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If lung cancer is most often caused by exposure to solid particles and gases, then what is most often caused by exposure to solid particles and gases? Answer choices: - syphilis - diabetes - contamination - scattered light - lung cancer - hair color - global warming - Pollution
The answer to this question is: | lung cancer | qasc_qa_with_combined_facts_1 |
|
If evaporation cools the body, then what is used to cool the body? Answer choices: - vaporization - exercise - Animal fur - magnetism - Solar energy - dry and hot - sun - evaporation
evaporation
If force that requires opposing motion causes the speed of an object to decrease, then what causes the speed of an object to decrease? Answer choices: - kilometers - kinetic energy - Electrical energy - increase h2o - principals of aerodynamics - basic building blocks of life - opposing motion force - increase oxygen
opposing motion force
Q: If exposure to tobacco smoke causes tumors, then what causes lung tumors? Answer choices: - oxidation reaction - cancer - Pollution - rays or beams - fossil fuels - diabetes - Pesticides - tobacco smoke
A: tobacco smoke
Question: If arefrigerator is used for keeping chicken fresh, then what does a refrigerator keep fresh? Answer choices: - animals - heat - salt - oysters - canned food - grass - chicken - trout
Answer: chicken
*Question*
If saving energy reduces the resources needed to make something, then what reduces the resources needed to make something? Answer choices: - water conservation - A computer - saving energy - Pollution - electron microscope - power stations - Fuel cells - Electrical energy
**Answer**
saving energy
If roller coaster work the same as any object having mass being pulled down on a planet, then roller coaster work the same as any object having mass being pulled how on a planet? Answer choices: - body - trains - left - intermittently - down - feet - Lift - sideways
| down | qasc_qa_with_combined_facts_1 |
|
If diabetes is caused by a lack of hormone that helps cells absorb sugar from the blood, then what is caused by a lack of a hormone that helps cells absorb sugar from the blood? Answer choices: - glucose - cancer - resistance - diabetes - fever - serotonin - epilepsy - Dehydration
diabetes
If the skin is used for protecting the body from contamination, then what does the skin protect the body from? Answer choices: - cigarettes - pain - discoloration - sun's heat - disease - blood - rays or beams - contamination
contamination
Q: If flowers attract insects, then flowers attract? Answer choices: - bees - parasites - electrons - insects - pollen - plant life - carbon - honeybees
A: insects
Question: If the movement of tectonic plates can lower the average temperature of the earth, then what effect could more active plate tectonics have on the earth? Answer choices: - rapid expansion - Decreased precipitation - a tree falling - the production of heat - Lower average temperature - Physical weathering - a lot of human deaths - Plant growth is reduced
Answer: Lower average temperature
*Question*
If moss is the strongest in tropical enviornments, then where is moss the strongest? Answer choices: - near the shoreline - looseness of dirt or compost - The area was once underwater - It used to be covered by water - dead organisms - tropical environments - our nearest star - the body's largest organ
**Answer**
tropical environments
*Question*
If using renewable resources to generate power reduces carbon dioxide, then what does using renewable resources to generate power reduce? Answer choices: - lowered energy cost - solar power - climate - evergreen trees - Heat energy - oxygen - carbon dioxide - kinetic energy
**Answer**
| carbon dioxide | qasc_qa_with_combined_facts_1 |
|
*Question*
If fur causes an organism to keep warm, then what does fur do? Answer choices: - it serves as food - refract or absorb. - It helps them survive - absorb light energy - it catches fire - it drowns the organism - structure and function - it keeps an organism warm
**Answer**
it keeps an organism warm
*Question*
If insulin helps cells take up sugar from the blood, then what does insulin help take up from the blood? Answer choices: - fat - diabetes - sugar - Joules - red blood cells - plasma - Energy. - Energy
**Answer**
sugar
*Question*
If evolution occurs through birth and death, then what occurs through birth and death? Answer choices: - sleep - illness - anemia - tearing - Leptospirosis - nature - starvation - evolution
**Answer**
evolution
*Question*
If animals can communicate with visual cues, chemicals, or something that is a wave, then animals communicate through what? Answer choices: - chemicals - A wave - fur - nerves - A vacuum - A telephone - A particle - Movement
**Answer**
| A wave | qasc_qa_with_combined_facts_1 |
|
If insulin helps cells to lower the blood sugar, then what helps cells to lower the blood sugar? Answer choices: - sugar - candy - sweating - blood draws - Energy - insulin - pancreas - exercise
insulin
If atulip's purpose is to produce seeds, then what is a tulip's purpose? Answer choices: - to produce water - spread flower seeds - It remains dormant - to produce sunlight - Reproduction - to produce carbon - to produce seeds - Plant reproduction
to produce seeds
Q: If condensation in clouds is similar to humidity in the air, then condensation in the air and humidity are caused by? Answer choices: - Sun - kinetic - heat - Joules - climate - sweat - boiling - water
A: water
Question: If nematoda reproduce sexually, then what reproduces sexually? Answer choices: - viruses - humans - insects - orchids - the Sun - Nematoda - ferns - plants
Answer: Nematoda
*Question*
If something that can be smooth can only contract, then something that can be described as what can only contract? Answer choices: - Smooth - the skin - Rough - strong - Sweet - Loud - complex - alveoli
**Answer**
Smooth
(Q).
If insulin helps cells take up sugar from the blood, then what does insulin help take up from the blood? Answer choices: - fat - diabetes - sugar - Joules - red blood cells - plasma - Energy. - Energy
(A).
| sugar | qasc_qa_with_combined_facts_1 |
|
Answer the following question: If influenza causes widespread disease, then what does influenza cause? Answer choices: - amoeba - diabetes - anemia - extinction - shingles - disease - measles - propagate
Answer: | disease | qasc_qa_with_combined_facts_1 |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
--------
Question: and the lay public in understanding the progress of Ebola virus disease and the continuing outbreak.
Answer: background
Question: Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
Answer: background
Question: On the other hand , viruses has evolved many strategies to combat or utilize the host autophagy for their own benefit.
Answer: | background
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Example Input: Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
Example Output: background
Example Input: the development of vaccines and antiviral agents for SARS-CoV is essential for improving control and treatment of future outbreaks.
Example Output: background
Example Input: and to examine associations between PWD and other dam-related characteristics ( age , litter size , body mass index , and weight and number of active mammary glands of the dam ).
Example Output: | purpose
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Let me give you an example: Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
The answer to this example can be: background
Here is why: The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
OK. solve this:
have been traditionally consumed in various forms by Philippinos for treatment of diabetes and kidney related diseases.
Answer: | background | task1163_coda19_section_classification |
|
You will be given a definition of a task first, then some input of the task.
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
However , respondents with pre-outbreak respiratory problems and diabetes did not more often take preventive measures.
Output: | finding | task1163_coda19_section_classification |
|
Given the task definition and input, reply with output. In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
P-value < 0.001 ) and diabetes ( AOR = 1.68 ; 95 % CI ( 1.346-1.848 ) , P-value = 0.002.
| finding | task1163_coda19_section_classification |
|
Instructions: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Input: and infectious diseases ( 53-64 ) ; immune disorders ( 65-69 ) ; diabetes ( 70 -72 ) ; and hereditary diseases ( 73-77 ).
Output: | purpose | task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Example Input: reference is made to law cases which often settle view disputes by the extent of daylight obstruction.
Example Output: background
Example Input: The detectability of different methods as well as the auxiliary diagnosis value of antibodies test for SARS-CoV-2 infection were analyzed.
Example Output: method
Example Input: and infectious diseases ( 53-64 ) ; immune disorders ( 65-69 ) ; diabetes ( 70 -72 ) ; and hereditary diseases ( 73-77 ).
Example Output: | purpose
| task1163_coda19_section_classification |
|
You will be given a definition of a task first, then an example. Follow the example to solve a new instance of the task.
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
Solution: background
Why? The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
New input: This study aims to determine the safety and effectiveness of rosiglitazone in inadequately controlled type 2 diabetes patients with NAFLD.
Solution: | purpose | task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Example: Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
Example solution: background
Example explanation: The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
Problem: P-value < 0.001 ) and diabetes ( AOR = 1.68 ; 95 % CI ( 1.346-1.848 ) , P-value = 0.002.
| Solution: finding | task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Ex Input:
Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
Ex Output:
background
Ex Input:
This review attempts to identify potentially important genes that show some consistency in ( relative ) up or downregulation in key tissues between the resistant and susceptible chickens.
Ex Output:
purpose
Ex Input:
and CA3 and CA1 pyramidal cells were examined for spine density and morphology.
Ex Output:
| method
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
[Q]: inhibit growth of vaccinia virus ( VACV ) in vitro.
[A]: purpose
[Q]: lactoferrin as a treatment for calf diarrhea was not beneficial.
[A]: finding
[Q]: P-value < 0.001 ) and diabetes ( AOR = 1.68 ; 95 % CI ( 1.346-1.848 ) , P-value = 0.002.
[A]: | finding
| task1163_coda19_section_classification |
|
instruction:
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
question:
inhibit growth of vaccinia virus ( VACV ) in vitro.
answer:
purpose
question:
Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
answer:
background
question:
exhibits potent antiviral activity against FIV.
answer:
| background
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Example input: Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
Example output: background
Example explanation: The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
Q: and infectious diseases ( 53-64 ) ; immune disorders ( 65-69 ) ; diabetes ( 70 -72 ) ; and hereditary diseases ( 73-77 ).
A: | purpose | task1163_coda19_section_classification |
|
instruction:
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
question:
We constructed speci ¢ c siRNAs targeting the S gene in SARS-CoV.
answer:
method
question:
Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
answer:
background
question:
political , and economic policies as the foci of upstream drivers of the public 's health.
answer:
| method
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Ex Input:
have highlighted the importance of infection control.
Ex Output:
background
Ex Input:
Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
Ex Output:
background
Ex Input:
Peripheral or central inflammation is characterized by an upregulation of cytokines and their receptors in the brain.
Ex Output:
| background
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
emergence and eventual evolution of a plethora of infectious pathogens.
background
Background : The potential risks associated with `` toilet plume '' aerosols produced by flush toilets is a subject of continuing study.
background
This study aims to determine the safety and effectiveness of rosiglitazone in inadequately controlled type 2 diabetes patients with NAFLD.
| purpose
| task1163_coda19_section_classification |
|
Teacher: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Teacher: Now, understand the problem? If you are still confused, see the following example:
Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
Solution: background
Reason: The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
Now, solve this instance: HMA has become an important target in the treatment of type-2 diabetes.
Student: | background | task1163_coda19_section_classification |
|
Teacher:In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Teacher: Now, understand the problem? Solve this instance: Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
Student: | background | task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Input: Consider Input: Objectives : This work presents a new approach to selecting proper health-based thresholds for a heat warning system which are different from thresholds of heat-health relationship.
Output: purpose
Input: Consider Input: alone as an effective method for the routine prevention of disease transmission.
Output: method
Input: Consider Input: HMA has become an important target in the treatment of type-2 diabetes.
| Output: background
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Q: BMI , diabetes , and hypercholesterolemia with mild flu in an Iranian population.
A: | purpose | task1163_coda19_section_classification |
|
TASK DEFINITION: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
PROBLEM: Since then , researchers have conducted numerous in vitro and in vivo studies that consistently confirmed the antidiabetic activity of banaba.
SOLUTION: background
PROBLEM: single mismatch detection and low current response.
SOLUTION: background
PROBLEM: The average diameter of the silver colloids was approximately 10 nm.
SOLUTION: | method
| task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
This study aims to determine the safety and effectiveness of rosiglitazone in inadequately controlled type 2 diabetes patients with NAFLD. | purpose | task1163_coda19_section_classification |
|
Detailed Instructions: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
See one example below:
Problem: Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
Solution: background
Explanation: The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
Problem: BMI , diabetes , and hypercholesterolemia with mild flu in an Iranian population.
Solution: | purpose | task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Q: have highlighted the importance of infection control.
A: background
****
Q: Our data reinforce the idea that culture-adapted laboratory virus strains can have reduced fitness in vivo.
A: finding
****
Q: BMI , diabetes , and hypercholesterolemia with mild flu in an Iranian population.
A: | purpose
****
| task1163_coda19_section_classification |
|
Definition: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Input: HMA has become an important target in the treatment of type-2 diabetes.
Output: | background | task1163_coda19_section_classification |
|
In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
[Q]: Further , our results indicate that age factors should be considered when investigating the vaccination and therapeutic strategies for severe IAV infection.
[A]: finding
[Q]: replication , virion assembly and eventual egress of the NPEV from the infected cells.
[A]: method
[Q]: Conclusions : MERS-Cov infection is more common in male , advanced age and diabetes.
[A]: | finding
| task1163_coda19_section_classification |
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In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Example: Efforts to control future SARS outbreaks depend on the accurate and early identification of SARS-CoV infected patients.
Example solution: background
Example explanation: The sentence provides the background information regarding how they could control future SARS outbreaks depending on the accuracy of identification of some infected patients having SARS-CoV.
Problem: Conclusions : MERS-Cov infection is more common in male , advanced age and diabetes.
| Solution: finding | task1163_coda19_section_classification |
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Given the task definition and input, reply with output. In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Conclusions : MERS-Cov infection is more common in male , advanced age and diabetes.
| finding | task1163_coda19_section_classification |
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TASK DEFINITION: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
PROBLEM: The polymorphisms of IL-10 and TNF-α were not associated with SARS susceptibility.
SOLUTION: finding
PROBLEM: None of the 30 influenza-positive travellers had tympanic temperature $ 37.8 uC at screening ( 95 % CI 0 % to 12 % ) ; three had no influenza symptoms.
SOLUTION: finding
PROBLEM: have been traditionally consumed in various forms by Philippinos for treatment of diabetes and kidney related diseases.
SOLUTION: | background
| task1163_coda19_section_classification |
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Q: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
All the six AMI patients were aged > 60 years ; five of them had two or more underlying comorbidities ( hypertension , diabetes , cardiovascular diseases , and chronic obstructive pulmonary disease ).
A: | finding | task1163_coda19_section_classification |
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Detailed Instructions: In this task, you are given a sentence from the research paper and your task is to classify the given sentence into the following categories: Background (Why is this problem important? What relevant works have been created before? What is still missing in the previous works? What are the high-level research questions? How might this help other research or researchers?), Purpose (What specific things do the researchers want to do? What specific knowledge do the researchers want to gain? What specific hypothesis do the researchers want to test?), Method (How did the researchers do the work or find what they sought? What are the procedures and steps of the research?), or Finding (What did the researchers find out? Did the proposed methods work? Did the thing behave as the researchers expected?).
Problem:have been traditionally consumed in various forms by Philippinos for treatment of diabetes and kidney related diseases.
Solution: | background | task1163_coda19_section_classification |
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You will be given a definition of a task first, then some input of the task.
In this task, you are given a sentence. You are expected to recognize the name of any form of chemical substances. Although there might be several correct answers, you need to write one of them.
25-Hydroxyvitamin D in Obese Youth Across the Spectrum of Glucose Tolerance From Normal to Prediabetes to Type 2 Diabetes.
Output: | Glucose | task1483_chemical_extraction_chemprot_dataset |
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In this task, given a sentence in the English language, your task is to convert it into the Lao (Laotian) language.
--------
Question: Some aid came in the form of food, while other aid came as cash which would be used by the aid agencies to buy grain from Ethiopian farmers.
Answer: ບາງການຊ່ວຍເຫລືອ ແມ່ນມາໃນຮູບແບບອາຫານ ຂະນະທີ່ການຊ່ວຍເຫລືອອື່ນໆ ແມ່ນຈະເປັນເງິນສົດ ເຊິ່ງຈະຖືກໃຊ້ໂດຍອົງກອນຊ່ວຍເຫລືອ ເພື່ອຊື້ເຂົ້າຈາກຊາວນາໂອທິໂອເປຍ.
Question: While insulin resistance, a characteristic of diabetes, is linked with neurodegeneration, the new finding provides a strong connection between diabetes and Alzheimer's disease.
Answer: ຂະນະທີ່ ຄວາມຕ້ານທານຕໍ່ສານອິນຊູລິນ ລັກສະນະຂອງໂລກເບົາຫວານ ແມ່ນກ່ຽວຂ້ອງກັບການເຊື່ອມໂຍງຂອງສະໝອງ ການຄົ້ນພົບໃໝ່ໄດ້ສະໜອງການເຊື່ອມໂຍງທີ່ເຂັ້ມແຂງລະຫວ່າງໂລກເບົາຫວານ ແລະ ພະຍາດສະໝອງເຊື່ອມ.
Question: It is believed that the fire was started by an electrical fault, the Xinhua news agency reports.
Answer: | ສໍານັກຂ່າວ ຊິນຫົວ ລາຍງານວ່າ ເຫດໄຟໄໝ້ຄັ້ງນີ້ເຊື່ອວ່າເກີດຈາກໄຟຟ້າລັດວົງຈອນ.
| task554_alt_translation_en_la |
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Teacher: In this task, given a sentence in the English language, your task is to convert it into the Lao (Laotian) language.
Teacher: Now, understand the problem? If you are still confused, see the following example:
The government has reiterated its long standing opposition to the death penalty.
Solution: ລັດຖະບານໄດ້ເນັ້ນຍ້ຳການຄັດຄ້ານຕໍ່ໂທດປະຫາມາໂດຍຕະຫລອດ.
Reason: The above sentence is correctly translated from English to Lao.
Now, solve this instance: While insulin resistance, a characteristic of diabetes, is linked with neurodegeneration, the new finding provides a strong connection between diabetes and Alzheimer's disease.
Student: | ຂະນະທີ່ ຄວາມຕ້ານທານຕໍ່ສານອິນຊູລິນ ລັກສະນະຂອງໂລກເບົາຫວານ ແມ່ນກ່ຽວຂ້ອງກັບການເຊື່ອມໂຍງຂອງສະໝອງ ການຄົ້ນພົບໃໝ່ໄດ້ສະໜອງການເຊື່ອມໂຍງທີ່ເຂັ້ມແຂງລະຫວ່າງໂລກເບົາຫວານ ແລະ ພະຍາດສະໝອງເຊື່ອມ. | task554_alt_translation_en_la |
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Definition: In this task, given a sentence in the English language, your task is to convert it into the Lao (Laotian) language.
Input: While insulin resistance, a characteristic of diabetes, is linked with neurodegeneration, the new finding provides a strong connection between diabetes and Alzheimer's disease.
Output: | ຂະນະທີ່ ຄວາມຕ້ານທານຕໍ່ສານອິນຊູລິນ ລັກສະນະຂອງໂລກເບົາຫວານ ແມ່ນກ່ຽວຂ້ອງກັບການເຊື່ອມໂຍງຂອງສະໝອງ ການຄົ້ນພົບໃໝ່ໄດ້ສະໜອງການເຊື່ອມໂຍງທີ່ເຂັ້ມແຂງລະຫວ່າງໂລກເບົາຫວານ ແລະ ພະຍາດສະໝອງເຊື່ອມ. | task554_alt_translation_en_la |
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In this task, given a sentence in the English language, your task is to convert it into the Lao (Laotian) language.
Input: Consider Input: Other Republicans are starting to get jittery about their reelection hopes if DeLay is allowed to retain power.
Output: ສະມາຊິກພັກລິພັບບິກັນເລີ່ມກັງວົນໃຈກ່ຽວກັບຄວາມຫວັງຂອງພວກເຂົາໃນການເຮັດການເລືອກຕັ້ງໃໝ່ຖ້າທ່ານ ດີເລ ຍັງມີບົດບາດຢູ່.
Input: Consider Input: Alexandre Vinokourov of Kazakhstan has won stage 15 of the 2007 Tour de France in a time of 5h 34' 28".
Output: ອະເລັກຊອງ ວິໂນຄູຣອບ ຈາກຄາຊັດສະຖານໄດ້ຊະນະດ່ານທີ 15 ໃນການແຂ່ງຂັນຕູ ເດີ ຟອງ 2007 ດ້ວຍເວລາ 5ຊມ.34 ນາທີ 28 ວິນາທີ.
Input: Consider Input: While insulin resistance, a characteristic of diabetes, is linked with neurodegeneration, the new finding provides a strong connection between diabetes and Alzheimer's disease.
| Output: ຂະນະທີ່ ຄວາມຕ້ານທານຕໍ່ສານອິນຊູລິນ ລັກສະນະຂອງໂລກເບົາຫວານ ແມ່ນກ່ຽວຂ້ອງກັບການເຊື່ອມໂຍງຂອງສະໝອງ ການຄົ້ນພົບໃໝ່ໄດ້ສະໜອງການເຊື່ອມໂຍງທີ່ເຂັ້ມແຂງລະຫວ່າງໂລກເບົາຫວານ ແລະ ພະຍາດສະໝອງເຊື່ອມ.
| task554_alt_translation_en_la |
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In this task, given a sentence in the English language, your task is to convert it into the Lao (Laotian) language.
Input: Consider Input: There have been over 1000 reactions on the blog so far.
Output: ມີຄວາມຄິດເຫັນຕອບສະຫນອງວ່າ 1,000 ຄວາມຄິດເຫັນໃນຕອນນີ້.
Input: Consider Input: While insulin resistance, a characteristic of diabetes, is linked with neurodegeneration, the new finding provides a strong connection between diabetes and Alzheimer's disease.
Output: ຂະນະທີ່ ຄວາມຕ້ານທານຕໍ່ສານອິນຊູລິນ ລັກສະນະຂອງໂລກເບົາຫວານ ແມ່ນກ່ຽວຂ້ອງກັບການເຊື່ອມໂຍງຂອງສະໝອງ ການຄົ້ນພົບໃໝ່ໄດ້ສະໜອງການເຊື່ອມໂຍງທີ່ເຂັ້ມແຂງລະຫວ່າງໂລກເບົາຫວານ ແລະ ພະຍາດສະໝອງເຊື່ອມ.
Input: Consider Input: Investing in its communication tool may strengthen the company's leading position on the Chinese market.
| Output: ການລົງທືນໃນອຸປະກອນການສື່ສານອາດຊ່ວຍໃຫ້ບໍລິສັດຢູ່ໃນຕຳແຫນ່ງຜູ້ນຳໄດ້ຫມັ້ນຄົງຂື້ນໃນຕະຫລາດຈີນ.
| task554_alt_translation_en_la |
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Here is a news article: Teen killer George Zimmerman has a new painting, his brother announced on Twitter tonight. It's called "Angie" and it's of Angela Corey, the prosecutor in his murder trial.
He'll post details on "sale info" tomorrow, but a sneak preview of the "art" shows something that looks an awful lot like an AP photo, as Twitter user "Justice Calls" pointed out:
Yet again George Zimmerman @therealgeorgez PLAGIARIZES,TRACES and PHOTOSHOPS painting. (Photo:Rick Wilson, AP) pic.twitter.com/J76PjfI6OB — Justice Calls (@CallsForJustice) January 23, 2014
Lest you forget, Shepard Fairey paid quite the price when he used an AP photo of Barack Obama without permission: $1.6 million. Zimmerman doesn't have that kind of cash (he claimed to be indigent in November), but he did sell his first painting for $100,000, so, you know, if a photo agency were to sue him for copyright infringement, there could be some money there. Just saying.
We've emailed the AP for comment and will update if they respond.
Update, Friday: They've responded. Director of Media Relations Paul Colford doesn't seem happy. ||||| Tweet with a location
You can add location information to your Tweets, such as your city or precise location, from the web and via third-party applications. You always have the option to delete your Tweet location history. Learn more ||||| Obama 'HOPE' poster artist Shepard Fairey gets probation
LARRY NEUMEISTER Sept. 7, 2012
Shepard Fairey hugged his lawyers, was kissed by wife and shook hands with friends and supporters after his sentence was pronounced.The government had said in a presentence memorandum that Fairey, 42, should serve some time for destroying documents and fabricating others in a civil lawsuit he brought against The Associated Press in 2009. No prison term, it said, would send a "terrible message" to others who might engage in similar conduct."After spending a great amount of time, energy and legal effort, all of us at The Associated Press are glad this matter is finally behind us," AP President and CEO Gary Pruitt said in a statement. "We hope this case will serve as a clear reminder to all of the importance of fair compensation for those who gather and produce original news content."Prosecutors had told U.S. Magistrate Judge Frank Maas in Manhattan that Fairey had "both an ideological and financial motive" to alter evidence in his favor after basing his poster on one of the AP's photographs. They said he did so over several weeks, engaging in behavior that "cannot be dismissed as remotely impulsive or the product of a moment of bad judgment.""This was not a mere failure to preserve documents," the government wrote. "This was the intentional destruction of evidence and the intentional manufacture of false evidence. The defendant knew exactly what he was doing when he created the fake documents and sought to destroy the deleted documents."They noted that revenues at three companies he controlled doubled from roughly $3 million in 2007 to $6 million in 2009 while he was honored repeatedly, including being chosen to design the official poster of Obama's 2009 inauguration and commissioned to create the cover image of Obama for Time magazine's 2008 Person of the Year, which was displayed in an exhibition at the National Portrait Gallery.Defense attorneys argued that a prison term was not warranted, noting that the misdemeanor charge carries a potential of only six months in prison.They said Fairey is contrite and noted that he settled his civil case with the AP on unfavorable terms that included sanctions. The government outlined in its court papers that the deal required Fairey to pay the AP $1.6 million, with an insurance company contributing about $450,000 of that amount.In their sentencing memorandum, defense lawyers described Fairey as a devoted husband and father of two young daughters who runs companies that employ almost 30 people and who serves as the creative force behind a clothing line that employs another 80 people.They called his crime the "worst mistake of his life" and said he altered evidence "not to better his chances of winning the lawsuit or to enrich himself, but out of fear of embarrassment."The lawyers wrote that Fairey, who has diabetes, has already suffered "significant damage to his reputation," adding that an Internet search of his name "now produces results not just about his artistic and civic accomplishments, but also many web sites degrading him for his misconduct." |||||
A summary of this is? | – The artist George Zimmerman has unveiled his latest painting: a fire engine-red portrait of the special prosecutor who brought second-degree murder charges against him in the Trayvon Martin case. The painting is a re-creation of the very moment Angela Corey made her April 2012 announcement of those charges, reports the New York Daily News. But the artist took one tiny creative liberty: She's shown pinching her fingers together, and this text appears in the upper right: "I have this much respect for the American Judicial System." The painting was debuted to the world via his brother Robert's Twitter feed last night, along with the following: "Very proud to introduce @TherealGeorgeZ's latest...'Angie'. Sale info & details available tomorrow." But the Wire introduces an interesting wrinkle: The painting is essentially identical to an AP photo of the moment taken by Rick Wilson, or so @CallsforJustice pointed out, accusing Zimmerman of plagiarizing, tracing, and photoshopping the AP photo—which AP could have an issue with, if history is any indicator. Shepard Fairey, famed for using an AP photo as the basis for his famed HOPE poster, ended up settling his civil case with the AP for $1.6 million. Unlike Fairey, Zimmerman probably won't make millions off this painting, though: His blue flag painting went for $100,099.99 on eBay last month. | multi_news_1_0_0 |
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Article:
The memorial service for Justice Antonin Scalia concludes at the Basilica of the National Shrine of the Immaculate Conception in Washington.
Feb. 20, 2016 The memorial service for Justice Antonin Scalia concludes at the Basilica of the National Shrine of the Immaculate Conception in Washington. Marvin Joseph/The Washington Post
Scalia is laid to rest at the Basilica of the National Shrine of the Immaculate Conception in Washington.
Scalia is laid to rest at the Basilica of the National Shrine of the Immaculate Conception in Washington.
Scalia is laid to rest at the Basilica of the National Shrine of the Immaculate Conception in Washington.
A Texas sheriff’s department released an incident report late Tuesday that revealed new details of the discovery of Supreme Court Justice Antonin Scalia’s body, as well as the name of the friend who accompanied him on the hunting trip and the items found inside the ranch bedroom where the justice was found.
In response to a public records request made by The Washington Post, the Presidio County Sheriff’s Office released an incident report from the sheriff’s investigation of Scalia’s death at the Cibolo Creek Ranch on Feb. 13. The report stated that the justice’s body was found in bed with a pillowcase covering his eyes. A breathing apparatus was on the table next to the bed, but it was switched off. Scalia was lying on three pillows “stacked up to elevate his head.”
[Read the incident report here]
Scalia’s sheets and pillows “were still in the creased position from that day’s room service, indicating that there was no struggle involved,” the report said. The top pillowcase “appeared to have shifted at some point in the night due to the weight of his pillow, causing the pillow case to slide down and cover his eyes.”
The sheriff noted that the position of the pillow “did not seem to have inhibited Scalia’s breathing.”
Antonin Scalia died on Saturday, Feb. 13. Here's a look back on his tenure, his judicial philosophy and the legacy he leaves behind. (Monica Akhtar,Natalie Jennings/The Washington Post)
About 12:14 p.m., the owner of the ranch, John Poindexter, called Presidio County Sheriff Danny Dominguez to report the death but would not give him the name of the deceased person. There was then a disagreement between them about who should handle the death report. Poindexter told Dominguez that he wanted to report the death to the U.S. Marshals Service, but Dominguez said that it was under his jurisdiction.
“He then stated to me that this death was way beyond my authority and that it should go the Feds (USMS),” Dominguez said in the report. “I then replied it doesn’t matter who it is, it was still under my jurisdiction.”
Dominguez called U.S. Marshal Ken Roberts, and they agreed to meet at the ranch, south of Marfa, Tex. The sheriff arrived about 12:35 p.m.
When Dominguez arrived, he met Poindexter and Allen Foster, who is described in the report as “a close friend of Scalia” who had flown in with him the day before.
C. Allen Foster is a prominent Washington lawyer who has argued before the Supreme Court. It was not immediately clear whether C. Allen Foster was the Scalia friend referred to in the report. A representative from his law firm said that he was traveling and that she would try to reach him.
Since Scalia’s death at the remote West Texas ranch, questions have been raised about how the death investigation was handled and why an autopsy wasn’t performed on the 79-year-old Supreme Court justice.
The Presidio County judge and the manager of the funeral home that handled Scalia’s body said Scalia’s family insisted on not having an autopsy done.
Supreme Court Justice Antonin Scalia (Kevin Lamarque/Reuters)
Scalia suffered from coronary artery disease, obesity, diabetes and other ailments, according to a letter from his Supreme Court doctor.
Presidio County District Attorney Rod Ponton told the Associated Press there was nothing suspicious about Scalia’s death and cited a letter from Rear Adm. Brian P. Monahan, the attending physician for members of Congress and the Supreme Court. The Feb. 16 letter said Scalia’s many “significant medical conditions led to his death,” Ponton said.
Monahan listed ailments including “sleep apnea, degenerative joint disease, chronic obstructive pulmonary disease and high blood pressure,” the AP said. Scalia was also a smoker, the letter said.
According to the Presidio County sheriff’s report, Poindexter, Foster and the ranch manager took Dominguez to the room where Scalia died.
“All seemed to be in order,” he wrote. Scalia was face-up on the bed, covered with sheets up to his chin. Both of his hands were “resting at his side.”
A hose for the breathing machine was found on the left side of Scalia’s bed, but was not attached to him. Scalia’s briefcase was found closed, on a recliner. On the kitchen counter, the sheriff found a “blue stretch band exercise device.” A shaving kit was on the counter in the bathroom. And his shoes were placed next to the bathtub.
Scalia’s suitcase was open, and the contents were neatly folded. A shirt was folded on the sofa. On the table to the right of his bed, the sheriff found a flashlight and a pitcher of water with a napkin folded over the top. On a table in the room, there was an “orange cap, a set of keys, a pen, a watch, and a bottle of water.”
Poindexter and Foster told the sheriff that Scalia had arrived at the ranch the day before to go hunting. Poindexter has told reporters that about 35 guests were at the ranch for the weekend together.
Poindexter told the sheriff that they “had supper and talked for a while” that evening.
Scalia “said that he was tired and was going to his room for the night,” the sheriff wrote in his report. ||||| FILE - In this Oct. 18, 2011 file photo, U.S. Supreme Court justice Antonin Scalia looks into the balcony before addressing the Chicago-Kent College Law justice in Chicago. A letter from the Supreme Court's... (Associated Press)
FILE - In this Oct. 18, 2011 file photo, U.S. Supreme Court justice Antonin Scalia looks into the balcony before addressing the Chicago-Kent College Law justice in Chicago. A letter from the Supreme Court's doctor says Scalia suffered from coronary artery disease, obesity and diabetes, among other ailments... (Associated Press)
DALLAS (AP) — Antonin Scalia suffered from coronary artery disease, obesity and diabetes, among other ailments that probably contributed to the justice's sudden death, according to a letter from the Supreme Court's doctor.
Presidio County District Attorney Rod Ponton cited the letter Tuesday when he told The Associated Press there was nothing suspicious about the Feb. 13 death of the 79-year-old jurist. He said the long list of health problems made an autopsy unnecessary.
Ponton had a copy of the letter from Rear Adm. Brian P. Monahan, the attending physician for members of Congress and the Supreme Court. The letter was to Presidio County Judge Cinderela Guevara, who conducted a death inquiry by phone and certified Scalia's death.
The letter dated Feb. 16 said Scalia's many "significant medical conditions led to his death," Ponton said.
In the letter, Monahan listed more than a half-dozen ailments, including sleep apnea, degenerative joint disease, chronic obstructive pulmonary disease and high blood pressure. Scalia also was a smoker, the letter said.
Ponton declined to provide a copy of the letter, saying an open-records request must be made to Guevara.
The AP filed a records request with the judge last week, but she did not provide the letter or respond to a reporter's phone message Tuesday. The Texas Department of State Health Services has declined to release a copy of the death certificate.
Scalia was found dead in his bed at the Cibolo Creek Ranch, not far from the Mexico border, where he had gone on a hunting trip.
Dr. Mark Hlatky, professor of cardiovascular medicine at Stanford University, said a 79-year-old man with those conditions, especially coronary artery disease and sleep apnea, would be at risk for a potentially fatal heart arrhythmia.
"A lot of people do die in their sleep, and they're found the next day."
The conditions are also associated with pulmonary embolism and stroke, which could also "kill somebody very suddenly."
Scalia's death, he said, was unexpected, "but it sounds like it wasn't suspicious."
The justice's many ailments, taken together, were "quite dangerous," said Dr. David Zich, a physician of internal and emergency medicine at Northwestern Memorial Hospital.
Zich said he would advise a patient with those conditions who was still smoking to stop smoking first and then lose weight.
"Those are the main two things someone in his position can do himself," Zich said. "The rest falls on the physician to medically manage blood pressure and make sure their blood sugar levels are controlled well."
Zich said he would also want such a patient to use a continuous positive airway pressure machine, or CPAP, at night for sleep apnea "to make sure the heart and body aren't stressed while sleeping."
A breathing apparatus was found on the night stand next to Scalia's bed when his body was found, but he was not hooked up to it and it was not turned on when he died, according to a Presidio County Sheriff's Office incident report obtained late Tuesday by The Washington Post.
Nothing appeared out of place around Scalia's bed, according to the report. Three pillows were stacked to elevate Scalia's head. A top pillow appeared to have toppled onto his eyes and forehead but didn't appear positioned to impede his breathing, the report stated.
His arms were at his side atop the bed covers, which were pulled up to his chin. The bed covers were smooth and creased and showed no sign of a struggle, according to the report.
His suitcase was open and contained neatly folded clothing. On the kitchen counter rested a blue stretch exercise band.
Guevara, who as county judge is the top administrator in the area, previously said she conferred by phone with Sheriff Danny Dominguez and a U.S. marshal before certifying the death. On the day Scalia died, she also conferred with Monahan by phone before determining the cause of death.
Scalia's death "was handled in a similar fashion as the cases of other elderly people who have died in Presidio County," Ponton said.
In rural Texas, justices of the peace investigate deaths, among other duties, but the two justices in the region were out of town and unavailable. Guevara was also out of town, more than 60 miles away, but agreed to conduct the death inquiry by phone.
The Supreme Court does not provide regular reports about the justices' health. It is left to each court member to decide how much to make public about medical conditions.
Some justices, including Ruth Bader Ginsburg, have released detailed reports of hospital stays and surgeries. The Supreme Court's press office could find just one release in 29 years pertaining to Scalia's health, a report of surgery in 2003 to repair a torn rotator cuff in his right shoulder.
___
Associated Press writers Carla K. Johnson in Chicago and Mark Sherman in Washington contributed to this report. |||||
What is a summary? | – Supreme Court Justice Antonin Scalia suffered from a host of ailments that contributed to his death, including coronary artery disease, obesity, and diabetes, according to a letter from his physician. The letter—addressed to Presidio County Judge Cinderela Guevara, who determined Scalia died of a heart attack and no autopsy was needed—also mentions Scalia was a smoker who had sleep apnea, degenerative joint disease, chronic obstructive pulmonary disease, and high blood pressure, a Presidio County DA tells the AP, noting the letter is proof there was nothing fishy about the 79-year-old justice's death. The letter was dated three days after Scalia died, though Guevara says she also spoke to the doctor by phone on Feb. 13. A doctor who did not treat Scalia says the cited conditions would have put him at risk for heart arrhythmia, pulmonary embolism, and stroke. Another doctor notes a breathing machine used for sleep apnea would "make sure the heart and body aren't stressed while sleeping." A sheriff's report notes a breathing machine was found turned off next to Scalia's bed, but he was not hooked up to it, per the Washington Post. "All seemed to be in order," the sheriff wrote. Scalia's clothes were neatly folded and the sheets covering him were smooth and creased. His head was elevated on three pillows and his hands were at his sides. A pillowcase "appeared to have shifted at some point in the night" and was covering his eyes but "did not seem to have inhibited Scalia's breathing." | multi_news_1_0_0 |
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Here is a news article: Body-mass index (BMI) has a strong genetic component (40 to 80% heritability) involving several genes that have expression in the hypothalamus and fulfill roles in appetite regulation. 10,11 The strongest genomewide association signal lies in introns 1 and 2 of the gene FTO 12,13 ; this region contains 89 common variants ( Figure 1A Figure 1 Activation of a Superenhancer in Human Adipocyte Progenitors by the FTO Obesity Risk Haplotype.Panel A shows the genetic association with body-mass index (BMI) for all common FTO locus variants, 14 including the reported single-nucleotide variant (SNV) rs1558902 (red diamond) and the predicted causal SNV rs1421085 (red square). Gray shading delineates consecutive 10-kb segments. CEU denotes a population of Utah residents with northern and western European ancestry, and LD linkage disequilibrium. Panel B shows chromatin state annotations for the locus across 127 reference epigenomes (rows) for cell and tissue types profiled by the Roadmap Epigenomics Project. 15,16 For information on the colors used to denote chromatin states, see Figure S1A in the Supplementary Appendix . Vertical lines delineate the consecutive 10-kb segments shown in Panel A. ESC denotes embryonic stem cell, HSC hematopoietic stem cell, and iPSC induced pluripotent stem cell. Panel C shows human SGBS adipocyte enhancer activity, for 10-kb tiles, of the risk and nonrisk haplotypes with the use of relative luciferase expression. The boxes indicate means from seven triplicate experiments, and T bars indicate standard deviations. ) that are in high linkage disequilibrium in Europeans (r 2 ≥0.8) 12,13 across approximately 47,000 nucleotides, which makes the identification of the likely causal variant challenging. The associated region lacks protein-altering variants, which has prompted numerous gene-regulatory studies 17-21 ; these studies have predicted diverse and conflicting target genes and tissues, including FTO itself in a whole-body knockout, 17 IRX3 in pancreas 20 or brain, 19 RBL2 in lymphocytes, 21 and RPGRIP1L in brain. 18 However, the identification of a mechanistic basis for the association between the FTO locus and obesity in humans has been elusive, the relevant cell types and target genes remain unresolved, and the causal variant remains uncharacterized. In this study, we sought to identify a causal variant with regulatory roles, its upstream regulator, and its downstream target gene in order to provide a candidate mechanistic basis for the association between FTO and obesity.
Obesity affects more than 500 million people worldwide and contributes to type 2 diabetes, cardiovascular disorders, and cancer. 1 Obesity is the result of a positive energy balance, whereby energy intake exceeds expenditure, resulting in the storage of energy, primarily as lipids in white adipocytes. Energy balance is modulated by food consumption and physical activity, as well as by the dissipation of energy as heat through constitutive thermogenesis in mitochondria-rich brown adipocytes in brown fat and through inducible thermogenesis in beige adipocytes in white fat. 2-6 Thermogenesis is triggered by mechanisms within the cells themselves or by the sympathetic nervous system (e.g., through β-adrenergic receptor agonists), in response to exercise, diet, or exposure to cold. Regulators of mitochondrial thermogenesis (including IRF4, PGC1α, PRDM16, and TBX15) control the expression of the gene encoding uncoupling protein 1 (UCP1), 4,7-9 which depolarizes the inner mitochondrial membrane, causing proton transfer and heat dissipation.
We predicted the single-nucleotide variant (SNV) responsible for dysregulation of the target genes on the basis of a quantitative analysis of regulatory-motif conservation, and we used experimental alterations of the predicted causal nucleotide to validate its causality for enhancer activity and regulator binding. To predict the upstream regulator, we examined regulatory motif matches and regulator expression levels in adipocytes from obese and nonobese participants; we then experimentally validated its causality and epistasis with the risk haplotype by means of knockdown and overexpression in adipocytes from risk-allele carriers and nonrisk-allele carriers. Finally, we established the cell-autonomous causality of the predicted driver variant with the use of bidirectional CRISPR–Cas9 editing in primary adipocytes from risk-allele carriers and nonrisk-allele carriers, followed by measurement of target-gene expression, expression levels of energy-balance genes, and cellular phenotypic signatures of obesity in humans. Additional information on our methods is provided in the protocol (available at NEJM.org) and in the Supplementary Appendix .
On the basis of epigenomic annotations across 127 human cell types, we predicted the cell type in which the genetic variant was likely to act, and we validated the prediction with the use of haplotype-specific enhancer assays. We analyzed long-range chromatin interactions in the region surrounding FTO to define potential target genes, and to validate genetic targets, we conducted an expression quantitative-trait-locus (eQTL) analysis in primary human adipocytes from risk-allele carriers and nonrisk-allele carriers. We predicted the cellular processes affected by the obesity-associated variants on the basis of correlated expression with the target genes across participants, and we validated their genetic control with the use of a trans-eQTL analysis of energy-balance genes (i.e., an eQTL analysis of energy-balance genes at large genomic distances from the FTO locus) in adipocytes, as well as by measuring cellular phenotypes in risk-allele carriers and nonrisk-allele carriers. To examine the causal roles for the predicted target genes, we first used knockdown and overexpression of each target gene in primary human adipocytes from the subcutaneous fat of risk-allele carriers and nonrisk-allele carriers, followed by cellular phenotyping; second, we used generation of mice with a dominant negative allele of one of the target genes expressed in adipose tissue, followed by organism-level phenotyping, histologic measurements, and gene-expression profiling in major fat stores; and third, we used knockdown, overexpression, and knockout in three mouse adipocyte models.
We used techniques of epigenomics, comparative genomics, human genetics, genome editing, and directed perturbations in samples from patients and from mice to dissect the regulatory circuitry and mechanistic basis of the FTO obesity-associated locus. Our methods are described in detail in the Methods section in the Supplementary Appendix , available with the full text of this article at NEJM.org.
Primary human adipose–derived progenitor cell cultures were obtained from the subcutaneous adipose tissue of 100 healthy Europeans who were 20 to 50 years of age and had a BMI (the weight in kilograms divided by the square of the height in meters) of 20 to 24, which was in the normal range. The sample included 52 participants (hereafter referred to as risk-allele carriers) who were homozygous for the risk allele for the tag variant rs9930506 (which has been reported in genomewide association studies), as well as for the associated variants rs1421085 and rs1558902; together, these variants make up part of the risk haplotype, which in its entirety includes 89 variants in introns 1 and 2 of FTO that are common in European populations. The sample also included 48 participants who were homozygous for the nonrisk allele for all three of these variants (hereafter referred to as nonrisk-allele carriers). Primary cell cultures were used for the preparation of mitochondrial and nuclear messenger RNA, quantitative polymerase-chain-reaction (PCR) gene-expression analysis, assays of mitochondrial function and thermogenesis, determination of lipolysis rates, small interfering RNA–mediated knockdown, doxycycline-mediated overexpression, and CRISPR–Cas9 genome editing. In addition, whole adipose tissue and adipose-derived progenitor cells were obtained and RNA was isolated from a second European cohort of nongenotyped participants, including 12 severely obese patients (BMI, 35 to 52) who were undergoing bariatric surgery and 22 healthy nonobese participants (BMI, 18 to 28) who were undergoing elective surgery. We received approval from the local ethics committees in Germany, Norway, and Sweden. All participants gave written informed consent.
Results
Effect of the FTO Locus on IRX3 and IRX5 in Human Adipocyte Progenitor Cells To identify the cell types in which the causal variant may act, we examined chromatin state maps15,16 of the FTO obesity region across 127 cell types. An unusually long enhancer (12.8 kb) in mesenchymal adipocyte progenitors indicated a major regulatory locus (Figure 1B; and Fig. S1A, S1B, and S1C in the Supplementary Appendix). Haplotype-specific enhancer assays showed activity in association with the risk haplotype that was 2.4 times as high as that associated with the nonrisk haplotype in human SGBS adipocytes (i.e., adipocytes derived from a patient with the Simpson–Golabi–Behmel syndrome), which indicated genetic control of enhancer activity (Figure 1C). Enhancers in brain cells and other cell types were considerably shorter than those in mesenchymal adipocyte progenitors and lacked allelic activity (Fig. S1C and S1D in the Supplementary Appendix). To predict putative target genes, we examined large domains that had long-range three-dimensional chromatin interactions surrounding FTO and identified eight candidate genes (Figure 2A and 2BFigure 2 Activation of IRX3 and IRX5 Expression in Human Adipocyte Progenitors by the FTO Obesity Risk Genotype.Panel A shows gene annotations and LD with array tag variant rs9930506 in a 2.5-Mb window; LD is expressed as r2 values in the CEU population. Arrows indicate the direction of transcription of annotated genes in the locus. Panel B shows chromosome conformation capture (Hi-C) interactions contact probabilities in human IMR90 myofibroblasts,22 revealing a 2-Mb topologically associating domain, and LD mean r2 statistics for all SNV pairs at 40-kb resolution. Panel C shows box plots for expression levels, after 2 days of differentiation, in human adipose progenitors isolated from 20 risk-allele carriers and 18 nonrisk-allele carriers, evaluated by means of a quantitative polymerase-chain-reaction analysis for all genes in the 2.5-Mb locus. The horizontal line within each box represents the median, the top and bottom of each box indicate the 75th and 25th percentile, and I bars indicate the range. ). Among them, the developmental regulators IRX3 and IRX5 had genotype-associated expression, which indicated long-range (1.2-Mb) genetic control in primary preadipocytes (Figure 2C). Genotype-associated expression was not observed in whole-adipose tissue, a finding consistent with previous reports23,24; this indicated that the effect was cell type–specific and restricted to preadipocytes, which represent a minority of cells in adipose tissue (Fig. S2A in the Supplementary Appendix).
Effect of the FTO Locus on Mitochondrial Thermogenesis and Lipid Storage To identify the biologic processes affected by altered IRX3 and IRX5 expression in adipocytes, we used genomewide expression patterns in brown adipocyte–containing perirenal adipose tissue from a separate cohort of 10 nongenotyped, healthy kidney donors to identify genes with expression that was positively or negatively correlated with IRX3 and IRX5 expression. Genes that are associated with mitochondrial functions were found to have a negative correlation with IRX3 and IRX5, and genes with FXR and RXR lipid-metabolism functions were found to have a positive correlation, which suggests that IRX3 and IRX5 may play roles in energy dissipation and storage (Figure 3AFigure 3 Regulation of Obesity-Associated Cellular Phenotypes in Human Adipocytes by IRX3 and IRX5.Panel A shows the mitochondrial and FXR and RXR activation genes with strongest positive (in red) or negative (in green) correlation with IRX3 and IRX5 in human perirenal adipose tissue from 10 participants. Panels B and C show box plots of the increased adipocyte diameter and decreased mitochondrial DNA content in isolated differentiated adipocytes from risk-allele carriers (16 and 8 participants, respectively) relative to nonrisk-allele carriers (26 and 8, respectively). The vertical line within each box represents the median, the left and right margins of each box indicate the interquartile range, and I bars indicate the range. Panel D shows box plots of the altered basal and isoproterenol-stimulated oxygen consumption rate (OCR) on small interfering RNA (siRNA) knockdown and doxycycline (DOX)–mediated overexpression of IRX3 and IRX5 in 8 risk-allele carriers and 10 nonrisk-allele carriers. The siRNA efficiency was 62% for IRX3 and 71% for IRX5. The horizontal line within each box represents the median, the top and bottom of each box indicate the interquartile range, and I bars indicate the range. , and Table S1 in the Supplementary Appendix). IRX3 and IRX5 had consistently higher mean expression in white adipose tissue from nine participants, as well as negative correlation with PGC1A and UCP1 expression, as assessed with the use of interindividual expression patterns in perithyroid brown adipose tissue (Fig. S2B and S2C in the Supplementary Appendix); these findings indicated potential roles for IRX3 and IRX5 in the repression of thermogenesis. To examine the trans-eQTL genetic control of energy balance by the FTO obesity locus, we used primary preadipocytes from risk-allele carriers and nonrisk-allele carriers to evaluate the genes with mitochondrial and FXR and RXR functions that had expression patterns most closely correlated with those of IRX3 and IRX5, as well as several known markers of energy-balance regulation (Fig. S2D and S2E in the Supplementary Appendix). As compared with nonrisk-allele carriers, risk-allele carriers had lower expression of mitochondrial, browning, and respiration genes and higher expression of lipid-storage markers, which indicated a shift from energy dissipation to energy storage. These differences in expression were also reflected in the cellular signatures of obesity. Risk-allele carriers had increased adipocyte size, reduced mitochondrial DNA content, and a loss of UCP1 response to β-adrenergic stimulus or cold exposure (Figure 3B and 3C, and Fig. S2F in the Supplementary Appendix), as well as resistance to isoproterenol-mediated uncoupling, a decreased basal oxygen consumption rate, and a reduction in mitochondrial thermogenesis by a factor of 5 (Fig. S2G in the Supplementary Appendix); this indicated excessive accumulation of triglycerides, reduced mitochondrial oxidative capacity, reduced white adipocyte browning, and reduced thermogenesis.
Adipocyte-Autonomous Effects of IRX3 and IRX5 on Energy Balance We next quantified the effect that manipulation of IRX3 and IRX5 expression had on thermogenesis in primary preadipocytes that were isolated from both risk-allele carriers and nonrisk-allele carriers. In preadipocytes from risk-allele carriers, IRX3 and IRX5 knockdown restored oxygen consumption and thermogenesis response to nonrisk levels, increased thermogenesis by a factor of 7 (Figure 3D), and restored UCP1 expression levels (Fig. S3A in the Supplementary Appendix). In preadipocytes from nonrisk-allele carriers, IRX3 and IRX5 overexpression reduced basal respiration and thermogenesis to risk-allele levels (with thermogenesis reduced by a factor of 8) (Figure 3D) and decreased the expression of UCP1, other regulators of mitochondrial function and thermogenesis (PGC1A, PGC1B, and PRDM16), and the β-adrenergic receptor (ADRB3), which also regulates UCP1-independent thermogenesis programs (Fig. S3B and S3C in the Supplementary Appendix). These manipulations had no significant effect on preadipocytes from participants with the reciprocal genotypes, which indicated that IRX3 and IRX5 levels recapitulate the effect that the FTO genetic variant has on thermogenesis. To examine the organism-level effects of the repression of Irx3 in adipose tissue, we used adipose Irx3 dominant-negative (aP2-Irx3DN) mice. These mice had pronounced antiobesity characteristics, including reduced body size, body weight, fat mass, white and brown fat depots, and adipocyte size (Fig. S4A through S4G in the Supplementary Appendix). These aP2-Irx3DN mice also had resistance to weight gain on a high-fat diet, increased energy expenditure both at night and during the day, and increased oxygen consumption both at room temperature (22°C) and in thermoneutral conditions (30°C), but they did not have significant differences from control mice in food intake or locomotor activity (Fig. S4A and S4H through S4L in the Supplementary Appendix). At the molecular and cellular levels, these mice had increased mitochondrial activity and thermogenesis marker expression, reduced lipid-storage marker expression in both white and brown fat compartments, and markedly smaller adipocytes than did control mice (Fig. S4M, S4N, and S4O in the Supplementary Appendix). We next evaluated the tissue-autonomous versus brain-mediated roles of Irx3 by comparing the aP2-Irx3DN mice with hypothalamus dominant-negative Ins2-Irx3DN mice.19 The aP2-Irx3DN mice had a reduction in fat-mass ratio that was 3 times as great as that in Ins2-Irx3DN mice (a reduction of 57% vs. 19%), despite the fact that transgene expression in the hypothalamus was 3 times lower than that in Ins2-Irx3DN mice (Fig. S4P and S4Q in the Supplementary Appendix), which indicated that Irx3 has a hypothalamus-independent regulatory role in whole-body energy regulation. The phenotypic effects of Irx3 repression in aP2-Irx3DN mice were also stronger than those in whole-body Irx3 knockout mice, which suggested potential dominant repressor effects in adipocytes or other tissues, and were independent of Fto gene expression, which did not change (Fig. S4P and S4R in the Supplementary Appendix). Our findings indicate that both Irx3 and Irx5 have cell-autonomous roles: manipulation of Irx3 and Irx5 led to energy-balance differences in three mouse cellular models, including mouse embryonic fibroblast–derived adipocytes, white 3T3-L1 preadipocytes, and β-adrenergic–stimulated beige ME3 preadipocytes (Fig. S5 in the Supplementary Appendix). In each case, our results indicated that Irx3 and Irx5 induced adipocyte lipid accumulation and repressed thermogenesis in a cell-autonomous way.
Determination of the Causal Variant and Disruption of Repression by ARID5B To predict the causal variant, the disruption of which is necessary and sufficient to cause IRX3 and IRX5 dysregulation in human preadipocytes, we used phylogenetic module complexity analysis (PMCA)25 (Figure 4A and 4BFigure 4 Disruption of a Conserved ARID5B Repressor Motif by Causal SNV rs1421085 in Humans.Panel A shows disruption of an ARID5B repressor motif in the evolutionarily conserved motif module surrounding rs1421085. The sequences shown at the top of the panel indicate the frequencies of each nucleotide, with the size scaled to indicate the information content (measured as entropy) at each position. Panel B shows adapted phylogenetic module complexity analysis (PMCA)25 scores in the FTO region for all 82 noncoding SNPs in LD (r2≥0.8) with tag SNV rs1558902, which was identified in a genomewide association study26; rs1421085 had the maximal score. Chromatin state annotation is shown for Roadmap Epigenomics reference genome E025, which corresponds to adipose-derived mesenchymal stem cells; for information on the colors used to denote chromatin states, see Figure S1A in the Supplementary Appendix. Panel C shows increased endogenous expression of IRX3 and IRX5 on single-nucleotide T-to-C editing of rs1421085 in the nonrisk haplotype of a nonrisk-allele carrier, using CRISPR–Cas9 (five clonal expansions). CRISPR–Cas9 re-editing from the engineered C risk allele back to a T nonrisk allele with the use of an alternative single guide RNA restores low endogenous IRX3 and IRX5 gene expression. Panel D shows reduced expression of IRX3 and IRX5 on C-to-T editing of the risk allele in adipocyte progenitors from a risk-allele carrier. Knockdown of ARID5B increases IRX3 and IRX5 levels, as compared with the nontargeting control (siNT), only in the rescued allele, but not in the risk allele. , and Fig. S6A and S6B in the Supplementary Appendix). The highest PMCA score was found for the rs1421085 T-to-C SNV, which is in perfect linkage disequilibrium with the most significant reported SNV, rs1558902, across multiple populations (1000 Genomes Phase 1 data), a finding that is consistent with a potentially causal role. To evaluate whether rs1421085 plays a causal role in enhancer activity, we introduced the C allele into the nonrisk haplotype in our luciferase reporter assay. The T-to-C single-nucleotide alteration increased enhancer activity levels for 10-kb and 1-kb segments centered on the variant, in both orientations and both upstream and downstream of the transcription start, which indicated a gain of enhancer activity in association with the rs1421085 risk allele (Fig. S6C and S6D in the Supplementary Appendix). To evaluate the effect of the variant on regulator binding, we used electrophoretic mobility-shift assays (EMSAs) of adipocyte nuclear extract with probes for the risk allele and the nonrisk allele of rs1421085. We found binding for the nonrisk allele, T, which lacked enhancer activity, but no binding for the risk allele, C; this indicated that the increased enhancer activity associated with the risk allele is probably due to a loss of repressor binding rather than to a gain of activator binding (Fig. S6E in the Supplementary Appendix). We examined disrupted motifs and regulator expression to identify potential upstream regulators. The T-to-C substitution disrupted conserved motifs for NKX6-3, LHX6, and the ARID family of regulators (Figure 4A). Among them, ARID5B had the highest expression in adipose tissue and adipocytes and was bound specifically to the nonrisk allele in EMSA competition experiments (Fig. S6E and S6F in the Supplementary Appendix). ARID5B is known to play both repressive and activating roles and was previously implicated in adipogenesis and lipid metabolism in mice.27,28. Among nonrisk-allele carriers, expression of ARID5B was negatively correlated with expression of IRX3 and IRX5, a finding consistent with ARID5B having a repressive role. No correlation was found in risk-allele carriers, which indicates a loss of ARID5B regulation (Fig. S6G in the Supplementary Appendix). To evaluate the causal role of ARID5B, we next examined the effects of its knockdown and overexpression on IRX3 and IRX5. ARID5B knockdown increased IRX3 and IRX5 expression in primary preadipocytes from nonrisk-allele carriers to risk-allele levels, which indicates a loss of repression, but it had no effect on preadipocytes from risk-allele carriers, which indicates epistasis with the obesity-risk haplotype (Fig. S6H in the Supplementary Appendix). Consistent with this finding, in SGBS enhancer assays, ARID5B knockdown increased the activity of preadipocytes with the nonrisk allele to risk-allele levels, which indicates a loss of repression, but had no effect on risk-allele constructs, indicating epistasis with the rs1421085 risk allele (Fig. S6I in the Supplementary Appendix). ARID5B overexpression further reduced IRX3 and IRX5 levels in nonrisk-allele carriers, which indicated that repression was strengthened, but had no significant effect on risk-allele carriers, a finding consistent with impaired ARID5B repression in association with the risk haplotype (Fig. S6J in the Supplementary Appendix). We also evaluated the cellular effects of ARID5B-directed perturbations in primary preadipocytes from risk-allele carriers and nonrisk-allele carriers. In preadipocytes from nonrisk-allele carriers, ARID5B knockdown reduced basal oxygen consumption and lipolysis (Fig. S6K and S6L in the Supplementary Appendix) and shifted expression patterns from mitochondrial to lipid markers (Fig. S2E in the Supplementary Appendix), which indicated that ARID5B plays causal roles in energy-balance regulation. In contrast, ARID5B knockdown had no effect on preadipocytes from risk-allele carriers, a finding consistent with a loss of ARID5B control. These results suggest that the FTO obesity variant acts through disruption of ARID5B binding in the risk haplotype, leading to a loss of repression, a gain of enhancer activity, and increases in IRX3 and IRX5 expression (Fig. S6M in the Supplementary Appendix). ||||| A cure for obesity could be just an injection away after scientists at Harvard and MIT discovered that a tiny DNA tweak causes the metabolism to burn up excess fat.
Although it was thought that piling on the pounds was largely due to overeating and lack of exercise, researchers now think that genetics play a crucial role in whether fat is stored or used up as energy.
People with higher BMIs (Body Mass Index) often carry a variant of the FTO gene, which has been dubbed the ‘obesity gene.’
Now researchers at Harvard and MIT have discovered that the ‘obesity gene’ switches on two other genes which stop fat being burned up as heat – a process called thermogenesis.
And, crucially they have shown it is possible to turn off those genes using a ground breaking gene editing technique which snips out bad DNA code and replaces it with the correct sequence.
The scientists believe the technique could prevent or even cure obesity in those people with the faulty gene and negate the effects of a high-fat diet.
"Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual's metabolism," said senior author Professor Manolis Kellis, of MIT's Computer Science and Artificial Intelligence Laboratory (CSAIL) and of the Broad Institute.
"Knowing the causal variant underlying the obesity association may allow genome editing as a therapeutic avenue for individuals as risk.
"By manipulating this new pathway, we could switch between energy storage and energy dissipation providing new hope for a cure against obesity.”
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In Britain, 25 per cent of adults are obese — 12 million people — compared with fewer than three per cent in the Seventies. The proportion is predicted to grow to one in three by 2030 and more than half by 2050.
Weight gain is a risk factor for many health problems, including diabetes, heart disease, stroke and some cancers. Obesity and diabetes already costs the UK over £5 billion every year which is likely to rise to £50 billion in the next 36 years.
To test the theory that a faulty gene was driving weight gain, researchers gathered fat samples from Europeans carrying both the ‘obesity’ variant and a normal copy of the FTO gene.
They found that in people with the variant one letter of DNA code had been replaced by another. The wrong code was causing genes IRX3 and IRX5 to turn on when they should have been off.
Photo: Alamy
Previous studies have shown that IRX3 and IRX5 switch on during times of fat loss in the body, such as during periods of starvation to conserve fat.
Researchers used a new technology called the Crispr/Cas9 system to edit the DNA code and repair the sequence in mice and human cells. The technique sees a modified protein (Cas9) injected into the body where it can snip away specific sections of DNA.
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Mice which had been bred to obese saw a reduction of body weight and all major fat stores, and complete resistance to a high-fat diet.
The researchers are now looking at how to make the process useful for humans.
The research was published in the New England Journal of Medicine. ||||| Scientists have finally figured out how the key gene tied to obesity makes people fat, a major discovery that could open the door to an entirely new approach to the problem beyond diet and exercise.
The work solves a big mystery: Since 2007, researchers have known that a gene called FTO was related to obesity, but they didn't know how, and could not tie it to appetite or other known factors.
Now experiments reveal that a faulty version of the gene causes energy from food to be stored as fat rather than burned. Genetic tinkering in mice and on human cells in the lab suggests this can be reversed, giving hope that a drug or other treatment might be developed to do the same in people.
The work was led by scientists at MIT and Harvard University and published online Wednesday by the New England Journal of Medicine.
The discovery challenges the notion that "when people get obese it was basically their own choice because they choose to eat too much or not exercise," said study leader Melina Claussnitzer, a genetics specialist at Harvard-affiliated Beth Israel Deaconess Medical Center. "For the first time, genetics has revealed a mechanism in obesity that was not really suspected before" and gives a third explanation or factor that's involved.
Independent experts praised the discovery.
"It's a big deal," said Dr. Clifford Rosen, a scientist at Maine Medical Center Research Institute and an associate editor at the medical journal.
"A lot of people think the obesity epidemic is all about eating too much," but our fat cells play a role in how food gets used, he said. With this discovery, "you now have a pathway for drugs that can make those fat cells work differently."
Several obesity drugs are already on the market, but they are generally used for short-term weight loss and are aimed at the brain and appetite; they don't directly target metabolism.
Researchers can't guess how long it might take before a drug based on the new findings becomes available. But it's unlikely it would be a magic pill that would enable people to eat anything they want without packing on the pounds. And targeting this fat pathway could affect other things, so a treatment would need rigorous testing to prove safe and effective.
The gene glitch doesn't explain all obesity. It was found in 44 percent of Europeans but only 5 percent of blacks, so other genes clearly are at work, and food and exercise still matter.
Having the glitch doesn't destine you to become obese but may predispose you to it. People with two faulty copies of the gene (one from Mom and one from Dad) weighed an average of 7 pounds more than those without them. But some were obviously a lot heavier than that, and even 7 pounds can be the difference between a healthy and an unhealthy weight, said Manolis Kellis, a professor at MIT.
He and Claussnitzer are seeking a patent related to the work. It was done on people in Europe, Sweden and Norway, and funded by the German Research Center for Environmental Health and others, including the U.S. National Institutes of Health.
Obesity affects more than 500 million people worldwide and contributes to a host of diseases. In the U.S., about one-third of adults are obese and another one-third are more modestly overweight.
The FTO gene turns out to influence obesity indirectly, as a master switch that affects two other genes that control thermogenesis, or burning off energy. It's long been known that brown or beige fatty tissue — the so-called "good fat" — burns calories, while the more common white fat stores them. The body constantly makes fat cells, and the two genes determine whether they become brown or white ones.
In one experiment described in the medical journal, researchers blocked the faulty gene's effect in mice and found they became 50 percent leaner than other mice despite eating a high-fat diet, and burned more energy even when asleep.
In other tests on human cells, blocking the gene's effect increased energy burning in fat cells. Editing out the problem gene in human cells in the lab also restored normal metabolic function.
Researchers don't know the impact of having just one faulty copy of the gene but think it has less of an effect than having two copies.
Several companies are trying to develop treatments to stimulate brown fat, and the new research suggests a novel approach.
"It's a potential target" for drug development, said Dr. Sam Klein, an obesity researcher at Washington University in St. Louis. He called the work "an amazing study" and "a scientific tour de force."
Dr. Rudolph Leibel, an obesity expert at Columbia University in New York, used the same term — "tour de force." Still, some earlier research suggests the FTO gene may influence other aspects of obesity such as behavior and appetite.
"It's possible there are several mechanisms being affected," and that fat-burning is not the whole story, he said.
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Marilynn Marchione can be followed at http://twitter.com/MMarchioneAP ||||| In 1929, presidential candidate Herbert Hoover ran under the slogan "a chicken in every pot and a car in every garage." These items might seem common enough today, but Hoover was basically promising what were then considered luxuries to every American household. At the time of Hoover's campaign, "the few chickens raised for meat were sold directly to high-end restaurants, first-class dining cars, and luxury caterers," according to the Smithsonian Museum of American History . Chickens were instead kept for their eggs, which are a valuable source of protein and other nutrients. Egg consumption peaked mid-century, and has been in decline ever since. The overblown connection between cholesterol in eggs and heart disease certainly contributed to Americans turning their back on eggs. But a decline in prices of another protein source, specifically chicken, also contributed to eggs falling out of favor. In the last half of the 20th century, poultry consumption went up more than three-fold, according to USDA data. Red-meat consumption saw a steady decline over the same period, with Americans eating roughly 10 percent fewer pounds per capita every year. VIDEO: Stop Eating Food: The Soylent Experiment
As Americans increasingly eat out at restaurants more and consume more processed foods, salt intake has steadily increased across all age groups. The average American between ages 20 and 74 consumed close to 1,500 mg more sodium per day in 2006 than in 1971, according to the Institute of Medicine of the National Academies . The Centers for Disease Control and Prevention (CDC) recommends everyone ages 2 and up consume less than 2,300 mg per day, which is about a teaspoon a day. Some people with certain health risks, such as diabetes or high blood pressure, should limit that further to 1,500 mg per day. Eating too much salt increases water intake in the body, which leads to high blood pressure. Kidneys work overtime to deal with the excess sodium, and the increased blood volume puts a strain on the heart and blood vessels. At worst, a lifetime of a sodium surplus could lead to heart failure or stroke, according to the Harvard School of Public Health . Fast Food Is Less Salty Abroad
Go to the snack aisle of any supermarket or convenience store in the United States, and you'll find a wide array of potential options to satisfy any junk food craving. What do all of these foods have in common? They're all made of refined grains, in addition to other nutritionally deficient ingredients. Refined grains do not offer the same nutritional benefits as whole grains. The process by which refined grains are produced removes fiber, iron, vitamins and other nutrients, according to the American Heart Association . Examples of refined grains include white flour, corn flour and white rice. Not only have Americans turned to unhealthier grains for a greater share of their calories; modern wheat is also less nutritious than heritage grain varieties. Why You Should Probably Stop Eating Wheat
Beginning in 1980, when USDA issued the first federal dietary guidelines implicating fats and cholesterol as a major source of Americans' health woes, particularly heart disease, the food industry began shifting formulas in their products that moved away from saturated fat and toward vegetable oils and carbohydrates. Low-fat diets became all the rage, with a bevy of product lines offering low-fat alternatives. What happened after Americans got turned on to low-fat foods? They got even fatter and less healthy. Foods may not have had as much saturated fat, but they made that up with an increase in sugar and refined grains, which kept calorie counts the same. The switch to hydrogenated vegetable oils and margarines also only increased health risks. Heart disease is still the number one killer in the United States, and we also have rising numbers of diabetes and obesity to contend with. In fact, despite numerous studies since the 1990s showing that low fat diets are ineffective at best and harmful at worst, the government continues to recommend a low fat diet. FDA Bans Trans Fats - More Chemicals to Consider?
Americans aren't just eating more sugars than they used to; we're also drinking more. According to the Harvard School of Public Health , before the 1950s, the standard soft drink size was 6.5 ounces. That decade, manufacturers started selling larger sizes, and by 1960 the 12-ounce can was everywhere. Fast forward 30 years, and 20-ounce bottles are ubiquitous. Today, single-use soft drinks can reach up to 64 ounces and have up to 700 calories. Since the 1970s, sugary drinks have grown from 4 percent of Americans' daily calorie intake to 9 percent. A quarter of Americans get at least 200 calories a day from soft drinks. Teens and children are particularly high consumers, too. Sugar drinks are the top calorie source for teenagers, and are consumed daily by an estimated 91 percent of children. Does Soda Cause Violence?
, between the 1950s and 2000, Americans consumed on average 39 percent more refined sugars. Consumption of corn sweeteners, with high-fructose corn syrup leading the charge, octupled. On average, Americans consume an estimated 156 pounds -- yes, pounds -- of added sugar per capita every year. Excessive sugar intake can lead to all kinds of negative health outcomes, including but not limited to dental problems, obesity, diabetes, liver failure and more. These concerns are what led the Food and Drug Administration (FDA) recently to propose a change in food labeling that would recommend the daily intake of calories from added sugars not exceed 10 percent of total consumption. More than 70 percent of U.S. adults get over 10 percent of their daily calories from sugar. 7 Facts About Sugar That May Surprise You
View Caption + #3: According to the U.S. Department of Agriculture (PDF)
While calorie counts have been on the downswing, calorie intake is still far above where it once stood. Americans' daily average caloric intake is over 500 calories higher than it was in 1970, when the average hovered around 2,169 calories per day. What does a more than 20 percent increase in caloric intake mean for the average American? Consider that a pound a fat contains 3,500 calories. Assuming that even a quarter of those calories represent excess energy beyond what's needed for daily maintenance levels, that translates into a pound of stored fat gained every month, or 12 additional pounds per year. Portion sizes have seen a similar increase over time. According to the U.S. Department of Health & Human Services , in the last two decades alone, food portions in American restaurants have doubled or in some cases tripled. Portion sizes began increasing in the 1970s and rose sharply in the 1980s. Many food portions greatly exceed USDA and FDA standard servings, according to a study published in the American Journal of Public Health . "The largest excess over USDA standards (700 percent) occurred in the cookie category, but cooked pasta, muffins, steaks and bagels exceeded USDA standards by 480 percent, 333 percent, 224 percent and 195 percent, respectively," the study found. VIDEO: 4 Common Diet Myths Debunked
"A characteristic of the American dietary that has persisted throughout years has been its abundance." This sentence is no less true today than when it was published in the American Journal of Clinical Nutrition in 1959 . That abundance, however, comes with a cost: Americans eat too much. That excess consumption and often poor nutrition has brought with it a multitude of life-changing and often life-threatening diseases and conditions, including obesity, diabetes, heart disease, cancer and more. Although the number of Americans who are overweight or obese has been on a steady climb since the middle of the 20th century, a recent report by the New York Times suggests that efforts to abate this health crisis might be gaining ground thanks to a shift in public attitudes. For the first time since the federal government began tracking dietary intake over more than four decades of data collecting, the daily calorie intake of the average American showed a sustained decline. Read on to see how the American diet has changed since the middle of the 20th century. Americans Falsely Believe Their Diet Is Healthy
Scientists have identified a genetic master-switch that makes some people more prone to obesity than others, and research out Wednesday suggests it can be turned off, possibly leading to weight loss.
So far, researchers have been able to manipulate the genes of mice and human cells in the lab in order to reverse obesity, but the approach has not yet been tested in people.
Play Video New Picture Emerging of Young Brains on Sugar Scientists are discovering that neurological changes that create addictive brains can begin at a very young age, while the brain is still developing. What does that mean for children and sweets? Could some of them be addicted to sugar? DCI
If future studies are successful, the method could offer a novel way to cure obesity, a major public health problem that experts say affects some 500 million people around the world and can lead to cardiovascular disease, Type 2 diabetes and cancer.
Sugary Drinks Kill 184,000 People Every Year
“Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual’s metabolism,” said senior author Manolis Kellis, a professor of computer science at the Massachusetts Institute of Technology (MIT).
The study, co-authored by scientists at MIT and the Harvard University Medical School, appears in the New England Journal of Medicine.
Researchers focused on a gene region known as “FTO,” which has been probed widely since it was discovered in 2007 but has remained poorly understood.
Previous research tried to link the FTO region with brain circuits that control appetite, but researchers now believe the action takes place in fat cells and affects how much fat is stored, independently of the brain.
Specifically, the study found that a higher expression of two distant genes, IRX3 and IRX5, meant more fat was stored.
Pizza Prescription: Kids Should Eat Less
Then, they showed that they could manipulate this new pathway to reverse the signatures of obesity.
Using a DNA editing technology known as CRISPR/Cas9, researchers could switch between lean and obese signatures.
When researchers inhibited the corresponding gene in the fat cells of mice, the animals’ metabolism soared and they shed weight without eating less or exercising more.
“The results at the organism level were dramatic,” said lead author Melina Claussnitzer, a visiting professor at MIT.
“These mice were 50 percent thinner than the control mice, and they did not gain any weight on a high-fat diet. Instead they dissipated more energy, even in their sleep, suggesting a dramatic shift in their global metabolism,” she added.
Why Some Lose More Weight From Exercise
“The circuitry underlying the FTO region functions like a master regulatory switch between energy storage and energy dissipation.”
Researchers said they are currently forming partnerships with academics and industry to explore therapeutic options — and perhaps a cure — for obesity. |||||
A summary of this is? | – Fighting obesity is a lot more complicated than simply eating less and exercising more, according to researchers who have made a major breakthrough in studying the FTO "obesity gene." The gene was linked to obesity years ago, and scientists say they've now figured out how it works, as well as how it can be reversed, the AP reports. According to research published in the New England Journal of Medicine, the gene acts as a "switch" for other genes that affect whether energy from what people eat is stored as fat or burned off. People who inherited a faulty version of the gene from one parent, and especially those who inherited faulty versions from both parents, are a lot more likely to be obese. The researchers discovered that a gene editing sequence can reverse the effect, reports the Telegraph, which predicts that "a cure for obesity could be just an injection away," though the AP notes that a lot of testing lies ahead before a safe treatment can hit the market—and since the gene problem is widespread in white people but is found in only 5% of black people, "other genes are clearly at work." Still, experts call the finding a "big deal" with plenty of promise for treating obesity. "Obesity has traditionally been seen as the result of an imbalance between the amount of food we eat and how much we exercise, but this view ignores the contribution of genetics to each individual's metabolism," an MIT researcher tells Discovery. | multi_news_1_0_0 |
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Results During 3 500 004 person years of follow-up between 2004 and 2013 (median 7.2 years), a total of 11 820 men and 8404 women died. Absolute mortality rates according to spicy food consumption categories were 6.1, 4.4, 4.3, and 5.8 deaths per 1000 person years for participants who ate spicy foods less than once a week, 1 or 2, 3 to 5, and 6 or 7 days a week, respectively. Spicy food consumption showed highly consistent inverse associations with total mortality among both men and women after adjustment for other known or potential risk factors. In the whole cohort, compared with those who ate spicy foods less than once a week, the adjusted hazard ratios for death were 0.90 (95% confidence interval 0.84 to 0.96), 0.86 (0.80 to 0.92), and 0.86 (0.82 to 0.90) for those who ate spicy food 1 or 2, 3 to 5, and 6 or 7 days a week, respectively. Compared with those who ate spicy foods less than once a week, those who consumed spicy foods 6 or 7 days a week showed a 14% relative risk reduction in total mortality. The inverse association between spicy food consumption and total mortality was stronger in those who did not consume alcohol than those who did (P=0.033 for interaction). Inverse associations were also observed for deaths due to cancer, ischemic heart diseases, and respiratory diseases.
The beneficial effects of spices and their bioactive ingredients such as capsaicin have long been documented in experimental or small sized population studies. For example, an ecological study showed that populations with a higher consumption of spices have a lower incidence of cancer. 4 The ingestion of red pepper was found to decrease appetite and energy intake in people of Asian origin and white people and might reduce the risk of overweight and obesity. 5 6 In addition, the bioactive agents in spices have also shown beneficial roles in obesity, cardiovascular and gastrointestinal conditions, various cancers, neurogenic bladder, and dermatological conditions. 7 8 9 Moreover, spices exhibit antibacterial activity and affect gut microbiota populations, which in humans have been recently related to risks of diabetes, cardiovascular disease, liver cirrhosis, and cancer. 10 11 12 These data collectively suggest that spices may have a profound influence on morbidities and mortality in humans; however, the evidence relating daily consumption of spicy foods and total and disease specific mortality from population studies is lacking.
Spices have been an integral part of culinary cultures around the world and have a long history of use for flavoring, coloring, and preserving food, as well as for medicinal purposes. The increased use of spices as flavorings in foods is a major trend worldwide. 1 2 In China, chilli pepper is among the most popular spicy foods consumed nationwide. 3
Subgroup analyses were conducted separately among participants who did and did not report fresh chilli pepper as one of their commonly used spices. We compared both with those who ate spicy foods less than once a week. We also examined the associations of spicy food consumption with total mortality among prespecified baseline subgroups based on age (<50, 50 to 59, or ≥60), smoking status (regular smoker, or not), alcohol consumption (regular drinker, or not), level of physical activity (categorized using tertile cut-offs), and body mass index (<24.0, 24.0 to 27.9, or ≥28.0). The tests for interaction were performed by means of likelihood ratio tests, which involved comparing models with and without cross product terms between the baseline stratifying variable and spicy food consumption as an ordinal variable.
To examine the robustness of our findings, we also conducted several sensitivity analyses: additionally adjusting for occupation and household income; additionally adjusting for histories of chronic hepatitis or cirrhosis, peptic ulcer, and gallstone or cholecystitis; adjusting for a 13 level detailed smoking variable, which incorporated the information on amount of smoking in regular smokers and the time since quitting in former smokers, instead of a four level smoking variable; excluding participants dying during the first two years of follow-up; excluding participants who had diabetes at baseline; excluding participants who reported exclusive use of other spices instead of any types of chilli; stratifying analyses by rural or urban residence; and stratifying analyses by follow-up duration (<3 or ≥3 years).
Multivariate models were adjusted for established and potential risk factors for death: age (continuous, serving as the underlying timescale); sex (male or female); level of education (no formal school, primary school, middle school, high school, college, or university or higher); marital status (married, widowed, divorced or separated, or never married); alcohol consumption (non-drinker, occasional drinker, former drinker, or regular drinker); smoking status (never smoker, occasional smoker, former smoker, or regular smoker); physical activity in MET hours a day (continuous); body mass index (continuous); intake frequencies of red meat, fresh fruits, and vegetables (daily, 4-6 days/wk, 1-3 days/wk, monthly, or rarely or never); prevalent hypertension and diabetes at baseline (presence or absence); menopausal status (for women only, premenopausal, perimenopausal, or postmenopausal); and status of family history of cancer, heart attack, stroke, or diabetes (presence or absence). We adjusted for the family history variables only in the corresponding analysis of cause specific mortality.
We measured person years from baseline (2004–08) until the date of death, loss to follow-up, or 31 December 2013, whichever occurred first. Cox proportional hazards regression models were used to estimate the hazard ratios and 95% confidence intervals of mortality for spicy food consumption, with age as the underlying time scale. We accounted for the group specific effect of 10 survey sites on the hazard function by stratifying on the survey site variable in the Cox model.
Trained staff blinded to baseline information classified any deaths occurring among participants by using ICD-10 codes (international classification of diseases, 10th revision). The deaths were grouped into seven categories: cancer (C00-C97), ischemic heart diseases (I20-I25), cerebrovascular diseases (I60-I69), diabetes mellitus (E10-E14), diseases of the respiratory system (J00-J99), infections (A00-B99), and all other causes. Losses to follow-up in this study refer to participants whose permanent registered residence was no longer in the study area, who could not be contacted after at least three reasonable efforts within one year, or who could be contacted but their new residence was out of the jurisdiction of the regional coordinating center.
We ascertained vital status by means of linkage with local disease surveillance points system death registries 15 and residential records. To minimize the under-reporting of deaths and to identify participants who had moved permanently out of the study areas, we also carried out separate active follow-up annually by reviewing residential records, visiting local communities, or directly contacting participants. 14 The causes of death were sought chiefly from official death certificates that were supplemented, if necessary, by a review of the medical records or undertaking a verbal autopsy using a validated instrument for those with an ill defined or unknown cause of death reported. The electronic linkage to the national health insurance claim databases started in 2011, which has become an important means of follow-up and helped to improve the accuracy of diagnosis and phenotyping of reported conditions, outcome adjudication, and further data collection. Linkage to local health insurance databases has been achieved for about 95% of the participants in 2013. Participants from both urban and rural areas had similar proportions of successful linkage to health insurance databases. Linkage to local health insurance database was renewed annually. Participants who failed to be linked to local health insurance database were actively followed annually by staff to ascertain their status, including hospital admission, death, and moving out of the study area. Linkage to a local health insurance database has become an important supplementary way of ascertaining deaths.
At baseline, trained staff measured body weight, height, and blood pressure using calibrated instruments. Body mass index was calculated as weight (kg)/(height (m) 2 . A stepwise on-site testing of plasma glucose level was undertaken using the SureStep Plus meter (LifeScan; Milpitas, CA). Prevalent hypertension was defined as a measured systolic blood pressure of 140 mm Hg or more, a measured diastolic blood pressure of 90 mm Hg or more, self reported diagnosis of hypertension, or self reported use of antihypertensive drugs at baseline. Prevalent diabetes was defined as a measured fasting blood glucose concentration of 7.0 mmol/L or more, a measured random blood glucose concentration of 11.1 mmol/L or more, or self reported diagnosis of diabetes.
We obtained covariates from the baseline questionnaire, including sociodemographic characteristics (age, sex, education, occupation, household income, and marital status), lifestyle behaviors (alcohol consumption, tobacco smoking, physical activity, and intakes of red meat, fresh fruits, and vegetables), personal health and medical history (hypertension, diabetes, chronic hepatitis or cirrhosis, peptic ulcer, gallstones or cholecystitis, and menopausal status for women only), and information on family members, including biological parents and siblings who had had cancer, heart attack, stroke, or diabetes. The daily level of physical activity was calculated by multiplying the metabolic equivalent tasks (METs) value for a particular type of physical activity by hours spent on that activity per day and summing the MET hours for all activities. Habitual dietary intake in the past year was assessed by a qualitative food frequency questionnaire. A participant was considered as having a family history of a particular disease if they reported at least one first degree relative with the disease.
After completion of the baseline survey in July 2008, about 5% randomly chosen surviving participants in 10 survey sites were resurveyed during August and October of 2008. 14 To test the reproducibility of the frequency of spicy food consumption, we included 1300 participants who completed the same questionnaire twice at an interval of less than 1.5 years (median 1.4 years). Spearman’s coefficient for the correlation between the two questionnaires was 0.71, indicating that spicy food consumption was reported consistently.
In the baseline questionnaire we asked the participants “During the past month, about how often did you eat hot spicy foods?”: never or almost never, only occasionally, 1 or 2 days a week, 3 to 5 days a week, or 6 or 7 days a week. The participants who selected the last three categories were further asked “When you eat spicy foods, what are the main sources of spices usually used?” (multiple choices allowed fresh chilli pepper, dried chilli pepper, chilli sauce, chilli oil, and other or don’t know).
The China Kadoorie Biobank is a prospective cohort study of over 0.5 million adults from 10 geographically diverse areas across China; participants were enrolled between 2004 and 2008 and have been followed up ever since for morbidities and mortality. Further details of the China Kadoorie Biobank study have been described elsewhere. 13 14 Briefly, a total of 512 891 adults aged 30-79 years had valid baseline data—that is, completed questionnaire, physical measurements, and a written informed consent form.
Fig 2 Subgroup analysis of associations between consumption of spicy foods ≥6 days a week and total mortality according to potential baseline risk factors. Hazard ratios for total mortality are for comparison of men and women who ate spicy foods ≥6 days a week with those who ate spicy foods less than once a week. Risk estimates for other categories of spicy food consumption are shown in appendix table 2. Horizontal lines represent 95% confidence intervals
We also analyzed the associations between spicy food consumption and total mortality according to other potential baseline risk factors for death; the inverse associations between spicy food consumption and total mortality were generally similar across subgroups stratified according to age, smoking status, level of physical activity, and body mass index (all P values for interaction >0.05) (fig 2 ⇓ and appendix table 2). Significant differences across stratums were observed for alcohol consumption, with a stronger inverse association among participants who did not consume alcohol than those who did (P=0.033 for interaction).
Fig 1 Subgroup analysis of associations between consumption of spicy foods ≥6 days a week and total and cause specific mortality according to consumption of fresh chilli pepper. Hazard ratios for death from all causes and from specific causes are for comparison of men and women who ate spicy foods ≥6 days a week with those who ate spicy foods less than once a week. Appendix table 1 shows the risk estimates for other categories of spicy food consumption. Horizontal lines represent 95% confidence intervals
We further performed stratified analyses according to whether the participants reported using fresh chilli pepper as their predominant spice. We found that the inverse associations of daily spicy food consumption with death due to cancer, ischemic heart diseases, and diabetes seemed stronger in the fresh chilli group than in the non-fresh chilli group in the whole cohort of women and men, and the results were statistically significant in the fresh chilli group (fig 1 ⇓ and appendix table 1).
In the sensitivity analyses, the associations of spicy food consumption with total and cause specific mortality did not change appreciably with additional adjustment for occupation and household income; or additional adjustment for histories of chronic hepatitis or cirrhosis, peptic ulcer, and gallstone or cholecystitis; or adjustment for a 13 level detailed smoking variable instead of a four level smoking variable; or excluding participants dying during the first two years of follow-up; or excluding participants with prevalent diabetes at baseline; or excluding participants with exclusive use of other spices instead of any types of chilli (data not shown). The associations of spicy food consumption with total and cause specific mortality were consistently observed in participants from both rural and urban areas and for different follow-up durations (<3 or ≥3 years).
After multivariate adjustment, spicy food consumption was inversely associated with the risks of death due to cancer, ischemic heart diseases, and respiratory diseases in the whole cohort (table 2). No statistically significant heterogeneity was observed in the associations between spicy food consumption and cause specific mortality by sex (all P>0.05). Nevertheless, the associations seemed to be less evident in men than in women (table 3). In addition, more frequent consumption of spicy foods in women was also significantly associated with a reduced risk of death due to infections.
During a median follow-up of 7.2 years (interquartile range 1.84 years; total person years 3 500 004), we documented 11 820 deaths among men and 8404 deaths among women. Absolute mortality rates according to spicy food consumption categories were 6.1, 4.4, 4.3, and 5.8 deaths per 1000 person years for participants who ate spicy foods less than once a week and 1 or 2, 3 to 5, and 6 or 7 days a week, respectively. Age adjusted and multivariate adjusted analyses showed a statistically significant inverse association between spicy food consumption and total mortality. In the whole cohort, compared with participants who ate spicy foods less than once a week, the adjusted hazard ratios for death were 0.90 (95% confidence interval 0.84 to 0.96) for those who ate spicy foods 1 or 2 days a week, 0.86 (0.80 to 0.92) for 3 to 5 days a week, and 0.86 (0.82 to 0.90) for 6 or 7 days a week (table 2 ⇓ ). Compared with participants who ate spicy foods less than once a week, those who consumed spicy foods 6 or 7 days a week showed a 14% relative risk reduction in total mortality. The multivariate adjusted hazard ratios for total mortality among men, compared with men who ate spicy foods less than once a week, were 0.90 (0.83 to 0.98) for those who ate spicy food 1 or 2 days a week, 0.90 (0.83 to 0.99) for 3 to 5 days, and 0.90 (0.85 to 0.96) for 6 or 7 days a week; the respective hazard ratios among women were 0.88 (0.79 to 0.98), 0.78 (0.69 to 0.88), and 0.81 (0.75 to 0.87) (table 3 ⇓ ). There was no heterogeneity between men and women in any of the associations (P=0.723).
Table 1 ⇓ presents the age and site adjusted baseline characteristics of the participants according to the categories of spicy food consumption. Compared with participants who consumed spicy foods less frequently (3 to 5 days a week or less), those who consumed spicy foods almost every day were more likely to be rural residents, more likely to smoke tobacco and consume alcohol, and more frequently to consume red meat, vegetables, and fruits. Fresh and dried chilli peppers were the most commonly used types of spices in those who reported consuming spicy foods weekly (table 1).
Discussion
In this large prospective study, we observed an inverse association between consumption of spicy foods and total mortality, after adjusting for potential confounders. Compared with those who ate spicy foods less than once a week, those who consumed spicy foods almost every day had a 14% lower risk of death. Inverse associations were also observed for deaths due to cancer, ischemic heart diseases, and respiratory diseases. The associations were consistent in men and women.
Strengths and limitations of this study The strengths of this study include a large sample size, a prospective cohort design, and careful control for established and potential risk factors for death. This study does have a few limitations. Consumption of spicy foods may be correlated with other dietary habits and lifestyle behaviors. For example, in Chinese cuisine the cooking of chilli pepper and the production of chilli sauce and oil usually requires more oil, and intake of pungent foods may be accompanied by an increased intake of carbohydrate-rich foods such as rice to relieve the burning sensation. However, the lack of detailed dietary information in this study limited our ability to comprehensively adjust for total energy intake and other specific dietary factors. In addition, spicy food consumption may be correlated with socioeconomic status,16 which we partly controlled for in our analyses. Residual confounding by other unmeasured or unknown biological and social factors was still possible, although we carefully adjusted for several established and potential risk factors for death. However, residual confounding by the aforementioned or other confounding factors might have attenuated the inverse associations between spicy food consumption and mortality toward the null. Although chilli pepper was the most commonly used spice in our population, the use of other types of spices usually increases as the use of chilli pepper increases. Thus the health benefits of these spices apart from chilli pepper may also contribute to the observed inverse associations. Reverse causality is another possible explanation for our findings because people with chronic disease might abstain from spicy foods. However, we excluded participants who had cancer, heart disease, or stroke at baseline. Moreover, the results remained largely unchanged when we excluded participants dying during the first two years of follow-up from analyses or additionally adjusted for several major digestive system diseases that might deter people from consuming spicy foods. Although we employed multiple ways to maximize death ascertainment of participants, under-reporting of deaths might have occurred. However, the proportion of participants under-reported on death status would not depend on the levels of spicy food consumption. Considering that specificity of outcome detection is nearly perfect and sensitivity is lower than 100% in both exposure groups, outcome misclassification would produce little bias in estimating hazard ratio.17 The consumption of spicy foods was self reported; therefore, some measurement error is inevitable. The questionnaire on spicy food consumption used in our study has not yet been validated directly; however, previous studies have shown that using similar food frequency questionnaires could produce valid estimates of food consumption in a Chinese population.18 In addition, in a prospective study design, measurement errors may be non-differential and the measure of association is more likely to be biased toward the null. The consumption of spicy foods reported for a short period may not necessarily reflect the long term patterns of consumption. However, repeated collections of dietary information averaged 1.4 years in our cohort and have shown that the reported intakes of dietary factors including spicy foods were highly consistent over time. In addition, information was not available on how spicy foods were prepared and cooked. Such information would have enabled us to perform further analyses on the relation between spicy food consumption and mortality more extensively.
