO8hy3oCl — Marisol Gonzalez (@MarisolKZTV) August 26, 2017
Large shipping boats in Port Aransas have broken away from their moorings, leading to significant damage, KZTV reports.
Storm surges up to 13 feet are predicted in some places with up to 40 inches of rain over several days. The National Weather Service warns some residents may not be able to return to their homes for weeks or months.
Friday
11:05 p.m.: Harvey makes landfall
The eye of Harvey made landfall just after 11 p.m. between Port Aransas and Port O'Connor as a Category 4 storm with 130 mph winds, the National Weather Service said.
#Harvey made landfall at 10 PM CDT as a category 4 hurricane near Rockport, Texas, with max winds of 130 mph and min pressure of 938 mb. pic.twitter.com/98y5wpKmBw — NHC Atlantic Ops (@NHC_Atlantic) August 26, 2017
9:51 p.m.: President Trump signs disaster proclamation
President Trump tweeted shortly before 10 p.m. that he had signed a disaster proclamation, which Texas Gov. Greg Abbott said earlier Friday he had requested. The disaster proclamation will allow federal funds to flow into state and local relief efforts.
According to the National Hurricane Center, the storm is expected to make landfall "very soon."
Eye of Category 4 #Harvey almost onshore in Texas. Hurricane force winds reported at many observing stations. Landfall expected very soon. pic.twitter.com/JZ4tE1Bvbx — NHC Atlantic Ops (@NHC_Atlantic) August 26, 2017
8:20 p.m.: Evacuees seek refuge in San Antonio
Hundreds of evacuees seeking shelter from Hurricane Harvey arrived in San Antonio on Friday, CBS affiliate KENS-TV reports.
Two shelters opened their doors Friday morning, and city officials announced they would make room for at least 6,000 evacuees.
"I get deep anxiety when it comes to stuff like this," Justine Vela of Corpus Christi told the station. Vela packed up her four children and left for San Antonio.
"My kids don't kinda know what's going on because they are little," she said. "I'm trying to keep them calm and safe. This is the best place for us to be right now."
7:45 p.m.: Trump prepares to face first major natural disaster as president
Trump prepares for first major natural disaster as president
Hurricane Harvey will be the first major natural disaster of President Trump's administration. The White House is saying FEMA has changed since the organization's dismal response to Hurricane Katrina in 2005, CBS News' chief White House correspondent Major Garrett reports.
The failures of Katrina haunt emergency planners to this day, so much so, White House Homeland Security Adviser Tom Bossert felt compelled to say "now is not the time to lose faith in your government institutions."
"All the mayors and governors saw what happened at Katrina and they're not gonna let that happen," says David Paulison, who headed FEMA after Katrina and until 2009. He says that Katrina changed management procedures.
"Before we waited for the local community to become overwhelmed before the state stepped in, and waited for the state to become overwhelmed before the federal government stepped in," Paulison tells Garrett.
7:40 p.m.: FEMA urges residents to follow future orders
Federal Emergency Management Agency (FEMA) officials are encouraging residents and visitors in Hurricane Harvey's path to follow directions from local and state officials.
"I encourage residents who will be affected to follow directions from their local officials," Administrator Brock Long said in a statement. "Know your threats, heed the warnings, and if you're in the path of the storm, ensure your family is prepared for possible prolonged disruptions to normal services."
The agency has set up bases near Seguin, Texas, and areas closer to the storm's path to store supplies including more than 96,000 liters of water, 306,000 meals and 4,500 tarps and blankets, the Associated Press reports. State and local officials will be responsible for distributing the materials as needed.
7:20 p.m.: 20-30 inches of rain expected in Victoria, Texas
Hurricane Harvey could dump feet of rain in Texas
Victoria, Texas, is about 20 miles from the coast, but the distance is not expected to shield it from the worst impacts of Hurricane Harvey. Aside from winds up to 105 miles per hour, the biggest threat is the rain, CBS News' Manuel Bojorquez reports.
Victoria is in the bull's eye of Hurricane Harvey's rain, with 20-30 inches expected over the next 72 hours. that's a year's worth of rain for this city.
The flooding is expected to be worse than Victoria's 1998 disaster.
"We've never seen a forecast for that kind of localized rain, and I've been working hurricanes and emergencies here for several years. It's the most dangerous forecast we've ever seen," said O.C. Garza the Victoria Office of Emergency Management.
7:15 p.m.: Corpus Christi police stop responding to emergency calls
Millions flee for safety ahead of Hurricane Harvey
Corpus Christi police are not responding to calls for emergency service because of the current weather conditions. If you live in the area and you want to get out, the free bus rides are over and the city has discontinued the service, CBS News correspondent David Begnaud reports.
The National Weather Service says winds could leave homes uninhabitable for weeks or even months. Storm surge could reach 12 feet -- that's strong enough to wash away vehicles, Begnaud reports.
Fears of a power outage forced the sickest babies at a children's hospital to be moved out of the hurricane's path. Others are heeding the warnings and evacuating on their own.
7:02 p.m.: Hurricane Harvey upgraded to Category 4 storm
The National Hurricane Center has upgraded Hurricane Harvey to a Category 4 storm with maximum sustained winds of 130 mph and is moving northwest at a speed of 8 miles an hour. The storm is about 45 miles outside of Corpus Christi.
NEW: #Harvey continues to intensify and is now a category 4 #hurricane with maximum sustained winds of 130 mph. https://t.co/tW4KeGdBFb pic.twitter.com/7CkJkuafTb — NHC Atlantic Ops (@NHC_Atlantic) August 25, 2017
6:09 p.m.: Houston officials resist calls for evacuation
Houston is bracing for dozens of inches of rain, but officials are urging residents to stay put.
Judge Ed Emmett, Harris County's top official, said "no mass evacuations" would be called because the hurricane would not "directly" hit the area.
"Always say run from water, hide from wind, we mean storm surge, not rain. [It's] not the kind of water we would ask people to evacuation from," Emmett said.
Mayor Sylvester Turner also urged residents to stay off roads and in their homes. Turner said there might be "greater danger" in having residents who don't need to be evacuated onto roads that could possibly flood, the Associated Press reports.
6:13 p.m.: NWS issues "EXTREME WIND WARNING"
The National Weather Service in Corpus Christi has issued a warning for southwestern Calhoun County in south Texas, urging residents to "TAKE COVER NOW!"
"Widespread destructive winds of 115 to 145 mph will spread across Calhoun County, Aransas County, Nueces County, San Patricio County, Refugio County, producing swaths of tornado-like damage," the advisory says. "TAKE COVER NOW! Treat these imminent extreme winds as if a tornado was approaching and move immediately to the safe room in your shelter. Take action now to protect your life!"
5:08 p.m.: Wind speeds reach 125 mph, officials warn of "catastrophic flooding"
The National Hurricane Center (NHC) says in an update that Harvey now has wind speeds of 125 mph. It's now about 60 miles southeast of Corpus Christi.
The NHC also says some areas of Texas could get 40 inches of rain and cause "catastrophic flooding." The storm surge is expected to be between 6 to 12 feet along parts of the coast.
5:06 p.m.: Feds won't question families about immigration status at shelters
Immigration and Customs Enforcement (ICE) and U.S. Customs and Border Protection (CBP) issued a joint statement Friday saying they won't question the immigration status of families arriving to hurricane shelters in Texas and Louisiana.
The agencies said their "highest priorities are to promote life-saving and life-sustaining activities, the safe evacuation of people who are leaving the impacted area, the maintenance of public order, the prevention of the loss of property to the extent possible, and the speedy recovery of the region."
The joint statement said that routine "non-criminal immigration enforcement operations" would not be conducted at evacuation sites or assistance centers such as shelters or food banks.
It also warned that immigration laws would not be suspended, and the agencies would "be vigilant against any effort by criminals to exploit disruptions caused by the storm."
5:03 p.m.: President Trump arrives at Camp David
The president has arrived at Camp David, where he will be monitoring the storm over the weekend:
Just arrived at Camp David where I am closely watching the path and doings of Hurricane Harvey, as it strengthens to a Category 3. BE SAFE! — Donald J. Trump (@realDonaldTrump) August 25, 2017
4:50 p.m.: National Weather Service director: "The impacts will be extreme"
National Weather Service Director Louis Uccellini issued a warning to Louisiana and Texas residents on Friday, calling the impact of Hurricane Harvey "extreme" and "devastating."
"Catastrophic inland flooding due to incredible rainfall amounts and damaging wind will also be associated with this storm," Uccellini said in a statement Friday. "The flooding will be catastrophic and life threatening. The economic impact will likely be devastating."
4:46 p.m.: NASA posts photos of storm from space
NASA posted new photos of Harvey from the International Space Station taken by astronaut Jack Fischer:
.@Astro2fish orbited over Hurricane #Harvey2017 and photographed the storm bearing down on the Texas coast. pic.twitter.com/eBzNc7NlMZ — Intl. Space Station (@Space_Station) August 25, 2017
4:38 p.m.: Coast Guard rescues 12
The U.S. Coast Guard says it has rescued 12 people from the storm near Corpus Christi.
Breaking News: @USCG Air Station Corpus Christi rescued 12 as #HurricaneHarvey nears. Updates to follow soon at https://t.co/AJyH7tl8P9. pic.twitter.com/WRA8KzFQdy — USCG Heartland (@USCGHeartland) August 25, 2017
4:30 p.m.: Corpus Christi mayor: "You can't force people to leave"
Corpus Christi Mayor Joe McComb told CBSN that he hadn't issued a mandatory evacuation order citywide because "you can't force people to leave and send police out there and drag them out."
He added, "you can highly recommend it, and we've done that, and say they need to get out of low-lying areas."
McComb said he'd received a positive response of residents who were seeking higher grounds. "Many people have gone to San Antonio and points beyond," he said Friday.
4:15 p.m.: Tornado threats in Louisiana and Texas
The National Weather Service has issued a tornado watch for for parts of Louisiana and Texas lasting until 3:00 a.m. on Saturday.
A tornado watch has been issued for parts of Louisiana and Texas until 2 AM CDT pic.twitter.com/WjHxXSSDFt — NWS Houston (@NWSHouston) August 25, 2017
4:00 p.m.: Vice President Pence halts travel
Vice President Mike Pence will remain in Washington D.C. during the storm, his spokesman Marc Lotter announced on Twitter. Pence will coordinate with President Trump as he visits Camp David with first lady Melania Trump on Friday.
The White House said Marine One landed at Camp David at 3:46 p.m. on Friday, according to the pool report.
Due to #HurricaneHarvey, @VP Pence will remain in DC this wknd, coordinating with @POTUS Trump at Camp David, monitoring storm & response. — Marc Lotter (@VPPressSec) August 25, 2017
3:18 p.m.: President Trump tweets about Harvey
President Trump addressed the threat of Hurricane Harvey on Friday, urging residents to follow the advice of local and state officials.
I encourage everyone in the path of #HurricaneHarvey to heed the advice & orders of their local and state officials. https://t.co/N6uEWCZUrv — Donald J. Trump (@realDonaldTrump) August 25, 2017
3:15 p.m.: Texas governor requests disaster declaration
Texas Gov. Greg Abbott held an afternoon news conference warning residents that Harvey is going to be a "very major disaster." Abbott said Friday that he's asked President Trump for a federal disaster declaration.
Abbott warned residents in coastal areas to evacuate their homes, even if local officials hadn't issued an official warning.
"Even if an evacuation order has not been issued by your local official," Abbott said, "if you are in areas between Corpus Christi and Houston, and maybe even some other areas, especially low lying areas, you need to strongly consider evacuating."
He added, "You don't want to put yourself in a situation where you could be subject to a search and rescue."
3:00 p.m.: Hurricane Harvey reaches Category 3
Harvey became a Category 3 hurricane Friday afternoon, with sustained winds of 120 miles per hour, the National Hurricane Center said in an advisory. ||||| Houston (CNN) Harvey is no longer a hurricane, but life-threatening flooding continued in and around Houston on Sunday night as citizens with boats assisted authorities in search and rescue efforts.
Flooding from Tropical Storm Harvey is overburdening resources in the country's fourth-largest city, prompting authorities to call on volunteers with watercraft for help in rescuing those trapped in homes and buildings.
An immediate respite from Harvey's wrath seems unlikely to come. The National Weather Service calls the flooding "unprecedented," and warns things may become more dire if a forecasted record-breaking 50 inches of rain does fall on parts of Texas in coming days. In anticipation of a worsening situation, Dallas is turning its main convention center into a "mega-shelter" that can host 5,000 evacuees.
The rainfall threatens to exacerbate an already dangerous situation, as Harvey's rains have left many east Texas rivers and bayous swollen to their banks or beyond.
"The breadth and intensity of this rainfall are beyond anything experienced before," the weather service said. "Catastrophic flooding is now underway and expected to continue for days."
The storm killed two people in Texas, authorities said, and the death toll will likely rise. More than 1,000 people were rescued overnight, and Houston Mayor Sylvester Turner warned that some 911 calls are going unanswered as operators "give preference to life-threatening calls."
From 10pm Sat to 1pm Sun., Houston 911 received over 56,000 calls. During an average day, they usually handle about 8,000. #harvey — Houston OEM (@HoustonOEM) August 27, 2017
Here are the latest developments:
A woman who drove her vehicle into high water in Houston was killed, and fire killed a man in Rockport.
Several states and the US military are sending emergency workers and equipment to Texas. In Harris County, though, authorities are having issues mobilizing those resources. "We've requested boats, all the things that would normally happen in a well-planned response to an event like this, but they can't get here," Harris County Judge Ed Emmett said.
Dallas announced its plans to open a "mega-shelter" capable of accommodating 5,000 evacuees at the Kay Bailey Hutchison Convention Center. County officials, charitable groups and local hospitals are working to open the shelter by Tuesday morning.
While Turner warned the rain could exacerbate flooding for "four to five days," Federal Emergency Management Agency Director Brock Long said he expects his agency "is going to be there for years."
The Houston Independent School District has canceled school for the week.
Houston's George Bush Intercontinental and William P. Hobby airports are closed until further notice, officials said. Corpus Christi International reopened at 4 p.m. Sunday, officials said. Jack Brooks Regional Airport in Beaumont, Ellington Airport in Houston, Mustang Beach Airport in Port Aransas and McCampbell-Porter Airport in Aransas Pass are also temporarily closed, the Federal Aviation Administration says.
Ben Taub Hospital, which houses a Level I trauma center, is being evacuated after flooding in the basement "disrupted the power source," Emmet said.
316,000 customers have lost electricity, Gov. Greg Abbott said.
The Red Cross is serving about 130,000 meals a day, the governor said.
President Donald Trump will travel to Texas on Tuesday, press secretary Sarah Huckabee Sanders said.
Trapped
JUST WATCHED Woman trapped in home: 911 told us not to call Replay More Videos ... MUST WATCH Woman trapped in home: 911 told us not to call 01:28
Among those stranded by the storm is Ify Echetebu, 30, who spoke to CNN from her aunt's house in Dickinson, not far from Galveston Bay. Along with her fiancé, grandparents, a friend and several teenagers, Echetebu is trapped on the second floor of the house as floodwaters creep up the staircase. She can see the rooftops of submerged cars in driveways, she said.
On the first floor, the water is up to her waist, she said. Emergency services know she and 10 others are holed up in the home, she said, but because emergencies take priority, she doesn't expect to be rescued until tomorrow, Echetebu said.
The severity of the situation just hit me. I'm overcome with grief due to how helpless I feel in all of this. This is truly devestating. #PrayForTexas #PrayForGalvestonCounty #TropicalStormHarvey #HurricaneHarvey A post shared by Lotenné I. E. (@1whitenigerian) on Aug 27, 2017 at 7:42am PDT
"We're nervous to stay here, but we are sleeping in shifts," she said. "Now we're having to deal with sewage in the water, river water, bayou water, water moccasins, snakes, gators."
Not far away, a rescue operation saved 20 to 25 residents of La Vita Bella assisted-living facility in Dickinson.
"They were up to their waist," Galveston County Commissioner Ken Clark said. "If they were in a wheelchair, they could have been up to their neck."
Residents of a nursing home in Dickinson, Texas, were rescued Sunday.
After a record 22 inches fell on the county in one day, rescuers set out before dawn Sunday to save those who braved the storm. Officials quickly realized they did not have enough boats for the rescue operations and asked private boat owners to help, said County Judge Mark Henry, responsible for disaster response in the county.
As of Sunday evening, between 800 and 1,200 people had been rescued from their homes in Galveston County, Henry said.
As authorities warned people not to take shelter in attics, unless they have axes handy to break through their roofs, several residents provided CNN with their accounts of riding out the storm.
"We are still stranded in our home with little kids and the water keeps rising," Houston resident Janet Castillo said Sunday morning. "We have (tried calling several numbers), but their lines are all busy or they don't answer."
We are going on fumes & our hearts ache for community we serve, but we will not stop! We are leveraging more assets with every passing hour. — Chief Art Acevedo (@ArtAcevedo) August 27, 2017
Jake Lewis of New Braunfels, Texas, said he woke up to ankle-deep water in the Houston hotel where he is staying.
"We have nowhere to go," he said. "I have a 2016 Chevy Silverado and the water is up to the door panels. The water keeps rising."
One of two confirmed fatalities happened in Houston when a woman drove her vehicle into high water and couldn't make it across, city police said. She got out of her vehicle, was overtaken by floodwaters and drowned.
Many roads impassable
Photos: Hurricane Harvey slams Texas Downtown Houston is reflected in the flooded Buffalo Bayou on Wednesday, August 30, five days after Hurricane Harvey made landfall in Texas. The Category 4 storm came ashore late Friday, August 25, just north of Port Aransas, and has caused historic flooding. Correction: Previous versions of this gallery incorrectly reported that Hurricane Harvey is the strongest storm to make landfall in the United States since Wilma in 2005. Harvey is actually the strongest storm to make landfall in the United States since Charley in 2004. Hide Caption 1 of 74 Photos: Hurricane Harvey slams Texas Members of the Louisiana Department of Wildlife and Fisheries, the Florida Fish and Wildlife Conservation Commission and the Louisiana National Guard help rescue elderly people from a flooded assisted living home in Orange, Texas, on August 30. Hide Caption 2 of 74 Photos: Hurricane Harvey slams Texas A baby sits with family belongings at a Gallery Furniture store in Houston being used as a temporary shelter on August 30. Hide Caption 3 of 74 Photos: Hurricane Harvey slams Texas Floodwaters engulf homes in Port Arthur on August 30. Hide Caption 4 of 74 Photos: Hurricane Harvey slams Texas Janice Forse cries at an emergency shelter in Beaumont on August 30. Her home in Beaumont was flooded Wednesday morning. "Even Katrina wasn't this bad," Forse told the Austin American-Statesman. Hide Caption 5 of 74 Photos: Hurricane Harvey slams Texas Tammy Dominguez, left, and her husband, Christopher Dominguez, sleep on cots at the George R. Brown Convention Center, where nearly 10,000 people are taking shelter in Houston, on August 30. Hide Caption 6 of 74 Photos: Hurricane Harvey slams Texas A cat tries to find dry ground around a flooded apartment complex on August 30 in Houston. Hide Caption 7 of 74 Photos: Hurricane Harvey slams Texas Volunteer rescue workers help a woman from her flooded home in Port Arthur on August 30. Hide Caption 8 of 74 Photos: Hurricane Harvey slams Texas The Florida Air Force Reserve Pararescue team from the 308th Rescue Squadron helps evacuees board a helicopter in Port Arthur on August 30. Hide Caption 9 of 74 Photos: Hurricane Harvey slams Texas Water from the Addicks Reservoir flows into neighborhoods in Houston as floodwaters rise Tuesday, August 29. Hide Caption 10 of 74 Photos: Hurricane Harvey slams Texas Chris Gutierrez, second from right, helps his grandmother, Edelmira Gutierrez, down the stairs of their flooded house and into a waiting firetruck in the Concord Bridge neighborhood of Houston on August 29. Hide Caption 11 of 74 Photos: Hurricane Harvey slams Texas Members of the National Guard rest at a furniture store in Richmond, Texas, on August 29. Hide Caption 12 of 74 Photos: Hurricane Harvey slams Texas Alexis Hernandez holds her daughter Faith at the George R. Brown Convention Center, which is serving as a shelter in Houston. Hide Caption 13 of 74 Photos: Hurricane Harvey slams Texas Evacuees make their way though floodwaters in Houston on August 29. Hide Caption 14 of 74 Photos: Hurricane Harvey slams Texas President Donald Trump takes part in a briefing on Harvey as he visits Corpus Christi on August 29. In a stop in Austin, Trump spoke of the long-term effort and stiff costs that will be needed to rebuild the region. "Nobody's seen this kind of water," he said. "Probably, there's never been something so expensive in our country's history." While talking about recovery and relief efforts, Trump said, "We want to do it better than ever before." Hide Caption 15 of 74 Photos: Hurricane Harvey slams Texas Civilian rescuers put a boat into a flooded road to search for people in Cypress on August 29. Hide Caption 16 of 74 Photos: Hurricane Harvey slams Texas Volunteers organize items donated for Hurricane Harvey victims in Dallas on August 29. Hide Caption 17 of 74 Photos: Hurricane Harvey slams Texas An overview of downtown Houston on August 29 shows the scale of the catastrophic flooding. Hide Caption 18 of 74 Photos: Hurricane Harvey slams Texas Matthew Koser searches for important papers and heirlooms inside his grandfather's house in Houston's Bear Creek neighborhood on August 29. The neighborhood flooded after water was released from nearby Addicks Reservoir. Hide Caption 19 of 74 Photos: Hurricane Harvey slams Texas Shane Johnson removes items from a family home in Rockport, Texas, on August 29. Hide Caption 20 of 74 Photos: Hurricane Harvey slams Texas Airplanes sit at a flooded airport in Houston on August 29. Hide Caption 21 of 74 Photos: Hurricane Harvey slams Texas People set up a shelter for volunteer rescue workers at Fairfield Baptist Church in Cypress, Texas, on August 29. Hide Caption 22 of 74 Photos: Hurricane Harvey slams Texas Shardea Harrison looks at her 3-week-old baby, Sarai, as Dean Mize, right, and Jason Legnon use an airboat to rescue them from their home in Houston on Monday, August 28. Hide Caption 23 of 74 Photos: Hurricane Harvey slams Texas Thousands take shelter at the George R. Brown Convention Center in Houston on August 28. Hide Caption 24 of 74 Photos: Hurricane Harvey slams Texas Rescue boats fill Tidwell Road in Houston as they help flood victims evacuate the area on August 28. Hide Caption 25 of 74 Photos: Hurricane Harvey slams Texas People wait to be rescued from their flooded home in Houston on August 28. Hide Caption 26 of 74 Photos: Hurricane Harvey slams Texas A firefighter helps Sara Golden and her daughters Paisley, Poppy and Piper board a Texas Air National Guard C-130 at Scholes International Airport in Galveston, Texas, on August 28. Hide Caption 27 of 74 Photos: Hurricane Harvey slams Texas People make their way out of a flooded neighborhood in Houston on August 28. Hide Caption 28 of 74 Photos: Hurricane Harvey slams Texas Sam Speights removes possessions from his damaged home in Rockport on August 28. Hide Caption 29 of 74 Photos: Hurricane Harvey slams Texas Flood victims wait to unload from the back of a heavy-duty truck after being evacuated from their homes in Houston on August 28. Hide Caption 30 of 74 Photos: Hurricane Harvey slams Texas People leave a flooded area of Houston on August 28. Hide Caption 31 of 74 Photos: Hurricane Harvey slams Texas People are rescued in Houston on August 28. Hide Caption 32 of 74 Photos: Hurricane Harvey slams Texas Bridget Brundrett presents an American flag to Texas Gov. Greg Abbott while he was in Rockport on August 28. The flag had been recovered from city hall after flying during the hurricane. Hide Caption 33 of 74 Photos: Hurricane Harvey slams Texas A Coast Guard helicopter hoists a wheelchair on board after lifting a person to safety from a flooded area of Houston on August 28. Hide Caption 34 of 74 Photos: Hurricane Harvey slams Texas Houston flood victims eat and rest at the George R. Brown Convention Center on August 28. Hide Caption 35 of 74 Photos: Hurricane Harvey slams Texas Belinda Penn holds her dogs Winston and Baxter after being rescued from their home in Spring, Texas, on August 28. Hide Caption 36 of 74 Photos: Hurricane Harvey slams Texas A firefighter is wheeled to a waiting ambulance after he became fatigued while fighting an office-building fire in downtown Houston on August 28. Hide Caption 37 of 74 Photos: Hurricane Harvey slams Texas People evacuate a neighborhood in west Houston on August 28. Hide Caption 38 of 74 Photos: Hurricane Harvey slams Texas Julie Martinez, right, hugs her daughter, Gabrielle Jackson, in front of a relative's damaged apartment in Rockport on August 28. Hide Caption 39 of 74 Photos: Hurricane Harvey slams Texas Cattle are stranded in a flooded pasture in La Grange, Texas, on August 28. Hide Caption 40 of 74 Photos: Hurricane Harvey slams Texas Volunteer rescue boats make their way into a flooded subdivision in Spring, Texas, on August 28. Hide Caption 41 of 74 Photos: Hurricane Harvey slams Texas Houston police officer Daryl Hudeck carries Catherine Pham and her 13-month-old son, Aiden, after rescuing them from floodwaters on Sunday, August 27. Hide Caption 42 of 74 Photos: Hurricane Harvey slams Texas People push a stalled pickup through a flooded street in Houston on August 27. Hide Caption 43 of 74 Photos: Hurricane Harvey slams Texas Residents of Rockport return to their destroyed home on August 27. Hide Caption 44 of 74 Photos: Hurricane Harvey slams Texas The Buffalo Bayou floods parts of Houston on August 27. Hide Caption 45 of 74 Photos: Hurricane Harvey slams Texas Two men try to beat the current that was pushing them down an overflowing Brays Bayou in Houston on August 27. Hide Caption 46 of 74 Photos: Hurricane Harvey slams Texas Jane Rhodes is rescued by neighbors in Friendswood, Texas, on August 27. Hide Caption 47 of 74 Photos: Hurricane Harvey slams Texas Volunteers at Sacred Heart Catholic Church prepare cots for evacuees in Elgin, Texas, on August 27. Hide Caption 48 of 74 Photos: Hurricane Harvey slams Texas Damage to a home is seen in the Key Allegro neighborhood of Rockport on August 27. Hide Caption 49 of 74 Photos: Hurricane Harvey slams Texas Melani Zurawski cries while inspecting her home in Port Aransas on August 27. Hide Caption 50 of 74 Photos: Hurricane Harvey slams Texas Wilford Martinez, right, is rescued from his flooded car along Interstate 610 in Houston on August 27. Assisting him here is Richard Wagner of the Harris County Sheriff's Department. Hide Caption 51 of 74 Photos: Hurricane Harvey slams Texas A car is submerged by floodwaters on a freeway near downtown Houston on August 27. Hide Caption 52 of 74 Photos: Hurricane Harvey slams Texas A resident of the Bayou on the Bend apartment complex watches its first floor flood in Houston on August 27. Hide Caption 53 of 74 Photos: Hurricane Harvey slams Texas A city flag, tattered by the effects of Hurricane Harvey, flaps in the wind over the police station in Rockport on August 27. Hide Caption 54 of 74 Photos: Hurricane Harvey slams Texas Fort Bend County Sheriff Troy Nehls and Lucas Wu lift Ethan Wu into an airboat as they evacuate the Orchard Lakes subdivision in Fort Bend County, Texas, on August 27. Hide Caption 55 of 74 Photos: Hurricane Harvey slams Texas Damage is seen at a boat storage building in Rockport on August 27. Hide Caption 56 of 74 Photos: Hurricane Harvey slams Texas Water rushes from a large sinkhole along a highway in Rosenberg, Texas, on August 27. Hide Caption 57 of 74 Photos: Hurricane Harvey slams Texas Evacuees wade through a flooded section of Interstate 610 in Houston on August 27. Hide Caption 58 of 74 Photos: Hurricane Harvey slams Texas Evacuees are loaded onto a truck on an Interstate 610 overpass in Houston on August 27. Hide Caption 59 of 74 Photos: Hurricane Harvey slams Texas A graveyard is flooded in Pearland, Texas, on August 27. Hide Caption 60 of 74 Photos: Hurricane Harvey slams Texas A driver works his way through a maze of fallen utility poles in Taft, Texas, on Saturday, August 26. Hide Caption 61 of 74 Photos: Hurricane Harvey slams Texas Steve Culver comforts his dog Otis on August 26 as he talks about what he said was the "most terrifying event in his life." Hurricane Harvey destroyed most of his home in Rockport while he and his wife were there. Hide Caption 62 of 74 Photos: Hurricane Harvey slams Texas People walk through flooded streets in Galveston on August 26. Hide Caption 63 of 74 Photos: Hurricane Harvey slams Texas Aaron Tobias stands in what is left of his Rockport home on August 26. Tobias said he was able to get his wife and kids out before the storm arrived, but he stayed there and rode it out. Hide Caption 64 of 74 Photos: Hurricane Harvey slams Texas Brad Matheney offers help to a man in a wheelchair in Galveston on August 26. Hide Caption 65 of 74 Photos: Hurricane Harvey slams Texas Jessica Campbell hugs Jonathan Fitzgerald after riding out Hurricane Harvey in an apartment in Rockport. Hide Caption 66 of 74 Photos: Hurricane Harvey slams Texas Boats are damaged in Rockport on August 26. Hide Caption 67 of 74 Photos: Hurricane Harvey slams Texas A damaged home in Rockport on August 26. Hide Caption 68 of 74 Photos: Hurricane Harvey slams Texas Donna Raney makes her way out of the wreckage of her home as Daisy Graham assists her in Rockport on August 26. Raney was hiding in the shower after the roof blew off and the walls of her home caved in. Hide Caption 69 of 74 Photos: Hurricane Harvey slams Texas A laundromat's machines are exposed to the elements in Rockport on August 26. Hide Caption 70 of 74 Photos: Hurricane Harvey slams Texas A semi-truck is overturned on a highway south of Houston on August 26. Hide Caption 71 of 74 Photos: Hurricane Harvey slams Texas An American flag flies in front of a damaged mobile-home park in Rockport on August 26. Hide Caption 72 of 74 Photos: Hurricane Harvey slams Texas NASA astronaut Jack Fischer photographed Hurricane Harvey from the International Space Station on Friday, August 25. Hide Caption 73 of 74 Photos: Hurricane Harvey slams Texas Waves pound the shore as Harvey approaches Corpus Christi, Texas, on August 25. Hide Caption 74 of 74
In a Sunday news conference, Abbott said, "We want to stress when there is heavy rainfall and flooding, the importance of staying off the road. If you drive into water, you're taking your life into your own hands."
Portions of major highways, including Interstates 10, 45 and 610, were submerged and unnavigable. Houston resident Dion Laurent said the White Oak Bayou flooded I-10 and I-45.
White Oak Bayou flooding I-10 and I-45 #Harvey from Quitman St. Bridge A post shared by dion laurent (@dionrlaurent) on Aug 27, 2017 at 11:57am PDT
Harris County Sheriff Ed Gonzalez said he understands the compulsion to find safer ground, but urged people to think twice before venturing out into high water and to consider unforeseen dangers, such as manhole covers being lifted from their holes.
Lt. Craig Cummings of the Texas Department of Public Safety said attempts to drive to safety may be futile anyway, as it took him two and a half hours to drive 20 miles in Houston on Sunday.
"There's 60 barricaded locations as of midnight. Most thoroughfares are impassable. Several hundred structures are flooded, and we are expecting that number to rise," he said.
In Brazoria County, south of Houston, officials set up an evacuation route for all residents living west of State Highway 288 and south of State Highway 6, ordering them to "LEAVE NOW!" under a mandatory evacuation order. Those in need of shelter can take refuge in the Bell County Expo Center in Belton, officials said.
The 911 dispatchers in the nation's fourth-most populous city have received 2,000 requests for rescue, Mayor Turner said. Houston Fire Chief Samuel Peña said his department had responded to 2,500 calls and have about 1,000 more waiting to be serviced.
Gonzalez tweeted that many high-water rescues were performed overnight in Houston, some involving children or residents with medical issues, including one person suffering from cardiac arrest. Stranded residents were saved from vehicles on the highway. Airboats were employed in some instances, he said.
We need help!! My house is flooded and my dad has heart disease my mom diabetic — Juanita Arreguin (@JuanitaArregui4) August 27, 2017
People are taking to social media to announce their locations and ask for help.
One person, whose mom is diabetic and dad has heart disease, tweeted, "We need help!! My house is flooded."
24 inches of rain in 24 hours
JUST WATCHED Slow moving storm Harvey drenching Texas Replay More Videos ... MUST WATCH Slow moving storm Harvey drenching Texas 01:58
Harvey blasted ashore as a Category 4 hurricane just north of Corpus Christi. It brought with it 132-mph winds but was quickly downgraded to a tropical storm. Still, it continued to spawn tornadoes and lightning.
A flash flood emergency was declared for sections of Houston, where more than 24 inches of rain fell in 24 hours, the National Weather Service said.
The weather service said maximum sustained winds Sunday would be near 45 mph. While Harvey could become a tropical depression by Sunday night, residents are warned to remain vigilant.
The slow-moving storm is expected to drop 15 to 25 inches of rain over the Texas coast through Thursday. Isolated storms could drop up to 50 inches of rain, the weather service said.
"What is unique in Harvey is that as the storm moved inland, a large high pressure built in to the north and, basically, the steering currents, which guide Harvey, collapsed," said CNN senior meterologist Dave Hennen. "This has caused the extremely slow movement of the storm, moving only around 60 miles, less than 2 miles per hour. This has allowed the bands of storms to move over the same areas over and over."
The weather service says rainfall of this magnitude "will cause catastrophic and life-threatening flooding."
Some residents are comparing Harvey to Allison, a storm that struck the Texas coast in 2001 and killed 23 people.
"Allison was bad -- really, really bad," Houston resident Pat Napolio said, "but if (the water) creeps up anymore, Harvey will surpass (Allison)."
Rockport hit hard
A damaged home sits amid floodwaters Saturday after Hurricane Harvey slammed Rockport, Texas.
Another fatality was reported in the battered coastal city of Rockport. A person died in a house fire during the storm, Aransas County Judge Burt Mills said Saturday.
Warnings of tornadoes, torrential downpours and potentially historic flooding means extra bad news for broad swaths of southeast Texas, already littered with uprooted trees, toppled signs, flagpoles snapped like toothpicks and homes missing rooftops and patches of brick walls.
Hurricane Harvey took the walls off many Rockport homes.
Additional fatalities were feared in Rockport, where an estimated 5,000 residents rode out the storm, Aransas County Sheriff Bill Mills said.
Brock Long, director of the Federal Emergency Management Agency, said that Harvey would leave areas "uninhabitable for weeks or months," echoing language last heard ahead of Hurricane Katrina in 2005.
"FEMA is going to be there for years," Long said. ||||| Texas Gov. Greg Abbott said flooding in Houston from Tropical Storm Harvey may be the worst the city has ever seen.
“Houston is an area that is prone to flood at least once a year,” Abbott told ABC News Chief Anchor George Stephanopoulos on “This Week” Sunday, “but this is one of the worst, if not the worst that Houston has suffered.”
Harvey, which hit the Texas coast Friday night as a Category 4 hurricane with 130 mph winds and has since been downgraded to a tropical storm, has so far left at least two people dead. The storm is lingering over the Houston area, causing severe flooding that is expected to grow worse over the next few days, with a total of up to about three feet in rain possible through Wednesday.
Abbott said he appreciates the federal government's help in responding to Harvey.
“We could not be more appreciative of what the federal government has done, from the president on down,” Abbott, a Republican, told Stephanopoulos.
President Trump granted Governor Abbott’s request for a disaster proclamation on Friday, activating response from the Federal Emergency Management Agency for relief to the state.
“FEMA has been very active, involved, and engaged in this whole process long before the hurricane even hit ground,” said Abbott. “Because of their assistance it means that Texas will be able to begin the rebuilding process very swiftly.”
Ralph Barrera/Austin American-Statesman via AP
Asked by Stephanopoulos if it makes sense for the president to visit Texas this week, or if it will divert resources from the relief effort, Abbott said, “it depends on where he goes.”
“We are already involved in the cleanup process in Corpus Christi, if the president were to visit there it wouldn’t hinder any efforts. We’ll just have to wait and see where the storm goes, understanding that this entire storm has been very unpredictable in its movement, and I couldn’t tell you right now where it will be in two days,” he said.
The president tweeted Sunday morning that he will visit Texas once he can do so without disrupting emergency response efforts.
I will be going to Texas as soon as that trip can be made without causing disruption. The focus must be life and safety. — Donald J. Trump (@realDonaldTrump) August 27, 2017
The White House point man on the storm, Homeland Security Adviser Tom Bossert echoed the president’s tweet in a separate interview on “This Week” Sunday saying that Trump “doesn't want to get in the way” of relief efforts.
“We’ll go where we can without getting in the way of the operators,” said Bossert. “We certainly won’t go in a place where we would prevent lifesaving activities from taking place. The president wants to go to show support. He doesn’t want to go to get in the way.” ||||| A daily crawl of more than 200,000 home pages of news sites, including the pages linked from those home pages. Site list provided by The GDELT Project
These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites.
Sorry, the product specified was not found within the database. Products older than one year are purged to conserve space on our server.
The Iowa Environmental Mesonet maintains a similiar archive to that found on this website.
You can optionally try to find this product on their website here. |||||
What is a shorter version of the above article? | – As "catastrophic" flooding batters Texas in the wake of Hurricane Harvey, President Trump says he will be traveling to Texas "as soon as that trip can be made without causing disruption" in the wake of Hurricane Harvey, reports the AP. Trump tweeted that the "focus must be life and safety." Trump has been complimenting the response to the storm on his Twitter feed, commending "Great coordination between agencies at all levels of government." Trump adds that: "Many people are now saying that this is the worst storm/hurricane they have ever seen. Good news is that we have great talent on the ground." As much as 40 inches of rain could hit cities including Houston. Other developments: The National Weather Service is advising residents to not leave their homes, but if the highest floor becomes dangerous, to get on the roof and call 911, reports CBS News. More than 1,000 people have been rescued so far, reports CNN. "We could not be more appreciative of what the federal government has done, from the president on down," Texas Gov. Greg Abbott tells ABC News of the response. "FEMA has been very active, involved, and engaged in this whole process long before the hurricane even hit ground. Because of their assistance it means that Texas will be able to begin the rebuilding process very swiftly." "Houston is an area that is prone to flood at least once a year, but this is one of the worst, if not the worst that Houston has suffered," Abbott says. | multi_news_1_0_0 |
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Sharafat Khan has reportedly been living outside his house, mostly on the front lawn, since his wife kicked him out of the house in March and left him with only the clothes on his back. (Photo: KHOU)
Neighbors in the upscale waterfront development of Taylor Lake Shores in Lakeview are asking authorities, and a reclusive doctor, to find a solution to a months-long dispute that has left a 69-year-old man camped out in his million dollar front yard after a dispute with his wife.
Sharafat Khan has reportedly been living outside his house, mostly on the front lawn, since his wife – a Friendswood-area doctor – kicked him out of the house in March and left him with only the clothes on his back.
“I’m really weak, but otherwise OK,” he said Tuesday, seated underneath the palm trees in his front yard on Ray Shell Court.
His wife has placed a sign on the front door asking people not to feed him.
“If you want to feed him, take him to your house. If you want to, you can keep him at your house. Thanks for your sympathy, but do not bring anything on this property,” the sign reads.
Neighbors continue to bring him food anyway.
“It just seems the man is elderly and it seems inhumane to leave him stranded out there,” said neighbor Laurel Stout.
Sharafat Khan has reportedly been living outside his house, mostly on the front lawn, since his wife kicked him out of the house in March and left him with only the clothes on his back. (Photo: KHOU)
It was an everyday argument that got him kicked out of the house, Khan said.
Problem is, they can’t.
Lakeview Police report a series of arguments have brought them to the million dollar home as many as 30 times in the last six months. Khan says his 61-year-old wife kicked him out, changed the locks and demanded police to remove him from her property.
The property is in both their names. And police say that if he wants to loiter in his own front yard, there’s nothing they can do.
“My emotions are with this house. I could live on the floor over there,” he said, admitting he has had offers from friends and could afford to stay in a hotel if he chose to. “But I’m on my own property.”
Khan is clearly in frail health, and neighbors question his mental state. When we met him Tuesday morning, he was still wearing hospital scrubs, hospital socks and the hospital bracelets from a recent stay.
Khan says he has diabetes and blood pressure and neighbors and police confirm multiple ambulance calls to the home to take him to the hospital. Doctors treat him, but each time he ends up back in his front yard.
Sharafat Khan has reportedly been living outside his house, mostly on the front lawn, since his wife kicked him out of the house in March and left him with only the clothes on his back. (Photo: KHOU)
“I just know that she’s the stronger one in the family,” David Flores said after stopping by to check on his friend.
Flores says he was the general contractor for the Khan family home about a decade ago.
“I don’t understand why somebody wouldn’t come help their father, even if mom tells you no,” Flores said.
We’ve learned from one of his sons that the wife finally got tired of years of verbal and physical abuse. There are also allegations of theft. Harris County Criminal Court records show that Khan was arrested for domestic violence in 2008 and civil court records show his wife received a protective order in December 2014 and that she filed for divorce in June. She's also asked for multiple restraining orders. Records show that a final judgment has not yet been signed.
The wife has repeatedly asked police for help. Sources say she was at the Lakeview Police Station again on Tuesday afternoon and Adult Family Services has also been notified. But while Khan’s actions and frail health might suggest the need for mental health services, he remains camped outside his home.
Multiple attempts to reach his wife at her doctor’s office and the home were not successful. She returned home early Tuesday afternoon, drove her SUV through the circular driveway past Khan, parked in her garage and entered the home without comment to us or her husband.
We asked Khan one final question: What is he trying to accomplish?
“To realize whatever she is doing she’s doing bad,” he said. “People will know, the neighbors and everything else. People will ask her, put her down. Let her know what you’re doing to your husband.”
Read or Share this story: http://on.khou.com/1RsTKdv ||||| HOUSTON, KEITH GARVIN, KPRC CHANNEL 2 NEWS. NEW AT 10:00, A DISPUTE BETWEEN A DOCTOR AND HER HUSBAND HAS A NEIGHBORHOOD UP IN ARMS, AND POLICE TRYING TO KEEP THE PEACE HERE. THE HUSBAND HAS BEEN FORCED TO LIVE ON HIS FRONT YARD FOR THE LAST SIX MONTHS. CHANNEL 2'S JENNIFER BAUER IS LIVE FOR US IN TAYLOR LAKE VILLAGE, HARRIS COUNTY, WITH THE STORY YOU'LL SEE ONLY ON 2 TONIGHT. JEN? Reporter: YOU KNOW, THIS IS A VERY PRIVATE MATTER THAT HAS NOW BECOME VERY PUBLIC. MR. CANN SPENDS MOST OF HIS NIGHTSANNED IN A WHITE SHEET SITTING ON THE FRONT PORCH OF HIS MILLION-DOLLAR HOME. IN FACT, JUST ABOUT 10 MINUTES MINUTES AGO A CAME NEIGHBOR AND HELPED HIM WALK TO THE BACK OF THE HOUSE BECAUSE BACK THERE HE HAS MORE PRIVACY. NEIGHBORS ARE WORRIED ABOUT HIM AND THEY WANT TO HELP HIM. AS SOON AS WE PULLED UP IN FRONT OF THE MILLION-DOLLAR HOME, MR. KAHNEN ASKED US FOR HELP. HE DIDN'T KNOW WHO WE WERE BUT HE SAID HE NEEDED OUR HELP GETTING UP. HIS FRAGILE STATE IS WHAT HAS NEIGHBORS SO WORRIED. WEARING THE SAME CLOTHING. IT'S DIRTY. HE HAS NO BATHROOM FACILITIES, NO SHOES. THE WEATHER IS STARTING TO GET COLDER. HE'S VERY FRAIL. HE CAN'T EVEN WALK. Reporter: HE'S BEEN SLEEPING OUTSIDE ON AND OFF FOR SIX MONTHS. HE TELLS US THE FEUD WITH HIS WIFE OF 32 YEARS HAS BEEN GOING ON MUCH LONGER. BEEN GOING ON LIKE LAST SIX YEARS. Reporter: AND HOW COME YOU DON'T FILE FOR DIVORCE? I NEED MONEY. Reporter: HE SAYS HIS WIFE, WHO IS A DOCTOR, KICKED HIM OUT. SHE TOOK AWAY HIS KEYS AND WON'T LET HIM IN. THERE ARE SIGNS POSTED ALL OVER THE PLACE INSTRUCTING PEOPLE NOT TO FEED HIM OR HELP HIM. SHE DIDN'T WANT ME TO HAVE ANY KIND OF COMFORT. I'M AFRAID THAT HE'S GOING TO DIE OUT HERE, YOU KNOW, IN HIS YARD. Reporter: HE SAYS IT'S SIMPLE. HE OWNS THIS HOME AND HALF OF EVERYTHING INSIDE. HE DOESN'T FEEL HE SHOULD HAVE TO LEAVE. AND CLAIMS HIS WIFE WON'T FILE FOR DIVORCE BECAUSE SHE DOESN'T WANT TO GIVE UP HALF OF HER FORTUNE. THE POLICE TELL US THEY'VE BEENññ CALLED OUT HERE AS MANY AS 30ññ TIMES IN THE LAST SIX MONTHS. AND NOW NEIGHBORS ARE GETTING INVOLVED. DESPERATE TO HELP THE MAN WHO IS ESSENTIALLY HOMELESS BUT WHO OWNS HALF OF THIS MANSION. JUST HOPING THAT, YOU KNOW, WE CAN FIND HELP FOR HIM. ALLOWING THIS TO CONTINUE IS IN THE BEST INTEREST OF ANYONE. Reporter: AND TONIGHT WE DID HAVE A CONVERSATION WITH THE POLICE. THEY TELL ME THERE ISN'T MUCH LEGAL LOY THEY CAN DO BECAUSE MR. -- LEGALLY THEY CAN DO BECAUSE HE HAS EVERY RIGHT TO BE HERE AND THEY CAN'T FORCE HIS WIFE TO LET HIM INSIDE. OFFICERS TELL ME THEY HAVE CONTACTED ADULT PROTECTIVE SERVICES. AND THEY CONFIRM THAT THEY'RE INVOLVED BUT THEY CAN'T RELEASE THE SPECIFICS OF THIS CASE. HOWEVER, THEY DID TELL ME THEY ARE UNABLE TO FORCE ANYONE TO GET HELP. MR. CANN TELLS ME HE AND HIS WIFE HAVE TWO CHILDREN WHO LIVE OUT OF STATE. WE SPOKE WITH DR. CANN. SHE DIDN'T ANSWER THE DOOR WHEN WE TRIED SPEAKING WITH HER EARLIER. SHE DID GET US ON THE PHONE AND TOLD US THIS IS A PRIVATE MATTER AND SHE DOES NOT WANT TO SPEAK
SEABROOK, Texas -
A private family matter has become very public in the Taylor Lake Village community.
A dispute between a husband and his doctor wife has left him outside, sleeping and living in the yard of his million dollar mansion. According to the police, it’s been going on for the last six months and Sharafat Khan has been forced to live outdoors on and off during that time.
Neighbors are very worried because he is elderly, in poor health and in a fragile state.
"He’s wearing the same clothing, it’s dirty,” neighbor Debbie Scoggins said. “He has no bathroom facilities, no shoes."
"The weather is starting to get colder,” Laurel Stout, who lives across the street, said. "He’s very frail, he can’t even walk. I’m afraid he is going to die out here in his yard."
Khan told KPRC 2 his wife kicked him out of the house several months ago, took away his keys and had the locks changed. He said he doesn’t have access to their money and is basically homeless even though he owns half of their mansion.
Khan doesn’t feel like he should have to leave because the home and property are just as much his. He said he wants to be allowed inside and he’s hoping he can pressure her into changing her mind.
"She doesn’t want me to have any sort of comfort," he said.
Night after night he sleeps on the front porch wrapped in a sheet. During the day he tries to find shade under the trees. On Monday he was eating saltine crackers and drinking a warm bottle of water.
Neighbors said if they take him blankets and pillows, the wife takes them away.
There are signs posted all over the home instructing the neighbors not to help him or feed him.
Khan said the dispute is over his relationship with other family members. She wanted him to cut ties but he refused.
Police officers who are familiar with the situation said they have been called out to the home 20 to 30 times in the last six months. There is nothing legally they can do because Khan has every right to be there and they can’t force his wife to let him in.
"Our hands are tied," one officer said.
Someone close to the situation said Khan's wife claims she can't file for divorce because she and her husband practice Islam and they strictly follow Sharia law. Khan told KPRC this has nothing to do with religion and everything to do with money.
"She doesn’t want to hand over half her fortune," he said.
He can’t file for divorce because he claims he can't afford to.
Adult Protective Services are involved but can’t release specific information about the case because of confidentiality laws. A spokesperson for the agency said they cannot force someone to get help.
"I’m just hoping we can find help for him," Scoggins said.
"Allowing this to continue is not in the best interest of anyone," Stout said.
KPRC 2 reached out to the doctor for comment, she said it was a private matter and did not wish to speak about it.
Some problems stemmed from a 2008 assault charge, that's when Sharafat Khan was accused of hitting his wife, according to court documents.
Family members also said they have tried to get Khan help but he refuses. They've spoken with social workers and he's been in and out of certain facilities but often leaves against medical advice. |||||
Write a summary. | – Sharafat Khan, 69, has been living on the front lawn of the million-dollar Texas home he shares with his wife ever since she kicked him out in March, KHOU reports. Now neighbors are starting to become concerned for his mental and physical health. "He's wearing the same clothing, it's dirty," one neighbor tells KPRC. "He has no bathroom facilities, no shoes." "He's very frail, he can't even walk," says another. "I'm afraid he is going to die out here in his yard." KHOU reports Khan's doctor wife kicked him out with only the clothes he was wearing after a series of fights and changed the locks. A sign outside the house warns concerned neighbors: "If you want to feed him, take him to your house. If you want to, you can keep him at your house." KHOU reports police were called to the home up to 30 times in the past six months for arguments between Khan and his wife. Khan tells KPRC his wife is mad at him for staying in contact with certain relatives. But the couple's son tells KHOU Khan verbally and physically abused his wife for years. Records show Khan was arrested for domestic violence in 2008 and his wife filed for divorce in 2014. In between, she filed for multiple restraining and protective orders. She has demanded police remove Khan from the property, but they have no legal ability to do so. Khan is in bad health, and has been taken to the hospital numerous times since March but always ends up back on the lawn. KPRC reports Adult Protective Services is getting involved. | multi_news_1_0_0 |
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NEW DELHI (Reuters Life!) - A hardline Hindu organization, known for its opposition to "corrupting" Western food imports, is planning to launch a new soft drink made from cow's urine, often seen as sacred in parts of India.
The Rashtriya Swayamsevak Sangh (RSS), or National Volunteer Corps, said the bovine beverage is undergoing laboratory tests for the next 2 to 3 months but did not give a specific date for its commercial release.
The flavor is not yet known, but the RSS said the liquid produced by Hinduism's revered holy cows is being mixed with products such as aloe vera and gooseberry to fight diseases such as diabetes and cancer.
Many Hindus consider cow urine to have medicinal properties and it is often drunk in religious festivals.
The organization, which aims to transform India's secular society and establish the supremacy of a Hindu majority, said it had not decided on a name or a price for the drink.
"Cow urine offers a cure for around 70 to 80 incurable diseases like diabetes. All are curable by cow urine," Om Prakash, the head of the RSS Cow Protection Department, told Reuters by phone.
Prakash, who is based in Hardwar, one of four holy Hindu cities on the river Ganges where the world's largest religious gathering takes place, said the product will be sold nationwide but did not rule out international success.
"It is useful for the whole country and the world as well. It will be done through shops and through corporates," he said.
The Hindu group has campaigned against foreign imports such as Pepsi and Coca Cola in the past, which it sees as a corrupting influence and a tool of Western imperialism.
The RSS was temporarily banned after a Hindu mob tore down a mosque in 1992 which lead to bloody religious riots.
The Shiv Sena, a hardline Hindu political party also known for attacking what it sees as threats to Indian culture such as Valentine's Day, started a similar initiative last year to appeal to its powerbase in Mumbai.
To promote the food of the native Marathi culture, the Shiv Sena said it was "making a chain like McDonalds" to sell a popular local fried snack.
(Additional reporting by Vipul Tripathi)
(Editing by Miral Fahmy)
([email protected]; +91-997 111 0254; Reuters Messaging: [email protected])) ||||| Though it may never move into the mainstream, an alternative medicine promoted by a Hindu group in India is getting some attention: cow urine as a treatment for numerous diseases, including cancer, diabetes and tuberculosis.
But not any old cow urine will do, according to the followers of the hardline Rashtriya Swayamsevak Sangh (RSS) sect — only the urine collected from a female virgin cow will suffice, and it's best when collected before dawn.
"Cow urine offers a cure for around 70 to 80 incurable diseases like diabetes," Om Prakash, of the RSS Cow Protection Department, told Reuters. "All are curable by cow urine." [7 Medical Myths Even Doctors Believe]
Cow urine soda?
Though Westerners may find the practice surprising — if not outright disgusting — the therapeutic use of cow urine has a long history in India, particularly in Ayurvedic medicine, an ancient health care tradition that has been practiced in India for at least 5,000 years.
For people who would rather not drink their cow urine straight, the RSS has developed a cow-urine-based soft drink called Gomutra Ark. The drink is promoted as a "healthy" alternative to Coca-Cola, Pepsi and other soft drinks, which are seen as part of a wider problem resulting from corrupt Western influences.
"We refer to gau ark (cow urine) as gau jal (cow water), as it has immense potential to cure various diseases," Prakash told The Telegraph. "We have developed a soft-drink formula with gau jal as the base."
Science weighs in
Health experts, however, are less enthusiastic about the health benefits of drinking cow urine, especially when anti-cancer properties are claimed. "I think I'm perfectly comfortable in saying that I'm aware of no data that cow's urine — or any other species' urine — holds any promise ... in treating or preventing cancer," Dr. Donald Hensrud of the Mayo Clinic told ABC News.
Nonetheless, the product has been studied by a handful of researchers. A 2012 study published in the journal Ancient Science of Life suggested rats with diabetes that were fed Gomutra Ark had significantly lower blood glucose levels than rats in a control group did. "This study supports the traditional use of Gomutra Ark in diabetes," the researchers wrote, noting that it has a "high therapeutic index and is safe for chronic use."
And a 2013 study in the International Brazilian Journal of Urology claimed that distilled cow urine might help to prevent the development of kidney stones in rats.
However, these and other studies may not convince skeptics to start drinking urine anytime soon, even if it is part of a tasty soft drink.
"Just trust me on this — this drink really will require flavoring," Keith-Thomas Ayoob, nutritionist at the Albert Einstein College of Medicine, told ABC News. "If they use sugar or a caloric sweetener, then the world probably doesn't need another drink that's just a source of sugar calories, although this drink will probably have its 15 minutes [of fame] because of its novelty."
Follow Marc Lallanilla on Twitter and Google+. Follow us @livescience, Facebook & Google+. Original article on LiveScience. ||||| Chin chin: Urine-drinking Hindu cult believes a warm cup before sunrise straight from a virgin cow heals cancer - and followers are queuing up to try it
The Hindu believers regard the cow as a holy animal and say her urine has divine healing properties
In the north Indian city of Agra, dozens gather at the cow shelter of DD Singhal to have a fresh glass of cow urine
A growing cult of Hindu worshippers in India claim that drinking fresh cow urine will help cure them of all diseases - including cancer.
The Hindu believers regard the cow as a holy animal and say her urine has divine healing properties.
Jairam Singhal, 42, has been drinking cow pee for over a decade and was keen to testify to its health benefits.
Scroll down for video
A cult of Hindu worshippers in India is claiming that drinking fresh cow urine can help cure all diseases - including cancer
The Hindu believers regard the cow as a holy animal and say her urine has divine healing properties
In the north Indian city of Agra, dozens gather at the cow shelter of DD Singhal to have a fresh glass of cow urine
'I had diabetes, but ever since I have started drinking cow urine, my diabetes levels have been under control,' Jairam said.
'Someone told me drinking cow urine is good for health.
'We have had cows here for over 12 years now, so first thing in the morning we take cow urine and drink it.'
In the north Indian city of Agra, dozens gather at the cow shelter of DD Singhal to have a fresh glass of cow urine.
'Lots of people come here. And of late, the numbers have been rising. We all gather in the morning and drink fresh urine that Mother cow offers us,' Singhal said.
'Just a few years ago, there would hardly be anyone interested in taking cow urine from our shelter.
'But today lots of people come to our cow shelter. There are cancer patients sometimes - they want to see the benefits of cow urine.'
Many say the recent increase in the number of people drinking cow urine can be attributed to campaigns run by spiritual leaders.
Followers of the cult claim cow urine can successfully be used to combat cancer, diabetes, tumours, tuberculosis, stomach problems and much more.
They also claim that drinking cow pee is the only effective solution for treating baldness.
DD Singhal, founder of the Agra Gaushala Foundation, seen with some locals and his wife, worships a cow at his house in Agra, India
Followers of the cult claim cow urine can successfully be used to combat cancer, diabetes, tumours, tuberculosis, stomach problems and much more. They also claim that drinking cow pee is the only effective solution for treating baldness
'Lots of people come here. And of late, the numbers have been rising. We all gather in the morning and drink fresh urine that Mother cow offers us,' Singhal said
Many say the recent increase in the number of people drinking cow urine can be attributed to campaigns run by spiritual leaders
Two little girls pose with a cow at a cow shed in Agra, India
Cows seen on the roof of D.D Singhal's house. 'Only two things are pure in this universe, in this world. One is the water from the Holy Ganges river and the other is urine from mother holy cow,' Ramesh Gupta, a Hindu priest, said
'Only two things are pure in this universe, in this world. One is the water from the Holy Ganges river and the other is urine from mother holy cow,' Ramesh Gupta, a Hindu priest, said.
'Cow urine has been mentioned in ancient Hindu scriptures. No one can doubt the good effects it has on the human body. It is a divine gift from God.'
Followers like Gupta, however, insist that urine from every cow cannot be beneficial.
'The cow, whose urine one has to drink, should be a virgin - she must not have delivered a calf. Also, the urine is to be collected just before sunrise - that urine has the best effect,' he said.
However, there are people who oppose the claims made by preachers.
'People keep saying all kinds of things about cow urine, but we don't mind. People don't know what this is. They have never experienced the taste of cow urine or its effects, so how can they judge it,' Singhal said.
'It is just a matter of time before people realise the utility of cow urine.'
He is now eyeing to cash in on the growing trend and has plans to start manufacturing cow urine products on a commercial scale.
'We can manufacture eye drops, medicines for stomach ailments, toothpaste, bathing soaps, herbal powdered medicine, among other things, from cow urine,' he said.
||||| In a country where cows are sacred, drinking their urine is close to godliness. And better yet, it's marketable.
Along with protecting the bovine beast, the Cow Protection Department of the Rashtriya Swayamsevak Sangh (RSS) wants to make a cola from the cow's urine, which they say has curative properties.
"It has been established that cow urine is capable of curing even cancer, so imagine a drink which would not only be tasty but also healthy," Om Prakash, leader of RSS, told ABC News.
Curing cancer with cow urine? Cancer prevention experts said this seems like an unlikely stretch.
"It's a claim from somebody that does not have any distinction or credentials, and it's an empty claim without scientific basis," said Dr. Sam Epstein, emeritus professor of environmental and occupational medicine at the University of Illinois Chicago School of Public Health.
Dr. Donald Hensrud, chairman of the Division of Preventive Medicine at the Mayo Clinic in Rochester, Minn., agreed. "I think I'm perfectly comfortable in saying that I'm aware of no data that cow's urine -- or any other species' urine -- holds any promise ... in treating or preventing cancer."
So How's It Taste?
The cola concoction is currently undergoing laboratory testing in the northern city of Lucknow. The group hopes it will be launched in the market by the end of this year. The RSS does not have the budget to compete with other major soda companies, but Prakash believes the product is unique.
"It won't be like carbonated drinks and would be devoid of any toxics or pesticides. What do you get by drinking colas? Nothing. It's all gas, and that too is not good for health," he said.
Keith-Thomas Ayoob, nutritionist at the Albert Einstein College of Medicine, said there are a couple of potential problems with the drink, including the taste.
"Just trust me on this -- this drink really will require flavoring," Ayoob said. "If they use sugar or a caloric sweetener, then the world probably doesn't need another drink that's just a source of sugar calories, although this drink will probably have its 15 minutes because of its novelty."
Cow Urine Cola May Not Live Up to Claims
Pasteurization may also be necessary, he said.
One thing the cola does have going for it: cost.
"It won't be possible to make any guess or give you a rough idea about the price, but it will be cheap," said Prakash.
Dan Childs contributed to this report.
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Write a summary. | – An Indian Hindu group says it has a cure for some "70 to 80 incurable diseases," but it might not appeal to everyone. The miracle medicine is cow urine—specifically, pee from a virgin female taken before sunrise, LiveScience reports. The head of a cow shelter in northern India tells the Daily Mail: "We all gather in the morning and drink fresh urine that mother cow offers us." But you don't have to drink it neat: "We have developed a soft-drink formula with gau jal," or cow water, "as the base," Om Prakash told the Telegraph in 2009. Prakash is part of the Cow Protection Department of the Rashtriya Swayamsevak Sangh sect of Hinduism. Does it work? Some data seems to support it. In 2012, a study on diabetic rats given the soda, called Gomutra Ark, showed that they had significantly lower blood glucose than rats in a non-soda-drinking control group. It said the drink has a "high therapeutic index and is safe for chronic use." "I had diabetes, but ever since I have started drinking cow urine, my diabetes levels have been under control," a longtime user tells the Mail, which has a long series of fairly unappetizing photos of people drinking the urine. Last year, another study suggested distilled cow pee could help prevent rats from getting kidney stones. It's even said to cure cancer. But a Mayo Clinic doctor pooh-poohed that claim in a 2009 interview: "I think I'm perfectly comfortable in saying that I'm aware of no data that cow's urine—or any other species' urine—holds any promise ... in treating cancer." (As far as the pee of humans goes, scientists finally know what's in it.) | multi_news_1_0_0 |
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Article:
People with type 1 diabetes who used a bionic pancreas instead of manually monitoring glucose using fingerstick tests and delivering insulin using a pump were more likely to have blood glucose levels consistently within the normal range, with fewer dangerous lows or highs. The full report of the findings, funded by the National Institutes of Health, can be found online June 15 in the New England Journal of Medicine.
The researchers - at Boston University and Massachusetts General Hospital - say the process of blood glucose control could improve dramatically with the bionic pancreas. Currently, people with type 1 diabetes walk an endless tightrope. Because their pancreas doesn't make the hormone insulin, their blood glucose levels can veer dangerously high and low. Several times a day they must use fingerstick tests to monitor their blood glucose levels and manually take insulin by injection or from a pump.
In two scenarios, the researchers tested a bihormonal bionic pancreas, which uses a removable tiny sensor located in a thin needle inserted under the skin that automatically monitors real time glucose levels in tissue fluid and provides insulin and its counteracting hormone, glucagon, via two automatic pumps. In one scenario, 20 adults wore this device combination and carried a cell phone-sized wireless monitor around Boston for five days, unrestricted in their activities. In the other, 32 youth wore the device combination for five days at a camp for children with type 1 diabetes. Both groups were also monitored for five days wearing their own conventional pumps that deliver insulin.
"The bionic pancreas system reduced the average blood glucose to levels that have been shown to dramatically reduce the risk of diabetic complications," said co-first author Steven Russell, M.D., Ph.D., assistant professor of medicine at Massachusetts General Hospital. "This is tremendously difficult with currently available technology, and so most people with diabetes are unable to achieve these levels."
The researchers found about 37 percent fewer interventions for low blood glucose (hypoglycemia) and a more than twofold reduction in the time in hypoglycemia in adults using the bionic pancreas than with the manual pump. For adolescents using the bionic pancreas, results showed more than a twofold reduction in the need for interventions for hypoglycemia. As well, both groups had significant improvements in glucose levels with the bionic pancreas, particularly during the night.
"The performance of our system in both adults and adolescents exceeded our expectations under very challenging real-world conditions," said Ed Damiano, Ph.D., the paper's senior author, an associate professor of biomedical engineering at Boston University and the parent of a son with type 1 diabetes.
"A cure is always the end goal," he said. "As that goal remains elusive, a truly automated technology, which can consistently and relentlessly keep people healthy and safe from harm of hypoglycemia, would lift an enormous emotional and practical burden from the shoulders of people with type 1 diabetes, including my child and so many others."
Just as a thermostat helps control a home's temperature, the normal pancreas senses blood glucose levels and adjusts the hormones that control it. People with type 1 diabetes, whose pancreas produces little or no insulin, have been using the equivalent of a manual thermostat, needing constant checking and adjustment. A bionic pancreas - like the one used in these studies - would function more like an automated thermostat, automatically monitoring blood glucose and delivering insulin or glucagon when needed to keep glucose within the normal range. As well, these bionic pancreas devices could be monitored remotely by the patient's medical provider or parent.
"With promising results such as these, we plan to support larger multicenter trials of the artificial pancreas in the near future," said Guillermo Arreaza-Rubín, M.D., the project officer for artificial pancreas studies funded by the NIH's National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). "Within the next few years, we hope these technologies will go beyond experimental trials and be available to benefit more people with type 1 diabetes."
"The landmark Diabetes Control and Complications study - also funded by NIDDK - has long shown that maintaining as normal a blood glucose level as possible early on can stave off complications, including heart, kidney and eye diseases, decades later," said NIDDK Director Griffin P. Rodgers, M.D. "By funding research on the artificial pancreas, we aim to help people with type 1 diabetes maintain healthy blood glucose levels, prevent painful and costly complications, and lead freer, healthier lives."
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Among other funding sources, this research was supported by NIDDK grants R01DK085633 and R01DK097657, and was made possible by the Special Statutory Funding Program for Type 1 Diabetes Research. The program was established by Congress for research to prevent and cure type 1 diabetes.
The NIDDK, part of the NIH, conducts and supports basic and clinical research and research training on some of the most common, severe and disabling conditions affecting Americans. The Institute's research interests include: diabetes and other endocrine and metabolic diseases; digestive diseases, nutrition, and obesity; and kidney, urologic and hematologic diseases. For more information, visit http://www. niddk. nih. gov/ .
About the National Institutes of Health (NIH): NIH, the nation's medical research agency, includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. NIH is the primary federal agency conducting and supporting basic, clinical, and translational medical research, and is investigating the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit http://www. nih. gov .
NIH...Turning Discovery Into Health ||||| A portable artificial pancreas built with a modified iPhone successfully regulated blood sugar levels in a trial with people who have Type 1 diabetes, researchers reported Sunday.
Type 1 diabetes, which usually starts in childhood or young adulthood, is a chronic condition in which the pancreas produces little or no insulin, the hormone that lowers blood sugar levels. Insulin works in conjunction with glucagon, a hormone that raises blood sugar. Together, they keep blood sugar in a healthy range.
Currently about one-third of people with Type 1 diabetes rely on insulin pumps to regulate blood sugar. They eliminate the need for injections and can be programmed to mimic the natural release of insulin by dispensing small doses regularly.
But these pumps do not automatically adjust to the patient’s variable insulin needs, and they do not dispense glucagon. The new device, described in a report in The New England Journal of Medicine, dispenses both hormones, and it does so with little intervention from the patient.
“The data address some of the most difficult problems in diabetes management,” said Dr. Kevan Herold, director of the Yale Diabetes Center, who was not involved in the study. “I’d say that the effects are quite significant and noteworthy.”
Dr. Fredric E. Wondisford, director of the diabetes institute at Johns Hopkins, also found the results encouraging. “To me, it’s a clear advance,” he said. But he cautioned that the effectiveness and practicality of the device had still not been tested in large numbers of patients over long periods of time. He also raised the issue of cost and insurance coverage.
Treatment of Type 1 diabetes is complicated. Patients not using pumps need two or more insulin injections a day, and all have to monitor blood sugar several times a day by pricking their skin and testing their blood.
Maintaining safe blood sugar levels requires precise adjustments, especially to prevent hypoglycemia, or extremely low blood sugar. Hypoglycemia can occur quickly, without the patient’s awareness, and can be a life-threatening emergency.
For patients with adequate treatment, elevated blood sugar is usually not an emergency, but can cause vascular damage over time that can lead to eye problems and amputations.
The artificial pancreas is the latest version of a device that researchers have been refining for several years. The system consists of an iPhone 4S with an attached glucose monitoring device, two pumps, and reservoirs for insulin and glucagon.
A sensor implanted under the skin on one side of the patient’s abdomen measures the glucose in the fluid between the cells, which corresponds closely to blood glucose levels. The sensor delivers the reading to the smartphone, and the phone’s software calculates a dose of insulin and glucagon every five minutes.
The medicine is then pumped through thin tubes to two tiny infusion points embedded just under the skin on the other side of the patient’s abdomen.
The phone also has an app with which a patient can enter information immediately before eating, indicating whether the meal is breakfast, lunch or dinner, and whether the carbohydrate content will be small, large or typical. The device then calculates and dispenses the proper dosages.
The device still requires a finger stick twice a day to get an accurate blood reading, which the patient enters into the phone.
The developers tested the device over five days in two groups of patients, 20 adults and 32 adolescents, comparing the results with readings obtained with conventional insulin pumps that the participants were using.
The adults in the trial each had the constant attention of a nurse, and they lived in a hotel for the five-day study. Most of the time they were free to travel around and pursue normal activities.
The adolescents, 16 boys and 16 girls, lived under supervision in a summer camp for youths with diabetes.
“We need to do a true home-use study, give people the device and send them home,” said the lead author, Dr. Steven J. Russell, an assistant professor of medicine at Massachusetts General Hospital. “Let them do whatever it is they’re going to do without supervision.”
Several authors of the new report have received payments from medical device companies and hold patents on blood sugar monitoring technology.
The artificial pancreas performed better than the conventional pump on several measures. Among the adolescents, the average number of interventions for hypoglycemia was 0.8 a day with the experimental pump, compared with 1.6 a day with the insulin pumps. Among adults, the device significantly reduced the amount of time that glucose levels fell too low.
And the artificial pancreas worked well at calculating mealtime doses without the patient having to use (often inaccurate) estimates and correct a too high or too low reading after eating.
Much more work needs to be done before the device can be marketed, Dr. Russell said. The senior author, Edward R. Damiano, an associate professor of biomechanical engineering at Boston University, has a 15-year-old son with Type 1 diabetes. He said he was determined to get the new device working and approved in time for his son to go off to college carrying one. ||||| An artificial pancreas developed by Boston researchers shows considerable promise to dramatically change the treatment of type 1 diabetes, potentially enabling 2 million Americans to eat what they want without counting carbohydrates or calculating insulin injections, researchers announced Sunday.
Investigators from Massachusetts General Hospital and Boston University developed the experimental device, which consists of an automated pump that releases the hormones insulin and glucagon and a glucose monitoring system controlled by an iPhone app.
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“We encouraged them to eat whatever they wanted while they wore the bionic pancreas,” said Dr. Steven Russell, an endocrinologist at Massachusetts General Hospital who led the study. “They went on a diabetes vacation, eating ice cream, candy bars, and other things they normally wouldn’t eat — like taking out a new sports car and seeing what it can do.”
In a new study published online in the New England Journal of Medicine, the researchers found that 52 adults and teens who used the mobile system for five days had healthier blood sugar levels compared to when they used standard treatments that required them to check their own blood sugar levels and determine how much insulin to inject via a pump device.
“This is not a cure,” said study coauthor Edward Damiano, an associate professor of biomedical engineering at Boston University who holds a patent on the software that makes the automatic dosing decisions. “It’s taking diabetes management to its ultimate potential and unburdens people with type 1 diabetes from thinking about all the things that go into managing diabetes every day of their lives.”
Damiano, whose 15-year-old son developed type 1 diabetes during his first year of life, said he wakes up two to three times a night to check his son’s blood sugar to prevent it from falling to a dangerously low level, called hypoglycemia, which can cause seizures, a coma, and sometimes even death. Having an automated device, which is expected to become available by 2017 after more testing and upgrades, would save Damiano and other parents from having to wake up in the middle of the night to avoid medical emergencies, he said.
Children with type 1 diabetes are eight times more likely to die from severe hypoglycemia at night — called dead in bed syndrome — than in a car accident.
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Diabetes experts who were not involved in the study cautioned that automated devices need far more rigorous testing to determine if they’ll be safe enough to become widespread.
“Quite a few things need to be addressed,” added Dr. David Harlan, chief of the diabetes division at the UMass Memorial Medical Center in Worcester. “The chances of the pump failing with two difference hormone infusions are great and it doesn’t remove constant diligence from lives of people with diabetes.”
The rate of type 1 diabetes — in which the body’s immune cells attack and destroy a healthy insulin-producing pancreas — has, for unknown reasons, been surging over the past few decades, with nearly 16,000 children under age 18 now diagnosed with the condition every year. (Type 2 diabetes, by comparison, is a more common condition, and tends to occur well into adulthood and has far more explainable causes, such as genetics, obesity, and a lack of exercise.)
In the new study, all of the study participants were closely monitored — adults were accompanied by nurses round-the-clock and the teens were in a summer camp for those with type 1 diabetes — to ensure that their blood sugar levels wouldn’t rise too high or fall too low, which could cause seizures or other complications.
The research found that adult patients with type 1 diabetes who used the experimental device had lower blood sugar levels overall than the control group while also spending 67 percent less time in a state of hypoglycemia.
Children who used the device experienced a 50 percent reduction in carbohydrate use to treat hypoglycemia, though they did not experience a significant difference in their blood sugar measurements. That’s likely because children who participated in the study were closely monitored even when they used their usual treatments, said Russell.
He and his colleagues presented their results Sunday evening at the American Diabetes Association meeting in San Francisco.
“The initial proof of concept is very strong,” said Dr. Guillermo Arreaza-Rubin, a director at the National Institute of Diabetes and Digestive and Kidney Diseases which funded the trial. “Parents of children with type 1 live in permanent fear and maybe this device can free them from that burden and increase the quality of life of those with this disease.”
A few other groups of researchers presented findings on similar automated devices at the diabetes conference, he said, which, like the device developed in Boston, are also about three or four years away from widespread use.
Christopher Herndon, 13, a study participant who tried the bionic pancreas last summer while at Camp Joslin in Charlton, said for the first time in his life he “felt steady the whole day” rather than shaky when his blood sugar levels dropped too low and “really talkative” when it was too high.
Despite using an insulin pump and continuous glucose monitoring device, which many diabetes experts consider to be gold standard therapies, the Newburyport teen said he has never been able to achieve the kind of blood sugar control that he had while using the bionic pancreas.
While his mother, Christina, often wakes him at 2 a.m. to have some juice if his blood sugar drops too low, he was never woken by his counselors at the camp during the five days he used the device.
Mark Lorenz for The Globe Christopher Herndon said he has never been able to achieve the kind of blood sugar control that he had while using the bionic pancreas.
Colby Clarizia, another study participant, said he consumed three blueberry muffins for breakfast while wearing the artificial pancreas and was surprised to see how well the device worked. The 21-year-old from Amesbury also found it easy to use.
“Instead of measuring every carb in a glass of milk or serving of rice, I just had to input whether I was going to eat a large meal or small one,” he said.
Such a device, he added, would make it far easier for him to eat in restaurants where carbohydrate counts aren’t posted on menus.
The bionic pancreas automatically monitors blood sugar using a wireless glucose monitoring system that sends a signal every five minutes to an iPhone adapted with software. The iPhone app determines how much insulin to dispense — to make high blood sugar levels decrease — and how much of the hormone glucagon to dispense to make blood sugar levels rise; it also learns over time how to adjust the release of the two hormones based on input from the monitoring system.
Harlan plans to test the device in conjunction with Russell’s team in a large multicenter study launching this week that will have less rigorous monitoring. Participants will need to stay within an hour’s drive of the study site but won’t need to be accompanied by a health professional wherever they go.
“I think it’s an important step forward, but it’s going to be quite challenging to see whether this device can function safely and effectively without close supervision,” said Dr. Howard Wolpert, director of the institute for technology translation at the Joslin Diabetes Center in Boston, who reviewed the paper before publication. “An analogy I would present is that they climbed a flight of stairs but now the next stage will be like climbing a hill or even a mountain.” |||||
What is a summary? | – While you were using your iPhone to browse Facebook and read Newser, a group of researchers was modifying an iPhone 4S to be used as a portable artificial pancreas—and in a recent trial, the device successfully regulated the blood sugar levels of people with Type 1 diabetes. About a third of people with Type 1 diabetes, which is typically diagnosed in childhood, use an insulin pump to regulate their blood sugar rather than giving themselves insulin injections. But unlike those pumps, the bionic pancreas adjusts both insulin and glucagon, a hormone that works with insulin to regulate blood sugar, automatically, the New York Times reports. It performed better than a regular pump for both adults and adolescents, according to the press release. The device is comprised of more than just the iPhone: The patient has a sensor implanted under the skin near the abdomen, which sends readings of blood glucose levels to the attached phone. The phone then calculates and sends the correct dosage of insulin and glucagon through attached pumps and tubes every five minutes. Patients can also enter information about meals before they eat, and the phone will calculate and deliver the correct dose. Twice-daily finger pricks are still required, with the blood sugar readings entered into the phone. Adult participants had about 37% fewer incidents during which low blood glucose levels required intervention—incidents that can be dangerous in the moment as well as cause health complications down the line—and the device could even allow patients to eat what they want, the Boston Globe notes. (During the trial, participants "went on a diabetes vacation, eating ice cream, candy bars, and other things they normally wouldn’t eat," explains the lead researcher.) It could be available by 2017, but larger trials are the next step. | multi_news_1_0_0 |
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– It's probably a bad sign when investors react to news of your CEO's departure by buying like crazy. Microsoft dropped a bombshell this morning by announcing that Steve Ballmer would retire within 12 months, the AP reports. The company gave no indication of who might succeed the longtime executive, saying only that the board had appointed a special committee to find someone. Word of his departure was enough to send the stock up about 9% in premarket trading. "There is never a perfect time for this type of transition, but now is the right time," Ballmer said in a press release. "My original thoughts on timing would have had my retirement happen in the middle of our company's transformation to a devices and services company. We need a CEO who will be here longer term for this new direction." The move comes about a month after Microsoft released a grisly fourth-quarter report that saw it take a $900 million write-down on its Surface RT tablet.
Let's expand this into a news article: This will appear next to all of your comments
This will NOT appear anywhere on Newser ||||| NEW YORK ( TheStreet ) --shares are surging in pre-market trading, gaining 7.87% to $34.94 on news CEO Steve Ballmer will retire within the next 12 months.
Here is the company press release, announcing the decision:
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– Former mob boss Thomas "Tommy Shots" Gioeli wants $10 million from the federal government over a Ping-Pong injury. Gioeli, once a high-ranking member of the Colombo crime family, is suing over an injury he suffered during a game at the Metropolitan Detention Center in Brooklyn in 2013, according to court papers seen by the New York Daily News. He says he slipped on a wet floor while playing a game and fractured a kneecap. His suit argues that the prison is negligent because employees ignored complaints about a leaky pipe that led to the slippery conditions in the recreation area. The federal government, however, says that even Ping-Pong comes with risks, and Gioeli chose to take them. Gioeli needed surgery and rehab after the fall. The 64-year-old is three years into an 18-year sentence on racketeering charges, though he was acquitted of murder charges that included the 1997 slaying of a New York City police officer. At his sentencing in 2014, his attorney argued unsuccessfully for a light sentence because his client suffered from arthritis, diabetes, and heart disease, and thus probably wouldn't live beyond his early 70s, the New York Times reported. The story also noted that Gioeli had become a colorful fan of Twitter, with tweets such as: "The FBI spends it's limited resources on terminal Italian book-makers while terrorist & cartels flourish." So how did Gioeli wind up in prison? His own cousin ratted him out, reported the New York Post. (The late Anthony Colombo had a specific influence on the Godfather films.)
| Let's expand this into a news article: The mob boss had been at the federal jail in Brooklyn longer than any other inmate: four years awaiting trial and, after his conviction in 2012 on racketeering charges, nearly two more waiting to be sentenced. By the time his sentencing date arrived on Wednesday, the mobster, Thomas Gioeli, had been considered for the death penalty, convicted of conspiring to murder three mobsters and acquitted of killing a police officer; he had multiple angioplasties and, with the help of his family, even became an avid blogger and user of Twitter who taunted prosecutors and two mayors.
The measure of those six years behind bars for Mr. Gioeli — highly unusual for someone who has not yet been sentenced — were central to arguments in Federal District Court in Brooklyn on Wednesday over how much prison time Mr. Gioeli should get: the maximum 20 years, or something less.
One of Mr. Gioeli’s lawyers, Adam D. Perlmutter, said the six years had taken an especially hard toll. “He is now the senior-most person at the M.D.C.,” Mr. Perlmutter said, referring to the Metropolitan Detention Center. He named a host of medical conditions that Mr. Gioeli, 61, is living with, including diabetes, heart disease and arthritis. “People who suffer from chronic health conditions do harder time in prison than people who are healthy,” Mr. Perlmutter said. “A 20-year sentence for Thomas Gioeli is, in fact, a life sentence.”
The judge, Brian M. Cogan, said that with a 20-year sentence, credit for time served and good behavior, Mr. Gioeli would be out by his early 70s. “He’s not going to live to his early 70s?” Judge Cogan asked.
“I don’t think so,” Mr. Perlmutter answered.
A prosecutor, James Gatta, said, “Such time should not count against the sentence that the defendant should receive for his criminal conduct.”
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As the argument unfolded, Mr. Gioeli, who since his conviction last year grew a giant tuft of white hair on his chin, leaned back in his chair, twisting his white mustache, waving warmly and making baby faces at his family in the courtroom. It was odd behavior that would have been more at home at a child’s birthday party than at a sentencing for gangland murders.
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Judge Cogan knocked 16 months off the 20-year maximum and ordered Mr. Gioeli to pay $360,000 in restitution.
At the murder and racketeering trial, prosecutors said Mr. Gioeli, whom they called the former acting boss of the Colombo family, ordered the ambush and murder of an off-duty police officer, Ralph C. Dols, and ordered the killings of several other men in the 1990s. Prosecutors called admitted mob killers to testify against Mr. Gioeli (they described surprise shootings in basements, dissolving dead bodies with lye and burying them on Long Island), but the jury acquitted Mr. Gioeli of many charges, including the murder of Officer Dols. He was found guilty of one count of racketeering for conspiring to kill three mobsters.
The acts that the prosecutors described hardly meshed with Mr. Perlmutter’s portrayal of Mr. Gioeli as a family man, or “Tommy, the person,” as he called him in a long argument that roused sniffles among two or three dozen family members who showed up. “I look at their marriage and I’m jealous,” Mr. Perlmutter said of Mr. Gioeli’s relationship with his wife. It was an image that Mr. Gioeli also put forth on his blog during his years in jail, that of a family man who was wronged by zealous prosecutors.
His Twitter messages and blog posts, which family members posted after he wrote them using his prison email account, espoused a liberal vision of society, coming to the defense of the working poor, speaking out against sexism, when he was not opining on current events.
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Last month, Mr. Gioeli wrote on Twitter, “The FBI arrests old Italians for decades old robberies while allowing bankers to steal billions everyday. TSG #FBI #America #wallstreet,” signing his initials, T.S.G.
Judge Cogan, who said the evidence was overwhelming that Mr. Gioeli was a manager of the crime family and found it was more likely than not he had participated in other murders, said Mr. Gioeli was like many mobsters who are “absolutely schizophrenic in their personalities.” Judge Cogan said, “They go out there and they do things to get people murdered, and at the same time they are wonderful to their families and their communities.”
“They are vicious crimes, and they take a vicious person to do them. I recognize that’s not all there is to Mr. Gioeli.”
Judge Cogan said that Mr. Gioeli’s time served and the “wonderful” way he treated his family were mitigating factors. But he also said: “I haven’t seen any remorse. I’ve just seen self-righteousness.”
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Whether he will live to make it out after more than 18 years in prison, the judge said, “only God knows.”
A Selection of Twitter Messages From Thomas Gioeli ||||| A triple-murder suspect-turned-mob informant whose colorful stories led to the arrest of 39 underworld operators was sentenced to time served Friday — and he was even heralded by the judge for his bravery.
Thomas McLaughlin, 46, was 15 when he taken under the wing of a “bad” relative and nurtured to join the Colombo crime family, according to defense lawyer Stuart Grossman.
After getting pinched for drug trafficking and firearms possession, he went to jail for 16 years without cooperating, earning the trust of his criminal colleagues.
But in 2008 when he was released, the feds came to him and told him he would be charged with conspiracy in planning three mob hits and asked for his cooperation. Facing life in prison, he agreed to help and recorded more than 200 conversations between 2009 to 2011, leading to 39 arrests and two convictions.
He nearly put Sammy “The Bull” Gravano’s record to shame. Gravano helped jail 36 people.
‘I want to apologize for my past… I look forward to the future and continuing to be a husband and father.’ - Thomas McLaughlin
Brooklyn federal court Judge Brian M. Cohan on Friday sentenced him to the 16 years he already served and thanked him for wearing a wiretap for the government. “The number of criminal activities that were able to be prosecuted with Mr. McLaughlin’s cooperation is beyond anything I’ve ever seen… and let’s not forget the risk,” Judge Cohan said.
McLaughlin was also instrumental in the conviction of his own cousin, when he was called to testify at former Colombo boss Tommy “Tommy Shots” Gioeli 2012 trial and fingered his role in a murder.
Grossman called his client “a totally changed man,” and prosecutor Elizabeth Geddes applauded his cooperation with the government calling it “historic.”
Today McLaughlin is a family man with a “hard job. Not the kind of job you’re going to get rich on,” according to the judge, who did not say what his new employment entails.
McLaughlin addressed the court. “I want to apologize for my past, Your Honor,” he said.
“I look forward to the future and continuing to be a husband and father.”
“I’m not skeptical,” Judge Cohan said. “I’m dealing with someone who has not only gone straight but who will stay straight.” ||||| Leave the ping pong paddles, file the lawsuit.
That’s what former Colombo crime boss Thomas (Tommy Shots) Gioeli has done — suing the federal government for $10 million over injuries from a game of prison ping-pong.
The table tennis tumble happened Aug. 29, 2013, while Gioeli was being held at Metropolitan Detention Center in Brooklyn.
More than a year earlier, a Brooklyn Federal Court jury had found him guilty of racketeering conspiracy connected to murder plots.
Mob rat Thomas McLaughlin sentenced to zero jail time
Gioeli, 64, and fellow defendant Dino (Little Dino) Saracino also were accused of carrying out murders, including the killing of a police officer, but acquitted on the murder charges.
According to government court papers, Gioeli argues his slip and fall occurred because of prison officials’ negligence. They knew — or should have known — about the hazardous wet floor in recreation area, pointing to the proximity of showers and an allegedly leaky slop sink pipe.
Thomas (Tommy Shots) Gioeli, Colombo acting boss. (Jesse Ward/for New York Daily News)
The leak was reported to prison employees for days, if not weeks before the accident, Gioeli claims.
The burly Gioeli fractured his right kneecap and had to be hospitalized. The injury required surgery, physical therapy and occupational therapy, court papers obtained by the Daily News show.
Ex-Colombo hitman gets 12 years for murder of NYPD cop Dols
The government rejects any charge of negligence, saying it acted with necessary care at all times. And part of its defense is that there’s some risk that comes with playing table tennis — and Gioeli chose to take that risk.
The case has been assigned to Brooklyn Federal Court Judge Kiyo Matsumoto.
A bench trial is estimated to take about three days, though the case docket shows no trial date yet.
Gioeli is expected to make it up from his low-security North Carolina prison to testify about his spill and subsequent suffering, according to court papers.
Crime boss claims he got solitary for religious scapular
He did not take the stand at his criminal case.
The doctor who examined Gioeli is scheduled to testify about the mafioso’s mishap.
Another person who had been held at the lockup is expected to talk about the floor layout, prisoners tracking in water from the showers, and his complaints about the alleged leak.
The government said it plans to put on witnesses including a Metropolitan Detention Center general foreman.
Gioeli claims he slipped on a wet floor while playing table tennis. He's accusing prison officials of negligence. (wsantina/Getty Images/iStockphoto)
The man is expected to say he searched for records of reported water leaks or repair orders for leaks around the time of the incident, but found none.
Another planned government witness is a correction officer who says he found Gioeli on the wet floor, near the showers.
Gioeli is serving an 18-year prison sentence.
Both Gioeli’s lawyer Martin Schiowitz and the Bureau of Prisons declined comment Monday. ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. ||||| | multi_news_1_0_0 |
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Summarize this article:
If you've fallen asleep at your desk lately, it's no wonder. More than a third of Americans get less than seven hours of sleep each night -- a deficit that could put their health at risk, a new report says.The U.S. Centers for Disease Control and Prevention analyzed sleep surveys of 74,571 adults in 12 states and is offering up its findings in a report released Thursday. In questions about habits within the prior 30 days, almost 38% of respondents said they had fallen asleep by accident and almost 5% said they had nodded off or fallen asleep while driving.Whoa! Let's hope some of this can be attributed to dozing off late at night in front of the TV and not in the middle of the freeway. Take the test yourself with these sleep survey questions For multi-taskers pushing the envelope, it's worth noting that the National Sleep Foundation recommends seven to nine hours of sleep per day for adults and 10 to 11 hours for school-age children. (Parents can stop laughing now.)"Sleep difficulties, some of which are preventable, are associated with chronic diseases, mental disorders, health-risk behaviors, limitations of daily functioning, injury and mortality," says the report, officially named the Morbidity and Mortality Weekly Report.The news coincides (how convenient) with National Sleep Awareness Week from March 7 to 13. And let's hope no one annoyingly asks: "Got sleep?" ||||| Persons using assistive technology might not be able to fully access information in this file. For assistance, please send e-mail to: [email protected]. Type 508 Accommodation and the title of the report in the subject line of e-mail.
Unhealthy Sleep-Related Behaviors --- 12 States, 2009
An estimated 50--70 million adults in the United States have chronic sleep and wakefulness disorders (1). Sleep difficulties, some of which are preventable, are associated with chronic diseases, mental disorders, health-risk behaviors, limitations of daily functioning, injury, and mortality (1,2). The National Sleep Foundation suggests that most adults need 7--9 hours of sleep per night, although individual variations exist. To assess the prevalence and distribution of selected sleep difficulties and behaviors, CDC analyzed data from a new sleep module added to the Behavioral Risk Factor Surveillance System (BRFSS) in 2009. This report summarizes the results of that analysis, which determined that, among 74,571 adult respondents in 12 states, 35.3% reported having <7 hours of sleep on average during a 24-hour period, 48.0% reported snoring, 37.9% reported unintentionally falling asleep during the day at least 1 day in the preceding 30 days, and 4.7% reported nodding off or falling asleep while driving in the preceding 30 days. Continued public health surveillance of sleep quality, duration, behaviors, and disorders is needed to understand and address sleep difficulties and their impact on health. As a first step, a multifaceted approach that includes increased public awareness and education and training in sleep medicine for appropriate health-care professionals is needed; however, broad societal factors, including technology use and work policies, also must be considered.
BRFSS is a state-based, random-digit--dialed telephone survey of the noninstitutionalized U.S. civilian population aged ≥18 years, conducted by state health departments in collaboration with CDC (3). Based on Council of American Survey and Research Organizations (CASRO) guidelines, response rates* for 12 states† that used the optional sleep module in 2009§ ranged from 40.0% (Maryland) to 66.9% (Nebraska). Cooperation rates¶ ranged from 55.5% (California) to 83.9% (Georgia).
The following questions from the sleep module were asked: "On average, how many hours of sleep do you get in a 24-hour period? Think about the time you actually spend sleeping or napping, not just the amount of sleep you think you should get (categorized as <7 hours and ≥7 hours**)." "Do you snore? (can have been told by spouse or someone else; categorized as yes or no)?" "During the past 30 days, for about how many days did you find yourself unintentionally falling asleep during the day (categorized as none or at least 1 day reported)?" and "During the past 30 days, have you ever nodded off or fallen asleep, even just for a brief moment, while driving (categorized as yes or no)?" Age-standardized (to the projected U.S. 2000 population) prevalence estimates were calculated by state and by selected characteristics; 95% confidence intervals were calculated, and statistical significance (at p<0.05) was determined by t-test.
Among respondents, 35.3% reported sleeping <7 hours on average during a 24-hour period (Table). Adults aged ≥65 years were significantly less likely to report sleeping <7 hours (24.5%) than persons in all other age categories. Non-Hispanic blacks (48.3%) and non-Hispanic persons of other races (38.7%) were more likely to report sleeping <7 hours than non-Hispanic whites (34.9%). No significant differences were observed by sex. Compared with employed adults (37.4%), those unable to work (46.4%) were significantly more likely to report <7 hours of sleep, but retired adults (25.0%) and homemakers and students (30.8%) were less likely. Adults with at least some college education (35.8%) were significantly more likely to report <7 hours of sleep than those with less than a high school diploma (32.0%) as were divorced, widowed, or separated (39.1%) and never married adults (37.9%), compared with married adults (35.1%).
Snoring was reported by 48.0% of respondents (Table). Persons aged 18--24 years were least likely (25.6%) to report snoring. Hispanics (50.6%) were more likely to report snoring than non-Hispanic whites (46.8%), as were men (56.5%) compared with women (39.6%). Compared with employed persons (50.5%), retired adults (37.9%) and homemakers/students (37.0%) were significantly less likely to report snoring. Persons with less than a high school diploma (51.2%) and with a high school diploma or General Educational Development certificate (GED) (49.9%) were significantly more likely to report snoring than those with at least some college or a college degree (47.0%), as were married persons (49.5%) compared with never married (43.5%) persons.