Comparison with other studies and potential mechanism Our study is the first to analyze the association between daily consumption of spicy foods and mortality in a prospective cohort. Our findings are in line with previous evidence showing potential protective effects of spicy foods on human health. Capsaicin is the main active component of chilli pepper. The beneficial roles of capsaicin have been extensively reported in relation to anti-obesity, antioxidant, anti-inflammatory, anticancer, and antihypertensive effects, and in improving glucose homeostasis, largely in experimental or small sized population studies.7 8 9 Additionally, the antimicrobial function of spices, including chilli pepper, has long been recognized,3 19 and such a property may have an important effect on the gut microbiota in humans. In recent years, rapidly emerging evidence has implicated gut microbiota as a novel and important metabolic factor that affects the health of the host,20 and several studies in humans have related abundance, composition, and metabolites of gut microbiota to risk of obesity,21 22 23 diabetes,12 24 liver cirrhosis,11 and cardiovascular disease.10 25 However, how spicy foods and their bioactive ingredients may affect the composition and activity of gut microbiota has yet to be further investigated. In addition, our study suggested a threshold of around 1 or 2 days a week of spicy food consumption, beyond which the risk for mortality did not decrease further. Possible mechanisms might involve the bioaccessibility and bioavailability of bioactive ingredients and nutrients of spicy foods26; but further studies are needed to verify our findings. Our study indicated that spicy food consumption was particularly related to the reduced risk of mortality due to cancer, ischemic heart diseases, and respiratory diseases. Several previous epidemiological studies have suggested protective effects of capsaicin consumption on stomach or gallbladder cancer,7 9 27 although such effects were not consistently observed. The cardiovascular system is rich in capsaicin sensitive sensory nerves, which have an extensive role in regulating cardiovascular function.28 The antioxidant and antiplatelet properties of capsaicin and the important role of capsaicin in regulating energy metabolism may also contribute to its beneficial effects on the cardiovascular system.7 9 28 29 30 31 32 Less well known are the possible mechanisms underlying the potentially beneficial effect of spicy foods on respiratory diseases. However, the anti-obesity, antioxidant, anti-inflammatory, and antihypertensive effects of spicy foods would generally protect all these specific systems. Because the number of deaths from infections was relatively small, our study might not have had enough statistical power to rule out a possible relation between spicy food consumption and infections specific mortality. Compared with non-fresh spicy foods such as dried chilli pepper, chilli sauce, or chilli oil, fresh chilli pepper is richer in bioactive ingredients, including capsaicin, vitamin C, and other nutrients such as vitamin A, K, and B6, and potassium. In our stratified analyses we found that the inverse associations of spicy food consumption with certain cause specific deaths (cancer, ischemic heart disease, and diabetes) seemed to be stronger in those who consumed fresh chilli pepper than those who consumed non-fresh spicy foods. These data suggest that some of the bioactive ingredients are likely to be effective in driving the observed associations. Interestingly, a statistically significant inverse association between the daily consumption of spicy foods and diabetes, which was not observed in the whole cohort, was found in the subgroup that consumed fresh chilli pepper. This was consistent with previous evidence showing that dietary capsaicin may provide beneficial effects on glucose homeostasis.33 However, it remains unclear whether other nutrients abundant in fresh chilli pepper also have roles in lowering the risk of mortality. Intriguingly, we found that the inverse association was stronger in those who did not than did drink alcohol. Alcohol consumption has been related to an increased risk of mortality in some but not all previous studies.34 35 36 Even though moderate alcohol consumption has been related to a reduced risk of certain chronic diseases such as diabetes, moderately high alcohol consumption may increase energy intake37 and has been associated with increased mortality.38 In addition, alcohol intake also affects the metabolism of gut microbiota.39 40 Even though the precise mechanism remains unclear, the interaction between spicy foods and alcohol intake is biologically possible. We acknowledge that disease status might affect both alcohol and spicy food intakes, and we excluded participants with chronic diseases such as cancer, heart disease, or stroke at baseline from our analyses. Further investigations are warranted to validate our findings and explore the mechanisms. ||||| TIME Health For more, visit TIME Health
People who love chili peppers might be eating their way to a longer life, according to a new study published in The BMJ.
“We know something about the beneficial effects of spicy foods basically from animal studies and very small-sized human studies,” says study author Lu Qi, associate professor at the Harvard School of Public Health. Some of those preliminary studies have found that spicy food and their active components—like capsaicin, the compound found in chili peppers—might lower inflammation, improve metabolic status and have a positive effect on gut bacteria and weight, he says.
But human evidence remains scant. So Qi and a team of researchers looked at questionnaire data from about half a million adults all across China who participated in the China Kadoorie Biobank study between 2004-2008. Each person in the study reported their health status, alcohol consumption, spicy food consumption, main source of chili intake (fresh or dried, in a sauce or in an oil) as well as meat and vegetable consumption.
The researchers followed up with them about seven years later. Compared to people who ate spicy foods less than once a week, people who ate them just once or twice a week had a 10% reduced risk of death. Bumping up the spice consumption didn’t make much of a difference; those who ate spicy food 3-7 days a week were at 14% reduced risk of death compared to the most spice-averse group.
Eating chili-rich spicy foods was also linked to a lower risk of death from certain diseases, including cancer, ischemic heart diseases and respiratory diseases, they found. Further analysis revealed that fresh chili had a stronger protective effect against death from those diseases.
More research is needed to make any causal case for the protective effects of chili—this does not prove that the spicy foods were the reason for the health outcomes—but Qi finds this observational research valuable. “It appears that increasing your intake moderately, just to 1-2 or 3-5 times a week, shows very similar protective effect,” he says. “Just increase moderately. That’s maybe enough.”
MORE: 3 Reasons You Should Eat More Spicy Food |||||
What is a shorter version of the above article? | – People who like a little heat in their meals just might be doing their longevity a favor. So report researchers this week in the British Medical Journal after studying the health, diets, and alcohol consumption of more than 485,000 people in China. Controlling for many variables, including family medical history, age, education, diabetes, and smoking, they found that those who ate spicy foods—mainly via chili peppers—once or twice a week enjoyed a 10% reduced overall risk for death than those who ate spicy foods less than once a week, reports the New York Times. And that reduction improved to 14% when people ate spicy foods six or seven times a week. "We know something about the beneficial effects of spicy foods basically from animal studies and very small-sized human studies," study author Lu Qi of Harvard tells Time. Some findings focus on active components like capsaicin found in chili peppers that appears to reduce inflammation and improve metabolic status, gut bacteria, and weight, he adds. "It appears that increasing your intake moderately, just to one to two or three to five times a week, shows very similar protective effect. Just increase moderately. That’s maybe enough." Of course, more research is needed to demonstrate actual causation, but for now the link between the consumption of spicy foods and lower risk of death appears strong. (This man says hot sauce saved his life.) | multi_news_1_0_0 |
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A 46-year-old Orlando woman has become the oldest woman to give birth to a healthy baby through in vitro fertilization using her biological eggs, according to medical literature.
A 46-year-old from Orlando has become the oldest woman to have a baby through in vitro fertilization using her own fresh — not frozen — biological eggs.
Belinda Slaughter delivered her first child — a healthy baby boy — last September. Her son, Jackson, "is wonderful and perfectly healthy," said the proud mom.
She wasn't trying to set a record.
"I didn't think this was so special," said Slaughter, now 47, who is a dental hygienist. "I thought, 'There are women older than I am having babies.'"
That's true, but not with their own eggs.
While many women older than 46, even into their 60s, have delivered babies through in vitro using donor eggs or frozen embryos from when they were younger, Slaughter made medical history because of the age of her eggs, not the age of her uterus, said Dr. Mark Trolice, founder and medical director of Vivere-Winter Park Fertility Laboratory, who worked with Slaughter and her husband, Torrance Slaughter, 42, to conceive.
The case was published in the May issue of Fertility and Sterility, a journal of the American Society for Reproductive Medicine.
Such firsts are hard to verify, but the fact that this birth was reported in the medical literature gives it credibility, said Dr. Richard Paulson, a well-known fertility expert and medical director of the fertility program at the University of Southern California's Keck School of Medicine.
"What's remarkable about this case is not the age of the mother so much as the age of the egg, which was 46 years old," he said.
"If a woman freezes her eggs at age 40, and at age 47 has those eggs implanted trough in vitro fertilization and has a baby, that would not be as scientifically remarkable as if she got pregnant using an egg harvested at that day and age," Paulson said.
The oldest person on record to have a baby naturally, without infertility treatment, was a 59-year-old British woman who gave birth in 1997, according to Guinness World Records.
A New York infertility doctor claims that in 2011 his patient had a baby at age 49 using eggs she had frozen when she was 48, but that case was never verified in medical literature.
"People can make claims," Paulson said. "Many do press releases. But scientific journals validate them."
Slaughter, who had a history of infertility, knew her chances of getting pregnant with her own egg were slim.
"Dr. Trolice said that because of my age, I had only a 1 percent chance of conceiving, but I still wanted to try."
In March 2013, Trolice harvested eggs from Slaughter's ovary, fertilized them with her husband's sperm and three days later transferred four embryos into Slaughter's uterus. One took.
Against the odds
A woman is born with all the eggs she will ever have. As she ages, so do her eggs, which not only dwindle in number, but also have a greater chance of conferring a chromosomal defect.
For instance, at age 30, a woman's chance of having a baby with any chromosomal abnormality, including Down syndrome, is one in 385, said Trolice.
By 35 — the age at which doctors recommend women have genetic testing — the risk jumps to one in 192. By age 46, it's one in 16.
"In the world of reproduction, nothing gets better with age," Paulson said.
Nonetheless, thanks to women's desire to postpone pregnancy and advances in infertility treatment, the number of women having their first child at age 35 or older has increased ninefold from 1970 to 2012, according to the Centers for Disease Control and Prevention.
Still, fertility experts don't encourage women to defer pregnancy.
"In no way does a women want to use this example to defer fertility until they are older," said Trolice. "After age 40, women still face huge hurdles. Their risk of complication gets higher every step of the way."
If an older woman does conceive, her chances of miscarriage, high blood pressure, diabetes and problems with the placenta go up, so much so that the American Society for Reproductive Medicine tells doctors not to implant embryos in women beyond age 54.
Even Slaughter's pregnancy was not without complication. Halfway through her pregnancy, her cervix grew weak and needed suturing to prevent a too-early arrival. After that, she stayed in the hospital for 10 weeks, until at 31.5 weeks (8.5 weeks shy of full term), she had a cesarean section and delivered baby Jackson, who weighed 3 pounds, 8 ounces.
"I always knew it was going to work," she said, offering this advice to other women: "Pray for direction, then go for it. Don't live with regrets."
[email protected] or 407-420-5158 ||||| A 46-year-old Orlando woman has become the oldest mother in the United States, and possibly in the world, to give birth to a healthy baby through in-vitro fertilization using her own fresh eggs.
Belinda Slaughter, now 47, gave birth to her first child in September, her doctor, Mark Trolice of Winter Park, said in an interview on Tuesday. Key to the record is that the eggs were fresh, just a few days old, rather than frozen or donated. Slaughter, who named the boy Jackson, also beat the odds of delivering a child with chromosomal abnormalities, such as Down Syndrome, which increase with maternal age.
"She had a guardian angel watching over this pregnancy from the get-go," Trolice said.
The case should be considered an anomaly, said Stan Williams, chairman of the department of obstetrics and gynecology at the University of Florida's medical school, in Gainesville. Williams said the university's in-vitro program does not accept women over 43, because the low probability of success, and medical and financial risks exceed potential benefits. Slaughter had been turned away by another clinic, Trolice said.
"I'm hoping that women in their mid-40s aren't going to look at this and say 'Oh, I can do that too.' Being a world's record, people need to understand this is a very rare event," Williams said.
Trolice said Slaughter's success at least rivals and might exceed that of a woman in Italy who gave birth several years ago, also at around age 46. Her doctor reported the feat but not the woman's precise age at conception and birth - details needed to determine which woman was oldest.
Trolice said the birth reflects the continued improvement of in-vitro pregnancy rates since the first such successful birth in 1978 but agreed it should not provide false hope to women over 45.
The news was first reported in the May issue of the Fertility and Sterility, a journal of the American Society for Reproductive Medicine. |||||
What is a one-paragraph summary of the above article? | – A 46-year-old Florida woman became a new mom to a healthy baby boy last year via IVF—and though it's not unheard of for a woman to deliver a baby at her age, what's medically remarkable is that Belinda Slaughter didn't use frozen or donated embryos, but her own 46-year-old egg. And she's the oldest American woman verified to do so, NBC News reports. Son Jackson was born in September, the Orlando Sentinel reports, but the case was just published in a medical journal this month. Slaughter—who had fertility issues—was told she had a 1% chance of conceiving, but one of the four fresh, fertilized eggs implanted in her uterus latched on. "I didn't think this was so special," Slaughter, now 47, tells the Sentinel. "I thought, 'There are women older than I am having babies.'" She’s right. NBC lists one past success a few years ago—an unverified 46-year-old Italian woman. The Sentinel lists a couple more: a 59-year-old Brit who conceived her child naturally without IVF, and another unverified case in 2011 of a 49-year-old woman who gave birth after using her year-old frozen eggs. But doctors emphasize just how rare a feat this was. Fertility expert Dr. Richard Paulson remarks that “in the world of reproduction, nothing gets better with age." Indeed, Slaughter’s pregnancy was rife with complications, and she delivered at 31.5 weeks. "In no way does a woman want to use this example to defer fertility until they are older,” her doctor says. | multi_news_1_0_0 |
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News article:
Actor Dick Van Patten died this morning due to complications from diabetes, his publicist confirmed to ABC News. He was 86 years old.
"He was the kindest man you could ever meet in life," his rep, Jeff Ballard, said. "They don't make them like him anymore."
Best known for playing patriarch Tom Bradford in the series "Eight Is Enough," Van Patten most recently appeared in a 2011 episode of "Hot In Cleveland." In the past decade, he also appeared in "Arrested Development, "That '70s Show" and other programs.
"I like to do TV series. I think they're so comfortable. You're doing the same part every week," he once told Emmy TV Legends. "You're working with the same people and there's a lot of recognition. I like to do series best. I really do."
Born Richard Van Patten in New York City, the actor began working as a child and reportedly made his Broadway debut at seven.
Eventually, he moved to Hollywood, where he found success in TV and film, including several movies directed by Mel Brooks, such as "High Anxiety," Spaceballs" and "Robin Hood: Men In Tights."
The actor is survived by his wife, Pat, and their three sons, according to reports. ||||| Skip Ad Ad Loading... x Embed x Share 'Eight is Enough' star Dick Van Patten died today due to complications from diabetes. Jasper Colt, USA TODAY
Dick Van Patten in August 2006 in Los Angeles. (Photo: RENE MACURA/ AP)
Dick Van Patten, the venerable comic character actor who made millions chuckle on Eight is Enough and The Love Boat, has died. He was 86.
His death was confirmed by his publicist, Jeff Ballard, who said he died at a Santa Monica hospital early Tuesday from complications from diabetes.
Van Patten was a familiar face on American TV for decades, with a star on the Hollywood Walk of Fame.
But his best known role was that of beloved patriarch Tom Bradford on the family sitcom Eight is Enough, about the goofy dad of a family with eight kids that ran from 1977 to 1981.
The show was based on the real-life journalist Tom Braden, who had eight children and wrote a book about it, and later became one of the commentators on CNN's Crossfire.
Van Patten reprised the role in the 1987 TV movie Eight Is Enough: A Family Reunion and in 1989's An Eight Is Enough Wedding.
Van Patten's 2009 autobiography was titled Eighty is Not Enough.
We'll forever miss your sincere smile and devoted friendship, Dick Van Patten. Thank you for the love you gave so freely.
Rest in peace. — RUTH BUZZI (@Ruth_A_Buzzi) June 23, 2015
He was born in New York and started out as a child model and actor, billed as Dickie Van Patten. He appeared on the Broadway stage starting at age 7 (his first role was in 1935's Tapestry in Gray) and continued through his teen years, before moving to Hollywood and embarking on a long film and TV career, mostly in comic roles.
Among other shows, he also appeared on Happy Days, Sanford & Son, and Adam-12. He was a regular for six years on The Love Boat, starting in 1978 and playing a politician on the wacky cruise ship, and earlier played the ship doctor in the TV movie that preceded the show.
His numerous film roles included Soylent Green and a number of Mel Brooks films, including High Anxiety, Spaceballs, and Robin Hood: Men in Tights.
An animal enthusiast, Van Patten founded National Guide Dog Month, which began in 2008 to raise awareness and money for non-profit guide-dog schools in the U.S.
Van Patten was the older brother of actress Joyce Van Patten, the older half-brother of film director Tim Van Patten, and the uncle of actress Talia Balsam, George Clooney's first wife.
Van Patten is survived by his wife Patricia Van Patten, a former June Taylor dancer, to whom he had been married for 62 years, and his three actor sons, Nels, Jimmy and Vincent.
Read or Share this story: http://usat.ly/1LrG0zx |||||
What is a shorter version of the above article? | – Dick Van Patten, who starred as the patriarch of the Bradford family in the late 1970s show Eight is Enough, is dead at 86 from diabetes complications, reports ABC News. Van Patten also was a regular on the Love Boat for six years and "was a familiar face on American TV for decades," notes USA Today. Though he was partial to TV roles, Van Patten also starred in several movies, especially of the Mel Brooks variety, including High Anxiety, Spaceballs, and Robin Hood: Men in Tights. More recently, he appeared in Hot in Cleveland and Arrested Development. He is survived by his wife, Pat, and three sons. "He was the kindest man you could ever meet in life," says his rep, Jeff Ballard. "They don't make them like him anymore." | multi_news_1_0_0 |
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Article:
These findings on actual smartphone screen-time build upon prior work based on self-report and confirm that adults spend a substantial amount of time using their smartphones. Screen-time differs across age and race, but is similar across socio-economic strata suggesting that cultural factors may drive smartphone use. Screen-time is associated with poor sleep. These findings cannot support conclusions on causation. Effect-cause remains a possibility: poor sleep may lead to increased screen-time. However, exposure to smartphone screens, particularly around bedtime, may negatively impact sleep.
Total screen-time over 30 days was a median 38.4 hours (IQR 21.4 to 61.3) and average screen-time over 30 days was a median 3.7 minutes per hour (IQR 2.2 to 5.5). Younger age, self-reported race/ethnicity of Black and "Other" were associated with longer average screen-time after adjustment for potential confounders. Longer average screen-time was associated with shorter sleep duration and worse sleep-efficiency. Longer average screen-times during bedtime and the sleeping period were associated with poor sleep quality, decreased sleep efficiency, and longer sleep onset latency.
We performed a cross-sectional analysis in a subset of 653 participants enrolled in the Health eHeart Study, an internet-based longitudinal cohort study open to any interested adult (≥ 18 years). Smartphone screen-time (the number of minutes in each hour the screen was on) was measured continuously via smartphone application. For each participant, total and average screen-time were computed over 30-day windows. Average screen-time specifically during self-reported bedtime hours and sleeping period was also computed. Demographics, medical information, and sleep habits (Pittsburgh Sleep Quality Index–PSQI) were obtained by survey. Linear regression was used to obtain effect estimates.
Funding: Research reported in this publication was supported by the Office of Behavioral Social Sciences (OBSSR), National Institute of Biomedical Imaging and Bioengineering (NIBIB), National Institute of Neurological Disorders and Stroke (NINDS), National Heart Lung and Blood Institute (NHLBI), and National Institute on Alcohol Abuse and Alcoholism (NIAAA) of the National Institutes of Health under award number 1U2CEB021881 ( https://grants.nih.gov/grants/oer.htm ). MAC is a research fellow supported by the Sarnoff Cardiovascular Research Foundation ( http://sarnofffoundation.com ). KTN is a fellow supported by National Institute on Minority Health and Health Disparities (NIMHD) under award number R25MD006832 ( http://www.nimhd.nih.gov/ ). Ginger.io Incorporated ( https://ginger.io ) provided support in the form of salaries for authors LK and STM, but did not have any additional role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript. The specific roles of these authors (LK, STM) are articulated in the ‘author contributions’ section. The other funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Smartphones are increasingly integrated into everyday life [ 1 ]. At the same time, the prevalence of insomnia and sleep deprivation have risen [ 2 ]. Poor sleep (too little or too much, and poor quality) has been shown to be a risk factor for obesity, diabetes, cardiovascular disease, depression, and overall mortality [ 3 , 4 ]. Light in the blue spectrum, such as light produced from a smartphone, can suppress production of melatonin, leading to decreased drowsiness, difficulty initiating sleep, and non-restorative sleep [ 5 , 6 ]. In addition, engrossing activities during smartphone use may result in stimulation that is counter-productive to sleep preparation. Limiting the use of TV and computers near bedtime is commonly recommended as an important part of good sleep hygiene [ 7 ], but direct measurements of “screen-time” in native (or home) environments have not previously been available.
Hypothesis-driven analyses related to screen-time and sleep were restricted to participants that completed the PSQI. Age, sex, and a history of sleep apnea were a priori “forced” into adjusted linear regression models along with other covariates that were significant (p<0.05) in the hypothesis-free multivariate model. Based on a priori hypotheses, select measures from the PSQI were compared to the average screen-time in the hours near self-reported bedtime (1 hour before participant-reported bedtime, the hour of participant-reported bedtime, 1 hour after the participant-reported bedtime) and during the sleep period (bedtime hour to wake-up hour) in a subgroup with no missing screen data. Statistical analyses were performed using STATA 13 (College Station, TX). Two tailed p values <0.05 were considered statistically significant.
Associations between average screen-time and baseline demographics, medical history, and behaviors were assessed first in a bivariate manner using linear regression models. Variables that were associated with average screen-time with two-tailed p < 0.10 in the bivariate analyses were retained in a single multivariate linear regression model where significance was considered at the standard two-tailed p < 0.05 level. Variables that remained statistically significantly associated with screen-time in the multivariate model were interpreted as independent predictors of screen-time. Variables that were no longer associated with screen-time in the multivariable model were considered to have been confounded by other variables, and were interpreted as not being key independent predictors. A sensitivity analysis was performed by restricting to those with complete screen-time data (no missing data) over the 30-day window.
Participants provided baseline personal, demographic, and medical information via several online surveys once during their initial “eVisit.” Race and ethnicity were combined into a single mutually exclusive covariate (“race/ethnicity”), where Hispanic ethnicity, if present, took precedence over selected race. Self-reported height and weight were used to calculate body mass index (BMI). The validated Patient Health Questionnaire Overview (PHQ-9) was used to assess mood [ 8 ]. The validated International Physical Activity Questionnaire (IPAQ) was used to assess physical activity [ 9 ]. The validated Pittsburg Sleep Quality Index (PSQI) was used to assess sleep duration, quality, and the sleeping period (bedtime and wake-up time) [ 10 , 11 ]. The total PSQI score and component sub-scores were analyzed as continuous variables and “poor sleep” was defined as dichotomous variable by PSQI total > 5, per instrument protocol [ 12 ].
Screen-time data was collected on existing and new participants between September 1, 2014 and September 30, 2015. The amount of missing data (due to phone-off, airplane mode, or app-off) in 30-day rolling windows was computed and the windows with the minimum level of missing data were identified and selected for analysis. In the event of ties, the earliest window with the minimum amount of missing data for each participant was selected for analysis. Participants with no screen-time data (100% missing data) or less than 30 days of observation were excluded. Within the selected 30-day window, the overall average screen-time (averaged over all hours in 30 days) and the hourly average screen-time (during each hour of the day, averaged over 30 days) were computed for each participant.
On September 1, 2014, participants with smartphones were invited to download a mobile application (“app”) developed by Ginger.io (San Francisco, CA); this mobile app was capable of recording screen-time on Android-based smartphones. Once downloaded, the app automatically operated in the background without disrupting normal use of the smartphone. The app recorded screen-time continuously as the number of minutes in each hour that the screen was turned on as long as the smartphone was not in “airplane mode” and the app was not actively turned off. This screen-time measure was stored locally on the smartphone and transmitted over the Internet to the study database daily.
The Health eHeart Study ( www.health-eheartstudy.org ) is an internet-based prospective cohort that began enrolling any interested adult age ≥ 18 years with an active email address on March 8th, 2013. Participants were recruited via online and social media advertisements, email campaigns with research and advocacy organizations, and directly in person at University of California, San Francisco medical clinics. Consent was obtained electronically through the study website. We initially performed comparisons between prospectively collected screen-time and baseline demographics, medical history, and health behaviors in a hypothesis free manner. We then focused on participants who had completed a baseline sleep survey to specifically test the hypothesis that more screen-time would be associated with reduced sleep quality. The study was approved by the University of California, San Francisco Committee on Human Research.
Abbreviations: PSQI, Pittsburg Sleep Quality Index; SD, standard deviation. Among participants with a sleep survey and full screen-time data (N = 56), self-reported bedtime and wakeup-time was used to compute average screen-time (over 30 days) during the hour before bedtime, the hour of bedtime, the hour after bedtime, and during the sleeping period (all hours from bedtime to wakeup-time). All markers represent point estimates for linear regression coefficients after adjustment for age, sex, race/ethnicity, and history of obstructive sleep apnea. Coefficients correspond to the increase in average screen-time, during the indicated period, for a unit change in the corresponding sleep measure. Whiskers give 95% confidence intervals.
There were 56 participants that both completed the PSQI sleep survey and had complete screen-time data (0% missing). After adjustment for age, sex, race/ethnicity, and sleep apnea, poor sleep (by PSQI total > 5) was statistically significantly associated with longer average screen-time during the reported sleeping period and during the hour after bedtime ( Fig 5 ). Both decreased sleep efficiency and increased sleep onset latency were associated with longer average screen-time during the reported sleeping period, the hour of bedtime, and the hour after bedtime. Total sleep duration was not associated with average screen-time during the reported sleeping period or during any of the 3 hours near reported bedtime.
Abbreviations: PSQI, Pittsburg Sleep Quality Index; SD, standard deviation. Diamonds (unadjusted) and circles (adjusted) represent point estimates for linear regression coefficients, which correspond to the increase in average screen-time for a unit change in the corresponding variable. Whiskers give 95% confidence intervals. Each PSQI score was analyzed as a continuous variable. Coefficients for PSQI total score are reported per SD increase, coefficients for Poor sleep and other PSQI component scores are reported per unit increase. a PSQI sub-scores range from 0 (good) to 3 (poor) for each component of sleep. The total score is the sum of the sub-scores (0–21). PSQI total score > 5 is a standard dichotomous measure for overall poor sleep. Decreased sleep duration and decreased sleep efficiency correspond to higher component scores. b Adjusted for age, sex, race/ethnicity, and history of obstructive sleep apnea.
In the hypothesis-driven analyses in the subgroup who also completed the sleep survey (n = 136), decreased sleep quality, shorter sleep duration, lower sleep efficiency, and longer sleep onset latency were each significantly associated with greater overall average screen-time in unadjusted analyses ( Fig 4 ). After adjustment for age, sex, race/ethnicity, and history of sleep apnea, a greater score on the PSQI sleep duration component (less sleep) and reduced sleep efficiency were each statistically significantly associated with longer average screen-time ( Fig 4 ).
Abbreviations: BMI, body mass index; AF, atrial fibrillation; CAD, coronary artery disease; CHF, congestive heart failure; HTN, hypertension; OSA, obstructive sleep apnea. Boxes (bivariate) and circles (multivariate) represent point estimates for linear regression coefficients, which correspond to the increase in average screen-time for a unit change in the corresponding variable. Whiskers give 95% confidence intervals. For categorical covariates (race/ethnicity, smoking, activity level) p values for the overall effect of the variable are presented. a Factors significantly associated with average screen-time at the p < 0.10 level in bivariate linear models were included in a multivariate linear model. b Education and income were both ascertained with 9 levels and analyzed as continuous variables. c PHQ-9 score is scaled to a unit increase of 5, the width of each category of depression. d Data were available on 267 participants. e White circles are regression coefficients adjusted for all other variables in the model.
In pursuing the hypothesis-free approach to identify predictors of screen-time, crude analyses revealed that younger participants, females, blacks, Hispanics, those self-reporting as “other” race, those of lower socioeconomic status (less education and lower income), those without a past history of smoking, those with a higher PHQ-9 score (more depressed mood), and those without atrial fibrillation, hyperlipidemia, or hypertension exhibited a longer overall average screen-time ( Fig 3 ). After multivariate adjustment, only younger participants, blacks, and those reported to be of an “other” race demonstrated statistically significantly longer average screen-times ( Fig 3 ). For instance, an individual 10 years older in age, on average after multivariable adjustment, had an average overall screen-time that was lesser by 0.7 minutes/hour (95% confidence interval 0.5 to 0.8, p < 0.001).
Within the selected 30-day windows, the app recorded screen-time for a median 29.9 (IQR 27.3 to 30.0) days, during which total screen-time was a median 38.4 (IQR 21.4 to 61.3) hours and average screen-time was a median 3.7 (IQR 2.2 to 5.5) minutes per hour. This average screen-time is equivalent to 1 hour and 29 minutes (IQR 53 minutes to 2 hours and 12 minutes) per day. The relative distribution of screen-time within participants and hourly average screen-time across the population are shown in Fig 2 .
Abbreviations: AK, Alaska; HI, Hawaii. Dots represent the number of participants that resided in the zip-code corresponding to the placement on the map. All 50 states were represented and 147 (23%) resided in California. Created with Tableau Software ( www.tableau.com ) and published with permission of the company ( S1 File ). The U.S. map was used under a CC BY-SA copyright from OpenStreetMap contributors ( www.openstreetmap.org/copyright ).
Among 23,187 Health eHeart participants enrolled by September 1, 2015, there were 3,566 that had downloaded the Ginger.io app of which 761 had Android-based phones that enabled capture of screen-time. Of these, 653 completed the core surveys in eVisit 1, had the app downloaded for at least 30 days, and had at least some (i.e., not 100% missing) screen-time data. Participants represented all 50 U.S. states and 147 (23%) resided in California ( Fig 1 ). The baseline characteristics of the study population are presented in Table 1 . Those with an average screen-time above the population median tended to be younger, female, Black, Hispanic, or “other” race/ethnicity, and have a higher PHQ-9 depression score. A sensitivity analyses restricted to a subgroup with 0% missing screen data (n = 292) revealed similar results (data not shown).
Discussion
Participants' smartphone screen-time exposure was on average approximately 3.7 minutes per hour, centered as expected primarily during the daytime. Those who were younger, Black, and Other race/ethnicity had greater screen-time exposure. Longer average screen-time was associated with shorter duration of sleep and reduced sleep efficiency. Given that screen-time after self-reported sleeping hours and near an individual’s bedtime was associated with reduced sleep efficiency and greater sleep onset latency, the relationship between overall smartphone use and sleep may be driven by exposure near bedtime.
Since the advent of the modern smartphone in 2007, the adoption and use of these devices has been rapid and widespread [13]. As of 2015, approximately 64% of all American adults owned a smartphone, including 85% of those aged 18 to 29 [1]. While the demographics of individuals that purchase smartphones has been studied, the frequency of use based upon an objective measure has not previously been described. We found that younger individuals on average have greater screen-time, in agreement with survey-based demographic and marketing research [1,13]. Our finding that African Americans and Hispanics exhibit longer screen-time is consistent with the fact that racial and ethnic minorities have fewer desktop and laptop computers at home and are more frequently dependent on their smartphone for internet access [1]. Of interest, neither income nor education was associated with average screen-time after multivariable adjustment, suggesting that something cultural aside from socio-economic status may be driving increased smartphone use in these populations.
While there has been concern for both the negative and positive impact of smartphones on depression [14,15], screen-time exposure was not associated with mood after multivariable adjustment. It is also noteworthy that unlike TV watching [16,17], smartphone screen-time was not associated with physical activity level or BMI. This may in part be due to the multi-functionality of smartphones, different modes of media consumption, or perhaps the use of smartphones during physical activities (i.e., running apps). Finally, despite the fact that searching for medical information is one of the most common activities carried out with smartphones [1], none of the medical conditions evaluated were associated with average screen-time.
In addition to how smartphones are changing modern life, the impact of screen exposure on sleep is a major concern. Poor sleep has been shown to decrease performance at school and work, is associated with depressed mood, and is established as a risk factor for obesity, cardiovascular disease, stroke, and death [4,18,19]. Smartphones are often nearby at night, and 68% of owners store their phone on a bedside table while they sleep [20]. Prior studies regarding watching television, conventional computer use, and video-games have demonstrated that use at nighttime and particularly in the bedroom is associated with poor sleep and insomnia [2,7]. Exposure to blue light from such backlit screens suppresses production of melatonin, thereby delaying sleep onset and reducing sleep duration and quality [21]. A recent randomized cross-over trail found hospitalized patients took longer to fall asleep and had reduced quality of sleep after reading a backlit eReader compared to a paper book before bedtime [22]. However, this and other experimental studies may not generalize to typical at-home screen exposure and experiences with eReaders may not extrapolate to smartphone use. At-home screen-time obtained by self-report has been associated with poor sleep [23], but a study that used an app to measure smartphone screen-time in a small group of Taiwanese university students found that participants underestimated their screen-time by approximately 9 hours per week (equivalent to an average of 3.2 minutes/hour) [24].
Our objectively measured screen-time was associated with reduced quality of sleep. That increased screen-time in the hour of and after bedtime, but not the hour before, was associated with greater sleep onset latency agrees with the notion that screen use just before attempting to fall asleep may be particularly problematic.
This study has several important limitations. First, we analyzed a self-selected group of participants that elected to enroll in the Health eHeart Study and download the Ginger.io app, which may not be representative of the general population. Compared to the U.S. census, the cohort is better educated, wealthier, and consists of a greater proportion of whites and females [25,26]. The relative older age of our cohort may be surprising in a study requiring smartphone ownership. However, as demonstrated by the standard deviations in age, the cohort generally represented those in their early 30s to those in their mid 60s. This likely demonstrates the age groups most representative not only of smartphone ownership, but also those most willing, interested, and able to engage with an internet-based research study. On the other hand, we could only record screen-time on Android phones, owners of which tend to have lower socio-economic status compared to iPhone owners [27,28]. Similarly, analyses on screen-time and sleep were limited to a subset who had both types of data available, and analyses on screen-time near bedtime were in a further subset with no missing screen-time data, both of which are susceptible to selection bias. Demographic, medical, and sleep information were obtained by self-report, although well-validated standardized scales (PSQI, PHQ-9, IPAQ) were used. In addition, self-report of medical conditions within the Health eHeart Study has previously proven to exhibit high accuracy [29]. App-recorded screen-time is subject to some measurement error. Screen-time when the app was actively turned off or the phone was in airplane mode was not captured, there could be multiple users of a single smartphone, or the screen could be on while a participant was not aware (such as when the screen is on while in a pocket). We also focused specifically on smartphone screen-time exposure and did not have information on the use of other back-lit devices (TV, computer, tablets). We analyzed 30-day windows with the least amount of missing screen data in an attempt to maximize the accuracy of the screen-time measure, but this could also have induced bias. Still, incomplete capture of smartphone screen exposure, and the absence of data on exposure to other types of screens, should only decrease sensitivity for associations with other participant characteristics. Finally, in regards to the analyses related to screen-time and sleep; although screen-time was collected prospectively and compared to sleep characteristics at baseline, we cannot exclude “effect-cause”—poor sleep could lead to more screen-time.
Our study also has some notable strengths. This is the first time smartphone screen-time exposure has been recorded prospectively and compared to demographic and medical information. Screen-time was measured unobtrusively during “at home” use over a 30 day period and thus is more comparable to every-day long term use than prior experimental studies. Furthermore, since enrollment and consent in the Health eHeart study is performed remotely, the cohort is not limited to a particular geographic location or clinical population.
Our findings suggest that smartphone screen-time is an important exposure associated with worse sleep. Since poor sleep has important health consequences, further investigation to determine the causal relationship between smartphone use and sleep is necessary. This study took advantage of an app to measure smartphone screen-time, but sleep habits were measured once via a survey. Future work may benefit from using an app to collect data on nightly sleep quality. A measure of overall screen-time from multiple devices would also be helpful in this regard. Since certain activities may be more stimulating (e.g. thumbing through Facebook posts), future work might explore how screen-time, smartphone activities, and sleep interact. Ultimately, a deeper understanding of the situational and cultural factors driving smartphone use will be needed to guide studies on interventions aimed at reducing screen-time to improve sleep. ||||| The more time you spend on your smartphone, the worse you'll sleep, a new study suggests.
People in the study who used their smartphones for more time during the month-long study period got less sleep and were less likely to sleep well than those who spent less time on their phones, according to the study.
And people who used their smartphones right before bedtime took longer to fall asleep, according to the study, published today (Nov. 9) in the journal PLOS ONE.
The findings suggest that "exposure to smartphone screens, particularly around bedtime, may negatively impact sleep," the researchers wrote.
In the study, researchers asked 653 adults to install an app on their Android phones that recorded how many minutes the phone's screen was turned on, whenever the phone was not in airplane mode. The researchers collected the data from each person's phone over 30 days. Two of the study's authors work for the company that made the app. [9 Odd Ways Your Tech Devices May Injure You]
The people in the study were part of a larger, ongoing project called the Health eHeart Study and had provided information about their medical histories and lifestyle habits. In addition, some of the people in the study completed a questionnaire about their sleep habits, the researchers wrote.
Results showed that the participants used their phones, on average, for 1 hour and 29 minutes each day, the researchers found. There was no link between smartphone use and people's amount of physical activity, mood or body mass index, according to the study.
However, smartphone use was linked to sleep.
Among the 136 study participants who also provided information about their sleep habits, the researchers found that more smartphone screen time was associated with decreased sleep quality, a shorter amount of sleep time and a longer amount of time needed to fall asleep. More screen time was also linked to lower "sleep efficiency," which is a ratio of the amount of time spent in bed compared to the amount of time actually sleeping.
But in particular, smartphone use around bedtime was linked to lower sleep efficiency and longer time needed to fall asleep, according to the study. This finding suggests that "the relationship between overall smartphone use and sleep may be driven by exposure near bedtime," the scientists, led by Matthew Christensen, a researcher at the University of California, San Francisco, wrote.
"That increased screen time in the hour of and after bedtime, but not the hour before, was associated with [a longer time needed to fall asleep] agrees with the notion that screen use just before attempting to fall asleep may be particularly problematic," the researchers wrote.
Indeed, previous studies have suggested that screen time at night is associated with poor sleep and shorter sleep time, according to the study. This may be due to exposure to the blue light from screens, which may suppress the brain's production of the hormone melatonin, which is involved in sleep, the researchers wrote.
Apple, for example, is trying to address this problem with the "Night Shift" feature on the company's phones, which shifts the display from blues to warmer tones at night.
The researchers noted that there are several limitations to the study. For example, the participants, all of whom decided to join an app-driven study, may not be representative of the general population. In addition, it is possible that the measurements of screen time were not entirely accurate, because people may have let others use their phones for part of the time, or may have been unaware that their phone was "on," such as when it was in a pocket.
The investigators also noted that the study does not prove there is a cause-and-effect between smartphone use and worse sleep. It could be, for example, that people who generally have trouble going to sleep are more likely to turn to their phones at bedtime, the authors wrote.
Originally published on Live Science. ||||| (Reuters Health) - Using smartphones to measure how much time people spend looking at those phones confirms that more screentime is tied to poorer sleep, researchers say.
A man uses a smartphone in New York City, in this picture taken November 6, 2013. REUTERS/Mike Segar
“This is the first study to directly measure actual screen time in natural environments and compare it to sleep quality,” said senior author Dr. Gregory M. Marcus of the University of California, San Francisco. “We did not rely on participant self-report, but rather utilized a mobile app that ran in the background and could capture exact screen time duration.”
The researchers analyzed data on 653 adults enrolled in the internet-based Health eHeart Study.
Participants’ smartphones were provided with a mobile application that recorded screen time, or the number of minutes in each hour that the phone screen was on. This app collected data continuously over a 30-day window.
Some participants self-reported their bedtime and sleeping period as well as personal demographics and medical information.
Total screen time averaged 38.4 hours per 30 days, and average screen time per hour was 3.7 minutes, equivalent to one hour and 29 minutes per day, according to the report in the journal PLoS ONE.
“At first glance, that we on average spend about an hour and a half of our time interacting with our phone every day may not seem surprising,” Marcus told Reuters Health by email. “But in thinking about the fact that this is an hour and a half of uninterrupted time, that is a pretty significant part of our day.”
Younger people tended to have longer screen time. Screen time varied by age and race but was similar for people with the same socioeconomic background.
As in previous studies of self-reported screen time, as screen time increased, sleep quality decreased, including taking more time to fall asleep and getting less time asleep overall.
“This is a lot better than the usual surveys where people estimate how much they use their phone,” said Michael Gradisar of Flinders University School of Psychology in Adelaide, Australia. “I was surprised that people are using their phones for one to two hours per day. I thought it would be more than that.”
Television, which also involves a screen but is not interactive, may not be linked to sleep in the same way, Gradisar told Reuters Health by email.
“More screen time right around participant-reported bedtime was particularly associated with longer sleep latency (or a longer time to fall asleep) and reduced sleep quality,” Marcus said.
The light produced by smart phones might suppress production of melatonin, which is related to sleep, Marcus said.
“However, it is also possible that engrossing activities that result in stimulation, such as following the latest post on Facebook or a bothersome tweet, might be counter to productive sleep preparation,” he said.
But this study does not prove causality, as people with difficulty sleeping may spend more time on their phone as a result of their inability to sleep, he said.
“We know that poor sleep leads to many health problems, and we are only now beginning to fully recognize the negative impact on the cardiovascular system,” Marcus said.
“Avoiding smart phone screens is almost certainly low risk,” he said. “Therefore, if an individual is having difficulty falling asleep or maintaining an adequate quality of sleep, I think our observations support a good trial of screen time avoidance to determine if it helps that person obtain a good night’s sleep.”
SOURCE: bit.ly/2fD8M54 PLoS ONE, online November 9, 2016. |||||
What is a summary? | – The more time we spend on our smartphones, the more our quality of sleep suffers. So conclude researchers in a new study in the journal PLoS ONE. "This is the first study to directly measure actual screen time in natural environments and compare it to sleep quality," the senior author tells Reuters. "We did not rely on participant self-report, but rather utilized a mobile app that ran in the background and could capture exact screen time duration." And what they found backs previous research suggesting that screen time close to bedtime is "particularly problematic" as it was "associated with longer sleep latency (or a longer time to fall asleep) and reduced sleep quality," the researcher says. The researchers tracked 653 adults over 30 days and found that subjects used their phones for an average of 89 minutes a day. They saw no link between screen time and amount of physical exercise or body mass index or even mood, but they did when it came to quality of sleep, reports Live Science—and use right around bedtime seemed to have the greatest impact. The researchers are careful to note that their study doesn't prove causation or even explain why smartphone use might impact sleep; they hypothesize that the screens' blue light could be suppressing the sleep hormone melatonin, or that using the phone simply keeps the brain more active. Previous research has also linked smartphone use with poor sleep. (Orange-tinted eyewear can help block the blue light.) | multi_news_1_0_0 |
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Summarize this article:
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. |||||
Summary: | – 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:
Welcome!
As a member of the Utah Food Allergy Network (UFAN) and mom of an allergic kid, I've learned food allergies are easier to handle with information, a few handy tools, and a community of friends who “get it.” I post a new article most Mondays. Thanks for stopping by!
Kelley
||||| FILE - This image released by Columbia Pictures shows Peter Rabbit, voiced by James Corden and Cottontail in a scene from "Peter Rabbit." The filmmakers and the studio behind it are apologizing for insensitively... (Associated Press)
FILE - This image released by Columbia Pictures shows Peter Rabbit, voiced by James Corden and Cottontail in a scene from "Peter Rabbit." The filmmakers and the studio behind it are apologizing for insensitively depicting a character's allergy in the film that has prompted backlash online. Sony Pictures... (Associated Press)
FILE - This image released by Columbia Pictures shows Peter Rabbit, voiced by James Corden and Cottontail in a scene from "Peter Rabbit." The filmmakers and the studio behind it are apologizing for insensitively depicting a character's allergy in the film that has prompted backlash online. Sony Pictures... (Associated Press) FILE - This image released by Columbia Pictures shows Peter Rabbit, voiced by James Corden and Cottontail in a scene from "Peter Rabbit." The filmmakers and the studio behind it are apologizing for insensitively... (Associated Press)
LOS ANGELES (AP) — "Peter Rabbit" filmmakers and the studio behind it are apologizing for insensitively depicting a character's allergy in the film that has prompted backlash online.
Sony Pictures says Sunday in a joint statement with the filmmakers that "food allergies and are a serious issue" and the film "should not have made light" of a character being allergic to blackberries "even in a cartoonish, slapstick way."
In "Peter Rabbit" which was released this weekend, the character of Mr. McGregor is allergic to blackberries. The rabbits fling the fruit at him in a scene and he is forced to use an EpiPen.
The charity group Kids with Food Allergies posted a warning about the scene on its Facebook page Friday prompting some on Twitter to start using the hashtag #boycottpeterrabbit. The group said that allergy jokes are harmful to their community and that making light of the condition "encourages the public not to take the risk of allergic reactions seriously."
Kenneth Mendez, the president and CEO of the Asthma and Allergy Foundation of America, wrote an open letter to the studio Saturday asking for the opportunity to educate the company and the film's cast on the realities of food allergies and urged the studio to "examine your portrayal of bullying in your films geared toward a young audience."
The studio and filmmakers say that they, "Sincerely regret not being more aware and sensitive to this issue, and we truly apologize." ||||| There has been a lot of talk in the food allergy community about the new The Smurfs 2 movie because of a certain scene involving peanut allergy. Allergic Living asked me to see the movie and review it, from the allergy perspective. Along for her point of view was my 12-year-old daughter, who has severe allergies to dairy, egg, peanut, all tree nuts and most legumes.
So off we went. While I was prepared to be outraged, I also wondered whether the movie would prove a sign that the entertainment industry was starting to pay lip service to food allergies. With statistics like 1 in 13 children having food allergies, would this turn out to be an example of tokenism?
Let’s cut to the big scene in question: the birthday party. In the scene, the Smurf’s human friends, Patrick and Grace Winslow, are hosting the party for their son and are reviewing their checklist of cautions. The food is gluten-free, vegan, no peanuts or strawberries, produced humanely and served on BPA-free dishes. So far, so good.
When the man’s stepfather, the owner of a corndog company, arrives with corndogs for partygoers, parents ask about peanuts. He assures everyone that his company does not put peanuts in the corndogs. The peanut-allergic child takes a bite before the man can finish his sentence – that they are, though, cooked in peanut oil. With lips swollen, the child is rushed off to the hospital. Later the audience learns that he’s OK. This is portrayed as a relief to the host because both of the child’s parents are lawyers, and that was mildly annoying.
I asked my daughter what she thought as someone with allergies. She felt that the birthday party scene was important as it helped to define the stepfather’s character – he’s an insensitive man who pushes his way into situations and manages to cause problems. Her one major issue was that no one administered epinephrine the allergic child. That would have been easy to include.
If this scene was the only reference to allergies, I might have felt that the writers had gone for a cheap laugh. But the concept of allergies runs through this film in a respectful way. In fact allergies play a pivotal role in a touching turning point that ties up several subplots.
So no, we didn’t have a big issue with the depiction of food allergies in The Smurfs 2. My daughter did not notice the fact that the stepfather didn’t take the reaction very seriously, and I simply found it realistic. Not all of our relatives ‘get it’ either and this reflected poorly on the older man. I’m pleased to report that I doubt many parents or kids living with food allergies would be offended by this movie.
As for the film as a whole, we thoroughly enjoyed it. There is plenty going on in the subplots to keep the adults’ attention. For the children, they will no doubt enjoy the juvenile humor with plenty of references to farts and name-calling. There isn’t any real violence but poor Gargamel is the butt of a lot of slapstick comedy. Hank Azaria and Neil Patrick Harris return to their roles and don’t disappoint. So yes, it was worth the price of admission.
Susan Clemens is the moderator of Allergic Living’s online Forum and Facebook page. Please let us know your own thoughts of how allergies were depicted in the movie – in the comments below or on our social media.
||||| Image copyright Columbia/Sony Pictures/Kobal/REX/Shutterstock Image caption The scene in the new Peter Rabbit film involving blackberries led to calls for a boycott
The makers of the new film Peter Rabbit have apologised after facing a backlash over their depiction of a character's allergy.
A scene in the film shows a character who suffers a blackberry allergy being pelted with them by a gang of bunnies.
In a joint statement, Sony Pictures and the filmmakers said they "should not have made light" of the issue.
Campaigners condemned the scene and some Twitter users adopted the hashtag #boycottpeterrabbit.
The charity Kids with Food Allergies Foundation said in a Facebook post "food allergy 'jokes' are harmful to our community".
A petition calling on Sony Pictures to apologise also attracted thousands of signatures.
Image copyright Columbia/Sony Pictures/REX/Shutterstock Image caption Characters Cottontail, Flopsy and Mopsy use catapults to fire fruit and vegetables in one scene
The offending scene is shown in a film adaptation of the Beatrix Potter book Peter Rabbit, which was released in US cinemas this weekend.
The human character Tom McGregor, who has an allergy to the berries, is attacked by Peter and his friends who shower him with the fruit, even shooting one into his mouth, until he is forced to use an EpiPen to treat his reaction.
On Sunday, Sony Pictures said in a statement that it was wrong for the filmmakers to include the segment, "even in a cartoonish, slapstick way".
"We sincerely regret not being more aware and sensitive to this issue, and we truly apologise," the statement said.
Food allergies ||||| You probably remember Peter Rabbit as the lovable, impish star of wholesome childhood stories, but is he now a bully?
That’s what some parents are arguing after seeing the new Peter Rabbit film starring James Corden and directed by Will Gluck. The film, released on Friday in the U.S., grossed an estimated $25 million in its first weekend, out-earning every other film except the decidedly more grown-up Fifty Shades Darker, the final installment of the Fifty Shades of Grey trilogy.
The latest update to the classic children’s story features Peter Rabbit engaged in battle with the nephew of his traditional nemesis, the farmer Mr. McGregor. This nephew, as it turns out, has a blackberry allergy, a weakness Peter and his accomplices exploit in one battle scene. The rabbits pelt the younger Mr. McGregor with the berries and one goes into his mouth, causing him to go into anaphylactic shock and administer an EpiPen to himself.
Parents and advocacy groups have taken exception to this portrayal, calling it “allergy bullying” and saying it mocks allergy sufferers. The CEO of Allergy UK told The Telegraph the scene is irresponsible as it doesn’t portray the life-threatening danger of allergies and anaphylactic shock. On Saturday, the U.S.-based Food Allergy Research & Education organization warned on its Facebook page that the scene “might be upsetting” for viewers who have allergies.
Calls to boycott the film soon took off on Twitter, with people using #BoycottPeterRabbit to air their disappointment.
#PeterRabbitMovie @SonyPictures Would you laugh at a person with diabetes force fed sugar? No. But that's exactly what you're doing in your movie: continuing to marginalize people with #foodallergies. So throw an allergen at someone? I’m coming for you.#BoycottPeterRabbit — ☘️ Jamie ☘️ (@jamiefid) February 10, 2018
As a mother of a toddler allergic to several foods, I am disgusted that Sony would make a joke out of flicking an allergen at a food allergic individual. Doing so is felony aggravated assault! What kind of message does that scene send to kids?! #boycottpeterrabbit — hydrogirl71 (@hydrogirl71) February 10, 2018
But others soon began using the hashtag to criticise those encouraging a boycott for being too sensitive.
Just read this drivel today, #boycottpeterrabbit people getting offended over kids films. I remember violent cartoons as a child and I don’t recall brutally killing anyone growing up. Have some faith in your kids, breathe, and remember its just a stupid film about talking rabbits — Nick Fitzpatrick (@nicknogger) February 11, 2018
Sony Pictures and the filmmakers have issued an apology for the scene, saying they “should not have made light” of the issue. |||||
What is a summary? | – If you're wondering why there's a hashtag to boycott a new children's movie, ask parents of kids with allergies. The BBC reports on the pushback against Sony Pictures' Peter Rabbit, which includes a scene in which Mr. McGregor, who's allergic to blackberries, gets the fruit hurled at him by the title character and his bunny pals. One berry ends up in McGregor's mouth, causing him to go into anaphylactic shock and forcing the use of his EpiPen. "I'm pretty sure Beatrix Potter will be turning in her grave about now," one mom of a child with allergies tells the New York Times. She notes allergies are already often dismissed or ignored by people who aren't affected by them, and that "to have them trivialized on the big screen by such a popular character is immensely disappointing." Other parents and advocacy groups agree the film, with James Corden voicing Peter, is partaking in "allergy bullying," per Fortune. Kenneth Mendez, president of the Asthma and Allergy Foundation of America, penned an open letter to the filmmakers and Sony, noting that "we strongly urge you to refrain from the type of programming that mocks food allergies in the future." Mendez also points out that Sony has portrayed food allergies as a "punchline" before in children's films, citing one of the Smurfs movies and Cloudy With a Chance of Meatballs as two examples. Per the AP, Sony has issued a joint statement with the filmmakers apologizing for the scene, admitting the flick shouldn't have "made light" of the character's allergy, "even in a cartoonish, slapstick way." (New guidelines are out on giving babies peanuts.) | 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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Article:
A Hattiesburg mother turned her own grief into a life-saving miracle for the worship pastor at her church.
"Only the best screen writers could have attempted to write this script," Pastor Michael Minor said.
Minor was diagnosed with diabetes as a young adult in 1996. As the disease progressed, Minor's kidneys began to shut down, and eventually completely stopped functioning properly.
Minor was in end-stage renal failure.
He began home dialysis about two years ago, but the best long-term solution was a kidney transplant.
Minor was on donation lists for three area hospitals, and while organ donation lists usually come with significant wait time, Minor's blood type made his wait even longer.
"I'm O positive," Minor said. "That's a rarer type than the As, Bs and ABs and all of that."
Minor said he was told he could wait as long as nine years at one hospital before he had the possibility of a transplant.
But, this would soon change thanks to church member Adrian Murry.
Murry lost her son, Kendrick, after a tragic accident at work on Sept. 5, 2015.
"My son was at work, fell and hit his head," Murry said. "(He) had massive brain swelling, and had to have emergency surgery. He was eventually placed on life support in ICU, and just never responded."
Murry described her son as a typical big brother always looking to help others.
It was not until after her son's death that Murry found out he was an organ donor.
"We went through the information, and found out that I can pick a person in particular if I wanted to donate a certain organ to," Murry said. "I knew from coming to a service that our minister of music needed a kidney, so I said, 'hey, if he can use it.' I told her just like that. 'If he can use it, you know, we can try.'"
The hospital began the six-hour match testing and told Murry she would get a call if Minor was a match for her son's kidney.
"It was amazing because I wasn't expecting a phone call," Murry said. "It's like a made-for-TV movie. You never expect to be on the end of a happy ending. In spite of my son's loss, it's also a gain."
The hospital said Murry needed to move quickly to get in touch with Minor to move forward with the transplant.
Meanwhile, Minor was in Starkville for the LSU vs. Mississippi State Saturday night football game.
"I started getting calls about the possibility of having a kidney donor," Minor said. " I was like 'cool, you know sounds great. I would love a kidney.' I didn't really take it as serious as normal because I thought there was more to the process."
Minor says he got a call around 2:30 the next morning from his transplant coordinator at University of Mississippi Medical Center in Jackson.
"He said 'do you still want this kidney? We have one available for you.' And I'm like 'yeah,'" Minor said. "They asked me could I be in Jackson by 8 a.m."
So Minor made the trip from Starkville home to Hattiesburg and then from Hattiesburg to Jackson to get his new kidney.
"(I) got to UMC, had the transplant, I think, early Monday morning," Minor said. "That's how fast it went. I couldn't have scripted it like this."
Minor was back at West Point church for the first time Wednesday night.
Murry said she is thrilled Minor is doing so well post-transplant, but said it is hard to see him and think of her son.
"It's bittersweet, but day by day, it's just something that I'll grow to learn to live with," Murry said.
Minor said he was both thankful and surprised the Murry family thought of him during their loss.
"That's what kind of blew me away," Minor said. " I was like 'wow,' you know, 'they're thinking about me and my needs during their time of bereavement.'"
Murry said all of Kendrick's major organs were donated successfully to six people across the country.
Minor said he is looking forward to attending church services and and getting back to his music ministry.
Copyright 2015 WDAM. All rights reserved. ||||| Months after she lost her son and found out he was an organ donor, a Hattiesburg mom wanted to know who received his heart as her Mother's Day gift.
But she soon found she did not need to look further than her own family.
Adrian Murry lost her son, Kendrick, on a Saturday in September 2015 after he had an accident at work.
After his death, she found out he was an organ donor. She was able to donate his kidney to the worship pastor, Michael Minor, at her church, but wanted know who had her son's heart.
"I said ‘I want to know where his heart is,’" Murry said. "I designated the kidney. That was fine. But I wanted to know where his heart is, and I would be OK.”
Clintoria Johnson, Murry's cousin, said her heart was only functioning at 10 percent and had been waiting on a transplant for almost two years.
"It had gotten where, the last time I went to the doctor, they said ‘we’re going to have to put you in a hospital and give you a vac,’" Johnson said. "That’s how bad my heart had gotten that Friday. I prayed that Friday when I came (back home) from Jackson. I mean, Sunday morning before that day, I had gotten that call. They called me and asked how quick I could get to Jackson. I said as quick as I can. You tell me the time, I’ll be there.'”
But neither Johnson nor Murry immediately knew Johnson's transplant came from Kendrick. Murry said she would see Johnson wearing oxygen tubes at monthly family birthday gatherings, but did not know what was wrong or that she needed a transplant.
“It was a surprise," Murry said. "I didn’t know she was on the list. I didn’t know what she needed. I really didn’t know what was wrong. We have Sunday birthdays once a month over here, and she would come. I would see her with the tubes on her nose. There was this one particular time in August she asked me about my son. She said, ‘where’s your son?’ I said, ‘he’s at work. You know how kids are.’ She said, ‘well when you see him, tell him I said hello.’ And I said 'OK.' It’s odd, but that’s exactly what happened. Then that next month, he had the accident, and he passed.”
Johnson said, "Didn’t know at all. They kept saying a 25-year-old young heart, you know. I said OK, but we didn’t know what was going on. But everything just got to working together. It happened too quick. I said, ‘it’s got to be something. Got to be something. I just started putting my pieces together after they had said he got critical and he wasn’t going to make it, but it still didn’t dawn on me at that time that he was a donor.”
Murry knew who received her son's kidney because she specially designated Michael Minor, the pastor at her church, to be the recipient, but the process is more complicated when the donation is anonymous.
According to the Mississippi Organ Recovery Agency (MORA), donor and recipient families "may receive such information as age, gender, occupation and state of residence," and "the donation agencies facilitate anonymous correspondence and meetings initiated by either the donor family or recipient and only if agreed to by both parties. It is only after extended anonymous communication, and the agreement of both parties, that the names are released."
“Maybe a few days later (after his death), they were like ‘you know Clintoria went to the hospital, and I’m kind of thinking that’s Kendrick.,’" Murry said about her family. "I said ‘You think so?’ So I was trying to find out, but I was told I had to write a letter and sign a release. It took me awhile to get to that point, but I said for Mother’s Day, that’s what I wanted to know. It’s just too coincidental that my son passed that Saturday, and then here she is on her way. I said ‘we’re going to see.’ It took me awhile to get to that point, to start writing, but I said ‘yeah. We’re going to have to find out.’”
Murry and Johnson received the letter with the donor's identity heart the Monday before Mother's Day.
“I was so nervous," Johnson said. "I wanted to know so bad, I didn’t want to be by myself to open the letter.”
Murry said that Monday was also the day before her son's birthday. She said she could not contain her emotions when she found out Johnson received his heart.
“I just lost it," she said. "I was hollering and screaming. My dad came and (asked), ‘what’s wrong? What’s wrong?’ I was like I’m OK. It just came at a perfect time. It was like that was his birthday gift, but to me. It was a pretty good Mother’s Day.”
Murry and Johnson said they have a newfound closeness, and support each other through difficult days.
“We are family in more ways than one," Murry said. "I think about her a lot. I call her and check on her. She’ll call and check on me. I call her my son sometimes, my daughter."
Johnson said, “It means a lot to me. I just feel great. I’m just happy it’s in the family. It’s somebody I know. If I get depressed or whatever, I don’t have far to go. I know where she stays. I can be there in five minutes.”
Murry said, “I wanted to know it was in the family, and he is still in the family. That meant a lot to me. We were on a mission to find out, and we did. We did.”
Now, Murry said she wants to find out who received his other kidney, lungs and liver.
“We’ve got to get to Florida because his other recipients are in Florida," she said. “I know there were some children involved, so that makes me even more excited to find out. Children, you know, they are the future, so to know that some children live because of him is just…,” she said trailing off.
Murry said Johnson is coming with her.
“I told her she has to go," Murry said. "She has to go. We’ve got to figure something out, but we’re going to do it.”
Murry said she is taking classes with MORA to be able to teach others about organ donation and sign people up to become donors. She said despite her loss, she is thankful she has now bonds with so many because of it.
“Not just people directly related to his organs, but people in general," Murry said. "People that I meet and talk to about being an organ donor now because of his story. That means a lot to me. That means that he set out to do what he said which is bring people to Christ and save lives, and that’s exactly what he did and what he’s doing.”
Copyright WDAM 2016. All rights reserved. |||||Summary:
| – "I just lost it," Adrian Murry says—not of the day she lost her son in a workplace accident, but of the day she found out his heart went to a family member. When 25-year-old Kendrick Murry died from a head injury in September 2015, his mother learned he was an organ donor and ensured a kidney was given to the pastor at her Mississippi church, who was battling end-stage renal failure, reports WDAM. But unbeknownst to Murry, her own cousin had been waiting for a heart transplant for nearly two years. Murry tells WDAM she would see Clintoria Johnson at family events with tubes on her nose, but "I didn’t know what she needed. I really didn't know what was wrong." Shortly after Kendrick's death, however, Johnson received a 25-year-old heart and relatives started to suspect that it was Kendrick's. "They were like, 'You know Clintoria went to the hospital, and I'm kind of thinking that's Kendrick,'" Murry says. To find out, "I was told I had to write a letter and sign a release. It took me awhile to get to that point, but I said for Mother's Day, that's what I wanted to know," she says. Johnson agreed to find out the name of her donor and the news arrived just a day before Kendrick's birthday. It confirmed what the family had suspected: his heart had gone to Johnson. "I was hollering and screaming … It just came at a perfect time," says Murry. "It was like that was his birthday gift, but to me. It was a pretty good Mother's Day." Murry and Johnson have since grown much closer. "I call her my son sometimes, my daughter," says Murry. "It means a lot to me," adds Johnson. "I'm just happy [the heart is] in the family." | multi_news_1_0_0 |
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– As companies flee from Paula Deen amid controversy over a racial slur, the chef has broken with her agent. Barry Weiner was a key figure in Deen's professional life: The Wall Street Journal calls him her "chief adviser" and a business strategist who helped direct her company, Paula Deen Enterprises. The two had worked together for more than 10 years, the AP reports. Weiner and his firm also represent her sons and producer; it's not known whether those relationships will continue. The move may offer a chance for a new start, the Journal notes, but can Deen pull it off? A PR expert, citing the example of Michael Vick, thinks it's possible: "The American public is very forgiving. If she could really learn empathy, I think she could salvage her career."
Let's expand this into a news article: Paula Deen announced Thursday that she has cut business ties with the agent who helped make her a Food Network star and launch a media and merchandising empire that has largely crumbled in the wake of her admission that she used racial slurs in the past.
FILE - In this Dec. 30, 2010 file photo, Paula Deen speaks in Pasadena, Calif. Sears Holdings Corp. announced Friday, June 28, 2013, that it is cutting ties with Southern celebrity chef Deen, adding to... (Associated Press)
FILE - In this Jan. 17, 2012 file photo, celebrity chef Paula Deen poses for a portrait in New York. Deen announced Thursday, July 4, 2013 that she has cut business ties with the agent who helped make... (Associated Press)
Deen had worked with New York agent Barry Weiner for more than a decade. She has said he was instrumental in getting her show "Paula's Home Cooking" on the Food Network in 2002. She gave no reason for her parting with Weiner in a prepared statement.
"Paula Deen has separated from her agent," Deen's spokeswoman, Elana Weiss, said in an email Thursday. "She and her family thank him for the tireless effort and dedication over the many years."
Deen's breakup with one of her key partners comes after a turbulent two weeks that have left the celebrity chef's network of business deals in shambles. It all started within days of the public disclosure of a legal deposition in which Deen admitted under oath to having used the N-word.
The Food Network passed on renewing Deen's contract and yanked her shows off the air. Smithfield Foods, the pork producer that paid Deen as a celebrity endorser, dropped her soon after. Retailers including Wal-Mart and Target said they'll no longer sell Deen's products and publisher Ballantine scuttled plans for her upcoming cookbook even though it was the No. 1 seller on Amazon. Even the diabetes drug company that made the much-criticized deal to hire Deen as a paid spokeswoman dumped her.
Weiner worked to turn Deen into a comfort-food queen since she was little more than a Savannah restaurant owner and self-publisher of cookbooks who earned raves for her fried chicken.
In her book "Paula Deen: It Ain't All About the Cookin,'" Deen recalled meeting Weiner through TV producer Gordon Elliott, who was convinced they could turn her into a star.
"Barry and Gordon felt like there was a show somewhere inside this Paula character that could be very successful," Deen wrote. "They probably courted Food Network for two years trying to push me at them."
Deen also noted in her book: "Barry is affectionately known in my family as Barry Cuda. Perfect name for an agent."
Deen's business deals began falling apart after she was questioned under oath in May as part of a civil lawsuit filed last year by Lisa Jackson, a former manager of Uncle Bubba's Seafood and Oyster House, which Deen co-owns with her brother, Bubba Hiers. Jackson says she was sexually harassed and worked in an environment rife with racial slurs and innuendo.
Ultimately it was Deen's own words that proved damaging. Asked in her deposition if she had ever used the N-word, she replied: "Yes, of course." That she also insisted "it's been a very long time" seemed to matter little to the companies paying to use her name and image with their products. Neither were they swayed by Deen's apologies in online videos and in person with the "Today" show's Matt Lauer.
Forbes magazine last year ranked Deen as the fourth-highest-earning celebrity chef last year, figuring she had hauled in $17 million. Her company Paula Deen Enterprises generates total annual revenue of nearly $100 million, according to Burt Flickinger III, president of retail consultancy Strategic Resource Group.
Deen cast no blame in her statement announcing her split with Weiner. It ended by saying, "Paula wishes him well in all future endeavors." ||||| Dow Jones Reprints: This copy is for your personal, non-commercial use only. To order presentation-ready copies for distribution to your colleagues, clients or customers, use the Order Reprints tool at the bottom of any article or visit www.djreprints.com |||||
– A new federal report points to the environmental benefits of a vegan diet, and the meat industry is not exactly happy about it. Industry representatives say sustainability isn't within the purview of the Dietary Guidelines Advisory Committee, whose recommendations factor into guidelines by the federal agriculture and health departments, the Hill reports. "The same concern would exist if an expert sustainability committee were making nutrition policy recommendations," says a rep for the North American Meat Institute. "It is not appropriate for the person designing a better light bulb to be telling Americans how to make a better sandwich." Indeed, Secretary of Agriculture Tom Vilsack seemed to agree in an interview last month with the Wall Street Journal, the Hill notes. "I read the actual law," he noted. "Our job ultimately is to formulate dietary and nutrition guidelines." But earlier this year, the committee noted a need to address the "complete challenge" in order "to ensure a healthy food supply will be available for future generations," the Journal reported. The chair of the committee also points out that the committee outlines three separate diets, with one vegetarian-focused, one Mediterranean, and one American. "If people took the time to understand, this is not a meat-free diet and this is not [a] vegan approach," she tells the Hill. "They'd realize this is a healthy dietary pattern with three models that offers consumers a lot of choice." The group is accepting public comment until next month.
| Let's expand this into a news article: A federal panel that helps set federal dietary guidelines is recommending Americans eat less meat because it’s better for the environment, sparking outrage from industry groups representing the nation’s purveyors of beef, pork and poultry.
The Dietary Guidelines Advisory Committee, a federally appointed panel of nutritionists created in 1983, decided for the first time this year to factor in environmental sustainability in its recommendations. They include a finding that a diet lower in animal-based foods is not only healthier, but has less of an environmental impact.
The meat industry is lashing back, contending the panel has neither the authority nor the expertise to make such a judgment.
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“When you talk about the lens of the dietary guidelines it’s just not appropriate for the advisory committee to enter that conversation when they were asked to look at nutrition and health science,” said Kristina Butts, executive director of legislative affairs for the National Cattlemen’s Beef Association.The North American Meat Institute (NAMI) agrees, saying sustainability is a complex issue best left to a body that specializes in the environment.“The same concern would exist if an expert sustainability committee were making nutrition policy recommendations,” Betsy Booren, NAMI’s vice president of scientific Affairs, said in a public meeting last week. “It is not appropriate for the person designing a better light bulb to be telling Americans how to make a better sandwich.”The Agriculture Department and Department of Health and Human Services will use the committee’s report and recommendations to draft the final guidelines for 2015, due out later this year.But even Agriculture Secretaryhas said sustainability is an issue that falls outside the scope of the guidelines.“I read the actual law,” he was quoted saying in an interview with The Wall Street Journal. “And what I read … was that our job ultimately is to formulate dietary and nutrition guidelines. And I emphasize dietary and nutrition because that’s what the law says. I think it’s my responsibility to follow the law.”But members of the committee say they had free reign to discuss food supply in recommending what people should and shouldn’t be eating.“The scope is ours to fully define,” said Barbara Millen, chairwoman of the advisory committee and a professor in the Department of Family Medicine at Boston University School of Medicine.“Because we are encouraging Americans to eat more seafood, we felt we needed to look at the sustainability of that issue as well.”In response to the claims about a lack of expertise, Millen said the panel did bring in two domestic sustainability experts to work with the committee members.The 571-page report says the average U.S. diet has a larger environmental impact in terms of increased greenhouse gas emissions, land use, water use and energy use than the healthy dietary pattern it suggests — one that’s rich in vegetables, fruit, whole grains, seafood, legumes and nuts; moderate in low- and non-fat dairy products and alcohol; and lower in red and processed meat, sugar-sweetened foods and beverages, and refined grains.In its review of scientific studies, the committee highlighted research concluding that a vegan diet had the most potential health benefits."The organically grown vegan diet also had the lowest estimated impact on resources and ecosystem quality, and the average Italian diet had the greatest projected impact,” according to the report. “Beef was the single food with the greatest projected impact on the environment; other foods estimated to have high impact included cheese, milk, and seafood."The committee’s report says people should eat less red and processed meat because it contains saturated fats, which when over-consumed can lead to cardiovascular disease, and instead recommends Americans eat more vegetables and nuts.But industry groups argue that meat contains protein, which helps people feel fuller for longer periods of time. Eating meat, Butts said can help people stick to their diets better.Though consumers have never been known to strictly follow the final guidelines, NAMI’s spokesman Eric Mittenthal said the recommendations do impact federal programs like school lunches, WIC, the special supplemental nutrition program for women, infants and children, and military rations.But Millen said industry is misunderstanding their report, and overreacting.She said the committee mapped out three diets for Americans to use as guidelines – a vegetarian-style, a Mediterranean-style and a healthy U.S.-style diet.“If people took the time to understand, this is not a meat-free diet and this is not vegan approach, they’d realize this is a healthy dietary pattern with three models that offers consumers a lot of choice,” she said.The committee’s Vice Chairwoman Alice Lichtenstein said there’s also a misunderstanding in the meat industry about what the committee actually does.“We’re tasked with delivering a report to HHS and USDA,” she said. “We don’t know how much will be factored into the final guidelines or not. Our job is to collate and review the evidence out there and deliver it to the secretaries.”On Tuesday, Rep. Vicky Hartzler (R-Mo.) and 70 House Republicans sent a letter to HHS and USDA urging the final dietary guidelines to be based on sound nutritional science and adhere to the charter authorized by Congress.In the letter, the lawmakers said they believe the advisory committee “greatly exceeded their scope in developing the recommendations for the secretaries of USDA and HHS.”“It is the responsibility of the secretaries to ensure that this advisory committee stay focused on nutritional recommendations and not the wider policy realm of sustainability and tax policy, in which members of this committee had neither expertise, evidence, nor charter,” they wrote.HHS and USDA have extended the written comment period from April 8 to May 8 to give the public additional time to comment on the advisory committee’s report.An HHS representative said the departments would review the report, along with input from federal agencies and public comments to develop the final 2015 guidelines.The department would not answer questions about whether the topic of sustainability was within the committee’s purview or whether the agency plans to factor sustainability into the final guidelines. ||||| Healthy eating habits can also protect the environment, according to recommendations from the Dietary Guidelines Advisory Committee. The panel's vice chair Alice Lichtenstein discusses with Sara Murray.
U.S. dietary guidelines, the government’s benchmark for balanced nutrition, have long advised Americans to eat dark, leafy greens. Now, there is another way the standards could be going green.
A panel of nutrition experts recruited by the Obama administration to help craft the next set of guidelines, to be issued this year, said in long-awaited recommendations Thursday that the government should consider the environment when deciding what people should eat.
... ||||| Scientific Report of the 2015 Dietary Guidelines Advisory Committee
In February 2015, the 2015 Dietary Guidelines Advisory Committee (Advisory Committee) submitted the Scientific Report of the 2015 Dietary Guidelines Advisory Committee (Advisory Report) to the Secretaries of the U.S. Departments of Health and Human Services (HHS) and Agriculture (USDA).
The Advisory Report helps to inform the federal government of the body of scientific evidence on topics related to diet, nutrition, and health. The Advisory Report is not the Dietary Guidelines policy or a draft of the policy. Access the complete 2015–2020 Dietary Guidelines for Americans.
Download Advisory Report PDF – 22.8MB
Online-Only Supplementary Material
Appendices E-2 and E-3 contain links to additional report content that is available online only, and cannot be found in the printed or PDF versions of the Advisory Report. This supplementary material can be accessed through the links below:
Suggested Citation
Dietary Guidelines Advisory Committee. 2015. Scientific Report of the 2015 Dietary Guidelines Advisory Committee: Advisory Report to the Secretary of Health and Human Services and the Secretary of Agriculture. U.S. Department of Agriculture, Agricultural Research Service, Washington, DC. ||||| | multi_news_1_0_0 |
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- Top ranked pages (up to a max of 100) from every linked-to domain using the Wide00012 inter-domain navigational link graph ||||| Pat Conroy, the best-selling novelist and proud adoptive son of the Lowcountry who wrote lyrically about Charleston and unflinchingly about The Citadel, died Friday. He was 70.
The author of “The Great Santini,” “The Lords of Discipline” and “The Prince of Tides” and eight other books passed away shortly after being diagnosed with pancreatic cancer. He died at 7:43 p.m., surrounded by loved ones and family.
It was an ironic turn worthy of a novelist, as Conroy — who had had health problems in the past — in recent years had taken serious steps to improve his health.
But pancreatic cancer often goes undetected until it is too late. Conroy announced his illness last month, and vowed to fight.
“I feel that Pat in many ways had more than 100 years of life. He made his days count and accomplished so much in such a short amount of time,” said Joe Riley, Conroy’s friend and the former mayor of Charleston. “Pat Conroy was a treasure as a friend – a gracious, joyful, generous spirit. His heart just entertained you and lifted you up. Even if you were involved in a serious conversation, he found a way to make you laugh. He was a very good man, a good person, and he cared about right and wrong.”
Conroy was perhaps South Carolina’s most famous man of letters in this or any period of its history. His gushing, over-the-top prose introduced people “from off” to the wonders of pluff mud, the great saltmarsh and the Carolina sea islands.
He told stories of sprawling, dysfunctional families — flawed, wounded people — but managed to find the humor and joy in everything that was the South.
“He was a wonderful human being who, notwithstanding the many mountains he climbed, which he shared with us in his stories, probably had the best two years of his life recently,” said his friend, Beaufort Mayor Bill Keyserling. “He had cleaned up his act, been working out at the fitness center, been involved with USC’s Story River Press, and he was out and about speaking. He was just sideswiped by cancer and it took him fast. We’ll always miss him, but he’s lifted all of us up.”
Military roots
The son of a Chicago-born career Marine pilot and a Southern belle, Donald Patrick Conroy was born in Atlanta in 1945. The military family moved often during his childhood, sometimes twice a year. But when his father — the model for Santini — was eventually stationed in Beaufort during Conroy’s high school years, the future writer swore he had found his true home.
All of Conroy’s books were set in the South Carolina Lowcountry. In the opening line of “The Prince of Tides,” he wrote, “My wound is geography. It is also my anchorage, my port of call.”
Although he lived briefly in Rome and San Francisco, for most of his life he resided in Beaufort and on Fripp Island.
“When I finally got to South Carolina I said, ‘Mom,’ it was my twenty-third move, and I was 15 when I came here, and I said, ‘Mom, I ain’t movin’ again,” Conroy told historian Walter Edgar in 2014. “So poor Beaufort, through no fault of their own, I latched like a barnacle on that town.”
Conroy and his six siblings had a tumultuous childhood, suffering at the hands of an abusive and often violent father. For years, the family kept quiet about their turmoil.
Conroy’s high school English teacher, Gene Norris, became a good friend and introduced the young military brat to a larger world of literature — as well as the famous South Carolina writer Archibald Rutledge and a young civil rights leader named Martin Luther King Jr.
It instilled in him a lifelong love of teachers, and briefly led him into the profession. But he became a writer, Conroy said, because of his mother reading to him as a child.
“Reading has changed my life utterly,” he said in 2014. “Because I read, I wanted to write. Because I lived and read, I wanted to write stories, ‘cause I lived in South Carolina, ‘cause I went to The Citadel — and my Lord, The Citadel — I had stories flying out of me from everywhere. And because of this I wanted to write it down and have young kids read me the way I once read Thomas Wolfe.”
The Citadel mourned his passing Friday night.
“This is a very sad day for The Citadel family. Pat Conroy was a world-renowned author, active in his community and a passionate alumnus of The Citadel. He will be missed,” Lt. Gen. John Rosa, Citadel President said.
He wore The Ring
Although Conroy had no particular calling to the military, he enrolled as an English major at The Citadel because he thought it would make his father proud. There, he was most notable as a star of the Bulldogs basketball team, which he wrote about nearly 40 years later in a memoir, “My Losing Season.”
He grew to have a love-hate relationship with the military college, but gained an unabiding love of Charleston, a city he returned to time and again in his books.
“There is no city on Earth quite like Charleston,” Conroy wrote in his foreword to “The Mayor,” the biography of Joe Riley. “From the time I first came there in 1961, it’s held me in its enchanter’s power, the wordless articulation of its singularity, its withheld and magical beauty. Wandering through its streets can be dreamlike and otherworldly, its alleyways and shortcuts both fragrant and mysterious, yet as haunted as time turned in on itself.”
Shortly after graduation from The Citadel in 1967, he wrote his first book, a short ode to commandant of cadets Lt. Col. Thomas Nugent Courvoisie, whom the Corps affectionately called “The Boo.”
Unable to find a publisher, Conroy and Courvoisie published “The Boo” themselves, but not before having it vetted by a young Charleston attorney and Citadel alumnus named Joe Riley. The two became lifelong friends.
The Citadel banned the book initially. But it would seem mild in comparison to what would come later.
Conrack the teacher
Conroy took work as a teacher in the Beaufort County School District, where he was assigned a one-room schoolhouse on Daufuskie Island. He soon came to realize he was expected to be nothing more than a baby sitter to an island full of underprivileged black children. He made it his mission to give them a good education.
His unorthodox methods and ambitious plans led to his dismissal, but he got his revenge by writing a memoir of his experiences called “The Water is Wide.” When his agent told him the publisher offered $8,000, Conroy said he couldn’t afford it. The young writer did not realize that was what they would pay him as an advance on royalties.
Soon, Conroy turned to fiction, bringing the horrors of his childhood to life in his first novel, “The Great Santini,” which was later filmed as a movie starring Robert Duvall and Blythe Danner. The book was controversial in his family for its harsh look at his early life, although his siblings later said it was a much kinder version of the story than reality.
His second novel, “The Lords of Discipline,” centered on a thinly veiled version of the Citadel and its troubles with integration, involving a fictional secret group on campus devoted to making sure the college did not have black cadets. In the novel, Conroy found his novelist’s voice in the opening line, “I wear the ring.”
“His writing about Charleston and The Citadel was so powerful,” Riley said. “His pen was so passionate and descriptive.”
“The Lords of Discipline” illustrated his pride in the school but also offered a brutally honest appraisal of its shortcomings. The book began an open war with The Citadel that would not subside until years later, years after he championed the first female cadet in the early 1990s.
When a movie company wanted to film its version of “The Lords of Discipline” on campus — which, like “The Great Santini,” was partially written at Riley’s house South of Broad — The Citadel refused because of the book’s perceived negative portrayal of the school. Conroy chided the school’s board of trustees in The News and Courier for forgoing the easiest money they would have ever made.
A famously sharp wit
At the time, Conroy was living in Rome and writing “The Prince of Tides,” which would become his most successful and famous novel, spawning the Barbra Streisand and Nick Nolte movie. Conroy co-wrote the screenplay.
Conroy became known as South Carolina’s most famous liberal, championing equal rights, women at The Citadel. He marched alongside Riley in 2000 on a successful campaign to take the Confederate flag off the Statehouse dome.
“South Carolina lost a beloved son tonight,” Gov. Nikki Haley tweeted Friday night. “Pat Conroy will be missed. We can find comfort knowing his words and love for SC will live on.”
In the early 2000s, his cold war with The Citadel thawed and he was back on campus often, attending ball games and commencements. When Courvoisie passed away, he delivered the eulogy in Summerall Chapel.
Conroy’s books were routinely best-sellers after the 1986 publication of “The Prince of Tides.” He became so famous that, ultimately, the estate of Margaret Mitchell approached him about writing a sequel to the most famous Southern novel, “Gone With the Wind” – a book that he admired.
But his sharp wit was on full display when he reacted to the trustees’ stipulation that he could not mention homosexuality, miscegenation or kill Scarlett.
“I told them that if they insisted on that,’’ Conroy famously said, “I’d write the novel with this first sentence: After they made love, Rhett turned to Ashley Wilkes and said, ‘Ashley, have I ever told you that my grandmother was black?’”
Despite his wicked and often off-color sense of humor, Conroy was a gentle soul, generous and encouraging to other writers. He often supplied effusive praise that ended up on the jackets of first-time novelists’ books.
“The water is wide and he has now passed over.” said his wife, the novelist Cassandra King Conroy,
At the end of “The Prince of Tides,” the main character, Tom Wingo, offered what is a fitting epitaph to Conroy’s life:
“He was a coach, a teacher and a well-loved man. And it is enough, Lord. It is enough.” ||||| FILE - In this Oct. 13, 2010 file photo, author Pat Conroy announces the finalists for the National Book Foundations annual awards during a gathering at the Flannery O'Connor House, in Savannah, Ga. Conroy,... (Associated Press)
Pat Conroy, the beloved author of "The Great Santini" and "The Prince of Tides" and other best-sellers who drew upon his bruising childhood and the vistas of South Carolina and became one of the country's most compelling and popular storytellers, died Friday evening. He was 70.
Conroy, who announced last month that he had pancreatic cancer, died at home among family and loved ones in Beaufort, South Carolina, according to his publisher. The heavy-set author had battled other health problems in recent years, including diabetes, high blood pressure and a failing liver.
"The water is wide and he has now passed over," his wife, novelist Cassandra Conroy, said in a statement from publisher Doubleday.
South Carolina Gov. Nikki Haley tweeted: "We can find comfort knowing his words and love for SC will live on."
Funeral arrangements were still being made.
Few contemporary authors seemed more knowable to their readers over than Conroy. An openly personal writer, he candidly and expansively shared details of growing up as a "military brat" and his anguished relationship with his abusive father, Marine aviator and military hero Donald Conroy. He also wrote of his time in military school and his struggles with his health and depression.
"The reason I write is to explain my life to myself," Conroy said in a 1986 interview. "I've also discovered that when I do, I'm explaining other people's lives to them."
His books sold more than 20 million copies worldwide, but for much of his youth he crouched in the shadow of Donald Conroy, who "thundered out of the sky in black-winged fighter planes, every inch of him a god of war," as Pat Conroy would remember. The author was the eldest of seven children in a family constantly moving from base to base, a life readers and moviegoers would learn well from "The Great Santini" as a novel and film, which starred Robert Duvall as the relentless and violent patriarch.
The 1976 novel initially enraged Conroy's family, but the movie three years later made such an impression on his father that he claimed credit for boosting Duvall's career (The actor had already appeared in two "Godfather" films), saying, "The poor guy got a role with some meat on it."
But the book also helped achieve peace between father and son.
"I grew up hating my father," Conroy said after his father died in 1998. "It was the great surprise of my life, after the book came out, what an extraordinary man had raised me." The author would reflect at length on his relationship with his father in the 2013 memoir "The Death of Santini."
"The Prince of Tides," published in 1986, secured Conroy a wide audience, selling more than 5 million copies despite uneven reviews for its story of a former football player from South Carolina with a traumatic past and the New York psychiatrist who attempts to help him.
"Inflation is the order of the day. The characters do too much, feel too much, suffer too much, eat too much, signify too much and, above all, talk too much," said The Los Angeles Times Book Review.
But Conroy focused on the advice he once got from "the finest writer I ever encountered," novelist James Dickey, who taught him at the University of South Carolina.
"He told me to write everything I did with all the passion and all the power you could muster," Conroy recalled. "Don't worry about how long it takes or how long it is when you're done. You know, he was right."
"The Prince of Tides" was made into a hit 1991 film starring Nick Nolte and Barbra Streisand, who also produced and directed it. Conroy worked on the screenplay and shared an Oscar nomination, one of seven Oscar nominations it earned, including best picture.
Conroy's much-anticipated "Beach Music," published in 1995, was a best-seller that took nine years to complete. Conroy had been working on "The Prince of Tides" screenplay, but he also endured a divorce, depression, back surgery and the suicide of his youngest brother.
Conroy had other demons. After attending (at his father's insistence) The Citadel, South Carolina's state military college, he avoided the draft and went into teaching. In 2013, he wrote on his blog www.patconroy.com/wp that he had begun his life as "a draft dodger and anti-war activist" while his classmates "walked off that stage and stepped directly into the Vietnam War."
"When I talk to Ivy Leaguers or war resisters of that era, I always tell them that Vietnam was not theoretical to me, but deeply and agonizingly painful. Eight of my Citadel classmates died in that war," he wrote.
For years, he was alienated from The Citadel, which he renamed the Carolina Military Institute in his 1980 novel "The Lords of Discipline." A harsh tale of the integration of a Southern military school, the book was adapted into a film in 1983, but had to be made elsewhere because The Citadel's governing board refused to allow any crews on campus.
While "The Lords of Discipline" had made him unpopular with Citadel officials, reconciliation came in 2000 when he was awarded an honorary degree. In 2002, he visited during homecoming weekend and fans lined up to get him to autograph copies of his books.
"I never thought this would happen," Conroy said. "This is my first signing at the Citadel. That's amazing." He had recently published "My Losing Season," about his final year of college basketball at The Citadel.
The good feelings deepened when Conroy's cousin Ed Conroy, a 1989 Citadel grad, became the Citadel's basketball coach in 2006 — and within a couple of years brought about a remarkable improvement in the team's fortunes.
Pat Conroy's other books included "South of Broad," set in Charleston's historic district, and "My Reading Life", a collection of essays that chronicled his lifelong passion for literature.
He was born Donald Patrick Conroy on Oct. 26, 1945. The Conroy children attended 11 schools in 12 years before the family eventually settled in Beaufort, about an hour from Charleston. He read obsessively as a child and called fellow Southerner Thomas Wolfe his inspiration to become a writer.
"Thomas Wolfe was the first writer I felt was writing for me," Conroy said. "He was articulating a vision of the world that seemed ready for me."
Following graduation in 1967, he worked as a high school teacher in Beaufort. While there, he borrowed $1,500 to have a vanity press publish "The Boo," an affectionate portrait of Col. Thomas Courvoisie, an assistant commandant at The Citadel.
For a year he taught poor children on isolated Daufuskie Island, not far from the resort of Hilton Head. The experience was the basis for his 1972 book, "The Water Is Wide," which brought him a National Endowment for the Arts award and was made into the movie "Conrack."
Conroy was married three times and had two daughters. Although he lived around the world, he always considered South Carolina his home and lived since the late 1990s on Fripp Island, a gated community near Beaufort.
"Make this university, this state, yourself and your family proud," Conroy told University of South Carolina graduates in a 1997 commencement speech.
"If you have a little luck, any luck at all, if you do it right, there's a great possibility you can teach the whole world how to dance." |||||
Summary: | – Pat Conroy, the beloved author of The Great Santini, The Prince of Tides, and other best-sellers who drew upon his bruising childhood and the vistas of South Carolina and became one of the country's most compelling and popular storytellers, died Friday evening. He was 70. The Post & Courier frames his death as "an ironic turn worthy of a novelist." Though Conroy—who had battled diabetes, high blood pressure, and a failing liver—had lately "taken serious steps to improve his health," he died less than a month after announcing that he had pancreatic cancer. His death came at home, among family and loved ones in Beaufort, South Carolina, reports the AP. "The water is wide and he has now passed over," his wife, novelist Cassandra Conroy, said in a statement. His books sold more than 20 million copies worldwide, but for much of his youth he crouched in the shadow of his abusive father, Marine aviator and military hero Donald Conroy, who "thundered out of the sky in black-winged fighter planes, every inch of him a god of war," as Pat Conroy would remember. The author was the eldest of seven children in a family constantly moving from base to base, a life readers and moviegoers would learn well from The Great Santini as the 1976 novel and subsequent film, which starred Robert Duvall as the relentless and violent patriarch. The Prince of Tides, published in 1986, secured Conroy a wide audience, despite uneven reviews for its story of a former football player from South Carolina with a traumatic past and the New York psychiatrist who attempts to help him. It was made into a hit 1991 film starring Nick Nolte and Barbra Streisand. | multi_news_1_0_0 |
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Is alcohol good or bad for your health? With no shortage of contradictory findings, it's understandable if you're left feeling like you've had a little too much to drink.