An estimated 37.9% of adults reported unintentionally falling asleep during the day at least 1 day in the preceding 30 days (Table). Adults aged 18--24 years (43.7%) and ≥65 years (44.6%) were significantly more likely to report this behavior than all other age groups, as were persons from all other racial/ethnic categories compared with non-Hispanic whites (33.4%). No significant difference was observed by sex. Compared with employed persons (33.5%), those who were unemployed (44.0%), unable to work (57.3%), and homemakers/students (39.3%) were significantly more likely to report unintentionally falling asleep during the day. Persons with at least some college education (35.9%) were significantly less likely to report unintentionally falling asleep than those with a high school diploma or GED (39.6%) or less education (43.4%). Never married adults (42.9%) were significantly more likely to report unintentionally falling asleep during the day than married adults (35.9%).
Nodding off or falling asleep while driving in the preceding 30 days was reported by 4.7% of adults (Table). Persons aged ≥65 years (2.0%) were significantly less likely to report this behavior than persons aged 25--34 years (7.2%), 35--44 years (5.7%), 18--24 years (4.5%), 45--54 years (3.9%), and 55--64 years (3.1%). Hispanics (6.3%), non-Hispanic blacks (6.5%), and non-Hispanics of other races (7.2%) all were significantly more likely to report this behavior than non-Hispanic whites (3.2%). Men were more likely (5.8%) to report this behavior, compared with women (3.5%), and employed persons were more likely (5.4%), compared with homemakers and students (2.2%). No significant differences were observed by educational level or marital status.
Persons who reported sleeping <7 hours on average during a 24-hour period were more likely to report unintentionally falling asleep during the day at least 1 day in the preceding 30 days (46.2% versus 33.2%) and nodding off or falling asleep while driving in the preceding 30 days (7.3% versus 3.0%) (Figure). They also were more likely to report snoring (51.4% versus 46.0%).
Among adults in the 12 states surveyed, reports of <7 hours of sleep ranged from 27.6% in Minnesota to 44.6% in Hawaii. Snoring estimates ranged from 44.8% in California to 54.0% in Hawaii. Estimates of unintentionally falling asleep during the day in the preceding 30 days ranged from 33.0% in Wyoming to 42.8% in Hawaii. Finally, estimates of nodding off or falling asleep while driving in the preceding 30 days ranged from 3.0% in Illinois to 6.4% in Hawaii and Texas.
Reported by
LR McKnight-Eily, PhD, Y Liu, MS, MPH, AG Wheaton, PhD, JB Croft, PhD, GS Perry, DrPH, Div of Adult and Community Health, National Center for Chronic Disease Prevention and Heath Promotion; CA Okoro, MS, T Strine, PhD, Public Health Surveillance Program Office, Office of Surveillance, Epidemiology, and Laboratory Science, CDC.
Editorial Note
This report is the first to present estimates of the prevalence of unhealthy sleep-related behaviors based on responses to questions added to BRFSS in 2009. The results highlight two prevalences of self-reported sleep-related behaviors with potentially dangerous consequences: 37.9% of adults in 12 states reported unintentionally falling asleep during the day at least 1 day in the preceding 30 days, and 4.7% reported nodding off or falling asleep while driving during the same period. The sleep module, consisting of questions derived from surveillance-system and clinically validated sleep surveys, was developed by CDC and the National Sleep Awareness Roundtable†† in response to an Institute of Medicine recommendation to expand surveillance and monitoring of sleep loss and sleep disorders and to increase public awareness of unhealthy sleep behaviors (1).
Nationwide surveillance has not previously assessed the prevalence of either unintentionally falling asleep during the day or nodding off or falling asleep while driving. Drowsy driving, one of the most lethal consequences of inadequate sleep, has been responsible for an estimated 1,550 fatalities and 40,000 nonfatal injuries annually in the United States (4). In the analysis summarized in this report, the prevalence of falling asleep while driving ranged from 2.0% among persons aged ≥65 years to 7.2% among persons aged 25--34 years. Populations previously found at greatest risk included persons aged 16--29 years (particularly males), those with untreated sleep apnea syndrome or narcolepsy, and those who work shifts, particularly night shifts or extended shifts (4). Sleepiness reduces vigilance while driving, slowing reaction time, and leading to deficits in information processing, which can result in crashes (4). Differences among adults in the 12 states in the prevalence of nodding off or falling asleep while driving were substantial (range: 3.0% in Illinois to 6.4% in Hawaii and Texas) and might result from differences in the prevalence of populations at greater risk or differences in the use of safety measures, such as road rumble strips, an evidenced-based intervention that alerts inattentive drivers through vibration and sound.§§
Unintentionally falling asleep during the day can be indicative of narcolepsy or hypersomnia and has been associated with obstructive sleep apnea, which, in turn, has been associated with hypertension, cardiovascular disease, stroke, diabetes, and obesity (1). Falling asleep on the job can result in productivity losses for employers and dismissal for workers. In addition, depending on circumstances and level of responsibility, unintentionally falling asleep during the day can have dangerous consequences (e.g., while child caretaking, lifeguarding, or operating heavy equipment). To assess the potential impact of unintentionally falling asleep during the day, additional inquiry regarding the circumstances of this behavior is required.
Snoring, reported by 48.0% of participating adults, is a symptom of increased upper airway resistance during sleep and generally considered a marker for obstructive sleep apnea (1,5); pregnant women who snore can be at risk for preeclampsia (5). The finding in this report regarding average hours slept per 24-hour period is similar to findings in other reports. In this analysis, 35.3% of U.S. adults in 12 states reported having <7 hours of sleep on average during a 24-hour period, compared with approximately 29% in the 2004--2006 National Health Interview Survey (6), and compared with 37.1% in the 2005--2008 National Health and Nutrition Examination Survey who said they had <7 hours of sleep on workday and weekday nights (7).
Differences in prevalence by sociodemographic characteristics and state were observed for all four sleep-related behaviors. Adults in Hawaii had the highest prevalences for all four behaviors. The reasons for higher prevalences in Hawaii and other variations are unclear and might be subjects for further examination.
The findings in this report are subject to at least three limitations. First, the increase in the number of households with cellular telephones only and the increase in telephone number portability continue to decrease BRFSS response rates, reducing the precision of state estimates and potentially introducing bias. Although in 2009 all states conducted BRFSS surveys for cellular-only households in addition to households with landline telephones, cellular telephone data were not included for the sleep module and other optional modules. Second, institutionalized persons and persons residing in households without landline telephones are not included in the survey, nor are adults from all 50 states and U.S. territories, thereby limiting the generalizability of these findings. Finally, all estimates were based on self-report rather than physiologic measures of sleep behaviors with actigraphy (use of a movement-detection device with software that uses movement patterns to diagnose sleep disorders) (1) or polysomnography.
Substantial increases in the percentage of U.S. adults reporting an average of <7 hours of sleep per 24-hour period were observed from 1985 to 2004¶¶ and can be attributed in part to broad societal changes, including increases in technology use and shift work (1). Sleep disorders are common health concerns that can be evaluated and treated. However, many health-care professionals might have only limited training in somnology and sleep medicine, impeding their ability to recognize, diagnose, and treat sleep disorders or promote sleep health to their patients (1). The results described in this report indicate that a large percentage of adults in 12 states reported unhealthy sleep behaviors that can be related to disease comorbidity (e.g., obstructive sleep apnea and obesity), including nearly one in 20 persons who reported nodding off or falling asleep while driving in the preceding 30 days. Expanded surveillance is needed to understand and address the public health burden of sleep loss and disorders (1) and their associations with health problems and chronic diseases among adults in all 50 states and U.S. territories, which will enable further assessment of state and nationwide trends.
Healthy People 2020 includes a sleep health section, with four objectives: increase the proportion of persons with symptoms of obstructive sleep apnea who seek medical evaluation, reduce the rate of vehicular crashes per 100 million miles traveled that are caused by drowsy driving, increase the proportion of students in grades 9--12 who get sufficient sleep, and increase the proportion of adults who get sufficient sleep.*** Promoting sleep health, including optimal sleep durations, and reducing the prevalence and impact of sleep disorders will require a multifaceted approach. This approach should consider 1) sleep environments (i.e., living conditions and proximity to noise); 2) type, scheduling, and duration of work (8); 3) associated health-risk behaviors such as smoking, physical inactivity, and heavy drinking (1,9); 4) chronic conditions such as obesity and depression and other comorbid mental disorders (1,5); 5) stress and socioeconomic status (8); and 6) validation of new and existing therapeutic technologies (1). Drowsy driving also should be addressed, and additional effective interventions developed and implemented. As a first step, greater public awareness of sleep health and sleeping disorders is needed.
Acknowledgments
The findings in this report are based, in part, on contributions by BRFSS state coordinators in California, Georgia, Hawaii, Illinois, Kansas, Louisiana, Maryland, Minnesota, Nebraska, New York, Texas, and Wyoming; and DP Chapman, PhD, and LR Presley-Cantrell, PhD, Div of Adult and Community Health, National Center for Chronic Disease Prevention and Heath Promotion, CDC.
References
What is already known on this topic? An estimated 50--70 million U.S. adults have chronic sleep and wakefulness disorders, and the percentage who report <7 hours of sleep on average has increased since the 1980s to approximately one third of all U.S. adults. What is added by this report? This report provides the first prevalence estimates from nationwide (12 states) surveillance of unintentionally falling asleep during the day (37.9%) at least 1 day in the preceding 30 days, and nodding off or falling asleep while driving (4.7%) during the same period; in addition, 35.3% reported <7 hours of sleep in a typical 24-hour period. What are the implications for public health? Increased public awareness, expanded surveillance and research, training of health-care professionals, and a multifaceted approach that considers related health, employment, lifestyle, and environmental factors will be needed to improve sleep health among U.S. adults and reduce the prevalence of unhealthy sleep-related behaviors and sleep disorders.
TABLE. Age-specific and age-adjusted* percentage of adults reporting certain sleep-related behaviors, by selected characteristics --- Behavioral Risk Factor Surveillance System, 12 states, 2009 Characteristic No.† Sleeping on average <7 hrs in 24-hr period (n = 74,571) Snoring
(n = 68,462) Unintentionally fell asleep during the day at least 1 day in the preceding 30 days
(n = 74,063) Nodded off or fell asleep while driving in the preceding 30 days
(n = 71,578) % (95% CI) % (95% CI) % (95% CI) % (95% CI) Total 74,571 35.3 (34.5--36.1) 48.0 (47.2--48.8) 37.9 (37.1--38.7) 4.7 (4.2-- 5.1) Age group (yrs) 18--24 2,330 30.9 (27.8--33.9) 25.6 (22.7--28.6) 43.7 (40.4--47.1) 4.5 (3.0--5.9) 25--34 6,637 39.4 (37.3--41.6) 39.6 (37.4--41.8) 36.1 (34.0--38.2) 7.2 (5.8--8.6) 35--44 10,645 39.3 (37.7--41.0) 51.0 (49.2--52.7) 34.0 (32.3--35.6) 5.7 (4.9--6.6) 45--54 15,407 39.0 (37.6--40.5) 59.3 (57.8--60.8) 35.3 (33.8--36.7) 3.9 (3.3--4.6) 55--64 16,385 34.2 (32.7--35.7) 62.4 (60.9--63.9) 36.5 (35.0--38.0) 3.1 (2.4--3.8) ≥65 23,167 24.5 (23.4--25.6) 50.5 (49.2--51.9) 44.6 (43.4--45.9) 2.0 (1.6--2.3) Race/Ethnicity White, non-Hispanic 55,773 34.9 (33.9--35.9) 46.8 (45.9--47.8) 33.4 (32.5--34.4) 3.2 (2.8--3.6) Black, non-Hispanic 5,583 48.3 (45.7--51.0) 48.3 (45.8--50.8) 52.4 (49.7--55.1) 6.5 (5.1--7.9) Hispanic 6,198 33.0 (31.2--34.8) 50.6 (48.8--52.5) 41.9 (40.0--43.8) 6.3 (5.3--7.3) Other, non-Hispanic§ 6,484 38.7 (35.8--41.5) 48.2 (45.4--51.1) 41.0 (38.1--43.9) 7.2 (5.1--9.3) Sex Men 28,330 35.3 (34.2--36.5) 56.5 (55.3--57.8) 38.4 (37.2--39.7) 5.8 (5.1--6.5) Women 46,241 35.2 (34.2--36.2) 39.6 (38.7--40.6) 37.3 (36.3--38.4) 3.5 (3.1--3.9) Employment status Employed 38,814 37.4 (36.2--38.5) 50.5 (49.4--51.6) 33.5 (32.4--34.6) 5.4 (4.8--6.0) Unemployed 3,996 35.1 (32.2--38.0) 50.9 (47.9--54.0) 44.0 (41.0--47.0) 4.6 (3.2--6.0) Retired 20,304 25.0 (16.8--33.2) 37.9 (31.6--44.1) 27.3 (19.7--34.9) ---¶ --- Unable to work 4,001 46.4 (41.2--51.5) 55.8 (50.1--61.4) 57.3 (51.9--62.7) 9.5 (4.4--14.6) Homemaker/Student 7,134 30.8 (28.9--32.8) 37.0 (35.0--39.0) 39.3 (37.3--41.4) 2.2 (1.6-- 2.9) Education level Less than high school diploma or GED 6,393 32.0 (29.8--34.2) 51.2 (48.7--53.7) 43.4 (40.9--45.9) 5.4 (4.2--6.5) High school diploma or GED 20,504 37.0 (35.4--38.6) 49.9 (48.3--51.5) 39.6 (38.1--41.2) 4.0 (3.4--4.7) At least some college 47,426 35.8 (34.8--36.8) 47.0 (46.0--47.9) 35.9 (34.9--36.9) 4.8 (4.2-- 5.4) Marital status Married 42,965 35.1 (33.5--36.6) 49.5 (47.9--51.1) 35.9 (34.3--37.5) 4.3 (3.8--4.8) Divorced/Widowed/Separated 21,199 39.1 (36.5--41.8) 46.4 (43.0--49.9) 39.7 (35.9--43.5) 4.4 (3.3--5.5) Never married 8,590 37.9 (35.9--40.0) 43.5 (41.3--45.7) 42.9 (40.8--45.0) 4.6 (3.5--5.6) Member of unmarried couple 1,638 34.2 (30.2--38.2) 51.6 (47.4--55.8) 39.5 (35.4--43.6) 5.8 (3.5--8.1) State California 11,713 34.5 (33.3--35.8) 44.8 (43.6--46.1) 37.5 (36.3--38.8) 4.9 (4.3--5.5) Georgia 5,387 36.9 (34.5--39.2) 51.0 (48.8--53.1) 39.4 (37.1--41.8) 4.2 (3.2-- 5.2) Hawaii 6,288 44.6 (42.6--46.5) 54.0 (52.0--56.0) 42.8 (40.8--44.7) 6.4 (5.4-- 7.4) Illinois 5,549 36.1 (34.3--37.9) 49.3 (47.4--51.1) 38.6 (36.7--40.4) 3.0 (2.3-- 3.7) Kansas 8,703 30.0 (28.6--31.5) 53.9 (52.3--55.5) 35.4 (33.8--36.9) 3.3 (2.8-- 3.9) Louisiana 8,415 35.8 (34.1--37.5) 53.6 (51.9--55.4) 38.1 (36.4--39.8) 4.0 (3.3-- 4.7) Maryland 3,910 39.9 (37.4--42.4) 48.9 (46.4--51.4) 40.7 (38.1--43.3) 4.6 (3.4-- 5.7) Minnesota 5,519 27.6 (25.7--29.4) 51.6 (49.6--53.6) 33.7 (31.8--35.6) 3.1 (2.4-- 3.7) Nebraska 4,939 30.7 (27.9--33.4) 48.7 (45.6--51.7) 35.0 (32.0--38.1) 3.3 (2.3-- 4.2) New York 3,139 40.7 (38.1--43.2) 50.5 (47.8--53.1) 38.9 (36.4--41.4) 3.9 (2.8-- 5.0) Texas 5,310 34.0 (31.5--36.4) 52.1 (49.6--54.6) 38.6 (36.0--41.1) 6.4 (4.5-- 8.3) Wyoming 5,699 31.6 (29.8--33.5) 52.2 (50.4--54.1) 33.0 (31.1--34.9) 4.0 (3.1-- 4.9) ||||| | – Feeling tired? You're not alone. Some 35% of Americans average less than seven hours of sleep a night, according to a survey of nearly 75,000 adults in 12 states by the CDC. And the stats don't get rosier from there: 38% said they had fallen asleep by accident during the day in the last month, and close to 5% nodded off while driving, reports the LA Times. "Sleep difficulties, some of which are preventable, are associated with chronic diseases, mental disorders, health-risk behaviors, limitations of daily functioning, injury and mortality," says the report. "Drowsy driving, one of the most lethal consequences of inadequate sleep, has been responsible for an estimated 1,550 fatalities and 40,000 nonfatal injuries annually in the United States," wrote the report. The survey also revealed that nearly half of Americans snore; that people who are unable to work are much more likely to get less than 7 hours of sleep compared to employed people; and people who are divorced or single tend to be slightly more likely to get less sleep than their married counterparts. (Luckily, you may not need eight hours of sleep ... in a row.) | multi_news_1_0_0 |
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News article:
Frankie the dog delivers the diagnosis through smelling patients’ urine samples, according to a study conducted by the Arkansas University for Medical Sciences.
A group of researchers in Arkansas have trained a dog to detect thyroid cancer by smelling patients’ urine samples.
The german shepherd-mix named Frankie predicted with 88% accuracy which patients had thyroid cancer and which had a benign disease. The formerly stray pup was rescued from a busy street in Little Rock, Arkansas.
The study is researchers’ first crack at using canines to diagnose thyroid cancer through scent imprinting – a way of training dogs to recognize a particular smell. It follows an earlier study that showed dogs could reliably distinguish between the urine samples of healthy people and those with cancer.
“We’ve all looked at it from a skeptical, scientific standpoint, but the data just keeps leading us to the fact that this has remarkable clinical potential,” said Arny Ferrando, one of the lead researchers, said in a press release from Arkansas University for Medical Sciences, where the study was conducted.
Over six months, researchers at UAMS scent-imprinted Frankie with samples of blood, tissue and urine from patients with cancerous thyroid growths. Frankie was trained to turn away when benign thyroid disease was smelled, and lie down at the scent of metastatic thyroid carcinoma, a common thyroid cancer.
Researchers gave Frankie samples of patients who came to the university clinic with symptoms of thyroid cancer. The results of Frankie’s diagnosis, which was blinded to researchers, was compared with surgical pathologies, according to the study.
Of 34 patients, Frankie accurately predicted the diagnosis 30 times.
“Detecting and diagnosing thyroid cancer can be difficult, because it’s often looking for a very small number of occurrences in a very large background of benign nodules. It is also difficult to say with certainty that a patient is cancer-free after surgery,” said Donald Bodenner, director of the thyroid center at the university and chief of endocrine oncology, in a statement. He was also a lead researcher in the study.
Thyroid cancer is one of the fastest-growing cancer diagnoses worldwide, though the death rate has remained stable for years – leading some to believe that doctors are detecting growths that don’t need treatment. Diagnosis rates have risen especially fast in countries such as South Korea where health officials have started mass screening.
Compared with other cancers in the United States, thyroid cancer has a relatively low death rate. The American Cancer Society predicts that the cancer, which grows in the thyroid gland located in the neck, will result in 1,950 deaths in 2015, most of which (about two out of three) are diagnosed in people younger than 55.
“Having a technique with which to do these things with a higher degree of certainty would be a tremendous advance in thyroid cancer,” he said.
Researchers said they were interested in the future in determining what olfactory elements are present in the samples that allows Frankie to determine which are cancerous. Dogs’ sense of smell is often cited as being up to 100,000 times more acute than that of humans, according to PBS.
The findings were presented at the Endocrine Society’s annual conference Endo.
||||| This horse is completely relaxed. "There is no tension in the mouth and in the chewing muscles," said Dalla Costa. "The nostrils are relaxed." The horse was happy to be chilling out on a pleasant day in an open field.
While perhaps not as uncomfortable as the previous horse, this horse was also photographed while experiencing temporary, minor discomfort. In this case, the horse’s nostrils are wide open, while its lower lip is drawn back. Even its "ears are held passively backward," Dalla Costa said. PHOTOS: World's Ugliest Dog Winner for 2014
This unfortunate horse was photographed while in pain, which, thankfully, turned out to be only temporary. In this moment, however, Dalla Costa noted that the horse's ears are in a sideways position. Its eyes are partially closed, and its "chewing muscles are strained and prominent." Even the horse’s nostrils are stiff over its tightly shut mouth.
Horse expressions, meanwhile, share similar qualities with dogs. This horse, similar to the dogs happily looking at their owners, is attentive and awaiting direction. "The eyes are open and focused on the environment, ears are moving in the direction of sounds, and there is no muscle tension in the mouth," said Dalla Costa. VIDEO: Why Dogs Spin Before They Poop
If this dog could talk, the canine would likely be saying, "Oh, please -- feed me." The photo was snapped as the dog looked longingly at its owner, who was holding a favorite food treat. Dalla Costa explained that there is no visible tension in the dog’s face. Its expression cleverly communicates desire and gentleness, while also revealing a sense of hopeful expectation.
Every aspect of this dog’s face communicates concern and worry. "The mouth is opened and the dog is panting," Dalla Costa said. "The dog’s lips are partly drawn back, with no teeth exposure. The facial muscles show some degree of tension, visible through ridges that emerge on the lateral side of the face and near the eyes." His ears are up, yet not fully open, an indication that he’s attentive but also worried. VIDEO: Dogs Have Feelings, Too
This dog's gaze is riveted on its owner, who is holding food. "This emotional condition is considered positive, and we can assume that this dog is happy," said Dalla Costa, adding that "there is no visible tension in the facial muscles." Even though the eyes, ears and face are pointed in one direction, just as they were for the worried and lonely dog in the previous slide, this hopeful canine feels no anxiety. Dogs Know When You're Sad
This poor pooch "is tense, due to the departure of his owner," Dalla Costa said. Every part of the dog's face is turned in the direction of his owner's recent exit, maximizing the pup's ability to find him. The dog's eyes and tense mouth convey his worry and loneliness. The Dog Paddle Is Just an Underwater Jog
Here is another happy dog. In this case, Dalla Costa explained, the dog's "lips are retracted, but with no exposure of the teeth." The dog is thrilled that its owner has just returned and eagerly looks to the human for guidance. Dogs Were a Prehistoric Woman's Best Friend, Too
Facial expressions among social animals appear to have universal qualities, to the point where humans and other animals can discern how certain species feel just by looking at their faces. That's the suggestion in two new studies -- published in the Journal of Veterinary Behavior and PLOS ONE -- that help explain how humans can have such close, understanding relationships with animals such as dogs and horses, the subjects of the investigations. The research confirmed, through animal behavioral analysis, the underlying meaning of dog and horse facial expressions and also demonstrated that people have a natural knack for figuring out what they mean. For example, "this dog is experiencing a positive emotional state, as his owner has just come back," Emanuela Dalla Costa told Discovery News. She led both studies and is a researcher in the Department of Veterinary Science and Public Health at the Università degli Studi di Milano. She explained that the dog’s eyes are wide open, as is his mouth, yet his facial muscles are somewhat tense. Together, these features and others suggest that he is happy, eager and hopeful. Why Dogs Find Some Toys Boring
What Your Dog (or Horse) Is Trying to Tell You: Photos
A rescued male German shepherd-mix named Frankie (not shown here) recognized the smell of cancer in thyroid tissue obtained from multiple patients.
A scent-trained dog was able to identify the presence or absence of thyroid cancer in human urine samples 88.2 percent of the time, a new study concluded.
The study out of the University of Arkansas for Medical Sciences (UAMS) gathered urine samples from 34 university thyroid clinic patients before they underwent a biopsy for suspicion of thyroid cancer.
Fifteen of those biopsies came back positive for thyroid cancer, while the remaining 19 were diagnosed as benign thyroid disease.
Enter Frankie, a male German shepherd mix that had been trained to recognize the scent of cancer in thyroid tissue. Frankie's sharp nose matched 30 out of 34 samples with their pathology diagnoses.
"Frankie is the first dog trained to differentiate benign thyroid disease from thyroid cancer by smelling a person’s urine," said study co-author Arny Ferrando, PhD at UAMS, in a release.
The study's senior investigator, Donald Bodenner, M.D., PhD, and chief of endocrine oncology at UAMS, said Frankie was only slightly less accurate than a standard thyroid biopsy with a needle. The dog's results offer the possibility of a cheaper, less invasive approach to diagnosis of the illness.
"Current diagnostic procedures for thyroid cancer often yield uncertain results, leading to recurrent medical procedures and a large number of thyroid surgeries performed unnecessarily," Bodenner explained. "Scent-trained canines could be used by physicians to detect the presence of thyroid cancer at an early stage and to avoid surgery when unwarranted."
Bodenner is not yet using canines in formal diagnoses outside of the study and said the next step will be to collaborate with Auburn University's College of Veterinary Medicine on an expansion of the scent-training program. The veterinary center plans to train two of its bomb-sniffing dogs to learn how to sniff out thyroid cancer, using samples from UAMS patients. ||||| Researchers are looking to create a breakthrough method of detecting ovarian cancer - by using dogs to sniff out the disease.
A group of researchers collaborated to investigate using canine olfaction and chemical and nanotechnology analysis as a means of detecting early-stage ovarian cancer.
The collaboration was between the Working Dog Center of the University of Pennsylvania School of Veterinary Medicine, the physics and astronomy department of Penn's School of Arts and Science, Penn's Gynecologic Oncology division and the Monell Chemical Senses Center.
Physicians currently use the senses of light, sound and touch to help diagnose ovarian cancer in women. But the researchers say the sense of smell will now play an important part.
Volatile organic compounds (VOC) - or odorants, are altered in the early stages of ovarian cancer. The researchers say that previous studies have shown that trained detection dogs, alongside specific electronic devices, are able to detect minute quantities of odorants.
Patients from Penn Medicine, with and without ovarian cancer, have donated tissue and blood samples to the Working Dog Center to assist in their research.
Dr. Cynthia Otto hopes to develop a new system of screening ovarian cancer using the dogs' enhanced sense of smell.
The project is already under way, with three dogs being trained to sniff out the odorants that indicate a woman has ovarian cancer:
A springer spaniel called McBaine
A labrador retriever called called Ohlin, and
Tsunami - a German shepherd.
George Preti, an analytical chemist at the Monell center and adjunct professor in Penn Medicine's Department of Dermatology, says:
"Prior to the advent of modern quantitative clinical testing, physicians used olfaction to help with disease diagnosis. In this research, we are reaching back to move forward by using sensitive biological and analytical sensors to detect ovarian cancer's odorous signature."
Ovarian cancer accounts for around 3% of all cancers in women, and mainly develops in older women aged over 63. According to the American Cancer Society, 22,240 women in the US will receive a new diagnosis of ovarian cancer this year, and 14,230 women will die from the disease.
The researchers say that an effective screening strategy does not currently exist for the detection of ovarian cancer. Any advancement in diagnosis of ovarian cancer could have an important impact on overall survival from the disease.
Researchers at the Working Dog Center have begun training three dogs to sniff out odorants that indicate the presence of ovarian cancer.
Cynthia Otto, director of the Working Dog Center, says:
"These odorants remain a relatively untapped source for cancer detection information.
By utilizing the acute sense of smell in detection dogs in conjunction with chemical and nanotechnology methods, we hope to develop a new system of screening for ovarian cancer using analysis of odorants to facilitate early detection and help decrease future cancer deaths."
The researchers add that future studies will look at determining the most suitable tissue for evaluation, and measuring odor differences among various tumor grades.
Written by Honor Whiteman ||||| share
Inquiry: AN OCCASIONAL COLUMN
Dogs' Dazzling Sense of Smell
By Peter Tyson
Posted 10.04.12
NOVA scienceNOW
What lies behind their exceptional gift of sniff?
They haven't got no noses,
The fallen sons of Eve;
Even the smell of roses
Is not what they supposes;
But more than mind discloses
And more than men believe.
—from "The Song of the Quoodle," G.K. Chesterton
My dog Jones used to do the most curious thing whenever my friend Burk visited my house. Jones was a mutt from the pound, so before we adopted him he might have picked up some unsavory habits. But he'd sidle over to Burk, rub up against him, and start to lift his leg on him.
Your average dog's nose is tens of thousands of times as sensitive to odors as yours. What accounts for this stunning piece of machinery? Enlarge Photo credit: © Image Source/Corbis
Jones, a greyhound-black lab mix who, bless his big heart, passed on at age 15 a few years ago, never did that with any other visitor. Burk didn't smell or wear stinky clothes, and he didn't antagonize or otherwise provoke Jones. Burk did have a dog of his own, a redbone coonhound named Hattie, but other visitors had dogs. In short, he shouldn't have stood out in any way from anyone else. But to Jones, Burk was like a fresh wall to a graffiti artist.
Why? For me, Jones's behavior—which even a dog-cognition expert acknowledged was unusual—epitomizes the mystery that is dogs' sense of smell. What lies behind this astonishing capability of theirs, one that makes the world not a visual one as it is to us but a richly odoriferous one? How do their noses differ from ours, and what do their brains do differently? Finally, is there an answer to why Jones tried to pee on Burk every time he set foot in my place?
Olympic sniffers
Dogs' sense of smell overpowers our own by orders of magnitude—it's 10,000 to 100,000 times as acute, scientists say. "Let's suppose they're just 10,000 times better," says James Walker, former director of the Sensory Research Institute at Florida State University, who, with several colleagues, came up with that jaw-dropping estimate during a rigorously designed, oft-cited study. "If you make the analogy to vision, what you and I can see at a third of a mile, a dog could see more than 3,000 miles away and still see as well."
Figure 1: When a dog breathes in, the air separates into distinct paths, one (red) flowing into the olfactory area and the other (blue) passing through the pharynx (black) to the lungs. Enlarge Photo credit: © Courtesy of Brent Craven
Put another way, dogs can detect some odors in parts per trillion. What does that mean in terms we might understand? Well, in her book Inside of a Dog, Alexandra Horowitz, a dog-cognition researcher at Barnard College, writes that while we might notice if our coffee has had a teaspoon of sugar added to it, a dog could detect a teaspoon of sugar in a million gallons of water, or two Olympic-sized pools worth. Another dog scientist likened their ability to catching a whiff of one rotten apple in two million barrels.
"I find it really astonishing that they're able to detect such minute odor discriminations."
Experts have reported incredible true stories about the acuteness of dogs' sense of smell. There's the drug-sniffing dog that "found" a plastic container packed with 35 pounds of marijuana submerged in gasoline within a gas tank. There's the black lab stray from the streets of Seattle that can detect floating orca scat from up to a mile away across the choppy waters of Puget Sound. There's the cancer-sniffing dog that "insisted" on melanoma in a spot on a patient's skin that doctors had already pronounced cancer-free; a subsequent biopsy confirmed melanoma in a small fraction of the cells. And so on.
A nose for odors
What do dogs have that we don't? For one thing, they possess up to 300 million olfactory receptors in their noses, compared to about six million in us. And the part of a dog's brain that is devoted to analyzing smells is, proportionally speaking, 40 times greater than ours.
Dogs' noses also function quite differently than our own. When we inhale, we smell and breathe through the same airways within our nose. When dogs inhale, a fold of tissue just inside their nostril helps to separate these two functions. "We found that when airflow enters the nose it splits into two different flow paths, one for olfaction and one for respiration," says Brent Craven, a bioengineer at Pennsylvania State University who modeled airflow and odor transport using high-resolution MRI scans of a lab cadaver's nose (see Figure 1). Craven and colleagues are working to reverse-engineer the canine nose, in part to aid in the design of artificial "noses" that can sniff out odors as well as man's best friend can.
Figure 2: In the rear of a dog's nose lies the olfactory region (yellowish-brown), with its scroll-like tissues bristling with smell receptors. Respiratory regions appear in pink. Enlarge Photo credit: © Courtesy of Brent Craven
In us humans, the sense of smell is relegated to a small region on the roof of our nasal cavity, along the main airflow path. So the air we smell just goes in and out with the air we breathe. In dogs, about 12 percent of the inspired air, Craven's team found, detours into a recessed area in the back of the nose that is dedicated to olfaction, while the rest of the incoming air sweeps past that nook and disappears down through the pharynx to the lungs. Within the recessed area, the odor-laden air filters through a labyrinth of scroll-like bony structures called turbinates (see Figure 2). Like a whale's baleen sifting out krill, the turbinates sieve odor molecules based on different chemical properties. Olfactory receptors within the tissue that lines the turbinates, in turn, "recognize" these odor molecules by their shape and dispatch electrical signals to the brain for analysis.
Exit strategy
When we exhale through our nose, we send the spent air out the way it came in, forcing out any incoming odors. When dogs exhale, the spent air exits through the slits in the sides of their noses. The manner in which the exhaled air swirls out actually helps usher new odors into the dog's nose. More importantly, it allows dogs to sniff more or less continuously. In a study done at the University of Oslo in Norway, a hunting dog holding its head high into the wind while in search of game sniffed in a continuous stream of air for up to 40 seconds, spanning at least 30 respiratory cycles.
"It is a really big issue as to how in the heck dogs are doing it."
We can't wiggle our nostrils independently. Dogs can. This, along with the fact that the so-called aerodynamic reach of each of their nostrils is smaller than the distance between the nostrils (see Figure 3), helps them to determine which nostril an odor arrived in. This aids them in locating the source of smells—we've all seen dogs on an interesting scent weave back and forth across its invisible trail.
A second olfactory system
On top of all this, dogs have a second olfactory capability that we don't have, made possible by an organ we don't possess: the vomeronasal organ, also known as Jacobson's organ. Located in the bottom of a dog's nasal passage, Jacobson's organ picks up pheromones, the chemicals unique to each animal species that advertise mating readiness and other sex-related details.
Figure 3: When a dog breathes in (far left), it can tell which nostril an odor arrived in because each nostril's "aerodynamic reach" (blue) is so small. When a dog breathes out (near left), the expired air blows out the side slits in such a way as to augment the sampling of new odors. Enlarge Photo credit: © Courtesy of Brent Craven
The pheromone molecules that the organ detects—and their analysis by the brain—do not get mixed up with odor molecules or their analysis, because the organ has its own nerves leading to a part of the brain devoted entirely to interpreting its signals. It's as if Jacobson's organ had its own dedicated computer server.
Track masters
If dog's basic smelling skills amaze us, what they manage to achieve with those skills is truly astounding.
Take tracking, for example. Deborah Wells and Peter Hepper of the Animal Behaviour Centre at Queen's University Belfast, in Northern Ireland, showed in one study that dogs brought in at right angles to a trail recently walked by a person could determine the direction that person took from as few as five steps. In other words, the first step in the direction the person walked has a little less odor than subsequent steps, because its odor molecules have begun to diffuse into the air. "I find it really astonishing, kind of mind-boggling, that they're able to detect such minute odor discriminations," Horowitz says.
Scent-tracking dogs take such tracking to the extreme, routinely accomplishing remarkable feats in unfamiliar environments and on the trail of unfamiliar people such as missing persons. "It is a really big issue as to how in the heck dogs are doing it, that is, how they are tracking a so-called gradient," Walker says. "They're able to come to a branch point in the woods and say, 'Okay, I think little Sally ran this way. Something happened, and I need to make a decision.' That's pretty amazing if you think about it from an engineering standpoint, because little Sally's odors aren't the only thing there. There's changing wind, changing humidity. There are other odors—a deer defecated over here, and over here there's some urine from a rabbit. And somehow that dog is able to say, 'Yeah, but I'm focusing on little Sally.'"
As it moves along the ground, the bloodhound's giant, flappy ears help fan up odors to its nose, one reason the breed is the superstar of scent-tracking. Enlarge Photo credit: © Luis Santana/iStockphoto
Open questions
Such mysteries are the spice for dog researchers. In a 2003 study, for instance, Wells and Hepper found that dogs led at right angles to a human-laid trail one hour after the trail was walked identified the correct direction of those trails that had been laid from left to right more frequently than those laid from right to left.
"The dog has distinguished you."
"This was an interesting result, and I'm not too sure what is going on here," Wells told me in an email. "It is possibly related to lateral bias—we know that dogs show strong motor preferences, with male dogs using their left paws more than female dogs, who, by contrast, tend to use their right paws more." Some studies on other species show that lateral biases can extend to the olfactory system, she says, and further research is in order with dogs.
A marked man
And what of Jones and my friend Burk? When I told Horowitz about my dog's behavior—which always caught me and Burk equally off guard—and I asked why Jones might have done it, she laughed and said, "I cannot tell you. There are some places my science does not go." She could theorize, she said: Dogs mark with urine at places they think a lot of other dogs are going to smell, or maybe because there's something desirable or interesting about that place. Perhaps Burk already smelled pretty fragrantly of something else, she offered.
Regardless of why, I said, Burk should have felt honored by such treatment, right? Horowitz laughed again. "He certainly shouldn't have seen it as an insult," she said. "The dog has distinguished you."
Peter Tyson is former editor in chief of NOVA Online. ||||| Image copyright AM Hinson Image caption Dogs have 10 times the number of smell receptors as people
A dog has been used to sniff out thyroid cancer in people who had not yet been diagnosed, US researchers say.
Tests on 34 patients showed an 88% success rate in finding tumours.
The team, presenting their findings at the annual meeting of the Endocrine Society, said the animal had an "unbelievable" sense of smell.
Cancer Research UK said using dogs would be impractical, but discovering the chemicals the dogs can smell could lead to new tests.
The thyroid is a gland in the neck that produces hormones to regulate metabolism.
Thyroid tumours are relatively rare and are normally diagnosed by testing hormone levels in the blood and by using a needle to extract cells for testing.
Smelly job
Cancers are defective, out-of-control cells. They have their own unique chemistry and release "volatile organic compounds" into the body.
The canine approach relies on dogs having 10 times the number of smell receptors as people and being able to pick out the unique smells being released by cancers.
The man's best friend approach has already produced promising results in patients with bowel and lung cancers.
A team at the University of Arkansas for Medical Sciences (UAMS) had previously showed that a dog could be trained to smell the difference between urine samples of patients with and without thyroid cancer.
Image copyright AM Hinson Image caption Frankie gave the correct diagnosis in 30 out of 34 cases
The next step was to see if it could be used as a diagnostic test.
Frankie the German Shepherd was trained to lie down when he could smell thyroid cancer in a sample and turn away if the urine was clean.
Thirty-four patients, who were going to hospital for conventional testing, took part in the trial.
Frankie gave the correct diagnosis in 30 out of 34 cases. There were two false positives and two patients who would have been incorrectly given the all-clear.
Dr Donald Bodenner, the chief of endocrine oncology at UAMS, said: "The capability of dogs to smell minute amounts is unbelievable.
"The medical community over the next few years is going to have a great appreciation [for them].
E-nose
Some researchers are trying to strip out the canine-element and test for the unique pong of cancer with an "electronic nose".
This approach is also being trailed outside of cancer and has been used to find dangerous infections such as Clostridium difficile.
Dr Bodenner added: "We would like to know what Frankie is smelling, nobody knows."
Commenting on the findings Dr Jason Wexler, an endocrinologist in Washington, DC, argued: "This is a fascinating, interesting study and it has high potential in areas of the world that may not have access to biopsy techniques.
"There are many patients who are reluctant to undergo fine needle aspiration so I think that if you could design a technique where you have no invasive procedure that can have tremendous widespread appeal."
But Dr Emma Smith, from Cancer Research UK, cautioned: "Although there's some evidence that some trained dogs can sniff out the smelly molecules given off by cancers, there have been mixed results on how accurate they are and it's not really practical to think about using dogs on a wide scale to detect the disease.
"But carrying out lab tests to understand what the dogs are smelling might help to inform the development of 'electronic noses' to detect the same molecules, which could lead to better diagnostic tests in the future."
Dr Bodenner says it is an approach that he is actively pursuing.
Meanwhile, the lab is also trying to find a new home for canine-veterans from Iraq and Afghanistan.
Instead of sniffing out bombs, they will be trained to hunt for cancer.
Symptoms of thyroid cancer
A painless lump or swelling at the front of the neck below the Adam's apple
Unexplained hoarseness that doesn't get better after a few weeks
Sore throat or difficulty swallowing that doesn't get better
Pain in the neck
Source: NHS Choices ||||| Dogs are often referred to as "man's best friend," and a new study brings further strength to this term after revealing how a rescue dog called Frankie was able to detect the presence of thyroid cancer in human urine samples with almost 90% accuracy.
The study reveals that Frankie - a male German Shepherd-mix - correctly identified the thyroid cancer status of 30 out of 34 human urine samples. The study reveals that Frankie - a male German Shepherd-mix - correctly identified the thyroid cancer status of 30 out of 34 human urine samples.
According to the research team, from the University of Arkansas for Medical Sciences (UAMS) in Little Rock, Frankie - a male German Shepherd-mix - is the first dog that has been trained to differentiate benign thyroid disease and thyroid cancer by sniffing human urine samples.
Thyroid cancer is a cancer that begins in the thyroid gland, situated just below the thyroid cartilage in the front of the neck. Approximately 62,450 new cases of thyroid cancer will be diagnosed in the US this year, and around 1,950 Americans will die from the disease.
Unlike most other cancers, thyroid cancer is more common among younger adults, with almost 2 in 3 cases diagnosed in people under the age of 55.
Diagnostic techniques for thyroid cancer include fine-needle aspiration biopsy, which involves the patient having a thin needle inserted into the thyroid gland in order to obtain a tissue sample.
Senior investigator Dr. Donald Bodenner, chief of endocrine oncology at UAMS, says the diagnostic accuracy of canine scent detection is almost on par with that of fine-needle aspiration biopsy, but it would be an inexpensive and noninvasive alternative.
What is more, he notes many current methods for diagnosing thyroid cancer can be inaccurate, causing some patients to undergo needless surgery.
"Scent-trained canines could be used by physicians to detect the presence of thyroid cancer at an early stage and to avoid surgery when unwarranted," he adds.
Frankie trained to sniff out cancer in human urine samples
For their study, recently presented at The Endocrine Society's 97th Annual Meeting in San Diego, CA, Dr. Bodenner and colleagues obtained urine samples from 34 patients who attended the UAMS thyroid clinic.
All patients showed abnormalities in their thyroid nodules and went on to have biopsies and diagnostic surgery. Thyroid cancer was identified in 15 patients while 19 had benign thyroid disease.
Frankie - who the researchers say had been previously trained to recognize the smell of cancer in human thyroid tissue - was presented with the urine samples to sniff one at a time by a gloved dog handler.
While humans have around 5 million smell receptors, or olfactory cells, dogs possess around 200 million, making their sense of smell around a thousand times stronger than that of humans.
Frankie alerted the handler to a cancer-positive urine sample by lying down, while turning away from the urine sample alerted the handler to a benign status.
The authors note that the cancer status of each urine sample was unknown to both the dog handler and the study coordinator.
The handler also presented Frankie with urine samples with a known cancer status in between the study samples so the dog could be rewarded for achieving a correct answer.
30 out of 34 samples correctly identified with canine scent detection
On comparing Frankie's results with those of the final surgical pathology report for the samples, the team found the dog correctly identified the status of 30 out of 34 samples.
The sensitivity, or true-positive rate, of the canine scent detection came in at 86.7%, while specificity, or true-negative rate, was 89.5%. This means Frankie correctly identified a benign sample almost 9 in every 10 times.
The team notes that canine scent detection led to two false-negative and two false-positive results. The researchers now plan to expand their research by teaming up with Auburn University College of Veterinary Medicine, AL, who have agreed to assign two of its bomb-sniffing dogs to thyroid cancer detection training.
This is not the first time Medical News Today have reported on the cancer-detection talent of dogs. In May 2014, a study by Italian researchers revealed how specially trained dogs were able to detect prostate cancer in urine samples with 98% accuracy.
And in August 2013, MNT reported on a US study in which researchers detailed how three dogs are being trained to detect ovarian cancer. ||||| It is estimated that 233,000 men in the US will be diagnosed with prostate cancer this year. Although current screening methods for the disease - such as digital rectal exams - aid early detection, they are not always accurate. But with the help of "man's best friend," a new screening technique could be in the cards.
A new study from Italian researchers, presented at the 109th Annual Scientific Meeting of the American Urological Association in Orlando, FL, found that specially trained dogs were able to detect prostate cancer from urine samples with 98% accuracy.
There is no denying a dog's extraordinary sense of smell. While we have around 5 million olfactory cells in our noses - receptors that detect different odors - dogs have approximately 200 million. It is dogs' acute ability to trace scents that has made them so attractive to the medical world.
In November last year, a spotlight feature from Medical News Today delved into the world of medical detection dogs. The feature looked at how the animals can help alert a diabetic owner to high or low blood sugar levels through being trained to detect a specific scent in their breath or sweat.
The feature also explored how dogs are now being used for detection of various cancers. One study revealed that trained detection dogs were able to detect ovarian cancer in tissue and blood samples through sniffing out volatile organic compounds (VOCs). A 2011 study, conducted by researchers at UK charity Medical Detection Dogs, found that such compounds could also be biomarkers of bladder cancer.
The authors of this latest research note that in 2010, a study demonstrated that specially trained dogs were able to smell VOCs released into urine from prostate cancer tumors. But this study only involved 33 patients. Therefore, the Italian research team set out to determine dogs' detection accuracy in a larger sample.
A 'promising approach' to cancer detection
For their study, the team wanted to see whether two highly trained dogs were able to detect prostate cancer-specific VOCs in the urine samples of 677 participants. Of these, 320 had prostate cancer ranging from low-risk to metastatic and 357 were healthy controls.
Researchers found that two highly trained dogs were able to detect prostate cancer in urine samples with a combined 98% accuracy. Researchers found that two highly trained dogs were able to detect prostate cancer in urine samples with a combined 98% accuracy.
All testing was carried out in an environment that was free of olfactory disturbance, according to the team.
They found that the dogs were able to detect prostate cancer-specific VOCs in the urine samples with a combined accuracy of 98%. Sensitivity to the compounds was 99% accurate, while specificity was 97% accurate.
The first dog's overall accuracy for detecting VOCs was 99%, while sensitivity was 100% and specificity was 98%. The second dog was able to detect VOCs with 97% accuracy, while sensitivity was 99% accurate and specificity was 96% accurate.
Dr. Brian Stork, a urologist as West Shore Urology in Muskegon and Grand Haven, MI, who was not involved in the study but conducted the presentation, comments:
"These data show analysis of volatile organic compounds in urine is a promising approach to cancer detection. The possibility of using dogs to identify cancer is something most would never have considered possible a decade or two ago. It's an interesting concept that 'man's best friend' could help save your life."
It is not only dogs' intricate sense of smell that has caught the interest of medical researchers. Earlier this year, Medical News Today reported on a study revealing that dogs could provide new insight into Chiari malformation in humans - a condition that occurs when the lower parts of the brain are pushed down toward the spinal cord.
Other research published in Genome Biology found that dogs could serve as a model for obsessive compulsive disorder (OCD) in humans. |||||
What is a shorter version of the above article? | – Scientists seeking a quick and affordable way to detect thyroid cancer have trained a dog to smell it on people, with really good results. In a US study, a German shepherd mix named Frankie detected thyroid cancer (or lack thereof) in urine samples with nearly 90% accuracy, Medical News Today reports. Trained to lie down if he smelled cancer and turn away if he didn't, Frankie got it right 30 out of 34 times in patients who'd already undergone biopsies and diagnostic surgery for abnormal thyroid nodules. The study's top investigator, Donald Bodenner, tells Discovery that Frankie was nearly as accurate as thyroid biopsies done with a needle. He's also cheaper and less annoying. "We would like to know what Frankie is smelling, [but] nobody knows," Bodenner tells the BBC. His research team now plans to work with veterinarians in training two other dogs who already sniff bombs to detect thyroid cancer. Researchers also want to figure out what the dogs are smelling and possibly design "electronic noses" to do the job. All this would help people avoid invasive diagnostic procedures that "often yield uncertain results," Bodenner says, which lead to "a large number of thyroid surgeries performed unnecessarily." Meanwhile, thyroid cancer is spiking worldwide as the death rate remains stable, meaning doctors may be spotting thyroid growths that don't need treatment, the Guardian reports. Bodenner's dog-sniffing approach has worked before—with ovarian and prostate cancer—because, as PBS notes, a dog's sense of smell is up to 100,000 times better than ours. (But like other animals, their short-term memory stinks.) | multi_news_1_0_0 |
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– Science may be closer to figuring out why some people live so darn long. Researchers studying 1,800 people over the age of 100 and another 5,400 over the age of 90 discovered four genes linked to their longevity, Live Science reports. "There's a reasonably strong genetic component to becoming a centenarian, and we want to find out what that is," researcher Stuart Kim says. "We're beginning to unravel the mystery." Kim's study—published in PLOS Genetics—identified genes related to blood type, cell division, and Alzheimer's, as well as one known to make fruit flies live longer, that were either more or less common in the extremely old. In short, centenarians seem to have fewer genes connected to major diseases, according to Time. “It seems intuitively obvious that avoiding disease is part of the strategy of becoming a centenarian,” Time quotes Kim as saying. But he notes that conclusion goes against "really strong dogma in the field." Most researchers tend to believe undiscovered anti-aging genes are responsible, but Kim posits it could be much simpler: Centenarians may just get fewer diseases. According to Live Science, one of the four genes causes type O blood, which is known to be negatively associated with heart disease and cancer. Another of the genes is related to whether organ transplants are rejected or accepted, Time reports. According to Live Science, researchers hope further studies will turn up even more genetic similarities in centenarians. (This study says young blood can reverse the aging process.)
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If you live to be 100, you’re in a special group, one that longevity scientists are eagerly studying for clues to battling aging. But are these centenarians long-lived because they don’t get the diseases that fell the rest of us—heart problems, diabetes, dementia, arthritis and more—or because they are protected somehow against the effects of aging? Based on the data so far, most experts have concluded that centenarians get to where they are because they have some anti-aging secret that shields them against the effects of aging. That’s because studies found that centenarians had just as many genes that contribute to disease as those with more average life spans.
MORE: The Cure for Aging
But in a paper published in PLOS Genetics, researchers led by Stuart Kim, professor of developmental biology and genetics at Stanford University, questions that dogma. He found that on the contrary, centenarians may have fewer of the genes that contribute to major chronic diseases. That doesn’t mean that people who live to their 100s also don’t possess some protective anti-aging genes as well, but Kim’s study shows that they don’t experience as much disease as people who are shorter-lived.
Kim’s team came to that conclusion after conducting a novel type of genetic analysis. Most attempts to look for genes related to aging compare the genomes of centenarians and people with average life spans and pick out the regions where the maps differ. Those are potential targets for aging, but, as Kim notes, they could also be red herrings. “Because you search through hundreds of thousands, and now millions of variants, there is a lot of noise. So it makes it difficult to see the signal amidst all the noise.”
MORE: How to Live Longer
To purify the signal, Kim layered another piece of information on this comparison. He made the assumption that disease genes can reduce the chances of someone reaching their 100s, and focused just on known disease-causing genes in his analysis. “With that, we can make better guesses about what is really bad for becoming a centenarian,” he says.
The filtered analysis pumped out five major regions of interest for longevity. Four are familiar; they involve the gene connected to Alzheimer’s, an area involved with heart disease, the genes responsible for the A-B-O blood type and the immune system’s HLA region that needs to be matched for organ transplants to avoid rejection. These four have known connections to longevity. The Alzheimer’s gene, ApoE, for example, is linked to shorter life span, while the heart disease variants are involved in directing a cell’s life span and the O blood type is known to be connected to better health outcomes and survival.
MORE: How to Live 100 Years
The fifth region was one that had never been linked to longevity before, and Kim admits that not much is known about how it might contribute to longer life, except that mutations in the gene region can contribute to neurological diseases such as ALS and that in fruit flies, other mutations help the insects to live longer.
“It seems intuitively obvious, that avoiding disease is part of the strategy of becoming a centenarian,” says Kim. “But there is a really, really strong dogma in the field that there was no depletion of disease genes in centenarians, and that all of their survival benefit was coming from protection from anti-aging genes. I think they were wrong.”
Those previous studies that pointed to this anti-aging effect over the effect of fewer disease-causing genes were generally smaller, and might not have isolated the signal from the noise.
Kim’s team shows that the way centenarians reach their second century may involve more than just being blessed with anti-aging genes. “We found that, at least in part, they live longer because they don’t get sick,” he says. He also readily admits that they may also benefit from some anti-aging factor that researchers haven’t uncovered—yet. ||||| Several new genes linked to an exceptionally long life have been discovered, according to a new study that examined the genomes of people living into their 100s, known as centenarians.
Using a new method, the researchers found four genes linked with a very long life: A gene called ABO, which is involved in determining blood type; a gene called CDKN2B, which regulates cell division; a gene called APOE, which is linked with Alzheimer's disease; and a gene called SH2B3, which was previously found to extend life in fruit flies.
The researchers hope that future studies will uncover even more genes linked with longevity, and figure out how these genes may affect the aging process.
"There's a reasonably strong genetic component to becoming a centenarian, and we want to find out what that is," said study researcher Stuart Kim, a professor in the Department of Developmental Biology and Genetics at Sanford University. "We're beginning to unravel the mystery" of why some people age so successfully compared to the normal population, Kim said. [Extending Life: 7 Ways to Live Past 100]
Previous studies have attempted to find variations in genes that are more common in the very old compared with younger people, but haven't had much luck. These studies looked through millions of variations in the human genome, but they might have missed some important associations.
The new study aimed to narrow the search for genes linked with long life by focusing on ones that are known to strongly affect a person's risk of age-related disease, like heart disease and Alzheimer's. The thinking is that these diseases increase a person's risk of dying early, and so genetic variants that increase the risk of these diseases would also decrease the chances of a long life, the researchers said.
The researchers first searched for longevity-linked genes in a population of about 800 people over age 100 and 5,400 people over age 90.
They found eight genes that were linked with a long life span, and were able to confirm four of these genes in a follow-up analysis of about 1,000 people ages 100 or over.
The study found that certain variants in the ABO, CDKN2B, APOE and SH2B3 genes were more common in centenarians than in people with a typical life span. (Adults in the United States have an average life expectancy of about 79 years, according to the Centers for Disease Control and Prevention.)
For example, the study found that the a genetic variation associated with type O blood was more common in centenarians than in the study's control group, meaning that there were slightly more centenarians with type O blood, compared to people with a typical life span. Previous studies have found that people with type O blood have a lower risk of coronary heart disease and cancer, and have lower cholesterol levels than people with other blood types.
Another genetic variant in the CDKN2B gene seems to play a role in whether cells continue to divide, or stop dividing. Given that the stoppage of cell division, called senescence, is thought to contribute to aging, having a gene variation that reduces cell senescence could be a factor that contributes to successful aging, Kim said.
Kim suspects that there are still more genes linked with a longer life span.
"I hope our paper inspires other people to continue searching for" genes linked with longevity, Kim said.
The study was published yesterday (Dec. 17) in the journal PLOS Genetics.
Follow Rachael Rettner @RachaelRettner. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science. ||||| | multi_news_1_0_0 |
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News article:
North Korean leader Kim Jong Un (4th R) visits the Kumsusan Palace of the Sun to pay tribute to founding President Kim Il Sung and former leader Kim Jong Il to mark the 61st anniversary of the victory of the Korean people in the Fatherland Liberation War, in this photo...
BEIJING/SEOUL North Korean leader Kim Jong Un is in firm control of his government but has hurt his leg, a source with access to the secretive North's leadership said, playing down speculation over the 31-year-old's health and grip on power.
North Korea's state media, which usually chronicles Kim's whereabouts in great detail, has not made any mention of his activities since he attended a concert with his wife on Sept. 3, and Kim was absent from early state media coverage of a major political anniversary on Friday.
In the previous two years, Kim marked the anniversary of the founding of North Korea's Workers' Party with a post-midnight visit to the Pyongyang mausoleum where the bodies of his father and grandfather are interred.
Last year, that visit was covered about four hours later by the state's KCNA news agency, and by the daily Rodong Sinmun newspaper. As of about 8 a.m. (7.00 p.m. EDT) on Friday, there was no KCNA report of an event at the mausoleum. Friday's Rodong Sinmun could not yet be seen on its website.
Kim's father, Kim Jong Il, did not always attend the Oct. 10 memorial event when he was in power.
The source, who has close ties to Pyongyang and Beijing, said on Thursday that Kim hurt his leg while inspecting military exercises.
"He ordered all the generals to take part in drills and he took part too. They were crawling and running and rolling around, and he pulled a tendon," the source told Reuters on condition of anonymity.
"He injured his ankle and knee around late August or early September while drilling because he is overweight. He limped around in the beginning but the injury worsened," the source said.
Kim, who has rapidly gained weight since coming to power after his father died of a heart attack in 2011, had been seen walking with a limp since an event with important officials in July, which would imply he may have aggravated an earlier injury.
Kim needs about 100 days to recuperate, said the source, whose information could not be independently verified.
"Kim Jong Un is in total control," said the source.
Kim's absence from public view is fuelling speculation over the state of his health and whether he may have been sidelined in a power struggle.
"The longer he remains out of the public eye, the more uncertainty about him, and the status of his regime, will grow," said Curtis Melvin, a researcher at the U.S.-Korea Institute at the Johns Hopkins School of Advanced International Studies in Washington.
NOT KIM'S FIRST ABSENCE
North Korean officials have denied that Kim's public absence since early September is health-related and a U.S. official following North Korea said this week there were no indications he was seriously ill or in political trouble.
It remains unclear why a leg injury would keep Kim out of the public eye for so long, although this is not the first time he has been missing from public view.
In June 2012, six months after coming to power, state media failed to report on or photograph him for 23 days.
He re-surfaced the next month at a dolphinarium.
Speculation that Kim's unusually long absence from public view may be due to ill health was fueled by a North Korean television report late last month that said he was suffering from "discomfort".
Some North Korea watchers also suggest that Kim may have been sidelined in a power struggle, a scenario they say was reinforced by the unexpected visit on Saturday of a high-level delegation to the closing ceremony of the Asian Games in Incheon, South Korea.
Another interpretation of that visit holds that it was meant to convey stability in Pyongyang.
The source with knowledge of Kim Jong Un's health said rumors of a coup were "rubbish".
"It would have to be a very subtle coup indeed not to disrupt international travel plans," said Andray Abrahamian of the Choson Exchange, a Singapore-based group running a program for North Koreans in Southeast Asia.
North Korea is a hereditary dictatorship centered on the ruling Kim family. Kim's sister, Kim Yo Jong, is known to have an official role within the ruling party. His brother, Kim Jong Chol, and his estranged half-brother are not in the public eye.
Kim was absent from a Sept. 25 meeting of the Supreme People's Assembly, or parliament, the first he has not attended since coming to power three years ago.
However, Kim's name has not disappeared from state propaganda.
Thursday's edition of the Rodong Sinmun carried three letters to Kim from overseas allies on its front page, and has reported on returning athletes from the Asian Games who thanked "the Marshal" for his support during the competition.
Abrahamian said it was unlikely Kim had been usurped.
"Kim Jong Un has always shared power with other key figures and even if the internal balance of power has shifted, it is unlikely that they would want to remove him, given his unmatchable symbolic value. Again, though, everyone is guessing," he said.
(Writing by Tony Munroe; Editing by Mike Collett-White and Raju Gopalakrishnan) ||||| With the North Korean leader not seen in public for more than a month, rumours of a palace coup are rife. But evidence from inside the country suggests otherwise, says Christopher Green
The appearance of three senior North Koreans in South Korea at the closing ceremony of the Asian Games has caused quite a stir. One of them has links to sport and another to relations with Seoul, so both had reasons to make the trip. But it’s the presence of the third, Hwang Pyong-so, that has caused the most consternation.
Hwang is a member of the North Korea’s Organisation and Guidance Department (OGD), which wields immense power in the country, with some observers claiming it represents a rival source of authority to the young leader, Kim Jong-un.
Kim Jong-un’s absence from the victory parade in Pyongyang for athletes returning from the Games only added to the speculation.
The leader has not been seen in public since 3 September, missing high-profile events including the celebrations for founding day of the Democratic People’s Republic of North Korea on 9 September and a legislative session of the Supreme People’s Assembly on the 25th. Just yesterday he missed a meeting to mark the 17th anniversary of Kim Jong-il’s election as general secretary of the ruling party.
Facebook Twitter Pinterest North Korea’s Asian Games athletes welcomed back to Pyongyang. Photograph: KCNA/EPA
Formal acknowledgement in a television documentary that Kim is suffering from “discomfort” did nothing to dampen the rumours that he has been subject to a palace coup.
The speculation stems from remarks from a former high-ranking North Korean official turned defector, Jang Jin-sung, suggesting the OGD has seized control, leaving Kim as a figurehead.
For many commenters, Hwang’s surprise appearance at the closing ceremony of the Asian Games was enough to provide evidence of Kim Jong-un’s downfall – both because of Hwang’s seniority and the unlikeliness of his trip to the south.
Neither of Hwang’s two public titles, director of the Korean People’s Army general political department and vice-chair of the National Defence Commission, have anything to do with sport. His position within the OGD is not well known, but the fact that a person with these ties would appear in the heart of South Korean territory was seen as proof of a powerful shake-up at the top.
Facebook Twitter Pinterest Hwang Pyong-so arrives in Incheon for the closing ceremony of the Incheon Asian Games. Photograph: YONHAP/EPA
But there is a less dramatic explanation. Based on the video evidence of his limp, it is widely accepted that Kim is now receiving medical treatment – possibly at one of the family’s well-appointed villas. The Seoul-based defector group, North Korea Intellectuals’ Solidarity, claims that Kim Yo-jong, his younger sister who acted as an aide to their father Kim Jong-il during his final years, is signing off on decisions in his absence.
Yet claims that Kim has been toppled are not supported by reports of internal North Korean lectures explaining the surprise visit to the Games. DailyNK, a South Korean media organisation staffed in part by defectors who have sources in the North, says civilians were gathered at workplaces and housing complexes on Saturday afternoon to hear the government’s explanation for the trip.
“Senior party and military cadres were dispatched all the way [to the Asian Games] for our athletes, who, without exception, honoured the Fatherland with their indomitable fighting spirit,” one lecturer explained. “With his great love and compassion, Marshal Kim Jong-un personally organised their dispatch, and provided them with a special plane,” she added.
The text for these lectures, a regular feature of life in North Korea, is produced centrally for dispatch throughout the land, and delivered without deviation. Not attending public lectures and teaching sessions is, officially at least, not an option – as mandated by the Ten Principles for the Establishment of the One-ideology System.
Facebook Twitter Pinterest North Korean athletes pay tribute to statues of former leaders on their return from the Asian Games. Photograph: KCNA/EPA
The result is that almost all North Koreans hear the same stories and lies, and remain on-message, however far they may be from the capital. In the absence of verifiable information on Kim’s status, they offer vital insight into what Pyongyang wants the country’s people to believe.
The suggestion that he is still at the helm, nominally at least, is supported by Choson Sinbo, an online publication run by the pro-North association of Korean residents in Japan, which reported that the visit to Incheon was “made possible by the resolve of Kim Jong-un”.
Also, the domestic North Korean media has barely reported on the trip at all. However, it has focused on the medal winning exploits of the country’s athletes at the Asian Games, with the official mouthpiece Rodong Sinmun singing one song loudly and clearly: the country’s sporting prowess is all down to the “energetic guidance” of one man: Kim Jong-un.
So despite the rumour mill, the North Korean message is still of Kim’s benevolent greatness. In elite circles his authority may be fragile, but that is a different question, one of the distribution of power in a dictatorship. It should not be confused with control over society. Publicly at least, the Kim dynasty remains in complete control. ||||| SEOUL, South Korea — In most countries, footage showing the leader with a limp might have generated some curiosity. But in tightly controlled North Korea, those images — coupled with the disappearance of the country’s ruler, Kim Jong-un, from public view for five weeks — have generated endless debate among foreign officials and analysts always on the lookout for upheaval in one of the world’s most dangerous police states.
The disappearance is especially notable because Mr. Kim, like his father and grandfather before him, has used public appearances accompanied by fawning subjects as a key tool of the propaganda machine that has long held the state together.
For now, American and South Korean officials say that while they think the young leader might be ailing, there is no sign that there has been a coup. After three generations of Kims, any shift away from dynastic rule would probably involve unusual movements of the country’s million-plus military or its people, and none have been detected by the South.
And the fact that North Korea sent three officials widely seen as the Nos. 2, 3 and 4 in the country’s hierarchy to attend the recent closing ceremony of the Asian Games in South Korea, and that during their visit they agreed to resume official dialogue with Seoul, suggests that Mr. Kim remains in control, according to officials and analysts in South Korea.
In Washington, officials have waved off coup rumors as the wishful thinking of people who have spent years looking for signs of regime collapse and been serially disappointed.
“The last time was when everyone was predicting that Kim Jong-un would be pushed aside by his more experienced uncle,” said one senior official. “And look what happened to him.”
That uncle, Jang Song-thaek, 67, got on his nephew’s bad side over business deals and power plays involving some in the elite, and was executed last year, according to accounts pieced together by American and South Korean officials at the time. That has spawned rumors that disaffected members of the ruling party or military, eager to settle scores, are at it again, but officials say there is far more speculation of such a plot than evidence.
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But given the secretive nature of the North Korean government, and the consequences of turmoil in a nuclear-armed and often belligerent country, the official doubts about any power shifts have done little to stop speculation.
Some of the rumors are relatively benign, suggesting that the corpulent Mr. Kim is simply recovering from that nemesis of many a leader with a soft spot for rich food: gout. But others suggest that Mr. Kim, who is believed to be about 30, has finally lost power to older North Korean power brokers more schooled in the country’s treacherous politics, either through a planned revolt or a more subtle takeover that would leave him as a figurehead.
In an indication of the breathless nature of the online rumor mill, one story circulated on social media in China went so far as to name the engineer of the purported coup, Vice Marshal Jo Myong-rok. The only catch: Mr. Jo was reported to have died several years ago.
One reason for the proliferation of theories is that rumors in North Korea have sometimes turned out to be true. These include news of the country’s devastating famine in the 1990s as well as the more recent (and unpopular) currency reform, which in both cases first surfaced in poorly sourced reports.
But there is also always the temptation to believe the worst of a family-ruled country that has little exposure to the outside world and has displayed its share of oddities, and cruelties. At least in earshot of their many minders, regular North Koreans credit the Kims with godlike feats. And although experts say Mr. Kim did not feed his uncle to dogs as one Chinese blog post suggested, South Korean intelligence officials said some of the uncle’s lieutenants were executed by machine gun.
In gauging what has happened to Mr. Kim, some analysts have noted that his father and grandfather also disappeared for weeks on end.
“Kim Jong-un’s disappearing act over the past month, in the North Korean context, is not an aberration,” said Lee Sung-yoon, a North Korea expert at Tufts University’s Fletcher School of Law and Diplomacy. “Such vanishing acts would be most unusual in democracies, but in totalitarian North Korea, Kim is the state. He is free to come and go as he pleases.”
Mr. Kim, however, has never been gone from sight this long and, until now, had been notably visible, visiting farms, factories and military units more frequently than his reclusive father did.
The visits are always covered prominently in the North’s state-controlled news media and include what passes for statecraft in North Korea; like his father and grandfather, Mr. Kim is followed on the “on-site guidance tours” by party functionaries and generals about twice his age who furiously scribble down his thoughts on how to make improvements.
For now, foreign officials and analysts are anxiously waiting for Friday, the anniversary of the founding of the ruling Workers’ Party, to see if Mr. Kim will make a public appearance. Speaking at a parliamentary hearing this week, Han Min-koo, the South Korean defense minister, said that his country’s intelligence had determined that Mr. Kim was “at a certain place north of Pyongyang.” Mr. Han gave no further details, citing the sensitivity of the intelligence. His remark was widely taken as meaning that Mr. Kim was recuperating at a family villa in Gangdong, north of the North Korean capital, and that the government in Seoul did not believe that Mr. Kim had lost power in a coup.
North Korean diplomats in New York and Geneva have dismissed reports about Mr. Kim’s absence as part of efforts by their country’s external enemies to spread disinformation to undermine the Pyongyang government. One of the three North Korean officials visiting the South last Saturday, the party secretary Kim Yang-gon, told Unification Minister Ryoo Kihl-jae of South Korea that there was “no problem at all” with Kim Jong-un’s health, according to Mr. Ryoo.
Other than Mr. Kim’s absence, there are few outward signs of trouble in the North. The North Korean media is brimming, as usual, with propaganda extolling his leadership. On Tuesday, the North’s main party newspaper, Rodong Sinmun, intoned that the people and military of North Korea “knew no other leader than the marshal.” Daily NK, a Seoul-based website that says it uses anonymous sources within the North, reported North Korean citizens watching the Asian Games on large screens in central Pyongyang in recent weeks while the media there attributed any victory by North Korean athletes to the “greatness” of Mr. Kim.
Most analysts in South Korea conclude that Mr. Kim has been kept from the cameras since Sept. 3 simply because he is suffering from some ailment.
With so much internal propaganda focused on Mr. Kim, John Delury, a North Korea expert at Yonsei University in Seoul, said that if Mr. Kim had surgery and was recuperating, the North would probably not want to release images of him in a wheelchair. North Korea kept Mr. Kim’s father, Kim Jong-il, out of public view for months after he suffered a stroke in 2008.
In any case, Mr. Delury said the speculation would not end until the young Mr. Kim appeared in public.
“At some point if Kim fails to appear in public, then we can assume there is a serious problem,” he said. “The question is how long?” ||||| Story highlights With North Korea's leader out of public eye, sister's profile increases
A think-tank run by defectors says she may be temporarily leading the government
Kim Yo Jong is in her twenties; she attended private school in Switzerland
The mystery surrounding North Korea's erratic young leader, Kim Jong Un, only deepens by the day.
He has not been seen publicly in more than a month. Rumors are flying that Kim is ill with gout, diabetes, even possible problems with his ankles. Now, a group of defectors say they believe Kim's younger sister, Kim Yo Jong, may be running the country while he recuperates.
The North Korea Intellectuals' Solidarity, a think-tank run by defectors, says Kim Yo Jong may be at least temporarily leading the government. The group has not revealed the source of its information, and CNN cannot independently confirm it. But Kim Yo Jong's star appears to be rising.
Michael Madden, who runs the blog North Korea Leadership Watch, says Kim Yo Jong has been identified in North Korean media as deputy director of the Workers' Party, a very powerful position.
Victor Cha, an analyst with the Center for Strategic and International Studies who previously handled the North Korea account with the National Security Council, says Kim Yo Jong began surfacing publicly earlier this year at party functions.
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"Clearly it's an effort to slow-track her into becoming somebody who is important within the system," Cha says. "I can see how it's possible that she's in some sort of temporary position. It's very difficult for the North Korean system to run without one of the Kim family at least titularly in charge. So, if Kim Jong Un is indisposed, she's really the only available body that's left, in terms of a direct Kim family line."
Who is Kim Yo Jong?
Madden says Kim Yo Jong was born in 1987 or 1988, and attended private school in Switzerland with Kim Jong Un. They both stayed at the North Korean embassy while attending the Swiss school, Madden says, and lived there under assumed names.
Madden says Kim Yo Jong is the youngest of seven siblings their father, Kim Jong Il, had with four women. Many of them are half-siblings, but Kim Jong Un and Kim Yo Jong have the same mother.
Madden says Kim Yo Jong was always close to her father, and after returning from Switzerland, she was appointed to positions of responsibility in the government. She would act as an advance-team leader, inspecting sites before official visits, and had administrative duties as well.
Now, he says, she continues those duties and has taken on more responsibility under her brother's rule: dealing with policy and receiving intelligence briefings. She acts "almost like a White House chief-of-staff would," Madden says.
He says he believes she had a large role in planning the recent trip by three top North Korean officials to South Korea while her brother was absent from the scene.
Ready for prime time?
Given her age and that so little is known about Kim Yo Jong, North Korea-watchers are concerned about her being in the top leadership spot, if only temporarily. The stress and palace intrigue inside the North Korean regime, they say, may be overwhelming.
"If in fact she is running the country -- as someone in their early to mid twenties, to me that is quite alarming," Cha says. "It means there is something seriously wrong with Kim Jong Un and there is some sort of void that they're desperately trying to fill."
All eyes will be on a significant event this Friday, October 10. That's the 69th anniversary of the founding of the ruling Workers' Party. Kim Jong Un attended the anniversary event last year. If he doesn't show up at Friday's ceremonies, concern over his public disappearance will only grow.
If he does attend, intelligence analysts will be looking at his appearance, his body language -- every detail -- very carefully. |||||
What is a shorter version of the above article? | – As Kim Jong Un remains out of sight—and North Korean officials do unusual things like admit the country has labor camps—Pyongyang-watchers are starting to wonder who's running the place. Amid rumors of a "palace coup," a think tank run by North Korean defectors suspects that his 27-year-old sister Kim Yo Jong is in charge, at least while Kim recuperates from what some observers believe is gout or fractured ankles. Not much is known about Kim Yo Jong, the youngest of the leader's six siblings, but if she is indeed making national decisions, that "means there is something seriously wrong with Kim Jong Un and there is some sort of void that they're desperately trying to fill," an analyst with the Center for Strategic and International Studies tells CNN. He says she was first spotted at official functions earlier this year. A surprise visit to South Korea by the country's No. 2 and No. 3 leaders last week fueled more rumors of Kim's downfall, but analysts believe that while there may have been a shake-up at the top, he is still at the top, at least as a figurehead, the Guardian reports. Kim's father and grandfather also dropped out of sight for long periods, so Kim's "disappearing act over the past month, in the North Korean context, is not an aberration," a North Korea expert at Tufts University tells the New York Times. "Such vanishing acts would be most unusual in democracies, but in totalitarian North Korea, Kim is the state. He is free to come and go as he pleases." Tomorrow is the 69th anniversary of the founding of the ruling Workers' Party—described by Reuters as a "key political event"—and analysts will be closely watching to see if Kim makes an appearance at his family's mausoleum as he has done the past two years. | multi_news_1_0_0 |
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For Chris Christie, there was no way around it. "In case you haven't noticed, I'm slightly overweight," he said during a debate in his successful campaign for governor.
Two years later, Christie is the man of the moment in presidential politics, with many powerful Republicans clamoring for him to run. But it has been 100 years since Americans sent a true heavyweight to the White House, when William Howard Taft tipped the scales at well over 300 pounds.
Nor is Christie just "slightly overweight." So there is no delicate way to ask this: Is Chris Christie too fat to win?
Politics, after all, is a business of image and first-impressions -- and study after study shows that people judge the hefty more harshly than they judge those who are thin.
"Overweight people have much less of a chance of getting a job, they have much less of a chance of keeping a job ... they are paid less than those who are thin," said David Birdsell, dean of the School of Public Affairs at Baruch College in New York.
"In this era of exercise, we impute moral failings to people who don't rein in their weight," he said. "Those prejudices are just intensified for people who seek elected office."
Indeed, John McLaughlin, a New York-based Republican political consultant, said he routinely advises his clients to watch what they eat.
"You don't want them to gain weight, to look poorly on television," he said.
The political stage is filled with candidates who have heard that message loud and clear.
Mike Huckabee, the Republican former governor of Arkansas, famously shed 110 pounds and penned a self-help book, "Quit Digging Your Grave With a Knife and Fork," before plunging into the 2008 presidential race. He went on to tout his weight loss endlessly during the campaign.
In New York, more than a dozen overweight state legislators went on a very public battle of the bulge last year as they prepped for re-election.
"Voters would rather see someone whose belly isn't, you know, huge -- someone who is fit and trim," Assemblyman Sam Hoyt, an upstate Democrat, said at the time.
If a candidate is not "fit and trim," he might even face ridicule, as Christie recently did from late night talk show host David Letterman.
"You know who the Republicans want as their candidate is the tubby guy across the river, Chris Christie," Letterman said on "The Late Show," taped across the Hudson River from New Jersey in New York City. "You talk about tons of fun, here we go.
"I want Chris Christie in this race because just I want to be able to meaningfully say, 'Hey, bring it, fat boy!'" Letterman said later. "He's got to be close to 400 pounds. ... Take a look. ... Go to Google Earth."
Political scientists and strategists said they could not recall a truly heavy American politician finding great national success in the television age.
"Our candidates tend to be tall, they tend to have great hair," said Russell Riley, a presidential scholar at the University of Virginia's Center of Public Affairs. "This doesn't seem to be a business that, at the presidential level, willingly accepts people who are demonstrably overweight.
"Most people would look at Ronald Reagan say, 'This is a guy who looks like he could be president,'" he added.
Christie is an old hand in the political weight wars. In the 2009 race for New Jersey governor, incumbent Democratic Gov. Jon Corzine not-so-subtly made Christie's plus size an issue.
Corzine broadcast a television ad showing unflattering images of Christie as the narrator intoned that Christie "threw his weight around" to avoid getting traffic tickets. To drive home the comparison, Corzine, a fitness buff, ran in 5K and 10K races during the campaign.
"I have struggled with my weight for the last 30 years on and off, and that's the way it is, and so I think there are a lot of people out in New Jersey who have the same kind of struggles," Christie told one interviewer.
Earlier this year, Christie talked openly with ABC News' Diane Sawyer about his weight and his effort to exercise more.
"What do you say to yourself to psych yourself into it?" Sawyer asked.
"Just look in the mirror, Diane," Christie replied. "OK, I have to get healthier and this job has really forced me, because it's such a draining job from the energy perspective."
Chris Christie's Weight: Disadvantage or Advantage?
Ironically, many strategists say Christie's weight could work to his advantage if he enters the presidential race.
At a time when many Americans are angry with Washington and fed up with politicians, Christie's weight allows him to stand apart from the political crowd, they said. It is an image Christie played to when he warned New Jerseyans to "get the hell off the beach" as Hurricane Irene approached in late August.
"People want something different, something out of the ordinary ... someone who is willing to stand up and confront problems," McLaughlin said "Being a picture-perfect candidate I don't think is as important anymore."
Doug Muzzio, a political scientist at Baruch College, said Christie's weight could help him subliminally with voters, too.
"Maybe this is a time when you need someone to be a bull in a china shop," Muzzio said. "Well, bulls are big."
If there is a danger for Christie, it is that his weight might leave voters wondering about his health. In July, he went to the hospital with breathing problems and lightheadedness, forcing doctors to run an EKG test, take blood and x-ray his chest. The diagnosis: a bout of asthma.
Asked if rivals might use such episodes against him, Christie said at the time, "My political enemies are never at rest ... and if this is what they want to use, I think I'm having a pretty good week.
"Despite the well-chronicled issues with my weight, I've been relatively healthy by all objective indicators," he said.
McLaughlin, the Republican strategist, said he relishes the idea of Christie challenging President Obama.
"It would be a real visual contrast, where you have Barack Obama, who is in good shape, perceived as being buff and athletic, going against Chris Christie, who has problems with asthma, who is overweight," McLaughlin said.
"I'd argue it's a vision of government that is big, fat and out of control -- in contrast Christie, who is putting the government of New Jersey on a diet," he said, "The paradox is very interesting." ||||| Whether or not he lets himself be persuaded to run for president, Chris Christie needs to find some way to lose weight. Like everyone else, elected officials perform best when they are in optimal health. Christie obviously is not.
You could argue that this is none of my business, but I disagree. Christie’s problem with weight ceased being a private matter when he stepped into the public arena — and it’s not something you can fail to notice. Obesity is a national epidemic whose costs are measured not just in dollars and cents but also in lives. Christie’s weight is as legitimate an issue as the smoking habit that President Obama says he has finally kicked.
On rare occasions, Christie speaks candidly about his weight. “I’m really struggling, been struggling for a long time with it,” he told CNN’s Piers Morgan in June. “And I know that it would be better for my kids if I got it more under control, and so I do feel a sense of guilt at times about that.”
Six weeks later, the New Jersey governor was briefly hospitalized for asthma — a condition that he has had for most of his life. Researchers say that many respiratory problems, including asthma, are worsened by obesity.
As he left the hospital, Christie acknowledged the connection. He described himself as “relatively healthy by all objective indicators,” but added that “if I weighed less, I’d be healthier.”
“The weight exacerbates everything,” he said.
And it does. According to the National Institutes of Health, obesity puts people at greater risk for Type 2 diabetes, coronary heart disease and stroke, certain types of cancer, sleep apnea, osteoarthritis, and gallbladder and liver disease.
The NIH estimates that nearly 34 percent of U.S. adults can be classified as “obese,” meaning they have a body mass index of more than 30. By this standard, a man who stands 5-foot-11 — Christie’s reported height — would be obese if his weight reached 215 pounds. While Christie does not disclose his weight, it appears to exceed the 286 pounds that would place him among the 5.7 percent of American adults whom NIH classifies as “extremely obese.”
I refer to obesity as an epidemic because the percentage of obese adults has doubled in the past 40 years — and childhood obesity is increasing even more rapidly. Again according to the NIH, “obesity is associated with over 112,000 excess deaths due to cardiovascular disease, over 15,000 excess deaths due to cancer, and over 35,000 excess deaths due to non-cancer, non-cardiovascular disease causes per year.”
On average, health-care costs for obese persons are 42 percent higher than costs for individuals whose weight falls into the “normal” range. It costs Medicare $1,723 more a year for an obese beneficiary than a non-obese one. For Medicaid the differential is $1,021, and for private insurers it’s $1,140. In other words, obesity is helping propel the rise in health-care costs, which are fueling the long-term rise in the national debt.
My intention is not to blame Christie for the federal government’s deficit spending — or, in fact, to blame him for his own obesity. Blame is not the point. Christie is just 49 and has four young children; politics aside, I’m sure he wants to be around to share the milestones in their lives. He prides himself on bullheaded determination and speaks often about the need for officials to display leadership. Well, Gov. Christie, lead thyself.
“I weigh too much because I eat too much,” he said after his hospitalization this summer, “and I eat some bad things, too.”
If only it were that simple. Yes, the basic arithmetic of calories ingested vs. calories expended is inescapable. But the science of weight control now takes into account the role that genetics might play, along with psychological factors that lie outside our conscious control. There are new options, including gastric surgery, beyond the dieting roller coaster — lose 40 pounds, gain it all back — that Christie says he has been riding for years.
Those who have lost weight and kept it off for extended periods, including former Arkansas governor Mike Huckabee, say they have succeeded by making proper diet and exercise part of their lives — not just unpleasant chores that have to be endured.
Politically, I disagree with Christie on almost everything. I’ll have plenty of opportunities to tell him why. Today, I’d just like to offer him a bit of unsolicited, nonpartisan, sincere advice: Eat a salad and take a walk.
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Sargent: The other jobs fight to watch
Stromberg: Rick Perry backs down, but on what? |||||
What is a one-paragraph summary of the above article? | – Is Chris Christie too fat for the White House? His extra girth could serve him well in an election—to a point. It makes him look like one of the gang, if the gang is the growing number of obese Americans. And his pounds prove he's a guy not listening to the diet nags of the "nanny state," a plus for Tea Party fans. It's also ... different. "People want something different, something out of the ordinary, someone who is willing to stand up and confront problems," political consultant John McLaughlin tells ABC News. "Being a picture-perfect candidate I don't think is as important anymore." But it's been 100 years since our last hefty prez, William Howard Taft, tipped the scales at more than 300 pounds. We have a monster prejudice against fat people. "Overweight people have much less of a chance of getting a job, they have much less of a chance of keeping a job, they are paid less than those who are thin," says David Birdsell of the School of Public Affairs at New York's Baruch College. "In this era of exercise, we impute moral failings to people who don't rein in their weight. Those prejudices are just intensified for people who seek elected office." Then, there's the potentially deadly impact of his extra weight—not good for him, or the nation. "I’d like to offer him a bit of unsolicited, nonpartisan, sincere advice," writes Eugene Robinson in the Washington Post. "Eat a salad and take a walk." | multi_news_1_0_0 |
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– An apple a day keeps the blues away? According to a new study, eating fruits and vegetables increases happiness. "However," researcher Andrew Oswald tells the New York Daily News, "French fries will not count." Researchers from England's University of Warwick and the University of Queensland in Australia examined the food journals of more than 12,000 people. "Happiness benefits" were noted for each extra portion of produce consumed each day. For people who went from eating little to no fruit and vegetables each day to eating eight portions, the "feel-good factor" was on par with that experienced when going from being jobless to employed. While the health benefits of eating produce are well-known, they don't offer immediate gratification: The "well-being improvements" kick in after about two years of adopting a high-produce diet. According to an earlier CDC study, 76% of Americans failed to eat enough fruit, while 87% didn't eat their recommended daily amount of veggies. "People’s motivation to eat healthy food is weakened by the fact that physical-health benefits, such as protecting against cancer, accrue decades later," Oswald says in a press release. "However, well-being improvements from increased consumption of fruit and vegetables are closer to immediate.” As for why fruit and vegetable consumption may boost happiness, the authors say more research is needed. However, they do speculate that increased antioxidants in the blood may play a role. (These researchers found that butter consumption could reduce diabetes risk.) | The adage of “an apple a day” has new bite.
Everybody knows that eating fruits and vegetables is good for you in the long run as it reduces risks for cancer and heart attacks. But a new study found that munching produce boosts happiness even quicker. The associated feel-good factor kicks in within two years. Granted, that’s still not fast as other things will make you feel better, like, say, a bag of Doritos or a vodka and tonic. But yeah, dive into that kale.
So urge researchers who followed 12,385 randomly selected subjects as they kept food diaries and had their psychological well-being monitored. The collaborative effort was by the University of Warwick, England, and the University of Queensland, Australia.
Subjects were observed in 2007, 2009 and 2013. Changes in their income, employment and personal factors were figured into findings. Happiness benefits were detected for each extra daily portion of fruit and vegetables — “tinned, frozen, dried and fresh,” per the study — up to eight portions per day. "The fruits and vegetables do not have to be prepared in any special way," Warwick researcher Andrew Oswald told the Daily News. "However, French fries will not count."
Many experts suggest eating 5-9 servings of fruits and vegetables on a daily basis. The more produce that was consumed, the bigger the feel-good increase.
Subjects who changed from eating almost no fruit and vegetables to munching eight portions a day experienced an increase in life satisfaction equivalent “to moving from unemployment to having a job.”
Veggies are a source of a "more immediate" feel-good boost. (Brigitte Sporrer/Getty Images)
“Eating fruit and vegetables apparently boosts our happiness far more quickly than it improves human health,” said Oswald.
“People’s motivation to eat healthy food is weakened by the fact that physical-health benefits, such as protecting against cancer, accrue decades later,” Oswald added. “Well-being improvements ... are closer to immediate.”
Further study is needed to explain why eating fruits and veggies makes people feel good. A possible explanation is that fruits and veggies are rich in antioxidants, substances in the body that other research has linked with optimism.
“Perhaps our results will be more effective than traditional messages in convincing people to have a healthy diet,” said researcher Redzo Mujcic. “There is a psychological payoff now from fruit and vegetables, not just a lower health risk decades later.”
Good luck with that. Americans, at any rate, aren’t anywhere close to eating fruits and veggies in recommended numbers. And, again, French fries don’t count. ||||| New research suggests up to eight-a-day can make you happier
University of Warwick research indicates that eating more fruit and vegetables can substantially increase people’s later happiness levels.
To be published shortly in the prestigious American Journal of Public Health, the study is one of the first major scientific attempts to explore psychological well-being beyond the traditional finding that fruit and vegetables can reduce risk of cancer and heart attacks.
Happiness benefits were detected for each extra daily portion of fruit and vegetables up to 8 portions per day.
The researchers concluded that people who changed from almost no fruit and veg to eight portions of fruit and veg a day would experience an increase in life satisfaction equivalent to moving from unemployment to employment. The well-being improvements occurred within 24 months.
Cancer
The study followed more than 12,000 randomly selected people. These subjects kept food diaries and had their psychological well-being measured. The authors found large positive psychological benefits within two years of an improved diet.
Professor Andrew Oswald said: “Eating fruit and vegetables apparently boosts our happiness far more quickly than it improves human health. People’s motivation to eat healthy food is weakened by the fact that physical-health benefits, such as protecting against cancer, accrue decades later. However, well-being improvements from increased consumption of fruit and vegetables are closer to immediate.”
The work is a collaboration between the University of Warwick, England and the University of Queensland, Australia. The researchers found that happiness increased incrementally for each extra daily portion of fruit and vegetables up to eight portions per day. The study involved an examination of longitudinal food diaries of 12,385 randomly sampled Australian adults over 2007, 2009, and 2013 in the Household, Income, and Labour Dynamics in Australia Survey. The authors adjusted the effects on incident changes in happiness and life satisfaction for people’s changing incomes and personal circumstances.
Western diet
The study has policy implications, particularly in the developed world where the typical citizen eats an unhealthy diet. The findings could be used by health professionals to persuade people to consume more fruits and vegetables.
Dr Redzo Mujcic, research fellow at the University of Queensland, said: “Perhaps our results will be more effective than traditional messages in convincing people to have a healthy diet. There is a psychological payoff now from fruit and vegetables -- not just a lower health risk decades later.”
The authors found that alterations in fruit and vegetable intake were predictive of later alterations in happiness and satisfaction with life. They took into account many other influences, including changes in people’s incomes and life circumstances. One part of the study examined information from the Australian Go for 2&5 Campaign. The campaign was run in some Australian states which have promoted the consumption of two portions of fruit and five portions of vegetables each day.
Antioxidants
The academics think it may be possible eventually to link this study to current research into antioxidants which suggests a connection between optimism and carotenoid in the blood. However they argue that further research is needed in this area.
8 July 2016
Notes to Editors
“Evolution of well-being and happiness after increases in the consumption of fruit and vegetables” by Redzo Mujcic and Andrew Oswald, forthcoming in the August issue of the American Journal of Public Health.
The paper will be available here http://ajph.aphapublications.org/doi/abs/10.2105/
DOI: AJPH.2016.303260
The paper will also be downloadable here: www.andrewoswald.com
Andrew Oswald PhD is Professor of Economics and Behavioural Science, University of Warwick, UK. He is also a member of the University’s Centre for Competitive Advantage in the Global Economy (CAGE). Established in January 2010, CAGE is a research centre in the Department of Economics at the University of Warwick. Funded by the Economic and Social Research Council (ESRC), CAGE is carrying out a 10 year programme of innovative research.
The centre’s research programme is focused on how countries succeed in achieving key economic objectives such as improving living standards, raising productivity, and maintaining international competitiveness, which are central to the economic wellbeing of their citizens. ||||| Adults Meeting Fruit and Vegetable Intake Recommendations — United States, 2013
Latetia V. Moore, PhD1; Frances E. Thompson, PhD2 (Author affiliations at end of text)
Eating more fruits and vegetables adds nutrients to diets, reduces the risk for heart disease, stroke, and some cancers, and helps manage body weight when consumed in place of more energy-dense foods (1). Adults who engage in <30 minutes of moderate physical activity daily should consume 1.5–2.0 cup equivalents of fruit and 2–3 cups of vegetables daily.* However, during 2007–2010, half of the total U.S. population consumed <1 cup of fruit and <1.5 cups of vegetables daily; 76% did not meet fruit intake recommendations, and 87% did not meet vegetable intake recommendations (2). Although national estimates indicate low fruit and vegetable consumption, substantial variation by state has been observed (3). Fruit and vegetable intake information from the Behavioral Risk Factor Surveillance System (BRFSS) is the sole source of dietary surveillance information for most states, but frequency of intake captured by BRFSS is not directly comparable to federal intake recommendations, which are expressed in cup equivalents. CDC analyzed median daily frequency of fruit and vegetable intake based on 2013 BRFSS data for the 50 states and the District of Columbia (DC) and applied newly developed prediction equations to BRFSS to calculate the percentage of each state's population meeting fruit and vegetable intake recommendations. Overall, 13.1% of respondents met fruit intake recommendations, ranging from 7.5% in Tennessee to 17.7% in California, and 8.9% met vegetable recommendations, ranging from 5.5% in Mississippi to 13.0% in California. Substantial new efforts are needed to build consumer demand for fruits and vegetables through competitive pricing, placement, and promotion in child care, schools, grocery stores, communities, and worksites.
BRFSS is an ongoing state-based random-digit–dialed telephone survey of noninstitutionalized, civilian adults aged ≥18 years residing in the United States. BRFSS collects data on health risk behaviors and conditions, chronic diseases and conditions, access to health care, and use of preventive health services and practices related to the leading causes of death and disabilities in the United States (4). BRFSS asks respondents how many times per day, week, or month they consumed 100% fruit juice, whole fruit, dried beans, dark green vegetables, orange vegetables, and other vegetables over the previous month as part of the rotating core questionnaire administered every other year. For these analyses, respondents were excluded if they did not reside in the 50 states or DC, were missing responses to one or more questions, or had implausible reports of fruit or vegetable intake (reported eating fruit >16 times per day or vegetables >23 times per day) (5); after excluding these 118,193 (24%) respondents, the resulting analytic sample size was 373,580. The 2013 median American Association of Public Opinion Research response rate across the 50 states and DC was 45.9%.
Intake recommendations appropriate for adults who engage in <30 minutes of moderate physical activity daily are based on the Dietary Guidelines for Americans (1) and are expressed in cup equivalents, whereas BRFSS captures frequency of intake. To estimate the percentage of each state's population meeting fruit and vegetable intake recommendations, previously developed prediction equations were applied to the frequency of intake data from BRFSS (6); these analyses are fully described elsewhere (6). In summary, 24-hour dietary recall data from the National Health and Nutrition Examination Survey (NHANES) for the period 2007–2010 were used to fit age- and sex-specific logistic regression models that estimate probabilities of meeting recommendations as functions of reported daily frequency of consumption, race/ethnicity, and income-to-poverty ratio, adjusting for day-to-day dietary variation. Reported daily frequencies of fruit and vegetable intake from BRFSS were calculated by dividing weekly frequencies by seven, monthly frequencies by 30, and yearly frequencies by 365. BRFSS respondents' race/ethnicity (Hispanic, non-Hispanic black, and all others) and income-to-poverty ratio (<125%, 125%–349%, and ≥349%) were defined consistent with previous analyses (6). For income-to-poverty ratio, poverty was defined according to federal poverty guidelines.† Respondents' reported daily frequencies of fruit juice and whole fruit intake, race/ethnicity, and income-to-poverty ratio were used as predictors in the models to estimate each respondent's predicted probability of meeting the fruit intake recommendations. Reported daily intake frequencies of dried beans, dark green vegetables, orange vegetables, and other vegetables, along with demographic information, were used as predictors in the models to estimate probabilities of meeting vegetable intake recommendations. Predicted probabilities were weighted and averaged across all respondents and in each state to obtain the percentage of each state's population meeting recommendations, using statistical software to account for the complex survey design. Balanced repeated replication technique, replicate weights, and Taylor linearization were used to compute standard errors and confidence intervals accounting for variation in the prediction models and BRFSS.
Median frequency of reported fruit intake across all respondents was once per day, ranging from 0.9 in Arkansas to 1.3 times per day in California (Table). Median frequency of reported vegetable intake was 1.7 times per day, ranging from 1.4 in Louisiana, Mississippi, and North Dakota to 1.9 times per day in California and Oregon. Based on prediction equations, 13.1% of respondents met fruit recommendations, and 8.9% met vegetable recommendations. The percentage of state populations meeting recommendations for fruits ranged from 7.5% in Tennessee to 17.7% in California, and for vegetables, from 5.5% in Mississippi to 13.0% in California.
Discussion
In 2013, most adults consumed too few fruits and vegetables, with substantial variation by state. This analysis enhances current surveillance efforts by enabling the comparison of fruit and vegetable intake from the BRFSS survey module with federal recommendations. Ongoing collection of relevant state-level nutritional status and program data help identify public health nutrition problems in each state and support the design, evaluation, and management of nutrition intervention programs, in addition to catalyzing local interest in nutrition programs and policies (7).
Because fruit and vegetable consumption affects multiple health outcomes (1) and is currently low across all states, continued efforts are needed to increase demand and consumption. Improving fruit and vegetable consumption for adults might start with improving intake during childhood. During 2007–2010, 60% of children consumed fewer cup equivalents of fruit than recommended, and 93% consumed fewer vegetables than recommended (2). Better dietary practices earlier in life might lead to better practices later in life, and places where children learn and play can have an integral role in improving intake. For example, school districts, schools, and early care and education providers can help increase children's fruit and vegetable consumption by meeting or exceeding current federal nutrition standards for meals and snacks, serving fruit and vegetables whenever food is offered, and training staff to make fruit and vegetables more appealing and accessible.§ Improving fruit and vegetable accessibility, placement, and promotion in grocery stores, restaurants, worksites, and other community settings might improve intake in adults (8,9). For example, work sites can make it easier for employees to make healthy food choices and create social norms that support healthy eating by creating policies to ensure that fruits and vegetables are provided at work-site gatherings, including meetings, conferences, and other events (8). CDC funds state, local, tribal, and territorial health departments to improve environments in worksites, schools, child care, and community settings to expand access to fruits and vegetables and other healthy food and beverage choices for persons of all ages.¶
The findings in this report are subject to at least five limitations. First, self-reports of intake are based on a limited set of questions and are prone to measurement error and recall bias (10). Self-reported intake might overestimate intake in some populations and underestimate intake in others (10). Second, these results might not be generalizable to the entire U.S. adult population (4). BRFSS excludes those living in nursing homes, long-term care facilities, military installations, and correctional institutions (4), but the overall effect this would have on the estimation of intake is unclear. Moreover, territories were excluded because prediction models were derived from NHANES, which excludes territories.** Third, estimates do not include non-100% fruit juice or fried potatoes because BRFSS respondents are instructed not to include them. Including these sources results in 4%–6% higher estimates for fruit and 30%–44% higher estimates for vegetables (6) but federal dietary guidelines recommend limiting foods and beverages with added sugars and solid fats (1). Fourth, relatively low response rates for BRFSS might have biased the sample. Finally, using prediction equations to estimate intake might have resulted in measurement error. However, previous analyses showed that applying prediction equations to 2011 BRFSS frequency data yielded estimates comparable to 2007–2010 national estimates that used more accurate 24-hour recalls (6).
These results indicate that <18% of adults in each state consumed the recommended amount of fruit and <14% consumed the recommended amount of vegetables. Increased attention to food environments in multiple settings, including child care, schools, communities, and worksites, might help improve fruit and vegetable intake, and thus help prevent chronic disease.
1Division of Nutrition, Physical Activity, and Obesity Prevention and Control, National Center for Chronic Disease Prevention and Health Promotion, CDC; 2Division of Cancer Control and Population Sciences, National Cancer Institute, National Institutes of Health.
Corresponding author: Latetia V. Moore, [email protected], 770-488-5213.
References
Summary What is already known about this topic? Although national estimates indicate low fruit and vegetable intake, substantial variation by state has been observed. Fruit and vegetable intake information from the Behavioral Risk Factor Surveillance System (BRFSS) is the sole source of dietary information for most states, but the frequency of fruit and vegetable intake it captures cannot be directly compared to federal intake recommendations, which are expressed in cup equivalents. What is added by this report? CDC analyzed the percentage of each state's population meeting fruit and vegetable intake recommendations from the most recent BRFSS survey for the 50 states and the District of Columbia, using a new scoring procedure. In 2013, 13.1% of respondents met fruit intake recommendations, ranging from 7.5% in Tennessee to 17.7% in California, and 8.9% met vegetable recommendations, ranging from 5.5% in Mississippi to 13.0% in California. What are the implications for public health practice? Substantial new efforts are needed to build consumer demand for fruits and vegetables through competitive pricing, placement, and promotion in child care, schools, grocery stores, communities, and worksites. ||||| | multi_news_1_0_0 |
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Physical activity may be as effective as drugs in treating heart disease and should be included as a comparison in the development of new medicines, according to a review published today in the British Medical Journal.
No statistically detectable differences were evident between exercise and drug treatment for patients with coronary heart disease or prediabetes, and exercise was more effective among patients recovering from a stroke, according to a review of 16 meta-analyses that included 305 studies involving 339,274 participants. The review was conducted by researchers at Harvard University and Stanford University.
The analysis adds to evidence showing the benefit of non-medical approaches to disease through behavior and lifestyle changes. Given the cost of drug treatment, regulators should consider requiring pharmaceutical companies to include exercise as a comparator in clinical trials of new medicines, according to authors Huseyin Naci of Harvard and John Ioannidis of Stanford.
“In cases where drug options provide only modest benefit, patients deserve to understand the relative impact that physical activity might have on their condition,” Naci and Ioannidis said in the published paper. In the meantime, “exercise interventions should therefore be considered as a viable alternative to, or, alongside, drug therapy.”
Drug Types
The definition of exercise and their frequency, intensity and duration varied across the list of studies included in the analysis, which limits the ability to generalize the findings to different forms of physical activity, said the authors, who received no funding for the review.
Drug treatments in the studies included statins and beta blockers for coronary heart disease; anticoagulants and antiplatelets for stroke; and diuretics and beta blockers for heart failure.
A landmark study by Dean Ornish, founder of the Preventive Medicine Research Institute, found that a low-fat vegetarian diet, increased exercise and stress management can reduce heart disease more than standard medical care. Patients who receive training from medical professionals on Ornish’s program for reversing heart disease have been reimbursed by Medicare since January 2011.
Cardiovascular disease is the leading cause of death globally, killing at least 17 million people a year with fatalities predicted to rise to more than 23 million by 2030, according to the World Health Organization.
Deaths linked to heart disease and stroke would be reduced by 25 percent if people quit smoking, limited salt intake and adopted other healthy habits, the U.S. Centers for Disease Control and Prevention said last month.
Not all patients benefit more from exercise than from drugs. For those recovering from heart failure, diuretic medicines were more effective, according to the analysis.
To contact the reporter on this story: Makiko Kitamura in London at [email protected]
To contact the editor responsible for this story: Phil Serafino at [email protected] ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. ||||| | – A lot of heart patients would be just as well off—and some potential stroke victims even better off—if their doctors prescribed physical activity instead of drugs, according to a new study. Researchers say they crunched the numbers from hundreds of studies involving 340,000 patients to pit medication against exercise—what they call a "blind spot" in research—and they found exercise as effective as drugs to prevent repeat heart attacks and Type 2 diabetes, the Wall Street Journal reports. Exercise proved to be more effective than drugs for preventing repeat strokes, but medication was more effective for patients recovering from heart failure. "Exercise is a potent strategy to save and extend life in coronary heart disease and other conditions," say the researchers, who suggest regulators consider requiring drug companies to compare the relative benefits of exercise during clinical trials of new medicines, reports Bloomberg. Experts called the study results "exciting"—but stressed that heart patients should use exercise in tandem with medication instead of as a substitute, and talk to their doctor before stopping medication or beginning an exercise program. | multi_news_1_0_0 |
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input: Story highlights Nearly 33% of Mexicans are obese, a United Nations report says
That's the highest level of the world's industrialized nations
Cheap, high-calorie food and lack of exercise are to blame, experts say
Mexico heads the list of the world's most overweight industrialized nations. Fat chance you say? Exactly.
Nearly a third of Mexican adults are obese, a recent United Nations Food and Agricultural Organization report says, topping even the United States, which comes in a close second at 31.8%.
The United States has long been a fixture atop the chubby list.
The culprit? High-calorie, low-cost, processed foods and an increasingly sedentary lifestyle as Mexican incomes rise and more people move into metropolitan areas.
The danger, according to the World Health Organization, is an increased risk of cardiovascular disease, diabetes, degenerative joint diseases and some cancers.
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The obesity epidemic is a double whammy for Mexican children, who can be both malnourished and overweight.
"They are exposed to high-fat, high-sugar, high-salt, energy-dense ... foods, which tend to be lower in cost but also lower in nutrient quality," the World Health Organization reports.
It's a growing problem -- and not just for Mexico. Since 1980, obesity rates worldwide have doubled.
In 2008, more than 1.4 billion adults were overweight and 500 million were obese.
The solution is simple but not always easy to accomplish, especially as nutritional options are limited in many parts of the world.
The WHO recommends:
-- Limiting your intake of fats and sugars
-- Increasing consumption of fruit and vegetables, as well as legumes, whole grains and nuts
-- Engaging in regular physical activity: 60 minutes a day for children and 150 minutes per week for adults ||||| WARCZone is a collection of outsider-uploaded WARCs, which are contributed to the Internet Archive but may or may not be ingested into the Wayback Machine. They are being kept in this location for reference and clarity for the Wayback Team, while also being accessible to the general public who are seeking any particular items they can regarding certain websites. |||||
summary: – Amid near-constant news of the obesity epidemic, you'd be forgiven for thinking the US led the developed world when it comes to weight—but by at least one measure, you'd be wrong. Mexico actually has a higher percentage of obese adults, with 32.8% of its grown-up population meeting the description, a UN report finds. The US isn't far behind, however, with 31.8% of adults considered obese. In Mexico, some 70% of adults are overweight, al-Jazeera notes. Keeping fit isn't easy for Mexican children in particular, who face both obesity and malnourishment, CNN reports. "They are exposed to high-fat, high-sugar, high-salt, energy-dense ... foods, which tend to be lower in cost but also lower in nutrient quality," says the World Health Organization. Amid climbing incomes and shifts to city life, Mexico is also seeing a more sedentary lifestyle among its population. Across the planet, obesity has doubled since 1980.
input: With last year's NKOTBSB tour (that's New Kids on the Block and Backstreet Boys) still fresh in our minds, we finally might be getting the ’N Sync reunion we really wanted all along. MTV has announced that along with receiving the Video Vanguard Award, Justin Timberlake will be joined onstage by his former bandmates (that's JC Chasez, Lance Bass, Joey Fatone, and Chris Kirkpatrick) for a "reunion performance." Whether that's a quick harmonizing of the "Bye Bye Bye" chorus, or putting back on the puppet strings, we cannot tell you, but one thing is for sure: ’N Sync's "sixth member," Lou Pearlman, will not be invited (or released from jail) to the reunion.
UPDATE: Turns out this rumor might not be true. On his SirusXM show, Lance Bass explained that some of the boys were in Miami together to see Justin and Jay Z's last stadium show and Page Six might have mistaken that for an upcoming reunion. ||||| Is she waiting Till the World Ends?
Britney Spears turned her website into a ticking clock this week, counting down the days, hours, minutes, and seconds til September 17, 2013, when we can only assume something Brit-rrific will occur!
But what??? Seems too soon for the Vegas show. (We WISH!)
So is it her new album? A new single? Another Charlie Brown homage?
Gimme Gimme More info, Brit!
The countdown is titled All Eyes On Me — as though we ever look ANYWHERE else!
We put our thinking caps on: Could this be the name of the new album?
Britney DID tweet earlier this month:
It's coming sooner than you think ;) But this album is for my diehard fans so it needs to be perfect!!!! http://t.co/OMTlLGMyuI — Britney Spears (@britneyspears) August 2, 2013
So we DEF know it’s coming soon, and the only question we have is WHEN!
But maybe now we know that, too!!!
Can’t wait to see what September 17 brings! We’ll be In the Zone til then!
[Image via FayesVision/WENN.]
Tags: album, all eyes on me, britney spears, countdown, music minute, website |||||
summary: | – The Internet is abuzz with the most exciting news since New Kids on the Block and the Backstreet Boys went on tour together: *NSYNC is back ... reportedly. According to the New York Post's sources, the boy band will reunite Sunday night at the VMAs. MTV has already announced Justin Timberlake will be performing at the awards show, but the sources say he'll be joined by JC Chasez, Lance Bass, Joey Fatone, and Chris Kirkpatrick. And all of the above were in Timberlake's VIP section Friday night at the Jay Z concert in Miami... A sampling of the amusingly breathless Twitter reaction: @asingleton138: "Crying because #nsync is reuniting for the VMA's and I've never been so happy ever" @shesliketexasss: "OMG OMG OMG. I CAN'T EVEN.... Ahhhh THIS IS THE BEST DAY OF MY LIFE" @LisaKasha: "Dear God, I hope this is true. My life will be complete." @WhoaGxD: "IS THIS REAL LIFE I THINK I'M HAVING A HEARTATTACK. WHAT IS AIR. PLEASE TELL ME THIS ISN'T A SICK JOKE" @MaggieTyma: "WHATTTT?! This is the best news I've ever heard in my whole life ever." @SDCCnerdsattack: "So a possible #NSync reunion at the VMA's?! Excuse me as a I FLAIL AROUND." @iitsbrittney: "I would literally fall on the floor, dead." @ctonies: "Guys, #Nsync is going to be at the VMAs! I cannot handle being at work after hearing this news I should tell my boss I have to go #byebyebye" @lesliejeannene: "I will not get too excited for this #nsync reunion - it can only lead to heartbreak when they don't sing Digital Get Down." And our favorite, from @zeemuffin: "I DIDN'T EVEN KNOW CHRIS WAS STILL ALIVE!!!" Not to be outdone, Britney Spears has started some sort of countdown clock on her website, meaning what must certainly be BIG NEWS, Perez Hilton reports. | multi_news_1_0_0 |
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News article:
Starting in 1996, Alexa Internet has been donating their crawl data to the Internet Archive. Flowing in every day, these data are added to the Wayback Machine after an embargo period. ||||| In addition to causing illness, viruses leave indelible footprints behind, because infection permanently alters the immune system. Blood tests that detect antiviral antibodies can provide information about both past and present viral exposures. Typically, such tests measure only one virus at a time. Using a synthetic representation of all human viral peptides, Xu et al. developed a blood test that identifies antibodies against all known human viruses. They studied blood samples from nearly 600 people of differing ages and geographic locations and found that most had been exposed to about 10 viral species over their lifetime. Despite differences in the rates of exposure to specific viruses, the antibody responses in most individuals targeted the same viral epitopes.
Structured Abstract
Introduction The collection of viruses found to infect humans can have profound effects on human health. In addition to directly causing acute or chronic illness, viral infection can alter host immunity in more subtle ways, leaving an indelible footprint on the immune system. This interplay between virome and host immunity has been implicated in the pathogenesis of complex diseases such as type 1 diabetes, inflammatory bowel disease, and asthma. Despite the growing appreciation for the importance of interactions between the virome and host, a comprehensive method to systematically characterize these interactions has yet to be developed.
Rationale Current serological methods to detect viral infections are predominantly limited to testing one pathogen at a time and are therefore used primarily to address specific clinical hypotheses. A method that could simultaneously detect responses to all human viruses would allow hypothesis-free analysis to detect associations between past viral infections and particular diseases or population structures. Humoral responses to infection typically arise within 10 to 14 days of initial exposure and can persist over years or decades, thus providing a rich source of the history of pathogen encounters. In this work, we present VirScan, a high-throughput method that allows comprehensive analysis of antiviral antibodies in human sera. VirScan uses DNA microarray synthesis and bacteriophage display to create a uniform, synthetic representation of peptide epitopes comprising the human virome. Immunoprecipitation and high-throughput DNA sequencing reveal the peptides recognized by antibodies in the sample. The analysis requires less than 1 μl of blood.
Results We screened sera from 569 human donors across four continents, assaying a total of over 108 antibody-peptide interactions for reactivity to 206 human viral species and >1000 strains. We found that VirScan’s performance in detecting known infections and distinguishing between exposures to related viruses is comparable to that of classical serum antibody tests for single viruses. We detected antibodies to an average of 10 viral species per person and 84 species in at least two individuals. Our approach maps antibody targets at 56–amino acid resolution, and our results nearly double the number of previously established viral B cell epitopes. Although rates of specific virus exposure varied depending on age, HIV status, and geographic location of the donor, we observed strong similarities in antibody responses across individuals. In particular, we found multiple instances of single peptides that were recurrently recognized by antibodies in the vast majority of donors. We performed tiling mutagenesis and found that these antibody responses targeted substantially conserved “public epitopes” for each virus, suggesting that antibodies with highly similar specificities, and possibly structures, are elicited across individuals. |||||
What is a shorter version of the above article? | – Blood tests can reveal a lot about you, from your suicide risk to your need for antibiotics. Now, researchers at Howard Hughes Medical Institute say a simple blood test can identify every virus you've ever had. From just a single drop of blood, VirScan can detect the remains of more than 1,000 strains of 206 viruses that are infecting or have ever infected a patient, Discover reports via a Science study. The cost: about $25, reports RedOrbit. Essentially, the immune system creates new B cells designed to battle a particular virus; those cells make the antibodies that bind to and inactivate the virus, and identifiable traces of those antibodies remain in the blood—ready to fight the virus again should it return. Previously, doctors could only test for antibodies to one virus at a time. But VirScan can search for hundreds of antibody reactions simultaneously, Popular Science reports. After screening blood from 569 people on four continents, experts found people were exposed to 10 viruses on average; two had antibodies for 84 different viruses. Study author Tomasz Kula makes clear one advantage of VirScan: "You can look at viral exposures in an unbiased way without having to suspect a particular infection ahead of time." That could help patients with undiagnosed diseases, including, for instance, Hepatitis C. Kula points out Hepatitis C can spur liver damage and cancer, often "because patients do not show symptoms for many years and so they did not get tested for this particular virus." (Read how a college dropout revolutionized blood tests.) | multi_news_1_0_0 |
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– It's a Star Wars avalanche: In addition to the coming Episodes VII, VIII, and IX, Disney plans to produce a number of spinoff movies that revolve around certain characters, CEO Robert Iger tells CNBC. No word yet on which characters will be featured in the standalone films (rumor is Yoda is up first), but Iger says they are "great ... characters that are not part of the overall saga." Lawrence Kasdan (who wrote Return of the Jedi, The Empire Strikes Back, Raiders of the Lost Ark, The Big Chill, The Bodyguard, the list goes on...) is working on the new films with Simon Kinberg (Mr. and Mrs. Smith, Sherlock Holmes), and JJ Abrams recently confirmed he will in fact be directing Episode VII, E! notes. "The implications for Star Wars fans will be great," Iger promised. "There are these good ideas out there and good creators interested in fleshing out these ideas, and we're going for it."
Let's expand this into a news article: Disney posted quarterly earnings and revenue that beat Wall Street's expectations on Tuesday amid strong revenue growth in its media networks business and its theme parks. But earnings slipped from a year ago, given higher programming costs at ESPN.
And, big news "Star Wars" fans: Disney, which announced it would buy Lucasfilm last year, plans to make spinoff movies based on characters in addition to the three sequels it had previously announced, CEO Bob Iger told CNBC in an interview after the earnings report.
After the announcement, the company's shares rose in extended-hours trading. (Click here to get the latest quotes for the company's shares.) ||||| CTRL-C or CMD-C, then press Enter. Click/tap elsewhere to exit, or press ESC.
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Ready for some brand-new lore?
A new hope became a reality today when Disney CEO Robert Iger confirmed that the studio is going to be making a number of Star Wars spinoff films in addition to the planned trilogy that will pick up after the action of Return of the Jedi.
"We are working on a few stand-alone films, derived from great Star Wars characters that are not part of the overall saga," the chief executive said in a sit-down with CNBC.
Star Wars responds to White House Death Star rejection letter
Lawrence Kasdan, who penned Jedi and The Empire Strikes Back, and Simon Kinberg are working on the new projects as well as consulting with J.J. Abrams, who, after giving fans the slick run-around about his intentions, recently confirmed that he is directing Episode VII.
"The implications for Star Wars fans will be great," Iger promised—though he would not divulge details about which characters would be getting the feature treatment, saying he would leave the creative process to executive producer Kathleen Kennedy and Lucasfilm.
"We have these great opportunities," he said, "because there are these good ideas out there and good creators interested in fleshing out these ideas, and we're going for it."
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– Breakfast may or may not be for champions, but skipping breakfast is for people who want a greater risk of a heart attack, reports CBS News. A Harvard study tracked the habits of 27,000 men for 16 years, and found that those who did without a morning meal were more likely to have a heart attack later in life. Researchers extrapolated that into a 27% greater risk for the general population, saying the results should apply to women as well as men, reports USA Today. They didn't get into why that is, only that the correlation exists. "The short answer may be that skipping the early meal keeps your body in the stressful state of fasting for longer, which can disrupt your metabolism in considerable and, apparently, life-threatening, ways," writes Alice G. Walton at Forbes. Lots of questions remain, but the lead researcher sums it up simply: "Don't skip breakfast," he writes. And try it to make it a reasonably healthy one.
| Let's expand this into a news article: Here's more evidence why breakfast may be the most important meal of the day: Men who reported that they regularly skipped breakfast had a higher risk of a heart attack or fatal coronary heart disease in a study reported in the American Heart Association journal Circulation.
Researchers analyzed food frequency questionnaire data and tracked health outcomes for 16 years (1992-2008) on 26,902 male health professionals ages 45-82. They found:
Men who reported they skipped breakfast had a 27 percent higher risk of heart attack or death from coronary heart disease than those who reported they didn't.
The men who reported not eating breakfast were younger than those who did, and were more likely to be smokers, employed full time, unmarried, less physically active and drank more alcohol.
Men who reported eating late at night (eating after going to bed) had a 55 percent higher coronary heart disease risk than those who didn't. But researchers were less convinced this was a major public health concern because few men in the study reported this behavior.
During the study, 1,572 of the men had first-time cardiac events.
"Skipping breakfast may lead to one or more risk factors, including obesity, high blood pressure, high cholesterol and diabetes, which may in turn lead to a heart attack over time," said Leah E. Cahill, Ph.D., study lead author and Postdoctoral Research Fellow in the Department of Nutrition at Harvard School of Public Health in Boston, Mass.
"Our study group has spent decades studying the health effects of diet quality and composition, and now this new data also suggests overall dietary habits can be important to lower risk of coronary heart disease," said Eric Rimm, Sc.D., senior author and Associate Professor of Epidemiology and Nutrition, Harvard School of Public Health and Associate Professor of Medicine at the Harvard Medical School.
Men who reported eating breakfast ate on average one more time per day than those who skipped breakfast, implying that those who abstained from breakfast were not eating additional make-up meals later in the day. Although there was some overlap between those who skipped breakfast and those who ate late at night, 76 percent of late-night eaters also ate breakfast, researchers said.
The study collected comprehensive questionnaire data from the participants and accounted for many important factors such as TV watching, physical activity, sleep, diet quality, alcohol intake, medical history, BMI, and social factors like whether or not the men worked full-time, were married, saw their doctor regularly for physical exams, or smoked currently or in the past.
While the current study group was composed of men who were of 97 percent white European descent, the results should also apply to women and other ethnic groups, but this should be tested in additional studies, researchers said.
"Don't skip breakfast," Cahill said. "Eating breakfast is associated with a decreased risk of heart attacks. Incorporating many types of healthy foods into your breakfast is an easy way to ensure your meal provides adequate energy and a healthy balance of nutrients, such as protein, carbohydrates, vitamins and minerals. For example, adding nuts and chopped fruit to a bowl of whole grain cereal or steel-cut oatmeal in the morning is a great way to start the day."
###
Other co-authors are Stephanie Chiuve, Sc.D.; Rania Mekary, Ph.D.; Majken Jensen, Ph.D.; Alan Flint, M.D., Dr.Ph.; and Frank Hu, M.D., Ph.D. The authors had no relevant disclosures.
The National Institutes of Health and a Canadian Institutes of Health Research Postdoctoral Research Fellowship to Dr. Cahill funded the study.
Try these American Heart Association tips for eating breakfast and these heart-healthy breakfast options.
For the latest heart and stroke news, follow us on Twitter: @HeartNews.
For updates and new science from Circulation, follow @CircAHA. ||||| Skipping breakfast has pretty consistently been linked to health risks – high blood pressure, overweight, and an unhealthy assortment of blood-fats, among them. But what’s interesting is that the health effects of skipping breakfast – even being overweight – don’t seem to be the result of indulging in extra “make-up” meals throughout the day. So it’s not about just the calories: There seems to be something else at play. The short answer may be that skipping the early meal keeps your body in the stressful state of fasting for longer, which can disrupt your metabolism in considerable and, apparently, life-threatening, ways.
The new study out of Harvard looked at the health records of nearly 27,000 men, all healthcare professionals 45-82 years old when the study began. The team looked for correlations in lifestyle choices – e.g., skipping breakfast – and health outcomes over a period of about 16 years.
Men who skipped breakfast were 27% more likely to experience heart attack or to die as the result of coronary heart disease. The men who skipped breakfast were more likely to be single, smokers, employed full-time, to drink more alcohol, were younger, and were less likely to be physically active than people who ate breakfast. Controlling for a slew of these and other risk factor for heart disease – like alcohol consumption, smoking history, body mass index, regular doctor visits, quality of diet, TV watching, activity level, and sleep habits – did reduce the link between skipping breakfast and heart disease, but didn’t obliterate it. The number of times per day the men ate wasn’t linked to heart risk.
As study author Leah Cahill tells me, the reason that skipping breakfast is linked to coronary heart disease is because it seems to give rise to a group of risk factors that collectively raise heart risk. “Prolonged fasting,” she says, “leads to increases in diastolic and systolic blood pressure, blood concentrations of insulin, triglycerides, free fatty acids and LDL-cholesterol, and to decreases in blood concentrations of HDL-cholesterol.” These are all the textbook risk factors for major heart trouble.
The question then is why skipping breakfast is linked to all of these issues. Cahill says that fasting is a stressful state for the body, so prolonging the fast by not eating when you wake up amplifies the stress. “As we sleep all night we are fasting, and so if we regularly do not 'break fast' in the morning, it puts a strain on our bodies that over time can lead to insulin resistance, hypercholesterolemia and blood pressure problems, which can then lead to heart disease.”
She and her team think that it’s all about when that first meal of the day is eaten.
“We believe that it is the timing of how breakfast 'breaks fast' in the morning that provides the protection against heart attack that we observed,” says Cahill. “Our bodies need to be fed food regularly in order to maintain healthy levels of blood lipids such as cholesterol, hormones such as insulin, and normal blood pressure." Perhaps eating earlier reduces the strain on the body that comes of fasting, and/or resets the metabolism.
It’s worth pointing out that this study and others like it seem to question the diets that encourage periodic fasting to reduce weight and/or heart risk factors. There’s also some fairly convincing evidence that calorie restriction can actually help the heart and longevity. But Cahill says that there’s a difference between skipping breakfast and other forms of fasting or restriction, and even the diets that include “fasting days” still make room for breakfast. Additionally, many studies that look at calorie consumption and restriction are done in rodents, which have fundamentally different metabolisms from humans’.
What’s important to note is that metabolism isn’t static – it can change depending on how and when you feed your body. And your cardiovascular health will feel the effects. Of course, eating doughnuts for breakfast probably counteracts the effect somewhat, so choosing reasonable ways in which to break your fast is essential.
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More on Forbes: ||||| People who don't eat breakfast are more likely to be hungrier later and eat larger meals.
Skipping breakfast may increase the risk of a heart attack, a study finds. (Photo: Pennsylvania State University Food Lab) Story Highlights Larger meals may spike blood sugar levels and lead to clogged arteries
It was an observational study of older men
Researcher: "Breakfast is an important meal"
ATLANTA — Another reason to eat breakfast: Skipping it may increase your chances of a heart attack.
A study of older men found those who regularly skipped breakfast had a 27% higher risk of a heart attack than those who ate a morning meal. There's no reason why the results wouldn't apply to other people, too, the Harvard researchers said.
Other studies have suggested a link between breakfast and obesity, high blood pressure, diabetes and other health problems seen as precursors to heart problems.
"But no studies looked at long-term risk of heart attack," said Eric Rimm, one of the study authors at the Harvard School of Public Health.
Why would skipping breakfast be a heart attack risk?
Experts aren't certain, but here's what they think: People who don't eat breakfast are more likely to be hungrier later in the day and eat larger meals. Those meals mean the body must process a larger amount of calories in a shorter amount of time. That can spike sugar levels in the blood and perhaps lead to clogged arteries.
But is a stack of syrupy pancakes, greasy eggs and lots of bacon really better than eating nothing?
The researchers did not ask what the study participants ate for breakfast, and were not prepared to pass judgment on whether a fatty, sugary breakfast is better than no breakfast at all.
Other experts agreed that it's hard to say.
"We don't know whether it's the timing or content of breakfast that's important. It's probably both," said Andrew Odegaard, a University of Minnesota researcher who has studied a link between skipping breakfast and health problems like obesity and high blood pressure.
"Generally, people who eat breakfast tend to eat a healthier diet," he added.
The new research was released Monday by the journal Circulation. It was an observational study, so it's not designed to prove a cause and effect. But when done well, such studies can reveal important health risks.
The researchers surveyed nearly 27,000 men about their eating habits in 1992. About 13% of them said they regularly skipped breakfast. They all were educated health professionals — like dentists and veterinarians — and were at least 45.
Over the next 16 years, 1,527 suffered fatal or non-fatal heart attacks, including 171 who had said they regularly skipped breakfast.
In other words, over 7% of the men who skipped breakfast had heart attacks, compared to nearly 6% of those who ate breakfast.
The researchers calculated the increased risk at 27%, taking into account other factors like smoking, drinking, diet and health problems like high blood pressure and obesity.
As many as 18% of U.S. adults regularly skip breakfast, according to federal estimates. So the study could be important news for many, Rimm said.
"It's a really simple message," he said. "Breakfast is an important meal."
Copyright 2013 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.
Read or Share this story: http://usat.ly/12cP1HJ ||||| You've heard it before: Breakfast is the most important meal of the day. A new study suggests it can be a life-saving one as well, especially for men.
Men who regularly skip breakfast were found in a new study to be at higher risk of a heart attack or death caused by heart disease than their counterparts who eat the meal daily.
"Don't skip breakfast," warned study author Dr. Leah E. Cahill, a postdoctoral research fellow in the nutrition department at Harvard School of Public Health in Boston, Mass., in a statement.
Eating breakfast may help lower diabetes risk
A healthy breakfast is linked to benefits like a lower risk for diabetes and obesity, and has also been shown to give eaters a daily boost of energy.
The U.S. Department of Agriculture adds that kids who eat a healthy breakfast are more likely to behave better in school, earn higher test scores for math and reading, pay attention, problem solve and be less likely to become overweight than kids who skip the meal.
To find out whether skipping a morning meal messed with the heart, researchers at the Harvard School of Public Health enlisted nearly 27,000 men between the ages of 45 and 82, who were enrolled in a study of male health professionals. They were tracked for 16 years.
Why calories count: 10 common myths busted
During the study, nearly 1,600 men suffered heart attacks.
They found men who skipped breakfast were 27 percent more likely to have a heart attack or die from heart disease than men who ate breakfast regularly.
A closer look revealed younger men were more likely to skip breakfast than older ones, as were smokers, the unmarried, alcohol drinkers, people who were less physically active and those who had full-time jobs. They also found men who reported waking up to eat at night after they went to bed had a 55 percent higher risk of heart disease than men who didn't, but they warned the overall risk was small since few men reported this night-owl behavior.
"Skipping breakfast may lead to one or more risk factors, including obesity, high blood pressure, high cholesterol and diabetes, which may in turn lead to a heart attack over time," said Cahill.
The study was published July 22 in Circulation, the journal of the American Heart Association.
The study did not look at what specifically these men ate for breakfast or whether it was healthy.
"We don't know whether it's the timing or content of breakfast that's important. It's probably both," Andrew Odegaard, a public health researcher at the University of Minnesota researcher who has studied links between skipping breakfast and obesity, high blood pressure, said to USA Today. "Generally, people who eat breakfast tend to eat a healthier diet." Odegaard was not involved in the research.
If their findings are replicated in women and across different races and ethnic groups, it could lead doctors to start recommending breakfast for their patients to improve public health, the researchers wrote.
A New England Journal of Medicine study this year called the notion that eating breakfast reduces obesity risk a "presumption," in a recent study looking at myths surrounding weight gain. The researchers cited two studies that found no evidence of a reduction in obesity risk among breakfast eaters. ||||| | multi_news_1_0_0 |
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Write a summary based on this article:
Bret Michaels -- Making An 'Amazing Recovery'
Bret Michaels continued to make tremendous progress in his recovery this weekend -- and one source close to the singer tells us the whole thing is nothing short of "amazing."
We're told Bret was "very aware" and in a "good mood" this weekend during an evaluation with a specialist -- the singer was even described as "somewhat talkative."
It's a major improvement from the "critical" state Bret was in after suffering a massive hemorrhage near his brain stem back on April 23 -- a condition that can often be fatal if not treated quickly by experienced professionals.
||||| The 47-year-old's will to live is "undeniable," said Dr. Joseph Zabramski, chief of cerebrovascular surgery at the Barrow Neurological Institute at St. Joseph's Hospital and Medical Center in Phoenix, who has been leading the team treating "The Celebrity Apprentice" contestant since he suffered a brain hemorrhage last week.
"Mr. Michaels will continue to undergo testing considering we have hit a few roadblocks, including hyponatremia, severe cranial and back pain suffered from blood drainage, an emergency appendectomy performed a week earlier and a lifelong history of Type 1 diabetes," Zabramski said in a statement released Friday by Michaels' publicist, Joann Mignano.
Michaels, who was diagnosed with Type 1 diabetes at age 6 and underwent an emergency appendectomy April 12, was rushed to St. Joseph's Hospital last week with a severe headache. He was later diagnosed with a subarachnoid hemorrhage, which causes bleeding in the fluid-filled spaces around the base of the brain. The cause of the hemorrhage is still unknown.
"There is no doubt that Mr. Michaels' condition is serious," Zabramski added.
He said Michaels, who has two daughters, 9-year-old Raine Elizabeth and 4-year-old Jorja Bleu, "did not want his family to wake up and see him lying unconscious in the middle of the floor." He also said immediate medical attention and Michaels' "fight to stay conscious during the hemorrhage" enabled doctors to stabilize his condition.
Other doctors said it is possible that Michaels could be healthy enough to appear on "The Celebrity Apprentice" live finale May 23. He is one of seven contestants remaining on Donald Trump's competitive reality series, including pop singer Cyndi Lauper, reality TV diva Sharon Osbourne, celebrity chef Curtis Stone and actress Holly Robinson Peete.
"If all the studies he had done show no evidence of an aneurysm being found, it would really just depend on his energy level," said Dr. Ronald Benitez, director of cerebrovascular surgery at Overlook Hospital in New Jersey. "If all the tests were negative, and I was watching the show at the end of May, I personally wouldn't be surprised if he was on it."
Michaels already filmed most of "The Celebrity Apprentice" last fall. However, the finale requires the last two contestants to debate against each other live in front of Trump. If Michaels ascends to the final showdown, it would be unprecedented in "The Apprentice" franchise history if he is not present to defend himself in the boardroom.
"We've never been confronted with anything like this," Trump told Matt Lauer on NBC's "Today" show Tuesday. "He is still in the show. He's doing really, really well, and all of sudden ... I can't imagine. It's going to be live for two hours, and it's going to be in four weeks. I can't imagine he's going to be on the finale, but he very well might be."
Whether he's fired or hired by Trump during the May 23 finale or in an earlier installment, Michaels' representatives are still giving his music fans something to believe in. While his appearances scheduled through May 21 have already been postponed, Michaels' other concert dates, including his summer tour with Lynyrd Skynyrd, are going ahead as scheduled.
"At this time, we are planning to resume the tour May 26 in Ft. Smith, Ark., provided there are no further complications or setbacks," said a statement posted Thursday on Michaels' website by his tour manager, Janna Elias. "We will then continue with all scheduled dates throughout the summer and fall, including the June and July tour with Lynyrd Skynyrd."
It certainly wouldn't be Michaels' first comeback tour. After glam-rock was edged out in the 1990s, the "Unskinny Bop" singer found renewed fame on reality TV. He starred as a judge on the third season of USA's singing contest "Nashville Star" in 2005, then as the bad-boy bachelor looking for lust on VH1's tawdry dating show "Rock of Love" from 2007 to 2009.
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On the Net:
Bret Michaels, http://www.bretmichaels.com/
"Celebrity Apprentice", http://www.nbc.com/the-apprentice/
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On the Net:
Bret Michaels, http://www.bretmichaels.com/
"Celebrity Apprentice", http://www.nbc.com/the-apprentice/ ||||| | – Bret Michaels is recovering so well from his brain hemorrhage that one friend calls it “amazing.” During a recent evaluation, he was “very aware,” “somewhat talkative,” and even in a “good mood,” the source tells TMZ. On Friday, his doctor said Michaels is expected to make a full recovery and called his will to live “undeniable"—adding that he may even be able to appear on the Celebrity Apprentice finale May 23, the AP reports. | multi_news_1_0_0 |
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Paula Deen is coming back.
Less than a year after her association with a racist slur led to the loss of her TV contract and many sponsors, Deen has created a new company. Paula Deen Ventures includes all the restaurants, cruises, cookbooks, cookware and other products that focus on her touting of traditional Southern cuisine.
Deen is partnering with Phoenix-based Najafi Media, which specializes in consumer distribution. Jahm Najafi, founder and chief executive officer, said in a statement Wednesday that he has "a deep respect for the hard work, unique content and quality products which Paula has built around her brand."
A spokeswoman for the company declined comment to CNNMoney when asked for details about the partnership.
Deen's sponsors dropped the food mogul like a hot potato last June after she admitted, during testimony in a racial discrimination lawsuit, that she had once used a racist slur to describe an African-American man. She later offered a tear-soaked apology via YouTube and NBC's "The Today Show."
The Food Network, owned by Scripps Networks Interactive (SNI), let her contract run out , and she was dumped by a slew of sponsors and business partners, including pork producer Smithfield Foods, the casino chain Caesars (CZR), the diabetes drugmaker Novo Nordisk (NVO) and retailers Wal-Mart (WMT), Target (TGT), Home Depot (HD), Sears (SHLD) and JCPenney (JCP).
Related: Duck Commander launches line of guns
Deen was already worth $10 million when the scandal hit, according to Brian Warner, managing editor of celebritynetworth.com.
Najafi is clearly betting on the zeal of loyal fan base, with costumers continuing to packing into her restaurants in Savannah, Ga., and buying her branded products. For example, Amazon (AMZN) pre-sales for her "New Testament" cookbook surged 1,300% in the wake of her scandal before Ballantine Books decide to cancel the release. ||||| Paula Deen is trying to reheat her career.
A recently formed new company, Paula Deen Ventures, said it has received an investment of between $75 million and $100 million from Najafi Cos., a private-equity company led by Jahm Najafi, who owns BMG Music Service and the Book-of-the-Month Club.
Phoenix-based Najafi Cos. said the cash... ||||| Paula Deen $75 MIllion For Huge Comeback
Breaking News
-- like the Phoenix -- is rising again ... thanks to a $75 MILLION infusion of cash from a Phoenix-based investment company that could put Paula's wares in the back pocket of airplane seats.Jahm Najafi clearly thinks the Paula Deen brand is still a marketable commodity, because his company is fronting the cash.As for Najafi's plan ... we found it extremely interesting that in 2012 he bought SkyMall magazine ... which you've probably leafed through and then failed to buy anything from inside. So the question -- will Paula's pots and pans end up in the mag?As you know ... Paula was unceremoniously dumped by virtually all of her sponsors after confessing she used the N word to describe a person who robbed the bank she was a teller at in the 80s.By the way ... in addition to SkyMall, Najafi owns the Book of the Month Club and Columbia House. |||||
What is a one-paragraph summary of the above article? | – Get ready to see much more of Paula Deen. The celeb chef seems to have rebounded from last year's mess over her use of a racist slur with an investment of $75 million from a private-equity firm, reports CNN Money. Deen is teaming with Najafi Cos. to create Paula Deen Ventures, and she's reportedly in talks with retail chains and TV networks about partnerships. (The Food Network says it is not among those talking to Deen.) Deen tells the Wall Street Journal that she's confident she will succeed given that "hundreds of thousands of my fans sent me messages of love and support," especially through the We Support Paula Deen Facebook page. TMZ notes that Jahm Najafi, owner of the company backing Deen, also owns SkyMall magazine and wonders whether "Paula's pots and pans (will) end up in the mag." | multi_news_1_0_0 |
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– The plant tequila is derived from could play a role in fighting obesity, and it doesn't involve getting people so drunk they forget to eat, researchers say. Natural sugars found in agave appear to protect mice against obesity and type 2 diabetes, Fox News reports. The sugars, known as agavins, acted as a dietary fiber and were not absorbed into the bloodstream, leading researchers to believe they could be an ideal artificial sweetener for obese or diabetic people. "In certain circumstances, artificial sweeteners are useful in helping people maintain glucose control," an expert tells MedPage Today. "If this is all true, it sounds like it could be another additional tool for people with diabetes." The researchers say "agavins have a great potential as a light sweetener," though two big obstacles exist: They aren't that widely available, and they aren't very sweet. And if you're an agave syrup fan, take note: That syrup is very different from agavins; the researchers liken it more to high-fructose corn syrup. (In more booze- and health-related news, click to read about the case of a man whose body produces its own alcohol.)
Let's expand this into a news article: Tequila shots may do more than lighten the mood at a party; the drink may be beneficial for your health as well.
According to researchers from Mexico, natural sugars derived from the agave plant, called agavins, greatly protected a group of mice against diet-induced obesity and type 2 diabetes, MedPage Today reported.
In a new study presented at the American Chemical Society (ACS) annual meeting in Dallas, mice were distributed into seven groups. One group received a diet of plain water, while the other groups received water supplemented with either aspartame, glucose, fructose, sucrose, agave syrup or agavins.
The mice that consumed agavins showed a reduction in food intake and weight and a decrease in blood glucose levels. These findings were similar to the control group that received standard water.
Because agavins act as dietary fibers and do not raise blood sugar, the researchers believe the ingredient could be used as an alternative sweetening agent.
"We believe agavins have a great potential as a light sweetener," Mercedes G. López, of the Centro de Incetagcioan y de Estudios Avanzados, Biotechnology and Biochemistry Irapuato, in Guanajuato, Mexico wrote in the ACS abstract. "They are sugars, highly soluble, with a low glycemic index and a neutral taste…This puts agavins in a tremendous position for their consumption by obese and diabetic people."
The alcoholic beverage tequila is made from the blue agave plant, primarily around the Mexican city of Tequila. However, Lopez noted that agavins are not widely available and not as sweet as regular sugars.
Click for more from MedPage Today. ||||| Action Points Note that this study was published as an abstract and presented at a conference. These data and conclusions should be considered to be preliminary until published in a peer-reviewed journal.
Agavins, natural sugars derived from the stem of the agave plant, reduced weight and blood sugar in mice prone to diet-induced obesity and type 2 diabetes, according to researchers from Mexico.
In the study, male C57BL/6J mice were randomly distributed into seven groups of four mice. One group received a standard diet plus plain water. The others received a standard diet plus water supplemented with either glucose, fructose, sucrose, agave syrup, agavins, or aspartame.
Mice that consumed agavins in their water reduced their food intake, lost weight, and showed a reduction in blood glucose levels, said Mercedes G. López, PhD, of the Centro de Investigacion y de Estudios Avanzados, Biotechnology and Biochemistry Irapuato, in Guanajuato, Mexico, at the American Chemical Society (ACS) annual meeting in Dallas.
"They were, most of the time, not different from the control," she said in an email to MedPage Today.
The study is the first to attempt to evaluate agavins -- fructans that are made of long branched chains of fructose that act as a dietary fiber and do not raise blood sugar -- as an alternative sweetener.
"We believe agavins have a great potential as a light sweetener," wrote López in the ACS abstract. "They are sugars, highly soluble, with a low glycemic index and a neutral taste."
Most importantly, she noted, they are nondigestable and act as dietary fiber. "This puts agavins in a tremendous position for their consumption by obese and diabetic people."
López's past research has shown that agavins reduce glucose levels and increase glucagon-like peptide-1 (GLP-1), a hormone that slows stomach emptying and stimulates production of insulin.
"In certain circumstances, artificial sweeteners are useful in helping people maintain glucose control," Nora Saul, MS, RD, CDE, manager of nutrition services at Joslin Diabetes Center in Boston, who was not involved in the study, told MedPage Today. "If this is all true, it sounds like it could be another additional tool for people with diabetes."
One potential challenge with agavins is that they are not widely available. Also, while agavins have half the calories of regular sugars, they are not as sweet, noted López in her email. The latter could be solved at least somewhat by partial hydrolysis, she said.
"People must somehow understand that we cannot have the best of both worlds," in terms of finding an alternative sweetener that is still very sweet, she commented.
There's a significant difference between agavins and the agave syrup and nectar that are marketed as an alternative to sugar, López explained. Those agave products are made of fructans that have been broken down into individual fructoses and are similar to high-fructose corn syrup, she said.
High sugar intake contributes to cardiovascular disease, obesity, and type 2 diabetes. The American Heart Association and the American Diabetes Association have said they are not sure whether sugar alternatives are a solution.
In a joint statement in 2012, the organizations said the data is "still inconclusive about whether using non-nutritive sweeteners to displace caloric sweeteners, such as added sugars, can reduce carbohydrate intake (important for diabetes control), calorie intake or body weight, benefit appetite, or lower other risk factors associated with diabetes and heart disease in the long run. "
The study was supported by Mondelez International and Agavaceae Produce. López is on a patent for the methodology to extract agavins.
1969-12-31T19:00:00-0500 |||||
– China is engaged in something more than mere mischief on Mischief Reef in the disputed Spratly Islands, new satellite images have revealed. The Center for Strategic and International Studies says photos show that China is building an airstrip on an artificial island it has created, which would be its third large airstrip in the strategic South China Sea island chain, reports CNN, which notes that the photos were taken after China promised to halt land reclamation in the area. CSIS analysts say the nearly 2-mile airstrip will be big enough to take any plane the Chinese military has. Earlier satellite images revealed the construction of airstrips at Subi and Fiery Cross, and a CSIS analyst tells Reuters that with a third airstrip, China will be able to have "more or less constant" patrols in the area, which is also claimed in full or in part by Taiwan, Vietnam, the Philippines, Malaysia, and Brunei. Over the last year, China has rapidly built what worried US commanders have called the "Great Wall of Sand." "All of these places have gone from being outposts on stilts to full islands, potentially with airstrips, within the space of a year or just over a year," a CSIS analyst tells CNN. The US has repeatedly expressed concerns about the construction, which is expected to be high on the agenda when Chinese President Xi Jinping visits the US next week.
| Let's expand this into a news article: Story highlights Images appear to show new airstrip being built in South China Sea
China had said that land reclamation almost complete
Chinese President Xi Jinping will visit U.S. next week
Hong Kong (CNN) China appears to building a third airstrip in disputed waters in the South China Sea, according to new satellite images analyzed by the Washington-based Center for Strategic and International Studies (CSIS).
The images, taken September 8, come after China pledged to bring land reclamation in those waters to a halt, and will make for uncomfortable discussions when Chinese President Xi Jinping visits Washington next week.
Greg Poling, the director of CSIS's Asia Maritime Transparency Initiative , said that China had reclaimed a flat rectangle of land with a retaining wall about 3,000 meters (3,280 yards) in length on Mischief Reef. It's similar to airstrips that China has been building on artificial islands at the Fiery Cross and Subi reefs in the contested Spratly Islands.
"If it does turn out to be a runway, China will have three airstrips that can carry any plane the PLA (People's Liberation Army) has to offer," he said.
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"All of these places have gone from being outposts on stilts to full islands, potentially with airstrips, within the space of a year or just over a year," he added. ||||| Chinese dredging vessels are purportedly seen in the waters around Mischief Reef in the disputed Spratly Islands in the South China Sea in this still image from video taken by a P-8A Poseidon surveillance aircraft provided by the United States Navy May 21, 2015.
WASHINGTON China appears to be building a third airstrip in contested territory in the South China Sea, a U.S. expert said on Monday, citing satellite photographs taken last week.
The photographs taken for Washington's Center for Strategic and International Studies (CSIS) think tank on Sept. 8 show construction on Mischief Reef, one of several artificial islands China has created in the Spratly archipelago.
The images show a rectangular area with a retaining wall, 3,000 meters (3,280 yards) long, matching similar work by China on two other reefs, Subi and Fiery Cross, said Greg Poling, director of CSIS's Asia Maritime Transparency Initiative (AMTI).
"Clearly, what we have seen is going to be a 3,000-meter airstrip and we have seen some more work on what is clearly going to be some port facilities for ships," he said.
Security experts say the strip would be long enough to accommodate most Chinese military aircraft, giving Beijing greater reach into the heart of maritime Southeast Asia, where it has competing claims with several countries.
News of the work comes ahead of a visit to Washington next week by Chinese President Xi Jinping. U.S. worries about China's increasingly assertive territorial claims are expected to be high on the agenda.
A spokesman for the U.S. Defense Department, Commander Bill Urban, declined to comment specifically on Poling's assessment, but repeated U.S. calls for a halt to land reclamation, construction and militarization of South China Sea outposts to "ease tensions and create space for diplomatic solutions."
"China's stated intentions with its program, and continued construction, will not reduce tensions or lead to a meaningful diplomatic solution," he added.
A new airstrip at Mischief Reef would be particularly worrying for the Philippines, a rival claimant in the South China Sea. It would allow China to mount "more or less constant" patrols over Reed Bank, where the Philippines has long explored for oil and gas, Poling said.
Three airstrips, once completed, would allow China to threaten all air traffic over the features it has reclaimed in the South China Sea, he said, adding that it would be especially worrying if China were to install advanced air defenses.
Satellite photographs from late June showed China
had almost finished a 3,000-meter airstrip on Fiery Cross.
Satellite images from earlier this year showed reclamation work on Subi Reef creating land that could accommodate another airstrip. Poling said the latest images made it obvious that such an airstrip was being built at Subi.
China stepped up creation of artificial islands in the South China Sea last year, drawing strong criticism from Washington.
Asked about Mischief Reef on Monday, China's Foreign Ministry spokesman Hong Lei repeated China's claim to "indisputable sovereignty" over the Spratly Islands and its right to establish military facilities there.
(Additional reporting by Ben Blanchard in Beijing; Editing by Jonathan Oatis and Christian Plumb) ||||| | multi_news_1_0_0 |
|
News article:
Abstract Objective In contrast to proposals that physical activity (PA) can be a substitute for alcohol use, people who engage in greater overall PA generally consume more alcohol on average than less-active peers. Acknowledging that both PA and alcohol use vary considerably from day-to-day, this study evaluated whether established associations reflect daily behavioral coupling within-person, are an artifact of procedures that aggregate behavior over time, or both. Methods A lifespan sample of 150 adults (aged 19–89 years) completed three 21-day measurement bursts of a daily diary study. At the end of each day, they reported on their PA and alcohol consumption. Data were analyzed in a negative binomial multilevel regression. Results As expected, both behaviors exhibited limited between-person variation. After controlling for age, sex, and seasonal and social calendar influences, daily deviations in PA were significantly associated with daily total alcohol use. Once the within-person process linking PA and alcohol use was controlled, usual PA and total alcohol use were not associated. Conclusions The established between-person association linking PA and alcohol use reflects the aggregation of a daily process that unfolds within-people over time. Further work is needed to identify mediators of this daily association and to evaluate causality, as well as to investigate these relations in high-risk samples. Keywords: exercise, substance use, intraindividual, smartphone
Methods Participants Data are drawn from the Intraindividual Study of Aging, Health, and Interpersonal Behavior (Ram et al., 2014), a study of 150 community-dwelling adults (51% women) recruited from The Pennsylvania State University and surrounding community. Purposively stratified by gender and across the adult life span, they were between 19 and 89 years of age (M = 47.64, SD = 18.85) in bins from 18–24 (n=22), 25–34 (n=27), 35–49 (n=30), 50–64 (n=41), and 65+ (n=30). Participants had obtained between 2 and 24 years of formal education (M = 16.36, SD = 3.90), and between 0 and 6 children (M = 1.5, SD = 1.41). Largely mirroring the local population, participants self-identified as Caucasian (91%), African American (4%), Asian American (1%), and Mixed or Other (4%) ethnicity; and as heterosexual (93%) or bisexual, gay, or lesbian (6%), with less than 1% of the participants declining to indicate sexual orientation. Participants described their employment status as full time employed (49%), retired (18%), students (15%), part-time employed (15%), or unemployed (3%). Participants’ yearly family income ranged from ‘under $20,000’ to ‘$200,000 and over’ (Median = ‘$50,000 – $74,999’, Mode = ‘$20,000 – $49,999’), with 8.7% declining to answer. Comprehensive information about the study can be found elsewhere (Ram et al., 2014). Methodological details relevant to the present study are included below. Procedures Participants completed three 21-day measurement bursts at regular intervals (mean interval between bursts = 124 days, SD = 38) with lab visits at the beginning and end of each measurement burst. During those lab visits, participants completed a series of web-based surveys that included demographic characteristics (distributed throughout the study to minimize burden during any single lab visit). During each 21-day measurement burst, participants used a custom smartphone survey application to provide end-of-day reports of their alcohol use and PA. In the first lab visit, a research assistant trained participants how to answer each question on the survey and specifically provided definitions of serving sizes and examples of different intensities of PA (this information was also available in the study handbook given to participants as well as in a help screen linked to those questions on the smartphone). Upon completing each daily report, participants’ time- and date-stamped data were transmitted wirelessly to a secure server and backed-up locally on the phone to minimize missing data due to transmission errors. When participants returned to the lab at the end of each burst, data were downloaded from their phones to fill in any non-transmitted observations. Participants’ compensation was pro-rated based on their compliance with study procedures. In total each person contributed an average of 57.1 days (SD = 12.68) of data. All procedures were approved by the institutional review board and participants provided written informed consent for all procedures prior to data collection. Measures Daily alcohol use was measured using three items where participants were asked to indicate the number of standard servings of beer (12 fl oz), wine (5 fl oz), and liquor (1.5 fl oz) consumed that day. The response scale included 0, 1, 2, 3, 4, and 5+ as options. Along with number of drink type-specific servings consumed, number of total servings of alcohol was calculated for each day as the sum of the three drink types. Daily physical activity was measured using items adapted from the Leisure Time Exercise Questionnaire (Godin & Shephard, 1985). This measure was adapted from a previous-week recall to a same-day recall – an adaptation that should reduce error variance due to recall failures and reliance on heuristics (Matthews et al., 2012). Participants reported the number of 10+ min bouts of mild-, moderate-, and vigorous-intensity PA that they engaged in each day. Weights corresponding to the metabolic equivalents of each level of activity were applied (mild = 3, moderate = 5, vigorous = 9) and weighted responses were summed to create a daily PA score. Following usual practice (see Schwartz & Stone, 1998) the daily measures of PA were person-centered and split into time-invariant and time-varying components. Usual PA was calculated as the person-specific mean across all days, and daily PA deviations as day-to-day differences from those means. Demographic characteristics were assessed using self-reports of personal (e.g., age, sex, race and ethnicity, sexual orientation, employment status, education) and family characteristics (e.g., household income, number of children). Drawing from time stamps on each record, within-person dummy variables were created for each day of the week and month of the year except Tuesday and November (which served as reference categories because they had the lowest mean alcohol consumption). Data Analysis Generalized multilevel models were used to accommodate the data structure with days nested within people (Snijders & Bosker, 1999) and to test hypotheses about both the within- and between-person associations between PA (daily and aggregate [usual], respectively) and alcohol use. All models were fit to the data using Mplus 5.2 (Muthén & Muthén, 1998). Although the missingness (≪ 1%) mechanism was unknown, we treated incomplete data within available records as missing at random based on the null correlations between the number of days with observations and person-level scores for key study variables. In the first step of the analysis we evaluated the utility of different distributional assumptions for accommodating the count nature of the alcohol servings variable. Specifically, we fit a series of unconditional models to participants’ total servings and compared the resulting fit indices to evaluate the relative fit of models that treated the outcome variable as Gaussian, Poisson, zero-inflated Poisson, or negative binomial (Coxe, West, & Aiken, 2009; Hilbe, 2011).1 As an example, the most complex of these, the negative binomial model, is given as E ( y it ) = log ( μ i t ) = γ 00 + u 0 i (1) where μ it is the expected number of alcohol servings for person i on day t, u 0i are residuals that are assumed normally distributed with mean 0 and variance σ2 u0 and γ 00 is the fixed effect intercept coefficient. The number of alcohol servings for person i on day t, y it , is assumed to be negative binomial distributed with a variance given by μ i t + α μ i t 2 , where α is the dispersion parameter. In the second step of the analysis (unadjusted model), we expanded the best-fitting model by adding daily and usual PA as predictors of alcohol use. For example, following the negative binomial model above, Equation 1 became E(y it ) = log(μ it ) + β 0i + β 1i (Daily PA it ) (2) with β 0 i = γ 00 + γ 01 ( Usual PA i ) + u 0 i (3) β 1i = γ 10 (4) where γ 10 = β 1i represents the average within-person association between daily deviations in PA and alcohol use, γ 01 represents the between-person association between usual PA (centered) and alcohol use, and β 0i represents average alcohol servings adjusted for daily deviations in PA. In practice, coefficients are converted to readily-interpretable incident rate ratios by exponentiation. In the third step of the analysis (adjusted model), equations (3) and (4) were expanded to include the control variables. Specifically, previous-day PA, previous-day alcohol use, day of week (via a set of dummy variables), and season (via a set of dummy variables) were included as additional predictors in Equation 2, and age (centered), sex (0=female, 1 = male), and their two-way interactions with each other and usual PA were included as additional predictors in Equations 3 and 4.
Results The dataset comprised 8574 daily records which represented 91% of 9450 (=150 participants × 21 days/burst × 3 bursts) possible daily records. Alcohol use data were available in 99.6% of these records. The upper portion of shows that beer accounted for the majority of daily alcohol servings; however, zero was both the mode and median for daily consumption of all three drinks as well as total servings. Participants consumed one or more total servings of alcohol on an average of 1.91 days/week (SD = 2.20; mode = 0, median = 1, range = 0 – 7). The average number of daily standard servings of alcohol (beer, wine, and liquor combined across all days) was 0.66 (SD = 1.32; mode = 0, median = 0, range = 0 – 12). When drinking days were examined separately, participants drank an average of 2.24 total servings (SD = 1.54; mode = 1, median = 2). According to the definition of heavy drinking (i.e., ≥ 5 servings/day for men, ≥ 4 servings/day for women; Wechsler, Dowdall, Davenport, & Rimm, 1995), only 3.7% of the days qualified as heavy drinking days; however, 35% of participants had at least one heavy drinking day during the study. Table 1 M SD Median Mode Range % Days Zero ICC Alcohol Use Total servings 0.66 1.32 0 0 0 – 12 70.2% .40 Beer 0.32 0.88 0 0 0 – 5 83.7% .31 Wine 0.21 0.68 0 0 0 – 5 87.8% .47 Liquor 0.14 0.54 0 0 0 – 5 91.6% .21 Physical Activity Light 1.47 1.49 1 0 0 – 10 29.5% .40 Moderate 0.77 1.12 0 0 0 – 10 56.4% .27 Vigorous 0.35 0.80 0 0 0 – 10 76.3% .21 Total (raw) 11.46 12.46 8 0 0 – 170 19.4% .33 Total (transformed) 2.63 1.68 2.76 0 0.00 – 8.98 19.4% .40 Open in a separate window PA data were available in 99.9% of the daily records. The lower portion of shows that both mean scores and the proportion of between-person variation (estimated by the intraclass correlation) decreased as the intensity of activity increased. Daily PA exhibited significant positive skew (skewness = 2.66, SE = 0.03, p < .05) so a Box-Cox transformation was implemented to normalize the distribution. With λ = 0.20, the resulting skew was −0.10. Correlations among key study variables were estimated at the within- and between-person levels of analysis. It is best to interpret these correlations descriptively rather than inferentially because of the inherent limitations of each (i.e., within-person correlations disregard the nesting of observations within people, and between-person correlations were based on behavioral aggregates and disregard the daily fluctuations in scores for alcohol use and PA). Correlations with age and sex suggested that alcohol use was only weakly associated with greater PA (within-person r = .03, between-person r = .01) and more likely for younger adults (r = −.06) and men (r = .18). Levels of usual consumption were correlated with age, such that younger people tended to consume more beer (r = −.25, p < .01) and less wine (r = .18, p < .05) than older people, with no systematic relation between age and usual levels of liquor consumption. The fit of an unconditional means model was estimated using a variety of distributions to characterize total servings of alcohol (i.e., Gaussian, Poisson, zero-inflated Poisson, negative binomial, or zero-inflated negative-binomial). Fit was best, as indicated by lower AIC and BIC statistics, for the negative binomial model (AIC = 15,121, BIC = 15,142) compared to the Gaussian (AIC = 25,297, BIC = 25,318), Poisson (AIC = 22,459, BIC = 22,467), or zero-inflated Poisson (AIC = 18,398, BIC = 18,412). The zero-inflated negative binomial model exhibited a similar fit (AIC = 15,063, BIC = 15,091), but did not offer sufficient improvement to justify the added complexity of differentiating two data generation processes. All subsequent analyses treated outcome variable residuals as following a negative binomial distribution. presents estimated parameters from the unadjusted and adjusted multilevel models of total servings of alcohol. A subset of 21 participants did not drink at all during the study but conclusions were the same whether they were included or excluded so results from the entire sample are presented. In both the unadjusted and adjusted models, people drank more on days when they were more active than usual (unadjusted γ = 0.05; adjusted γ = 0.04), and between-person differences in usual PA levels were unassociated with alcohol use. We also tested a quadratic association between these variables at both the within- and between-person levels, but these were not statistically significant and thus were not included in the final model. Daily alcohol consumption was positively associated with previous-day consumption but not with previous-day PA. Total alcohol consumption was greatest over the social weekend (Thursday through Sunday) but did not vary by season (as indicated by the month of the year). At the between-person level, age, sex, and their interactions (both with each other and with usual PA) were not associated with total alcohol consumption. Table 2 Unadjusted Model Adjusted Model γ SE IRR γ SE IRR Intercept −1.43** 0.16 0.24 −2.16** 0.43 0.11 Daily physical activity 0.05* 0.02 1.05 0.04* 0.02 1.04 Usual physical activity 0.20 0.14 1.22 0.07 0.19 1.07 Previous-day alcohola 0.06** 0.02 1.06 Previous-day physical activity 0.00 0.02 1.00 Sunday 0.25** 0.09 1.28 Monday 0.13 0.08 1.14 Wednesday 0.12 0.08 1.13 Thursday 0.34** 0.09 1.41 Friday 0.77** 0.10 2.17 Saturday 0.88** 0.11 2.42 January 0.13 0.13 1.14 February 0.10 0.14 1.11 March 0.02 0.11 1.02 April −0.11 0.09 0.90 May 0.16 0.11 1.18 June 0.08 0.09 1.09 July 0.15 0.14 1.17 August 0.15 0.12 1.16 September 0.24 0.20 1.27 October 0.16 0.10 1.17 December −0.04 0.12 0.96 Age −0.02 0.02 0.98 Sex 0.99 0.68 2.70 Age × Sex −0.01 0.02 1.00 Age × Usual physical activity −0.01 0.01 0.99 Sex × Usual physical activity 0.18 0.27 1.20 Dispersion, α 0.59** 0.19 0.44** 0.15 Random effects, σ2 u0 3.03** 0.46 2.60** 0.43 Open in a separate window Additional analyses were conducted to evaluate whether the daily coupling of PA and alcohol consumption varied as a function of age or the day of week. Neither age nor day of week moderated associations between daily PA and alcohol consumption (all p > .05). Thus, the daily coupling between these behaviors appeared to be relatively uniform across slow (age) and fast (day of week) timescales. Another analysis was conducted that controlled for both the burst number (0–2) and the sequence of the day within burst (0–20); neither predictor was significant and our conclusions from the model did not change. Another set of additional analyses were conducted to predict the binary outcome of heavy episodic drinking using two versions of the dataset: one with all observed days and one with drinking days only. In both cases, PA was not associated with heavy drinking at the within- or between-person level; however, only 3.7% of total days involved heavy drinking so these results may not be conclusive. Finally, an analysis was conducted to predict the binary incident rate of drinking on a given day and findings led to conclusions that were consistent with those outlined above based on count data.
Acknowledgments This work was supported by the National Institute on Aging grant AG035645 and the National Institute on Drug Abuse grant P50 DA010075. ||||| It had long been thought an antiquated concept associated with a slower, unproductive working world and Nigel Farage, but the boozy lunch is back.
Figures released by M&C Allegra Foodservice have revealed that the lunchtime pint is enjoying a surprising upturn in popularity. The study, which asked 18,000 people in-depth questions about their drinking habits, showed alcohol sales continuing to decline but a 2pc rise in the number consumed with food during the daytime. In the same period soft drinks and tap water sales fell by 3pc.
It's officially a trend, and you need to catch that train before it pulls out of town. To stop you from drinking alone, however, here are seven watertight scientific reasons available to convince your colleagues to join you.
1. It boosts your creativity
Are you prone to looking out of the window for extended periods of time, desperately searching for ideas? Do you find yourself easily bored and distracted when looking for answers, chatting to colleagues and reading articles that excuse daytime drinking? The only remedy is to have a pint at lunch.
It has been proven over and over again that a limited amount of alcohol aids creativity and problem solving. Beer, specifically, has just the right amount of kick to get the creative juices flowing without turning your brain to mush.
"Alcohol manipulates focus," Professor Jennifer Wiley of the University of Illinois at Chicago has said. “We have this assumption that being able to focus on one part of a problem or having a lot of expertise is better for problem solving. But that’s not necessarily true. Innovation may happen when people are not so focused. Sometimes it’s good to be distracted.”
So, if you're stuck on something, you'll always find the answer in the bottom of a glass. Just remember to write that idea down before you blackout.
This man is about to have an idea Credit: Alamy
2. It's better at hydrating you than water
In April this year, The Telegraph reported that "Not drinking enough water has the same effect as drink driving" – which is problematic, given that beer is actually better at hydrating you than water. Sort of.
Impish scientists at Granada University in Spain conducted an experiment in 2007 in which a group of students was asked to complete strenuous exercise routines until their temperatures reached 40ºC. Half the group were then given water to cool down with, and the other half beer. Emphatically, the hydration effect in the latter was "slightly better" than those on traditional agua. Gracias, students.
Still sceptical? British scientists have backed it up, too. Dr James Betts, an expert on nutrition and metabolism at Bath University, said at the time: "If you are dehydrated to start with following exercise, a beer, as opposed to a spirit, probably does not have a high enough concentration of alcohol to induce a diuretic effect."
So next time the health and safety bods suggest you drink 9 litres of water a day to keep your brain sharp, place a firm palm in their chest and bellow "NO. I AM GOING TO THE PUB, DARREN."
Thanks to his beer habit, Nigel Farage will technically live forever Credit: Getty
3. You will live longer
Should your boss ever berate you for wobbling back in to the office at 3pm after an extended conference call in JD Wetherspoon, riddle her this: had you not drunk those two pints at lunch, you could die early. So rather than wasting valuable working hours, you were in fact investing in more time further down the line.
A study by researchers at Virginia Tech University found that during a period of five years, non-drinkers were 19pc more likely to die than those who enjoy one or two drinks a day for half the week. What's more, the tee-totallers were 56pc more likely to be diagnosed with coronary heart disease. If you want to see your grandchildren grow up, go for a pint at lunch.
4. It complements food better than wine
Looking to liven up that Pret sandwich? Pair it with a fine, full-bodied pint of bitter.
Wine may bring out certain qualities in more sophisticated or flavoursome foods for evening meals, but lunchtime fare is better enhanced by beer. Curry notwithstanding (Cobra or Kingfisher being the obvious marriage partner), beer is reckoned to complement sandwiches, fried foods, cheese, pasta and chocolate.
"Beer is a great match for food because of the complexity of its flavors, its ability to provide refreshment and to interact with many food flavors," Marc Stroobandt, a beer sommelier, told Men's Fitness. "Even before the meal, beer already is doing its work for food pairing as the hops stimulate the appetite."
So if you truly want to enjoy your lunch, you will do so with a pint.
"We like to drink with Xi, 'cos Xi is our mate..." Credit: Andy Rain/EPA
5. Everyone back at the office will suddenly like you
It does not take us, nor scientists, to tell you that beer has properties that make it a useful social lubricant, but the University of Washington proved it so anyway.
In 2011 the faculty conducted a survey of nearly 500 students and asked them how often they had experienced a list of negative (hangovers, regretful sexual awakenings and so on) and positive effects of drinking (a greater ability to tell jokes, heightened bravery, singing quality etc). Not only did the majority say they experienced the positives far more, they also claimed not to take the negatives seriously.
Need more evidence? People who drink have more friends and are more likely to be keep a healthy marriage. Get the Special Brew; it's time to make friends.
This group of colleagues had not spoken before sipping these beers Credit: Alamy
6. It'll help you sleep
As nine out of ten health articles posted on the internet will tell you, getting a poor night's sleep is about as good for your overall wellbeing as skinny-dipping in lava. How fortunate, then, that a pint at lunch will do wonders for nodding off easily that night. Eight of them would do the job even faster, of course, but the sleep quality wouldn't be quite tip-top. A moderate amount each day, however, has been shown to help.
As well as helping us relax and fall asleep faster (not entirely helpful going in to the work afternoon, but worth bearing in mind), a small amount of alcohol each day could be beneficial to the quality of your rest, especially if you keep it to late afternoon.
Know your limits. This man's is one and one half. Credit: Alamy
7. It's far better for you than most other options
Consider what else is on offer at lunchtime. Coca-cola? Tap water? Wine? Panda pops? In the health stakes, all are thrashed by beer.
Water, as we have discovered, is utterly worthless when it comes to hydration. Wine triggers migraines. Coca-Cola will start to dissolve your soul after less than an hour. And Panda Pops? They died four years ago.
Beer, on the other hand, has been proven to lower the risk of type-2 diabetes, shrink the risk of gallstones, delay muscle deterioration and keep your bones strong. This isn't pub chat; these are facts. Look them up. ||||| Exercise provides a wealth of benefits to brain and body, and is regarded as a protective factor against disease. Protective factors tend to cluster together - that is, people who engage in one healthy behavior, such as exercise, also engage in other healthy behaviors, such as maintaining a nutritious diet and getting sufficient sleep. In contrast to exercise, alcohol consumption is not typically regarded as a health-promoting behavior, although moderate intake has been associated with a lower risk of cardiovascular disease. Surprisingly, several large, population-based studies have shown a positive association between physical activity and alcohol intake. The present review focuses on what is known about this relationship, including potential neural bases as well as moderating factors, and discusses important directions for further study, such as a more thorough characterization of people who both drink and exercise. We focus on ramifications for intervening with people who have alcohol use disorders, as exercise has been assessed as both a treatment and preventive measure, with mixed results. We believe that, in order for such interventions to be effective, clinical trials must distinguish treatment-seeking populations from non-treatment-seeking ones, as well as ensure that the use of exercise as a tool to decrease alcohol consumption is made explicit. We posit that a better understanding of the relationship between physical activity and alcohol intake will maximize intervention efforts by informing the design of clinical trials and research-driven prevention strategies, as well as enable individuals to make educated decisions about their health behaviors. ||||| Photo
Phys Ed Gretchen Reynolds on the science of fitness.
For many people, working out and alcohol are closely linked. Sports teams and training partners celebrate victories, bemoan defeats or mark the end of training sessions with a beer or three. Beer, in fact, provides a substantial portion of some exercisers’ fluid intake after workouts.
But whether exercise encourages people to drink and, likewise, whether drinking encourages people to exercise has been in dispute.
Now two new studies suggest that exercise may well influence when and how much people drink. Drinking may even affect whether people exercise, and, the findings suggest, the interplay between exercise and alcohol could be a good thing.
Past epidemiological studies have shown that people who exercise tend numerically also to be people who drink, and vice versa. In a typical study from 2001, for example, researchers found that men and women who qualified as moderate drinkers, meaning they downed about a drink a day, were twice as likely to exercise regularly as teetotalers.
But most of these previous studies had limitations. They relied, for instance, on people’s ability to recall their exercise and drinking habits over the course of, say, the past year, which can be notoriously unreliable. They also rarely took into account participants’ ages and gender, which affect how much people exercise and drink.
And perhaps most problematic, these past studies rarely determined whether people’s exercise and drinking tended to go hand in hand, suggesting a strong link. In other words, someone might work out on a Thursday and then imbibe on Friday evening with friends, providing no obvious connection between the activities. But in many earlier studies, he or she probably would have been categorized as an exerciser who drinks.
So to better untangle the relationship between drinking and sweating, researchers at Pennsylvania State University, in the most scientifically ambitious of the new studies, turned to a representative group of 150 adult men and women age 18 to 75 who already were enrolled in an ongoing, long-term health study at the university.
They asked these volunteers to visit the lab and fill out extensive questionnaires about their lifestyles, and then provided each of them with a simple smartphone app that could be used to record a day’s drinking and exercise activities. The app would automatically send each day’s report to the scientists.
The volunteers agreed to use the app for 21 consecutive days. Over the course of about a year, covering different seasons, each participant completed three of these 21-day reports.
When the researchers collated and compared the data from their volunteers, they found, for the first time, an unequivocal correlation between exercising on any given day and subsequently drinking, especially if someone exercised more than usual. As the scientists write in their study, which was published recently in Health Psychology, “people drank more than usual on the same days that they engaged in more physical activity than usual.”
This relationship held true throughout all seasons of the year and whether someone was a man or a woman, a collegian or a retiree. Age and gender did not affect the results.
Thankfully, the data did not show that exercise incited or exacerbated problem drinking. Only very rarely during the study did anyone report drinking heavily, which the researchers defined as downing more than four drinks in succession for a woman and five for a man.
But of course this kind of epidemiological study cannot determine why working out and drinking should be associated at all, which makes the second study, a newly published review of past, related experiments, especially those involving animals, so compelling.
In the review, published in Frontiers in Psychiatry, the authors point out that in lab rodents, both exercise and alcohol have been shown to increase activity in parts of the brain related to reward processing. The animals seem, in animal fashion, to get a kick out of both exercise and drinking.
But while the animals’ brains responded similarly to the two activities, they did not respond identically, the past studies show. There are aspects of reward processing related to exercise that differ from reward processing related to drinking, and those differences may help to explain why, if given the opportunity, animals will avidly engage in both running and ethanol sipping. The resulting neurological high appears to be generally more pervasive and lasting than with either activity alone.
It’s possible, although not proved, that something similar happens in people who exercise and imbibe, said J. Leigh Leasure, an associate professor at the University of Houston, director of the school’s behavioral neuroscience lab and the lead author of the new review.
Feeling a slight buzz after a workout, she said, we may, without overt volition, look to extend and intensify that feeling with a beer, a glass of wine or a cocktail.
But we also are more complicated and opaque in our behavior than rodents and likely to conjoin workouts and alcohol for many additional and sometimes tangled reasons, Dr. Leasure said. Many people, for instance, exercise in large part to burn the calories associated with drinking, meaning that, for them, drinking drives exercise behavior. Social bonding also plays an outsize role in the two activities for many of us, Dr. Leasure said. The camaraderie created on the practice field or among workout partners can nudge exercisers to reconvene convivially at the local bar, and those gatherings may motivate reluctant exercisers to stick with their routines, because they feel rewarded afterward.
But while the available evidence suggests that exercise may encourage people to drink, it does not indicate that this relationship is necessarily worrisome for the vast majority of us, Dr. Leasure said. Someone who drinks moderately is unlikely to become a problem drinker as a result of exercise.
“But it’s good to be aware,” she said, that the two activities frequently intersect. “Many people may not have noticed” that they indulge in an extra beer or two on those days when they visit the running trail or the gym.
Related: |||||
What is a shorter version of the above article? | – If you ever crave a beer after sweating it out on the trail or at the gym, you're not alone. Two new studies suggest that there's a link between exercise and drinking, and that it "could be a good thing," reports the New York Times. What's more, neither study showed that exercise incites heavy drinking (defined as four or more drinks for a woman, five or more for a man). In one study, researchers at Pennsylvania State University report in the journal Health Psychology an "unequivocal correlation," as the Times puts it, between exercising and then drinking, most notably when the workout was particularly strenuous. As the authors found, "People drank more than usual on the same days that they engaged in more [physical activity] than usual." In the other study out of the University of Houston, researchers report in the journal Frontiers in Psychiatry that the brains of lab rodents tend to respond very similarly, though not identically, to exercise and alcohol—and that the neurological high is markedly stronger when both activities are performed instead of just one. It's possible, one researcher posits, that by drinking after a workout we're subconsciously seeking to extend the euphoria of the workout. And the authors of the first study observe that while exercise "has intuitive appeal as an alternative activity" for drinking, "the literature does not support this approach as a universal, primary prevention strategy." Meanwhile, drinking during the daytime is on the rise, reports the Telegraph. (One study has found that moderate drinking is associated with longer life expectancy.) | multi_news_1_0_0 |
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– Amid near-constant news of the obesity epidemic, you'd be forgiven for thinking the US led the developed world when it comes to weight—but by at least one measure, you'd be wrong. Mexico actually has a higher percentage of obese adults, with 32.8% of its grown-up population meeting the description, a UN report finds. The US isn't far behind, however, with 31.8% of adults considered obese. In Mexico, some 70% of adults are overweight, al-Jazeera notes. Keeping fit isn't easy for Mexican children in particular, who face both obesity and malnourishment, CNN reports. "They are exposed to high-fat, high-sugar, high-salt, energy-dense ... foods, which tend to be lower in cost but also lower in nutrient quality," says the World Health Organization. Amid climbing incomes and shifts to city life, Mexico is also seeing a more sedentary lifestyle among its population. Across the planet, obesity has doubled since 1980.
Let's expand this into a news article: Story highlights Nearly 33% of Mexicans are obese, a United Nations report says
That's the highest level of the world's industrialized nations
Cheap, high-calorie food and lack of exercise are to blame, experts say
Mexico heads the list of the world's most overweight industrialized nations. Fat chance you say? Exactly.
Nearly a third of Mexican adults are obese, a recent United Nations Food and Agricultural Organization report says, topping even the United States, which comes in a close second at 31.8%.
The United States has long been a fixture atop the chubby list.
The culprit? High-calorie, low-cost, processed foods and an increasingly sedentary lifestyle as Mexican incomes rise and more people move into metropolitan areas.
The danger, according to the World Health Organization, is an increased risk of cardiovascular disease, diabetes, degenerative joint diseases and some cancers.
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The obesity epidemic is a double whammy for Mexican children, who can be both malnourished and overweight.
"They are exposed to high-fat, high-sugar, high-salt, energy-dense ... foods, which tend to be lower in cost but also lower in nutrient quality," the World Health Organization reports.
It's a growing problem -- and not just for Mexico. Since 1980, obesity rates worldwide have doubled.
In 2008, more than 1.4 billion adults were overweight and 500 million were obese.
The solution is simple but not always easy to accomplish, especially as nutritional options are limited in many parts of the world.
The WHO recommends:
-- Limiting your intake of fats and sugars
-- Increasing consumption of fruit and vegetables, as well as legumes, whole grains and nuts
-- Engaging in regular physical activity: 60 minutes a day for children and 150 minutes per week for adults ||||| WARCZone is a collection of outsider-uploaded WARCs, which are contributed to the Internet Archive but may or may not be ingested into the Wayback Machine. They are being kept in this location for reference and clarity for the Wayback Team, while also being accessible to the general public who are seeking any particular items they can regarding certain websites. |||||
– A Long Beach, Calif., man has filed a lawsuit after he was denied a $5 million Scratchers ticket prize on a technical measure: his teenage son bought the ticket. Per the Daily Bulletin, Ward Thomas’ suit filed Friday against the California Lottery Commission alleges breach of contract among other complaints. Thomas says he sent his 16-year-old son Benjamin into a Mobil gas station to exchange and cash out 12 winning tickets in October, reports ABC 7. The father and son took home $230 along with five $20 Scratchers tickets, which they played when they returned home. One of those tickets yielded a $5 million prize, which he says he validated that night at a 7-Eleven and later again at a Santa Ana lottery office. Ward says that after submitting his claim, the lottery commission confirmed the winning, but come December, denied his claim for the cash prize because his son was not of legal age (18) to purchase the ticket. The suit claims that workers at the gas station, also a defendant, never said Benjamin was too young to buy the tickets and failed to enforce this rule. It also accuses the commission of false advertising since there were no signs at the store stating age requirements. The California Lottery Commission and Mobil station did not comment on the pending litigation.
| Let's expand this into a news article: A Long Beach resident is suing the California State Lottery Commission and a local liquor store for failing to honor a winning Scratchers ticket worth $5 million.Ward Thomas is suing the commission and Los Altos Mobil gas station along Bellflower Boulevard for damages resulting from the loss and denial of the winning ticket.In the lawsuit, Thomas claims on or around Oct. 16 at 8 p.m. he and his 16-year-old son Benjamin went to the Mobil Mart to buy California Lottery tickets, which they had done in the past.At Ward's request, he sent his son inside with 12 "Deluxe 7's" Scratchers that totaled $330 in winnings. He asked his son to exchange the tickets for more Scratchers, according to the lawsuit.Benjamin bought five Scratchers tickets at $20 each and was given the remaining $230 to take home. When Ward and his son went home, they played the tickets and a "100X The Money" ticket resulted in a winning amount of $5 million.According to Thomas's claim, he validated the ticket at a 7-Eleven in the 1700 block of Palo Verde Avenue around 9:54 p.m. that night. He then validated the ticket again the next day at the state's Lottery District in Santa Ana.Ward said he then submitted the claim for the winning ticket and was told by the commission he was the winner of the $5 million prize.But on Dec. 5, the commission denied his claim for the money, stating the ticket was purchased by his son who could not legally play the lottery, according to the suit.The plaintiff claims that at no time did the store tell his son he could not purchase Scratchers tickets because of his age. He also claims his son was not asked to have an adult present to buy the tickets or that he provide his identification.In the lawsuit, it claims the commission failed in operating by its own rules properly and failed to have Benjamin informed that he could not buy a ticket because of his age. It also states his son was not asked for an ID by the store, which means the store failed to verify his son's age before allowing him to get a ticket and that Benjamin was not informed any winnings would be invalidated.The suit goes on to say there were no signs at the store, that the commission failed to honor Ward's winning ticket, it improperly trained retailers about the lottery rules, especially when it comes to the age of the buyer, and not having stores properly enforce those rules.The lawsuit states Ward has suffered and will continue to suffer financial losses including interest and other damages because of the ongoing issue. It also said Ward suffers emotionally, which totals about $50,000 in damages.The California Lottery Commission said it could not comment because of pending litigation. The Mobil station also did not comment. ||||| A Long Beach man sued the state and California Lottery Commission Friday, alleging he was wrongfully denied a $5 million Scratchers ticket prize because his 16-year-old son bought the winning ticket.
Ward Thomas’ Los Angeles Superior Court lawsuit alleges failure to discharge a mandatory duty, breach of contract, negligence and both intentional and negligent representation. The suit seeks unspecified damages.
A California Lottery representative did not immediately reply to a request for comment.
Thomas says his son bought five Scratchers tickets at a Mobil station on Bellflower Boulevard in Long Beach on Oct. 16 by exchanging other winning tickets. One of the five was a winning ticket with a $5 million prize, the suit states.
Thomas validated the ticket at a 7-Eleven store in Long Beach that same day and then validated it again the next day at the lottery office in Santa Ana, the suit states.
However, on Dec. 5, the Lottery Commission told Thomas that his award was being denied because his son was a minor and therefore was “not legally able to play the lottery,” the suit states.
The complaint does not state how the commission knew Thomas’ son bought the tickets and that the purchaser was under age 18.
No one at the gas station, which also is a defendant, told Thomas’ son that he was too young to buy a lottery ticket, the suit states.
The suit further alleges the commission failed to enforce its own rules in the operation of the lottery and that the commission engaged in false advertising by not publicizing that lottery ticket buyers had to be at least 18 years old. ||||| | multi_news_1_0_0 |
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Write an article based on this summary:
– Five city and state officials were charged Wednesday with involuntary manslaughter over the water crisis in Flint, Michigan, the Detroit Free Press reports. They are Michigan Department of Health and Human Services Director Nick Lyon—the highest-ranking official to be charged in the water crisis so far, per the Detroit News—former Flint Emergency Manager Darnell Earley, former City of Flint Water Department Manager Howard Croft, plus Michigan Department of Environmental Quality’s Drinking Water Chief Liane Shekter-Smith and Water Supervisor Stephen Busch. Twelve people died after the city's water supply was changed to the Flint River in April 2014 and there was an outbreak of Legionnaires' disease. Prosecutors allege that Lyon knew about the outbreak by at least Jan. 28, 2015, yet did not make the news public until a year later; he is charged with causing the Dec. 13, 2015, death of Robert Skidmore. All of the involuntary manslaughter charges are linked to Skidmore's death; the 85-year-old died after many cases of Legionnaires' disease had been diagnosed, but the public still had not been notified of the outbreak. Lyon is also charged with misconduct in office for allegedly telling an official to halt an analysis that would have helped figure out what caused the outbreak, the Detroit Free Press reports. Also Wednesday, Chief Medical Executive Dr. Eden Wells was charged with obstruction of justice and lying to a police officer; she is accused of giving false testimony to a special agent, lying to a peace officer about when she knew of the outbreak, and threatening to withhold funding for the Flint Area Community Health and Environment Partnership if it did not stop investigating the outbreak. Flint residents are still advised to use a filter if they plan to drink the city's tap water, and many use bottled water instead, which is distributed for free in the city.
Article: |
CLOSE The ongoing Flint water crisis has taken a toll on residents of this iconic Michigan city, who have been living with lead-tainted tap water for over two years. One Flint resident describes the experience as, “like being in war, but without violence.”
Buy Photo Attorney General Bill Schuette takes questions after announcing new charges against two high-ranking state health officials in the Flint drinking water crisis on Wednesday June 14, 2017. (Photo: Ryan Garza, Detroit Free Press)Buy Photo
Michigan Attorney General Bill Schuette today filed new, more serious charges in the Flint Water Crisis investigation, but also said the case is shifting to a new phase.
"We will turn to the prosecution of this investigation," Schuette said at a news conference in Flint this morning. "We are confident that the charges that we have filed will be upheld in the courts."
Schuette's statement came after he announced involuntary manslaughter charges against Nick Lyon, director of the Michigan Department of Health, as well as Darnell Earley, Flint's former emergency manager; Howard Croft, the city's former director of public works; Liane Shekter-Smith, the state's former top drinking water official and water supervisor Stephen Busch of the Department of Environmental Quality.
Those charges, felonies punishable by up to 15 years in prison, stem from the death of 85-year-old Robert Skidmore, who December 2015 death is tied to the Legionnaire's Disease outbreak in Flint.
State officials, they said, knew about the outbreak but refused to sound a public alarm that could have saved lives. At least 12 people died from complications related to the outbreak.
In all, 15 people have been charged with 51 counts. Two have plead no contest to lesser charges and agreed to help with the investigation, but none of the cases have gone to court yet.
Todd Flood, a former Wayne County Prosecutor who is serving as special counsel in the investigation, said today's charges stem from the deadly inaction of government officials.
"There are two types of people: those who give a damn and those who don't," Flood said. "I have run across many public servants who do care, but this is a case where there is willful disregard."
Andrew Arena, a former head of the Detroit FBI branch who is serving as lead investigator, said he began the probe thinking perhaps people just made mistakes, but concluded otherwise as the investigation continued.
"Many people attempted to do what is right," Arena said. "People didn't just make mistakes, they willfully and intentionally failed to do what they were supposed to do."
And Schuette said that while no charges currently are planned against Gov. Rick Snyder, his investigation continues, and "we have attempted to interview the governor," but "we were not successful."
More Flint water crisis coverage:
Michigan health director Nick Lyon, 4 others charged with involuntary manslaughter over Flint water
Flint water crisis: 5 officials face manslaughter charges
Criminal charges against top Michigan officials extremely rare
Watch: Manslaughter charges announced in Flint water crisis probe
Buy Photo Attorney General Bill Schuette announces new charges against two high-ranking state health officials in the fourth round of criminal charges in the Flint drinking water crisis on Wednesday June 14, 2017 during a press conference at Riverfront Banquet Center in downtown Flint. (Photo: Ryan Garza, Detroit Free Press)
Here are the list of additional charges announced today:
Michigan Health and Human Services Director Nick Lyon is charged with involuntary manslaughter and misconduct in office, both felonies.
Chief Medical Executive Eden Wells is charged with obstruction of justice and lying to a police officer.
Four defendants charged earlier -- former Flint emergency manager Darnell Earley, former Michigan Department of Environmental Quality drinking water chief Liane Shekter-Smith; DEQ drinking water official Stephen Busch; and former City of Flint Water Department manager Howard Croft -- were each charged with involuntary manslaughter.
All of the new charges are in connection with the Legionnaires' disease outbreak in the Flint area that led to 12 deaths after the city's water supply was switched to the Flint River in April 2014.
Read more Free Press coverage of the Legionnaires' disease outbreak:
Read the Free Press investigation from April 2016: Why were officials silent on Legionnaires' in Flint?
Here are all the victims of the Legionnaires' disease outbreak in Flint
Database: Search all of the Legionnaires' disease cases by county
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EDITOR'S NOTE: Here is the full news release sent by Michigan Attorney General Bill Schuette this morning regarding five people charged with involuntary manslaughter in the Flint water crisis.