Now, new research from Denmark suggests that moderate levels of alcohol drinking — not binge drinking — may be linked to a lower risk of developing diabetes. But it's not just how much people drink, but how often they drink, that plays a role, the researchers said.
It's important to note, however, that most experts recommend that if you don't already drink alcohol, you shouldn't start because of possible health benefits.
In the study, published today (July 27) in the journal Diabetologia, researchers found that drinking alcohol three to four days a week was associated with a lower risk of diabetes compared with drinking less than one day a week. [7 Ways Alcohol Affects Your Health]
The "findings suggest that alcohol drinking frequency is associated with risk of diabetes, and that consumption of alcohol over three to four days per week is associated with the lowest risk of diabetes, even after taking average weekly alcohol consumption into account," the researchers, led by Charlotte Holst, a doctoral student of public health at the University of Southern Denmark, wrote.
In the study, the researchers looked at data on more than 76,000 adults who participated in the Danish Health Examination Survey in 2007 to 2008. The people in the study filled out questionnaires about their drinking habits, including how much and how often they drank alcohol, and what type of alcohol they drank. Using information from the Danish National Diabetes Register, the researchers determined if the people in the study developed diabetes.
The researchers noted that they weren't able to distinguish between type 1 diabetes and type 2 diabetes using the available data. However, it's more common to develop type 2 diabetes as an adult than type 1 diabetes, which usually develops during childhood.
The people in the study were tracked for a median of 4.9 years, the researchers wrote. Over this time period, about 850 men and 890 women developed diabetes.
In men, drinking alcohol three to four days per week was associated with a 27 percent lower risk of diabetes compared with drinking less than one day per week, the researchers found. For women, the same frequency was associated with a 32 percent lower risk.
The researchers also looked at the amount of alcohol consumed. Their findings were similar to those of earlier studies, which have shown that drinking a moderate amount of alcohol is associated with the lowest risk of diabetes. Specifically, the study found that for men, drinking 14 drinks per week was associated with a 41 percent lower risk of diabetes compared with no drinks, and for women, drinking nine drinks per week was associated with a 58 percent lower risk of diabetes.
When the researchers looked at alcohol type, they found that different alcohol types were associated with different levels of risk. For example, drinking seven or more glasses of wine per week was associated with a 25 to 30 percent lower risk of diabetes compared with drinking less than one glass of wine per week.
There were also differences between men and women: For beer, for example, drinking between one and six brews was associated with a 21 percent lower risk of diabetes in men compared with drinking less than one beer a week, and there was no link found between beer consumption and diabetes risk in women. Drinking seven or more drinks made with liquor per week, on the other hand, was associated with an 83 percent increased risk of diabetes in women compared with one liquor-based drink per week. [Here's How Much Alcohol Is OK to Drink in 19 Countries]
The study only looked at the association between drinking alcohol and risk of diabetes — it didn't prove cause and effect. However, the researchers hypothesize that wine's beneficial effects may stem from compounds called polyphenols, which may help the body control blood sugar levels and, in turn, lower a person's risk of diabetes, according to the study.
The researchers noted that they didn't find an association between binge drinking (defined in the study as drinking five or more drinks at a time) and diabetes risk, but this may be because there weren't enough binge drinkers in the study to observe a link. In other words, it's possible that binge drinking is linked to diabetes risk, but more research is needed.
One limitation of the study was that the people self-reported their alcohol consumption, which means that it could be inaccurate, the researchers wrote.
Originally published on Live Science. ||||| Drinking alcohol three to four times per week could significantly reduce a person's chances of developing diabetes, according to a new study.
Wine is tipped to be the most beneficial, followed by beer, but researchers warn that clear spirits, such as gin and vodka, could substantially increase a woman's chances of succumbing to the condition.
Experts argue, however, that the health impacts of alcohol consumption can vary from person to person and the study should not be taken as a "green light" for excessive drinking.
The new research, published in European medical journal Diabetologia, surveyed more than 70,000 Danish participants on their drinking habits over the course of five years.
Of the 859 men and 887 women who developed diabetes over this period – either type 1 or type 2 – those who drank frequently emerged as the least at risk.
The lowest risk of diabetes was observed at 14 drinks per week in men and nine drinks per week in women.
"Our findings suggest that alcohol drinking frequency is associated with the risk of diabetes and that consumption of alcohol over three to four weekdays is associated with the lowest risks of diabetes, even after taking average weekly alcohol consumption into account," Professor Janne Tolstrup from the University of Southern Denmark noted in the report. ||||| TIME Health For more, visit TIME Health
Drinking alcohol—especially wine—every few days may help protect against type 2 diabetes, suggests a new study published in the journal Diabetologia. People in the study who drank three to four days a week were about 30% less likely to develop diabetes than those who drank less than once a week.
This isn’t the first study to find a link between drinking moderately—having up to 7 drinks a week for women and up to 14 drinks a week for men—and a reduced diabetes risk, compared to not drinking at all. (Heavy drinking, however, is known to increase the risk of diabetes.)
For the new study, researchers analyzed data from more than 70,000 healthy Danish adults who were surveyed about their health and drinking habits around 2007. They tracked them for five years to see who developed type 2 diabetes.
People who had the lowest risk for diabetes were those who drank alcohol at moderate—and slightly more than moderate—levels. Men who drank 14 drinks a week had a 43% lower risk of diabetes than men who did not drink at all; women who drank nine drinks a week had a 58% reduced risk.
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The timing of those drinks also mattered. Drinking three to four days a week was linked to the biggest risk reduction. For women, very infrequent drinking (less than one day a week) was also associated with slightly lower diabetes rates, compared to being a lifetime abstainer.
“For the same total weekly amount of alcohol, spreading it out on more days is better than drinking it all together,” said lead author Janne Tolstrup, professor of epidemiology and intervention research at the University of Southern Denmark’s National Institute of Pubic Health, in an email.
Wine seemed to have a special edge. This study, and previous ones, found that moderate-to-high intake of wine was associated with lower diabetes risk—possibly because the polyphenol compounds in red wine may help manage blood sugar, the authors wrote.
MORE: Here’s What Happens When You Drink Red Wine Every Night
Moderate consumption of beer was also linked to lower diabetes risk for men in the study, but not for women. The researchers say that may be because not enough women in their sample reported drinking beer to show a strong association. (Most drank wine.)
As for spirits, the researchers found no association with diabetes risk in men—but women who had at least seven hard-liquor drinks per week had an 83% increased risk of diabetes compared to those who had less than one. These results are also uncertain, says Tolstrup, since fewer people in the study reported drinking spirits regularly.
While the study suggests a link between alcohol and a lower risk of type 2 diabetes, the study cannot determine that alcohol causes these protective effects. Tolstrup also points out that alcohol is related to more than 50 different diseases and conditions—in both positive and negative ways. The study did not, for example, take into account the increased risk of breast cancer that’s been associated with even low levels of alcohol consumption.
“Any recommendations about how to drink and how much to drink should not be inferred from this study,” she says, “or any study investigating associations between alcohol and a single outcome such as diabetes.” Alcohol affects virtually every organ system in the body, Tolstrup says. She recommends that people stick to current guidelines for moderate drinking, and doesn’t advise current abstainers to start drinking for health reasons.
MORE: Alcohol Is Good for Your Heart — Most of the Time
The results, while interesting, call for more research.
Dr. Ronald Tamler, medical director at the Mount Sinai Clinical Diabetes Institute, was not involved in the new study, but says it confirms observations from previous research. He also recommends drinking in moderation, “up to one drink a day for women and two drinks a day for men,” he said in an email.
“My patients are happy when they ‘confess’ that they have a glass of wine with dinner, and I tell them they should feel free to continue their evening routine,” Tamler says. “However, I do not advise patients to start drinking just to reduce risk of developing diabetes.”
Tamler also points out that the study focused on people developing a new diagnosis of diabetes. “Once somebody has diabetes, different forms of alcohol can have very different effects,” he says. “Beer may increase blood sugar levels (carbs!) while hard liquor may lead to dangerously low glucose levels.” ||||| | – Good news, wine and beer lovers: A new study finds that "moderate but regular" alcohol consumption appears to be linked to a lower risk of developing diabetes. Researchers surveyed more than 70,000 Danish participants over a five-year period and found that men who reported drinking 14 drinks a week and women who reported drinking nine per week were at the lowest risk (41% lower for men than those who did not drink, 58% lower for women), CNBC reports. "Our findings suggest that alcohol drinking frequency is associated with the risk of diabetes and that consumption of alcohol over three to four weekdays is associated with the lowest risks of diabetes," a researcher says. The lead author adds, "For the same total weekly amount of alcohol, spreading it out on more days is better than drinking it all together." Overall, drinking three to four days a week was linked to a 27% lower risk of diabetes (men) or 32% lower risk (women) than drinking less than one day a week, LiveScience reports. A caveat: While wine was found to be the best choice (the researchers hypothesize this could be because the polyphenol compounds in red wine could help with blood sugar management), followed by beer (for men only), clear spirits including gin and vodka were found to be linked with an increased risk of developing diabetes for women. Of course, outside health experts are warning people to be careful and not take this study as an excuse to over-indulge. And Time notes that while other studies have found a link between moderate drinking and a reduced risk, heavy drinking is known to increase diabetes risk. | multi_news_1_0_0 |
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– Today marks World AIDS Day, and there's no shortage of fascinating, hopeful, and dour pieces to read. The four things we found most interesting to know: America remains "in danger of losing the war on AIDS." That opinion belongs to CDC Director Thomas Frieden. He makes his case in the New England Journal of Medicine today, but the New York Times' reporting of it is the piece to read. Sample: "While the article's language was dry and academic, some AIDS experts said it amounted to a call for radical changes ... [that] can be made only by state and local health departments, over which the CDC has little control." The name Jeff Schmalz. The "journalistic prodigy" was a New York Times reporter who, as KERA's headline puts it, "reported on AIDS while he fought the disease." He died in 1993, having learned about his diagnosis after having a seizure while in the newsroom on Dec. 21, 1990. "His reporting helped transform coverage of AIDS." More on Schmalz here and here. Oscar Villareal's experience: He's one of two dozen people featured in the new book Tomorrow Is a Long Time: Tijuana’s Unchecked HIV/AIDS Epidemic, but for those looking for an abbreviated version, Slate shares the sex worker's story (with photos). During his days he lived as "Beto, a gay man who cruised the park. At night he became a transgender woman, Alessandra, Alé for short." The piece by book author Jon Cohen "shows the challenges of ending the AIDS epidemic." "Everyone laughed." So writes Slate of an Oct. 15, 1982, exchange in which White House Press Secretary Larry Speakes was asked about AIDS. Speakes was unfamiliar with it, and reporter Lester Kinsolving told him it was referred to as the "gay plague." The laughter erupted, and continued. A documentary short that captures the exchange debuted today on Vanity Fair. The 7.5-minute When AIDS Was Funny contains audio from two other press conferences.
Expand this summary. | About Jeff Schmalz
Jeff Schmalz was a journalistic prodigy. He was hired by The New York Times while still a college student, and he was essentially running its metropolitan coverage by his mid-20s. From his crisply pressed trousers and shirts to his unerring sense of how to structure a feature story, he was a consummate Timesman. People in the newsroom speculated that someday he could be “on the masthead” – the list of the top editors on the world’s most important newspaper. All the while, though, Jeff was struggling with his identity as a gay man. He came out to many friends and peers on the Times, but he kept his sexual orientation secret from the newsroom management, the people who had control over his professional life. Under the executive editor A.M. Rosenthal, the Times newsroom of the 1970s and 80s was a homophobic place, and journalists known to be gay or lesbian were stalled or even demoted in their careers.
Then, one day in December 1990, Jeff collapsed in the newsroom with a brain seizure. It was the first evidence that he had full-blown AIDS – a death sentence in these years before drug cocktails were available to victims of the disease. With AIDS, Jeff was endangered and he was outed. Yet he was also cracked wide open in positive ways. He found his calling in writing about HIV and AIDS, doing memorable portraits of Magic Johnson, Mary Fisher, and Harold Brodkey, among others, and chronicling his own experience reporting on the most personal beat imaginable. As Jeff himself said at the time, having AIDS stirred an empathy in him that he had long obscured beneath a witty, cynical, hard-driven exterior.
Who Jeff was and what he did deeply changed The New York Times, sensitizing it as never before to the humanity of gay people. The Times of today – publishing same-sex wedding announcements, editorializing in favor of marriage equality – is the fruition of changes that Jeff helped set into motion but never lived long enough to fully see.
And now, 22 years after Jeff died at age 39, his contributions have been largely forgotten. “Dying Words” will restore his name and work to the annals of gay history and journalistic history.
About Our Project
Dying Words: The AIDS Reporting of Jeffrey Schmalz is a project with two parts – an audio documentary and a book. Both were based on our contemporary interviews with many of Jeff’s friends and colleagues, existing recordings of Jeff himself, and excerpts from his AIDS coverage. The project features interviews with major journalists as Anna Quindlen, Adam Moss, Arthur Sulzberger, Jr., and Elizabeth Kolbert, as well as the AIDS activist Mary Fisher and the LGBT historian Eric Marcus. Our project had the full and enthusiastic support of Wendy Schmalz, Jeff’s sister, who is his closest living relative. Thanks to Wendy, we had access to original microcassette recordings of Jeff’s interviews with Larry Kramer, Magic Johnson, Randy Shilts, and Bill Clinton, among others.
The audio documentary was produced by Kerry Donahue and edited by Ben Shapiro, both award winning journalists. It was distributed by PRX to more than 125 public radio stations, including eight of the top 10 markets. It is also available for download. The Dying Words book was published by CUNY Journalism Press and released on December 1, 2015 to coincide with World AIDS Day. ||||| The two come into conflict, for example, when an infectious patient willfully refuses treatment and keeps passing on a disease. In the 1990s, during an outbreak of drug-resistant tuberculosis in New York City, Dr. Frieden famously detained patients who refused to take their pills, locking them in hospitals for months until they were cured.
In 2005, he advocated H.I.V.-control measures that he said would “offend both sides of the political establishment.” Condoms and clean syringes were needed even if conservatives disliked them, he said, and the tracing of sexual partners needed to be done even if H.I.V. activists opposed it.
Some of those goals have become law.
Although H.I.V. testing is not mandatory except in the military and under a few other circumstances, the counseling requirement has been dropped. Many hospitals test all patients unless they specifically refuse, and some cities even pay people applying for driver’s licenses to take H.I.V. tests.
Lab results are now reported by name almost everywhere. That makes it possible for local health workers to contact patients to make sure they receive help and to ask for the names of their sex partners so they, too, can be treated.
But that is failing, Dr. Frieden said in the interview. Only about half of those testing positive for H.I.V. are ever asked for names, and those who choose to answer “named relatively few.”
Local health departments lack the staff to trace contacts. “To be fair, it’s legitimately hard,” Dr. Frieden added. Some people find sex partners through apps like Grindr without ever learning their names.
New tests can detect the virus within 10 days of infection, but they are not being used enough, he said. An estimated 155,000 Americans with H.I.V. do not know it. And of those who are tested, 20 percent already have AIDS or are close to it — meaning they may have been spreading the virus for years. ||||| “I have come to the realization that I will almost certainly die of AIDS," New York Times reporter Jeff Schmalz wrote more than two decades ago. He died in 1993.
Schmalz reported on AIDS while he battled the disease. His reporting helped transform coverage of AIDS.
Kerry Donahue is director of the radio program at Columbia Journalism School. She produced the documentary “Dying Words," which explores Schmalz' career and airs on KERA 90.1 FM at 8 p.m. Tuesday, World AIDS Day.
Donahue talked with KERA about Schmalz' life and legacy.
Interview Highlights: Kerry Donahue ...
... on Jeff Schmalz' passion for journalism: "He was a very driven man. He grew up in a small town in Willow Grove, Penn., about an hour north of Philadelphia. He decided somewhere in high school, he worked on the high school newspaper, and he decided when he got to Columbia University that he would get a job at The New York Times. He worked as a copyboy. He immediately fell in love with it, so much so that he dropped out of Columbia and started working at the Times full-time, and he was very very ambitious about it.
... on how being gay affected his career: "He was a gay man and he stayed in the closet to people above him. To his colleagues and people below him, he was very out and open. But there was a consequence at the Times for being gay in much of the '70s and '80s. It was a very homophobic newsroom. Often, for gay staffers, if it was found out you were gay, [there was] a punishment or a sort of setback. That happened to Jeff Schmalz in 1983. He was passed over for promotion and about four months after that he was sent out to be a reporter - what would have been after a significant number of years of being an editor at The New York Times - a very entry-level reporter job - he felt he had been exiled a bit."
... on when Schmalz realized he had AIDS: "He had a seizure while at work on Dec. 21, 1990. He was just at his desk and he collapsed. He had a grand mal seizure, at which point the entire newsroom came running. When he got the diagnosis, it was quite severe. He had PML, a brain infection which typically was very fatal, is very fatal, often killing people within months. He really thought he would die almost immediately."
... on Schmalz' reporting changing after his diagnosis: "When he came back to work, I think he still in some ways was a bit in denial. He wanted to cover the 1992 presidential campaign, which he did - and in the course of that I think he started to find a way ... to cover AIDS. It took him a little while to figure out what angle on AIDS he wanted to cover. He was always a newspaper man thinking of how to make the story the most compelling and he ultimately settled on a series of profiles of people like himself who were living with AIDS and working and being in the world."
Kerry Donahue is director of the radio program at Columbia Journalism School.
“Dying Words," which explores the life and legacy of Jeff Schmalz, airs on KERA 90.1 FM at 8 p.m. Tuesday, World AIDS Day.
Video: Jeff Schmalz on "The Charlie Rose Show" in 1992
Jeff Schmalz on The Charlie Rose Show, November 19, 1992. from Kerry Donahue on Vimeo. ||||| World AIDS Day is, like other world disease days, a publicity gambit that has a distinctly absurd pageantry. But there is substance beyond candlelight vigils, a red ribbon hung from the White House portico, and proclamations from politicians and public health officials. Most tangibly, each World AIDS Day, held annually on Dec. 1, broadcasts official updates about the damage caused by HIV, which at last count had infected 78 million people since the epidemic surfaced in 1981 and had killed half of them. And beginning in 2012, World AIDS Day began to trumpet a new possibility that a few years earlier would have seemed preposterous, even delusional: ending the epidemic.
A growing number of locales on this World AIDS Day can rightly claim to have made important steps toward ending their epidemics. Key to this progress is the recent evidence that treatment is prevention: Anti-HIV drugs can reduce the virus to such low levels in appropriately treated people that they rarely infect others, whether it be through sex, mother-to-child transmission, or even sharing needles. Pre-exposure prophylaxis, or PrEP, protects uninfected people with the same drugs. San Francisco and New York state both have explicit plans to end their epidemics by more aggressively exploiting treatment as prevention and PrEP in concert with staples such as condom promotion, education, clean needle provision, and behavior change.
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To retain its epidemic status, AIDS requires that each infected person spread the virus to at least one other. If interventions can reduce transmissions such that, say, only 75 percent of people with HIV infect someone else, an epidemic will sputter and, eventually, stop. But for millions of people, a great distance separates the aspiration to end AIDS from the achievement of that goal.
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Photo by Malcolm Linton/Polaris
In the summer of 2014, Oscar, 28, earned his living as a sex worker in Tijuana, the Mexican border town that abuts San Diego. During the day Oscar was Beto, a gay man who cruised the park. At night he became a transgender woman, Alessandra, Alé for short, who worked the clubs and the streets in the red-light district known as the Zona Norte. “Alé makes more money than Beto,” Oscar said, adding that the life he shared with his two alter egos was “very balanced.”
Photo by Malcolm Linton/Polaris
Oscar lived in Tijuana as a young child but moved to Wisconsin at age 8 on a visa with his aunt and a sister. “I went supposedly to go to school, but then I ended up working, and I liked the money, so I forgot about school,” he said. A Greek restaurant hired him as a dishwasher when he was 12, and his aunt could not persuade him to continue with his studies. “I was young and hardheaded. I regret that now.” The restaurant owners treated him like one of their own children, he said, eventually promoting him to crew leader.
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Oscar married and had a son, entertained as a female impersonator, and bought a new Ford Focus. “Over there, I used to do cocaine, because I was making a lot of money,” he said. Then in 2010 he had a car accident. He had no license or insurance, which led to his arrest and the discovery that his visa had expired. After six months at a detention center run by the U.S. Immigration and Customs Enforcement, a judge granted Oscar a “voluntary departure,” which meant he would leave the United States but not be barred from re-entering.
Oscar returned to Tijuana without his family, and he started to smoke crystal methamphetamine, a powerful aphrodisiac used by many sex workers.
Photo by Malcolm Linton/Polaris
Oscar had his first HIV test in Wisconsin when he was 18. He was negative. When he took another test on Tijuana’s Gay Pride Day in 2013, he was still uninfected.
Photo by Malcolm Linton/Polaris
Gay men and transgender women have the highest HIV infection rates of any group in Tijuana. Selling sex further increases risk, as does smoking crystal meth. “Alé gets horny and crazy and wild,” said Oscar.
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A meta-analysis in 2008 that looked at 25 studies of transgender women in 14 countries found an HIV prevalence of 27.3 percent in those who sold sex and 14.7 percent in those who did not. The overall estimated prevalence of HIV in Tijuana adults is 0.6 percent, about the same as in the United States.
Photo by Malcolm Linton/Polaris
Oscar said Alé scared him: “Alé gets whatever she wants. She is a very spoiled girl. She’s a very dangerous girl. She is very, very strong. She is my boss. I listen to her sometimes. And Oscar, he is kind of like Alé but more mellow, not that aggressive.”
Photo by Malcolm Linton/Polaris
When Oscar was a boy, he regularly returned to Tijuana to see his mother, and he had his first sexual experience there when he was 10. “I was on the streets most of the time playing around, and there were a lot of old guys,” he remembered. “They’d say, ‘Play with my thing, and I’ll give you a candy.’ ” Back in Wisconsin, he continued to trade sex with older men for treats and money. “It was normal to me.”
Photo by Malcolm Linton/Polaris
Oscar was appalled that so many deportees, like onetime gang member from Los Angeles Lesly Zulema Sanchez, ended up living in the Tijuana River Canal. “I think those people are nuts,” said Oscar. “Sometimes people ask me for a coin or whatever, and they say, ‘Oh, I’m deported.’ I’m like, I’m deported, too, and I try to survive in a different way.”
Photo by Malcolm Linton/Polaris
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Oscar said Alé mainly had U.S. clients. “They confuse me because they want Alé, but then they want Alé to behave like Oscar. I don’t like that. Why? Why do they do that?”
Often, Oscar explained, the clients wanted Alé to be the insertive partner. “That’s strange, weird. It bothers me when I’m Alé and they try to touch Beto’s things. I don’t like that. They’re supposed to be locked in a safe.”
Male-to-female transgender people often have male clients who like to receive anal sex but do not identify themselves as gay. In their minds, there is no stigma if they are having sex with a woman, even if she has a penis.
Photo by Malcolm Linton/Polaris
In September 2014, the police arrested Oscar, who was coming out of a weeklong meth binge. A search allegedly found that he was carrying half a kilo of crystal meth, and he was locked up at Tijuana’s La Mesa prison, which houses 6,000 inmates. “The police put the drug on me,” he said. “With no witnesses, my lawyer said I’m going to get five years.”
Logically, places like Tijuana would be at the top of the list for campaigns to ending AIDS epidemics.
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Centro de Servicios, a nongovernmental organization commonly referred to as SER, is the main HIV prevention program in Tijuana that serves gay men and transgender women. Its staff regularly visits La Mesa prison to conduct rapid tests for the virus and to educate inmates about how to protect themselves. SER’s Kristian Salas tested Oscar and found that he was positive.
The prison moved Oscar to a cell with six other HIV-infected inmates, who received double helpings of food. “Kristian told me I shouldn’t be sad,” said Oscar. “He told me it was like diabetes, and people don’t die as long as they take the medication. I’m not sure about that. Only time will tell me the truth.”
In February, when we last checked in with Oscar, he was still in prison and said his CD4 white blood cells—HIV’s main target—numbered 353 per microliter of blood. (Normal CD4 counts range from 600 to 1,200.) He complained that he was not yet receiving antiretrovirals. Mexico’s guidelines call for treating all HIV-infected people, regardless of their CD4 counts.
* * *
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Tijuana as a whole does not have a particularly severe HIV/AIDS problem—especially considering the other health issues it faces. In Tijuana, as in the United States and much of the world outside of sub-Saharan Africa, the virus primarily has made headway in “high-risk” groups, creating what scientists call a “micro hyperepidemic.” This limited spread makes places like Tijuana especially amenable to ending AIDS. It is far more difficult to launch treatment and prevention campaigns for a general population than it is to target smaller and interconnected communities of transgender women, gay men, sex workers, and people who inject drugs, the main groups infected with HIV in Tijuana.
Logically, places like Tijuana would be at the top of the list for campaigns to ending AIDS epidemics. But no coordinated effort exists in Tijuana to test people at the highest risk, the cornerstone of any such effort. When people do test negative, they are not offered PrEP. And for those who are infected, a recent study found that only 3.7 percent were receiving anti-HIV drugs. Treatment as prevention doesn’t have a hope if it’s not used.
The reasons why Tijuana has not jumped on the ending AIDS bandwagon reach far beyond the problem of limited resources—and they are common to other places that have similarly scaled, easier-to-contain micro hyperepidemics. There are two essential obstacles, and they overlap. First, there is no strong leadership. This in part reflects the reality that the communities most affected by HIV have weak political muscle: Tijuana has no advocacy movement loudly chanting in front of government buildings on behalf of gay men, transgender women, drug users, and sex workers. And the rampant stigma and discrimination these groups face is compounded because many are deportees from the United States or migrants from Central America, most are poor, and some are homeless.
In September, the World Health Organization issued guidelines that for the first time recommended treating all HIV-infected people in the world with antiretroviral drugs and offering PrEP to everyone at “substantial risk” of becoming infected. The guidelines explicitly state that if countries adopt these recommendations, they will contribute to “ending the AIDS epidemic as a major public health threat by 2030.” This is a glorious vision that on this World AIDS Day surely will receive more rah-rahism than ever before. ||||| On Oct. 15, 1982, at a White House press briefing, reporter Lester Kinsolving asked Press Secretary Larry Speakes about a horrifying new disease called AIDS that was ravaging the gay community.
“What’s AIDS?” Speakes asked.
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“It’s known as the ‘gay plague,’ ” Kinsolving replied.
Everyone laughed.
“I don’t have it,” Speakes replied. “Do you?” The room erupted in laughter again. Speakes continued to parry Kinsolving’s questions with quips, joking that Kinsolving himself might be gay simply because he knew about the disease. The press secretary eventually acknowledged that nobody in the White House, including Reagan, knew anything about the epidemic.
“There has been no personal experience here,” Speakes cracked. The room was in stitches.
On Dec. 1, 2015—World AIDS Day—Vanity Fair debuted a short documentary by Scott Calonico about this now-infamous exchange. Calonico has finally unearthed audio of the galling colloquy between Speakes and Kinsolving. Their exchange—and the accompanying laughter—is as horrifying now as it must have been to those dying of the disease in 1982. ||||| Study in The New England Journal of Medicine concludes improvements to education, lifestyle and health are contributing to decline in overall number of new cases of dementia. MORE
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News article:
Importance Foods that have similar carbohydrate content can differ in the amount they raise blood glucose. The effects of this property, called the glycemic index, on risk factors for cardiovascular disease and diabetes are not well understood.
Objective To determine the effect of glycemic index and amount of total dietary carbohydrate on risk factors for cardiovascular disease and diabetes.
Design, Setting, and Participants Randomized crossover-controlled feeding trial conducted in research units in academic medical centers, in which 163 overweight adults (systolic blood pressure, 120-159 mm Hg) were given 4 complete diets that contained all of their meals, snacks, and calorie-containing beverages, each for 5 weeks, and completed at least 2 study diets. The first participant was enrolled April 1, 2008; the last participant finished December 22, 2010. For any pair of the 4 diets, there were 135 to 150 participants contributing at least 1 primary outcome measure.
Interventions (1) A high–glycemic index (65% on the glucose scale), high-carbohydrate diet (58% energy); (2) a low–glycemic index (40%), high-carbohydrate diet; (3) a high–glycemic index, low-carbohydrate diet (40% energy); and (4) a low–glycemic index, low-carbohydrate diet. Each diet was based on a healthful DASH-type diet.
Main Outcomes and Measures The 5 primary outcomes were insulin sensitivity, determined from the areas under the curves of glucose and insulin levels during an oral glucose tolerance test; levels of low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, and triglycerides; and systolic blood pressure.
Results At high dietary carbohydrate content, the low– compared with high–glycemic index level decreased insulin sensitivity from 8.9 to 7.1 units (−20%, P = .002); increased LDL cholesterol from 139 to 147 mg/dL (6%, P ≤ .001); and did not affect levels of HDL cholesterol, triglycerides, or blood pressure. At low carbohydrate content, the low– compared with high–glycemic index level did not affect the outcomes except for decreasing triglycerides from 91 to 86 mg/dL (−5%, P = .02). In the primary diet contrast, the low–glycemic index, low-carbohydrate diet, compared with the high–glycemic index, high-carbohydrate diet, did not affect insulin sensitivity, systolic blood pressure, LDL cholesterol, or HDL cholesterol but did lower triglycerides from 111 to 86 mg/dL (−23%, P ≤ .001).
Conclusions and Relevance In this 5-week controlled feeding study, diets with low glycemic index of dietary carbohydrate, compared with high glycemic index of dietary carbohydrate, did not result in improvements in insulin sensitivity, lipid levels, or systolic blood pressure. In the context of an overall DASH-type diet, using glycemic index to select specific foods may not improve cardiovascular risk factors or insulin resistance.
Trial Registration clinicaltrials.gov Identifier: NCT00608049 ||||| If you generally eat a heart-healthy diet, then you might have one fewer factor to worry about: the "glycemic index" of the carbs you eat, new research suggests.
In a new study, researchers looked at how people's health is affected by the types of carbs they eat, using one measure of carbohydrates called the glycemic index. This index is a number, between 1 and 100, that reflects how much a given carb raises your blood sugar levels. For example, carbs such as apples and oatmeal have a low glycemic index, meaning they raise blood sugar less than carbs with a higher glycemic index, such as white bread and corn flakes.
The researchers at Johns Hopkins University School of Medicine and Harvard Medical School set out to examine whether healthy diets with a low glycemic index would provide more heart health benefits compared with similarly healthy diets that have a higher glycemic index. [5 Diets That Fight Diseases]
The researchers gave special diets to 163 overweight men and women for five weeks, and tracked their blood pressure, cholesterol levels and sensitivity to insulin. The participants were on four different diets that all contained the same number of calories, but two were high in carbohydrates and two were low in carbohydrates. Among the two that were high in carbs, one had a high glycemic index and the other had a low index. Similarly, of the two diets that were low in carbs, one had a high glycemic index and the other had a low one.
The results showed that the glycemic index of the diet didn't matter. The participants on diets with a low glycemic index did not have improvements in their insulin sensitivity, cholesterol levels or blood pressure during the study, according to the findings published today (Dec. 16) in the journal JAMA.
"We were really surprised," says co-author Dr. Lawrence Appel, a professor of medicine at Johns Hopkins. "We did not detect any clear benefit of the low glycemic index diets on the major risk factors for heart disease, and we found no evidence of benefit for diabetes prevention."
All four diets in the study were based on the Dietary Approaches to Stop Hypertension (DASH) diet. The DASH diet is designed to help treat or prevent high blood pressure by reducing people's salt intake and including foods rich in nutrients that help lower blood pressure, such as potassium, calcium and magnesium.
"The unexpected findings" of the study suggest that the concept of glycemic index is less important than previously thought," Dr. Robert Eckel, a professor of medicine at the University of Colorado, wrote in an editorial accompanying the study. "These findings should therefore direct attention back to the importance of maintaining an overall heart-healthy lifestyle, including diet pattern," he said.
An overall heart-healthy lifestyle includes the basic rules that most people already know, Appel said. "Don't drink sugar-sweetened drinks. Try to eat fruits, vegetables and whole grains. Try to avoid sweets, salt and foods high in saturated and trans fats. People who follow these principles will reap the benefits," he said.
Email Bahar Gholipour. Follow Live Science @livescience, Facebook & Google+. Originally published on Live Science. |||||
What is a shorter version of the above article? | – Eating too many carbohydrates is largely considered to be bad for our health—leading to weight gain, higher cholesterol levels, and more heart disease risk factors. But when people follow a low-carb diet, the types of carbs they eat may not be so important, finds a new study out of Harvard and Johns Hopkins published this week in the journal JAMA. Following the highly regimented diets of 163 participants (each assigned to one of four diets, all of which contained the same calories but had different carbs), researchers were surprised to find that when overall carb levels were low, the glycemic level of the carbs consumed didn't seem to matter, reports LiveScience. Some argue that low glycemic diets, with lots of whole grains and low-starch veggies, are better for blood sugar levels and insulin sensitivity. But the New York Times reports that the new findings suggest that low glycemic diets actually worsened insulin sensitivity. "The dogma out there is that a high glycemic index is bad," a former president of the American Heart Association not involved in the study tells the Times. "I hope that ultimately the glycemic index will be left on the shelf." Still, the findings only relate to short-term health effects and didn't take into account the effects on the growing population of adults with Type 2 diabetes. (Diets low in carbs overall also appear to lower blood pressure.) | multi_news_1_0_0 |
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The Godfather of House Music was 59 years old.
Sad news: legendary house DJ Frankie Knuckles has reportedly passed away, with both DJ Deeon and Paul Johnson confirming the news.
Knuckles was born in The Bronx in 1955 and began DJing in New York in the ’70s with Larry Levan. After moving to Chicago in 1977 he played at the famed Warehouse and then his own club, The Power Plant. He remained an integral part of house music throughout the decades, producing seminal records ‘Your Love’, ‘Baby Wants To Ride’ and ‘Tears’ and continuing his DJing career to the present day. In 2004, Chicago named a street after him where the old Warehouse once stood.
RBMA and Bill Brewster have already paid tribute with a playlist of 50 classic tracks from The Warehouse. You can also stream a radio recording of Knuckles DJing in 1986.
It’s not yet clear how Knuckles died, but a statement is expected to be released today (April 1). ||||| Nobody can agree on who invented the blues or birthed rock & roll, but there is no question that house music came from Frankie Knuckles, who died Monday afternoon of as-yet-undisclosed causes at age 59. One of the Eighties and Nineties' most prolific house music producers and remixers, Knuckles is, hands down, one of the dozen most important DJs of all time. At his Chicago clubs the Warehouse (1977-82) and Power Plant (1983-85), Knuckles’ marathon sets, typically featuring his own extended edits of a wide selection of tracks from disco to post-punk, R&B to synth-heavy Eurodisco, laid the groundwork for electronic dance music culture—all of it.
Frankie Knuckles: 5 defining tracks from the Chicago house pioneer
Knuckles made an abundant number of dance classics, including early Jamie Principle collaborations "Your Love"(1986) and "Baby Wants to Ride"(1987); "Tears"(1989), with Satoshi Tomiiee and Robert Owens; "The Whistle Song"(1991); and his remixes of Chaka Khan’s "Ain’t Nobody"(1989), Sounds of Blackness’s "The Pressure" (1992), and Hercules and Love Affair’s "Blind" (2008).
Born Francis Nicholls in the Bronx on January 18, 1955, Knuckles began hitting New York’s after-hours spots such as the Loft, the Sanctuary, Better Days, and Tamburlaine—the clubs where disco was born—as a teenager, along with his best friend, Larry Philpot. By the mid-Seventies, both of them were DJs themselves, and Philpot had changed his surname to Levan. The duo worked together at two of the most important early discos: the Gallery (presided over by Nicky Siano, whose smooth on-beat mixing style was enormously influential) and the Continental Baths, a multi-room gay bathhouse on Manhattan’s West Seventy-fourth Street. (Two other entertainers got their start there: Bette Midler and her pianist, Barry Manilow.)
By 1977, both started their own clubs in difference cities. While Levan (who died in 1992) helmed the Paradise Garage in Soho, Knuckles moved to Chicago, where Robert Williams, an old friend of both, was opening what became the Warehouse. A narrow building with oblong windows at 206 South Jefferson St. (today it’s a law office), the Warehouse was where Knuckles began honing his sound and style—"a wide cross-section of music," as he told The Guardian in 2011. His mélange of disco classics, weird indie-label soul curiosities, the occasional rock track, European synth-disco and all manner of rarities would eventually be codified (at Importes, Etc., the record shop where Knuckles bought much of his music) as "House Music"—short, of course, for the Warehouse. (In 2004, the block where the Warehouse stood was renamed Honorary Frankie Knuckles Way.)
Frankie Knuckles Live @ The Warehouse - 28-08-1981 by R_Co on Mixcloud
At a time when Saturday Night Fever had cranked up disco’s profile till it blanketed pop culture, Knuckles favored the music’s weirdoes and rebels. He spun tracks on independent labels like Salsoul and cheesy-exotic synth-disco from Italy. He liked things floridly dramatic and stark (First Choice’s "Let No Man Put Asunder," Black Ivory’s "Mainline"); he liked party conviviality (Positive Choice’s wonderfully loose "We Got the Funk"); he liked genuine strangeness (Two Man Sound’s heavily phased "Que Tal America"). Working with reel-to-reel tape, he’d re-edit his favorite tracks to extend the grooves for his dance floor. "It wasn’t traditional disco like Donna Summer," Jesse Saunders, another Chicago DJ of the time, said in 1995. "It was really R&B."
It was also enormously influential. Chicago was a DJ town, with local radio broadcasting several mix shows starting in the late Seventies, and nearly every jock in the city bowed to Frankie. One of the city’s most popular jocks was Farley Keith Williams—then "Funkin'" Farley Keith of WBMX-FM’s Hot Mix 5 DJ team, and later a Chicago house hit-maker as Farley "Jackmaster" Funk. "Honestly, when I started, I didn't go out buying new records," Farley said in 2008. "I went out and regurgitated what Frankie Knuckles would play."
Knuckles was so popular that the Warehouse—initially a members-only club for largely black gay men—began attracting straighter, whiter crowds, leading its owner, Robert Williams, to eschew memberships. Knuckles left in November 1982, opening the Power Plant a few months later. Not long after that, a fast-talking young DJ from Detroit named Derrick May, who’d recently been knocked flat after hearing Knuckles for the first time, sold Frankie a drum machine to further enhance his mixes—something several DJs in Chicago (and Detroit) were already doing.
That combination of bare, insistent drum machine pulse and an overlay of cult disco classics just about defines the sound of early Chicago house music—a sound many young local producers were beginning to mimic in the studio by 1985. That year, Knuckles made his first recordings with an ethereal-voiced, Prince-obsessed singer-songwriter named Byron Walford, a.k.a. Jamie Principle. The pair’s early tracks were recorded in the Power Plant DJ booth, but they soon graduated to local studios. Several of their songs together wound up released by the local label Trax Records—without the artists’ permission, as both Knuckles and Principle later insisted; it's just one example of the cutthroat business practices at the dark heart of early house music.
Frankie Knuckles - WBMX Friday Night Jams 1986 by Sarah Davies on Mixcloud
But the music wasn’t just popular in the city’s clubs or party-rental spaces. Chicago house blew up in England in 1986, with Farley "Jackmaster" Funk and Daryl Pandy's "Love Can’t Turn Around," hitting the U.K. Top Ten and J.M. Silk’s "Jack Your Body" going to Number One in January 1987. "I remember being interviewed by a journalist in '86," Knuckles told Bill Brewster and Frank Broughton in The Record Players: DJ Revolutionaries. "And I remember telling her this music’s gonna be around for a while. It’s gonna take it a long time for it to get to where it needs to be at, but it’ll be around for a long time."
Though the dance charts were about as far as most Chicago house titles went in their home country, house music—as well as Detroit techno, the style Derrick May was helping pioneer—not only yielded actual chart hits overseas, they fueled a new style of clubbing. In the summer of 1987, a group of English DJs—including Paul Oakenfold and Danny Rampling—traveled to the Mediterranean island of Ibiza and were turned on to both a more expansive playlist than usual, thanks to DJ Alfredo of the open-air club Amnesia, and a new drug: MDMA, or Ecstasy. Bringing that combo back to England, Rampling’s Shoom club, followed by Oakenfold’s Spectrum, birthed what the Brits called "raves": enormous gatherings, usually in warehouses or open fields, of kids wearing smiley-face T-shirts while dancing all night, often on Ecstasy, to house and techno.
Knuckles wasn't interested. In 1988, he returned home to New York and took on a series of club residencies—the World, the Roxy, the Sound Factory, and Sound Factory Bar (a different venue) among them—and teamed up with manager Judy Weinstein and fellow DJ David Morales (who’d filled in for Levan at the Paradise Garage) to form Def Mix Productions, a studio umbrella that altered the job description of a club remixer. Rather than simply change the arrangement or even grafting a new track onto an existing song, Knuckles and Morales would remake the source material from the ground up, even bringing the artist back in to cut a new vocal. Eric Kupper, a keyboardist and producer who worked on many of Knuckles’ great Nineties recordings, said that Frankie’s work "had a little more of an arrangement going on" than Morales'.
"[When] you’ve got someone as big as Luther Vandross and Michael Jackson sitting there saying, 'Whatever you want, however you want it, I’ll stay here as long as you need me,' that’s the reward right there," Knuckles said in 2011. "All the programmers I worked with were all classically trained musicians . . . I was teaching them a different side of what it is they do. Infusing certain ideas like Debussy-esque piano over a very thick house track or bass line is something that blew their minds. It blew mine, too, but it’s something they never imagined and/or heard of before . . . We didn’t know if it would work or not, but it did."
Though Knuckles kept up a heavy DJ schedule throughout his career, health problems, as well as the waning popularity of his type of traditionalist house music, led to his quieting down on the production front in the 2000s. In July 2008, Knuckles’ right foot was amputated: He’d broken it during a 2000 snowboarding accident in Switzerland, leading to a bone disease exacerbated by late-breaking diabetes.
But that year, Knuckles' profile got a significant bump. For one thing, younger DJs and producers were discovering vintage Chicago house music, from Knuckles’ tracks to mid-Nineties "ghetto house" on labels like Dance Mania. For another, Knuckles released his remix of Hercules and Love Affair’s "Blind" that year—a deeply moving version that tops an already great original. Knuckles was "considered a huge risk" to work on the track, DFA co-head Jonathan Galkin said in 2011: "Is he gonna get it? He's a main room remixer a lot of times . . . So going to that guy for our indie leftfield disco record? He knocked it out of the park."
More recently, Knuckles was regularly hitting the global club and (occasionally) festival circuit—and regularly converting kids who’d never heard of the Warehouse. Exhibit A: His sizzling Boiler Room session from April 2013. "When he was defining house music, all of us were running around the Christmas tree with a fucking toy drum," went the introduction. "So show some love, show some respect—throw yourself in the dirt for Frankie!" ||||| The "Godfather of House Music" Frankie Knuckles has passed away today at age 59, as confirmed by fellow Chicago house artists DJ Deeon and Paul Johnson.
Born in the Bronx in 1955, Knuckles first began DJing in New York alongside Larry Levan. He then moved to Chicago in the 1970's to become the premiere DJ at The Warehouse, the nightclub that would birth the dance music genre "house." Knuckles then opened up his own club, The Power Plant, in 1983. Knuckles was also a producer on such famous songs as James Power's "Your Love" and "Baby Wants to Ride." |||||
Write a summary. | – He's been called the "Godfather of House Music," and Rolling Stone says he "laid the groundwork for electronic dance music culture—all of it." Frankie Knuckles, who died yesterday at 59, was the top DJ at the Warehouse in Chicago, where house music was effectively invented, Gawker reports. Born in the Bronx, Knuckles launched his DJing career in New York before moving to Chicago, where a street was eventually named after him, FACT reports. After five years at the Warehouse, he moved on to open the Power Plant in 1983. At the Warehouse, Knuckles blended disco, indie, and rock to create house music, named for the club. He left his mark on hits ranging from 1982's "Your Love" to 2008's "Blind." "Hands down," Knuckles is "one of the dozen most important DJs of all time," writes Michaelangelo Matos in Rolling Stone. The cause of death hasn't been been revealed. | multi_news_1_0_0 |
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South Nassau Hospital alerting 4,247 patients of possible blood contamination
South Nassau Communities Hospital is sending out 4,247 letters to patients recommending they be tested for hepatitis B and C and HIV because of the risk of infection from an insulin pen.
In the letter dated Feb. 22, the Oceanside hospital said the patients may have received insulin from an insulin pen reservoir -- not the pen's single-use disposable needle -- that could have been used with more than one patient.
An insulin pen for those with diabetes is a pre-filled syringe meant to be used to dispense insulin in a single patient. Because of potential backflow of a patient's blood into the pen cartridge after injection, using a pen on multiple patients may expose them to blood-borne infections.
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Hospital spokesman Damian Becker said no one was observed reusing the insulin pen reservoir on more than one patient, but a nurse was heard saying it was all right to do so.
"Once that was said, we then followed through with a report to the state Department of Health," Becker said.
The hospital said risk of infection is "extremely low."
"Nonetheless, out of an abundance of caution, the hospital is recommending that patients receiving the notification be tested for hepatitis B, hepatitis C and HIV. While the testing is voluntary, it is recommended," the hospital said.
Becker said Tuesday the hospital, which is sending the letters out in phases, has received about 200 phone calls so far. The last letters should be received by March 17, Becker said.
It will take patients about two weeks to receive test results, he said.
The hospital said it has since banned the use of insulin pens and permits only the use of single-patient-use vials.
The state Department of Health said that last year three health facilities reported potential insulin pen re-use: two state-regulated facilities and the Veterans Administration's medical center in Buffalo.
South Nassau is offering free and confidential blood testing and has set up a dedicated telephone line for those patients notified. To arrange a test, call 516-208-0029.
Insulin pen misuse is not uncommon.
In May 2008, Nassau University Medical Center in East Meadow notified 840 patients that nurses may have been using insulin pens on multiple patients.
In 2009, following reports of improper use of insulin pens in hospitals, the U.S. Food and Drug Administration issued an alert reminding health care workers that insulin pens are meant for use on a single patient only.
In 2012, the U.S. Centers for Disease Control and Prevention said that "in spite of this alert, there have been continuing reports of patients placed at risk through inappropriate reuse and sharing of insulin pens," and it put out a clinical reminder on their proper use.
Last year, the VA issued an alert systemwide following the report of insulin pen misuse at its Buffalo hospital. Of 395 patients tested, 12 were found with hepatitis B and six with hepatitis C. ||||| Patients at South Nassau Communities hospital are being urged to get tested for hepatitis and HIV after a possible contamination of insulin shots. Greg Cergol reports. (Published Wednesday, March 12, 2014)
A Long Island hospital says some patients may be at risk of exposure to hepatitis B, hepatitis C and HIV after authorities found that an insulin pen may have been used on more than one patient.
South Nassau Communities Hospital says the risk of infection is extremely low but is recommending that patients get tested.
The hospital sent a letter to that effect to more than 4,000 patients, according to Newsday. It is offering free blood testing and has set up a toll-free hotline that patients can call to schedule a blood test.
The number is 516-208-0029.
Newsday reports that no one was observed reusing the insulin pen reservoir but a nurse was heard saying it was OK to do so.
"Once that was said, we then followed through with a report to the state Department of Health," hospital spokesman Damian Becker told the newspaper.
In the meantime, the hospital has instituted a policy banning the use of insulin pens, permitting only single-use vials to administer prescribed insulin treatments to patients. |||||
What is a one-paragraph summary of the above article? | – More than 4,000 people on Long Island are getting the most unwelcome kind of letter from a local hospital—a warning that they might have been inadvertently exposed to HIV. As ABC News explains, the risk is low, but it stems from improper use of an insulin pen. It seems a nurse at South Nassau Communities Hospital was overheard saying, incorrectly, that it was OK to reuse the pen on multiple patients, reports Newsday via NBC News. "Once that was said, we then followed through with a report to the state Department of Health," says a spokesperson. The hospital is urging all those who might have been exposed to get tested for HIV, hepatitis B, and hepatitis C. In the meantime, the hospital is ditching the pens—which can indeed be used multiple times provided it's the same patient—in favor of single-use insulin vials. | multi_news_1_0_0 |
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Paula Deen’s longtime powerhouse publicist, Nancy Assuncao, has quit after six years over the butter-loving chef’s plan to plug a diabetes drug.
Assuncao faithfully stuck with Deen through years of hearty drama, including her battle with rival chef Anthony Bourdain, who called her “the most dangerous woman in America.” But she quit as Deen’s spokeswoman and chief marketer last month as Deen negotiated her deal to hawk the drug Victoza.
Deen, now under siege by diabetics, nutritionists and fellow chefs for keeping her own Type 2 diabetes secret for three years, even as she pushed recipes full of sugar and fat, probably could use Assuncao’s help now. Deen only revealed her diagnosis last week.
A source said Assuncao “strongly disagreed with Deen’s dramatic turnabout, after years of promoting fatty foods, to announcing she has a deal with a diabetes drug company [Novo Nordisk] and will be promoting lighter food and ‘diabetes in a new light.’
“While Paula did tell some people at her live appearances about her diabetes, she certainly didn’t talk about it on her show. Nancy disagreed with Paula’s plan to be a drug-company spokesman and challenged her decision. But this wasn’t a battle Nancy felt she was going to win. She couldn’t be part of it.”
Assuncao, whose past clients have included Ian Schrager, told us last night, “I’m very grateful for the six years that I worked with Paula in helping her build the Deen brand.
“Although we had a great deal of fun along the way, I could not agree with the new business strategy going forward. Nonetheless, I wish them continued success.”
Deen’s new rep could not be reached last night, with a staffer at her office telling us, “She is on the Paula Deen cruise.” The chef’s Web site said Celebrity Cruises’ Eclipse would be a “tasty journey” in the Caribbean with a group buffet dinner, a cooking demo and a personal photo with Deen (one per family). ||||| Let Food Network chefs plan what's for dinner, with quick and easy recipes delivered to your inbox daily.
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Summary: | – What do you do when your celebrity chef client continues churning out dishes like Deep-Fried Stuffing on a Stick or Cheesy Ham and Banana Casserole three years after she learns she has Type 2 diabetes, only to start shilling for a drugmaker? If you're Paula Deen's publicist, you walk. Nancy Assuncao, who worked with Deen for six years, quit over Deen's plan to hawk a diabetes drug, the New York Post reports. Assuncao “strongly disagreed with Deen’s dramatic turnabout, after years of promoting fatty foods, to announcing she has a deal with a diabetes drug company and will be promoting lighter food and 'diabetes in a new light,'" says a source. Assuncao herself adds, "I could not agree with the new business strategy going forward." Deen's new rep was "on the Paula Deen cruise" and unavailable; the Post notes that that jaunt is a "'tasty journey' in the Caribbean with a group buffet dinner, a cooking demo, and a personal photo with Deen (one per family)." If you can't get enough, click to see Deen's last meal before announcing her diagnosis, or her unfortunate "six-word memoir." | multi_news_1_0_0 |
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Photographer: Daniel Acker/Bloomberg Photographer: Daniel Acker/Bloomberg
The aloe vera gel many Americans buy to soothe damaged skin contains no evidence of aloe vera at all.
Samples of store-brand aloe gel purchased at national retailers Wal-Mart, Target and CVS showed no indication of the plant in various lab tests. The products all listed aloe barbadensis leaf juice — another name for aloe vera — as either the No. 1 ingredient or No. 2 after water.
There’s no watchdog assuring that aloe products are what they say they are. The U.S. Food and Drug Administration doesn’t approve cosmetics before they’re sold and has never levied a fine for selling fake aloe. That means suppliers are on an honor system, even as the total U.S. market for aloe products, including drinks and vitamins, has grown 11 percent in the past year to $146 million, according to Chicago-based market researcher SPINS LLC.
“You have to be very careful when you select and use aloe products,” said Tod Cooperman, president of White Plains, New York-based ConsumerLab.com, which has done aloe testing.
Aloe’s three chemical markers — acemannan, malic acid and glucose — were absent in the tests for Wal-Mart, Target and CVS products conducted by a lab hired by Bloomberg News. The three samples contained a cheaper element called maltodextrin, a sugar sometimes used to imitate aloe. The gel that’s sold at another retailer, Walgreens, contained one marker, malic acid, but not the other two. That means the presence of aloe can’t be confirmed or ruled out, said Ken Jones, an independent industry consultant based in Chapala, Mexico.
23,000 Stores
Target Corp. declined to comment. Spokesmen for Wal-Mart Stores Inc., CVS Health Corp. and Walgreens Boots Alliance Inc. said their suppliers confirmed to them that their products were authentic. The four retailers have 23,000 outlets between them.
Walmart Equate brand Aloe After Sun Gel Photographer: Daniel Acker/Bloomberg
The four gels that Bloomberg had analyzed were Wal-Mart’s Equate Aloe After Sun Gel with pure aloe vera; Target’s Up & Up Aloe Vera Gel with pure aloe vera; CVS Aftersun Aloe Vera Moisturizing Gel; and Walgreens Alcohol Free Aloe Vera Body Gel. The lab that did the testing requested anonymity to preserve its business relationships.
The tests used a technique called nuclear magnetic resonance. It found additives such as maltodextrin and other ingredients, like triethanolamine, an emulsifier. In all the samples, lactic acid, a component that indicates degraded aloe vera, was absent.
Fruit of the Earth, a Fort Worth, Texas-based aloe brand founded in 1980, said it made the gels for Wal-Mart, Target and Walgreens. Fruit of the Earth said its aloe supplier was Ormond Beach, Florida-based Concentrated Aloe Corp., which said it uses fair trade, organic aloe that’s farmed and processed in Guatemala.
Both companies disputed Bloomberg’s findings.
Raw Ingredients
“We’ve been in the business a long time and we know where the raw ingredients come from,’’ John Dondrea, Fruit of the Earth’s general counsel, said in a telephone interview. “We stand behind our products.’’
CVS brand Aftersun Aloe Vera Moisturizing Gel Source: CVS
Tim Meadows, president of Concentrated Aloe Corp., said that nuclear magnetic resonance isn’t reliable for cosmetics because the presence of multiple ingredients can cause interference and there’s no way to test for aloe in finished products. He added that maltodextrin isn’t an adulterant because it can be used in the drying process, and while some ways of processing aloe remove acemannan, that doesn’t mean the aloe isn’t real, he said.
“Acemannan has been misinterpreted,’’ Meadows said. “The cosmetics industry requires highly processed aloe. How that affects acemannan is anybody’s guess.’’
Though it’s true that nuclear magnetic resonance isn’t a test that’s designed to study aloe vera in cosmetics, the lab results suggest that the plant “is not a major component” of the products, said James Neal-Kababick, director of Flora Research Labs in Grants Pass, Oregon, which tests and researches natural products. Jones, the consultant who also reviewed some of the tests, said he didn’t see evidence of aloe or interfering substances.
The CVS aloe gel was made by Product Quest Manufacturing LLC. The Daytona Beach, Florida-based firm declined to comment or identify its supplier.
Lawsuits Filed
Several law firms, including Bloomfield Hills, Michigan-based Barbat, Mansour & Suciu PLLC, have filed lawsuits against the four retailers after separate testing failed to find aloe in the companies’ private-label products. They’re seeking class-action status and restitution for all the customers who they say were misled.
See also: The Parmesan Cheese You Sprinkle on Your Penne Could Be Wood
“No reasonable person would have purchased or used the products if they knew the products did not contain any aloe vera,’’ attorneys wrote in a complaint filed in September in Illinois on behalf of plaintiffs represented by 10 law firms.
Fruit of the Earth, Wal-Mart, Target, CVS and Walgreens denied the allegations.
Independently, ConsumerLab.com said it had Fruit of the Earth brand Aloe Vera 100% Gel tested using nuclear magnetic resonance and found no evidence of aloe, while a competing brand, Aubrey Organics, did contain the markers that indicate aloe. ConsumerLab said it tested a dozen aloe products, including pills and juices, and just half the items appeared to meet the claims on their labels.
Beneficial Properties
Acemannan is thought to give the plant its beneficial properties, said Jane Wilson, executive director of the International Aloe Science Council in Silver Spring, Maryland, which represents the industry.
Walgreens Well brand alcohol free Aloe Vera Body Gel Photographer: Daniel Acker/Bloomberg
Jesper Hummeluhr, founder of Copenhagen-based cosmetics maker Aloe Vera Group APS, said that if acemannan isn’t detected, the aloe was degraded during the manufacturing process or the product contains no aloe. He’s been making aloe products since 1989.
“What you have there is not aloe,’’ said Hummeluhr, who reviewed some of the results without being told the name of the brands. “It could be a lot of water and a little bit of aloe added.’’
Reliability Questioned
Acemannan is as much as 15 percent of aloe’s makeup. Levels below 0.01 percent of dry weight won’t register in the tests. Fruit of the Earth’s Dondrea declined to say how much aloe is in the firm’s gels, citing proprietary formulations.
Aloe vera is a succulent farmed in hot climates like Texas and Mexico. Its spiky leaves contain a clear goo that people have used as a topical ointment to treat burns and other skin problems for millennia. Known as the “plant of immortality” in ancient Egypt, it was depicted on stone carvings 6,000 years ago, a burial gift for pharaohs, and it’s been used as a folk remedy for conditions from diabetes to epilepsy, according to the National Center for Complementary and Integrative Health.
Imitation Aloe
Concerns over imitation aloe aren’t new. The industry created the International Aloe Science Council in the 1980s as more and more products hit store shelves that contained little or no aloe, said Wilson, the group’s executive director. Maltodextrin, a light-colored powder that looks like aloe powder and is used as a food additive, was a common filler or substitute. Maltodextrin is cheaper than aloe, Wilson said.
Target brand Aloe Vera Gel Photographer: Daniel Acker/Bloomberg
Jeff Barrie, a Keene, New Hampshire-based sales manager at AloeCorp, one of the biggest suppliers of raw aloe powder, said he’s seen competitors beat his lowest prices by half. That means they’re not selling aloe, he said. Aloe powder can cost as much as $240 a kilogram, he said, while the same amount of maltodextrin can cost a few dollars.
Making just 1 kilogram of aloe powder, the ingredient used in finished goods like gels and drinks, requires 400 kilos (882 pounds) of aloe leaves, Barrie said. The process involves removing rinds from the leaves and dehydrating the remaining aloe into a powder form.
“Aloe is all harvested by hand,” Barrie said. “It’s an involved process and it’s not cheap.”
There’s no conclusive body of scientific research affirming aloe’s healing properties. While some studies have shown a benefit for burns and cuts, “there’s nothing to hang your hat on” in terms of clear evidence, partly because there hasn’t been enough research, said D. Craig Hopp, a program director at the National Center for Complementary and Integrated Health in Bethesda, Maryland.
Loving Aloe
“There’s a lot of people that swear by aloe and love it, and if you put it in your product, you’ll sell more of it whether it’s a cream or a lotion for sunburns,’’ said Gary Shreeve, a vice president of global operations at Scottsdale, Arizona-based Forever Living Products, which sells aloe certified by the International Aloe Science Council.
Some people are old school about aloe. Rather than buying aloe products, they just keep the succulent around the house.
Meredith Zielke, a documentary filmmaker in Chicago, is one of many aloe lovers who have a simple remedy. She keeps the plant in her home to cool her skin when her Lyme disease acts up. And it works, she said.
“I like just having it at home to snip it from there,” Zielke said. “I just like the comfort and the knowledge of having a plant in your house that can actually heal you.” ||||| The aloe vera plant is known for its ability to heal sunburn and other skin ailments, but customers who bought aloe gel might now have reason to feel even more burned.
Store-branded aloe gel sold at Walmart (WMT), Target (TGT) and CVS (CVS) appears to lack one essential ingredient: aloe vera, according to a new study from Bloomberg News, which commissioned lab to test the products. While all of the products listed aloe vera juice as either their first or second ingredient, none of them included the three chemical markers that signify the presence of aloe vera, the report found.
The findings come amid increased questions about whether more government oversight is required for cosmetics and body-care products, although the Federal Food, Drug and Cosmetic Act bars companies from mislabeling ingredients. Cosmetic products and ingredients don’t require approval from the Food and Drug Administration, other than for color additives.
Questions about such products are regulated were raised last year in the case of Wen Hair Care, a shampoo line that has sparked lawsuits after some customers suffered rashes and hair loss. As for the supposedly aloe-less aloe products, customers have already filed lawsuits that allege false advertising and negligent misrepresentation, among other problems.
“No consumer would have purchased the product had they known it contained no aloe vera,” alleges one of the lawsuits, which was filed in August against Target.
Citing pending litigation, Target said it was unable to comment on Bloomberg’s report.
Walmart isn’t planning to remove the aloe gel product from its shelves, spokesman Randy Hargrove said. “We hold our suppliers to high standards and are committed to providing our customers the quality products they expect. We contacted our supplier, and they stand behind the authenticity of their products,” he said.
The retailer’s supplier, aloe maker Fruit of the Earth, said it disputed Bloomberg’s findings. “We have also had tests conducted on the raw aloe material used in our gel products, which show the presence of the alleged marker (acemannan) that Bloomberg reported finding no evidence of,” general counsel John Dondrea wrote in an email. He
CVS also defended the quality of its aloe gel. “We are committed to bringing high quality products to consumers, and maintain ongoing contact with suppliers to ensure that they meet our high standards,” the company said in a statement. “We have reviewed with the supplier, and they have affirmed the product’s authenticity.”
The aloe vera market is a bright spot for drug stores and other retailers, with the U.S. market for aloe products growing 11 percent in the last year to $146 million, according to Bloomberg, which cites market researcher SPINS LLC.
If there is no aloe vera in the products, as Bloomberg alleges, what’s actually inside the bottles? The testing found maltodextrin, which the report notes is a cheaper ingredient that is sometimes used as a filler in aloe products. The aloe vera gel samples tested by Bloomberg found no trace of acemannan, malic acid and glucose, the three chemical markers for aloe. Walgreens’ aloe gel included malic acid, but lacked the other two, Bloomberg noted.
ConsumerLab.com, a company that conducts independent tests on health and nutrition products, said that its testing found that only about half of aloe products contained satisfactory levels of aloe, with many having only a small amount or none at all.
Aloe vera users have one way to make sure they are applying the real deal: Use an actual aloe vera plant. Many consumers keep one in their home, and cut a leaf on the succulent when they want to rub some gel on a cut or burn.
Even so, it might be best to take its healing properties with a grain of salt, since the National Center for Complementary and Integrated Health notes that there’s not enough evidence to conclude whether it’s as useful as devotees of the plant believe. |||||
What is a shorter version of the above article? | – Tests conducted on the aloe vera gels sold by some of America's biggest retailers failed to detect any trace of the ingredient you would most expect to find in a product calling itself aloe vera gel. Bloomberg says the lab it hired to test aloe vera products from Walmart, Target, and CVS couldn't find the three chemical markers associated with the plant, but it did find maltodextrin, a much cheaper product sometimes used in place of genuine aloe. Tests on aloe vera gel from another retailer, Walgreens, found just one of the markers, malic acid, which experts say isn't enough to confirm the presence of the plant. The products all listed the plant at the No. 1 or No. 2 ingredient, after water. The FDA has never levied a fine for using fake aloe, putting retailers on what Bloomberg calls an "honor system." Aloe gel supplier Fruit of the Earth has disputed the finding, and CVS and Walmart both say they are standing by their suppliers. Target declined to comment, citing pending lawsuits, one of which states: "No consumer would have purchased the product had they known it contained no aloe vera," per CBS News. Aloe vera has been used as an ointment for thousand of years. Joe Barrie of AloeCorp, one of the the biggest suppliers of aloe vera powder, tells Bloomberg that some competitors are selling for half of his lowest price, suggesting that what they're selling isn't aloe. He says it can take more than 200 pounds of aloe leaves to make a single pound of the powder. "Aloe is all harvested by hand," he says. "It’s an involved process and it’s not cheap." (A study of herbal supplements found a disturbing lack of herbs.) | multi_news_1_0_0 |
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Carbohydrates: How carbs fit into a healthy diet Carbohydrates aren't bad, but some may be healthier than others. See why carbs are important for your health and which ones to choose. By Mayo Clinic Staff
Carbohydrates often get a bad rap, especially when it comes to weight gain. But carbohydrates aren't all bad. Because of their numerous health benefits, carbohydrates have a rightful place in your diet. In fact, your body needs carbohydrates to function well.
But some carbohydrates might be better for you than others. Understand more about carbohydrates and how to choose healthy carbohydrates.
Understanding carbohydrates
Carbohydrates are a type of macronutrient found in many foods and beverages. Most carbohydrates occur naturally in plant-based foods, such as grains. Food manufacturers also add carbohydrates to processed foods in the form of starch or added sugar.
Common sources of naturally occurring carbohydrates include:
Fruits
Vegetables
Milk
Nuts
Grains
Seeds
Legumes
Types of carbohydrates
There are three main types of carbohydrates:
Sugar. Sugar is the simplest form of carbohydrate and occurs naturally in some foods, including fruits, vegetables, milk and milk products. Types of sugar include fruit sugar (fructose), table sugar (sucrose) and milk sugar (lactose).
Sugar is the simplest form of carbohydrate and occurs naturally in some foods, including fruits, vegetables, milk and milk products. Types of sugar include fruit sugar (fructose), table sugar (sucrose) and milk sugar (lactose). Starch. Starch is a complex carbohydrate, meaning it is made of many sugar units bonded together. Starch occurs naturally in vegetables, grains, and cooked dry beans and peas.
Starch is a complex carbohydrate, meaning it is made of many sugar units bonded together. Starch occurs naturally in vegetables, grains, and cooked dry beans and peas. Fiber. Fiber also is a complex carbohydrate. It occurs naturally in fruits, vegetables, whole grains, and cooked dry beans and peas.
More carbohydrate terms: Net carbs and glycemic index
Terms such as "low carb" or "net carbs" often appear on product labels. But the Food and Drug Administration doesn't regulate these terms, so there's no standard meaning. Typically "net carbs" is used to mean the amount of carbohydrates in a product excluding fiber, or excluding both fiber and sugar alcohols.
You probably have also heard talk about the glycemic index. The glycemic index classifies carbohydrate-containing foods according to their potential to raise your blood sugar level.
Weight-loss diets based on the glycemic index typically recommend limiting foods that are higher on the glycemic index. Foods with a relatively high glycemic index ranking include potatoes and white bread, and less healthy options such as snack foods and desserts that contain refined flours.
Many healthy foods, such as whole grains, legumes, vegetables, fruits and low-fat dairy products, are naturally lower on the glycemic index.
How many carbohydrates do you need?
The Dietary Guidelines for Americans recommends that carbohydrates make up 45 to 65 percent of your total daily calories.
So, if you get 2,000 calories a day, between 900 and 1,300 calories should be from carbohydrates. That translates to between 225 and 325 grams of carbohydrates a day.
You can find the carbohydrate content of packaged foods on the Nutrition Facts label. The label shows total carbohydrates — which includes starches, fiber, sugar alcohols, and naturally occurring and added sugars. The label might also list separately total fiber, soluble fiber and sugar.
Carbohydrates and your health
Despite their bad rap, carbohydrates are vital to your health for a number of reasons.
Providing energy
Carbohydrates are your body's main fuel source. During digestion, sugars and starches are broken down into simple sugars. They're then absorbed into your bloodstream, where they're known as blood sugar (blood glucose).
From there, glucose enters your body's cells with the help of insulin. Glucose is used by your body for energy, and fuels all of your activities — whether it's going for a jog or simply breathing. Extra glucose is stored in your liver, muscles and other cells for later use, or is converted to fat.
Protecting against disease
Some evidence suggests that whole grains and dietary fiber from whole foods help reduce your risk of cardiovascular diseases. Fiber may also protect against obesity and type 2 diabetes. Fiber is also essential for optimal digestive health.
Controlling weight
Evidence shows that eating plenty of fruit, vegetables and whole grains can help you control your weight. Their bulk and fiber content aids weight control by helping you feel full on fewer calories. Contrary to what low-carb diets claim, very few studies show that a diet rich in healthy carbohydrates leads to weight gain or obesity.
Choose your carbohydrates wisely
Carbohydrates are an essential part of a healthy diet, and provide many important nutrients. Still, not all carbs are created equal.
Here's how to make healthy carbohydrates work in a balanced diet:
Emphasize fiber-rich fruits and vegetables. Aim for whole fresh, frozen and canned fruits and vegetables without added sugar. Other options are fruit juices and dried fruits, which are concentrated sources of natural sugar and therefore have more calories. Whole fruits and vegetables also add fiber, water and bulk, which help you feel fuller on fewer calories.
Aim for whole fresh, frozen and canned fruits and vegetables without added sugar. Other options are fruit juices and dried fruits, which are concentrated sources of natural sugar and therefore have more calories. Whole fruits and vegetables also add fiber, water and bulk, which help you feel fuller on fewer calories. Choose whole grains. Whole grains are better sources than refined grains of fiber and other important nutrients, such as B vitamins. Refined grains go through a process that strips out parts of the grain — along with some of the nutrients and fiber.
Whole grains are better sources than refined grains of fiber and other important nutrients, such as B vitamins. Refined grains go through a process that strips out parts of the grain — along with some of the nutrients and fiber. Stick to low-fat dairy products. Milk, cheese, yogurt and other dairy products are good sources of calcium and protein, plus many other vitamins and minerals. Consider the low-fat versions, to help limit calories and saturated fat. And beware of dairy products that have added sugar.
Milk, cheese, yogurt and other dairy products are good sources of calcium and protein, plus many other vitamins and minerals. Consider the low-fat versions, to help limit calories and saturated fat. And beware of dairy products that have added sugar. Eat more legumes. Legumes — which include beans, peas and lentils — are among the most versatile and nutritious foods available. They are typically low in fat and high in folate, potassium, iron and magnesium, and they contain beneficial fats and fiber. Legumes are a good source of protein and can be a healthy substitute for meat, which has more saturated fat and cholesterol.
Legumes — which include beans, peas and lentils — are among the most versatile and nutritious foods available. They are typically low in fat and high in folate, potassium, iron and magnesium, and they contain beneficial fats and fiber. Legumes are a good source of protein and can be a healthy substitute for meat, which has more saturated fat and cholesterol. Limit added sugars. Added sugar probably isn't harmful in small amounts. But there's no health advantage to consuming any amount of added sugar. The Dietary Guidelines for Americans recommends that less than 10 percent of calories you consume every day come from added sugar.
So choose your carbohydrates wisely. Limit foods with added sugars and refined grains, such as sugary drinks, desserts and candy, which are packed with calories but low in nutrition. Instead, go for fruits, vegetables and whole grains.
||||| Bacon became my new best friend on the ketogenic diet. Business Insider
A viral diet that's been found to burn up to 10 times as much fat as a standard diet is gaining momentum among Silicon Valley tech workers. And it involves eating a lot of fat.
The ketogenic, or "keto," diet — which first became popular in the 1920s as a treatment for epilepsy and diabetes— limits carbohydrates to no more than 50 grams a day, which is the rough equivalent of a plain bagel or a cup of white rice. By comparison, dietary guidelines from the US Department of Agriculture recommend from 225 to 325 grams of carbs a day.
On the keto diet, the body goes into starvation mode and taps its fat stores for fuel. Studies suggest the low-carb, high-fat diet may promote weight loss, improve focus, and stave off age-related diseases. More research is needed on its long-term effects, especially among healthy people.
A small study recently published in the journal Diabetes and Metabolic Syndrome found that adults who had been diagnosed with metabolic syndrome (a precursor of diabetes) and ate a ketogenic diet had resting metabolic rates (a measure of how much energy your body burns when at rest) more than 10 times as high as people who ate a standard diet.
Last year, I spent two months eating bacon, butter, and avocados to see why the keto movement is so popular with tech workers. Here's what it was like. ||||| I am no stranger to diets. I've cut sugar, counted points on Weight Watchers, and swapped solid food for Soylent, a venture-capital-backed meal-replacement shake. I gave up breakfast for a week and drank this caffeinated meal-replacement shake instead »
But those usually don't last long. I love food. I'm a chronic snacker.
When I learned about the keto diet, it caught my interest because dieters could eat seemingly unlimited amounts of healthy fats, like cheese, nuts, avocado, eggs, butter — foods that have high "point values" on Weight Watchers and are severely restricted. The keto diet reorganizes the building blocks of the food pyramid. It cuts down carbs to 20 to 50 grams a day, depending on a person's medical history and insulin sensitivity. (There are about 30 grams in one apple or half of a plain bagel.) On the diet, healthy fats should be about 80% of a person's daily calories, while protein should be about 20%. On average, Americans get about 50% of their calories from carbs, 30% from fat, and 15% from protein, according to the Centers for Disease Control and Prevention.
The keto diet is like Atkins on steroids. It turns the body into a fat-burning machine. The human body breaks down carbohydrates into glucose, which is used for energy or stored as glycogen in liver and muscle tissue. But it has a plan-B fuel supply. When carbs go missing from a person's diet, the body uses up its glucose reserves and then breaks down stored fat into fatty acids, which, when they reach the liver, are converted into an organic substance called ketones. The brain and other organs feed on ketones in a process called ketosis, which gives the diet its name. Keto dieters eat lots of fat to maintain this state. While the low-carb diet dates back to the 1920s, when it was found to reduce seizures in people living with epilepsy, Dr. Robert Atkins popularized a version of it in the '60s and '70s. Like the keto diet, the Atkins diet restricts carb consumption to 20 to 25 grams a day during an introductory phase, but then ramps up to 80 to 100 grams a day. So it's less strict than keto.
But the keto diet is not for everyone, so I sought medical supervision. Dr. Priyanka Wali is an internal-medicine physician with specialty training in obesity medicine. She uses the keto diet routinely for her patients who have insulin resistance, pre-diabetes, and diabetes. In 2014, Wali was moonlighting at a weight-loss clinic in San Francisco, where she saw her patients struggle to stick to their strict diet programs and maintain their weight loss. She started reading studies on low-carb diets and became convinced it was the solution. Wali made herself a guinea pig before she prescribed the diet. And it worked. She said she "expected to feel a lot of adverse side effects" from eating so much fat, "but what ended up happening was I felt great." "I started to have more energy and concentration," Wali said. "I didn't lose weight, but my fat distribution changed, so I lost weight from my hips."
After asking me about my family history and my reasons for trying the keto diet, Wali determined I was an "optimizer," like the healthy tech workers who rely on the diet. Tech workers living in the Bay Area sometimes go to extreme lengths to improve their bodies and minds. For example, at the supplements startup HVMN (formerly known as Nootrobox), most employees don't eat on Tuesdays — a ritual they say improves ketone production and productivity. Intermittent fasting has been found to assist ketosis. To see whether I was a good fit for the keto diet, Wali requested I have some lab work done, including a cholesterol panel and a fasting-insulin-level test. My results came back normal, meaning there was no medical necessity for me to go on the diet. If I were pre-diabetic or insulin-resistant, Wali would likely have made the keto diet part of my treatment.
Wali introduced me to the "keto food pyramid," via this image that went viral on Reddit. We agreed that for my first week on the keto diet, I would aim for 30 to 50 grams of carbs during the day and eat regular, carb-heavy dinners, even if they took me over the limit. "Sugar addiction is a real thing," Wali told me in our first meeting. She wanted me to ease into ketosis to avoid "carbohydrate withdrawal," which can cause irritability, depression, headaches, lethargy, and nausea. I was happy to take it slow. As I was learning the carb loads of different foods in those first few weeks, I tracked my meals on the Fitbit and Weight Watchers apps, but Wali says paper and pen works just as well.
She taught me how to count carbs the smart way: Carbohydrates - dietary fiber = net carbs. Fiber is a carbohydrate that the body can't digest. It doesn't raise blood-sugar levels, so there's no use in counting grams of dietary fiber toward a daily carbohydrate goal. A cup of almonds has about 20 grams of carbohydrates, but 12 of those come from dietary fiber. As a result, I had to count only 8 grams for the serving. What a bargain!
Pasta was off the menu. A cup of cooked whole-wheat noodles has about 41 net carbs, which would blow through my daily carb allowance in one small portion.
I had to be careful even with fruits and starchy vegetables. A cup of blueberries has about 11.5 net carbs. It's also low in fiber, so it's not very filling for long.
When I got home from my visit with Wali, I was forced to rethink all my dietary staples. I let my boyfriend finish off our supply of apples, bananas, bread, pasta, rice, and potatoes.
And I said yes to fat. A typical breakfast included a coffee with half-and-half, along with cheesy eggs cooked in butter and two slices of bacon. Some mornings I scrambled to find 20 minutes to make breakfast. Few restaurants had dishes that met my dietary restrictions. I ate a sad, tortilla-less breakfast burrito once. I managed to find one restaurant, La Boulangerie in San Francisco, that makes scrambled eggs with mix-ins to order. I swapped potatoes for a side salad and tossed the toast. It cost $11.
For lunch, I ate a lot of "sad desk salads." Two cups of leafy greens, an ounce of cheddar cheese, a handful of nuts, and avocado or cauliflower rang up about 6 net carbs.
Our office has the best snacks — Goldfish, Nature Valley bars, animal crackers, and peanut-butter-filled pretzels (my personal brand of indulgence). I thought of them often. I used to snack every hour between 10 a.m. and dinner. Food was always on my mind. In my first week, I dug up the willpower to resist those sugar binges. But it was not without consequences. My headaches pounded for hours on end. My mind said, "Eat something." Wali recommended I drink more water and salt my food to ease the headaches.
I scoured keto blogs for high-fat snacks — called "fat bombs" — to power me through the sugar cravings. Loaded cauliflower made with butter, sour cream, cheddar cheese, and bacon became my go-to treat. The keto comfort food didn't make me feel deprived. Here's the recipe for loaded cauliflower »
During Week 2, my ketone-testing meter kit arrived in the mail. The pocket-sized medical device uses a small blood sample to measure the presence of ketones. A doctor can prescribe a ketone-testing meter to people with diabetes, but insurance may not cover it. Optimizers like me turn to Amazon for third-party sellers. I bought the Precision Xtra glucose-meter kit (which also measures ketones) for $22, and a 10-pack of ketone testing strips for $42. The meter has since gone up to about $60 on Amazon. Keto adherents use ketone-testing meters to check whether they're in a state of nutritional ketosis — generally considered to be above 0.3 millimoles per liter of blood, according to Wali. Entrepreneurs sometimes share their ketone levels on social media. It's the biohacking community's equivalent of posting photos of a bathroom scale to celebrate recent weight loss.
My first encounter with a lancing device, a tool that draws blood from the fingertip, was not particularly pleasant. Afterward, I held the ketone-testing meter to the drop of blood.
I got 0.4 mmol/L, a low-level state of nutritional ketosis. In less than two weeks on the diet, my body had flipped the switch from burning carbs to burning fat as its primary fuel source.
Three weeks in, I felt the difference. Even on days when I ate bun-less cheeseburgers for lunch, my energy was sky-high. I no longer needed coffee to stay awake in the afternoon.
I suddenly could go three, four, even five hours without thinking about food. My snacking became much less frequent, and I became more focused on work as a result. Dr. Jason Fung, who specializes in kidney care, offers an analogy in his book "The Obesity Code." Imagine sitting down to an all-you-can-eat buffet. At some point, the idea of eating one more pork chop becomes sickening. But if the dessert cart passes, it's hard to resist. That's because highly refined carb-filled foods, like cake and pie, don't trigger hormones in the brain that say: "You're full. Stop eating." Proteins and fat can signal when you've had enough.
When I splurged on a bagel or pizza, which did happen, I wanted to curl up under my desk and nap within 30 minutes of eating. I felt uncomfortably full and groggy. The worst part of cheating was that it had the potential to reverse a state of nutritional ketosis. When my parents came to town over one weekend and I went rogue, I wound up with a ketone reading of 0.3 mmol/L, meaning my body was burning more carbs than fat. I returned to the diet that Monday, but it takes an average of five days for the body to use up the leftover glycogen reserves and return to nutritional ketosis, Wali says.
To avoid the ill feelings that carbs gave me, I experimented more in the kitchen. I learned that pizza made with a baked cauliflower crust was not pizza. It tastes like a vegetable casserole, but at least I don't wake up feeling bloated.
Eating at restaurants was the hardest part. I ate taco fillings out of tortillas and scraped the breading off fried chicken. Every menu had just one or two things I could order guilt-free.
After eating mostly fat, protein, and leafy vegetables for one month, I reached my peak ketone reading of 0.9 mmol/L — a strong indication that I reached a state of ketosis. By this point in my journey, most of the negative side effects had subsided. (I experienced leg cramps and tingling sensations in my feet, which Wali said was from eating too little salt. She suggested I try magnesium supplements, and the problem went away within days.) A ketone reading of 0.9 mmol/L indicates a mild state of ketosis. Dieters can reach higher levels — "go deeper" into ketosis — by restricting carbs to fewer than 20 grams a day or fasting. But there isn't consensus in the medical community that doing so unlocks additional benefits. Geoff Woo, the cofounder and CEO of HVMN, said he aimed for 3.0 mmol/L or higher, which he achieves through intermittent fasts that spike ketone production, for "optimal mental flow." When I started to obsess over the numbers my ketone testing meter gave me, Wali encouraged me to instead focus on how I felt.
It was then that I realized why I loved eating keto — it made me feel like a superhero. When I lost 30 pounds on Weight Watchers in college, I celebrated the numbers on the scale and how my clothes fit. But because I continued to eat carbs in smaller portions, I was still prone to sugar crashes and afternoon "brain fog." The transformation was incomplete. The keto diet made over my mind and my body. The sense of mental clarity and energy that came on about three to four weeks into eating keto was unlike anything I've experienced. I woke up feeling strong, confident, and capable of taking on whatever the day threw at me. "This is how you're supposed to feel as a human being," Wali said during a follow-up visit. |||||Summary:
| – Silicon Valley techies adopt some unusual eating habits to boost productivity, including one firm where workers fast on Tuesdays. Melia Robinson wanted to see how one of these dieting regimens would affect her, and she concludes for Business Insider that it "vastly improved my life." The course she followed: the ketogenic, or keto, diet, which deprives the body of carbohydrates—just 50 grams a day instead of the recommended 225 to 325 grams daily—and sends it into "starvation mode." What it then burns instead: a person's fat stores, which are broken down into organic byproducts called ketones, which then become the body's main fuel supply. To keep the fat stores well stocked, that means individuals on this diet have to scarf down plenty of cheese, eggs, and avocados. Off the menu: pasta, bread, rice, and other carb-heavy foods, including some fruits. And so, under the direction of a doctor, Robinson followed a routine she calls "Atkins on steroids." That meant breakfasts of butter-fried eggs and greasy bacon, as well as lunches consisting of "sad desk salads." Robinson sated hunger pangs in between with "fat bomb" snacks (her favorite: cauliflower smothered in butter, sour cream, and cheese). After just two weeks, she says her body "flipped the switch" and started using up her body fat to replace the carbs it had previously burned. Then her energy spiked, she no longer needed coffee as an afternoon pick-me-up, and her obsession with snacking waned. One month in, Robinson reached a "state of ketosis," with few remaining side effects. She not only lost 8 pounds over two months, but she experienced better concentration and more energy. "It made me feel like a superhero," she writes. More on Robinson's eating experiment here. | multi_news_1_0_0 |
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– A new study suggests that a woman's diet plays a role in when menopause begins. UK researchers emphasize that their research doesn't show cause and effect—meaning they're not advocating that anyone change their diet—but the bottom-line findings are drawing attention. The average age of menopause in the study was 51, but women who ate a diet high in refined white pasta or rice tended to see it start about a year and a half earlier, reports New Scientist. On the other hand, those who ate a lot of oily fish (salmon, sardines, and mackerel) generally saw it begin three years later than usual, reports Live Science. A diet rich in legumes (think peas and beans) also was associated with a later onset, though to a lesser degree than oily fish. "This study doesn't prove a link with the foods mentioned, but certainly contributes to the limited knowledge we currently have on why some women go through menopause earlier than others," a nurse who serves as chairwoman of the British Menopause Society tells the BBC. In their study in the Journal of Epidemiology and Community Health, the researchers theorize that legumes and oily fish keep menstruation going because they contain or stimulate antioxidants, while the refined carbs have the opposite effect by raising the risk of insulin resistance and interfering with sex hormones. While early menopause is linked to a higher risk of osteoporosis and heart disease, it's also linked to protection against breast and ovarian cancer, notes Live Science.
Article: |
The limited number of studies and contradictory results 10–12 in this area suggests the need for further cohort studies with detailed dietary intake measures to clarify this association. The aim of this analysis was to explore the associations between food groups and nutrient intake in a large cohort of British women with age at incident natural menopause. We hypothesised that intake of healthier food groups such as fruits and vegetables would be associated with an earlier menopause while a high consumption of meat and processed meat would delay the onset of menopause.
A number of causes have been postulated for the relationship between age at menopause and these health outcomes, such as genetic factors, behavioural and environmental exposures, socio-demographic factors, hormonal mechanisms and health-related factors. 9 Diet can also be an underlying factor. 9 Two large cohort studies have also hypothesised an association 10 11 but reported conflicting findings.
The average age of menopause in the UK is reported to be 51 years. 1 Menopause is an important phase in a woman’s life indicating the end of the reproductive life span with reduction in oestrogen and increased progesterone levels. 2 3 Several studies have documented an association between earlier age at natural menopause and lower bone density, osteoporosis, depression and premature death. 4 5 Other studies have shown increased risk of cardiovascular and coronary diseases. 6 7 In contrast, a late menopause has been associated with a higher risk for breast, ovarian and endometrial cancers. 8
Descriptive statistics were used to explore the socio-demographic and obstetric history of the women. Linear regression models were used to determine the relationships between the various food groups (continuous exposure in g/day) as well as nutrients (continuous exposure) and age at natural menopause (continuous outcome in years). In addition, because younger women at baseline have less chance of a later menopause we evaluated the associations by stratifying on age at baseline (≤50 vs >50 years). An estimate >0 was considered as a later age at natural menopause. Assumptions for linear regression were checked by plotting the residuals against fitted values which showed a constant variance and a histogram demonstrated a normal distribution of the residuals. Due to the differences in age at natural menopause by vegetarian status and parity as evidenced by previous studies, 10 18 sensitivity analysis exploring that relationship was undertaken stratified by vegetarian status and parity (nulliparous vs multiparous). Moreover, since presence of diabetes might influence both diet and age at natural menopause, we also adjusted for diabetes. To take account of multiple testing, the significance level was set at 1% with 99% CIs. All analyses were conducted using Stata V. 14.0 (StataCorp).
A directed acyclic graph (DAG) (online supplementary figure 1 ) with diet (food groups) as the main exposure and age at natural menopause (continuous) as the outcome was generated to determine confounding variables. Based on available literature and data collected, potential confounding variables (age, parity, energy intake, body mass index (BMI), social class, age at first full-term pregnancy, age at menarche, smoking, alcohol consumption and physical activity) were included in the DAG. According to the minimal sufficiency set of adjustments, physical activity (MET-hours/week), smoking status (current vs not current smoker), alcohol consumption (g/day) and social class (routine and manual, intermediate, professional and managerial) were identified as confounders and were thus adjusted for in the regression models. For the associations between nutrient intake and age at natural menopause, total energy intake was also adjusted for the non-energy-containing nutrients (women were excluded if they had extremely high (>6000 kcal/day) or low (<500 kcal/day) energy intake) and energy from other macronutrients was adjusted for specific macronutrients.
Dietary assessment at baseline involved a detailed 217-item food frequency questionnaire (FFQ) derived from the FFQ which was validated on a subsample of 303 cohort subjects against a 4-day food diary as well as fasting blood measures of specific nutrients. 13 15 16 Using the different frequency categories of the FFQ, the number of daily portions for the 217 food items was defined. These were consequently converted into weight of each food consumed per day based on the Food Standards Agency portion sizes book. 17 For the current study, the individual food items were collated into food groups according to their culinary uses (eg, Mediterranean vegetables, cruciferous vegetables, citrus family fruits) and nutrient profile (eg, fat or fibre content) (online supplementary table 1 ). In total, 15 food items were considered individually. Seven food items were considered individually due to their specific nutrient profile such as textured vegetable proteins, oily fish, shellfish, grapes, herbal tea, tea and wines, which have antioxidant properties and might separately affect age at natural menopause. The remaining eight food items (eg, tomatoes, sauces, low calorie salad cream, etc) were considered indivdually because they could not be collated under any of the other food groups. Furthermore, in order to have a better estimate for the difference in mean age at natural menopause across the different food groups, results were presented per portion size.
In total, 14 172 women who participated at both baseline and follow-up were considered for this study. Information was collected on demographic details, weight history, physical activity, reproductive history (age at last period; number of periods in last 12 months; use of hormone replacement therapy (HRT)), anthropometric and other health-related factors at baseline as well as at follow-up. Participants who experienced a natural menopause at follow-up were identified through comparison of baseline and follow-up data. Natural menopause was defined as the permanent cessation of the menstrual periods for at least 12 consecutive months. 2 Menstruating women, that is, those having one or more menstrual period in the last 12 months at baseline and who became naturally postmenopausal at follow-up were included in the final analysis. Inclusion criteria also comprised never used HRT at baseline and currently not using HRT at follow-up (as HRT use may influence the bleeding pattern among premenopausal women 14 ). Women who ever used HRT after reaching menopause at phase II were also included. Women who had bilateral oophorectomy and hysterectomy at baseline as well as pregnant women at baseline were excluded from the study. In addition, only women with an age at natural menopause between ≥40 and ≤65 years were included (as no menstruation before the age of 40 might be chemically induced or due to surgical procedures). In addition, participants with missing data on the main study outcome, age at natural menopause and confounders were also excluded from the study ( figure 1 ).
The UK Women’s Cohort Study (UKWCS) is a large prospective study consisting of 35 372 women aged between 35 and 69 years. Recruited participants were from England, Scotland and Wales. 13 Baseline data were collected between the years 1995 and 1998 via postal questionnaire. Follow-up data were collected on average 4 years later, between the years 1999 and 2002. 13
Sensitivity analysis by parity demonstrated a difference for the association between the various food groups and age at natural menopause for nulliparous against the multiparous participants. In multiparous women, a later onset of age at natural menopause was found to be associated with an increased intake of oily fish (per portion/day: 3.3 years, 99% CI 0.3 to 6.3) and fresh legumes (per portion/day: 1.1 years, 99% CI 0.1 to 2.01) while an increase in intake of refined pasta and rice (per portion/day: −1.9 years, 99% CI −3.3 to −0.4) as well as savoury snacks (per portion/day: −1.0 years, 99% CI −2.1 to −0.0) was associated with an earlier age at natural menopause. For nulliparous women, a higher consumption of grapes (per portion/day: 2.5 years, 99% CI 0.0 to 4.9) and poultry (per portion/day: 5.2 years, 99 % CI 0.1 to 10.3) was found to be significantly associated with a later age at natural menopause (online supplementary table 3 ).