FLINT – Michigan Attorney General Bill Schuette today announced that he has charged Michigan Department of Health and Human Services Director Nick Lyon, former Flint Emergency Manager Darnell Earley, former City of Flint Water Department Manager Howard Croft, as well as Michigan Department of Environmental Quality’s Drinking Water Chief Liane Shekter-Smith and Water Supervisor Stephen Busch with involuntary manslaughter related to their alleged failure to act in the Flint Water Crisis. Involuntary manslaughter is punishable by up to 15 years in prison, and/or a $7,500 fine. In addition to the involuntary manslaughter charges, Schuette also charged Lyon with Misconduct in Office, a felony, subject to 5 years in prison and/or a $10,000 fine. MDHHS Chief Medical Executive Eden Wells has also been charged with lying to a peace officer and obstruction of justice related to an alleged attempt to stop an investigation into the health crisis in Flint and later misleading investigators as to her actions. Schuette was joined at the announcement by Genesee County Prosecutor David Leyton, Flint Water Investigation Special Prosecutor Todd Flood, and Chief Investigator Andrew Arena. INVESTIGATION INTERIM REPORT
With more than a dozen people now having been charged, and pre-trial hearings and other legal proceedings occurring, Schuette released the initial results of the more than yearlong investigation. Included in the report is a comprehensive look at today’s and past charges made, as well as a review of the facts and evidence in the case. NOTE: The report is attached to this press release. DEFENDANTS
Multiple Flint-area residents died of Legionnaires’ disease in the time immediately following the switch from Detroit Water and Sewer Department to the Flint River. All defendants charged with involuntary manslaughter are charged in relation to the death of Robert Skidmore, 85, of Mt. Morris, Michigan. Skidmore died of Legionnaires’ disease after many others had been diagnosed with the illness, yet no public outbreak notice had been issued. The charges allege failure to notify and lack of action to stop the outbreak allowed the disease to continue its spread through Flint’s water system. NICK LYON
As the Director of the Michigan Department of Health and Human Services, a position whose duties are outlined in the Michigan Constitution, Lyon has a duty to protect public health. The investigation has shown that Lyon allegedly received notice of a deadly Legionnaires’ Disease outbreak in Genesee County nearly one year before he informed the public. After being informed about a potentially fatal health risk, Lyon allegedly deliberately failed to inform the public of a deadly Legionnaires’ Disease outbreak, which resulted in the death of Robert Skidmore. Furthermore, Lyon allegedly participated in covering up the source of Genesee County’s Legionnaires’ Disease outbreak by repeatedly attempting to prevent an independent researcher from looking into the cause of the outbreak. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. COUNT 2 – MISCONDUCT IN OFFICE Did between February 2015 and May 2017, commit misconduct in office, an indictable offense at common law, in violation of his duty to protect the health of the citizens of the County of Genesee, State of Michigan and to protect the public health enjoined upon him by the Michigan Public Health Code, MCL 333.5111(1); MCL 333.5111(2)(f);MCL 333.2251(1): MCL 333.2251(3); and MCL 333.20531 and the Critical Health Problems Reporting Act; contrary to MCL 750.505. [750.505] FELONY: 5 Years and/or $10,000.00. EDEN WELLS
As the Chief Medical Executive of the Michigan Department of Health and Human Services, Dr. Eden Wells has a responsibility to protect the health and welfare of Michigan residents. During the course of the investigation of the Flint Water Crisis, it is alleged that Wells attempted to withhold funding for programs designed to help the victims of the crisis, and then lied to an investigator about material facts related to the investigation. Charges:
COUNT 1 – OBSTRUCTION OF JUSTICE Did commit the common law offense of obstruction of justice by knowingly providing false testimony to a Special Agent and by threatening to withhold funding for the Flint Area Community Health and Environment Partnership if the partnership did not cease its investigation into the source of the Legionnaires’ Disease outbreak in Flint, Michigan; contrary to MCL 750.505. FELONY: 5 Years or $10,000. DNA to be taken upon arrest. COUNT 2 – LYING TO A PEACE OFFICER – 4 YEAR OR MORE CRIME INVESTIGATION After being informed by Special Counsel Todd Flood, in the presence of Special Agent Arthur Wimmer, that they were conducting a criminal investigation, did knowingly and willfully make a statement or statements to the officer that he or she knew was false or misleading regarding the following material fact or facts relating to the investigation: the date she knew of the Legionnaires’ Disease outbreak in Flint, Michigan, and the officer was conducting a criminal investigation regarding involuntary manslaughter; contrary to MCL 750.479c(2)(c). [750.470C2C]. HIGH COURT MISDEMEANOR: 2 Years and/or $5,000.00. STEPHEN BUSCH
Stephen Busch served as the Michigan Department of Environmental Quality District 8 Water Supervisor, a position which would have allowed him to order the Flint Water Treatment Plant be shut down because it was not producing safe water. In January of 2015, Busch was made aware of the Legionnaires’ Disease outbreak, yet he allegedly represented to the public that Flint’s drinking water was safe. Busch was previously charged with felony Misconduct in Office, Tampering with Evidence, Conspiracy to Tamper with Evidence, and two misdemeanor counts for both a treatment and monitoring violation of the Michigan Safe Water Drinking Act. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. LIANE SHEKTER-SMITH
As the Chief of the Office of Drinking Water and Municipal Assistance at the Department of Environmental Quality, Shekter-Smith had the ability to order the Flint Water Treatment Plant shut down for failure to produce safe water. Shekter-Smith was previously charged with a felony of Misconduct in Office and a misdemeanor charge of Willful Neglect of Duty. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. HOWARD CROFT
As Director of Public Works for the City of Flint, Croft had the ability to mandate changes to the treatment processes at the WTP to ensure proper disinfection was occurring, or switch back to DWSD. Mike Glasgow, former Flint Water Treatment Plant Operator, was allegedly pressured by Croft to start using the Flint Water Treatment Plant. Croft’s alleged failure to treat the water properly contributed to the bacterial outbreaks found in Flint, including the legionella in the spring of 2015. Croft was previously charged with felony False Pretenses and Conspiracy to Commit False Pretenses. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. DARNELL EARLEY
As an appointed Emergency Manager for the City of Flint, Earley was tasked with ensuring the health and welfare of the City. During his terms as Emergency Manager, Earley contributed to the decisions that allegedly caused the death of Robert Skidmore by keeping the City on the water source even as it became obvious the source should be switched back to Detroit Water & Sewer. Earley was previously charged with felony False Pretenses, Conspiracy to Commit False Pretenses, Misconduct in Office and a misdemeanor charge of Willful Neglect of Duty. Charges:
COUNT 1 – HOMICIDE – MANSLAUGHTER – INVOLUNTARY Did cause the death of Robert Skidmore on December 13, 2015, by failing to alert the public about a Legionnaires’ Disease outbreak in Flint, Michigan when he had notice that another outbreak would occur; contrary to MCL 750.321. [750.321-C] FELONY: 15 Years and/or $7,500.00. DNA to be taken upon arrest. Acriminal charge is merely an accusation and the defendants are presumed innocent until proven guilty.
Read or Share this story: http://on.freep.com/2t1Kvv3 ||||| Buy Photo Clockwise from upper left, Dr. Eden Wells, Nick Lyon, Darnell Earley and Howard Croft (Photo: Detroit Free Press, Michigan Attorney General)Buy Photo
FLINT — Attorney General Bill Schuette charged two high-ranking state health officials today in the fourth round of criminal charges in the Flint drinking water crisis.
He also said he will be adding new, serious felony charges against four defendants who were charged earlier in the investigation.
And Schuette said that while no charges currently are planned against Gov. Rick Snyder, his investigation continues, and "we have attempted to interview the governor," but "we were not successful."
Michigan Health and Human Services Director Nick Lyon is charged with involuntary manslaughter and misconduct in office, both felonies.
More Flint water crisis coverage:
Michigan health director Nick Lyon, 4 others charged with involuntary manslaughter over Flint water
Flint water crisis: 5 officials face manslaughter charges
Criminal charges against top Michigan officials extremely rare
Watch: Manslaughter charges announced in Flint water crisis probe
Chief Medical Executive Dr. Eden Wells is charged with obstruction of justice and lying to a police officer.
Buy Photo Michigan Health and Human Services Director Nick Lyon is charged with involuntary manslaughter and misconduct in office, both felonies. (Photo: Ryan Garza, Detroit Free Press)
And four defendants charged earlier -- former Flint emergency manager Darnell Earley, former Michigan Department of Environmental Quality drinking water chief Liane Shekter-Smith, DEQ drinking water official Stephen Busch, and former City of Flint Water Department manager Howard Croft -- each will faced additional charges of involuntary manslaughter. Schuette said.
All of the new charges are in connection with the Legionnaires' disease outbreak in the Flint area that led to 12 deaths after the city's water supply was switched to the Flint River in April 2014.
Read more Free Press coverage of the Legionnaires' disease outbreak:
Read the Free Press investigation from April 2016: Why were officials silent on Legionnaires' in Flint?
Here are all the victims of the Legionnaires' disease outbreak in Flint
Database: Search all of the Legionnaires' disease cases by county
Health department officials released a statement from Gov. Rick Snyder saying he stands behind Lyon and Wells, and that they would remain in their jobs pending trial.
Lyon, 49, of Marshall is accused of causing the death of Robert Skidmore on Dec. 13, 2015 by failing to alert the public about a foreseeable outbreak of Legionnaires' disease. It's a 15-year felony.
All of the other involuntary manslaughter charges also relate to the death of Skidmore, who was 85 at the time of his death.
Buy Photo Chief Medical Executive Eden Wells is charged with obstruction of justice and lying to a police officer. (Photo: Ryan Garza, Detroit Free Press)
"Defendant Lyon was aware of Genesee County's Legionnaires' disease outbreak at least by Jan. 28, 2015, and did not notify the public until a year later," the charging documents allege.
Lyon "exhibited gross negligence when he failed to alert the public about the deadly outbreak and by taking steps to suppress information illustrating obvious and apparent harms that were likely to result in serious injury."
According to the charging documents, Lyon "willfully disregarded the deadly nature of the Legionnaires' disease outbreak," later saying he "can't save everyone," and "everyone has to die of something."
Chip Chamberlain and Larry Williey, Lyon's Grand Rapids attorneys, sai: "We are confident in our defense of Nick Lyon," and "the true facts simply do not support the prosecution’s claims." they said the case "appears to be a misguided theory looking for facts that do not exist," and Schuette's news conferences are prejudical and include false statements.
"We absolutely and vehemently dispute the charges," the attorneys said. "They are baseless. We intend to provide a vigorous defense of Nick Lyon and we expect the court system to vindicate him entirely."
Schuette said that he's heard from many people frustrated and angry that he has not brought charges against Snyder, the state's Republican governor since 2011. But he said he's also heard from those who feel he's been too hard on the Snyder administration, and charges are only being filed when the evidence warrants them.
Tuesday's charges, while they do not end the investigation, mark the end of one phase of the investigation and "a significant milestone," he said.
Buy Photo Former Flint emergency manager Darnell Earley will face additional charges of involuntary manslaughter. (Photo: Jessica J. Trevino, Detroit Free Press)
Andrew Arena, Schuette's chief criminal investigator and the former FBI director in Detroit, said what he has found most shocking is that "people had information in their possession" about the Legionnaires' disease outbreak, "and just failed to act."
Charges were authorized Wednesday morning by 67th District Court Judge G. David Guinn, in Flint.
On the misconduct in office charge, a five-year felony, Lyon is accused of instructing an official to discontinue an analysis that would help determine the cause of the outbreak.
Related:
Wells, 54, of Ann Arbor is accused in connection with the obstruction of justice charge of providing false testimony to a special agent and threatening to withhold funding for the Flint Area Community Health and Environment Partnership if the partnership did not cease its investigation into the source of the outbreak. That's a five-year felony.
Wells also is charged with lying to a peace officer about the date she knew of the outbreak of Legionnaires' disease. That's a two-year misdemeanor.
"Dr. Wells vehemently denied the charges and the charges will be vigorously defended," Wells' lawyer, Jerold Lax told the Free Press in a statement.
Buy Photo Former City of Flint Water Department manager Howard Croft will face additional charges of involuntary manslaughter. (Photo: Ryan Garza, Detroit Free Press)
According to the charging documents, Wells gave a statement to Schuette's investigators on April 12, 2016, pursuant to an agreement under which she would not be charged, provided she made no false statements.
Wells allegedly lied by saying she had no knowledge of the Legionnaires' disease outbreak until late September or early October of 2015, when in fact she knew about the outbreak in March 2015.
Watch our mini-documentary on the Flint water crisis, winner of a Michigan Emmy:
CLOSE The ongoing Flint water crisis has taken a toll on residents of this iconic Michigan city, who have been living with lead-tainted tap water for over two years. One Flint resident describes the experience as, “like being in war, but without violence.”
Wells was appointed chief medical executive in May 2015. She previously served as medical consultant to the department's Bureau of Epidemiology from 2004 to 2011.
There were 12 deaths linked to Legionnaires' disease during a 17-month period in 2014 and 2015 in the Flint area. Dozens more were sickened by the disease, a severe type of pneumonia.
In previous years, six to 13 cases were typically confirmed annually in the county.
So far, 15 current or former state or City of Flint officials have been charged, including two emergency managers who were appointed by the governor and reported to the state treasurer.
Flint Mayor Karen Weaver issued a statement that said "manslaughter is a serious charge," and "it’s good to see that state Attorney General Schuette and his team are taking this matter seriously by bringing such serious charges against those who they believe didn’t do enough to address this public health threat, or to alert the Flint community about it."
Flint's drinking water became contaminated with lead in April 2014 after the city switched from treated Lake Huron water supplied from Detroit to raw water from the Flint River, which was treated at the Flint Water Treatment Plant.
Michigan Department of Environmental Quality officials have acknowledged a mistake in failing to require corrosion-control chemicals be added to the more corrosive water. As a result, lead leached from pipes, joints and fixtures into Flint households.
Though lead levels in the water have come down significantly since the state acknowledged the contamination around Oct. 1, 2015, residents are still advised not to drink tap water without a filter. Many still rely on bottled water, which can be picked up free at distribution centers in Flint.
Five of the current or former state employees charged previously are from the DEQ. Three are from the Department of Health and Human Services (DHHS).
DEQ drinking water official Stephen Busch will face additional charges of involuntary manslaughter. (Photo: Michigan Attorney General)
Outbreaks of Legionnaires' disease in the Flint area following the water switch were tied to the deaths. Officials haven't definitely linked the water switch to the disease, but Schuette and his investigators have come close to doing so in public statements and documents related to the criminal charges.
Lyon was told in September by state investigators that he was a focus of the investigation, Lyon's lawyer Willey of the Grand Rapids criminal defense firm Willey & Chamberlain told the Free Press in October.
"We haven't heard from them for months," Willey said late Tuesday. "I've received no notification ... that anything is in the offing."
Snyder named Lyon director of DHHS in April 2015 when he created a new agency that merged the former departments of community health and human services.
Previously, Lyon had served as health director beginning in September 2014, Before that, he was the agency's chief deputy director beginning in 2011.
Contact Paul Egan: 517-372-8660 or [email protected]. Follow him on Twitter @paulegan4.
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Flint — Michigan’s health department director and four other officials involved with Flint’s lead-contaminated water were charged Wednesday with involuntary manslaughter, the most serious charges to date in the criminal investigation.
Nick Lyon was accused of misconduct in office and involuntary manslaughter, becoming the highest-ranking member of Gov. Rick Snyder’s administration to be targeted in the criminal probe. The manslaughter charges carries a penalty of up to 15 years in prison and a $7,500 fine, while the misconduct charge carries a prison sentence of up to five years and a $10,000 fine.
Lyon, former Flint Emergency Manager Darnell Earley, former Michigan Department of Environmental Quality Drinking Water Chief Liane Shekter-Smith, state Water Supervisor Stephen Busch and former Flint Water Department Manager Howard Croft are accused of failing to alert the public about an outbreak of Legionnaires’ disease in the Flint area. Earley, Shekter-Smith, Busch and Croft already have been charged with less-serious crimes.
There were 12 deaths and 79 other people sickened by Legionnaires’ disease in 2014-15, which some experts have linked to the contaminated water after the city switched to Flint River water in April 2014.
One legal expert said the “aggressive” manslaughter charges will be challenging to prove to juries.
But Michigan Attorney General Bill Schuette remained undeterred and indicated during a Wednesday press conference that he is continuing not to rule out possible charges against Snyder. When asked why Snyder has not been charged, Schuette said no “crime has been established,” and “we’re not filing charges at this time.”
Lyon and four others failed to protect the residents of Flint, said Schuette, who was joined by Genesee County Prosecutor David Leyton, Special Prosecutor Todd Flood and investigator Andy Arena. Lyon’s failure to act resulted in the death of at least one person, 85-year-old Robert Skidmore of Genesee Township, the attorney general said.
Skidmore’s death certificate shows that he died Dec. 13, 2015, from “end stage congestive heart failure.” Only diabetes is listed as a contributing cause to the death of Skidmore, according to the certificate.
But the charging document indicates that a McLaren Flint Hospital doctor on June 2, 2015, collected a sample from Skidmore that tested positive for Legionella and that the Genesee County medical examiner will “not refute the medical doctor’s findings that Legionnaires’ Disease was a cause of Robert Skidmore’s death.”
The state’s chief medical officer, Dr. Eden Wells, was charged Wednesday with obstruction of justice and lying to a police officer. The obstruction charge carries a prison term of up to two years. Wells’ lawyer was not immediately known.
“People have died because of the decisions people made,” Schuette said.
“There are two types of people in the world: Those who give a damn and those who don’t. This is a case where there has been willful disregard” for the health and safety of others, Flood said.
Lyon attorneys Chip Chamberlain and Larry Willey fired back that the case “appears to be a misguided theory looking for facts that do not exist.”
“To that point, we’ve witnessed numerous press conferences by the prosecution that have been intentionally prejudicial to the process and unfair to those targeted. Worse yet, they have made many statements that are completely false. ... We expect the court system to vindicate him entirely.”
Michigan’s health department director and four other individuals involved with Flint’s lead-contaminated water were charged Wednesday with involuntary manslaughter (Photo: Detroit News file photos)
Snyder fires back
Email records released by Snyder’s administration show Lyon was aware of a spike in Legionella — bacteria that causes Legionnaires’ disease, a form of pneumonia — as early as January 2015 but didn’t put out a public alert. Snyder informed the public about the Legionnaires’ outbreak in January 2016.
Lyon has said he knew about Legionnaires’ for months but wanted to wait until investigators in the Health and Human Services Department finished their own probe.
Snyder fired back at Schuette’s office while keeping Lyon and Wells on the job, telling Health and Human Services employees in an email that “I am standing behind Nick and Eden.”
“Director Lyon and Dr. Eden Wells, like every other person who has been charged with a crime by Bill Schuette, are presumed innocent unless and until proven guilty beyond a reasonable doubt,” Snyder said in a statement.
“Some state employees were charged over a year ago and have been suspended from work since that time. They still have not had their day in court. That is not justice for Flint nor for those who have been charged. Director Lyon and Dr. Wells have been and continue to be instrumental in Flint’s recovery.”
Senate Minority Leader Jim Ananich, D-Flint, called Snyder’s response to the charges “tone deaf” and argued the governor should be focused on the harm done to Flint residents rather than state employees.
Ananich questioned if Lyon can continue leading the state health department “if he has not been protecting the public and not been informing his superiors” about real or potential threats.
“I think it’s very troubling, and I think he probably should step down,” he said about Lyon. “I think the question needs to be why the governor doesn’t think so.”
Schuette charges face hurdles
Wayne State University law professor Peter Henning said the attorney general’s office will have to prove that any public warning he may have made about Legionnaires’ disease could have prevented deaths.
“For any homicide charge, you have to prove causation and that there is a direct linkage for what he did or failed to do and the death,” said Henning, a former federal prosecutor. “That will certainly be a hurdle for the attorney general’s office.”
Prosecutors may also have to prove a link between Flint water and the Legionnaires’ disease outbreak, Henning added. Experts and the state have debated whether the water itself is to blame or a local hospital where many of the cases originated.
“This case is going to turn very much on expert testimony,” Henning said. “It’s not a whodunit. It’s: Did he do anything that caused the death? The death occurred; now it’s a matter of tracing it back, and there’s a challenge there.”
But in a Wednesday interview, Leyton said he and Schuette had a “duty to bring those charges.”
“Every single case you bring to court as a prosecuting attorney is a challenge because of so many factors,” he said. “But our job is provide justice for the people of Michigan and, in this specific instance, the city of Flint.”
About 15 state and Flint officials have been charged in what Schuette called “the most comprehensive investigation in Michigan history.” The longtime Republican elected official has been considering a run for governor in 2018.
“I am duty bound to uphold the laws in the state of Michigan,” Schuette said.
Flint official, residents react
Flint Mayor Karen Weaver was watching the press conference on a livestream from her chief of staff and said “wow” when the involuntary manslaughter charges were announced.
“It’s terrible what has occurred but it’s a good day for the people of the city of Flint,” Weaver later said. “We’ve had people die as a result of this water crisis. And for justice to be had is wonderful.”
The charges are “a measure of justice,” said U.S. Rep. Dan Kildee, a Flint Township Democrat who has gained national attention speaking out on the crisis. He told MSNBC host Rachel Maddow on Wednesday. “… It’s somewhat comforting to know that the system works, that when you see a state government do something as bad as they did to the city of Flint, that individuals will be held accountable for it. But we need more. We need other forms of justice, we need people to make it right. We need the state government to step up and make it right.”
Flint resident Shelby Offord, 28, said the charges filed Wednesday are “a good start,” but wishes officials would do more.
“I feel there should be more charges coming because the ones who have been affected and got the lead poisoning, that’s something they’ve got to deal with the rest of their lives,” Offord said as she walked in downtown Flint with her two 10-year-old girls, both of who had some form of lead in their system because of the water.
Doug McGruder, 75, of Flint Township, said Earley is the “scapegoat” and that others such as the governor need to be held accountable by Schuette. But he said he is not holding his breath.
“Earley shouldn’t have been charged because like me, on my job, I have a boss,” McGruder said. “The person that’s in charge of me should be charged. And that’s the governor.”
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This breakfast burger is loaded with cholesterol. But new dietary guidelines may say that this doesn't matter as much as we thought. (Photo: Aramark)
Longstanding advice about avoiding cholesterol for heart health may be on the way out.
In a draft report issued in December, an influential federal panel — the Dietary Guidelines Advisory Committee — scrapped longstanding guidelines about avoiding high-cholesterol food. In the draft, cholesterol — found in foods such as egg yolks — is no longer listed as a "nutrient of concern."
The panel hasn't yet filed its final report, but it ncludes the same comment on cholesterol, according to a report in The Washington Post.
The committee is not reversing advice about the risks of having a high level of LDL cholesterol, the "bad" cholesterol, in the blood. People with high LDL levels are at greater risk of a heart attack.
The committee will send its final recommendations to the Department of Health and Human Services and the U.S. Department of Agriculture, which issue the dietary advice. Those departments are expected to issue Dietary Guidelines for Americans, 2015 later this year.
Spokesmen for the USDA and HHS declined to comment on the Post story. In a written statement, the USDA said, "The committee's activities are solely advisory in nature. We look forward to reviewing the recommendations from the advisory committee, as well as public comments and the views of other experts, as we formulate the 2015 Dietary Guidelines for Americans over the course of the next year."
The proposed change on cholesterol would be in line with the positions of other health groups, said Robert Eckel, past president of the American Heart Association. The heart association and American College of Cardiology issued dietary guidelines in 2013 and did not include advice about cholesterol. That's because there wasn't definitive evidence to tell the average person to reduce how much cholesterol they consume, Eckel said.
People with diabetes should still be careful about consuming too much cholesterol, which may increase their heart risks, Eckel says.
Other cardiologists agree it's time to stop telling people to limit cholesterol from food.
"It's the right decision," said Steven Nissen, chairman of cardiovascular medicine at the famed Cleveland Clinic. "We got the dietary guidelines wrong. They've been wrong for decades."
He noted that only 20% of a person's blood cholesterol — the levels measured with standard cholesterol tests — comes from diet. The rest comes from genes, he said.
"We told people not to eat eggs. It was never based on good science," Nissen said.
Advice to avoid foods high in fat and cholesterol led many Americans to switch to foods high in sugar and carbohydrates, which often had more calories. "We got fatter and fatter," Nissen says. "We got more and more diabetes."
Recent studies even suggest that longtime advice on saturated fat and salt may be wrong, Nissen says.
Marion Nestle, a professor in the department of nutrition, food studies and public health at New York University, noted that the federal government doesn't have to follow the committee's advice.
The last set of advice, the 2010 guidelines, advised Americans to consume less than 300 milligrams a day of dietary cholesterol, about the amount in one egg. Nestle said she has no inside knowledge of the committee's decision.
"If the committee is dropping this recommendation, it may be because so many people are taking statins that dietary cholesterol doesn't matter so much anymore," Nestle said. "In the last study I saw that exonerated eggs from raising heart disease risk, 90% of the study subjects were taking statins. But I think we need to wait and see what the committee actually says before saying too much about this."
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Time to put eggs back on the menu? (Deb Lindsey for The Washington Post)
The nation’s top nutrition advisory panel has decided to drop its caution about eating cholesterol-laden food, a move that could undo almost 40 years of government warnings about its consumption.
The group’s finding that cholesterol in the diet need no longer be considered a “nutrient of concern” stands in contrast to the committee’s findings five years ago, the last time it convened. During those proceedings, as in previous years, the panel deemed the issue of excess cholesterol in the American diet a public health concern.
The finding follows an evolution of thinking among many nutritionists who now believe that, for healthy adults, eating foods high in cholesterol may not significantly affect the level of cholesterol in the blood or increase the risk of heart disease.
The greater danger in this regard, these experts believe, lies not in products such as eggs, shrimp or lobster, which are high in cholesterol, but in too many servings of foods heavy with saturated fats, such as fatty meats, whole milk, and butter.
The new view on cholesterol in food does not reverse warnings about high levels of “bad” cholesterol in the blood, which have been linked to heart disease. Moreover, some experts warned that people with particular health problems, such as diabetes, should continue to avoid cholesterol-rich diets.
While Americans may be accustomed to conflicting dietary advice, the change on cholesterol comes from the influential Dietary Guidelines Advisory Committee, the group that provides the scientific basis for the “Dietary Guidelines.” That federal publication has broad effects on the American diet, helping to determine the content of school lunches, affecting how food manufacturers advertise their wares, and serving as the foundation for reams of diet advice.
The panel laid out the cholesterol decision in December, at its last meeting before it writes a report that will serve as the basis for the next version of the guidelines. A video of the meeting was later posted online and a person with direct knowledge of the proceedings said the cholesterol finding would make it to the group’s final report, which is due within weeks.
After Marian Neuhouser, chair of the relevant subcommittee, announced the decision to the panel at the December meeting, one panelist appeared to bridle.
“So we’re not making a [cholesterol] recommendation?” panel member Miriam Nelson, a Tufts University professor, said at the meeting as if trying to absorb the thought. “Okay ... Bummer.”
Members of the panel, called the Dietary Guidelines Advisory Committee, said they would not comment until the publication of their report, which will be filed with the Department of Health and Human Services and the Department of Agriculture.
While those agencies could ignore the committee’s recommendations, major deviations are not common, experts said.
Five years ago, “I don’t think the Dietary Guidelines diverged from the committee’s report,” said Naomi K. Fukagawa, a University of Vermont professor who served as the committee’s vice chair in 2010. Fukagawa said she supports the change on cholesterol.
Walter Willett, chair of the nutrition department at the Harvard School of Public Health, also called the turnaround on cholesterol a “reasonable move.”
“There’s been a shift of thinking,” he said.
But the change on dietary cholesterol also shows how the complexity of nutrition science and the lack of definitive research can contribute to confusion for Americans who, while seeking guidance on what to eat, often find themselves afloat in conflicting advice.
Cholesterol has been a fixture in dietary warnings in the United States at least since 1961, when it appeared in guidelines developed by the American Heart Association. Later adopted by the federal government, such warnings helped shift eating habits -- per capita egg consumption dropped about 30 percent -- and harmed egg farmers.
Yet even today, after more than a century of scientific inquiry, scientists are divided.
Some nutritionists said lifting the cholesterol warning is long overdue, noting that the United States is out-of-step with other countries, where diet guidelines do not single out cholesterol. Others support maintaining a warning.
***
The forthcoming version of the Dietary Guidelines -- the document is revised every five years -- is expected to navigate myriad similar controversies. Among them: salt, red meat, sugar, saturated fats and the latest darling of food-makers, Omega-3s.
As with cholesterol, the dietary panel’s advice on these issues will be used by the federal bureaucrats to draft the new guidelines, which offer Americans clear instructions -- and sometimes very specific, down-to-the-milligram prescriptions. But such precision can mask sometimes tumultuous debates about nutrition.
“Almost every single nutrient imaginable has peer reviewed publications associating it with almost any outcome,” John P.A. Ioannidis, a professor of medicine and statistics at Stanford and one of the harshest critics of nutritional science, has written. “In this literature of epidemic proportions, how many results are correct?”
Now comes the shift on cholesterol.
Even as contrary evidence has emerged over the years, the campaign against dietary cholesterol has continued. In 1994, food-makers were required to report cholesterol values on the nutrition label. In 2010, with the publication of the most recent “Dietary Guidelines,” the experts again focused on the problem of "excess dietary cholesterol."
Yet many have viewed the evidence against cholesterol as weak, at best. As late as 2013, a task force arranged by the American College of Cardiology and the American Heart Association looked at the dietary cholesterol studies. The group found that there was “insufficient evidence” to make a recommendation. Many of the studies that had been done, the task force said, were too broad to single out cholesterol.
“Looking back at the literature, we just couldn’t see the kind of science that would support dietary restrictions,” said Robert Eckel, the co-chair of the task force and a medical professor at the University of Colorado.
The current U.S. guidelines call for restricting cholesterol intake to 300 milligrams daily. American adult men on average ingest about 340 milligrams of cholesterol a day, according to federal figures. That recommended figure of 300 milligrams, Eckel said, is " just one of those things that gets carried forward and carried forward even though the evidence is minimal.”
"We just don't know," he said.
Other major studies have indicated that eating an egg a day does not raise a healthy person’s risk of heart disease, though diabetic patients may be at more risk.
“The U.S. is the last country in the world to set a specific limit on dietary cholesterol,” said David Klurfeld, a nutrition scientist at the U.S. Department of Agriculture. “Some of it is scientific inertia.”
***
The persistence of the cholesterol fear may arise, in part, from the plausibility of its danger.
As far back as the 19th century, scientists recognized that the plaque that clogged arteries consisted, in part, of cholesterol, according to historians.
It would have seemed logical, then, that a diet that is high in cholesterol would wind up clogging arteries.
In 1913, Niokolai Anitschkov and his colleagues at the Czar’s Military Medicine Institute in St. Petersburg, decided to try it out in rabbits. The group fed cholesterol to rabbits for about four to eight weeks and saw that the cholesterol diet harmed them. They figured they were on to something big.
“It often happens in the history of science that researchers ... obtain results which require us to view scientific questions in a new light,” he and a colleague wrote in their 1913 paper.
But it wasn’t until the 1940s, when heart disease was rising in the United States, that the dangers of a cholesterol diet for humans would come more sharply into focus.
Experiments in biology, as well as other studies that followed the diets of large populations, seemed to link high cholesterol diets to heart disease.
Public warnings soon followed. In 1961, the American Heart Association recommended that people reduce cholesterol consumption and eventually set a limit of 300 milligrams a day. (For comparison, the yolk of a single egg has about 200 milligrams.)
Eventually, the idea that cholesterol is harmful so permeated the country's consciousness that marketers advertised their foods on the basis of "no cholesterol."
***
What Anitschkov and the other early scientists may not have foreseen is how complicated the science of cholesterol and heart disease could turn out: that the body creates cholesterol in amounts much larger than their diet provides, that the body regulates how much is in the blood and that there is both “good” and “bad” cholesterol.
Adding to the complexity, the way people process cholesterol differs. Scientists say some people -- about 25 percent -- appear to be more vulnerable to cholesterol-rich diets.
“It’s turned out to be more complicated than anyone could have known,” said Lawrence Rudel, a professor at the Wake Forest University School of Medicine.
As a graduate student at the University of Arkansas in the late 1960s, Rudel came across Anitschkov’s paper and decided to focus on understanding one of its curiosities. In passing, the paper noted that while the cholesterol diet harmed rabbits, it had no effect on white rats. In fact, if Anitschkov had focused on any other animal besides the rabbit, the effects wouldn't have been so clear -- rabbits are unusually vulnerable to the high-cholesterol diet.
“The reason for the difference -- why does one animal fall apart on the cholesterol diet -- seemed like something that could be figured out,” Rudel said. “That was 40 or so years ago. We still don’t know what explains the difference.”
In truth, scientists have made some progress. Rudel and his colleagues have been able to breed squirrel monkeys that are more vulnerable to the cholesterol diet. That and other evidence leads to their belief that for some people -- as for the squirrel monkeys -- genetics are to blame.
Rudel said that Americans should still be warned about cholesterol.
“Eggs are a nearly perfect food, but cholesterol is a potential bad guy,” he said. “Eating too much a day won’t harm everyone, but it will harm some people.”
***
Scientists have estimated that, even without counting the toll from obesity, disease related to poor eating habits kills more than half a million people every year. That toll is often used as an argument for more research in nutrition.
Currently, the National Institutes of Health spends about $1.5 billion annually on nutrition research, an amount that represents about 5 percent of its total budget.
The turnaround on cholesterol, some critics say, is just more evidence that nutrition science needs more investment.
Others, however, say the reversal might be seen as a sign of progress.
“These reversals in the field do make us wonder and scratch our heads,” said David Allison, a public health professor at the University of Alabama at Birmingham. “But in science, change is normal and expected.”
When our view of the cosmos shifted from Ptolemy to Copernicus to Newton and Einstein, Allison said, “the reaction was not to say, ‘Oh my gosh, something is wrong with physics!’ We say, ‘Oh my gosh, isn’t this cool?’ ”
Allison said the problem in nutrition stems from the arrogance that sometimes accompanies dietary advice. A little humility could go a long way.
“Where nutrition has some trouble,” he said, “is all the confidence and vitriol and moralism that goes along with our recommendations.”
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– It looks like Americans will be able to eat their eggs guilt-free soon. The Washington Post reports that the federal government is poised to drop its decades-long warning about eating foods high in cholesterol. In classic bureaucrat-speak, the Dietary Guidelines Advisory Committee has concluded that cholesterol is no longer a "nutrient of concern." The finding is currently in a draft report, but it is expected to be included in official USDA dietary guidelines that will be released within weeks. "The move reflects updated scientific thinking on cholesterol," explains a post at Reason. "While high cholesterol levels in the blood can still be a bad health indicator, scientists no longer view high blood cholesterol as a direct result of eating a cholesterol-rich diet, at least not for most people." A cardiologist quoted by USA Today echoes the point: "We told people not to eat eggs," he says. "It was never based on good science." The change will not reverse warnings that high levels of "bad cholesterol," or LDL, pose a health risk, but the panel is embracing the evolving view that dietary cholesterol is not the culprit. Instead, most nutritionists now think that trans fats and saturated fats are the bigger dangers in regard to heart disease, notes the Post. | multi_news_1_0_0 |
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On Feb. 5, 2013, just weeks before her 13th birthday, Syble Rossiter was at home in Albany, Oregon, gasping for breath and in critical condition. For most of the afternoon, her family had watched as she vomited violently and lost control of her bowels, eventually becoming so weak she could no longer stand. In the hours leading up to her final, fevered breaths, as Syble slowly drifted into unconsciousness and ultimately death, her parents never called a doctor or rushed her to an emergency room. As members of the General Assembly Church of the First Born, a faith-healing Christian sect, they believed that seeking medical help for their daughter would be a sign of spiritual weakness and an affront against God’s will. Instead, Travis and Wenona Rossiter tried to cure her with prayer.
Inside the Linn County Courthouse this month, the Rossiters and their defense attorneys watched silently as prosecutor Keith Stein presented images of Syble that authorities had taken at the crime scene. Gaunt and pale, the girl’s body was seated upright on her family’s living room couch in a red shirt and a pair of urine-soaked jeans. Her eyes were sunken, and her body looked dehydrated. From the witness stand, Dr. Gary Goby, the county’s medical examiner, told the jury that Syble had died from complications of a chronic and undiagnosed case of Type 1 diabetes, adding that a simple treatment of insulin and fluids could have saved her life.
Because of their inaction, the prosecutor argued, Travis and Wenona Rossiter were directly responsible for their daughter’s death. “This case is not about their religion,” he told the jurors. “It’s about the minimum standard of medical care that our laws will tolerate when it comes to our children.” The Rossiters’ defense lawyers claimed that the family had thought she only had the flu, but the jury was ultimately unmoved. Last week, the Rossiters were convicted of first- and second-degree manslaughter, which in Oregon carries a 10-year mandatory minimum sentence.
Travis and Wenona Rossiter in Oregon's Linn County Circuit Court, where they stood trial for manslaughter last week in the faith-healing death of their daughter, Syble, whom they denied medical care. KOIN 6 News
The verdict is the latest in a string of convictions of faith healers who endanger their children in Oregon, where officials have been empowered by some of the strictest laws in the country since 2011, when the state eliminated the last of its religious-defense statutes. Oregon has successfully prosecuted three similar cases in the last three years, putting mothers and fathers in jail on charges of criminal mistreatment, negligent homicide and manslaughter, and sending a message to other faith-healing families that they must seek medical care for their children.
Just across the state line in Idaho, however, there are no such deterrents. During the same period of time, at least 12 children have died at the hands of faith-healing parents in the state, yet not a single charge has been filed. In Idaho, authorities do not investigate or prosecute faith-healing deaths, which occur largely without scrutiny from the public or media. Of the dozen documented cases in the last three years—and there are likely many more that have gone unreported—all were members of the Followers of Christ, a faith-healing group with a doctrine nearly identical to the Church of the First Born. The Followers are also active in Oregon, where they gained notoriety in the 1990s after a series of high-profile child deaths.
The stark contrast over a span of a few highway miles is not lost on Linda Martin, an Idaho native and former member of the Followers of Christ who attended the Rossiters’ trial in Oregon.
“When they described the way Syble was found, I immediately knew what had transpired the night she died,” says Martin, who moved to Oregon in 1999 but maintained contact with members of her church. “It was like watching a Followers death scene all over again. I hate that sick feeling of knowing what’s going to come next.”
Of the 604 people buried in Idaho's Peaceful Valley Cemetery, 208 appear to be children, more than 35 percent. 149 of those children—a full 70 percent—were buried there after Idaho adopted its religious defense to manslaughter laws in 1972. Courtesy of Linda Martin
To Martin, what’s going on in Idaho “makes Oregon look like a bunch of boy scouts.” Last year, after watching too many children needlessly suffer and die, Martin broke her silence about the unpunished deaths in Idaho, and she has since become one of the few activists devoted to the issue there. Though it would lead to her being shunned by family and friends, she reached out to a reporter who had covered the Followers in Oregon, Dan Tilkin of Portland’s KATU News, and urged him to dig further in Idaho. The investigation led to the Peaceful Valley Cemetery outside of Boise, where Tilkin made the startling discovery that among the 553 marked graves at the cemetery, 144 appeared to be those of children, more than 25 percent.
Martin says a more extensive review of burial records at Peaceful Valley using the Idaho State Archives, obituaries and interviews with family and next of kin shows that among the 604 people buried at the cemetery, including unmarked graves, 208 are children, which means the figure is closer to 35 percent. Those findings are documented on the Find a Grave website, an online database of cemetery records. While the graves of deceased children in the cemetery date back to 1905, 149 children, more than 70 percent, were buried there in or after 1972, the year that Idaho enacted a law providing a religious defense to manslaughter.
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Autopsy records show that all 11 Followers children buried in Peaceful Valley since 2011 succumbed to medically preventable conditions. There were infants who slowly perished from sepsis, respiratory failure and diabetes, and teens who battled pneumonia for weeks. One 16-year-old, Pamela Eells, drowned in her own fluids after suffering from a bone infection commonly associated with leukemia, according to her coroner’s report. The medical examiner in that case, Dr. Charles Garrison, said he found it inexplicable “to comprehend how anyone can watch a child die and do nothing.”
Perhaps worst of all was the fate of 15-year-old Arrian Granden, whose family stood by for three days in 2012 as their daughter suffered fits of vomiting and diarrhea. Arrian’s esophagus eventually ruptured from her retching, which was brought on by an easily treatable case of food poisoning. She gradually fell unconscious before going into cardiac arrest. A 205-word case summary from the Canyon County Coroner’s Office is the only official record of her death.
***
Nearly every state includes some form of religious exemption from charges against faith-healing parents in its criminal or civil codes. Most of these laws are remnants of a decision by the federal government in the 1970s—granted at the urging of the Christian Science Church, the nation’s largest faith-healing denomination—to withhold funding for child abuse programs in states that did not enact some form of religious immunity for parents who favored spiritual healing over medical care. While the federal government later rescinded its regulation, most states left the laws in place.
Currently, 32 states, including Idaho, provide a religious defense to felony or misdemeanor crimes specifically against children, including neglect, endangerment and abuse, according to state statutes compiled by Children’s Healthcare Is a Legal Duty (CHILD), a national advocacy group. There are 38 states that provide religious exemptions in their civil codes on child abuse and neglect, which can prevent Child Protective Services from investigating and monitoring cases of religion-based medical neglect and discourage reporting.
More Study Says Religious Kids Are Easier to Fool
Of the states that still provide a religious defense to felonies against children, Idaho remains in a league of its own. It is one of only six states that provide a religious exemption to manslaughter, negligent homicide or capital murder (the others being Arkansas, Iowa, Louisiana, Ohio and West Virginia). But of those six, it is the only state where children are known to have died at the hands of faith-healing parents in the last 20 years. Rita Swan, CHILD’s co-founder, describes Idaho as “the worst in the country,” and she attributes the state’s high number of deaths to its overreaching religious exemption laws, which were enacted in 1972.
Swan and other child advocates argue that Idaho’s laws, and those like them, are in direct contradiction with the Supreme Court’s 1944 decision in Prince v. Massachusetts, which ruled that parental authority cannot jeopardize a child’s welfare, even in cases of religious expression. “The right to practice religion freely,” the court concluded, “does not include liberty to expose…[a] child…to ill health or death.”
“Parents may be free to become martyrs themselves,” the decision continued. “But it does not follow they are free, in identical circumstances, to make martyrs of their children.”
Idaho’s religious exemption law describes prayer as a spiritual “treatment” that can act as a legal substitute for medical care. In other words, it can’t be neglect if the child is receiving treatment, even if that treatment consists exclusively of asking God for a miracle. What’s more absurd, according to Swan, is that the state’s laws inadvertently promote the most extreme behavior among faith-healing parents because of how they’re written: Parents can lose their religious protections the minute they use any other means of care beyond spiritual treatment to help cure a child.
“If the parent combines prayer with orange juice or a cool bath to bring down a fever,” Swan says, “the parent loses the exemption.”
Yet, because of the profound chilling effect Idaho’s religious exemption laws have had on the authorities who might enforce them, those claims have never been put to the test. Not a single criminal charge has been filed in cases of religion-based medical neglect in the state since legislators enacted the law four decades ago. Boise police declined to even report two faith-healing parents in 2010 after they refused medical care for their critically injured son, citing the religious exemption statute. The following year, Canyon County Coroner Vicki DeGeus-Morris told reporters that she had stopped doing autopsies on children who belonged to the Followers of Christ altogether.
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Few with power or political will in Idaho have been compelled to stop the growing body count. With the exception of one local television station in Boise, the revelations, which have been coming to light since last year, attracted scant media attention in the state. Idaho’s largest papers didn’t touch the story, nor did the state’s public radio or alternative weeklies.
Earlier this year, a proposal was introduced in Idaho’s state legislature to amend its religious shield laws, but it never got to the floor. Scott Bedke, the state’s House speaker, prevented the bill from having a hearing. Even the Governor’s Task Force on Children at Risk, a nonpartisan advisory group, declined to support the bill, which became red meat for conservative state legislators who saw it as government intrusion and an assault on religious freedom.
The Followers of Christ Church in Marsing, Idaho, about 6 miles from Peaceful Valley Cemetery. KATU
“This is about religious beliefs, the belief God is in charge of whether they live, and God is in charge of whether they die,” said Republican Rep. Christy Perry. “This is about where they go for eternity.”
There is currently no sponsor for a new bill, and the chance of one gaining traction in next year’s legislature is slim. Reached by phone, the original sponsor, Boise Democrat John Gannon, indicates that it’s not exactly on the top of his to-do list. “It’s honestly not something that I’ve thought a lot about lately,” he says.
Bryan Taylor, the lead prosecutor in Canyon County, where Arrian Granden died, would not respond to multiple requests for comment. He has previously stated that his hands are tied by current law. “If they don’t want to have their children go to a doctor, as long as they haven’t caused the injuries, then we don’t really have a leg to stand on in exploring criminal charges,” he told KBOI 2 News.
Outside of Oregon and Idaho, there have been 20 documented faith-healing fatalities of minors since 2008 in 10 different states, including Texas, Colorado and Pennsylvania, according to CHILD. But the death count among Followers of Christ puts Idaho well out in front as the deadliest state in the country. That distinction actually once belonged to Oregon, until a highly publicized child death in 1998 ultimately prompted prosecutors and lawmakers to act.
Oregon, like Idaho, had a religious defense to manslaughter on the books when 11-year-old Bo Phillips died from untreated diabetes that year. His family, who were members of the Followers of Christ, prayed over him and anointed his body with oil instead of taking him to a doctor. It was the first time authorities felt they had a clear case of abuse in a faith-healing child death. But the district attorney for the county, Terry Gustafson, declined to prosecute the boy’s parents because of ambiguities in the state law.
Gustafson’s decision triggered public outcry across the state. The Oregonian newspaper in Portland, the state’s largest paper, launched an investigative series on faith-healing deaths, which found that of the 78 children buried in one Followers cemetery in Oregon City since 1955, 21 had died from treatable illnesses. Shortly after, ABC’s 20/20 and Diane Sawyer brought national attention to the state’s faith-healing controversy with a prime-time segment on the Followers. By 1999, legislators had eliminated religious protections in cases of manslaughter and criminal mistreatment.
Alayna Wyland nearly went blind when a massive growth consumed the left side of her face. Her parents, Timothy and Rebecca Wyland, who are members of the Followers of Christ, were convicted of criminal mistreatment in 2011 for not providing her with medical care. Clackamas County Sheriff's Office
In 2011, the state eliminated all remaining religious exemptions for denying medical care. Within a few months, Followers of Christ members Timothy and Rebecca Wyland were convicted of criminal mistreatment for allowing a growth the size of a baseball on their infant daughter’s face to go untreated. They were sentenced to 90 days in jail and eventually lost custody of their daughter. While six states have now struck all religious protections for crimes against children, Oregon’s reforms have shown to be the most sweeping in their transformation. With the Rossiters’ conviction, the state has now won every faith-healing child death case it has prosecuted.
Advocates like Martin believe that without publicity and stiff legal repercussions, children will continue to suffer and die at the hands of faith-healing parents in Idaho. And they are praying that they will find a way to make the issue resonate with lawmakers and the public in the state.
“If we can change the laws there, we might be able to give some of these kids a chance at growing up,” says Martin. “The torture of these children has got to stop.” ||||| BOISE, Idaho – Peaceful Valley Cemetery sits on a windswept hill 30 miles east of Boise.
Some of The Followers of Christ faith healers bury their dead there.
The same last names appear over and again, going back decades. Some - like Beagley - are the same names you’ll see in a similar cemetery in Oregon City.
In 2010, jurors in Clackamas County convicted Jeff and Marci Beagley of letting their son Neal die of an untreated urinary tract infection.
KATU’s Dan Tilkin covered that story, as he has so many faith-healing stories. That’s why he traveled to Idaho to trace the connections between Followers members in both states, and a new trail of dead children.
A former member of the Followers of Christ advised him to go to Peaceful Valley and look for two specific names.
He found them. He found many more.
Garrett Dean Eells.
The coroner’s report says Garrett was a 6-day-old baby who died of interstitial pneumonitis. That’s pneumonia, untreated.
Jackson Scott Porter.
Jackson was a baby girl. She lived only 20 minutes. The coroner’s report said she received no pre-natal care.
Her grandfather, Mark Jerome, says she died in his house three months ago after his daughter went into labor.
“Well, when she came over, she was just sick - like a kidney infection or something like that,” Jerome said. “So she just wanted to come to the house for a couple days. And when she had the baby no one expected it, it just happened that quick."
The coroner used the words “extreme prematurity” to describe the labor.
Jerome said he doesn’t regret the lack of pre-natal care. That gets to the heart of faith-healing.
“That's the way we believe,” he said. “We believe in God and the way God handles the situation, the way we do things."
Preston Bowers and Rockwell Sevy.
The Canyon County coroner believes Preston had Down’s Syndrome, and that the 2-year-old died of pneumonia.
KATU reported on his death in 2011, along with that of 14-year-old Rocky.
Rocky isn’t buried in the cemetery, but he lived nearby with his parents, Sally and Dan.
They didn’t want to talk about not getting him treatment.
"What I will talk to you about is the law,” Dan Sevy said. “I would like to remind you this country was founded on religious freedom, and on freedom in general. I would like to say, I picture freedom as a full object. It's not like you take "a" freedom away. It's that you chip at the entire thing. Freedom is freedom. Whenever you try to restrict any one person, then you're chipping away at freedom. Yours and mine."
That was that. Sevy didn’t want to talk any more about it.
“I told you I'm not going to do that,” he said. “You don't understand the full story, and I'm not going to stand in front of a camera and give you the whole story. It's just not going to happen. I see the way these things get edited out.
“All I see is an aggressive campaign against Christianity in general, it’s amazing to me in this day and age where Muslims get soft pedaled and Christians are under attack. It just blows my mind.”
Unfortunately, those weren’t the only names in the cemetery. There are 10 new graves that look as though they belong to children that have appeared since KATU’s last report in 2011.
Arrian Jade Granden.
Arrian was 15 years old. She ran track at Parma Middle School.
In June 2012, she got food poisoning.
She vomited so badly she ruptured her esophagus.
She slipped into unconsciousness and went into cardiac arrest.
She died.
Micah Taylor Eells.
The autopsy says Micah died of “likely an intestinal blockage.”
Micah was four days old.
None of the parents of the children who are buried at Peaceful Valley Cemetery will be prosecuted. Oregon wiped out its laws protecting faith-healers. Idaho did not.
Read more: Faces of the fallen - Autopsy reports for the 12 dead children (Warning: graphic content)
Pamela Jade Eells.
Doctor Charles Garrison performed the autopsy on 16-year-old Pamela. She died of pneumonia.
"If you’ve ever been in a situation where you can’t breathe, it’s pretty desperate.
"You’re drowning in your own fluids.”
Watch: Raw interview with Dr. Charles Garrison:
The coroner’s report says Pamela died after a long chronic battle with an infection in her pelvic bone.
Garrison hasn’t forgotten.
“It's inexplicable to me to comprehend how anyone can watch a child die and do nothing,” he said.
Linda Martin has seen it before. She’s a former Followers of Christ who grew up near Boise. She left when she was a teenager, and lives in Oregon now.
She contacted KATU when she realized more children were dying. She said she is related to many of them.
She keeps their obituaries in an album.
“Everybody hears about the Oregon City trials and the Oregon City churches,” she said. “What they don't understand is the Idaho churches are more rigid, they are unbending, and they are more ruthless then the Oregon churches are.
“It happens one at a time, and the church is so good at covering up that most people don't even know what's going on next door to them."
Jerry Gardener.
Jerry was Linda’s cousin. In 1980, he died from diabetes at the age of 11.
Both Martin and Dr. Garrison are frustrated Idaho hasn’t followed Oregon’s lead.
In Idaho, you can use faith-healing as a defense when it comes to children.
In Oregon, you can’t.
Syble Rossiter.
Syble was 12 when she died in Albany, Ore., last February.
Her parents, Travis and Wenona Rossiter, face manslaughter charges.
They belong to a congregation called “Church of the First Born” in Brownsville, Ore. According to Linda Martin’s family tree and other historical sources, that church is related to the Followers of Christ.
There’s at least one significant difference between the churches: When a child dies in Idaho due to lack of medical care, the parents aren’t breaking any laws.
“The state of Idaho has the religious shield laws to where you can just about murder your child in cold blood and claim religious exemptions and get away with it,” Martin said.
So many more names.
Of the 553 marked graves at Peaceful Valley Cemetery, 144 appear to be children under 18. That’s more than 25 percent.
Those deaths happened primarily in three different counties, which are manned by three different coroners who aren’t bringing the information to the public.
Very few people had a good idea how many children were dying until now. Linda Martin started a Facebook page to keep track of them. That’s still probably not a complete reckoning.
There are four such churches in Idaho, and they don’t get along.
Followers of Christ church in Marsing, Idaho.
“Difference of opinions, difference of religion, different ideas - we follow the word for what it is, what the bible says,” said Mark Jerome, who attends the Followers of Christ Church in Marsing, Idaho.
Followers members use at least two more cemeteries.
The caretaker at Star Cemetery in Star, Idaho said a Followers member recently showed up saying he needed to bury a baby. The baby was in the back seat of his car. The caretaker said he made the church member get a death certificate before he buried the child.
A spokesman for Idaho Governor Butch Otter asked to see the results of this investigation.
The state recently put together a child death review team, which will likely be looking at faith-healing deaths soon.
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Despite the deaths of least 12 children from “faith healing” Christian families in their state, lawmakers and public officials in Idaho have refused to challenge a state law providing a religious exemption from manslaughter and murder charges, Vocativ reported.
The childrens’ families belonged to a Pentecostal group known as the Followers of Christ, which punishes members who seek medical care by shunning them from their church. According to state law, parents can substitute prayer as a form of treatment. The religious exemption covers manslaughter, capital murder and negligent homicide charges, but cannot be cited if a parent uses any other form of treatment on top of praying for the child.
“If the parent combines prayer with orange juice or a cool bath to bring down a fever, the parent loses the exemption,” Rita Swan, co-founder of the advocacy group Children’s Healthcare Is a Legal Duty, said.
According to Swan’s organization, Idaho is one of 32 states that have religious exemptions to felony or misdemeanor charges involving children.
A bill calling for a change to the law did not advance in the state legislature earlier this year. The bill’s sponsor, state Rep. John Gannon (D), told Vocativ that pursuing a new bill is “honestly not something that I’ve thought a lot about lately.”
Similarly, Republicans appear unwilling to push for a change to the religious exemption.
“This is about religious beliefs, the belief God is in charge of whether they live, and God is in charge of whether they die,” state Rep. Christy Perry (R) said. “This is about where they go for eternity.”
KATU-TV reported last year that, out of 553 marked graves at a cemetery outside of Boise, 144 of them appeared to be burial spots for children, constituting about 26 percent of the deceased.
Among those buried was Jackson Scott Porter, a newborn girl who lived for just 20 minutes before dying in her grandfather’s home. The girl’s mother did not receive any pre-natal care. Her cause of death was listed as untreated pneumonia.
“That’s the way we believe,” the grandfather, Mark Jerome, told KATU at the time. “We believe in God and the way God handles the situation, the way we do things.”
KATU also reported that local officials believe that another minor, 14-year-old Rockwell Sevy, had undiagnosed Down’s syndrome before he also died from pneumonia, in 2011.
Sevy’s father, Dan Sevy, refused to discuss his son’s death with KATU last year, citing his right to freedom of religion.
“I would like to say, I picture freedom as a full object. It’s not like you take ‘a’ freedom away,” Dan Sevy said. “It’s that you chip at the entire thing. Freedom is freedom. Whenever you try to restrict any one person, then you’re chipping away at freedom. Yours and mine.”
Vocativ reported that, according to autopsy records, each of the children from “faith healing” families who have died over the past three years succumbed to conditions that could have been treated medically. No charges have been filed in any of their deaths.
Watch KATU’s report, as aired last year, below. |||||
What is a one-paragraph summary of the above article? | – Thirty-two states have religious exemptions to some crimes against children; six of those allow a religious exemption in cases including manslaughter, negligent homicide, or capital murder. But Idaho has earned a disturbing distinction: In the past two decades, it's the only one of those six states where kids have died due to parents' adherence to healing by faith alone. The past three years have seen at least 12 children's deaths in faith-healing cases, Vocativ reports. All the deaths were of members of a religious group called Followers of Christ. In a Followers cemetery near Boise, almost 35% of the graves belong to children, says a former member of the group who's now fighting for change. Among the deaths since 2011 are infants who died of sepsis and teens who died of pneumonia; one 15-year-old died after an "easily treatable case of food poisoning." According to Idaho's 1972 religious-exemption laws, prayer is a form of treatment. No criminal charges have been filed in such cases since the laws came into existence. Activists say such laws contradict a 1944 Supreme Court decision that notes that while "parents may be free to become martyrs themselves … it does not follow they are free, in identical circumstances, to make martyrs of their children." The Vocativ report comes after parents in Oregon were convicted of first- and second-degree manslaughter in their daughter's death last year. A Followers of Christ member who lost a son defends the group's practices: "I would like to remind you this country was founded on religious freedom," he told KATU last year, as Raw Story notes. "It's not like you take 'a' freedom away. It's that you chip at the entire thing." | multi_news_1_0_0 |
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– After an acquisition that brings it deep into people's homes, Google is getting up close and personal with people's bodies. The latest project from the firm's secretive Google X facility is a "smart" contact lens that monitors the glucose levels of diabetics with a tiny wireless chip and sensor, reports PC World. It notes that the move into the rapidly expanding field of wearable medical technology brings Google even further away from its online software roots. "We've always said that we’d seek out projects that seem a bit speculative or strange, and at a time when the International Diabetes Federation is declaring that the world is 'losing the battle' against diabetes, we thought this project was worth a shot," Google said in a blog post. The company says a lot more work needs to be done before the lens can reach consumers, but it is already looking for partners who can help bring it to market, reports the BBC. (In other Google news, a Google Glass legal precedent was set yesterday.)
Expand this summary. | Google started giving back Thursday with an announcement on its official blog that it has begun testing on a smart contact lens. Yeah, you read that right: a smart contact lens.
And while that might initially seem like a mad scientist’s side project, it’s actually incredibly cool: The smart contact lens is designed to assist diabetes patients by measuring glucose levels in their tears, using a mini glucose sensor, and transmitting that data to a phone via a tiny wireless chip.
Both the chip and the sensor are embedded between two layers of soft lens material, and the prototypes can generate a reading once per second.
While clinical research studies have already been completed, Google is still in discussions with the FDA, and the company is also looking for partners to help bring the lens to market. Google is additionally seeking partners who can help leverage the technology to develop apps that would make glucose levels available to both patients and their doctors.
Additionally, there’s some interest in integrating LED lights which would light up to indicate various glucose levels. The blog post reports that one of every 19 people on the planet suffers from diabetes, and many patients do not test their glucose levels often enough because the methods to do so have been cumbersome, or painful.
While this is an amazing medical advancement, and certain to help scores of people, it seems curious that the initial feedback to the announcement is so positive overall, in contrast to the blowback from Google’s purchase of Nest earlier this week—which was met with dozens of privacy concerns. Perhaps we’re just less worried about what we put in our eyes?
This story, "Googly eyes: Smart contact lens would test glucose in diabetics' tears" was originally published by TechHive . ||||| Media playback is unsupported on your device Media caption Google said the sensors on the smart contact lens are so small they look like bits of glitter
Google has said it is testing a "smart contact lens" that can help measure glucose levels in tears.
It uses a "tiny" wireless chip and a "miniaturised" glucose sensor embedded between two layers of lens material.
The firm said it is also working on integrating tiny LED lights that could light up to indicate that glucose levels have crossed certain thresholds.
But it added that "a lot more work" needed to be done to get the technology ready for everyday use.
"It's still early days for this technology, but we've completed multiple clinical research studies which are helping to refine our prototype," the firm said in a blogpost.
"We hope this could someday lead to a new way for people with diabetes to manage their disease."
'Exciting development'
It is likely to spur a range of other innovations towards miniaturizing technology and using it in wearable devices to help people monitor their bodies better Manoj Menon, Frost & Sullivan
Many global firms have been looking to expand in the wearable technology sector - seen by many as a key growth area in the coming years.
Various estimates have said the sector is expected to grow by between $10bn and $50bn (£6bn and £31bn) in the next five years.
Within the sector, many firms have been looking specifically at technology targeted at healthcare.
Google's latest foray with the smart contact lens is aimed at a sector where consumer demand for such devices is expected to grow.
According to the International Diabetes Federation, one in ten people across the world's population are forecast to have diabetes by 2035.
People suffering from the condition need to monitor their glucose levels regularly as sudden spikes or drops are dangerous. At present, the majority of them do so by testing drops of blood.
Google said it was testing a prototype of the lens that could "generate a reading once per second".
"This is an exciting development for preventive healthcare industry," Manoj Menon, managing director of consulting firm Frost & Sullivan told the BBC.
"It is likely to spur a range of other innovations towards miniaturizing technology and using it in wearable devices to help people monitor their bodies better."
Open innovation?
Google said it was working with the US Food and Drug Administration (FDA) to bring the product to mainstream use.
It added that it would look for partners "who are experts in bringing products like this to market".
Google said it would work with these partners to develops apps aimed at making the measurements taken by the lens available to the wearer and their doctor.
Mr Menon said it was "commendable" that Google was willing to work with other partners even before the product was commercially ready.
Image copyright Sensible Baby Image caption Sensible Baby showcased a prototype baby sleep monitoring system at this year's CES
"Their open innovation approach is going to help accelerate the development of this product and get it out to the market much faster," he said.
Other firms have also been looking towards wearable products that help monitor the health of the wearer.
Earlier this month, a gadget called Sensible Baby was unveiled at the Consumer Electronics Show (CES) in Las Vegas. It is a sensor put in an infant's night clothes that tracks their temperature, orientation and movement.
It sounds a smartphone app alarm if it detects a problem.
Several smartwatches that can monitor data by studying key indicators such as the the wearer's heart rate and temperature have also been launched.
Last year, Japanese firm Sony filed a patent for a 'SmartWig', with healthcare cited as one of its potential uses.
It said the wig could use a combination of sensors to help collect information such as temperature, pulse and blood pressure of the wearer. ||||| | multi_news_1_0_0 |
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BALTIMORE — A key alibi witness for Adnan Syed, the Maryland man whose 2000 murder conviction was the subject of the first season of the true-crime podcast, "Serial," testified on his behalf for the first time on Wednesday, telling a judge that she'd seen him at a public library on the day of the killing.
Asia Chapman, a high school classmate, appeared as a witness in Syed's post-conviction hearing in Baltimore City Circuit Court, where his lawyers argued that he deserved a new trial because his original defense team failed him.
Syed seemed "completely normal" when they ran into each other at the Woodlawn library branch on Jan. 13, 1999, Chapman said. She heard later that he'd been arrested for strangling his ex-girlfriend, Hae Min Lee, that same day in a fit of jealous rage after she began dating someone new. Chapman realized she may have worthwhile evidence. But it was never used.
On the stand, Chapman, 34, repeated the story she told in 2014's "Serial," when she went by her maiden name, McClain. She is now married with two children, and pregnant with a third, and lives in Washington. She laughed nervously as she testified.
While Chapman spoke, Syed, 34 and serving a life sentence, sat still in the courtroom in a blue-gray jumpsuit, chains around his ankles. His family sat behind him, on the right side of the courtroom.
Chapman's testimony came on the first day of a hearing to determine whether Syed will be given a new trial based on evidence that wasn't previously presented. Testimony is expected to continue through Friday.
Meanwhile, Lee's family released a statement Wednesday saying she remained "the true victim" and that the reopened case was forcing them to "relive a nightmare." They said they believed in Syed's guilt and "look forward to bringing this chapter to an end so we can celebrate the memory of Hae instead of celebrating the man who killed her."
Adnan Syed enters Courthouse East in Baltimore prior to a hearing on Wednesday, Feb. 3, 2016 in Baltimore. Barbara Haddock Taylor / The Baltimore Sun via AP
Chapman testified that after she realized her library encounter with Syed might be of value, she wrote him two letters offering to help and signed a notarized affidavit. But his defense lawyer never contacted her.
Not long after, she went to college, and lost track of Syed's case.
In 2010, Syed's new lawyer, Justin Brown, contacted Chapman, who in turn sought advice from prosecutor Kevin Urick. The prosecutor allegedly called Brown "BS" and dissuaded Chapman from returning his call. But Chapman took notes on the conversation, which were entered into evidence as she testified Wednesday.
In January 2014, "Serial" host Sarah Koenig contacted Chapman for an interview. Chapman agreed, but said Wednesday that she didn't know what a podcast was, and thought it was for a written article. Later, when the podcast went viral, she heard from friends on Facebook that her voice was in it. She was shocked.
"Serial" became a sensation in the fall of 2014, raising new questions about Syed's innocence.
Chapman said she listened to the show, and began to rethink her involvement in the case. She also grew angry about her conversation with Urick.
Before "Serial," Chapman said, "I didn't think I was very important at all." The podcast, she said, "placed a great weight on my heart." She then contacted Brown herself.
When Brown asked her why she wanted to testify, Chapman responded: "I felt it was the right thing to do. For justice to be served, all the information needs to be on the table."
Related: 'Serial' Star in Court for Hearing That Could Lead to Retrial
Earlier on Wednesday, Brown argued that his client's original defense attorney, Cristina Gutierrez, was too ill and stressed to adequately represent him during his 2000 trial.
Brown called on Phillip Dantes, a friend and colleague of Gutierrez, to highlight how sick she had become. Gutierrez died in 2004 after first suffering the effects of multiple sclerosis in 1999. Her condition was also complicated by diabetes. In 2001, the state disbarred her as an attorney following complaints from clients whom she represented; she agreed to be disbarred.
Dantes testified that he saw her change from a "zealous" star defender to a physically incapacitated lawyer who "looked like she had a high level of anxiety" around the time leading up to Syed's trial.
Brown, meanwhile, also pointed to Gutierrez's failure to contact Chapman, and also Gutierrez's inability to bring evidence showing that critical cellphone records may have been unreliable.
Maryland Deputy Attorney General Thiruvendran Vignarajah vigorously opposed Brown's assessment during his opening statement, saying that a jury convicted Syed on "overwhelming evidence."
"Mr. Syed was convicted because he did it," Vignarajah said.
It wasn't immediately clear if Brown plans to call on his client to testify.
The judge also ordered that several witnesses be sequestered during the post-conviction hearing, meaning they cannot watch the hearing proceedings until they are called to the stand. Chapman and Rabia Chaudry, Syed's most notable advocate, were among those sequestered. ||||| The convicted killer at the center of the wildly popular investigative podcast "Serial" finally got his day in court today, after questions were raised about his guilt and whether he had a fair trial in Maryland 16 years ago.
Lawyers for Adnan Syed argued at a court hearing for a new trial, and called a key witness who was featured in the podcast but was never called to testify during Syed's original trial.
Asia McClain is a potential “alibi witness” who said she was with Syed at the public library near Baltimore’s Woodlawn High School at the time prosecutors previously said they believe his ex-girlfriend Hae Min Lee was murdered.
McClain, who goes by her married name now, Chapman, said she previously wrote to Syed twice to say she was with him that afternoon and that she was willing to speak up if needed. During her testimony today, she was asked why she is speaking out now.
"I felt it was the right thing to do. All the information needs to be on the table in the interest of telling the truth," she said today in court, sounding confident on the stand.
Brown had described McClain as a “big piece of the puzzle” at the beginning of the three-day, post-conviction hearing.
Syed's new defense team, led by Justin Brown, is arguing that Syed’s former lawyer, the late Cristina Gutierrez, failed to provide him with effective counsel during his 2000 trial and the cellphone tower evidence used by prosecutors was unreliable.
Syed, now 35, is serving a life sentence for Lee's death in 1999. Syed walked into court today wearing shackles and a blue jumpsuit, and sporting a long beard and a prayer cap.
Family, supporters and journalists were in attendance during the opening statements by the state and Syed’s defense team. “Serial” podcast creator Sarah Koenig, and former Baltimore Sun reporter, sat in the front row of the courtroom.
Syed and Lee were both students at Woodlawn High School. Lee went missing in January 1999, and was found weeks later, strangled and buried in Leakin Park, a few miles from the school.
The defense called two witnesses to the stand this morning, both of whom had worked with Gutierrez. Brown and his team say Gutierrez failed to provide Syed with effective counsel because of health issues, financial hardships and a family life in turmoil.
Phillip Dantes, who worked with and mentored Gutierrez, called her a “zealous” worker, but that she struggled with health issues, including multiple sclerosis. His testimony was largely denied because of numerous sustained objections from the state, who said the character-take down was a form of “smearing.”
The state also says Syed received a fair trial.
“He was convicted because he did it and the state proved it,” said Maryland Deputy Attorney General Thiruvendran Vignarajah, who is leading the charge against Syed.
The second witness, William Kanwisher, worked as an investigator for Gutierrez. During a somewhat testy testimony, Kanwisher called Gutierrez “accomplished,” but also says he noticed a lack of energy, and a decrease in focus from the lawyer because of her crumbling health.
“She became more erratic,” he said. “I had to do more of her cases,” going on to say that often times, Gutierrez would hand over entire cases for him to take on with just a handful of days to prepare. She died in 2004.
The post-conviction proceedings are meant to determine whether Syed will receive a new trial.
The Maryland Court of Special Appeals issued an order in May directing Syed’s case to a lower court so the testimony of McClain could be added to the record. After his conviction, McClain, another high school classmate, wrote him letters in jail, saying she had seen him in the library around the same time Lee was killed.
In November, Retired Circuit Court Judge Martin P. Welch granted Syed’s request to introduce the alibi witness testimony, as well as cell tower records that were later claimed to be unreliable, according to the carrier, saying it would “be in the interests of justice.” (It is not unusual for retired judges to hear cases).
“I don’t want to say it’s unusual, but he’s definitely beating the odds here,” said Becky Feldman, chief of the post-conviction defenders division at the Maryland Office of the Public Defender. “Filing motions to reopen a post-conviction are fairly common. We probably get hearings on motions to reopen on maybe 20 percent of the cases. Most of them are just denied.”
So what happens next?
“I would be shocked if we get a ruling on Friday,” Feldman said. “There’s no time requirement on when a court must issue a post-conviction ruling.”
Syed’s fate rests in the hands of Welch, who could issue an oral ruling on Friday, determining if Syed will get a new trial or not. The likelihood is that he will issue a written decision at a later time, which could take weeks to months. If Syed is granted a new trial, the state will likely appeal, Feldman says. Syed could be stuck in this process for months – even years, should the court take its time.
Syed’s lawyer tweeted last week about the hearing. ||||| For more than a decade, Asia McClain was confident that she had seen Adnan Syed at a Woodlawn library during the time when prosecutors said he had killed his former girlfriend.
Defense attorneys never asked about her account, she said, and a prosecutor later dismissed the potential alibi as irrelevant. But before a packed courtroom on Wednesday, McClain described how a popular podcast about the case had persuaded her that she needed to speak up.
"In order for justice to be served, all information has to be out on the table," McClain testified in Baltimore Circuit Court.
It was the first day of a three-day hearing. Syed's attorneys argued Wednesday that he should receive a new trial in the 1999 murder of his ex-girlfriend and Woodlawn High School classmate Hae Min Lee. The hearing was the first since the "Serial" podcast raised questions about Syed's conviction.
A hush fell over the courtroom full of supporters, spectators and news media as Syed, 34, was escorted in, shackled at the hands and feet.
Syed's attorneys say McClain's account should not have been dismissed. They say her testimony and newly scrutinized cellphone tower evidence provide grounds for a new trial.
Attorneys for the state urged retired Judge Martin P. Welch to deny the request. Deputy Maryland Attorney General Thiru Vignarajah said Syed received sufficient representation during his trial in 2000 and that any decision by his attorneys not to follow up on McClain's account then was strategic.
"Mr. Syed was convicted on the basis of overwhelming evidence," Vignarajah said. "Mr. Syed was convicted because he did it, and the state proved it."
A jury convicted Syed of kidnapping and strangling the 18-year-old Lee, and he was sentenced to life in prison. No physical evidence tied Syed to the crime, but a witness testified that he helped Syed bury her body.
Lee's family did not participate in the "Serial" podcast and has not spoken out in any of the articles, spinoff podcasts and websites that followed. After the hearing concluded for the day, Vignarajah read a statement from the family from the courthouse steps, in which they said the new proceedings were forcing them to "relive a nightmare we thought was behind us."
"We believe justice was done when Adnan was convicted in 2000, and we look forward to bringing this chapter to an end so we can celebrate the memory of Hae instead of celebrating the man who killed her," the family said.
The family said Lee was the "true victim."
Much of the testimony Wednesday centered on the effectiveness of M. Cristina Gutierrez, Syed's trial attorney. Gutierrez died in 2004.
Two former associates testified that Gutierrez had begun to fall apart physically and mentally, and was no longer the same top attorney when she took on Syed's case.
Welch dismissed arguments to reopen Syed's case in 2012, when the defense raised questions about Gutierrez's work and introduced McClain's account as an alibi.
Kevin Urick, a prosecutor in Syed's case, testified at the 2012 hearing that McClain had told him she had claimed in an affidavit that she had seen Syed at the library on the day of Lee's killing "because she was getting pressure" from Syed's family.
McClain did not testify then, and now says that Urick misrepresented the case to her — and misrepresented her position to the court.
"He flat out said, 'He killed that girl,'" McClain testified Wednesday. She said Urick told her that defense attorneys were trying to game the system and that he was confident of Syed's guilt.
Witnesses in the hearing have been sequestered and directed not to speak to reporters. Urick told The Baltimore Sun last year that he never dissuaded McClain from testifying. He did say he told her that the evidence was "strong" against Syed.
Urick, now a prosecutor in Cecil County, is listed as a potential state witness in the current hearing.
McClain first raised the potential alibi immediately after Syed's arrest in 1999. She testified that she was stuck at the Woodlawn library on Jan. 13 waiting for her boyfriend and struck up a conversation with Syed.
He was "completely normal," she said.
McClain wrote a letter to Syed after his arrest, offering to help him if he thought the information would be useful in mounting a defense. She wrote a second letter a day later, she said, but never heard from Syed's defense.
Vignarajah provided notes from Gutierrez's case file. He had obtained them in recent weeks by arguing that the contents had been shared widely with the public through the "Serial" podcast, which was downloaded millions of times.
The files, he said, showed Gutierrez dividing up tasks, assigning clerks and attorneys to pursue them, and making strategic decisions about what to pursue and what to withhold.
Gutierrez determined that the "pursuit of Ms. McClain would not be a worthwhile endeavor," Vignarajah said, countering the contention that Gutierrez was not of sound mind.
Vignarajah said McClain's account did not mesh with Syed's own account to police of his movements that day, and raised a number of "warning signs and red flags" that Gutierrez could reasonably have chosen to shy away from.
He told Welch that the defense must prove not only that Gutierrez made questionable decisions in defending Syed, but was "constitutionally deficient" and "below the standard of conduct."
McClain sat just feet from Syed, whom she described as a former acquaintance. By the time his trial started a year after his arrest, she said, she was concentrating on college and did not follow the proceedings.
Syed has been incarcerated for 16 years. He entered the courtroom wearing a blue prison top, jeans, work boots, and a round gray-and-white skullcap, or topi.
McClain, meanwhile, has moved to Washington state, where she said she is married with two children, and expecting a third.
McClain described participating in the "Serial" podcast unwittingly. She said she assumed it was a sparsely followed Internet radio show. But her account became a crucial chapter in the 12-episode series, and she "binge-listened" to the program.
Before "Serial," "I didn't think I was very important at all," McClain testified. "I came to find out, as [creator] Sarah [Koenig] said, maybe it is important."
Koenig, the former Baltimore Sun reporter who produced and narrated "Serial," also attended the hearing. ||||| | – A woman who says she saw Serial subject Adnan Syed at a library at a time when prosecutors said he was murdering his ex-girlfriend took the stand on Wednesday—16 years after he received a life sentence for the crime. Asia McClain told the Baltimore courtroom that Syed seemed "completely normal" when she saw him on Jan. 13, 1999, NBC News reports. She testified that she wrote two letters offering to help his defense but was never contacted by defense lawyer Cristina Gutierrez. McClain said she lost track of the case for years, but the Serial podcast convinced her to speak out, reports the Baltimore Sun. "In order for justice to be served, all information has to be out on the table," she told the hearing, which will determine whether Syed gets a new trial. The Sun reports that Syed's current lawyer, Justin Brown, argued that Gutierrez, who died in 2004, was too ill to represent him properly in 2000 because of stress and health problems, including multiple sclerosis. Deputy Maryland AG Thiru Vignarajah used notes from Gutierrez's case file to counter that she was of sound mind and had decided against using McClain's testimony because it raised "warning signs and red flags" and didn't match Syed's account of his movements the day Hae Min Lee was murdered. Lee's family issued a statement saying they believe justice was done in 2000 and they are now having to "relive a nightmare we thought was behind us." The hearing concludes Friday, though a decision could take weeks or months, ABC News reports. | multi_news_1_0_0 |
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Article:
Our study provides a comprehensive, prospective analysis of the contemporary risks of death associated with cigarette smoking in the United States. The rate of death from any cause was 2 to 3 times as high among current smokers as among persons who never smoked, a finding that is consistent with the results in our previous report.3 Approximately 17% of this excess mortality was due to associations with causes that have not been formally established as attributable to smoking.
The rate of death from renal failure was twice as high among current smokers as among persons who never smoked, a finding that is consistent with results from case–control studies.11,12 Smoking is an important cause of the cardiovascular risk factors for renal failure but may also directly impair kidney function.12 Even in patients without underlying renal or cardiovascular diseases, urinary albumin, a marker of potential renal damage, increases in a dose-dependent manner with the number of cigarettes smoked per day.13
Current smoking was associated with an increased risk of death from hypertensive heart disease (according to ICD-10 coding), which is the only category of heart disease not already formally established as attributable to smoking.1 Criteria for attributing a death from heart disease to hypertensive heart disease are not well defined.14 Hypertensive heart disease can include both hypertensive heart failure and other types of heart disease. However, this association is relevant for assessing the public health burden of smoking, since a considerable number of deaths in the United States are attributed to hypertensive heart disease.15
Mortality from intestinal ischemia was strongly associated with current smoking in this cohort, as it was in the Million Women Study.2 The relative risk was approximately 6 among current smokers and decreased with increasing number of years since quitting. To our knowledge, no other large studies have examined this association. Smoking acutely reduces blood flow to the intestines,16 and evidence suggests that smoking causes risk factors that can often lead to intestinal ischemia, including atherosclerosis, platelet aggregation, and congestive heart failure.17
Mortality from infections was more than twice as high among current smokers as among persons who never smoked, and the risk increased with smoking intensity and declined with increasing number of years since cessation. Previous studies have documented higher rates of many infectious diseases among smokers.18,19 The Surgeon General has concluded that cigarette smoke adversely affects immune function and may accelerate the progression of many infectious diseases.1
Current smoking was associated with more than double the risk of death from diseases included in the category of other digestive diseases (ICD-10 codes K00–K54, K56–K69, and K78–K93). The Surgeon General recently concluded that the evidence linking smoking to Crohn’s disease was suggestive but still insufficient.1 Moreover, smoking is an important modifiable risk factor for peptic ulcers20,21 and acute pancreatitis.22,23 Other diseases in this group include paralytic ileus and bowel obstructions, cholelithiasis, diverticulitis, and gastrointestinal hemorrhages. Although these diseases are not common causes of death, they account for millions of hospitalizations each year.24
There is broad agreement that cigarette smoking causes cancers at a minimum of 12 different sites.25,26 This study updates the relative risks of death from cancer at these sites in a contemporary population. We also found additional significant associations with death from breast cancer and from prostate cancer. The Surgeon General has not yet concluded that smoking causes breast cancer.1 We found that the risk of death increased significantly with smoking intensity and declined after cessation of smoking, findings that were similar to results from previous analyses of data from the individual cohorts that were pooled for the current analysis.27-30 Numerous studies have examined the relationship between smoking and breast cancer; however, confounding by alcohol use remains a concern. An analysis of the Million Women Study showed a 13% higher risk of fatal breast cancer among current smokers after adjustment for the number of drinks per week, but no association was observed among women who consumed fewer than three drinks per week.2 In our analysis, smoking remained significantly associated with death from breast cancer among women who were not current drinkers. However, associations between smoking and death from breast cancer may also be biased by differences in screening31 or treatment32 patterns among smokers, and information on these variables was not available in this study. Additional studies with detailed information on these factors may be useful in clarifying whether smoking is causally associated with death from breast cancer.
Mortality from prostate cancer in this population was 43% higher among current smokers than among those who had never smoked, a finding that is consistent with most previous analyses of prostate-cancer mortality.33 The Surgeon General concluded that although there was insufficient evidence that smoking increases the incidence of prostate cancer, the available evidence suggested that current or recent smoking increases the risk of advanced-stage disease and of death from prostate cancer.1 Higher mortality from prostate cancer among smokers could be caused by delayed diagnosis owing to less intense medical surveillance or by a promoting effect of smoking on later stages of carcinogenesis and progression.34 This latter hypothesis is supported by analyses showing associations between smoking and both progression of prostate cancer35 and prostate-cancer–specific mortality among men with prostate cancer.36 Results from our analysis appear to be consistent with an influence of smoking on later stages of carcinogenesis, since we observed no increase in prostate-cancer mortality among men who had recently quit smoking.
We found significantly higher mortality from liver cirrhosis among smokers than among persons who never smoked but did not observe a dose–response pattern with respect to smoking intensity or years since quitting. In a recent analysis of the Million Women Study, mortality from liver cirrhosis was increased by a factor of 3, a finding that was unchanged when the analysis was restricted to women who reported consuming fewer than three drinks per week.2 In our analysis, current smoking was significantly associated with death from liver cirrhosis even among persons who were not current drinkers, although the relative risk was lower in that subgroup than in the overall study population. This association may be confounded by past alcohol use, but it could plausibly be attributed, at least in part, to smoking. Future studies should focus on the risks associated with smoking among persons who have never drunk alcohol.
Overall, associations between smoking and death from the 14 disease categories shown in Table 3 accounted for virtually all the excess mortality associated with smoking that was not already accounted for by diseases previously established as attributable to smoking. We think there is strong evidence for a causal association between smoking and at least 5 of these disease categories — infections, hypertensive heart disease, renal failure, intestinal ischemia, and other respiratory diseases. The associations with respiratory diseases and infections have strong biologic plausibility. Hypertensive heart disease, renal failure, and intestinal ischemia are related to poor vascular function, and the adverse effects of smoking on vascular function in general are well established.17
In addition to these five disease categories, smoking was associated with mortality from cancers of unknown primary site that was increased by a factor of nearly 3. No cancer that has not already been established as caused by smoking is likely to be as strongly associated with smoking as that. Therefore, the excess risk of death from these cancers is likely to have resulted from cancers already established as caused by smoking. The same holds true with respect to deaths from unknown causes. Since the great majority of deaths are from causes established as attributable to smoking, this category probably includes substantial numbers of deaths from known smoking-related diseases. Deaths from the five disease categories we consider likely to be causal combined with deaths from unknown cancers and unknown causes accounted for approximately 10% of the total excess mortality among smokers in this cohort, or about half of all the excess mortality not accounted for by diseases already established as caused by smoking.
Our results suggest that the Surgeon General’s recent estimate of smoking-attributable mortality may have been an underestimate. The Surgeon General’s estimate, which took into account only the 21 diseases formally established as caused by smoking, was that approximately 437,000 deaths among adults are caused each year by active smoking (not including secondhand smoke). However, the Surgeon General’s report presents an alternative estimate of 556,000 deaths among adults on the basis of the excess mortality from all causes. The difference between these two estimates is nearly 120,000 deaths.1 If, as suggested by the results in our cohort, at least half of this difference is due to associations of smoking with diseases that are causal but are not yet formally established as such, then at least 60,000 additional deaths each year among U.S. men and women may be caused by cigarette smoking.
The primary strength of this study is its large size, which enabled us to examine causes of death that are too rare to examine in smaller studies; nonetheless, these outcomes are responsible for a sizable number of smoking-related deaths. This analysis includes mortality data that are updated from our original report and thus provides more precise estimates of the contemporary risks of death associated with smoking.
A notable limitation of this study is that most members of the study population were white, and on average, they were better educated than the general population. Another limitation is that the associations observed in this study could be confounded by differences between smokers and nonsmokers with respect to risk factors including diet, physical activity, and access to medical care. The potential for confounding varies depending on the specific mortality outcome. However, in an earlier study of smoking and mortality, adjustment for demographic and behavioral factors had a minimal effect on risk estimates.37
In conclusion, this comprehensive examination of cause-specific mortality in a large contemporary population identified associations between smoking and increased mortality from several diseases that are not currently established as caused by smoking. Although these associations should be investigated further, our results suggest that the number of persons in the United States who die each year as a result of smoking cigarettes may be substantially greater than currently estimated. ||||| The U.S. surgeon general says about 480,000 Americans die each year as a result of smoking. But a new analysis suggests the true figure may be closer to 575,000.
The 21 causes of death that have been officially blamed on smoking accounted for 83% of the actual deaths among smokers who were tracked in a study published in Thursday’s edition of the New England Journal of Medicine.
Additional diseases -- including breast cancer, prostate cancer, hypertensive heart disease and renal failure -- were responsible for most of the rest of the observed deaths. A very small number of deaths were due to things such as accidents and suicide, which have a more tenuous link to smoking.
Researchers from the American Cancer Society, the National Cancer Institute and elsewhere combined data from five large, ongoing health studies: the Nurses’ Health Study I, the Women’s Health Initiative, the Health Professionals Follow-up Study, the Cancer Prevention Study II and the National Institutes of Health-AARP Diet and Health Study. The researchers included 954,029 men and women who were being tracked as of Jan. 1, 2000, and who had told interviewers about their smoking status.
Between 2000 and 2011, 16,475 (19%) of the 88,616 smokers died, as did 108,253 (23%) of the 469,141 former smokers and 56,649 (14.3%) of the 396,272 people who had never smoked, according to the study.
Smokers were more likely than nonsmokers to have died from one of the established smoking-related diseases, the researchers found. These included most kinds of heart disease; stroke; chronic obstructive pulmonary disease; pneumonia, influenza and tuberculosis; atherosclerosis; aortic aneurysms and other arterial diseases; diabetes; acute myeloid leukemia; and cancers of the lung, pancreas, colon and rectum, kidney, liver, bladder, larynx, lip and oral cavity, stomach and esophagus.
These diseases were responsible for the overwhelming majority of deaths among men and women who were still smoking at the end of their lives.
But not all of them. Another 17% of deaths among female smokers and 15% of the deaths of male smokers were traced to other causes.
In nearly every case, the diseases in this second group were more likely to kill current smokers than nonsmokers, according to the study.
For instance, female smokers were 30% more likely to die of breast cancer than their non-smoking counterparts, and men who smoked were 40% more likely to die of prostate cancer than their non-smoking peers. Rare cancers were 60% more likely to kill men if they were smokers, the researchers found.
The risk of death due to infections was more than twice as high for smokers than for nonsmokers. Ditto for hypertension, hypertensive renal disease and a range of digestive diseases.
Smokers were 2.6 to 3.6 times more likely than nonsmokers to die of liver cirrhosis and 1.9 to 2.1 times more likely to die of kidney failure. Hypertensive heart disease, some kinds of respiratory diseases and ischemic disorders of the intestines were also more likely to kill smokers than nonsmokers, the study authors calculated.
The more cigarettes a person smoked per day, the greater his or her risk of dying from infections, breast cancer or kidney failure. Among those who quit, the longer it had been since the last cigarette, the lower the risk of dying from infections or breast cancer, according to the report.
The researchers laid out the biological mechanisms that could plausibly explain why some of these diseases would be more likely to kill smokers. In the case of infections, for example, cigarette smoke is known to hinder immune function. Smoking is also known to reduce blood flow to the intestines, potentially explaining the link to intestinal and digestive diseases.
Compared to the U.S. population as a whole, the people included in this study were more likely to be white and to be highly educated. That limits researchers’ ability to generalize the findings to the entire country.
Still, the study authors didn’t hesitate to say that the surgeon general should go back and check the math.
“Our results suggest that the number of persons in the United States who die each year as a result of smoking cigarettes may be substantially greater than currently estimated,” they wrote.
For more medical news you can use, follow me on Twitter @LATkarenkaplan and "like" Los Angeles Times Science & Health on Facebook. ||||| About 42 million Americans smoke — 15 percent of women and 21 percent of men — according to the Centers for Disease Control and Prevention. Research has shown that their death rates are two to three times higher than those of people who have never smoked, and that on average, they die more than a decade before nonsmokers. Smokers are more than 20 times as likely as nonsmokers to die of lung cancer. Poor people and those with less formal education are the most likely to smoke.
Mr. Carter said he had been inspired to dig deeper into the causes of death in smokers after taking an initial look at data from five large health surveys being conducted by other researchers. The participants were 421,378 men and 532,651 women 55 and older, including nearly 89,000 current smokers.
As expected, death rates were higher among the smokers. But diseases known to be caused by tobacco accounted for only 83 percent of the excess deaths in people who smoked.
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“I thought, ‘Wow, that’s really low,’ ” Mr. Carter said. “We have this huge cohort. Let’s get into the weeds, cast a wide net and see what is killing smokers that we don’t already know.”
The research was paid for by the American Cancer Society, and Mr. Carter worked with scientists from four universities and the National Cancer Institute.
The study was observational, meaning that it looked at people’s habits, like smoking, and noted statistical correlations between their behavior and their health. Correlation does not prove a cause-and-effect relationship, so this kind of research is not considered as strong as experiments in which participants are assigned at random to treatments or placebos and then compared. But people cannot ethically be instructed to smoke for a study, so a lot of the data on smoking’s effects on people comes from observational studies.
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Analyzing deaths among the participants from 2000 to 2011, the researchers found that, compared with people who had never smoked, smokers were about twice as likely to die from infections, kidney disease, respiratory ailments not previously linked to tobacco, and hypertensive heart disease, in which high blood pressure leads to heart failure. Smokers were also six times more likely to die from a rare illness caused by insufficient blood flow to the intestines.
Mr. Carter said he had confidence in the findings because, biologically, it made sense that those conditions were related to tobacco. Smoking can weaken the immune system, increasing the risk of infection, he said. It is also known to cause diabetes, high blood pressure and artery disease, all of which can lead to kidney problems. Artery disease can also choke off the blood supply to the intestines. Lung damage from smoke, combined with increased vulnerability to infection, can lead to multiple respiratory illnesses.
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Two other observations supported the findings, he said. One was that the more heavily a person smoked, the greater the added risks. The second was that among former smokers, the risks diminished over time. In general, such effects, known as a dose response, suggest that an observed correlation is more than a coincidence.
The study also found small increases in the risks of breast and prostate cancer among smokers. Mr. Carter said those findings were not as strong as the others, adding that additional research could help determine whether there were biological mechanisms that would support a connection.
A 2014 report by the surgeon general’s office said the evidence for a causal connection between smoking and breast cancer was “suggestive but not sufficient.” The same report found no evidence that smoking caused prostate cancer, but it noted that in men who did have prostate cancer, smoking seemed to worsen the outcome.
The diseases that had previously been established by the surgeon general as caused by smoking were cancers of the esophagus, stomach, colon, liver, pancreas, larynx, lung, bladder, kidney, cervix, lip and oral cavity; acute myeloid leukemia; diabetes; heart disease; stroke; atherosclerosis; aortic aneurysm; other artery diseases; chronic lung disease; pneumonia; influenza; and tuberculosis. ||||| A new study suggests that smoking may be responsible for 60,000 to 120,000 more deaths in the U.S. each year than previously thought.
The examination of 181,377 fatalities logged in five large databases found that many of the excess deaths among smokers were due to causes not previously linked to smoking, such as kidney failure, infections and possibly breast and prostate cancers.
Until now, 21 common diseases have been associated with cigarette smoking, including diabetes, 12 cancers and six forms of cardiovascular disease. The new research, published in the New England Journal of Medicine, may expand that list.
"We were interested in whether smoking causes more than these diseases that are on the list. And we certainly did find some," coauthor Eric Jacobs told Reuters Health. "The fact that about 17 percent of the extra deaths that occur in smokers were due to causes that were not on the Surgeon General's list was a bit of a surprise to me."
If the findings are applied nationwide, he said, the number of previously-unrecognized smoking-related deaths could be greater than the total number of Americans who die each year of influenza or liver disease.
Until this study, about 480,000 U.S. deaths each year were believed to be attributable to cigarettes.
The researchers also found that the elevated risks faded as smokers stayed off cigarettes.
The findings derive from databases following nearly a million people over age 54 for about a decade.
The researchers expected to see smokers dying faster than nonsmokers, and they did.
But when they looked beyond conventional causes, they found that smoking doubled the risk of death from kidney failure and from various respiratory diseases. It also seemed to pose a six-fold risk of death from intestinal ischemia, where the intestine is damaged by reduced blood flow.
The risk of death from infections was 2.3 times higher and the likelihood of death from cirrhosis of the liver was 3.1 times higher.
Breast cancer deaths were 30 percent higher among the smokers. Prostate cancer death rates were elevated by 40 percent.
In many cases, the more people smoked, the greater the risk. That wasn't seen in prostate cancer, "but the risk of death decreased significantly as the number of years since quitting smoking increased," said Dr. Graham Colditz of the Washington University School of Medicine, St. Louis, in an editorial.
"It's not a surprise that smoking kills. We've known that for years," said Jacobs, who is director of pharmacoepidemiology at the American Cancer Society. "But it's important for people to realize the full impact that smoking has in terms of the national deaths. So eliminating smoking needs to be a national priority."
In his editorial, Colditz points out that 18 percent of the U.S. population, 42 million Americans, smoke, and public health efforts to help them quit have not done enough to change “social norms.”
In the U.S., smoking has become a habit of the poor and the poorly-educated, Colditz told Reuters Health. He said that "in 2013, a total of 29 percent of adults below the poverty line smoked, whereas 16 percent at or above the poverty level did. In addition, only 6 percent of adults with advanced college degrees smoked, whereas 41 percent of those with a general equivalency degree did."
Colditz writes in the editorial, “The Affordable Care Act provides expanded access to cessation support for many, but holes in Medicaid coverage in many states leave numerous smokers without as much evidence-based support as they need.”
SOURCE: bit.ly/1xJnCqb New England Journal of Medicine, online February 11, 2015. |||||
What is a summary? | – How many Americans does smoking kill each year? If you're going by the surgeon general, the answer is about 480,000. But a new study published in the New England Journal of Medicine suggests the number is actually more like 575,000. The issue is that only 21 causes of death are officially blamed on smoking, the Los Angeles Times explains—think heart disease, stroke, COPD, and certain cancers, including lung and esophageal. But those causes of death actually only account for 83% of deaths among smokers that the study tracked. The rest were caused by things like renal failure, infections, other cancers, and even accidents and suicide, which, the Times notes, "have a more tenuous link to smoking." Researchers looked at five large studies involving nearly a million people to compile the information. The diseases not officially caused by smoking were more likely to kill current smokers than nonsmokers: Breast cancer was 30% more likely to kill female smokers; prostate cancer was 40% more likely to kill male smokers; smokers were twice as likely to die of infections, hypertension, and certain digestive diseases than nonsmokers—and they were as much as 3.6 times more likely to die of cirrhosis. The comparisons go on, and in some cases, a smoker's risk was even greater the more cigarettes he or she smoked per day. Why? The study didn't actually establish a cause-and-effect relationship, the New York Times notes, but researchers offer explanations: in the case of infections, possibly because smoking hampers the immune system. For intestinal or digestive illnesses, possibly because smoking reduces blood flow to the intestines. The good news? If you quit, the higher risks fade the longer you stay away from cigarettes, Reuters reports. (If you do quit, you may have trouble finding "magic" lozenges.) | multi_news_1_0_0 |
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You’re not alone if a big bowl of pasta puts a smile on your face, but according to new research, that sense of happiness may be short-lived. A new study links pasta and other carbohydrates to a risk of being diagnosed with depression.
According to the Centers for Disease Control and Prevention, carbohydrates are essential to the human body as a source of glucose. Carbohydrates can be found in both healthy and unhealthy foods, such as fruits, vegetables, grains, milk, cookies, and soda.
A research team led by Michel Lucas, Ph.D., from the Harvard School of Public Health, has finished conducting a 12-year study to determine carbohydrate-rich food’s association with depression. A total of 43,000 women with no history of depression were recruited for the study. Researchers asked participants about their daily eating habits and oversaw blood testing.
Results indicated that women who ate red meat and refined grains such as bread, pasta, and chips were at a 29 to 41 percent increased risk of being diagnosed with or receiving treatment for depression. Dr. Lucas and his colleagues were also surprised by the effect that carbohydrates had on inflammation, Prevention reports.
Although Dr. Lucas was unable to explain the specific cause of carbohydrates' effect on mental health and the body’s immune response, he did provide a list of foods known to reduce the risk of depression and inflammation. Olive oil, coffee, wine, fish, and certain vegetables can help boost your mood and control inflammation.