Our findings demonstrated that non-vegetarians reach a natural menopause 0.8 years later compared with vegetarians (99% CI 0.2 to 1.4). Exploring associations for non-vegetarians alone showed they had an earlier age at natural menopause associated with an increased consumption of savoury snacks (per portion/day: −1.7 years, 99% CI −3.1 to −0.4) and soft drinks (per portion/day: −1.3 years, 99% CI −2.5 to −0.2) while an increase in intake of oily fish (per portion/day: 3.4 years, 99% CI 0.2 to 6.5) and fresh legumes (per portion/day: 1.4 years, 99% CI 0.2 to 2.7) were associated with a later onset of menopause (online supplementary table 2 ).
For the association between nutrients and age at natural menopause, a later age at natural menopause by approximately 0.6 years was found with a higher intake of vitamin B6 per mg (99% CI 0.1 to 1.2). Similarly, a higher intake of zinc was associated with a delayed age at natural menopause by 0.3 years per mg (99% CI −0.0 to 0.6) ( table 3 ). Stratification by age at baseline further demonstrated that a higher intake of carbohydrates was associated with an earlier age at natural menopause by 0.2 years (99% CI −0.4 to −0.0) among women 50 years or below.
An increase in portion size of refined pasta and rice as well as savoury snacks was associated with an earlier age at natural menopause by 1.8 years (99% CI −3.0 to −0.5) and 0.9 years (99% CI −1.7 to −0.1), respectively in the unadjusted model ( table 2 ). In the adjusted model, for each additional portion of oily fish and fresh legumes, age at menopause was increased by 3.3 years (99% CI 0.8 to 5.8) and 0.9 years (99% CI 0.0 to 1.8), respectively. On the other hand, a higher intake of refined pasta and rice (per portion/day: 1.5 years; 99% CI −2.8 to −0.2) was associated with an earlier menopause. Stratification by age at baseline led to reduced associations between the various food groups and age at natural menopause. The CIs were wider because of the smaller samples in these subgroups.
Of the 1874 women who were premenopausal at baseline survey (and had self-reported age at natural menopause at follow-up), 914 had become postmenopausal at 4-year follow-up. Baseline characteristics of the participants are outlined in table 1 . The mean age at natural menopause at follow-up was 50.5 years (95% CI 50.3 to 50.8). Participants had a mean BMI of 23.9 kg/m 2 (95% CI 23.6 to 24.1) and 9.6% were categorised as obese. Physical activity level was quite low among the participants with a mean of 15 min/day. This study also included 38% vegetarian participants. Most of the women were married, parous and of professional and managerial class. In this study, only 8% of women smoked and the mean alcohol consumption was 9 g/day (around one unit).
Discussion
This is the first study of women in the UK to report on food and nutrient intake in relation to age at incidence of natural menopause. Of 14 172 women who were followed up for approximately 4 years, 914 women went through a natural menopause. The mean age at natural menopause was 50.5 years with a median age of 51 years. We found that intakes of oily fish and fresh legumes were associated with later age at menopause and intake of refined pasta/rice was associated with an earlier menopause. Only a few previous studies have reported diet in relation to age at natural menopause with a limited number of food items/groups included.10 12 Previous research has mainly been focused on the relationship between socio-demographic as well as lifestyle factors (education status, marital status, parity, etc) and age at natural menopause.18–21
Our results demonstrate that each additional increment in fresh legumes portion/day was associated with a later age at natural menopause by 0.9 years. Fresh legumes are a good source of antioxidants, which can partly explain this association. This has been supported by the biochemical and molecular analyses undertaken by Matamoros et al.22 Similarly, in a Japanese prospective study the antioxidant properties of green and yellow vegetables were postulated for the association between a higher intake of the green and yellow vegetables and a later age at natural menopause.12 Oocyte maturation, ovulation, luteolysis and follicle atresia are affected by reactive oxygen species (ROS). Phenolic compounds, vitamins and carotenoids in vegetables counteract the ROS and may thus decrease the proportion of follicles undergoing follicular atresia.23 24 Further support of this theory from our findings was a later age at natural menopause with a high intake of vitamin B6 and zinc as both of these have antioxidant properties.23 25 Likewise, Stepaniack et al 26 demonstrated an association between use of vitamin and mineral supplements and a later menopause.
Our findings demonstrate a later age at natural menopause by approximately 3 years for each additional portion/day of oily fish. However, in contrast to our findings, a recent review article as well as a 10-year follow-up study reported an earlier onset of menopause with high intake of polyunsaturated fats.27 28 Nagel et al 10 reported no association between fish intake and age at natural menopause but it was not clear if oily fish was considered separately. Oily fish is a rich source of the omega-3 fatty acid which can potentially improve antioxidant capacity.29 Therefore, in a similar way to the fresh legumes and vitamins described above, the antioxidant properties exerted by the oily fish intake could possibly offset ROS, therefore decreasing the proportion of follicles undergoing follicular atresia and delaying onset of natural menopause.
In the present study, increasing refined pasta and rice consumption was associated with an earlier age at natural menopause. The EPIC-Heidelberg study also reported a similar association.10 High consumption of refined carbohydrates (classified as high glycaemic index foods) increases the risk of insulin resistance. Insulin resistance can lead to decreased sex hormone binding globulin levels (SHBG) as a result of the inhibitory effect of insulin on the SHBG production in the liver30 as well as increased oestrogen levels.31 High oestrogen levels cause release of the luteinising hormones which triggers ovulation, which might imply more cycles and rapid depletion of oocytes, consequently leading to an earlier menopause.32 This can be supported by a recent review study which reported that women with type II diabetes mellitus tend to have an earlier menopause although additional evidence is required to clarify this association.33
Although we found that fresh legumes are associated with a later menopause, our study further demonstrated that women who were vegetarian had an earlier age at natural menopause compared with non-vegetarians. This finding is in line with other studies which also reported an earlier age at natural menopause among vegetarians.34 35 The vegetarian diet, which normally consist of high fibre and no animal fat-containing foods, may affect the levels of the luteinising hormone, follicle stimulating hormone and the length of the menstrual cycle.36 Previous studies have demonstrated that high fibre and decreased fat intakes were both associated with a lower oestrogen level, which may account for the earlier age at natural menopause among vegetarians.37 38 However, caution should be taken in interpreting this finding as vegetarian status was self-reported in this study.
It is possible that results for younger women may differ from those for older women. This could result from different diets between younger and older women,39 and that younger women have less opportunity to report a later menopause. To explore this, stratifying on age at baseline showed reduced associations within each subgroup.
This is the first study looking prospectively at the relationship between diet and age at natural menopause in the UK. Strengths of this study include the investigation of the association between individual nutrients and a wide variety of food groups and age at natural menopause compared with similar few previous studies. Careful adjustment for likely confounders was also carried out in the regression modelling using the DAG. A limitation of this prospective cohort study is that diet was reported by the participants using an FFQ and may thus be subjected to recall bias. However, FFQ enables recording of a long-term diet, thus showing its cumulative influence on the outcome while food diaries/24-hour recall give only a snapshot of the diet. Our sample was also more health conscious given the high number of vegetarians in our sample population and more well-off participants than the general population as shown in the descriptive table (table 1). However, our study still includes women from a range of different background which implies that findings of this study may be extrapolated to other countries.
Women with an earlier menopause spend more years deprived from the benefits of oestrogen compared with women who become menopausal around the normal menopausal age range, which puts them at a greater risk of some future poor health outcomes such as osteoporosis and heart disease. On the other hand, women with a later onset of menopause are at greater risk of breast, endometrial and ovarian cancers. Our findings confirm that diet may be associated with the age at natural menopause. This may be relevant at a public health level since age at natural menopause may have implications on future health outcomes. Health practitioners might thus also need to take into account the diet of women when dealing with menopause-related issues.
In summary, our study is the first to demonstrate that diet is associated with age at natural menopause in a large cohort of British women. Intakes of oily fish and fresh legumes were found to be associated with a later onset of natural menopause while higher intake of refined pasta and rice was associated with younger age at natural menopause. The nutrients vitamin B6 and zinc were also found to be associated with a later age at natural menopause. Women who were vegetarian had an earlier age at natural menopause compared to non-vegetarians.
What is already known on this subject Several factors including socio-demographic and reproductive factors are associated with age at natural menopause. Limited existing studies present conflicting evidence between diet and age at natural menopause. ||||| Eating certain foods may be linked to a delayed or hastened onset of menopause, a new study from England finds.
Chowing down on fresh legumes, such as peas and green beans; and oily fish, such as salmon, sardines and mackerel; may be linked to a delay in the onset of menopause, while eating refined carbs, such as rice and pasta, may be linked to an earlier onset, the researchers found.
However, the study found only a correlation between diet and the timing of menopause; the study didn't look at what mechanisms, exactly, would enable a woman's diet to influence menopause. In other words, the study didn't prove cause and effect. [5 Key Nutrients Women Need As They Age]
What's more, it's not yet clear whether delaying menopause is a good thing. Early menopause is linked to an increased risk of heart disease, osteoporosis and depression, but it also protects against certain cancers, including breast, endometrial and ovarian cancers, the researchers said.
"As such, we cannot really recommend women to consume these specific foods to influence their onset of natural menopause," said lead study researcher Yashvee Dunneram, a doctoral student in the School of Food Science and Nutrition at the University of Leeds in England.
Previous studies have shown that diet may influence menopause, but results from different studies had contradictory findings, Dunneram told Live Science. So, she decided to use survey data from the U.K. Women's Cohort Study, which allowed her and her colleagues to examine the eating habits of women before they reached menopause and then compare that information with the women's actual age of menopause. This ongoing survey made the data more reliable than a retrospective study, in which people try to remember what they ate years afterward, she said.
To investigate, the researchers looked at survey data collected from more than 35,000 women, ages 35 to 69, from England, Scotland and Wales. On the survey, the women answered questions about health factors that might influence menopause, including diet, weight history, exercise levels, reproductive history and the use of hormone replacement therapy.
Then, four years later, the researchers followed up with the women and asked at what age the women had reached menopause. About 14,000 women responded at both time points, and of those, 914 reported that they had gone through natural menopause during that four year period, when they were between ages 40 and 65.
On average, the women reached menopause at age 51, the researchers found.
Each additional daily portion of oily fish, including trout and herring, was associated with a delay of menopause by about three years, and each additional daily portion of fresh legumes was associated with a menopause delay of about a year, the researchers found. What's more, a higher intake of vitamin B6 and zinc (from diet, not from supplements) in general was associated with later menopause, the researchers said.
In contrast, each additional daily portion of refined carbs was associated with a 1.5-year-earlier menopause start date — a finding that took into account other possible influential factors, the researchers said.
The researchers also broke down the data into smaller groups, looking at mothers versus nonmothers and vegetarians versus nonvegetarians.
Among the women who were not vegetarian, eating more unhealthy snacks every day — such as chips and baked goods — was associated with starting menopause almost two years earlier compared with vegetarian women who ate fewer unhealthy snacks every day, the researchers found. Meanwhile, childless women who ate more grapes and poultry tended to start menopause later.
Perhaps certain foods, such as grapes, legumes and oily fish, are associated with later menopause because they contain or stimulate antioxidants, which may play a role in egg maturation and release, the researchers said.
Conversely, refined carbs increase the risk of insulin resistance, which can interfere with sex hormone activity and boost estrogen levels — factors that may increase the number of menstrual cycles and deplete egg supply faster, the researchers said. [5 Myths About Women's Bodies]
The study was published online today (April 30) in the Journal of Epidemiology and Community Health.
Original article on Live Science. ||||| plainpicture/Cavan Images
A study of more than 900 women in the UK has found that eating more white pasta and rice is linked to getting menopause earlier, while a diet rich in oily fish is linked to later menopause. However, it is not possible to tell if these diets directly affect the onset of menopause, or if they merely reflect some other, hidden factor.
Janet Cade, at the University of Leeds, UK, and colleagues analysed data from 900 women who experienced menopause between the ages of 40 and 65. They found that the average age of menopause was 51, but that certain foods were associated with when menopause begun.
Women who ate an additional daily portion of refined white pasta or rice tended to reach menopause around one-and-a-half years earlier than average, while an extra daily serving of oily fish was associated with a delay of more than three years.
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Diets high in fresh legumes – such as peas and beans – were linked with women reaching the menopause around a year later. Higher intake of vitamin B6 and zinc were also associated with later menopause.
Health implications
“The age at which menopause begins can have serious health implications for some women,” says Cade. Women who go through menopause early can have an increased risk of osteoporosis and heart disease, while those who do so later can be more likely to develop breast, womb and ovarian cancers.
Cade and her colleagues suggest that the antioxidants in legumes may help keep the menstrual cycle going for longer, and that omega 3 fatty acids – which are abundant in oily fish – may boost this. It’s possible that refined carbohydrates increase the risk of insulin resistance, which may interfere with sex hormones.
“The body’s metabolism plays an important role regulating ovulation and periods,” says Channa Jayasena, at Imperial College London. But he warns against inferring a dietary recipe for delaying the menopause from this study. “Unfortunately, a big limitation of these observational studies is their inability to prove that dietary behaviour actually causes early menopause. Until we have that type of proof, I see no reason for people to change their diet.”
Journal reference: Journal of Epidemiology and Community Health
Read more: All you need to know about the menopause (but nobody tells you) ||||| Image copyright Getty Images
A diet high in carbs could bring on an earlier menopause, a study suggests.
Eating lots of pasta and rice was associated with reaching menopause one-and-a-half years earlier than the average age of women in the UK of 51.
However, the University of Leeds study of 914 UK women, also found that a diet rich in oily fish and peas and beans may delay natural menopause.
But experts say many other factors, including genes, influence timing of the menopause.
It's not clear how big a contribution dietary choices might make and women should not worry about changing what they eat based on the findings, they add.
Food findings
The research was published in the Journal of Epidemiology & Community Health and the women were asked what their typical diet contained.
A diet high in legumes, which includes peas, beans, lentils and chickpeas, delayed menopause by one-and-a-half years, on average.
Eating lots of refined carbs, particularly rice and pasta, was linked to menopause coming earlier by one-and-a-half years.
Image copyright Getty Images
The researchers took into account other potentially influencing factors, such as a woman's weight, reproductive history and use of HRT, but they weren't able to consider genetic factors, which can influence age of menopause.
The study is observational and cannot prove any cause, but the researchers offer some possible explanations behind their findings.
For example, legumes contain antioxidants, which may preserve menstruation for longer.
Omega-3 fatty acids, which are in oily fish, also stimulate antioxidant capacity in the body.
Refined carbs boost the risk of insulin resistance, which can interfere with sex hormone activity and boost oestrogen levels. This might increase the number of menstrual cycles leading to the egg supply running out faster.
Health implications
Study co-author Janet Cade, professor of nutritional epidemiology, said the age at which menopause begins can have "serious health implications" for some women.
"A clear understanding of how diet affects the start of natural menopause will be very beneficial to those who may already be at risk or have a family history of certain complications related to menopause."
Women who go through the menopause early are at increased risk of osteoporosis and heart disease, while women who go through it late are at increased risk of breast, womb, and ovarian cancers.
Kathy Abernethy, menopause specialist nurse and chairwoman of the British Menopause Society, said: "This study doesn't prove a link with the foods mentioned, but certainly contributes to the limited knowledge we currently have on why some women go through menopause earlier than others."
Image copyright Getty Images
Prof Saffron Whitehead, emeritus professor of endocrinology at St George's University of London and Society for Endocrinology member, said: "It is an interesting approach to investigate the timing of the menopause but I am not yet convinced that diet alone can account for the age of the onset of the menopause. There are too many other factors involved."
Dr Channa Jayasena, clinical senior lecturer and consultant in reproductive endocrinology and andrology at Imperial College, points out "the body's metabolism plays an important role regulating ovulation and having periods".
"It is tempting to speculate that this provides a recipe for delaying menopause. Unfortunately, a big limitation of these observational studies, is their inability to prove that dietary behaviour actually causes early menopause. Until we have that type of proof, I see no reason for people to change their diet." ||||| | 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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– Odds are, your New Year’s resolution involves losing weight. Most everyone’s does. Well good news: US News & World Report has just released its second annual diet rankings, with the top 25 diets you can jump on to get healthy. The list isn’t haphazard either—the magazine says it spent months combing medical journals, government reports, and more to compile it. Here’s the cream of the crop: DASH Diet—It was originally developed to combat high blood pressure, but DASH ranks as the best all-around balanced diet, with loads of nutritional benefits. Just don’t try it if you’ve got a salt tooth. TLC Diet—This government-endorsed diet focuses on cutting back on fat, and boasts great nutritional benefits, especially for cardiovascular health. Mayo Clinic Diet—This multi-stage diet eases you into a new eating routine, breaking your bad habits. It’s especially effective at fending off diabetes. Mediterranean Diet—This sensible dieting mindset scores big with experts thanks to its emphasis on fruits and vegetables and an overall healthy lifestyle. Weight Watchers Diet—This household name came in well ahead of the other commercial diet plans, proving both better at helping adherents lose weight and easier to follow.
Expand this summary. | Easy omelet
Combine eggs, chives and reduced fat cheddar cheese into a quick breakfast that can provide you with a foundation for the day. You may also consider adding veggies, such as spinach or asparagus. (Getty Images)
Bran flakes
Breakfast needn’t be complicated. Pour a bowl of bran flakes or shredded wheat, douse in low-fat milk and top with blueberries or sliced peaches to sweeten without added sugar. (Getty Images)
Chicken salad sandwich
Between two slices of whole-wheat bread, and paired with lettuce and tomato, unsalted chicken salad topped with regular Dijon mustard can satisfy without leading to a post-lunch afternoon slump. (Getty Images)
Minestrone soup
From tomatoes to diced carrots and chopped celery, plus red kidney beans or chickpeas – this hearty garden in a bowl, which also includes pasta, will satisfy any lunchtime craving. (Getty Images)
Yogurt
For a quick snack on the run, grab a nonfat yogurt with no added sugar – for the healthiest option and more protein, choose plain Greek yogurt – and add fruit for sweetness. (Getty Images)
Salad with chicken and berries
For a green and lean dinner, try a leafy salad topped with grilled chicken and strawberries. Dress lightly with oil and vinegar or your favorite vinaigrette dressing. (Getty Images)
Asian pork tenderloin
Spice it up with this traditional dish featuring roasted pork that incorporates sesame seeds coriander, minced onion and other savory flavoring. Pair with steamed peas. (Getty Images)
Spaghetti squash with meat sauce
Although DASH isn't a low-carb diet, you might still like to enjoy a spaghetti dinner without all of the carbs and calories. For a lighter alternative, try spaghetti squash topped with meat sauce. (Getty Images)
Apples with cottage cheese dip
You don't have to wait until midnight for a snack. Slice up some apples and grab a small bowl of fat-free cream cheese, then add orange juice, peanuts, vanilla and brown sugar for a tasty treat whether it's midmorning or late in the afternoon. (Getty Images)
Tuna salad on a bed of lettuce
Tuna is a healthy lunch or dinner choice that can be used in a wide variety of dishes. A tuna salad on top a bed of lettuce is one option that is a delicious source of protein and vitamins. (Getty Images)
Vegetable kabobs
If you're looking for a vegetarian-friendly dish, throw together some vegetable kabobs. Great for parties or a night at home, these can be made on a grill or in an oven. (Getty Images)
Strawberry banana smoothie with soy milk
A strawberry banana soy smoothie is a great snack for any time of the day, whether you're running out the door in the morning or just finishing your afternoon workout. (Getty Images) ||||| (Getty Images) What is Mediterranean Diet? This diet has been reviewed by U.S. News' team of expert panelists. Learn more » Balanced These diets fall within accepted ranges for the amount of protein, carbs, fat and other nutrients they provide. Pros & Cons Nutritionally sound
Diverse foods and flavors
Lots of grunt work
Moderately pricey It's generally accepted that the folks in countries bordering the Mediterranean Sea live longer and suffer less than most Americans from cancer and cardiovascular ailments. The not-so-surprising secret is an active lifestyle, weight control, and a diet low in red meat, sugar and saturated fat and high in produce, nuts and other healthful foods. The Mediterranean Diet may offer a host of health benefits, including weight loss, heart and brain health, cancer prevention, and diabetes prevention and control. By following the Mediterranean Diet, you could also keep that weight off while avoiding chronic disease. There isn't "a" Mediterranean diet. Greeks eat differently from Italians, who eat differently from the French and Spanish. But they share many of the same principles. Working with the Harvard School of Public Health, Oldways, a nonprofit food think tank in Boston, developed a consumer-friendly Mediterranean diet pyramid that offers guidelines on how to fill your plate – and maybe wineglass – the Mediterranean way.
How does Mediterranean Diet work? Do's & Don'ts Do: Load up on whole grains and veggies. Because this is an eating pattern – not a structured diet – you're on your own to figure out how many calories you should eat to lose or maintain your weight, what you'll do to stay active and how you'll shape your Mediterranean menu. The Mediterranean diet pyramid should help get you started. The pyramid emphasizes eating fruits, veggies, whole grains, beans, nuts, legumes, olive oil, and flavorful herbs and spices; fish and seafood at least a couple of times a week; and poultry, eggs, cheese and yogurt in moderation, while saving sweets and red meat for special occasions. Top it off with a splash of red wine (if you want), remember to stay physically active and you're set. While certainly not required, a glass a day for women and two a day for men is fine if your doctor says so. Red wine has gotten a boost because it contains resveratrol, a compound that seems to add years to life – but you'd have to drink hundreds or thousands of glasses to get enough resveratrol to possibly make a difference. Do's & Don'ts Do's & Don'ts Do: Load up on whole grains and veggies.
What Can I Eat? x of x | Full Screen Buckwheat pancakes
Top a small stack with sliced bananas or a cup of blueberries, and drizzle on a couple tablespoons of light maple syrup. (Getty Images) Greek yogurt
Add strawberries or raspberries and a teaspoon of honey to sweeten. To make it a more complete breakfast, this can be paired with a slice of whole-grain toast "buttered" with smashed avocado. (Getty Images) Mediterranean pasta salad
Get your carb fix without guilt. This lunch option combines pasta noodles tossed in extra-virgin olive oil with red peppers, sun-dried tomatoes and crumbled feta cheese. (Getty Images) Chicken souvlaki
Pocket the good stuff: chicken and veggies, in a wrap. Pair with a side of couscous to eat lunch fast or slow. (Getty Images) Roasted almonds
Grab a handful for a protein-packed snack that will keep you from loading up on sugary junk later in the day. (Getty Images) Grilled salmon
Make a mark on seafood by searing it over an open flame. Make it a meal by adding a side salad of arugula and spinach or wild greens. (Getty Images) Quinoa salad
This ancient edible source of plant-based protein can be combined with a wide array of other filling foods that spring from the dirt, from eggplant to onion. (Getty Images) Chocolate mousse
If you're in the mood for something sweet after dinner, treat yourself to a delicious chocolate mousse. The recipe calls for extra bitter dark chocolate, extra virgin olive oil, eggs, sugar, salt, orange zest and orange liqueur. (Getty Images) Steamed mussels
Try steamed mussels for a fresh seafood meal that can be prepared in about a half hour. Cook them in dry white wine for extra flavor. (iStockPhoto) Pumpkin soup
If you go crazy for all things pumpkin in the fall, "spicy pumpkin soup" is the perfect dish for an appetizer, lunch or dinner. (Getty Images) French fries
You don't have to give up french fries to eat healthy. Keep this favorite in your diet by roasting them in your oven the Mediterranean way rather than frying them. (Getty Images) Banana bread with peanuts
Make "peanut banana bread" on Sunday, and you will have an easy breakfast option or snack throughout the week. (Getty Images) x of x x of x Buckwheat pancakes
Top a small stack with sliced bananas or a cup of blueberries, and drizzle on a couple tablespoons of light maple syrup. (Getty Images) Greek yogurt
Add strawberries or raspberries and a teaspoon of honey to sweeten. To make it a more complete breakfast, this can be paired with a slice of whole-grain toast "buttered" with smashed avocado. (Getty Images) Mediterranean pasta salad
Get your carb fix without guilt. This lunch option combines pasta noodles tossed in extra-virgin olive oil with red peppers, sun-dried tomatoes and crumbled feta cheese. (Getty Images) Chicken souvlaki
Pocket the good stuff: chicken and veggies, in a wrap. Pair with a side of couscous to eat lunch fast or slow. (Getty Images) Roasted almonds
Grab a handful for a protein-packed snack that will keep you from loading up on sugary junk later in the day. (Getty Images) Grilled salmon
Make a mark on seafood by searing it over an open flame. Make it a meal by adding a side salad of arugula and spinach or wild greens. (Getty Images) Quinoa salad
This ancient edible source of plant-based protein can be combined with a wide array of other filling foods that spring from the dirt, from eggplant to onion. (Getty Images) Chocolate mousse
If you're in the mood for something sweet after dinner, treat yourself to a delicious chocolate mousse. The recipe calls for extra bitter dark chocolate, extra virgin olive oil, eggs, sugar, salt, orange zest and orange liqueur. (Getty Images) Steamed mussels
Try steamed mussels for a fresh seafood meal that can be prepared in about a half hour. Cook them in dry white wine for extra flavor. (iStockPhoto) Pumpkin soup
If you go crazy for all things pumpkin in the fall, "spicy pumpkin soup" is the perfect dish for an appetizer, lunch or dinner. (Getty Images) French fries
You don't have to give up french fries to eat healthy. Keep this favorite in your diet by roasting them in your oven the Mediterranean way rather than frying them. (Getty Images) Banana bread with peanuts
Make "peanut banana bread" on Sunday, and you will have an easy breakfast option or snack throughout the week. (Getty Images) ×
How much does Mediterranean Diet cost? The cost of the Mediterranean diet, like most aspects of the diet, depends on how you shape it. While some ingredients ( olive oil, nuts, fish and fresh produce in particular) can be expensive, you can find ways to keep the tab reasonable – especially if you're replacing red meats and meals with plant-based home cooking, some research suggests. Your shopping choices matter, too. Can't spring for the $50 bottle of wine? Grab one for $15 instead. And snag whatever veggies are on sale that day, rather than the $3-a-piece artichokes.
Will Mediterranean Diet help you lose weight? The Mediterranean diet might help you lose weight. While some people fear that eating a diet like the Mediterranean diet that is relatively rich in fats (think olive oil, olives, avocado and some cheese) will keep them fat, more and more research is suggesting the opposite is true. Of course, it depends on which aspects you adopt and how it compares to your current diet. If, for instance, you build a "calorie deficit" into your plan – eating fewer calories than your daily recommended max or burning off extra by exercising – you should shed some pounds. How quickly and whether you keep them off is up to you. Here's a look at a few studies addressing weight loss on the Mediterranean diet: A 2016 study in The Lancet Diabetes & Endocrinology journal that analyzed data from Predimed – a five-year trial including 7,447 adults with Type 2 diabetes or at risk for cardiovascular disease who were assigned either a Mediterranean diet supplemented with olive oil, the same diet supplemented with nuts or a control diet – found that people on the Mediterranean versions added the fewest inches to their waistlines. The olive oil folks lost the most weight.
A 2010 study in Diabetes, Obesity and Metabolism assigned 259 overweight diabetics to one of three diets: a low-carb Mediterranean diet, a traditional Mediterranean diet or a diet based on recommendations from the American Diabetes Association. All groups were told to exercise 30 to 45 minutes at least three times per week. After a year, all groups lost weight; the traditional group lost an average of about 16 pounds while the ADA group dropped 17 pounds and the low-carb group lost 22 pounds.
Another study, published in the New England Journal of Medicine in 2008, assigned 322 moderately obese adults to one of three diets: calorie-restricted low-fat; calorie-restricted Mediterranean; and non-calorie-restricted low-carb. After two years, the Mediterranean group had lost an average of 9 7/10 pounds; the low-fat group, 6 4/10 pounds; and the low-carb group, 10 3/10 pounds. Although weight loss didn't differ greatly between the low-carb and Mediterranean groups, both lost appreciably more than the low-fat group did.
A 2008 analysis of 21 studies in the journal Obesity Reviews concluded the jury is still out on whether following the Mediterranean diet will lead to weight loss or a lower likelihood of being overweight or obese.
How easy is Mediterranean Diet to follow? Because Mediterranean diets don't ban entire food groups, you shouldn't have trouble complying long term. The Mediterranean diet can be convenient. When you want to cook, there's a recipe and complementary wine that'll transport you across the Atlantic. Oldways' consumer-friendly tips will make meal planning and prepping easier. And you can eat out, as long as you bring someone along to share the hefty entrees. Oldways offers numerous Mediterranean recipes, including this guide featuring meals that all cost $2 or less a serving. Otherwise, a simple Google search will turn up lots of healthy Mediterranean meal ideas. Want more inspiration? Oldways recommends the "4-Week Mediterranean Diet Menu Plan." If you eat out while following the Mediterranean diet, embrace the diet's affinity for sharing by ordering one entree for the two of you. And be sure to start with a house salad or order extra veggies a la carte to get your fill. [RELATED: 10 Ways to Stay on Track With Your Weight-Loss Goals When Life Goes Crazy] Recommended Article Recommended Article 10 Ways to Stay on Track With Your Weight-Loss Goals When Life Goes Crazy Stressed? Busy? Here’s how to keep life from sidelining your weight-loss progress. You may save time on the Mediterranean diet by cooking and storing meals ahead of time; otherwise, you'll have to hire somebody to plan, shop for and prepare your meals, if your time is more valuable than your wallet. You'll find lots of free Mediterranean diet resources on the Oldways website, including an easy-to-understand food pyramid; a printable grocery list; gender- and age-specific tips on making the Mediterranean switch; a quick-read "starter" brochure; a recipe newsletter; and even a glossary defining Mediterranean staples, from bruschetta to tapenade. Hunger shouldn't be a problem on this diet; fiber and healthy fats are filling, and you'll be eating lots of fiber-packed produce and whole grains, and cooking with satiating fats like olive oil. Nutrition experts emphasize the importance of satiety, the satisfied feeling that you've had enough. You're making everything, so if something doesn't taste good, you know who to blame. ||||| (Getty Images) What is Mayo Clinic Diet? This diet has been reviewed by U.S. News' team of expert panelists. Learn more » Balanced These diets fall within accepted ranges for the amount of protein, carbs, fat and other nutrients they provide. Pros & Cons Nutritionally sound
You shape your diet
Lots of grunt work
Somewhat pricey Weight loss and a healthier lifestyle go hand in hand on the Mayo Clinic Diet. You recalibrate your eating habits, breaking bad ones and replacing them with good ones with the help of the Mayo Clinic's unique food pyramid. The pyramid emphasizes fruits, veggies and whole grains. In general, these foods have low energy density, meaning you can eat more but take in fewer calories. Think of it this way: For about the same amount of calories you could have a quarter of a Snickersbar or about 2 cups of broccoli. By sticking with the Mayo Clinic Diet, you’re expected to shed 6 to 10 pounds in two weeks and continue losing 1 to 2 pounds weekly until you’ve hit your goal weight. In 2013, Mayo Clinic published "The Mayo Clinic Diabetes Diet," which our experts did not evaluate. A new edition of this book will be available Jan. 1, 2019. This spin on the standard eating plan is designed for people with prediabetes and Type 2 diabetes, and its advice is specific to lowering blood sugar and keeping levels stable.
How does Mayo Clinic Diet work? Do's & Don'ts Do: Raid the produce section of your supermarket. The newest (and second) edition of the "Mayo Clinic Diet" book was published in 2017. Use it, as well as the Mayo Clinic Diet website , as your guides to work your way through two parts: "Lose it!" and "Live it!" Part one focuses on 15 key habits – ones to add and ones to ditch. You don't count calories, and you can snack all you want on fruits and veggies. After two weeks, you begin part two, learning how many calories you should eat to either lose or maintain weight and where those calories should come from. No food group is completely off-limits – you're developing a pattern of healthy eating you'll follow for life. [Check out the DASH diet, which aims to help prevent and lower high blood pressure.] In "Lose it!" you'll add a healthy breakfast, lots of fruits and veggies, whole grains, healthy fats and at least 30 minutes of physical activity a day. You'll ban eating while watching TV, sugar (except what's found in fruit), snacking (except on fruits and veggies), consuming too much meat and full-fat dairy, and eating out (unless the food you order follows the rules). If you're really motivated, you'll also adopt bonus habits such as keeping food, activity and goal diaries; exercising 60 or more minutes per day; and eating natural or minimally processed "real food."
In "Live it!" you'll use what you learned in the first phase but be allowed to occasionally break the rules. You'll also calculate the number of calories you can eat while still losing a couple of pounds a week. But instead of counting the calories in every grain of (brown) rice you eat, you'll focus on servings. On a 1,400-calorie plan, for example, you're allowed four or more servings each of fruits and veggies, five servings of carbs, four of protein/dairy and three of fats. What's a serving? For fruit, it's the size of a tennis ball; for protein, no bigger than a deck of cards. Round out "Live it!" with regular physical activity and you're set for life. If you’re interested in following the Mayo Clinic Diabetes Diet, it's heavy on food that's naturally rich in nutrients and low in fat and calories, and the diet emphasizes fruits, veggies and whole grains. Recommended foods include healthy carbs (think fruit, legumes, vegetables, whole-wheat flour and wheat bran); fiber-rich foods such as nuts and beans; heart-healthy fish such as salmon, mackerel and tuna; and "good" fats, which include avocados, almonds, olives and walnuts. Foods to avoid include saturated fats, trans fats, cholesterol and sodium. Do's & Don'ts Do's & Don'ts Do: Raid the produce section of your supermarket.
How much does Mayo Clinic Diet cost? Whether it's pricier than your current grocery tab depends, of course, on what you put in your cart. Fruits, veggies and whole-grain products are generally more expensive than sugary cereal, white bread and frozen pizzas. But there's no membership fee, and the diet's individualized nature gives you financial wiggle room – by making dinner from whatever produce is on sale, for example. The "Mayo Clinic Diet" book is an essential guide and should be purchased.
Will Mayo Clinic Diet help you lose weight? Most likely, Mayo Clinic Diet will help you lose weight, provided you follow the rules. Although the only research specifically evaluating the diet comes from the Mayo Clinic itself, preliminary results are promising. The principles behind it are backed by substantial research, which suggests its potential for weight loss and weight maintenance. In a 2008 pilot program of 53 obese Mayo Clinic employees who followed "Lose it!" for two weeks, average weight loss was 8 pounds. Nearly all of the 46 who finished lost 4 or more pounds, and most lost between 6 to 10 pounds. There was no control group. In general, diets rich in low-energy-dense foods have been shown to deliver weight loss, promoting fullness on fewer calories, according to the Centers for Disease Control and Prevention. In a study of 97 obese women, published in the American Journal of Clinical Nutrition in 2007, researchers randomly assigned dieters to either a low-energy-dense, low-fat diet or a low-energy-dense, low-fat diet that emphasized fruits and vegetables. After a year, both groups lost weight, and the fruits-and-vegetables dieters lost even more – 14 pounds compared with 11 pounds. More studies, particularly large controlled trials, are needed to confirm the findings.
How easy is Mayo Clinic Diet to follow? Most dieters will find the restrictive "Lose it!" phase difficult. That's why it only lasts two weeks. Once you develop your plan in "Live it!" and find no foods completely off limits, you'll be more likely to stay on the wagon. You're free to eat out, as long as you let Mayo's food pyramid direct your menu choices. Alcohol might be restricted a little more than you'd prefer. And while a slew of Mayo guides make developing your plan easier, there's just no way to avoid the grocery store and stove. Mayo's companion "The New Mayo Clinic Cookbook, Second Edition," is packed with recipe ideas. Once you understand healthy eating and serving sizes, you can scour outside recipe websites for free. Eating out is discouraged in Mayo’s "Lose it!" phase, but the fine print says you technically still can if you don't stray from the guidelines. There are no timesavers, unless you hire somebody to plan your meals, shop for them and prepare them. And you can't pay someone to exercise for you. The book provides meal planning, grocery shopping and dining out guides; a crash course in nutrition basics; and advice for staying motivated. Mayo doesn't have any book-specific resources online, but you can peruse its large database of diet-related articles . Nutrition experts emphasize the importance of satiety, the satisfied feeling that you’ve had enough. You shouldn’t feel hungry on the Mayo Clinic Diet. In part one, you can snack on unlimited veggies and fruits, and later, when you've got a calorie cap, the emphasis on low-energy-dense fruits, veggies and high-fiber whole grains should keep you feeling fuller longer. You're making everything, so if something doesn't taste good, you know who to blame. ||||| Roast beef sandwich
Meat lovers can craft a roast beef sandwich with leafy greens and a tomato. Add a half cup of pasta salad with a quarter cup of mixed vegetables and an apple for a balanced lunch. (Getty Images)
Popcorn
Need a snack? Try popcorn – but stick to two cups cooked with canola oil. (Getty Images)
Apple oatmeal
One cup of oatmeal is a delicious, heart-healthy way to start your morning. Add apple slices or your favorite fruit to sweeten. (Getty Images)
Eggs
Eggs are fine for breakfast, but limit yourself to two yolks per week on this cholesterol-friendly diet. (Egg whites and substitutes aren’t limited.) (Getty Images)
Skinless poultry
Skinless poultry is a great way to add protein to your lunch salad or dinner plate. Just remember not to eat more than five ounces per day. Consider substituting a quarter cup of cooked dry beans or peas for one ounce of meat. (Getty Images)
Vegetables
Leafy greens, cooked or raw vegetables and raw vegetable juices are great ways to get your required three to five servings of vegetables each day. Incorporate squash into your soups or make a radish salad. The choice is yours. (Getty Images)
Whole grains
Don’t shy away from healthy whole grains like English muffins for breakfast if that’s what you crave. The TLC Diet calls for six servings of bread, cereals, pasta, rice and other grains each day. Just remember to limit yourself to one teaspoon of soft margarine. (Getty Images) ||||| Egg, bacon and avocado sandwiches
Serve this ultra‐satisfying breakfast sandwich with hot sauce on the side. For less mess on the go, use whole wheat pita pockets instead. (Courtesy of Weight Watchers)
Chopped spinach salad and pear salad with sherry vinaigrette
Pomegranate seeds add a pop of color and flavor to salads. Cut back on prep work by buying them prepackaged. (Courtesy of Weight Watchers)
Classic lasagna
Dig into this gooey version of meat lasagna. It's rich and flavorful, good enough to be called a classic. (Courtesy of Weight Watchers)
Chocolate mousse espresso shots
Espresso‐spiked chocolate pudding is layered with crushed chocolate wafers in this so‐simple dessert recipe. (Courtesy of Weight Watchers)
Toast with avocado and red pepper flakes
If you usually just throw a slice of bread in the toaster for breakfast, you don't have to stop there. Spread fresh mashed avocado on top and add some red pepper flakes to transform your basic toast into a scrumptious treat. (Getty Images)
Chicken noodle soup
Chicken noodle soup isn't only for when you're sick. You can enjoy this winter favorite as a light lunch or dinner. Add frozen vegetables like peas, corn, green beans and carrots to give it a boost of flavor and vitamins. (Getty Images)
Cheeseburger with tomatoes and grilled onions
If you get a craving for a succulent burger, go ahead and grill one up using 93-percent lean ground beef. Fresh tomatoes and grilled onions make great toppings that are delicious and healthy. If you like your burger extra juicy, don't press down on the patty when you cook it. (Getty Images)
Roasted baby potatoes
Roasted baby potatoes are a great side to any meal. Cook with oregano and lemon to give them a zesty taste. (Getty Images)
Apple pie
Always a popular dessert, apple pie is a delicious option for summer cookouts, holiday dinners or just a night on the couch. For an extra touch, add a crumble made with oats, flour and sugar. (Getty Images)
Butternut squash with sage and orange
The next time you're in your local grocery store or at the farmers market, grab some butternut squash and add orange zest and fresh sage to make a yummy side dish. You can buy pre-cut butternut squash as a time-saver. (Getty Images)
Cucumber slices and dip
If you love snacking on cucumber slices, try them with a dip made from low-fat cottage cheese, sour cream, chives and black pepper for a light option. (Getty Images)
Oatmeal chocolate chip cookies
Just because you're watching your weight doesn't mean you can't enjoy fresh cookies from the oven. Oatmeal chocolate chip cookies are a baked treat you can indulge in without the guilt. (Getty Images) ||||| | multi_news_1_0_0 |
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Article:
Health Tennessee Will Now Criminally Charge Pregnant Women Who Use Drugs CREDIT: Shutterstock
Tennessee Gov. Bill Haslam (R) has approved a measure that will allow Tennessee to bring criminal charges against pregnant women who use drugs for potentially harming their fetuses, even though there isn’t conclusive scientific evidence that being exposed to illicit drugs in the womb causes long-term harm to children.
The governor’s approval of the legislation comes despite a massive outcry from reproductive rights and criminal justice groups across the country, who say that criminalizing pregnant women is the wrong policy approach. Threatening to bring charges against women who are struggling with substance abuse dissuades them from coming forward to seek the medical treatment they need. It’s also a policy that disproportionately harms low-income and non-white women.
“Today, the Tennessee governor has made it a crime to carry a pregnancy to term if you struggle with addiction or substance abuse,” Alexa Kolbi-Molinas, a staff attorney with the ACLU Reproductive Freedom Project, said. “This deeply misguided law will force those women who need health care the most into the shadows. Pregnant women with addictions need better access to health care, not jail time.”
In a statement accompanying his signature on the bill, Haslam claimed that he had “extensive conversations with experts including substance abuse, mental health, health and law enforcement officials” and will “be monitoring the impact of the law through regular updates with the court system and health professionals.”
But most experts — including the American Medical Association, the American Academy of Pediatrics, the American College of Obstetricians and Gynecologists, and the American Public Health Association — oppose efforts to arrest pregnant women who use drugs. Medical professionals are concerned about women getting the prenatal care they need, since skipping out on those services actually leads to a greater risk of miscarriage, stillbirth, and infant death. Specialists in obstetric medicine and drug addiction called on Haslam to veto the measure.
Although drug possession and drug sales can result in criminal charges, states typically do not arrest people simply for using drugs. Addiction is considered to be a medical issue, and under the Constitution’s definition of cruel and unusual punishment, states aren’t allowed to criminalize those types of disorders. But Tennessee is making an exception for pregnant people.
“Do we arrest new fathers who come into the emergency room who test positive for drugs? This is not really about arresting pregnant women because they use drugs. This is arresting women because they became pregnant, making them vulnerable to charges of child endangerment for risking harm to a newborn,” Lynn Paltrow, the executive director of National Advocates for Pregnant Women (NAPW), one of the groups that’s been fighting against the criminalization of pregnant women for years, told ThinkProgress in an interview earlier this month.
Two years ago, Tennessee barred the use of criminal charges against pregnant women for using drugs, opting to encourage drug-addicted women to enter treatment. Advocates are frustrated that the state is backtracking on that policy, which they supported. “Now we’re seeing the General Assembly take two big steps back,” Farah Diaz-Tello, a staff lawyer for NAPW, recently told the New York Times. “It’s going from a state with some of the best practices to one of the worst.” ||||| Buy Photo Dr. Stephen Patrick, right, and Michael Botticelli, deputy director of the White House Office of National Drug Control Policy, take a close look at a baby inside the NICU on Monday while touring the Monroe Carell Jr. Children’s Hospital at Vanderbilt University. (Photo: Jae S. Lee, The Tennessean)Buy Photo
Tennessee women who use drugs while pregnant can be criminally charged for harm done to their infants beginning July 1.
Gov. Bill Haslam signed the legislation Tuesday after "extensive conversations with experts including substance abuse, mental health, health and law enforcement officials," he wrote in a statement. "The intent of this bill is to give law enforcement and district attorneys a tool to address illicit drug use among pregnant women through treatment programs."
The governor's decision comes after a week of mounting nationwide opposition from civil and reproductive rights groups. They argued that criminalization would drive vulnerable women away from drug addiction treatment.
"I understand the concerns about this bill, and I will be monitoring the impact of the law through regular updates with the court system and health professionals," Haslam wrote.
Simple Answer: What's best for babies born to drug-addicted mothers?
The law brings back criminalization, which lawmakers had eliminated two years ago as the state moved toward programs that incentivize expecting mothers to get into treatment.
Tennessee officials have wrestled with what to do about the growing numbers of infants born dependent on drugs and who often suffer from a condition known as neonatal abstinence syndrome.
The legislation would allow mothers to avoid criminal charges if they get into one of the state's few treatment programs. Haslam said he wants doctors to encourage women to get into treatment before delivering their babies so they can avoid charges.
The proposal also includes an unusual sunset provision, which means the criminal penalty will be in effect until 2016. At that time, lawmakers will have to revisit the issue.
Opponents, including five national medical organizations and local doctors who treat pregnant women, worry that criminalization will scare women away from treatment and reverse last year's Safe Harbor Act, which protected the custody rights of mothers and gave them priority placement into the state's limited number of treatment programs.
The director of the American Civil Liberties Union of Tennessee — joined by the national ACLU — said she was "extremely disappointed" by the governor's decision.
"A pregnant woman struggling with drug or alcohol dependency will now be deterred from seeking the prenatal care she needs," said Hedy Weinberg.
Abuse of prescription painkillers has fueled a tenfold increase in such births in the past decade, sending health officials scrambling. There were 921 drug-dependent births in 2013 and 253 so far this year.
Reach Tony Gonzalez at 615-259-8089 or on Twitter @tgonzalez.
MOMS AND DRUGS
921: The number of drug-dependent births in Tennessee in 2013
253: The number of drug-dependent births so far this year.
The legislation would allow mothers to avoid criminal charges if they get into one of the state's few treatment programs.
Read or Share this story: http://tnne.ws/1kqiiEn ||||| Public Health
Tennessee Bill Could Send Addicted Moms To Jail
itoggle caption Katie Collins/PA Photos/Landov
Pregnant women addicted to illegal narcotics or prescription pain pills could soon be jailed in Tennessee under a bill awaiting the governor's signature. The strict proposal enjoys bipartisan support — despite objections from doctors.
The medical term for what happens when a newborn has withdrawal symptoms a day or two after birth is "neonatal abstinence syndrome." At its worst, these babies suffer from seizures; it's not clear whether there might also be lasting effects.
Tennessee last year forced every hospital to start reporting such cases, and the numbers have only been going up. As health officials have made drug-dependent babies a priority, the Legislature has taken a more punitive approach.
"It's always somebody else's fault," says state Rep. Terri Lynn Weaver. "What's wrong with: 'You screwed up, you're wrong, you've got to pay the consequences.' What's wrong with that?"
It's always somebody else's fault. ... What's wrong with: You screwed up, you're wrong, you've got to pay the consequences?
Weaver initially wanted to make it possible to charge women with homicide if their drug-dependent newborn died, but ultimately she had to tone it down. The women would now have the option to seek treatment.
"We can't make her get help herself," says Weaver, "but, by golly, we can give her an option and a choice."
Weaver is a conservative Republican, but Democrats jumped on board too. State Rep. John DeBerry admits it seems unnatural to punish a pregnant woman for harming her unborn child.
"We are always trying to save children who should be saved by their families, and I have said if there is a better way, bring it to me," he says. "I haven't seen it yet."
In some other states, prosecutors have gone after addicts whose newborn dies, trying to charge them with murder. Farah Diaz-Tello of the National Advocates for Pregnant Women points to a case in Mississippi.
"What Tennessee is doing is creating a law that would permit this kind of prosecution — not for murder," says Diaz-Tello, "but it would allow for reckless endangerment, which is a misdemeanor, all the way up to aggravated assault."
And an assault charge could mean 15 years behind bars for the mother.
Being a poorly controlled diabetic is terrible for pregnancy — probably equally as bad as drug addiction — and we don't legislate those choices.
New mother Jackie Bains has returned to a Nashville women's clinic for a checkup. Her son is 7 weeks old and perfectly healthy. Bains says she was hooked on narcotic pain pills when she found out she was pregnant — but she got help. She says it was hard to tell people, but it would have been even harder if she thought she could be punished for her addiction.
"I mean, some people are worried about going to jail and what it could do. But then you also have to worry about what it would do to the baby, too," she says. "I do think it will deter people from wanting to come in to seek help."
It's a concern that worries many in the medical community — that the punitive approach, even with its treatment option, will drive away women or encourage more abortions.
Jessica Young, an obstetrician at Vanderbilt University Medical Center who specializes in drug treatment during pregnancy, says lawmakers don't fully understand that addiction can be a sickness.
"Being a poorly controlled diabetic is terrible for pregnancy — probably equally as bad as drug addiction — and we don't legislate those choices," says Young. "I just think this is an easy group to pick on because addiction has such a stigma."
Tennessee Gov. Bill Haslam, a relatively moderate Republican, has been hearing from women's groups around the country asking him to veto the bill, but he says he's comfortable with the final language, given that a woman always has a way to avoid jail time, even after giving birth to a child going through drug withdrawal. |||||
What is a summary? | – Starting July 1, if you're pregnant and use drugs while living in Tennessee, you can be charged with a crime for causing harm to your unborn baby. Gov. Bill Haslam signed the controversial law yesterday, the Tennessean reports. Civil and reproductive rights groups had opposed it, saying it would scare women away from getting treatment for drug addiction, but Haslam said he talked to "experts including substance abuse, mental health, health, and law enforcement officials" before signing the legislation, and will closely monitor its impact. Critics also say the law disproportionately affects low-income and non-white women, ThinkProgress notes. Using drugs while pregnant was previously criminalized in the state, but decriminalized two years ago as lawmakers moved toward programs encouraging pregnant women to get treatment. But the law is back as the number of babies born dependent on drugs is on the rise. Pregnant drug users can avoid criminal charges if they enter a treatment program, and Haslam is asking doctors to encourage women to enter treatment programs before delivery to avoid being charged. If they don't enter treatment, women charged under the law could face as many as 15 years in jail, NPR reported last week. | multi_news_1_0_0 |
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Nothing tops an office with a door on the universal workplace wish list, but a desk near a window that lets in natural light probably ranks a close second. Outside views are often badges of seniority or achievement in the work world—understandably, given that they're in short supply. But new evidence suggests employers should look at daylight exposure less as a mark of accomplishment and more as a matter of public health.
Employers should look at daylight exposure less as a mark of accomplishment and more as a matter of public health.
So says an interdisciplinary team of architects and medical researchers that recently conducted a small case study comparing people exposed to natural light at their jobs with those who aren't. The window workers scored better on common self-report health and sleep surveys; they also slept 46 minutes more a night, on average, as measured by a sleep monitor. The findings will be reported in the Journal of Clinical Sleep Medicine.
"We really wanted to look at some health issues related to lack of natural light in people's lives in general," Mohamed Boubekri, study leader and architectural scholar at the University of Illinois, told Co.Design. "The reason why we selected office buildings is because … that's where most of us spend a good chunk of our lives."
The study found that 27 workers who sat in windowless offices (or so far from a window as to get no natural light) scored worse than 22 workers who did get daylight on all eight dimensions of a health survey known as the Short Form 36. The windowless group fared significantly worse on two particular areas, including "vitality." Workers without daylight exposure also showed worse overall sleep quality on a well-established self-report sleep index.
To go beyond self-report measures, Boubekri and collaborators arranged for 21 of the study participants to wear a watch capable of tracking light exposure and activity patterns. These actigraphy measures confirmed that the windowless workers received less daylight, were less physically active during the work day, and slept an average of 46 minutes less on work nights. Windowless workers also fared worse on five other sleep measures, including sleep fragmentation (or waking up during the night), though these differences weren't statistically significant.
The health benefits of exposure to daylight during the work day extend beyond the work week.
Interestingly, window workers slept more soundly than windowless workers on non-work nights—roughly 8.5 hours versus 6.5 hours—according to the actigraphy measures. And workers in the window group also received significantly more natural light than those in the windowless group after work and on free days. That finding caught the researchers by surprise and is tough to explain, but Boubekri speculates that workers who get daylight at the office may have more energy to go outside during their off time.
Overall, the findings suggest that the health benefits of exposure to daylight during the work day extend far beyond quitting time and even beyond the work week. In addition to more overall light exposure, these workers sleep better, seem more active, and have higher quality-of-life ratings than those who work in artificial light all day. The source of the sleep troubles, in particular, might be disruption of their circadian rhythms—the internal clocks that operate best when exposed to sufficient daylight.
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"Some say we spend 90% of our lives indoors," says Boubekri, who's also written a book on the role of lighting in architectural design. "It's very, very significant."
The new findings extend what little research already exists on daylight and worker health, including a 1997 study that looked at lighting as a matter of "preventive medicine" and challenged designers to improve the situation. That work proposed naming the problem "ill-lighting syndrome" to draw more attention to it. Evidently the label never stuck, but more architects and design critics have sounded the alarm of late.
Commercial buildings without windows are worth an estimated 20% less per square foot.
Writing earlier this year in the magazine Architectural Lighting, Kevin Van Den Wymelenberg of the University of Idaho's Integrated Design Lab championed better daylighting not only for the purposes of better health and productivity, but real estate value. (Commercial buildings without windows are worth an estimated 20% less per square foot, though they cost more to build.) The energy savings are also significant, though energy-efficient bulbs have made this point less powerful in recent years.
Boubekri says designing well-lit buildings isn't nearly as much of a challenge as convincing designers it's important to do. "In an era where we're trying to limit consumption of fossil energy resources, we really should be thinking in a different way about these things," he says. "Not just using electric light to light our lives." ||||| Work in an office with no windows? It could cost you 46 minutes of sleep a night
Workers who sit near a window also found to have less broken sleep
Are also more likely to exercise, having got a good night's sleep
Body 'needs exposure to daylight to keeps its sleeping patterns on track'
Forget milky drinks, hot water bottles or curling up with a good book - th e real secret to a good night's sleep may be where you sit at work.
New research shows office staff stuck in w indowless rooms - or with little exposure to daylight - get on average 46 fewer minutes of sleep a night.
Those who sit near a window were also found to have less broken sleep and a better quality of life than employees deprived of daylight.
Workers in windowless rooms, or with little daylight exposure, may lose up to 46 minutes of sleep a night
The findings, published in the Journal of Clinical Sleep Medicine, suggest the working environment may be crucial to setting the body's own internal clock.
Researchers say better designed offices could boost the physical and mental health of workers.
One in three Britons suffers from poor sleep, with stress, computers and taking work home often blamed for the lack of quality slumber.
However, the cost of all those sleepless nights is more than just bad moods and a lack of focus.
Regular poor sleep raises the risk of serious medical conditions like obesity, heart and diabetes - and can even shorten life expectancy.
Adequate exposure to natural daylight is known to be crucial for governing the body's circadian rhythm - the built-in clock which dictates our sleeping and waking patterns.
Researchers from the University of Illinois, Northwestern University in Chicago and the
Hwa-Hsia Institute of Technology in Taiwan, teamed up to investigate the role of workplace windows in aiding sleep.
They recruited 49 office employees, just over half of whom spent the day in mostly windowless environments, while the rest enjoyed frequent exposure to daylight through windows.
Each one was quizzed on sleeping patterns, physical activity and general lifestyle.
Some of the volunteers also wore hi-tech watches round-the-clock for a fortnight to measure their light exposure, levels of physical activity and sleep/wake times.
The results showed those with the most work-time light exposure snoozed an average of 46 minutes more per night than their light-deprived colleagues.
They also scored better on a sleep quality scale and reported fewer night-time disturbances - and were more likely to exercise, having got a good night's sleep.
Exposure to daylight also meant better sleep quality and fewer night-time disturbances
In a report on their findings they said: 'Workers in offices with windows not only had significantly more light exposure during work hours but also slept an average of 46 minutes more per night during the week than those without (access to) windows.
'Office workers with more light exposure at the work place also tended to have better sleep quality, more physical activity and a better quality of life.
'We suggest that architectural design of office environments should place more emphasis on sufficient daylight exposure for workers in order to promote health and well-being.'
The study backs up earlier research suggesting that nurses are less likely to face burnout from work-related stress and more likely to achieve job satisfaction if they have exposure to at least three hours of daylight a day.
Sleep expert Dr Neil Stanley said the body needs exposure to daylight to keeps its sleeping patterns on track. 'Light is essentially the thing that tells our bodies to be awake and dark tells them to go to sleep.
'The problem with office lighting is that it is not made up of 'blue' light, which is the wavelength of light you get from the sun and which controls your body clock. ||||| Scientific Investigations
http://dx.doi.org/10.5664/jcsm.3780
Mohamed Boubekri, Ph.D.1; Ivy N. Cheung, B.A.2; Kathryn J. Reid, Ph.D.2; Chia-Hui Wang1,3; Phyllis C. Zee, M.D., Ph.D., F.A.A.S.M.2
1School of Architecture, University of Illinois at Urbana-Champaign, Champaign, IL; 2Department of Neurology, Northwestern University, Chicago, IL; 3Department of Architecture, Hwa-Hsia Institute of Technology, Taipei, Taiwan
Workers in windowless environments reported poorer scores than their counterparts on two SF-36 dimensions—role limitation due to physical problems and vitality—as well as poorer overall sleep quality from the global PSQI score and the sleep disturbances component of the PSQI. Compared to the group without windows, workers with windows at the workplace had more light exposure during the workweek, a trend toward more physical activity, and longer sleep duration as measured by actigraphy.
Participants (N = 49) included 27 workers working in windowless environments and 22 comparable workers in workplaces with significantly more daylight. Windowless environment is defined as one without any windows or one where workstations were far away from windows and without any exposure to daylight. Well-being of the office workers was measured by Short Form-36 (SF-36), while sleep quality was measured by Pittsburgh Sleep Quality Index (PSQI). In addition, a subset of participants (N = 21; 10 workers in windowless environments and 11 workers in workplaces with windows) had actigraphy recordings to measure light exposure, activity, and sleep-wake patterns.
Since the sick building syndrome of the 1970s and the World Health Organization's Declaration on Occupational Health for All in 1994,1 occupational health has become a salient issue among health professionals and architects alike. With the increased interest today in green architecture, daylighting is becoming an important design consideration. Typically, daylighting recommendations are made in the form of daylight factor levels ranging between 2% to 6% depending on building types and activities. A daylight factor is a percentage of indoor illuminance compared to the outdoor illuminance on a horizontal surface. The daylight factor principle is valid for stable overcast sky conditions only; sunny conditions are too dynamic and changing to be considered.
Although there are many studies that have explored the relationship between daylighting, psychological well-being, and workers' productivity or school children's performance,2–4 few have addressed the impact of daylight at the workplace on sleep, quality of life, and overall health. Exposure to light-dark patterns is one of the main environmental cues for circadian rhythms that influence approximately 24-hour biological, mental, and behavioral patterns such as sleep and activity.5 The timing of light exposure is very influential on these rhythms, and previous research has shown that office environment lighting during work hours can act as a regulator of circadian physiology and behavior, with blue-enriched artificial lighting even competing with natural light as an entrainer.6 Given that office hours occur during biologically natural daylight hours, we posit that light exposure in the office environment will have effects on sleep, and via sleep and other influences also have effects on physical and mental health.
BRIEF SUMMARY Current Knowledge/Study Rationale: Both the amount and timing of light exposure is important for physical and mental health. While research indicates possible links between light exposure in workplaces and workers' productivity and performance, less is known about the role of workplace light exposure on workers' quality of life and sleep quality. Study Impact: Office workers with more light exposure at the workplace tended to have longer sleep duration, better sleep quality, more physical activity, and better quality of life compared to office workers with less light exposure at the workplace. Office workers' physical and mental well-being may be improved via enhanced indoor lighting for those with insufficient daylight in current offices as well as increased emphasis on light exposure in the design of future offices.
There is much evidence that links insufficient sleep and/ or reduced sleep quality to a range of significant short-term impairments such as memory loss, slower psychomotor reflexes, and diminished attention.7–9 If windowless environments or lack of daylight affect office workers' sleep quality, there will be subsequent effects not only individually but also on a societal level, leading to more accidents, workplace errors, and decreased productivity. Sleep quality is also an important health indicator that may have effects on, and interactions with mood, cognitive performance, and health outcomes such as diabetes and other illnesses.10–13 Therefore, it is crucial to investigate the effects of daylight as it may provide a profound way to improve office workers' productivity and health as well as the safety of the community they work and live in. Deprivation to light damages monoamine neurons and produces a depressive behavioral phenotype in rats.14 In humans, a direct correlation between the severity level of seasonal affective disorder and exposure to natural light is well documented.15–17 Results of several studies suggest that both natural and artificial bright light, particularly in the morning, can improve significantly health outcomes such as depression, agitation, sleep, circadian rest-activity, and seasonal affective disorder.18–26
These effects of light exposure, or the lack thereof, illustrate the importance of proper light exposure for physical well-being and mental health. In our modern society, many responsibilities at the workplace and at home dictate self-imposed alterations and/or loss of daylight in our daily lives. Findings from the previously discussed research suggest that the light exposure determined by our daily schedules will have subsequent consequences on our mood, cognitive performance, and overall well-being. However, studies exploring the impact of daylight exposure, or the lack thereof, on the health of office workers are very scarce. Therefore, the aim of this study was to examine the influence of light exposure at the workplace, through the existence or absence of windows and of daylight, on office workers' sleep patterns, physical activity, and quality of life via actigraphy and subjective measures. In our study we compared two groups of office workers—those with windows and abundant levels of daylight and those without windows and with no direct contact with daylight at their workstations— in terms of overall health and well-being and subjective sleep quality using well-validated scales, and objective measures of sleep, activity levels, and light exposure via actigraphy. We hypothesized that office workers with windows in the work-place would have more light exposure, better sleep quality, more physical activity, and higher quality of life ratings compared to office workers without windows in the workplace.
METHODS Participants A total of 49 participants were recruited, including 27 day-shift workers in windowless workplaces and 22 comparable day-shift workers in workplaces with windows. Workers were selected from volunteers within administrative support staff and other office workers on the campus of the University of Illinois at Urbana-Champaign (UIUC) whose work schedule was from 08:00 to 17:00. The typical recruitment process was done by contacting an office manager, who in turn provided names of volunteers from his/her group. The participants were not told about the specific objectives of the study but were informed that the study was about the impact of workplace physical and social conditions on productivity and well-being. In addition, a subset of the participants had actigraphy recordings to measure light exposure, activity, and sleep. A total of 21 participants had actigraphy recordings, including 10 office workers in windowless workplaces and 11 office workers in workplaces with windows. Participants were selected for actigraphy based on a convenience sample with volunteers from office locations with and without windows. Once the volunteers were identified, daylight factors at their workstations were measured. Only daylight factors > 2% were kept in the study for workers in workplaces with windows. Generally, daylight factors < 2% are deemed not useful for task performance illumination. In this study, we define a windowless workplace as one without any windows or one where workstations were far away from windows and therefore had no exposure to daylight and no views to the outside world. The Institutional Review Board of the University of Illinois at Urbana-Champaign (UIUC) approved the research study, and all volunteers gave informed written consent as required by UIUC regulations and standards. The cities of Urbana-Champaign are relatively small, and the commute for most participants is generally less than 15 minutes by car. Nearly all participants drove individual cars to work. Measures - Questionnaires Office workers' health related quality of life was measured by Short Form 36 (SF-36), a questionnaire with 36 items related to the physical and psychosocial domains of health influenced by a person's experiences, beliefs, and perceptions of health. The SF-36 survey is a well-validated health status questionnaire that measures an individual's physical functioning, bodily pain, and perception of the ability to perform physical, social, and emotional role functions.27 The Pittsburgh Sleep Quality Index (PSQI) was utilized to evaluate subjective sleep quality of the participants. This self-rated questionnaire assesses sleep quality and disturbances over a 1-month time interval.28 The PSQI is composed of 19 self-rated questions and 5 questions rated by a bed partner or roommate. Only the self-rated items were used in scoring the scale. The 19 questions generate 7 component scores: subjective sleep quality, sleep latency, sleep duration, habitual sleep efficiency, sleep disturbances, use of sleeping medication, and daytime dysfunction. Each component score ranges from 0 (no difficulty) to 3 (severe difficulty). The component scores are summed to produce a global score with a range of 0–21. A higher score indicates lower sleep quality. A PSQI global score > 5 is considered suggestive of significant sleep disturbance. A daylight deprivation survey was administered that includes questions pertaining to demographic characteristics (age, gender, race, and working experience) and behavioral characteristics (self-reported amount of exposure to daylight on a scale of 1-10 [with 1 being always exposed and 10 being never exposed], hours of outdoor activities per day, eating behavior prior going to bed, and duration of current light exposure level). Measures - Actigraphy Participants wore an Actiwatch-L (Minimitter) on their non-dominant wrist. An actiwatch device is an ambulatory physiological data logger often used in research and clinical settings to detect and record motion during wake and sleep. The Actiwatch-L has an accelerometer sensitivity of 0.05 g-force and is equipped with a photodiode for measuring amount and duration of light illuminance. Participants were instructed to continuously wear these actiwatches for 2 weeks without removing them (except for bathing) during the period of time they were answering the questionnaires. Participants were also instructed to leave the actiwatches exposed to the environment at all times and to avoid covering them with clothing. The questionnaires and actiwatches were administered during late spring and summer seasons. Valid data were recorded for a range of 6 to 10 workdays and 2 to 4 free days in participants, with the average participant yielding 8.4 workdays and 3.4 free days of actigraphy data meeting inclusion criteria for analysis, as determined by < 4 h off-wrist time per day. Analysis was conducted on Actiware software version 5 (Philips Respironics) with 30-sec sampling epochs and wake threshold value of 40 activity counts. Sleep start was defined as the first 10-min period in which no more than one epoch was scored as mobile. Sleep end was defined as the last 10-min period in which no more than one epoch was scored as immobile. Wake threshold selection was set at medium. Actigraphy measures were calculated as the average of each participant's valid workdays (split into wake time to 08:00 for workday mornings, 08:00 to 17:00 for work hours, and 17:00 to sleep start for workday evenings) and valid free days for activity and light exposure variables, and for nighttime hours following workdays and free days for sleep variables. Actigraphy variables analyzed include total activity counts (sum of all valid physical activity counts for all epochs in the active period from wake time to 08:00 for workday mornings, 08:00 to 17:00 on workdays for work hours, 17:00 to sleep start for workday evenings, and for wake periods during free days), sleep onset time (clock time of sleep start on nights following workdays and free days), sleep onset latency (time elapsed between the start time of a given rest interval and the following sleep start time on nights following workdays and free days), sleep efficiency (the percentage of scored total sleep time to interval duration minus total invalid time for the given rest period on nights following workdays and free days), wake after sleep onset (total minutes between the start time and end time of a given sleep interval scored as wake on nights following workdays and free days), sleep time (total minutes between the start time and end time of a given interval scored as sleep on nights following workdays and free days), sleep fragmentation (sum of percent mobile and percent immobile bouts < 1 min duration to the number of immobile bouts for the given interval on nights following workdays and free days), and average light exposure (sum of all valid illuminance data in lux on a logarithmic scale for all epochs from the start time to the end time of a given interval multiplied by the epoch length in minutes from wake time to 08:00 for workday mornings, 08:00 to 17:00 on workdays for work hours, 17:00 to sleep start for workday evenings, and for wake periods during free days). Statistical Methods First, we performed a χ2 test (homogeneity for proportions) to compare distributions of the demographics and behavioral characteristics as measured by the daylight deprivation survey (age, race, gender, working experience, self-reported amount of exposure to daylight, hours of outdoor activities per day, eating behavior prior to going to bed, and duration of current light level exposure) between participants working in workplaces without windows and participants working in workplaces with windows. Secondly, we performed t-tests to determine any statistical difference between the two groups in terms of office workers' health related quality of life and sleep quality as measured on the SF-36 and PSQI. For the subset of participants with actigraphy recording, distributions of the demographics and behavioral characteristics as measured by the daylight deprivation survey between workers in workplaces with no windows and workers in work-places with windows were compared to distributions in the overall group. T-tests were then utilized to gauge differences between the two groups in terms of the following previously defined actigraphy measures: total activity counts, sleep onset time, sleep onset latency, sleep efficiency, wake after sleep onset, sleep time, fragmentation index, and light exposure. Pearson bivariate correlations were run between work hour light exposure as measured by actigraphy and subjective questionnaires and other actigraphy variables.
RESULTS Demographics and Behavioral Characteristics of the Two Groups of Workers Results of the χ2 test show no significant differences between these two groups in terms of distributions of age, race, gender, working experience, hours of outdoor activities per day, eating behavior prior to going to bed, and duration of current light level exposure (Table 1). Therefore, these two groups were comparable except in their amount of self-reported amount of exposure to daylight (Table 2). Table 1 Demographic and behavioral characteristics of the two groups (more ...) Table 2 Self-reported amount of exposure to daylight between the two groups (more ...) For the subset of participants with actigraphy recording, distributions of the demographic and behavioral characteristics as measured by the daylight deprivation survey between workers in workplaces with no windows and workers in work-places with windows are comparable to respective distributions in the overall group, again with no significant differences in these distributions between groups except in their amount of self-reported amount of exposure to daylight. Light Exposure of the Two Groups of Workers The self-reported amount of exposure to daylight scale shows office workers in workplaces without windows perceived they had significantly less exposure to daylight than office workers in workplaces with windows, as expected (Table 2). Results from actigraphy confirm average light exposure differences during work hours for the two groups, with workers in workplaces with windows receiving more light exposure than workers in workplaces without windows (Table 3 and Figure 1A; 3.00 log lux versus 2.58 log lux; p = 0.02). There was no significant difference in light exposure from wake time to start of the work period (Table 3; 2.57 log lux versus 2.38 log lux; p = 0.32); however, workers with windows in the workplace had more light exposure during workday evenings (Table 3; 2.50 log lux versus 1.93 log lux; p = 0.008) and during free days (Table 3; 3.30 log lux versus 2.37 log lux; p = 0.003) than workers without windows in the workplace. While we cannot say from our data collection whether this difference is from natural daylight or artificial lighting in the office building, workers without windows at the workplace had significantly lower average light exposure than workers with windows during workday work hours and evenings as well as during free days. Table 3 Results of t-tests for actigraphy measures between the two groups (more ...) Figure 1 Actigraphy measures of light exposure, total activity, and sleep time between workers in workplaces with windows (N = 11) and without windows (N = 10). Actigraphy data collected in a subset of the office workers show that those with windows in the workplace had higher light exposure (A), more total activity... (more ...) Physical and Mental Conditions of the Two Groups of Workers Workers in workplaces without windows had significantly worse scores on two of the SF-36 dimensions—role limitation due to physical problems (RP) and vitality (VT)—than workers in workplaces with windows (Figure 2; p = 0.001 and p = 0.004, respectively). There was also a positive correlation between light exposure during work hours and role limitation due to physical problems (R = 0.503, p = 0.02). Overall, both the physical component summary (PCS) (p = 0.09) and mental component summary (MCS) (p = 0.11) scores of those in workplaces without windows were lower than scores of those working in workplaces with windows (Table 4). Participants in workplaces without windows reported poorer scores on all time on workday nights (R = 0.483, p = 0.03). While there were no significant differences between workers with windows and workers without windows in sleep onset time (21:46 versus 22:04), sleep onset latency (10 min vs 19 min), sleep efficiency (91% vs 89%), wake after sleep onset (30 min vs 37 min), and sleep fragmentation (19 vs 22) on workday nights, the averages point toward better measures of sleep quality for workers with windows at the workplace than workers without windows at the workplace during the workweek. Similarly, workers with windows at the workplace slept more than their counterparts on free day nights (506 min vs 389 min; p = 0.005), and although there were no differences in sleep onset time (22:06 vs 22:48), sleep onset latency (15 min vs 20 min), sleep efficiency (91% vs 90%), wake after sleep onset (31 min vs 36 min), and sleep fragmentation (20 vs 22) on free day nights, the averages point toward better measures of sleep quality for workers with windows at the workplace than workers without windows at the workplace during free day nights. Figure 2 Short Form 36 (SF-36) measures of vitality and role limitation due to physical problems between workers in workplaces with windows (N = 22) and without windows (N = 27). Workers with windows in the workplace reported better scores on vitality (A) and role limitation due to physical problems (B) on the... (more ...) Table 4 Results of t-tests for Short Form-36 between the two groups (more ...) Table 5 Results of t-tests for Pittsburgh Sleep Quality Index between the two groups (more ...) Figure 3 Pittsburgh Sleep Quality Index (PSQI) measures between workers in workplaces with windows (N = 22) and without windows (N = 27). Workers with windows in the workplace reported better overall global score on the PSQI (A) compared to workers with no windows in the workplace. The difference in global score is... (more ...)
DISCUSSION These results demonstrate a relationship between work-place light exposure and office workers' sleep quality, activity patterns, and quality of life. Workers in workplaces with windows not only had significantly more light exposure during work hours but also slept an average of 46 minutes more per night during the workweek than workers in workplaces without windows. Workers with windows in the workplace also had more light exposure during the workday evenings and during free days, as well as longer sleep time compared to workers without windows in the workplace. However, there were no differences in light exposure in the mornings before the work period. Workers without windows also reported poorer scores than their counterparts on the global PSQI score and the PSQI component score for sleep disturbances. None of the other component scores of the PSQI were significantly different between groups, nor were actigraphy sleep variables other than sleep time different between the groups. These findings suggest that light exposure, or the lack thereof, during work hours may have effects beyond the workplace that impact sleep duration and quality, which may then have further effects on other health factors. Research indicates that insufficient sleep and reduced sleep quality have myriad health and safety consequences. For example, insufficient sleep and reduced sleep quality have been associated with higher evening levels of cortisol, impaired glucose metabolism, increases in appetite via decreased leptin and increased ghrelin levels, and higher body mass index, as well as increased fatigue and deterioration of performance, alertness, and mental concentration, which can lead to increased error rates and subsequent risk of injury.7–9,29–32 These health and performance consequences may affect perceived health related quality of life, as measured by the SF-36. Our results from the SF-36 show workplaces without windows have significantly negative impact on workers' role limitation due to physical problems (RP) and vitality (VT), as well as a marginal negative impact on workers' mental health compared to workplaces with windows. These results are similar to the findings of a study that examined five dimensions (GH, V, SF, RE, and MH) of the SF-36 and found that the scores of vitality (VT), social functioning (SF), and mental health (MH) for those working in dark offices are lower than scores for those working in offices with more lighting.33 Another study focusing on predictors of burnout among nurses found that exposure to at least three hours of daylight per day resulted in less stress and higher satisfaction at work.34 While those with more daylight in the workplace also have higher daily physical activity during work hours and workday evenings, our analysis cannot determine whether the workers get more activity because of the daylight or whether they have more daylight exposure due to activity. There was no difference in physical activity between the two groups during free days despite differences in light exposure during free days, and correlations between physical activity levels and light exposure during work hours, workday evenings, and free days did not suggest a strong relationship. Nonetheless, it remains a possibility that differences in activity level may influence light exposure and also sleep, yet the tendency towards higher activity levels indicates workers with more daylight exposure may have fewer physical problems or complaints regarding vitality in parallel with our findings on subjective measures of the SF-36. Prior to this study, little was known about how architectural features such as windows impact light exposure and subsequent effects on physical and mental factors. Via examination of the influence of office settings with and without windows on office workers' light exposure, sleep, physical activity, and quality of life via actigraphy and subjective measures, this research study shows office workers in workplaces with windows may have more light exposure, better sleep quality, more physical activity, and higher quality of life ratings than office workers in work-places without windows. This study has some limitations that could be addressed in future work. For example, the small sample size and sampling methodology could be addressed in a larger study. Participants for this study were volunteers based on a convenience sample, which may have introduced bias. The amount of light in an office may be associated with position or level of experience in the workplace; however, we found no differences in age, race, gender, years at current job, and duration of working in current light levels between workers in office settings with and without windows. We also do not have data from the participants on caffeine use, measurements of stress levels, and chronotype, which is of interest given the outcome measures of this study. Although we observed no differences in sleep onset time between the two groups of workers on workday nights and free day nights, the possibility remains that chronotype, circadian timing, or other behavioral measures may be responsible for some of the differences observed in the two groups of workers. This warrants further investigation. The objective measures of wrist actigraphy support the subjective findings; however, actigraphy data were collected for only 21 of the 49 total participants. Furthermore, although actigraphy has reasonable validity and reliability and is often used as a sleep assessment tool in sleep medicine, this methodology has some limitations. Sleep diaries were not collected in this study, and therefore were unavailable for the actigraphy analysis. For sleep-wake periods, actigraphy has low specificity for detecting wakefulness within sleep periods. Actigraphy is also neither sensitive to low light levels nor calibrated for artificial fluorescent lighting. As such, light exposure measurements for workers in office settings without windows may be an underestimate. In addition, since light exposure data are collected from the wrist, there is the possibility that error may be introduced by covering of the actiwatch, and therefore, reported values may not be fully representative of the light levels reaching the retina. Our data collection methods also do not allow for differentiation between natural daylight and artificial lighting, and do not allow for analysis of specific wavelengths of light exposure. Future studies would benefit from using devices that collect spectral distribution for comparison between the two workplace groups. Lastly, additional benefits of workplaces with windows, such as the roles of views and other dimensions, were not taken into account in this study. Views may bring some psychological dimension while daylight may have physiological effects. Future research may be able to dissociate the different roles of views and daylighting of windows. This can be done, for example, by exploring the differences between skylights that provide very limited views to the sky only versus side windows. Despite these limitations, significant differences are seen with light exposure levels and subsequent measures of sleep quality and physical and mental well-being. As emphasized in the World Health Organization's Declaration on Occupational Health for All,1 the focal point for practical occupational health activities is the workplace. Therefore, employers have a social responsibility to plan and design a safe and healthy working environment for their employees. Some countries (such as Canada, Germany, and France) recommend certain amounts of daylight in schools and offices. Yet even in these countries it is not a requirement. In the United States, the national building code lists windows primarily as a means of emergency escape and rescue as opposed to natural lighting. Given the results of this study, we conclude that emphasizing daylight exposure and lighting in the workplace may positively affect the well-being of people working in those spaces. Lower amounts of light exposure in the workplace was associated with reduced sleep duration, poorer sleep quality, lower activity levels, and reduced quality of life in this sample of office workers. Light exposure in the workplace may therefore have long-lasting and compounding effects on the physical and mental health of the workers not only during but also beyond work hours. Enhanced indoor lighting for those with insufficient lighting in current offices as well as increased emphasis on light exposure in the architectural design of future office environments is recommended to improve office workers' sleep quality and physical well-being. Workers with limited or no access to windows in the workplace may increase their light exposure during work hours in various ways. Taking a walk during a break and enjoying lunch outdoors are simple ways to increase daytime natural light exposure. Further research is needed to determine what light exposure durations or intensities are sufficient or optimal for benefits to well-being. |||||
What is a one-paragraph summary of the above article? | – No windows in your office? You may be losing sleep over it—literally. Researchers surveyed 22 workers getting natural light exposure and 27 others missing it; they found that those who were getting the exposure at work got an extra 46 minutes of sleep during the work week and reported better health overall, Fast Company reports. That could be because their circadian rhythms were altered due to lack of light, the magazine suggests. Data was based on self-reporting as well as light-tracking devices worn by participants. Even on nights when "windowless" workers hadn't been at the office, they still got less sleep. Another odd finding: Workers with windows actually got more light exposure even when they weren't at work. Maybe that's because they have more energy to move around, a researcher suggests. "We suggest that architectural design of office environments should place more emphasis on sufficient daylight exposure for workers in order to promote health and well-being," the experts say in the Journal of Clinical Sleep Medicine, via the Daily Mail. (Click to see why seven hours of sleep might be better than eight.) | 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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– If you smoke for most of your life and still live to a ripe, old age, you might have more than luck on your side. Though smokers can generally expect to live 10 years less than non-smokers, this is by no means a hard and fast rule. Jeanne Calment, for example, smoked every day from the age of 21, yet was the oldest person in the world when she died at age 122 in 1997, reports the Washington Post. To understand such cases, scientists at UCLA carried out a study on long-lived smokers, comparing 90 smokers who lived past 80 with 730 who died before 70. They identified genetic markers that allows some to endure damage from stressors such as cigarette smoke better than the rest of us. In fact, the markers "seem to promote longevity," study author Morgan Levine says in a release. "Many of these markers are in pathways that were discovered to be important for aging and lifespan in animal models," says Levine, noting the genes "may facilitate lifespan extension by increasing cellular maintenance and repair." When researchers compared those with the gene variants to 6,447 non-smokers, they found the former group was 22% more likely to survive into their 90s, and three times more likely to reach 100, reports UPI. They also had a lesser risk of cancer. Genetic tests might someday allow people to easily learn whether they are among this "biologically distinct" group. Just don't bet on good news: Levine notes it's "extremely small," and "even among those who are genetically predisposed to longevity, smoking cessation is likely still one of the best things they can do for their health." (Want to live longer? You might try chili peppers.) | LOS ANGELES, Sept. 9 (UPI) -- Smoking cigarettes is universally regarded as bad for health, but not everybody who smokes develops cancer or other diseases linked to the habit. New research shows that a proportion of lifelong smokers live to extreme ages despite the long list of negative effects cigarettes have on the body.
Researchers found a set of genetic markers that promote longevity in cells and mitigate damage to them, which may be the explanation for preventing diseases tied to cell dysfunction.
"Many of these markers are in pathways that were discovered to be important for aging and lifespan in animal models," said Dr. Morgan Levine, a researcher at the University of California Los Angeles, in a press release. "There is evidence that these genes may facilitate lifespan extension by increasing cellular maintenance and repair. Therefore, even though some individuals are exposed to high levels of biological stressors, like those found in cigarette smoke, their bodies may be better set up to cope with and repair the damage."
Researchers used data from the Health and Retirement Study to conduct a genome-wide study comparing 90 long-lived smokers with 730 smokers between the ages of 52 and 69. They found a set of 215 nucelotide polymorphisms, which together make up a functional interaction network that allows people with them to better withstand environmental damage and mitigate the damage to cells.
The set of nucleotide polymorphisms was then used to compare the smokers with 6,447 non-smokers, which showed people with the polymorphisms were 22 percent more likely to survive into their 90s and and triple the chance of making it 100 years old. The same comparison also found the group with the genetic differences had an 11 percent reduction in cancer prevalence.
The set of genetic differences may play into future research working to prevent cancer because genetic instability is a key part of developing tumors, researchers said.
The study is published in The Journals of Gerontology. ||||| Abstract
Human longevity and diseases are likely influenced by multiple interacting genes within a few biologically conserved pathways. Using long-lived smokers as a phenotype ( n = 90)—a group whose survival may signify innate resilience—we conducted a genome-wide association study comparing them to smokers at ages 52–69 ( n = 730). These results were used to conduct a functional interaction network and pathway analysis, to identify single nucleotide polymorphisms that collectively related to smokers’ longevity. We identified a set of 215 single nucleotide polymorphisms (all of which had p <5×10 −3 in the genome-wide association study) that were located within genes making-up a functional interaction network. These single nucleotide polymorphisms were then used to create a weighted polygenic risk score that, using an independent validation sample of nonsmokers ( N = 6,447), was found to be significantly associated with a 22% increase in the likelihood of being aged 90–99 ( n = 253) and an over threefold increase in the likelihood of being a centenarian ( n = 4), compared with being at ages 52–79 ( n = 4,900). Additionally, the polygenic risk score was also associated with an 11% reduction in cancer prevalence over up to 18 years (odds ratio: 0.89, p = .011). Overall, using a unique phenotype and incorporating prior knowledge of biological networks, this study identified a set of single nucleotide polymorphisms that together appear to be important for human aging, stress resistance, cancer, and longevity.
Over time, nearly all biological organisms experience a progressive decline of cellular structure and function, resulting in a decreased ability for systems to adequately respond to environmental perturbations and maintain homeostasis. This process known as aging is the number one risk factor for mortality among humans, contributing to an individual’s susceptibility to a number of distinct conditions such as cardiovascular disease, cancer, diabetes, neurodegenerative diseases, sarcopenia, lung disease, vision/hearing impairment, and frailty ( 1 , 2 ). Accordingly, it has been suggested that slowing the aging process would not only increase life span but also postpone most major illnesses and disability ( 3 ).
In 1993, a paper by Schächter and coworkers discussed the enormous potential for identifying alleles that influence aging and longevity in humans ( 4 ). Since then, with the growing availability of sequencing data, the search for genes that regulate human aging and longevity has gained significant momentum ( 5–8 ). Using twin data, researchers have estimated that genetic differences account for 20%–30% of the variance in human life span, with the remainder being under the influence of environmental or stochastic factors ( 9 , 10 ). However, it has been suggested that the degree of genetic influence may also vary as a function of environment ( 11 ). Evidence from animal models suggests that genetic factors which influence longevity may be linked to innate stress resistance ( 12–15 ); if so, genetic endowment may contribute differentially to variability in life span within populations, as a function of environmental conditions. For instance, genes that promote somatic maintenance and repair may exhibit a larger effect among individuals who accumulate increased exposure to adverse environmental conditions. Exposure to damaging environmental stressors would likely result in significant reductions in life span for the majority of individuals; however, individuals genetically endowed with genes promoting somatic maintenance and repair may be able to better mitigate damage and thus would experience little to no reduction in life span. Conversely, the majority of those living under advantageous environmental conditions may have relatively long survival, due to minimal damage accumulation, and thus genetic differences would have less of an effect on life-span variability.
Smoking is one of the most consistent biological stressors among humans and has been shown to have drastic consequences for life span and disease progression, most notable heart disease and cancer ( 16 , 17 ). It is suggested that cigarette exposure may impact the risk of death and disease via its acceleration of the aging process ( 18 , 19 ). Yet, not all smokers experience earlier mortality—in fact, a small proportion manage to survive to extreme ages. For instance, centenarians have been shown to exhibit the same poor health behaviors as other members of their birth cohort ( 20 ). There is reason to believe that these long-lived smokers may represent a biologically distinct group, endowed with genetic variants allowing them to respond differentially to environmental stressors. In previous work, we showed that current heavy smokers who had survived to age 80 and beyond had mortality risks and inflammatory levels similar to nonsmoking individuals of the same age—suggesting that they may be innately equipped to offset the harmful effects of cigarette exposure ( 21 ).
In experimental studies, many of the genes associated with stress resistance and longevity in animal models have been found to be comprised within pathways, such as the insulin-like growth factor-I/insulin signaling pathway, that are evolutionarily conserved among yeast, drosophila, Caenorhabditis elegans , mice, and humans ( 14 , 22 ). However, most of these mutations occur so rarely in nature that it is unlikely that they would contribute to the variability of life span within the general population. Furthermore, most of these mutations were discovered in organisms with identical genetic backgrounds, which will certainly not be the case when identifying polymorphisms that influence life span in humans. For humans, it is likely that multiple polymorphisms may simultaneously influence life span. For this reason, we hypothesize that multiple genes, potentially within these conserved pathways, influence longevity in a polygenic manner. While work by Sebastiani and coworkers ( 8 ) successfully used Bayesian networks to quantify genetic signatures that were predictive of longevity, most genome-wide association studies (GWAS) of human longevity investigate the individual influences of single nucleotide polymorphisms (SNPs). Incorporating a priori information on networks may allow us to identify functionally related genes whose effects are too small to observe individually, yet jointly influence aging, longevity, and disease risks. Therefore, the current study aims to (a) investigate genes associated with the long-lived smoker phenotype, drawing on previous knowledge of functional interaction networks and pathways, in order to conceptualize GWAS results; (b) generate a polygenic risk score (PRS) based on GWAS and network-selected SNPs; (c) examine how the genetic score is related to age in the nonsmoking population of middle-aged and older adults; (d) examine how the genetic score is related to prevalence of disease within both the smoking and nonsmoking populations.
Methods
Discovery and Validation Samples
Participants were part of the 2006 and 2008 waves of the Health and Retirement Study (HRS), a nationally representative longitudinal study of health and aging in the United States ( 23 ). Our discovery sample was limited to white current smokers only. Cases ( N = 90) were participants who reported that they currently smoked and who had survived to at least age 80 at the last wave they were interviewed, while controls ( N = 730) were participants who reported that they currently smoked and who were less than 70 years of age at the last wave they were interviewed. It is well known that on average, smokers’ life expectancy is reduced by 10 years. Thus, one would expect that the mortality selection of smokers aged 80+ is similar to the mortality selection of nonsmokers aged 90+ (an age cutoff commonly used in longevity studies). Furthermore, we based our age cutoffs on our previous work, which provided evidence that heavy/current smokers who survived to age 80+ were a distinct group ( 21 ). We showed that a nationally representative group of 80+-year-old smokers did not have higher mortality rates (during up to 18 years of mortality follow-up) compared to 80+-year-old never smokers. They also had similar physiological functioning measures—inflammation, blood pressure, and immune function. On the other hand, smokers who were aged 50–69 had significantly higher mortality rates during follow-up and worse contemporaneous physiological functioning measures than never smokers of the same age. Finally, the mortality rates of the younger group suggested that the majority of 50- to 69-year-old current smokers will not survive to ages 80+. Overall, this suggests that smokers in their 80s and beyond likely represent a biologically resilient group ( 21 ).
Our validation sample ( N = 6,447) was made up of HRS participants who self-reported as nonsmokers at the time of their last interview, were aged 52 and older, and who had complete genetic data from which to generate a PRS. Participants younger than 52 were excluded, given that HRS collects data on a nationally representative sample of older adults (aged 52 and older), and their spouses, and as a result, younger participants represent spouses of persons aged 52 and older and therefore may not be representative of the population their age. In the validation sample, 4,501 had missing genotype information for at least one of the SNPs used to create the PRS. When comparing excluded individuals (aged 50 and older) to our validation sample, we found that they did not significantly differ in age, sex, or smoking status (former vs never). However, our validation sample was made up of significantly more participants who self-reported their race as white (86%) than the excluded sample (83%).
Genotyping and Quality Control
Genotyping was performed for participants who provided saliva samples and signed consent forms in 2006 and 2008 and was carried out by the NIH Center for Inherited Disease Research (CIDR) using the Illumina Human Omni-2.5 Quad Beadchip, with coverage of approximately 2.5 million SNPs. Quality control filters were performed by CIDR and the Genetics Coordinating Center of the University of Washington ( http://hrsonline.isr.umich.edu/sitedocs/genetics/HRS_QC_REPORT_MAR2012.pdf ). These filters consisted of removal of: duplicate SNPs; missing call rates more than or equal to 2%; more than 4 discordant calls in 423 study duplicates; more than one Mendelian error; Hardy–Weinberg equilibrium p values less than 10 −4 in European or African samples; sex differences in all allelic frequency more than or equal to 0.2; and sex differences in heterozygosity greater than 0.3. As a result, 2,201,371 SNPs remained. However, given our small sample of cases which could inflate p values for SNPs with small minor allele frequencies, we set our minor allele frequency cutoff at 0.05, which left us with a total of 1,224,285 SNPs for our analysis.
Principal components analysis was conducted by the HRS to account for population structure in accordance with the methods described by Patterson and coworkers ( 24 ). This analysis produced sample eigenvectors (EV). A screen plot generated by HRS showed that the 20 components produced by the principal components analysis only accounted for a small fraction of the overall genetic variance (<4%) for the full HRS genetic sample and that most of this was contained within the first two components ( 23 ). We used a logistic regression model to examine the relationship between the 20 EV and our phenotype and found that none of the EV were significantly associated with being a long-lived smoker. Nevertheless, we ultimately decided to adjust for the first four EV in all subsequent analyses. More information on QC checks and the principal components analysis is provided by HRS ( 25 ).
Functional Interaction Network
PLINK’s gene report command ( 26 ) was used to map SNPs with p less than 5×10 −3 to Genes based on GRCh37/hg19 coordinates. Start and end genome positions from RefSeq genes were provided by the UCSC table browser ( http://genome.ucsc.edu/cgi-bin/hgTables ). For our analysis, we did not assign upstream or downstream SNPs to a gene; only those SNPs that fell within the designated GRCh37/hg19 coordinates of the gene were assigned to the gene—no border was added to the start and stop coordinates of each gene.
Cytoscape plugin Reactome FI ( 25 ) was used to identify and examine functional interaction networks based on results from the GWAS. The functional interaction networks in the Reactome FI plugin are based on data from the Reactome database ( 27 , 28 ), which contains information on manually curated human pathways—DNA replication, transcription, translation, the cell cycle, metabolism, and signaling cascades. “Reactions” encompass a number of biological processes, including binding, activation, translocation, degradation, and classical biochemical reactions. The information in the database comes from published research and is peer-reviewed and regularly updated by expert biologists. More information on the database is available through the Reactome website ( http://www.reactome.org/ ).
Two gene sets—those whose assigned SNPs had p less than 5×10 −3 in the GWAS and those whose assigned SNPs had p less than 5×10 −4 in the GWAS—were selected for incorporation in the network analysis. These two thresholds were chosen to allow for more lenient significance criteria, which may address the problem of missing heritability ( 29 ), yet limiting the potential of overfitting which could weaken predictive ability in validation studies ( 30 ). After examining the network structures of both sets, the subset with p less than 5×10 −3 was selected for further analysis and validation, given that the network comprised of genes from SNPs with p less than 5×10 −4 significance had too few SNPs to generate large enough functional interaction networks to produce a meaningful PRS.
Using the genes which formed a functional interaction network, and whose assigned SNPs had p less than 5×10 −3 in the GWAS, we ran pathway enrichment analysis using Reactome FI. This analysis examines whether the number of networked genes in a given pathway is significantly higher than what would be expected by chance alone. Probability and p value for the pathway enrichment analysis is determined by binomial test and false discovery rate based on 1,000 permutation test. The possible pathways are curated from a number of resources including Reactome, KEGG, CellMap, NCI PID, and BioCarta.
Polygenic Risk Score
PRS were developed as a means of examining the aggregate influence of multiple genetic markers ( 31 ). A PRS can be thought of as a measure of “genetic burden” ( 32 ) and has become increasingly used to facilitate understanding genetic associations with complex traits. To generate a PRS, the 215 genes in our final network were mapped back to the original SNPs. For those mapping to more than one SNP, the SNP with the lowest p value was selected to represent that gene. Next PRS were calculated for the discovery (smokers) and the validation samples (nonsmokers) from the HRS population.
The PRS assumes a dose–response effect, where for each SNP, persons who are homozygous for the negatively associated allele (major allele if the beta coefficient was positive, and minor allele if the beta coefficient was negative) are coded as 0, persons who are heterozygous are coded as 1, and persons who are homozygous for the positively associated allele are coded as 2. Finally, the allele counts for each SNP were weighted by the log of their odds ratio (OR) from the GWAS and summed across the 215 SNPs from our FI network, to generate the total and component PRS. Scores were then standardized to have a mean of 0 and a SD of 1.
Statistical Analysis
Study methodology is outlined in Figure 1 . A case–control GWAS (long-lived vs normal lived smokers) was used to identify SNPs that are potentially associated with longevity and biological stress resistance. Moderately significant SNPs from the GWAS were then mapped to genes and used to build a genetic network based on a priori experimental proteomic evidence of identified genetic pathways and gene interactions. SNPs included within the gene network were used to calculate composite PRS for the entire HRS genetic sample. Using multinomial logistic regression, controlling for the first four EV and sex, we examined the association between PRS and longevity—operationalized as the probability of being in an older age group: ages 80–89, 90–99, or 100+, relative to being at ages 50–79 during the most recent wave interviewed—using a validation sample of nonsmokers from the HRS ( n = 6,447). We then examined whether using the network-based approach to SNP selection for inclusion in the PRS improved predictive ability, we compared the association between being very old and our final PRS to the associations between being very old and four other PRS which utilized other SNP selection criteria—top hits, a random subset with p less than 5×10 −3 , a random subset of the 784 SNPs with p less than 5×10 −3 that also mapped to genes, and the top hits of the 784 SNPs ( p < 5×10 −3 that also mapped to genes). To compare the PRS, logistic regression models controlling for the first four EV and sex were used, with participant aged 50–79 coded as 0 and participants aged 90 and older coded as 1. The cutoff age was increased to 90 versus 80, which was used in the initial GWAS, given that our validation sample was made up of nonsmokers for whom survival to age 80 is much more likely. Finally, we tested the association between PRS and disease prevalence for three major diseases of aging: heart disease, cancer (other than skin), and diabetes. Over 10 waves spanning from 1992 to 2010, participants were asked whether they had ever been diagnosed with each condition. Three logistic regression models incorporating the panel data and adjusting for repeated observations using random effects were run to assess the association between PRS and each of the three conditions. These models were run controlling for age, sex, the first four EV, self-reported race, education, smoking status at each wave, body mass index at each wave, and sample classification (discovery cases, discovery controls, or validation sample).
Figure 1. View largeDownload slide Study approach. The study utilized data from the HRS to run a GWAS and network analysis using long-lived smokers as the phenotype of interest. SNPs identified through these processes were then used to create PRS. For validation and replication, we examined the association between the score and age or longevity among nonsmokers in the nationally representative population in HRS. GWAS = genome-wide association study; HRS = Health and Retirement Study; PRS = polygenetic risk score; SNP = single nucleotide polymorphism.
Figure 1. View largeDownload slide Study approach. The study utilized data from the HRS to run a GWAS and network analysis using long-lived smokers as the phenotype of interest. SNPs identified through these processes were then used to create PRS. For validation and replication, we examined the association between the score and age or longevity among nonsmokers in the nationally representative population in HRS. GWAS = genome-wide association study; HRS = Health and Retirement Study; PRS = polygenetic risk score; SNP = single nucleotide polymorphism.
Results
Genome-Wide SNP Analysis
Our GWAS differentiating long-lived smokers from younger smokers was run controlling for sex and four EV which control for population stratification. Although no SNPs met the genome-wide significant threshold—which is not surprising given our small sample size—20 SNPs met the threshold for “suggestive” association ( Figure 2a ). Also, as shown in our Q-Q plot ( Figure 2b ), we observed a moderate departure from the null hypothesis of no association, beginning between p = 10 −3 and 10 −4 . Studies of “missing heritability” have suggested that while for the most part, the SNPs meeting statistical significance cutoffs in GWAS only account for a relatively small proportion of the variance in a phenotype, there is evidence that the additional consideration of less significant loci may capture more of the association with phenotypic heterogeneity. Two p value thresholds were considered ( p < 5×10 −3 and p < 5×10 −4 ) based on previous studies suggesting that the proportion of the variance explained for a phenotype increases when allowing p value threshold to relax to such levels ( 26 ), but that allowing for variables with higher p values than this reduced predictive power ( 33 ).
Figure 2. View largeDownload slide GWAS results. We found that while no SNPs met the criteria for genome-wide significance, a number of SNPs had “suggestive” association with longevity among smokers (a). Additionally, our Q-Q plot shows that we had more SNPs that had p values <5×10 −4 than might be expected by chance (b). GWAS = genome-wide association study; SNP = single nucleotide polymorphism.
Figure 2. View largeDownload slide GWAS results. We found that while no SNPs met the criteria for genome-wide significance, a number of SNPs had “suggestive” association with longevity among smokers (a). Additionally, our Q-Q plot shows that we had more SNPs that had p values <5×10 −4 than might be expected by chance (b). GWAS = genome-wide association study; SNP = single nucleotide polymorphism.
Network and Pathway Analysis
SNP locations were mapped to Genes—for SNPs with p less than 5×10 −3 and p less than 5×10 −4 from the GWAS. Overall, there were 535 SNPs with p less than 5×10 −4 , which mapped to 115 genes, and 5,184 SNPs with p less than 5×10 −3 , which mapped to 784 unique genes. Cytoscape plugin Reactome FI was used to construct functional interaction networks and run subsequent pathway enrichment analyses. Reactome FI was designed to identify network patterns that relate to disease. The database covers more than 50% of human proteins which are used to build functional interaction networks based on a set of input genes.
Using the 2013 FI network build, we found that 215 of our 784 genes ( p < 5×10 −3 ) made up functional networks that had five or more genes each, the largest of which was encompassed by 202 genes ( Figure 3 ). The other 569 genes were either not functionally connected to any other genes that had SNPs with p less than 5×10 −3 or formed networks of three or fewer genes. On the other hand, only three genes were comprised in the network that utilized a p value cutoff of p less than 5×10 −4 , therefore, the network with p less than 5×10 −3 was selected for use in further investigation and validation.
Figure 3. View largeDownload slide Functional interaction network. After mapping SNPs with p values <5×10 −3 to genes, we found that 215 of them were comprised within functional interaction networks of five or more genes—200 genes were in a single network and 15 genes made up 3 networks of 5 genes each. Of the 215 SNPs (represented by their respective genes in the network), the majority had p values between 5×10 −4 and 5×10 −3 , associations that would have been overlooked using a normal GWAS approach. GWAS = genome-wide association study; SNP = single nucleotide polymorphism.
Figure 3. View largeDownload slide Functional interaction network. After mapping SNPs with p values <5×10 −3 to genes, we found that 215 of them were comprised within functional interaction networks of five or more genes—200 genes were in a single network and 15 genes made up 3 networks of 5 genes each. Of the 215 SNPs (represented by their respective genes in the network), the majority had p values between 5×10 −4 and 5×10 −3 , associations that would have been overlooked using a normal GWAS approach. GWAS = genome-wide association study; SNP = single nucleotide polymorphism.
Next, we ran Reactome FI’s pathway enrichment analysis for these 215 genes in the network using p less than 5×10 −3 as the significance threshold and found 21 pathways that were enriched at false discovery rate less than 5×10 −3 . The 10 most highly enriched pathways, in order, included: P13K-Akt signaling, pathways in cancer, signaling by platelet-derived growth factor, glutamatergic synapse, Ras signaling pathway, Rap1 signaling pathway, L1CAM interactions, focal adhesion, Netrin-1 signaling, and Netrin-mediated signaling ( Supplementary Table S1 ).
Validation Using a PRS
A standardized PRS was generated based on a weighted composite score of the 215 SNPs from the selected interaction network and was evenly distributed ( Figure 4a ), with a range from −3.68 to 6.02 in the overall HRS population (discovery and validation sample). Mean PRS were compared between our original cases and controls—smokers aged 80+ and smokers younger than 70, respectively—to determine how much of variation in the original phenotype was explained using a composite SNP score of only 215 SNPs from the original 1,224,285 SNPs. Results showed that the score completely accounted for group membership, with no overlap between the two groups ( Figure 4b ). Of our original 90 cases of long-lived smokers, 49 had complete data on all the SNPs needed to generate the overall PRS, and we found that for this group, PRS ranged from 2.34 to 6.02, with a mean of 4.17 and a SD of 0.78. Among the 730 controls, 422 had no missing genotype data for the 215 SNPs, and these participants had PRS ranging from −3.41 to 2.32, with a mean of −0.55 and a SD of 0.95. Not only were scores significantly higher for the long-lived group, but scores also appeared to be more homogeneous.
Figure 4. View largeDownload slide Associations between PRS and longevity. Overall, the weighted PRS was found to be fairly evenly distributed and ranged between −3.68 and 6.02 (a). When comparing the scores of our GWAS cases and controls, we found that there was no overlap between the two groups (b)—cases all had scores of 2.34 or greater (with a mean of 4.17), while controls had scores ranging between −3.41 and 2.32 (with a mean of −0.55). A multinomial logistic regression model was used to examining the association between PRS and age in a validation sample ( n = 6,447). Results were used to predict the proportion of centenarians in the population by PRS (c). We found that among individuals with a PRS of −2.0 (2 SD s below the mean), only 3.2 in 100,000 persons are predicted to be a centenarian. On the other hand, for individuals with a PRS of 2.0 (2 SD s above the mean), 340.3 in 100,000 persons are predicted to become centenarians. GWAS = genome-wide association study; PRS = polygenetic risk score; SNP = single nucleotide polymorphism.
Figure 4. View largeDownload slide Associations between PRS and longevity. Overall, the weighted PRS was found to be fairly evenly distributed and ranged between −3.68 and 6.02 (a). When comparing the scores of our GWAS cases and controls, we found that there was no overlap between the two groups (b)—cases all had scores of 2.34 or greater (with a mean of 4.17), while controls had scores ranging between −3.41 and 2.32 (with a mean of −0.55). A multinomial logistic regression model was used to examining the association between PRS and age in a validation sample ( n = 6,447). Results were used to predict the proportion of centenarians in the population by PRS (c). We found that among individuals with a PRS of −2.0 (2 SD s below the mean), only 3.2 in 100,000 persons are predicted to be a centenarian. On the other hand, for individuals with a PRS of 2.0 (2 SD s above the mean), 340.3 in 100,000 persons are predicted to become centenarians. GWAS = genome-wide association study; PRS = polygenetic risk score; SNP = single nucleotide polymorphism.
Next using our validation sample, we performed a multinomial logistic regression, controlling for the four EV, sex, and race to determine if the PRS was associated with the probability of being in an older age group—aged 80–89 ( n = 1,290), 90–99 ( n = 253), and 100+ ( n = 4)—relative to those aged 52–79 ( n = 4,900). Our results showed ( Table 1 ) that among these 6,447 participants, a higher PRS was associated with an increased likelihood of being at ages 90–99 or being a centenarian, relative to being in the youngest age group (50–79). Results showed that a one unit increase was associated with 20% greater likelihood of being at ages 90–99 compared to 29–79 (OR = 1.20, p = .007), and a 3.3-fold increases in the likelihood of being a centenarian (OR = 3.27, p = .027). Based on the parameter from Table 1 , we estimated the predicted proportion of centenarians in the population of nonsmokers, by PRS ( Figure 4c ). We found that for individuals with a PRS that was 2 SD s below the mean (PRS = −2), only 3.2 in 100,000 were predicted to be centenarians. For individuals with a mean PRS (PRS = 0), 33.2 in 100,000 were predicted to be centenarians, and for individuals with a PRS that was 2 SD s above the mean (PRS = 2), 340.3 in 100,000 were predicted to be centenarians.
Table 1. Age Category Odds Ratio p Value 80–89 1.04 0.204 90–99 1.20 0.007 100+ 3.27 0.027 <80 (Reference category) Age Category Odds Ratio p Value 80–89 1.04 0.204 90–99 1.20 0.007 100+ 3.27 0.027 <80 (Reference category) View Large
Table 1. Age Category Odds Ratio p Value 80–89 1.04 0.204 90–99 1.20 0.007 100+ 3.27 0.027 <80 (Reference category) Age Category Odds Ratio p Value 80–89 1.04 0.204 90–99 1.20 0.007 100+ 3.27 0.027 <80 (Reference category) View Large
To provide evidence that using a network-based approach to select candidate SNPs improved our predictive measure, we compared the strength of the association between longevity and our measure to the associations between longevity and four other weighted PRSs from 215 SNPs selected via other means—top hits (the 215 most significant SNPs from the GWAS), a random subset of 215 SNPs with p less than 5×10 −3 from the GWAS, a random subset of 215 SNPs that were part of the 784 SNPs that had p less than 5×10 −3 from the GWAS and that also mapped to genes, and the 215 most significant SNPs out of the subset of 784 SNPs (those with p < 5×10 −3 that also mapped to genes). To validate our approach, we used five separate logistic regression models—one per individual PRS—with the outcome being 1 if an individual was 90+ years old and 0 if he/she was aged 52–79. Models were run using our validation sample only and controlling for the four EV, sex, and self-reported race ( Table 2 ). Of the five models, our original measure which utilized the functional interaction network to select SNPs for inclusion in the PRS was the only PRS variable found to be statistically significant (OR = 1.22, p = .005)—and it remained significant even after Bonferroni adjustment ( p < .01). On the other hand, the four other PRSs were not significantly associated with being at ages 90 and older and had OR between 0.83 and 1.10 with p values ranging from .122 to .872. Lists of SNPs and corresponding gene sets used for the other PRS measures are available upon request.
Table 2. PRS Method Odds Ratio p Value Network-based PRS a 1.21 .005 Top SNPs b 0.95 .649 Random SNPs c 0.83 .122 Random genes d 0.98 .872 Top genes e 1.10 .253 PRS Method Odds Ratio p Value Network-based PRS a 1.21 .005 Top SNPs b 0.95 .649 Random SNPs c 0.83 .122 Random genes d 0.98 .872 Top genes e 1.10 .253 View Large
Table 2. PRS Method Odds Ratio p Value Network-based PRS a 1.21 .005 Top SNPs b 0.95 .649 Random SNPs c 0.83 .122 Random genes d 0.98 .872 Top genes e 1.10 .253 PRS Method Odds Ratio p Value Network-based PRS a 1.21 .005 Top SNPs b 0.95 .649 Random SNPs c 0.83 .122 Random genes d 0.98 .872 Top genes e 1.10 .253 View Large
Given that the replication and discovery sets both came from the same population sample (HRS), we also examined the association between the PRS and longevity (90+) in a completely independent sample. Data for this analysis came from the English Longitudinal Study of Aging (ELSA). ELSA is a sister-study of the HRS and there has been an attempt to harmonize the sample design, the questions, and the genetic approach. Both are nationally representative panel studies of individuals aged 50 years and older. Our validation sample from ELSA consisted of 264 long-lived individuals (aged 90+) and 4,521 controls (aged 50–79). Approximately 11% of long-lived individuals were current smokers, whereas for controls, approximately 13% were current smokers. Genotyping was performed using the Illumina Omni 2.5-8 Beadchip and the same QC criteria that were used for HRS. The majority of the SNPs used in the original PRS were available for ELSA ( n = 205). The 10 SNPs that were not genotyped in ELSA (and their corresponding genes) are listed in Supplementary Table S3 . After standardizing the PRS, so that it had a mean of 0 and SD of 1, we used a logistic regression to test whether the PRS was associated with an increased probability of being at ages 90+ compared to ages 50–79. The model was run using all subjects, adjusting for population stratification (EV1–EV4). Results showed that a 1 SD increase in PRS was associated with a 7% increase in the likelihood of being at ages 90+, relative to ages 50–79 (OR = 1.07, p = .018). We were not able to test centenarian status given that ELSA top-codes mortality at 90, making it impossible to differentiate who survived to 100+. Subsequent models adjusting for smoking status (never, current, and former) were also run and did not appear to impact results (OR = 1.08, p = .014). Next, we examined whether the association between PRS and longevity was dependent on smoking status. We found that the interaction between PRS and smoking was not significant, and in stratified models, the effect size was similar for the never (OR = 1.06), former (OR = 1.08), and current smoking (OR = 1.08) groups.
Finally, using the HRS validation sample (nonsmokers), we examined the association between our original PRS and disease prevalence measures for heart disease, cancer, and diabetes. This analysis was restricted to participants who reached at least age 70 or older during the study, to ensure we were picking up aging-related disease. Over the 10 waves, 22.5% of participants self-reported having been diagnosed with heart disease, 15.3% self-reported having been diagnosed with diabetes, and 13.6% self-reported having been diagnosed with cancer other than skin cancer at some point during their lifetime. Logistic regression models were run on the validation sample. Repeated-measures data across all waves were pooled over time and nonindependence for repeated measures were accounted for using clustering. Our results showed that a higher PRS was significantly associated with lower prevalence of cancer ( Table 3 ). For each 1 SD increase in the PRS, the likelihood that an individual had ever been diagnosed with cancer was reduced by nearly 11% (OR = 0.89; p = .011). When examining the association between PRS and either heart disease or diabetes, we found no statistically significant relationships ( Table 3 ).
Table 3. Cancer (nonskin) a Heart Disease b Diabetes c Odds Ratio p Value Odds Ratio p Value Odds Ratio p Value PRS 0.89 .011 0.987 .732 1.035 .260 Age (y) 1.06 <.001 1.073 <.001 1.044 <.001 EV1 2.18E-06 .026 4.22E-04 .089 9.88E+10 <.001 EV2 2.96E-06 .079 2.19E-09 <.001 8.62E+04 .008 EV3 1.38E+03 .355 7.509 .687 9.48E+02 .102 EV4 73.44 .303 80.830 .225 9.16E-03 .216 BMI Underweight (<18.5) 1.242 .344 0.942 .776 1.156 .711 Overweight (25–29.9) 1.000 .998 1.144 .043 1.813 <.001 Obese (30+) 1.136 .200 1.438 <.001 4.045 <.001 Education GED 0.981 .932 1.210 .264 0.767 .150 High school 1.324 .026 0.855 .113 0.795 .036 Some college 1. 286 .065 0.782 .025 0.709 .004 College and above 1.651 <.001 0.631 <.001 0.606 <.001 Sex (female = 1) 0.945 .523 0.543 <.001 0.731 <.001 Ever smoked 1.156 .098 1.311 <.001 1.096 .260 Constant 0.001 <.001 0.002 <.001 0.006 <.001 Cancer (nonskin) a Heart Disease b Diabetes c Odds Ratio p Value Odds Ratio p Value Odds Ratio p Value PRS 0.89 .011 0.987 .732 1.035 .260 Age (y) 1.06 <.001 1.073 <.001 1.044 <.001 EV1 2.18E-06 .026 4.22E-04 .089 9.88E+10 <.001 EV2 2.96E-06 .079 2.19E-09 <.001 8.62E+04 .008 EV3 1.38E+03 .355 7.509 .687 9.48E+02 .102 EV4 73.44 .303 80.830 .225 9.16E-03 .216 BMI Underweight (<18.5) 1.242 .344 0.942 .776 1.156 .711 Overweight (25–29.9) 1.000 .998 1.144 .043 1.813 <.001 Obese (30+) 1.136 .200 1.438 <.001 4.045 <.001 Education GED 0.981 .932 1.210 .264 0.767 .150 High school 1.324 .026 0.855 .113 0.795 .036 Some college 1. 286 .065 0.782 .025 0.709 .004 College and above 1.651 <.001 0.631 <.001 0.606 <.001 Sex (female = 1) 0.945 .523 0.543 <.001 0.731 <.001 Ever smoked 1.156 .098 1.311 <.001 1.096 .260 Constant 0.001 <.001 0.002 <.001 0.006 <.001 View Large
Table 3. Cancer (nonskin) a Heart Disease b Diabetes c Odds Ratio p Value Odds Ratio p Value Odds Ratio p Value PRS 0.89 .011 0.987 .732 1.035 .260 Age (y) 1.06 <.001 1.073 <.001 1.044 <.001 EV1 2.18E-06 .026 4.22E-04 .089 9.88E+10 <.001 EV2 2.96E-06 .079 2.19E-09 <.001 8.62E+04 .008 EV3 1.38E+03 .355 7.509 .687 9.48E+02 .102 EV4 73.44 .303 80.830 .225 9.16E-03 .216 BMI Underweight (<18.5) 1.242 .344 0.942 .776 1.156 .711 Overweight (25–29.9) 1.000 .998 1.144 .043 1.813 <.001 Obese (30+) 1.136 .200 1.438 <.001 4.045 <.001 Education GED 0.981 .932 1.210 .264 0.767 .150 High school 1.324 .026 0.855 .113 0.795 .036 Some college 1. 286 .065 0.782 .025 0.709 .004 College and above 1.651 <.001 0.631 <.001 0.606 <.001 Sex (female = 1) 0.945 .523 0.543 <.001 0.731 <.001 Ever smoked 1.156 .098 1.311 <.001 1.096 .260 Constant 0.001 <.001 0.002 <.001 0.006 <.001 Cancer (nonskin) a Heart Disease b Diabetes c Odds Ratio p Value Odds Ratio p Value Odds Ratio p Value PRS 0.89 .011 0.987 .732 1.035 .260 Age (y) 1.06 <.001 1.073 <.001 1.044 <.001 EV1 2.18E-06 .026 4.22E-04 .089 9.88E+10 <.001 EV2 2.96E-06 .079 2.19E-09 <.001 8.62E+04 .008 EV3 1.38E+03 .355 7.509 .687 9.48E+02 .102 EV4 73.44 .303 80.830 .225 9.16E-03 .216 BMI Underweight (<18.5) 1.242 .344 0.942 .776 1.156 .711 Overweight (25–29.9) 1.000 .998 1.144 .043 1.813 <.001 Obese (30+) 1.136 .200 1.438 <.001 4.045 <.001 Education GED 0.981 .932 1.210 .264 0.767 .150 High school 1.324 .026 0.855 .113 0.795 .036 Some college 1. 286 .065 0.782 .025 0.709 .004 College and above 1.651 <.001 0.631 <.001 0.606 <.001 Sex (female = 1) 0.945 .523 0.543 <.001 0.731 <.001 Ever smoked 1.156 .098 1.311 <.001 1.096 .260 Constant 0.001 <.001 0.002 <.001 0.006 <.001 View Large
Discussion
For most individuals, environment may play a major role in their probability of postponing disease and reaching old age. However, for those under chronic exposure to exogenous stressors, such as cigarette smoke, genetic variants may act as key factors in determining whether individuals are able to delay the age-related progressive decline in physiological functioning by offsetting damage though activation of somatic maintenance and repair mechanisms. As a result, survival among smokers may serve as a unique model for examining the genetics of stress resistance, aging, and longevity. Using long-lived smokers as our phenotype, we were able to identify a network of SNPs that, collectively, were strongly associated with extreme survival and lower cancer rates in an independent validation sample or nationally representative nonsmokers.
Our findings suggest that a 1 SD increase in the genetic load of the 215 SNPs we identified was associated with a 20% increase in the likelihood that an individual was aged 90–99 and an over threefold increase in the likelihood of being a centenarian. Additionally, our model predicted that approximately 340 in 100,000 individuals who had a PRS that was 2 SD s above the mean would be a centenarian, compared to only 33 and 3 in 100,000 who had a PRS at the mean or was 2 SD s below the mean, respectively. It has been reported in the literature that in 2010, there were just over 17 centenarians per 100,000 people in the United States ( 34 ), which appears similar to our estimate for mean PRS, taking into account that our validation sample is made up of participants aged 52 and older and only includes nonsmokers. However, additional studies utilizing different samples that include larger numbers of centenarians should be conducted to better understand the association between the PRS we generated in the current study and an individual’s likelihood of surviving to age 100 and beyond.
One of the major physiological risks of exogenous genotoxic exposure that accompanies smoking is the accumulation of DNA damage ( 35 ). However, it is likely that long-lived smokers possess variants which prevent genomic instability and allow them to survive to more extreme ages. Genomic instability also happens to be one of the hallmarks of cancer pathogenesis ( 36 ), thus the same genes that may promote survival among smokers may also be important for cancer prevention. This is consistent with our findings which showed that the genes we identified through our GWAS and network analysis on long-lived smokers were collectively associated with a nearly 11% lower cancer prevalence in the validation sample. Additionally, our functional interaction network of 215 genes was significantly enriched with pathways in cancer, as well as Ras signaling, Rap1 signaling pathways, and signaling by platelet-derived growth factor—all of which have implications for cancer pathogenesis ( 37–39 ).
Pathways which are believed to be potential regulators of the aging process were also enriched in our network. Overall, results showed that the PI3K/AKT signaling pathway had the highest enrichment score. This pathway has previously been shown to comprise genes related to stress resistance, DNA repair, cell death, protein turnover, and antioxidants ( 40 ). PI3K/AKT pathway is activated via insulin/insulin-like growth factor signaling. Insulin/insulin-like growth factor signaling is evolutionarily conserved has been shown to elicit a strong influence on life span in model organisms ( 14 ) and there is further evidence to suggest it may play an important role in human longevity ( 41 ). In worms, transcription factor Daf-16 (abnormal DAuer Formation-16) is a key regulator of insulin/insulin-like growth factor signaling and has been found to be fundamental for extreme life-span extension ( 42 ). The FOXO family of transcription factors are the human homolog for DAF-16 , and FOXO3a has been shown to be one of the most consistently cited longevity genes in human populations ( 43 ). Our network analysis and PRS included SNP rs12203834 (Chr6:108975562), which is an intron variant in FOXO3a . While rs12203834 has not been previously cited, two SNPs in FOXO3 have been previously associated with extreme longevity in two distinct populations—American men of Japanese ancestry from Hawaii (rs13217795) and German men and women (rs9400239) ( 44 , 45 ). Furthermore, a SNP (rs10457180) in FOXO3 was one of only two markers to reach genome-wide significance in the longevity consortium ( 46 ). The other was an APOE marker, which unfortunately was not directly genotyped in our data.
Although there is evidence to suggest that FOXO3 is an important gene for aging and longevity, it is likely that additional genes may simultaneously be important for extreme survival, especially under adverse conditions. Previous studies have provided evidence that suggest life span is a polygenic trait ( 47 ), influenced by multiple alleles with individual small effects. Furthermore, Kirkwood and coworkers provide three explanations for why aging is likely polygenic: (a) aging is not programmed, (b) genes that influence life span are probably byproducts of selection for other traits, and (c) aging and life span are driven, for the most part, by stochastic damage accumulation ( 48 ). Using traditional single-SNP GWAS approaches, many alleles with small individual effects will go unnoticed due to the reliance on strict significance criteria, thus contributing to what is being termed the “missing heritability problem” ( 49 ). There is an urgent need for employing methods that both allow for the examination of cumulative associations across SNPs as well as reliable methods for selecting SNPs for inclusion in predictive measures. Our and others’ result illustrate the usefulness of polygenic measures ( 30 , 50 ); nevertheless best practices for SNP selection in the creation of these measures has been less concrete. Network-based analyses may be a useful tool for variant selection when creating polygenic scores ( 51 ). Given the evidence that phenotypes like longevity may be influenced by genes within specific pathways and networks ( 22 ), we believe that the use of prior knowledge, such as functional interaction network analysis, provides better inclusion criteria for composite scores than methods that only consider top GWAS hits. This is consistent with the present study which showed that PRSs composed of SNPs identified using other means—top hits—were not significantly associated with longevity, while the PRS made up of SNPs in a functional interaction network was found to be a significant predictor of whether an individual was 90 years or older. Furthermore, the strength of this association increased further when predicting whether a participant was a centenarian, remaining significant even with a very small sample size. This is consistent with previous studies reporting that genes may be more important for extreme longevity versus variations in life span within typical ranges ( 45 ).
There are limitations to the present study that should be noted. First, our discovery sample consisted of a very small number of cases, which could limit our ability to detect true associations that have small effect sizes. Second, smoking, age, and disease status were based on self-reports. Third, the network was based on curated information, which did not allow for the discovery of novel gene–gene interactions. Fourth, the p value threshold used to select SNPs for inclusion in the network analysis was based on the GWAS, which did not take into account gene–gene interactions. In moving forward, it will be important to incorporate network structure into the calculation of PRS and use statistical network-based methods to identify sets of functionally related genes.
Through our use of a unique phenotype, functional interaction networks to select SNPs, and methods allowing examination of associations with aging-related phenotypes using composite measures of multiple genetic variants, we developed a genetic risk score that was significantly associated with an individual’s likelihood of surviving to extreme old age and also found to predict lower cancer prevalence. Overall, our findings suggest that longevity may be under the regulation of complex genetic networks which influence stress resistance and genomic stability. In moving forward, it will be important to examine how functional variants associated with the SNPs in our score interact with one another to impact signaling within their respective pathways and how these alterations translate into differences in life span and cancer risk.
Funding
This research was supported by the National Institute on Aging (NIA): P30AG017265 and T32AG0037. The HRS is supported by NIA (U01AG009740) and the Social Security Administration.
Acknowledgment
Electronic resources: PLINK 1.9, Shaun Purcell: http://pngu.mgh.harvard.edu/purcell/plink/ and Cytoscape v3.1.0: http://www.cytoscape.org/
References
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Aging and DNA damage in humans: A meta-analysis study . Aging . 2014 ; 6 ( 6 ): 432 – 439 . ): 36. Negrini S Gorgoulis VG Halazonetis TD Genomic instability–an evolving hallmark of cancer . Nat Rev Mol Cell Biol . 2010 ; 11 ( 3 ): 220 – 228 . doi: ):. doi: 37. Shields JM Pruitt K McFall A Shaub A Der CJ Understanding Ras: 'it ain't over 'til it's over' . Trends Cell Biol . 2000 ; 10 ( 4 ): 147 – 154 . ): 38. Largaespada DA A bad rap: Rap1 signaling and oncogenesis . Cancer Cell . 2003 ; 4 ( 1 ): 3 – 4 . ): 39. Wang Z Ahmad A Li Y et al. Emerging roles of PDGF-D signaling pathway in tumor development and progression . Biochim Biophys Acta . 2010 ; 1806 ( 1 ): 122 – 130 . doi:10.1016/j.bbcan.2010.04.003 ):. doi:10.1016/j.bbcan.2010.04.003 40. Mercken EM Crosby SD Lamming DW et al. Calorie restriction in humans inhibits the PI3K/AKT pathway and induces a younger transcription profile . Aging Cell . 2013 ; 12 ( 4 ): 645 – 651 . doi:10.1111/Acel.12088 ):. doi:10.1111/Acel.12088 41. Suh Y Atzmon G Cho MO et al. Functionally significant insulin-like growth factor I receptor mutations in centenarians . Proc Natl Acad Sci USA . 2008 ; 105 ( 9 ): 3438 – 3442 . doi:10.1073/pnas.0705467105 ):. doi:10.1073/pnas.0705467105 42. Kwon ES Narasimhan SD Yen K Tissenbaum HA A new DAF-16 isoform regulates longevity . Nature . 2010 ; 466 ( 7305 ): 498 – 502 . doi:10.1038/Nature09184 ):. doi:10.1038/Nature09184 43. Tazearslan C Cho M Suh Y Discovery of functional gene variants associated with human longevity: Opportunities and challenges . J Gerontol A Biol Sci Med Sci . 2012 ; 67 ( 4 ): 376 – 383 . doi:10.1093/gerona/glr200 ):. doi:10.1093/gerona/glr200 44. Willcox BJ Donlon TA He Q et al. FOXO3A genotype is strongly associated with human longevity . Proc Natl Acad Sci USA . 2008 ; 105 : 13987 – 13992 . doi:10.1073/pnas.0801030105 . doi:10.1073/pnas.0801030105 45. Flachsbart F Caliebe A Kleindorp R et al. 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© The Author 2015. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: [email protected]. ||||| Smoking has been shown to have drastic consequences for lifespan and disease progression, and it has been suggested that cigarette exposure may impact the risk of death and disease via its acceleration of the aging process. Not all smokers experience early mortality, however, and a small proportion manage to survive to extreme ages.
Using long-lived smokers as their phenotype, the authors of a study published today in The Journals of Gerontology, Series A: Biological Sciences & Medical Sciences identified a network of SNPs (a DNA sequence variation occurring commonly within a population) that allow certain individuals to better withstand environmental damage (like smoking) and mitigate damage. Collectively, these SNPs were strongly associated with high survival rates.
Morgan E. Levine, corresponding author of the study, said: "We identified a set of genetic markers that together seem to promote longevity. What's more, many of these markers are in pathways that were discovered to be important for aging and lifespan in animal models. There is evidence that these genes may facilitate lifespan extension by increasing cellular maintenance and repair. Therefore, even though some individuals are exposed to high levels of biological stressors, like those found in cigarette smoke, their bodies may be better set up to cope with and repair the damage."
These findings suggest that longevity, rather than being entirely determined by environmental factors, may be under the regulation of complex genetic networks which influence stress resistance and genomic stability. Therefore, there is reason to believe that long-lived smokers represent a biologically distinct group, endowed with genetic variants allowing them to respond differentially to environmental stressors.
Genomic instability also happens to be one of the hallmarks of cancer pathogenesis, and so the same genes that may promote survival among smokers may also be important for cancer prevention. This is consistent with the findings of the study, which showed that the genes identified were associated with a nearly 11% lower cancer prevalence.
###
The full report, "A Genetic Network Associated with Stress Resistance, Longevity, and Cancer in Humans" is available online here: http://biomedgerontology. oxfordjournals. org/ content/ early/ 2015/ 09/ 08/ gerona. glv141. full
Correspondence should be directed to:
Morgan E. Levine
Department of Human Genetics, Gonda Research Center, David Geffen School of Medicine
(818) 437-6791
[email protected] ||||| Jeanne Calment, the French doyenne believed to be oldest person in the world when she died at the extreme age of 122, was known for three things: her quick wit, her fondness for bicycling around the small city where she grew up -- and the fact that she was a daily smoker.
Before her death in 1997, Calment was often asked the secret to her good health. She would respond with a laugh and describe how she would frequently consume two pounds of chocolate a week, drank generous amounts of port wine and became a smoker at age 21.
At a time when public health messages emphasize just how important it is to carefully balance diets and fitness regimes in order to live long lives, Calment is a reminder of that no matter what we do there may always be a part of our health that is beyond our control.
In an intriguing study published this week, researchers delved into the genetic makeup of long-lived smokers like Calment and found that their survival may be due to an innate resilience they were born with.
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Slides sit in a bay waiting to be sequenced at the Complete Genomics research facility in Mountain View, Calif. (David Paul Morris/Bloomberg News)
Morgan E. Levine, a post-doctoral fellow in human genetics and biostatistics at the University of California-Los Angeles, and Eileen Crimmins, a gerontology professor at the University of Southern California, discovered a set of genetic markers in these smokers that they believe may allow them to better withstand and mitigate environmental damage from stressors.
Smoking is known to be one of the worst things you can do to your body, with drastic consequences on life span and the progression of disease. On average, smokers' life expectancy is 10 years less than non-smokers. The long-lived smokers are the exception and the researchers said that their findings suggest that they may be a "biologically distinct group" that is endowed with genetic variants that allow them to respond differently to exposure.
"There is evidence that these genes may facilitate lifespan extension by increasing cellular maintenance and repair," Levine said.
The study, which was published Wednesday in the Journals of Gerontology, Series A: Biological Sciences & Medical Sciences, involved participants of the longitudinal Health and Retirement Study in the United States. The researchers compared 90 participants who were smokers and lived to past age 80, with 730 people who were smokers and lived to less than 70 years of age.
They found that those in the age 80-plus group had similar physiological function as measured by inflammation, blood pressure and immune function as non-smokers in their age group. Smokers who died at a younger age had had worse physiological function than their same-age non-smoking counterparts at the time they were measured.
Levine told The Washington Post that the work is important because "the more we know about why we age, the more equipped we will be to intervene."
"Aging is an extremely complex process, and I think we are only beginning to uncover some of the mechanisms that regulate it. However, it also happens to be the biggest risk factor for most of the diseases that people suffer and die from," she said.
The 46 human chromosomes, where DNA resides and does its work. (National Cancer Institute/AP)
While the study has a number of limitations -- its small sample size for one and the fact that things like disease status were self-reported -- the researchers had enough information to develop a genetic risk score for smokers. They reported that they were not only able to predict an individual's likelihood of surviving to a very old age -- but a person's risk of cancer, which, not surprisingly, was significantly lower in those with the protective gene variants.
An important question smokers may have is whether they carry the genetic variants identified in the study.
While there are a number of companies that offer direct-to-consumer tests for genetic information, Levine said not all of them measure the same markers and "therefore, they may not have all the markers we presented in this paper."
Such a test may possible in the future, however. Levine is collaborating with other researchers at the University of Southern California's Davis School of Gerontology to develop tools that would allow individuals to calculate their health risks based on information from blood tests and genetics.
Levine emphasized, however, that the “proportion of people who have a ‘genetic signature’ that would help them cope with the biological stresses of smoking is extremely small, and therefore, nobody should use this paper as an excuse to continue smoking.”
“Even among those who are genetically predisposed to longevity, smoking cessation is likely still one of the best things they can do for their health,” she said.
With the focus on wellness in modern society, Levine said she's currently working on new research into people's "health spans" (as opposed to life spans), a term that refers to the length of a person’s life that is disease and disability free.
"Our society has been conditioned to associate a very negative image with being old," she said. "However, we have seen that some people are able to live to be centenarians without ever suffering from disease and disability. This is the goal." Read more:
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– Ten thousand steps. It's easy to remember, and a goal lauded by several wearable fitness trackers, but is it actually a good daily target for fitness? The number is too simplistic and not for everyone, reports the Huffington Post. For instance, for the extremely sedentary, taking 10,000 steps—which works out to roughly five miles—every day is so lofty a goal it might actually work as a deterrent. And for people who are already active and, say, jogging a few times a week, 10,000 steps could amount to slowing down. Meanwhile, the number is probably too low for kids in general, one exercise researcher says. In a 2014 article, LiveScience pointed out the CDC doesn't actually specify a step count, but recommends 2.5 hours of moderate activity each week; that translates into roughly 7,000 to 8,000 steps. So where does the number come from? It appears to have originated in Japan in the lead-up to the 1964 Olympics in Tokyo, with one company developing a pedometer called a man-po-kei, where "man" means 10,000, "po" means step, and "kei" means gauge. "It was a business slogan, like 'Just Do It' for Nike, but it resonated with people," Professor Catrine Tudor-Locke tells the BBC. And while there's certainly no downside to shooting for the 10,000-mark, it won't necessarily make you thin. US News & World Report last year flagged a 2008 meta-analysis of nine studies in which overweight or obese participants upped their steps by an average of 4,000 each day. After logging those extra miles for an average of four months, participants lost an average 3.13 pounds, "an amount that was just barely deemed statistically significant," US News observed. (There is such a thing, though, as running too much.) | Have you ever started a walking program in order to lose weight? While no doubt there are huge health benefits to regular exercise, unfortunately the ability of exercise to cause weight loss without you changing your diet has proven itself to be disappointing – to say the least. And yet, many take on walking programs with that express aim – often aiming at those much vaunted 10,000 steps. The question is, will those steps help?
First off, as far as walking and health goes – I’m a huge fan. Walking is free, it’s exceedingly accessible, it absolutely affects fitness and it requires no special planning, preparation or gear. On the surface, it might also seem to be integral to weight loss. Consider a group of more than 10,000 individuals (who on average have lost 66 pounds and kept them off for more than five years) in the National Weight Control Registry. The vast majority exercise, and among the group, walking is their most common means to do so. Did those folks’ steps translate into their pounds lost? A recent meta-analysis has the answer.
The meta-analysis specifically looked at studies of folks with overweight or obesity who undertook pedometer-based walking programs that didn’t include specific dietary change components. The authors identified nine studies that met their inclusion criteria, and they then pooled the studies’ results together. On average, participants increased their average daily number of steps by close to 4,000 and did so for a 16-week period. So did they lose weight? Well, yes, after spending four months walking an extra one to two miles per day, the average walker was seen to have lost 3.13 pounds – an amount that was just barely deemed statistically significant.
To help appreciate those numbers, the meta-analysis’ authors put them into perspective and state that for every 10.5 additional miles you walk, you might expect to lose a hair over 1/10 of one pound. Putting this another way, if you walk an extra 1.5 miles each and every day, you might expect that after 10 weeks of not missing a single walk, you’ll have lost a single pound – or that at the end of the year, your 547.5 miles of hiking will have lost you 5 pounds. Of course, I’m guessing that most people who undertake a walking program in the hopes of losing weight will quit in disappointment long before they reach that 10-week mark, let alone a year.
Perhaps the most amazing aspect of the study was that the authors stubbornly elected to present their findings positively, suggesting quite firmly that walking programs could be very beneficial to weight loss. Yet what this study really helped to prove wasn’t that you can walk your weight off, but rather that weight is lost through food – and if you start walking with the expectation of losing, it’s probably also fair for you to expect that pretty soon you’ll sit back down. On the other hand, if you start your walking program with hopes of improving your cardiovascular health, strength, mobility, mood and sleep, I’d bet you’ll be much more likely to keep on walking, as those are benefits you can fairly count on. Ultimately, reading this study I couldn’t help but wonder when will researchers stop suggesting that exercise is the ticket to the weight-loss express and instead shift the focus to exercise’s rightful and non-disappointing role as the ticket to health? ||||| Image copyright Thinkstock
Fitbit and other fitness trackers set a default goal of 10,000 steps a day. But just how valid is this aim if you're trying to stay active, asks Chris Stokel-Walker.
Late in the day, as you take a step, your wrist starts buzzing. Congratulations. You've hit your target.
Fitbit, which is going public, makes wearable devices that track your fitness levels, such as calories burned and distance travelled. You can customise it, but the default goal is 10,000 steps each day.
That vibration as you reach the landmark figure is "oddly rewarding", says Nath Buck, 26, a media support officer who has been using Fitbit for just over a year.
"I initially bought it purely out of curiosity to see how active I was," he says. Now he's convinced his flatmate and three colleagues to invest in similar gadgets and competes with them to see who can walk the furthest fastest.
The market for wearable fitness tracking devices is big business, with the number produced expected to increase from 17.7 million in 2014 to 40.7 million this year. According to research firm IDC, more than 100 million fitness devices that fit on your wrist like a watch will be sold across the globe by 2019.
A third of such devices currently sold are manufactured by Fitbit, and a further 4% by Jawbone, a competitor. Its default goal is also 10,000 steps - roughly equivalent to around five miles each day.
Image copyright Getty Images Image caption The Fitbit Flex
The Misfit Shine tracker sets users a target of 1,000 points, equivalent to around 10,000 steps. Azumio's Argus fitness tracking app for the iPhone sets targets for the number of steps users should take at between 8,000 to 10,000 per day.
So where does the magic number come from? It's believed that the concept of 10,000 steps originated in Japan in the run-up to the 1964 Tokyo Olympics, says Catrine Tudor-Locke, an associate professor at the Pennington Biomedical Research Centre at Louisiana State University.
Pedometers became all the rage in the country as Olympic fever swept through Japanese society. One company came out with a device called a manpo-kei, which means 10,000 step meter.
"It was a business slogan, like 'Just Do It' for Nike, but it resonated with people," Tudor-Locke says.
Since then 10,000 steps has become a commonly-acknowledged goal for daily fitness across the world. Various targets around that figure have been published by public bodies.
Japan's Ministry of Health, Labour and Welfare, for example, recommends "a daily walk of 8,000 to 10,000 steps". The UK National Obesity Forum says that a person who walks between 7,000 to 10,000 steps a day qualifies as "moderately active".
Image copyright Thinkstock Image caption Only another 9,997 footsteps to go...
The target appears to be a relatively arbitrary figure. Human, another iOS app, inspires users to be active for 30 minutes a day instead. But the 10,000-steps-a-day goal does have some basis in scientific advice.
Also, 10,000 steps is "a nice, round number" - much like Malcolm Gladwell's much-lauded promise that 10,000 hours of practice in any field is sufficient to make you an expert - even if the reality is much more nuanced.
It "latches onto people better than the vague 7,000 to 8,000 number", says Laura Williams, a diet and fitness expert. As well as being easily digestible, it's challenging while also realistic.
"For most people, 150 minutes of exercise a week sounds like an awful lot," she adds.
Image copyright Thinkstock
But the 10,000 steps figure need not be taken too literally. For one thing, not all steps are equal.
As Dale Esliger, a senior lecturer in the measurement of physical activity at Loughborough University, explains: "If you've got short or long legs there are differences there."
For a long-legged woman, 10,000 steps is unlikely to be as tough as it would be for someone shorter. Plus people's gaits differ as much as their eye colour or personalities.
Besides, a device on your wrist recording digital motion in your legs is not infallible. Some of those 10,000 steps recorded on your fitness tracker might include you bending down to tie your shoelaces, says Esliger.
"The best kind of device to track steps taken is one placed on the ankle, looking for an actual step biomechanically," notes Esliger.
According to the NHS, the average Briton walks between 3,000 and 4,000 steps a day - significantly less than the Fitbit target. Yet many people do significantly more, and for them 10,000 steps might not be much of a target.
"If you run three times a week, you're not going to get fitter by walking 10,000 steps," Williams explains. "You're already quite fit. You're going to need to do more to get fitter than someone who is chronically unfit and inactive. For them, walking 5,000 or 10,000 steps a day will improve their fitness."
Wearable devices instead offer people a challenging goal they can attain to, and a simple-to-understand baseline roughly equivalent to the minimum suggested amount of exercise.
Image copyright ALAMY Image caption Other fitness devices are available
Buck, for example, swims and runs regularly, and is unlikely to be challenged by 10,000 steps - yet still keeps his target at that level. "I've thought about changing it but 10,000 seems a good 'basic' target to reach," he says. "You know you're doing at least the minimum then."
To reach 10,000 steps you have to create some structure in your walking routine, says Williams. That might involve walking a mile one way and a mile another when you go out for lunch.
"If you do too little, like park two car parking spaces further away from the supermarket entrance, you're not going to reach the target," she says. "You also need to make sure you keep challenging yourself. Pace and intensity is key to getting fitter."
Tudor-Locke agrees that the 10,000-step target is "laudable". She says: "Go for it if you want to. In fact, go for 12,000 - go to 14,000. There is no limit we know of that is detrimental to health."
But, she warns, don't treat it as an absolute target. "Rather than be obsessed with a number," she says, "it's just important to not be sedentary."
And though you may feel triumphant upon reaching your 10,000-step target, remembering that snaffling a chocolate cake will undo the day's work is vital, too.
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Image copyright ALAMY
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By Jesse Singal
If you pluck someone off the street, whether in New York or Wichita or Seattle or Sacramento, and ask them how many steps people should aim for per day in order to get enough physical activity, they'll probably tell you 10,000. In an age in which pedometers are cheaper, more accurate, and more feature-rich than ever, this number has taken on almost mythical proportions -- a lofty-sounding goal (in reality, it's approximately five miles, and a reasonably active person can pull it off fairly easily) that separates the active-lifestyle haves from the slothful have-nots.
But is there any medical reason to embrace this number? Not really. That's because the 10,000-steps-a-day recommendation has nothing to do with sedentary, fast-food-drenched circa-2015 America. Rather, the recommendation first popped up in a very different food and environment: 1960s Japan.
"It basically started around the Tokyo Olympics" in 1964, said Catrine Tudor-Locke, a professor who studies walking behavior at LSU's Pennington Biomedical Center. "A company over there created a man-po-kei, a pedometer. And man stands for '10,000,' po stands for 'step,' and kei stands for 'meter' or 'gauge.'" Ten thousand, it turns out, "is a very auspicious number" in Japanese culture, said Theodore Bestor, a Harvard researcher of Japanese society and culture, in an email. "That is, it seems likely to me that the 10,000 steps goal was subsidiary to having a good-sounding name for marketing purposes." Whatever the reason for the adoption of this particular number, "It resonated with people at the time, and they went man-po-kei-ing all over the place," said Tudor-Locke.
The problem, which barely needs stating, is that circa-1964 Japan was markedly different from the circa-2015 U.S. "By all accounts, life in Japan in the 1960s was less calorie rich, less animal fat, and much less bound up in cars," said Bestor. Data from the Food and Agriculture Organization of the United Nations shows that the average per-capita food supply for Japanese people in 1964 was 2,632 calories, while the average for Americans in 2011 was 3,639. That's a difference of about 1,000 calories -- or, if you're keeping track, about 20,000 steps for an average-size person. (Jean Buzby of the USDA said in an email that food supply is a commonly used rough proxy for food consumption.)
These sorts of numbers all vary hugely, of course, depending on region, social demographics, and a variety of other factors. But the point is no one can argue that Japanese people in the 1960s lived in the same sort of nutritional environment as Americans in 2015.
More broadly, 10,000 steps is just a bit too simplistic a figure, say nutrition researchers. All the ones I spoke to agreed that there's nothing wrong with shooting for 10,000 steps, per se, and that on paper, walking (or doing any physical activity) more is better than walking less. But Tudor-Locke said that, "The one-size-fits-all [approach] doesn't necessarily work."
Her work focuses on the most sedentary slice of the population (a rather big slice slice in the U.S.), and there, it can be a challenge to get people to take 5,000 steps, let alone 10,000. But moving from 2,500 steps a day, say, to 5,000, is a small but important victory for people who don't get any exercise, and can have important health ramifications. "We know that you get the biggest bang for your buck by just moving from a sedentary state up a little bit," she said. "Your biggest bang comes from rolling off the couch and being active." A big European study published in January that looked at the mortality rates for people with different activities levels, in fact, found that "a markedly reduced hazard was observed between those categorized as inactive and those categorized as moderately inactive" -- a 20 to 30 percent reduction.
People in these categories, who at the moment are getting almost no exercise, aren't going to benefit from the 10,000 steps recommendation. In fact, it might deter them from exercising, said Tudor-Locke. "For people who are very inactive or chronically ill or whatever have you, that might be a huge jump for them," she said, "and that might be intimidating for them." If the 10,000 steps goal has this effect, "then it loses its purpose." From a public-health perspective, she said, a more pressing, realistic goal is "to get people away from taking less than 5,000" steps a day.
In a country where people eat really, really poorly, there's also a chance that fixating on the 10,000-step milestone will lead people to neglect other, potentially important factors like their diet. "Focusing exclusively on how many steps you're getting and neglecting those other aspects isn't going to lead to an overall improvement in health, unless you're addressing those other factors simultaneously," said Jeff Goldsmith, a biostatistics professor at Columbia's Mailman School of Public Health.
In other words: Yeah, 10,000 steps is great, but if you follow up those 10,000 steps by buying a 500-calorie hamburger -- and, more generally, spend the rest of your day eating junk -- you can still gain weight and face all sorts of unpleasant negative health outcomes. "What we know from the scientific evidence is that diet and physical activity are relatively separate domains," said Dr. Eric Rimm of the Harvard School of Public Health. "There are people who are overweight and eat poorly and still exercise, and on the other hand, there are people who eat really well but sit on the couch." An overly narrow focus on 10,000 doesn't encourage an integrated approach to getting healthier.
Finally, 10,000 steps might "be too low for children," said Jean Philippe-Walhin, an exercise researcher at the University of Bath -- and kids these days, as you're probably already aware, aren't doing so hot on the obesity front.
So while 10,000 steps is fun and easy to remember and a catchy marketing tool in (at least) two languages, maybe it's time, given just how unhealthy so many people are and how much they'd benefit from moving around just a little more, to embrace an incremental-improvement approach to exercise. But even if the science of nutrition and exercise is complicated, that doesn't mean the take-home message needs to be. "Stand rather than sit, walk rather than stand, jog rather than walk, and run rather than jog," wrote Ulf Ekelund, lead author of the European mortality study, in an email. Tudor-Locke distilled things even further: "Just move more than before," she said. "Keep moving more than before."
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Also on HuffPost: ||||| If you buy a smart pedometer or fitness tracker like a Fitbit, chances are the device will encourage you to take 10,000 steps a day. But do you really have to walk this much to be healthy?
Experts say that while 10,000 steps a day is a good number to reach, any amount of activity beyond what you're currently doing will likely benefit your health.
The origins of the 10,000-steps recommendation aren't exactly scientific. Pedometers sold in Japan in the 1960s were marketed under the name "manpo-kei," which translates to "10,000 steps meter," said Catrine Tudor-Locke, director of the Walking Behavior Laboratory at Pennington Biomedical Research Center in Baton Rouge, La. The idea resonated with people, and gained popularity with Japanese walking groups, Tudor-Locke said. [The Best Pedometers of 2014]
Studies conducted since then suggest that people who increased their walking to 10,000 steps daily experience health benefits.
One study found that women who increased their step count to nearly 10,000 steps a day reduced their blood pressure after 24 weeks. Another study of overweight women found that walking 10,000 steps a day improved their glucose levels.
Walking 10,000 steps a day is not an official recommendation from the Centers for Disease Control and Prevention. Instead, the agency recommends adults engage in 150 minutes of moderate activity a week, such as brisk walking. To meet the CDC's recommendation, you need to walk about 7,000 to 8,000 steps a day, Tudor-Locke said.
If you normally walk about 5,000 steps a day, getting in an extra 30-minute, brisk walk into your day would take you to about 8,000 steps, Tudor-Locke said. The average U.S. adult walks about 5,900 steps daily, she said.
Still, there's no reason to stop at 8,000 steps if you can do more, Tudor-Locke told Live Science. "We do know that more is better."
The Mayo Clinic recommends that people using pedometers first set short-term goals, such as taking an extra 1,000 steps daily for one week, and then build up to a long-term goal such as 10,000 steps.
Tudor-Locke said that there's not a single strategy to increase your step count, each person has to find what works for them. The most important thing is to increase your activity beyond what you were doing before.
Dr. Clay Marsh, chief innovation officer at Ohio State University Wexner Medical Center, agreed, and said that people don't need to feel like they have to achieve 10,000 steps to be active.
"We just want people to get up, and get started," Marsh told Live Science in an interview in February. "Any amount of activity that you can do today that you didn’t do yesterday, you're probably going to start benefiting from it."
Follow Rachael Rettner @RachaelRettner. FollowLive Science @livescience, Facebook & Google+. Original article on Live Science. ||||| RESULTS Nine studies met the study inclusion criteria. Cohort sample size ranged from 15 to 106, for a total of 307 participants, 73% of whom were women and 27% of whom were men. The duration of the intervention ranged from 4 weeks to 1 year, with a median duration of 16 weeks. The pooled estimate of mean weight change from baseline using a fixed-effects model and combining data from all 9 cohorts was −1.27 kg (95% confidence interval, −1.85 to −0.70 kg). Longer intervention duration was associated with greater weight change. On average, participants lost 0.05 kg per week during the interventions.
METHODS In this meta-analysis, we searched 6 electronic databases and contacted pedometer experts to identify pedometer-based walking studies without a dietary intervention that reported weight change as an outcome. We included randomized controlled trials and prospective cohort studies published after January 1, 1995, in either English or Japanese, with 5 or more adult participants and at least 1 cohort enrolled in a pedometer-based walking intervention lasting at least 4 weeks.
PURPOSE Cross-sectional studies show that individuals who walk more tend to be thinner than those who walk less. This does not mean, however, that the association between higher step counts and lower weight is causal or that encouraging sedentary individuals to increase step counts helps them lose weight.
Key Words:
In this meta-analysis, we examined the effects of pedometer-based walking interventions on weight loss. We included in the analysis studies of walking programs without dietary intervention that used pedometers as motivational tools and that were conducted among overweight or obese, sedentary adults.
Most simple pedometers only provide feedback on total daily steps taken; feedback on intensity, duration, or frequency of walking is not provided. In contrast to walking programs that use time-based walking goals, pedometer-based walking programs make it possible to meet a relatively high step-count goal either by going for 1 long walk or by taking lots of very short walks spread throughout the day. It is in part the flexibility to fit in walking whenever it is convenient for the individual participant that makes pedometer-based walking programs popular. At the same time, the flexibility also adds some uncertainty with respect to the health benefits of pedometer-based walking programs. The amount of weight loss that a sedentary adult can expect to achieve from these programs in the absence of dietary modification or other nonexercise interventions is not known.
Cross-sectional observational studies have shown that people who walk more tend to be thinner than those who walk less. 5 – 9 In a typical pedometer-based walking intervention, participants are given a pedometer to wear every day, all day, as they go about their usual activities. Pedometers are small, inexpensive devices about the size of a pager that are worn at the waist and that count every step the wearer takes during the day. Participants are also given an assigned or negotiated total daily step-count goal. Pedometer-based walking programs show promise as an adjunct both in dietary weight loss interventions 10 and in preventing weight regain after substantial weight loss. 8 , 11
Obesity is increasing in prevalence among adults in the United States at an alarming rate. 1 The prevalences of type 2 diabetes 2 , 3 and other obesity-related chronic illnesses are increasing along with the prevalence of obesity. Both obesity and type 2 diabetes are preventable with diet and exercise modifications. 4
We used a mixed-effects meta-regression model to assess whether there was any association of study duration and quality scores with the weight change effect size. Both duration of intervention and quality scores were entered in the model as fixed effects, and study was considered as a random effect.
Because the Cochran test demonstrated heterogeneity, we used a random-effects model to calculate the pooled estimate of mean weight change from baseline, combining data from all cohorts, and generated a forest plot to illustrate both the study-specific effect sizes (along with an associated 95% confidence interval) and the pooled effect estimate based on this model. The weights used in combining estimates equal the reciprocal of the sum of 2 variances: (1) the estimated variance associated with the study and (2) the estimated component of variance due to variation between studies. To further test the overall significance based on a more general method of combining P values, we calculated the Fisher log-likelihood ratio statistic and the associated P value for the statistic using a χ 2 test with twice the total number of studies for degrees of freedom.
To test for heterogeneity between studies in the analysis, we used the Cochran Q statistic, 17 which is simply the sum of squared deviations of the study-specific estimates from the overall pooled estimate, weighting each study’s contribution in the same manner as in the meta-analysis. P values were obtained by comparing the statistic Q with a χ 2 distribution with k – 1 degrees of freedom, where k is the number of studies considered.
To test for evidence of publication bias, we examined a standard funnel plot. 14 A funnel plot is simply a scatterplot of the measure of interest against the reciprocal of the corresponding standard error. Publication bias refers to the preferential publication of only those studies with significant results. Nonsignificant results would typically be accompanied by larger variability and vice versa. A lack of publication bias would thus be indicated by a rough inverted funnel shape of the above plot, thereby showing the presence of both significant and nonsignificant results in the data. In addition to this graphical check for bias, we also used the rank-correlation test of Begg and Mazumdar 15 and the test of Egger et al, 16 both of which are formal statistical tests of bias that are based on the same consideration underlying the funnel plot.
We used a within-participant correlation of 0.98 for studies that had an intervention duration of less than 3 months (12 weeks) and 0.95 for studies that had an intervention duration of 3 to 9 months (12–36 weeks). These correlation values were computed exactly for a few studies and were assumed to hold for the studies that were similar in duration.
In using this strategy, we made the assumption that the correlation of within-participant preintervention and postintervention weights was similar across studies. This assumption allowed us to estimate effect sizes for all of the cohorts included in the analysis. The strategy we adopted is similar to that recommended by Follmann et al. 13
To conduct a meta-analysis, one must have a standard deviation of the outcome being measured in each study. This value allows for calculation of the effect size for each study. Many of the included studies did not report the standard deviation of the change in weight but instead reported the standard deviation for the preintervention and postintervention weights. For those studies that reported exact P values for the preintervention-postintervention comparison, we could easily derive the standard deviation of the change in weight. For studies without exact P values, or t statistics, we imputed the standard deviation of the change using the individual preintervention and postintervention standard deviations as well as the within-participant correlation of the weight measures, with the formula displayed in Figure 1 ⇓ .
To ascertain within-participant weight change from preintervention assessment to postintervention assessment, we either obtained it directly from the study results or calculated it by determining the difference between reported mean weights before and after the intervention. All weights were converted to kilogram units. All statistics were computed using STATA 9.0 (StataCorp LP, College Station, Texas, 2005) and MINITAB 14.0 (Minitab Inc, State College, Pennsylvania, 2004).
Because our analysis focused on preintervention-postintervention weight change, we were able to include both controlled and uncontrolled trials. To rate study quality, we used a modified version of the Downs and Black quality-scoring system. 12 Items rated in the quality-scoring system included sample size, sample selection, outcome assessment quality, rate of dropout, quality of the statistical analysis, adjustment for confounding, and reporting details. Because blinding is not possible in an intervention based on self-monitoring and because the analysis was based on preintervention-postintervention comparisons rather than a comparison between randomized groups, we omitted items in the quality scale related to randomization and blinding. Two raters (C.R.R., J.J.A.) rated all included studies, and discrepancies were resolved by consensus.
Additionally, we contacted experts in the pedometer research field to find other studies that might be eligible for inclusion. Some of the studies identified by the experts that did meet inclusion criteria were published after the date of the automated database search.
We used 2 different methods to identify studies to include in this meta-analysis. First, 2 of the authors (C.R.R., T.L.N.) conducted a systematic search of 6 databases for citations related to walking or pedometers. The databases searched were CINAHL, EMBASE, MEDLINE, PsycINFO, SportDiscus, and Web of Science. The search was conducted on July 8, 2005, using search terms that included “walking,” “pedometer,” “step count,” and “sedentary.” An updated search was conducted on September 12, 2006, using CINAHL, MEDLINE, PsycINFO, SportDiscus, and Web of Science; EMBASE was no longer accessible from our institution. Once the search was completed, 1 author (T.L.N.) reviewed abstracts to screen out papers that clearly did not meet the inclusion criteria. Several authors (T.L.N., C.R.R., J.J.A.) reviewed in more detail studies that could not be excluded based on the abstract alone or studies without abstracts to determine if they met our inclusion criteria.
The study was published (whether as a complete manuscript, a brief report, or an abstract alone), and the report had sufficient detail to confirm that the study met other meta-analysis inclusion criteria.
The scatterplot in Figure 4 ⇓ shows the strong relationship between intervention duration and weight change. The straight line drawn through the plot is the predicted least squares line based on the meta-regression results with the quality value fixed at 62.8 (the average quality score of the 9 studies).
We found a strong linear association between the duration of intervention and the magnitude of weight change (β = −0.05, P = .003), with interventions of longer duration being associated with greater weight change. Weight change was not significantly associated with study quality (P = .08).
The Cochran Q statistic for testing heterogeneity was 19.16. Based on a χ 2 with 8 degrees of freedom, the Q value was statistically significant at the 5% level (P=.01). We therefore chose to use a random-effects model for our meta-analysis. The pooled estimate of mean weight change from baseline using a random-effects model and combining data from all 9 cohorts was −1.27 kg (95% confidence interval, −1.85 to −0.70 kg), with an overall intervention effect (P <.001). Figure 3 ⇓ shows a forest plot of effect sizes and confidence intervals for all 9 cohorts, again based on the random-effects meta-analysis. The Fisher statistic for the significance of the weight change effect was 87.06, with P<.001.
Results of the 3 tests to look for evidence of publication bias showed no evidence of such bias. Figure 2 ⇓ shows the results of a funnel plot, which showed no evidence of publication bias. This lack of bias was further confirmed by both the rank-correlation test of Begg and Mazumdar 15 (P = .75) and the test of Egger et al 16 (P = .74). Although these 3 tests are reassuring, they cannot rule out publication bias.
Table 2 ⇓ shows results of the studies. All but 1 of the cohorts examined had a small decrease in weight at the end of the intervention. The range of weight change for the 9 cohorts was +0.30 to −3.70 kg, with an unadjusted mean weight change across the cohorts of −1.42 kg. In 5 of the 9 cohorts, the weight change was statistically significant comparing postintervention with preintervention weight at the P = .05 level.
Table 1 ⇓ gives an overview of each of the 9 studies included in the final analysis, with studies listed in ascending order according to the average postintervention step count. Among the 9 cohorts examined, the sample size ranged from 15 to 106 participants, for a total of 307 participants, 73% of whom were women and 27% of whom were men. The duration of the intervention ranged from 4 weeks to 1 year, with a median duration of 16 weeks.
After compiling search results across all databases and eliminating duplicates, we found 1,405 articles that were published between January 1, 1995, and September 12, 2006, that were about pedometers or walking. By reviewing the abstracts for these 1,405 articles to exclude articles that were not intervention trials involving pedometer-based walking programs, we identified 86 studies for more extensive review and inclusion criteria screening. Of these 86 studies reviewed in detail, 9 met our inclusion criteria.
DISCUSSION
The average participant in a pedometer-based walking program without dietary change can expect to lose a modest amount of weight, on the order of 1 kg. Results from the 9 cohorts we examined were remarkably consistent and did not vary by the population targeted or the goal-setting strategies used. These findings are consistent with previous research showing that increasing moderate-intensity physical activity tends to result in a modest amount of weight loss.27–30
The amount of weight loss attributable to pedometer-based walking programs is small but important from a clinical perspective. According to the meta-regression results, the average participant adhering to a pedometer-based walking program can expect to lose about 0.05 kg per week. That translates to a weight loss of about 1 lb every 10 weeks. Over a year, participants can expect to lose about 5 lb. Although a 5-lb weight loss for an overweight participant may represent only 2% to 3% of that person’s body weight, if the participant continues with the pedometer program and if the rate of weight loss is sustained over several years, the target of 7% of body weight loss used in the Diabetes Prevention Program study4 could be achieved.
Such modest amounts of weight loss, no matter how clinically important, may be discouraging to participants whose primary motivation for starting a walking program is to shed pounds. Unrealistic expectations of dramatic weight loss from such a program may result in early dropout. Helping participants set realistic and obtainable goals may be an important part of helping them stick with a walking program. Additionally, encouraging participants who are motivated by weight loss goals to add a dietary component to their walking program may yield more weight loss and thus may increase adherence.10,31,32
Average daily step-count increases varied from slightly less than 2,000 steps per day to more than 4,000 steps per day across these studies. For the average person, a 2,000-step walk is approximately equal to a 1-mile walk.33 The daily increase in physical activity above baseline thus varied across these studies from an increase of 1 mile to slightly more than 2 miles of walking. At an average pace of 3 miles per hour, that represents an additional 20 to 40 minutes of walking a day and is in the range recommended by national guidelines.34 This increase in physical activity can be expected to result in health benefits that are independent of weight loss. Increasing physical activity reduces the risk of adverse cardiovascular events,31,35–38 lowers blood pressure,23 and helps dieters maintain lean muscle tissue during diet-induced weight loss.39 Additionally, a pedometer-based walking program can improve glucose tolerance in people with impaired glucose tolerance or type 2 diabetes.23,40
Unfortunately, we know very little about the long-term sustainability of weight loss from pedometer-based walking programs. More long-term studies of such programs are needed to better delineate their weight loss outcomes in that time frame.
There are several important limitations to this study. Because the analysis was based on preintervention-postintervention comparisons rather than on a comparison between randomized groups, there are a number of potential threats to validity, and the pooled estimate of approximately a 1.30-kg weight loss may either overestimate or underestimate the effect of the pedometer-based walking intervention. Participants who elect to join a walking program may be particularly motivated to change both their diet and exercise habits. Although none of the study interventions included in the meta-analysis had a dietary component, participants may have decreased their caloric intake on their own; therefore, the real cause of the weight loss might be dietary change rather than increased physical activity. To the extent that the weight loss observed in this review is attributable to participants’ self-initiated diet changes, we would be overestimating the impact of the increased energy expenditure due to the pedometer-based walking program on weight loss. It would not take much of a change in dietary intake to cause a 1-kg weight loss. Only a study in which meticulous records of dietary intake are kept for all participants could ensure that the weight loss we observed was not due to changes in diet. Evidence supporting the theory that walking programs can result in weight loss includes the results of 1 study that examined preintervention and postintervention strength and fitness levels.20 This study showed improved cardiorespiratory fitness and leg strength in addition to weight loss, suggesting that the exercise was of sufficient intensity to have a training effect.
It is more likely, however, that we have underestimated the impact of a pedometer-based walking program on weight loss. To the extent that individuals who did not start a walking program would have continued to slowly gain weight rather than maintain a stable weight, our weight loss estimate is lower than the actual change in weight attributable to the walking program. A large randomized controlled trial with a no-walking-program control arm for comparison would allow us to measure both the decreased weight gain and the weight lost from the walking program. The findings of a dose-response association with interventions that lasted longer resulting in larger amounts of weight loss adds evidence to our conclusion that the weight loss detected in this meta-analysis was in fact caused by the intervention itself.
In this study, we pooled the results from 9 cohorts of overweight or obese and sedentary individuals, all of whom participated in a pedometer-based walking program. All of the studies included in this meta-analysis were published since 2001, and most are preliminary investigations with small numbers of participants. As we learn more about pedometer-based walking programs and how to study them, both the quality of individual studies and the robustness of meta-analytic results will improve.
In conclusion, pedometer-based walking programs without a dietary intervention component do result in a modest amount of weight loss. Pedometer-based walking programs also do increase step counts and thus can be expected to confer health benefits that are associated with both a modest decrease in weight and an increase in physical activity. ||||| | multi_news_1_0_0 |
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News article:
How do you feel about eating cloned meat?
While the rest of the world sorts out its feelings about the safety and ethics of cloning animals for food production, China is charging ahead and building the world’s largest animal cloning factory, set to begin operations in 2016. The 200 million yuan (over $31 million) commercial animal cloning center will be located in the Tianjin Economic-Technological Development Area, a government-sponsored business area about 100 miles from Beijing.
Feelings are decidedly mixed about whether we should be eating cloned meat. On one hand, the European Parliament recently voted by a large margin to outlaw the sale of cloned livestock. On the other hand, the FDA has said that “there are no complications that are unique to cloning” and the meat is safe to eat, despite evidence that cloned animals may not live as long as those birthed in the old-fashioned way. In the US, no special labeling is required for cloned meat, and no one really seems to know how common the practice of cloning meat for food is. Still, some say that most of the cattle cloned in the US are used to breed stock and are not sold for food.
But China is going full steam ahead. The new facility will focus on cloning cattle to feed China’s burgeoning population, which likes its meat.
Xu Xiaochun, the chief executive of BoyaLife, the company behind the new operation, told The Guardian, “We are going [down] a path that no one has ever travelled. We are building something that has not existed in the past.” The company intends to produce 100,000 cow embryos per year and hopes to provide 5 percent of the meat eaten in China.
In addition to cattle, BoyaLife will be cloning champion racehorses and dogs used to sniff out victims of natural disasters or stashes of illegal drugs. Xu told The Guardian that the new clone factory would also rescue endangered species from extinction.
Xu is pretty confident that cloned animals are safe to eat and will benefit humanity: “This is going to change our world and our lives. It is going to make our life better. So we are very, very excited about it.”
The cloning factory will be a partnership involving Sooam Biotech, a South Korean company that will clone your dog for you so that you can replicate your best friend and cheat your way out of a dog’s short lifespan. Sooam Biotech is run by the scientist Hwang Woo-suk, once known as “the pride of Korea” and the “king of cloning.” Problem is, he was found to have fabricated a series of experiments back in 2006, and was dismissed from his post at Seoul National University. His transgressions had to do with “research fraud and gross ethical lapses in the way he obtained human eggs for his experiments.”
His partners in China’s new cloning factory are evidently not alarmed by his checkered past. Xu said the world’s largest animal cloning factory was now almost complete. “We want it to be modern, we want it to be cutting edge. We want it to represent the future,” he said.
Let’s just hope Wayne Knight doesn’t get his Jurassic Park on and screw this up for humanity too. ||||| Tianjin facility aims to produce thousands of cow embryos as well as racehorses and sniffer dogs
The scientist behind plans to build the world’s largest animal cloning factory in China has hailed the venture as an “extremely important” contribution that could help save critically endangered species from extinction.
Xu Xiaochun, the chief executive of BoyaLife, the company behind the 200m yuan (£20.6m) project, said it would begin operations in the first half of 2016 in Tianjin, a city about 160km (100 miles) from Beijing.
“We are going [down] a path that no one has ever travelled,” he told the Guardian following the unveiling of the factory’s blueprint this week. “We are building something that has not existed in the past.”
£1,000 for a micro-pig. Chinese lab sells genetically modified pets Read more
The main focus of the 14,000-square-metre facility will be cloning cattle to feed China’s rocketing demand for beef.
BoyaLife initially hopes to produce 100,000 “top quality” cow embryos a year and to eventually be responsible for 5% of the premium cattle slaughtered in China.
The intended size of the operation dwarfs that of US companies allowed by the Food and Drug Administration (FDA) to sell meat and dairy from cloned livestock since 2008. After a lengthy debate over cloned livestock, the FDA ruled that clones were as safe to eat as any other cattle, pigs or goats. But most cloned cattle in the US are used as breeding stock, to raise the quality of herds, rather than to sell for food.
In the UK, meat and milk from cloned cows are considered “novel foods” and suppliers need special permission to sell them. In 2010, beef from the offspring of a cow cloned in the US entered the food chain, leading to an investigation by the Food Standards Agency.
In its latest statement on cloned animals, the European Food Safety Authority said there was no evidenceof differences between meat and dairy products from clones or their offspring and healthy, conventionally bred animals, but reiterated its concerns that the cloning process can cause animal health and welfare problems. “Animal health and welfare remain a matter of concern, mainly due the increased number of deaths at all stages of development,” the organisation said.
Scientists at BoyaLife will also focus on cloning champion racehorses and sniffer dogs capable of locating victims of natural disasters or stashes of illegal drugs.
Facebook Twitter Pinterest The world’s largest animal cloning factory, which is set to open in Tianjin, China, in 2016. Photograph: Boyalife
Xu said the clone factory would also serve humanity and nature by helping rescue endangered species from the brink of extinction.
“This is going to change our world and our lives,” he said. “It is going to make our life better. So we are very, very excited about it.”
The factory is the latest step in Chinese attempts to become a world leader in cloning technology.
Scientists in mainland China have been cloning cattle, pigs and sheep for about 15 years, Hong Kong’s South China Morning Post reported.
In 2014, the BBC said a Chinese company called BGI was cloning animals on an industrial scale in the southern city of Shenzhen.
There, scientists working out of a former shoe factory were reportedly churning out 500 cloned pigs every year.
“We can do cloning on a very large scale,” Yutao Du, a scientist at the project, was quoted as saying. “Thirty to 50 people together doing cloning so that we can make a cloning factory here.”
The Tianjin factory is a partnership with Sooam Biotech, a South Korean company run by the Seoul-based scientist Hwang Woo-suk. Hwang, a once-revered veterinarian known as the “king of cloning”, was disgraced in 2006 after he was found guilty of research fraud and gross ethical lapses in the way he obtained human eggs for his experiments.
Sooam has been cloning puppies for about a decade and has been operating in China since 2014, cloning Tibetan mastiff puppies in the city of Weihai in partnership with BoyaLife. Hwang’s team was the first in the world to clone a dog, an Afghan hound named Snuppy, born in 2005. The same year, scientists in Italy unveiled the first cloned champion racehorse, created from a skin cell taken from a multiple endurance race winner.
“In China we do things on a massive scale,” Xu told Bloomberg in 2014. “We want to do all this not just for profit, but also for history.”
The Chinese scientist suggested his company might one day be able to produce the world’s first cloned giant panda at its Weihai facility.
In China, which has witnessed a series of devastating food safety scandals, state media sought to convince the public there was no risk in consuming the cloned cattle Xu’s company plans to produce.
“Beef from cloned cattle is safe to eat,” Zhang Yong, a professor at the veterinary medicine college of Shaanxi province’s Northwest A&F University, told the China Daily.
In a conference call with reporters, BoyaLife’s chief executive said: “I can tell you, cloned beef is the tastiest beef I’ve had.”
Xu said the construction of the world’s largest animal cloning factory was now almost complete. “We want it to be modern, we want it to be cutting edge. We want it to represent the future,” he said.
Additional reporting by Christy Yao ||||| Features
(Corrects Daesung Group chairman’s name in 38th paragraph.)
Behind glass in a never-before-used operating room inside a just-built cabin at the end of a freshly paved road, Dr. Hwang Woo Suk is chasing rogue flies with an electrified bug swatter that looks like a small tennis racket. He wears baby blue scrubs branded with the logo of Sooam Biotech, his South Korea-based research company, and is making final checks of this temporary facility, erected from scratch in eight days in the Chinese city of Weihai. Here, in a few hours, he’ll deliver the first cloned puppies in the country’s history.
Originally the procedure had been scheduled for Sooam’s headquarters in Seoul, where Hwang, 61, runs the only facility on earth that clones dogs for customers willing to pay $100,000. He led the team that cloned the first dog in 2005, and he’s produced more than 550 cloned puppies since, increasing the efficiency of a complicated process to a point where he can guarantee an exact genetic copy of a client’s dog, provided he has healthy tissue to work with. Today’s delivery, however, is a special case, and at the last minute, Chinese officials asked Hwang to relocate the operation to Weihai, in Shandong province.
For starters, the puppies are Tibetan mastiffs, a breed of ancient, aloof guard dogs so hallowed in China that owning the best specimens is an assertion of status almost without rival. The donor of the cells used to clone these puppies was an 8-year-old champion stud from Qinghai province whose owner turned down a $5 million offer for him last year. He can earn nearly that much in one breeding season. Earlier this year, a developer paid $2.6 million for a single, gold-colored puppy, and a scarcity of top-quality puppies in China means that the run on mastiffs costing more than mansions is unlikely to abate anytime soon.
In 2005, Hwang was named Korea’s first “Supreme Scientist.” By 2009, he was “penniless and devastated”
Beyond the symbolic importance of the breed, Chinese officials wanted the operation staged in Weihai because it provided a backdrop for the announcement of a partnership between Sooam and BoyaLife, a fast-growing Chinese biotechnology company with 28 subsidiaries and operations in 16 provinces. Sometime early next year, ground will be broken for a 667,000-square-foot research laboratory on a spectacular plateau of yellow grass and scrubby pines facing the Yellow Sea. There, scientists from both companies will operate China’s first commercial animal cloning facility on grounds landscaped to look like a park. “The point is to expand cloning in China,” says Dr. Xu Xiao-chun, chairman and chief executive officer of BoyaLife, whose excellent English is the product of 17 years in the U.S.
Rare breeds, dogs cloned for devoted owners, and specialized working dogs (for police and bomb-sniffing work, as well as cancer detection) will be a part of that business, he says, but only a small one. “Dogs are the entry point,” he says. The far larger and more important focus will be cloning cows to help China deal with a growing appetite for beef. Currently the Chinese favor pork and consume just 5 kilograms (11 pounds) a year of beef per capita, half the global average and one-tenth what Americans consume. But the population is acquiring a taste, so Xu wants to “expedite the production of high-quality beef” through cloning.
Beyond that, he envisions a renowned research facility to explore the various biomedical applications of cloning and stem cells, another area of focus for Sooam and BoyaLife. “In China we do things on a massive scale,” he says. “But we want to do all this not just for profit, but also for history.” He smiles. “Maybe we can deliver the first cloned giant panda in Weihai.” (In 2004, the Chinese government built a special gene bank and began collecting cells from existing pandas with the idea that such a thing might one day be possible.)
Photograph by Ka Xiaoxi for Bloomberg BusinessweekHwang with a Yorkie clone in a play area outside Sooam’s lab in Seoul
As of this September, though, the lab exists as a collection of architectural drawings and a plot of land selected for optimal feng shui, so Hwang and his surgical team will make do with the temporary facility tucked into a wooded hollow. It’s a handsome three-room structure with cedar paneling, hardwood floors, and a fully equipped operating room, but construction had been completed only the night before, and cleaning was still under way. Thus the dust and a few rogue insects. “My apologies. This is temporary,” Hwang says, fly zapper in hand. “Don’t ask how we did it,” Xu adds.
At around 1 p.m., the various dignitaries are ushered in and scramble for spots along the windows. Only the district’s ranking party secretary, as well as Xu and his father, Xu Zhihong, the former president of Peking University, are given scrubs and allowed into the OR. Every single person raises a smartphone as Hwang, wearing a Madonna-style headset mic, assesses the sleeping surrogate. She lies on a surgical table, belly up, in preparation for a Caesarean delivery, which Hwang insists is safer in the case of large breeds. Hwang uses large mutts to gestate his clones because they have big wombs and are better able to handle the stress of surgery.
Eleven minutes later, Hwang pulls the first puppy out of the uterus, followed by the second, and finally, after some rooting around, the third. “They’ve already started to cry,” he says, and passes them to an assistant, who cleans them and places them near a microphone so that the crowd outside the windows can hear the adorable whines and whimpers. Each is given a tiny bow and laid on a metal tray that a nurse holds up to the window.
“This is too magic,” my translator says. “Wow.”
Hwang is famous—and infamous—in the world of genetics. A decade ago, he became one of the most celebrated scientists in the world when he published two studies in the journal Science that announced the first successful cloning of a human embryo. Hwang, then a Seoul National University (SNU) professor, said he’d been able to extract stem cells from the embryo, apparently creating a new and potentially unlimited source for these important cells, which were becoming recognized as a possible treatment for all kinds of diseases. Time named him one of its “People Who Mattered” in 2004, and in June 2005, Korea’s Ministry of Science and Technology declared Hwang the first “Supreme Scientist” in the country’s history. He was honored on a postage stamp.
Then it all came undone. An American researcher who’d been one of the co-authors on the Science papers disavowed the work later that year. In Korea, a member of Hwang’s team went public, claiming that he’d paid women, including underlings at the university, for their eggs—a major ethical breach. An inquest launched by SNU subsequently determined that Hwang’s group hadn’t actually cloned an embryo, despite harvesting cells from 288 different human eggs. Pictures of the results, investigators learned, were fakes—merely multiples of the same photo—and government funds had been misused. Hwang called a news conference to apologize and announced that he would resign from his numerous posts. “I was blinded by work and my drive for achievement,” he said.
It wasn’t over. The government assigned a prosecutor to the case and eventually convicted Hwang of bioethical violations and embezzlement of $700,000 in public research funds. It also stripped him of his license to practice stem cell research. In 2009 a judge gave Hwang a two-year suspended prison sentence, claiming that he’d owned up to his crimes and hadn’t used the misappropriated funds for personal use; he’d used them to purchase human eggs. Hwang refuses to talk about the scandal and leaves it to Kwoun Young Chul, executive director at HBion, Sooam’s commercial division, to address the matter. Kwoun, 43, asserts that the fabrication of the data at SNU’s partner institution, MizMedi Hospital, was the result of poor oversight by Hwang, as principal investigator, but wasn’t part of some intentional plot to falsify data and fool the public. The episode “sank Dr. Hwang to an abyss,” Kwoun adds.
Hwang was, in his own words, “penniless and devastated” after the scandal, but a sizable portion of the Korean public never turned against him and continued to support him and his work. Donors included sympathetic citizens, who mailed in checks for as little as $100 or sent him food and clothes, as well as investors, who still believed in his ability to do important research. “Thanks to all of them, I was able to start Sooam,” he says.
At Sooam he resumed his work on animal cloning, using a technique known as somatic cell nuclear transfer (SCNT), in which the nucleus of an oocyte (egg cell) is removed and replaced by that of a somatic (body) cell from the mature specimen being cloned. Typically, these cells are fibroblasts, the cells that make up the body’s connective tissue. They’re taken via skin biopsy from the abdomen and cultured in a lab. Once the somatic cell nucleus is in place, a lab worker uses electricity to fuse the nucleus and oocyte together into a reconstructed embryo that’s implanted into a surrogate mother.
This is how Dolly the sheep was created in 1996, and it’s the way scientists have replicated cows, pigs, goats, mice, and many other animals since. Every scientist who does mammal cloning, including Hwang, licenses the so-called Dolly patent from ViaGen, a U.S. company that acquired the intellectual property from Dolly’s creator, Dr. Ian Wilmut.
Hwang used SCNT to create Snuppy, the world’s first cloned dog, born in April 2005 at Seoul National University. In the process he added a few steps specific to canines that he subsequently patented. An Afghan hound clone, Snuppy was gestated in a Labrador retriever surrogate. His arrival at SNU was somewhat lost in the furor over Hwang’s stem cell work, but it was a major achievement, as no one had ever before cloned a dog. (Snuppy still lives in Korea.)
Dogs have some peculiar and complicated reproductive traits that make the species difficult to clone; most problematic, their ovulation cycles are irregular, and the eggs are in a mature state and optimal for cloning for only a few hours. In the case of Snuppy, it took 123 attempts to produce a single viable puppy. That inefficiency led most observers—and even Hwang—to suggest that this wasn’t something likely to scale for pets.
In 2007, Hwang met an American named Lou Hawthorne who had led the unsuccessful effort to clone a border collie mix named Missy in the late 1990s through a now-defunct company called Genetics Savings & Clone. Despite several years and millions of dollars devoted to the so-called Missyplicity project, scientists failed to clone Missy before she died in 2002. They had collected and stored samples of her cells, however, and when Hawthorne met Hwang, he asked if Sooam could try again. Hwang took the samples and cloned Missy on the first attempt, producing four pups. Hawthorne brought all four Missys back to California.
One year later, Sooam sold its first cloned dog to Edgar and Nina Otto, a Florida couple so distraught over the death of Lancelot, their beloved Labrador, that they were willing to pay $155,000 in an auction for the opportunity to receive the world’s first commercially cloned dog. They named him Lancelot Encore. Six years and hundreds of cloned dogs later, Sooam has streamlined the process enough so that anyone with $100,000 and the patience to wait in line for up to six months can have a dog cloned. A team of scientists works under Hwang with the ability to carry out every part of the painstaking process, and the lab has the capacity to produce 150 to 200 commercial clones a year for clients who so far have included celebrities, Middle Eastern royals, and a few proud, non-anonymous buyers such as Dr. Philip Dupont, a veterinarian in Lafayette, La.
Photograph by Thomas Prior for Bloomberg BusinessweekMelvin’s legacy lives on in Ken and Henry, pictured with owner Dupont in Lafayette, La.
Dupont and his wife saw Hwang’s work on a Discovery Channel program called I Cloned My Pet and were so taken with the idea that they immediately called Sooam and arranged to have Melvin, their Catahoula leopard dog mix, cloned. Dupont had paid $50 for Melvin to a guy on a dirt road deep in the bayou, and the puppy was so sickly that he lost a full pound of worms in the first 24 hours. “I thought about putting him to sleep a few times, and he turned out to be the best dog I ever had,” Dupont says. “You feel like you’re talking to a person. The dog does things that are weird.” Dupont was using the present tense, even though Melvin had died just a week before our conversation—but not before he enjoyed nearly two full years with his clones, Ken and Henry. “It’s like having two Melvins running around all the time,” Dupont says.
To prove its work, Sooam instructs clients to take a tissue sample and send it to the University of California at Davis for genetic analysis. The Duponts did that, but they didn’t need to; it was obvious to them just by hanging around the clones that they were for real.
“These puppies are just like him,” Dupont says. “They love to hunt moles. They love to hunt field rats. They will come in and sneeze on command when we say, ‘You got a cold?’ Melvin did that. It’s like having Melvin around the house, but two. Sometimes, too much Melvin.”
Sooam’s Korean headquarters sits at the foot of a hill in the western suburbs of Seoul, in the shadow of a towering, multilevel golf driving range and across the road from another. The facility looks like a series of shirt boxes stacked irregularly atop one another. The front yard, about a half-acre of manicured grass, is fenced so that the clones-in-residence have a place to chase Frisbees and act like normal puppies.
All visitors must remove their shoes just inside the foyer and switch to a set of borrowed sandals, which is a matter of Korean custom and not some sterility protocol. (If you want to use the bathroom, you change footwear a second time, from the sandals to a special set of toilet slippers.)