A recent study out of Emory University also focused on the connection between depression and inflammation. Researchers tested an anti-inflammatory drug’s effect on people with high levels of untreatable depression. The medication successfully blocked a key molecule in inflammation that may also induce depression-like symptoms.
"Inflammation is the body's natural response to infection or wounding," said Andrew H. Miller, M.D., the study’s lead researcher and professor of psychiatry and behavioral sciences at Emory University School of Medicine. "However when prolonged or excessive, inflammation can damage many parts of the body, including the brain." ||||| Transcript for Pasta Linked to Depression in New Study
Now, to possible bad news for pasta lovers. According to a new study from the harvard school of public health, there may be a link between pasta and depression. Women who ate diets heavier in refined grains like pasta, will be one-third more likely to suffer from depression. Abc news chief medical correspondent, dr. Richard besser, is going to break it down for us. Do that for us. This study? It's an interesting study. The connection here is between food, inflammation in their bodies and depression. There's some studies that show inflammation in our bodies is one thing that drives depression. These researchers want to see, are there certain foods we eat that cause inflammation that put us at greater risk than for depression. They found a group of foods that cause inflammation. And they asked women did they become more depressed. Women who ate more pasta, red meat and sodas, had a 29% to 41% increased risk of depression. People that ate food of less inflammation, have lower rates of depression. Were there problems with the study that you found, rich? You can't take a group of people and say you're going to eat this. You look at what people normally eat. And then, you try to control it for everything else. It could be the other way around. People who are starting to see changes in their mood go to confident food. I know after a downer day, i like to reach for the pint of ice cream. It may be driven the opposite direction altogether. But it is interesting to look at. And this study only with women? How about men and children? It's a famous study out of harvard. They follow over 100,000 women. They find the inflammation like this. You can't apply it to men, or children, either. Recommendation? I'm a fan of the mediterranean diet. Rich in whole grains, fish. If it's good for the heart and good for the brain, as well. Thanks so much.
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NEW YORK (CBSNewYork) — Pasta already has been maligned as a carb-heavy, fattening foodstuff in recent years, and now, a new study suggests that it might be linked to depression.
The study in the journal, “Brain, Behavior and Immunity” concluded that a dietary pattern high in carbs such as pasta can lead to a diagnosis of depression. The Nurses’ Health Study spent 12 years following 43,685 women between the ages of 50 and 77, who did not have depression when the study began.
The study concluded that women who ate refined grains such as pasta, drank soft drinks, and ate fatty red meat – in what has been termed an “inflammatory dietary pattern” – were more likely to be treated for depression, according to published reports.
The high-carb diet pattern revealed increased inflammatory biomarkers in blood tests, the study said.
Out-of-control inflammation also has been linked to heart disease, stroke, diabetes, and cancer, according to published reports.
In the past decade, pasta has been maligned along with other high-carb foods as a catalyst for obesity. But Live Science argued that pasta is actually a healthy carbohydrate, and a major component of the Mediterranean diet that is considered a useful way to maintain a healthy weight.
You May Also Be Interested In These Stories ||||| Brain, Behavior, and Immunity, founded in 1987, is the official journal of the Psychoneuroimmunology Research Society (PNIRS). This innovative journal publishes peer-reviewed basic, experimental, and clinical studies dealing with behavioral, neural, endocrine, and immune system interactions in humans and animals. It is an international, interdisciplinary journal devoted to original research in neuroscience, immunology, integrative physiology, behavioral biology, psychiatry, psychology, and clinical medicine and is inclusive of research at the molecular, cellular, social, and whole organism level. The journal features online submission and review. Manuscripts are typically peer-reviewed and returned to authors within 30 days of submission, leading to timely publication of experimental results. There are no submission fees or page charges for Brain, Behavior, and Immunity, which is published eight times a year. Detailed instructions for authors can be found at http://ees.elsevier.com/bbi/.
Research areas include: |||||
Write a summary. | – A Harvard study that followed 43,000 women over 12 years has found that some of your favorite foods may not just be hurting your physical health, but your mental health, too. The research team looked at the women's diets and discovered those who consumed more red meat, soda, and refined grains, like pasta, white bread, and chips, were 29% to 41% more likely to be diagnosed with depression than those who consumed more wine, coffee, and leafy greens, Medical Daily reports. The women, aged 50 to 77, had no prior history with depression before the study, notes CBS New York. Exactly how the carb-rich foods are linked to depression isn't known: ABC News points out that those suffering from depression may head to comfort foods, like pasta, which could account for the higher rates. But it may also be that carb-rich diets lead to more inflammation, something that has already been pegged as a possible link to depression, Prevention reports, noting that women who ate more carb-rich foods also tested higher for three biomarkers of inflammation. How to keep your risk down? The study author suggests a Mediterranean-style diet, heavy in olive oil, fish, and veggies, like carrots and sweet potatoes. | multi_news_1_0_0 |
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This is the first study to quantify associations of mutually exclusive categories of objectively measured physical activity and sedentary time with markers of cardiometabolic health in a nationally representative sample of English adults. Overall, adults who engaged in at least 150 min of MVPA per week, including those with concomitant high sedentary time (‘Sedentary Exercisers’), had more favourable health profiles compared to physically inactive individuals with high sedentary time (‘Couch Potatoes’). Low sedentary time independent of physical activity (‘Light Movers’) had positive associations with HDL-cholesterol. These findings were consistent with the sensitivity and continuous analyses.
The approach to categorising the population into one of four mutually exclusive categories extends previous research using HSE. For example, previous analysis of HSE has reported associations between both self-reported and objectively assessed sedentary time with markers of health in working age and older adults and between MVPA and markers of health [25–27]. The wider evidence has increasingly demonstrated that objectively measured sedentary time is independently associated with markers of cardiometabolic health [16–20, 41, 42], although not all studies have demonstrated this link [43]. Whilst these previous analyses have adjusted for MVPA, the associations of sedentary time with health across physical activity levels are less well understood. Therefore, this study adds to the evidence by investigating associations of sedentary status with health across categories of physical activity.
Our findings are in broad agreement with the only other study to have used a similar methodology [36]. Using national survey data from the USA, Loprinzi and colleagues found that in comparison to individuals (aged ≥20 years) who engaged in <150 min/week of MVPA with high sedentary time (sedentary time > light-intensity physical activity time), individuals engaging in ≥150 min/week of MVPA had a more favourable cardiometabolic profile (BMI, waist circumference, C-reactive protein, white blood cells and neutrophils) regardless of their sedentary status. [36] Participants in the most desirable group (≥150 min/week of MVPA with low sedentary time) also had better HDL-cholesterol, triglyceride and insulin levels. Similar to our study, participants in the physically inactive group with low sedentary time had fewer beneficial associations, although more favourable profiles for triglycerides and insulin levels were still observed.
Our findings, alongside those of Loprinzi and colleagues [36], are also consistent with the emerging evidence that levels of fitness or physical activity may modify the associations between sedentary time and markers of health in adults [35, 41, 44, 45], with sedentary behaviour only emerging as a determinant of health in those who are inactive or unfit. Together, these studies suggest that being physically active may confer some protection from the potentially deleterious impact of high sedentary behaviour.
In our study, low sedentary time in the absence of being physically active (‘Light Movers’) was associated with higher levels of HDL-cholesterol (+0.11 mmol/L), suggesting that physical inactivity in a combination with low sedentary time may have some positive relationships with health. However, the potential benefits appeared to be less numerous and consistent than those observed for physically active categories (‘Busy Bees’ and ‘Sedentary Exercisers’). One reason for this could be in the assessed markers of cardiometabolic health. Although our study included a measure of glycaemia (HbA1c), more sensitive measures of insulin resistance, which have shown stronger associations with sedentary time [6, 19, 20, 46], were not available.
Although sedentary behaviour and MVPA have been hypothesised to be distinctive health behaviours, it is unclear to what extent the underlying mechanisms act through the same or independent pathways. This reflects a limitation in the evidence more generally where mechanisms underpinning the benefits of sedentary behaviour have not been adequately elucidated. To date, the only evidence-based independent mechanism for sedentary behaviour has been through the activation of lipoprotein lipase which has been shown to change by a factor of 10 in animal models following hind limb suspension [47]. This supports the observation in our study where low sedentary time was associated with higher HDL-cholesterol levels, even in those who were physically inactive (‘Light Movers’). In contrast to sedentary behaviour, acute and chronic physiological adaptions have been well established linking higher levels of physical activity to cardiometabolic health [48–50]. ||||| A new study of over 1 million people finds that doing at least one hour of physical activity per day, such as brisk walking or cycling for pleasure, may eliminate the increased risk of death associated with sitting for 8h a day.
Physical inactivity is linked to an increased risk of heart disease, diabetes and some cancers and is associated with more than 5 million deaths per year [1] and, as the first global economic analysis of physical inactivity shows, costs the world economy over US$67.5 billion per year in health care costs and lost productivity.
The findings come from a new four-paper Series published today in The Lancet and launched in London ahead of the Summer Olympic Games. The authors of the Series warn there has been too little progress in tackling the global pandemic of physical inactivity since the 2012 Olympics, with a quarter of adults worldwide still failing to meet current recommendations on physical activity.
Sitting time, physical activity and risk of death (paper 1)
Researchers analysed data from over 1 million people from 16 studies. The research team wanted to see how many hours of daily physical activity would be required to eliminate the association between prolonged sitting time and increased risk of death. Examples of physical activity were brisk walking at 5.6 km/h or cycling for pleasure at 16 km/h.
The researchers classified individuals into four equally sized groups according to how active they were - less than 5 mins a day for the least active, up to 60-75 mins a day for the most active [2].
People who sat for 8 hours a day but were physically active had a much lower risk of death compared to people who sat for fewer hours a day, but were not physically active (figure 2A). This suggests that physical activity is particularly important, no matter how many hours a day are spent sitting. In fact, the increased risk of death associated with sitting for 8 hours a day was eliminated for people who did a minimum of 1 hour physical activity per day. The greatest risk of death was for people who sat for long periods of time and were inactive.
WHO guidelines recommend that adults should do at least 150 mins of physical activity per week [3], which is much lower than the 60-75 mins per day identified in this analysis. The study also warns of the progress that remains to be made in increasing levels of physical activity since only about 25% of people in the analysis did an hour or more physical activity per day.
"There has been a lot of concern about the health risks associated with today's more sedentary lifestyles," says lead author Professor Ulf Ekelund, the Norwegian School of Sports Sciences, Norway and the University of Cambridge, UK "Our message is a positive one: it is possible to reduce - or even eliminate - these risks if we are active enough, even without having to take up sports or go to the gym."
He adds: "For many people who commute to work and have office-based jobs, there is no way to escape sitting for prolonged periods of time. For these people in particular, we cannot stress enough the importance of getting exercise, whether it's getting out for a walk at lunchtime, going for a run in the morning or cycling to work. An hour of physical activity per day is the ideal, but if this is unmanageable, then at least doing some exercise each day can help reduce the risk." [4]
The research team also looked at time spent watching TV per day - a specific type of sedentary behaviour - in a subgroup of approximately half a million people. They found similar results: sitting watching TV for over 3h per day was associated with an increased risk of death in all activity groups, except the most active (figure 2B). The authors stress that the association is likely not because of a causal link between watching TV and an increased risk of death, but simply that watching TV is a specific type of sedentary behaviour. The increased risk of death associated with sitting watching TV for many hours a day was slightly greater than the increased risk of death associated with total sitting time. The authors say that this could be due to a number of factors - for instance, long hours watching TV may be a marker of a more unhealthy lifestyle in general including being less likely to take exercise. Also, because people usually watch TV in the evenings after dinner which might affect their metabolism, or because people may be more likely to snack while watching TV.
The authors warn that the study mainly included data from people aged over 45 years old from the USA, Western Europe and Australia, so may not apply to other populations.
Economic burden of physical inactivity (paper 2)
In the first study to estimate the global economic burden of physical inactivity, researchers estimated the total cost of physical inactivity to be at least INT$67.5 billion in 2013 [5] - equivalent to what US$67.5 billion could buy in the United States in 2013, or the total Gross Domestic Product of Costa Rica in the same year. In the USA alone, the economic burden of physical inactivity in 2013 was US$27.8 billion, compared to R$3.3 billion in Brazil, £1.7 billion in the UK and AUS$805 million in Australia.
The study found that high-income countries bear a much larger proportion of the economic burden associated with physical inactivity (80.8% of health-care costs in high income countries and 60.4% of indirect costs), whereas low-income and middle-income countries have a larger proportion of the disease burden (75.0% of the global burden of disease for physical inactivity is borne by low and middle income countries) (table 3).
"The current economic cost of physical inactivity is borne mainly by high income countries. However, as low and middle income countries develop, and if the current trajectory of inactivity continues, so too will the economic burden in low and middle income countries who are currently poorly equipped to deal with chronic diseases linked to physical inactivity," says lead author Dr Melody Ding, University of Sydney, NSW, Australia. "Our study makes the economic case for a global response to promote physical activity to tackle diseases such as diabetes, heart disease and some cancers, with the aim of reducing health inequalities." [4]
The authors note that the study only included costs for the five major diseases associated with physical inactivity (coronary heart disease, stroke, type 2 diabetes, breast cancer, and colon cancer), therefore the cost calculations are based on conservative estimates, and the true cost may be even higher.
Progress since the 2012 Olympic Games (paper 3)
Although there has been progress in developing national policies, the authors found these were too often not being put into practice. In 2010, 75% of countries reported having a physical activity policy but only 44% reported it being operational. In 2015, over 90% had a policy and 71% reported it being operational (figure 2). But there has been little progress in increasing levels of physical activity with 23% of the global adult population and 80% of school-going adolescents failing to meet the WHO recommendation of 150 minutes of moderate-intensity exercise per week in 2015.
"In the past four years, more countries have been monitoring progress in physical activity, but evidence of any improvements is scarce. We know that physical inactivity is linked to diseases including heart disease, diabetes and some cancers, and new evidence also shows that 300000 cases of dementia could be avoided annually if all people were physically active. The global pandemic of physical inactivity remains, and the global response has been far too slow" says lead author Professor Jim Sallis, University of California San Diego, San Diego, CA, USA [4].
Smarter approaches to physical activity (paper 4)
Increasing levels of physical activity will require collaboration between schools, urban planning, transport, sports and recreation and the environmental sectors, and greater efforts should be made to actively monitor physical activity as a risk factor in clinical practice. The authors point to several successful examples such as the Bus Rapid Transit (BRT) System introduced in Curitiba (Brazil), Bogota (Colombia) and Cambridge (UK) which puts stops further apart than traditional bus stops to encourage walking; or the Coordinated Approach to Child Health (CATCH) in the USA which promotes a healthy school environment including physical activity, food, nutrition and sun protection (see panels 1, 2, 3).
"Large-scale problems require large-scale solutions, and we need commitment from governments, as well as international organisations to tackle the global public health challenge of physical inactivity. Science and practice are providing important evidence, but now is the time for action," says Professor Rodrigo Reis, Washington University in St Louis, St Louis, MO, USA [4].
Writing in a linked Comment, Dr Pam Das, Senior Executive Editor and Dr Richard Horton, Editor-in-chief of The Lancet say: "The world needs to get serious about physical activity. And that means money--for capacity in public health departments to undertake adequate surveillance, cross sector partnerships, interventions, policy monitoring, and research, especially the cost-effectiveness of interventions. There is extensive evidence about the need for action to improve physical activity, what actions are most promising, and who needs to be involved. But capacity and funding remains insufficient because physical activity is not taken seriously enough to rise to the top of the funding priorities."
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NOTES TO EDITORS:
[1] Findings come from The Lancet Physical Activity Series 2012 http://www. thelancet. com/ series/ physical-activity
[2] Physical activity was expressed in metabolic equivalent of task (MET)-hours per week. The four quartiles were 2·5 MET-h per week (equivalent to about 5 min of moderate intensity activity per day), 16 MET-h per week (25-35 min per day) and 30 MET-h per week (50-65 min per day), and 35·5 MET-h per week (60-75 min per day).
[3] http://www. who. int/ dietphysicalactivity/ factsheet_recommendations/ en/
[4] Quotes direct from authors and cannot be found in the text of the Articles
[5] Estimates are provided in International Dollars (INT$) which corresponds to the cost adjusted for purchasing power in the USA in 2013. It is widely used in economics to compare costs in different countries over time. Table 1 provides costs for 142 countries in INT$. ||||| There’s been a lot of finger-wagging of late about the health risks associated with sitting at a desk all day, or binge-watching our favorite TV shows. Now couch potatoes can rejoice because a new study has found that just an hour of moderate activity a day wipes out all the negative impacts of sedentary behavior—contrary to some prior studies claiming exercise didn’t help much at all.
“Our message is a positive one,” lead author Ulf Ekelund, of the Norwegian School of Sports Science and the University of Cambridge, said in a statement. “It is possible to reduce, or even eliminate, these risks if we are active enough, even without having to take up sports or go to the gym.”
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The study is part of a new four-paper series published today in The Lancet, along with several commentaries, timed to appear just before the start of the Olympic games. That’s not a coincidence. It’s a follow-up to a 2012 series in The Lancet declaring physical inactivity a “global pandemic,” and estimating that 5.3 million people die each year due to inactivity. The 2016 series examines how much progress has been made over the last four years to counter this. [You can listen to a full Lancet podcast about the whole series here.]
Sitting for long periods—as many of us do for work—and binge-watching TV is the new smoking when it comes to human health risks. Over the last few years, there have been countless studies claiming links between our sedentary lifestyles and heart attacks, kidney diseases, chronic diseases, and colorectal cancer. Others warned that this behavior shortens our life expectancy and gives us mental health issues. And even for those who exercise regularly, a 2014 Mayo Clinic study found that every hour you sit reduces the gains of your daily workout by eight percent.
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Now for the good news: that last bit might not be true after all. Earlier this year, yet another study, this time by researchers from the University of Leicester, found that people who exercise regularly really do offset the unhealthy side effects of sitting all day. And the latest meta-analysis published today in The Lancet supports that conclusion.
Granted, an hour a day of moderate exercise is twice the amount of exercise recommended by the current World Health Organization (WHO) guidelines. Even 30 minutes a day can be beneficial, but if you really want to offset all that sitting and binge-watching, the researchers agreed that you’ll need to double that. This doesn’t mean intense gym workouts or hardcore training for marathons. Anything that boosts your heart rate qualifies, including a nice brisk walk to work or leisurely bike ride.
Bear in mind that this is a meta-analysis of prior research. According to Ekelund, he and his colleagues first combed through the existing scientific literature and picked out 13 studies relating to how much time people spend sitting and mortality (defined as premature death). Then they contacted the original authors and asked them all to reanalyze their data using the same parameters. This gave them a huge sample size: over 1 million subjects in all.
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Ekelund and his colleagues divided the subjects into four equal groups, based on their level of physical activity—anywhere from less than 5 minutes a day, to an hour or more per day (60-70 minutes, on average). They found that those who were sedentary for eight hours a day, yet countered this with an hour of physical activity, had a much lower risk than those who maybe didn’t sit for as long a period, but were not as physically active. That suggests it’s not the sitting, it’s the exercise that is the most relevant factor. (Needless to say, people who sat the most and exercised the least had the highest risk.)
So what about binge-watching our favorite TV shows, which can be an even more passive activity than sitting at a computer typing? There have been a lot of hysterical headlines in recent years about how watching too much TV is totally going to kill you.
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There’s some grounds for the concerns. A 2014 Spanish study found that if you’re watching three or more hours per day, you’re twice as likely to die in the next few years. Sitting in front of the TV has also been linked to higher risk of colon and lung cancers. Just this week, yet another study appeared warning about the dangers of excessive binge-watching—this time showing an increased risk of dying from a blood clot in the lungs among the Japanese subjects.
More good news: An hour of exercise a day also helps reduce this risk, according to Ekelund, although the beneficial impact is not quite as strong. He attributes the difference to what he calls “residual confounding”—that is, other factors are likely influencing the outcome of the analysis. Some people might have a more unhealthy lifestyle overall, or perhaps we snack or drink more while watching TV, all of which could adversely impact our health.
As for those who might protest that an hour a day of moderate exercise just isn’t reasonable for very busy people, Ekelund pointed out in a London press conference earlier today that the average amount of time adults in the United Kingdom spend watching TV is 3 hours and 6 minutes. “I don’t know if it’s too much to ask that maybe a little of those three hours be devoted to physical activity,” he said. The general rule of thumb, as Ekelund succinctly advised: “Sit less and move more, and the more the better.”
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[The Lancet] |||||
Write a summary. | – If you think squeezing an hour of exercise in per day can't come close to making up for the other 23 hours when you're relatively sedentary—and so you don't bother at all—rethink that strategy. A study by Cambridge University and the Norwegian School of Sports Sciences published in the Lancet journal finds that even if you're sitting in front of a computer monitor or watching soap operas during the 9-to-5, just one hour of physical activity could nix the increased death risk, per a press release. The findings support a University of Leicester study done earlier this year that found regular exercise can fend off the detrimental effects of daylong sitting sessions, including increased risk of diabetes, certain cancers, and heart disease. "Our message is a positive one: It is possible to reduce—or even eliminate—these risks if we are active enough, even without having to take up sports or go to the gym," Ulf Ekelund, the study's lead author, says. Researchers examined data from 1 million people from 16 studies, dividing them into four groups based on activity level, from less than five minutes a day up to 60 to 75 minutes per day; activities included such exercise as brisk walking at around 3.5mph or leisurely cycling at 10mph. Those who were physically active had a significantly lower risk of death than those who kept up their couch potato habits. And those who put in a minimum of one hour a day of exercise got rid of the risk altogether from sitting for eight hours. That means even if you can't put in the full hour to wipe the slate clean, you'll still derive some benefit from even a bit of exercise, scientists say. Gizmodo notes it's no happy accident that this new study, part of a four-paper series, is emerging right on the eve of the Summer Olympics: It examines how much progress has been made since a Lancet series from four years ago that said lack of exercise was a "global pandemic" that contributed to the deaths of 5.3 million people annually. (Ten thousand steps a day might not be the magic number for fitness.) | multi_news_1_0_0 |
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– With chaos reigning and scores of travelers being held in the nation's airports in the wake of President Trump's executive order banning travelers from seven countries, a federal judge issued an injunction barring the government from deporting anyone, reports Politico. During an emergency hearing Saturday night in Brooklyn, US District Court Judge Ann Donnelly appeared to focus on the timing, and Politico notes that the scope of her ruling is limited, applying to people who were already in transit when the executive order was made. "If they had come in two days ago, we wouldn't be here, am I right? ... These are all people who have been through a vetting process," she said. A federal judge in Alexandria, Va., also moved to block the deportation of green card holders being held at Dulles airport, as well as force the government to provide them with lawyers, while another judge in Seattle blocked the deportation of two immigrants being held until a hearing could take place. The Department of Homeland Security, meanwhile, said that green card holders from the affected nations were granted special exemption Saturday and allowed to enter the country, reports the AP. For his part, Trump had this to say: "It’s not a Muslim ban, but we were totally prepared. It’s working out very nicely. You see it at the airports, you see it all over."
Expand this summary. | President Donald Trump: "It’s working out very nicely. You see it at the airports, you see it all over.” | Getty Judge blocks deportations as Trump order sparks global outrage White House faces legal challenges over executive order after travelers with visas to enter the U.S. were detained.
NEW YORK — A judge has blocked the federal government from deporting citizens of seven countries who were detained at U.S. airports over the past day or so as a result of an executive order President Donald Trump issued Friday.
Advocates said 100 to 200 travelers from those Muslim-majority countries were being held at various airports around the U.S. as a result of Trump’s order, which was billed as an anti-terrorism measure. The detentions sparked protests outside many international airports, including John F. Kennedy Airport in New York and Dulles Airport outside Washington.
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U.S. District Court Judge Ann Donnelly issued her injunction over the government’s objection during an emergency hearing Saturday night as several hundred people opposed to Trump's order chanted and milled about outside the Brooklyn, N.Y., federal courthouse.
During the brief court session, the judge said it was difficult to see the harm in allowing the newly arrived immigrants to stay since they were being routinely admitted just a couple of days ago.
"If they had come in two days ago, we wouldn't be here, am I right? ... These are all people who have been through a vetting process," the judge said.
"Explain to me how these petitioners won't suffer irreparable damage if I don't grant this stay?" Donnelly asked.
Assistant U.S. Attorney Susan Riley complained that the court proceeding was unduly rushed. "This has unfolded with such speed, we haven't had an opportunity to address any of the important legal issues," Riley said.
However, American Civil Liberties Union lawyer Lee Gelernt said the immigrants affected were essentially the victims of bad timing that caused them to be caught in limbo just as Trump's order was being issued.
"These people were caught in transit," Gelernt said. "The government is putting someone back on a plane to Syria now."
Donnelly, an appointee of President Barack Obama, said she was freezing the status quo by blocking the deportations.
"The whole point of this hearing is to preserve the status quo. I don't think it's unduly burdensome to identify people we are talking about here," the judge declared. "Nobody is to be removed in this class."
The White House had no immediate comment on the legal setback for one of the new president's signature policy moves. Justice Department spokespeople did not immediately indicate whether an appeal was planned.
Donnelly's order does not appear to interfere with most of Trump's directive, since the judge only moved to protect a limited number of individuals who were already on or were about to board flights to the U.S. when Trump signed his measure. Now, such travelers will likely be blocked from boarding flights in the first place.
Several other judges also stepped into the legal fray over the implementation of Trump’s executive order Saturday night and into the wee hours of Sunday morning. A federal judge in Alexandria, Va., issued an order barring the deportation of all green card holders being detained at Dulles Airport In Virginia for seven days. Judge Leonie Brinkema’s order also required that Customs and Border Protection grant lawyers access to those individuals.
"Department of Homeland Security officials are refusing to allow lawyers to talk with the detained people, who are legal permanent residents, even though the judge’s order requires the government to permit lawyer access,” one of the attorneys involved, Andrew Pincus, said later Saturday night.
Also, a federal judge in Seattle blocked the deportation of two immigrants from the airport there until a hearing set for Friday.
Early Sunday morning, two federal judges in Massachusetts issued an edict that seemed to further undermine Trump’s order. The restraining order from U.S. District Court Judge Susan Burroughs and Magistrate Judge Judith Dein appeared to be the first one to require the actual release of people being detained under Trump’s order.
Burroughs and Dein ruled that for the next seven days immigration officials “shall not by any manner or means detain or remove individuals” with valid visas, or green cards, or refugees who would be permitted to enter the U.S. in the absence of Trump’s order.
The Massachusetts federal judges’ order appeared to apply nationwide, although a portion of it focused on instructions for airlines serving Boston’s Logan Airport. The judges instructed Customs and Border Protection to advise those airlines that “individuals on these flights will not be detained or returned based solely on the Executive Order.”
The early-morning judicial order came shortly after the Department of Homeland Security issued a statement indicating plans to release all green-card holders who had arrived in the United States on Friday or Saturday who were detained under the Trump order. However, the Massachusetts judges’ order included categories beyond green-card holders. It was not immediately clear whether the Massachusetts federal judges’ order effectively guaranteed the rights of green-card holders to board flights headed for the U.S. or even for Boston.
If that order doesn't free all the immigrants being detained as a result of Trump’s executive action, the legal battle will likely move to a series of individual cases filed in New York, Chicago and elsewhere Saturday, where immigrants will be seeking to be released from detention to travel or settle in the U.S.
Donnelly acted on a petition filed early Saturday in the Eastern District of New York, seeking to release Hameed Khalid Darweesh and Haider Sameer Abdulkhaleq Alshawi from detention at JFK Airport. The case was filed by the ACLU, the International Refugee Assistance Project the National Immigration Law Center and a Yale Law School legal clinic.
Darweesh was released early Saturday afternoon, according to aides to New York Democratic Reps. Jerry Nadler and Nydia Velazquez, who went to JFK to try and free the men. Alshawi was released Saturday night, said a Nadler spokesman who indicated earlier that at least 10 others had been detained at the airport.
“This should not happen in America," the two lawmakers said in a statement earlier Saturday. "We shouldn’t have to demand the release of refugees one by one. We must fight this executive order in the streets, in the courts, anywhere, anytime. We must resist. We must fight. We must keep working to keep America the land of the free and the home of the brave.”
Pandemonium over Trump's new executive order erupted at airports nationwide on Saturday, with reports of dozens of immigrants and travelers stranded or turned back in Philadelphia, Washington, D.C., New York and Dallas as demonstrators flooded airports to denounce Trump's directive. One Syrian Christian family who had been working with Rep. Charlie Dent (R-Pa.) were detained at Philadelphia International Airport and then subsequently forced to leave, according to the congressman.
During a press conference at Dulles International Airport, Virginia Gov. Terry McAuliffe said one family had been detained as he slammed Trump's order as one that will "breed hatred toward Americans around the globe." Fifty people were being held at Dallas/Fort Worth International Airport, according to local reports.
Protesters rally at a demonstration against the new ban on immigration issued by President Donald Trump at Logan International Airport in Boston on Jan. 28. | Getty
But at the White House, Trump said his order was being carried out just as he planned.
“It’s not a Muslim ban, but we were totally prepared," Trump said. "It’s working out very nicely. You see it at the airports, you see it all over.”
Customs and Border Protection agents who detained the men at JFK pointed to Trump’s executive order, telling the immigrants’ attorneys: “Mr. President. Call Mr. Trump,” according to the 20-page lawsuit.
Darweesh, now 53, worked on behalf of the U.S. military in Iraq for a decade as an interpreter and electrical engineer, earning him a so-called “special immigrant visa” that are allotted to Iraqi nationals who aided the U.S. government during the Iraq War and now face threats staying there. Darweesh applied for the visa in Oct. 1, 2014, which was issued on Jan. 20, the same day Trump was inaugurated.
And Alshawi, 33, was granted a visa Jan. 11 to join his wife and son, who have already been resettled as refugees in Houston.
The lawsuit argues that the detention of two men is “part of a widespread pattern applied to many refugees and arriving aliens detained after the issuance of” Trump’s executive order on Friday.
On a call with reporters Saturday, Abed Ayoub, legal and policy director for the American-Arab Anti-Discrimination Committee, said CBP officials had told advocates dozens of people were being held at JFK as a result of the executive order.
He also cited reports of people being held at airports in Atlanta, Detroit, Houston and Washington, D.C.
“We’re already hearing about hundreds of people being detained at airports,” said Marielena Hincapie, the executive director of the National Immigration Law Center. “It got issued late on a Friday afternoon, it was not released to the public for several hours and then here on a Friday night over the weekend, we’re dealing with hundreds of people who have been arriving with no guidance to Border Patrol personnel.”
Trump’s far-reaching executive order does allow for some exemptions at the discretion of administration officials, including “when the person is already in transit and denying admission would cause undue hardship.” But advocates such as Hincapie say the messy rollout of Trump’s controversial directive is triggering confusion and chaos at airports nationwide, since border patrol officers have received little guidance on how to implement the order.
“They failed to inform airports about what to do,” Hincapie said.
Darweesh’s wife and three children were also granted visas and traveled with him, but were not detained. They are supposed to resettle in Charlotte, N.C. And neither men had been allowed to contact their lawyers, the lawsuit says.
Iraq is one of seven countries whose citizens, under Trump’s executive order released late Friday, are barred from entering the United States for 90 days, along with Iran, Libya, Somalia, Sudan, Syria and Yemen.
Ted Hesson contributed to this report. ||||| President Donald Trump speaks on the phone with German Chancellor Angela Merkel, Saturday, Jan. 28, 2017, in the Oval Office at the White House in Washington. (AP Photo/Andrew Harnik) (Associated Press)
President Donald Trump speaks on the phone with German Chancellor Angela Merkel, Saturday, Jan. 28, 2017, in the Oval Office at the White House in Washington. (AP Photo/Andrew Harnik) (Associated Press)
WASHINGTON (AP) — The Latest on U.S. President Donald Trump and his ban on refugees from Muslim-majority countries (all times local):
3 a.m.
The Homeland Security Department says a New York court order temporarily barring the U.S. from deporting people from nations subject to President Donald Trump's travel ban will not affect the overall implementation of the White House executive action.
The agency said the court order affected a relatively small number of travelers who were inconvenienced by security procedures upon their return.
The department's statement said: "President Trump's Executive Orders remain in place— prohibited travel will remain prohibited, and the U.S. government retains its right to revoke visas at any time if required for national security or public safety," according to the DHS statement.
Stephen Miller, a senior adviser to the White House, said that nothing in the judge's order "in anyway impedes or prevents the implementation of the president's executive order which remains in full, complete and total effect."
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11 p.m.
Foreign-born U.S. residents who could have been barred from re-entering the United States under President Donald Trump's immigration order have been allowed back into the country.
That's according to a Department of Homeland Security official who briefed reporters on Saturday night. The official spoke on condition of anonymity because the official wasn't authorized to publicly discuss details of the matter.
Trump's order Friday barred citizens of seven Muslim-majority nations from entering the United States for 90 days. That meant that even those with permanent residency "green cards" or other visas risked not being let back in to the United States.
However, the official said all green card holders from the seven countries who sought to enter the U.S. Saturday were granted special permission.
It's not clear if other green card holders will be admitted. The official said cases are being reviewed individually.
— Alicia Caldwell
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9:40 p.m.
A federal judge in New York has issued an emergency order temporarily barring the U.S. from deporting people from nations subject to President Donald Trump's travel ban.
U.S. District Judge Ann Donnelly issued the order Saturday evening after lawyers for the American Civil Liberties Union filed a court petition on behalf of people from seven predominantly Muslim nations who were detained at airports across the country as the ban took effect.
Cheers broke out in a crowd of demonstrators outside a Brooklyn courthouse as the decision, effective nationwide, was announced.
The order barred U.S. border agents from removing anyone who arrived in the U.S. with a valid visa from Iraq, Syria, Iran, Sudan, Libya, Somalia and Yemen.
It also covered anyone with an approved refugee application.
It was unclear how quickly the order might affect people in detention.
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7 p.m.
New York City's Kennedy Airport became a scene of anguish Saturday for relatives of people detained after arriving in the U.S. from nations subject to President Donald Trump's travel ban.
Lawyers and advocates working at the airport say they didn't have a hard count on the number of people taken into custody after getting off their flights.
Yosre Ghaled was among about a dozen distraught people waiting at a terminal Saturday to see if loved ones would be released or deported.
She says her mother-in-law's sister had been detained.
The 67-year-old Yemeni citizen had flown to the U.S. to live with family because she is sick from heart problems and diabetes.
Two members of congress joined hundreds of protesters at the airport, demonstrating against the detentions.
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1 a.m.
The government of Mexican President Enrique Pena Nieto is taking exception to the Israeli prime minister's praise of a border wall to keep out illegal immigration.
Prime Minister Benjamin Netanyahu said on Twitter Saturday that "President Trump is right" for building a wall.
"I built a wall along Israel's southern border," he wrote. "It stopped all illegal immigration. Great success. Great idea."
Mexico's Foreign Ministry said in a communique that it had expressed its "profound surprise, rejection and disappointment in the prime minister's message on Twitter" to Israel's ambassador. "Mexico is Israel's friend and should be treated as such."
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12:20 a.m.
President Donald Trump says his crackdown on refugees and citizens from seven majority-Muslim countries "is not a Muslim ban."
A day after signing an executive order implementing the ban immediately, Trump says it's "working out very nicely."
But confusion, worry and outrage boiled over Saturday as airlines blocked people from traveling to the United States and legal challenges were mounted.
Included is a 90-day ban on travel to the U.S. by citizens of Iraq, Syria, Iran, Sudan, Libya, Somalia and Yemen. The U.S. refugee program is suspended for 120-days.
Trump's order imposed the most aggressive ban on Syrians, indefinitely blocking entry to the U.S. by anyone from that country, including those fleeing civil war.
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12:10 a.m.
Airlines around the world are turning away passengers, refunding tickets and rebooking flights in the aftermath of President Donald Trump's immigration order.
The order signed Friday included a 90-day ban on travel to the U.S. by citizens of Iraq, Syria, Iran, Sudan, Libya, Somalia or Yemen. It also suspended the U.S. refugee program for four months.
That forced airlines to tell some customers they couldn't proceed on flights to the U.S.
Dubai-based Emirates said a small number of its passengers were affected Saturday, and it was helping them rebook. Delta Air Lines and British Airways both said they were offering refunds for passengers who couldn't complete their trips.
Several airlines, including Qatar Airways, posted travel alerts on their websites warning customers about the changes.
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11:50 p.m.
In Tehran, Iranian Foreign Minister Mohammad Javad Zarif says his country's decision to not issue give Americans visas will not be retroactive.
Zarif says on Twitter: "Unlike the U.S., our decision is not retroactive. All with valid Iranian visa will be gladly welcomed."
U.S. visa restrictions that took effect on Saturday for people from several countries, including Iran, ban travel even for those who already had American visas.
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11:20 p.m.
Canadian Prime Minister Justin Trudeau has a message for refugees rejected by U.S. President Donald Trump: Canada will take you.
Trudeau tweeted Saturday "To those fleeing persecution, terror & war, Canadians will welcome you, regardless of your faith. Diversity is our strength #WelcomeToCanada ."
Trudeau also tweeted a picture of him greeting a Syrian child at Toronto's airport.
Trudeau oversaw the arrival of more than 39,000 Syrian refugees soon after he was elected in late 2015.
The young prime minister has been reluctant to criticize President Donald Trump. His government has been trying to balance his liberal view of the world while not offending the new Trump administration.
More than 75 percent of Canada's exports are to the U.S.
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10:20 p.m.
An Iraqi who was detained overnight at a New York City airport because of President Donald Trump's ban on refugees from certain Muslim nations has called America "the land of freedom" after being released from custody.
Hameed Khalid Darweesh worked as an interpreter for the U.S. Army when it invaded Iraq in 2003. Later he was a contract engineer for the U.S.
He was granted permission to relocate to the U.S., but was detained along with another traveler from Iraq after arriving at John F. Kennedy Airport Friday night.
Lawyers petitioned a federal court early Saturday to let them go. Two Democratic U.S. Representatives, Nydia Velazquez and Jerrold Nalder, were at the airport trying to get 11 other detainees released.
After he was freed Saturday, Darweesh told a waiting crowd that "America is the greatest nation, the greatest people in the world."
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9:50 p.m.
In Somalia, people are reacting with dismay and warnings that countries could retaliate against the United States' new immigration and visa policies with restrictive policies of their own.
"I am shocked beyond words. This will mean that my new husband will never be able to join me in the U.S.," said Fatima Ashkir, a Somali-American woman from Florida who came to Mogadishu to marry her Somali boyfriend.
Others say they are not surprised at President Donald Trump's executive order imposing a three-month ban on refugees from seven Muslim-majority countries, including Somalia.
"His intentions of hurting rather than to help were clear from the very beginning," said Ahmed Abdullahi, a university student in Mogadishu. "But you have to know that this will have a serious effect on relations between Americans and the Muslim world. A tit-for-tat response by Muslim countries, in which Americans could be barred from entering countries affected, is likely to be seen."
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8:30 p.m.
Iran's foreign ministry is suggesting the country will limit issuing visas to American tourists in retaliation for U.S. President Donald Trump's suspension of immigration and visas for nationals from Muslim countries including Iran.
The official IRNA news agency Saturday carried a statement by the Iranian foreign ministry that says Iran will resort to "counteraction" to Trump's executive order.
The statement says: "Iran, to defend the dignity of the great Iranian nation, will implement the principle of reciprocity until the removal of the insulting restriction against Iranian nationals."
The statement adds: "It will apply corresponding legal, consular and political actions."
The two countries have had no diplomatic relations since 1979 when militants stormed the U.S. embassy.
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8 p.m.
Cairo airport officials say five U.S.-bound Iraqi migrants from one family who have been prevented from boarding an EgyptAir flight to New York's John F. Kennedy airport would return to Iraq.
They said the five will spend Saturday night at Cairo airport and leave for Irbil, capital of Iraq's Kurdish region, Sunday morning.
They added that the sixth U.S.-bound migrant, a Yemeni national, left the airport to return to Cairo, where he resides.
The officials said Saturday's action by the airport was the first since President Donald Trump imposed a three-month ban on refugees from seven Muslim-majority countries: Iraq, Syria, Iran, Sudan, Libya, Somalia and Yemen.
The officials said the six migrants, escorted by officials from the U.N. refugee agency, were stopped from boarding the plane after authorities at Cairo airport contacted their counterparts in JFK airport.
The officials spoke on condition of anonymity because they were not authorized to brief the media.
(This story corrects the number of U.S.-bound Iraqi migrants to five, not six)
— Hamza Hendawi.
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7:05 p.m.
Dutch airline KLM says it has had to turn away seven would-be passengers because they would no longer have been accepted into the United States under President Donald Trump's ban on immigration from seven Muslim-majority nations.
Manel Vrijenhoek, at KLM's press office, said: "We would love to bring them there. That's not the problem. It's just that this is what the U.S. sprang on the rest of the world — that these people are no longer welcome."
She said the seven were due to fly with KLM from different airports around the world. Vrijenhoek said she had no specifics on their nationalities, although she confirmed they were from countries affected by the three-month immigration ban: Iraq, Syria, Iran, Sudan, Libya, Somalia and Yemen.
Trump signed the order Friday.
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6:40 p.m.
A U.S. federal law enforcement official says any non-U.S. citizen from Iraq, Syria, Iran, Sudan, Libya, Somalia or Yemen is now barred from entering the United States.
That covers legal permanent residents — green card holders — and visa-holders from those seven countries who are out of the United States after Friday, when President Donald Trump signed an executive order with the temporary ban. They cannot return to the U.S. for 90 days.
The official says there's an exemption for immigrants and legal permanent residents whose entry is in the U.S. national interest, but it's unclear how that exemption will be applied.
The official says visa and green card holders already in the U.S. will be allowed to stay.
The official wasn't authorized to publicly discuss the details of how Trump's order is being put in place and spoke only on condition of anonymity.
Customs and Border Protection is notifying airlines about passengers whose visas had been canceled or legal residents scheduled to fly back to the U.S., and the airlines are being told to keep them off those flights.
— Alicia Caldwell
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6:35 p.m.
Israel's leader has endorsed President Donald Trump's plan to build a wall along the Mexican border.
Prime Minister Benjamin Netanyahu tweeted Saturday that Israel's wall along its border with Egypt has been successful in stopping a swell of African migrants.
"President Trump is right. I built a wall along Israel's southern border. It stopped all illegal immigration. Great success. Great idea," he wrote, with images of the Israeli and American flag.
The tweet marked a rare public foray for the Israeli leader into a charged American domestic affair. The two leaders spoke earlier this week and Netanyahu is planning to visit Trump in the White House next month.
After repeated clashes with President Obama, Netanyahu has high expectations for Trump, who has signaled he will take a kinder approach.
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5:45 p.m.
Malala Yousafzai, shot in the head by the Pakistani Taliban in 2012 to stop her campaigning for girls' education and co-winner of the 2014 Nobel peace prize, says she is heart-broken by U.S. President Donald Trump's ban on refugees from entering the United States for four months.
The order Friday suspends a program that saw around 85,000 people displaced by war, political oppression, hunger and religious prejudice resettled in the U.S. last year. Trump indefinitely blocked people fleeing Syria's civil war, and imposed a 90-day ban on U.S. entry from seven Muslim majority nations.
In a statement Saturday, Yousafzai implores Trump "not to turn his back on the world's most defenseless children and families."
Refugees and immigrants, she says, have "helped build your country."
Trump's mother was born in Scotland.
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5:15 p.m.
Qatar Airways is advising passengers bound for the United States from seven newly banned majority Muslim countries that they need to have either a U.S. green card or diplomatic visa to travel.
A statement on the company's website says: "Nationals of the following countries: Sudan, Libya, Somalia, Syria, Iran, Iraq, Yemen ... may travel to the U.S. only if they are in possession of a permanent resident card (Green card) or any of the below visas."
It listed foreign government, United Nations, international organization and NATO visas.
President Donald Trump has issued a 90-day ban on all entry to the U.S. from countries with terrorism concerns, including Syria, Iraq and Libya.
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3 p.m.
Cairo airport officials say seven U.S.-bound migrants — six from Iraq and one from Yemen — have been prevented from boarding an EgyptAir flight to New York's John F. Kennedy Airport.
The officials said the action Saturday by the airport was the first since President Donald Trump imposed a three-month ban on refugees from seven Muslim-majority countries: Iraq, Syria, Iran, Sudan, Libya, Somalia and Yemen.
The officials said the seven migrants, escorted by officials from the U.N. refugee agency, were stopped from boarding the plane after authorities at Cairo airport contacted their counterparts at the Kennedy airport.
The officials spoke on condition of anonymity because they were not authorized to brief the media.
— Hamza Hendawi.
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2:45 p.m.
The head of a leading refugee aid agency says President Donald Trump's decision to ban Syrian refugees hurts innocents fleeing violence.
Jan Egeland of the Norwegian Refugee Council tells The Associated Press on Saturday that Trump's decision "will not make America safer, it will make America smaller and meaner."
Trump on Friday suspended refugee admissions for four months and indefinitely banned those from war-torn Syria, pending program changes that are to ensure refugees won't harm national security.
Egeland says the decision dealt a "mortal blow" to the idea of international responsibility for those fleeing persecution. He says the U.S. is leading a "race to the bottom" in which politicians in wealth countries provide "zero moral leadership."
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1 p.m.
Iran's President Hassan Rouhani says the time has come for removing walls between nations rather that building new ones.
Rouhani did not name any particular country but his remarks come shortly after President Donald Trump's executive order Friday suspending all immigration and visa processes for nationals from a handful of countries with terrorism concerns, including Iran, for 90 days.
Rouhani said Saturday that, "It is not the day for creating distance among nations."
Speaking at a tourism conference broadcast on state TV, Rouhani said that those seeking to create such walls, "have forgotten that the Berlin Wall collapsed years ago."
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12:30 p.m.
The International Rescue Committee is calling President Donald Trump's suspension of the U.S. refugee resettlement program a "harmful and hasty" decision.
In a statement issued late Friday night after the suspension was announced, IRC President David Miliband said, "America must remain true to its core values. America must remain a beacon of hope."
The IRC statement declared that the U.S. vetting process for prospective refugees is already robust — involving biometric screening and up to 36 months of vetting by "12 to 15 government agencies."
Miliband praised The United States' record as a resettlement destination and said, "This is no time for America to turn its back on people ready to become patriotic Americans." ||||| | multi_news_1_0_0 |
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Here is a news article: You've heard the term "hangry," right? People who are hungry often report being unreasonably angry until they're fed.
"Hangry" is a relatively new buzz word, but science is backing it up. A new study published in the journal PNAS suggests married couples are more aggressive when they have low blood sugar levels.
Background
Everyone gets upset at their spouse or significant other sometimes. But self-control hopefully prevents you from taking that anger out on them in a physical manner.
Yet scientists know that self-control is a limited resource. You have a tank of it, so to speak, in your brain. Each time you use self-control to avoid telling off your boss or to skip the dessert bar, that tank becomes less full.
And "aggression often starts when self-control stops," says Brad Bushman, a psychologist at Ohio State University who's studied aggression for 25 years.
What refills your self-control tank? Energy, which comes in part from the food you eat.
The study
Researchers recruited 107 married couples to participate in the study. The husbands and wives measured their glucose (or blood sugar) levels every morning and night for 21 days.
Each night they were asked to stick up to 51 pins in a voodoo doll, depending on how angry they were at their spouse. The researchers compared this aggression level to the participants' average glucose levels over the study period.
At the end of the 21 days, researchers had the couples come into the lab for another test. They asked each husband and wife to compete against their significant other in a virtual game. The couples were told the winner got to blast the loser with a loud, obnoxious noise. (In reality, their partner was not on the receiving end.)
Researchers measured how long and how intense the winner chose to blast the noise, and compared that aggression level to their average blood sugar level.
The results
Study participants with lower nightly blood sugar levels were more aggressive - both in "pinning" their voodoo doll and in blasting their partner with a louder noise for longer. These findings remained true even after researchers controlled the data for relationship satisfaction.
More evidence
This study supports previous research done by Bushman's lab at Ohio State University. In an earlier study, Bushman and his colleagues found participants who drank a sugar-sweetened beverage behaved less aggressively than those who drank a beverage sweetened with a sugar substitute.
Another study linked diabetes to more aggressive behavior. Because glucose increases self-control, people who have difficulty metabolizing glucose should have less self-control, the researchers theorized.
In a separate series of studies, Bushman showed diabetics were less inclined to forgive others. "These findings provide the first evidence that forgiveness depends on how efficiently the body uses glucose," the study authors wrote.
Takeaway
The study authors say giving people more access to food could reduce aggression in certain settings, such as prisons or psychiatric hospitals. As for the rest of us:
"I would recommend couples discuss sensitive issues over dinner," Bushman said. "Or better yet, after dinner." ||||| New study finds that spouses are more likely to get angry with each other if they're dealing with low blood sugar levels. So have a snack, and chill out.
Brad Bushman, professor of communication and psychology at Ohio State University, holds one of the voodoo dolls used in the study. (Photo: Jo McCulty, Ohio State University)
The next time you get annoyed at your spouse, you might want to grab something to eat. That's the take-home message from a new study that found marital hostility is at its highest when blood sugar is at its lowest.
Spouses of both genders jabbed more pins into a voodoo doll on evenings when their blood sugar was the lowest, according to the new study, published online Monday in the Proceedings of the National Academy of Sciences.
Lead researcher Brad Bushman of Ohio State University said his own marriage has improved since he took his study's advice: "When you discuss a sensitive topic with your spouse, you should do so over dinner, or better yet after dinner – but you should definitely not do it on an empty stomach."
Bushman and his colleagues paid $100 each to 107 married couples, found through public advertisements, to participate in the study.
This is one of the voodoo dolls used in the study to measure participants' anger with their spouses. (Photo: Jo McCulty, Ohio State University)
To measure aggressiveness, each husband and wife was given a voodoo doll and 51 pins. They were told to check their blood glucose level before bed each night for three weeks, and to stick any number of pins into the doll, depending on how angry they were with their spouse that day. They didn't see each other's dolls.
After three weeks, the couples were invited back to the lab, placed in separate rooms and told to compete against each other to see who could press a computer button faster after a given command. The winner could blast the loser with a loud, ugly sound.
The spouses who stabbed their voodoo doll more freely also were more likely to turn up the volume on the punishing sounds, the study found. The results did not differ between couples who said their marriages were weak or strong, he said.
Angry people are more impulsive, more likely to lash out, both verbally and physically, said Bushman, adding that anger is the leading cause of homicide.
Ann Goebel-Fabbri, a psychologist with the Joslin Diabetes Institute in Boston, praised the creativity of the study but said she thinks the researchers went too far in suggesting that low blood sugar could lead to violence.
People with diabetes – who are prone to large swings in blood glucose – do complain about being moody, she said. But they are certainly not any more likely to be violent than the general population.
"There is no connection between diabetes and aggression," said Goebel-Fabbri, also an assistant professor at Harvard Medical School.
"I think the translation from voodoo doll and loud noise to domestic violence, I think is way overstating it," she said. "It would be lovely if we could solve the domestic violence problem by feeding people better, but…there's no data that would support that."
Read or Share this story: http://usat.ly/1kqc5Jm ||||| Husbands and wives reported being most unhappy with their spouses when their blood-sugar levels were lowest, usually at night, according to research released today in the Proceedings of the National Academy of Sciences.
Husbands and wives reported being most unhappy with their spouses when their... Read More
Husbands and wives reported being most unhappy with their spouses when their blood-sugar levels were lowest, usually at night, according to research released today in the Proceedings of the National Academy of Sciences. Close
Serious discussions between spouses shouldn’t take place on an empty stomach, a study suggests.
Husbands and wives reported being most unhappy with their spouses when their blood-sugar levels were lowest, usually at night, according to research released today in the Proceedings of the National Academy of Sciences. Missing a meal, dieting or just being hungry may be the reason, researchers said.
Sugar, or glucose, is used by the brain as fuel to help regulate self-control. Without the fuel, it is more difficult for people to control emotions like anger and aggression, researchers said. Today’s findings are among the first to show how low sugar levels in the body may play a part in marital arguments, confrontations and even domestic violence, said Brad Bushman, the lead study author.
“Self-control comes in part from the fuel we give our brains. This is one of the few physiological aspects we can control,” said Bushman, a professor of communication and psychology at Ohio State University in Columbus, in a telephone interview today. “People who are hungry are often very cranky.”
Researchers in the study included 107 married couples who for 21 days had to test their blood-sugar levels before breakfast in the morning and before bed in evening. They were also given voodoo dolls representing their spouses and told to insert as many as 51 pins daily depending on how angry they were with their partner. The researchers were testing aggressive impulses.
Measuring Aggression
Those with the lowest nighttime blood-sugar levels inserted the most pins, while those with the highest glucose levels inserted the least, the study found. Women tended to stick more pins into their husband voodoo doll, but the finding wasn’t significant. The authors only found the association for nighttime blood glucose levels as the amount of sugar in the body drops throughout the day, Bushman said.
After 21 days, the couples went into a laboratory where they were told they would compete with their spouse to see who could press a button the fastest to test aggressive behavior. The winners could blast their spouse with a loud noise through headphones. The spouses in reality were playing against a computer, not each other.
The researchers found that those with the lowest average nighttime blood-sugar levels sent louder and longer noises to their spouse no matter how good their relationship was or whether they were male or female.
Timing Important
“If couples have a sensitive topic to discuss, it would be really smart to do it over dinner or better yet after dinner,” Bushman said. “They should definitely not do it on an empty stomach.”
Low blood sugar can trigger hormones that activate the body’s “fight or flight” system and cause people to become more aggressive, anxious and irritable, said Timothy Graham, who wasn’t an author of today’s study.
For families with someone who has diabetes, where swings between highs and lows can occur more often, he suggests counseling. For others, regular, small meals throughout the day may help keep blood sugar levels consistent and help prevent dips that can cause aggression.
“Probably more regular and healthy meals could improve the dynamics of a relationship,” Graham, an assistant professor of medicine at the University of Utah in Salt Lake City, said in a telephone interview.
To contact the reporter on this story: Nicole Ostrow in New York at [email protected]
To contact the editors responsible for this story: Reg Gale at [email protected] Andrew Pollack, Angela Zimm |||||
A summary of this is? | – "If couples have a sensitive topic to discuss, it would be really smart to do it over dinner or better yet after dinner," say researchers who have linked low blood sugar to marital hostility. "They should definitely not do it on an empty stomach." Researchers tracked the blood sugar levels—and, using voodoo dolls, the aggression levels—of 107 married couples and found that those with the lowest nighttime blood sugar were the most likely to stick pins in the doll representing their partner, CNN reports. In laboratory tests, people with low blood sugar were also the most willing to blast their partner with a loud, obnoxious noise in what they were told was a game, USA Today reports. The results were similar no matter how strong a couple said their marriage was. Low blood sugar can trigger hormones that cause people to become aggressive and irritable, a professor of medicine explains to Bloomberg. "Probably more regular and healthy meals could improve the dynamics of a relationship," he says, adding that counseling should be considered when diabetes is involved. | multi_news_1_0_0 |
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Article:
WASHINGTON (AP) — Food companies and restaurants could soon face government pressure to make their foods less salty — a long-awaited federal effort to try to prevent thousands of deaths each year from heart disease and stroke.
FILE - This May 30, 2014, file photo shows Food and Drug Administration Commissioner Dr. Margaret Hamburg in Washington. Food companies and restaurants could soon face government pressure to make their... (Associated Press)
FILE - This Feb. 7, 2012 file photo shows a shopper walking down the canned soup aisle at a grocery store in Cincinnati. Food companies and restaurants could soon face government pressure to make their... (Associated Press)
The Food and Drug Administration is preparing voluntary guidelines asking the food industry to lower sodium levels, FDA Commissioner Margaret Hamburg told The Associated Press. Hamburg said in a recent interview that the sodium is "of huge interest and concern" to the agency.
"We believe we can make a big impact working with the industry to bring sodium levels down, because the current level of consumption really is higher than it should be for health," Hamburg said.
It's still unclear when FDA will release the guidelines, despite its 2013 goal to have them completed this year.
Hamburg said she hoped the agency would be able to publicly discuss the issue "relatively soon." On Tuesday, FDA spokeswoman Erica Jefferson said there is no set timeline for their release.
The food industry has already made some reductions, and has prepared for government action since a 2010 Institute of Medicine report said companies had not made enough progress on making foods less salty. The IOM advised the government to establish maximum sodium levels for different foods, though the FDA said then — and maintains now — that it favors a voluntary route.
Americans eat about 1½ teaspoons of salt daily, about a third more than the government recommends for good health and enough to increase the risk of high blood pressure, strokes and other problems. Most of that sodium is hidden inside common processed foods and restaurant meals.
In addition to flavor, companies use sodium to increase shelf life, prevent the growth of bacteria, or improve texture and appearance. That makes it more difficult to remove from some products, Hamburg noted.
Once the guidelines are issued, Americans won't notice an immediate taste difference in higher-sodium foods like pizza, pasta, bread and soups. The idea would be to encourage gradual change so consumers' taste buds can adjust, and to give the companies time to develop lower-sodium foods.
"I think one of the things we are very mindful of is that we need to have a realistic timeline," Hamburg said.
Health groups would prefer mandatory standards, but say voluntary guidelines are a good first step.
Still, Michael Jacobson of the Center for Science in the Public Interest says he is concerned companies may hesitate, worried that their competitors won't lower sodium in their products.
If that happens, "then FDA should start a process of mandatory limits," Jacobson says.
That's what companies are worried about. Though the limits would be voluntary, the FDA is at heart a regulatory agency, and the guidelines would be interpreted as a stern warning.
Brian Kennedy of the Grocery Manufacturers Association, which represents the country's biggest food companies, says the group is concerned about the FDA setting targets and any guidelines should be based on a "rigorous assessment of all available scientific evidence."
The food industry has pointed to a separate 2013 IOM report that said there is no good evidence that eating sodium at very low levels — below the 2,300 milligrams a day that the government recommends — offers benefits. The government recommends that those older than 50, African-Americans and people with high blood pressure, diabetes or chronic kidney disease eat 1,500 milligrams a day. The American Heart Association recommends that everyone eat no more than 1,500 milligrams a day.
Lanie Friedman of ConAgra Foods, one of the companies that would be subject to the voluntary guidelines, says the newer IOM report is a "paradigm change" and more research is needed. But those pushing for sodium limits say it's pointless to debate how low the recommendations should go — Americans are still eating around 3,400 milligrams a day.
Many food companies and retailers already have pushed to reduce salt. Wal-Mart pledged to reduce sodium in many items by 25 percent by next year, and food giant ConAgra Foods says it made a 20 percent reduction. Subway restaurants said it has made a 30 percent reduction restaurant-wide.
The companies say that in some cases, just removing added salt or switching ingredients does the trick. Potassium chloride can also substitute for common salt (sodium chloride), though too much can cause a metallic taste.
Levels of sodium in food can vary widely. According to the Centers for Disease Control and Prevention, sodium in a slice of white bread ranges from 80 milligrams to 230 milligrams. Three ounces of turkey deli meat can have 450 milligrams to 1,050 milligrams.
Those ranges give health advocates hope.
"Those differences say to me that the companies that make the highest-sodium products could certainly reduce levels to the same as the companies that make the lower-sodium products," Jacobson says.
Still, the guidelines could be a hard sell. In recent years, congressional Republicans have fought the Obama administration over efforts to require calorie labels on menus and make school lunches healthier. When the administration attempted to create voluntary guidelines for advertising junk food for children, the industry balked and Republicans in Congress fought the idea, prompting the administration to put them aside.
Other members of Congress are pushing the agency to act.
"As the clock ticks, America's blood pressure, along with health costs due to chronic disease, continues to rise," says Sen. Tom Harkin, chairman of the Senate committee that oversees the FDA.
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Find Mary Clare Jalonick on Twitter at http://twitter.com/MCJalonick ||||| Food and restaurant companies are under increasing pressure to make products healthier, but sometimes they don't want customers to know when they have cut the salt or fat.
Companies have employed the tactic, which some executives call "stealth health," in tweaking products including Hamburger Helper, Oreo cookies and McDonald's french... |||||Summary: |
– In the minds of customers, healthy food often means less-tasty food. At the same time, however, many clamor for healthier options. All this puts restaurants and food makers in a bind—and the solution, the Wall Street Journal reports, is "stealth health." This refers to companies secretly improving the healthiness of their offerings without telling the customers, at least not until they've already gotten used to the altered version. "When you tell people something's healthy, they think it doesn't taste good," says an exec at Boston Market. In the fourth quarter of last year, that restaurant chain reduced sodium in several products; it finally told customers about it in February. Kraft didn't tell anyone when it cut trans fats from Oreos in 2006. And General Mills kept quiet about sodium cuts over six years in Hamburger Helper, using ingredients such as garlic to maintain flavor. "It takes multiple months, if not years, to get the right equation between taste and health," says a company health officer. But it all depends on the product and its audience: Fans of Progresso Soups, also made by General Mills, want to eat more healthily—so when sodium was cut in the soups, the company made sure customers knew. Like it or not, we may be seeing lower salt levels in our food soon: The FDA is readying new sodium guidelines, the AP reports. | multi_news_1_0_0 |
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(Reuters) - Omar Abdel-Rahman, the Muslim cleric known as “the blind sheikh” who was convicted of conspiracy in the 1993 World Trade Center bombing and of planning a broader “war of urban terrorism” in the United States, died on Saturday in a North Carolina prison, authorities said.
Abdel-Rahman, 78, died of natural causes at 9:40 a.m. (1440 GMT) at a medical center at a federal prison compound in Butner, North Carolina, according to Greg Norton, a spokesman.
The cleric, who had diabetes and coronary artery disease, had been incarcerated at the complex for nearly 10 years, Norton said.
Earlier, the cleric’s son Ammar said his family had received a phone call in Eygpt from a U.S. representative saying his father had died.
The Egyptian-born Abdel-Rahman remained a spiritual leader for radical Muslims even after more than 20 years in prison.
With his long gray beard, sunglasses and red and white clerical cap, the charismatic Abdel-Rahman was the face of radical Islam in the 1980s and 1990s. He preached a fiery brand of Islam that called for the death of people and governments he disapproved of and the installation of an Islamic government in Egypt. His following was tied to fundamentalist killings and bomb attacks around the world.
“Abdel-Rahman was at the vortex of some of the bloodiest and most consequential terrorist incidents of the 1990s - incidents that would establish the patterns of global terrorism that continue to bedevil us today,” said Bruce Hoffman, a terrorism expert at Georgetown University in Washington.
“He was a tireless and enthusiastic in projecting his message of violence and hatred,” said Hoffman, who served on the U.S. government’s commission that reviewed the Sept. 11, 2001, attacks in New York and Washington and over Pennsylvania.
Abdel-Rahman, who was born in a village along the Nile on May 3, 1938, lost his eyesight due to childhood diabetes and grew up studying a Braille version of the Koran.
As an adult he became associated with the fundamentalist Islamic Group and was imprisoned and accused of issuing a fatwa leading to the 1981 assassination of Egyptian President Anwar Sadat, against whom he had railed for years. The sheikh said he was hung upside-down from the ceiling, beaten with sticks and given electric shocks while held but he was eventually acquitted and went into self-imposed exile in 1990.
He managed to get to New York after the U.S. Embassy in Sudan granted him a tourist visa in 1990 - despite the fact that he was on the State Department’s list of people with ties to terror groups.
U.S. authorities blamed a computer error for the visa, but the mistake was compounded in 1991 when Abdel-Rahman was given a green card and permanent U.S. resident status. The New York Times reported the CIA had approved the visa application for Abdel-Rahman, who had supported the anti-Soviet mujahedin in Afghanistan during the 1980s.
Abdel-Rahman preached his radical message and lived in the New York City borough of Brooklyn and nearby Jersey City, New Jersey, building a strong following among fundamentalist Muslims. Even in exile, he remained a force in the Middle East, where followers listened to cassette tapes and radio broadcasts of his sermons decrying the Egyptian government and Israel.
While in the United States Abdel-Rahman and his disciples would be linked to the 1990 slaying in New York of militant Rabbi Meir Kahane, the 1992 killing of an anti-fundamentalist writer in Egypt and attacks on foreign tourists in Egypt.
U.S. authorities took action in 1992 by revoking Abdel-Rahman’s green card on the grounds that he had lied about a bad check charge in Egypt and about having two wives when he entered the country. He was facing the possibility of deportation when a truck bomb went off in the basement parking garage of the World Trade Center on Feb. 26, 1993, killing six people and injuring more than 1,000 in an attack that made Americans realize that they were not immune to international terrorism.
Four months later Abdel-Rahman was arrested and went on trial with several followers in 1995, accused of plotting a day of terror for the United States - assassinations and synchronized bombings of the U.N. headquarters, a major federal government facility in Manhattan and tunnels and a bridge linking New York City and New Jersey.
The indictment said Abdel-Rahman and his followers planned to “levy a war of urban terrorism against the United States” as part of a jihad - or holy war - to stop U.S. support for Israel and change its overall Middle East policy.
The defendants were not directly charged with the 1993 World Trade Center attack but were convicted of conspiring with those who did carry out the bombing.
Abdel-Rahman’s convictions also included plotting to kill Egyptian President Hosni Mubarak during a visit to the United States in 1993, a Jewish New York state legislator and a Jewish New York State Supreme Court justice.
Much of the case against Abdel-Rahman and his followers was based on video and audio recordings made with the help of a bodyguard for the sheikh who became an FBI informant. A video also showed four defendants mixing fertilizer and diesel fuel for bombs.
After a nine-month trial, the sheikh and nine followers were found guilty in October 1995 on 48 of 50 charges.
He did not testify at his trial but at a sentencing hearing Abdel-Rahman gave a passionate speech of more than 90 minutes through a translator, proclaiming his innocence and denouncing the United States as an enemy of his faith.
Egyptian Omar Abdel-Rahman speaks during a news conference in this still image taken from February 1993 video footage on January 18, 2013. REUTERS/Reuters TV/Files
“I have not committed any crime except telling people about Islam,” he said.
Abdel-Rahman was still an important figure in radical Islam even after years in prison. A year before his al Qaeda followers pulled off the most destructive assault on U.S. soil, the Sept. 11, 2001, attacks, Osama bin Laden had pledged a jihad to free Abdel-Rahman from prison. When Mohammed Mursi, a leader of the Muslim Brotherhood, began his short-lived presidency of Egypt in 2012, he said winning the sheikh’s freedom would be a priority and the jihadists who attacked an Algerian oilfield and took hostages in 2013 also demanded his release.
In 2006 one of Abdel-Rahman’s lawyers, Lynne F. Stewart, was sentenced to 28 months in prison for helping smuggle messages from the cleric to his followers in Egypt. ||||| FILE - This April 6, 1993 file photo shows Sheik Omar Abdel-Rahman in New York. Kenneth McKoy of the Federal Correction Complex in Butner, N.C., said Abdel-Rahman died Saturday, Feb. 18, 2017, after... (Associated Press)
FILE - This April 6, 1993 file photo shows Sheik Omar Abdel-Rahman in New York. Kenneth McKoy of the Federal Correction Complex in Butner, N.C., said Abdel-Rahman died Saturday, Feb. 18, 2017, after a long battle with diabetes and coronary artery disease. Abdel-Rahman was sentenced to life in prison... (Associated Press)
FILE - This April 6, 1993 file photo shows Sheik Omar Abdel-Rahman in New York. Kenneth McKoy of the Federal Correction Complex in Butner, N.C., said Abdel-Rahman died Saturday, Feb. 18, 2017, after a long battle with diabetes and coronary artery disease. Abdel-Rahman was sentenced to life in prison... (Associated Press) FILE - This April 6, 1993 file photo shows Sheik Omar Abdel-Rahman in New York. Kenneth McKoy of the Federal Correction Complex in Butner, N.C., said Abdel-Rahman died Saturday, Feb. 18, 2017, after... (Associated Press)
BUTNER, N.C. (AP) — Omar Abdel-Rahman, the so-called Blind Sheik convicted of plotting terror attacks in the United States in the 1990s, has died. He was 78.
Kenneth McKoy of the Federal Correction Complex in Butner, North Carolina, said Rahman died at 5:40 a.m. after suffering from diabetes and coronary artery disease. Abdul-Rahman had been at the complex for seven years.
Rahman was a key spiritual leader for a generation of Islamic militants and became a symbol for radicals during a decade in American prisons.
Abdel-Rahman, blind since infancy from diabetes, was the leader of one of Egypt's most feared militant groups, the Gamaa Islamiya, which led a campaign of violence aimed at bringing down ex-President Hosni Mubarak.
Abdel-Rahman fled Egypt to the U.S. in 1990 and began teaching in a New Jersey mosque. A circle of his followers were convicted in the Feb. 26, 1993 truck bombing of New York's World Trade Center that killed six people — eight years before al-Qaida's suicide plane hijackers brought the towers down.
Later in 1993, Abdel-Rahman was arrested for conspiracy to carry out a string of bombings against the United Nations, the Lincoln and Holland tunnels, the George Washington Bridge and other New York landmarks. |||||
What is a one-paragraph summary of the above article? | – The man known as the "blind sheikh," who was convicted of plotting the 1993 World Trade Center bombing and other terrorist attacks in New York City, died Saturday in a North Carolina jail, CBS News reports. According to the AP, Omar Abdel-Rahman, born in Egypt, had been blind since he was an infant due to childhood diabetes. He became a leader of the militant group Gamaa Islamiya and, Reuters reports, was the "face of radical Islam" during the 80s and 90s. Despite being on a State Department list of people with terror connections, Rahman arrived in the US on a tourist visa in 1990 then received a Green Card and permanent resident status. The CIA may have pulled some strings for him. In 1993, a truck bomb exploded under the World Trade Center, killing six people and injuring a thousand more. Rahman was sentenced to life in prison in 1995 for planning that attack and an expanded "war of urban terrorism" that would include the bombings of New York City bridges and the UN. Rahman sought to end the US' support of Israel and Egypt. He continued as a leader for radical Muslims while in prison. Osama bin Laden had even vowed to free him at one point. Officials say Rahman died of natural causes following a history of coronary artery disease and diabetes. He was 78. | multi_news_1_0_0 |
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Image copyright AP Image caption Tariq Aziz (right) was the instantly-recognisable face of Saddam Hussein's regime
As former Iraqi President Saddam Hussein's main link with the world, Tariq Aziz became a familiar figure around the globe, most notably during the Gulf wars of 1991 and 2003.
With his cheery, urbane manner and passing resemblance to Groucho Marx, Tariq Aziz was the instantly-recognisable face of Saddam Hussein's regime.
But, behind the scenes, the Iraqi foreign minister and deputy prime minister proved to be a formidable negotiator and diplomat.
A fluent English speaker, Tariq Aziz was the only Christian - a Chaldean Catholic - in Iraq's cabinet.
He was born Michael Yuhanna in 1936 near Mosul in northern Iraq. His family circumstances were humble - his father was a waiter.
The young Yuhanna read English literature at Baghdad University before pursuing a career as a teacher of English, then as a journalist.
Kuwait invasion
He also joined the Baath party, changed his name to Tariq Aziz, and was involved in propaganda work after the 10-month Baathist coup in 1963.
After the Baathists took power in 1968, he became editor of the regime's newspaper and then information minister.
In 1977, he joined the Revolutionary Command Council - the committee of senior Baath Party officials which effectively ruled Iraq. In 1983 Saddam, who shied away from travelling abroad, made Aziz his foreign minister.
Image copyright AP Image caption Tariq Aziz with then UN Secretary General Kofi Annan in 1998
Within months he had rebuilt diplomatic bridges with the United States, after a hiatus of 17 years. He managed to convince Donald Rumsfeld, then a private emissary from President Ronald Reagan, that Iraq was a crucial buffer against the Islamist state of Iran, which Iraq was then fighting.
Then, after the invasion of Kuwait in August 1990, when Iraq was almost totally isolated, Aziz deftly negotiated a pact with Iran.
In a series of drawn-out meetings with the-then UN Secretary-General, Perez de Cuellar, and the US Secretary of State, James Baker, Aziz consistently put forward the view that Kuwait was part of Iraq and that any negotiations must take in the whole Palestinian question.
Afterwards Aziz said: "When it comes to the Arabs, you raise the stick, and we are fed up with this policy of double standards."
Prison plea
But the US-led attack which followed did little to damage Aziz's career.
In the run-up to the 2003 Gulf War, he once more played a leading role in negotiations. While arguing that Iraq posed no military threat, he believed that conflict was inevitable and laid the blame squarely on two factors - "oil and Israel".
He surrendered to US troops on 24 April 2003 despite having previously declared that he would rather die than become a prisoner of war.
Image copyright AP Image caption Tariq Aziz with then Russian Foreign Minister Igor Ivanov at a press conference in Baghdad
In a letter published in the Observer newspaper in May 2005, Aziz wrote: "We have been in prison for a long time and we have been cut off from our families. No contacts, no phones, no letters. Even the parcels sent to us by our families are not given to us. We need a fair treatment, a fair investigation and finally a fair trial. Please help us."
In October 2005, evidence allegedly given by Aziz formed the basis of a claim in a US Senate report that the UK MP, George Galloway, had lied while under oath in a Senate hearing.
Mr Galloway, a friend of Tariq Aziz, has vigorously denied claims that he received 23 million barrels of oil from Saddam Hussein, which should have formed part of Iraq's oil-for-food programme.
In April 2008, Aziz finally went on trial accused of complicity in the execution of 42 Iraqi traders who had been accused of manipulating food prices while Iraq was subject to international trade sanctions.
He was convicted in March 2009 of crimes against humanity and sentenced to 15 years imprisonment. Five months later he was convicted of having been involved in the forced displacement of Kurds in northern Iraq and given another seven years behind bars.
Though Saddam Hussein was said to listen to him, Aziz was never a powerful or influential member of the regime.
This was reflected in his lowly ranking as the eight of spades in the US military's famous "deck of cards" that was used to identify the most-wanted members.
Above all, Aziz was loyal to his master, who trusted him to act as his mouthpiece before the world. ||||| Tariq Aziz, Iraq's former deputy prime minister and foreign minister, has died in prison aged 79 years old.
Iraqi officials said Aziz, who was one of the former Iraqi leader Saddam Hussein's top deputies, died on Friday afternoon after suffering a heart attack on Thursday.
Al Jazeera has learned that Aziz's son, Ziad, expressed outrage that Iraqi officials had not informed him of his father's death, and he had instead found out through local media reports.
Aziz was Iraq's foreign minister between 1983 and 1991 and deputy prime minister between 1979 and 2003.
Born Mikhail Yuhanna in 1936, Aziz was the highest ranking Christian official under Saddam's presidency and a member of the former ruling Baath Party's inner circle.
He was sentenced to death by the Iraqi High Tribunal in 2010 for his role in human rights abuses committed under the former government, which was overthrown in 2003 when Iraq was invaded by a US-led alliance.
Iraq's public face
Aziz surrendered to US forces shortly after the invasion and had been a prisoner since.
Al Jazeera's Imran Khan, reporting from Baghdad, said Aziz was one of the most hated figures from the old regime and Iraqi TV stations had largely ignored his death.
"There will be no eulogies for him, no day of mourning for him. He was hated as a member of the former regime," he said.
One of the best known faces of Saddam's Iraq, Aziz travelled globally where he defended his leader against the many accusations of alleged human rights abuses.
When the US prepared for its campaign to end the Iraqi occupation of Kuwait prior to the first Gulf War, Aziz hit out at Arab states, calling them "subservient Arab weaklings".
Aziz remained loyal to his boss in the aftermath of defeat during that war, and through the 12 years of sanctions that followed.
In the run-up to the US-led invasion of Iraq in 2003, Aziz was the "eight of spades" on the famous deck of cards of Iraq's most wanted released by US authorities.
"He was always seen as someone who could try and prevent the impending US invasion. He was always seen as a diplomat," Al Jazeera's Khan said. ||||| Image copyright AFP Image caption Tariq Aziz (right) played a prominent role in Saddam Hussein's reign as Iraq's president
Tariq Aziz, known as the face of Saddam Hussein's regime on the world stage for many years, has died in an Iraqi hospital, officials say.
Aziz, 79, served as foreign minister and deputy prime minister and was a close adviser to the former leader.
He was sentenced to death by the Iraqi Supreme Court in 2010 for the persecution of religious parties under Saddam's rule but was never executed.
He surrendered to US troops in 2003 shortly after the fall of Baghdad.
A local health official told reporters that he was taken to hospital from prison after suffering a heart attack. Initial reports said he had died in prison.
He had long been in poor health, suffering from heart and respiratory problems, high blood pressure and diabetes, and his family repeatedly called for his release from custody.
Media playback is unsupported on your device Media caption The BBC's Caroline Hawley: "He surrendered shortly after the regime was toppled"
His wife, Violet, had visited him in prison on Thursday, their daughter Zeinab told the AP news agency.
She said her father had suffered several strokes that left him confined to a wheelchair and unable to speak during her parents' final meeting.
"He didn't move. He couldn't talk. He didn't say a word to her. He just looked at her," said Zeinab, adding: "It is so sad that he had to go this way."
'Eight of spades'
Aziz, who was known for his black-rimmed glasses and love of cigars, first came to prominence while serving as foreign minister during the first Gulf War in 1991.
As a Christian in a mainly Sunni Muslim government, he was not considered a member of Saddam Hussein's innermost circle.
A fluent English speaker, he played a vocal role before the US invasion of Iraq in 2003, meeting Pope John Paul II in the Vatican to call for peace.
But when Baghdad fell, his lack of influence was reflected in his lowly ranking as the eight of spades in the US military's famous "deck of cards" used to identify the most-wanted players in Saddam's regime.
Analysis: Paul Adams, BBC diplomatic correspondent
Image copyright AFP Image caption As a fluent English speaker, Aziz was often deployed to explain Saddam's actions
Tariq Aziz was one of the most visible of Saddam Hussein's lieutenants and, it seems, one of the most loyal.
He frequently represented Iraq on the international stage, speaking fluent English and giving a monstrous regime an urbane, often charming face. And like Saddam, he was often seen puffing on fat Cuban cigars.
When Iraq found itself in dock, as it did after its invasion of Kuwait in 1990, it invariably fell to Tariq Aziz to explain Saddam's actions to an exasperated world. He did it doggedly, often infuriatingly, for decades.
As an ethnic Chaldean from northern Iraq, he was also the only Christian member of Saddam's entourage, which made him useful as an envoy for an secular regime. It also made him an outsider in Baghdad.
Western diplomats never doubted his loyalty to Saddam, but wondered how much he really knew about his master's secrets.
Obituary: Tariq Aziz
Tariq Aziz: Saddam's dangerously loyal courtier
In 2009, Aziz was sentenced to 15 years for the execution of 42 Iraqi traders who had been accused of manipulating food prices while Iraq was subject to international trade sanctions.
Five months later, he was sentenced to another seven years in prison for his role in the forced displacement of Kurds.
Despite being sentenced to death in 2010, there never seemed any huge pressure to carry out the sentence, according to BBC Arab affairs editor Sebastian Usher. ||||| Tariq Aziz, the debonair Iraqi diplomat who made his name by staunchly defending Saddam Hussein to the world during three wars and was later sentenced to death as part of the regime that killed hundreds of thousands of its own people, has died in a hospital in southern Iraq, officials said. He was 79.
Aziz, who had been in custody in a prison in the south awaiting execution, died Friday afternoon after he was taken to the al-Hussein hospital in the city of Nasiriyah following a heart attack, according to the provincial governor, Yahya al-Nassiri.
Aziz, the highest-ranking Christian in Saddam's regime, was its international face for years. He was sentenced in 2010 to hang for persecuting members of the Shiite Muslim religious parties that now dominate Iraq.
His wife, Violet, had visited him in prison Thursday, their daughter Zeinab told The Associated Press in the Jordanian capital, Amman, where most of the family lives.
Her father had suffered several strokes that left him confined to a wheelchair and unable to speak during their parents' final meeting, she said.
"He didn't move. He couldn't talk. He didn't say a word to her. He just looked at her," said Zeinab, 46, fighting back tears.
"It is so sad that he had to go this way," she said, speaking outside the family's Amman home, where friends and relatives gathered. "So sad that he didn't see his grandchildren, so sad that he had to spend his last years alone, sick and alone, and in this very humiliating circumstance."
"But I want people to remember what he did," she added. "He really fought for his country, in his own way."
Al-Nassiri, the governor of Dhi Qar province, said doctors could not save Aziz at the hospital in Nasiriyah, about 320 kilometers (200 miles) southeast of Baghdad.
"The medical staff did their best to rescue him, but they failed. It is God's will," he said, adding that Aziz had been a chain smoker and suffered from diabetes and high blood pressure for a long time. Local Iraqi authorities later told the family it can take Aziz's body from the hospital morgue.
The only Christian among Saddam's inner circle, Aziz's religion rescued him from the hangman's noose that was the fate of other members of the top regime leadership.
After he was sentenced to death, the Vatican asked for mercy for him as a Christian. Iraq's president at the time, Jalal Talabani, then refused to give the death sentence his required signature, citing Aziz's age and religion.
Even before he was sentenced, the ailing Aziz appeared to know that he would die in custody. He had had several strokes while in custody undergoing trial multiple times for various regime crimes.
"I have no future. I have no future," Aziz told The AP, looking frail and speaking with difficulty because of a recent stroke, in a jailhouse interview in September 2010. At that stage, he had been sentenced to more than two decades in prison.
"I'm sick and tired but I wish Iraq and Iraqis well," he said.
Elegant and eloquent, Aziz spoke fluent English, smoked Cuban cigars and was loyal to Saddam to the last, even naming one of his sons after the dictator. His posts included that of foreign minister and deputy prime minister, and he sat on the Revolutionary Command Council, the highest body in Saddam's regime. ||||| This will appear next to all of your comments
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Write a summary. | – Tariq Aziz, who during his years as Iraq's foreign minister and deputy prime minister was one of Saddam Hussein's close advisers, has died at the age of 79, the BBC reports. Iraqi officials say Aziz suffered a heart attack yesterday at the Iraqi prison where he had been jailed, and he died earlier today, per al-Jazeera. The AP notes he died in a hospital in southern Iraq. The highest-ranked Christian in Hussein's regime surrendered to US troops in 2003 and was sentenced to death in 2010 by the Iraqi Supreme Court for religious persecution; he had been imprisoned since then. With his large glasses and what the BBC calls a "passing resemblance to Groucho Marx," Aziz was a recognizable face around the world during the Gulf War in the early '90s and the 2003 US invasion of Iraq. His status as a Christian may have played a role in saving his life: After his death sentence was handed down, the Vatican asked for mercy for him, and Iraq's then-president opted not to sign the paperwork to greenlight his hanging, the AP notes. But Aziz appeared to realize he would die behind bars: He had multiple strokes while imprisoned, per the news agency, and spoke with difficulty during a 2010 jailhouse interview with the AP. "I have no future. I have no future," he said at the time. "I'm sick and tired, but I wish Iraq and Iraqis well." | multi_news_1_0_0 |
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News article:
INDIANAPOLIS - One of the co-founders of Lucas Oil has put out an explanatory advertisement after his wife and co-founder created a negative social media post about minorities last week.
Forrest Lucas, husband of Charlotte Lucas, wrote the letter, published as an advertisement this week, after RTV6 broke the story of her Facebook post. The post talked about how minorities should not be running the country.
"I'm sick and tired of minorities running our country!" Lucas wrote in the post. "As far as I'm concerned, I don't think that atheists (minority), muslims [sic] (minority) nor any other minority group has the right to tell the majority of the people in the United States what they can and cannot do here. Is everyone so scared that they can't fight back for what is right or wrong with his country?"
The next day, Charlotte issued an apology for the post.
Thursday morning, Forrest Lucas put out an ad (in the form of a letter), explaining what had happened and how he and Charlotte were trying to move forward.
The advertisement read:
Dear Friends:
Many of you know the story of how Charlotte and I started Lucas Oil from nothing in 1989. Over the last 25 years, Lucas Oil has achieved success with many oil products, developed a strong, supportive presence in motorsports, expanded into ranching and media operations, and became naming rights holder for the stadium that the Indianapolis Colts call home. Lucas Oil remains a family-owned business with manufacturing and distribution facilities in our home state of Indiana. Lucas Oil is proud to have employees, friends, customers and business partners reflecting ethnic and racial diversity.
Charlotte and I have been extremely fortunate, and we have found many ways to give back to the community. Among many other things, we have funded groups that provide opportunities and benefits for veterans, women, minorities and disadvantaged youth. We have supported causes that promote education and seek cures for cancer, diabetes, paralysis and other health problems.
Unfortunately, this week, Lucas Oil has been in the news for all the wrong reasons. The media reported a story about a posting Charlotte made on her Facebook page in which she included statements directed to minority special interest groups. Although it was not Charlotte's intent to offend anyone, her comments were harsh and insensitive. Her words were hurtful to many and disappointing to all. Make no mistake, Charlotte feels extremely saddened by her actions and regrets the posting. She has issued an apology with the hope that it will be accepted as sincere.
The reality is that the message posted on Charlotte's Facebook page does not reflect the feelings in her heart. Those who know Charlotte appreciate that she is a caring and loving person who has great respect for everyone. We thank those who have consoled Charlotte in this time of turmoil and have encouraged her to learn from her mistake.
Lucas Oil will continue to focus on all of its positive business activities and events. We will use this opportunity to examine our diversity efforts and to strengthen our relationships with minority leaders and organizations. We appreciate the patience and understanding of the community as we make progress in these areas.
Sincerely,
Forrest Lucas, Lucas Oil Products ||||| Photo: Michael Hickey/WireImage
Forrest Lucas, the co-founder of Lucas Oil, has discovered an innovative new way for newspapers to make money in this challenging media climate: charging people for full-page ads they can use to apologize for their wife's racist Facebook rants.
Lucas's wife, Charlotte Lucas, caused a little bit of a stir when she posted then deleted this message to her Facebook page last week:
"I'm sick and tired of minorities running our country! As far as I'm concerned, I don't think that atheists (minority), muslims (minority)n or any other minority group has the right to tell the majority of the people in the United States what they can and cannot do here. Is everyone so scared that they can't fight back for what is right or wrong with this country?"
Lucas was so embarrassed by his wife's behavior that he paid to have a full-page ad taken out in the Indianapolis Star, where he apologized on her behalf.
"Her words were hurtful to many and disappointing to all," the ad reads. "Make no mistake, Charlotte feels extremely saddened by her actions and regrets the posting. She has issued an apology with the hope that it will be accepted as sincere."
Next up: paying for sponsored tweets to apologize for that time your son got a DUI! |||||
What is a shorter version of the above article? | – Some Facebook posts are costlier than others. After the wife of a co-founder of Lucas Oil posted a diatribe against "minorities," her husband took out a full-page ad in the Indianapolis Star today to apologize, reports WRTV. This is the original post by Charlotte Lucas that prompted Forrest Lucas to shell out: "I'm sick and tired of minorities running our country! As far as I'm concerned, I don't think that atheists (minority), muslims (minority) nor any other minority group has the right to tell the majority of the people in the United States what they can and cannot do here. Is everyone so scared that they can't fight back for what is right or wrong with his country?" Charlotte deleted the post fairly quickly and apologized, saying that she was trying to vent her anger at the sway of special interest groups over elected officials, reports the Star. Today, husband Forrest took out the ad, which said in part: "Although it was not Charlotte's intent to offend anyone, her comments were harsh and insensitive. Her words were hurtful to many and disappointing to all. Make no mistake, Charlotte feels extremely saddened by her actions and regrets the posting." (You can see it in full via this link; go to page A12.) New York's Daily Intelligencer thinks the idea could help the struggling newspaper industry make some money if it catches on. "Next up: paying for sponsored tweets to apologize for that time your son got a DUI!" | multi_news_1_0_0 |
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PRAGUE (AFP) -
Czech President Milos Zeman, known for showing hostility towards journalists, taunted them on Thursday, saying he regretted making them look like "little idiots" during a bizarre event in which he set a huge pair of red underpants on fire.
The visibly frail 73-year-old Zeman abruptly announced a press conference on Thursday afternoon, raising speculation about his possible resignation.
"I apologise to the journalists whose intelligence I tested, unsuccessfully as always," Zeman told reporters gathered for the briefing the gardens of Prague Castle where he was flanked by his spokesman, assistants and several firemen.
To their amazement, Zeman then proceeded to burn a huge pair of red underpants in a fire pit, assisted by two firemen dressed in full gear.
"The time of underwear in politics is over," Zeman declared. "I'm sorry to make you look like little idiots, you really don't deserve it," he told reporters before leaving in his car.
The red underpants, measuring roughly one square metre, resembled a pair that Czech pranksters had flown from a flag pole atop the presidential palace in 2015 in protest against Zeman.
The pranksters said that the red colour of their boxer-short style protest flag symbolised the unhealthily close link they believed Zeman, a former communist, had with China and Russia.
Staunchly pro-Russian and pro-Chinese, Zeman once dubbed journalists "manure" and "superficial" before telling Russian President Vladimir Putin in China in May 2017 that "journalists should be liquidated".
He also showed up at a press conference in October 2017 with a toy Kalashnikov in his hand labelled "for journalists".
Zeman narrowly won a second consecutive term in January elections, beating his pro-European liberal rival Jiri Drahos in a knife-edge run-off that underscored deep divisions in the EU and NATO state.
Zeman's stunt drew a barrage of criticism on Thursday, with Jiri Pospisil, leader of the right-wing TOP 09 party, exclaiming "let us wake up from this nightmare!"
Zeman's health has come under heavy scrutiny in recent months.
He walks with a cane, is diabetic and is a former heavy drinker and smoker.
© 2018 AFP ||||| PRAGUE (AP) — A fiery stunt by the Czech president has really stunned journalists this time.
Milos Zeman announced a press conference for Thursday, but instead of briefing reporters, he had two firefighters in protective gear burn a huge pair of red underpants in front of them.
Czech media said the boxer shorts in question had been hoisted by activists in 2015, replacing the official presidential flag on Prague Castle. The red underwear was meant to symbolize Zeman's close relationships with Russia and China and has since become a symbol for criticism of his presidency.
After the incineration, Zeman told reporters: "I'm sorry to make you look like little idiots, you really don't deserve it."
Zeman, 72, has often clashed with the press, even waving a fake machine gun at reporters last year. |||||
Write a summary. | – A fiery stunt by the Czech president has really stunned journalists this time. Milos Zeman announced a press conference for Thursday, but instead of briefing reporters, he had two firefighters in protective gear help him burn a huge pair of red underpants in front of them, the AP reports. Per AFP, a "visibly frail" Zeman did the deed on a 10-foot-by-10-foot pair of boxer shorts, and he had some words after the incineration. "The time of underwear in politics is over," he declared to reporters. "I'm sorry to make you look like little idiots, you really don't deserve it." Czech media said the boxer shorts in question resembled a pair that had been hoisted by activists in 2015, replacing the official presidential flag on Prague Castle. The red underwear was meant to symbolize Zeman's close relationships with Russia and China and has since become a symbol for criticism of his presidency. Zeman, 73, has often clashed with the press, even waving a fake machine gun at reporters last year. | multi_news_1_0_0 |
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Here is a news article: The seed for this crawl was a list of every host in the Wayback Machine
This crawl was run at a level 1 (URLs including their embeds, plus the URLs of all outbound links including their embeds)
The WARC files associated with this crawl are not currently available to the general public. ||||| Focused crawls are collections of frequently-updated webcrawl data from narrow (as opposed to broad or wide) web crawls, often focused on a single domain or subdomain. ||||| New evidence recently found that many ER doctors fail to recognize signs and symptoms of a stroke, which can leave patients at a higher risk for a potentially life-threatening "brain attack." Although patients should still rely on their physician for a complete cognitive and cardiovascular checkup, they should also be wary of their own warning signs. A study published in the American Heart Association’s journal Stroke has revealed a patient’s ability to stand on one leg can determine their risk for a stroke.
"One-leg standing time is a simple measure of postural instability and might be a consequence of the presence of brain abnormalities," Dr. Yasuharu Tabara, associate professor at the Center for Genomic Medicine at Kyoto University Graduate School of Medicine in Kyoto, Japan, said in a statement.
Tabara and his colleagues recruited 841 women and 546 men at an average age of 67. Participants were asked to stand on one leg with their eyes open for a maximum of 60 seconds. This examination was performed twice and researchers used the better of the two times for their research. The research team used brain magnetic resonance imaging to evaluate cerebral small vessel disease.
Ability to stand on one leg can predict stroke risk. Photo courtesy of Shutterstock
Participants who were unable to balance on one leg for more than 20 seconds were at a higher risk for cerebral small vessel disease, most notably small infarctions — a type of ischemic stroke that occurs when blood supply to the brain is blocked or leaks outside vessel walls. These small infarctions did not show any symptoms, such as lacunar infarction and microbleeds. The presence of both lacunar infarction and microbleeds is usually associated with cognitive decline.
Findings revealed that 34.5 percent of participants with more than two lacunar infarction legions had trouble balancing on one leg, while 16 percent of those with one lacunar infarction lesions also struggled with balancing. Thirty percent of participants with more than one microbleed lesion had trouble balancing on one leg and 15.3 percent of those with one microbleed lesion had trouble balancing. On average, patients with cerebral disease were older and those who were unable to stand on one leg for over 20 seconds recorded lower cognitive scores.
"Our study found that the ability to balance on one leg is an important test for brain health," Tabara added. "Individuals showing poor balance on one leg should receive increased attention, as this may indicate an increased risk for brain disease and cognitive decline."
According to the American Stroke Association, small vessel disease is a condition in which already small arteries in the heart become even narrower. It is often a common occurrence of aging; however, factors such as high blood pressure and diabetes can worsen this condition. Patients with small vessel disease are at a higher risk for lacunar infarction and intracerebral hemorrhage.