Photograph by Thomas Prior for Bloomberg BusinessweekKen and Henry, Melvin’s clones
On the research floor, a junior scientist directs us to put on scrubs, then leads us through an air lock, where jet fans blast stray particles off our clothing, and into the lab, where men and women carry vials and peer into microscopes. A camera atop one microscope projects the invisible work going on: A technician carefully manipulates two joysticks to do the delicate work of enucleating an embryo and injecting the nucleus of a live cell in its place—the key components of cloning an egg that will soon be implanted into a surrogate in the operating theater downstairs.
Work at Sooam is divided into three sections: canine, porcine, and bovine. The canine team focuses on commercial cloning, as well as on transgenic clones, which are genetically engineered to express certain traits. Last year scientists on that team successfully manipulated the genes of one beagle clone to develop Alzheimer’s disease, and all 18 clones from that cell line have been born with the disease. The project remains in the study phase, but if it can be commercialized, it would allow Sooam to produce dogs with Alzheimer’s on demand, potentially opening up a huge business catering to pharmaceutical companies doing research in that space—which use 7,500 beagles a year in the U.S. alone, according to Sooam. A second project is under way to produce clones born with diabetes, another epidemic disease that affects both humans and dogs.
Transgenic research has tremendous potential for Sooam, and for the many other scientists pursuing it around the world, but it’s expensive and time-intensive. Sooam’s bovine team is at work on dairy cow clones engineered to express glycoproteins, such as interferon, which are released by cells in the presence of viruses to trigger immune response. These are widely sought by pharmaceutical manufacturers for obvious reasons, but difficult to obtain. Sooam’s plan is to create the clones and harvest the proteins via the 10,000 gallons of milk a dairy cow generates in a year. The team managed to produce a single cow that expressed interferon last year, but the animal didn’t survive. Work continues.
Closer to market is Sooam’s effort to help restore the Han-woo cow population. The Han-woo is Korea’s equivalent of Wagyu or Kobe, and stocks were devastated by an outbreak of foot and mouth disease three years ago. The morning after the delivery of the precious puppies in China, Hwang met on a farm with Nam Kyung Pil, the governor of Gyeonggi, Korea’s largest province, to celebrate the birth of the first set of cow clones from a Sooam project sponsored by the provincial government. If the pilot program is successful, Sooam is likely to get a much larger contract to take the program national. “It would be a very big piece of business for us,” says Kwoun of Sooam’s sister company.
Cloning’s DNA 1 of 13 Photograph by Getty Images 1902
German embryologist Hans Spemann uses a hair from his infant daughter to separate a salamander embryo into two. Each develops normally.
Photograph by Getty Images 1938
Spemann proposes a “fantastical experiment” to clone via nuclear transfer but can’t perform the experiment because baby hairs don’t cut it.
Photograph by Getty Images 1958
Oxford’s John Gurdon clones tadpoles using the intestinal cell of an African clawed frog.
Photograph by Getty Images 1981
Karl Illmenese and Peter Hope clone a mouse at the University of Geneva.
Photograph by Getty Images 1996
Hello, Dolly! Ian Wilmut and Keith Campbell of the Roslin Institute use the nucleus from a sheep’s udder cell to replace that of an egg. Only 1 of 277 transfers takes, and Dolly’s it.
Courtesy Advanced Cell Technology 2001
Scientists at Advanced Cell Technology use a surrogate to clone the first endangered species: Noah, a bull gaur (wild ox). He dies of an infection unrelated to cloning.
Photograph by Texas A&M University/Getty Images 2001
The first cloned cat, CopyCat, is born at Texas A&M under the direction of Dr. Mark Westhusin, in collaboration with Dr. Taeyoung Shin, later a Sooam founder.
Photograph by Getty Images 2003
Goodbye, Dolly. The celebrity sheep is euthanized after developing lung cancer.
Photograph by Park Ji-Hwan/AFP via Getty Images 2004
A group of scientists at Seoul National University (SNU) led by Hwang Woo Suk announce the cloning of a human embryo. This is later exposed as a fraud.
Photograph by Getty Images 2005
The first dog, an Afghan hound named Snuppy, is cloned by Hwang and his team at SNU.
Photograph by Getty Images 2008
Sooam clones the first pet dog for an American couple. They pay $155,000 for the historic privilege.
2009
Closer to Jurassic Park, French and Spanish scientists clone a Pyrenean ibex, extinct since 2000. Ten minutes after her birth, she dies—and the species goes extinct all over again.
2013
An Oregon team led by Shoukhrat Mitalipov appears to achieve what Hwang claimed in 2004: It uses SCNT to clone a human embryo that can be used as a source of stem cells.
The porcine team is pursuing transgenic clones that could one day provide a safe source of organs for humans in need. Pig organs are similar to ours, which makes them an attractive potential substitute for patients awaiting transplants. Our immune systems, however, tend to reject foreign organs. One solution is to fuse human genetic material into the pig clone embryo, so that the recipient’s immune system doesn’t reject the transplanted organ. Eventually, says Jeong Yeon Woo, Sooam’s 39-year-old director of research, Sooam will have to collaborate with a hospital or university, because “we are not immune specialists.”
One of Hwang’s biggest dreams is to revive his work on human stem cells. To this day, he asserts that the cell line he created back at Seoul National University was from a cloned embryo, not cultured from an existing embryo as investigators determined. Sooam still owns the line. There’s just one problem: The Korean government, in response to the scandal, banned research on human stem cells. “We will keep knocking on the doors,” Hwang says, “not only in South Korea but also in other countries, until we can continue our human stem cell research.”
Broadening Sooam’s reach is the primary responsibility of Kwoun, a former investment banker. Hwang hired him early this year to put him in charge of all things financial, freeing up Hwang to focus on research, and especially to head HBion, the sister company that was founded to commercialize the technologies developed by Sooam. For now, that means mostly canines, but also a NASA-discovers-Velcro type spinoff: a high-end skin-care line called Dracell that was created from the patented culture medium in which Sooam grows and stores all of its cloned embryos.
“A tiger has the exact same number of chromosomes as a pig, so we might try that”
Some projects are even more audacious. In 2012, Hwang and his team cloned a litter of seven rare Asian coyotes using a mutt as a surrogate. That same year he announced a partnership with North-Eastern Federal University in Russia to work on the so-called Mammoth Restoration Project. The National Geographic Channel filmed the initial expedition into Siberia in search of a frozen carcass from which genetic material might be taken and turned the footage into an hourlong special, “Mammoth: Back From the Dead.” It’s a compelling idea—and not as outrageous as it might seem, Director of Research Jeong explains. “Principally it’s possible because we use stem cells stored in nitrogen already,” he says. “So they’re frozen.” Scientists in Japan managed to clone a mouse using cells harvested from a specimen that had been frozen for 10 years, proving that prolonged freezing isn’t an insurmountable barrier. What’s critical is that the mouse cells were frozen in a steady state. In the instance of the mammoths, the tissues have been through a series of freezes and thaws.
And where would Sooam gestate a mammoth, if it ever obtained the right samples? “Probably an elephant,” Jeong says. The coyote project proved that scientists can use one species as a surrogate for another, and Sooam plans to push this line of inquiry further. It’s been suggested that if the Chinese ever allowed the giant panda to be cloned, a dog could be used as a surrogate because the two species are genetically similar enough, and there’s no way that Beijing is going to take the risk of offering up full-grown pandas to serve as surrogates. Hwang is also working to persuade the Spanish government to let him clone the rare Spanish ibex, using the Korean black goat as a surrogate. Numerous other endangered species, including African wild dogs and various wolves, are on his wish list. Could they save the Siberian tiger, which would require some other huge and ferocious cat? “A tiger has the exact same number of chromosomes as a pig, so we might try that,” Jeong says. “Our future plan is to clone all extinct animals,” says Kwoun, who’s been listening. “In the future. But we are out of hands.”
On the morning of my last day in Seoul, Kwoun is late picking me up. “I’m very sorry,” he says. “We had a bit of a panic situation.” An e-mail arrived overnight from a man in France whose dog had died unexpectedly the previous day. The man wrote that he had “loved this dog very much” and that he wished to be able to “keep some part of him,” so he’d put its dead body into his freezer and bought himself a ticket to Korea. He required only instructions on how to proceed from there. Kwoun chuckles. “We told him there was no need to panic and that he should take the dog out of the freezer immediately,” he says.
There is no precise rule for how much time an owner has to harvest his dog’s cells for cloning after death; it varies depending on the specimen and how it’s handled. As a general rule, Sooam tells people they have five days to arrange a biopsy and ship a few vials of cells to Korea, though in some cases samples can be viable for days beyond that. The Frenchman was told to wrap his dog in wet towels, refrigerate it—freezing can actually damage cells—and find a vet or hospital to snip a bit of tissue and sign the paperwork stating that the biological material was for research purposes, so that it wouldn’t get confiscated in transit. Once a sample has been received, the client can relax and put the clone on what amounts to layaway. Sooam requires only $3,000 to arrange storage of the tissue in perpetuity—“so that people can do cloning later on, when they have money,” Kwoun explains.
At the lab, the staff is preparing for a group of Americans coming to pick up two special puppies, cloned from the DNA of a Belgian Malinois that’s currently deployed with a unit of the U.S. Army Special Forces (which Sooam isn’t permitted to name). The donor dog was chosen because he was a standout among Special Forces canines—elite even among the elite, something like the soldier-dog equivalent of LeBron James—and these three-month-old puppies were heading to the U.S. to undergo training as part of an experiment.
Photograph by Thomas Prior for Bloomberg BusinessweekTwo Belgian Malinois puppies, cloned from the DNA of a dog that’s currently deployed with a unit of the U.S. Army Special Forces
At this point, cloning a pet is straightforward for Sooam. Given fresh cells, Hwang says, “we have never failed cloning a specific dog, regardless of its size or breed.” In turn, that part of the business is fairly mature. Orders are healthy. There’s a waiting list.
What’s most intriguing to Hwang now is the study of clone performance, particularly among what Sooam calls special purpose dogs. He wants to know if a puppy cloned from a truly exceptional working dog will end up performing at that job as well as his genetic twin. If he does, it could seriously disrupt the process of breeding and training police dogs, explosives detection dogs, and others that serve in jobs that help save human lives.
Recently, Sooam secured a contract to provide 40 cloned special purpose dogs to the South Korean national police, and several are already in service at the Incheon International Airport near Seoul. But Hwang’s scientists lack proof that the donor dogs were truly special. That’s why they sought out the Americans, to find empirically great dogs to clone.
The four Americans arrive after lunch, in the company of some powerful South Koreans, including Younghoon (David) Kim, chairman of the Daesung Group, one of the country’s largest multinationals, and his managing director. Daesung has interests in energy and defense and is invested in this particular project as the Korean liaison to the American company that will, if this experiment proves out, sell cloned super dogs to police departments and military units around the globe.
Known as BioPremium K9, the startup was founded by Peter Hwang, a Korean American who served 25 years with the Illinois State Police and the FBI. Hwang (no relation to the doctor) has known Daesung’s chairman since they were both young men, and Kim came to him with an unusual request: He needed to find “the best working dog in the U.S.” for a special project. Hwang recruited an Illinois-based cop and canine specialist named Bert Badertscher to help him, and the two set out to locate just such a dog.
Photograph by Thomas Prior for Bloomberg BusinessweekBrannon holds Special Ops clones Ghost and Echo between bite-training sessions in Sharpsville, Pa.
Eventually, they settled on Shallow Creek Kennels, a small facility north of Pittsburgh that trains elite dogs for numerous police departments and U.S. government agencies, including Special Operations. The owner, John Brannon, loved the idea and had just the dog in mind. He arranged for fibroblasts to be collected from the dog, which is currently working in Afghanistan and whose identity is classified. Sooam cloned him, resulting in Ghost and Echo, the adorable clone brothers that the Americans had all come to Seoul to collect.
Because every day matters when your goal is to turn a puppy with potential into a dependable, battle-ready working dog, Brannon had given Sooam staffers a strict training and socialization regimen to follow from birth, but it isn’t until the dogs are bounding around on the front lawn after a short adoption ceremony that Brannon is able to get his first good look at them. “I’m impressed. They seem advanced for their age. But you don’t really know until a dog is 12 months what you have physically and mentally,” Brannon says, which is why he doesn’t bother with the imprecise and wasteful process of breeding. It’s far more effective for him to travel to Europe a few times a year to source year-old dogs from one of several kennels he knows and trusts.
One of the most challenging things about great police dogs, Badertscher says, is finding the right puppies and then training them, only to have to retire them eight or nine years later. “Now we have a chance, an idea—it’s only a theory,” he says. Every time you breed a dog naturally, you lose some portion of its greatness, because the genes are diluted by the contribution of the mate. And you’re lucky if one or two dogs out of a litter of eight might have the drive and focus to become the kind of dogs who can find bombs, take fire, and work independently on command—let alone jump out of airplanes at night.
“Ghost and Echo are the first research study to see if this idea works: Can we reproduce these top-quality dogs through cloning” and eliminate most of the margin for error, Badertscher says. Beyond that, he believes, “the next step is giving these dogs a chance to live longer” by using cloning to eliminate problems such as cancer, hip dysplasia, and bad eyesight that can prematurely end a working dog’s career. Two extra years of work would be an incredible boost in productivity, keeping the best dogs working longer and offsetting the increased costs of cloning. “The biggest thing we’ll have to fight,” he says, “is the word ‘cloning.’ ” |||||
What is a shorter version of the above article? | – Facing a serious meat shortage as its population continues to grow and industrialize, China is set to open the world's largest animal-cloning factory in the first half of 2016. But it's not just cloning and raising cattle for beef. Commercial genetics company BoyaLife, which is building the center with South Korea's Sooam Biotech, Sinica, Peking University's Institute of Molecular Medicine, and the Tianjin International Joint Academy of Biomedicine, says it also plans to clone racehorses and dogs—the latter not just for pets but to sniff out illegal drugs and victims of natural disasters, reports Vice. It may even help rescue endangered species from the brink of extinction. "In China we do things on a massive scale," BoyaLife CEO Xu Xiaochun told Bloomberg back in 2014. "We want to do all this not just for profit, but also for history." And in spite of some controversy on the use of cloned animals, he tells the Guardian he's confident the move is a positive one: "We are going [down] a path that no one has ever traveled. We are building something that has not existed in the past. This is going to change our world and our lives. It is going to make our life better. So we are very, very excited about it." The European Parliament has voted to outlaw the sale of cloned livestock, while in the US the FDA has long taken the stance that cloned meat is safe and harbors no complications "unique to cloning." (The US is already in the cloning racehorses game.) | multi_news_1_0_0 |
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– The fittest city in the US also happens to be the capital. So says this year's American Fitness Index, the work of the American College of Sports Medicine. The report scores cities based on a range of factors, including chronic health problems like diabetes; healthy and not-so-healthy behaviors, like diet and smoking; local recreational spots, like playgrounds; use of public transportation; and amount of parkland, USA Today reports. Washington, DC, comes out on top after three years of victory for Minneapolis-St. Paul, which this year comes in second. The rest of the top five: Portland, Oregon Denver San Francisco And the bottom five of the country's 50 biggest cities: Nashville Indianapolis Oklahoma City Louisville Memphis Click for the full list.
Expand this summary. | Thank you, Anthem Foundation, for helping us create healthy and fit communities!
The Anthem Foundation has invested more than one million dollars for AFI data research and technical assistance to communities since 2006.
Want to be a part of the next 10 years of AFI? Sign up to receive quarterly program resources and updates! ||||| A jogger runs along the walking path below the Washington Monument in Washington, DC. The Washington metro area is the fittest city in the nation according to an annual ranking by the American College of Sports Medicine. (Photo: Jack Gruber, USA TODAY)
The Washington metropolitan area has reclaimed the top spot in an annual ranking of health and community fitness, bumping Minneapolis-St. Paul, last year's three-peat winner, to second place.
Portland, Ore.; Denver; and San Francisco round out the Top 5 on the 2014 American Fitness Index report, released today. Memphis is ranked last among the nation's 50 largest metropolitan areas.
Published by the American College of Sports Medicine, the report uses federal and other data to compare Metropolitan Statistical Areas (MSA) based on 31 indicators in four categories: chronic health problems (diabetes, asthma); health behaviors (cigarette smoking and fruit consumption); physical or built environments (parkland acreage and number of farmer's markets); and recreational facilities (swimming pools and playgrounds). A new indicator this year is a city's "Walk Score," a measurement of how easy it is to walk to amenities and services.
Developed by a team of leading sports medicine professionals and exercise scientists, the fitness index offers a snapshot of the state of health in the community and an evaluation of the infrastructure, community assets and policies that encourage healthy and fit lifestyles, according to the report.
The Washington metro area achieved a high of 77.3 out of 100 possible points with notable strengths listed in the areas of personal health behaviors and amenities that support physical activity and healthy living, says Walter Thompson, chairman of the advisory board that created the index and a professor of exercise physiology at Georgia State University in Atlanta.
Thompson points to Washington's top marks for parkland as a percentage of city land (19.5% vs. the target goal of 10.6%); park-related expenditures ($398 per resident; target goal: $101.80 per resident); farmers' markets per capita (28.5 per 1,000,000; target goal: 13.1 per 1,000,000); percent of commuters using public transportation (14.1%; target goal: 4.3%); average percent of commuters biking and walking (4.0%; target goal: 2.8%); and an excellent Walk Score (74.0; target goal 51.1).
Washington's public amenities were cited as above average, with more recreation centers, more swimming pools and more tennis courts per capita than target goals. On the health front, the region was at or better than the target goal for lower death rates from cardiovascular disease and diabetes.
"Measures for the top five MSAs are very similar, suggesting that the 'fitness' levels of these cities are very similar and the differences among them are probably not remarkable," says Thompson.
As for cities at the bottom of the index: No. 45 San Antonio (35.6 out of 100 points); No. 46 Nashville (32.5 points); No. 47 Indianapolis (32.3 points); No. 48 Oklahoma City (31.6 points); No. 49 Louisville (25.7 points); and No. 50 Memphis (24.8 points). It's important to remember "that the ranking merely points out that relative to each other, some metro areas scored better on the indicators than the other," says Thompson. The index "was created for communities to assess their level of health and fitness, assess areas that could use improvement, and to increase their scores over time," he says.
Cities, states and businesses are often in need of the kinds of metrics that this report pulls together, says physician Timothy Church, director of preventive medicine research at the Pennington Biomedical Research Center in Baton Rouge. He was not involved in the new report. "I've worked with a number of those groups and they want to know how do we judge ourselves, how do we know if we're doing the right things, what should we be working on?"
In addition, the attention associated with this report "helps creates an awareness" that factors associated with fitness, health and environment "make a difference in people's lives," says Church. "These are important topics to talk about. (The report) clearly can be a call to action for certain places."
With a grant from the WellPoint Foundation, (the charitable arm of health plan provider WellPoint) the American College of Sports Medicine will use data from the AFI report to work with community organizations in Cincinnati, Las Vegas and Miami in 2014 to initiate locally driven health improvement efforts.
Read or Share this story: http://www.usatoday.com/story/news/nation/2014/05/28/fit-cities-index/9483563/ ||||| | multi_news_1_0_0 |
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Article:
Nonetheless, the use of a chokehold in subduing a large but unarmed man during a low-level arrest raises for Mr. Bratton the same questions about police training and tactics that he faced 20 years ago, in his first stint as New York City’s police commissioner.
In 1994, the year after the Police Department banned chokeholds, a man named Anthony Baez died in the Bronx after a police officer put him in a chokehold during a dispute over a touch football game.
At City Hall on Friday, Mr. Bratton said he did not believe that the use of chokeholds by police officers in New York City was a widespread problem, saying this was his “first exposure” to the issue since returning as police commissioner in January.
Mayor Bill de Blasio, standing next to Mr. Bratton, said, “Like so many New Yorkers I was very troubled by the video,” referring to a bystander’s recording of the incident, which was posted on the website of The New York Daily News. The two police officers who initially confronted Mr. Garner have been temporarily taken off patrol duty. The police declined to name the officers but said one of them had been on the force for eight years and the other for four years.
Late Friday, the mayor’s office announced that Mr. de Blasio was postponing his family’s departure on a planned vacation to Italy from Friday evening until Saturday. The postponement was to allow Mr. de Blasio to spend more time making calls to elected officials, community leaders and members of the clergy, and talking to the police, about Mr. Garner’s death, the mayor’s press secretary, Phil Walzak, said.
The encounter between Mr. Garner and plainclothes officers, from the 120th Precinct, began after the officers accused Mr. Garner of illegally selling cigarettes, an accusation he was familiar with. He had been arrested more than 30 times, often accused of selling loose cigarettes bought outside the state, a common hustle designed to avoid state and city tobacco taxes. In March and again in May, he was arrested on charges of illegally selling cigarettes on the sidewalk.
For years, Mr. Garner chafed at the scrutiny by the police, which he considered harassment. In 2007, he filed a handwritten complaint in federal court accusing a police officer of conducting a cavity search of him on the street, “digging his fingers in my rectum in the middle of the street” while people passed by. ||||| Photo: New York Daily News
An unarmed 43-year-old father of six from Staten Island died yesterday after at least five NYPD officers choked and smothered him during an arrest. Eric Garner, who suffered from chronic asthma, diabetes, and sleep apnea, was about six-foot-four, 400 pounds, the Daily News reports, and had a history of arrests for selling untaxed cigarettes. “I’m minding my business,” he says when confronted in the deeply disturbing video shot by a neighbor. “Are you serious? I didn’t do nothin’. What’d I do?”
“Every time you see me, you’re messing with me. I’m tired of it. This stops today,” says Garner. “Every time you see me, you wanna harass me. I told you last time, please just leave me alone.”
When the officers move to arrest him, Garner struggles until he’s choked from behind by a man not in uniform, who then pushes Garner’s head into the concrete. “I can’t breathe!” says Garner in a muffled scream. “I can’t breathe!” He repeats it over and over again, at least nine times audibly. Witnesses say the incident started when Garner tried to break up a fight.
Photo: New York Daily News
An NYPD spokesperson would only tell the Daily News that Garner “was being placed in custody, went into cardiac arrest and died.” Internal affairs has launched an investigation, with Garner’s wife saying a detective has been in touch. “I’m sorry for your loss,” he said, noting that he was involved “because there is wrongdoing.” That much seems obvious.
Update: In a very un-Bloomberg move, the mayor has taken to Twitter to acknowledge the incident.
On behalf of all New Yorkers, I extend my deepest condolences to the family of Eric Garner. — Bill de Blasio (@BilldeBlasio) July 18, 2014
His full statement:
On behalf of all New Yorkers, I extend my deepest condolences to the family of Mr. Garner, who died yesterday afternoon while being placed in police custody. We have a responsibility to keep every New Yorker safe, and that includes when individuals are in custody of the NYPD. That is a responsibility that Police Commissioner Bratton and I take very seriously. We are harnessing all resources available to the City to ensure a full and thorough investigation of the circumstances of this tragic incident. The NYPD’s Internal Affairs Bureau is working closely with the Office of the Richmond County District Attorney, which is leading this investigation.
Update II: At a press conference today, Mayor de Blasio said he was “deeply troubled” after watching the Garner video.
BdB says it's too early to jump to conclusions. But he promises New Yorkers there will be a complete investigation of the incident. — Michael Howard Saul (@MichaelHwrdSaul) July 18, 2014
NYPD Commissioner Bill Bratton added that the chokehold “appears” to be in violation of department policies, which can be read here. ||||| (This story was originally published on July 18, 2014)
A 400-pound asthmatic Staten Island dad died Thursday after a cop put him in a chokehold and other officers appeared to slam his head against the sidewalk, video of the incident shows.
“I can’t breathe! I can’t breathe!” Eric Garner, 43, repeatedly screamed after at least five NYPD officers took him down in front of a Tompkinsville beauty supply store when he balked at being handcuffed.
Within moments Garner, a married father of six children with two grandchildren, stopped struggling and appeared to be unconscious as police called paramedics to the scene. An angry crowd gathered, some recording with smartphones.
“When I kissed my husband this morning, I never thought it would be for the last time,” Garner’s wife, Esaw, told the Daily News.
She got no details from police until after she had gone to the hospital to identify his body, she said.
“I saw him with his eyes wide open and I said, ‘Babe, don’t leave me, I need you.’ But he was already gone,” she said.
A family friend searching for her in the hospital ran into detectives from the NYPD’s Internal Affairs Division. The friend put them on the phone with her, the grieving widow said.
ERIC GARNER: A YEAR LATER
She spoke with a Detective Howard, who told her, “I’m sorry for your loss,” she said. He said his office was involved “because there is wrongdoing,” she said.
Police officials said Garner had a history of arrests for selling untaxed cigarettes. Cops said they observed him selling his wares Thursday on Bay St. and moved in for an arrest.
Within moments Garner, a married father of six children with two grandchildren, ceased struggling and appeared to become unconscious as police called paramedics to the scene. (New York Daily News) Within moments Garner, a married father of six children with two grandchildren, ceased struggling and appeared to become unconscious as police called paramedics to the scene. (New York Daily News) Within moments Garner, a married father of six children with two grandchildren, ceased struggling and appeared to become unconscious as police called paramedics to the scene.
An NYPD spokesman would only say the man “was being placed in custody, went into cardiac arrest and died” at Richmond University Medical Center.
But Esaw Garner and other family members said it was a trumped up claim.
“They’re covering their asses, he was breaking up a fight. They harassed and harassed my husband until they killed him,” she said. Garner’s family said he didn’t have any cigarettes on him or in his car at the time of his death.
She said she pleaded with police at the hospital to tell her what happened, but they brushed her off.
“They wouldn’t tell me anything,” she said.
An angry crowd gathered, some recording with smartphones. (Ken Murray/NEW YORK DAILY NEWS)
Officials confirmed that NYPD Internal Affairs officers launched an investigation Thursday night.
Records show Garner was due in court in October on three Staten Island cases, including charges of pot possession and possession or selling untaxed cigarettes.
Esaw Garner said her husband was unable to work because he suffered from a host of ailments, including chronic asthma, diabetes and sleep apnea.
Garner’s mother, Gwen Carr, 65, added, “I want justice.”
'When I kissed my husband this morning, I never thought it would be for the last time,' Garner’s wife, Esaw Garner, told the Daily News. Esaw Garner holds a photo of her late husband with sons Emery (left) and Eric. (Sam Costanza for New York Daily News)
Police said Garner was not armed.
The Staten Island resident was sitting in front of Bay Beauty on Bay St. and Victory Blvd. just before 5 p.m. when two plainclothes cops began questioning him about selling untaxed cigarettes, a video obtained by the Daily News shows.
Ramsey Orta, 22, shot the shocking footage. (Ken Murray/NEW YORK DAILY NEWS)
“I didn’t do s---!” the 6-foot-4 Garner, wearing a sweaty T-shirt and khaki shorts, told the officers from the 120th Precinct when they approached him. “I was just minding my own business.
“Every time you see me you want to mess with me. I’m tired of it. It stops today!” he yelled.
'He’s the nicest guy. I can’t believe what I saw. That’s no way to do an arrest,' said Douglas, 50, about Garner. Douglas would only give his first name. (acquired by: TOMAS E. GASTON)
Ramsey Orta, 22, who shot the video, tried to intervene, telling the cops his friend had just broken up a fight between three men and had not been selling cigarettes.
But when backup uniformed officers arrived, the cops moved in to cuff Garner, the video shows.
“Don’t touch me, please,” he said.
Friends of Eric Garner set up a memorial at the spot where he died. (Sam Costanza) The candle memorial reads 'BIG E.' (Sam Costanza) Eric Garner recently attended the circus with friends and family members. (Sam Costanza) Eric Garner and his wife Esaw Garner. (Sam Costanza)
When Garner refused orders to put his hands behind his back, one of the plainclothes cops, wearing a green T-shirt with a yellow No. 99 on the back, got behind him and put him in a chokehold, the footage shows.
A struggle ensued as three uniformed officers joined in on the arrest, knocking the man to the ground.
He screamed, “I can’t breathe!” six times before he went silent and paramedics were called.
“They jumped him and they were choking him. He was foaming at the mouth,” Orta told The News. “And that’s it, he was done. The cops were saying, ‘No, he’s OK, he’s OK.” He wasn’t OK.”
“They were choking him. He kept saying, ‘I can’t breathe, I can’t breathe! Get off of me, get off of me!’ and I didn’t hear any more talking after that,” said witness Valencia Griffin, 50, of Staten Island. “He died right there.”
Another witness, who would only give his first name, Douglas, said he’d known Garner for four years.
“He’s a very big man, very intimidating, but he’s just a big teddy bear,” said Douglas, 50. “He’s the nicest guy. I can’t believe what I saw. That’s no way to do an arrest.”
Eric Garner's family including (from left) son Eric, 18, daughter Erica, 24, daughter Emerald, 22, wife Esaw, 46, mother Gwen Carr, 65, and son Emery, 14, are mourning the loss of him. (Sam Costanza for New York Daily News) Eric Garner's sister, MTA bus operator Lisha Flagg, 38, wants justice for Eric Garner's death. (TOMAS E. GASTON)
At the video’s end, the cop who had choke-held Garner can be seen staring at the camera that was videotaping him.
“This had nothing to do with the fight, this had something to do with something else,” the cop said, and walked away.
A law enforcement source said the incident was troubling.
“A guy is dead in our custody. That is always a potential problem,” the source said.
With Patrick McCarron and Bill Hutchinson
UPDATE: The Staten Island district attorney is investigating the shocking death of a 400-pound asthmatic dad after a city cop placed him in a chokehold.
Eric Garner, 43, died Thursday after a sidewalk takedown by five NYPD officers making an arrest outside a Tompkinsville beauty parlor.
“My office is working along with the NYPD to do a complete and thorough investigation into the circumstances surrounding Mr. Garner's death,” said District Attorney Daniel M. Donovan Jr. in a Friday statement.
Click here to read Friday's full story
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What is a summary? | – An unarmed Staten Island man died yesterday after police put him in a choke-hold and he shouted "I can't breathe!" at least nine times, New York reports. Eric Garner, 43, a father of six and a grandfather, can be seen in an eyewitness video standing on a street corner when police approached him. "Every time you see me, you're messing with me," said Garner, who stood six-foot-four and weighed over 300 pounds. "I'm tired of it. This stops today. ... Please just leave me alone." But officers moved in, pinning Garner down with a choke-hold and apparently slamming his head against the sidewalk, the Daily News reports. Garner, who suffered from chronic asthma, sleep apnea, and diabetes, was dead within minutes. Police say Garner sold untaxed cigarettes, and had just been seen doing so. Garner was also due in court on three cases, including pot possession and illegal cigarette sales. But according to his wife, Esaw—and a friend of Garner's who shot the video—police really moved in because Garner had broken up a fight. Either way, Mayor Bill de Blasio has vowed a full investigation (the New York Times notes that the NYPD rulebook forbids choke-holds). Meanwhile, Esaw sounds like she's still grasping what just happened. "When I kissed my husband this morning, I never thought it would be for the last time," she said. At the hospital, "I saw him with his eyes wide open and I said, 'Babe, don’t leave me, I need you.' But he was already gone." | multi_news_1_0_0 |
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FILE - This Oct. 10, 2013, file photo, shows an EpiPen epinephrine auto-injector, a Mylan product, in Hendersonville, Texas. Mylan, now in the crosshairs over severe price hikes for its EpiPen, said Thursday,... (Associated Press)
FILE - This Oct. 10, 2013, file photo, shows an EpiPen epinephrine auto-injector, a Mylan product, in Hendersonville, Texas. Mylan, now in the crosshairs over severe price hikes for its EpiPen, said Thursday, Aug. 25, 2016, it will expand programs that lower out-of-pocket costs by as much as half. (AP... (Associated Press)
FILE - This Oct. 10, 2013, file photo, shows an EpiPen epinephrine auto-injector, a Mylan product, in Hendersonville, Texas. Mylan, now in the crosshairs over severe price hikes for its EpiPen, said Thursday, Aug. 25, 2016, it will expand programs that lower out-of-pocket costs by as much as half. (AP... (Associated Press) FILE - This Oct. 10, 2013, file photo, shows an EpiPen epinephrine auto-injector, a Mylan product, in Hendersonville, Texas. Mylan, now in the crosshairs over severe price hikes for its EpiPen, said Thursday,... (Associated Press)
NEW YORK (AP) — Mylan, in the face of heated criticism over price hikes for its EpiPen emergency allergy treatment, is bulking up programs that help patients pay for the drug.
The generic drugmaker laid out a plan on Thursday to expand its patient assistance program and offer $300 savings cards for its EpiPen 2-Pak.
There is no change in the price of the treatment, however, which is what has drawn ire both in Congress and from families that have had to shell out increasingly large sums for the potentially life-saving treatment.
Mylan has hiked prices for EpiPen as frequently as three times a year over the past nine years. A two-dose EpiPen package cost around $94 nine years ago but has climbed more than 600 percent to an average cost of $608 in May, according to the Elsevier Clinical Solutions' Gold Standard Drug Database.
Mylan did not immediately return calls from The Associated Press early Thursday about the drug's price.
Mylan N.V. said it's doubling eligibility for its patient assistance program, which it said will get rid of out-of-pocket costs for uninsured and underinsured patients and families. It also noted that the $300 savings card will cover about half the cost patients who would otherwise have to pay the full list price.
Patients will also be able to order the injected emergency medicine for severe allergic reactions directly from the company, to help lower costs, Mylan said.
Democratic presidential candidate Hillary Clinton and members of Congress from both parties have been calling on Mylan to address the pricing.
Pharmaceutical and biotech industries can fuel American innovation, and combat debilitating diseases, Clinton said in the statement Wednesday. But she added that "it's wrong when drug companies put profits ahead of patients, raising prices without justifying the value behind them."
Last year, more than 3.6 million U.S. prescriptions for two-packs of EpiPens were filled, according to data firm IMS Health. That earned Mylan nearly $1.7 billion.
EpiPens are used in emergencies to treat severe allergies that can lead to anaphylactic shock. Roughly 40 million Americans have severe allergies to spider bites, bee stings and foods like nuts, eggs and shellfish. ||||| Drugmaker Mylan is promising to double the eligibility for its EpiPen assistance program following a pricing backlash from consumers, but the company stopped shorted of reducing or capping prices of the emergency allergy treatment. WSJ’s Austen Hufford joins Lunch Break with Tanya Rivero. Photo: Reuters
Mylan NV responded Thursday to backlash over price increases for its EpiPen emergency allergy treatment by promising to reduce the costs that some patients pay, though the drugmaker stopped short of saying it would roll back prices or limit future increases.
EpiPen is a lifesaving treatment for millions whose allergies can send them into severe shock, including many schoolchildren who are advised to keep an injector handy at all... ||||| Mylan Taking Immediate Action to Further Enhance Access to EpiPen® (Epinephrine Injection, USP) Auto-Injector
Mylan doubling the eligibility for patient assistance, effectively eliminating out-of-pocket expense for uninsured and under-insured patients
Company to cover up to $300 of out-of-pocket cost at pharmacy; reducing patient cost by 50% off Mylan list price
Mylan also to open pathway to provide EpiPen® Auto-Injector directly to patients
HERTFORDSHIRE, England and PITTSBURGH, Aug. 25, 2016 /PRNewswire/ -- Mylan N.V. (NASDAQ, TASE: MYL) today announced it is taking immediate action to further enhance access to EpiPen® (epinephrine injection, USP) Auto-Injector by expanding already existing programs in recognition of those patients who are facing the burden of higher out-of-pocket costs. The company is reducing the patient cost of EpiPen® Auto-Injector through the use of a savings card which will cover up to $300 for their EpiPen 2-Pak®. For patients who were previously paying the full amount of the company's list price for EpiPen®, this effectively reduces their out-of-pocket cost exposure by 50%. Mylan also is doubling the eligibility for its patient assistance program, which will eliminate out-of-pocket costs for uninsured and under-insured patients and families as well.
Mylan CEO Heather Bresch said, "We have been a long-term, committed partner to the allergy community and are taking immediate action to help ensure that everyone who needs an EpiPen® Auto-Injector gets one. We recognize the significant burden on patients from continued, rising insurance premiums and being forced increasingly to pay the full list price for medicines at the pharmacy counter. Patients deserve increased price transparency and affordable care, particularly as the system shifts significant costs to them. However, price is only one part of the problem that we are addressing with today's actions. All involved must also take steps to help meaningfully address the U.S. healthcare crisis, and we are committed to do our part to drive change in collaboration with policymakers, payors, patients and healthcare professionals."
Mylan has worked to help patients with commercial insurance pay as little as $0 for EpiPen® Auto-Injector using the My EpiPen Savings Card®. In 2015, this resulted in nearly 80% of these patients paying nothing out of pocket for their EpiPen® Auto-Injector. However, as the health insurance environment has evolved, driven by the implementation of the Affordable Care Act, patients and families enrolled in high deductible health insurance plans, who are uninsured, or who pay cash at the pharmacy, have faced higher costs for their medicine.
Mylan is taking the following immediate actions to help further address the needs of patients and families:
For patients in health plans who face higher out-of-pocket costs, the company is providing immediate relief by offering a savings card for up to $300 . This will effectively reduce by 50% the cost exposure for patients who would have otherwise paid the full list price for EpiPen ® Auto-Injector.
. This will effectively reduce by 50% the cost exposure for patients who would have otherwise paid the full list price for EpiPen Auto-Injector. Mylan also is doubling eligibility for our patient assistance program to 400% of the federal poverty level. This means a family of four making up to $97,200 would pay nothing out of pocket for their EpiPen ® Auto-Injector.
would pay nothing out of pocket for their EpiPen Auto-Injector. Further, Mylan will continue to offer the EpiPen4Schools ® program. The program, launched in August 2012 , has provided more than 700,000 free epinephrine auto-injectors and educational resources to more than 65,000 schools nationwide to help them be prepared for anaphylaxis events among students.
program. The program, launched in , has provided more than 700,000 free epinephrine auto-injectors and educational resources to more than 65,000 schools nationwide to help them be prepared for anaphylaxis events among students. Mylan also is opening a pathway so that patients can order EpiPen® Auto-Injector directly from the company, thereby reducing the cost.
These programs will apply to EpiPen® and EpiPen Jr® (epinephrine injection, USP) Auto-Injectors.
In the interest of fostering greater price transparency in the healthcare system, Mylan is providing the entire economic story of the EpiPen® supply chain on our website.
About EpiPen® (epinephrine injection, USP) Auto-Injector
EpiPen® (epinephrine injection, USP) and EpiPen Jr® (epinephrine injection, USP) Auto-Injectors are used for the emergency treatment of life-threatening allergic reactions. Each EpiPen 2-Pak® and EpiPen Jr 2-Pak® contains two single auto-injectors, instructions for use and a training device, with no drug product or needle, to help patients become familiar with the administration technique. EpiPen® Auto-Injector should be administered immediately at the first sign of an anaphylactic reaction. EpiPen® Auto-Injector is not a substitute for emergency medical treatment. Patients should seek emergency medical attention immediately following administration. For more information about EpiPen® Auto-Injector, visit epipen.com.
About Mylan
Mylan is a global pharmaceutical company committed to setting new standards in healthcare. Working together around the world to provide 7 billion people access to high quality medicine, we innovate to satisfy unmet needs; make reliability and service excellence a habit; do what's right, not what's easy; and impact the future through passionate global leadership. We offer a growing portfolio of more than 2,700 generic and branded pharmaceuticals, including antiretroviral therapies on which approximately 50% of people being treated for HIV/AIDS in the developing world depend. We market our products in more than 165 countries and territories. Our global R&D and manufacturing platform includes more than 50 facilities, and we are one of the world's largest producers of active pharmaceutical ingredients. Every member of our more than 40,000-strong workforce is dedicated to creating better health for a better world, one person at a time. Learn more at mylan.com
Indications
EpiPen® (epinephrine injection, USP) 0.3 mg and EpiPen Jr® (epinephrine injection, USP) 0.15 mg Auto-Injectors are for the emergency treatment of life-threatening allergic reactions (anaphylaxis) caused by allergens, exercise, or unknown triggers; and for people who are at increased risk for these reactions. EpiPen® and EpiPen Jr® are intended for immediate administration as emergency supportive therapy only. Seek immediate emergency medical help right away.
Important Safety Information
Use EpiPen® or EpiPen Jr® Auto-Injectors right away when you have an allergic emergency (anaphylaxis). Get emergency medical help right away. You may need further medical attention. Only a healthcare professional should give additional doses of epinephrine if you need more than two injections for a single anaphylactic episode. EpiPen® or EpiPen Jr® should only be injected into the middle of your outer thigh (upper leg), through clothing if necessary. Do not inject into your veins, buttocks, fingers, toes, hands or feet. Hold the leg of young children firmly in place before and during injection to prevent injuries. In case of accidental injection, please seek immediate medical treatment.
Rarely, patients who have used EpiPen® or EpiPen Jr® may develop an infection at the injection site within a few days. Some of these infections can be serious. Call your healthcare professional right away if you have any of the following at an injection site: redness that does not go away, swelling, tenderness, or the area feels warm to the touch.
Tell your healthcare professional about all of your medical conditions, especially if you have asthma, a history of depression, thyroid problems, Parkinson's disease, diabetes, high blood pressure or heart problems, have any other medical conditions, are pregnant or plan to become pregnant, or are breastfeeding or plan to breastfeed. Be sure to also tell your healthcare professional all the medicines you take, especially medicines for asthma. If you have certain medical conditions, or take certain medicines, your condition may get worse or you may have longer lasting side effects when you use EpiPen® or EpiPen Jr®.
Common side effects include fast, irregular or "pounding" heartbeat, sweating, nausea or vomiting, breathing problems, paleness, dizziness, weakness, shakiness, headache, feelings of over excitement, nervousness or anxiety. These side effects usually go away quickly if you lie down and rest. Tell your healthcare professional if you have any side effect that bothers you or that does not go away.
Please see the full Prescribing Information and Patient Information.
You are encouraged to report negative side effects of prescription drugs to the FDA.
Visit www.fda.gov/medwatch or call 1-800-FDA-1088.
For additional information, please contact us at 800-395-3376.
EpiPen®, EpiPen Jr®, EpiPen 2-Pak®, EpiPen Jr 2-Pak®, EpiPen4Schools® and My EpiPen Savings Card® are registered trademarks owned by Mylan Inc.
© 2016 Mylan Specialty L.P. All rights reserved.
Photo - http://photos.prnewswire.com/prnh/20160825/401225-INFO
Photo - http://photos.prnewswire.com/prnh/20160825/401226-INFO
SOURCE Mylan N.V. ||||| | – The public scolding of drugmaker Mylan over the soaring price of EpiPen seems to have worked: The company on Thursday didn't lower the price, but it made the allergy injections cheaper for many by expanding its assistance programs. Specifically, it doubled eligibility for relief to 400% of the poverty level, declaring on its website that a family of four that earns $97,200 would pay no out-of-pocket expenses, reports the Wall Street Journal. It also said it is offering a savings card that will cover up to $300 for a two-pack of the allergy injections, amounting to a savings of 50% for those who were otherwise paying the full price, reports the AP. “We recognize the significant burden on patients from continued, rising insurance premiums and being forced increasingly to pay the full list price for medicines at the pharmacy counter,” says CEO Heather Bresch. “However, price is only one part of the problem that we are addressing with today’s actions.” On Wednesday, Hillary Clinton joined those calling for Mylan to lower the price, which has risen about 500% since 2008, notes Reuters. | 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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Write an article based on this summary:
– A new study out of Harvard puts forward what the New York Times calls a "startling hypothesis" about Alzheimer's. The research published in Science Translational Medicine suggests that old infections in the brain—or, more specifically, the body's attempt to fight them off—may be at the root of the disease. The study revolves around the telltale plaque in the brain associated with Alzheimer's, which is caused by a buildup of a protein called amyloid beta. Scientists have never been sure why the protein begins to build up as people age. “Does it play a role in the brain, or is it just garbage that accumulates?" is how Harvard's Rudolph Tanzi frames the question per New Scientist. His study suggests that it does indeed play a role, and an important one: The body produces the protein to fight off infections that pass into the brain through the blood-brain barrier; the problem occurs when it doesn't get properly cleared away after the fight. “It’s interesting and provocative,” an Alzheimer's researcher at the University of California, San Francisco, tells the Times of theory. It's been tested on mice and roundworms but not humans yet. "Most shocking of all," writes Scientific American, "was that when they injected bacteria into the brains of Alzheimer’s mouse models, amyloid plaques—the hallmark of the disease—formed within 48 hours." If further research backs up the notion, it could lead to new ways of treating the disease. For example, if this protein that eventually causes trouble comes into being originally as a way to fight pathogens, "you could vaccinate against those pathogens, and potentially prevent this problem arising later in life,” says Tanzi's co-author, Robert Moir of Massachusetts General Hospital. (Maybe memories lost to Alzheimer's aren't gone forever?) | General consensus among Alzheimer’s researchers has it that the disease’s main culprit, a protein called amyloid beta, is an unfortunate waste product that is not known to play any useful role in the body—and one that can have devastating consequences. When not properly cleared from the brain it builds up into plaques that destroy synapses, the junctions between nerve cells, resulting in cognitive decline and memory loss. The protein has thus become a major drug target in the search for a cure to Alzheimer’s.
Now a team of researchers at Harvard Medical School and Massachusetts General Hospital are proposing a very different story. In a study published this week in Science Translational Medicine, neurologists Rudolph Tanzi and Robert Moir report evidence that amyloid beta serves a crucial purpose: protecting the brain from invading microbes.
“The original idea goes back to 2010 or so when Rob had a few too many Coronas,” Tanzi jokes. Moir had come across surprising similarities between amyloid beta and LL37, a protein that acts as a foot soldier in the brain’s innate immune system, killing potentially harmful bugs and alerting other cells to their presence. “These types of proteins, although small, are very sophisticated in what they do,” Moir says. “And they’re very ancient, going back to the dawn of multicellular life.”
Just as amyloid beta is known to do, these antimicrobial proteins can build up and form fibrils that, when not properly regulated, have harmful effects. Yet unlike amyloid beta, their role in the immune system has been widely accepted: They prevent microbes from adhering to host cells, and ultimately trap them. So five years ago the pair of researchers set out to determine whether amyloid beta could also act as a natural antibiotic. They had previously explored their hypothesis in vitro, but in this new study they used worms and mice. For these animal models they compared what happened when amyloid beta was overexpressed to when it was not produced, and found that the former led to increased resistance to infection and longer survival rates.
The team first infected cultured human and hamster cells with a type of fungus called Candida albicans and found that high expression of amyloid beta had a protective effect, doubling the number of cells that were not infected. The researchers then moved on to roundworms, or nematodes, which usually do not survive for more than two to three days once the fungus takes hold. The nematodes with overexpressed amyloid beta, however, were still going strong five to six days after they were infected. Finally, the researchers infected the brains of mice with a strain of salmonella to cause meningitis. Mice that were genetically altered to overproduce human amyloid beta survived nearly twice as long as mice that did not have the protein at all.
Most shocking of all, according to Tanzi and Moir, was that when they injected bacteria into the brains of Alzheimer’s mouse models, amyloid plaques—the hallmark of the disease—formed within 48 hours. “We didn’t know this was even possible,” Tanzi says, “that amyloid plaques would form rapidly overnight.” And in the middle of each plaque was one Salmonella bacterium, supporting the theory that the amyloid deposition had formed around the microbe as an entrapment mechanism—just like LL37 and other established antimicrobial proteins.
“These results are particularly intriguing,” says Anna Palamara, a microbiologist at the Sapienza University of Rome who was not involved in the study. “Previous [research] shows that several infectious agents, including viruses, trigger amyloid beta production and accumulation.” Herpes and influenza are just two of the infections that have been tested by other research teams.
The Harvard team’s new findings provide further evidence that Alzheimer’s could be inadvertently spurred by an infection that causes the formation of too much amyloid. As people get older the immune system and blood-brain barrier become increasingly compromised, making it easier for microbes to sneak into the brain. It wouldn’t take many of these pathogens, according to Tanzi, to cause amyloid buildup. “And that could rapidly start the cascade toward the disease,” he says, “causing tangles and inflammation. You’ve got all three pillars of Alzheimer’s right there.”
“It is possible to speculate that during a mild infection the production of amyloid beta may help,” Palamara says. “But in the presence of persistent or repeated infections, amyloid beta levels may accumulate, exceeding a threshold. In this case its protective role might change to the well-known neurotoxic one.”
The idea that amyloid beta has a positive function in the body could potentially change how scientists approach potential treatments. Instead of attempting to completely eliminate the protein, “we might want to think about just dialing it down,” Tanzi says. Moreover, Moir adds, the drugs in trials now are for the most part designed to reduce inflammation by targeting pathways in the adaptive immune system. But if amyloid production and deposition are innate immune responses, then targeting pathways of innate immunity or the microbes themselves may be the way to go.
They do not expect convincing the scientific community of this to be easy. “This is really going to cause a lot of unrest in the field,” Tanzi says. “Any new revolutionary discovery is first ridiculed, then violently opposed, and finally taken to be self-evident. We’re ready for the ridicule and the violent opposition, and we think we have enough data so that we can look forward to self-evident.”
But the pair has a long way to go. They are now moving forward with a plan to systematically characterize the microbes found in the aging brain. From there they hope to identify the pathogens that may be involved in the onset of Alzheimer’s—as well as those that potentially play a role in other amyloid diseases, such as diabetes.
“We’re at the top of a mountain with a freshly formed layer of snow,” Moir says. “Where you go is where you choose. There’s so much to explore.” ||||| Juan Gaertner/Science Photo Library
It’s a double-edged sword. The protein plaques in the brain associated with Alzheimer’s disease could be created as our immune system fights off invading microbes.
Alzheimer’s disease has long been linked to the accumulation of sticky plaques of beta-amyloid proteins in the brain, but their function – if any – has remained unclear.
“Why does beta-amyloid accumulate in people as they get older? Does it play a role in the brain, or is it just garbage that accumulates,” asks Rudolph Tanzi of Harvard Medical School.
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Tanzi’s team has been working with Robert Moir at the Massachusetts General Hospital in Boston to look at the protein in other animals. The group has found that a certain sequence of particular amino acids in human beta-amyloid is shared widely – among 70 per cent of vertebrates, including in the coelacanth, an ancient type of fish.
That this sequence is shared so widely, and has not changed over time, suggests there is a reason it has been conserved. “This is a very old peptide doing something that’s important,” says Moir.
Brain defence
Moir had previously found that beta-amyloid kills microbes as well as does an anti-microbial peptide called LL-37. This molecule is a foot soldier for the primitive part of our immune system, which we share with many other animals.
So the team tested whether the purpose of beta-amyloid is also to kill microbes in the brain. When they injected bacteria into the brains of mice bred to be able to develop plaques much as humans do, the mice developed amyloid plaques overnight.
“When you look in the plaques, each one had a single bacterium in it,” says Tanzi. “A single bacterium can induce an entire plaque overnight.”
This suggests that microbial infection could be triggering the formation of plaques that cause Alzheimer’s disease. Somehow, bacteria, viruses or other pathogens may be crossing the blood-brain barrier and getting into the brain. The brain may be responding by using beta-amyloid to trap and kill them. But if these plaques aren’t cleared away fast enough, they may then lead to inflammation and tangles of another protein, called tau, causing neurons to die and the progression towards Alzheimer’s disease.
“The stickiness of amyloid is both a godsend and a curse,” says Samuel Gandy at the Mount Sinai Hospital in New York.
Alzheimer’s vaccination
Other work has suggested that infections can cause Alzheimer’s disease, arguing that microbes lead to inflammation, directly causing neuron death and cognitive decline. Chlamydia and the herpes virus are among the suggested culprits.
But Tanzi and Moir believe it is beta-amyloid that causes the damage, not the microbes themselves.
The team now plans to look at the brains of people who have died from Alzheimer’s disease. If the team finds microbial DNA or RNA inside the plaques, the discovery could open up a new way to think about Alzheimer’s disease and how it might be treated.
“You could vaccinate against those pathogens, and potentially prevent this problem arising later in life,” says Moir.
Journal reference: Science Translational Medicine, DOI: 10.1126/scitranslmed.aaf1059
Read more: Universal plaque-busting drug could treat various brain diseases ||||| | multi_news_1_0_0 |
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Article:
Future of Paula Deen's Deals Uncertain Amid Racial Slur Scandal
Another serving of drama may be coming for Paula Deen, who could lose more deals on the heels of her firing from the Food Network.A representative for the shopping network QVC, which sells her cookware, released a statement Sunday to PEOPLE that expressed "concerns [over] the unfortunate Paula Deen situation," adding, "QVC does not tolerate discriminatory behavior."Following the celebrity chef's admission that she used a racial slur in the past, the network is "closely monitoring these events and the ongoing litigation," continues the representative's statement, which was first reported by TMZ . "We are reviewing our business relationship with Ms. Deen, and in the meantime, we have no immediate plans to have her appear on QVC."Deen, 66, issued a statement less than 24 hours after the Food Network announced on Friday it was dropping the longtime star."I have had the pleasure of being allowed into so many homes across the country and meeting people who have shared with me the most touching and personal stories," she said . "This would not have been possible without the Food Network. Thank you again. Love and best dishes to all of y'all."Deen also has a book, titled Paula Deen's New Testament: 250 Favorite Recipes, All Lightened Up, due to arrive in stores this October. Her publisher, Random House, Inc., has not cancelled her contract. However, a spokesman for Random House, whose imprints include Ballantine Books, tells PEOPLE, "We are monitoring the situation closely."Deen's cookware is also sold at Target, Sears, Walmart, J. C. Penney, and Kmart. Last January, she announced a partnership with Novo Nordisk when she revealed she has type 2 diabetes. The drug maker is standing by her."Paula Deen's still a product spokesperson for the Victoza brand. We recognize the seriousness of these allegations and will follow the legal proceedings closely, staying in contact with her. As a company committed to improving the lives of people with diabetes, Novo Nordisk engaged Deen as a spokeswoman because of Paula's commitment to increasing awareness about diabetes to millions of people in this country."And they aren't the only ones watching the situation. Sears Holdings told PEOPLE late Sunday that "the company is currently exploring next steps as they pertain to Ms. Deen's products." ||||| Paula Deen to Face Matt Lauer on Today Show After Food Network Firing
Paula Deen is usually the one doing the cooking when she appears on TV, but on Wednesday, June 26, she'll be in the hot seat as Matt Lauer grills her on the details of her recent racial slur scandal. The beleaguered chef, 66, was supposed to appear on the TODAY show last Friday but bailed at the last minute because she was too "exhausted"; she has since rescheduled the interview.
"She has told us she will be here this time," Lauer announced on Monday, June 24.
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The news comes just a few days after Deen's Food Network firing. On Friday, June 21, the Southern chef was dropped by her longtime employers amid controversy over her admission in a deposition last month that she had used racial slurs -- including the N-word. A few hours after her termination, Deen thanked the network for 11 "great years."
"I have had the pleasure of being allowed into so many homes across the country and meeting people who have shared with me the most touching and personal stories," she said in a statement. "This would not have been possible without the Food Network. Thank you again. Love and best dishes to all of y'all."
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That statement followed two video apologies earlier in the day. In the second -- which was posted after the first clip was removed -- Deen said she had canceled her TODAY show appearance because she "was physically not able" to go on camera.
"The pain has been tremendous that I have caused to myself and to others," she explained. "So I'm taking this opportunity, now that I've pulled myself together and am able to speak, to offer an apology to all those that I have hurt."
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"I want people to understand that my family and I are not the kind of people that the press say we are," she continued. "I've spent the best of 24 years to help myself and others. Your color of skin, your religion, your sexual preference does not matter to me."
Deen's apology came too late for the Food Network, which pulled her hour-long block of programming from the Saturday, June 22, schedule after her Friday firing. She is also at risk of being dropped by QVC, which markets and sells her cookware products. On Sunday, June 23, a rep for the home shopping corporation told Us Weekly that the company "shares the concerns being raised around the unfortunate Paula Deen situation."
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"QVC does not tolerate discriminatory behavior," the rep said. "We are closely monitoring these events and the ongoing litigation. We are reviewing our business relationship with Ms. Deen, and in the meantime, we have no immediate plans to have her appear on QVC." |||||Summary: |
– Yet another company has dropped Paula Deen in the wake of the Food Network giving her the boot and QVC apparently thinking about doing the same. Smithfield, a major pork company (that was recently purchased by a Chinese company), says it will no longer partner with Deen for her line of "Paula Deen Collection" hams in the wake of her n-word controversy, TMZ reports. "Smithfield is determined to be an ethical food industry leader and it is important that our values and those of our spokespeople are properly aligned," reads a statement from the company. As such, "we are terminating our partnership with Paula Deen." (Hilariously, it was a Smithfield ham Deen was once hit in the face with.) Meanwhile, the racism flap grows: A black man who used to work with Deen and her brother says Paula often used him and other workers from her brother's restaurant to staff parties at her mansion, but rarely paid them. "She just gave us beer and alcohol for working all those days," he tells Radar. In one case, he says, he didn't want to work a party "but they threatened our jobs and put it on the line." He claims he and a few other black men were forbidden from talking to the guests. It seems the Paula Deen Apology Tour is about to begin: She's appearing on Today Wednesday, after she canceled her originally scheduled appearance last Friday, Us reports. But in more bad news for Deen, the publisher of her upcoming cookbook tells People it is "monitoring the situation closely," and Sears says it is "exploring next steps" with regard to her line of products. | multi_news_1_0_0 |
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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.
JUST WATCHED Sugary drinks linked to 180,000 deaths Replay More Videos ... MUST WATCH Sugary drinks linked to 180,000 deaths 02:16
JUST WATCHED Coca-Cola pledges to tackle obesity Replay More Videos ... MUST WATCH Coca-Cola pledges to tackle obesity 04:12
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. | multi_news_1_0_0 |
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Here is a news article: FACEBOOK PAGE: https://www.facebook.com/groups/864431573661266/ This ordinance has been in place for many years. Many families have had to give up their family pets due to this law. It is important for all of us to come together and be a voice for not only Diggy the American Bulldog, but all of the pets and people that have suffered heartache in the past years. We must remember, it is not the animal that is the beast, it is man that creates the beast. Aggressive dogs come in all shapes, sizes, and BREEDS. This should be handled on a case-by-case basis. Please sign this petition so that these wonderful, intelligent, and LOYAL dogs can call Waterford, Michigan their home too!
Diggy is an American Bulldog that was at the Detroit Dog Rescue for 100 days before Dan Tillery came and adopted him. Dan snapped the photo above to show their joy for becoming a family, and the photo immediately went viral on the Internet. But now, the Waterford Township is threatening to take Diggy away because they claim owning him violates a local ordinance that bans specific breeds.
To whom it may concern,
In light of "Diggy", the American Bulldog owned by Mr. Daniel Tillery and the ban against "dangerous dogs/ "pit bulls"",
Please take action to remove/revise Article 3, Section 3 "Pitbull Breeds, et al" in the Township Code of Ordinances.
Please make our community safer by creating a dog ordinance that does not single out specific breeds. We can make the community safer through dog ordinances that all dog owners have to follow, no matter what their dog looks like.
Dangerous dogs are a problem. Irresponsible dog owners are causing the problem, and our laws should target the people.
Included is website address where you will find a model ordinance as published by the American Veterinary Medical Association which serves to equally protect animals as well as victims of dangerous animals and their irresponsible owners. Please take this into serious consideration. https://www.avma.org/KB/Policies/Documents/Model-Dog-Cat-Control-Ord-Policy.pdf
The signatures you will find attached are in support of Diggy STAYING in Waterford Township, AND removing the ban on "pit bull" dogs.
This petition was started Friday June 10, 2016, and as of today, Monday June 13, 2016, it has gotten 49,781 total signatures. 2,312 of those signatures are from WATERFORD RESIDENTS. This number is steadily climbing.
Sincerely,
Tara Vitale and Tiffany Robertson (former residents of Waterford)
and Susan Roberson, 5754 Pontiac Lake Rd., Waterford 48327 ||||| WATERFORD TOWNSHIP (WWJ) – Diggy the dog has been given three days to vacate his brand new Metro Detroit home.
A Waterford Township dog owner says local officials are threatening to take away his newly adopted dog, all because the dog’s breed was misidentified in a photo that swept the internet by storm.
“Sir Wiggleton” sat in a shelter for almost 100 days waiting for someone, anyone to make him a part of their family. On Monday, his dreams came true when local musician Dan Tillery made it official and adopted the dog, now named Diggy.
When the two met, they instantly became best friends. Staff at Detroit Dog Rescue knew this was a match made in heaven, so they snapped a photo of the grinning best friends and posted it to Facebook, saying: “We know this photo is going to break the internet and we apologize, but we had to share.”
And were they ever right. The photo quickly went viral, spreading across the internet and reaching a national television audience.
But it also drew the eyes of officials in Waterford Township. The township has an ordinance banning pit bull breed dogs and when officials saw the photo, they apparently assumed Diggy was a pit bull.
On Thursday afternoon, just days after Diggy moved in, police showed up on Tillery’s doorstep and asked to see the dog. Police told WWJ they received several complaints of a pit bull being housed at the home, which violates a city ordinance.
“They asked if he’s a friendly dog, I said he’s the friendliest dog,” Tillery told WWJ’s Jon Hewett. “When they went to the gate the actually see him, he licked their face, was very kind. They said, we’re dog lovers, that’s cool, he seems like a good boy. Took some pictures of him.”
Tillery said he got a call about an hour later and was told, based on their visual inspection alone, the officers concluded Diggy was a pit bull.
“He said, you know, we don’t really need much more than I think he’s a pit, and that’s enough, so, he looks like a pit, I think he’s a pit, he’s got to go. You have three days to have him out of your home,” Tillery said.
The deadline is Monday.
The dog rescue is standing behind Tillery, who registered and obtained a proper license for Diggy shortly after he was adopted. The rescue and Tillery say Diggy is an American Bulldog, not a pit bull, and they have supporting adoption papers from the City of Detroit Animal Control and Welfare and their veterinarian who all confirm the dog’s breed.
In a statement, police said Tillery indicated he had another place to take the dog and that he would comply with the ordinance by Monday.
Violation of the township’s ordinance, which prohibits any person from owning, possessing or maintaining a pit bull/pit bull terrier, can result in a civil infraction and a fine of $500. ||||| A picture of a man and his newly adopted pit bull went viral because of the dog's big smile, but the attention brought local police to the man's door demanding he return the dog as pit bulls are prohibited in the town.
Stop and frisk: Why are police departments moving away from it?
When musician Dan Tillery’s joyous photo with his smiling new dog, Diggy, went viral last week, it looked as though the story of a dog held in a shelter for nearly 100 days would have a happy ending.
But a pit bull ban in Mr. Tillery’s hometown, Waterford Township, Michigan, threatens to separate the two and has raised questions regarding the ethics of such bans.
The police say that Diggy, the smiling dog in this viral photo, must leave town. 😠 https://t.co/Oc1tjPHAwy pic.twitter.com/DD3mO1YoMg — The Dodo (@dodo) June 12, 2016
On Thursday, Waterford Township police said Diggy may not be allowed in the town because he might be pit bull, which violates an ordinance banning pit bulls and pit bull mixes, according to ABC News.
Tillery is contending that Diggy is an American Bulldog, and got a dog license from the town stating that he was. A veterinarian from the Detroit Dog Rescue also classified the dog as an American Bulldog. However, the Detroit Dog Rescue had previously classified the dog as a pit bull mix.
The town’s ordinance allows police officers to ban any dog they believe is a pit bull at their personal discretion, the Huffington Post reported. Police Chief Scott Underwood told The Oakland Press that its “a pretty clear case of an ordinance that makes it clear what’s permissible and what’s not, and our job is to enforce the ordinance.”
This development has brought renewed attention to bans against pit bulls. Proponents of such bans say the pit bulls are a dangerous breed, while opponents say humans are responsible when their pets become violent.
Proponents of such bans point to the reputation of pit bulls as dangerous animals. The April 2011 issue of Annals of Surgery asserted that one person is killed by a pit bull every 14 days, two people are injured every day, with children at a higher risk. The report concluded that pit bull attacks are associated with "higher morbidity rates, higher hospital charges, and a higher risk of death than are attacks by other breeds of dogs," and suggested that strict regulation of the breed could "substantially reduce" deaths from dog bites in the United States.
Colleen Lynn, the president and founder of DogsBite.org, a national dog-bite-victims group dedicated to reducing dog attacks, told Time violence is not a learned behavior in pit bulls, it is something they are born with.
"Pit bulls were specifically bred to go into that bite with incredible aggression and fight," she said.
A petition from opponents of Waterford's ban has 42,179 signatures as of Sunday afternoon.
"We must remember, it is not the animal that is the beast, it is man that creates the beast," part of the petition reads. "Aggressive dogs come in all shapes, sizes, and BREEDS. This should be handled on a case by case basis."
In a response to the Time article, Sara Enos, the founder and executive director of the American Pit Bull Foundation argued that the problem is with people, not with pit bulls.
Ms. Enos wrote that pit bulls have many positive traits and serve in many capacities, such as being search-and-rescue dogs, companions, helping kids with reading disabilities, serving as seizure watch dogs, diabetic alert dogs, and comforting nursing home residents.
“Eradicating Pit Bull dogs will affect more than just our family dogs; it will affect the much larger number of citizens that these dogs help, as opposed to attack,” she wrote.
As for Diggy, it is unclear whether or not he will be allowed to stay in town. Kristina Millman-Rinaldi, the executive director of Detroit Dog Rescue, told the Huffington Post that the group is waiting to hear back from the township. ||||| Notice
You must log in to continue. ||||| The mutt, part American bulldog and part who-knows-what-else, was scooped up off the Detroit streets and kept in a small animal control enclosure. There, he waited. And waited. For nearly 100 days, the pooch had little new to explore except different corners of his cage.
Enter a no-kill animal shelter, Detroit Dog Rescue, which transferred the dog out of animal control in March and gave him his first name, Sir Wiggleton. “He had a sparkle in his eye that he needed to get out,” Kristina Rinaldi, Detroit Dog Rescue executive director, told the Detroit News. “I definitely did not want to see him euthanized.”
The group posted a picture of Sir Wiggleton to its Facebook page at the end of May, and almost immediately his future seemed to change. In the photo — the kind of picture social media gurus might describe as “highly shareable” — a goofy grin splits Sir Wiggleton’s face, revealing a long tongue as pink as a fresh tuna steak. His friendly visage accrued genial anthropomorphism and likes aplenty.
To one particular Facebook user, the animal’s smile evoked a fellow mammal with an equally goofy grin. The man passed Sir Wiggleton’s photo along to a local musician named Dan Tillery, citing the similarity in their smiles. In Sir Wiggleton — renamed Diggy, post-adoption — Tillery saw the very animal companion he had been looking for.
“It was like, ‘We need this guy. He looks like he has a lot of personality,’ ” Tillery said to the Detroit News.
On their first day together at Tillery’s home in Waterford, Mich., Tillery and Diggy took a goofball selfie and gave it to Detroit Dog Rescue. The group, which understands that photos of well-groomed men and cute animals have great power, decided that the joint Tillery-Diggy snapshot was destined for nothing less than breaking the Internet, putting Diggy in the same company as Taylor Swift, color-changing dresses and Kim Kardashian as would-be destroyers of the delocalized communications technology.
The Internet remained intact, but the photo caught social media fire, as fans shared it thousands of times. The duo scored celebrity treatment by People magazine and wound up on ABC News, with Tillery on the guitar and Diggy chewing on a stick.
“Every time I see him, I get a big dumb smile, and every time he sees me he gets a big dumb smile,” Tillery told ABC on Tuesday morning, which filmed the musician singing affectionate pop tunes to his new pooch.
“I’ve only had him one night,” Tillery said, “but he’s totally cool.”
Such total coolness was, unfortunately, not destined to last. As the photo gaveth — skyrocketing Tillery and Diggy’s relationship into the animal Facebook exosphere — it threatened to taketh away, once the news of the pooch landed in the hands of the Waterford Township Police Department.
[Being labeled a pit bull can doom a shelter dog’s chances of adoption]
Waterford, Mich., is a township where certain dog breeds are outlawed, under a type of ordinance known as breed-specific legislation, or BSL. The Waterford ban has its roots in a 1988 incident in which a pit bull pair severely injured a woman’s arm and killed her pet Airedale terrier. A few months afterward, the township passed its first ban on pit bull terriers, eventually prohibiting dogs with characteristics that “substantially conform to the breed standards established by the American Kennel Club for American Staffordshire Terriers or Staffordshire Bull Terriers.”
Supporters of BSL argue that some dog breeds are inherently riskier to own than others, because of their size or propensity for aggression. In a 2014 interview with Time, Colleen Lynn, the creator of DogsBite.org, an organization that aims to reduce dog attacks and advocates against pit bull ownership, blames human selection of certain traits. “Why do herding dogs herd? Why do pointing dogs point? They don’t learn that behavior, that’s selective behavior,” Lynn said. “Pit bulls were specifically bred to go into that pit with incredible aggression and fight.”
[‘Oh my God. He’s lifeless’: Detroit preschooler dies after attack by pack of 4 neighborhood pit bulls]
Pit bull defenders say that reports of the animal’s death-lock jaws are exaggerated and that its bred-for-violence history is a recent invention. In fact, one WWI-era depiction shows a pit bull defending an American flag chock-full of kittens, as The Washington Post reported in May; in her new book, “Pit Bull: The Battle Over An American Icon,” author Bronwen Dickey interviews a geneticist who argues that, even if the dogs fought in pits a century ago, claims that fighting DNA remains baked into their genomes are “ludicrous.”
[It’s time to stop demonizing pit bulls]
Other dog breed experts note that too many dogs are painted with the “pit bull” brush; one study of four Florida shelters determined that every other pooch labeled a pit bull had no such genetic ancestry.
The Waterford Police visited Tillery at his home on Thursday, asking if Diggy was friendly. Tillery said yes. “When they went to the gate,” Tillery told CBS News, the pooch “was very kind” and licked the cops’ faces. “They said, ‘we’re dog lovers, that’s cool, he seems like a good boy.’ Took some pictures of him.”
An hour after that, the police told him Diggy was unwelcome.
Neighbors had complained, the police said, that Tillery had violated the pit bull ban. Per a statement via the Detroit Free Press, Waterford Police Chief Scott Underwood said that, “Based on their observations, it was determined the dog was part pit bull/pit bull terrier.” The police department did not cite Tillery — violations of the pit bull ordinance come with up to a $500 penalty — but insisted that, by Monday, Diggy would have to go. If a court hearing were to agree that Diggy is a prohibited animal, according to the ban, he would be “subject to destruction.”
[Dog law, pit bulls, and “breed-specific presumptions”: When must a dog who bites be destroyed]
Rinaldi described the ordinance as “the craziest” in an interview with the Huffington Post. Detroit Dog Rescue had called Waterford Township prior to Diggy’s adoption, to make sure that an American bulldog would be welcome in Tillery’s home. And the veterinary assessment determined that Diggy was an American bulldog — distinct from a Staffordshire terrier. Town officials, she said, told her that only dogs determined to be pit bulls are forbidden.
Tillery may have to relocate Diggy if the township does not budge. “I don’t like controversy,” he wrote on Facebook on Friday. “I hate it actually. I just love dogs. I just wanted a dog. This feeling in my stomach is awful. I hate this.”
By early Monday morning, an online petition to overturn the ban had roughly 49,000 signatures. ||||| ...
day at Union Lake Veterinary Hospital ! He’s improved his range of motion after being hit by a car and now this guys is ready for a home. Stories like these are all thanks to your donations in action! ||||| See more of Detroit Dog Rescue on Facebook |||||
A summary of this is? | – Dan Tillery was so excited to adopt his pup, Diggy (nee Sir Wiggleton), who had spent 100 days in a Detroit shelter, that they made a music video and took a beaming photo together that went viral on social media. "We know this photo is going to break the internet and we apologize, but we had to share!" Detroit Dog Rescue's Facebook page gushed June 6. But that thrill was short-lived when Waterford Township cops got wind of the adoption and informed the Michigan man he had until Monday to "relocate" Diggy because they say he's a pit bull—a breed banned by a local ordinance, MLive.com reports. Waterford police tell WWJ they received multiple complaints about Diggy and headed to Tillery's house Thursday. "When they went to the gate [to] actually see him, he licked their face," Tillery says, noting officers took photos of Diggy. They informed him later that day that they had concluded Diggy was a pit bull. But Detroit Dog Rescue says in a follow-up post that Diggy isn't a pit bull, but an "American Bulldog who can't stop smiling." Supporting documents from a vet and Detroit's animal control department also contend Diggy is a bulldog. Some experts say "too many dogs are painted with the 'pit bull' brush," the Washington Post notes, and others maintain pit bull bans are unethical to begin with, per the Christian Science Monitor. For now, however, Waterford officials are sticking with their pit bull definition (they used guidelines from the American Kennel Club) and say Diggy has to go. Police say Tillery has indicated he'll comply; he could face a civil infraction and $500 fine if he refuses. Meanwhile, more than 50,000 have signed an online petition to overturn Waterford's "dangerous dog" ban. The Post notes that if Diggy is found to be a prohibited pup, he can be destroyed. (A pit bull burned in a fire is now an honorary firefighter.) | multi_news_1_0_0 |
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Article:
Image copyright Thinkstock Image caption A Mediterranean diet is rich in fruit, vegetables and healthy fats like olive oil
A Mediterranean diet can help older adults maintain bigger brains, new research has suggested
A study of pensioners in Scotland found that those with a diet rich in fresh fruit, vegetables and olive oil had healthier brains than those with different eating habits.
They suffered less brain shrinkage than those who regularly ate meat and dairy products.
The study was carried out by University of Edinburgh researchers.
They carried out brain scans on 401 people in their 70s who did not have dementia and who provided information about what they ate.
Learning and memory
The Mediterranean diet is rich in vegetables, fruits, olive oil, beans and cereal grains and includes moderate amounts of fish, dairy products and wine while limiting consumption of red meat and poultry.
Scientists found that those who adhered most closely to the diet retained significantly greater brain volume after three years than those who did not.
Lead researcher Dr Michelle Luciano said: "As we age, the brain shrinks and we lose brain cells, which can affect learning and memory.
"This study adds to the body of evidence that suggests the Mediterranean diet has a positive impact on brain health."
Image copyright Thinkstock Image caption People who follow a Mediterranean diet eat a limited amount of red meat and poultry
Diet accounted for about half the variation in brain volume seen across all the study participants.
The results were the same when researchers adjusted for other factors that could affect brain volume, such as age, education and having diabetes or high blood pressure.
Eating more fish and less meat was not associated with differences between people's brains, contrary to earlier findings.
"It's possible that other components of the Mediterranean diet are responsible for this relationship, or that it's due to all of the components in combination," Dr Luciano said.
Dr Luciano said previous studies carried out measurements in a single "snapshot", while the new research followed participants over time.
She said: "In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain. Larger studies are needed to confirm these results.
Cognitive ability
The findings appear in the journal Neurology.
Dr David Reynolds, chief scientific officer at Alzheimer's Research UK, said: "This study adds to previous research highlighting the importance of this kind of well-balanced diet in maintaining a healthy brain as we age.
"While the study points to diet having a small effect on changes in brain size, it didn't look at the effect on risk of dementia. We would need to see follow-up studies in order to investigate any potential protective effects against problems with memory and thinking."
Prof Peter Passmore, professor of ageing and geriatric medicine at Queen's University Belfast, said: "While it would seem that the loss of brain volume over time is not what anyone would want to see and therefore that preservation of volume should be a good thing in terms of cognitive ability, it is still not fully clear exactly what this could mean in terms of memory and dementia.
"The authors do point out that further research is needed."
The study is published in the 4 January online issue of Neurology, the medical journal of the American Academy of Neurology. ||||| 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. ||||| Breaking News Emails Get breaking news alerts and special reports. The news and stories that matter, delivered weekday mornings.
/ Updated By Maggie Fox
A Mediterranean diet that’s loaded with fresh vegetables, fruit and the occasional drink could help preserve your brain into old age, researchers reported Wednesday.
It’s the latest in a series of studies showing that a healthy diet can preserve health, including brain health.
This one’s a little different because it doesn’t seem to show that adding fish to the diet makes any difference. It’s not clear why, but it adds another piece of evidence in favor of dumping junk food and turning instead to fresh salads dressed with olive oil, plenty of fresh fruit, hummus, beans and pasta.
Everyone’s brain shrinks as they get older. This study, published in the journal Neurology, found that people in their mid-70s who ate a Mediterranean-style diet lost less brain mass than people who ate a diet more typical of their native Scotland.
“A bigger brain is in general better for you because at least in late life, it makes a person more resistant to the effects of brain diseases."
“We found that lower adherence to the Mediterranean diet was associated with greater three-year reduction in total brain volume,” Michelle Luciano of the University of Edinburgh in Scotland and colleagues wrote.
Related: Vegan diet may save your life and the planet, too
The team used a group of Edinburgh residents who were born in 1936 and have been followed ever since. For this round, the volunteers filled out a food diary and then many of them agreed to have a series of magnetic resonance imaging (MRI) scans of their brains.
Mediterranean Foods STUDIO BOX / Getty Images
The study took them from age 70 to around 76 and the MRIs allowed the researchers to see just when and how their brains changed as they moved from late middle age into early old age. About 400 of the volunteers made it through two MRIs over three years.
Those who ate more fruits, vegetables, olive oil and the like, and less fried food, red meat and cheese had less brain shrinkage, the team found. On average, their brains shrank at about half the rate that would normally be expected over three years for people this age, they said.
Related: Tasty Diet Cuts Heart Disease
“In our study, eating habits were measured before brain volume was, which suggests that the diet may be able to provide long-term protection to the brain,” Luciano said in a statement. “Still, larger studies are needed to confirm these results.”
People got points for light to moderate drinking-- in this case about a third of drink a day to no more than three drinks a day on average for men and two for women.
Dr. David Knopman, a professor of neurology at the Mayo Clinic in Minnesota who was not involved in the study, said this could translate to real-life benefits.
“Loss of brain volume is an inevitable part of the aging process,” Knopman told NBC News.
Related: This Diet Helps You Live Longer
“A bigger brain is in general better for you because at least in late life, it makes a person more resistant to the effects of brain diseases,” he added. “People who have bigger brains in general can tolerate more brain pathology, more brain disease, than those who have smaller brains. So the reduced loss in the people who adhered to the Mediterranean diet in general would be expected to protect them from developing dementia.”
“We found that lower adherence to the Mediterranean diet was associated with greater three-year reduction in total brain volume."
Everyone who took part in the study was healthy and living independently, and the study was not designed to show whether healthier eating reduced the risk of dementia. But other studies have shown that good diets can prevent Alzheimer’s and other types of dementia.
Related: Could a Mediterranean diet keep your brain from shrinking?
A 2015 study done at Columbia University also found that people who ate Mediterranean diets had bigger brains. But it also found this may have been caused in part because people who ate Mediterranean diets also are more fish and less of other types of meat.
The Edinburgh team didn’t find any effect from eating meat or fish, and they found education did not seem to matter, either.
Previous research has linked a Mediterranean diet to a reduced risk of heart disease and some cancers, as well as stroke and to a longer life in general.
“People who eat healthy are often healthier in many other respects,” Knopman pointed out.
“They're much less likely to be obese, they're much less likely to have diabetes, hypertension, much less likely to smoke, more likely to exercise. And they're probably more likely to adhere to good health behaviors in general.”
Related: Mediterranean Diet May Slow Brain Aging
But a series of studies done in Spain finds the effects are clear even when people are already starting out with healthier diets. The team in Barcelona adds extra olive oil and nuts to the standard diets of Spaniards and finds the benefits on heart health and brain health are clear.
The Edinburgh study only asked people once – when they were 70 – what they ate. So it’s not entirely clear if it takes a lifetime of eating better to help the brain. ||||| Abstract
Objective: To assess the association between Mediterranean-type diet (MeDi) and change in brain MRI volumetric measures and mean cortical thickness across a 3-year period in older age (73–76 years).
Methods: We focused on 2 longitudinal brain volumes (total and gray matter; n = 401 and 398, respectively) plus a longitudinal measurement of cortical thickness (n = 323), for which the previous cross-sectional evidence of an association with the MeDi was strongest. Adherence to the MeDi was calculated from data gathered from a food frequency questionnaire at age 70, 3 years prior to the baseline imaging data collection.
Results: In regression models adjusting for relevant demographic and physical health indicators, we found that lower adherence to the MeDi was associated with greater 3-year reduction in total brain volume (explaining 0.5% of variance, p < 0.05). This effect was half the size of the largest covariate effect (i.e., age). Cross-sectional associations between MeDi and baseline MRI measures in 562 participants were not significant. Targeted analyses of meat and fish consumption did not replicate previous associations with total brain volume or total gray matter volume. |||||
What is a summary? | – A healthy diet isn't just good for your waistline, but also your brain, say scientists in a study in Neurology—the latest to tout the benefits of the Mediterranean diet. About 400 healthy Scottish volunteers kept a food diary at age 70, then underwent MRI scans of their brains at 73 and 76, per the Los Angeles Times. All brains shrink with age, but researchers found those who ate a Mediterranean diet lost less brain mass than others. In fact, their brains appeared to shrink at half the rate of those who ate less healthy food, says study author Michelle Luciano of the University of Edinburgh. What's so great about having a bigger brain? "People who have bigger brains in general can tolerate more brain pathology, more brain disease, than those who have smaller brains," a doctor not involved in the study tells NBC News. "So the reduced loss in the people who adhered to the Mediterranean diet in general would be expected to protect them from developing dementia," he continues. The study, however, didn't look at the effects of a larger brain on memory or thinking. A 2015 study also found people who followed a Mediterranean diet had larger brains, but it attributed that to a high intake of fish over meat and poultry. In what should be good news for steak lovers, this latest study found participants' habits of eating meat or fish didn't affect brain size. "It's possible that other components of the Mediterranean diet are responsible for this relationship, or that it's due to all of the components in combination," Luciano tells the BBC. (This diet may cut your Alzheimer's risk.) | multi_news_1_0_0 |
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News article:
wlky An 8-month-old Kentucky boy died in a hot car on Monday after his father forgot to drop him at day care, authorities said.
An 8-month-old Kentucky boy died in a hot car on Monday after his father forgot to drop him at day care, authorities said. He was found in his car seat.
Authorities were still investigating the case, but ruled the death an accident, The Associated Press reported.
Louisville police said Lincoln Lindsay's father left the boy strapped in his car seat when he went to work, about five miles from his home in Louisville’s East End neighborhood.
The father later found the boy’s lifeless body still strapped in the seat and rushed him to their home, hoping the boy’s mother, who worked in medicine, could revive him, local station WDRB reported.
Ambulances eventually arrived at the family’s house, and the boy was pronounced dead there at 6:17 p.m.
Authorities haven’t nailed down how long the boy was stranded in the punishing heat, but said it appeared to be several hours.
The mercury in Louisville hovered around 90 degrees all day, and authorities said temperatures inside the car easily topped 100.
Lincoln's parents, who were not identified, were questioned by police, but no charges have been filed.
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Experts said it was common for busy parents to leave children behind in cars.
Numbers from Forget Me Not USA, an Oklahoma-based organization that raises awareness about the problem, said 532 children have died after being left in hot cars since 1998.
wlky An 8-month-old Kentucky boy died in a hot car on Monday after his father forgot to drop him at day care, authorities said.
Kentucky had 18 hot car deaths from 1998 to 2011, according to the group’s website.
“A lot of the times it is a parent that might not have the child with them at all times and so if they’ve got work or other things on their mind the child might fall asleep in the backseat so they don’t hear them. It’s easy to do.” Kristin Norris, of Exploited Children’s Help Organization in Louisville, told WDRB.
Last month, a Texas mom was arrested for allegedly leaving her 2-year-old boy in the car while she downed margaritas at a Dallas Tex-Mex joint for 30 minutes.
That mom, Jessica Christian, had cracked the windows. The boy survived. She was charged with child abandonment and child endangerment.
Warnings about children left in hot cars come as the Northeast was bracing for the massive heat wave.
Temperatures in cities from Boston to Washington, D.C. were expected to reach triple digits starting Wednesday, the official beginning of summer and the longest day of the year.
New York was under a hot weather advisory, with the mercury expected to hit 94 degrees on Wednesday and 98 degrees on Thursday.
The heat wave was expected to snap over the weekend.
With News Wire Services
||||| Story highlights "Few areas (will be) below 90 degrees in the Northeast," weather service says
Last year, the weather service reported 206 heat-related deaths nationwide
In the past decade, heat has been the second-leading cause for weather-related deaths
The first major heat wave of the summer blanketed the U.S. East Coast on Wednesday with scorching temperatures that swept across the region.
Hot air -- often in excess of 90 degrees -- stretched from Maine to North Carolina, with the highest temperatures hitting parts of Connecticut, Massachusetts, New York, New Jersey, Pennsylvania and Maryland, according to the National Weather Service.
"Very few areas are forecast to be below 90 degrees in the Northeast," said agency spokeswoman Susan Buchanan.
5 tips to survive extreme heat
States across the mid-Atlantic also had heat indices that reached 105 degrees, said the National Weather Service, which issued warnings and advisories across the region.
Heat indices combine temperature and relative humidity to indicate how hot the body feels.
JUST WATCHED The heat is on today in the Northeast Replay More Videos ... MUST WATCH The heat is on today in the Northeast 01:35 PLAY VIDEO
New York City and parts of northeast New Jersey are expecting the heat index to reach even higher. Actual temperatures reached the mid-90s on Wednesday.
"I wouldn't say this is highly abnormal," said meteorologist Rick Watling. "Having heat advisories or even warnings this time of the year is not too unusual."
The National Weather Service advises residents to wear lightweight and loose-fitting clothing, drink plenty of water, take frequent breaks in shaded or air-conditioned environments, stay out of the sun and check on relatives and neighbors.
Young children and the elderly are especially at risk for heat-related injuries, the service said.
Last year, it reported 206 heat-related deaths. In the past decade, heat has been the second-leading cause for weather-related fatalities, the service said.
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Cities across the Northeast designated cooling centers and have issued advisories in an effort to help keep residents safe, according to emergency management officials in several cities.
"For the most part, they're places that are already open and they're designated for when the heat rises," said New York Emergency Management spokeswoman Judith Kane. "The centers are places like senior centers that will be open to the public. It's an effective way to get access to air conditioning if you don't have it."
Residents are advised to call 311 or to go to their city's website online to find cooling centers and to get further information on how to keep cool as the heat rises. ||||| It was the longest day of the year Wednesday, and with temperatures in New York hitting the mid-90s, the hottest one, too.
But Thursday could be even more unbearable.
With temperatures projected to hit 98 degrees and a heat index of well over 100, Mayor Michael R. Bloomberg urged New Yorkers to seek air-conditioning, drink plenty of water and check on friends and neighbors.
The city has opened 455 air-conditioned cooling centers through Thursday, with extended hours, at places like senior centers, Salvation Army community centers and public libraries. Residents can call 311 or go to nyc.gov to find a convenient location.
In a heat advisory, the city’s Education Department asked principals to limit outdoor recess and exercise during the warmest hours, from 10 a.m. to 2 p.m.
“Please pay special attention to children who may be more susceptible to heat-related illness, including those who are obese, have chronic medical conditions such as diabetes and asthma, or are suffering from a gastrointestinal illness,” the advisory said.
Consolidated Edison said that it had about 1,000 power failures in the city and Westchester County on Wednesday, most of which had been restored, and that it had begun to reduce the voltage in the system to prepare for the demand expected on Thursday.
“Tomorrow will definitely exceed today’s,” said Michael Clendenin, a spokesman for Con Ed.
The last time the temperature broke 90 in New York was in August, as part of a heat wave that claimed at least 31 lives in the city. (The heat spell at the end of last month came close, topping out at 89 degrees.)
In a news conference at a senior center in the Bronx, Mr. Bloomberg focused on ways to prevent heat-related illness and warned that the conditions could be “very dangerous.”
“It’s crucial that all New Yorkers take the necessary precautions to protect themselves and their families from the heat,” he said.
The city’s public pools will not open until June 28, the day after school ends. But many educators indicated that they were prepared for the heat, with 9 of 16 schools contacted on Wednesday saying they had already altered their normal routines.
Employees at several elementary and middle schools said they were keeping students inside for recess and encouraging them to stay in air-conditioned areas. Others said they were giving students extra water breaks or even, in one case, free fruit ices.
Maria Resto, secretary at Middle School 45 in Manhattan, said that students were not allowed to go outside for recess and that a planned field trip to Central Park was canceled because of the heat.
At Public School 110 in the Bronx, Melva Morton, an intervention counselor, said that because only half of the building had air-conditioning, teachers in the uncooled half were propping their doors open.
Not that the children noticed.
“For some reason, the children don’t feel the heat,” Ms. Morton said. “We’re the ones that are sweltering. The kids are running around like you wouldn’t believe. Some of us said, ‘Maybe we shouldn’t let you outside,’ but they said, ‘No, we want to go outside!’ To them, it’s like a regular day.” |||||
What is a shorter version of the above article? | – Summer started off with a bang in the Northeast yesterday, with temperatures often higher than 90 degrees up and down the East Coast. In some states, the heat index hit as high as 105 degrees, and New York City and parts of New Jersey expect that number to get higher, CNN reports. The New York Times notes that it was the city's hottest day of the year—the temperature hasn't cracked the 90-degree mark since August—but today could be worse, with temps expected to reach 98 degrees. Relief is expected over the weekend, the New York Daily News adds, but expect triple digits in some areas before then. In Kentucky, high temperatures contributed to a tragedy this week: Lincoln Lindsay, eight months old, died after his father forgot to drop him off at day care and instead left him in his car seat while he went to work Monday. The temperature was around 90 degrees that day, meaning inside the car it was over 100 degrees; Lindsay was likely in the car for several hours. Authorities ruled the death an accident. | multi_news_1_0_0 |
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Article:
Radiation treatment for breast cancer can increase a woman’s risk of heart disease, doctors have long known. But the size of the added risk has not been clear.
Now, a new study offers a way to estimate the risk. It finds that for most women the risk is modest, and that it is outweighed by the benefit from the treatment, which can halve the recurrence rate and lower the death rate from breast cancer by about one-sixth.
According to the study, a 50-year-old woman with no cardiovascular risk factors has a 1.9 percent chance of dying of heart disease before she turns 80. Radiation treatment for breast cancer would increase that risk to between 2.4 percent and 3.4 percent, depending on how much radiation hits the heart.
“It would be a real tragedy if this put women off having radiotherapy for breast cancer,” said Sarah Darby, a professor of medical statistics at the University of Oxford in Britain, and the lead author of the study, published Wednesday in The New England Journal of Medicine.
Dr. Silvia Formenti, the chairwoman of radiation oncology at New York University Langone Medical Center, said she worried that women with cancer would misconstrue the findings to mean that radiation is dangerous and that they should have their breasts removed instead of having lumpectomies, in order to avoid radiation.
“There is a wave toward mastectomy in this country,” Dr. Formenti said.