Source: Okada Y, Ohara M, Tabara Y, et al. Stroke. 2014. ||||| Your Balance on One Leg & Your Stroke Risk Linked
Inability to stand on one foot for 20-plus seconds could suggest brain vessel damage, study contends
WebMD News from HealthDay
WebMD News Archive
By Steven Reinberg
HealthDay Reporter
THURSDAY, Dec. 18, 2014 (HealthDay News) -- If you can't balance on one leg for at least 20 seconds you may be at risk of a stroke, Japanese researchers suggest.
Difficulty standing on one leg may indicate that small strokes or tiny bleeds have already occurred, which means the risk for more serious strokes is high, the investigators reported online Dec. 18 in the journal Stroke.
"Individuals showing instability while standing on one leg, as well as problems walking, should receive increased attention, as this physical frailty may signal potential brain abnormalities and mental decline," said lead author Yasuharu Tabara, an associate professor in the Center for Genomic Medicine at the Kyoto University Graduate School of Medicine.
Stroke, a leading cause of disability and death, occurs when blood flow to a part of the brain is interrupted because of a clot or bleeding.
For the study, Tabara's team had nearly 1,400 men and women, average age 67, try to balance on one leg for a minute. The researchers also took MRI scans to assess disease in the small blood vessels of participants' brains, in the form of "silent" strokes -- or microbleeds.
The researchers found that the inability to balance on one leg for more than 20 seconds was linked to having had tiny strokes or small bleeds in the brain. Balance problems were also associated with reduced thinking and memory skills.
Dr. Richard Libman, chief of vascular neurology at North Shore-LIJ Health System in Manhasset, N.Y., said that "narrowing or blockages of tiny blood vessels deep within the brain can give rise to small strokes or tiny amounts of bleeding."
These small strokes, which are a major contributor to mental decline and dementia, have also been associated with walking and balance difficulty and falling, he explained.
"The authors of this study have devised a simple test of balance, which seems to be able to reflect 'small vessel disease' of the brain," Libman said.
"This test may be an inexpensive, low-tech method to screen people for small vessel disease who are most likely at risk for further strokes and brain damage," Libman added. |||||
A summary of this is? | – Think you're at risk of a stroke? Then try standing on one one leg for at least 20 seconds, a new study says. Japanese researchers had nearly 1,400 women and men, with an average age of 67, try the balancing act for at least a minute—and found that those who lasted less than 20 seconds were more likely to have already suffered a small stroke, WebMD reports. Such strokes are considered a serious contributor to dementia and mental decline. People who can't go 20 seconds "should receive increased attention, as this physical frailty may signal potential brain abnormalities and mental decline," says chief study author Yasuharu Tabara. Those who failed the test were at greater risk of small vessel disease like "infarctions"—ischemic strokes caused by a block or leak in the brain's blood supply, Medical Daily reports. Worse, such strokes show no symptoms. So the one-leg test "may be an inexpensive, low-tech method to screen people for small vessel disease who are most likely at risk for further strokes and brain damage," says a vascular neurologist. Published in the journal Stroke, the study recalls a finding earlier this year that 53-year-old men and women who could rapidly stand and sit in a chair for a minute, and stand on one leg for more than 10 seconds, were at less risk of an early death, the Telegraph reports. (Another study shows that half of Dr. Oz's advice is all wrong.) | multi_news_1_0_0 |
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Eating a Mediterranean-style diet pops up again and again as a health booster. The latest study to look at its benefits suggests following the diet may delay brain shrinkage as we age.
People who ate a diet rich in fresh fruits and vegetables, fish, legumes, and olive oil, along with small to moderate amounts of alcohol, and who consumed less meat and dairy, had less brain shrinkage than people who did not follow a Mediterranean eating style, according to a study published today in the journal Neurology. The researchers also found that Mediterranean diet followers had a larger brain volume than those who didn't eat this way.
The difference between the two groups added up to about five years of aging, the scientists reported.
Study author Yian Gu, of Columbia University, in New York, said the results are exciting because they raise the possibility that people may potentially be able to prevent brain shrinking and the effects of aging on the brain by following a healthy diet.
"The more you adhere to the Mediterranean diet, the better protection you get for your brain," she told CBS News.
Dishing up more fish and less meat was linked with less brain shrinkage. "Eating at least three to five ounces of fish weekly or eating no more than 3.5 ounces of meat daily may provide considerable protection against loss of brain cells," Gu said in a press statement.
The study included 674 people with an average age of 80 who did not have dementia. They completed questionnaires about their diet over the past year and then had brain scans an average of seven months after answering the diet survey. The participants were divided into two groups based on how closely their dietary habits followed the Mediterranean diet basics.
The people who more closely followed a Mediterranean-like diet had total brain volume that was 13.11 milliliters larger than those who did not follow the Mediterranean diet. Their gray matter volume was 5.0 milliliters larger, and their white matter volume was 6.41 milliliters larger.
Dr. Gayatri Devi, an attending neurologist at Lenox Hill Hospital, in New York, told CBS News, "The freshest thing here in this study shows that people on a Mediterranean diet, their brains actually shrunk less than people not on Mediterranean diet. And the shrinkage translated to an advantage of five years of brain aging. Persons who said that they were having a diet high in fruits, vegetables and fish and high in different kinds of polyunsaturated fats like olive, had plumper more healthy brains, less-shrunk brains than people who reported having a diet of food that was high in dairy and high in red meats and low in vegetables and fruits."
The less shrinkage there is in your brain, said Devi, the more brain cells there are available, and "the more brain cells you have available, the more likely you are to be protected against illnesses of the brain related to aging, like Alzheimer's."
Devi said the omega 3 fatty acids found in fish seem to keep nerve cells healthy, while the B vitamins found in a lot of vegetables and fruits may help prevent the buildup of plaque in the brain seen in Alzheimer's disease. "The foods that are high in saturated fat may actually promote the laying down of plaques seen in Alzheimer's," she said.
Devi said it was interesting that in two equally slender people, the one eating the more Mediterranean-like diet was more likely to have a brain that shrunk less.
The research, said Devi, "gives us another tool in our toolbox to help keep us more functional as we get older."
The study, supported by the National Institutes of Health, does not prove that the Mediterranean diet prevents brain shrinkage, it only showed an association, study author Gu said.
Following a Mediterranean-style diet has also been linked with a range of other benefits, including better heart health and a reduced risk of diabetes. ||||| US survey shows older people who follow vegetable-rich diet have brain volume greater than those who do not
Eating a Mediterranean diet rich in fish and vegetables may help prevent your brain shrinking for as long as five years, new research suggests.
People who follow such a diet, which also involves consuming less meat and dairy products than average, end up with bigger brains and slow down the ageing process, according to the US study.
“These results are exciting, as they raise the possibility that people may potentially prevent brain shrinking and the effects of ageing on the brain simply by following a healthy diet,” said the lead author, Yian Gu, of Columbia University in New York.
Researchers looked at 674 people with an average age of 80 who lived in northern Manhattan and did not have dementia.
They found that the total brain volume of those who had closely followed a Mediterranean-style diet was on average 13.11 millilitres greater than that of those who had not done so.
Their grey matter volume was 5 millilitres greater, and their white matter 6.4 millilitres greater, than those who had not stuck to Mediterranean foods.
The difference between the two groups is equivalent to about five years of ageing, the authors said.
“The magnitude of the association with brain measures was relatively small. But when you consider that eating at least five of the recommended Mediterranean diet components has an association comparable to five years of age, that is substantial,” said Gu.
Having fish regularly and eating little meat was particularly effective. “Eating at least 3 to 5 ounces of fish weekly, or eating no more than 3.5 ounces of meat daily, may provide considerable protection against loss of brain cells equal to about three to four years of ageing,” Gu added.
The Mediterranean diet typically consists of large amounts of vegetables, pulses, fruit, cereal, fish and monounsaturated fatty acids such as olive oil. It also includes small amounts of meat, poultry, dairy products and saturated fatty acids, plus mild to moderate alcohol consumption.
The authors cautioned that their findings, published in the journal Neurology, do not prove conclusively that the Mediterranean diet prevents brain shrinkage and that it is merely an association.
However, two British dementia charities said it was further evidence that the Mediterranean diet may improve brain health.
“There is an increasing amount of evidence that eating a healthy diet rich in fish, vegetables, legumes and nuts is good for your brain,” said Dr James Pickett, the head of research at the Alzheimer’s Society. “This study delves further into the potential benefits that diet could have, but it does not prove that a Mediterranean-style diet can stop your brain from shrinking as you age.”
People hoping to reduce their risk of developing dementia should also quit smoking, exercise regularly and keep their blood pressure low, he said.
But Dr Laura Phipps, a spokeswoman for Alzheimer’s Research UK, expressed caution: “While this study suggests there is an association between eating a Mediterranean diet and brain volume in healthy older people, we don’t know whether these particular food choices alter dementia risk. It’s hard to know from this study what the underlying reason for the link between diet and brain volume might be, and what other factors may be involved.”
Age remains the biggest risk factor for dementia, but genetics and lifestyle also play a part, Phipps added. |||||
What is a one-paragraph summary of the above article? | – Hoping to avoid brain shrinkage, cognitive impairment, and dementia? Gobble up lots of fish, veggies, and nuts. A new study shows those who follow the increasingly well-regarded Mediterranean diet have less brain atrophy than those who don't. Researchers scanned the brains of 674 Manhattan residents over 80 who showed no signs of dementia, and analyzed their diets based on a questionnaire, reports the Guardian. The patients who kept to a Mediterranean diet had a brain volume that was 13.11 milliliters larger than others, their gray matter volume was 5 milliliters larger, and their white brain matter was 6.41 milliliters larger. Since people's brains shrink with age, researchers say the difference in brain volume is equal to about five years of aging. This doesn't mean the Mediterranean diet slows brain aging, but it does show an association. And with greater brain volume comes more brain cells. "The more brain cells you have available, the more likely you are to be protected against illnesses of the brain related to aging, like Alzheimer's," a doctor tells CBS News, adding omega-3 fatty acids found in fish may benefit nerve cells, while B vitamins in fruits and veggies may prevent the buildup of plaque in the brain. "These results are exciting, as they raise the possibility that people may potentially prevent brain shrinking and the effects of aging on the brain simply by following a healthy diet," lead author Yian Gu says. One aspect of the diet stood out, though. "Eating at least three to five ounces of fish weekly or eating no more than 3.5 ounces of meat daily may provide considerable protection against loss of brain cells equal to about three to four years of aging," Gu adds. (The diet might also add years to your life.) | multi_news_1_0_0 |
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Article:
The mob boss had been at the federal jail in Brooklyn longer than any other inmate: four years awaiting trial and, after his conviction in 2012 on racketeering charges, nearly two more waiting to be sentenced. By the time his sentencing date arrived on Wednesday, the mobster, Thomas Gioeli, had been considered for the death penalty, convicted of conspiring to murder three mobsters and acquitted of killing a police officer; he had multiple angioplasties and, with the help of his family, even became an avid blogger and user of Twitter who taunted prosecutors and two mayors.
The measure of those six years behind bars for Mr. Gioeli — highly unusual for someone who has not yet been sentenced — were central to arguments in Federal District Court in Brooklyn on Wednesday over how much prison time Mr. Gioeli should get: the maximum 20 years, or something less.
One of Mr. Gioeli’s lawyers, Adam D. Perlmutter, said the six years had taken an especially hard toll. “He is now the senior-most person at the M.D.C.,” Mr. Perlmutter said, referring to the Metropolitan Detention Center. He named a host of medical conditions that Mr. Gioeli, 61, is living with, including diabetes, heart disease and arthritis. “People who suffer from chronic health conditions do harder time in prison than people who are healthy,” Mr. Perlmutter said. “A 20-year sentence for Thomas Gioeli is, in fact, a life sentence.”
The judge, Brian M. Cogan, said that with a 20-year sentence, credit for time served and good behavior, Mr. Gioeli would be out by his early 70s. “He’s not going to live to his early 70s?” Judge Cogan asked.
“I don’t think so,” Mr. Perlmutter answered.
A prosecutor, James Gatta, said, “Such time should not count against the sentence that the defendant should receive for his criminal conduct.”
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As the argument unfolded, Mr. Gioeli, who since his conviction last year grew a giant tuft of white hair on his chin, leaned back in his chair, twisting his white mustache, waving warmly and making baby faces at his family in the courtroom. It was odd behavior that would have been more at home at a child’s birthday party than at a sentencing for gangland murders.
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Judge Cogan knocked 16 months off the 20-year maximum and ordered Mr. Gioeli to pay $360,000 in restitution.
At the murder and racketeering trial, prosecutors said Mr. Gioeli, whom they called the former acting boss of the Colombo family, ordered the ambush and murder of an off-duty police officer, Ralph C. Dols, and ordered the killings of several other men in the 1990s. Prosecutors called admitted mob killers to testify against Mr. Gioeli (they described surprise shootings in basements, dissolving dead bodies with lye and burying them on Long Island), but the jury acquitted Mr. Gioeli of many charges, including the murder of Officer Dols. He was found guilty of one count of racketeering for conspiring to kill three mobsters.
The acts that the prosecutors described hardly meshed with Mr. Perlmutter’s portrayal of Mr. Gioeli as a family man, or “Tommy, the person,” as he called him in a long argument that roused sniffles among two or three dozen family members who showed up. “I look at their marriage and I’m jealous,” Mr. Perlmutter said of Mr. Gioeli’s relationship with his wife. It was an image that Mr. Gioeli also put forth on his blog during his years in jail, that of a family man who was wronged by zealous prosecutors.
His Twitter messages and blog posts, which family members posted after he wrote them using his prison email account, espoused a liberal vision of society, coming to the defense of the working poor, speaking out against sexism, when he was not opining on current events.
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Last month, Mr. Gioeli wrote on Twitter, “The FBI arrests old Italians for decades old robberies while allowing bankers to steal billions everyday. TSG #FBI #America #wallstreet,” signing his initials, T.S.G.
Judge Cogan, who said the evidence was overwhelming that Mr. Gioeli was a manager of the crime family and found it was more likely than not he had participated in other murders, said Mr. Gioeli was like many mobsters who are “absolutely schizophrenic in their personalities.” Judge Cogan said, “They go out there and they do things to get people murdered, and at the same time they are wonderful to their families and their communities.”
“They are vicious crimes, and they take a vicious person to do them. I recognize that’s not all there is to Mr. Gioeli.”
Judge Cogan said that Mr. Gioeli’s time served and the “wonderful” way he treated his family were mitigating factors. But he also said: “I haven’t seen any remorse. I’ve just seen self-righteousness.”
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Whether he will live to make it out after more than 18 years in prison, the judge said, “only God knows.”
A Selection of Twitter Messages From Thomas Gioeli ||||| A triple-murder suspect-turned-mob informant whose colorful stories led to the arrest of 39 underworld operators was sentenced to time served Friday — and he was even heralded by the judge for his bravery.
Thomas McLaughlin, 46, was 15 when he taken under the wing of a “bad” relative and nurtured to join the Colombo crime family, according to defense lawyer Stuart Grossman.
After getting pinched for drug trafficking and firearms possession, he went to jail for 16 years without cooperating, earning the trust of his criminal colleagues.
But in 2008 when he was released, the feds came to him and told him he would be charged with conspiracy in planning three mob hits and asked for his cooperation. Facing life in prison, he agreed to help and recorded more than 200 conversations between 2009 to 2011, leading to 39 arrests and two convictions.
He nearly put Sammy “The Bull” Gravano’s record to shame. Gravano helped jail 36 people.
‘I want to apologize for my past… I look forward to the future and continuing to be a husband and father.’ - Thomas McLaughlin
Brooklyn federal court Judge Brian M. Cohan on Friday sentenced him to the 16 years he already served and thanked him for wearing a wiretap for the government. “The number of criminal activities that were able to be prosecuted with Mr. McLaughlin’s cooperation is beyond anything I’ve ever seen… and let’s not forget the risk,” Judge Cohan said.
McLaughlin was also instrumental in the conviction of his own cousin, when he was called to testify at former Colombo boss Tommy “Tommy Shots” Gioeli 2012 trial and fingered his role in a murder.
Grossman called his client “a totally changed man,” and prosecutor Elizabeth Geddes applauded his cooperation with the government calling it “historic.”
Today McLaughlin is a family man with a “hard job. Not the kind of job you’re going to get rich on,” according to the judge, who did not say what his new employment entails.
McLaughlin addressed the court. “I want to apologize for my past, Your Honor,” he said.
“I look forward to the future and continuing to be a husband and father.”
“I’m not skeptical,” Judge Cohan said. “I’m dealing with someone who has not only gone straight but who will stay straight.” ||||| Leave the ping pong paddles, file the lawsuit.
That’s what former Colombo crime boss Thomas (Tommy Shots) Gioeli has done — suing the federal government for $10 million over injuries from a game of prison ping-pong.
The table tennis tumble happened Aug. 29, 2013, while Gioeli was being held at Metropolitan Detention Center in Brooklyn.
More than a year earlier, a Brooklyn Federal Court jury had found him guilty of racketeering conspiracy connected to murder plots.
Mob rat Thomas McLaughlin sentenced to zero jail time
Gioeli, 64, and fellow defendant Dino (Little Dino) Saracino also were accused of carrying out murders, including the killing of a police officer, but acquitted on the murder charges.
According to government court papers, Gioeli argues his slip and fall occurred because of prison officials’ negligence. They knew — or should have known — about the hazardous wet floor in recreation area, pointing to the proximity of showers and an allegedly leaky slop sink pipe.
Thomas (Tommy Shots) Gioeli, Colombo acting boss. (Jesse Ward/for New York Daily News)
The leak was reported to prison employees for days, if not weeks before the accident, Gioeli claims.
The burly Gioeli fractured his right kneecap and had to be hospitalized. The injury required surgery, physical therapy and occupational therapy, court papers obtained by the Daily News show.
Ex-Colombo hitman gets 12 years for murder of NYPD cop Dols
The government rejects any charge of negligence, saying it acted with necessary care at all times. And part of its defense is that there’s some risk that comes with playing table tennis — and Gioeli chose to take that risk.
The case has been assigned to Brooklyn Federal Court Judge Kiyo Matsumoto.
A bench trial is estimated to take about three days, though the case docket shows no trial date yet.
Gioeli is expected to make it up from his low-security North Carolina prison to testify about his spill and subsequent suffering, according to court papers.
Crime boss claims he got solitary for religious scapular
He did not take the stand at his criminal case.
The doctor who examined Gioeli is scheduled to testify about the mafioso’s mishap.
Another person who had been held at the lockup is expected to talk about the floor layout, prisoners tracking in water from the showers, and his complaints about the alleged leak.
The government said it plans to put on witnesses including a Metropolitan Detention Center general foreman.
Gioeli claims he slipped on a wet floor while playing table tennis. He's accusing prison officials of negligence. (wsantina/Getty Images/iStockphoto)
The man is expected to say he searched for records of reported water leaks or repair orders for leaks around the time of the incident, but found none.
Another planned government witness is a correction officer who says he found Gioeli on the wet floor, near the showers.
Gioeli is serving an 18-year prison sentence.
Both Gioeli’s lawyer Martin Schiowitz and the Bureau of Prisons declined comment Monday. ||||| These crawls are part of an effort to archive pages as they are created and archive the pages that they refer to. That way, as the pages that are referenced are changed or taken from the web, a link to the version that was live when the page was written will be preserved.Then the Internet Archive hopes that references to these archived pages will be put in place of a link that would be otherwise be broken, or a companion link to allow people to see what was originally intended by a page's authors.The goal is to fix all broken links on the web . Crawls of supported "No More 404" sites. |||||
What is a summary? | – Former mob boss Thomas "Tommy Shots" Gioeli wants $10 million from the federal government over a Ping-Pong injury. Gioeli, once a high-ranking member of the Colombo crime family, is suing over an injury he suffered during a game at the Metropolitan Detention Center in Brooklyn in 2013, according to court papers seen by the New York Daily News. He says he slipped on a wet floor while playing a game and fractured a kneecap. His suit argues that the prison is negligent because employees ignored complaints about a leaky pipe that led to the slippery conditions in the recreation area. The federal government, however, says that even Ping-Pong comes with risks, and Gioeli chose to take them. Gioeli needed surgery and rehab after the fall. The 64-year-old is three years into an 18-year sentence on racketeering charges, though he was acquitted of murder charges that included the 1997 slaying of a New York City police officer. At his sentencing in 2014, his attorney argued unsuccessfully for a light sentence because his client suffered from arthritis, diabetes, and heart disease, and thus probably wouldn't live beyond his early 70s, the New York Times reported. The story also noted that Gioeli had become a colorful fan of Twitter, with tweets such as: "The FBI spends it's limited resources on terminal Italian book-makers while terrorist & cartels flourish." So how did Gioeli wind up in prison? His own cousin ratted him out, reported the New York Post. (The late Anthony Colombo had a specific influence on the Godfather films.) | multi_news_1_0_0 |
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Article:
Importance Between 40% and 50% of women in Western countries use complementary therapies to manage menopausal symptoms.
Objective To determine the association of plant-based therapies with menopausal symptoms, including hot flashes, night sweats, and vaginal dryness.
Data Sources The electronic databases Ovid MEDLINE, EMBASE, and Cochrane Central were systematically searched to identify eligible studies published before March 27, 2016. Reference lists of the included studies were searched for further identification of relevant studies.
Study Selection Randomized clinical trials that assessed plant-based therapies and the presence of hot flashes, night sweats, and vaginal dryness.
Data Extraction Data were extracted by 2 independent reviewers using a predesigned data collection form.
Main Outcomes and Measures Hot flashes, night sweats, and vaginal dryness.
Results In total, 62 studies were identified, including 6653 individual women. Use of phytoestrogens was associated with a decrease in the number of daily hot flashes (pooled mean difference of changes, −1.31 [95% CI, −2.02 to −0.61]) and vaginal dryness score (pooled mean difference of changes, −0.31 [95% CI, −0.52 to −0.10]) between the treatment groups but not in the number of night sweats (pooled mean difference of changes, −2.14 [95% CI, −5.57 to 1.29]). Individual phytoestrogen interventions such as dietary and supplemental soy isoflavones were associated with improvement in daily hot flashes (pooled mean difference of changes, −0.79 [−1.35 to −0.23]) and vaginal dryness score (pooled mean difference of changes, −0.26 [−0.48 to −0.04]). Several herbal remedies, but not Chinese medicinal herbs, were associated with an overall decrease in the frequency of vasomotor symptoms. There was substantial heterogeneity in quality across the available studies, and 46 (74%) of the included randomized clinical trials demonstrated a high risk of bias within 3 or more areas of study quality.
Conclusions and Relevance This meta-analysis of clinical trials suggests that composite and specific phytoestrogen supplementations were associated with modest reductions in the frequency of hot flashes and vaginal dryness but no significant reduction in night sweats. However, because of general suboptimal quality and the heterogeneous nature of the current evidence, further rigorous studies are needed to determine the association of plant-based and natural therapies with menopausal health. ||||| Women who have already passed through the menopause may be able to have children following a blood treatment usually used to heal wounds
Peter Dazeley/Getty
MENOPAUSE need not be the end of fertility. A team claims to have found a way to rejuvenate post-menopausal ovaries, enabling them to release fertile eggs, New Scientist can reveal.
The team says its technique has restarted periods in menopausal women, including one who had not menstruated in five years. If the results hold up to wider scrutiny, the technique may boost declining fertility in older women, allow women with early menopause to get pregnant, and help stave off the detrimental health effects of menopause.
“It offers a window of hope that menopausal women will be able to get pregnant using their own genetic material,” says Konstantinos Sfakianoudis, a gynaecologist at the Greek fertility clinic Genesis Athens.
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“It is potentially quite exciting,” says Roger Sturmey at Hull York Medical School in the UK. “But it also opens up ethical questions over what the upper age limit of mothers should be.”
Women are thought to be born with all their eggs. Between puberty and the menopause, this number steadily dwindles, with fertility thought to peak in the early 20s. Around the age of 50, which is when menopause normally occurs, the ovaries stop releasing eggs – but most women are already largely infertile by this point, as ovulation becomes more infrequent in the run-up. The menopause comes all-too-soon for many women, says Sfakianoudis.
The age of motherhood is creeping up, and more women are having children in their 40s than ever before. But as more women delay pregnancy, many find themselves struggling to get pregnant. Women who hope to conceive later in life are increasingly turning to IVF and egg freezing, but neither are a reliable back-up option (see “The pregnancy pause“).
The menopause also comes early – before the age of 40 – for around 1 per cent of women, either because of a medical condition or certain cancer treatments, for example.
“It offers hope that menopausal women will be able to get pregnant using their own genetic material“
To turn back the fertility clock for women who have experienced early menopause, Sfakianoudis and his colleagues have turned to a blood treatment that is used to help wounds heal faster.
Platelet-rich plasma (PRP) is made by centrifuging a sample of a person’s blood to isolate growth factors – molecules that trigger the growth of tissue and blood vessels. It is widely used to speed the repair of damaged bones and muscles, although its effectiveness is unclear. The treatment may work by stimulating tissue regeneration.
Sfakianoudis’s team has found that PRP also seems to rejuvenate older ovaries, and presented some of their results at the European Society of Human Reproduction and Embryology annual meeting in Helsinki, Finland, this month. When they injected PRP into the ovaries of menopausal women, they say it restarted their menstrual cycles, and enabled them to collect and fertilise the eggs that were released.
“I had a patient whose menopause had established five years ago, at the age of 40,” says Sfakianoudis. Six months after the team injected PRP into her ovaries, she experienced her first period since menopause.
Sfakianoudis’s team has since been able to collect three eggs from this woman. The researchers say they have successfully fertilised two using her husband’s sperm. These embryos are now on ice – the team is waiting until there are at least three before implanting some in her uterus.
The team isn’t sure how this technique works, but it may be that the PRP stimulates stem cells. Some research suggests a small number of stem cells continue making new eggs throughout a woman’s life, but we don’t know much about these yet. It’s possible that growth factors encourage such stem cells to regenerate tissue and produce ovulation hormones. “It’s biologically plausible,” says Sturmey.
Fertilised eggs
Sfakianoudis’s team says it has given PRP in this way to around 30 women between the ages of 46 and 49, all of whom want to have children. The researchers say they have managed to isolate and fertilise eggs from most of them.
“It seems to work in about two-thirds of cases,” says Sfakianoudis. “We see changes in biochemical patterns, a restoration of menses, and egg recruitment and fertilisation.” His team has yet to implant any embryos in post-menopausal women, but hopes to do so in the coming months.
PRP has already been helpful for pregnancy in another group of women, says Sfakianoudis. Around 10 per cent of women who seek fertility treatment at his clinic have a uterus that embryos find difficult to attach to – whether due to cysts, scarring from miscarriages or having a thin uterine lining. “They are the most difficult to treat,” says Sfakianoudis.
But after injecting PRP into the uteruses of six women who had had multiple miscarriages and failed IVF attempts, three became pregnant through IVF. “They are now in their second trimester,” says Sfakianoudis.
Fertility aside, the technique could also be desirable for women who aren’t trying to conceive. The hormonal changes that trigger menopause can also make the heart, skin and bones more vulnerable to ageing and disease, while hot flushes can be very unpleasant. Many women are reluctant to take hormone replacement therapy to reduce these because of its link with breast cancer. Rejuvenating the ovaries with PRP could provide an alternative way to boost the supply of youthful hormones, delaying menopause symptoms.
Steve Gschmeissner/SPL
However, Sfakianoudis’s team hasn’t yet published any of its findings. “We need larger studies before we can know for sure how effective the treatment is,” says Sfakianoudis.
“One woman had been in menopause for 5 years. Six months after treatment, she had a period“
Some have raised concerns about the safety and efficacy of the procedure, saying the team should have tested the approach in animals first. “This experiment would not have been allowed to take place in the UK,” says Sturmey. “The researchers need to do some more work to make sure that the resulting eggs are OK,” says Adam Balen at the British Fertility Society.
To know if the technique really does improve fertility, the team will also need to carry out randomised trials, in which a control group isn’t given PRP.
Virginia Bolton, an embryologist at Guy’s and St Thomas’ Hospital in London, is also sceptical. “It is dangerous to get excited about something before you have sufficient evidence it works,” she says. New techniques often find their way into the fertility clinic without strong evidence, thanks to huge demand from people who are often willing to spend their life savings to have a child, she says.
If the technique does hold up under further investigation, it could raise ethical questions over the upper age limits of pregnancy – and whether there should be any. “I lay awake last night turning this over in my mind,” says Sturmey. “Where would the line be drawn?”
Health issues like gestational diabetes, pre-eclampsia and miscarriage are all more common in older women. “It would require a big debate,” says Sturmey.
Sperm home test kit How are the little swimmers doing? Low sperm counts or poor sperm quality are behind around a third of cases of couples who can’t conceive. A visit to a clinic for a test can be awkward, but a smartphone-based system lets men determine whether that’s necessary by checking their fertility at home. Men often find it embarrassing to give a semen sample at a clinic, says Yoshitomo Kobori at the Dokkyo Medical University Koshigaya Hospital in Japan. So Kobori devised an alternative. “I thought a smartphone microscope could be an easy way to look at problems with male fertility,” he says. Kobori and his colleagues came up with a lens less than a millimetre thick that can be slotted into a plastic “jacket”. Clipped on to the camera of a smartphone, it magnifies an image by 555 times – perfect for looking at sperm. To do a home test, a man would apply a small amount of semen to a plastic sheet around five minutes after ejaculation and press it against the microscope. Watch them swim The phone’s camera can then take a 3-second video clip of the sperm. When viewed enlarged on a computer screen, it is easy for someone to count the total number of sperm and the number that are moving – key indicators of fertility. Kobori says the system works as well as the software used in fertility clinics. When the team ran 50 samples through both systems, they got almost identical results. The work was presented at the European Society of Human Reproduction and Embryology meeting in Helsinki this month. The system can’t assess the ability of sperm to fertilise an egg. “This method is only the simple version of semen analysis,” says Kobori. But that could be enough for men to identify potential fertility problems, and decide whether to seek help from a doctor.
This article appeared in print under the headline “Reversing the menopause”
Leader: “Who should we believe when it comes to fertility?” |||||Summary:
| – The hot flashes, night sweats, and vaginal dryness characteristic of menopause may no longer also signal the end of a woman's fertility thanks to a blood treatment used to heal wounds. Presenting their findings at the European Society of Human Reproduction and Embryology annual meeting in Helsinki, Finland, this month, researchers in Greece said they were able to reverse menopause in roughly 30 women, including one who entered menopause at 40 but five years later menstruated again, reports New Scientist. The team has collected three eggs from her and, using her husband's sperm, fertilized two into embryos that they plan to implant into her uterus. Still, an outside researcher says, the development "opens up ethical questions over what the upper age limit of mothers should be." The team reports that roughly 1% of women become infertile before they turn 40 thanks to certain medical conditions and cancer treatments. "It offers a window of hope that menopausal women will be able to get pregnant using their own genetic material," says gynecologist Konstantinos Sfakianoudis. The team injected a woman's ovaries with a platelet-rich plasma—or PRP, which is made with a person's own blood to trigger tissue and blood vessel growth and has been used by the likes of Tiger Woods to speed healing from soft-tssue injuries, notes Forbes—to effectively rejuvenate them and trigger menstrual cycles. They're not yet sure exactly how it works, but they've managed to fertilize eggs from nearly all of the 30 women they studied, who are between 45 and 49 and want to have children. In related news, a meta analysis published in JAMA found that some "natural" remedies, though not Chinese "medicinal" herbs, may slightly improve certain symptoms of menopause. (Heard of snowflake moms?) | multi_news_1_0_0 |
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Sleep is a vital indicator of overall health and well-being. We spend up to one-third of our lives asleep, and the overall state of our "sleep health" remains an essential question throughout our lifespan.
Most of us know that getting a good night’s sleep is important, but too few of us actually make those eight or so hours between the sheets a priority. For many of us with sleep debt, we’ve forgotten what “being really, truly rested” feels like.
To further complicate matters, stimulants like coffee and energy drinks, alarm clocks, and external lights—including those from electronic devices—interferes with our "circadian rhythm" or natural sleep/wake cycle.
Sleep needs vary across ages and are especially impacted by lifestyle and health. To determine how much sleep you need, it's important to assess not only where you fall on the "sleep needs spectrum," but also to examine what lifestyle factors are affecting the quality and quantity of your sleep such as work schedules and stress.
To get the sleep you need, you must look at the big picture.
How Much Sleep Do We Really Need: Revisited
The National Sleep Foundation released the results of a world-class study that took more than two years of research to complete – an update to our most-cited guidelines on how much sleep you really need at each age. You can read the research paper published in Sleep Health .
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Eighteen leading scientists and researchers came together to form the National Sleep Foundation’s expert panel tasked with updating the official recommendations. The panelists included six sleep specialists and representatives from leading organizations including the American Academy of Pediatrics, American Association of Anatomists, American College of Chest Physicians, American Congress of Obstetricians and Gynecologists, American Geriatrics Society, American Neurological Association, American Physiological Society, American Psychiatric Association, American Thoracic Society, Gerontological Society of America, Human Anatomy and Physiology Society, and Society for Research in Human Development. The panelists participated in a rigorous scientific process that included reviewing over 300 current scientific publications and voting on how much sleep is appropriate throughout the lifespan.
“Millions of individuals trust the National Sleep Foundation for its sleep duration recommendations. As the voice for sleep health it is the NSF’s ||||| One way to have more time for work and play every day is to sleep a little bit less. But eventually, staying awake for longer periods can have a negative impact on the quality of our lives. So where does the break-even point lie, and can it be shifted?
What You Stand To Lose
Few things do your body better than a good night's rest. While many of its molecular and cellular mechanisms remain unresolved, we know that sleep helps us consolidate memories , fight infection and manage stress – all while contributing to the maintenance and repair of just about every tissue in our bodies. Meanwhile, a lack of sleep can affect everything from your performance at work to your performance in bed. Foregoing sleep for extended periods of time has been shown to cause your body's metabolism to go haywire. High blood pressure. Obesity. Heart disease. Diabetes. They're all tied to a lack of sleep and crummy sleep habits – what researchers refer to as poor sleep hygiene. "Sleep services all aspects of our body in one way or another: molecular, energy balance, as well as intellectual function, alertness and mood," says sleep expert Dr. Merrill Mitler, a neuroscientist at the National Institutes of Health.
One of the most extensive human sleep deprivation studies ever conducted sheds light on what happens when our bodies are deprived of the sleep they need. Researchers led by Hans Van Dongen, professor of sleep and chronobiology in the Department of Psychiatry at the University of Pennsylvania, limited study volunteers to various levels of sleep deprivation for 14 consecutive days (for example, 6 hours in bed per night for two weeks straight). The researchers then compared test participants' cognitive and physiological abilities at the end of this period to those of test participants who had gone one, two, and three nights without sleep.
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Their results showed that restricting sleep to six hours per night caused cognitive performance and reaction times to drop so dramatically, that by the end of the 2-week period, these test participants were performing as poorly as subjects who had forgone sleep entirely for two nights straight.
What little evidence there is for people acclimating to less sleep comes from a 2009 study conducted by scientists at Walter Reed Army Institute of Research. Researchers led by Thomas Balkin, chairman of the National Sleep Foundation, investigated the effects of "sleep banking" by having test subjects spending ten hours in bed every night for a week. When members of this "extended" sleep group were subsequently deprived of sleep, their performance on motor and attentional tasks suffered less than that of participants in the "habitual" sleep group, who had not been allowed to "bank" sleep in advance, but had rather stuck to their normal sleep schedule.
Photo Credit: Davide Cassanello via flickr | CC BY 2.0
It would be inaccurate, however, to say that members of the extended sleep group had conditioned themselves to require less sleep. They still performed worse on the motor and attentional tasks than they would have if they were fully rested. What' more, their dleep-deprived performance was only compared to that of the habitual sleep group for five days. It stands to reason that this performance gap would shrink to zero over time. Consider, also, that the average time in bed for test subjects who were not allowed to "bank" sleep was 7 hours. That's time in bed, not time spent sleeping. Given that sleep experts recommend most adults get between 7 and 8 hours of sleep a night, it's likely that members of the habitual group started the experiment with a handicap, and that that the test subjects who were forced to spend a few extra hours in bed were getting closer to the amount of sleep they actually needed.
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To summarize: Your body must have sleep. Full stop. As of 2014, there is no strong evidence that a person can condition his or her body over time to require less sleep. "The fact is," says Mitler, "when we look at well-rested people, they're operating at a different level than people trying to get by on 1 or 2 hours less nightly sleep."
But What Does Your Body Need?
Of course, what our bodies require and what we give them are two very different things.
An earlier headline for this post read "Can You Condition Your Body To Get By On Less Sleep?" The answer to that question – and it is, in case you missed it, a very different question than the one now posed – is yes.
In point of fact, society has been managing on less and less sleep for years. In 2005, a poll conducted by the National Sleep Foundation concluded that Americans averaged just 6.9 hours of sleep per night. According to the report, that's two hours less than people were sleeping on a nightly basis back in the 19th century; an hour drop per night compared to fifty years ago; and 15—25 minutes less per night since the turn of the century.
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Requirements vary from person to person, so there is, technically speaking, no "right" amount of sleep, but experts say the average adult needs between 7 and 8 hours per night. Babies, 16 hours. Children and teenagers, 10 and 9 hours, respectively.
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That the typical American is sleeping fewer hours than the minimum recommended average would suggest that many of us are already coping regularly with the side-effects of sleep deprivation.
What About People Who Function on Four Hours Per Night?
Margaret Thatcher is said to have averaged about four hours of sleep per night. This means one of two things. 1) The Iron Lady could have been more ferrous still, had she only gotten more sleep, or 2) Thatcher actually owed her political status and leadership style to her indefatigability.
It's impossible to say now, but it could be that Thatcher belonged to what the Wall Street Journal's Melinda Beck referred to in 2011 as "The Sleepless Elite," a small subset of the population – between 1 and 3% – that functions perfectly fine on less than six hours of sleep a night. Investigations conducted by University of California San Francisco researcher Ying-Hui Fu suggest there could be a genetic basis to lower sleep requirements. When a mutated gene called hDEC2, a variation found in the DNA of short sleepers, was replicated in mice, the animals required less sleep overall and needed less rest to recover from bouts of sleep deprivation.
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It is safe to say that most of us are not like Margaret Thatcher when it comes to our achievements or our reputations. It is equally safe to say that most of us are not members of "The Sleepless Elite." More likely is that we're simply not aware of how sleepy we really are.
In the sleep deprivation study led by by Van Dongen, mentioned earlier, test participants who were subjected to consecutive nights of decreased sleep were asked to rate their subjective feelings of sleepiness. Their self-assessments were terrible. While increases in self-rated sleepiness were observed, they were small. After two weeks of sleep deprivation, most volunteers believed themselves to be functioning relatively normally, even though their cognitive and physiological abilities were comparable to those of subjects who had gone days without sleeping whatsoever. |||||
Summary: | – There never seem to be enough hours in the day to take care of what we need to do (and maybe squeeze in an episode of Game of Thrones), and so a reader writing into the New York Times' Ask Well blog poses a question we've all likely pondered: Can we train our bodies to get by on less sleep? Dr. Sigrid Veasey, a sleep professor at U of Penn's Perelman School of Medicine, cuts to the chase: no, not really. Part of this reason is that humans simply need a certain amount of sleep to function properly, per the Sleep Foundation: Last year, the group published a study in Sleep Health that spells out the average amount people need: For most adults, seven to nine hours seems to be the sweet spot. The problem comes, Veasey notes, when sleep deprivation clouds our brains and makes us think we're doing OK after sleeping four hours at a time for weeks on end. "The more you deprive yourself of sleep over long periods of time, the less accurate you are of judging your own sleep perception," she says. And lack of sleep can wreak havoc on more than your perception: It can screw with your metabolism and contribute to a host of medical conditions such as diabetes, high blood pressure, and obesity, per io9. So how do you figure out how much sleep you really need, without being unduly influenced by your foggy, sleep-deprived mind? Go on vacation, advises the Times blog. Once you've spent a few days acclimating to your body's natural, non-deadline-driven rhythms, how many hours you snooze each night in St. Lucia is probably a decent gauge of just the right amount of shut-eye you need back home. (Here, new sleep guidelines just for kids.) | multi_news_1_0_0 |
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CHICAGO (Reuters) - While stroke is common in both men and women, guidelines released on Thursday for the first time address factors such as pregnancy, birth control pills and menopause that put women at particular risk for the deadly condition.
Issued by the American Heart Association and the American Stroke Association, the guidelines are designed to help doctors and patients recognize stroke risk factors early, when there is time to act.
"If you are a woman, you share many of the same risk factors for stroke with men, but your risk is also influenced by hormones, reproductive health, pregnancy, childbirth and other sex-related factors," said Dr Cheryl Bushnell, author of the new scientific statement published in the American Heart Association journal Stroke.
According to the report, stroke is the fifth-leading cause of death in men and the third-leading cause of death in women. Shared risk factors for stroke include high blood pressure, high cholesterol and smoking.
But other factors influence stroke risk in women. Many of these involve pregnancy. For example, women with a history of high blood pressure should take extra steps to control it during pregnancy, such as taking low-dose aspirin and possibly a calcium supplement. That helps reduce the risk of preeclampsia, a condition marked by high blood pressure and protein in the urine that can cause stroke during or after delivery and premature birth.
Women who have had preeclampsia have twice the risk of a stroke and four times the risk of high blood pressure later in life. As a result, they should address issues such as smoking, high cholesterol and obesity, which heighten their stroke risk even more.
Likewise, women should be screened for high blood pressure before using birth control pills, because that combination raises stroke risks.
Other risk factors more common in women than men include migraine with aura, atrial fibrillation, diabetes, depression and emotional stress.
These are signs 52-year-old Karen Rastenis from Solon, Ohio, wished she had been aware of a while back. Before her stroke two years ago, Rastenis was a smoker and more than 150 lbs overweight. When she woke up one morning with weakness on her right side, the busy single mother of two teenagers ignored the symptom. Then it kept getting worse.
By the time she went to the hospital a few days later, her blood pressure was dangerously high at 237 over 160. She had already had a stroke in her brain stem and "I was on the verge of having a massive stoke," she said.
Rastenis says she had always been overweight but she did not know she had high blood pressure before the stroke.
Still, there had been warning signs. She had had migraines with aura from the start of puberty until she had her first child. During that pregnancy, she also had preeclampsia.
Since her stroke, Rastenis has taken several steps to prevent another. She has quit smoking and had weight loss surgery. She has already lost 60 lbs.
Still, she wishes she had known about the risks earlier.
"It's about time that they looked at the differences in stroke between males and females," she said. "We've known that a woman's heart attack will present differently than a man's. It seems to follow that the same is true of stroke."
Dr Shazam Hussain, stroke section head at the Cleveland Clinic in Ohio, who was not involved in the study, said the guidelines were long overdue.
"Certainly, there is something in common between men and women in terms of stroke risk factors. It's also been recognized there are differences," he said, noting that women tend to do worse after a stroke and are also more likely to die from stroke than men.
"I think recognizing that, putting that on the table as a group that needs more focus when we do studies and when we care for women is very important," he said.
(Reporting by Julie Steenhuysen; editing by Gunna Dickson) ||||| The American Heart Association has released new guidelines for the unique risks women face for stroke. (American Heart Association/The Washington Post)
The American Heart Association has released new guidelines for the unique risks women face for stroke. (American Heart Association/The Washington Post)
Women of all ages should pay more attention to the risk of stroke than the average man, watching their blood pressure carefully before they think about taking birth-control pills or getting pregnant, according to a new set of prevention guidelines released Thursday.
Women are also more likely to have risk factors associated with stroke, such as migraines, depression, diabetes and the abnormal heart rhythm known as atrial fibrillation.
The guidelines from the American Heart Association and American Stroke Association were the first such recommendations aimed at preventing strokes in women. Stroke is the fourth-leading cause of death for all Americans and a leading cause of disability. It’s the third-leading cause of death for women, after heart disease and cancer.
Women share many of the same risk factors as men for stroke, but they have unique risks that come with pregnancy complications and hormone use, said Cheryl Bushnell, associate professor of neurology at Wake Forest Baptist Medical Center in Winston-Salem, N.C., who led a group of experts that developed the guidelines.
Previous guidelines about cardiovascular prevention in women have included some information about stroke. “But it was buried in there,” said Bushnell, who has been studying the topic for more than a decade. “We wanted to take topics that are really women-specific and emphasize stroke and put it all in one guideline.”
The recommendations, published in the journal Stroke, emphasize the importance of controlling blood pressure, especially in young women. They are aimed at a broader age range than most recommendations.
“We’re talking about being aware of blood pressure before you ever take birth-control medication, being aware of blood pressure before you ever get pregnant,” Bushnell said.
A stroke occurs when the blood supply to the brain is blocked or when a blood vessel in the brain ruptures, causing brain tissue to die.
The signs of stroke in women are similar to those in men, including drooping of the face, sudden numbness or weakness of the arm, and difficulty with speech or trouble understanding. But symptoms in women may be more vague or subtle, Bushnell said. Women are more likely to have a change in their ability to communicate with people, she said.
An estimated 6.8 million people in the United States have had a stroke, including 3.8 million women, according to the American Heart Association. Women make up more than half of the estimated 800,000 people who have a stroke each year.
As women increasingly outlive men, their lifetime risk of stroke becomes higher. Women are also more likely to be living alone as widows when they suffer a stroke, are more likely to be institutionalized and have poorer recovery than men, research shows.
“As the baby-boomer generation ages, more people are at risk for stroke, and women in particular as they enter their 50s, 60s and 70s,” said Alexander Dromerick, a neurology professor at Georgetown University who was not among the experts working on the guidelines.
The new recommendations, he said, raise the visibility of the issue.
“Women are more adversely affected by stroke than men,” according to the guidelines. “Now more than ever, it is critical to identify women at higher risk for stroke and initiate the appropriate prevention strategies.”
In some instances, the recommendations call for common-sense precautions that doctors and consumers should already be taking. These include regular physical activity, moderate alcohol consumption, no smoking, and a diet rich in fruits, vegetables, grains, nuts and olive oil and low in saturated fat.
Other recommendations are more specific :
●Women should be screened for high blood pressure before taking birth-control pills, because the combination raises stroke risks.
●Women with a history of high blood pressure before pregnancy should be considered for low-dose aspirin or calcium supplement therapy, or both, to lower preeclampsia risk.
●Women who have preeclampsia have twice the risk of stroke and a fourfold risk of high blood pressure later in life. Therefore, preeclampsia should be recognized as a risk factor well after pregnancy.
Preeclampsia and eclampsia are blood-pressure disorders during pregnancy that cause major complications, including stroke during or after delivery, premature birth and risk for stroke well after childbearing, in some cases as long as 40 years later. Preeclampsia is characterized by high blood pressure and high protein levels in the urine, and when seizure also occurs, it is called eclampsia, according to the American Heart Association.
The guidelines also recommend that women who have migraine headaches with aura — such as blinking lights or moving dots — stop smoking to avoid higher stroke risks. Women are four times more likely to have migraines than men, research shows. Women over age 75 should also be screened for atrial fibrillation.
One recommendation that could be controversial is treating pregnant women with moderately high blood pressure (150 to 159 over 100 to 109 millimeters of mercury) with blood pressure medication. That goes against a recommendation by the American Congress of Obstetricians and Gynecologists, Bushnell said.
“We are going out on a limb,” she said. “We don’t want women to develop severe blood pressure, and that has to be weighed with risks for the mom and the baby.”
James Roberts, who chaired the American Congress of Obstetricians and Gynecologists task force on hypertension in pregnancy, said the obstetrician group suggests that in general, women with moderately high blood pressure should not receive blood pressure medication. But, he added, “there might be situations where that might be appropriate for individuals.” ||||| | – Women need to be more vigilant about their stroke risk than their male counterparts, say new guidelines—the first geared specifically to the fairer sex. While both sexes share many risk factors (think high blood pressure, obesity, and smoking), women have an additional set all their own. Pregnancy, childbirth, and hormones from birth control pills or post-menopausal therapy boost the risk of stroke, the No. 3 killer of women, say the guidelines from the American Heart Association and American Stroke Association, per Reuters and the Washington Post. A few standout guidelines? Women should track and work to control their blood pressure from an early age via a healthy diet. "We're talking about being aware of blood pressure before you ever take birth-control medication, being aware of blood pressure before you ever get pregnant," says guidelines author Cheryl Bushnell. That's because combining high blood pressure with birth-control pills ups stroke risk; those with high blood pressure who become pregnant can suffer from preeclampsia, which can lead to stroke during or following delivery. Such pregnant women may want to take low-dose aspirin or calcium supplement therapy to reduce their risk of preeclampsia. More controversially, the guidelines recommend administering blood pressure medication to pregnant women with just moderately high blood pressure; the American Congress of Obstetricians and Gynecologists disagrees. "We are going out on a limb," says Bushnell. "We don't want women to develop severe blood pressure." | multi_news_1_0_0 |
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– This year's first Nobel Prize has been announced, and the award in medicine goes to a pair of Americans and a German. James Rothman of Yale, Randy Schekman of UC Berkeley, and Thomas Suedhof of Stanford won the prize for their work on cells' internal transportation, or "vesicle traffic," the AP reports. The group helped explain how "cargo is delivered to the right place at the right time," the Nobel committee said. "Through their discoveries, Rothman, Schekman, and Suedhof have revealed the exquisitely precise control system for the transport and delivery of cellular cargo," the committee noted, per Reuters. "Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes, and immunological disorders." The $1.2 million prize precedes upcoming announcements for Nobels in physics, chemistry, literature, peace, and economics, the AP notes. The Nobel committee explains more about the trio's findings here.
Expand this summary. | The Nobel Prize in Physiology or Medicine 2013
James E. Rothman, Randy W. Schekman, Thomas C. Südhof Share this:
English Swedish
Press Release
2013-10-07
The Nobel Assembly at Karolinska Institutet has today decided to award
The 2013 Nobel Prize in Physiology or Medicine
jointly to
James E. Rothman, Randy W. Schekman
and Thomas C. Südhof
for their discoveries of machinery regulating vesicle traffic,
a major transport system in our cells
Summary
The 2013 Nobel Prize honours three scientists who have solved the mystery of how the cell organizes its transport system. Each cell is a factory that produces and exports molecules. For instance, insulin is manufactured and released into the blood and signaling molecules called neurotransmitters are sent from one nerve cell to another. These molecules are transported around the cell in small packages called vesicles. The three Nobel Laureates have discovered the molecular principles that govern how this cargo is delivered to the right place at the right time in the cell.
Randy Schekman discovered a set of genes that were required for vesicle traffic. James Rothman unravelled protein machinery that allows vesicles to fuse with their targets to permit transfer of cargo. Thomas Südhof revealed how signals instruct vesicles to release their cargo with precision.
Through their discoveries, Rothman, Schekman and Südhof have revealed the exquisitely precise control system for the transport and delivery of cellular cargo. Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes, and immunological disorders.
How cargo is transported in the cell
In a large and busy port, systems are required to ensure that the correct cargo is shipped to the correct destination at the right time. The cell, with its different compartments called organelles, faces a similar problem: cells produce molecules such as hormones, neurotransmitters, cytokines and enzymes that have to be delivered to other places inside the cell, or exported out of the cell, at exactly the right moment. Timing and location are everything. Miniature bubble-like vesicles, surrounded by membranes, shuttle the cargo between organelles or fuse with the outer membrane of the cell and release their cargo to the outside. This is of major importance, as it triggers nerve activation in the case of transmitter substances, or controls metabolism in the case of hormones. How do these vesicles know where and when to deliver their cargo?
Traffic congestion reveals genetic controllers
Randy Schekman was fascinated by how the cell organizes its transport system and in the 1970s decided to study its genetic basis by using yeast as a model system. In a genetic screen, he identified yeast cells with defective transport machinery, giving rise to a situation resembling a poorly planned public transport system. Vesicles piled up in certain parts of the cell. He found that the cause of this congestion was genetic and went on to identify the mutated genes. Schekman identified three classes of genes that control different facets of the cell´s transport system, thereby providing new insights into the tightly regulated machinery that mediates vesicle transport in the cell.
Docking with precision
James Rothman was also intrigued by the nature of the cell´s transport system. When studying vesicle transport in mammalian cells in the 1980s and 1990s, Rothman discovered that a protein complex enables vesicles to dock and fuse with their target membranes. In the fusion process, proteins on the vesicles and target membranes bind to each other like the two sides of a zipper. The fact that there are many such proteins and that they bind only in specific combinations ensures that cargo is delivered to a precise location. The same principle operates inside the cell and when a vesicle binds to the cell´s outer membrane to release its contents.
It turned out that some of the genes Schekman had discovered in yeast coded for proteins corresponding to those Rothman identified in mammals, revealing an ancient evolutionary origin of the transport system. Collectively, they mapped critical components of the cell´s transport machinery.
Timing is everything
Thomas Südhof was interested in how nerve cells communicate with one another in the brain. The signalling molecules, neurotransmitters, are released from vesicles that fuse with the outer membrane of nerve cells by using the machinery discovered by Rothman and Schekman. But these vesicles are only allowed to release their contents when the nerve cell signals to its neighbours. How is this release controlled in such a precise manner? Calcium ions were known to be involved in this process and in the 1990s, Südhof searched for calcium sensitive proteins in nerve cells. He identified molecular machinery that responds to an influx of calcium ions and directs neighbour proteins rapidly to bind vesicles to the outer membrane of the nerve cell. The zipper opens up and signal substances are released. Südhof´s discovery explained how temporal precision is achieved and how vesicles´ contents can be released on command.
Vesicle transport gives insight into disease processes
The three Nobel Laureates have discovered a fundamental process in cell physiology. These discoveries have had a major impact on our understanding of how cargo is delivered with timing and precision within and outside the cell. Vesicle transport and fusion operate, with the same general principles, in organisms as different as yeast and man. The system is critical for a variety of physiological processes in which vesicle fusion must be controlled, ranging from signalling in the brain to release of hormones and immune cytokines. Defective vesicle transport occurs in a variety of diseases including a number of neurological and immunological disorders, as well as in diabetes. Without this wonderfully precise organization, the cell would lapse into chaos.
James E. Rothman was born 1950 in Haverhill, Massachusetts, USA. He received his PhD from Harvard Medical School in 1976, was a postdoctoral fellow at Massachusetts Institute of Technology, and moved in 1978 to Stanford University in California, where he started his research on the vesicles of the cell. Rothman has also worked at Princeton University, Memorial Sloan-Kettering Cancer Institute and Columbia University. In 2008, he joined the faculty of Yale University in New Haven, Connecticut, USA, where he is currently Professor and Chairman in the Department of Cell Biology.
Randy W. Schekman was born 1948 in St Paul, Minnesota, USA, studied at the University of California in Los Angeles and at Stanford University, where he obtained his PhD in 1974 under the supervision of Arthur Kornberg (Nobel Prize 1959) and in the same department that Rothman joined a few years later. In 1976, Schekman joined the faculty of the University of California at Berkeley, where he is currently Professor in the Department of Molecular and Cell biology. Schekman is also an investigator of Howard Hughes Medical Institute.
Thomas C. Südhof was born in 1955 in Göttingen, Germany. He studied at the Georg-August-Universität in Göttingen, where he received an MD in 1982 and a Doctorate in neurochemistry the same year. In 1983, he moved to the University of Texas Southwestern Medical Center in Dallas, Texas, USA, as a postdoctoral fellow with Michael Brown and Joseph Goldstein (who shared the 1985 Nobel Prize in Physiology or Medicine). Südhof became an investigator of Howard Hughes Medical Institute in 1991 and was appointed Professor of Molecular and Cellular Physiology at Stanford University in 2008.
Key publications: Novick P, Schekman R: Secretion and cell-surface growth are blocked in a temperature-sensitive mutant of Saccharomyces cerevisiae. Proc Natl Acad Sci USA 1979; 76:1858-1862. Balch WE, Dunphy WG, Braell WA, Rothman JE: Reconstitution of the transport of protein between successive compartments of the Golgi measured by the coupled incorporation of N-acetylglucosamine. Cell 1984; 39:405-416. Kaiser CA, Schekman R: Distinct sets of SEC genes govern transport vesicle formation and fusion early in the secretory pathway. Cell 1990; 61:723-733. Perin MS, Fried VA, Mignery GA, Jahn R, Südhof TC: Phospholipid binding by a synaptic vesicle protein homologous to the regulatory region of protein kinase C. Nature 1990; 345:260-263. Sollner T, Whiteheart W, Brunner M, Erdjument-Bromage H, Geromanos S, Tempst P, Rothman JE: SNAP receptor implicated in vesicle targeting and fusion. Nature 1993;
362:318-324. Hata Y, Slaughter CA, Südhof TC: Synaptic vesicle fusion complex contains unc-18 homologue bound to syntaxin. Nature 1993; 366:347-351.
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The Nobel Assembly, consisting of 50 professors at Karolinska Institutet, awards the Nobel Prize in Physiology or Medicine. Its Nobel Committee evaluates the nominations. Since 1901 the Nobel Prize has been awarded to scientists who have made the most important discoveries for the benefit of mankind.
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MLA style: "The 2013 Nobel Prize in Physiology or Medicine - Press Release". Nobelprize.org. Nobel Media AB 2014. Web. 10 Aug 2018. <http://www.nobelprize.org/nobel_prizes/medicine/laureates/2013/press.html>
Recommended: ||||| STOCKHOLM/CHICAGO Three scientists won the Nobel medicine prize on Monday for plotting how cells transfer vital materials such as hormones and brain chemicals to other cells, giving insight into diseases such as Alzheimer's, autism and diabetes.
Americans James Rothman, 62, Randy Schekman, 64, and German-born Thomas Suedhof, 57, separately mapped out one of the body's critical networks in which tiny bubbles known as vesicles enable cells to secrete chemicals such as insulin into the surrounding environment.
This cellular machinery, which has evolved over a billion years, is so sensitive that slight malfunctions in the mechanism can cause serious illness or death.
"Through their discoveries, Rothman, Schekman and Suedhof have revealed the exquisitely precise control system for the transport and delivery of cellular cargo," the Nobel Assembly at Sweden's Karolinska Institute said in a statement when awarding the prize of 8 million crowns ($1.2 million).
Their research on how cells transport material around sheds light on how insulin, which controls blood sugar levels, is made and released into the blood at the right place at the right time. Diabetes and some brain disorders have been attributed at least in part to defects in the vesicle transport systems.
The scientists' work explains an "absolutely essential" component of cell biology that helps scientists understand how the brain or hormone secretion works, said Dr. Jeremy Berg, who for years worked as director of the National Institute of General Medical Sciences, a part of the National Institutes of Health, which underwrote much of the research.
"It's one of the prizes for which there is not a treatment that came out of it directly, but there are probably literally thousands of laboratories around the world whose work would not be taking place the way it is without their work," said Berg, who is director of the Institute for Personalized Medicine at the University of Pittsburgh.
The Nobel committee said the work could help in understanding immuno-deficiency and brain disorders such as autism.
"HOW CELLS WORK"
"Their discoveries could perhaps have clinical implications in psychiatric diseases, but my guess is that they will be more useful for the understanding of how cells work," said Professor Patrik Rorsman of Oxford University.
Schekman, a geneticist, first became interested in how proteins move within cells in 1974. At the University of California, Berkeley, he began working on yeast, a single cell microorganism. Research showed his findings applied equally to human cells.
Among Schekman's research aims is to study whether the accumulation of the protein amyloid in the brains of Alzheimer's disease patients is due to disruption of the vesicle system.
Suedhof, a neuroscientist, has focused particularly on the brain and questions of human thought and perception, emotions and actions determined by signaling between neurons, cells which constitute the foundation of the nervous system.
"My major interest is in trying to understand how neurons in the brain communicate - how these processes get established during development, and how they become impaired in autism and schizophrenia," Suedhof said in an interview.
Suedhof said the work was really about "cell traffic," the ability of cells to move material around.
Medicine is the first of the Nobel prizes awarded each year. Prizes for achievements in science, literature and peace were first awarded in 1901 in accordance with the will of dynamite inventor and businessman Alfred Nobel.
"My first reaction was, `Oh, my god!`" said Schekman, who was woken with the good news. "That was also my second reaction," he added, according to a University of California, Berkeley, statement.
Schekman said in an interview that his work was born out of a desire to understand how it was possible for one cell to talk to the other. He said figuring that out would help deepen understanding of how the brain works, "one of the most important questions in biology today."
Suedhof said while he and his fellow prize winners had worked separately they had met each other "many, many times." They had "argued and sometimes agreed and sometimes disagreed," he said with a laugh.
(This story is refiled to amend sixteenth paragraph to read University of California, Berkeley instead of Berkeley University)
(Reporting by Stockholm Newsroom; Additional reporting by Kate Kelland in London; Editing by Alistair Scrutton, Ralph Boulton and Ross Colvin) ||||| Americans James Rothman and Randy Schekman and German-born researcher Thomas Suedhof won the 2013 Nobel Prize in medicine on Monday for discoveries on how proteins and other materials are transported within cells.
The Nobel committee said their research on "vesicle traffic" _ the transport system of our cells _ helped scientists understand how "cargo is delivered to the right place at the right time" inside cells.
"Disturbances in this system have deleterious effects and contribute to conditions such as neurological diseases, diabetes and immunological disorders," the committee said.
Rothman is a professor at Yale University while Schekman is at the University of California, Berkeley. Suedhof joined Stanford University in 2008.
The medicine prize kicked off this year's Nobel announcements. The awards in physics, chemistry, literature, peace and economics will be announced by other prize juries this week and next. Each prize is worth 8 million Swedish kronor ($1.2 million). ||||| | multi_news_1_0_0 |
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– The amount of weight a mom-to-be gains during pregnancy may have a link to the weight of the child she bears, a new study finds. Gaining either too much or too little weight can both result in a greater chance that child will be obese, LiveScience reports. The research followed 4,145 women and their kids between ages 2 and 5. What they found: Women with a normal body mass index before pregnancy are advised to gain 25 to 35 pounds; those who gained less were 63% more likely to have an overweight or obese kid. Moms in that group who gained more than that recommended amount were 80% more likely to have an overweight or obese kid. Of all women who gained less than the recommended amount of weight, some 19.5% had overweight or obese kids. Of those who gained more, 20.4% had kids in that category; that's compared to 14.5% of kids whose moms gained the recommended amount of weight. Why? "Gaining either too little or too much weight in pregnancy may permanently affect mechanisms that manage energy balance and metabolism in the offspring, such as appetite control and energy expenditure," a researcher says. The weight-gain recommendations came from the Institute of Medicine in Washington, DC, Medical Daily notes. | Like the fabled Goldilocks, a woman’s weight gain during pregnancy may be a matter of striking a middling balance. New research from Kaiser Permanente shows that women who gain too much or too little weight during pregnancy may predispose their children for the future development of obesity.
Published Sunday in the American Journal of Obstetrics and Gynecology, the study is one of the largest to examine the effects of neonatal weight on childhood obesity. Researchers reviewed the electronic health records of more than 4,100 obstetrical patients from diverse racial backgrounds in Northern California.
After reviewing the records of children born to these women by ages 2 and 5, they found a much higher incidence of obesity among children born to mothers who’d gained more than the recommended weight during pregnancy, at 20.4 percent compared to a “normal” rate of 14.5 percent. Conversely, mothers who’d gained less than the recommended weight gave birth to children with a higher chance of developing obesity, at 19.5 percent.
And healthy moms especially should take note. Women of normal body mass index (BMI) who gained less than the recommended amount of weight were 63 percent more likely than others to bear a child who became overweight or obese. Likewise, women with normal BMI who failed to gain the recommended weight during pregnancy were 80 percent more likely to birth a baby who develops a weight problem, senior researcher Monique M. Hedderson said in a news release.
"The stronger association we found among normal weight women who gained too much or too little weight during pregnancy suggests that perhaps weight gain in pregnancy may have an impact on the child that is independent of genetic factors," Hedderson said.
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The womb apparently sets the pace for certain metabolic functions, says study leader Sneha Sridhar. "Gaining either too little or too much weight in pregnancy may permanently affect mechanisms that manage energy balance and metabolism in the offspring, such as appetite control and energy expenditure," she said. "This could potentially have long-term effects on the child's subsequent growth and weight."
The researchers used BMI and pregnancy weight-gain recommendations from the Institute of Medicine, a nonprofit think-tank based in Washington, D.C. For obese women with BMIs of 30 or higher, health experts there recommend neonatal weight gain of 11 to 20 pounds, with 15 to 25 pounds for overweight women. Women who are underweight should gain the most at 28 to 40 pounds.
The researchers also defined childhood obesity at ages 2 and 5 as greater than the 85th percentile of child growth standards from the Centers for Disease Control and Prevention. ||||| About 1 in 4 women now are obese at the time they become pregnant. Credit: Pregnancy photo via Shutterstock
Women who gain either more or less weight than recommended during pregnancy may be more likely to have an overweight child, a new study has found.
Researchers looked at health records of 4,145 women, and the medical records of their children between ages 2 and 5.
They found that among women who had a normal body mass index (BMI) before pregnancy, those who gained less than the recommended amount (of 25 to 35 pounds) were 63 percent more likely to have a child who became overweight or obese, compared with those who gained the recommended amount. [7 Ways Pregnant Women Affect Babies]
Similarly, women with a normal BMI before pregnancy who gained more weight than recommended were 80 percent more likely to have an overweight or obese child, according to the study published today (April 14) in the American Journal of Obstetrics and Gynecology.
"Gaining either too little or too much weight in pregnancy may permanently affect mechanisms that manage energy balance and metabolism in the offspring, such as appetite control and energy expenditure," said study researcher Sneha Sridhar, a public health researcher at Kaiser Permanente division of research in Oakland, Calif.
"This could potentially have long-term effects on the child's subsequent growth and weight," Sridhar said.
Previous studies have shown that gaining too much weight during pregnancy can increase the risk of gestational diabetes for the mother, as well as increase the risk of health problems for the child, such as childhood obesity. But other studies have also shown that gaining too little weight during pregnancy can lead to complications such as preterm birth and small infants.
In the study, the researchers also found that among all women who gained more than the recommended weight during pregnancy, 20.4 percent had children who were overweight or obese, compared with 19.5 percent of women who gained less than the recommended weight and 14.5 percent of women who gained weight within the guidelines.
Women in the study were members of Kaiser Permanente health care plans in Northern California, and were racially diverse. They had completed a health survey between 2007 and 2009 and subsequently had a baby, the researchers said.
As for the children, the researchers considered a child overweight or obese if he or she had a BMI greater than 85 percent of children in their age group, following the Centers for Disease Control and Prevention child growth standards.
Obesity is partly genetic, but the finding that even normal weight women were more likely to have overweight children if they gained too much or too little weight during pregnancy, suggests that weight conditions during pregnancy may affect the child independently of genetic factors, said Monique Hedderson, another researcher on the study.
In fact, the impact of inappropriate weight gain during pregnancy on child's weight appeared to be stronger among normal weight women than among those who were obese or underweight before pregnancy, the researchers said.
According to the Institute of Medicine, the amount of weight that women are recommended to gain during pregnancy depends on their BMI before pregnancy. Obese women who have a BMI of 30 or greater are recommended to gain between 11 and 20 pounds during pregnancy, and overweight women (with a BMI between 25 and 29) are recommended to gain 15 to 25 pounds. Underweight women (with a BMI less than 18.5) are recommended to gain 28 to 40 pounds.
Email Bahar Gholipour or follow her @alterwired. Follow us @LiveScience, Facebook & Google+. Original article on Live Science. ||||| | multi_news_1_0_0 |
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Consumption of sugary drinks may lead to an estimated 184,000 adult deaths each year worldwide, according to research published today in the journal Circulation and previously presented as an abstract at the American Heart Association Council on Epidemiology and Prevention in 2013.
"Many countries in the world have a significant number of deaths occurring from a single dietary factor, sugar-sweetened beverages. It should be a global priority to substantially reduce or eliminate sugar-sweetened beverages from the diet," said Dariush Mozaffarian, M.D., Dr.P.H., senior author of the study and dean of the Friedman School of Nutrition Science & Policy at Tufts University in Boston.
In the first detailed global report on the impact of sugar-sweetened beverages, researchers estimated deaths and disabilities from diabetes, heart disease, and cancers in 2010. In this analysis, sugar sweetened beverages were defined as any sugar-sweetened sodas, fruit drinks, sports/energy drinks, sweetened iced teas, or homemade sugary drinks such as frescas, that contained at least 50 kcal per 8oz serving. 100 percent fruit juice was excluded.
Estimates of consumption were made from 62 dietary surveys including 611,971 individuals conducted between 1980 and 2010 across 51 countries, along with data on national availability of sugar in 187 countries and other information. This allowed capture of geographical, gender and age variation in consumption levels of sugar-sweetened beverages in different populations. Based on meta-analyses of other published evidence on health harms of sugar-sweetened beverages, the investigators calculated the direct impact on diabetes and the obesity-related effects on cardiovascular disease, diabetes and cancer.
In 2010, the researchers estimate that sugar-sweetened beverages consumption may have been responsible for approximately:
• 133,000 deaths from diabetes
• 45,000 deaths from cardiovascular disease
• 6,450 deaths from cancer
"Some population dietary changes, such as increasing fruits and vegetables, can be challenging due to agriculture, costs, storage, and other complexities. This is not complicated. There are no health benefits from sugar-sweetened beverages, and the potential impact of reducing consumption is saving tens of thousands of deaths each year," Mozaffarian said.
The impact of sugar-sweetened beverages varied greatly between populations. At the extremes, the estimated percentage of deaths was less than 1 percent in Japanese over 65 years old, but 30 percent in Mexican adults younger than 45. Of the 20 most populous countries, Mexico had the highest death rate attributable to sugar-sweetened beverages with an estimated 405 deaths per million adults (24,000 total deaths) and the U.S. ranked second with an estimated 125 deaths per million adults (25,000 total deaths).
About 76 percent of the estimated sugar-sweetened beverage-related deaths occurred in low- or middle-income countries.
In nations of the Caribbean and Latin America, such as Mexico, homemade sugary drinks (e.g. frescas) are popular and consumed in addition to commercially prepared sugar-sweetened beverages. "Among the 20 countries with the highest estimated sugar-sweetened beverage-related deaths, at least 8 were in Latin America and the Caribbean, reflecting the high intakes in that region of the world," said Gitanjali Singh, Ph.D., lead author of the study and a research assistant professor at the Friedman School.
Overall, in younger adults, the percent of chronic disease attributed to sugar-sweetened beverages was higher than the percent in older adults. "The health impact of sugar-sweetened beverage intake on the young is important because younger adults form a large sector of the workforce in many countries, so the economic impact of sugar-sweetened beverage-related deaths and disability in this age group can be significant. It also raises concerns about the future. If these young people continue to consume high levels as they age, the effects of high consumption will be compounded by the effects of aging, leading to even higher death and disability rates from heart disease and diabetes than we are seeing now," Singh said. ||||| Sugary drinks cause 184,000 deaths worldwide annually, including 25,000 deaths in the United States, according to a new study.
The finding — a revised estimate of numbers first presented at a scientific meeting in 2013 — represents a tally of deaths from diabetes, heart disease and cancer that scientists say can be directly attributed to the consumption of sweetened sodas, fruit drinks, sports/energy drinks and iced teas.
The numbers imply that sugary drinks can cause as many deaths annually as the flu.
"It should be a global priority to substantially reduce or eliminate sugar-sweetened beverages from the diet," said Dr. Dariush Mozaffarian, senior author of the study and dean of the Friedman School of Nutrition Science and Policy at Tufts University in Massachusetts. [7 Foods You Can Overdose On]
There is evidence that sugary drinks contribute to obesity and that obesity contributes to people's risk of these diseases, Mozaffarian said. Previous studies found that obesity-related diseases cause more than 17 million deaths per year.
For this latest study, led by Gitanjali Singh, an assistant professor at Tufts, researchers attempted to tease out the contribution that sugary drinks make to this global burden of obesity-related deaths. They calculated that there are 133,000 deaths yearly from type 2 diabetes; 45,000 deaths from cardiovascular disease; and 6,450 deaths from cancer.
The study is based on a complex statistical analysis of country-specific dietary habits and causes of death in more than 50 countries, coupled with information on the availability of sugar on the world market. The researchers' definition of sugary drinks included beverages sweetened with cane sugar, beet sugar and high-fructose corn syrup.
"Among the 20 countries with the highest estimated sugar-sweetened beverage-related deaths, at least eight were in Latin America and the Caribbean, reflecting the high intakes in that region of the world," Singh said.
In Mexico, where more than 10 percent of the population has diabetes, approximately 30 percent of the deaths among people under age 45 are due to sugary drinks, the researchers concluded. Mexico had the highest death rate attributable to sugar-sweetened beverages, the researchers said.
Conversely, in Japan, where unsweetened teas are among the most popular beverages, deaths from sugary drinks are negligible.
Americans consume 22.2 teaspoons of added sugar (equal to 355 calories) per day, on average, and sugar-sweetened beverages are the primary source of this sugar, according to the American Heart Association (AHA). The sugars are added to foods and drinks to improve their taste but provide no nutritional benefit, only calories, thus contributing to weight gain and heart disease, the AHA said.
A 12-ounce (355 milliliters) serving of regular soda has about 10 teaspoons of sugar, according to the American Diabetes Association, which recommends that people avoid drinking sugar-sweetened beverages to help prevent diabetes.
The researchers could not prove a direct cause and effect — for example, they cannot say that sugary beverages are the actual, primary cause of these 184,000 deaths on an individual level. Rather, they based their conclusions on national beverage consumption trends, death rates and sugar availability.
The beverage industry remains skeptical of the findings.
"This study does not show that consuming sugar-sweetened beverages causes chronic diseases and the authors themselves acknowledge that they are at best estimating effects of sugar-sweetened beverage consumption," the American Beverage Association, a trade association that represents the U.S. non-alcoholic beverage industry, said in a statement.
Mozaffarian said the connection between sugary drinks and obesity is well established. "They [the industry] have their heads in the sand," Mozaffarian told Live Science.
Follow Christopher Wanjek @wanjek for daily tweets on health and science with a humorous edge. Wanjek is the author of "Food at Work" and "Bad Medicine." His column, Bad Medicine, appears regularly on Live Science. ||||| In a statement, the American Beverage Association, a trade group representing soft drink manufacturers, said the study "does not show that consuming sugar-sweetened beverages causes chronic diseases."
"The authors themselves acknowledge that they are at best estimating effects of sugar-sweetened beverage consumption," said the statement. “America’s beverage companies are doing our part to offer consumers the fact-based information and the beverage options they need to make the right choices for themselves and their families.”
Some might argue that the study doesn’t prove beyond a doubt that soda is causing all those deaths because it’s not a randomized controlled trial.
“You could say that this isn’t perfect, but I think that if the beverage industry says we’re not sure that soda causes obesity, they’re just putting their heads in the sand,” Mozaffarian said. “And we’re not including all the other health impacts, like back pain, gallstones, joint disease, that are caused by obesity.”
The researchers fear that the problem is only going to get worse since these kinds of beverages are more popular with younger people.
Dr. Bruce Lee hopes that the study will heighten awareness.
“People should be looking more carefully at what this consumption is doing,” said Lee, an associate professor of international health and director of the Global Obesity Prevention Center at Johns Hopkins University. “Here you have a beverage where there isn’t anything on the label to suggest any nutritional value. This is an easy target.”
“The study is not a randomized controlled trial, so one can’t be certain that it was the sugar-sweetened beverages causing the deaths,” said Liz Ruder, a professor of nutrition and dietetics at the University of Pittsburgh Medical Center. “But because the authors have employed sophisticated statistical techniques and they have rich food consumption data I believe that these data are likely to be accurate.”
While there is some controversy over sugar substitutes, Mozaffarian would rather see people consuming drinks with artificial sweeteners than with sugar. “You can view it as a bridge to success,” he said.
Mozaffarian is hoping for changes at the governmental level and points to a recently released report showing how much sugar intake has declined in Mexico since the country adopted a sugar tax. “I think that shows that there is a really easy policy lever to pull that raises revenue while solving health problems.”
Back in March of 2013, news media reported on an early version of the study that was presented at that year's American Heart Association Council on Epidemiology and Prevention meeting. |||||
What is a one-paragraph summary of the above article? | – Need that extra push to kick your soda habit? This might be it: Sugary beverages are responsible for more than 184,000 deaths per year around the world, say researchers at Tufts University. Those include soda, fruit drinks, sports and energy drinks, and iced teas, they write in a post at Science Daily. The sugary drinks were linked to 133,000 deaths from type 2 diabetes, 45,000 from cardiovascular disease, and 6,450 from cancer in 2010. (The new total is an upward revision of an estimate presented previously.) Of those, 25,000 deaths were in the US, which equates to 125 deaths per million adults. The only country that fared worse was Mexico, which reported 405 deaths per million adults. In fact, sugary drinks were blamed for 30% of deaths in Mexicans younger than 45. The study—based on national consumption trends, death rates, and sugar availability—finds sugary drinks lead to as many deaths per year as the flu, and study author Dariush Mozaffarian says cutting back should be a "global priority," per LiveScience. It's a no-brainer, he says. "There are no health benefits from sugar-sweetened beverages, and the potential impact of reducing consumption is saving tens of thousands of deaths each year." The beverage industry asserts that "this study does not show that consuming sugar-sweetened beverages causes chronic diseases," but Mozaffarian says industry officials "have their heads in the sand." At this point, he tells NBC News, switching to drinks with artificial sweeteners can be considered "a bridge to success." (Some argue sugar is as bad as tobacco.) | multi_news_1_0_0 |
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Summarize this article:
As Mahmoud Ahmadinejad prepares to speak to the United Nations General Assembly in New York on Wednesday, an electronic billboard in Times Square and subway placards around the city will remind the Iranian president and U.N. delegates of an American who has been missing in Iran for more than five years.
"I'm trying to make the public realize that my husband is the second-longest held hostage in American history," said Christine Levinson, husband of former FBI agent Robert Levinson. "It's been five and a half years since he disappeared on Kish Island and two years since we received a video from his captors . . . and we still have no information about Bob since the day he disappeared."
"This week, with the UN General Assembly in New York," Christine Levinson told ABC News, "we are trying to get the whole world's attention. I am hoping we will finally be able to get him home."
Robert Levinson, a father of seven and grandfather of two, began working as a private detective after leaving the FBI. He disappeared in March 9, 2007 while on a business trip to the Iranian resort island of Kish. U.S. officials believe he is being held by unknown captors in Southwest Asia.
Five months after his disappearance, against the advice of the U.S. government, Christine Levinson and her son traveled to Tehran to conduct their own investigation, but the trip yielded no results.
The Levinson family received a so-called "proof of life" video in late 2010 showing Levinson, who suffers from diabetes and high blood pressure, in deteriorating health. Levinson, who was 62 at the time, addressed Christine as "my beautiful, my loving, my loyal wife" and referred to his 33 years of service to the federal government before pleading for help from U.S. authorities.
Christine Levinson is now appealing directly to Ahmadinejad, who is under the international spotlight as he prefers to give his final speech to the U.N. as Iranian president. He leaves office next year. "In the past he has said that he will investigate and he will have his people investigate," Levinson told CNN. "He has promised to help us. So we need to get him in touch with whoever can help us get the job done and get Bob home."
Pictures of Levinson began appearing on subway placards in Midtown Manhattan last week. The signs, and a Times Square billboard, feature a picture of Levinson next to the word "Missing" and ask United Nations delegates to "encourage the Islamic Republic of Iran to work with the U.S. to bring Bob home."
This year the FBI offered a $1 million reward for information. The case has frustrated investigators, whose diplomatic strategies have failed.
"We ask ourselves how is it possible that someone -- especially someone 6'4? and (then) 225 pounds -- disappears without a trace," reads a statement from the Levinsons on the family's website.
Iranian representatives did not respond immediately to a request for comment.
Click Here for the Blotter Homepage. ||||| Story highlights Ahmadinejad sits down for an interview with CNN's Piers Morgan
During the sometimes contentious conversation, he talks about the Holocaust, Syria
Ahmadinejad also discusses an anti-Islam film and Osama bin Laden
Iran's president is to address the U.N. General Assembly on Wednesday
Iranian President Mahmoud Ahmadinejad made clear what he meant when he said Israel should be "wiped off" the map and touched on everything from the Holocaust to homosexuality in a wide-ranging interview that aired Monday on CNN's "Piers Morgan Tonight."
The president, speaking through a translator, also said what his country would do if attacked by Israel, and he slammed an anti-Islam film that has triggered protests in the Muslim world.
"If a group comes and occupies the United States of America, destroys homes while women and children are in those homes, incarcerate the youth of America, impose five different wars on many neighbors, and always threaten others, what would you do? What would you say? Would you help it? ... Or would you help the people of the United States?" Ahmadinejad asked in response to whether Israel should be "wiped off" the face of the map, as he once said.
"So when we say 'to be wiped,' we say for occupation to be wiped off from this world. For war-seeking to (be) wiped off and eradicated, the killing of women and children to be eradicated. And we propose the way. We propose the path. The path is to recognize the right of the Palestinians to self-governance."
When asked whether he believes in a two-state solution to the Israeli-Palestinian conflict, Ahmadinejad declined to comment.
JUST WATCHED Ahmadinejad: Iran has right to defend itself Replay More Videos ... MUST WATCH Ahmadinejad: Iran has right to defend itself 01:39
JUST WATCHED Ahmadinejad: 'Very close' with Iran Jews Replay More Videos ... MUST WATCH Ahmadinejad: 'Very close' with Iran Jews 01:10
"I cannot express an opinion. That is their prerogative," Ahmadinejad said. "But the people of Palestine must be allowed by everyone, and helped by everyone, to allow them, to give them the right to choose for themselves."
In New York this week to visit the United Nations, Ahmadinejad spoke at a meeting on the rule of law Monday and is scheduled to address the U.N. General Assembly on Wednesday.
U.N. Secretary-General Ban Ki-moon met with the Iranian president over the weekend and warned him of the "potentially harmful consequences of inflammatory rhetoric," according to a U.N. statement.
During his speech Monday, Ahmadinejad accused "some members of the Security Council with veto rights" of having "chosen silence with regard to the nuclear warheads of a fake regime, while at the same time they impede scientific progress of other nations."
Though he didn't name the countries, he was clearly talking about the United States, Israel and his own country.
Some world powers, particularly Western nations, suspect that Iran is seeking to build nuclear weapons. Tehran insists its nuclear program is for peaceful purposes.
When asked by CNN's Morgan what Iran would do if Israel were to attack it, Ahmadinejad said, "Any nation has the right and will indeed defend herself."
"But my question is this: Why should the world be managed in such a way that an individual can allow himself to threaten a rich and deeply rooted historical, ancient country such as Iran? A great country, such as Iran, based on an excuse of his own fabrication. ... Another country can say, 'I am guessing that country B is doing activity X, therefore I will attack that country' ... can this be ... a successful formula for the management of the world?"
Again there, the president was likely referring to Iran's disputed nuclear program.
Asked whether he feared a war or military conflict with Israel was imminent, Ahmadinejad said: "The Zionists are very much, very adventuresome, very much seeking to fabricate things, and I think they see themselves at the end of the line and I do firmly believe that they seek to create new opportunities for themselves and their adventurous behaviors."
Among other topics the president touched on in the interview taped in New York over the weekend were:
Anti-Islam film
Ahmadinejad denounced the film, "Innocence of Muslims," that portrays the Prophet Mohammed as a womanizer, child molester and killer. The online video has led to a wave of global unrest.
"Fundamentally, first of all, any action that is provocative, offends the religious thoughts and feelings of any people, we condemn," he said.
"Likewise, we condemn any type of extremism. Of course, what took place was ugly. Offending the Holy Prophet is quite ugly. This has very little or nothing to do with freedom and freedom of speech. This is the weakness of and the abuse of freedom, and in many places it is a crime. It shouldn't take place, and I do hope the day will come in which politicians will not seek to offend those whom others hold holy," Ahmadinejad said.
"We also believe that this must also be resolved in a humane atmosphere, in a participatory environment, and we do not like anyone losing their lives or being killed for any reason, anywhere in the world."
The privately produced film sparked protests against the United States, where it was made. While most of the demonstrations have been peaceful, some were marred by violence that has left more than two dozen people dead -- among them U.S. Ambassador to Libya Chris Stevens and three other Americans killed in an attack on the consulate in Benghazi, Libya, that reportedly followed a demonstration against the film.
When asked by Morgan whether he thought protesters should stop threatening U.S. staff abroad, Ahmadinejad said he cannot say what other people or nations should do, but that he believes "extremism gives birth to following and subsequent extremists."
Syria
A long-time supporter of embattled Syrian President Bashar al-Assad, Ahmadinejad told CNN's Morgan the crisis in Syria must be resolved through dialogue, and without outside interference.
He condemned the violence, which has left more than 26,000 people dead since March 2011, according to opposition activists.
"We must all say enough of this violence, right now," Ahmadinejad said, adding that he is working to organize a group to bring the two sides together.
"We do believe that freedom, the right to choose, the right to vote, respect and justice is the fundamental right of all people. All people must obtain these rights. No one has the right to restrict a people and nation, but we believe as a friend of nations, we must help the nations around the world to obtain these rights through peaceful paths, though peaceful actions."
The Holocaust
The conversation was contentious at times, particularly when the topic turned to the Nazi Germany extermination of the Jews last century. Ahmadinejad has long questioned the existence of the Holocaust.
"I pass no judgment about historic events. I defend the human freedoms. Whatever event has taken place throughout history, or hasn't taken place, I cannot judge that. Why should I judge that? I say researchers and scholars must be free to conduct research and analysis about any historical event," the Iranian president said.
Homosexuality
"I'm sorry. Let me ask you this. Do you believe that anyone is giving birth through homosexuality? Homosexuality ceases procreation. Who has said that if you like or believe in doing something ugly, and others do not accept your behavior, that they're denying your freedom?" he asked Morgan.
"Proper education must be given ... the education system must be revamped. The political system must be revamped. And these must be also reformed, revamped along the way. But if you, if a group recognizes an ugly behavior or ugly deed as legitimate, you must not expect other countries or other groups to give it the same recognition."
Jews
When asked how he would feel if one of his children dated a Jew, Ahmadinejad replied, "I would have to see who that Jewish man or woman would be. I see love amongst people as completely acceptable. There are many Jews living in Iran with whom we are very close. There are ... some Muslims that marry into Jewish families or marry Christians."
"I -- we have no such problems," he added.
"Of course, I think none of us should represent the whole population of the United States, but we believe that color, religion, native tongue, ethnic background shouldn't create differences or distances between people, nor should it be the sole reason to bring people closer together. It has always been like this."
Osama bin Laden
Ahmadinejad also discussed his reaction to Osama bin Laden's death last year by American Navy Seals under President Barack Obama.
"I would have been happier to see a transparent trial, a formal trial, and find out the root causes of all of the events of the last few years," the Iranian president said. |||||
Summary: | – Mahmoud Ahmadinejad is in town, and the wife of a former FBI agent taken hostage in Iran in 2007 is taking advantage of that fact. The Iranian president "has said that he will investigate and he will have his people investigate," says Christine Levinson, whose husband, Robert, is believed to be held in Southwest Asia. "So we need to get him in touch with whoever can help us get the job done and get Bob home." With the UN General Assembly meeting in New York, Levinson has put up a billboard and subway signs to remind Ahmadinejad and UN delegates of her husband, ABC News reports. "I'm trying to make the public realize that my husband is the second-longest held hostage in American history," she says. Meanwhile, Ahmadinejad—who will address the General Assembly tomorrow—used his visit as an opportunity to sit down with Piers Morgan on CNN last night and revisit his favorite topics, including bashing Israel, denouncing homosexuality, and questioning the existence of the Holocaust, among other things. On the topic of homosexuality: "I'm sorry. Let me ask you this. Do you believe that anyone is giving birth through homosexuality? Homosexuality ceases procreation. Who has said that if you like or believe in doing something ugly, and others do not accept your behavior, that they're denying your freedom?" Ahmadinejad said. "If you, if a group recognizes an ugly behavior or ugly deed as legitimate, you must not expect other countries or other groups to give it the same recognition." Click for more from the interview. | multi_news_1_0_0 |
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Low-Gluten Diet May Be Linked to Diabetes Risk
Researchers in long-term study say avoiding gluten may increase the risk of type 2 diabetes, but other experts say a lack of fiber may be the real culprit.
Does a diet low in gluten increase the risk of type 2 diabetes?
Researchers involved in a new, long-term study think it might, but some dietitians argue the link could actually be due to a low intake of fiber.
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In the observational study commencing in 1984, researchers estimated the daily gluten intake for almost 200,000 participants through food questionnaires completed every two to four years.
The findings were presented today at the American Heart Association's Epidemiology and Prevention / Lifestyle and Cardiometabolic Health 2017 Scientific Sessions.
Read more: Is non-celiac gluten sensitivity a real thing? »
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What researchers discovered
In their study, researchers found that those who ate the most gluten had a lower risk for developing type 2 diabetes in the 30 years of follow-up study.
Participants in the highest 20 percent of gluten consumption had a 13 percent lower risk of developing type 2 diabetes compared with those with the lowest daily gluten consumption (fewer than 4 grams).
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“We wanted to determine if gluten consumption will affect health in people with no apparent medical reasons to avoid gluten,” Geng Zong, PhD, a research fellow in the Department of Nutrition at Harvard University’s T.H. Chan School of Public Health, said in a press release.
“Gluten-free foods often have less dietary fiber and other micronutrients, making them less nutritious, and they also tend to cost more. People without celiac disease may reconsider limiting their gluten intake for chronic disease prevention, especially for diabetes.”
Janelle Smith, MS, dietitian for the Celiac Disease Foundation, says those who are forced to be gluten-free due to celiac disease shouldn’t be concerned by the study.
“Those with celiac disease might worry that they are at an increased risk of type 2 diabetes based on these results. As of now, research does not show that celiac disease is associated with an increased risk of type 2 diabetes, but it is associated with type 1 diabetes,” she told Healthline.
“It is quite possible that it is not reduced gluten, but overall reduced fiber intake that would result in this correlation.”
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Read more: A gluten-free diet may not do you any good »
The fiber connection
Smith is not alone in suggesting a possible link between type 2 diabetes and a low-gluten diet could in fact be due to restricted fiber intake.
Susan Weiner, a registered dietitian and nutritionist, holds a similar view on the research.
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“My initial thought is that people who restricted gluten [also] restricted fiber from whole grains as well in their quest to limit their gluten intake,” Weiner told Healthline.
“Additionally, if they ate cake, crackers, and cookies which were gluten free without looking at carbohydrates or calories, that could have caused an increase in weight associated with an increased risk of type 2 diabetes. The cause is not conclusive, but this seems likely.”
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Following a gluten-free diet composed primarily of processed foods can lead to weight gain and detrimental long-term consequences. Susan Weiner, registered dietitian and nutritionist
Of those who participated in the study, individuals who ate less gluten also tended to eat less cereal fiber, which is considered a protective factor against the development of type 2 diabetes.
Weiner says it is important those who follow a gluten-free diet ensure they are not eating too much processed food.
“When folks go ‘gluten free’ for reasons other than a legitimate reason such as celiac disease or gluten sensitivity, they often purchase processed gluten-free foods such as cookies, crackers, and chips. These foods have low nutritional value, pack on calories, and are low in fiber,” she told Healthline.
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“The health consequences of following a gluten-free diet composed primarily of processed foods can lead to weight gain and detrimental long-term consequences associated with low fiber intake,” she said.
Read more: Pediatricians concerned about increase in gluten-free diets for children »
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Low-gluten diet popularity
Gluten is a type of protein found in wheat and rye that gives bread and baked goods elasticity and a chewy texture.
Only a small percentage of the population cannot eat gluten. About 1 percent must abstain due to celiac disease.
Despite a lack of evidence that reducing consumption of gluten provides long-term health benefits, gluten-free diets have been gaining popularity.
Experts say this isn’t necessarily a good thing.
I hope that the public will begin to realize that ‘gluten-free’ does not equate with ‘healthy.’ Janelle Smith, Celiac Disease Foundation
“The rise of popularity of the gluten-free diet is a double-edged sword for people with a medical necessity for it,” Alice Bast, chief executive officer of the patient advocacy group Beyond Celiac, told Healthline.
“The gluten-free fad has driven the increase in the availability of packaged food options and to some extent raised awareness of celiac disease and gluten sensitivity,” she added. “However, we’ve also seen the gluten-free fad overshadow the fact that it’s the only current treatment for celiac disease … For those of us for whom the gluten-free diet is not an option, it has resulted in our not being taken seriously in situations in which we don’t have 100 percent control over our food and beverages.”
Smith says the findings of the research may prompt those who abstain from gluten for reasons other than celiac disease and sensitivities to think carefully about doing so.
“I hope that the public will begin to realize that ‘gluten-free’ does not equate with ‘healthy,’ and that a healthy gluten-free diet takes planning and consideration,” she said. ||||| Study Highlights:
Diets higher in gluten were associated with a lower risk of developing Type 2 diabetes.
Study participants who ate less gluten tended to eat less cereal fiber, a known protective factor for developing Type 2 diabetes.
Embargoed until 8:30 a.m. PT/11:30 a.m. ET, Thursday, March. 9, 2017
PORTLAND, Oregon, March 9, 2017 — Eating more gluten may be associated with a lower risk of developing Type 2 diabetes, according to research presented at the American Heart Association’s Epidemiology and Prevention / Lifestyle and Cardiometabolic Health 2017 Scientific Sessions.
Gluten, a protein found in wheat, rye and barley, gives bread and other baked goods elasticity during the baking process and a chewy texture in finished products. A small percentage of the population cannot tolerate gluten due to Celiac disease or gluten sensitivity, but gluten-free diets have become popular for people without these conditions, even though there is lack of evidence that reducing gluten consumption provides long-term health benefits.
“We wanted to determine if gluten consumption will affect health in people with no apparent medical reasons to avoid gluten,” said Geng Zong, Ph.D., a research fellow in the Department of Nutrition at Harvard University’s T.H. Chan School of Public Health in Boston, Massachusetts. “Gluten-free foods often have less dietary fiber and other micronutrients, making them less nutritious and they also tend to cost more. People without Celiac disease may reconsider limiting their gluten intake for chronic disease prevention, especially for diabetes.”
Micronutrients are dietary components such as vitamins and minerals.
In this long-term observational study, researchers found that most participants had gluten intake below 12 grams/day, and within this range, those who ate the most gluten had lower Type 2 diabetes risk during thirty years of follow-up. Study participants who ate less gluten also tended to eat less cereal fiber, a known protective factor for Type 2 diabetes development.
After further accounting for the potential effect of cereal fiber, individuals in the highest 20 percent of gluten consumption had a 13 percent lower risk of developing Type 2 diabetes in comparison to those with the lowest daily gluten consumption (approximately fewer than 4 grams).
The researchers estimated daily gluten intake for 199,794 participants in three long-term health studies — 69,276 from the Nurses’ Health Study (NHS), 88,610 from the Nurses’ Health Study II (NHSII) and 41,908 from the Health Professionals Follow-up Study (HPFS) — from food-frequency questionnaires completed by participants every two to four years. The average daily gluten intake in grams was 5.8 g/d for NHS, 6.8 g/d for NHSII, and 7.1 g/d for HPFS, and major dietary sources were pastas, cereals, pizza, muffins, pretzels, and bread.
Over the course of the study, which included 4.24 million person-years of follow-up from 1984-1990 to 2010-2013, 15,947 cases of Type 2 diabetes were confirmed.
Study participants reported their gluten consumption and the study was observational, therefore findings warrant confirmation by other investigations. Also, most of the participants took part in the study before gluten-free diets became popular, so there is no data from gluten abstainers.
Co-authors are Benjamin Lebwohl, M.D., Frank Hu, M.D., Ph.D., Laura Sampson, Lauren Dougherty, Walter Willett, M.D., Dr.P.H., Andrew Chan, M.D., M.P.H., and Qi Sun, M.D., Sc.D.
Author disclosures are on the manuscript.
This study is funded by the National Heart, Lung, and Blood Institute.
Additional Resources:
###
Statements and conclusions of study authors that are presented at American Heart Association scientific meetings are solely those of the study authors and do not necessarily reflect association policy or position. The association makes no representation or warranty as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations and health insurance providers are available at www.heart.org/corporatefunding.
For media inquiries about this news release and AHA spokesperson perspective:
Darcy Spitz: (212) 878-5940; [email protected]
Carrie Thacker: (214) 706-1665; [email protected]
For public inquiries:
(800)-AHA-USA1 (242-8721)
heart.org and strokeassociation.org ||||| March 9 (UPI) -- Researchers from Harvard University found that a low- or gluten-free diet may increase a person's risk for developing type 2 diabetes.
The research findings were presented at the American Heart Association's Epidemiology and Prevention/Lifestyle and Cardiometabolic Health 2017 Scientific Sessions.
Gluten is a protein found in wheat, rye and barley, and gives bread and baked goods their elasticity during the baking process. Celiac disease is a gluten intolerance or gluten sensitivity in people and is linked to type 1 diabetes.
The availability of gluten-free products has increased in recent years, however, many people without Celiac disease are using gluten-free products more and more. Research has shown that reducing gluten consumption in people without Celiac disease provides no long-term health benefits.
"We wanted to determine if gluten consumption will affect health in people with no apparent medical reasons to avoid gluten," Geng Zong, a research fellow in the Department of Nutrition at Harvard University's T.H. Chan School of Public Health, said in a press release. "Gluten-free foods often have less dietary fiber and other micronutrients [vitamins and minerals], making them less nutritious and they also tend to cost more. People without Celiac disease may reconsider limiting their gluten intake for chronic disease prevention, especially for diabetes."
The large cohort study included data from three previous studies consisting of 4.24 million people followed from 1984-90 to 2010-13.
Researchers found most participants had gluten intake below 12 grams per day, and within that range, people who ate the most gluten had lower risk of developing type 2 diabetes during the 30 years of follow-up.
Participants who ate less gluten also tended to eat less cereal fiber, which is a known protective factor for type 2 diabetes.
Researchers found participants in the highest 20 percent of daily gluten consumption had a 13 percent lower risk of developing type 2 diabetes compared to participants with the lowest amount of daily gluten consumption. |||||
What is a one-paragraph summary of the above article? | – Unless you suffer from Celiac disease, you might want to forego the gluten-free products—a new study suggests they may bring a greater risk of type 2 diabetes. Harvard researchers presented their findings at an American Heart Association forum, reports UPI. After studying data from a long-term observational study of 4.24 million people, they found that most participants consumed less than 12 grams of gluten daily. Those who ate low amounts of gluten within that range were more likely to develop type 2 diabetes than at the upper end of the range, say the researchers in a press release. Gluten is a protein in wheat, rye, and barley, and though a small percentage of people cannot tolerate it, gluten-free diets have become popular with a wider range of people. "Gluten-free foods often have less dietary fiber and other micronutrients, making them less nutritious and they also tend to cost more," says one of the researchers. "People without Celiac disease may reconsider limiting their gluten intake for chronic disease prevention, especially for diabetes." The study finds correlation, not causation, but there are already a few theories floating around. One is that the gluten-free versions of foods that are typically made with gluten (cereals, cakes, crackers) often have lots of sugar, and thus attempting to go gluten-free could inadvertently result in a less healthy diet. One thing that could help: A dietitian tells Healthline that those who are on gluten-free diets should take care to make sure they don't eat too many processed foods. (Gluten-free pasta has even more carbs.) | multi_news_1_0_0 |
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News article:
Story highlights "I just feel like God's will will be done," victim's mother tells CNN
Randall Kerrick's attorneys say resubmitting same charge to grand jury illegal
Prosecutors have said first grand jury was not a full panel; defense contests that claim
Officer fatally shot Jonathan Ferrell after woman called 911 to report home invasion
A grand jury has indicted Officer Randall Kerrick of the Charlotte-Mecklenburg Police Department on a charge of voluntary manslaughter in the September 14 shooting death of Jonathan Ferrell, according to a statement from state Attorney General Roy Cooper.
The grand jury heard evidence from the state Bureau of Investigation and the police department.
"With the strength of the evidence in this case, we're not surprised," Charles Monnett, an attorney for Ferrell's family, said about Monday's indictment.
"We're all pleased and happy that the process is beginning now and that there's an end in sight," he said. "It is the first step towards justice."
JUST WATCHED Hear 911 call that led to man's death Replay More Videos ... MUST WATCH Hear 911 call that led to man's death 02:29
Ferrell's mother, Georgia, told CNN that she is prepared to wait as long as it takes for the case to wind its way through the justice system.
"I just feel like God's will will be done," she said.
The Charlotte, North Carolina, officer faced a second grand jury proceeding for the fatal shooting of Ferrell, an ex-college football player who was reportedly seeking assistance after a car accident.
Attorneys for Kerrick had denounced the prosecution's move to resubmit the case as unlawful and filed a motion to block it, but CNN affiliate News 14 Carolina reported the grand jury convened Monday morning
A grand jury last week declined to indict Kerrick . Prosecutors said afterward the grand jury was composed of less than a full panel and vowed to send the case back.
According to a handwritten statement filed with the court, the first grand jury requested that the prosecutor submit a "bill of indictment to a lesser-included or related offense," but the state attorney general said he would resubmit the voluntary manslaughter charge.
Chris Chestnut, another attorney for Ferrell's family, described relatives as "shocked and devastated" by the first grand jury's ruling and said they were concerned a "miscarriage of justice is imminent."
Kerrick's attorneys, however, filed a motion Friday saying that any miscarriage was on the prosecution's part.
Randall Kerrick faces a voluntary manslaughter charge.
North Carolina law states that a grand jury can be made up of 12 to 18 members, the defense attorneys said. Thus, the prosecution's claim that it could go back to the grand jury because fewer than 18 members initially heard Kerrick's case was spurious, the motion said.
There was "nothing irregular or improper" about the grand jury that heard last week's case, the attorneys said in a statement.
The motion further alleged that Cooper's statement to the media -- that "This is not over" -- and his announcement that he would resubmit the case was a "wholly improper and blatant attempt to influence the (second) grand jury."
The defense reiterated its claim that the shooting, "while tragic, was justified under the circumstances presented to Officer Kerrick at the time," according to its statement.
"We have seen news clips and interviews stating the community should be 'outraged' at the return of a No True Bill of Indictment," the statement continued. "Those outraged have simply not heard all of the facts and hasten to a position. The true outrage of this community should be at the Attorney General's complete disregard of the original findings of our first grand jury."
Ferrell's family disagreed and issued a statement saying, "It appears that this motion was filed solely because Randall Kerrick's attorneys feel their client will be indicted once the full Grand Jury properly considers the evidence in this case when it convenes on Monday."
Attorneys for Ferrell's family on January 13 filed a civil lawsuit connected to his death. It targets the city of Charlotte, Mecklenburg County, Charlotte-Mecklenburg Police Chief Rodney Monroe and Kerrick.
Kerrick shot an unarmed Ferrell , a 24-year-old ex-Florida A&M football player, after a woman -- home alone with her 1-year-old child -- called 911 and reported someone was trying to break down her front door.
It was 2:35 a.m., and according to the lawsuit, the woman "does not understand that Jonathon may be injured and is in need of assistance and becomes frightened by his presence on her doorstep at such a late hour. She quickly closes the door, calls 911 for assistance and activates her home security system."
The woman told police Ferrell was "yelling for her to turn her alarm off" but never reported that Ferrell harmed her, made threatening statements, brandished a weapon or stole or vandalized her property, the lawsuit further alleges.
Police were dispatched, and Ferrell walked down the street to seek assistance elsewhere, according to the lawsuit.
Kerrick and two other officers arrived on the scene about 11 minutes after the 911 call, but Kerrick didn't speak with the woman, the lawsuit says. He instead tracked down Ferrell, who "never engages in any conduct which can be objectively reasonably interpreted as aggravated active aggression," according to the lawsuit.
"Defendant Kerrick, in direct violation of written police department regulations, fires 12 high-velocity bullets at Jonathon, striking him 10 times in the chest and arms," the lawsuit continues.
The Charlotte-Mecklenburg Police Department has called the shooting unlawful.
"The evidence revealed that Mr. Ferrell did advance on Officer Kerrick and the investigation showed that the subsequent shooting of Mr. Ferrell was excessive," police said in a statement on September 14, the day of the shooting. "Our investigation has shown that Officer Kerrick did not have a lawful right to discharge his weapon during this encounter."
Kerrick is free on $50,000 bond. His attorneys said in their statement Friday, "The citizens of Mecklenburg County by and through its grand jury have spoken. We pray that if this case is reheard by a second Grand Jury, the same conclusion will be reached -- that there is no probable cause to sustain an indictment for voluntary manslaughter against Officer Kerrick." ||||| Given a second try, a Mecklenburg County grand jury indicted a police officer Monday in connection with the shooting death last fall of an unarmed Charlotte man.
Just before 4 p.m., the voluntary manslaughter indictment of Police Officer Randall Kerrick became public. The officer was arrested Sept. 14 after he shot Jonathan Ferrell 10 times during a predawn confrontation northeast of Charlotte. If convicted, the 28-year-old could spend between three and 11 years in prison.
As news of the grand jury’s decision reached a SouthPark law office, Ferrell’s mother and brother preached patience, faith and divine inevitability.
“God’s will must be done,” Georgia Ferrell, who was up from her home in Tallahassee, Fla., said. “That’s the first thing that popped into my head. God’s will must be done.”
Kerrick’s arrest and indictment mark the first time in more than 30 years that a Charlotte police officer has been charged in connection with an on-duty shooting.
Kerrick’s attorney, George Laughrun, said Monday evening that he has not seen the indictment and would not comment. He said he had delivered the news to Kerrick and his family but would not give details.
The indictment came after Kerrick’s case made a highly unusual second trip to a grand jury, and only because a judge refused to block it. Last week, a Mecklenburg grand jury declined to indict the officer on voluntary manslaughter and asked that a lesser charge be brought to them to consider.
Veteran prosecutors and defense attorneys say a grand jury refusing to indict is extremely rare. For example, the jurors who didn’t indict Kerrick issued “true bills” on all the 276 other cases they heard that day.
In response, Attorney General Roy Cooper announced last week that his prosecutors would resubmit the case to the county’s other sitting grand jury with the same voluntary manslaughter charges.
Kerrick’s defense team went to court Monday morning to block him. They argued that giving prosecutors a second crack at an indictment, coupled with Cooper’s comments about the case and the fact that demonstrators were protesting a block away, compromised their client’s chances at a fair hearing.
“How in the world is that grand jury supposed to go into that courtroom and make a decision when you’ve also got the NAACP outside?” defense attorney Michael Greene asked Superior Court Judge Bob Bell. “How is Randall Kerrick supposed to get a fair trial and due process?”
After the 30-minute debate, Bell said he found no legal basis to stop prosecutors from taking the case to a new grand jury.
This time, Cooper’s team, led by Senior Deputy Attorney General Jim Coman, sent twice as many witnesses to make the case against Kerrick than had testified before the first grand jury the week before. Two came from the State Bureau of Investigation. Two were CMPD detectives, and colleagues of Kerrick.
Twelve votes are required for an indictment. Last week, only 14 jurors were on hand to consider the Kerrick case, meaning that as few as three jurors could block the indictment. Cooper cited those absences as a factor in bringing the case back for a second time.
An attorney general spokeswoman did not respond to questions on whether the witnesses presented new evidence and whether grand jurors had watched video shot from a police car on the night of the shooting.
Charlotte attorney Charles Monnett, who is handling the Ferrell family’s lawsuit against Kerrick, the police department and the city and county, said lines of communication with the prosecutors have improved in recent days and that there was “a good possibility that the grand jury saw the video.”
Monnett earlier had spoken of what he described “as the tremendous sense of relief that the system is headed now in the right direction, that justice may be reached.”
Reasonable force
The indictment sets the stage for a trial on use of force in the city that helped set the national standard for how police are supposed to respond.
The Supreme Court’s landmark 1989 ruling on “objective reasonableness” grew out of a lawsuit on how Charlotte police allegedly mistreated a diabetic black man on West Boulevard five years before.
Police response must be “objectionably reasonable in light of the facts and circumstances confronting them,” Chief Justice William Rehnquist wrote. Among the considerations: “the severity of the crime at issue, whether the suspect poses an immediate threat to the officers or others, and whether he is actively resisting arrest.”
Rehnquist also added this: Would another “reasonable officer” react the same way?
The standard was used in jury instructions in the federal case against Los Angeles police officers who beat Rodney King, and in talk-show debates and online blogs surrounding the shooting death of Trayvon Martin.
As with those cases, Ferrell’s death brought national headlines and has taken on clear racial overtones. Ferrell, a former Florida A&M; football player, was black; Kerrick is white.
Not a ‘complete victory’
Activist John Barnette, who helped organize a Monday morning rally outside the Government Center calling for Kerrick’s indictment, said the grand jury’s decision is not a “complete victory” because the police officer has not been convicted and Ferrell is still dead.
Barnette also criticized a system that he says took almost five months to respond to Ferrell’s death.
Ferrell moved to Charlotte a year before his death from Tallahassee to be with his fiancee. On the night he died, he gathered with friends to drink at a bar, then gave a co-worker a ride home. Ferrell’s autopsy showed his blood-alcohol level was low enough for him to drive.
But Ferrell wrecked his car on his way out of the Bradfield Farms neighborhood. He kicked his way free, apparently losing his cellphone in the process, then walked more than a quarter of a mile to the nearest home. There, police say, he pounded on the front door.
The woman inside called 911, frantically describing how an unknown black man was trying to break into her home.
Kerrick was one of three officers to respond. As he approached the officers, Ferrell ignored their orders to stop, investigators say. One of the other officers fired his Taser but missed. Police say Ferrell then veered into Kerrick, who, with three years on the force, was the least experienced officer on the scene. Kerrick fired 12 shots from close range. He was the only officer to use his gun.
Charlotte police investigations into officer shootings typically last weeks, even months. But Police Chief Rodney Monroe ordered Kerrick’s arrest that same day, accusing the officer of using excessive force.
Laughrun, a former prosecutor, says the video from the police car shows his client acted appropriately.
Last week, when the first grand jury did not indict, Laughrun was declaring victory for Kerrick. Now he must begin preparing for his trial. Laughrun predicts one won’t be held before the end of the year at the earliest.
The fact that prosecutors needed two tries to get what is normally a routine indictment doesn’t necessarily portend a difficult path to a conviction, veteran Charlotte defense attorney James Wyatt said Monday.
But given the nature of the case and the publicity it has received, Wyatt acknowledged that finding an impartial jury could be a long and intense process.
“It will be a very different kind of case because a police officer is a defendant,” said Wyatt, who is not connected to the case. “Jurors are keenly aware of how dangerous a police officer’s job can be and how decisions have to be made on a split-second basis.
“They will have to decide whether the officer’s actions were appropriate or whether he went beyond the bounds of what a well-trained officer should have done.”
Georgia Ferrell and her son Willie say they plan to attend Kerrick’s trial. A week ago, when the grand jury refused to indict the police officer who shot her son, Ferrell asked supporters in Charlotte to keep fighting.
Now she asked for prayer.
“We are going to keep praying, not just for us, but for everyone involved in this case,” she said as she sat near a desk in Monnett’s office that held dozens of photos of her dead son taken over the course of his life.
Asked if that included Kerrick and his family, her eyes flashed.
“Of course, it does,” she said. Staff writers Cleve R. Wootson Jr. and Elisabeth Arriero contributed. |||||
What is a shorter version of the above article? | – A North Carolina police officer who shot an unarmed car crash victim 10 times was indicted yesterday for involuntary manslaughter on a grand jury's second try. Randall Merrick, who faces between three and 11 years in prison if found guilty, is the first Charlotte police officer to be indicted for an on-duty shooting in more than 30 years, reports the Charlotte Observer. A grand jury refused to indict the 28-year-old officer last week, but the case was sent back for a highly unusual second try after prosecutors said that there hadn't been a full panel present for the first attempt. The family of Jonathan Ferrell, who was shot after he crashed his car late at night and walked to a nearby house, where the homeowner called 911, filed a wrongful death lawsuit earlier this month. A lawyer for the family says the evidence is so strong that the indictment is no surprise. "We're all pleased and happy that the process is beginning now and that there's an end in sight," he tells CNN. "It is the first step towards justice." | multi_news_1_0_0 |
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Here is a news article: Excoriating prosecutors for deliberately withholding evidence, a court of appeals has ordered a new trial for Michael Johnson, better known as Tiger Mandingo, who was convicted last year for "recklessly" infecting a person with HIV and exposing or attempting to expose four others to the virus.
The Eastern District Court of Appeals of Missouri ruled on Tuesday that the prosecution rendered Johnson’s trial “fundamentally unfair” when it withheld, until the last minute, recordings of phone conversations Johnson had made from prison.
Johnson is currently serving a 30.5 year sentence and is one of the most highly publicized targets of America’s controversial HIV laws, which make it a crime for HIV-positive people to have sex without first disclosing that they have the virus. BuzzFeed News has written extensively about Johnson’s arrest and trial.
Many prosecutors defend HIV laws as offering just punishment for behavior that can help transmit the virus. But AIDS advocates contend the laws are outdated and harsh. If decades-long sentences ever were appropriate, they say, they aren’t anymore, given the tremendous medical advances in HIV care. Many epidemiologists and AIDS advocates say the laws — which single out HIV — can actually fuel the epidemic by making people afraid to get tested and treated, and by fostering the dangerous belief that only the HIV-positive person is responsible for preventing transmission of the virus.
When Johnson was arrested in 2013, he was a star wrestler at Lindenwood University, where he was also one of the only black students. His trial, held in the nearly all-white town of St. Charles, Missouri, featured a combination of race and sex that was as highly charged as the name he used online and while performing in drag balls: Tiger Mandingo. Prosecutors asked would-be jurors if being gay was a “choice,” and evidence presented to the court included graphic descriptions of Johnson’s “huge” penis — and even images of it.
The trial turned on whether Johnson had told his partners — most of whom were white — that he was HIV-positive. They all said he didn’t, but he insisted that he did. In one of the prison phone recordings, however, Johnson said he was only “pretty sure” he had let his partners know. That statement was crucial, the appeals court noted, because it was “the only evidence in the record of Johnson stating to anyone that he was not certain about whether he disclosed his HIV status to his sexual partners.”
After he was found guilty, Johnson appealed on two grounds: that his trial was unfair because those recordings had been effectively withheld from the defense until the morning the trial began, and that his long sentence was so disproportionate to the crime that it violated the constitutional ban on cruel and unusual punishments.
The appeals court made no ruling on whether the punishment fit the crime. But on the first point, the court was withering, lambasting the prosecution for engaging in “a trial-by-ambush strategy.”
About a year and a half before the trial, Johnson’s attorneys had requested that the prosecution hand over any “written or recorded statement” Johnson had made. Prosecutors are required to comply with such requests, and failing to do so is a serious violation of prosecutorial ethics.
But, the appeals court noted, the prosecution delivered the “tapes at defense counsel’s office on the Friday before the trial while the office was closed for a state holiday.” So Johnson’s attorneys received the voluminous recordings — totaling 24 hours of taped calls — the morning of the trial’s opening day, denying Johnson “a decent opportunity to prepare his case in advance of trial,” the court ruled.
That was no accident, the court found; instead, prosecutors “intentionally withheld the recordings from the defense to gain a strategic advantage.” The court quoted an unnamed prosecutor saying, “If we disclose them to the defense they'll tell their client. And I'm not impugning anyone's integrity, I'd do the same thing: Hey, they're listening to your conversation, shut up. So we don't disclose them until towards the end.” Transcripts of the trial obtained by BuzzFeed News reveal the speaker to be Assistant District Attorney Peter Groenweghe, the lead prosecutor on the case.
Because the prosecution had “purposely withheld the recordings,” the court found that “Johnson was forced to make critical strategic decisions — such as whether to seek to avoid trial by pursuing a plea bargain, whether to waive his right to silence and testify, and what particular defense to raise — without being timely furnished highly prejudicial, properly-requested discovery.”
The court decided to “reverse the judgment of the trial court” and send the case back for a new trial.
A spokesperson for the prosecutor did not respond to requests for comment. According to Johnson’s attorney, public defender Samuel Buffaloe, prosecutors can ask the appeals court to reconsider its decision to order a new trial. If the appeals court denies that request or reaffirms its ruling, prosecutors can appeal to the state’s supreme court. If Tuesday’s ruling stands, Buffaloe said, “Mr. Johnson will be put back in his position before his trial took place,” where he would have the opportunity to be tried from scratch or to pursue a plea bargain.
But for Johnson, nothing will change immediately. According to his lawyer, he will remain in prison until a decision is made if, and when, to have a new trial. Any possibility of a hearing about whether he can be released on bond will wait until that time.
As BuzzFeed News previously reported, Johnson has been in and out of solitary confinement — or “administrative segregation,” as the jail called it — for much of the time in the three years since he was first arrested. One of his closest advocates is Meredith Rowan, with whom Johnson had one of the recorded phone conversations at the heart of the new ruling. Rowan feels “cautiously optimistic,” but said she has been unable to see Johnson in person since he was transferred from the St. Charles County Jail into the Missouri state prison system more than a year ago.
Tony Rothert, legal director for the ACLU of Missouri, which filed an friend-of-the-court brief on Johnson's behalf, was “thrilled” at the news. Still, he is concerned that if the “case returned for a new trial, the problem remains that the prosecution is built on inflaming public fears about those individuals with HIV, gay people, and black men.”
He added, “Based on what we currently know about HIV and what treatment and prevention methods are available, Missouri's criminalization of sex is irrational and serves no purpose but to further stigmatize persons living with HIV.”
And what does Johnson himself think of this news?
Perhaps nothing. As of this writing, neither Rowen nor Akil Patterson, Johnson’s other closest advocate, had spoken to him. Even Johnson’s attorney hadn’t talked to his client yet — meaning Johnson himself may not yet know that he could get another day in court. ||||| Officially, former college wrestler Michael Johnson was on trial for not telling his sexual partners that he had HIV. But inside the courtroom, the man known as Tiger Mandingo was also up against America’s attitudes on race and sexuality.
SAINT CHARLES, Missouri — Michael Johnson was finally getting his day in court. Best known by his screen name, Tiger Mandingo, the black, gay, HIV-positive college wrestler with a chiseled body had been accused of infecting two men with the virus and of “recklessly” exposing four others to it. Under Missouri law, HIV-positive people must tell all their sexual partners that they are infected, even if they practice safe sex. Johnson was accused not merely of keeping his HIV status to himself, but of willfully lying to his partners, telling them he was HIV-negative before engaging in what the prosecutor would call the most “dangerous” form of sex: ejaculating without a condom into the rectums and mouths of his sex partners. As his lawyer tried to negotiate a plea deal, the 23-year-old Johnson rejected the idea, even after a friend visited him in jail and begged him to reconsider, and even though Johnson said he had spent months in solitary confinement, not even allowed to go to church. He was innocent, he said, and had confidence in the American criminal justice system. So on May 11, he was in St. Charles County court, where the judge and the lawyers began to choose the 12 jurors who would decide if he would spend the rest of his life in prison. No one had shown up to support him. His own mother wasn’t there; she would arrive late and leave before his trial ended. His only ally that morning was his public defender, Heather Donovan, a petite white woman in a gray suit, and she stood up in front of the pool of potential jurors and told them that her client was...guilty until proven innocent. Amid groans in the courtroom, the judge, Jon Cunningham, reminded Donovan that she’d meant to say the opposite: that her client was innocent until proven otherwise. Things never got better for Johnson, who has become one of the most highly publicized targets of America’s controversial HIV laws, which make it a crime for HIV-positive people to have sex without first disclosing that they have the virus. When actor Charlie Sheen announced that he is HIV-positive last month, he said that at least two of his sexual partners had been “warned” about his health status. But another of his sex partners came forth to say the actor never told her that he has HIV, potentially opening him up to prosecution under California’s law. Many prosecutors defend HIV laws as offering just punishment for behavior that can help transmit the virus. But critics say the laws unjustly place all responsibility on the person with the virus: While Johnson faced up to life in prison, his partners bore no legal liability, even though they all willingly engaged in unprotected sex acts during casual hookups with “Tiger.”
More fundamentally, AIDS advocates say, the laws are outdated and harsh. If decades-long sentences ever were appropriate, they say, they aren’t anymore, given the tremendous medical advances in HIV care. Indeed, many epidemiologists and AIDS advocates say the laws — which single out HIV — can actually fuel the epidemic by making people afraid to get tested and treated, and by fostering the dangerous belief that only the HIV-positive person is responsible for preventing transmission of the virus. But what propelled Johnson’s case into headlines as far away as Australia was the volatile combination of race and sex epitomized by his own screen name, Tiger Mandingo. Many of Johnson’s sex partners — including four of the men he was charged with exposing to HIV — were white. And almost every news account featured photos that Johnson had posted on social media of his dark-skinned, muscular, and often shirtless torso. That lurid fascination with Johnson’s black body carried over into his trial. Arrested and charged in an overwhelmingly white community where anti-gay beliefs are widespread, the gay, black “Tiger” never stood a chance. Over five days, as a procession of sex partners and medical experts, as well as Johnson himself, testified, what unfolded was a courtroom drama that on the surface pitted an aggressive prosecutor against a hapless public defender, but that in a deeper sense pitted Johnson against America’s deeply entrenched attitudes about race and sexuality.
View this photo on Instagram instagram.com A photo of Michael Johnson posted to his Instagram account.
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Characterized by his sexual partners as being “very large,” “too tight” for condoms, and too big to fit in a mouth “due to his large size,” Johnson/Tiger’s penis was described in unusually graphic and at times almost absurd detail in police reports and later on the stand. It would even be shown to jurors in still images from a sex tape that he and one of his partners made. The soft-spoken former university student had shown up to court in a blue shirt and a bright red tie, but standing trial was his black, ejaculating, HIV-positive penis. The Jury Of the 51 potential jurors, only one appeared to be nonwhite — a female, African-American retired nurse — and all identified as straight. Most looked to be in their fifties or older. During questioning, about half of the would-be jurors said being gay was a “choice.” Only a third agreed that being gay was “not a sin.” No potential juror acknowledged having HIV. All said they believed HIV-positive people who do not tell their sexual partners that they have the virus should be prosecuted. When asked, not a single person said they had any distrust of the police. (The quotations from this trial are from the reporter’s notes. Following directions from the court, BuzzFeed News did not record the proceedings, and the court has declined to make transcripts available.) When the prosecutor, Philip Groenweghe, made arguments from notes, he confidently lifted his eyes from his papers to make eye contact with whomever he was addressing. But much of the time, his arguments were so polished, and he seemed so confident in them, that he spoke eloquently and persuasively without notes. His hands went in and out of his pockets as he emphasized points, and he grabbed his lapels or took his glasses off with dramatic effect. He stalked the courtroom, never asking the judge for permission to approach the bench. He would drop his voice to sound reasonable while addressing jurors, but he sometimes yelled and jabbed his finger at witnesses. Donovan, who appeared many years Groenweghe’s junior, clutched her notes, the papers sometimes shaking. Donovan routinely asked Judge Cunningham for his permission to approach the bench (as did the female prosecutor), and she rarely made eye contact with anyone. When she spoke, she often stammered and stumbled over her words. (Donovan did not respond to requests for comment.) Groenweghe was backed up at all times by another attorney, Jennifer Bartlett, and an omnipresent paralegal, along with a rotating cast of four or five police detectives, assistants, specialists, and a victim’s advocate sitting right behind them in the first bench of the galley. All were dressed in somber business suits. Groenweghe’s boss, Republican St. Charles County Prosecuting Attorney Timothy Lohmar, is a rising attorney from a local political dynasty (the trial took a recess for the funeral of his father, a former judge). Meanwhile, save for an assistant who would come into the courtroom once or twice a day for a few minutes to deliver papers, and who was often dressed in casual jeans and a blouse, public defender Donovan was alone — except for her client, whom she often did not acknowledge, even neglecting to greet him most times he was led into court. Judge Cunningham, who had a soft, lilting voice, presided over the courtroom with a light air. He didn’t interject, and he would often pause in contemplation before overruling or sustaining an objection. But he usually ruled against Donovan. Weeding out whom he didn’t want on his jury, Groenweghe repeatedly asked the kinds of questions (and heard the kinds of answers) about homosexuals one can no longer ask about black people outright. A handful of the younger potential jurors said positive things about gay people, but many used words such as “sick,” “wrong,” and “immoral.” Groenweghe later told BuzzFeed News he was trying to weed out anyone who was anti-gay — but none of the younger potential jurors made it onto the jury. Later, during the actual trial, Groenweghe’s balding head and thick neck would turn almost red as he described the “lifestyle” of homosexuals. When talking about HIV and gay sexual acts, he spat out the words “semen,” “blood,” and “mucus membrane.” (He later said he was being “precise” about medical terminology.) But he spoke relatively evenly for nearly two hours during jury selection, using his time to build the central argument he wanted his eventual jurors to buy — and to screen out potential jurors who might not buy it: Whenever HIV-positive people don’t tell their sexual partners that they’re positive, that’s a crime, even if their partners didn’t ask or were promiscuous. Donovan spoke for only about 10 minutes during jury selection, and brought up prejudice and racism rarely, such as when she asked potential jurors if they would have a problem talking about interracial gay sex acts. When the jury was finally selected, it was made up of four white men, seven white women, and the black retired nurse, all proclaiming to be HIV-negative and straight. A couple of the jurors may have been in their forties, but most appeared to be in their fifties or sixties.
The Accusers Once the trial began, it quickly became clear that the State of Missouri v. Michael L. Johnson was not a case of “he said versus he said,” but of “he said versus they said.” Each of Johnson’s six sex partners called to the stand testified that they asked Johnson before they hooked up if he was “clean” or STD-free, and that he'd assured them he was. But their testimony occasionally contradicted what they had initially told police, sometimes on crucial points. The jury never heard about several of these discrepancies, because Donovan sometimes failed to pounce on them during cross-examination, and when she did, she was often overruled. Even when the accusers’ testimony wasn’t contradictory, it revealed the complicated, murky decision-making that happens in sexual hookups. The sex partners all said the sex was consensual — they willingly engaged in sex that could transmit HIV — yet they often used passive language to describe how it was they’d come to have unprotected sex with Johnson’s “huge” penis on the black sheets of his Lindenwood University dorm room. Dylan King-Lemons, a lithe young blonde man, was the person who first pressed charges against Johnson, prompting the prosecution to search for other alleged victims. And his accusation was one of the most serious: Johnson had not merely exposed him to HIV — Johnson had actually infected him.
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Lemons testified that he began his sexual relationship with Johnson on Jan. 26, 2013, when they were both students at Lindenwood’s suburban campus west of St. Louis. Lemons said he was regularly tested for HIV, always asked his partners if they were HIV-positive, and wanted to use a condom with Johnson. But, he testified, Johnson told him that he was HIV-negative, that the condom was “too tight and too small,” and that “they don’t make condoms in his size.” So, Lemons said, he agreed to have unprotected sex in the “traditional female role” and said that Johnson ejaculated inside his anus. About two weeks later, Lemons testified, he went to Mercy Hospital with severe stomach pains. He was hospitalized twice, for a total of 14 days, according to his testimony and that of his attending physician, Dr. Otha Miles. Lemons was eventually diagnosed with gonorrhea and HIV. The timing of what was said to be Lemons’ “HIV flu,” which can sometimes occur shortly after someone is exposed to the virus, and the fact that they both had gonorrhea formed the circumstantial basis of evidence tying Lemons’ diagnoses to Johnson’s. But no scientific tests, such as genetic fingerprinting of the virus, were performed to determine if Lemons’ strain of HIV was the same as Johnson’s. In his opening statement, Groenweghe said Lemons knew Johnson had to be the one who infected him because he was the only person he’d had sex with in the prior 11 months. On the stand, Lemons also testified that he hadn’t had sex with anyone else in nearly a year — meaning he wouldn’t have had sex with anyone but Johnson from January or February of 2012. But when he first went to police, Lemons said that he “had been able to narrow it down between two people” — Johnson and another sexual partner, a woman — “because of the time frame” his doctor had given him for the date he was likely infected, six months before his hospitalization. His relationship with the woman, he told Detective Stepp, lasted “from May 2012 until the end of November 2012.” He told Stepp that he had had sex with a total of six people in his life and that a state public health officer told him that all of them except Johnson had tested negative for HIV. In the police report, a woman described as Lemons’ “best friend,” who was questioned separately, told Detective Stepp she believed Lemons had been dating a third person, about “8.5-9 months prior” to Lemons getting sick. It could not be determined if this person was one of the five people the state public health officer said had tested negative. According to the police report, the friend said that both the other people Lemons had been seeing were “very promiscuous.”
Lemons declined to comment, as did one of his two other sex partners. The second one could not be reached, and Lemons’ friend did not respond to requests for comment. In her cross-examination, Donovan did not press Lemons on the discrepancies between his testimony and what he initially told the police, nor did she mention his other sexual partners — points that bear on Lemons’ credibility and cut to the very heart of the allegation that Johnson was the person who infected Lemons. (Later, she tried to ask his physician if Lemons had had sex with an “old friend,” but Groenweghe objected, successfully, on grounds that the doctor wouldn’t know who his sexual partners were.) In court, she did not point out that the prosecution offered no scientific evidence that Lemons’ and Johnson’s viral strains matched. In the police report there is a passage in which Lemons seems afraid that the tables will be turned and that he, the accuser, might become the accused. After Lemons finally got out of the hospital, he told Detective Stepp, he met up with Johnson and told him he was HIV-positive. They then had sex again, and again without a condom. Detective Stepp wrote: I asked Lemons if he was forced to have sex and if he thought he was raped. Lemons stated that he was not raped and he doesn’t want [Johnson] to “go down as a rapist.” Lemons proceeded to say, “I don’t think I was raped but I don’t want this to come back on me. I told him I was HIV positive and highly contagious.” Lemons advised that he told [Johnson] that he wasn’t going to fight having sex but it would be very stupid if they did. Lemons advised that he wanted to have sex but he didn’t want to infect [Johnson]. Lemons said several times that he wanted to be clear that he didn’t feel he was raped but he wants me to know he warned [Johnson] of his HIV diagnosis. At trial, Lemons testified that he is now engaged to marry a man who is HIV-negative and that they have never had sex — not even with condoms — out of fear of transmission. Lemons also testified that without health insurance, his hospitalization plunged him $100,000 into debt and that he had to declare bankruptcy. A search by BuzzFeed News of online court databases such as PACER turned up no record of him having filed bankruptcy, and Groenweghe told BuzzFeed News, “I didn’t check bankruptcy records.” Another witness, Andrew Tryon, was a tall, thin, blonde Lindenwood University cheerleader. He and Johnson consensually filmed their sexual encounter, and stills from the video were printed and handed out to to the jury. Groenweghe said they showed Johnson topping Tryon, ejaculating on his back, then using his fingers to feed Tryon what Groenweghe called “HIV-infected semen.” When the jurors looked at the stills, their faces were stoic and impassive. On the stand, Tryon testified that the sexual encounter he’d had with Johnson matched what the tape showed. But in his initial police report, Tryon describes having sex with Johnson on three different occasions, and none matched what the video showed. For example, in cross-examination, Donovan got Tryon to admit he’d first described jacking Johnson off before swallowing his semen, not having Johnson ejaculate on his back, as the video showed.
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Wiry and pale, Charles Pfoutz took the stand. He spoke in a clipped and breathless manner, and the portion of his head not covered by a hat looked shaved. His charges against Johnson were not filed until he’d been in jail for a year and a half, right before the trial. Pfoutz admitted to prosecutor Jennifer Bartlett that he had a previous criminal record, having pleaded guilty to a burglary in November 2009. Pfotuz testified that he’d told Detective Stepp that he got tested regularly for HIV — every other month, he said. Yet he also testified that he’d had unprotected receptive intercourse with “Tiger Mandingo” — at that point he didn’t know Johnson’s real name — the day they met on Jack’d, a gay hookup app similar to Tinder. In her cross-examination of Pfoutz, Donovan had her most effective moment. She lashed Pfoutz to his previous deposition, in which he had said under oath that when he’d first found out he was HIV-positive he’d told medical personnel that he’d been having sex with only one man — and it wasn’t Johnson. Pfoutz said he’d been having sex since 2007 with that man, and that they were monogamous. Donovan’s cadence sped up while parrying with Pfoutz, whose eyes got wider and speech got faster, in one of the only times in the trial in which Donovan looked the person she was addressing in the eye. Pfoutz looked shaken when he left the stand, and the next recess was the only occasion when chatter among court observers revealed any sense that the defense had discredited a witness.
Filip Cukovic, a slim Serbian exchange student, testified that he found Johnson “unusual because he was black,” and there were only white people in his home country. Johnson was charged with exposing him to HIV after having anal intercourse with and without a condom before ejaculating on the side of Cukovic’s head. Detective Stepp wrote that after being with Johnson, Cukovic was “scared to even touch himself.” Christian L. Green, a skinny African-American man, testified in a soft-spoken voice that he bottomed for Johnson, without ever considering using a condom: “After I asked him if he was clean, I didn’t think about it.” Montel Moore, another slim black man, testified that although he bottomed for Johnson without protection, he pushed Johnson off before he could ejaculate inside him. Moore initially told police that he “he did everything opposite that he would normally do” that night, including that he “doesn’t have random sex with strangers, is usually not the receiver of anal sex, doesn’t perform oral sex, and always wears a condom.” According to the police report, Moore also said that while having sex with Johnson, his roommate came home early and walked into the dorm room. Moore further stated that “Tiger” quickly jumped into the bathroom. Moore explained that his roommate is also gay and that they had been involved in a relationship last year. Moore advised he thought he had to deceive his roommate to avoid any drama. Moore explained that he had told his roommate that he had invited “Tiger” over to surprise him with a “three-way.” But the credibility of Johnson’s partners was not on trial — not as to whether they may have exposed themselves to HIV through other sexual encounters, or if they were to be believed about what they were saying about Johnson, and least of all if they bore any responsibility for the sex they consented to. Groenweghe kept the focus on whether or not Johnson told them he had HIV. The Doctors The doctors and medical experts who took the stand provided evidence that clearly hurt Johnson’s case. But when two of them tried to testify that HIV is a manageable disease — that with current therapies a person with the virus can expect to live almost as long as someone without it — Groenweghe objected vociferously. By doing so, he managed to curtail a crucial point: HIV today is nothing like the death sentence it was in 1988, when Missouri passed the law that Johnson was on trial for breaking. Those medical personnel who met and examined Johnson personally — nurse practitioners Marianne Adolf and Kelly Martin, and Missouri Department of Health epidemiologist Frank Lydon — testified that Johnson had indeed tested positive for HIV before he had sex with the six partners, and that he’d been treated for gonorrhea at least three times. They also confirmed that Johnson acknowledged his HIV infection and that he had received HIV counseling several times and been repeatedly told that failing to disclose was a felony. According to a police report, a health department document noted that Johnson was not informing his partners of his sexually transmitted infections. Groenweghe asked Adolf, a plump, middle-aged white woman with thinning straw hair and glasses, to describe how a condom could be blown up like a balloon until it was big enough to fit over someone’s head. This was designed to expose as bogus the excuse Tryon and Lemons said Johnson gave — that he was “too big” or the condoms were “too tight.” But the most damaging testimony came when Martin said Johnson told her he wasn’t sexually active when he clearly was, a lie that prosecutor Groenweghe hammered home. Dr. Otha Miles, an African-American doctor at Mercy Hospital who treated Lemons and testified for the prosecution, called HIV a “terminal” disease. But the defense’s medical witnesses — Dr. David Hardy of UCLA Medical School and Dr. Rupa Patel of Washington University in St. Louis and Barnes-Jewish Hospital — strongly disagreed that HIV is a “terminal” disease when treated properly. Patel testified that most people are afraid of HIV because of stigma and what they learned in the 1980s. But, when treated properly by taking as little as one pill a day, she said, “life expectancy should be normal.” She added that some patients need to see a doctor only every six to twelve months. Among HIV experts, Patel's and Hardy’s views are anything but controversial. A 2013 study estimated that a person in the United States or Canada who contracts HIV at age 20 and gets treatment “is expected to live into their early 70s, a life expectancy approaching that of the general population.” Even if Johnson had transmitted HIV to Lemons, Hardy's and Patel’s expert opinions were that it was the transmission of a treatable disease, and not of a death sentence. But when Patel attempted to compare HIV to other chronic medical conditions — arguing, for example, that HIV can be easier to treat than diabetes — Groenweghe successfully interrupted her arguments by objecting that she was trying to add unsolicited information to a yes-or-no question. Then, during cross-examination, Groenweghe attacked Patel, yelling, “You’re supposed to be a scientist!” Who, he demanded, did she work for: the public defender paying her, or objective science? Groenweghe pointed out that Dr. Patel had not examined Johnson personally and he accused her of not having reviewed all of Johnson’s medical records. Ultimately, he turned his ire on the public defender herself, accusing Donovan of withholding information from her witness. Donovan objected loudly, saying she “resented” Groenweghe’s accusations. Judge Cunningham called the lawyers to the bench. From about 20 feet away, Donovan could be heard crying, telling the judge she was doing the best she could and working with what she had, and that she was being personally attacked by Groenweghe. Her crying got louder as she said, “You are going to need to have a new trial in a few minutes because I am going to be disqualified.” Donovan then stormed out of the courtroom, abandoning an incredulous-looking Dr. Patel on the stand — and leaving Johnson looking bewildered. When Donovan came back in, her eyes still puffy, the bailiff brought her tissues. The judge called a recess for 15 minutes, which stretched to nearly an hour until Donovan returned. The Accused On the last day of testimony, Johnson took the stand in his own defense. His own mother and two of his friends said they didn’t want him to do so. He has learning disabilities and by his own account does not read or write very well. When Donovan asked him how he’d gotten to college, intending for him to explain his athletic scholarship, he answered her literally, saying he’d gotten to Lindenwood University by taking a bus. But he spoke calmly, deliberately, and slowly, testifying that he had disclosed his HIV status to each of his six of his partners prior to having sex and that he remembered doing so with each one. Still, while the jury never got to see how some of Johnson’s accusers contradicted what they said in police reports, the jury saw Johnson appear to contradict himself — on video. Groenweghe played a clip of Johnson being interviewed (without a lawyer present) by Detective Stepp in 2013. Johnson and Stepp, both in the courtroom, silently watched themselves onscreen. In the clip, Detective Stepp hands Johnson a photo and asks who it is. Johnson says he doesn’t know. Groenweghe pounced. The photo showed Lemons. How could Johnson not know when questioned in 2013 who Lemons was — yet on the stand in 2015 remember that he had disclosed to him? He must have been lying then, or lying now, or both. Groenweghe then played an audio tape of Johnson in jail talking with Meredith Mills, who befriended Johnson when he played soccer with her stepson and has remained close to him. On the tape, Johnson said it was difficult to tell her something. The clip was very short and the context unclear, but Groenweghe said the exchange was about how hard it was coming out to Mills as HIV-positive. Mills and Johnson later told BuzzFeed News that he was speaking about coming out as gay. By the time he left the stand, Johnson had admitted he was only “pretty sure” he had disclosed.
The Verdict Groenweghe smiled throughout the last day, his eyes twinkling as he delivered his closing arguments and recapped one piece of evidence against Johnson’s credibility after another: Johnson contradicting himself on video and audio, Detective Stepp’s testimony about how he investigated Johnson, the testimony of the medical personnel who said they explained to Johnson that not disclosing would be a felony several times, and the collective testimony of all six men who said Johnson had told them he was not infected. Groenweghe warned the jurors that they needed to keep the public safe from Johnson — who roamed the world with a “calling card” of “HIV with a tint of gonorrhea mixed in" — by convicting him and locking him up forever. In her closing statement, Donovan repeated that her client had testified that he had told his partners that he was HIV-positive, and she made points she had been unable to get in during her cross-examinations. For the most serious charges of HIV transmission, she highlighted Lemons’ contradictory stories on the stand and in previous statements, and she said he altered the date when he’d had an HIV test — all of which, she said, “bring reasonable doubt into when Mr. Lemons contracted HIV and from whom.” Regarding Pfoutz, she said he didn’t even approach the police until more than a year after he’d said his sole sex partner was someone other than Johnson. That evening, just about two hours after closing arguments were finished, the jurors signaled that they had reached a conclusion. They found Michael Johnson not guilty on all charges involving Pfoutz. But, they found Johnson guilty of recklessly transmitting HIV to Lemons and of exposing or attempting to expose the four other men to HIV. The Jury’s Sentence The following morning, the jury convened to hear evidence and arguments on what sentence they should give Johnson. For the transmission conviction alone, the minimum was 10 years, while the maximum, according to the statute, was “30 years to life.” “What you have seen and heard so far is only the tip of the iceberg,” Groenweghe said in his opening statement. “Now we can tell you more.” Groenweghe went on to say that although the charges were about the six people who’d given testimony, the jury was going to hear about 32 more sex videos made with other sex partners. They would also hear about people who had come forward after news broke about “Tiger Mandingo” but who had declined to press charges against Johnson, including an unnamed married man who, Groenweghe said, didn’t want to press charges because he didn’t want his wife to find out. Christine King-Lemons, the mother of Dylan King-Lemons, testified for the prosecution at sentencing and told the jury to send Johnson away for life in prison. “Dylan’s diagnosis is a life sentence without parole,” she said through tears. “So I ask each of you: Why does Michael Johnson deserve any less?” Mills, whose stepson had played soccer with Johnson, was the only witness to speak on his behalf. Mills described him as a “gentle giant” who had become a member of her family after he’d been befriended her stepson. Johnson, she added, was very good with her young daughter, who has severe emotional needs.
But on cross-examination, Groenweghe asked her why, after Johnson had been arrested and was in jail, she hadn’t instructed him to tell officials whom he had slept with. She said she knew her phone calls were being recorded and might be used against him — as they were. Groenweghe accused her of not caring about the mothers of the other affected young men. Johnson’s mother, Tracy Johnson, did not testify. In his final arguments to the jurors, Groenweghe called Johnson’s accusers “promiscuous.” Hands in his pockets, eyes downcast, he told the members of the jury that these young gay men “have a lifestyle I don't understand, that many of us don't understand.” But, he said that HIV criminalization laws weren’t put on the books by legislators just to protect them, but to protect the public health — including the health of the jurors. Compared with the murder cases he’d tried in his career, Groenweghe said, this one was worse: A murder ended when a gun or knife killed someone, but the AIDS virus that passed through Johnson could still be killing people for years. From the perspective of HIV and its “mindless agenda,” he said, Michael Johnson was the “perfect host,” because he helped the virus spread by having sex “with one young man after another.” HIV could wind up killing someone who had “never heard of Tiger Mandingo and who might not even be gay” — like, he said, the wife of the man who didn’t press charges. While the jury was sequestered to deliberate the sentence, spectators filled the courtroom for one of the only times during the trial. But not present was Mills, who had to return to Indianapolis to care for her children, or even Michael’s mother, who had hitched a ride back to her home in Indiana with Mills. Kimber Mallett — a professor of the class in which Johnson was arrested almost two years before — was the sole person present who knew him and would see what would happen to him. It took the jury about an hour to return with a sentence. As the gallery rose for them to file in for the last time, crying and sniffling were audible from several people in the warm room, including from the forewoman of the jury. When Judge Cunningham read that the jury was condemning Johnson to 30 years in prison for HIV transmission, there was an audible gasp in the chamber. There was absolute silence as he announced an additional 30.5 years of sentencing for three counts of exposure and one attempt to expose to HIV — meaning Johnson could serve 60.5 years in prison if the judge ordered the sentences to be served consecutively. Cunningham scheduled a final sentencing hearing for July, when he’d decide if Johnson would spend three decades or six in prison, and the trial of Tiger Mandingo was adjourned. In a post-trial interview in November, Groenweghe said that the jury’s verdict — not guilty on one count but guilty on the others — “showed that they were fair.” He added, “I think it shows how seriously they took the public health problem.” To think of HIV as anything other than a terminal disease was “awfully foolish,” he said. It could be “managed,” he conceded, but “has no cure.” Groenweghe also dismissed any suggestion of racial bias. His office had reviewed HIV prosecutions in St. Charles County and found that only two of the six defendants, or 33%, were African-Americans — clear evidence, he said, that there was no racial bias. But in Missouri, blacks make up less than 12% of the population — and in St. Charles, less than 5%. The Jailhouse Interview A few days after the trial, Johnson gave an exclusive hourlong interview to BuzzFeed News from behind a glass wall in the St. Charles County jail. Handcuffed, he had difficulty holding the black intercom phone to his ear. Johnson said he’d expected nothing worse than a hung jury. But, he said, the jurors didn’t believe him when he testified that he had told his sexual partners he was infected because “the jury didn’t believe a person would ever be with a person” sexually “who was HIV-positive.” Asked about the video that showed him denying he knew who Lemons was, Johnson said he was trying to remember who the person in the photo was and said that if the “prosecutor would have let the video go on,” it would have shown him eventually identify Lemons.
An email obtained by BuzzFeed News shows Johnson’s lawyer was negotiating a plea deal of 10 years, which Johnson nixed. But he had “no regrets,” he said. “I could have been home sooner with my family, and they’d have loved me to come home,” Johnson said. But “I was never going to take a plea” because “it would have been morally wrong,” he said. “I wasn’t raised to give up because something is hard.” Johnson said he was embarrassed that his family “heard things about my sex life” and about “me being promiscuous.” “No one was meant to see” the sex tapes, he said, and he was mortified that Groenweghe made it seem as if he’d made them with 30 people. Johnson said he made the videos with repeat partners who, like Tryon, agreed to be taped. Johnson said he was still being held in solitary confinement up to 23 hours a day, as he had been for several months. Yet he displayed a steadfast faith in the criminal justice system, along with a belief that he will ultimately be found innocent on appeal. “I couldn’t just let it be because I’m black, and I’m in a place where being gay and HIV-positive is hard, that you shouldn’t still believe that the system works.” Asked about facing 30 years in prison, Johnson said, “I’ve thought a lot about how this is something that could happen to other HIV-positive people. If I didn’t stand up, who would?” “I learned from this trial how wrong it is to criminalize people with HIV. Once you have it, you have it for the rest of your life. You will be looking over your shoulder forever, fearing someone could say, ‘This person didn’t tell me. Lock him up!’” The Final Sentence On July 13, Judge Cunningham ruled that Johnson could serve his sentences concurrently and sentenced him to 30 years in prison. His attorney filed for appeal a few days later, and he has been moved to the Fulton Reception and Diagnostic Center, a Missouri state prison about a two-hour drive west of St. Louis. Lawyers said it’s not clear when Johnson might be eligible for parole. If he serves his full sentence, he would be set free when he is 52 years old — but when released he would still be a registered sex offender. Johnson has no prior criminal record — something his public defender did not highlight for the jury. Still, his sentence is longer than the average sentence for almost every other crime in the state. According to the Missouri Department of Corrections, Johnson’s sentence exceeds the average for physical assault (19.9 years), forcible rape with a weapon (28.2 years), and even second-degree murder (25.2 years).
After the trial, Filip Cukovic, one of Johnson’s sex partners, said that while HIV laws should stay on the books, “Getting 30 years for exposing someone to HIV is just silly.” He added, “It would be better for him if he’d killed someone instead.” Recent prosecutions outside of Missouri involving HIV have resulted in far less severe punishments. In Washington in 2014, a Seattle man charged with transmitting HIV to eight men was was placed under court order and sent to counseling. In California this year, a San Diego man was given six months in jail for lying to his partner about having HIV and ordered to stay off of hookup apps such as Grindr. And in February, judges of the nation’s highest military court, the U.S. Military Court of Appeals, overturned the HIV conviction of an HIV-positive Air Force sergeant because “prosecutors failed to prove that any” of his sexual acts at a swingers’ party “were likely to transmit HIV to his partners.” But in Missouri, two months after Johnson was sentenced, David Lee Mangum of Dexter was sentenced to 30 years for exposing others to HIV. Missouri’s harsh sentences cut against a national trend in medicine, which is moving away from dealing with HIV as a criminal matter. A wide swath of medical authorities — including the American Medical Association, the Association of Nurses of AIDS Care, and even the medical director for corrections medicine for the Saint Louis County Department of Health — believe prosecuting people for not disclosing their HIV status could facilitate an increase in its transmission and harm the public health.
Even Charles Pfoutz, the accuser whose testimony did not lead to a conviction, said he didn’t think Johnson “deserved 30 years” and should have gotten “like in California, six months to a year.” In a phone interview in October, Pfoutz said he initially told the prosecuting attorney, “It's fifty-fifty. I’m responsible, he’s responsible” for his HIV transmission. Which raises a question: Who gave Johnson HIV? Johnson says he “can’t say who.” “There’s always an idea, but I wouldn’t want to say if I don’t know for sure.” If he did, would he want them prosecuted? “No, I wouldn’t wish harm on anyone,” he said, shaking his head slowly behind the thick jail glass. “I wouldn’t want this to happen to anyone.”
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Steven W. Thrasher was named Journalist of the Year 2012 by the National Lesbian and Gay Journalists Association. His work has appeared in the New York Times, the Village Voice, Rolling Stone and Newsweek. Contact Steven Thrasher at [email protected]. Got a confidential tip? Submit it here.
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A summary of this is? | – With HIV no longer a death sentence, decades-old HIV laws and the heavy sentences they carry have become more contentious. A prime and much publicized example was that of Michael L. Johnson, now 25, a Lindenwood University wrestling star at the time of his 2013 arrest who is serving 30.5 years for "recklessly" infecting a male partner with HIV and exposing four others to it. Or, was: On Tuesday, a new trial was ordered for Johnson by a Missouri appeals court, which overturned his conviction after finding the trial court did indeed "abuse its discretion" in airing portions of jailhouse phone calls Johnson made that the defense didn't get access to until the morning of the trial's first day. In Missouri's case, not disclosing your HIV status to a partner, as Johnson's accusers alleged and he denied, can be a felony. The ACLU of Missouri is backing Johnson, and as the St. Louis Post-Dispatch reports, flagged what it (and others) perceive to be problems with the conviction and sentence: that the "law under which he is charged is based on outdated science." Critics of such laws cite significant medical advances and note that while the person with HIV faces legal repercussions, the partner who chose to have unprotected sex does not, reported BuzzFeed last year. BuzzFeed separately reports on what was in those taped calls: Johnson saying his level of confidence that he had alerted his partners to his status was "pretty sure." The court pointed out it was "the only evidence in the record of Johnson stating to anyone that he was not certain," making it "highly prejudicial evidence" that Johnson's defense should have had time to prepare to for. (This woman fights to keep the man who gave her HIV behind bars.) | multi_news_1_0_0 |
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– After suffering 10 deaths from the West Nile virus so far this year, Dallas County has declared a state of emergency, setting the stage for aerial anti-mosquito spraying. The disease is surging in the state, which has seen at least 381 cases this year, compared to just 27 last year; 95% of tested Houston mosquitoes were carrying the virus, the Los Angeles Times reports. "Texas is on track to have the worst year ever for West Nile virus," an official says. The statewide death toll stands at 16. Officials blame a warm winter and wet spring; human and bird activity can also play a role, a CDC epidemiologist says. Though Texas' outbreak is the nation's worst, the state isn't the only one that's suffering: Louisiana and Mississippi have each seen 39 cases, including one death each, while Oklahoma has grappled with 22 cases. "We're probably hitting the peak nationally," notes the epidemiologist. The virus can turn into West Nile fever or a range of other, more threatening diseases—though "less than 1% develop a serious neurologic illness," says a CDC rep, according to CNN. An expert points out that 90% of the victims she has studied took no precautions (like wearing bug spray).
Expand this summary. | Dallas Mayor Mike Rawlings declared Wednesday that the city is facing an emergency as the West Nile virus spreads, killing at least 14 people in Texas and 26 nationwide, according to the Centers for Disease Control and Prevention.
The Dallas declaration clears the way for aerial spraying to kill the infected mosquitos that carry the disease.
The United States is experiencing its biggest spike in West Nile virus since 2004, with 241 cases of the disease reported nationwide this year so far, including four deaths, health officials said last weekend, before the latest totals.
Of the 42 states that have reported infections in people, birds or mosquitoes, 80% of them have been in Texas, Mississippi and Oklahoma, the U.S. Centers for Disease Control and Prevention said in a statement. The CDC listed a breakdown of infections by state.
"It is not clear why we are seeing more activity than in recent years," said Marc Fischer, a CDC medical epidemiologist. "Regardless of the reasons for the increase, people should be aware of the West Nile virus activity in their area and take action to protect themselves and their family."
The virus is transmitted through infected mosquitoes.
In the United States, most infections occur between June and September, and peak in August, according to the CDC.
Symptoms include fever, headache, body aches, joint pains, vomiting, diarrhea or rash.
"Less than 1% develop a serious neurologic illness such as encephalitis or meningitis (inflammation of the brain or surrounding tissues)," the CDC said.
Those at greater risk are people older than 50 and those with conditions such as cancer, diabetes and kidney disease, or with organ transplants.
There are no medications to treat West Nile virus or vaccines to prevent infection. People with milder illnesses typically recover on their own, but those more seriously affected may need hospital care.
Health experts say prevention measures include avoiding mosquito bites, using insect repellant and getting rid of insect breeding sites.
Symptoms of West Nile virus ||||| Mosquito technician Daryl Beckwith looks through the mosquitos at Dallas County Mosquito Lab. Officials are set to meet in Dallas to discuss options for responding to the growing number of West Nile virus cases in north Texas. (Evans Caglage, The Dallas Morning News / Associated Press / )
HOUSTON—Dallas County officials have declared a state of emergency after the West Nile virus infected at least 190 people, killing 10, as the nation’s worst outbreak hits Texas.
An unusually warm winter and rainy spring in the Dallas-Fort Worth area and elsewhere in Texas has provided ideal conditions for breeding mosquitoes, West Nile carriers, officials said.
The emergency declaration in Dallas clears the way for state money and resources to fight the outbreak. In the coming days the county will deploy small planes for aerial insecticide spraying over hard-hit neighborhoods, in addition to ground spraying already underway.
Texans have contracted the highest number of West Nile infections and have suffered more West Nile deaths than any other state in the nation, according to the Centers for Disease Control and Prevention.
Statewide 16 deaths—including the 10 in Dallas County—have been reported so far this year, compared with two in 2011 and seven the year before, according to the Texas Department of State Health Services.
And the virus is spreading at a faster pace this year across the state. As of Monday, 381 West Nile infections had been reported in more than two dozen Texas counties, compared with 27 infections reported statewide last year in a handful of counties.
In Houston alone, about 95% of tested mosquitoes are carrying the virus.
No other state comes close to Texas, according to the CDC. However, neighboring states are also reporting higher infection rates this year: Louisiana and Mississippi each reported 39 West Nile infections and one death. Oklahoma has had 22 infections, but no deaths.
Tarrant County, home to Fort Worth, has reported 171 West Nile infections and two deaths, (compared with two cases last year and no deaths) in what county medical director Dr. Sandra Parker described as “an atypical year.”
“Texas is on track to have the worst year ever for West Nile virus,” Christine Mann, a spokeswoman for the Texas Department of State Health Services, told The Times.
The Lone Star state’s worst West Nile year was 2003, one of the first years the virus was reported to have spread west from Northeastern states. That year, Texas saw 439 West Nile cases and 40 deaths, according to state figures.
Marc Fischer, a CDC medical epidemiologist based in Fort Collins, Colo., told The Times that tracing the roots of West Nile outbreaks is tough.
“It’s a pretty complicated story,” he said, a combination of the right warm, wet weather, mosquitoes, birds (another West Nile carrier) and human behavior.
“Each year we have seasonal outbreaks, and they tend to happen in different places because of those factors,” Fischer said, including recent outbreaks in the Los Angeles area.
Fischer said the CDC expects to release updated state-by-state West Nile surveillance figures Wednesday, and that, “We’re probably hitting the peak nationally.”
“People really should be aware of what they can do to prevent infections—primarily protect themselves from mosquito bites,” he said.
Those infected with West Nile virus may develop West Nile fever, with symptoms such as headache, fatigue, body aches, a skin rash on the trunk of the body and swollen lymph glands. The illness can last a few days to several weeks, according to the CDC.
They may also develop the more serious West Nile encephalitis, meningitis or poliomyelitis, with some of the same symptoms but also neck stiffness, disorientation, tremors, convulsions and muscle weakness that can lead to neurological damage, coma, paralysis and death. The elderly and those with weakened immune systems are most at risk of becoming seriously ill once infected.
Kristy Murray, an infectious disease specialist at Baylor College of Medicine's National School of Tropical Medicine, told The Times that Texas has seen an uptick in West Nile cases every three years, starting in 2003. It’s not clear why, she said, but ecology plays a role—perhaps all the rain in north Texas after a long-lasting drought.
“Up there it’s prime conditions. Three years ago the hot spot was El Paso. You end up having these hot zones where there’s just a lot of transmission going on,” Murray said.
Murray has been studying Texans infected with West Nile since 2003, and found 90% said they had done nothing to protect themselves from mosquitoes carrying the virus.
“People just become complacent,” she said.
West Nile infections appear to have increased in many states compared with recent years, including California.
California had its first reported West Nile death earlier this month, an 88-year-old woman in Kern County, and 18 West Nile infections reported statewide in eight counties, including one in Los Angeles. That’s almost double the number of West Nile infections reported statewide this time last year. California public health officials already expect this year’s West Nile totals to surpass last year, when the state had 159 infections and nine fatalities.
Nationwide, 241 West Nile infections were reported to the CDC as of the end of July, the most cases reported during that period since 2004.
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Sam Sianis, owner of the Billy Goat Tavern and son of the man ejected from Wrigley Field in 1945, acknowledges the crowd along with his goat prior to a playoff game in 1984. (AP Photo)
You’ve heard of the the Cubs’ Curse of the Billy Goat, right? Just to recap, during the 1945 World Series, the owner of Chicago’s Billy Goat Tavern owner was supposedly kicked out of Wrigley Field because of the smell of his pet goat, at which point he cursed the team to never win a title at that ballpark.
Sure enough, the Cubs haven’t so much as been to the World Series since then, and they haven’t won a championship since 1908. However, with this year’s team poised to make a postseason run, some Cubs fans did what they could Tuesday to lift the curse.
These weren’t just ordinary fans, though — they were a group of competitive eaters, including Takeru Kobayashi, famous for dominating the July 4 Nathan’s hot dog-eating contest from 2001 to 2006. And what did these eaters consume?
Why, a goat, of course.
About to watch the Hot Dog Champion Kobayashi break the Billy Goat Curse. #legend pic.twitter.com/5lzaa3JAt9 — Joe Difino (@Joe_Difino8) September 23, 2015
Four guys are about to eat 40 pounds of goat. This is happening. pic.twitter.com/hRKTXCnXI5 — Matt Lindner (@mattlindner) September 23, 2015
And this is what 40 pounds of cooked goat looks like. pic.twitter.com/RWh1GlYlkr — Matt Lindner (@mattlindner) September 23, 2015
The event took place at a Chicago restaurant owned by competitive eaters Pat “Deep Dish” Bertoletti and Tim Brown. They, along with Kobayashi, Kevin “L.A. Beast” Strahle and Bob “Notorious B.O.B.” Shoudt, took down 40 pounds of cooked goat in mere minutes.
Kobayashi with the aftermath. 40 pounds if goat gone in about twelve minutes. That was…disgusting. pic.twitter.com/ACnMgScwxT — Matt Lindner (@mattlindner) September 23, 2015
Only time will tell if the stunt was worth it. Of course, the Cubs first must reach the postseason, or else it was much ado about mutton.
The team, though, is very well-positioned to make the playoffs, with a 10-game lead over its closest competitor (the Giants) for the second wild-card spot. The Cubs have made the postseason six times since 1945, most recently in 2008, but they have only won one playoff series, in 2003.
(H/T The Score) ||||| Eduardo Perez and Keith Law discuss whether Cubs pitcher Jake Arrieta can beat out Dodgers pitcher Zack Greinke for the NL Cy Young Award. (1:53)
CHICAGO -- Jake Arrieta said he didn't feel sharp and that he was a little off Tuesday night.
The National League Cy Young Award candidate still tossed a three-hitter.
Arrieta became the first pitcher in the major leagues to reach 20 victories, Kris Bryant set the Cubs' rookie record for home runs and Chicago inched closer to a playoff berth with a 4-0 win over the Milwaukee Brewers.
Looking loose after manager Joe Maddon entertained the team with a petting zoo in the outfield at Wrigley Field before the game, Arrieta (20-6) struck out 11 for Chicago, whose magic number for making its first postseason in seven years dropped to three.
Editor's Picks Rogers: Cubs pitcher Jake Arrieta's historic season reaches 20 wins Chicago Cubs manager Joe Maddon opted to leave starter Jake Arrieta in for the ninth inning so he could make his 20th victory of the season a complete one.
Stats & Info: Arrieta rolls to 20th win of season Jake Arrieta became the first pitcher in the majors to 20 wins and continues his impressive dominance since the All-Star break.
Tuesday's Top 5: Jake Arrieta is good In his past 18 starts, Jake Arrieta has had 18 quality starts and is 14-1 with a 0.94 ERA. 2 Related
The right-hander retired 14 in a row in one stretch in becoming the first Cubs pitcher to win 20 games since Jon Lieber in 2001.
"I've alluded to it before but it just means that I'm putting my team in positions to win ballgames," Arrieta said. "At the end of the day, that's our goal, is to try and pile on as many as we can especially with where we're at in the season."
Bryant, whose April 17 debut was one of the most anticipated in years, hit a two-run homer in the third off Tyler Cravy (0-8) to give Chicago a 2-0 lead. It was Bryant's 26th long ball, besting Billy Williams' mark set in 1961. Bryant added a run-scoring double in the eighth.
He also relished a curtain call after his third-inning drive.
"That was a special moment for me to get up on the steps and get that recognition," Bryant said. "It was something I'll never forget."
Kyle Schwarber was credited with an RBI double in the fifth when shortstop Jean Segura couldn't catch his high popup to short right field, allowing Dexter Fowler to score.
But Tuesday belonged to Arrieta, who added another accomplishment to a fine season that included a no-hitter Aug. 30 at the Los Angeles Dodgers.
"Jake is good," Maddon deadpanned as he began his postgame news conference. "That was outstanding once again."
By beating Milwaukee, Arrieta became the first Chicago pitcher since Hall of Famer Fergie Jenkins in 1971 to win at least 20 games and strike out at least 200 in a season. He also lowered his ERA to 1.88, giving him a chance to become the Cubs' first qualifying starter with a sub-2.00 ERA since Grover Cleveland Alexander had a 1.91 mark in 1920.
"He's got four good pitches." Brewers manager Craig Counsell said of Arrieta. "How many guys have four good pitches?"
Arrieta also lowered his ERA to 0.86 since the All-Star break, which would be a major league record, and he continued perhaps his best stretch of the season.
"It's hard to say otherwise," Arrieta said. "It's been good. It's been consistent."
Cravy went four innings and allowed two runs and three hits for the Brewers, who lost their 10th in 11.
"At this point in the season, he's pretty much going to capitalize on a miss every time," Cravy said. "(Bryant) got me tonight."
WALKING IT BACK
On Monday, Maddon blamed a Starlin Castro error on the field conditions caused by a recent AC/DC concert at Wrigley Field. A day later, Maddon backtracked.
"I have no problem with the concerts whatsoever," Maddon said. "Big music fan."
Maddon said it was "an attempt at weak humor" Monday.
"I was very flippant," Maddon said.
THE CHASE TO 100
Bryant had three RBIs to reach 98 on the season, giving him a 98-95 lead on Anthony Rizzo.
TRAINER'S ROOM
Brewers: OF Ryan Braun (back) took batting practice but remained out of the lineup. Counsell didn't rule out Braun playing again this season. ... C Jonathan Lucroy (concussion) is getting closer and could see time at first base, but he will not catch for the remainder of the season. ... RHP Jimmy Nelson (head contusion) was placed on the 60-day disabled list, and RHP Michael Blazek (broken right hand) was transferred to the 60-day DL.
Cubs: INF Addison Russell didn't start but Maddon said it was to rest him. He entered as a defensive replacement in the seventh.
UP NEXT
Chicago RHP Kyle Hendricks (7-6, 4.22 ERA) faces Milwaukee RHP Zach Davies (1-2, 6.00). Hendricks has gone 3-0 with a 1.07 ERA in four starts against the Brewers. ||||| The big question as Major League Baseball starts up after the All-Star Game is: Can the Chicago Cubs win the World Series for the first time in 100 years? The Cubs will win if they can break the "Curse of the Billy Goat." What's that? Let's take a look at some Chicago baseball history.
In the very early days of professional baseball, the Cubs were a dynasty. The team was led by such Hall of Fame stars as first baseman Frank Chance and pitcher Mordecai "Three-Finger" Brown (folks called him that because he lost part of his index finger in a farm accident). The Cubs won a record 116 games in 1906 (a record they share with the Seattle Mariners), and they won the World Series in 1907 and 1908.
The Cubs won the National League pennant and appeared in seven more World Series after that but never won the big prize again. The last time the Cubs played in the World Series was 1945, the year of the curse.
The story is that there was a man, William Sianis, who owned a tavern in Chicago. Sianis was known as "Billy Goat" because he kept a goat named Murphy at his tavern. Sianis called his bar and restaurant Billy Goat Tavern.
On Oct. 6, 1945, with the Cubs leading the World Series two games to one, Sianis bought two tickets to Game 4 of the World Series. Sianis showed up at the ballpark with Murphy. The owners of the Cubs would not let Murphy into the game, saying animals were not allowed in the ballpark and besides, the goat smelled. Sianis was angry and supposedly stood outside the park and yelled, "The Cubs ain't gonna win no more!"
I don't believe in curses, but the Cubs lost the series in 1945, and though they have come close a few times, they have never returned to the World Series.
So can the Cubs break the curse? After all, the Red Sox broke the "Curse of the Bambino," the supposed string of bad luck Boston had because it traded Babe Ruth to the New York Yankees, when the Sox won the World Series in 2004 and 2007.
So far this season the Cubs have been terrific, putting together the best record in the National League. The Cubs have a solid everyday lineup including all-stars Geovany Soto at catcher, Aramis Ramirez at third base and Kosuke Fukudome in the outfield. But most important, the Cubs have five very good starting pitchers. So the Cubs should hold off the St. Louis Cardinals and the Milwaukee Brewers and win the tough National League Central Division to make the playoffs.
But to win the World Series, even a good team needs to be a little lucky. And luck is something the Chicago Cubs have not had for a long, long time.
Fred Bowen writes KidsPost's sports opinion column and is an author of sports novels for kids. ||||| "Cubbies" redirects here. For the minor league baseball team formerly known as the Rockford Cubbies, see Dayton Dragons
The Chicago Cubs are an American professional baseball team based in Chicago, Illinois. The Cubs compete in Major League Baseball (MLB) as a member club of the National League (NL) Central division. The team plays its home games at Wrigley Field, located on the city's North Side. The Cubs are one of two major league teams in Chicago; the other, the Chicago White Sox, is a member of the American League (AL) Central division. The Cubs, first known as the White Stockings, were a founding member of the NL in 1876, becoming the Chicago Cubs in 1903.[4]
The Cubs have appeared in a total of eleven World Series. The 1906 Cubs won 116 games, finishing 116–36 and posting a modern-era record winning percentage of .763, before losing the World Series to the Chicago White Sox ("The Hitless Wonders") by four games to two. The Cubs won back-to-back World Series championships in 1907 and 1908, becoming the first major league team to play in three consecutive World Series, and the first to win it twice. Most recently, the Cubs won the 2016 National League Championship Series and 2016 World Series, which ended a 71-year National League pennant drought and a 108-year World Series championship drought,[5] both of which are record droughts in Major League Baseball.[6][7] The 108-year drought was also the longest such occurrence in all major North American sports. Since the start of divisional play in 1969, the Cubs have appeared in the postseason nine times through the 2017 season.[5][8]
The Cubs are known as "the North Siders", a reference to the location of Wrigley Field within the city of Chicago, and in contrast to the White Sox, whose home field (Guaranteed Rate Field) is located on the South Side.
The Cubs have multiple rivalries. There is a divisional rivalry with the St. Louis Cardinals, a newer rivalry with the Milwaukee Brewers and an interleague rivalry with the Chicago White Sox.
History
Early club history
1876–1902: A National League
The 1876 White Stockings won the N.L. championship
The Cubs began playing in 1870 as the Chicago White Stockings, joining the National League (NL) in 1876 as a charter member. Owner William Hulbert signed multiple star players, such as pitcher Albert Spalding and infielders Ross Barnes, Deacon White, and Adrian "Cap" Anson, to join the team prior to the N.L.'s first season. The White Stockings played their home games at West Side Grounds and quickly established themselves as one of the new league's top teams. Spalding won forty-seven games and Barnes led the league in hitting at .429 as Chicago won the first ever National League pennant, which at the time was the game's top prize.
After back-to-back pennants in 1880 and 1881, Hulbert died, and Spalding, who had retired to start Spalding sporting goods, assumed ownership of the club. The White Stockings, with Anson acting as player-manager, captured their third consecutive pennant in 1882, and Anson established himself as the game's first true superstar. In 1885 and '86, after winning N.L. pennants, the White Stockings met the champions of the short-lived American Association in that era's version of a World Series. Both seasons resulted in matchups with the St. Louis Brown Stockings, with the clubs tying in 1885 and with St. Louis winning in 1886. This was the genesis of what would eventually become one of the greatest rivalries in sports. In all, the Anson-led Chicago Base Ball Club won six National League pennants between 1876 and 1886. As a result, Chicago's club nickname transitioned, and by 1890 they had become known as the Chicago Colts,[9] or sometimes "Anson's Colts", referring to Cap's influence within the club. Anson was the first player in history credited with collecting 3,000 career hits. After a disappointing record of 59–73 and a ninth-place finish in 1897, Anson was released by the Cubs as both a player and manager.[10] Due to Anson's absence from the club after 22 years, local newspaper reporters started to refer to the Colts as the "Orphans".[10]
After the 1900 season, the American Base-Ball League formed as a rival professional league, and incidentally the club's old White Stockings nickname (eventually shortened to White Sox) would be adopted by a new American League neighbor to the south.[11]
1902–1920: A Cubs dynasty
The 1906 Cubs won a record 116 of 154 games. They then won back-to-back World Series titles in 1907–08
In 1902, Spalding, who by this time had revamped the roster to boast what would soon be one of the best teams of the early century, sold the club to Jim Hart. The franchise was nicknamed the Cubs by the Chicago Daily News in 1902, although not officially becoming the Chicago Cubs until the 1907 season.[12] During this period, which has become known as baseball's dead-ball era, Cub infielders Joe Tinker, Johnny Evers, and Frank Chance were made famous as a double-play combination by Franklin P. Adams' poem Baseball's Sad Lexicon. The poem first appeared in the July 18, 1910 edition of the New York Evening Mail. Mordecai "Three-Finger" Brown, Jack Taylor, Ed Reulbach, Jack Pfiester, and Orval Overall were several key pitchers for the Cubs during this time period. With Chance acting as player-manager from 1905 to 1912, the Cubs won four pennants and two World Series titles over a five-year span. Although they fell to the "Hitless Wonders" White Sox in the 1906 World Series, the Cubs recorded a record 116 victories and the best winning percentage (.763) in Major League history. With mostly the same roster, Chicago won back-to-back World Series championships in 1907 and 1908, becoming the first Major League club to play three times in the Fall Classic and the first to win it twice. However, the Cubs would not win another World Series until 2016; this remains the longest championship drought in North American professional sports.
1913 Chicago Cubs
The next season, veteran catcher Johnny Kling left the team to become a professional pocket billiards player. Some historians think Kling's absence was significant enough to prevent the Cubs from also winning a third straight title in 1909, as they finished 6 games out of first place.[13] When Kling returned the next year, the Cubs won the pennant again, but lost to the Philadelphia Athletics in the 1910 World Series.
In 1914, advertising executive Albert Lasker obtained a large block of the club's shares and before the 1916 season assumed majority ownership of the franchise. Lasker brought in a wealthy partner, Charles Weeghman, the proprietor of a popular chain of lunch counters who had previously owned the Chicago Whales of the short-lived Federal League. As principal owners, the pair moved the club from the West Side Grounds to the much newer Weeghman Park, which had been constructed for the Whales only two years earlier, where they remain to this day. The Cubs responded by winning a pennant in the war-shortened season of 1918, where they played a part in another team's curse: the Boston Red Sox defeated Grover Cleveland Alexander's Cubs four games to two in the 1918 World Series, Boston's last Series championship until 2004.
Beginning in 1916, Bill Wrigley of chewing-gum fame acquired an increasing quantity of stock in the Cubs. By 1921 he was the majority owner, maintaining that status into the 1930s.
Meanwhile, the year 1919 saw the start of the tenure of Bill Veeck, Sr. as team president. Veeck would hold that post throughout the 1920s and into the 30s. The management team of Wrigley and Veeck came to be known as the "double-Bills."
The Wrigley years (1921–1945)
1929–1938: Every three years
Near the end of the first decade of the double-Bills' guidance, the Cubs won the NL pennant in 1929 and then achieved the unusual feat of winning a pennant every three years, following up the 1929 flag with league titles in 1932, 1935, and 1938. Unfortunately, their success did not extend to the Fall Classic, as they fell to their AL rivals each time. The '32 series against the Yankees featured Babe Ruth's "called shot" at Wrigley Field in game three. There were some historic moments for the Cubs as well; In 1930, Hack Wilson, one of the top home run hitters in the game, had one of the most impressive seasons in MLB history, hitting 56 home runs and establishing the current runs-batted-in record of 191. That 1930 club, which boasted six eventual hall of fame members (Wilson, Gabby Hartnett, Rogers Hornsby, George "High Pockets" Kelly, Kiki Cuyler and manager Joe McCarthy) established the current team batting average record of .309. In 1935 the Cubs claimed the pennant in thrilling fashion, winning a record 21 games in a row in September. The '38 club saw Dizzy Dean lead the team's pitching staff and provided a historic moment when they won a crucial late-season game at Wrigley Field over the Pittsburgh Pirates with a walk-off home run by Gabby Hartnett, which became known in baseball lore as "The Homer in the Gloamin'".[15]
After the "double-Bills" (Wrigley and Veeck) died in 1932 and 1933 respectively, P.K. Wrigley, son of Bill Wrigley, took over as majority owner. He was unable to extend his father's baseball success beyond 1938, and the Cubs slipped into years of mediocrity, although the Wrigley family would retain control of the team until 1981.[16]
1945/The Curse of the Billy Goat
The Cubs enjoyed one more pennant at the close of World War II, finishing 98–56. Due to the wartime travel restrictions, the first three games of the 1945 World Series were played in Detroit, where the Cubs won two games, including a one-hitter by Claude Passeau, and the final four were played at Wrigley. The Cubs lost the series, and did not return until the 2016 World Series. After losing the 1945 World Series to the Detroit Tigers, the Cubs finished with a respectable 82-71 record in the following year, but this was only good enough for third place.
In the following two decades, the Cubs played mostly forgettable baseball, finishing among the worst teams in the National League on an almost annual basis. From 1947 to 1966, they only notched one winning season. Longtime infielder-manager Phil Cavarretta, who had been a key player during the 1945 season, was fired during spring training in 1954 after admitting the team was unlikely to finish above fifth place. Although shortstop Ernie Banks would become one of the star players in the league during the next decade, finding help for him proved a difficult task, as quality players such as Hank Sauer were few and far between. This, combined with poor ownership decisions such as the College of Coaches, and the ill-fated trade of future Hall of Fame member Lou Brock to the Cardinals for pitcher Ernie Broglio (who won only seven games over the next three seasons), hampered on-field performance.
1969: Fall of '69
The late-1960s brought hope of a renaissance, with third baseman Ron Santo, pitcher Ferguson Jenkins, and outfielder Billy Williams joining Banks. After losing a dismal 103 games in 1966, the Cubs brought home consecutive winning records in '67 and '68, marking the first time a Cub team had accomplished that feat in over two decades.
In 1969 the Cubs, managed by Leo Durocher, built a substantial lead in the newly created National League Eastern Division by mid-August. Ken Holtzman pitched a no-hitter on August 19, and the division lead grew to 8 1⁄ 2 games over the St. Louis Cardinals and by 9 1⁄ 2 games over the New York Mets. After the game of September 2, the Cubs record was 84-52 with the Mets in second place at 77-55. But then a losing streak began just as a Mets winning streak was beginning. The Cubs lost the final game of a series at Cincinnati, then came home to play the resurgent Pittsburgh Pirates (who would finish in third place). After losing the first two games by scores of 9-2 and 13-4, the Cubs led going into the ninth inning. A win would be a positive springboard since the Cubs were to play a crucial series with the Mets the next day. But Willie Stargell drilled a two-out, two-strike pitch from the Cubs' ace reliever, Phil Regan, onto Sheffield Avenue to tie the score in the top of the ninth. The Cubs would lose 7-5 in extra innings.[6] Burdened by a four-game losing streak, the Cubs traveled to Shea Stadium for a short two-game set. The Mets won both games, and the Cubs left New York with a record of 84-58 just 1⁄2 game in front. More of the same followed in Philadelphia, as a 99 loss Phillies team nonetheless defeated the Cubs twice, to extend Chicago's losing streak to eight games. In a key play in the second game, on September 11, Cubs starter Dick Selma threw a surprise pickoff attempt to third baseman Ron Santo, who was nowhere near the bag or the ball. Selma's throwing error opened the gates to a Phillies rally. After that second Philly loss, the Cubs were 84-60 and the Mets had pulled ahead at 85-57. The Mets would not look back. The Cubs' eight-game losing streak finally ended the next day in St. Louis, but the Mets were in the midst of a ten-game winning streak, and the Cubs, wilting from team fatigue, generally deteriorated in all phases of the game.[1] The Mets (who had lost a record 120 games 7 years earlier), would go on to win the World Series. The Cubs, despite a respectable 92-70 record, would be remembered for having lost a remarkable 17½ games in the standings to the Mets in the last quarter of the season.
1977–1979: June Swoon
Following the 1969 season, the club posted winning records for the next few seasons, but no playoff action. After the core players of those teams started to move on, the 70s got worse for the team, and they became known as "the Loveable Losers." In 1977, the team found some life, but ultimately experienced one of its biggest collapses. The Cubs hit a high-water mark on June 28 at 47–22, boasting an 8 1⁄ 2 game NL East lead, as they were led by Bobby Murcer (27 HR/89 RBI), and Rick Reuschel (20–10). However, the Philadelphia Phillies cut the lead to two by the All-star break, as the Cubs sat 19 games over .500, but they swooned late in the season, going 20–40 after July 31. The Cubs finished in fourth place at 81–81, while Philadelphia surged, finishing with 101 wins. The following two seasons also saw the Cubs get off to a fast start, as the team rallied to over 10 games above .500 well into both seasons, only to again wear down and play poorly later on, and ultimately settling back to mediocrity. This trait became known as the "June Swoon". Again, the Cubs' unusually high number of day games is often pointed to as one reason for the team's inconsistent late season play.
Wrigley died in 1977. The Wrigley family sold the team to the Chicago Tribune in 1981, ending a 65-year family relationship with the Cubs.
Tribune Company years (1981–2008)
1984: Heartbreak
Ryne Sandberg set numerous league and club records in his career and was elected to the Hall of Fame in 2005.
After over a dozen more subpar seasons, in 1981 the Cubs hired GM Dallas Green from Philadelphia to turn around the franchise. Green had managed the 1980 Phillies to the World Series title. One of his early GM moves brought in a young Phillies minor-league 3rd baseman named Ryne Sandberg, along with Larry Bowa for Iván DeJesús. The 1983 Cubs had finished 71–91 under Lee Elia, who was fired before the season ended by Green. Green continued the culture of change and overhauled the Cubs roster, front-office and coaching staff prior to 1984. Jim Frey was hired to manage the 1984 Cubs, with Don Zimmer coaching 3rd base and Billy Connors serving as pitching coach.
Green shored[17] up the 1984 roster with a series of transactions. In December, 1983 Scott Sanderson was acquired from Montreal in a three-team deal with San Diego for Carmelo Martínez. Pinch hitter Richie Hebner (.333 BA in 1984) was signed as a free-agent. In spring training, moves continued: LF Gary Matthews and CF Bobby Dernier came from Philadelphia on March 26, for Bill Campbell and a minor leaguer. Reliever Tim Stoddard (10–6 3.82, 7 saves) was acquired the same day for a minor leaguer; veteran pitcher Ferguson Jenkins was released.
The team's commitment to contend was complete when Green made a midseason deal on June 15 to shore up the starting rotation due to injuries to Rick Reuschel (5–5) and Sanderson. The deal brought 1979 NL Rookie of the Year pitcher Rick Sutcliffe from the Cleveland Indians. Joe Carter (who was with the Triple-A Iowa Cubs at the time) and right fielder Mel Hall were sent to Cleveland for Sutcliffe and back-up catcher Ron Hassey (.333 with Cubs in 1984). Sutcliffe (5–5 with the Indians) immediately joined Sanderson (8–5 3.14), Eckersley (10–8 3.03), Steve Trout (13–7 3.41) and Dick Ruthven (6–10 5.04) in the starting rotation. Sutcliffe proceeded to go 16–1 for Cubs and capture the Cy Young Award.[17]
The Cubs 1984 starting lineup was very strong.[17] It consisted of LF Matthews (.291 14–82 101 runs 17 SB), C Jody Davis (.256 19–94), RF Keith Moreland (.279 16–80), SS Larry Bowa (.223 10 SB), 1B Leon "Bull" Durham (.279 23–96 16SB), CF Dernier (.278 45 SB), 3B Ron Cey (.240 25–97), Closer Lee Smith(9–7 3.65 33 saves) and 1984 NL MVP Ryne Sandberg (.314 19–84 114 runs, 19 triples,32 SB).[17]
Reserve players Hebner, Thad Bosley, Henry Cotto, Hassey and Dave Owen produced exciting moments. The bullpen depth of Rich Bordi, George Frazier, Warren Brusstar and Dickie Noles did their job in getting the game to Smith or Stoddard.
At the top of the order, Dernier and Sandberg were exciting, aptly coined "the Daily Double" by Harry Caray. With strong defense – Dernier CF and Sandberg 2B, won the NL Gold Glove- solid pitching and clutch hitting, the Cubs were a well balanced team. Following the "Daily Double", Matthews, Durham, Cey, Moreland and Davis gave the Cubs an order with no gaps to pitch around. Sutcliffe anchored a strong top-to-bottom rotation, and Smith was one of the top closers in the game.
The shift in the Cubs' fortunes was characterized June 23 on the "NBC Saturday Game of the Week" contest against the St. Louis Cardinals; it has since been dubbed simply "The Sandberg Game." With the nation watching and Wrigley Field packed, Sandberg emerged as a superstar with not one, but two game-tying home runs against Cardinals closer Bruce Sutter. With his shots in the 9th and 10th innings Wrigley Field erupted and Sandberg set the stage for a comeback win that cemented the Cubs as the team to beat in the East. No one would catch them.
In early August the Cubs swept the Mets in a 4-game home series that further distanced them from the pack. An infamous Keith Moreland-Ed Lynch fight erupted after Lynch hit Moreland with a pitch, perhaps forgetting Moreland was once a linebacker at the University of Texas. It was the second game of a double header and the Cubs had won the first game in part due to a three run home run by Moreland. After the bench-clearing fight the Cubs won the second game, and the sweep put the Cubs at 68–45.
In 1984, each league had two divisions, East and West. The divisional winners met in a best-of-5 series to advance to the World Series, in a "2–3" format, first two games were played at the home of the team who did not have home field advantage. Then the last three games were played at the home of the team, with home field advantage. Thus the first two games were played at Wrigley Field and the next three at the home of their opponents, San Diego. A common and unfounded myth is that since Wrigley Field did not have lights at that time the National League decided to give the home field advantage to the winner of the NL West. In fact, home field advantage had rotated between the winners of the East and West since 1969 when the league expanded. In even numbered years, the NL West had home field advantage. In odd numbered years, the NL East had home field advantage. Since the NL East winners had had home field advantage in 1983, the NL West winners were entitled to it.
The confusion may stem from the fact that Major League Baseball did decide that, should the Cubs make it to the World Series, the American League winner would have home field advantage unless the Cubs hosted home games at an alternate site since the Cubs home field of Wrigley Field did not yet have lights. Rumor was the Cubs could hold home games across town at Comiskey Park, home of the American League's Chicago White Sox. Rather than hold any games in the cross town rival Sox Park, the Cubs made arrangements with the August A. Busch, owner of the St. Louis Cardinals, to use Busch Stadium in St. Louis as the Cubs "home field" for the World Series. This was approved by Major League Baseball and would have enabled the Cubs to host games 1 and 2, along with games 6 and 7 if necessary. At the time home field advantage was rotated between each league. Odd numbered years the AL had home field advantage. Even numbered years the NL had home field advantage. In the 1982 World Series the St. Louis Cardinals of the NL had home field advantage. In the 1983 World Series the Baltimore Orioles of the AL had home field advantage.
In the NLCS, the Cubs easily won the first two games at Wrigley Field against the San Diego Padres. The Padres were the winners of the Western Division with Steve Garvey, Tony Gwynn, Eric Show, Goose Gossage and Alan Wiggins. With wins of 13–0 and 4–2, the Cubs needed to win only one game of the next three in San Diego to make it to the World Series. After being beaten in Game 3 7–1, the Cubs lost Game 4 when Smith, with the game tied 5–5, allowed a game-winning home run to Garvey in the bottom of the ninth inning. In Game 5 the Cubs took a 3–0 lead into the 6th inning, and a 3–2 lead into the seventh with Sutcliffe (who won the Cy Young Award that year) still on the mound. Then, Leon Durham had a sharp grounder go under his glove. This critical error helped the Padres win the game 6–3, with a 4-run 7th inning and keep Chicago out of the 1984 World Series against the Detroit Tigers. The loss ended a spectacular season for the Cubs, one that brought alive a slumbering franchise and made the Cubs relevant for a whole new generation of Cubs fans.
The Padres would be defeated in 5 games by Sparky Anderson's Tigers in the World Series.
Shawon Dunston was the Cubs shortstop for 10 years.
The 1985 season brought high hopes. The club started out well, going 35–19 through mid-June, but injuries to Sutcliffe and others in the pitching staff contributed to a 13-game losing streak that pushed the Cubs out of contention.
1989: NL East division championship
In 1989, the first full season with night baseball at Wrigley Field, Don Zimmer's Cubs were led by a core group of veterans in Ryne Sandberg, Rick Sutcliffe and Andre Dawson, who were boosted by a crop of youngsters such as Mark Grace, Shawon Dunston, Greg Maddux, Rookie of the Year Jerome Walton, and Rookie of the Year Runner-Up Dwight Smith. The Cubs won the NL East once again that season winning 93 games. This time the Cubs met the San Francisco Giants in the NLCS. After splitting the first two games at home, the Cubs headed to the Bay Area, where despite holding a lead at some point in each of the next three games, bullpen meltdowns and managerial blunders ultimately led to three straight losses. The Cubs couldn't overcome the efforts of Will Clark, whose home run off Maddux, just after a managerial visit to the mound, led Maddux to think Clark knew what pitch was coming. Afterward, Maddux would speak into his glove during any mound conversation, beginning what is a norm today. Mark Grace was 11–17 in the series with 8 RBI. Eventually, the Giants lost to the "Bash Brothers" and the Oakland A's in the famous "Earthquake Series."
1998: Wild card race and home run chase
Sammy Sosa was the captain of the Chicago Cubs during his tenure with the team.