But at the same time, she and other experts say that the cardiovascular risk is real and that when radiation is given, every effort should be made to minimize exposure of the heart.
In addition, women who have had radiation treatment need to be especially vigilant about controlling other factors that increase the odds of heart disease, like high blood pressure and cholesterol.
Dr. Lori Mosca, the director of preventive cardiology at NewYork-Presbyterian Hospital/Columbia University Medical Center, who was not involved in the study, said the findings meant that a history of breast irradiation should be added to the list of risk factors for heart disease and taken into consideration by all doctors who are treating such patients.
“We absolutely need to put on our radar screen that prior radiation to the breast may be a new and important risk factor for women,” Dr. Mosca said.
But she and other experts also warned that the results needed to be verified because the study was not a controlled experiment, but was based on an analysis of records and estimates of radiation exposure to the heart.
Dr. Javid Moslehi, co-director of the cardio-oncology program at the Dana-Farber Cancer Institute in Boston and the author of an editorial accompanying the study, said the research was the first to provide risk estimates correlated with doses in breast cancer treatment, over a long time period.
“This is a huge paper, both in terms of how many women it impacts, and how it opens the door for new studies that need to be done,” Dr. Moslehi said.
He said the study reflected the fact that many people with cancer are now living long enough to encounter long-term effects of both radiation and chemotherapy.
They have given rise to a new and fast-growing field in medicine, cardio-oncology.
About three million women in the United States have been treated for breast cancer, and the majority have had radiation.
Although doctors try to spare the heart, it still gets some of the dose, especially when the left breast is treated. Radiation can damage the linings of blood vessels and scar the heart muscle.
Dr. Darby’s study is based on the records of 2,168 women who had radiation for breast cancer from 1958 to 2001 in Sweden and Denmark; 963 of the women had “major cardiac events” sometime after their cancer treatment, meaning a heart attack or clogged coronary arteries that needed treatment or caused death.
From the treatment records, the researchers estimated the radiation dose to the women’s hearts. They found that the risk began to increase within a few years after exposure, and that it continued for at least 20 years. The higher the dose, the higher the risk, and there was some increase in risk at even the lowest level of exposure.
“It was certainly a surprise to us that the risk started within the first few years after exposure, as radiation-related heart disease has traditionally been thought of as usually occurring several decades after exposure,” Dr. Darby said.
Radiation is measured in units called Grays, and the researchers found that for each Gray to which the heart was exposed, the odds of heart attack or another coronary events rose by 7.4 percent. The average dose to the heart over an entire course of radiation treatment was 5 Gray, they said. For an individual woman, the net effect would depend on her baseline initial risk of heart disease and the total radiation dose to her heart.
Women who already had risk factors, especially those who had had heart attacks in the past, would have seen the largest absolute risk from radiation.
Some radiation oncologists say that nowadays, the dose to the heart is lower than 5 Gray.
Dr. Louis S. Constine, vice chairman of radiation oncology at the University of Rochester Medical Center, said that 2 Gray was more common and that doctors could now put shields in front of the heart and “curve radiation around the chest wall instead of shooting it through the heart and lungs.”
Dr. Formenti thinks that for most patients, the best way to protect the heart is to treat them while they are lying on their stomachs, instead of the usual way, lying on their backs. Women lie on a table or a mattress with openings that let the breasts drop away from the chest.
Anatomy differs, but in most women this prone position helps keep the radiation beams as far as possible from the heart and lungs. The heart still receives some radiation, but significantly less than when women lie on their backs, especially when the left breast is being treated.
“If you can keep it below 1 Gray, which is what we are doing, you are probably O.K. with the majority of patients,” Dr. Formenti said.
During the past 15 years, she said, she has treated several thousand patients this way.
Dr. Formenti and her colleagues also teach the technique to other doctors. But, she said, it is taking a long time to catch on. ||||| Radiotherapy regimens for breast cancer have changed since the women in these trials were irradiated, and the doses of radiation to which the heart is exposed are now generally lower. 4 Nevertheless, in most women, the heart still receives doses of 1 to 5 Gy. 5-11 Several studies have suggested that exposures at this level can cause ischemic heart disease, 12-14 but the magnitude of the risk after any given dose to the heart is uncertain, as are the time to the development of any radiation-related disease and the influence of other cardiac risk factors. We therefore conducted a study relating the risk of ischemic heart disease after radiotherapy to each woman's radiation dose to the heart and to any cardiac risk factors she had at the time of radiotherapy.
Randomized trials have shown that radiotherapy for early-stage breast cancer can reduce the rates of recurrence and of death from breast cancer. 1,2 However, long-term follow-up in some trials has shown that radiotherapy can also increase the risk of ischemic heart disease, presumably through incidental irradiation of the heart. 1,3
Rate ratios were estimated with the use of conditional logistic regression after stratification according to country and to age at the time of cancer diagnosis, year of cancer diagnosis, and years from cancer diagnosis to first subsequent major coronary event (for case patients) or the index date (for controls) (all in 5-year categories). 22,23 To estimate the proportional increase in the rate of major coronary events per gray of radiation, the data were also stratified according to presence or absence of a cardiac risk factor. The rate of major coronary events was modeled as B s (1+KX), where B s was the stratum-specific rate of major coronary events in the absence of radiotherapy, X was the dose (or EQD2) of cardiac radiation (in Gy), and K was the percentage increase in the rate of major coronary events per gray. The form 1+KX was chosen for the dose–response relationship because a wide variety of functions are approximately linear for small values of X. The adequacy of 1+KX for summarizing the dose–response relationship was examined by carrying out analyses based on categories of radiation dose. In these analyses and in tests for interactions between radiation dose and other factors, models similar to the model described above were used. Significance tests were two-sided, and both significance tests and confidence intervals were based on the likelihood ratio. For analyses in which the explanatory variable was categorical, the confidence intervals for every category, including the reference category, were estimated from the amount of information in that category. 24 Calculations were performed with the use of Stata Statistical Software, release 12 (StataCorp), 25 and EpiWin, release 1.8 (Hirosoft International). 26
Individual radiotherapy charts, including a diagram or photograph of the treatment fields and a dose plan (where available) were copied. Virtual simulation and planning based on computed tomography (CT) (or, for a few regimens, manual planning) were used to reconstruct each radiotherapy regimen on the CT scan of a woman with typical anatomy. Virtual simulation and CT planning involved the reconstruction of radiotherapy fields on a CT scan. Radiation doses to the structures of interest were then estimated with the use of the treatment-planning system Helax–TMS, version 6.1B (Nucletron). In manual planning, the doses were estimated on the basis of charts on which isodose curves (i.e., lines delimiting areas receiving the same radiation dose) had been drawn. As previously described, 18,19 dose-volume histograms for the whole heart and for the left anterior descending coronary artery (which often receives the highest dose of radiation from radiotherapy for cancer of the left breast) were obtained for the regimens used, and the mean doses received by these two structures were calculated. Equivalent doses delivered in 2-Gy fractions (EQD2) 20 were calculated from the dose-volume histograms as nd[(d+α/β)÷(2+α/β)], where n was the number of fractions, d was the dose to the heart per fraction (in Gy), and α/β was 2 Gy. 21
In both countries, women without histopathological confirmation of breast cancer, with bilateral or metastatic disease at the time of diagnosis, or with a history of cancer (excluding nonmelanoma skin cancer) or previous radiotherapy to the thoracic area were excluded. All other women who received radiotherapy were cross-matched with nationwide registers of diagnosis at the time of hospital discharge and cause of death (up to 2002 in Sweden and 2007 in Denmark). 17 Women whose primary diagnosis was a major coronary event that occurred after a diagnosis of breast cancer but before any recurrence or diagnosis of a second cancer were classified as case patients. Whenever possible, hospital cardiology or autopsy records were reviewed, and if the case-defining event was refuted, the woman was excluded from the study. For each remaining case patient, we defined “time period” as the time from breast-cancer diagnosis to the time of first major coronary event. Controls (one per case patient in Sweden and two per case patient in Denmark) were selected at random from all eligible women in the study population. Eligibility criteria for controls included fulfillment of the matching criteria (country of residence, age at the time of breast-cancer diagnosis, and year of diagnosis, with both age and year matched within 5 years); receipt of radiotherapy; and no recurrence of breast cancer, no diagnosis with another cancer, and no major coronary event before the index date (defined as the date of breast-cancer diagnosis plus the time period of the matched case).
A single study protocol was used, but the selection of case patients and controls varied slightly between the two countries. In Sweden, all women living in Stockholm for whom data were recorded in the Swedish National Cancer Register 15 were considered for the study if they received a diagnosis of breast cancer between 1958 and 2001, were younger than 70 years of age at the time of diagnosis, and had received radiotherapy. Because information on radiotherapy is not kept by the Swedish Register, hospital records were used to determine which women had received radiotherapy. In Denmark, all women for whom data were recorded in the register held by the Danish Breast Cancer Cooperative Group 16 were considered for the study if they received the diagnosis of breast cancer between 1977 and 2000, were younger than 75 years at the time of diagnosis, and received radiotherapy. The study was approved by the Danish Data Protection Agency and by the ethics review board of the Karolinska Institutet in Stockholm. The requirement for informed consent was waived because of the nature of the study.
A population-based case–control study of major coronary events was conducted in women in Sweden and Denmark who received external-beam radiotherapy for invasive breast cancer. Major coronary events were defined as a diagnosis of myocardial infarction (International Classification of Diseases, 10th Revision [ICD-10] codes I21–I24), coronary revascularization, or death from ischemic heart disease (ICD-10 codes I20–I25). Patients with a diagnosis of angina alone were not included, because pilot studies showed that we could not reliably identify angina. Patient records from hospital oncology departments were used to obtain data on each woman's medical history before her diagnosis of breast cancer, tumor characteristics, and radiotherapy.
The overall average of the mean EQD2 doses to the heart was 3.9 Gy (range, 0.1 to 30.4). The mean doses and the EQD2 doses to the heart were highly correlated (correlation coefficient, 0.98). The results of analyses based on dose and EQD2 dose were therefore similar (Fig. S1 in the Supplementary Appendix ). Estimated mean doses to the left anterior descending coronary artery and to the heart were also correlated (correlation coefficient, 0.76) (Table S9 in the Supplementary Appendix ). The mean dose of radiation to the heart was a better predictor of the rate of major coronary events than the mean dose to the left anterior descending coronary artery (P<0.001 for mean dose to the heart; P=0.001 for mean dose to the left anterior descending coronary artery). The mean dose of radiation to the heart remained significantly associated with the rate of major coronary events after the mean dose to the left anterior descending coronary artery was taken into account (P=0.04). However, the converse did not apply: the mean dose to the left anterior descending coronary artery was not significantly associated with the rate of major coronary events after the mean dose to the heart was taken into account (P=0.62).
The percentage increases in the rate of major coronary events per gray of radiation according to the number of years since radiation exposure were as follows: 0 to 4 years, 16.3% (95% CI, 3.0 to 64.3); 5 to 9 years, 15.5% (95% CI, 2.5 to 63.3); 10 to 19 years, 1.2% (95% CI, −2.2 to 8.5); and 20 or more years, 8.2% (95% CI, 0.4 to 26.6) ( Table 3 Table 3 Percentage Increase in the Rate of Major Coronary Events per Gray, According to Time since Radiotherapy.). The variation among these values was consistent with random variation (P=0.16 for heterogeneity; P=0.26 for trend). Findings were similar when the analysis was repeated separately according to age at the time of the breast-cancer diagnosis, the presence or absence of preexisting cardiac risk factors, whether the case patient had died from ischemic heart disease, and whether the case patient's hospital cardiology record or autopsy record had been reviewed (Tables S5 through S8 in the Supplementary Appendix ).
The overall average of the estimated mean doses of radiation to the heart was 6.6 Gy for women with tumors in the left breast, 2.9 Gy for those with tumors in the right breast, and 4.9 Gy overall (range, 0.03 to 27.72). The rate of major coronary events increased by 7.4% for each increase of 1 Gy in the mean radiation dose delivered to the heart (95% CI, 2.9 to 14.5; P<0.001) ( Figure 1 Figure 1 Rate of Major Coronary Events According to Mean Radiation Dose to the Heart, as Compared with the Estimated Rate with No Radiation Exposure to the Heart.). When women were grouped according to whether the mean radiation dose to the heart was less than 2 Gy, 2 to 4 Gy, 5 to 9 Gy, or 10 or more Gy, the percentage increases in the rate of major coronary events in these four categories, as compared with the estimated rate if the cardiac dose had been zero, were 10% (95% CI, −9 to 33), 30% (95% CI, 14 to 49), 40% (95% CI, 15 to 72), and 116% (95% CI, 59 to 195), respectively. The percentage increase per gray did not differ significantly according to any of the matching factors used in the selection of controls, tumor characteristics (including whether the tumor was in the left or right breast), or cancer treatments in addition to radiotherapy. Despite the fact that the rate of major coronary events was higher among women with cardiac risk factors than among those without such risk factors, the percentage increase in the rate of major coronary events per gray was similar for women with and those without a cardiac risk factor at the time of breast-cancer diagnosis ( Table 2 Table 2 Radiation Dose to the Heart and Percentage Increase in the Rate of Major Coronary Events per Gray, According to Risk Factors and Other Characteristics.).
Women irradiated for cancer of the left breast had higher rates of major coronary events than women irradiated for cancer of the right breast (P=0.002), but there were no other strong associations between the rate of major coronary events and tumor characteristics or the cancer treatments administered in addition to radiotherapy (rate ratio, 1.20; P=0.06 for nodal status and P≥0.10 for all other tumor or treatment characteristics) ( Table 1 Table 1 Characteristics of the Women in the Study at the Time of Breast-Cancer Diagnosis and Association between the Characteristics and the Subsequent Rate of Major Coronary Events.). In contrast, the overall rate ratio for a major coronary event among women with a history of ischemic heart disease as compared with women with no such history was 6.67 (95% confidence interval [CI], 4.37 to 10.18). The rate ratio was 13.43 (95% CI, 7.65 to 23.58) during the first 10 years after the cancer diagnosis as compared with 2.09 (95% CI, 1.05 to 4.13) during later years (P<0.001) (Table S4 in the Supplementary Appendix ). Rates of major coronary events were also elevated among women with a history of other circulatory diseases, diabetes, or chronic obstructive pulmonary disease; among women who smoked; and among women with a high body-mass index or a history of regular analgesic use. The rate ratio for the presence of one or more of these factors but no ischemic heart disease was 1.96 overall (95% CI, 1.60 to 2.40); during the first 10 years after the cancer diagnosis, the rate ratio was 2.60 (95% CI, 1.89 to 3.57) as compared with 1.63 (95% CI, 1.24 to 2.15) during later years (P=0.03).
A total of 963 women with major coronary events and 1205 controls were included in the study. Among the case-defining major coronary events (i.e., the event resulting in inclusion in the study), 44% occurred less than 10 years after breast cancer was diagnosed, 33% occurred 10 to 19 years afterward, and 23% occurred 20 or more years afterward. Hospital cardiology or autopsy records confirmed the case-defining major coronary event in 65% of case patients and were consistent with the event in 9% of case patients; for the remaining 26% of case patients, no relevant record could be found. A total of 54% of case patients were known to have died from ischemic heart disease, either at the time of their case-defining event or subsequently. (For further information, see Tables S1, S2, and S3 in the Supplementary Appendix , available with the full text of this article at NEJM.org.)
Discussion
Breast cancer is the most common cancer in women worldwide, with more than 1 million new diagnoses each year.27 Moreover, every year, tens of thousands of women worldwide receive a diagnosis of ductal carcinoma in situ. The overall 5-year survival rate for these two diagnostic groups combined is approximately 90%, and in both groups many of the survivors will have received radiotherapy.28 Current mean doses of radiation to the heart from radiotherapy for breast cancer are typically about 1 or 2 Gy for disease of the right breast. For disease of the left breast, the doses are usually higher but vary widely, and for some women, including those in whom the distance of the heart to the thoracic wall is small and those who require internal mammary irradiation, the mean dose may be around 10 Gy.5-11
Among the 2168 women in this study, the mean dose to the heart ranged from 0.03 Gy to 27.72 Gy, with an overall average of the mean doses of 4.9 Gy. The risk of a major coronary event increased linearly with the mean dose to the heart. The magnitude of the risk was 7.4% per gray, with no apparent threshold below which there was no risk. The risk started to increase within the first 5 years after exposure and continued for at least 20 years. The percentage increase in risk per gray was similar for women with and those without cardiac risk factors at the time of radiotherapy.
A strength of this study is that it relates the risk of ischemic heart disease among women who have received radiotherapy for breast cancer to individual doses of cardiac radiation and individual cardiac risk factors at the time of their cancer diagnosis. Other strengths of the study are that it was carried out in women with cancer that had not recurred (thus avoiding confusion with the influence of further treatment); that it was population-based, including all women recorded as receiving radiotherapy for breast cancer in Denmark or Stockholm during the period of interest (thus avoiding the tendency in randomized trials to omit patients in poor health); and that the majority of cardiac events were confirmed by a review of cardiology or autopsy records. Because health status may play a role in the selection of women for radiotherapy, we included in the study only women who had received radiotherapy; nonrandomized comparisons of women who underwent irradiation with those who did not could produce misleading estimates of risk.29
A limitation of our study was that individual CT-based information on radiotherapy was unavailable for the women studied, because they were treated before the era of three-dimensional CT-based planning. However, we have used 20 consecutive individual CT-based, three-dimensional planning scans to show that for left and right tangential radiotherapy and for left and right direct internal mammary fields, the patient-to-patient variation in mean radiation dose to the heart is small (coefficients of variation, 30%, 11%, 11%, and 21%, respectively).4 We have also confirmed that the patient with typical anatomy who was used to calculate the dose estimates in this study was average in terms of the radiation dose to her heart. Consideration of irradiated structures within the heart30,31 may prove fruitful in the future, but in the present study, inclusion of the estimated mean dose to the left anterior descending coronary artery did not improve prediction of the rate of major coronary events.
Since our study included few women who were younger than 40 years of age at the time of radiotherapy, caution is needed in applying our results to women in this age group, and the possibility of larger increases in the rate of major coronary events per gray of radiation for this group cannot be ruled out. Few women in this study were treated with anthracyclines, and none with taxanes or trastuzumab, all of which are known to affect the heart, even in the absence of radiotherapy.32
Studies comparing rates of cardiac disease among women who received radiotherapy for cancer of the left breast and women who received radiotherapy for cancer of the right breast have been reviewed elsewhere.33-35 Such studies are likely to underestimate the extent of any radiation-related risk because they rely on any difference in cardiac dose between women irradiated for tumors in the left breast and those irradiated for tumors in the right breast. In addition, these studies have generally not had information on whether a woman had prior heart disease, and thus could not account for any tendency to avoid irradiation in women with preexisting cardiac risk factors and cancer of the left breast or for the exclusion of women whose only diagnosis was angina (which may be unreliably recorded in routine records). In our study, the radiation-related increase in the risk of major coronary events began within the first 5 years after exposure. Early increases in risk have been reported in studies of patients with Hodgkin's lymphoma who received radiotherapy.36-38 The effect of preexisting cardiac risk factors on the risk of radiation-related ischemic heart disease has not been well studied, but one report on patients with breast cancer indicated that the absolute effect of radiotherapy was greater in smokers than in nonsmokers.39 Several studies have empirically investigated the relationship between cardiac radiation dose and risk of heart disease (Table S10 in the Supplementary Appendix). The estimates vary considerably, but this is to be expected, since both the populations studied and the end points reported were diverse.
The relevance of our findings to a woman receiving radiotherapy for breast cancer today is that they make it possible to estimate her absolute risk of radiation-related ischemic heart disease. This absolute risk can be weighed against the probable absolute reduction in her risk of recurrence or death from breast cancer that would be achieved with radiotherapy.2 The percentage increases in risk per unit increase in the mean dose of radiation to the heart are similar for women with and women without preexisting cardiac risk factors. Therefore, absolute radiation-related risks are greater for women with preexisting cardiac risk factors than for other women.
Data from a case–control study do not by themselves permit estimation of absolute risks. Therefore, we have illustrated our results on the risk of fatal ischemic heart disease by combining them with recent data on rates of death from ischemic heart disease for the 15 westernmost countries of the European Union combined (Table S11 in the Supplementary Appendix). We have also illustrated the effect of radiotherapy for breast cancer on the risk of an acute coronary event (i.e., a major coronary event or unstable angina) by assuming that for women younger than 50 years of age, those 50 to 59 years of age, those 60 to 69 years of age, and those 70 to 79 years of age, the rates of acute coronary events are 6 times, 5 times, 3 times, and 2 times the rates of death from ischemic heart disease, respectively.40 The resulting baseline lifetime risk estimates are similar to recent estimates for the United States.41
For a 50-year-old woman with no preexisting cardiac risk factors, radiotherapy involving a mean dose to the heart of 3 Gy would increase her risk of death from ischemic heart disease before the age of 80 years from 1.9% to 2.4% (i.e., an absolute increase of about 0.5 percentage points), and it would increase her risk of having at least one acute coronary event from 4.5% to 5.4% (i.e., an absolute increase of about 0.9 percentage points) (Figure 2Figure 2 Cumulative Risks of Death from Ischemic Heart Disease and of at Least One Acute Coronary Event.). If her mean cardiac dose were 10 Gy, her absolute risk of death from ischemic heart disease would increase from 1.9% to 3.4% (1.5 percentage points), and her absolute risk of having at least one acute coronary event would increase from 4.5% to 7.7% (3.2 percentage points).
For women with one or more preexisting cardiac risk factors, both the baseline risks and the absolute increases in risk are higher. For example, radiotherapy involving a mean dose of radiation to the heart of 3 Gy in a 50-year-old woman with one or more cardiac risk factors would increase her risk of death from ischemic heart disease before the age of 80 years from 3.4% to 4.1% (an absolute increase of 0.7 percentage points), and it would increase her absolute risk of having an acute coronary event by the age of 80 years by 1.7 percentage points. A mean dose of 10 Gy to her heart would result in radiation-related risks that were considerably higher.
In conclusion, we found that incidental exposure of the heart to radiotherapy for breast cancer increased the rate of major coronary events by 7.4% per gray, with no apparent threshold. The percentage increase per unit increase in the mean dose of radiation to the heart was similar for women with and women without preexisting cardiac risk factors, which indicates that the absolute increases in risk for a given dose to the heart were larger for women with preexisting cardiac risk factors. Therefore, clinicians may wish to consider cardiac dose and cardiac risk factors as well as tumor control when making decisions about the use of radiotherapy for breast cancer. ||||| Radiation, a component of breast cancer therapy, can penetrate to the heart, a new study finds.
A linear accelerator is used to treat cancer at a hospital. Women treated with radiation for breast cancer are more likely to develop heart problems later, even with the lower doses used today, new research suggests. (Photo: John Rucosky, AP) Story Highlights Radiation can keep breast cancer from returning, but also damage the heart
Breast cancer survivors face a number of long-term complications due to treatment
Chemotherapy can cause heart failure and can put women into early menopause
Women treated with radiation for breast cancer face an increased risk of heart attacks and death, even 20 years after the end of treatment, a new study shows.
The study is the latest to document the serious long-term health problems faced by cancer survivors. Although improved treatments allow more people today to survive their disease, these toxic therapies also lead many to suffer chronic health problems.
Radiation, for example, is a key component of breast cancer therapy and significantly reduces the risk that tumors will return. But beams of radiation can penetrate beyond the breast to the heart and the arteries that feed it, according to a study published online Wednesday in the New England Journal of Medicine.
In a study of 2,168 breast cancer patients who had radiation therapy between 1958 and 2001 in Sweden and Denmark, doctors found that any amount of radiation increased the risk of heart disease. Researchers defined heart disease to include heart attacks, surgeries such as a bypass or angioplasty, or a heart-related death.
"This is a major concern," says Ben Smith, an assistant professor of radiation oncology at M.D. Anderson Cancer Center in Houston, who was not involved in the new study. In spite of improvements in technology, Smith says many women around the country "still have a significant portion of their heart in the path of the radiation beam."
STORY: DNA from tumor could provide early warning
More than 232,000 American women will be diagnosed with breast cancer this year, according to the American Cancer Society. About 3 million American women today are survivors.
Women who received radiation to the left breast, which is slightly closer to the heart, were at especially high risk, the study says. Women with pre-existing heart disease also had a higher risk. Heart problems were generally most common in the first five to 10 years after treatment.
Over the course of 20 years, the risk of heart disease increased an average of 7.4% with each additional unit of radiation, called a gray. Women in the study received an average radiation dose of 4.9 gray to the heart, although some women received up to 27 gray.
Doctors have worked to reduce unnecessary radiation exposure over the years, experts note.
But American women being treated today may still receive radiation of about 2 to 5 gray to the heart, Smith says. New technology allows doctors at his hospital to reduce that exposure even further, to a fraction of 1 gray.
Yet the risks described in the new paper "may represent just the tip of the iceberg," wrote Javid Moslehi, a cardiologist specializing in the care of cancer patients at Boston's Dana-Farber Cancer Institute.
That's because radiation can cause not just narrowing of the arteries and heart attacks, but abnormal heart rhythms, malfunctioning heart valves and other serious issues, which weren't measured in this study, Moslehi writes.
Certain chemotherapy drugs also can cause heart failure, he writes. In the new study, only eight patients got chemo.
Lastly, chemo often throws women into early menopause, which causes many breast cancer survivors to gain weight, says Jody Schoger, a breast cancer survivor and advocate from The Woodlands, Texas. That puts further stress on the heart.
Because cancer treatment can damage the heart and blood vessels in so many ways, leading a healthy lifestyle — with a good diet, lots of exercise and no smoking — is critically important, Smith says.
Cardiologists and family doctors also can help women manage their risks, says cardiologist Christopher Cannon, a professor at Harvard Medical School. Breast cancer survivors could be screened early, for example. Doctors have a wide variety of medications, from aspirin to statins, that also can reduce women's risks, he says.
Eric Winer, director of breast medical oncology at Dana-Farber, says patients should not avoid potentially lifesaving radiation therapy because of the risk of heart disease.
"Radiation is remarkably safe and well-tolerated," Winer says. "It would be a mistake to conclude from this that we should use radiation less often."
But doctors agree that scientists should continue to look for ways to reduce women's risks.
At M.D. Anderson, women can now receive radiation therapy that is synchronized with their breath, Smith says. Inhaling deeply pushes the heart down, and out of the radiation beam. New technology starts and stops the radiation beam automatically as women breathe in and out, nearly eliminating exposure to the heart, he says.
Radiation's risks to the heart loom especially large when women have very early cancers that may not prove life-threatening, Smith says. About 60,000 women a year are diagnosed with a condition called DCIS, or ductal carcinoma in situe. Experts disagree on whether these "Stage O" tumors represent very early cancers or pre-cancers.
About 30% to 40% of DCIS progresses into invasive cancer, although not all of those tumors are life-threatening, Winer says.
Because of that uncertainly, women with DCIS are typically treated as if they have an early cancer, with a lumpectomy, radiation and sometimes hormone therapy.
While radiation reduces the risk that women will be diagnosed with a new case of DCIS or cancer, there's no evidence to show it improves survival, Winer says.
"Any concerns about radiation become an even bigger issue for women who have very early stage breast cancers like DCIS, where women have to very carefully weight the pros and cons of treatments," Winer says. "We need to figure out which women with DCIS need treatment to spare women from the side effects."
Smith encourages breast cancer patients to talk to their doctors about taking steps to reduce their risks.
"Some practices do amazing work to essentially spare the heart," says Smith, who serves as a consultant to review radiation plans from doctors around the country. "And there are others that pretend the heart isn't even there. This is a teachable moment for doctors."
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What is a summary? | – A new study looks at the heart dangers posed by radiation in breast cancer treatment, but despite the 2,168-woman, 43-year survey, the meaning of the results comes down to who you ask. "This is a major concern," one oncologist tells USA Today, while a cardiologist warns that the study "may represent just the tip of the iceberg." However, the New York Times calls the increased danger "modest," and says the study shows that radiation's benefits far outweigh the added heart risks. The study found the risk of heart disease increased by 7.4% for each "gray" (a unit that measures the absorption of radiation). The average woman in the study absorbed nearly 5 gray, but doctors point out that these days radiation absorption of 2 gray is more common, and new techniques can even keep it under 1. "It would be a real tragedy if this put women off having radiotherapy for breast cancer," says the lead author of the paper. You can see an abstract of the original paper at the New England Journal of Medicine. | multi_news_1_0_0 |
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Plastic surgeon Denis Boucq displays silicone gel breast implants as he poses at his office in a clinic in Nice December 16, 2011.
Silicone gel breast implants, manufactured by French company Poly Implant Prothese (PIP), are displayed at the office of plastic surgeon Denis Boucq in a clinic in Nice December 16, 2011.
Plastic surgeon Denis Boucq (R) operates on a patient to remove her silicone gel breast implants, manufactured by French company Poly Implant Prothese (PIP), at a clinic in Nice December 21, 2011.
Alexandra Blachere, who heads an association of women with faulty breast implants, displays silicone gel breast implants during an interview in Paris December 20, 2011.
PARISThe French government urged 30,000 women in France on Friday to seek removal of defective breast implants that a now-defunct company exported worldwide but it said there was no evidence that the product raised the risk of cancer.
The government said public healthcare funds would be used to finance the removals, which were recommended because of the risk of ruptures that could cause inflammation and irritation, at a cost which health officials estimated at 60 million euros.
Around 30,000 women in France have had breast implants made by the company Poly Implant Prothese SA (PIP), which is accused of using industrial-grade silicone normally used in anything from computers to cookware.
PIP, founded by one-time butcher Jean-Claude Mas, produced about 100,000 implants a year before its products were ordered off the market in early 2010.
As many as 300,000 women worldwide may have received PIP implants, which were exported to Latin American countries such as Brazil and Argentina, and Western European markets such as Britain, Germany, Spain and Italy.
Britain said on Friday it was not following the French recommendation and played down any cancer risks.
France has had reports of eight cases of cancer in women with breast implants made by PIP, but health officials stressed at a news conference that the product was not suspected of increasing cancer risk.
A health ministry statement said advice from medical experts showed that: "There is as of now no increased risk of cancer for women using implants of the PIP brand versus other implants."
The statement addressed to French women said new implants would be paid from public funds in cases where the initial implant was inserted for medical reasons, typically for reconstruction after breast cancer treatments.
Associations representing women with PIP implants have been demanding that all replacements, including cases of implants that were purely cosmetic, be publicly funded.
"This announcement is just a smokescreen and the victims of PIP are angry," said Alexandra Blachere, head of the association of PIP implant users in France. "PIP implants are dangerous even excluding cancer. The state can't simply order them to be removed and then leave women to get by afterwards."
Philippe Courtois, a lawyer for a French association of PIP implant users, gave a cautious welcome to Friday's government announcement, saying: "It's a common sense decision even if it unfortunately comes a bit late."
CHEAP SILICONE
PIP was placed into liquidation in March 2010 with losses of 9 million euros after the French medical safety agency, AFSSAPS, recalled its implants when surgeons reported abnormally high rupture rates.
During a subsequent inspection of its manufacturing site, officials found PIP was using a type of silicone that was not approved by health authorities, but was about 10 times cheaper.
An investigation found a majority of implants made by PIP since 2001 contained the unapproved gel.
A spokesman for the German company TUV Rheinland which provided quality certification of PIP's production facilities until March 2010 said its remit was to check the production process not the content of the silicone.
TÜV Rheinland sued PIP in February 2011, claiming it was "thoroughly and continuously misled" by PIP about a change in the silicone that was used.
Authorities in Britain, where women using PIP implants have also announced a court case, also played down any cancer risk.
"Women with PIP implants should not be unduly worried. We have no evidence of a link to cancer or an increased risk of rupture. If women are concerned they should speak to their surgeon," British Chief Medical Officer Dame Sally Davies said.
More than 2,000 women in France have filed legal complaints and another 250 women have recently done likewise in Britain, where the authorities have stopped short of recommending implant removals and sought to reassure on cancer risks too on Friday.
Several as yet unidentified executives of the company founded by Mas, are expected to face charges of aggravated fraud in an ongoing court case in France, which exposes them to possible sentences of up to five years in prison. French judicial inquiries tends to be extremely protracted and often highly secretive affairs.
The PIP scandal was rekindled in recent weeks by the death of a cancer victim who had such implants, prompting prosecutors to open another preliminary inquiry that will assess whether there are grounds for more serious charges of involuntary manslaughter.
(Additional reporting by Alexandria Sage in Paris, Jean Francois Rosnoblet in Marseilles, Kate Kelland in Britain, Ludwig Burger in Frankfurt) ||||| PARIS — French health authorities issued an extraordinary guideline on Friday urging 30,000 French women to have defective breast implants removed, deepening concerns in half a dozen countries and adding more unwelcome light to failings in French medical oversight.
While trying to dampen fears that the implants were linked to any kind of cancer, the French health minister, Xavier Bertrand, recommended that recipients have an “explant” procedure as a preventive, nonemergency measure, even if there were no clinical indications that the implants had been leaking substandard silicone. Medical experts said they were unable to think of any prior action on implants on the scale of the French decision.
The implants — made by a French company, Poly Implants Prothèses, that was closed last year — used an inferior, industrial-grade silicone and are more likely to rupture or ooze than those made from surgical silicone. The French authorities stressed that the leaked gel carries no known link to cancer, focusing instead on how it can irritate body tissues and cause damaging inflammation.
Questions over how low-grade silicone could have gone undetected in hundreds of thousands of implants sold in Western Europe, Australia and South America come on the heels of France’s largest public health scandal in years. That involves a diabetes medication, Mediator, that was also used as a diet drug. It remained in circulation despite at least a decade of warnings, and health officials say it may have caused as many as 2,000 deaths. The maker, Servier, has been charged with defrauding the health-care system and is being investigated for consumer fraud and manslaughter.
No PIP implants were known to have been used in the United States, but there are concerns over an unknown number of women who traveled to South American for less-expensive implants. So far, no country has reported a rupture rate as high as France’s — 5 percent — and most have issued statements meant to reassure implant recipients.
Anxieties rose sharply last month when a French woman whose implant had ruptured died from a rare cancer called anaplastic large-cell lymphoma, and French media reported that she was the eighth woman with the PIP implants to have died of cancer, a figure for which the statistical significance is unclear.
On Friday, the health authorities in Britain, where some 40,000 women received the implants, said it was not recommending “routine removal. ”
“We recognize the concern that some women who have these implants may be feeling, but we currently have no evidence of any increase in incidents of cancer associated with these implants and no evidence of any disproportionate rupture rates other than in France,” the British agency said in a statement.
In Brazil, where about 25,000 implants were used, the National Agency of Sanitary Vigilance recommended that recipients be examined by their doctors. Chile’s Public Health Institute asked doctors who performed implants to contact patients to explain the emerging concerns.
The healthy ministry in Venezuela, one of the region’s largest plastic surgery markets, did not comment, nor did that in Colombia, where nearly 15,000 women have had PIP implants.
Breast implants have had a contentious history, with critics saying they are overused and that women in the pursuit of a narrowly defined ideal of beauty end up subject to uncertain dangers from silicone leaks, including auto-immune problems and what animal studies suggest are possible links to cancer. In the United States, a 14-year moratorium in the United States on all silicone implants was lifted only in 2006, after two decades of litigation in American courts failed to show a conclusive link to cancer in humans. The United States Institute of Medicine and the Food and Drug Administration eventually determined that there was no evidence that standard silicone implants were harmful.
A spokeswoman for the French health products safety agency, known as Afssaps, said it was possible that the rupture rates in other countries were lower because reporting was still low, or because complaints had not yet reached some governments.
“We began in March 2010 to alert the authorities in the countries that had imported those implants,” she said. “But the question is whether they passed on the information to the population. We don’t know.”
France will foot the bill for the implant removals, but will only pay for new implants in women who had them for reconstructive surgery after breast cancer. Women who choose not to undergo the removal should have an ultrasound examination every six months, the authorities said, and should remove any implant that ruptures.
Some foreign doctors expressed approval for the French approach. ||||| | – The French government today advised women who got breast implants from Poly Implant Prothèse to have them removed post-haste, and even offering up public health care funds to finance the operation, over fears that they might rupture or cause irritation. The PIP boobs were yanked off the market last year, over accusations that they were filled with industrial-grade silicone—the stuff used in things like computer chips and spatulas, Reuters explains. France said that there was no evidence that the implants boosted cancer risk, but more than 1,000 French women have suffered ruptures, so they’re recommending their removal as a preventative measure. Some 30,000 women in France and 300,000 worldwide received PIP implants, though mainly in Europe and Latin America—none were sold in the US, according to the New York Times. Britain today added that it was not echoing France’s recommendation, citing the lack of cancer risk. | multi_news_1_0_0 |
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– The Justice Department may be gearing up to sue the state of South Dakota after a report released Monday found thousands of people with disabilities that could potentially be managed at home are being relegated to nursing homes or other long-term-care facilities instead, the New York Times reports. This most recent probe (the Times says there have been more than 50 around the country) is part of federal efforts to cut down on the 250,000 or so disabled people under the age of 65 "unfairly" placed in nursing homes—what a 2013 Senate committee report says flouts the Americans With Disabilities Act and violates a Supreme Court ruling made nearly two decades ago. "Regardless of their age, people with disabilities deserve privacy, autonomy, and dignity in their everyday lives," the head of the DOJ's Civil Rights Division says in the report. One 73-year-old tells the Times some nursing homes are nothing more than "warehouses," with the paper noting patients are often kept from cooking their own meals or going out with friends unless they're signed out—"like a kid," another resident says. The 1999 Supreme Court case anchoring this civil rights dilemma, Olmstead vs. LC, ruled that, under the ADA, people with disabilities have a right to receive help without being segregated from the rest of society. South Dakota Gov. Dennis Daugaard—who was sent a 35-page letter from the DOJ outlining his state's violations and calling for "corrective action," per Disability Scoop—tells the Times in a statement he agrees with federal efforts in theory but struggles with implementation because of the many rural communities in his state. (Some want online shopping more accessible.) | WASHINGTON — When patients in South Dakota seek help for serious but manageable disabilities such as severe diabetes, blindness or mental illness, the answer is often the same: With few alternatives available, they end up in nursing homes or long-term care facilities, whether they need such care or not.
In a scathing rebuke of the state’s health care system, the Justice Department said on Monday that thousands of patients were being held unnecessarily in sterile, highly restrictive group homes. That is discrimination, it said, making South Dakota the latest target of a federal effort to protect the civil rights of people with disabilities and mental illnesses, outlined in a Supreme Court decision 17 years ago.
The Obama administration has opened more than 50 such investigations and reached settlements with eight states. One investigation, into Florida’s treatment of children with disabilities, ended in a lawsuit over policies that placed those children in nursing homes. With its report Monday, the Justice Department signaled that it might also sue South Dakota.
While the administration has received widespread attention for investigating police abuses and supporting the rights of gay and transgender people, the Justice Department has also steadily made these cases part of its civil rights agenda. The government says that those efforts have allowed more than 53,000 Americans with disabilities to leave institutions or avoid them altogether. It is a small number compared with the 250,000 working-age people who are estimated to be needlessly living in nursing homes, but advocates say the federal campaign has had significant effects. ||||| This collaborative project is an extension of the 2016 End of Term project, intended to document the federal government's web presence by archiving government websites and data. As part of this preservation effort, URLs supplied from partner institutions, as well as nominated by the public, will be crawled regularly to provide an on-going view of federal agencies' web and social media presence. Key partners on this effort are the Environmental Data & Governance Initiative and the Data Refuge project. This collection is a continuation of the 2016 End of Term web archiving and, as such, is deduplicated against that collection. It allows for the ongoing archiving of publicly nominated websites beyond the "official" end of the End of Term project.
Interested members of the public, particularly government information specialists, are invited to submit selected web sites to be included in the collection using the public nomination tool.
For more information on partner institutions, web crawling and past End of Term projects, please visit the End of Term Archive. ||||| The Americans with Disabilities Act (ADA) prohibits discrimination against people with disabilities in several areas, including employment, transportation, public accommodations, communications and access to state and local government’ programs and services. As it relates to employment, Title I of the ADA protects the rights of both employees and job seekers. The ADA also establishes requirements for telecommunications relay services. Title IV, which is regulated by the Federal Communications Commission (FCC), also requires closed captioning of federally funded public service announcements.
While the U.S. Department of Labor's (DOL) Office of Disability Employment Policy (ODEP) does not enforce the ADA, it does offer publications and other technical assistance on the basic requirements of the law, including covered employers’ obligation to provide reasonable accommodations to qualified job applicants and employees with disabilities. For a quick overview of the ADA read “The Americans with Disabilities Act: A Brief Overview.”
In addition to the U.S. Department of Labor, several other federal agencies have a role in enforcing, or investigating claims involving, the ADA:
Two agencies within the U.S. Department of Labor enforce parts of the ADA. The Office of Federal Contract Compliance Programs (OFCCP) has coordinating authority under the employment-related provisions of the ADA. The Civil Rights Center (CRC) is responsible for enforcing Title II of the ADA as it applies to the labor- and workforce-related practices of state and local governments and other public entities. Visit the Laws & Regulations subtopic for specific information on these provisions.
DOL Resources on the ADA ||||| Following a comprehensive investigation, today, the Justice Department released its findings that South Dakota unnecessarily relies on nursing facilities to provide services to people with disabilities, in violation of the community integration mandate of the Americans with Disabilities Act (ADA) and the Supreme Court’s decision in Olmstead v. L.C.
South Dakotans with disabilities do not have a meaningful choice to receive the services they need in their own homes and communities. The ADA and the Olmstead ruling require states to make services available to people with disabilities in the most integrated setting appropriate to their needs, regardless of age or type of disability.
The department’s findings, detailed in a letter to South Dakota Governor Dennis Daugaard, follow an investigation into the state’s system of care for people who receive services and supports in nursing facilities. The department found that thousands of people who rely on South Dakota for needed services must live in nursing facilities to receive those services, isolated from their communities. With access to adequate home- and community-based services, these individuals could instead live in their homes and communities.
“Regardless of their age, people with disabilities deserve privacy, autonomy and dignity in their everyday lives,” said Principal Deputy Assistant Attorney General Vanita Gupta, head of the Justice Department’s Civil Rights Division. “Our findings reveal how South Dakota’s current system of long-term care violates federal law and fails to give people with disabilities the choice to live in their own homes and their own communities. South Dakota officials have expressed their desire to provide meaningful opportunities for people with disabilities to receive home- and community-based care, and we look forward to working with South Dakota to build a more effective, more efficient and more just service system for all.”
An analysis of South Dakota’s current spending and national data shows that South Dakota – which has one of the highest nursing facility utilization rates in the country – may even realize cost savings and be able to serve more people by increasing the state’s use of home- and community-based services. The state funds the placement of about 3,400 people in nursing facilities through Medicaid at any given time, and approximately 5,500 people over the course of one year.
Nursing facility residents in South Dakota range in age, and include many older adults and almost 450 people under the age of 65. In addition to older adults with age-related disabilities, many of these individuals have disabilities they were born with or acquired at a young age, such as cerebral palsy, multiple sclerosis and amputations due to diabetes or mobility impairments due to an accident.
The findings letter examines the widespread impact of the state’s nursing facility system. For example, one 51-year-old man told the Justice Department that he had entered the nursing facility to recover after a leg amputation, but had been trying to leave the nursing facility for months, without help.
The department’s findings letter includes the following key conclusions:
Thousands of people who need long-term care have no choice but a nursing facility because South Dakota does not adequately arrange for community-based services or identify residents appropriate for transition.
Many people who rely on state services do not know that they could choose community-based services instead of a nursing facility because the state has not informed them of or offered them these services.
South Dakota spends more than 80 percent of its long-term services budget on nursing facilities but could rebalance these funds to prioritize home- and community-based services.
Most residents have physical disabilities, chronic illnesses or cognitive disabilities and need some assistance with some day-to-day tasks, rehabilitative therapy or nursing –services that the state can provide in community-based settings rather than in institutions.
People with similar needs to those living in South Dakota’s nursing facilities successfully receive services at home in other states, and even in South Dakota. The state already offers many of the services people will need to live in their own homes and can increase community capacity and address service limitations to ensure all individuals can choose these services instead of nursing facility placement.
People with disabilities living in rural and frontier areas of the state, including those living on reservations, have particular difficulty accessing services in their homes and communities.
The full findings letter can be found at www.ada.gov. Please visit www.ada.gov/olmstead to learn more about the division’s ADA Olmstead enforcement efforts, and www.justice.gov/crt to learn more about the laws enforced by the Justice Department’s Civil Rights Division. Additional information about the U.S. Attorney’s Office of the District of South Dakota is available on its website at www.justice.gov/usao-sd.
The investigation was conducted by the Civil Rights Division with assistance by the U.S. Attorney’s Office of the District of South Dakota. The United States is represented by Trial Attorneys Alexandra Shandell, Joshua Rogers and Mathew Schutzer of the Civil Rights Division’s Special Litigation Section and Assistant U.S. Attorney Alison Ramsdell of the District of South Dakota.
South Dakota Findings Letter ||||| | multi_news_1_0_0 |
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– What looks like blood in your toilet bowl could actually be red ink seeping from your toilet paper, says colorectal surgeon Guy Nash—but he's still upset about it. That's because people who use toilet paper decorated in red may think they're seeing blood in the toilet when there isn't any, and vice versa. At stake is a possible colon-cancer diagnosis. "Those patients bleeding will miss real blood, and those not bleeding will report 'blood' in the toilet mistakenly," Nash tells LiveScience. "In my view, it is irresponsible of the makers to have not considered this," he said. But not all medical experts are on board: "I think it's nonsense," said a New York gastroenterologist who has never seen red blood confused with red-colored toilet paper. In any case, says Nash, "If someone sees blood, they should call their doctor, not panic, and have it appropriately evaluated." Even then, rectal bleeding is fairly common and is usually caused by a small anal tear or a swollen blood vessel—not colon cancer, notes WebMD.
Let's expand this into 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. ||||| Beware of decorative toilet paper that could hide signs of illness.
Credit: BMJ Case Reports View full size image
Toilet paper containing red ink could disguise a dangerous medical condition, one doctor believes.
Paper that is decorated with pictures or designs that include red ink could look bloody when wet, and traces of red blood in the toilet are one of the most common signs of colon cancer, colorectal surgeon Dr. Guy Nash of Poole Hospital, in England, wrote in a letter published Jan. 15 in the journal BMJ Case Reports.
"Those patients bleeding will miss real blood, and those not bleeding will report 'blood' in the toilet mistakenly," Nash said.
Colon cancer, or colorectal cancer, develops in the cells that line the large intestine (colon) or rectum. The condition caused about 50,000 deaths in the United States in 2013, according to the National Cancer Institute, and many people suffer few symptoms early on. [10 Do's and Don'ts to Reduce Your Risk of Cancer]
Nash said he saw what looked like blood in his own toilet, but it turned out to be red hearts adorning the bathroom tissue. He said manufacturers and the public should be aware of this risk.
"In my view, it is irresponsible of the makers to have not considered this," Nash told LiveScience in an email, adding that inks of other colors would not create this difficulty.
Not all medical professionals view it as a concern, however.
"I think it's nonsense," said Dr. David Bernstein, a gastroenterologist at North Shore University Hospital in Manhasset, N.Y. Bernstein said he has never seen a patient who confused colored toilet paper with signs of colon cancer.
"If someone sees blood, they should call their doctor, not panic, and have it appropriately evaluated," Nash said. He also said healthy people should have regular colonoscopies, which are widely recommended as a screening tool for colorectal cancer.
Bloody stool is much more commonly associated with hemorrhoids than colon cancer, both doctors said. Other causes could include an anal fissure, diverticular disease or colitis.
And red toilet paper isn't the only thing people may mistake for blood. Nash said some of his patients report bleeding that turns out to be beetroot eaten three days earlier.
Follow Tanya Lewis on Twitter and Google+. Follow us @livescience, Facebook & Google+. Original article on LiveScience. |||||
– It seems 2014 could be a very good year for Alexis Shapiro, the Texas 12-year-old whose plight got a wave of national attention over the weekend. Alexis suffers from hypothalamic obesity, a rare condition that causes her to constantly feel hungry; even with a strict diet, her 4-foot-7 frame carries 198 pounds, and she gains at least two pounds a week. Doctors believe gastric bypass surgery is the only thing that can help, but her insurer turned her down because of her age. Now, NBC News reports she could get the surgery within six weeks. Pediatric obesity expert Dr. Thomas Inge says that now that the family has the money for the surgery—thanks to nearly 1,800 donors who have given more than $73,000 to date on Alexis' GoFundMe site; four unnamed philanthropists have also offered assistance—Alexis could undergo it within six weeks at the Cincinnati Children's Hospital Medical Center. "The team is certainly in favor from a medical standpoint of moving forward as quickly as we can." Inge says than in addition to losing weight, the surgery should help soften the disconnect between her brain and her gut that causes her to feel so hungry. Click for more on her condition, which has worsened to the point that her mom says she told her psychologist "she wants to die."
| Let's expand this into a news article: A 12-year-old Texas girl who became morbidly obese after a rare illness triggered by brain surgery could get a potentially life-saving operation by February, thanks to a flood of donations from strangers.
More than 1,700 people have contributed more than $70,000 for Alexis Shapiro, of Cibolo, Texas, who weighs nearly 200 pounds and is gaining about 2 pounds a week because of a runaway condition called hypothalamic obesity.
That’s in addition to at least four anonymous philanthropists who have stepped forward to help. The response started within hours after NBC News first reported the story on Saturday.
“My goodness! It’s crazy,” said Jenny Shapiro, Alexis’ mother, who added that her family has been surprised and touched by the generosity. “Alexis really likes it. I think she feels like people aren’t looking at her anymore and people are rooting for her.”
Doctors say gastric bypass weight-loss surgery is the only thing that can help Alexis, but the U.S. military, which provides her family’s health insurance, says it won’t pay for the operation because Alexis is too young.
TRICARE and Humana Military, which provide family insurance for Alexis’ father, Air Force veteran Ian Shapiro, denied the request citing rules that say gastric bypass surgery may be covered, but only if the patient is 18 or has achieved full bone growth. Officials said the family could appeal the decision.
But Alexis’ parents — and doctors — say that an appeal could take too long and that there would be no guarantee the child would be approved for the $50,000 operation. Ian Shapiro, 34, is claims representative for USAA, a banking and insurance provider. Jenny Shapiro, 34, works part-time as a dog groomer at PetSmart.
“If nothing else, we have what’s required for the hospital,” Jenny Shapiro said. “If I need to make payments or whatever, then I will.”
Dr. Thomas H. Inge, an expert in pediatric obesity at the Cincinnati Children’s Hospital Medical Center, said Alexis could receive the surgery at his hospital within six weeks now that the funding appears to be in place.
“The team is certainly in favor from a medical standpoint of moving forward as quickly as we can,” he said.
Every extra pound gained is a risk to Alexis, who has developed Type 2 diabetes and other health problems in the past two years. She was just 9 when she developed a benign brain tumor called a craniopharyngioma, which affects at most 1 child per every million per year.
Surgery to remove the tumor went well, but it damaged her hypothalamus and pituitary gland, two organs that help regulate energy balance, appetite and weight.
Like more than half of children who get those tumors, Alexis developed hyperphagia and hypothalamic obesity, disorders that make her gain massive amounts of weight — even as her body thinks it’s starving.
Her parents have had to monitor her food intake and exercise extremely closely, sometimes limiting the child to 900 calories a day. In the past, they’ve had to padlock the kitchen cupboards because Alexis’ conditions cause cravings that make her want to eat an entire jar of peanut butter at one sitting, for instance.
Gastric bypass surgery could help Alexis lose between 20 percent and 30 percent of her body mass, and also curb the misfire between her brain and gut that makes her feel like she’s starving, Inge said.
What’s not clear now is, even if the initial surgery is paid for, whether TRICARE would cover any follow-up care that Alexis might need. Officials with the military insurer did not respond to NBC News requests for comment about the new developments in Alexis’ case.
The Shapiros and Inge said they were planning to talk on Monday to discuss the timing for surgery — and its aftermath. Bariatric surgery is a serious procedure with lifelong consequences. New research by Inge and others suggests that teens do about as well as adults after weight-loss surgery, with the risk of major complications in about 5 percent to 7 percent of cases.
The money raised by NBC News readers and others will help pay for the surgery, Jenny Shapiro said. Any extra will go toward the costs of travel, lodging and other expenses as the family of five travels to Cincinnati for the operation. The family had started an account last summer at GoFundMe, one of several websites that help people raise money for medical expenses. Site organizers charge 5 percent of the donated amount, plus another 2.9 percent and 30 cents per transaction goes to WePay, a payment site.
But it wasn't until Alexis' situation received national attention that the fund jumped, within hours, from a little more than $1,000 to more than $50,000. As of Monday evening, it had grown to more than $71,000.
"I am really amazed at the power of information to bring out the best in people in cases like this," said Inge.
Alexis and her family are cheered by the outpouring of goodwill and generosity, especially during the holidays, Jenny Shapiro added.
“It’s going to be a lot of hard work,” she said. “We know that it’s not going to be 'Have the surgery and, yay, everything’s fixed.' But it’s a start.”
JoNel Aleccia is a senior health writer with NBC News. Reach her on Twitter at @JoNel_Aleccia or send her an email. ||||| We want to thank everyone!!! People who have shared, donated, or left a nice supportive message. We have been trying to thank everyone personally. But, I am only to 900 out of 1,971 people. So I'm really sorry if you have not received a thank you message yet. Please know how thankful and grateful we are. It's an amazing feeling to know how many people have wanted to make sure Alexis gets her surgery. Which will be the end if March. Thank you to everyone!! We hold onto HOPE that this surgery will be successful. Alexis needs a better quality of life.As many of you know Alexis was diagnosed with a rare brain tumor called a craniopharyngioma in 2011. It caused damage to the most important parts of her brain. She has no function of her hypothalamus, or pituitary gland. This has left her with several life threatening conditions. Most we control with replacement hormones and medication. However, the one thing we have not been able to control is something called hypothalamic obesity. it is a beast and we have tried so hard to control it. but, it has been found that no amount of diet or exercise will stop this obesity. Alexis has gained about 140lbs in not even 2yrs. It has been heartbreaking for her and for us. She can not do the things she used to love.So i am seeking bariatric surgery for her. We found a dr. Who has done this with other patients similar to Alexis. He is very kind and experienced. We talked about it with Alexis and she Wants to do it even though she knows it will be hard work. But, she is used to hard work.If it was only that easy.we received the denial from Tricare. Frustrating!! We plan to appeal however, nothing with tricare is easy or fast. Alexis has had many hospital admissions. Problems caused by her weight which then causes more serious problems due to her panhypotuitarism . She needs to be as healthy as possible to keep from going into an adrenal crisis. This is so important to us. Alexis is suffering from this weight and we want to fight for her. Please join us. We met the team in Cincinnati and we love them. I fully trust them with Alexis. We will be making 3 more trips to Ohio at least. This fund will help us do that! We thank everyone.Alexis has made some grey ribbons ( brain tumor awarness) So if you donate please let us know how many you would like. she can make a pin or a magnet. ||||| | multi_news_1_0_0 |
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News article:
(CNN) Kim Jong Un is sending his younger sister to South Korea for the Winter Olympics, the first time any member of the Kim dynasty has visited the country.
South Korea's Unification Ministry said in a statement that Kim Yo Jong will be joining North Korea's high-level delegation to the South, headed by Kim Yong Nam , president of North Korea's parliament.
The 30-year-old, who has seen her profile rise steadily since 2014, was last year promoted to North Korea's Politburo. She and Kim Jong Un were born to the same mother, Ko Yong Hui.
Kim Yo Jong, right, sister of North Korean leader Kim Jong Un, at the official opening of the Ryomyong residential area, April 13, 2017.
Kim Yo Jong's inclusion in the North Korean delegation is likely to irritate the United States, which has sent its own delegation led by Vice President Mike Pence to counter North Korea's charm offensive.
Last year, the US Treasury Department included Kim Yo Jong on its list of blacklisted officials . As the vice director of the Workers' Party Propaganda and Agitation Department, she has been targeted by US sanctions.
On a refueling stop on his way to Asia, Pence said the aim of his trip was to show American "resolve" in rallying the international community against the Kim regime.
"We're traveling to the Olympics to make sure that North Korea doesn't use the powerful symbolism and the backdrop of the Winter Olympics to paper over the truth about their regime," Pence said.
JUST WATCHED Pence keeps door open for NK discussions Replay More Videos ... MUST WATCH Pence keeps door open for NK discussions 01:27
But South Korea welcomed the announcement, saying it was "significant that Kim had included his sister in the delegation.
"We believe that the North's announcement of the delegation shows its willingness to ease tensions on the Korean peninsula along with a message of celebration for the PyeongChang Olympic Winter Games," it said in a statement. "It is significant that the delegation also includes Kim Yo Jong, who is Chairman Kim Jong Un's sister and holds an important position in the Workers' Party of Korea."
Shadowy figure
Like most members of the Kim clan, little is known about Kim Yo Jong beyond her official rank. According to NK Leadership Watch, she is a close aide of her brother's "and since his accession manages his public events, itineraries and logistical needs, among other tasks."
JUST WATCHED Joint Korean ice hockey team plays first game Replay More Videos ... MUST WATCH Joint Korean ice hockey team plays first game 02:32
She was promoted to the country's Politburo as an alternate member in October.
Born September 26, 1987, Kim Yo Jong studied in Switzerland like her brother and is believed to have attended Kim Il Sung University and a western European school for her higher education.
Her position is such that, according to a Seoul-based think tank run by North Korean defectors, Kim Yo Jong briefly took charge of the country while her brother was reportedly ill with gout or diabetes in late 2014.
Hopes for a breakthrough
Kim's presence, alongside Kim Yong Nam (no relation), the 90-year-old ceremonial head of state in North Korea, will raise hopes for a potential breakthrough in relations with the US.
This week, Pence suggested he would be open to meeting North Korean politicians on the sidelines of the Olympics, saying President Donald Trump "always believes in talking."
"North Korea can have a better future than the militaristic path, the path of provocation and confrontation that it's on. Better for its own people, better for the region, and better for peace," Pence said.
However on Wednesday he also warned the US was about to impose the "toughest and most aggressive round of economic sanctions on North Korea ever."
"We will continue to isolate North Korea until it abandons its nuclear and ballistic missile programs once and for all," he said.
The Vice President's delegation includes the father of the late Otto Warmbier, an American student who died shortly after being released from North Korean custody.
Fred Warmbier and his wife Cindy were in the audience during US President Donald Trump's State of the Union address last month.
They looked on tearfully as the President cited their son's treatment as a example of the "menace that threatens our world."
The US delegation will be joined by the President's daughter and senior advisor Ivanka Trump , who will attend the closing ceremony on February 25, a White House official said Monday.
JUST WATCHED Trump: We honor Otto Warmbier's memory Replay More Videos ... MUST WATCH Trump: We honor Otto Warmbier's memory 02:34
Hundreds of North Koreans have arrived in South Korea ahead of the Opening Ceremony on Friday.
Though only 22 athletes will compete in events, the North's delegation will be among the largest at the Games.
It includes an 114-strong art troupe and 96-crew who arrived at South Korea's Mukho port on Wednesday aboard the Mangyongbong 92 cargo-passenger ferry.
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Kim's delegation includes Hyon Song Wol, the lead singer of Kim Jong Un's favorite girl band, whose every move was followed by a insatiable South Korean press during a pre-Games tour last month.
Hyon's the closest thing North Korea has to a celebrity and her presence in Pyeongchang is an indication of how seriously North Korea is taking its Olympic diplomatic mission.
Kim Jong Un's Olympic plans also include a massive military parade on Thursday through the streets of the North Korean capital Pyongyang. The display would be an attempt "to scare the hell out of the Americans," a diplomatic source told CNN last month. ||||| Image copyright KCNA Image caption Kim Yo-jong in a 2015 picture of her brother touring a military unit
The influential sister of North Korean leader Kim Jong-un is to attend the Winter Olympic Games which open in Pyeongchang in the South on Friday, ministers in Seoul say.
Kim Yo-jong, a senior Workers' Party official promoted to the politburo last year, will be the first immediate Kim family member to cross the border.
Both Koreas will march under one flag at the opening ceremony.
The North's participation has been seen as a thawing of bilateral ties.
However, the US, Japan and others have accused the North of using the Games for propaganda purposes.
Who is Kim Yo-jong?
Believed to have been born in 1987, she is the youngest daughter of late leader Kim Jong-il and is Kim Jong-un's full sister. She is about four years younger than her brother and is said to be very close to him.
She is reportedly married to the son of Choe Ryong-hae, the powerful party secretary.
Image copyright Reuters Image caption Kim Yo-jong at the opening of a residential complex in Pyongyang in 2017
Kim Yo-jong has been in the spotlight sporadically in recent years, with her main job being to protect her brother's image via her role in the party's propaganda department.
She remains blacklisted by the US over alleged links to human rights abuses in North Korea.
A message from her brother?
Analysis: BBC's Laura Bicker in Seoul
This is a huge surprise. There had been speculation Kim Yo-jong might be part of the delegation but few thought it would actually happen. It is being seen as a sign that Kim Jong-un is serious about improving ties with South Korea.
Kim Yo-jong is one of Kim Jong-un's closest aides and some are speculating that she might be bringing a message from her brother.
But there could be a number of obstacles to overcome if she is to make it to Pyeongchang. She is targeted by US sanctions for alleged human rights abuses, although she is not on the UN Security Council travel blacklist.
There is also the question of how she will get to the Games. Seoul has had to request special permission from the US and others in the international community to allow North Korean athletes and performers to travel south by bus and ferry. They may have to do so again and this time it will be for a member of Kim Jong-un's own family.
How rare is this visit?
It would be the first by a direct member of the Kim dynasty.
Chang Song-thaek, Kim Jong-un's uncle and brother in law of Kim Jong-il, did travel to the South but did not belong to the Baekdu blood line, which is considered significant.
There is speculation in the South that this is part of Kim Yo-jong's grooming for greater power, and that she could be bringing a letter from her brother to South Korean President Moon Jae-in, who she is likely to meet.
It is unclear whether Kim Yo-jong will be at the opening ceremony on Friday.
Who else is in the delegation?
Politically, four figures, including Kim Yo-jong, are key. The others are:
Kim Yong-nam . North Korea's ceremonial head of state, the president of its parliament. The diplomatically sure-footed 90-year-old has seen the rule of all three North Korean leaders and has travelled overseas before
. North Korea's ceremonial head of state, the president of its parliament. The diplomatically sure-footed 90-year-old has seen the rule of all three North Korean leaders and has travelled overseas before Ri Son-gwon . The head of the North Korean state agency in charge of inter-Korean affairs. A veteran negotiator, he was North Korea's chief delegate at the rare inter-Korean talks held in January
. The head of the North Korean state agency in charge of inter-Korean affairs. A veteran negotiator, he was North Korea's chief delegate at the rare inter-Korean talks held in January Choe Hwi. Vice-chairman of the Central Committee of the Workers' Party and chairman of the National Sports Guidance Committee. Under US state department sanctions
And the rest of the North Korean team?
It's a 280-strong delegation, most of whom arrived in the South on Wednesday.
Led by North Korean Sports Minister Kim Il-guk, it includes 229 cheerleaders, four officials from the National Olympic Committee, 26 taekwondo demonstrators and 21 journalists.
Media playback is unsupported on your device Media caption North Korean cheerleaders arrive in the South for the Games
The team arrived via a western border at 09:28 local time (00:26 GMT), the Yonhap news agency reported.
Only 10 athletes will compete for the North at the Games, along with another 12 as part of a unified Korean women's ice hockey team.
Drip, drip, drip of PR
Michael Madden, North Korea leadership expert
In announcing its delegates both to the 2018 Winter Olympics and the inter-Korean culture events on the sidelines, Pyongyang let out the information in a slow drip.
Part of this is Pyongyang maximising the positive PR effects. The announcement of the full delegation came following the arrival of its athletes to the Games late last week, and one day after 10 musicians arrived in South Korea.
So now North Korea has earned itself a third day of positive media coverage about its participation in the Olympics.
How have others reacted?
The US is scornful of the North's motives over the Olympics and is sending Vice-President Mike Pence to the opening ceremony in Pyeongchang to counter what it terms propaganda.
Image copyright Reuters Image caption Both the US and Japan have been critical of the North's Olympics policy
"We're travelling to the Olympics to make sure that North Korea doesn't use the powerful symbolism in the backdrop of the Winter Olympics to paper over the truth about their regime," he said.
He was in Tokyo on Wednesday and maintained the pressure, announcing that "the United States will soon unveil the toughest and most aggressive round of economic sanctions on North Korea".
Japan has been equally sceptical. Chief Cabinet Secretary Yoshihide Suga said: "We must not be fooled by North Korea's 'smile diplomacy'."
Where are we on North-South ties?
North Korea currently faces growing international pressure and sanctions over its nuclear and missile programmes.
Its latest ballistic missile test, on 28 November, sparked a new series of measures from the UN, targeting petrol shipments and travel for North Koreans, and a war of words between the North and US President Donald Trump.
Kim Jong-un then extended a New Year's olive branch to the South over participation in the Olympics, which run from 9 to 25 February.
The perceived warming of ties has not been without difficulties, not least the North's decision to move a military parade in Pyongyang from April to the day before the opening of the Games. ||||| FILE - This 2015, file photo provided by the North Korean government shows North Korean leader Kim Jong Un and his sister Kim Yo Jong, left, during their visit to a military unit in North Korea. South... (Associated Press)
FILE - This 2015, file photo provided by the North Korean government shows North Korean leader Kim Jong Un and his sister Kim Yo Jong, left, during their visit to a military unit in North Korea. South Korea’s Unification Ministry said North Korea informed Wednesday, Feb. 7, 2018, that Kim Yo Jong would... (Associated Press)
FILE - This 2015, file photo provided by the North Korean government shows North Korean leader Kim Jong Un and his sister Kim Yo Jong, left, during their visit to a military unit in North Korea. South Korea’s Unification Ministry said North Korea informed Wednesday, Feb. 7, 2018, that Kim Yo Jong would... (Associated Press) FILE - This 2015, file photo provided by the North Korean government shows North Korean leader Kim Jong Un and his sister Kim Yo Jong, left, during their visit to a military unit in North Korea. South... (Associated Press)
SEOUL, South Korea (AP) — North Korean leader Kim Jong Un's sister, an increasingly prominent figure in the country's leadership, will be part of the North's delegation to the South Korean Winter Olympics, officials said Wednesday.
Kim Yo Jong, believed to be around 30, will be the first member of North Korea's ruling family to visit South Korea since the end of the 1950-53 Korean War. Analysts say her inclusion in the Olympic delegation shows North Korea's ambition to use the Olympics to break out from diplomatic isolation by improving relations with the South, which it could use as a bridge for approaching the United States.
By sending a youthful, photogenic person who will undoubtedly attract international attention during the Olympics, North Korea is also trying to construct a fresher and warmer public image and defuse potential U.S. efforts to use the Pyeongchang Games to highlight the North's brutal human rights record, experts say.
Kim Jong Un might also have seen that U.S. President Donald Trump was sending his daughter, Ivanka, to the Olympics ceremony and decided to match the move by sending his sister, said Hong Min, an analyst at Seoul's Korea Institute for National Unification.
By sending a relative, "Kim Jong Un may be trying to present himself as an equal to Donald Trump," Hong said.
South Korea's Unification Ministry said North Korea informed it that Kim Yo Jong, first vice director of the Central Committee of North Korea's ruling Workers' Party, would be part of the delegation led by the country's nominal head of state, Kim Yong Nam.
The ministry said Kim Yo Jong's schedule in the South has yet to be determined, and it wasn't immediately clear whether she will meet with President Moon Jae-in, a liberal who has expressed a desire to reach out to the North.
Moon's office welcomed the decision to send Kim Yo Jong, which it said showed the North's willingness to cooperate in efforts to ease tensions in the Korean Peninsula.
"First Vice Director Kim Yo Jong is Chairman Kim Jong Un's sister who has an important role in the Workers' Party, (so her visit) is that much more meaningful," presidential spokesman Kim Eui-kyeom said in a statement read on television.
Koh Yu-hwan, a North Korea expert at Seoul's Dongguk University, said Kim Yo Jong, as Kim Jong Un's relative and apparently one of the few people who has earned his absolute trust, carries more weight as a dialogue partner for the South than any other official the North could send.
It's unclear whether any member of the North Korean government delegation will hold talks with U.S. officials during the Olympics. But Kim Yo Jong's presence would give North Korea a better opportunity to win South Korean help in reaching out to the United States, Hong said. He also said Washington may see Kim Yo Jong as an avenue to deliver messages to Kim Jong Un.
"With any other North Korean official, even the so-called No. 2 Choe Ryong Hae, you are getting a person who's just parroting orders given by Kim Jong Un," Hong said. "But with Kim Yo Jong, you are getting a person who's chiefly involved in designing Kim Jong Un's rule, a person whom the leader actually listens to."
North Korea said the delegation will also include Choe Hwi, chairman of the country's National Sports Guidance Committee, and Ri Son Gwon, chairman of the North's agency that deals with inter-Korean affairs.
Seoul previously said the delegation would arrive Friday, but Wednesday's statement was the first confirmation that a member of the North's ruling family will be included.
Kim Yo Jong and Kim Jong Un were born to the same mother, Ko Yong Hui. They had a half brother, Kim Jong Nam, who was murdered last year at a Malaysian airport.
Kim Yo Jong was promoted by her brother last year to be an alternate member of the decision-making political bureau of the ruling party's central committee, which analysts said showed that her activities are more substantive than previously thought.
The war-separated Koreas are cooperating on a series of conciliatory measures during the Olympics, which the South sees as an opportunity to ease tensions with the North following an extended period of animosity over its nuclear weapon and missile programs. Skeptics think North Korea is trying to use the Olympics to weaken U.S.-led sanctions and pressure against it and buy time to advance its weapons programs.
North Korea has 22 athletes competing in the Winter Olympics but also has sent performing artists and a large cheering group.
A decision by North Korea to send the artists by sea has triggered debate in the South, where conservatives see the move as a clear indication the North is trying to use the Olympics to ease sanctions against it.
South Korea is deciding whether to accept North Korea's request that it provide fuel for the ferry that transported the artists. Seoul exempted the ferry from sanctions to allow it in South Korean waters.
"We will closely discuss with the United States and other related nations the matter of providing convenience to the Mangyongbong ferry so that no problem regarding sanctions would occur," said Seoul's Unification Ministry spokesman, Baik Tae-hyun. |||||
What is a shorter version of the above article? | – In a move seen as a sign that North Korea is serious about improving relations with the South—and about thumbing its nose at the US—Kim Jong Un's powerful younger sister will be visiting South Korea as part of the North's high-level Olympic delegation. Kim Yo Jong, who is a full sibling of the North Korean leader and is believed to be around 30 years old, will be the first "direct member" of the Kim dynasty to visit the South, the BBC reports. South Korean officials welcomed the surprise announcement, saying it is "significant that the delegation also includes Kim Yo Jong, who is Chairman Kim Jong Un's sister and holds an important position in the Workers' Party of Korea." Analysts say Kim Jong Un appears to be trying to present a warmer image of North Korea. By sending his sister when President Trump is sending daughter Ivanka, Kim "may be trying to present himself as an equal to Donald Trump," Hong Min at Seoul's Korea Institute for National Unification tells the AP. Mike Pence, meanwhile, is on a visit to Asia aimed at counteracting Pyongyang's "charm offensive," as CNN puts it. He told reporters Wednesday that the US is about to impose the "toughest and most aggressive round of economic sanctions on North Korea ever." Kim Yo Jong was in January 2017 placed on the US Treasury Department's sanctions list over the country's human rights record, Reuters reported at the time; here's what else we know about her. | multi_news_1_0_0 |
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Summarize this article:
You may have heard the warning that sitting is the new smoking — that our sedentary lifestyles are a huge health threat and we could die an early death if we sit, tethered to our computers and our TVs, for too many hours each day.
But it’s not just the sitting that health experts are worried about; it’s our general lack of any physical activity. In a new paper, published in the journal JAMA, researchers at the Centers for Disease Control and Prevention looked at both how much we sit and how much we exercise — and they came to a painful, though predictable, conclusion: We’re not moving nearly enough.
They estimated that one in four adults sit for more than eight hours a day. That means most of our waking hours are spent sitting on our butts.
The data came from a nationally representative survey of 5,900 adults in the 2015-’16 National Health and Nutrition Examination Survey, where people were also asked how much exercise they get. Four in 10 Americans reported being physically inactive, meaning they get no moderate or vigorous exercise each week. And recall that the CDC recommends at least two hours and 30 minutes of moderate-intensity exercise every week, or 75 minutes of vigorous working out.
Unfortunately, though standing desks have been heavily promoted as the antidote to our sedentary lifestyle, their benefits have been grossly oversold. Standing doesn’t count as exercise, and, unlike running or cycling, there is there is no evidence that simply standing at work improves cardiovascular health.
In fact, the latest science suggests a lack of exercise, not sitting at work, might be the bigger health problem overall.
The problem with the evidence on sitting and health
The sit-and-die public health messages are based on a bunch of studies that have correlated sitting too much with a premature death and a higher risk of chronic diseases including cancer, diabetes, and heart disease.
But the link between sitting and death has been complicated in recent years. And it turns out the context may matter more than the sitting itself. Here’s Emmanuel Stamatakis, an associate professor at the University of Sydney, over at the Conversation:
In other words, the literature on sitting is likely confounded by these socioeconomic factors that may help explain why some sedentary people have worse health outcomes than other sedentary people.
The same kind of counterintuitive finding pops up in the research on people who stand a lot for work. As Aaron Carroll explained in the New York Times this week, a large, long-term study of 38,000 people found that those who stand or walk for more than six hours each day while working had at least double the risk of surgery for varicose veins, which are associated with a greater risk of arterial disease and heart failure.
So standing at work — just like sitting and watching too much TV — “could be a marker for other unhealthy demographic factors or habits, including lower socioeconomic status,” he added.
Exercise — not standing — protects against the potential harms of a sedentary lifestyle
There is one thing that protects against the potential ravages of a sedentary lifestyle: exercise. As Stamatakis explained, being physically inactive — not just sitting a lot — is what appears to heighten the risk of chronic disease. And researchers have found that the health harms of sitting seem to go away when people get about an hour of physical activity each day.
Regular physical activity can “prevent dementia, type 2 diabetes, some cancers, depression, heart disease and other common serious conditions — reducing the risk of each by at least 30%,” according to this 2015 report on the benefits of exercise from the Academy of Medical Royal Colleges. “This is better than many drugs.”
It also helps people live longer. “Many studies give an approximate 30% risk reduction in all-cause mortality. Smoking is the biggest contributor to early mortality and years living with chronic illness and disability.” Overall, the researchers found, regular exercise reduces cardiac death by 31 percent.
And right now, Americans aren’t getting enough. The new survey found four in 10 Americans reported being completely physically inactive each week, meaning they get no moderate or vigorous exercise.
Getting more exercise doesn’t necessarily require extra time
Americans often complain that they don’t have enough time to work out. A 2015 survey asked a group of 1,000 of them how they’d spend an extra four hours each week if they suddenly had the time. The No. 1 answer? Exercise. The desire for more time to work out trumped the wish for more time spent with family, sleeping, or even doing hobbies.
But this 2017 Lancet paper demonstrated that all kinds of physical activity were equally good for the heart. And it’s a reminder that we often overthink exercise — and we may not actually need to set aside extra time to work out.
Exercise doesn’t require a gym membership or fancy shoes. Exercise is something you can do throughout the day, every day. It also doesn’t need to be grueling, and it doesn’t have to cost anything, to see health benefits.
Simply walking more — while commuting, running errands, in a meeting, or on the phone — counts for a lot.
The researchers in the Lancet study also found there was a linear relationship between the amount of exercise and disease risk, meaning the more hours a person spent doing physical activity (again, of any kind), the lower their risk of disease and death. (The benefits seemed to taper off at 1.8 hours of brisk walking per day.) And the people who reported getting the most physical activity were the ones who had exercise built into their daily lives, through simple things like active transport to work, their jobs, or housework. Note: They weren’t just standing around at their desks. ||||| Let’s start with what we know about research on sitting, then explain why it can be misleading as it relates to work. A number of studies have found a significant association between prolonged sitting time over a 24-hour period and increased risk for cardiovascular disease. A 2015 study, for instance, followed more than 150,000 older adults — all of whom were healthy at the start of the study — for almost seven years on average. Researchers found that those who sat at least 12 hours a day had significantly higher mortality than those who sat for less than five hours per day.
A 2012 study in JAMA Internal Medicine followed more than 220,000 people for 2.8 years on average and found similar results. Prolonged sitting over the course of a day was associated with increased all-cause mortality across sexes, ages and body mass index. So did a smaller but longer (8.6 years on average) study published in 2015 in the Journal of Physical Activity & Health.
Another study from 2015, which followed more than 50,000 adults for more than three years, also found this relationship. But it found that context mattered. Prolonged sitting in certain situations — including when people were at work — did not have this same effect.
Why might that be? Sitting itself may not be the problem; it may be a marker for other risk factors that would be associated with higher mortality. Unemployed or poorer people, who would also be more likely to have higher mortality, may be more likely to spend large amounts of time sitting at home. For some, sedentary time is a marker, not the cause, of bad outcomes.
Studies looking specifically at work don’t find a causal pattern. One 2015 paper focused on workers age 50 to 74 in Japan, for more than 10 years on average per participant. It found that — among salaried workers, professionals and those in home businesses — there was no association between sitting at work and cardiovascular risk. A 2016 study examining Danish workers also failed to find a link. ||||| Standing desks are a trend sweeping many workspaces.
I tried using a standing desk at work for two weeks and found that I was much more mindful of my posture throughout the day, and was more productive overall.
I burned a few more calories than I would have while sitting and found that I seemed to be able to stand for longer with the right playlist.
Should you choose to try a standing desk, too, I recommend wearing comfortable shoes.
Whether you work in an office or not, you've probably heard of one trend sweeping many workspaces: standing desks. But standing desks are more than trendy. Many claim that there are real benefits that come from using a standing desk, from newfound energy to less back pain. To see for myself, I tried using a standing desk at work for two weeks. Here's what happened:
I became much more mindful of my posture throughout the day
What you probably don't realize when you're sitting at a desk is your posture while doing so. For me personally, I typically lean over to one side and often alternate between resting both forearms on my desk or only resting one arm at a time.
Standing desks can lead to less tension. Leah Rocketto/INSIDER
The moment I started using a standing desk, I realized just how off my posture was and began to be mindful of the way in which I carried myself while working. I tried to set myself up for success by keeping both feet side by side, my shoulders pulled down, and my body weight equally distributed rather than leaning off to or favoring one side.
As the days passed, I noticed less discomfort and tension overall in comparison to how I used to feel when I was working seated at a desk all day. My back bothered me less, and my neck felt less strained since my computer was more at eye-level.
I recommend wearing comfortable shoes
Standing with uncomfortable shoes can be hard. Shutterstock
I typically wear sneakers to work on a daily basis as my career is that of a fitness professional, but on days in which I opted for loafers or flatter shoes, I could certainly feel it by that evening. Standing for multiple hours a day takes its toll on you in ways in which you may not feel right away.
Standing all day, or too many hours throughout the day actually poses more risk factors than sitting all day does.
A study in the Journal of American Epidemiology found that a combination of standing and sitting actually produces the most benefits. Following a 20:8:2 regimen - sitting for 20 minutes, standing for 8 minutes, moving for two minutes, and then repeating throughout the workday is recommended.
It is recommended that you sit for 20 minutes, stand for eight minutes and move for two minutes. S_L/Shutterstock
I apparently burned a few more calories
A study performed by the American Heart Association determined that on average standing burns an extra 0.15 calories per minute compared to sitting. While this doesn't seem significant, the calories burnt certainly add up — about 54 calories per da y for the average 150-pound person.
I felt a bit more productive
There was an increase in productivity. Pixabay
One unexpected benefit of having a standing desk was that I actually became more productive. I felt more "free" overall, as it was easier for me to move from task to task. I could head over to a whiteboard and take a few notes manually, or run over to chat with a coworker, and then go back to my desk with ease. I felt more like a collaborator in my workspace and was unable to check off a few more things than usual on my daily to-do lists.
Music seemed to allow me to stand longer
Music really did seem to trick me into standing for longer periods of time. Whether it was because I could respond to emails while sidestepping and singing, or that it simply took my mind off of things, it worked. The right playlist can certainly increase productivity, and in this case increase endurance, too (and there's research to back it up).
According to Inc., assistant professor in the music therapy program at the University of Miami, Dr. Teresa Lesiuk, performed research with findings that "those who listened to music completed their tasks more quickly and had better ideas overall than those who didn't."
Based on my positive experiences using a standing desk at work, I plan to continue to do so more often than not moving forward. The benefits outweigh the cons, and as a fitness professional, it seems like a necessity more than an option.
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Summary: | – Standing desks were all the rage for a while, but a recent article in the New York Times pooh-poohs them as "overrated." You may have heard that all the sitting you do at work all day is slowly killing you, but if you look at the actual research, that's not really the case, writes Aaron E. Carroll, a professor of pediatrics. No, sitting for hours a day is not great, and yes, prolonged sitting has been found to be linked to poor health outcomes. But the evidence doesn't support the idea that it's prolonged sitting at work that is the problem. In fact, there are studies that have found prolonged sitting at work does not have the same adverse effects as prolonged sitting in other situations, and there are also studies finding too much standing or walking at work is linked to health problems. The real problem with prolonged sitting is when it's part of an overall sedentary lifestyle. As Carroll explains, it could very well be that prolonged sitting is a marker for other problems, such as unemployment, and it's those other problems that lead to a sedentary lifestyle. It's the type of prolonged sitting that's associated with an overall sedentary lifestyle that you want to avoid. The best way to combat it? Exercise, and standing at a desk is not exercise. There's also no proof that standing to work improves cardiovascular health, Vox reports. Rather than buying a standing desk and thinking you're getting the benefit of actual exercise, some experts suggest taking walking breaks throughout the day at work. There are, however, other benefits to sit-stand desks, including alleviating neck and back pain, and headlines like "I tried using a standing desk at work for a week and it instantly gave me more energy" still abound. (It's not the sitting that's killing you.) | multi_news_1_0_0 |
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Increased awareness of the health consequences of eating too much sugar has fueled a dramatic uptick in the consumption of zero-calorie artificial sweeteners in recent decades. However, new research finds sugar replacements can also cause health changes that are linked with diabetes and obesity, suggesting that switching from regular to diet soda may be a case of 'out of the frying pan, into the fire.'
Artificial sweeteners are one of the most common food additives worldwide, frequently consumed in diet and zero-calorie sodas and other products. While some previous studies have linked artificial sweeteners with negative health consequences, earlier research has been mixed and raised questions about potential bias related to study sponsorship.
This new study is the largest examination to date that tracks biochemical changes in the body--using an approach known as unbiased high-throughput metabolomics--after consumption of sugar or sugar substitutes. Researchers also looked at impacts on vascular health by studying how the substances affect the lining of blood vessels. The studies were conducted in rats and cell cultures.
"Despite the addition of these non-caloric artificial sweeteners to our everyday diets, there has still been a drastic rise in obesity and diabetes," said lead researcher Brian Hoffmann, PhD, assistant professor in the department of biomedical engineering at the Medical College of Wisconsin and Marquette University. "In our studies, both sugar and artificial sweeteners seem to exhibit negative effects linked to obesity and diabetes, albeit through very different mechanisms from each other."
Hoffmann will present the research at the American Physiological Society annual meeting during the 2018 Experimental Biology meeting, held April 21-25 in San Diego.
The team fed different groups of rats diets high in glucose or fructose (kinds of sugar), or aspartame or acesulfame potassium (common zero-calorie artificial sweeteners). After three weeks, the researchers saw significant differences in the concentrations of biochemicals, fats and amino acids in blood samples.
The results suggest artificial sweeteners change how the body processes fat and gets its energy. In addition, they found acesulfame potassium seemed to accumulate in the blood, with higher concentrations having a more harmful effect on the cells that line blood vessels.
"We observed that in moderation, your body has the machinery to handle sugar; it is when the system is overloaded over a long period of time that this machinery breaks down," Hoffmann said. "We also observed that replacing these sugars with non-caloric artificial sweeteners leads to negative changes in fat and energy metabolism."
So, which is worse, sugar or artificial sweeteners? Researchers cautioned that the results do not provide a clear answer and the question warrants further study. It is well known that high dietary sugar is linked to negative health outcomes and the study suggests artificial sweeteners do, too.
"It is not as simple as 'stop using artificial sweeteners' being the key to solving overall health outcomes related to diabetes and obesity," Hoffmann added. "If you chronically consume these foreign substances (as with sugar) the risk of negative health outcomes increases. As with other dietary components, I like to tell people moderation is the key if one finds it hard to completely cut something out of their diet."
Brian Hoffmann will present this research on Sunday, April 22, from 10 a.m.-noon in the San Diego Convention Center Exhibit Hall (poster A322) (abstract). Contact the media team for more information or to obtain a free press pass to attend the meeting.
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About Experimental Biology 2018
Experimental Biology is an annual meeting that attracts more than 14,000 scientists and exhibitors from five host societies and more than two dozen guest societies. With a mission to share the newest scientific concepts and research findings shaping clinical advances, the meeting offers an unparalleled opportunity for exchange among scientists from across the U.S. and the world who represent dozens of scientific areas, from laboratory to translational to clinical research. http://www. experimentalbiology. org #expbio
About the American Physiological Society (APS)
APS is a nonprofit organization devoted to fostering education, scientific research and dissemination of information in the physiological sciences. The Society was founded in 1887 and today represents more than 10,500 members and publishes 14 peer-reviewed journals. http://www. the-aps. org ||||| Artificial sweeteners may have zero calories, but do they offer zero additional risk for developing diabetes? Well, if you attended a presentation at the Experimental Biology 2018 conference in San Diego, you may say, rats, the risk may be far from zero.
To be fair, nothing has zero health risk. Even though eating broccoli in general is quite healthy, you could still bludgeon yourself with broccoli, and eating huge amounts of broccoli could lead to obesity as well as some serious gas and loss of friends. However, the main advertised benefit of artificial sweeteners, such as those in diet soda, is that they don't contain the calories and the accompanying obesity, diabetes, and other health-related risks of sugar.
The study presented by Brian Hoffmann, George Ronan, and Dhanush Haspula from the Medical College of Wisconsin suggested that things may not be that sweet for artificial sweeteners. They did a combination of in vitro (which essential means inside a test tube or similar equipment) and in vivo (meaning in a live animal) experiments using rats that were specially designed to be more susceptible to developing diabetes. For the in vitro experiments, the research team placed cells from the inside lining of the rats' small blood vessels into test tubes and exposed these cells to either sugar or a common artificial sweetener. Why the inside lining of blood vessels? Well, one of the effects of diabetes is to cause damage to small blood vessels, which then results in many of the complications of diabetes such as loss of eyesight, kidney function, and blood circulation to various parts of the body.
The in vitro experiments found that both sugars and artificial sweeteners interfered with glycosylation, a key step in which sugars are added to proteins that then affects how the proteins function. Therefore, messing up glycosylation could affect a number of functions that various proteins perform in the cells. The research team did find that sugar and artificial sweeteners seemed to affect the expression of different genes differently, which implies that the way that they affect glycosylation may be different. Nonetheless, the fact that both disrupt this key biochemical process raises concerns.
The second in vivo part of the study involved dividing rats into separate groups and feeding each group high doses of either a sugar (glucose or fructose) or an artificial sweetener (aspartame or acesulfame potassium) for 3 weeks. They then took blood samples from the rats and found that both sugar and artificial sweeteners affected the concentrations of fat, amino acids, and other biochemicals in their blood. In other words, in just 3 weeks, both sugar and artificial sweeteners seemed to be disrupting the way fats and proteins were being processed.
In a press release, Hoffmann said, "Despite the addition of these non-caloric artificial sweeteners to our everyday diets, there has still been a drastic rise in obesity and diabetes. In our studies, both sugar and artificial sweeteners seem to exhibit negative effects linked to obesity and diabetes, albeit through very different mechanisms from each other."
Of course, this was a presentation at a scientific meeting rather than a peer-reviewed publication in a scientific journal. So we'll have to wait until a subsequent publication (assuming that it makes it through the scientific peer-review process for a respectable journal) provides more details about the experiments and results before more rigorously evaluating how well the study was done. Also, as I have said before, there are humans who are rats. But rats are not humans. What happens in a rat may stay in a rat. Meaning that humans may handle artificial sweeteners differently. Moreover, the study showed changes that may be related to eventually developing diabetes but did not yet prove that the rats would develop diabetes. Running the experiment for longer periods of time may help offer better proof. ||||| Photo: CorrieMiracle (Pixabay)
For as long as artificial sweeteners have existed, people have been warned about their supposed health risks such as cancer and multiple sclerosis. But while these claims are routinely debunked as nothing more than junk science, some research—including a new study presented this week at the annual Experimental Biology conference—is beginning to indicate that sweeteners could actually contribute to health problems like type 2 diabetes.
Researchers at the Medical College of Wisconsin and Marquette University used rats vulnerable to developing diabetes for their experiments. For three weeks, different groups were fed high doses of two sugars, glucose and fructose, and two common artificial sweeteners, aspartame and acesulfame potassium. They then studied the rats’ blood using a large-scale technique that tracks minute metabolic changes, known as metabolomics.
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“Just after three weeks of giving these sweeteners and sugars to our diabetes-susceptible rats, we saw biochemical changes in the blood that could potentially lead to alterations in fat and energy metabolism,” lead author Brian Hoffman, a biomedical engineer at both institutions, told Gizmodo.
Diabetes is what happens when our bodies become unable to maintain proper glucose levels in the body—a process that’s largely regulated by the hormone insulin. This breakdown causes people to either stop responding to insulin as easily as they once did, or to stop producing insulin altogether. Excessive sugar in our diets is thought to help cause diabetes by overtaxing the body’s insulin-producing machinery, since it’s used to bring high blood glucose levels back to normal.
Because of that, artificial sweeteners have long been advertised as a way for people to eat treats and soft drinks safely and lose weight, without raising the risk of diabetes. But rates of diabetes and obesity have continued to skyrocket regardless, even as sweetener-rich foods and drinks became widely available starting in the 1950s. (There are currently six FDA-approved artificial sweeteners.)
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As a result, Hoffman and his team have not only tried to understand how sugar sparks the chain of events that leads to diabetes, but also tried to suss out whether sweeteners could do the same.
If sweeteners can raise our risk of diabetes, Hoffman says, they probably do it differently than sugar. Rather than overwhelming the body’s machinery, his and others’ research suggests, fake sugar wears it out. “Sweeteners kinda trick the body. And then when your body’s not getting the energy it needs—because it does need some sugar to function properly—it potentially finds that source elsewhere,” Hoffman said.