The 1998 season would begin on a somber note with the death of legendary broadcaster Harry Caray. After the retirement of Sandberg and the trade of Dunston, the Cubs had holes to fill, and the signing of Henry Rodríguez to bat cleanup provided protection for Sammy Sosa in the lineup, as Rodriguez slugged 31 round-trippers in his first season in Chicago. Kevin Tapani led the club with a career high 19 wins while Rod Beck anchored a strong bullpen and Mark Grace turned in one of his best seasons. The Cubs were swamped by media attention in 1998, and the team's two biggest headliners were Sosa and rookie flamethrower Kerry Wood. Wood's signature performance was one-hitting the Houston Astros, a game in which he tied the major league record of 20 strikeouts in nine innings. His torrid strikeout numbers earned Wood the nickname "Kid K," and ultimately earned him the 1998 NL Rookie of the Year award. Sosa caught fire in June, hitting a major league record 20 home runs in the month, and his home run race with Cardinals slugger Mark McGwire transformed the pair into international superstars in a matter of weeks. McGwire finished the season with a new major league record of 70 home runs, but Sosa's .308 average and 66 homers earned him the National League MVP Award. After a down-to-the-wire Wild Card chase with the San Francisco Giants, Chicago and San Francisco ended the regular season tied, and thus squared off in a one-game playoff at Wrigley Field. Third baseman Gary Gaetti hit the eventual game winning homer in the playoff game. The win propelled the Cubs into the postseason for the first time since 1989 with a 90–73 regular season record. Unfortunately, the bats went cold in October, as manager Jim Riggleman's club batted .183 and scored only four runs en route to being swept by Atlanta in the National League Division Series.[18] The home run chase between Sosa, McGwire and Ken Griffey, Jr. helped professional baseball to bring in a new crop of fans as well as bringing back some fans who had been disillusioned by the 1994 strike.[19] The Cubs retained many players who experienced career years in 1998, but, after a fast start in 1999, they collapsed again (starting with being swept at the hands of the cross-town White Sox in mid-June) and finished in the bottom of the division for the next two seasons.
2001: Playoff push
Despite losing fan favorite Grace to free agency and the lack of production from newcomer Todd Hundley, skipper Don Baylor's Cubs put together a good season in 2001. The season started with Mack Newton being brought in to preach "positive thinking." One of the biggest stories of the season transpired as the club made a midseason deal for Fred McGriff, which was drawn out for nearly a month as McGriff debated waiving his no-trade clause.[20] The Cubs led the wild card race by 2.5 games in early September, but crumbled when Preston Wilson hit a three run walk off homer off of closer Tom "Flash" Gordon, which halted the team's momentum. The team was unable to make another serious charge, and finished at 88–74, five games behind both Houston and St. Louis, who tied for first. Sosa had perhaps his finest season and Jon Lieber led the staff with a 20-win season.[21]
2003: Five more outs
The Cubs had high expectations in 2002, but the squad played poorly. On July 5, 2002, the Cubs promoted assistant general manager and player personnel director Jim Hendry to the General Manager position. The club responded by hiring Dusty Baker and by making some major moves in 2003. Most notably, they traded with the Pittsburgh Pirates for outfielder Kenny Lofton and third baseman Aramis Ramírez, and rode dominant pitching, led by Kerry Wood and Mark Prior, as the Cubs led the division down the stretch.
Mark Prior, along with Kerry Wood, led the Cubs' rotation in 2003.
Chicago halted St. Louis' run to the playoffs by taking four of five games from the Cardinals at Wrigley Field in early September, after which they won their first division title in 14 years. They then went on to defeat the Atlanta Braves in a dramatic five-game Division Series, the franchise's first postseason series win since beating the Detroit Tigers in the 1908 World Series.
After losing an extra-inning game in Game 1, the Cubs rallied and took a three-games-to-one lead over the Wild Card Florida Marlins in the National League Championship Series. Florida shut the Cubs out in Game 5, but the Cubs returned home to Wrigley Field with young pitcher Mark Prior to lead the Cubs in Game 6 as they took a 3–0 lead into the 8th inning. It was at this point when a now-infamous incident took place. Several spectators attempted to catch a foul ball off the bat of Luis Castillo. A Chicago Cubs fan by the name of Steve Bartman, of Northbrook, Illinois, reached for the ball and deflected it away from the glove of Moisés Alou for the second out of the eighth inning. Alou reacted angrily toward the stands and after the game stated that he would have caught the ball.[22] Alou at one point recanted, saying he would not have been able to make the play, but later said this was just an attempt to make Bartman feel better and believing the whole incident should be forgotten.[22] Interference was not called on the play, as the ball was ruled to be on the spectator side of the wall. Castillo was eventually walked by Prior. Two batters later, and to the chagrin of the packed stadium, Cubs shortstop Alex Gonzalez misplayed an inning-ending double play, loading the bases. The error would lead to eight Florida runs and a Marlin victory. Despite sending Kerry Wood to the mound and holding a lead twice, the Cubs ultimately dropped Game 7, and failed to reach the World Series.
The "Steve Bartman incident" was seen as the "first domino" in the turning point of the era, and the Cubs did not win a playoff game for the next eleven seasons.[23]
2004–2006
In 2004, the Cubs were a consensus pick by most media outlets to win the World Series. The offseason acquisition of Derek Lee (who was acquired in a trade with Florida for Hee-seop Choi) and the return of Greg Maddux only bolstered these expectations. Despite a mid-season deal for Nomar Garciaparra, misfortune struck the Cubs again. They led the Wild Card by 1.5 games over San Francisco and Houston on September 25. On that day, both teams lost, giving the Cubs a chance at increasing the lead to 2.5 games with only eight games remaining in the season, but reliever LaTroy Hawkins blew a save to the Mets, and the Cubs lost the game in extra innings. The defeat seemingly deflated the team, as they proceeded to drop six of their last eight games as the Astros won the Wild Card.
Dempster emerged in 2004 and became the Cubs' regular closer.
Despite the fact that the Cubs had won 89 games, this fallout was decidedly unlovable, as the Cubs traded superstar Sammy Sosa after he had left the season's final game early and then lied about it publicly. Already a controversial figure in the clubhouse after his corked-bat incident,[24] Sammy's actions alienated much of his once strong fan base as well as the few teammates still on good terms with him, (many teammates grew tired of Sosa playing loud salsa music in the locker room) and possibly tarnished his place in Cubs' lore for years to come.[citation needed] The disappointing season also saw fans start to become frustrated with the constant injuries to ace pitchers Mark Prior and Kerry Wood. Additionally, the 2004 season led to the departure of popular commentator Steve Stone, who had become increasingly critical of management during broadcasts and was verbally attacked by reliever Kent Mercker.[25] Things were no better in 2005, despite a career year from first baseman Derrek Lee and the emergence of closer Ryan Dempster. The club struggled and suffered more key injuries, only managing to win 79 games after being picked by many to be a serious contender for the N.L. pennant. In 2006, bottom fell out as the Cubs finished 66–96, last in the NL Central.
2007–2008: Back to back division titles
Alfonso Soriano signed with the club in 2007
After finishing last in the NL Central with 66 wins in 2006, the Cubs re-tooled and went from "worst to first" in 2007. In the offseason they signed Alfonso Soriano to a contract at eight years for $136 million,[26] and replaced manager Dusty Baker with fiery veteran manager Lou Piniella.[27] After a rough start, which included a brawl between Michael Barrett and Carlos Zambrano, the Cubs overcame the Milwaukee Brewers, who had led the division for most of the season. The Cubs traded Barrett to the Padres, and later acquired catcher Jason Kendall from Oakland. Kendall was highly successful with his management of the pitching rotation and helped at the plate as well. By September, Geovany Soto became the full-time starter behind the plate, replacing the veteran Kendall. Winning streaks in June and July, coupled with a pair of dramatic, late-inning wins against the Reds, led to the Cubs ultimately clinching the NL Central with a record of 85–77. They met Arizona in the NLDS, but controversy followed as Piniella, in a move that has since come under scrutiny,[28] pulled Carlos Zambrano after the sixth inning of a pitcher's duel with D-Backs ace Brandon Webb, to "....save Zambrano for (a potential) Game 4." The Cubs, however, were unable to come through, losing the first game and eventually stranding over 30 baserunners in a three-game Arizona sweep.[29]
Carlos Zambrano warming up before a game.
The Tribune company, in financial distress, was acquired by real-estate mogul Sam Zell in December 2007. This acquisition included the Cubs. However, Zell did not take an active part in running the baseball franchise, instead concentrating on putting together a deal to sell it.
The Cubs successfully defended their National League Central title in 2008, going to the postseason in consecutive years for the first time since 1906–08. The offseason was dominated by three months of unsuccessful trade talks with the Orioles involving 2B Brian Roberts, as well as the signing of Chunichi Dragons star Kosuke Fukudome.[30] The team recorded their 10,000th win in April, while establishing an early division lead. Reed Johnson and Jim Edmonds were added early on and Rich Harden was acquired from the Oakland Athletics in early July.[31] The Cubs headed into the All-Star break with the N.L.'s best record, and tied the league record with eight representatives to the All-Star game, including catcher Geovany Soto, who was named Rookie of the Year. The Cubs took control of the division by sweeping a four-game series in Milwaukee. On September 14, in a game moved to Miller Park due to Hurricane Ike, Zambrano pitched a no-hitter against the Astros, and six days later the team clinched by beating St. Louis at Wrigley. The club ended the season with a 97–64 record[32] and met Los Angeles in the NLDS. The heavily favored Cubs took an early lead in Game 1, but James Loney's grand slam off Ryan Dempster changed the series' momentum. Chicago committed numerous critical errors and were outscored 20–6 in a Dodger sweep, which provided yet another sudden ending.[33]
The Ricketts era (2009–present)
The Ricketts family acquired a majority interest in the Cubs in 2009, ending the Tribune years. Apparently handcuffed by the Tribune's bankruptcy and the sale of the club to the Ricketts siblings, led by chairman Thomas S. Ricketts, the Cubs' quest for a NL Central three-peat started with notice that there would be less invested into contracts than in previous years. Chicago engaged St. Louis in a see-saw battle for first place into August 2009, but the Cardinals played to a torrid 20–6 pace that month, designating their rivals to battle in the Wild Card race, from which they were eliminated in the season's final week. The Cubs were plagued by injuries in 2009, and were only able to field their Opening Day starting lineup three times the entire season. Third baseman Aramis Ramírez injured his throwing shoulder in an early May game against the Milwaukee Brewers, sidelining him until early July and forcing journeyman players like Mike Fontenot and Aaron Miles into more prominent roles. Additionally, key players like Derrek Lee (who still managed to hit .306 with 35 HR and 111 RBI that season), Alfonso Soriano, and Geovany Soto also nursed nagging injuries. The Cubs posted a winning record (83–78) for the third consecutive season, the first time the club had done so since 1972, and a new era of ownership under the Ricketts family was approved by MLB owners in early October.
2010–2014: The decline and rebuild
Starlin Castro during his 2010 rookie season.
Rookie Starlin Castro debuted in early May (2010) as the starting shortstop. However, the club played poorly in the early season, finding themselves 10 games under .500 at the end of June. In addition, long-time ace Carlos Zambrano was pulled from a game against the White Sox on June 25 after a tirade and shoving match with Derrek Lee, and was suspended indefinitely by Jim Hendry, who called the conduct "unacceptable." On August 22, Lou Piniella, who had already announced his retirement at the end of the season, announced that he would leave the Cubs prematurely to take care of his sick mother. Mike Quade took over as the interim manager for the final 37 games of the year. Despite being well out of playoff contention the Cubs went 24–13 under Quade, the best record in baseball during that 37 game stretch, earning Quade the manager position going forward on October 19.
On December 3, 2010, Cubs broadcaster and former third baseman, Ron Santo, died due to complications from bladder cancer and diabetes. He spent 13 seasons as a player with the Cubs, and at the time of his death was regarded as one of the greatest players not in the Hall of Fame.[34] He was posthumously elected to the Major League Baseball Hall of Fame in 2012.
Despite trading for pitcher Matt Garza and signing free-agent slugger Carlos Peña, the Cubs finished the 2011 season 20 games under .500 with a record of 71–91. Weeks after the season came to an end, the club was rejuvenated in the form of a new philosophy, as new owner Tom Ricketts signed Theo Epstein away from the Boston Red Sox,[35] naming him club President and giving him a five-year contract worth over $18 million, and subsequently discharged manager Mike Quade. Epstein, a proponent of sabremetrics and one of the architects of the 2004 and 2007 World Series championships in Boston, brought along Jed Hoyer from the Padres to fill the role of GM and hired Dale Sveum as manager. Although the team had a dismal 2012 season, losing 101 games (the worst record since 1966), it was largely expected. The youth movement ushered in by Epstein and Hoyer began as longtime fan favorite Kerry Wood retired in May, followed by Ryan Dempster and Geovany Soto being traded to Texas at the All-Star break for a group of minor league prospects headlined by Christian Villanueva, but also included little thought of Kyle Hendricks. The development of Castro, Anthony Rizzo, Darwin Barney, Brett Jackson and pitcher Jeff Samardzija, as well as the replenishing of the minor-league system with prospects such as Javier Baez, Albert Almora, and Jorge Soler became the primary focus of the season, a philosophy which the new management said would carry over at least through the 2013 season.
One of two Cubs building blocks, Anthony Rizzo, swinging in the box.
The 2013 season resulted in much as the same the year before. Shortly before the trade deadline, the Cubs traded Matt Garza to the Texas Rangers for Mike Olt, Carl Edwards Jr, Neil Ramirez, and Justin Grimm.[36] Three days later, the Cubs sent Alfonso Soriano to the New York Yankees for minor leaguer Corey Black.[37] The mid season fire sale led to another last place finish in the NL Central, finishing with a record of 66-96. Although there was a five-game improvement in the record from the year before, Anthony Rizzo and Starlin Castro seemed to take steps backward in their development. On September 30, 2013, Theo Epstein made the decision to fire manager Dale Sveum after just two seasons at the helm of the Cubs. The regression of several young players was thought to be the main focus point, as the front office said Sveum would not be judged based on wins and losses. In two seasons as skipper, Sveum finished with a record of 127–197.[38]
The 2013 season was also notable as the Cubs drafted future Rookie of the Year and MVP Kris Bryant with the second overall selection.
On November 7, 2013, the Cubs hired San Diego Padres bench coach Rick Renteria to be the 53rd manager in team history.[39] The Cubs finished the 2014 season in last place with a 73-89 record in Rentería's first and only season as manager.[40] Despite the poor record, the Cubs improved in many areas during 2014, including rebound years by Anthony Rizzo and Starlin Castro, ending the season with a winning record at home for the first time since 2009,[41] and compiling a 33–34 record after the All-Star Break. However, following unexpected availability of Joe Maddon, the Cubs relieved Rentería of his managerial duties on October 31, 2014. During the season, the Cubs drafted Kyle Schwarber with the fourth overall selection.
Hall of Famer Ernie Banks died of a heart attack on January 23, 2015, shortly before his 84th birthday.[42] The 2015 uniform carried a commemorative #14 patch on both its home and away jerseys in his honor.
2015-present: Championship run
On November 2, 2014, the Cubs announced that Joe Maddon had signed a five-year contract to be the 54th manager in team history.[43] On December 10, 2014, Maddon announced that the team had signed free agent Jon Lester to a six-year, $155 million contract. Many other trades and acquisitions occurred during the off season. The opening day lineup for the Cubs contained five new players including center fielder Dexter Fowler. Rookies Kris Bryant and Addison Russell were in the starting lineup by mid-April, and rookie Kyle Schwarber was added in mid-June. On August 30, Jake Arrieta threw a no hitter against the Los Angeles Dodgers.[44] The Cubs finished the 2015 season in third place in the NL Central, with a record of 97–65, the third best record in the majors and earned a wild card berth. On October 7, in the 2015 National League Wild Card Game, Arrieta pitched a complete game shutout and the Cubs defeated the Pittsburgh Pirates 4–0.[45]
The Cubs defeated the Cardinals in the NLDS three-games-to-one, qualifying for a return to the NLCS for the first time in 12 years, where they faced the New York Mets. This was the first time in franchise history that the Cubs had clinched a playoff series at Wrigley Field.[46] However, they were swept in four games by the Mets and were unable to make it to their first World Series since 1945.[47]
Before the season, in an effort to shore up their lineup, free agents Ben Zobrist, Jason Heyward and John Lackey were signed.[48] To make room for the Zobrist signing, Starlin Castro was traded to the Yankees for Adam Warren and Brendan Ryan, the latter of whom was released a week later.[49]
2016 Champions visit the White House in January 2017
2016 Champions visit the White House in June 2017
In a season that included a no-hitter on April 21 by Jake Arrieta,[50] the Cubs finished with the best record in Major League Baseball and won their first National League Central title since the 2008 season, winning by 17.5 games. The team also reached the 100-win mark for the first time since 1935 and won 103 total games, the most wins for the franchise since 1910. The Cubs defeated the San Francisco Giants in the National League Division Series and returned to the National League Championship Series for the second year in a row, where they defeated the Los Angeles Dodgers in six games. This was their first NLCS win since the series was created in 1969. The win earned the Cubs their first World Series appearance since 1945 and a chance for their first World Series win since 1908. Coming back from a three-games-to-one deficit, the Cubs defeated the Cleveland Indians in seven games in the 2016 World Series, They were the first team to come back from a three-games-to-one deficit since the Kansas City Royals in 1985. On November 4, the city of Chicago held a victory parade and rally for the Cubs that began at Wrigley Field, headed down Lake Shore Drive, and ended in Grant Park. The city estimated that over five million people attended the parade and rally, which made it one of the largest recorded gatherings in history.[51]
In an attempt to be the first team to repeat as World Series champions since the Yankees in 1998, 1999, and 2000, the Cubs struggled for most of the first half of the 2017 season, never moving more than four games over .500 and finishing the first half two games under .500. On July 15, the Cubs fell to a season-high 5.5 games out of first in the NL Central. The Cubs struggled mainly due to their pitching as Jake Arrieta and Jon Lester struggled and no starting pitcher managed to win more than 14 games (four pitchers won 15 games or more for the Cubs in 2016). The Cub offense also struggled as Kyle Schwarber batted near .200 for most of the first half and was even sent to the minors. However, the Cubs recovered in the second half of the season to finish 22 games over .500 and win the NL Central by six games over the Milwaukee Brewers. The Cubs pulled out a five-game NLDS series win over the Washington Nationals to advance to the NLCS for the third consecutive year. For the second consecutive year, they faced the Dodgers. This time, however, the Dodgers defeated the Cubs in five games.[52]
Prior to the 2018 season, the Cubs made several key free agent signings to bolster their pitching staff. The team signed starting pitcher Yu Darvish to a six-year, $126 million contract and veteran closer Brandon Morrow to two-year, $21-million contract,[53][54] in addition to Tyler Chatwood and Steve Cishek.[55][56] However, the Cubs struggled to stay healthy throughout the season. Anthony Rizzo missed much of April due to a back injury,[57] and Bryant missed almost a month due to shoulder injury.[58] However, Darvish, who only started eight games in 2018, was lost for the season due to elbow and triceps injuries.[59] Morrow also faced two injuries before the team ruled him out for the season in September.[60]
The team maintained first place in their division for much of the season. The injury-depleted only went 16–11 during September, which allowed the Milwaukee Brewers, to finish with the same record. The Brewers defeated the Cubs in a tie-breaker game to win the Central Division and secure the top-seed in the National League.[61] The Cubs subsequently lost to the Colorado Rockies in the 2018 National League Wild Card Game for their earliest playoff exit in three seasons.[62]
Ballpark
Wrigley Field and Wrigleyville
The Cubs have played their home games at Wrigley Field, also known as "The Friendly Confines" since 1916. It was built in 1914 as Weeghman Park for the Chicago Whales, a Federal League baseball team. The Cubs also shared the park with the Chicago Bears of the NFL for 50 years. The ballpark includes a manual scoreboard, ivy-covered brick walls, and relatively small dimensions.
Located in Chicago's Lake View neighborhood, Wrigley Field sits on an irregular block bounded by Clark and Addison Streets and Waveland and Sheffield Avenues. The area surrounding the ballpark is typically referred to as Wrigleyville. There is a dense collection of sports bars and restaurants in the area, most with baseball inspired themes, including Sluggers, Murphy's Bleachers and The Cubby Bear. Many of the apartment buildings surrounding Wrigley Field on Waveland and Sheffield Avenues have built bleachers on their rooftops for fans to view games and other sell space for advertisement. One building on Sheffield Avenue has a sign atop its roof which says "Eamus Catuli!" which is Latin for "Let's Go Cubs!" and another chronicles the time since the last Division title, pennant, and World Series championship. The 00 denotes the 2016 NL Central title, NL pennant, and the World Series championship. On game days, many residents rent out their yards and driveways to people looking for parking spots. The uniqueness of the neighborhood itself has ingrained itself into the culture of the Chicago Cubs as well as the Wrigleyville neighborhood, and has led to being used for concerts and other sporting events, such as the 2010 NHL Winter Classic between the Chicago Blackhawks and Detroit Red Wings, as well as a 2010 NCAA men's football game between the Northwestern Wildcats and Illinois Fighting Illini.
In 2013, Tom Ricketts and team president Crane Kenney unveiled plans for a five-year, $575 million privately funded renovation of Wrigley Field.[63][64] Called the 1060 Project, the proposed plans included vast improvements to the stadium's facade, infrastructure, restrooms, concourses, suites, press box, bullpens, and clubhouses, as well as a 6,000-square-foot (560 m2)t jumbotron to be added in the left field bleachers, batting tunnels, a 3,000-square-foot (280 m2) video board in right field, and, eventually, an adjacent hotel, plaza, and office-retail complex.[65] In previous years mostly all efforts to conduct any large-scale renovations to the field had been opposed by the city, former mayor Richard M. Daley (a staunch White Sox fan), and especially the rooftop owners.
Months of negotiations between the team, a group of rooftop properties investors, local Alderman Tom Tunney, and Chicago Mayor Rahm Emanuel followed with the eventual endorsements of the city's Landmarks Commission, the Plan Commission and final approval by the Chicago City Council in July 2013.[66] The project began at the conclusion of the 2014 season.[67]
Bleacher Bums
The "Bleacher Bums" is a name given to fans, many of whom spend much of the day heckling, who sit in the bleacher section at Wrigley Field. Initially, the group was called "bums" because it referred to a group of fans who were at most games, and since those games were all day game.[68] A Broadway play,[69] starring Joe Mantegna, Dennis Farina, Dennis Franz, and James Belushi ran for years and was based on a group of Cub fans who frequented the club's games. The group was started in 1967 by dedicated fans Ron Grousl, Tom Nall and "mad bugler" Mike Murphy, who was a sports radio host during mid days on Chicago-based WSCR AM 670 "The Score". Murphy alleges that Grousl started the Wrigley tradition of throwing back opposing teams' home run balls.[70][71]
Culture
Cubs Win Flag
Cubs Win Flag Cubs Lose Flag
Beginning in the days of P.K. Wrigley and the 1937 bleacher/scoreboard reconstruction, and prior to modern media saturation, a flag with either a "W" or an "L" has flown from atop the scoreboard masthead, indicating the day's result(s) when baseball was played at Wrigley. In case of a split doubleheader, both the "W" and "L" flags are flown.
Past Cubs media guides show that originally the flags were blue with a white "W" and white with a blue "L". In 1978, consistent with the dominant colors of the flags, blue and white lights were mounted atop the scoreboard, denoting "win" and "loss" respectively for the benefit of nighttime passers-by.
The flags were replaced by 1990, the first year in which the Cubs media guide reports the switch to the now familiar colors of the flags: White with blue "W" and blue with white "L". In addition to needing to replace the worn-out flags, by then the retired numbers of Banks and Williams were flying on the foul poles, as white with blue numbers; so the "good" flag was switched to match that scheme.
This long-established tradition has evolved to fans carrying the white-with-blue-W flags to both home and away games, and displaying them after a Cub win. The flags have become more and more popular each season since 1998, and are now even sold as T-shirts with the same layout. In 2009, the tradition spilled over to the NHL as Chicago Blackhawks fans adopted a red and black "W" flag of their own.
During the early and mid-2000s, Chip Caray usually declared that a Cubs win at home meant it was "White flag time at Wrigley!" More recently, the Cubs have promoted the phrase "Fly the W!" among fans and on social media. [72]
Mascots
Clark (left) with the Oriole Bird
The official Cubs team mascot is a young bear cub, named Clark, described by the team's press release as a young and friendly Cub. Clark made his debut at Advocate Health Care on January 13, 2014, the same day as the press release announcing his installation as the club's first ever official physical mascot.[73] The bear cub itself was used in the clubs since the early 1900s and was the inspiration of the Chicago Staleys changing their team's name to the Chicago Bears, because the Cubs allowed the football team to play at Wrigley Field in the 1930s.
The Cubs had no official physical mascot prior to Clark, though a man in a 'polar bear' looking outfit, called "The Bear-man" (or Beeman), which was mildly popular with the fans, paraded the stands briefly in the early 1990s. There is no record of whether or not he was just a fan in a costume or employed by the club. Through the 2013 season, there were "Cubbie-bear" mascots outside of Wrigley on game day, but none were employed by the team. They pose for pictures with fans for tips. The most notable of these was "Billy Cub" who worked outside of the stadium for over six years until July 2013, when the club asked him to stop. Billy Cub, who is played by fan John Paul Weier, had unsuccessfully petitioned the team to become the official mascot.[74]
Another unofficial but much more well-known mascot is Ronnie "Woo Woo" Wickers[75] who is a longtime fan and local celebrity in the Chicago area. He is known to Wrigley Field visitors for his idiosyncratic cheers at baseball games, generally punctuated with an exclamatory "Woo!" (e.g., "Cubs, woo! Cubs, woo! Big-Z, woo! Zambrano, woo! Cubs, woo!") Longtime Cubs announcer Harry Caray dubbed Wickers "Leather Lungs" for his ability to shout for hours at a time.[76] He is not employed by the team, although the club has on two separate occasions allowed him into the broadcast booth and allow him some degree of freedom once he purchases or is given a ticket by fans to get into the games. He is largely allowed to roam the park and interact with fans by Wrigley Field security.
Music
During the summer of 1969, a Chicago studio group produced a single record called "Hey Hey! Holy Mackerel! (The Cubs Song)" whose title and lyrics incorporated the catch-phrases of the respective TV and radio announcers for the Cubs, Jack Brickhouse and Vince Lloyd. Several members of the Cubs recorded an album called Cub Power which contained a cover of the song. The song received a good deal of local airplay that summer, associating it very strongly with that bittersweet season. It was played much less frequently thereafter, although it remained an unofficial Cubs theme song for some years after.
For many years, Cubs radio broadcasts started with "It's a Beautiful Day for a Ball Game" by the Harry Simeone Chorale. In 1979, Roger Bain released a 45 rpm record of his song "Thanks Mr. Banks", to honor "Mr. Cub" Ernie Banks.[77]
The song "Go, Cubs, Go!" by Steve Goodman was recorded early in the 1984 season, and was heard frequently during that season. Goodman died in September of that year, four days before the Cubs clinched the National League Eastern Division title, their first title in 39 years. Since 1984, the song started being played from time to time at Wrigley Field; since 2007, the song has been played over the loudspeakers following each Cubs home victory.
The Mountain Goats recorded a song entitled "Cubs in Five" on its 1995 EP Nine Black Poppies which refers to the seeming impossibility of the Cubs winning a World Series in both its title and Chorus.
In 2007, Pearl Jam frontman Eddie Vedder composed a song dedicated to the team called "All the Way". Vedder, a Chicago native, and lifelong Cubs fan, composed the song at the request of Ernie Banks. Pearl Jam has played this song live multiple times several of which occurring at Wrigley Field.[78][79] Eddie Vedder has played this song live twice, at his solo shows at the Chicago Auditorium on August 21 and 22, 2008.
An album entitled Take Me Out to a Cubs Game was released in 2008. It is a collection of 17 songs and other recordings related to the team,[80] including Harry Caray's final performance of "Take Me Out to the Ball Game" on September 21, 1997, the Steve Goodman song mentioned above, and a newly recorded rendition of "Talkin' Baseball" (subtitled "Baseball and the Cubs") by Terry Cashman. The album was produced in celebration of the 100th anniversary of the Cubs' 1908 World Series victory and contains sounds and songs of the Cubs and Wrigley Field.[81][82]
Popular culture
The 1986 film Ferris Bueller's Day Off showed a game played by the Cubs when Ferris' principal goes to a bar looking for him.
The 1989 film Back to the Future Part II depicts the Chicago Cubs defeating a baseball team from Miami in the 2015 World Series, ending the longest championship drought in all four of the major North American professional sports leagues. In 2015, the Miami Marlins failed to make the playoffs but the Cubs were able to make it to the 2015 National League Wild Card round and move on to the 2015 National League Championship Series by October 21, 2015, the date where protagonist Marty McFly traveled to the future in the film.[83] However, it was on October 21 that the Cubs were swept by the New York Mets in the NLCS.
The 1993 film Rookie of the Year, directed by Daniel Stern, centers on the Cubs as a team going nowhere into August when the team chances upon 12-year-old Cubs fan Henry Rowengartner (Thomas Ian Nicholas), whose right (throwing) arm tendons have healed tightly after a broken arm and granted him the ability to regularly pitch at speeds in excess of 100 miles per hour (160 km/h). Following the Cubs' win over the Cleveland Indians in Game 7 of the 2016 World Series, Nicholas, in celebration, tweeted the final shot from the movie: Henry holding his fist up to the camera to show a Cubs World Series ring.[84]
Tinker to Evers to Chance
"Baseball's Sad Lexicon," also known as "Tinker to Evers to Chance" after its refrain, is a 1910 baseball poem by Franklin Pierce Adams. The poem is presented as a single, rueful stanza from the point of view of a New York Giants fan seeing the talented Chicago Cubs infield of shortstop Joe Tinker, second baseman Johnny Evers, and first baseman Frank Chance complete a double play. The trio began playing together with the Cubs in 1902, and formed a double play combination that lasted through April 1912. The Cubs won the pennant four times between 1906 and 1910, often defeating the Giants en route to the World Series.
Joe Tinker, Johnny Evers, and Frank Chance are the three Cubs described in the poem.
These are the saddest of possible words: "Tinker to Evers to Chance." Trio of bear cubs, and fleeter than birds, Tinker and Evers and Chance. Ruthlessly pricking our gonfalon bubble, Making a Giant hit into a double – Words that are heavy with nothing but trouble: "Tinker to Evers to Chance."
The poem was first published in the New York Evening Mail on July 12, 1912. Popular among sportswriters, numerous additional verses were written. The poem gave Tinker, Evers, and Chance increased popularity and has been credited with their elections to the National Baseball Hall of Fame in 1946.
Playoffs/Championships
a Prior to 1969, divisions did not exist in MLB. The Chicago Cubs played in the National League East between 1969–1993 before moving to the newly created National League Central in 1994.
Prior to 1969, divisions did not exist in MLB. The Chicago Cubs played in the National League East between 1969–1993 before moving to the newly created National League Central in 1994. b Prior to 1995, only two divisions existed in each league. With the realignment into three divisions and the institution of the wild card in 1995, the Division Series was added. Division Series .
Prior to 1995, only two divisions existed in each league. With the realignment into three divisions and the institution of the wild card in 1995, the Division Series was added. . c Prior to 1969, the National League champion was determined by the best win–loss record at the end of the regular season. See League Championship Series .
Prior to 1969, the National League champion was determined by the best win–loss record at the end of the regular season. . d None of the World Series contested before 1903 are recognized by MLB. See List of pre-World Series baseball champions.
Distinctions
Throughout the history of the Chicago Cubs' franchise, fifteen different Cubs pitchers have pitched no-hitters; however, no Cubs pitcher has thrown a perfect game.[85][86]
Forbes value rankings
As of 2017, the Chicago Cubs are ranked as the 18th most valuable sports team in the world, 14th in the United States, fourth in MLB behind the New York Yankees, Los Angeles Dodgers, and Boston Red Sox, and second in the city of Chicago behind the Bears.[87]
Year World US MLB CHI Value Ref. 2010 46 37 5 2 $726,000,000 [88] 2011 42 34 4 2 $773,000,000 [89] 2012 36 29 4 2 $879,000,000 [90] 2013 31 25 4 2 $1,000,000,000 [91] 2014 21 16 4 2 $1,200,000,000 [92] 2015 17 13 4 2 $1,800,000,000 [93] 2016 21 17 5 3 $2,200,000,000 [94] 2017 18 14 4 2 $2,680,000,000 [87]
Team
Current roster
Retired numbers
The Chicago Cubs retired numbers are commemorated on pinstriped flags flying from the foul poles at Wrigley Field, with the exception of Jackie Robinson, the Brooklyn Dodgers player whose number 42 was retired for all clubs. The first retired number flag, Ernie Banks' number 14, was raised on the left field pole, and they have alternated since then. 14, 10 and 31 (Jenkins) fly on the left field pole; and 26, 23 and 31 (Maddux) fly on the right field pole.
There is also a movement to retire numbers for other players, most notably the uniform shirt of Gabby Hartnett. The Cubs first wore numbers on their shirts in 1932, and Hartnett wore #7 initially but switched to #9 for the next four seasons. From 1937 to 1940 he wore #2, which is the number considered for retirement. Petitions have been sent in to the team for Cap Anson (shirt), Hack Wilson (shirt), Phil Cavarretta (3), Andre Dawson (8) and, as well as more recent departures Kerry Wood (34), Sammy Sosa (21), and Mark Grace (17).
* Robinson's number was retired by all MLB clubs.
Hall of Famers
Minor league affiliations
Before signing a developmental agreement with the Kane County Cougars in 2012, the Cubs had a Class A minor league affiliation on two occasions with the Peoria Chiefs (1985–1995 and 2004–2012). Ryne Sandberg managed the Chiefs from 2006 to 2010. In the period between those associations with the Chiefs the club had affiliations with the Dayton Dragons and Lansing Lugnuts. The Lugnuts were often affectionately referred to by Chip Caray as "Steve Stone's favorite team." The 2007 developmental contract with the Tennessee Smokies was preceded by Double A affiliations with the Orlando Cubs and West Tenn Diamond Jaxx. On September 16, 2014 the Cubs announced a move of their top Class A affiliate from Daytona in the Florida State League to Myrtle Beach in the Carolina League for the 2015 season.[95] Two days later, the Cubs signed a four-year player development contract with the South Bend Silver Hawks of the Midwest League, ending their brief relationship with the Kane County Cougars and shortly thereafter renaming the Silver Hawks the South Bend Cubs.[96]
Spring training history
The Chicago White Stockings, (today's Chicago Cubs), began spring training in Hot Springs, Arkansas in 1886. President Albert Spalding (founder of Spalding Sporting Goods) and player/manager Cap Anson brought their players to Hot Springs and played at the Hot Springs Baseball Grounds. The concept was for the players to have training and fitness before the start of the regular season, utilizing the bath houses of Hot Springs after practices.[97][98][99] After the White Stockings had a successful season in 1886, winning the National League Pennant, other teams began bringing their players to Hot Springs for "spring training".[99][100] The Chicago Cubs, St. Louis Browns, New York Yankees, St. Louis Cardinals, Cleveland Spiders, Detroit Tigers, Pittsburgh Pirates, Cincinnati Reds, New York Highlanders, Brooklyn Dodgers and Boston Red Sox were among the early squads to arrive. Whittington Park (1894) and later Majestic Park (1909) and Fogel Field (1912) were all built in Hot Springs specifically to host Major League teams.[101]
The Cubs' current spring training facility is located in Sloan Park in Mesa, Arizona, where they play in the Cactus League. The park seats 15,000, making it Major League baseball's largest spring training facility by capacity. The Cubs annually sell out most of their games both at home and on the road. Before Sloan Park opened in 2014, the team played games at HoHoKam Park – Dwight Patterson Field from 1979. "HoHoKam" is literally translated from Native American as "those who vanished." The North Siders have called Mesa their spring home for most seasons since 1952.
In addition to Mesa, the club has held spring training in Hot Springs, Arkansas (1886, 1896–1900), (1909–1910) New Orleans (1870, 1907, 1911–1912); Champaign, Illinois (1901–02, 1906); Los Angeles (1903–04, 1948–1949), Santa Monica, California (1905); French Lick, Indiana (1908, 1943–1945); Tampa, Florida (1913–1916); Pasadena, California (1917–1921); Santa Catalina Island, California (1922–1942, 1946–1947, 1950–1951); Rendezvous Park in Mesa (1952–1965); Blair Field in Long Beach, California (1966); and Scottsdale, Arizona (1967–1978).
The curious location on Catalina Island stemmed from Cubs owner William Wrigley Jr.'s then-majority interest in the island in 1919. Wrigley constructed a ballpark on the island to house the Cubs in spring training: it was built to the same dimensions as Wrigley Field. The ballpark was called Wrigley Field of Avalon.[102] (The ballpark is long gone, but a clubhouse built by Wrigley to house the Cubs exists as the Catalina County Club.) However, by 1951 the team chose to leave Catalina Island and spring training was shifted to Mesa, Arizona.[103] The Cubs' 30-year association with Catalina is chronicled in the book, The Cubs on Catalina, by Jim Vitti, which was named International 'Book of the Year' by The Sporting News. The Cubs left Catalina after some bad weather in 1951, choosing to move to Mesa, a city where the Wrigleys also had interests.[104] Today, there is an exhibit at the Catalina Museum dedicated to the Cubs' spring training on the island.[105][106]
The former location in Mesa is actually the second HoHoKam Park; the first was built in 1976 as the spring-training home of the Oakland Athletics who left the park in 1979. Apart from HoHoKam Park and Sloan Park the Cubs also have another Mesa training facility called Fitch Park, this complex provides 25,000 square feet (2,300 m2) of team facilities, including major league clubhouse, four practice fields, one practice infield, enclosed batting tunnels, batting cages, a maintenance facility, and administrative offices for the Cubs.
Media
Radio
Cubs radio rights are held by CBS Radio; its acquisition of the radio rights effective 2015 ended the team's 90-year association with 720 WGN. During the first season of the contract, Cubs games aired on WBBM, taking over as flagship of the Chicago Cubs Radio Network. On November 11, 2015, CBS announced that the Cubs would move to WBBM's all-sports sister station, WSCR, beginning in the 2016 season. The move was enabled by WSCR's end of their rights agreement for the White Sox, who moved to WLS.[107][108][109]
The play-by-play voice of the Cubs is Pat Hughes, who has held the position since 1996, joined by Ron Coomer. Former Cubs third baseman and fan favorite Ron Santo had been Hughes' long-time partner until his death in 2010. Keith Moreland replaced Hall of Fame inductee Santo for three seasons, followed by Coomer for the 2014 season.[110]
The club also produces its own print media; the Cubs' official magazine Vineline, which has 12 annual issues, is in its third decade, and spotlights players and events involving the club. The club also publishes a traditional media guide.
Television
As of September 1, 2016, Cubs games air locally on the following outlets:
NBC Sports Chicago, a cable network owned in part by NBCUniversal and the Ricketts family. It broadcasts all Cubs games not broadcast over-the-air, or nationally by Major League Baseball's television partners. [111]
WGN-TV (channel 9.1), a Tribune Media-owned over-the-air station that has aired Cubs telecasts since its inception in 1948; WGN-TV's Cubs telecasts are produced by the station's sports department, WGN Sports. In November 2013, the team exercised an option to terminate its existing deal with WGN-TV after the 2014 season, requesting a higher-valued contract lasting through the 2019 season (which would be aligned with the end of its contract with CSN Chicago). WGN-TV announced on January 7, 2015 that it would maintain broadcast rights to 45 Cubs games through the 2019 season within the Chicago market only. [111] [112]
WLS-TV (channel 7.1), an ABC owned-and-operated station. It was announced on December 12, 2014 that the station would acquire rights to 25 games per season through 2019.[113][114]
Prior to September 1, 2016, when WGN-TV ended their CW affiliation to return to being an independent station, several games in the WGN package since 2015 were sub-licensed to Fox Television Stations-owned MyNetworkTV station WPWR-TV (channel 50.1), due to CW pre-emption limits which precluded airing on WGN-TV. These games returned full-time to WGN-TV upon that date, when WPWR assumed the market's CW affiliation and WGN was no longer limited by a network. In previous years, the sublicensed games were carried by WCIU-TV (channel 26.1) under the branding of "CubsNet" and "WGN Sports on The U".[115]
WGN's Cubs games formerly aired nationally on WGN America; however, prior to the 2015 season, the Cubs, as well as all other Chicago sports programming, was dropped from the channel as part of its re-positioning as a general entertainment cable channel.[116] To compensate, all games carried by over-the-air channels are syndicated to a network of other television stations within the Cubs' region, which includes Illinois and parts of Indiana and Iowa.[114][117][118][119]
All of the team's current television contracts end after the 2019 season. On November 16, 2015 in an interview with WSCR radio, the Cubs' president of business operations Crane Kenney stated that the team was seeking to launch its own in-house regional sports network.[111][120][121] On December 18, 2018, it was reported by the Chicago Sun-Times that the team was preparing to launch its RSN, "Marquee", in 2020, and that Sinclair Broadcast Group (which had previously attempted to purchase WGN's parent company Tribune Media, and runs the national sports network Stadium with the White Sox's investment arm Silver Chalice) was a frontrunner to serve as managing partner.[122]
Len Kasper has been the Cubs' television play-by-play announcer since 2005 and was joined by Jim Deshaies in 2013. Bob Brenly (analyst, 2005–12), Chip Caray (play-by-play, 1998–2004), Steve Stone (analyst, 1983–2000, 2003–04), Joe Carter (analyst for WGN-TV games, 2001–02) and Dave Otto (analyst for FSN Chicago games, 2001–02) also have spent time broadcasting from the Cubs booth since the death of Harry Caray in 1998.[123]
Ford C. Frick Award recipients
See also
References
Further reading ||||| The Cubs were born the Chicago White Stockings in 1876, one of eight inaugural teams. The team would go on to win the first National league Championship and would become one of sports first dynasties by winning six of the first eleven championship titles (1876, 1880-82, 1885-86). The modern day “Cubs” would come into existence in 1903, and continue their success posting a record in wins in 1906 with 116 games won. This would also be their first pennant win as the “Cubs.” The World Series title would be lost to their cross town rivals, the White Sox.
The following year, after a repeat pennant, they would go on to win their first World Series title in 1907. They returned the following year to win their second (and last) World Series becoming the first team in baseball to win back to back World Series Titles.
The Cubs continued their success capturing pennants in 1910, 1918 and an astounding four pennants in a ten year span (1929, 1932, 1935, 1938). The Cubs would play in the World Series in each of those years. Their final pennant would come in 1945, the year the Cubs faced the Detroit Tigers and a local Chicago saloon owner named William “Billy Goat” Sianis with his goat, Murphy.
From 1876 to 1945, The Chicago Cubs were one of the most successful baseball teams in the country. They would post a 5475-4324 (.559) record, with 51 winning seasons, 16 first place finishes, and 16 pennants and World Series appearances. They would win two World Series titles and six Championship titles in that span. This would come to a screeching halt in game four of the 1945 World Series. 1945- “Who Stinks Now?”
October 6th, a sad day in Cubs history. The Cubs entered game four of the World Series leading the Detroit Tigers 2 games to 1, and needing to win only two of the next four games played at Wrigley Field. A local Greek, William “Billy Goat” Sianis, owner of the Billy Goat Tavern and a Cubs fan, bought two tickets to Game four. Hoping to bring his team good luck he took his pet goat, Murphy, with him to the game. At the entrance to the park, the Andy Fran ushers stopped Billy Goat from entering saying that no animals are allowed in the park. Billy Goat, frustrated, appealed to the owner of the Cubs, P.K. Wrigley. Wrigley replied, “Let Billy in, but not the goat.” Billy Goat asked, “Why not the goat?” Wrigley answered, “Because the goat stinks.” According to legend, the goat and Billy were upset, so then Billy threw up his arms and exclaimed, “The Cubs ain’t gonna win no more. The Cubs will never win a World Series so long as the goat is not allowed in Wrigley Field.” The Cubs were officially cursed. Subsequently, the Cubs lost game four, and the remaining series getting swept at home and from the World Series. Billy Goat promptly sent a telegram to P.K. Wrigley, stating, “Who stinks now?” For the next twenty years, throughout the remainder of Billy Goat’s life the Cubs would finish each season at 5th place or lower, establishing a pattern that would reverse the Cubs luck and term the team “The Lovable Losers.” The World Series would become a dream, and “wait ’til next year” would become the team’s motto. From 1946 to 2003, the Cubs would post a 4250-4874 (.466) record, have only 15 winning seasons, finish in first place a mere 3 times, have no pennants, no World Series appearances let alone wins, with only four post season experiences (1984, 1989, 1998, 2003) resulting in a complete reversal of their fortunes. The Cubs were and are a cursed franchise.
1969- “Miracle” Mets or “Cursed” Cubs
In 1969, a year before he passed away, “Billy Goat” Sianis finally felt satisfied and claimed the curse is lifted, but the goat still was bitter. The Cubs began the season winning and coasted throughout the season into mid-August with a commanding first place lead. By the end of the season a surging “Miracle” Mets overtook the struggling “Cursed” Cubs to claim first place and knock the Cubs out of contention. This would become a pattern over the years.
1973- One limo, a red carpet, and a goat denied once again
In 1973, Billy Goat’s nephew and new Billy Goat Tavern owner, Sam Sianis, with the help of Tribune columnist, Dave Condon, brought the goat to Wrigley in an attempt to lift the curse. The goat was escorted to Wrigley in a white limousine, and given a red carpet entrance to the park with a sign saying, “All is forgiven. Let me lead the Cubs to the pennant.” The ushers at the entrance denied the goat “Socrates,” a descendant of Murphy, yet again. The Cubs saw their mid-season first place lead whither away to another unsuccessful season.
1984- Eight outs away
The Tribune Company, new owners of the Cubs, finally invited the goat to opening day at Wrigley Field in an attempt to lift the curse. Sam Sianis and his goat finally walked the grass of Wrigley Field, and in an effort to lift the curse Sam raised his hat and said, “The curse is lifted.” The Cubs won and won and won their way to their first post season game and division title in almost forty years. They continued their winning taking the first two games of the National League Championship Series against the San Diego Padres. They just needed to win one of the next three games at San Diego to finally reach the World Series. Sam and his goat waited for the call to go along with the team and ensure the victory, only to be left behind in Chicago.
After losing games three and four in San Diego, the Cubs were leading the Padres 3-2 in the seventh inning, with only eight outs needed to win the game and the ace pitcher Rick Sutcliffe at the helm. An eerie chain of events would ensue. A routine ground ball was hit to first baseman, Leon Durham, which dribbled through his legs allowing the tying run to score. An overworked Rick Sutcliffe, who dominated game one, yielded the remaining three runs. The Padres swept the Cubs in San Diego, and swept the Cubs out of the series. The Cubs were still cursed.
1989- So Close, So Far
Hoping for a repeat of 1984, Sam Sianis and his goat again walked the field of Wrigley on opening day. The Cubs again won their way to first place and their second division title in five years. But the goat was left behind once again in the post season, where the Cubs lost to the San Francisco Giants four games to one.
1994- “Let the Goat in!”
The Cubs started the 1994 season horribly, losing twelve home games in a row. Their worst home start in history. In an effort to end this streak, Sam Sianis and his goat went to Wrigley Field only to be denied entrance yet again. Amidst the chant of “Let the Goat in!” amongst the Wrigley crowd, Hall of Famer, Ernie Banks helped by escorting Sam and his goat into Wrigley. The Cubs won the game 5-2, ending their worst home start ever. A lesson learned?
1998- Bring in the Wild Card
In 1998, the Cubs finished the season with 89 wins, tied with the San Francisco Giants for the Wild Card. During the Tiebreaking game on Sept. 28th, the Cubs brought in their Wild Card, Sam and his goat. The Cubs would go on to win the game 5-3 and went into the post season as a Wild Card. But once again Sam and his goat were left behind in Chicago, while the Cubs got swept in Atlanta, and swept out of the post season.
2003- Five outs away
The Cubs ended the 2003 season in a tight race with the Houston Astros. When the goat was sent to Houston in an effort to reverse the curse, Houston lost while the Cubs won their first division title in fourteen years. The Cubs were on a roll. They would go on to beat the Atlanta Braves, winning their first post season series in almost 100 years. In the National League Championship Series against the Florida Marlins, the Cubs took a quick 3 game lead needing only one more victory to go to the World Series for the first time in almost sixty years. In game six of the series, with the ace Mark Prior at the helm, the Cubs entered the eighth inning leading 3-0. Once again the goat was left behind, and an eerie chain of events would ensue. With only five outs needed to secure a victory, a pop foul seemingly in play was interfered with by a fan taking away a sure out. That was followed by the next play, when a routine ground ball was hit to the sure handed Alex Gonzalez only to be bobbled, taking away an inning ending double play. Ace pitcher, Mark Prior, overworked, yielded the tying and leading runs, until the Marlins left the eighth leading 8-3. The Marlins ended up winning the game, then swept the Cubs at home and swept them out of the playoffs yet again.
What does the future hold in store for the Cubs? Many attempts have been made to lift the curse, yet the goat still has not seen his baseball game. One moment in time, one horrible mistake in game four of the 1945 World Series, has yielded years of pain and anguish for Cubs fans abroad. The Chicago Cubs prior to the curse were one of the best teams in baseball, and after the curse have become the “Lovable Losers.” If the Cubs are ever again in a situation, where they are outs away from the World Series, will the goat get the call? For the sake of the Cubs, “LET THE GOAT IN!”
2015 – Murphy’s Law
Under new Manager Joe Maddon, the 2015 Cubs fielded a team of exciting young players. They captured the Wild Card, won a single game playoff against the Pirates, and went on to beat the rival St. Louis Cardinals in the division series. Only the Mets stood between the Cubs and their first World Series appearance since 1945. However, their momentum came to a sudden halt when they ran into Daniel Murphy. He hit a home run in all four games of the series and the Cubs were once again swept out of the playoffs.
2015 wasn’t the first time “Murphy” played a role in Cubs’ history: ||||| A pair of competitive eaters will test the power of their skills Tuesday night as they attempt to reverse the Cubs' "billy goat curse" by eating a whole goat.
Famed Japanese competitive eater Takeru Kobayashi, who has won Nathan's Coney Island Hot Dog Eating Contest six times, and L.A. Beast, a competitive eater and YouTube star, plan to eat a 40-pound cooked goat in a single sitting at Lincoln Square's Taco In a Bag.
Kobayashi and L.A. Beast will be joined by Tim Brown and Patrick Bertoletti, the restaurant's co-owners, who have also indulged in competitive eating contests.
The hope is to reverse the 70-year "billy goat curse" as the North Side team inches closer and closer to making the playoffs this year.
The goat-eating challenge begins at 7:30 p.m. at Taco In A Bag, located at 4603 N. Lincoln Ave. ||||| The Cubs were born the Chicago White Stockings in 1876, one of eight inaugural teams. The team would go on to win the first National league Championship and would become one of sports first dynasties by winning six of the first eleven championship titles (1876, 1880-82, 1885-86). The modern day “Cubs” would come into existence in 1903, and continue their success posting a record in wins in 1906 with 116 games won. This would also be their first pennant win as the “Cubs.” The World Series title would be lost to their cross town rivals, the White Sox.
The following year, after a repeat pennant, they would go on to win their first World Series title in 1907. They returned the following year to win their second (and last) World Series becoming the first team in baseball to win back to back World Series Titles.
The Cubs continued their success capturing pennants in 1910, 1918 and an astounding four pennants in a ten year span (1929, 1932, 1935, 1938). The Cubs would play in the World Series in each of those years. Their final pennant would come in 1945, the year the Cubs faced the Detroit Tigers and a local Chicago saloon owner named William “Billy Goat” Sianis with his goat, Murphy.
From 1876 to 1945, The Chicago Cubs were one of the most successful baseball teams in the country. They would post a 5475-4324 (.559) record, with 51 winning seasons, 16 first place finishes, and 16 pennants and World Series appearances. They would win two World Series titles and six Championship titles in that span. This would come to a screeching halt in game four of the 1945 World Series. 1945- “Who Stinks Now?”
October 6th, a sad day in Cubs history. The Cubs entered game four of the World Series leading the Detroit Tigers 2 games to 1, and needing to win only two of the next four games played at Wrigley Field. A local Greek, William “Billy Goat” Sianis, owner of the Billy Goat Tavern and a Cubs fan, bought two tickets to Game four. Hoping to bring his team good luck he took his pet goat, Murphy, with him to the game. At the entrance to the park, the Andy Fran ushers stopped Billy Goat from entering saying that no animals are allowed in the park. Billy Goat, frustrated, appealed to the owner of the Cubs, P.K. Wrigley. Wrigley replied, “Let Billy in, but not the goat.” Billy Goat asked, “Why not the goat?” Wrigley answered, “Because the goat stinks.” According to legend, the goat and Billy were upset, so then Billy threw up his arms and exclaimed, “The Cubs ain’t gonna win no more. The Cubs will never win a World Series so long as the goat is not allowed in Wrigley Field.” The Cubs were officially cursed. Subsequently, the Cubs lost game four, and the remaining series getting swept at home and from the World Series. Billy Goat promptly sent a telegram to P.K. Wrigley, stating, “Who stinks now?” For the next twenty years, throughout the remainder of Billy Goat’s life the Cubs would finish each season at 5th place or lower, establishing a pattern that would reverse the Cubs luck and term the team “The Lovable Losers.” The World Series would become a dream, and “wait ’til next year” would become the team’s motto. From 1946 to 2003, the Cubs would post a 4250-4874 (.466) record, have only 15 winning seasons, finish in first place a mere 3 times, have no pennants, no World Series appearances let alone wins, with only four post season experiences (1984, 1989, 1998, 2003) resulting in a complete reversal of their fortunes. The Cubs were and are a cursed franchise.
1969- “Miracle” Mets or “Cursed” Cubs
In 1969, a year before he passed away, “Billy Goat” Sianis finally felt satisfied and claimed the curse is lifted, but the goat still was bitter. The Cubs began the season winning and coasted throughout the season into mid-August with a commanding first place lead. By the end of the season a surging “Miracle” Mets overtook the struggling “Cursed” Cubs to claim first place and knock the Cubs out of contention. This would become a pattern over the years.
1973- One limo, a red carpet, and a goat denied once again
In 1973, Billy Goat’s nephew and new Billy Goat Tavern owner, Sam Sianis, with the help of Tribune columnist, Dave Condon, brought the goat to Wrigley in an attempt to lift the curse. The goat was escorted to Wrigley in a white limousine, and given a red carpet entrance to the park with a sign saying, “All is forgiven. Let me lead the Cubs to the pennant.” The ushers at the entrance denied the goat “Socrates,” a descendant of Murphy, yet again. The Cubs saw their mid-season first place lead whither away to another unsuccessful season.
1984- Eight outs away
The Tribune Company, new owners of the Cubs, finally invited the goat to opening day at Wrigley Field in an attempt to lift the curse. Sam Sianis and his goat finally walked the grass of Wrigley Field, and in an effort to lift the curse Sam raised his hat and said, “The curse is lifted.” The Cubs won and won and won their way to their first post season game and division title in almost forty years. They continued their winning taking the first two games of the National League Championship Series against the San Diego Padres. They just needed to win one of the next three games at San Diego to finally reach the World Series. Sam and his goat waited for the call to go along with the team and ensure the victory, only to be left behind in Chicago.
After losing games three and four in San Diego, the Cubs were leading the Padres 3-2 in the seventh inning, with only eight outs needed to win the game and the ace pitcher Rick Sutcliffe at the helm. An eerie chain of events would ensue. A routine ground ball was hit to first baseman, Leon Durham, which dribbled through his legs allowing the tying run to score. An overworked Rick Sutcliffe, who dominated game one, yielded the remaining three runs. The Padres swept the Cubs in San Diego, and swept the Cubs out of the series. The Cubs were still cursed.
1989- So Close, So Far
Hoping for a repeat of 1984, Sam Sianis and his goat again walked the field of Wrigley on opening day. The Cubs again won their way to first place and their second division title in five years. But the goat was left behind once again in the post season, where the Cubs lost to the San Francisco Giants four games to one.
1994- “Let the Goat in!”
The Cubs started the 1994 season horribly, losing twelve home games in a row. Their worst home start in history. In an effort to end this streak, Sam Sianis and his goat went to Wrigley Field only to be denied entrance yet again. Amidst the chant of “Let the Goat in!” amongst the Wrigley crowd, Hall of Famer, Ernie Banks helped by escorting Sam and his goat into Wrigley. The Cubs won the game 5-2, ending their worst home start ever. A lesson learned?
1998- Bring in the Wild Card
In 1998, the Cubs finished the season with 89 wins, tied with the San Francisco Giants for the Wild Card. During the Tiebreaking game on Sept. 28th, the Cubs brought in their Wild Card, Sam and his goat. The Cubs would go on to win the game 5-3 and went into the post season as a Wild Card. But once again Sam and his goat were left behind in Chicago, while the Cubs got swept in Atlanta, and swept out of the post season.
2003- Five outs away
The Cubs ended the 2003 season in a tight race with the Houston Astros. When the goat was sent to Houston in an effort to reverse the curse, Houston lost while the Cubs won their first division title in fourteen years. The Cubs were on a roll. They would go on to beat the Atlanta Braves, winning their first post season series in almost 100 years. In the National League Championship Series against the Florida Marlins, the Cubs took a quick 3 game lead needing only one more victory to go to the World Series for the first time in almost sixty years. In game six of the series, with the ace Mark Prior at the helm, the Cubs entered the eighth inning leading 3-0. Once again the goat was left behind, and an eerie chain of events would ensue. With only five outs needed to secure a victory, a pop foul seemingly in play was interfered with by a fan taking away a sure out. That was followed by the next play, when a routine ground ball was hit to the sure handed Alex Gonzalez only to be bobbled, taking away an inning ending double play. Ace pitcher, Mark Prior, overworked, yielded the tying and leading runs, until the Marlins left the eighth leading 8-3. The Marlins ended up winning the game, then swept the Cubs at home and swept them out of the playoffs yet again.
What does the future hold in store for the Cubs? Many attempts have been made to lift the curse, yet the goat still has not seen his baseball game. One moment in time, one horrible mistake in game four of the 1945 World Series, has yielded years of pain and anguish for Cubs fans abroad. The Chicago Cubs prior to the curse were one of the best teams in baseball, and after the curse have become the “Lovable Losers.” If the Cubs are ever again in a situation, where they are outs away from the World Series, will the goat get the call? For the sake of the Cubs, “LET THE GOAT IN!”
2015 – Murphy’s Law
Under new Manager Joe Maddon, the 2015 Cubs fielded a team of exciting young players. They captured the Wild Card, won a single game playoff against the Pirates, and went on to beat the rival St. Louis Cardinals in the division series. Only the Mets stood between the Cubs and their first World Series appearance since 1945. However, their momentum came to a sudden halt when they ran into Daniel Murphy. He hit a home run in all four games of the series and the Cubs were once again swept out of the playoffs.
2015 wasn’t the first time “Murphy” played a role in Cubs’ history: |||||
What is a shorter version of the above article? | – The Cubs beat the Brewers 4-0 last night, gaining ground toward a wild-card spot in the National League playoffs, and if Chicago wins tonight, they may have a goat to thank. For 69 years, 11 months, and 17 days, the MLB team has labored under "The Billy Goat Curse," which the superstitious believe has kept the Cubs from winning a title in Wrigley Field—and that a group of competitive eaters hoped to break last night by devouring a 40-pound goat, NBC Chicago reports. The curse was supposedly cast during the 1945 World Series, when Billy Sianis, the owner of Billy Goat Tavern, is said to have shown up at the ballpark with his pet goat, Murphy. The goat wasn't allowed entry by Cubs owner PK Wrigley himself because it reeked, the Washington Post notes, and Sianis reportedly screamed in a rage outside the park: "The Cubs ain't gonna win no more!" The Cubs not only lost that World Series, but they haven't been back to the championships since, earning them the nickname the "Lovable Losers." Past attempts to lift the curse have proven futile, the tavern's website notes. Per the Post, hot dog-eating champ Takeru Kobayashi joined four other competitive eaters at a Chicago restaurant last night to break the spell, and their alchemy involved chowing down on a cooked 40-pound goat in a chowdown one observer said transpired in "about twelve minutes," adding, "That was … disgusting." And if the Cubs don't make the playoffs? As the Post puts it, the goat gorging will just have been "much ado about mutton." If they win the World Series, however, you could have a shot at an $85,000 DeLorean. (Read all about the curse here.) | multi_news_1_0_0 |
|
Women with insomnia or other sleep problems have an increased risk of giving birth prematurely, a new study suggests.
The observational study, in Obstetrics & Gynecology, included 2,172 women with a sleep disorder who gave birth between 2007 and 2012 to single children after 22 to 44 weeks of gestation. They were matched with the same number of women with the identical ethnic, health and behavioral characteristics, but who did not have a sleep disorder.
Over all, women with sleep disorders had a 14.6 percent prevalence of preterm birth (before 37 weeks of gestation), compared with 10.9 percent in those without a diagnosis. Those with insomnia had a 30 percent increased risk, and those with sleep apnea a 40 percent increased risk, compared with women without a sleep problem.
Women with insomnia were nearly twice as likely to deliver before 34 weeks gestation.
“More severe sleep disorders are often underdiagnosed, because poor sleep is common during pregnancy,” said the lead author, Jennifer N. Felder, a postdoctoral researcher in psychology at the University of California, San Francisco. “But for women having sleep problems that are severe, impairing and distressing, it’s important to talk to their health care providers.” ||||| (Reuters Health) - Women who experience sleep disorders like insomnia and apnea during pregnancy may be more likely to deliver premature babies than pregnant women who don’t have trouble sleeping, a U.S. study suggests.
Compared with women who didn’t have sleep problems, women with insomnia were 30 percent more likely to have a preemie and the odds for women with sleep apnea, a breathing disorder, were 50 percent higher, the study found.
“It is normal to experience sleep changes during pregnancy - often due to discomfort, pain or frequent trips to the bathroom,” said lead study author Jennifer Felder, of the University of California, San Francisco.
“The current study focused on more impairing sleep problems that were severe enough to result in a sleep disorder diagnosis,” Felder said by email.
Apnea, a potentially serious sleep disorder that involves repeated stops and starts in breathing, has been linked to high blood pressure during pregnancy, which is an independent risk factor for preterm births. Obesity and advanced age can make apnea more likely.
Even though many pregnant women have insomnia at some point, previous studies haven’t offered a clear picture of how this type of sleep deprivation influences the odds of preterm births.
Worldwide, preterm birth is the leading cause of death for children under 5 years old, the researchers note in the journal Obstetrics and Gynecology.
Pregnancy normally lasts about 40 weeks, and babies born after 37 weeks are considered full term. The new study focused on preterm infants, delivered at 34 to 36 weeks’ gestation, and extremely premature babies delivered before 34 weeks.
In the weeks immediately after birth, preemies often have difficulty breathing and digesting food. They can also encounter longer-term challenges such as impaired vision, hearing, and cognitive skills as well as social and behavioral problems.
The study team examined data on more than 3 million births in California from 2007 to 2012. They focused on 2,172 women who had a sleep disorder diagnosis and compared their birth outcomes to a randomly selected group of 2,172 mothers who were similar in many ways but had no sleep issues.
Women with sleep disorders were more likely to be black, age 35 or older, obese, and to have other medical issues like high blood pressure, diabetes and infections as well as higher odds of smoking or using drugs and alcohol while pregnant. They were also more likely to have a history of preterm birth.
Overall, almost 15 percent of women with sleep disorders had a preterm birth, compared with 11 percent of women without sleep issues.
The study wasn’t a controlled experiment designed to prove how or even whether sleep disorders directly cause preterm births.
Even so, the results offer fresh evidence of the link between sleep disorders and early arrivals, said Dr. Ghada Bourjeily, a researcher at Warren Alpert Medical School of Brown University in Providence, Rhode Island, who wasn’t involved in the study.
“Sleep appears to get worse in pregnancy in many, even women who do not have a preexisting sleep disorder,” Bourjeily said by email. “Unfortunately, we do not know yet whether improving sleep quality before or during pregnancy would prevent development of negative outcomes such as preterm birth.”
Starting pregnancy at a healthy weight, however, may make sleep disorders less likely, said Dr. Amos Grunebaum, director of obstetrics at NewYork-Presbyterian Hospital/Weill Cornell Medical Center in New York.
“Being overweight or obese increases your risk of having a sleep disorder,” Grunebaum, who wasn’t involved in the study, said by email. “It also increases pregnancy complications.”
When sleep disorders do surface during pregnancy, women should discuss symptoms in detail with their doctors, said Dr. Milena Pavlova, a researcher at Brigham and Women’s Hospital in Boston who wasn’t involved in the study. This includes any issues with breathing, gasping or choking at night or any uncomfortable leg or body sensations that prevent sleep.
Expectant mothers should also make sleep a priority in their schedules, Pavlova, who wasn’t involved in the study, said by email.
“Allow enough time for sleep - the life you save may be your baby’s,” Pavlova said.
SOURCE: bit.ly/2j2fR06 Obstetrics and Gynecology, online August 8, 2017. ||||| Andrew Lichtenstein/Corbis/Getty
Despite strides in maternal medicine, premature birth remains a vexing problem for obstetricians worldwide. But an analysis of medical records from almost 3 million pregnant women in California1 suggests that a surprisingly simple intervention — better sleep — might help to address the issue.
Researchers found that women who had been diagnosed with insomnia or sleep apnoea were about twice as likely as women without sleep disorders to deliver their babies more than six weeks early.
“It seems obvious, but strangely this study has not been done before,” says Laura Jelliffe-Pawlowski, an epidemiologist at the University of California, San Francisco (UCSF), and an author of the research, which was published on 8 August in the journal Obstetrics and Gynecology1. “Seeing this relationship is important because we are just starved for interventions that can make a difference.”
Public-health experts say that better treatment for pregnant women with serious sleep disorders could save babies' lives, and do so with approaches that avoid the use of medication. Every year, 15 million babies worldwide are born prematurely — more than three weeks before the typical full-term pregnancy of 40 weeks. These children have less time to develop in the womb, and 1.1 million will die from birth-related complications. Many others are left with hearing impairment, learning disabilities, cerebral palsy and other health issues.
The new study is part of the UCSF Preterm Birth Initiative, an ambitious US$100-million effort to study prematurity, focusing on California and East Africa. The researchers working on the effort plan to mine large quantities of historical data, ensuring that any findings are statistically significant. They hope to use these findings to identify medical and social interventions that could reduce preterm births, and test them in trials of pregnant women.The programme is funded by the Bill and Melinda Gates Foundation and philanthropists Lynne and Marc Benioff.
Forty winks for forty weeks
Jennifer Felder, a postdoctoral researcher in clinical psychology at UCSF who led the study, says that she had been troubled by the lack of research on sleep and pregnancy. Because pregnant women often have some difficulty sleeping, she suspects that doctors and researchers had not thought to examine the consequences of sleep disorders more closely.
Felder and her colleagues acquired the records of almost three million births that took place in California between 2007 and 2012, which were scrubbed of identifying information but linked to hospital-discharge papers from the women who had given birth. Each record contained a medical history of the mother and notes taken throughout her pregnancy and baby's delivery. Doctors had diagnosed about 2,300 of the women with a sleep disorder during their pregnancy. Insomnia and sleep apnoea were the main problems, although narcolepsy, excessive sleepiness and restless leg syndrome were also seen.
Insomnia, the researchers found, increased a woman's risk of preterm birth by 30%, while sleep apnoea increased the risk by 40%. Sleep disorders also increased the risk of very premature births: 5.3% of women with sleep issues delivered their babies at less than 34 weeks' pregnancy, compared to 2.9% for women without such a diagnosis.
Felder says that a lack of sleep is unlikely to be a direct cause of early births. But it could trigger other processes, such as inflammation, that eventually result in prematurity. A 2010 review of studies linked premature birth to the presence of the inflammatory proteins C-reactive protein and interleukin-6, in amniotic fluid2. To explore the idea, the UCSF initiative will soon begin to examine immune-system proteins in pregnant women using blood stored in a repository associated with California’s department of public health. The scientists will compare samples with an attention to premature birth and insomnia.
And in the meantime, sleep troubles in expectant mothers can alert doctors to potential danger. “I counsel women on how to have the best pregnancy outcome,” says Louis Muglia, the director of the Center for Prevention of Preterm Birth at Cincinnati Children’s Hospital Medical Center in Ohio. “Now I might start asking, 'do you get a good night’s sleep?'.” |||||
Write a summary. | – A new study suggests that one way to cut down on premature births is to make sure pregnant women get good sleep. The observational study, published in the journal Obstetrics & Gynecology, found that women diagnosed with some kind of sleep disorder were more likely to give birth early, reports the New York Times. Overall, 15% of such women had preemies, compared to 11% among women without a sleep disorder. More specifically, a diagnosis of insomnia raised the risk of having a pre-term birth by 30% and sleep apnea by 40%. Similarly, sleep disorders were associated with more births characterized as "very premature," reports Nature. The study found that 5.3% of women with such disorders delivered 34 weeks or earlier, compared with 2.9% for those without a disorder. “It seems obvious, but strangely this study has not been done before,” says co-author Laura Jelliffe-Pawlowski, an epidemiologist at the University of California, San Francisco. "Seeing this relationship is important because we are just starved for interventions that can make a difference.” The authors make clear they're referring to women with diagnosed problems, not merely to women who occasionally have trouble sleeping while pregnant, which is fairly common. They found that sleep disorders are more common among women who are black, 35 or older, obese, and have other medical issues, reports Reuters. Based on the study, one piece of advice for women planning to have kids is to try to start the pregnancy at a healthy weight. (Some evidence supports therapy over pills to treat insomnia.) | multi_news_1_0_0 |
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Methods: We conducted a cohort study of 1636 women from two prospective breast cancer cohorts. Intrinsic tumor subtype (luminal A, luminal B, human epidermal growth factor receptor 2 [HER2]–enriched, basal-like) was determined by the PAM50 gene expression assay. Breastfeeding history was obtained from participant questionnaires. Questionnaires and medical record reviews documented 383 recurrences and 290 breast cancer deaths during a median follow-up of nine years. Multinomial logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) between breastfeeding and tumor subtype. Cox regression was used to estimate hazard ratios (HRs) for breast cancer recurrence or death. Statistical significance tests were two-sided.
Results: Breast cancer patients with basal-like tumors were less likely to have previously breastfed than those with luminal A tumors (OR = 0.56, 95% CI = 0.39 to 0.80). Among all patients, ever breastfeeding was associated with decreased risk of recurrence (HR = 0.70, 95% CI = 0.53 to 0.93), especially breastfeeding for six months or more (HR = 0.63, 95% CI = 0.46 to 0.87, P trend = .01). Similar associations were observed for breast cancer death. Among women with luminal A subtype, ever breastfeeding was associated with decreased risks of recurrence (HR = 0.52, 95% CI = 0.31 to 0.89) and breast cancer death (HR = 0.52, 95% CI = 0.29 to 0.93), yet no statistically significant associations were observed among the other subtypes. Effects appeared to be limited to tumors with lower expression of proliferation genes. ||||| By Kathleen Doheny
HealthDay Reporter
TUESDAY, April 28, 2015 (HealthDay News) -- Women who breast-feed their babies and later develop breast cancer are less likely to have the cancer return or to die from it than women who do not breast-feed, new research shows.
"We found in this study of over 1,600 women with breast cancer that those who previously breast-fed had a 30 percent overall decreased risk of their breast cancer recurring," said study leader Marilyn Kwan, a research scientist at the Kaiser Permanente division of research in Oakland, Calif. "We also found those who previously breast-fed had a 28 percent reduced risk of dying from their breast cancer."
The study was published online April 28 in the Journal of the National Cancer Institute.
Previous research has found that breast-feeding is linked with a lower risk of developing breast cancer in the first place, the researchers said.
"If a woman breast-feeds, she reduces her risk of developing breast cancer by about 5 percent to 10 percent, although other factors come into play," Kwan said, such as the number of children she has had. "We think this is one of the first [studies] to examine the role of breast-feeding and breast cancer outcomes -- prognosis and survival," she added.
"Overall, our study confirms that breast-feeding is not only good for the baby, but has potential health benefits for the mom," Kwan said.
Her team found that breast-feeding's protective effect in lowering the chances of recurrence or death from breast cancer was strongest against the most commonly diagnosed breast cancers.
The study builds on previous evidence about the link between breast-feeding and breast cancer, said Dr. Joanne Mortimer, director of Women's Cancer Programs and co-director of the Breast Cancer Program at City of Hope Cancer Center, in Duarte, Calif.
The message that's reinforced in the new research, Mortimer explained, is that ''women who breast-feed get less aggressive breast cancer." While that has been known, the new study adds detailed findings about tumor types, she said.
Kwan's team looked at two groups of women, some diagnosed from 1997 to 2000 and others diagnosed from 2006 to 2013. Most were patients at Kaiser Permanente, a large health maintenance organization.
The researchers found an association between breast-feeding and a more favorable outcome for breast cancer patients, but the study didn't prove cause-and-effect. The investigators found the link to be statistically significant with breast cancers known as luminal A subtypes, including tumors known as estrogen receptor-positive (ER-positive), the most common of all breast cancers. However, they did not find the link to be statistically strong for other subtypes of breast cancer.
While Kwan found an overall 30 percent reduced risk of breast cancer recurrence among those who breast-fed, when they took the length of breast-feeding into account, any duration decreased risk, but the link was not as strong for those who did so for less than six months.
The American Academy of Pediatrics (AAP) recommends exclusive breast-feeding for about six months, followed by continued breast-feeding as foods are introduced, for up to a year or longer. Breast-feeding helps protect babies from diseases such as diabetes, from infection and from becoming overweight. Mothers who breast-feed have a lower risk of developing breast and ovarian cancers, according to the AAP.
Kwan and others speculate that breast-feeding may be protective for a number of reasons. For instance, it reduces a woman's lifetime number of menstrual cycles, and that lowers the accumulated exposure to hormones that can help some cancers grow. Breast-feeding also increases differentiation, or maturation, of the ductal cells in the breast, perhaps making them more resistant to cancer, Kwan explained.
Mortimer said that possible mechanism makes sense, based on a concept that the breast isn't fully developed until a woman has lactated.
More information
To learn more about breast-feeding, visit the U.S. Department of Health and Human Services. |||||
Write a summary. | – It appears that women who breastfeed are imparting health benefits not just to their children but to themselves as well. So suggests a new study out this week in the Journal of the National Cancer Institute involving 1,636 women with breast cancer; those who breastfed their babies were 30% less likely to have the cancer recur and 28% less likely to die from it than those who had never breastfed. The research builds on previous findings that breastfeeding reduces a woman's overall chance of getting breast cancer in the first place. "If a woman breastfeeds, she reduces her risk of developing breast cancer by about 5% to 10%, although other factors come into play," such as how many children she's had, study leader Marilyn Kwan at Kaiser Permanente tells HealthDay News. "We think this is one of the first [studies] to examine the role of breastfeeding and breast cancer outcomes—prognosis and survival." Of note: while any duration of breastfeeding improved prognosis and survival to some degree, doing so for less than six months was less protective. Kwan adds to the chorus of researchers who postulate that breastfeeding helps ductal cells fully mature and thus better resist cancer. (When it comes to getting breast cancer in the first place, the numbers are even more convincing.) | multi_news_1_0_0 |
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News article:
This photo provided by the Long Beach Fire Department shows Captain David Rosa who was fatally shot while responding to an emergency at a senior home on Monday, June 25, 2018 in Long Beach, Calif. Rosa,... (Associated Press)
This photo provided by the Long Beach Fire Department shows Captain David Rosa who was fatally shot while responding to an emergency at a senior home on Monday, June 25, 2018 in Long Beach, Calif. Rosa, a long-time veteran of the department and leaves behind a wife and two children. Another firefighter... (Associated Press)
LONG BEACH, Calif. (AP) — A 77-year-old man set a fire to lure firefighters to his Southern California retirement home so he could shoot them, authorities said. The attack killed one firefighter and wounded another.
Thomas Kim was arrested Monday on suspicion of murder, attempted murder and arson but investigators were still trying to determine a motive for the attack in the southern Los Angeles suburb, Police Chief Robert Luna said.
"There's still is a large puzzle we're trying to put together. There's still a lot of information we don't know," Luna said.
Kim remained jailed on $2 million bail and it was unclear whether he had an attorney.
Firefighters were called to the 11-story Covenant Manor at around 4 a.m. Monday by reports of an explosion. They found some second-floor windows blown out, activated sprinklers, the smell of gas and a fire that they extinguished, authorities said.
Firefighters were searching the building when shots rang out and the two firefighters were hit, Fire Chief Michael DuRee said.
Fire Capt. Dave Rosa, a 17-year veteran, died at a hospital, the chief said. He is survived by a wife and two children ages 16 and 25.
"Long Beach lost a hero today," Mayor Robert Garcia said.
Dozens of firefighters stood at attention and saluted as the flag-draped coffin carrying Rosa's body was brought out of a hospital Monday afternoon and loaded into a coroner's van. Community members waved American flags along the street outside the hospital as the procession of police and fire vehicles escorted the van to the coroner's office.
The other firefighter, Ernesto Torres, was released from the hospital and was expected to make a full recovery, officials said.
An elderly resident at the retirement home was also shot and was in critical but stable condition, Luna said. However, the circumstances of that shooting were not immediately known.
The police chief said a revolver was found after Kim was arrested. Investigators also called in a bomb squad to render two suspicious devices safe.
Luna didn't explain the nature of the devices but said detectives have "a lot of questions" about them and what Kim intended to do with them.
Eighty senior citizens were evacuated from the retirement home until it could be declared safe.
"This is a lot to deal with," said Pamela Barr, 73, as she sat with her son in a car, waiting to be allowed back in the tower.
Barr, who lives on the ninth floor, said she hadn't heard of any troubles involving residents of the facility, where she has lived for seven years. She described it as clean, well-run and secure.
The residential tower near downtown Long Beach has 100 apartments for low-income people age 62 and older as well as disabled adults, according to its website.
Long Beach is a major port city with a population of more than 400,000.
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Balsamo reported from Los Angeles. Associated Press writer John Antczak in Los Angeles contributed to this report. ||||| Firefighters pay their respects to Capt. Dave Rosa, 45, on Monday, June 25, 2018 during a procession taking his body from St. MaryÕs Hospital in Long Beach to the coronerÕs office. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Paul Bersebach, Orange County Register/SCNG)
A portrait of Long Beach Fire Captain Dave Rosa, 45, during a press conference after he was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
CHP escortes the fallen firefighter, Capt. Dave Rosa, to the L. A. County Coroners office in Los Angeles on Monday, June 25, 2018, on the 710 freeway as firefighters salute on the overpass. (ABC-7)
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The Los Angeles City Fire Department honor guard brings a wreath to St. Mary Medical Center after Long Beach Fire Captain David Rosa was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Firefighters pay their respects to Capt. Dave Rosa, 45, on Monday, June 25, 2018 during a procession taking his body from St. MaryÕs Hospital in Long Beach to the coronerÕs office. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Paul Bersebach, Orange County Register/SCNG)
Corinna Rowe of Long Beach said she was showing her support for all firefighters during a procession for Capt. Dave Rosa, 45, on Monday, June 25, 2018 to take his body from St. MaryÕs Hospital in Long Beach to the coronerÕs office. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Paul Bersebach, Orange County Register/SCNG)
The body of Long Beach Fire Captain David Rosa leaves St. Mary Medical Center inside a coroner’s van after he was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Adrian Duran of Boyle Heights came out to honor fallen Long Beach Fire Capt. Dave Rosa at the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters console each other outside St. Mary Medical Center after Fire Captain David Rosa was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Residents of the elderly living facility where the shooting of the Long Beach Fire Fighter took place are escorted away from the building for their safety on Monday June 25, 2018. (Photo by Tracey Roman)
Long Beach Assistant Fire Chief Xavier Espino outside St. Mary Medical Center after Fire Captain David Rosa was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach firefighters console each other outside St. Mary Medical Center after Fire Captain David Rosa was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach Fire Department Capt. Dave Rosa, 45, was killed after being struck by gunfire while responding to reports of an explosion at Covenant Manor in Downtown Long Beach. (Photo courtesy of Long Beach Fire Department)
LONG BEACH, CA – JUNE 25: Jenn Ochoa of Los Alamitos shows her support during a procession for Capt. Dave Rosa, 45, to take his body from St. Mary’s Medical Centerin Long Beach to the coroner’s office on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Paul Bersebach/Orange County Register/SCNG)
Long Beach firefighters salute as a van carrying the family of Fire Captain David Rosa leaves St. Mary Medical Center after his body left in a coroner’s van after he was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
A Long Beach Firefighter wears a black band over their badge in remembrance of Fire Captain Dave Rosa, 45, who was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach Firefighters CHP and Police escort the body of fallen Fire Captain David Rosa down the 710 Freeway Monday afternoon on Monday June 25, 2018. (Photo by Tracey Roman)
Officials investigate at Covenant Manor in the 600 block of E. 4th St. in Long Beach where Capt. Dave Rosa, 45, was killed on Monday, June 25, 2018 while responding to a fire call. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at the downtown Long Beach high-rise. (Photo by Paul Bersebach, Orange County Register/SCNG)
Officials investigate at Covenant Manor in the 600 block of E. 4th St. in Long Beach where Capt. Dave Rosa, 45, was killed on Monday, June 25, 2018 while responding to a fire call. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at the downtown Long Beach high-rise. (Photo by Paul Bersebach, Orange County Register/SCNG)
Windows blown out in explosion at Long Beach retirement home where a Long Beach Fire Department Capt. Dave Rosa, 45,was shot to death today. (Photo by Kelly Puente, Orange County Register/SCNG)
The scene from 3rd and Atlantic where firefighters responding to a report of an explosion in a high-rise apartment in downtown Long Beach shortly before 4 a.m. were met with gunfire, with two getting struck on June 25, 2018. (Photo by Megan Barnes)
Long Beach firefighters line 11th. Street as they wait for the body of Long Beach Fire Captain David Rosa to leave St. Mary Medical Center after he was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach Fire Department Capt. Dave Rosa, 45, who was killed in the line of duty on Monday, June 25, 2018, was active in the Capo Valley Little League as the Vice President and umpire for the league in this 2007 file photo. (Photo by David Bro, Contributing Photographer)
This .357 revolver was recovered at the scene where Long Beach Fire Captain Dave Rosa, 45, was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach Mayor Rober Garcia, left, and Fire Chief Mike Duree outside St. Mary Medical Center after Fire Captain David Rosa was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach firefighters line 11th. Street as they wait for the body of Long Beach Fire Captain David Rosa to leave St. Mary Medical Center after he was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. (Photo by Jeff Gritchen, Orange County Register/SCNG)
LAFD puts a flag in place for the arrival of Long Beach Capt. Dave Rosa at the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
The body of Long Beach Fire Capt. Dave Rosa arrives as the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters embrace as they await the arrival of the body of Capt. Dave Rosa at the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters embrace as they await the arrival of the body of Capt. Dave Rosa at the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Displaced Covenant Manor residents were shuttled to Silverado Park for medical evaluations and meals. The city and the American Red Cross set up cots in the gym. (Photo by Megan Barnes, Long Beach Press-Telegram/SCNG)
Long Beach firefighters salute as the body of Capt. Dave Rosa arrives as the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters salute as the body of Capt. Dave Rosa arrives as the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters salute as the body of Capt. Dave Rosa arrives as the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters embrace as they await the arrival of the body of Capt. Dave Rosa at the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach firefighters salute as the body of Capt. Dave Rosa arrives as the Los Angeles County Coroners office Monday afternoon. Rosa and other firefighters were shot at while responding to a fire call early Monday morning. Rosa died from his injuries and another firefighter was treated and released. No suspect has been named in the shooting. (Photo by David Crane, Daily News/SCNG)
Long Beach Fire Chief Mike Duree and Mayor Robert Garcia chat after a press conference for Fire Captain Dave Rosa, 45, who was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
A portrait of Long Beach Fire Captain Dave Rosa, 45, as Long Beach Fire Chief Mike Duree talks about him during a press conference after he was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach Fire Chief Mike Duree during a press conference after Fire Captain Dave Rosa, 45, was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Flowers and cards are left at Fire Station 10 in Long Beach where Capt. Dave Rosa, 45, worked. Rosa was killed on Monday, June 25, 2018 while responding to a fire call at a downtown Long Beach high-rise. (Photo by Paul Bersebach, Orange County Register/SCNG)
Long Beach Chief of Police Robert Luna during a press conference after Fire Captain Dave Rosa, 45, was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
Long Beach Fire Chief Mike Duree during a press conference after Fire Captain Dave Rosa, 45, was shot and killed responding to a fire in Long Beach, CA, on Monday, June 25, 2018. Rosa and another firefighter were struck by gunfire while responding to reports of an explosion at a downtown Long Beach high-rise. (Photo by Jeff Gritchen, Orange County Register/SCNG)
A decorated, widely respected Long Beach fire captain responding to an explosion at high-rise retirement home was gunned down early Monday morning in a puzzling attack that authorities said was orchestrated by a 77-year-old resident of the facility, who possibly planned the ambush but whose motive remained a mystery.
A second firefighter was grazed by gunfire and was expected to make a full recovery, and an elderly resident who was shot was in critical condition.
As firefighters and other law enforcement personnel across Long Beach, and the state, mourned the loss of veteran fire Capt. Dave Rosa, Long Beach police announced they had apprehended Thomas Kim, a second-floor resident of the building, in connection with both the explosion and the shootings. He was arrested on suspicion of murder, two counts of attempted murder and arson. He was held on $2 million bail.
Kim has a previous arrest years ago for auto theft, police said. But they were trying to figure out a motive for Monday’s attacks.
“We’re frustrated that there’s a large puzzle we’re trying to put together, and a lot of information we don’t know yet,” Police Chief Robert Luna said.
Police were investigating whether Kim set the fires prior to the attack on the two firemen, and said suspicious devices were found in his apartment.
Long Beach Fire Chief Mike DuRee identified the fallen firefighter as Rosa, a 45-year-old captain for the past 6½ years.
Rosa worked the busiest fire stations in the city, most recently Fire Station No. 10, DuRee said, and he trained new firefighters.
He leaves behind a wife and two sons ages 16 and 25.
“He was a staunch family man, a good husband, a good father, a joy to be around, just a wonderful wonderful person, as are most firefighters,” DuRee said. “It’s left quite a big void.”
Rosa’s death triggered an emotional outpouring of support from firefighters and police departments across the state, as well as from elected leaders, including. Gov. Jerry Brown.
“It was with great sadness that Anne and I learned Fire Captain David Rosa passed away today while protecting the residents of a retirement home,” the governor said in statement. “Our deepest condolences go out to Captain Rosa’s family, friends and the entire Long Beach Fire Department as they mourn his tragic death.”
The wounded firefighter was Ernesto Torres, 35, who has 12 years with the department. He suffered a graze wound and was discharged from the hospital and is expected to make a full recovery.
An elderly resident of the building was in a hospital listed in critical but stable condition.
The 11-story, 100-unit Covenant Manor houses low-income senior citizens in the 600 block of East Fourth Street near Atlantic Avenue.
When asked whether the attack was a planned ambush, Police Chief Luna said, “That is definitely on the table. … We’re going to be looking at that. That’s the environment we work in today as law enforcement and firefighters.
“You go to these scenes and you never know what’s on the other side of those doors,” he said. “These brave firefighters went through those doors and, unfortunately, they were met with gunfire.
“We’re brothers and sisters, so this is hitting us extremely hard,” the chief said.
Police recovered a revolver at the scene, and a sheriff’s department bomb squad examined two devices that were deemed to be “suspicious,” Luna said. They were rendered safe, he said, and flammable liquids believed to be gasoline were removed from the scene.
“We have a lot of questions about the devices that were found and the suspect’s intent, which we do not have a full picture of yet,” Luna said.
He said preliminary evidence and witness interviews point to an intentional set-up.
DuRee said that while he has heard of firefighters being targeted in other parts of the country, “this is the first time we’ve ever experienced anything like this.”
The last time a Long Beach firefighter was killed in the line of duty was in 1974.
Kim was arrested about 6 a.m., according to jail records.
“Patrol officers immediately started to search for the shooter as we normally do in these situations, we try and isolate him and save anybody else from being shot,” Luna said.
Thomas Kim’s only major vice is gambling and that cost him his marriage several years ago, according to his brother.
“His wife left him because he gambled,” George Kim, who hasn’t spoken to his brother in nearly 30 years, said. “That is the only thing that is a bad habit.” Thomas Kim and his ex-wife, who is a nurse, have one daughter.
Thomas Kim’s immigrated to the U.S. in the 1960’s, graduated from college and briefly worked as a civil engineer in the LA area.
He then worked in the construction industry in Korea and in Saudi Arabia before returning to the U.S. Thomas Kim, who is diabetic, would also buy clothing items at LA flea markets and then resell them in Mexico, George Kim said. He plans to visit his brother in jail.
“I don’t know what it will be like to see him. I haven’t seen him in almost 30 years,” he said. “I thought he was dead. I’m going to find out what happened to him.
About 3:49 a.m., firefighters received the initial report, said Jake Heflin, a spokesman for the Long Beach Fire Department, with residents reporting a strong smell of gasoline.
“They did notice some windows were blown out and sprinklers were on,” he said.
Within 10 minutes, firefighters had knocked down the fire, apparently on the second floor. Another 10 minutes later, shots were fired, with the victims hit by the gunfire, Heflin said.
Today is an incredibly sad day for Long Beach and the Long Beach Fire Department. We’ve lost one of our local heroes and another is injured but stable. We are all praying and sending love to the families and our @lbfd team. — Robert Garcia (@RobertGarciaLB) June 25, 2018
By late morning, 80 Covenant Manor residents had been bused to a nearby Covenant Presbyterian Church, where they were interviewed by police. Many were still in their pajamas.
Afterward, one woman, visiting her son, said she heard a loud boom on the second floor.
“I was so nervous,” said the woman, who would only give her name as Ms. Harris. “I slipped on my sweatpants and ran downstairs.”
She said she didn’t even know about the shooting, but added, “It looked like it blew a window clean out of the building.”
The residents were then bused to Silverado Park’s gym, where city employees and the American Red Cross set up green cots. They were expected to return home Monday evening.
The displaced residents were offered meals and evaluated for their medical needs. Many have chronic conditions, such as diabetes, or use walkers and wheelchairs to get around.
James Park, a spokesman for HumanGood, which operates Covenant Manor, said the nonprofit is “focusing on helping those residents who were displaced from their homes and assisting the authorities in their ongoing investigation.”
Ronald Keller, sitting barefoot in his wheelchair, said police rescued him from his apartment on the 9th floor, where he lives alone.
“I heard a bang, then I heard glass breaking or scattering across the floor,” he said. “I didn’t know what was going on.”
Keller started going down the hallway, when police told him to stay in his apartment and wait for them take him to safety. From his window while he waited about 15 minutes, he watched a flurry of police activity.
“I’m used to hearing gunshots in this area,” Keller said.
Then police came for him, he said: “They came and pushed me to the elevators.”
Adrian, who declined to provide his last name, said he, his dachshund mix and others escaped the building by going down the stairs. The elevator doors had automatically locked after the fire alarm sounded.
“I was woken by a big boom and initially thought there was an earthquake,” he said.
Friends who live on the second floor told Adrian they heard two gunshots after the blast. He was saddened to learn the gunfire claimed the life of a fireman: “I’m so sorry. There are crazy people all over the place, and good people lose their lives.”
Neal Day, a military veteran who lives next door to the building, said he slept through the explosion, but his neighbors were rattled and initially thought it was a bad car crash.
“It was pretty chaotic and confusing since they were trying to evacuate all of the seniors inside,” he said.
Late Monday morning, police and fire officials collected at St. Mary’s Medical Center, exchanging handshakes, hugs and tears. A large crowd gathered.
An honor guard with the Los Angeles Fire Department brought a wreath of white, yellow and red flowers, with two yellow stripes across it in honor of Capt. Rosa.
Then, at about 12:30 p.m., a 16-vehicle procession that included a coroner’s van began a procession to take the body to the coroner’s office in Los Angeles, heading westbound on 11th Street, to Long Beach Boulevard and then onto the 710 Freeway.
In front were three motorcycle officers. They were followed by Engine No. 10, from Rosa’s station.
Along the 710, firefighters and perhaps other officials positioned their emergency trucks on the overpasses, standing outside and saluting Rosa as the procession moved along just below them.
A few civilians stood with them on the sidewalk in solidarity. An 8 p.m. vigil was planned at Fire Station No. 10.
“My dad was a fireman, so I just wanted to pay my respects,” said Tim McCord, a local oil field operator.
At Fire Station 10 in Central Long Beach, where Rosa was based, residents left notes, candles and flowers.
“First responders have a dangerous job, but this one really brought it close to home,” said Jay Maupin, who lives across the street from the station.
Abraham Garcia, 21, stopped by with a bouquet of two dozen red roses. Garcia, an aspiring firefighter, said he was one of Rosa’s students in the Long Beach Explorers youth program.
“He was always so passionate about what he did,” Garcia said.
One anonymous Long Beach resident left a poem with a note at the bottom: “Thank you for all the lives you’ve saved. I’m so sorry you lost yours.”
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What is a shorter version of the above article? | – A firefighter in Long Beach, Calif., was killed in the line of duty on Monday, and the circumstances are especially jarring: Authorities suspect that a 77-year-old resident of a nursing home deliberately set off an explosion, then waited for firefighters to arrive so he could shoot them, reports the Long Beach Press-Telegram. Thomas Kim, a resident of the 11-story building, is jailed on suspicion of murder, attempted murder, and arson. Police say he killed veteran fire Capt. Dave Rosa, 45, and wounded 35-year-old firefighter Ernesto Torres, who was expected to make a full recovery. A resident of the home also was shot and is in critical condition. “We’re frustrated that there’s a large puzzle we’re trying to put together, and a lot of information we don’t know yet,” says Police Chief Robert Luna. Police have not speculated about a motive, and Kim "hasn't given us much of an explanation," says another police official, per the Los Angeles Times. Firefighters arrived at Covenant Manor about 4am Monday after getting a report about an explosion, reports the AP. They discovered blown-out windows on the second floor and extinguished a fire, and were searching the building when gunfire broke out. Authorities later recovered a revolver from the scene, and found two suspicious devices in Kim's apartment as well as what is believed to be gasoline. An ambush? "That is definitely on the table," says Luna. "These brave firefighters went through those doors and, unfortunately, they were met with gunfire." | multi_news_1_0_0 |
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