In the rats’ blood, his team found evidence of protein breakdown, likely meaning their bodies turned to burning away muscle as a source of energy. They also found higher levels of lipids and other fats, which over time could contribute to obesity and diabetes. Other research has suggested sweeteners alter the community of bacteria that call our guts home—the microbiome—in a way that could lead to harmful metabolic changes. And still more research has shown that diets high in artificial sweeteners are associated with a greater risk of diabetes and obesity.
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Hoffman is well aware of past efforts to tie sweeteners to dire health risks, but he says things are different in this case.
“Most of these sweeteners were approved well before we had the technology to perform studies like my lab is doing. So they weren’t able to look as in-depth at some of the potential effects being caused,” he said. “By knowing what biochemical changes these are causing through these large-scale studies, we can take a unbiased approach and see what’s changing to give us a better direction.”
Hoffman’s team plans to submit their current findings for consideration in several peer-reviewed journals, but they’re already in the middle of studying their sweetener-fed rats for longer periods of time. Future studies are likely to involve taking a peek at the rats’ microbiomes too. Ultimately, he believes their study method could be relatively easy to use with people, since all that would be needed is a blood sample to study small metabolic changes.
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In the meantime, though, he doesn’t necessarily want to scare anyone away from their diet drink habit.
“What I like to tell people is that most things in moderation are going to be fine. So if you enjoy your diet soda here and there, than have your diet soda here and there. If you like your normal soda here and there, have it here and there,” he said. “It’s when people start to chronically consume these—say, a person drinks two, three, four of [these drinks] everyday, that we should start to be concerned. Because you’re starting to introduce these biochemical changes and the body has no time to recover.”
[EB 2018]
Update: The American Beverage Association, a trade group that represents the non-alcoholic beverage industry, reached out to Gizmodo after this article was published, and offered this response to the study’s findings:
“Low-calorie sweeteners have been proven safe by worldwide government safety authorities as well as hundreds of scientific studies and there is nothing in this research that counters this well-established fact.” |||||
What is a summary? | – Guzzling diet soft drinks may seem like an easy workaround if you can't kick soda but want to fend off health problems spurred by sugar. A new study presented at the Experimental Biology conference over the weekend suggests otherwise—specifically when it comes to diseases like Type 2 diabetes. Gizmodo reports on research presented by Brian Hoffmann and his team, which carried out what a press release says is the largest study yet to follow the body's biochemical changes after consumption of both sugar and artificial sweeteners. For three weeks, scientists fed rats either high doses of fructose and glucose (two natural sugars), or the zero-calorie artificial sweeteners aspartame and acesulfame potassium. In the end, all the rats exhibited biochemical changes in their blood that are often seen as precursors to diabetes and obesity. Hoffmann notes sugars and artificial sweeteners appear to act differently on the body, though: Excess sugars likely overwhelm the system, while artificial sweeteners seem to change the metabolism of fat and energy. Forbes notes the study hasn't yet been peer-reviewed, no human studies have been done, and the research showed only changes that could lead to diabetes, not that the rats actually developed it. Meanwhile, Hoffmann doesn't want to scare anyone off their occasional indulgence. "If you enjoy your diet soda here and there, than have your diet soda here and there," he tells Gizmodo. "It's when people start to chronically consume these … that we should start to be concerned. Because you're starting to introduce these biochemical changes and the body has no time to recover." (Stroke and dementia may also result from too much diet soda.) | multi_news_1_0_0 |
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– If you've ever suffered a concussion, a new study suggests you may have a higher risk of developing Alzheimer's disease—or not. Mayo Clinic researchers performed brain scans on 141 people in their 70s and 80s who had memory problems and 448 who didn't. Some 18% and 17%, respectively, reported at one time suffering a brain injury in which they lost consciousness or memory. The latter group's scans came back normal, head injury or not. But the group with memory issues and a previous concussion were five times more likely to have an Alzheimer's-associated plaque buildup in the brain, the study author explains, per HealthDay News. Since both groups had the same rate of injury and only some showed a buildup of the protein beta amyloid, the findings show the link between head trauma and the plaque is complex and not all brain injuries lead to the disease. "If you do hit your head, it doesn't mean you are going to develop Alzheimer's," the study author says, but "it may increase your risk." A medical director agrees, and tells USA Today, "In my view, these findings are consistent with the idea that traumatic brain injury may lead to amyloid accumulation and Alzheimer's disease."
Article: |
Concussions Linked to Alzheimer's Risk in Study
Brain scans found seniors with both poor memory and prior head injury have more plaque buildup
WebMD News from HealthDay
WebMD News Archive
By Kathleen Doheny
HealthDay Reporter
THURSDAY, Dec. 26, 2013 (HealthDay News) -- Older adults with memory problems and a history of concussion have more buildup of Alzheimer's disease-associated plaques in the brain than those who also had concussions but don't have memory problems, according to a new study.
''What we think it suggests is, head trauma is associated with Alzheimer's-type dementia -- it's a risk factor," said study researcher Michelle Mielke, an associate professor of epidemiology and neurology at Mayo Clinic Rochester. "But it doesn't mean someone with head trauma is [automatically] going to develop Alzheimer's."
Her study is published online Dec. 26 and in the Jan. 7 print issue of the journal Neurology.
Previous studies looking at whether head trauma is a risk factor for Alzheimer's have come up with conflicting results, she noted. And Mielke stressed that she has found only a link or association, not a cause-and-effect relationship.
In the study, Mielke and her team evaluated 448 residents of Olmsted County, Minn., who had no signs of memory problems. They also evaluated another 141 residents with memory and thinking problems known as mild cognitive impairment.
More than 5 million Americans have Alzheimer's disease, according to the Alzheimer's Association. Plaques are deposits of a protein fragment known as beta-amyloid that can build up in between the brain's nerve cells. While most people develop some with age, those who develop Alzheimer's generally get many more, according to the Alzheimer's Association. They also tend to get them in a predictable pattern, starting in brain areas crucial for memory.
In the Mayo study, all participants were aged 70 or older. The participants reported if they ever had a brain injury that involved loss of consciousness or memory.
Of the 448 without any memory problems, 17 percent had reported a brain injury. Of the 141 with memory problems, 18 percent did. This suggests that the link between head trauma and the plaques is complex, Mielke said, as the proportion of people reporting concussion was the same in both groups.
Brain scans were done on all the participants. Those who had both concussion history and cognitive [mental] impairment had levels of amyloid plaques that were 18 percent higher than those with cognitive impairment but no head trauma history, the investigators found. ||||| Having a serious concussion could be a risk factor for developing Alzheimer's decades later – though not everyone with head trauma will lose their memory, a new study suggests.
PET scan of a brain in the early stages of Alzheimer's disease. (Photo: Gary Small, UCLA School of Medicine) Story Highlights Study shows link among those who had head injuries and later had memory problems
Scientists say more research needed to understand the relationship
Brain scans measure buildup of protein called beta amyloid
Having a serious concussion could be a risk factor for developing Alzheimer's decades later – though not everyone with head trauma will lose their memory, a new study suggests.
A team from the Mayo Clinic in Rochester Minn., conducted brain scans on 448 older Minnesotans who had no signs of memory problems and 141 who did. Roughly 17% in both groups had had a brain injury earlier in life involving some loss of consciousness or memory.
Those who had no signs of memory problems had normal brain scans, regardless of their history of brain injury. Scans of those with memory problems and a history of brain injury were five times more likely to show a buildup of a brain protein long associated with Alzheimer's Disease, says study author Michelle Mielke, an associate professor of epidemiology and neurology at the Mayo Clinic.
The study, published online today in the journal Neurology, examined people in their 70s and 80s who reported having an earlier head trauma – in most cases 50 or 60 years earlier when they were adolescents. In those days, only the sickest people went to the doctor, so the head injuries were probably quite significant, Mielke says.
This is one of the first studies to take advantage of new technology, allowing brain scans to measure the buildup of a protein called beta amyloid, long associated with Alzheimer's. Most previous studies of the connection between Alzheimer's and head injury had looked only at cadavers.
"In my view, these findings are consistent with the idea that traumatic brain injury may lead to amyloid accumulation and Alzheimer's disease," says Richard Lipton, director of the Division of Cognitive Aging and Dementia and the Montefiore Headache Center at Albert Einstein College Of Medicine in New York City.
More research is needed, he cautions, to help explain how one causes the other. "To more fully explore the causal links, we need not just brilliant snapshots but the movies which track brain changes and cognitive changes over time."
For people worried about their own head injuries, the study provides some comfort, Lipton says. Both groups of older adults – impaired and normal – had the same rate of head injury. So, clearly, not every head injury leads to Alzheimer's disease, he says.
Most head injuries are accidents and therefore unavoidable, though helmets and seat belts can make a difference in some cases.
Lipton says he hopes that learning more about the connection between head injury and Alzheimer's will lead to interventions to protect injured brains from long-term damage. "Drugs that block the development of amyloid or increase its removal from the brain may help protect persons with traumatic brain injury from Alzheimer's disease, though that has not been demonstrated," he says.
Until then, the best strategy is to minimize known risk factors for Alzheimer's – high blood pressure, diabetes and high cholesterol – by eating a healthy Mediterranean diet and exercising both mind and body, he says. ||||| | multi_news_1_0_0 |
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Image copyright Getty Images
Open heart surgery appears to be safer in the afternoon because of the body's internal clock, scientists have said.
The body clock - or circadian rhythm - is the reason we want to sleep at night, but it also drives huge changes in the way our bodies work.
The research, published in the Lancet, suggests the heart is stronger and better able to withstand surgery in the afternoon than the morning.
And it says the difference is not down to surgeons being tired in the morning.
Doctors need to stop the heart to perform operations including heart valve replacements. This puts the organ under stress as the flow of oxygen to the heart tissue is reduced.
The doctors and researchers looked for complications including heart attacks, heart failure or death after surgery. They found:
54 out of 298 morning patients had adverse events
28 out of 298 afternoon patients had adverse events
Afternoon patients had around half the risk of complications
One major event would be avoided for every 11 patients operated on in the afternoon
One of those involved in the research, Prof Bart Staels, from the Institut Pasteur de Lille, told the BBC News website: "We don't want to frighten people from having surgery - it's life saving."
He also said it would be impossible for hospitals to conduct surgery only after lunch.
But Prof Staels added: "If we can identify patients at highest risk, they will definitely benefit from being pushed into the afternoon and that would be reasonable."
Obesity and type 2 diabetes have been shown to increase the risk of complications after surgery.
Heart health is already known to fluctuate over the course of a day.
The risk of a heart attack or stroke is highest first thing in the morning, while the heart and lungs work at their peak in the afternoon.
Dr John O'Neill, from the UK Medical Research Council's Laboratory of Molecular Biology, said: "Scientifically it is not hugely surprising, because just like every other cell in the body, heart cells have circadian rhythms that orchestrate their activity.
"Our cardiovascular system has the greatest output around mid/late-afternoon, which explains why professional athletes usually record their best performances around this time."
Other possible explanations for the findings included surgeons being tired in the morning or their own body clock affecting their surgical skill, particularly if they are not "morning people".
But Prof Staels said the researchers had gone to great lengths to show that the difference in survival rates was not down to the surgeons.
The French team also experimented on cardiac tissue samples from patients and showed they beat more readily in the afternoon.
And an analysis of the DNA in the samples found 287 genes whose activity showed a circadian rhythm - waxing and waning during the day.
They then moved into mice and used experimental drugs to alter the activity of one of those genes and seemed to be able to reduce the risk of death.
Prof Staels said: "We believe we have identified a potential way to circumvent the disturbing observation that operations in the morning lead to more complications."
However, that will require more research to confirm.
The researchers are also investigating whether circadian rhythms have an impact on survival in other types of surgery.
Dr Mike Knapton, from the British Heart Foundation, said: "Thousands of people now have open heart surgery in the UK. If this finding can be replicated in other hospitals this could be helpful to surgeons planning their operating list, for non-urgent heart surgery.
Follow James on Twitter. ||||| Nobody wants to have open heart surgery. But if you do, you want to have it in that afternoon.
That's the conclusion of a major new study that found there is a significantly higher risk of damage for people having surgery in the morning.
And it's all because of the body clock, or circadian rhythms, which help keep us regulated through the day. It decides when we wake up, sleep and eat – and how ready we are to recover from major surgery.
The new study, published in the Lancet, found that there are almost 300 genes that link the body clock to heart damage.
And it found that there is a link between a person's body clock and how at risk they are of undergoing heart damage and major events like heart attacks after having heart surgery.
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17/20 Earth could be at risk of meteor impacts Earth could be in danger as our galaxy throws out comets that could hurtle towards us and wipe us out, scientists have warned. Scientists have previously presumed that we are in a relatively safe period for meteor impacts, which are linked with the journey of our sun and its planets, including Earth, through the Milky Way. But some orbits might be more upset than we know, and there is evidence of recent activity, which could mean that we are passing through another meteor shower. Showers of meteors periodically pass through the area where the Earth is, as gravitational disturbances upset the Oort Cloud, which is a shell of icy objects on the edge of the solar system. They happen on a 26-million year cycle, scientists have said, which coincide with mass extinctions over the last 260-million years
18/20 Genetically-engineered, extra-muscular dogs Chinese scientists have created genetically-engineered, extra-muscular dogs, after editing the genes of the animals for the first time. The scientists create beagles that have double the amount of muscle mass by deleting a certain gene, reports the MIT Technology Review. The mutant dogs have “more muscles and are expected to have stronger running ability, which is good for hunting, police (military) applications”, Liangxue Lai, one of the researchers on the project. Now the team hope to go on to create other modified dogs, including those that are engineered to have human diseases like muscular dystrophy or Parkinson’s. Since dogs’ anatomy is similar to those of humans’, intentionally creating dogs with certain human genetic traits could allow scientists to further understand how they occur
19/20 Researchers discover 'lost world' of arctic dinosaurs Scientists say that the new dinosaur, known as Ugrunaaluk kuukpikensis, “challenges everything we thought about a dinosaur’s physiology”. Florida State University professor of biological science Greg Erickson said: “It creates this natural question. How did they survive up here?”
20/20 A team of filmmakers in the US have made the first ever scale model of the Solar System in a Nevada desert Illustrations of the Earth and moon show the two to be quite close together, Mr Overstreet said. This is inaccurate, the reason being that these images are not to scale.
Study author Professor David Montaigne, University of Lille, France, said: "Our study found that post-surgery heart damage is more common among people who have heart surgery in the morning, compared to the afternoon.
"Our findings suggest this is because part of the biological mechanism behind the damage is affected by a person's circadian clock and the underlying genes that control it.
"As a result, moving heart surgery to the afternoon may help to reduce a person's risk of heart damage after surgery."
Researchers looked at the medical records of 596 people who had heart valve replacement surgery including half who had surgery in the morning, half in the afternoon.
They checked for any major cardiac events such as a heart attack, heart failure or death from heart disease in this research which took place between January 2009 to December 2015.
They found that 28 out of 298 afternoon patients had adverse events while 54 out of 298 morning patients experienced such events.
The researchers suggest this could equate to one major event being avoided for every 11 patients who have afternoon surgery and that people who had surgery in the afternoon had a 50% lower risk of a major cardiac event, compared with people who had surgery in the morning.
The team also tracked the health of 88 patients who were randomly scheduled for heart valve replacement surgery in the morning or afternoon between January 2016 to February 2017.
Those who had afternoon surgery had lower levels of heart tissue damage after surgery, compared with morning surgery patients, according to the researchers.
Tests on heart tissue samples from 30 of the patients - including 14 who had morning surgery and 16 from the afternoon surgery group - showed that the afternoon surgery samples more quickly regained their ability to contract when put in conditions similar to the heart refilling with blood.
Genetic analysis of these samples also showed that 287 genes linked to the circadian clock were more active in the afternoon surgery sample.
The researchers believe this suggests the heart is subject to the body's circadian clock and the post-surgery results highlight that the heart is maybe weaker at repairing in the morning than in the afternoon.
Larger trials are need to test the findings.
Professor Michel Ovize, Hopital Louis Pradel, France, said the scientists have "clearly shown that circadian rhythm is of clinical importance in aortic valve replacement surgery" but that more research is needed.
He added: "Even before we have drugs available to regulate the circadian clock, one might propose that high-risk patients should preferentially be operated on in the afternoon."
Additional reporting by agencies |||||Summary:
| – Should you ever need heart surgery, it might be worth pressing for an afternoon appointment. New research in the Lancet finds patients who undergo morning heart surgery are twice as likely to suffer heart issues and other complications as patients who have surgery in the afternoon, per the BBC. It's not that doctors are drowsy in the morning and therefore prone to mistakes. Rather, researchers say the body's circadian rhythm regulates genes that are in top form and better able to handle stress in the afternoon, a fact that also explains why one's risk of heart attack is highest in the morning. To discover this, researchers conducted several studies, one monitoring 596 patients who underwent an aortic valve replacement, half in the morning, half in the afternoon. After 17 months, they found 18% of morning patients had suffered a major adverse cardiac event, acute heart failure, cardiovascular death, or a heart attack during the operation, compared to 9% of afternoon patients. Morning patients also had twice the risk of other complications, per the study, which identified 287 genes linking the body clock to heart health, reports the Independent. A second study also found morning patients had significantly higher levels of troponin, a measure of heart damage, per the New York Times. This doesn't mean morning surgeries should be avoided, but "we should identify patients at high risk for complications—those with diabetes or other metabolic risks, for example—and operate on those in the afternoon," a study author tells the Times. | multi_news_1_0_0 |
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Your Health
People Have Misconceptions About Miscarriage, And That Can Hurt
i Illustration Works/Corbis Illustration Works/Corbis
Most people think a miscarriage is rare, and many believe that if a woman loses a pregnancy that she brought it upon herself. Neither of those things is true, but the enduring beliefs cause great pain to women and their partners.
In fact, almost half of people who have experienced a miscarriage or whose partner has had one feel guilty, according to a survey to be published Monday in Obstetrics & Gynecology. More than a quarter of them felt shame. Many felt they'd lost a child.
"It's irrational, but there is such a deep shame attached to not being able to carry a baby to term.... I don't want another baby, I want THIS baby."
When NPR asked visitors to its Facebook page to tell us what they wished people knew about miscarriage, the response was overwhelming — 200 emails and counting, many heartbreaking. Their sentiments often echoed what the survey found.
"I wish people knew how much it's possible to miss a person you have never met, and to mark time by their absence," wrote one woman. "I will always think about how old my baby would be now and what our lives would be like if I hadn't lost the pregnancy."
The survey came about after Dr. Zev Williams realized that many of his patients had misconceptions about miscarriage. "I'd tell them how common a miscarriage was, and they seemed shocked," says Williams, an OB-GYN who directs the Program for Early and Recurrent Pregnancy Loss at Einstein College of Medicine of Yeshiva University and Montefiore Medical Center in New York.
In fact, between 15 percent and 20 percent of clinically recognized pregnancies end in miscarriage, defined as a pregnancy loss earlier than 20 weeks of gestation. (Pregnancy loss after that point is called a stillbirth.) Miscarriage is actually "by far the most common complication of pregnancy," says Williams. He and his colleagues wanted to find out how widespread some of the mistaken beliefs about miscarriage are.
They asked 1,084 adults about miscarriage and its causes. They also asked the 15 percent of survey respondents who had suffered a miscarriage, or whose partner had, about their experience. The results echoed what he'd seen in his patients: Some 55 percent of all respondents believed that miscarriage occurred in 5 percent or less of all pregnancies.
"I felt, and feel, literally broken, and betrayed by my body."
The cultural silence around miscarriage contributes to those misunderstandings, Williams says. "A lot of other conditions that people used to speak of only in hushed tones, like cancer and AIDS, we speak about a lot more," he says.
Not so for miscarriage. Because early pregnancy loss is so common, women are often advised not to share their pregnancy news with friends and family until the start of the second trimester. At that point the chance of miscarriage has drastically declined. But that secrecy means women who do miscarry in the first trimester may not get the support they need, Williams says.
"It's bizarre that the topic is so taboo," wrote one reader on Facebook. "I really feel an obligation now, having had a miscarriage, to mention my miscarriage when I'm talking about fertility or the process of conceiving or childbirth." She added a sentiment that many other women expressed: "I felt alone until I realized there is this big, secret miscarriage club — one that nobody wants to be a member of — and when I realized it existed, I felt angry that no one told me they had active membership."
"Many women in my family had suffered one or more, and I had no idea until I had one myself."
Chromosomal abnormalities in the fetus cause 60 percent of miscarriages. A handful of other medical conditions are also known to cause miscarriage. Most survey respondents knew that genetic or medical problems were the most common cause of early pregnancy loss. But they also mistakenly believed that other factors could trigger a miscarriage: a stressful event (76 percent); lifting something heavy (64 percent); previous use of contraception like an IUD (28 percent) or birth control pills (22 percent); and even an argument (21 percent). Some 22 percent believed that lifestyle choices, like using drugs, tobacco or alcohol, were the single biggest cause of miscarriages. That's not true.
Those who shared their experiences with NPR said many of those myths were repeated back to them by friends, family or colleagues after their own miscarriages. One said someone blamed her high heels. That kind of talk can be incredibly painful, even if you know you have the facts on your side.
"I felt alone until I realized there is this big, secret miscarriage club — one that nobody wants to be a member of — and when I realized it existed, I felt angry that no one told me they had active membership."
"I wish people understood that miscarriages are the flip side of the coin," wrote one woman. "If you've had a healthy pregnancy that went full term — you won a lottery. Short of obvious substance abuse and bull riding — your healthy baby is not the result of anything you did or didn't do. As much as you want to think you are in control — you aren't. And the same goes when I lost each pregnancy — as much as I wish I could have been — it was not in my control."
The feelings of guilt, shame and enormous loss reported in the survey were a common theme among those who told their stories to NPR. "I felt, and feel, literally broken, and betrayed by my body," wrote one woman. "It's irrational, but there is such a deep shame attached to not being able to carry a baby to term.... I don't want another baby, I want THIS baby, the one I thought I would have, the one I started planning for, hoping for, dreaming about, talking to. All that got taken away from me."
Not everyone was so deeply affected; some said the miscarriage came as a relief, either because the pregnancy was unwanted, or because they'd known something wasn't quite right. Or they said it was painful at the time, but that they'd moved on and weren't particularly haunted by the loss. "You have every right to feel ALL of your emotions you have," wrote one person. "Whether you feel grief or relief, your emotions are never wrong."
But because the loss can be so great, people said they wished others would acknowledge a miscarriage without reverting to a laundry list of well-intentioned but hurtful lines: "Well, at least you know you can get pregnant." (One reader said this was particularly upsetting after her seventh miscarriage.) "You can always try again." "If you adopt, you'll get pregnant." "It happens for a reason." "It's God's plan." (That, wrote another reader, sounds an awful lot like "God doesn't want you to be a parent.")
My husband "had hopes and dreams and fears and so much joy tied up into 9.5 weeks of cells."
Far better, people said, is to simply say, "I'm sorry. Is there anything I can do for you?"
Over and over again, we heard a wish that there was more private and public discussion of miscarriage. "Many women in my family had suffered one or more, and I had no idea until I had one myself," wrote one woman. "I felt that no one I knew had gone through this."
Several readers said this code of silence was even stronger for the partners of women who miscarry. One reader wrote that her husband "had hopes and dreams and fears and so much joy tied up into 9.5 weeks of cells," but he didn't get time off work, flowers or well-wishes from colleagues or visits from friends to "listen to him cry," as she did. Instead, "He had to suffer alone."
The new survey found that 46 percent of respondents who'd miscarried said they felt less alone when friends talked about their own miscarriages. Even a celebrity's disclosure of miscarriage helped.
"I wish people knew how much it's possible to miss a person you have never met, and to mark time by their absence."
One person who recently suffered a miscarriage summed it up: "While I'm definitely still healing emotionally, I would be happy to talk more about it. So many people grieve silently, but I've found that talking really helps the most."
That's the kind of conversation that Williams says he and his co-authors would like to spark with their survey. "Miscarriage is ancient. It's always been there." And all too often, he says, "people often blame themselves and don't discuss it." ||||| Miscarriages are common, but the majority of Americans still think they occur rarely, a new survey finds.
The nationwide online survey found that 55 percent of people in the United States believe that miscarriage happens in 5 percent or less of all pregnancies. But in reality, miscarriages end 15 to 20 percent of reported pregnancies, according to the researchers.
Miscarriage myths affect more than just people in the United States; they are a universal problem, said the study's senior author, Dr. Zev Williams, the director of the Program for Early and Recurrent Pregnancy Loss at the Albert Einstein College of Medicine and Montefiore Health System in New York City. [Blossoming Body: 8 Odd Changes That Happen During Pregnancy]
People tend to treat miscarriage as a taboo subject, and many women blame themselves for losing a pregnancy, Williams said.
"I've taken care of sisters who didn't know that each of them were having recurrent miscarriages," because they didn't tell each other, Williams told Live Science. "But you don't see that with anything else. I ask for family histories, so everyone knows when their family has heart disease, diabetes and Alzheimer's. But miscarriages, people don't talk about them."
Here's a look at five lessons about miscarriages doctors and the public could learn, based on what the researchers found to be common misconceptions about miscarriages in their survey, set to be published on Monday (May 11) in the journal Obstetrics & Gynecology.
1. Miscarriages are common
In reality, about 1 out of 5 pregnancies, or between 750,000 and 1 million pregnancies yearly in the United States, end in miscarriage.
But according to the survey, 10 percent of participants said they thought that fewer than 2 percent of all pregnancies ended in miscarriage.
This misconception was 2.5 times more common among men than women, the researchers found.
One possible reason many people hold such mistaken beliefs is that few people talk about miscarriages, Williams said.
2. People don't understand its causes
The majority of miscarriages happen for medical or genetic reasons. For instance, about 60 percent of miscarriages occur because of aneuploidy, which is the presence of an incorrect number of chromosomes. Other causes can be related to the mother's health conditions, such as whether there are structural abnormalities in the uterus, or if she has an endocrine disorder or an autoimmune disorder.
But 22 percent of the survey participants incorrectly said that lifestyle choices, including drug, alcohol or tobacco use during pregnancy, were the single most common causes of miscarriage, the researchers found. Men were 2.6 times more likely to think this than women, the study found.
People also falsely attributed miscarriages to other factors. For instance, the majority of participants said that a stressful event (76 percent) or longstanding stress (74 percent) could cause a miscarriage.
A large number of participants said that a miscarriage could be caused by lifting a heavy object (64 percent of respondents), having a sexually transmitted disease in the past (41 percent), using an intrauterine device in the past (28 percent), using oral contraception in the past (22 percent) or getting into an argument (21 percent), the researchers found.
None of these factors cause miscarriages, the researchers said. [5 Myths About Fertility Treatments]
Williams said he treated one patient who said that, while pregnant, she had doubts about whether she'd be a good mother. "She miscarried a couple of days later" and was tormented by the thought that she miscarried because she "didn't want it enough," he said. In reality, there is no way that such thoughts could bring on a miscarriage.
3. Miscarriages make people feel guilt and shame
About 15 percent of the survey participants said they had been personally affected by miscarriage, and these participants answered additional questions about their experience, the researchers said.
Among those affected by a miscarriage, 47 percent said they felt guilty, 41 percent said they felt like they did something wrong, 28 percent reported feeling ashamed, and 38 percent said they felt like they could have prevented it somehow, the researchers found.
Most of them (57 percent) were not told what might have caused the miscarriage. Some were told, "It just happens," or "We don't know."
But knowing the possible cause can be helpful, the researchers wrote. A majority of respondents, 88 percent, said they would want to know the cause, even if it wasn't something they could have prevented, the researchers found.
Among the people who were given a reason for the miscarriage, 19 percent fewer felt as if they were to blame, compared to those who were not given a reason, the researchers found.
4. People who miscarry need support
Even among people who haven't miscarried, more than one-third said that a pregnancy loss would be "extremely upsetting, equivalent to the loss of a child," the researchers found.
Of the people who miscarried, 74 percent said they received emotional support from the people they told, but only 45 percent said the medical community had provided adequate emotional support.
Celebrities can also help. Of survey participants who miscarried, 28 percent said that public figures who shared their miscarriage stories, including Ann Romney, the wife of former presidential candidate Mitt Romney, and actress Gwyneth Paltrow, helped ease their feelings of isolation, the study found.
However, friends helped even more. When a friend revealed a miscarriage, 46 percent of study participants said they felt less isolation after their own miscarriages.
"When people start talking about it, it has a very positive effect," Williams said.
5. More awareness is needed
Few people advocate for greater public awareness of miscarriage because the topic can be emotionally difficult to discuss, Williams said.
"Because it's such a taboo subject, you don't see advocacy for it, you don't see these support groups, you don't see people lobbying Congress to get more funding," he said. "And so research in miscarriage is dwarfed by all of these other conditions, even in women's health."
Even doctors may unknowingly discourage open discussion.
"When a woman does become pregnant, we tell them keep it quiet," he said. "The subtext to that is you might miscarry, and you don't want people to find out about it."
Follow Laura Geggel on Twitter @LauraGeggel. Follow Live Science @livescience, Facebook & Google+. Original article on Live Science. |||||
Summary: | – For all its prevalence, miscarriage remains stubbornly taboo. So says Dr. Zev Williams, an OB-GYN and director of the Program for Early and Recurrent Pregnancy Loss at the Einstein College of Medicine of Yeshiva University and Montefiore Medical Center in New York. He set out to learn about the misconceptions that fill the silence, and in a survey of 1,084 adults published today in the journal Obstetrics & Gynecology, he learned that most Americans think miscarriage occurs in just 1 in 20 pregnancies—and men are 2.5 times more likely to think they're as rare as 1 in 50. In reality, 1 out of every 4 or 5 pregnancies actually end in miscarriage. "I've taken care of sisters who didn't know that each of them were having recurrent miscarriages" because they didn't tell each other, Williams tells LiveScience. Another major myth is that women cause miscarriages (e.g., via stress, lifting heavy objects, drinking, even having an argument or negative thoughts), and 22% of respondents believed lifestyle choices like drug use are the biggest cause. (Most miscarriages—60%—are caused by chromosomal abnormalities.) Guilt is a common reaction. "I felt, and feel, literally broken, and betrayed by my body," one woman wrote to NPR. "It's irrational, but there is such a deep shame attached to not being able to carry a baby to term." Among the survey respondents who've miscarried, nearly half said they felt less alone when friends talked about their own miscarriages. People "often blame themselves and don't discuss it," Williams said, but "miscarriage is ancient. It's always been there." (In El Salvador, one miscarriage was considered murder.) | multi_news_1_0_0 |
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Here is a news article: EMBED More News Videos This may be the most intense video you will see all day.
EMBED More News Videos A passenger told ABC13 people were pretty upset after a woman's outburst on a Spirit Airlines flight.
EMBED More News Videos Passenger describes woman's outbursts on Spirit Airlines flight from Houston.
EMBED More News Videos Woman detained after outburst on Spirit flight from Houston
A woman was taken off a Spirit Airlines flight from Houston after she had a mid-flight meltdown.Eyewitness video taken by passenger Chianti Washington shows the woman pacing frantically up the aisle of the Minneapolis-bound plane, screaming hysterically.During the intense one-minute, 20-second video, the woman curses, makes threats involving her brothers, and acts erratically before a plane full of stunned passengers."Get me the f*** off this (long string of expletives) plane!" the woman screams. "You want to be (expletive) and b**chy to me? You'll see me f***ing pissed."At one point, when a male passenger stands up to block the woman from getting to the front of the plane, she shakes her fist at the man before lashing out again."Do you know who my brothers are? They are f***ing Marine snipers. Do you want to f*** with a f***ing Marine?" she screams, before pushing her way toward the cockpit.In the video, passengers can be heard praying, consoling each other, some audibly in distress by the unsettling incident."Do you want to know what hell is? I've (expletive) been there 10 (expletive) times!" the woman continues to shout.According to authorities, the woman became irate after the flight landed in Rochester, Minnesota, due to a medical issue.A passenger who became ill was taken off the aircraft before the outburst. She was taken into custody, screaming while being escorted off by police.It was not immediately known if the woman had any relation to the sick passenger.Spirit Airlines released the following statement to ABC13 about the incident: ||||| HOUSTON – After a Spirit Airlines flight from Bush Intercontinental Airport made an emergency landing in Rochester, Minn., a passenger became enraged.
Watching and recording from Row 14 of Spirit Airlines flight 346, Stephanie Calder all but panicked herself. She was afraid of an irate fellow passenger’s erratic outburst over an unexpected delay.
“I was thinking I need to protect my 15-year-old daughter (who was headed to Detroit for a volleyball tournament),” Calder said. “I (was just) worried (the angry passenger was) going to go even more irate and so I just put my back toward my daughter and shielded my daughter in case this woman decided to. I was one row behind the emergency exit door. Now, we were landed but who knows what this woman could have done.”
Their flight left Houston around 8 a.m. headed for Minneapolis. The Calder’s had a connecting flight to Michigan. However, about an hour after takeoff their plane diverted to Rochester, Minnesota because a man near the front of the plane needed a doctor.
“The attendant thought that he was just sleeping but he was actually in a coma,” Calder said.
When the plane landed, paramedics had to call police for back up.
“All of a sudden that’s where the lady came running from the back of the plane,” Calder said. “She started saying she’s not going to calm down and wanted off the plane and such.”
Police sent that passenger to a hospital for mental health evaluation after they were told she is a military veteran battling PTSD.
“That saddens me,” Calder said. “Now looking back at it all you just wish there was somebody on that plane (who) could have helped at that moment.”
Along with the man needing a doctor a third passenger got off the plane in Rochester, police said. That passenger was upset with how the airline handled the woman’s situation.
“This morning a flight from Houston to Minneapolis had to land in Rochester, Minnesota due to a Guest experiencing a medical emergency,” Derek Dombrowski, spokesman for Spirit Airlines said in a statement. “On the ground in Rochester, another passenger became erratic and irate and was removed from the aircraft with the assistance of law enforcement. We apologize to our guests who had to witness this and for the inconvenience of the delay. Safety (is) our top priority at Spirit Airlines.”
© 2018 KHOU ||||| The passenger who took and posted the video, Chianti Washington, tells KSTP the woman started acting out after EMT's took the medical patient off the plane. She says the woman started "being irate" about 5 minutes later. Washington says at first she thought the woman was just a disgruntled passenger, but soon realized there was a legitimate issue, which put her and other passengers in fear.
A short time later, Rochester Police returned to the flight for another passenger who wanted to get off. The passenger told police she didn't agree with how Spirit Airlines had treated the woman.
Spirit Airlines released a statement to ABC News, saying in part that it apologizes to guests and that safety is its top priority.
Police said the passenger who suffered the diabetic reaction was taken to the hospital for further treatment. |||||
A summary of this is? | – A female passenger became enraged after a Spirit Airlines flight had to divert for a medical emergency Monday, and she was caught on video screaming to be let off the plane before ultimately being escorted off the plane by police, ABC 13 reports. Flight 346 took off from Houston heading for Minneapolis, but after a male passenger was discovered to be unconscious, the plane made an emergency landing in Rochester, Minn., KHOU reports. In video shot by fellow passengers, the woman can be seen storming up and down the aisle of the plane shouting, among other things, "Get me the f--- off this f---ing plane" and "Do you know who my brothers are? They are f---ing Marine snipers. Do you want to f--- with a f---ing Marine?" The man had already been taken off the plane for medical attention at the time, and the woman was eventually escorted off by police officers and taken to a hospital for a mental health evaluation. She ultimately made other arrangements to get home. A fellow passenger says the woman told him she is a military veteran with PTSD, and she reportedly told police she was traveling alone for the first time and panicked. Police say a third passenger, who was reportedly upset with the way the woman's situation was handled, also exited the plane in Rochester. As for the male passenger, his current condition was not being reported, but KAAL reports he was having a diabetic reaction and was taken to a nearby hospital for treatment. | multi_news_1_0_0 |
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– The CDC is out with its first report on mental disorders and kids, and the bottom line is a pretty heavy one: 13% to 20% of kids between ages 3 and 17 now suffer from a mental disorder, per the AFP. And that has costly implications: The disorders spur $247 billion in medical, special ed, and juvenile justice costs every year, says the report, which defines said disorders as "serious deviations from expected cognitive, social, and emotional development." The report noted such diagnoses are on the rise, a determination made after reviewing data spanning from 1994 to 2011. Authors didn't offer a definitive explanation for the increase in prevalence, but said improved diagnosis and "public perception" could be part of it, reports Reuters. ADHD was the most common disorder, affecting 6.8% of kids. Also on the list: behavioral conduct problems: 3.5% anxiety/phobias: 3% depression: 2.1% autism spectrum disorders: 1.1% Tourette syndrome: 0.2%
Let's expand this into a news article: NEW YORK Up to 20 percent of children in the United States suffer from a mental disorder, and the number of kids diagnosed with one has been rising for more than a decade, according to a report released on Thursday by the U.S. Center for Disease Control and Prevention.
In the agency's first-ever study of mental disorders among children aged 3 to 17, researchers found childhood mental illnesses affect up to one in five kids and cost $247 billion per year in medical bills, special education and juvenile justice.
Children with mental disorders - defined as "serious deviations from expected cognitive, social, and emotional development" - often have trouble learning in school, making friends, and building relationships later in life, the report said.
They are more likely to have other chronic health problems, such as asthma and diabetes, and are at risk for developing mental illnesses as adults.
"This is a deliberate effort by CDC to show mental health is a health issue. As with any health concern, the more attention we give to it, the better. It's parents becoming aware of the facts and talking to a healthcare provider about how their child is learning, behaving, and playing with other kids," Dr. Ruth Perou, the lead author of the study, told Reuters in an interview.
"What's concerning is the number of families affected by these issues. But we can do something about this. Mental health problems are diagnosable, treatable and people can recover and lead full healthy lives," Perou added.
The study cited data collected between 1994 and 2011 that showed the number of kids with mental disorders is growing. The study stopped short of concluding why, but suggested improvements in diagnoses as one possible explanation
"Changes in estimated prevalence over time might be associated with an actual change in prevalence, changes in case definition, changes in the public perception of mental disorders, or improvements in diagnosis, which might be associated with changes in policies and access to health care," the study said.
Perou told Reuters more research was needed to determine the specific causes of mental disorders, and that greater awareness could lead to an uptick in diagnoses. A host of environmental factors, including chemical exposure and poverty, can also affect a child's mental health, she said.
Lead, for example, is known to be "one of the biggest toxins to impact behavior and learning," Perou said. Poor children are at a higher risk for developing certain conditions, according to the study.
The most prevalent mental health diagnosis, as reported by parents, was Attention Deficit/Hyperactivity Disorder (ADHD), which affects 6.8 percent of children. Also common were behavioral conduct problems (3.5 percent), anxiety, which consists mostly of fears and phobias (3 percent), depression (2.1 percent) and autism spectrum disorders (1.1 percent). Many of these disorders occur together, the report said.
Boys were found more likely to have most of the listed disorders except for depression and alcohol abuse, which affect more girls.
The study also noted that suicide, which can be precipitated by an untreated mental illness, was the second leading cause of death (after accidents) among children 12 to 17 years old.
The CDC report was based on multiple other studies that collected data and interviewed children and their guardians about their diagnoses, habits, behaviors and other factors.
(Reporting by Atossa Araxia Abrahamian; Editing by Daniel Trotta and Bob Burgdorfer) ||||| Many US youth have mental disorder: CDC
WASHINGTON — As many as one-fifth of American children and teens suffer from a mental disorder such as anxiety or depression and the incidence of such ailments is rising, a study released Thursday said.
"A total of 13 percent to 20 percent of children living in the United States experience a mental disorder in a given year," according to the report examining the mental health of adolescents released by the Centers for Disease Control and Prevention (CDC).
The data, reported in the CDC's Morbidity and Mortality Weekly Report (MMWR), said mental problems among youth are "an important public health issue in the United States because of their prevalence, early onset, and impact on the child, family and community, with an estimated total annual cost of $247 billion."
The study found that the most prevalent mental ailment was Attention Deficit Hyperactivity Disorder (ADHD), which was found in 6.8 percent of the nation's youth, followed by behavioral or conduct problems (3.5 percent); anxiety (3.0 percent); depression (2.1 percent); autism spectrum disorders (1.1 percent); and Tourette syndrome (0.2 percent.
The data, which was compiled between 2005 and 2011, found that suicide was the second leading cause of death among adolescents aged 12 to 17 in 2010.
The report showed that boys were more likely than girls to have certain mental health ailments, including ADHD, autism spectrum disorders, anxiety, Tourette syndrome, and cigarette dependence.
Adolescent boys also were more likely than girls to die by suicide.
Adolescent girls, meanwhile, were more likely than boys to have depression or an alcohol use disorder.
The report called on health professionals to conduct "early diagnosis and appropriate treatment" to "better understand the impacts of mental disorders, inform needs for treatment and intervention strategies, and promote the mental health of children."
Copyright © 2013 AFP. All rights reserved. More » |||||
– It looks like Reese Witherspoon's hard work paid off. Critics and audiences alike are raving about Wild, a flick based on Cheryl Strayed's bestselling memoir about hiking 1,100 miles after the death of her mother and collapse of her marriage. Should Witherspoon prepare an Oscar speech? What the critics are saying: "Witherspoon uses her own undoubted discomfort with the physical demands of the role to make us feel Strayed’s predicament in our bones," writes Peter Rainer at the Christian Science Monitor. The film is broken up by flashbacks, as is Strayed's memoir, but here they "tend to dissipate rather than enhance Strayed's trek." Still, Witherspoon "may be bucking for another Oscar," Rainer writes. "Wild is a fierce path well-worth following," writes Claudia Puig at USA Today. It's "faithful to the book" and flaunts "stunning cinematography." Plus, "Witherspoon is terrific" as she "brings writer Strayed alive, with all her complexity, confusion and drive," Puig writes. "Her voice-over narration is evocative, sometimes heartbreaking." Wild is "like a physical, philosophical and moral odyssey jointly crafted by Nietzsche and John Muir," played out "against some of the most magnificent scenery on the planet," writes Andrew O'Hehir at Salon. Yet he's not totally feeling it. "The movie has a curiously unsticky and unmemorable quality," he writes. "It stops being a story of self-defining human freedom, and becomes instruction." Both Wild and Witherspoon deliver for Joe Morgenstern. Witherspoon gives "a sensational performance, by far the best one of her career," he writes at the Wall Street Journal. She not only carries a heavy backpack, she "carries the whole movie." However, he saw the flashbacks to rough sex and hard drugs as "interruptions."
| Let's expand this into a news article: The movie, based on Cheryl Strayed's memoir about hiking the Pacific Crest Trail, is broken up by flashbacks too much but Witherspoon makes us feel Strayed's predicament in our bones.
“Wild” is based on Cheryl Strayed’s passionately funny-sad, Oprah-approved, bestselling 2012 memoir, but it doesn’t come across as a “safe” project. Reese Witherspoon, who plays Strayed, may be bucking for another Oscar – and just to make sure we know it, she doesn’t wear any makeup – but, as Hollywood movies go, it’s fairly uncompromising.
The movie, like the book, employs a back-and-forth flashback structure to depict Strayed’s 1,100-mile solo hike on the Pacific Crest Trail from the Mojave Desert to Washington State, which she undertook in the summer of 1995 when she was 26 and despairing from the death of her mother (well played by Laura Dern) and a broken marriage. (Strayed legally changed her surname from Nyland in 1995.) The hike began impulsively, as a way to break off bouts of sex and heroin addiction, and turned into a grueling soul-searching lasting more than three months.
Jean-Marc Vallée (“Dallas Buyers Club”), directing from a script by Nick Hornby, begins the movie right in the middle of the hike, with Strayed agonizing over a bloody toe in a too-tight boot. Her backpack, nicknamed “the Monster,” is almost as big as she is. In visual terms, Vallée is constantly pitting the diminutive Strayed against the broad expanse of the wilderness.
Danger is ever-present, not only from wild animals and rattlesnakes and parched landscapes and freak snowstorms, but also from the many men she encounters on the trail. (And the hikers are almost all men.) The sense of a single woman as prey has rarely been so chillingly conveyed in a movie (at least in a movie that wasn’t intended as a thriller).
Witherspoon uses her own undoubted discomfort with the physical demands of the role to make us feel Strayed’s predicament in our bones. (At one point our heroine slogs 20 miles to a water tank only to discover it’s empty.) The film is another in a series of memoiristic recent movies – along with “Into the Wild,” “All is Lost,” and “127 Hours” – about how confronting the wilderness outside compels a showdown with the wilderness within. What makes this one different is that Strayed doesn’t abide by the strong-and-silent ethic governing those films. The strongest emotion in the movie, her main motivating force, is the deep love she still holds for her mother.
Too much of “Wild” is broken up by flashbacks that tend to dissipate rather than enhance Strayed’s trek. At times she is swallowed up almost to the point of vanishing by the immensity of the vistas. The various encounters she has along the way with hikers, both platonic and predatory, have a schematic feel, as if we were proceeding chapter by chapter through her journey.
I’m also not quite sure I buy the spiritual uplift Strayed derives from the hike’s completion. It could just be that she is naturally high from being royally pooped. But Witherspoon accomplishes a very difficult feat: Often wordlessly, she makes us understand how Strayed could be less lonely in the wild than in a city full of people. Grade: B (Rated R for sexual content, nudity, drug use, and language.) ||||| It seems to be Feminism Week in the fall movie season, and given our intense social focus on the nature and limits of female empowerment and women’s sexual agency at the moment, the timing is just about right. This week features a documentary about the founding of the modern women’s movement (“She’s Beautiful When She’s Angry”), a comic drama about female soldiers in the Israeli military (“Zero Motivation”) and an adaptation of Strindberg’s proto-feminist and/or anti-feminist classic “Miss Julie,” written and directed by Liv Ullmann and starring Jessica Chastain. But the star attraction and Oscar-season prospect, I suppose, is “Wild,” which features Reese Witherspoon as Cheryl Strayed, the real-life memoirist who turned her search for self on the Pacific Crest Trail into a best-selling book and something like a cultural moment.
“Wild” is a moving, engaging and deeply sincere story, set against some of the most magnificent scenery on the planet, and most of Strayed’s fans should be reasonably content. If you detect a note of caution there, you’re right. I really have nothing bad to say about Canadian director Jean-Marc Vallée’s clean and straightforward filmmaking or Nick Hornby’s script (which capably renders a subjective, first-person account into a dramatic arc), and Witherspoon gives us a transparent and compelling performance, on screen alone for most of the picture, with very little sense of star vanity. But “Wild” the movie has a curiously unsticky and unmemorable quality, as if it had melted along the journey, a Sierra Nevada snowball in the Mojave Desert. It has the same nearly invisible flaws as “Dallas Buyers Club,” Vallée’s last agreeable pop-anthropology fable of fall and redemption, but writ larger: It’s just that little bit prepackaged, it stands off from us a little too far. It wants us to feel, but not to feel anything dangerous.
I feel roughly the same about Cheryl Strayed as I do about “Eat Pray Love” author Elizabeth Gilbert (a former magazine colleague of mine), which has to begin with the observation that I will never understand, on a personal or intimate level, what it’s like to be a woman who feels imprisoned in her own life in a female-specific trap. On a broader level, there’s nothing wrong with the personal search for transcendence and reinvention; it’s one of humanity’s more admirable tendencies. There’s certainly nothing wrong with writing about one’s own quest, and there’s absolutely nothing wrong with writing an account that connects with millions of other people and gets you paid. But the problem with all self-help or inspirational literature, beginning with the doctrines handed down to Moses on the mountain (and probably quite a bit before that) is always the same: People want to take it literally, and we have a tendency to mistake the map for the journey.
I doubt that the park rangers along the PCT much appreciate Strayed’s book, or this movie. First of all, they’re depicted as leering, sexist boors who are alternately amazed and aroused by the prospect of a solitary female backpacker. Then there’s the possibility that as the “Wild” phenomenon spreads further into mass culture the 2,650-mile trail from Mexico to Canada will be flooded with ill-prepared spiritual seekers. To be clear, on the first count I have no sympathy. I’m not questioning Strayed’s account of what she observed and experienced, and I’m sure that backpacker culture circa 1995 was full of macho creeps. One of the real strengths of “Wild” is the way Vallée and Witherspoon capture the tremendous vulnerability of a woman alone in the wilderness, and the immense fortitude that was necessary for Strayed to complete her trek.
Every encounter Cheryl has on the trail is loaded with tension and possible menace. A scraggly-looking rancher in the desert seems to be propositioning her; it turns out he means to take her home to the trailer park for a home-cooked meal with his wife. But a bow-hunter she meets in the mountains – and whom she rescues from a dangerous situation, ironically enough – has a different end in view. Only the presence of his hunting companion, who is slightly more committed to social norms, saves Strayed from a likely sexual assault at that moment. In that one brief scene “Wild” conveys a truth of female existence that men hardly ever notice: There are times in every woman’s life where her safety depends on the goodwill, or just on the whims, of men. That can only be exhausting and depressing.
Because our public discourse is dominated by morons, and by preformed, lard-like slabs of ideology masquerading as thought, someone out there right now is writing an article inspired by this movie saying that women should be more sensible than to go hiking alone if they want to avoid sexual assault. First of all, of course Strayed didn’t want to get raped, and of course women should have the right to walk where they please, when they please. More to the point, they do have that right, and must take it, even when that involves the possibility of bad things happening. Strayed’s memoir expresses a fundamental truth, and Vallée’s film at least gestures toward it: You cannot reinvent yourself without taking risks, and furthermore that nothing expresses the debased moral code of our time – which spread relatively evenly across the “left” and the “right” – better than the superabundance of caution, the pathological desire to swaddle oneself and one’s loved ones from all possible dangers.
When we watch Witherspoon as Strayed on her own, or nearly so, against the spectacular desert, forest and mountain landscapes of California – she walked the entire Golden State portion of the PCT and into Oregon, about 1,100 miles in all – “Wild” is never less than captivating. It’s like a physical, philosophical and moral odyssey jointly crafted by Nietzsche and John Muir, with a light dusting of second-wave feminism and just enough humor to lift the dough. (The cinematography is by Yves Bélanger, Vallée’s customary collaborator, and as much as I like to complain about the Arri Alexa, the digital camera that has conquered the film industry, the results look great in this case.) When we get to the reasons why Strayed decided to go for a big long walk in the first place, the movie becomes more problematic, not to say formulaic.
Hornby’s script chops up the back story into digestible flashback fragments, which feature a lovely performance from Laura Dern as Cheryl’s long-suffering but relentlessly optimistic mother. But the overall effect feels a little canned: Cheryl was unable to grieve her mother properly, she retreated into booze and drugs and compulsive promiscuity, and the way to escape that cycle was to walk more than a thousand miles by herself, amid rattlesnakes and would-be rapists and temperature extremes. Whether Strayed knew this consciously or not, her story tapped into a deep cultural vein: The “I Walked Somewhere and Found Myself” narrative goes back at least as far as medieval pilgrimages like the Camino de Compostela, and has roots in the ancient world. In fairness, Hornby includes some of the more reflective and anti-moralistic insights from Strayed’s book, including the idea that all these things were part of the same process: At one point she needed cocaine and sex with random guys, and at another point she needed solitude in the wilderness. But in the end “Wild” is a Hollywood holiday movie “based on a true story,” meaning that its view of reality is conditioned by the three-act structure and the pop-Christian teleology of sin and repentance.
Of course I looked at the gorgeous images in “Wild” and told myself I’d love to hike the Pacific Crest Trail; anybody would. Hell, if the vicarious experience of this movie motivates a few people to go outside, it’s a positive social good. But if I feel driven to seek out specific places on a specific trail in imitation of someone else’s authentic experience, then I’m just following a script, and missing the point of her story. Cheryl Strayed is someone who threw the script away and tried to write her own, which is a marvelous example for women or men of all kinds. As her story of liberation gets iterated and reiterated and streamlined and metamorphosed into an inspiring movie produced by and starring a famous actress who has the best possible intentions, it suffers the same fate as the stories of Jesus and the Buddha and so many other seekers. It stops being a story of self-defining human freedom, and becomes instruction.
”Wild” opens this week nationwide. ||||| Reese Witherspoon is the angry, wounded soul of “Wild.” She commands the screen throughout her heroine’s 1,100-mile journey of self-discovery and self-repair, on foot and mostly alone, from the Mojave desert to Washington State along the Pacific Crest Trail. It’s a sensational performance, by far the best one of her career. The hiker, Cheryl, carries only a huge pack on her back. Ms. Witherspoon carries the whole movie. And she does so with unflagging intensity and remarkable verve, even though this screen adaptation of Cheryl Strayed’s autobiographical best-seller is burdened, out of fidelity to the book, with life lessons... ||||| | multi_news_1_0_0 |
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Here is a news article: LONDON (Reuters) - People with heightened activity in the amygdala, an area of the brain linked to stress, may be at greater risk of heart disease and stroke, scientists said on Thursday in research that could lead to new ways to treat stress-related heart problems.
Scans a brain, bone and artery used in a study carried out by Massachusetts General Hospital and Harvard Medical School which associates the brain region called the amygdala, an area linked to stress, to greater risk of heart disease and stroke are seen in an undated image released January 11, 2017 by The Lancet which published the reasearch. The Lancet Handout via REUTERS
Publishing their work in The Lancet medical journal, the researchers said the stress signaled in the amygdala is also linked to increased bone marrow activity and to inflammation in the arteries, which can cause heart attack and stroke.
Exploring the links, the scientists said a plausible biological mechanism could be that the amygdala triggers the bone marrow to produce extra white blood cells, which then cause the arteries to develop plaques and become inflamed.
“Our results provide a unique insight into how stress may lead to cardiovascular disease,” said Ahmed Tawakol of Massachusetts General Hospital and Harvard Medical School in the United States, who led the study.
“This raises the possibility that reducing stress could produce benefits that extend beyond an improved sense of psychological wellbeing.”
Smoking, high blood pressure and diabetes are well- established risk factors for heart disease, and anecdotal evidence has pointed to chronic stress as another possible risk.
Studies in animals have previously found a link between stress and higher activity in bone marrow and arteries, but until now scientists were unsure if this was the case in people.
Other research has found the amygdala is more active in people with post-traumatic stress disorder, anxiety and depression. But before this study, none had found the region of the brain that links stress to heart attack and stroke risk.
In this research, scientists gave 293 patients brain and body scans to record their brain, bone marrow and spleen activity and inflammation of their arteries.
The patients were then tracked for an average of 3.7 years to see if they developed heart disease. In this time 22 patients had cardiovascular events - including heart attack, angina, heart failure, stroke and peripheral arterial disease.
The researchers found that those with higher amygdala activity were more likely to have subsequent cardiovascular disease, and more likely to develop problems sooner than those with lower activity.
Emily Reeve, a cardiac nurse at the British Heart Foundation charity, said the study’s findings should lead to better understanding of how to prevent heart disease.
“The link between stress and increased risk of developing heart disease has previously focused on the lifestyle habits people take up when they feel stressed such as smoking, drinking...and overeating,” she said.
“Exploring the brain’s management of stress and discovering why it increases the risk of heart disease will allow us to develop new ways of managing chronic psychological stress.” ||||| Image copyright Science Photo Library Image caption Researchers say they have identified how stress can lead to inflamed arteries
The effect of constant stress on a deep-lying region of the brain explains the increased risk of heart attack, a study in The Lancet suggests.
In a study of 300 people, those with higher activity in the amygdala were more likely to develop cardiovascular disease - and sooner than others.
Stress could be as important a risk factor as smoking and high blood pressure, the US researchers said.
Heart experts said at-risk patients should be helped to manage stress.
Emotional stress has long been linked with an increased risk of cardiovascular disease (CVD), which affects the heart and blood vessels - but the way this happens has not been properly understood.
This study, led by a team from Harvard Medical School, points to heightened activity in the amygdala - an area of the brain that processes emotions such as fear and anger - as helping to explain the link.
The researchers suggest that the amygdala signals to the bone marrow to produce extra white blood cells, which in turn act on the arteries causing them to become inflamed. This can then cause heart attacks, angina and strokes.
As a result, when stressed, this part of the brain appears to be a good predictor of cardiovascular events.
But they also said more research was needed to confirm this chain of events.
Inflammation insight
The Lancet research looked at two different studies. The first scanned the brain, bone marrow, spleen and arteries of 293 patients, who were tracked for nearly four years to see if they developed CVD. In this time, 22 patients did, and they were the ones with higher activity in the amygdala.
The second very small study, of 13 patients, looked at the relationship between stress levels and inflammation in the body.
It found that those who reported the highest levels of stress had the highest levels of amygdala activity and more evidence of inflammation in their blood and arteries.
Dr Ahmed Tawakol, lead author and associate professor of medicine at Harvard Medical School, said: "Our results provide a unique insight into how stress may lead to cardiovascular disease.
"This raises the possibility that reducing stress could produce benefits that extend beyond an improved sense of psychological wellbeing.
Image copyright Science Photo Library Image caption The amygdala is one of the most primitive parts of the brain linked to strong emotions, such as fear and anger.
What does the amygdala do?
It's the part of the brain that prepares you for fight or flight, becoming activated by strong emotional reactions.
The amygdalae (because there are two of them - one on each side of the brain) are almond-shaped groups of cells located deep within the medial temporal lobes of the brain.
In humans and animals, the amygdala is linked to responses to both fear and pleasure.
The term amygdala - which means almond in Latin - was first used in 1819.
Dr Tawakol added: "Eventually, chronic stress could be treated as an important risk factor for cardiovascular disease, which is routinely screened for and effectively managed like other major cardiovascular disease risk factors."
Commenting on the research, Dr Ilze Bot, from Leiden University in the Netherlands, said more and more people were experiencing stress on a daily basis.
"Heavy workloads, job insecurity or living in poverty are circumstances that can result in chronically increased stress, which in turn can lead to chronic psychological disorders such as depression."
Emily Reeve, senior cardiac nurse at the British Heart Foundation, said reducing the risk of heart disease and stroke from stress normally focused on controlling lifestyle habits such as smoking, drinking too much alcohol and overeating - but this should change.
"Exploring the brain's management of stress and discovering why it increases the risk of heart disease will allow us to develop new ways of managing chronic psychological stress.
"This could lead to ensuring that patients who are at risk are routinely screened and that their stress is managed effectively." ||||| The mind-body connection is more than just a catchphrase: A new study finds that increased levels of stress are indeed linked to greater risk of a heart attack or stroke.
Researchers found that the people in the study who had more activity in an area of the brain that regulates the body's response to stress and fear, called the amygdala, were more likely to have a heart attack or stroke than those with less activity in the amygdala, according to the study.
"This study identifies, for the first time in animal models or humans, the region of the brain that links stress to the risk of heart attack or stroke," lead study author Dr. Ahmed Tawakol, a cardiologist at Massachusetts General Hospital in Boston, said in a statement. [Heart of the Matter: 7 Things to Know About Your Ticker]
In addition, the researchers also linked increased activity in the amygdala to several processes that play a role in the development of heart disease, according to the study, published today (Jan. 11) in the journal The Lancet.
"While the link between stress and heart disease has long been established, the mechanism mediating that risk has not been clearly understood," Tawakol said.
In the study, the researchers looked at two groups of patients, the first of which included nearly 300 adults ages 30 and up. At the start of the study, none of the patients had heart disease. The researchers performed brain scans on the patients using a technique that not only measured brain activity levels but also allowed the researchers to look at levels of blood vessel inflammation and bone marrow activity throughout the body.
During the average follow-up period of 3.7 years, 22 of the patients had a medical event related to heart disease, such as a heart attack, stroke or diagnosis of heart failure. The researchers found that increased activity levels in the amygdala at the beginning of the study were linked to a significantly higher risk of having a cardiovascular event later on.
And the higher the levels of activity were in the amygdala at the study's start, the sooner these events occurred, the researchers found.
In addition, heightened activity in the amygdala was associated with greater amounts of inflammation in the blood vessels and higher levels of activity in the parts of the bone marrow where new blood cells are made, according to the study.
Both inflammation in the blood vessels and increased bone marrow activity can contribute to a condition called atherosclerosis, which increases a person's risk for heart disease, according to the study. In animal studies, researchers have found that stress activates the bone marrow, prompting it to produce white blood cells, which leads to inflammation, Tawakol said. "This study suggests an analogous path exists in humans," he added.
The second, smaller group of patients in the study included 13 people with chronic stress disorders, such as post-traumatic stress disorder. These patients were asked to complete a questionnaire about their perceived stress levels, as well as undergo brain scans to measure the levels of activity in their amygdalae. The researchers also measured the patients' blood vessel inflammation levels.
They found that the patients' perceived stress levels were linked to increased activity in the amygdala as well as increased levels of inflammation in the blood vessels.
The new study "provides more evidence of a heart-brain connection" by elucidating a link between activity in the amygdala, which is a marker of stress, and subsequent cardiovascular events, Zahi Fayad, a senior author of the study and the director of the Translational and Molecular Imaging Institute at the Icahn School of Medicine at Mount Sinai in New York City, said in a statement.
The link between amygdala activity and risk of heart attack or stroke held up even after the researchers controlled for risk factors for heart disease, Fayad added.
Although more studies are needed to look into the effects of stress reduction on heart disease risk, Tawakol noted that the "findings suggest several potential opportunities to reduce cardiovascular risk attributable to stress."
For example, "it would be reasonable to advise" people with an increased risk of heart disease to try stress-reduction techniques if they feel they have a lot of stress, he said. [11 Tips to Lower Stress]
Additionally, drugmakers may be able to target some of the mechanisms highlighted in the study to develop new drugs to treat heart disease, Tawakol said.
Originally published on Live Science. |||||
A summary of this is? | – Scientists have long cautioned that stress is bad for the heart, and a new study provides insight into precisely why. In the Lancet, researchers lay out a chain of events: When people feel stress, the amygdala area of the brain—it processes emotions such as fear and danger—fires up with extra activity to help them cope. The problem is that the amygdala sends a signal to bone marrow to generate more white blood cells, and those blood cells in turn cause arteries to become inflamed, explains the BBC. That inflammation can then result in heart attacks and strokes. Researchers based their findings on two studies, the larger of which tracked nearly 300 people for about four years. The pattern seemed clear: Those with higher amygdala activity were more likely to develop heart disease of some kind. "While the link between stress and heart disease has long been established, the mechanism mediating that risk has not been clearly understood," says study leader Ahmed Tawakol of Massachusetts General Hospital and Harvard Medical School, per Live Science. A link between stress and higher activity in bone marrow and arteries had previously only been recorded in animals, but the new research suggests it applies to humans as well, reports Reuters. The takeaway: "Reducing stress could produce benefits that extend beyond an improved sense of psychological wellbeing," says Tawakol. Those at increased risk of heart disease should look into stress-reduction techniques, he adds. (Almost half of all heart attacks are silent.) | multi_news_1_0_0 |
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FILE - In this Aug. 14, 2006 file photo, music industry veteran Jerry Heller is photographed in New York. Heller who helped introduce N.W.A. to the masses has died. Heller’s cousin, Gary Ballen, said... (Associated Press)
FILE - In this Aug. 14, 2006 file photo, music industry veteran Jerry Heller is photographed in New York. Heller who helped introduce N.W.A. to the masses has died. Heller’s cousin, Gary Ballen, said Heller died Friday, Sept. 2, 2016 in Southern California. (AP Photo/Jim Cooper) (Associated Press)
FILE - In this Aug. 14, 2006 file photo, music industry veteran Jerry Heller is photographed in New York. Heller who helped introduce N.W.A. to the masses has died. Heller’s cousin, Gary Ballen, said Heller died Friday, Sept. 2, 2016 in Southern California. (AP Photo/Jim Cooper) (Associated Press) FILE - In this Aug. 14, 2006 file photo, music industry veteran Jerry Heller is photographed in New York. Heller who helped introduce N.W.A. to the masses has died. Heller’s cousin, Gary Ballen, said... (Associated Press)
LOS ANGELES (AP) — The music manager who helped introduce N.W.A to the masses has died. Jerry Heller was 75 years old.
Heller's cousin, Gary Ballen, says Heller died Friday night at a hospital in Thousand Oaks, California, after suffering a heart attack while driving earlier in the day.
Heller co-founded Ruthless Records with Eazy-E, which released N.W.A's seminal album "Straight Outta Compton" in 1988, launching the West Coast gangsta rap movement. Ruthless was also behind such artists as J.J. Fad, Michel'le and Bone Thugs-N-Harmony.
Actor Paul Giamatti played the veteran music manager in last year's hit film "Straight Outta Compton." Heller sued the film's producers for defamation after its release, claiming it portrayed him as a villain.
"It made him look bad, like he stole money from (Eazy) or something, which never happened," Ballen said Saturday. "They just rewrote history. And because of that, he had this lawsuit and it's been going on and on. It really stressed him out having to deal with all this stuff."
Ballen said his cousin was "always kind of tormented" by his parting with Eazy and the label. In 2006, Heller released "Ruthless: A Memoir," which Ballen said was being adapted for the screen.
Heller had a history of heart problems and suffered from diabetes.
Born in Ohio, Heller started his career in the 1960s as an agent and promoter, working with such acts as Pink Floyd, Marvin Gaye and Creedence Clearwater Revival. He set up Elton John's first U.S. performance, Ballen said.
Ballen remembered how excited Heller was to play him a cassette of N.W.A's early tracks.
"He said, 'You watch, this is going to be the biggest music ever. This is going to take over rock 'n' roll,'" Ballen recalled. "Jerry was a real visionary... As far as I'm concerned, there would never be a Dr. Dre or an Ice Cube if it wasn't for Jerry getting (N.W.A) their first deal, which was really difficult. Nobody wanted to sign them."
Besides Ballen, Heller is survived by a brother and a nephew. ||||| Jerry Heller, the longtime music manager that helped launch the career of N.W.A and the gangsta-rap movement, died Friday. He was 75. Heller's cousin confirmed Heller's death to Billboard. According to TMZ, Heller died after suffering a medical emergency while driving that resulted in him sustaining serious injuries after crashing his minivan in California. It's still unclear whether Heller died from the medical emergency or the injuries from the crash.
Heller started his career in the music industry as an agent and promoter, working with artists like Creedence Clearwater Revival, Marvin Gaye, the Who and Black Sabbath in the Sixties and Seventies.
By the mid-Eighties, as hip-hop swelled in popularity, Heller co-founded Ruthless Records with Eazy-E; the Compton rapper reportedly paid Alonzo Williams of the World Class Wreckin' Cru, another Heller-signed act that featured Dr. Dre, for an introduction to the manager.
N.W.A formed in 1986 with Eazy-E and Dre linking up with C.I.A.'s Ice Cube and Arabian Prince; a year later, in 1987, Ruthless released the supergroup's first single "Panic Zone. By the release of 1988's Straight Outta Compton, MC Ren and DJ Yella would join N.W.A, which was inducted into the Rock and Roll Hall of Fame in 2015.
"From God we come and to God we return," MC Ren told Rolling Stone following Heller's death.
In addition to N.W.A, Ruthless also became the one-time home of acts like J.J. Fad, Bone Thugs-N-Harmony, the D.O.C., Michel'le, Jimmy Z and more.
Heller served as the N.W.A's manager for four years, although the group began to disintegrate in 1989 after Ice Cube quit over royalty disputes with Heller, resulting in the rapper's scathing diss track "No Vaseline." By 1991, Dr. Dre would ditch Ruthless for Death Row and skewer Heller in the video for his "Dre Day." However, Heller and Eazy-E's partnership continued until the rapper's death in 1995.
"I was with him until the day of his untimely death," Heller told Rolling Stone in November 2015. "I still think about him every day. He was like my son. He was a visionary. He was the greatest, and I've always believed that only he and I really understood the significance of what N.W.A was."
Following the release of Straight Outta Compton, the N.W.A biopic that portrayed Heller – played by Paul Giamatti – in a negative light, the former manager filed a $110 million defamation lawsuit against the film's producers, including Dr. Dre and Ice Cube. Heller also spoke to Rolling Stone about what he perceived as the film's many inaccuracies. However, the majority of Heller's lawsuit was dismissed this June.
"As for the things that bothered me, I've been in the business for six decades. I've probably represented almost every major artist in the world, either directly or peripherally, at one time or another," Heller said. "I have a certain reputation, and that reputation certainly doesn't entail the things that they said about me. It was very hurtful. I thought 'No Vaseline' was hurtful. But actually, this was more hurtful. Look, I am what I am, but I'm not a thief. And I'm not scandalous. I did more for N.W.A ... I mean, it was just incredible, the success that we had. So for them to call me a thief is just terrible."
In 2006, Heller released Ruthless: A Memoir to tell his side of the story and address certain accusations he claimed were untrue.
This story is developing. |||||
What is a one-paragraph summary of the above article? | – The music manager who played a large and controversial role in the rise of gangsta rap is dead at age 75. Jerry Heller, who helped launch N.W.A. with rapper Eazy-E in the mid-'80s, suffered a heart attack while driving and died at a hospital in Thousand Oaks, California, his cousin tells AP. Heller co-founded Ruthless Records with Eazy-E, and the label's Straight Outta Compton by N.W.A.in 1988 has since become a classic. Heller, however, eventually parted on bad terms with the label and high-profile performers such as Ice Cube and Dr. Dre, all of which of was retold in the recent Straight Outta Compton movie. Heller hated how he was portrayed so much that he sued. (He comes off as a greedy villain who takes advantage of the label's stars.) In fact, his lawyer blames the film for his death. "Jerry Heller would be alive today if not for that movie," Mickey Shapiro tells TMZ. He says his client had been stressed, "heartbroken," and unable to sleep well because of the movie. Before his collaboration with Eazy-E, Heller worked with acts such as Creedence Clearwater Revival, Black Sabbath, Marvin Gaye, and the Who, notes Rolling Stone. But it was his work in rap that has largely defined him. "As far as I'm concerned, there would never be a Dr. Dre or an Ice Cube if it wasn't for Jerry getting (N.W.A) their first deal, which was really difficult," says cousin Gary Ballen. "Nobody wanted to sign them." | 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.
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(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. |||||
Summary: | – 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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The Mediterranean diet -- rich in fruits, vegetables, fish, olive oil, nuts and whole grains -- has long been hailed as a heart-healthy eating plan. But new research suggests its health benefits may be limited to the rich and well-educated.
For the study, a team of Italian scientists reviewed diets, income and education level of nearly 19,000 men and women.
The investigators found the Mediterranean diet was associated with about a 60 percent lower risk of heart disease and stroke among those with higher incomes and more education. The same was not true for those with fewer resources -- even though they followed a similar eating plan.
Healthy habits -- such as getting regular exercise, routine check-ups, and not smoking -- are more common among people with higher incomes. But the study findings held up even after the researchers accounted for these variables and others, such as marital status and body mass index (a measurement based on height and weight).
Will a Mediterranean diet help you live longer?
The team investigated other possible explanations for this healthy diet disparity. The findings showed that the wealthier participants ate less meat and consumed more fish and whole grains than those with lower incomes.
The more affluent people also ate a greater variety of fruits and vegetables, which provided more antioxidants and other essential nutrients. The researchers concluded that food quality may be as important for health as how much people eat and how often.
"Money may provide access to a larger variety of foods typical of the Mediterranean diet, such as fruits and vegetables, thus obtaining more adequate intake of essential nutrients," said the study's leader, Giovanni de Gaetano. He's head of the department of epidemiology and prevention at the I.R.C.C.S. Neuromed Institute in Pozzilli, Italy.
Many of the most nutritionally valuable foods in the Mediterranean diet -- including fish, olive oil and produce -- aren't cheap.
"Let's think about a five-member family who wants to attain to the five-a-day portion of fruits and vegetables," de Gaetano said. "This sounds quite expensive."
Cooking methods also differed among the study participants. The people with more money and education were more likely to prepare their vegetables in healthier ways, which preserve their nutritional value.
Joan Salge Blake is a clinical associate professor and dietetic internship director at Boston University. She said the more affluent "are more likely to have better health care, access to a variety of diverse fruits and vegetables, and an overall understanding about the role of lifestyle and diet in disease prevention."
So, she added, "costs and access to healthy foods will clearly impact the quality of a person's diet and lifestyle."
That doesn't mean individuals and families on a tight budget can't afford to follow the Mediterranean diet, Salge Blake stressed. She offered the following budget-friendly advice:
Look for variety and sales. When it comes to overall diet quality, the more fruit and veggies on your plate, the better. Choose produce that is on sale, which will stretch your food dollar.
Buy in-season. Produce tastes a lot better when it's in season. It's also much less expensive. Bottom line: you're more likely to eat fruit if it's sweet and you'll probably load up on veggies if they are more flavorful.
Don't overcook. How you cook vegetables can affect their nutritional value. "Typically, the less cooking time will cause the least loss of nutrients," Salge Blake said.
Consider frozen and canned foods. "Canned fish and frozen veggies and fruit are oftentimes more affordable than fresh, and can pack an equal, if not more, nutrient punch per bite," Salge Blake said.
Try affordable alternatives. Olive oil is considered a staple of the Mediterranean diet but it's pricey. "Other plant oils -- such as soybean oil -- are healthy and affordable, so you don't have to consume only olive oil," Salge Blake said. She noted the Mediterranean diet contains legumes, such as dried beans and peas, which are extremely affordable.
The study was published online July 31 in the International Journal of Epidemiology. ||||| Abstract
Background It is uncertain whether the cardiovascular benefits associated with Mediterranean diet (MD) may differ across socioeconomic groups. Methods Prospective analysis on 18991 men and women aged ≥35 years from the general population of the Moli-sani cohort (Italy). Adherence to MD was appraised by the Mediterranean diet score (MDS). Household income (euros/year) and educational level were used as indicators of socioeconomic status. Hazard ratios (HR) were calculated by multivariable Cox proportional hazard models. Results Over 4.3 years of follow-up, 252 cardiovascular disease (CVD) events occurred. Overall, a two-point increase in MDS was associated with 15% reduced CVD risk (95% confidence interval: 1% to 27%). Such association was evident in highly (HR = 0.43; 0.25–0.72) but not in less (HR = 0.94; 0.78–1.14) educated subjects (P for interaction = 0.042). Similarly, CVD advantages associated with the MD were confined to the high household income group (HR = 0.39; 0.23–0.66, and HR = 1.01; 0.79–1.29 for high- and low-income groups, respectively; P for interaction = 0.0098). In a subgroup of individuals of different socioeconomic status but sharing similar MDS, diet-related disparities were found as different intakes of antioxidants and polyphenols, fatty acids, micronutrients, dietary antioxidant capacity, dietary diversity, organic vegetables and whole grain bread consumption. Conclusions MD is associated with lower CVD risk but this relationship is confined to higher socioeconomic groups. In groups sharing similar scores of adherence to MD, diet-related disparities across socioeconomic groups persisted. These nutritional gaps may reasonably explain at least in part the socioeconomic pattern of CVD protection from the MD.
Introduction
Observational studies have documented the association of Mediterranean-like dietary patterns with reduced cardiovascular disease (CVD) incidence and mortality,1–4 along with lower rates of cancer,5 neurodegenerative diseases and all-cause mortality.6,7 More recently, evidence on cardiovascular protection from an MD was provided also by intervention studies showing reduced risk of CVD after allocation to MD-like patterns both in primary8 and in secondary cardiovascular prevention.9 Diet quality exhibits a socioeconomic (SES) gradient, with less advantaged groups reporting lower adherence to healthy dietary patterns including an MD10 generally associated with poor health outcomes and higher prevalence of non-dietary unhealthy behaviours, such as tobacco use and inadequate physical activity.11
So far, SES inequities in diet have been documented for several domains of dietary behaviours and beyond food and nutrient intake; disparities were found for nutrient density levels, percentage contribution of food to nutrition and energy and also for diet variety, access to organic foods and food purchasing behaviours.12,13 During recent years, increased attention has been paid to the food processing pertinent to the MD which can influence the nutritional quality of foods, with consequent impact on future health outcomes, especially in relation to oxidative stress and inflammation.14 Actually, when measuring adherence to an MD, a relatively large amount of diet-related information or dietary behaviours is left out, and nutritional gaps among SES groups may still hold even in the presence of an apparently similar adherence to the same eating pattern.13
The aim of the present study is 3-fold: first, to evaluate the association between adherence to the MD and the incidence of fatal and non-fatal CVD events among adults initially free from CVD and diabetes; second, to test whether the association of the MD with CVD differs across SES strata; finally, to explore possible persisting diet-related differences among SES groups reaching similar scores of adherence to the MD.
Methods
Study population
The Moli-sani study is a prospective cohort study of 24 325 men and women (aged ≥ 35) randomly recruited from the general population of a Southern Italian region from March 2005 to April 2010.15 For the purpose of this study, individuals with a history of CVD (7.1%), diabetes (10.6%), those reporting implausible energy intakes (<800 kcal/day in men and <500 kcal/day in women or >4000 kcal/day in men and >3500 kcal/day in women; 3.2%), subjects with missing information on educational level (0.2%), unreliable medical or dietary questionnaires (1% and 3.9%, respectively), subjects lost to follow-up (0.2%) or with incomplete personal data (1.7%) were excluded from the analyses. The final sample consisted of 18 991 individuals.
The Moli-sani study complies with the Declaration of Helsinki and was approved by the ethical committee of the Catholic University in Rome, Italy. All participants provided written informed consent.
Ascertainment of cases
Primary fatal and nonfatal incident cases of CHD (unstable angina, myocardial infarction, coronary revascularization and sudden death from unspecified cardiac event) and cerebrovascular disease which occurred in the cohort during follow-up were ascertained by linkage of the study cohort to the hospital discharge files and to the regional Registro Nominativo delle Cause di Morte (ReNCaM) registry and death certificates (Istituto Nazionale di Statistica (ISTAT) form), by using the International Classification of Diseases, ninth revision (ICD-9). For CHD, ICD-9 codes 410–414 and/or reperfusion procedure (ICD-9 codes 36.0–36.9) and for cerebrovascular disease, ICD9 codes 430–432, 434, 436–438 or procedure codes for carotid revascularization (ICD 9 code 38.12) were considered.
Suspected CHD deaths were identified when ICD-9 codes 410–414 or 798 and 799 were reported as the underlying cause of death or codes 250, 401–405, 420–429 as the underlying cause of death, associated with codes 410–414 as a secondary cause of death. Suspected cerebrovascular deaths were identified when ICD-9 codes 430–438 were reported as the underlying, antecedent or direct cause of death. All events were validated using procedures of the American Heart Association (AHA), World Heart Federation (WHF), European Society of Cardiology (ESC), Centres for Disease Control (CDC) and National Heart, Lung, and Blood Institute (NHLBI) for epidemiology and clinical research studies.16
Ascertainment of risk factors at baseline
History of CVD included documented angina, myocardial infarction, revascularization procedures and cerebrovascular events. History of cancer included self-reported diagnosis of cancer. Hypertension was defined as systolic blood pressure ≥140 mm Hg or diastolic blood pressure ≥90 mmHg or treatment for hypertension. Hypercholesterola emia was defined as total cholesterol ≥240 mg/dl or use of specific medication.17 Diabetes was defined as blood glucose ≥126 mg/dl or as specific pharmacological treatment.
Total physical activity was assessed by a structured questionnaire and expressed as daily energy expenditure in metabolic equivalent task-hours (MET-h/day). Body mass index (BMI) was calculated as kg/m2. Subjects were classified as never-smokers, current smokers or ex-smokers (having quitted for at least 1 year).
Socioeconomic indicators
Socioeconomic information was self-reported and collected by structured questionnaires administered by trained personnel. Detailed information on both education and household income are available; however, in this study, categories were chosen by taking into account the relatively low number of incident CVD events which do not permit consideration of these socioeconomic indicators in greater detail. Education was based on the highest qualification attained and was categorized as up to lower secondary (approximately ≤8 years of study), upper secondary education (≤13) and post-secondary or higher (>13). Household income, expressed as earned euros per year, was a four-level variable (<25 000; 25 000–40 000; >40 000 euro/year), with missing values collapsed into a non-respondent category. Marital status was considered as married/cohabiting, divorced/separated, single or widowed.
Dietary assessment and indices of diet quality
Food intake was assessed by the validated Italian EPIC food frequency questionnaire.18 Adherence to the MD was defined according to the Mediterranean Diet Score.7
Food antioxidant content (FAC) was appraised by a score determining the content in antioxidant vitamins and phytochemicals of each food group and ranged from −99 to 99, with higher values indicating increased consumption of foods rich in antioxidants.19 The polyphenol content of diet was measured by a polyphenol antioxidant content (PAC)-score calculated as in Pounis et al.20 Total antioxidant capacity of diet (TAC) was assessed as in Di Giuseppe et al.21
Variety of fruit and/or vegetable intake was assessed by four (fruit, vegetables, vegetables subgroups and fruit/vegetable combined) different diet diversity scores, following approaches similar to those tested within EPIC cohorts.22 Diversity was the total number of individual vegetable/fruit products eaten at least once in 2 weeks. Data on cooking procedures were collected for vegetables, meat and fish. A score was constructed to discriminate healthy (boiling, stewing) and hazardous (frying, roasting, grilling) cooking methods;23 the healthier the procedure, the higher the score. Organic food intake was limited to organic vegetables and categorized as yes/no. Whole-grain products consumption was restricted to whole-grain bread intake (yes/no).
Statistical analysis
Means with standard deviations (SDs) and percentages were used to describe the characteristics of the study population. Multivariable hazard ratios (HRs) with 95% confidence intervals (95% CIs) were calculated by using Cox proportional hazards models to analyse the association between adherence to the MD and incident vascular outcomes. The multivariable models were adjusted for sex, age, smoking status, education, household income, marital status, BMI (categorical), total physical activity (ordered quintiles), hypertension and/or hypercholesterolaemia at baseline, energy intake and consumption of eggs and potatoes.
Appropriate multiplicative terms for testing interaction of education and income with adherence to the MD, as measured as two-point increase in the MDS, were included in the multivariable models (alternately adjusted for education or income) to test for a difference of effect of the MD across SES strata. Analyses on income were run on 13 226 subjects after exclusion of the non-respondent category. Differences in diet-related indices or behaviours across SES strata were calculated only among individuals reporting high adherence to the MD (MDS ≥ 6).
Figure 1a and b shows differences in diet-related indices (highest vs lowest educational or income groups), divided by standard deviation of the difference. In these figures, individuals with intermediate educational or income values were eliminated. Dummy variables for missing values of each variable of interest were created. The data analysis was generated using SAS/STAT software, Version 9.4 of the SAS System for Windows©2010. SAS Institute Inc. and SAS are registered trademarks of SAS Institute Inc., Cary, NC, USA.
Figure 1 View largeDownload slide a. Mean differences in diet-related indices for highest vs lowest educational groups sharing similar adherence to the Mediterranean diet (MDS ≥ 6). Individuals with intermediate educational values were eliminated. Each difference was divided by its standard deviation. b. Mean differences in diet-related indices for highest vs lowest household income groups sharing similar adherence to the Mediterranean diet (MDS ≥ 6). Individuals with intermediate income values were eliminated. Each difference was divided by its standard deviation.
Figure 1 View largeDownload slide a. Mean differences in diet-related indices for highest vs lowest educational groups sharing similar adherence to the Mediterranean diet (MDS ≥ 6). Individuals with intermediate educational values were eliminated. Each difference was divided by its standard deviation. b. Mean differences in diet-related indices for highest vs lowest household income groups sharing similar adherence to the Mediterranean diet (MDS ≥ 6). Individuals with intermediate income values were eliminated. Each difference was divided by its standard deviation.
Results
Mediterranean diet and CVD risk
Over a median follow-up of 4.3 years (lower to upper quartile: 3.5–5.4; 82718 person-years), we ascertained a total of 256 CVD events of which were 207 CHD and 49 were strokes. Baseline characteristics of the study population according to adherence to the MD are presented in Table 1.
Table 1 Adherence to the Mediterranean diet Poor (0–3) Average (4–5) High (≥ 6) P-value N (%) 5812 (30.6) 8361 (44.0) 4818 (25.4) - Age (years, means ± SD) 52.4 (11.5) 54.4 (11.4) 56.0 (10.8) <0.0001 Sex (men, %) 41.1 44.2 49.7 0.92 Income (€/year; %) <0.0001 <25 000 34.2 36.3 35.4 25 000–40 000 19.7 21.7 23.2 >40 000 11.8 12.2 14.7 Non-respondents 34.2 29.8 26.7 Education (%) <0.0001 Up to lower secondary 50.2 50.2 48.6 Upper secondary 36.2 36.5 36.8 Post-secondary or higher 13.6 13.3 14.6 Marital status (%) <0.0001 Married/cohabiting 83.8 86.1 87.7 Separated/divorced 2.9 2.7 2.5 Single 6.3 5.4 4.6 Widowed 7.0 5.7 5.2 BMI (%) 0.027 Normal (<25) 32.3 29.2 28.8 Overweight (≥25 <30) 41.2 43.8 44.7 Obese (≥30) 26.5 27.0 26.5 Smokers (%) 24.4 24.0 23.0 0.0020 Total physical activity (means ± SD) 42.8 (8.1) 43.4 (8.6) 43.2 (8.6) 0.0004 Hypertension (%) 47.1 51.8 57.0 <0.0001 Hypercholesterolaemia (%) 27.4 27.5 32.0 0.0001 Cancer (%) 2.8 3.1 3.1 0.91 Aspirin use (%) 1.6 1.8 1.9 0.91 Blood glucose (mg/dl, means ± SD) 95.7 (11.5) 95.5 (11.6) 95.8 (11.5) 0.35 Energy intake (kcal/day, means ± SD) 1995 (531) 2094 (541) 2224 (517) <0.0001 Adherence to the Mediterranean diet Poor (0–3) Average (4–5) High (≥ 6) P-value N (%) 5812 (30.6) 8361 (44.0) 4818 (25.4) - Age (years, means ± SD) 52.4 (11.5) 54.4 (11.4) 56.0 (10.8) <0.0001 Sex (men, %) 41.1 44.2 49.7 0.92 Income (€/year; %) <0.0001 <25 000 34.2 36.3 35.4 25 000–40 000 19.7 21.7 23.2 >40 000 11.8 12.2 14.7 Non-respondents 34.2 29.8 26.7 Education (%) <0.0001 Up to lower secondary 50.2 50.2 48.6 Upper secondary 36.2 36.5 36.8 Post-secondary or higher 13.6 13.3 14.6 Marital status (%) <0.0001 Married/cohabiting 83.8 86.1 87.7 Separated/divorced 2.9 2.7 2.5 Single 6.3 5.4 4.6 Widowed 7.0 5.7 5.2 BMI (%) 0.027 Normal (<25) 32.3 29.2 28.8 Overweight (≥25 <30) 41.2 43.8 44.7 Obese (≥30) 26.5 27.0 26.5 Smokers (%) 24.4 24.0 23.0 0.0020 Total physical activity (means ± SD) 42.8 (8.1) 43.4 (8.6) 43.2 (8.6) 0.0004 Hypertension (%) 47.1 51.8 57.0 <0.0001 Hypercholesterolaemia (%) 27.4 27.5 32.0 0.0001 Cancer (%) 2.8 3.1 3.1 0.91 Aspirin use (%) 1.6 1.8 1.9 0.91 Blood glucose (mg/dl, means ± SD) 95.7 (11.5) 95.5 (11.6) 95.8 (11.5) 0.35 Energy intake (kcal/day, means ± SD) 1995 (531) 2094 (541) 2224 (517) <0.0001
Table 1 Adherence to the Mediterranean diet Poor (0–3) Average (4–5) High (≥ 6) P-value N (%) 5812 (30.6) 8361 (44.0) 4818 (25.4) - Age (years, means ± SD) 52.4 (11.5) 54.4 (11.4) 56.0 (10.8) <0.0001 Sex (men, %) 41.1 44.2 49.7 0.92 Income (€/year; %) <0.0001 <25 000 34.2 36.3 35.4 25 000–40 000 19.7 21.7 23.2 >40 000 11.8 12.2 14.7 Non-respondents 34.2 29.8 26.7 Education (%) <0.0001 Up to lower secondary 50.2 50.2 48.6 Upper secondary 36.2 36.5 36.8 Post-secondary or higher 13.6 13.3 14.6 Marital status (%) <0.0001 Married/cohabiting 83.8 86.1 87.7 Separated/divorced 2.9 2.7 2.5 Single 6.3 5.4 4.6 Widowed 7.0 5.7 5.2 BMI (%) 0.027 Normal (<25) 32.3 29.2 28.8 Overweight (≥25 <30) 41.2 43.8 44.7 Obese (≥30) 26.5 27.0 26.5 Smokers (%) 24.4 24.0 23.0 0.0020 Total physical activity (means ± SD) 42.8 (8.1) 43.4 (8.6) 43.2 (8.6) 0.0004 Hypertension (%) 47.1 51.8 57.0 <0.0001 Hypercholesterolaemia (%) 27.4 27.5 32.0 0.0001 Cancer (%) 2.8 3.1 3.1 0.91 Aspirin use (%) 1.6 1.8 1.9 0.91 Blood glucose (mg/dl, means ± SD) 95.7 (11.5) 95.5 (11.6) 95.8 (11.5) 0.35 Energy intake (kcal/day, means ± SD) 1995 (531) 2094 (541) 2224 (517) <0.0001 Adherence to the Mediterranean diet Poor (0–3) Average (4–5) High (≥ 6) P-value N (%) 5812 (30.6) 8361 (44.0) 4818 (25.4) - Age (years, means ± SD) 52.4 (11.5) 54.4 (11.4) 56.0 (10.8) <0.0001 Sex (men, %) 41.1 44.2 49.7 0.92 Income (€/year; %) <0.0001 <25 000 34.2 36.3 35.4 25 000–40 000 19.7 21.7 23.2 >40 000 11.8 12.2 14.7 Non-respondents 34.2 29.8 26.7 Education (%) <0.0001 Up to lower secondary 50.2 50.2 48.6 Upper secondary 36.2 36.5 36.8 Post-secondary or higher 13.6 13.3 14.6 Marital status (%) <0.0001 Married/cohabiting 83.8 86.1 87.7 Separated/divorced 2.9 2.7 2.5 Single 6.3 5.4 4.6 Widowed 7.0 5.7 5.2 BMI (%) 0.027 Normal (<25) 32.3 29.2 28.8 Overweight (≥25 <30) 41.2 43.8 44.7 Obese (≥30) 26.5 27.0 26.5 Smokers (%) 24.4 24.0 23.0 0.0020 Total physical activity (means ± SD) 42.8 (8.1) 43.4 (8.6) 43.2 (8.6) 0.0004 Hypertension (%) 47.1 51.8 57.0 <0.0001 Hypercholesterolaemia (%) 27.4 27.5 32.0 0.0001 Cancer (%) 2.8 3.1 3.1 0.91 Aspirin use (%) 1.6 1.8 1.9 0.91 Blood glucose (mg/dl, means ± SD) 95.7 (11.5) 95.5 (11.6) 95.8 (11.5) 0.35 Energy intake (kcal/day, means ± SD) 1995 (531) 2094 (541) 2224 (517) <0.0001
Highest adherence to the MD (MDS ≥ 6) was associated with reduced risk of CVD in the model controlled for age, sex and energy intake (Table 2) and also after further adjustment for a number of possible confounders (multivariable HR = 0.67; 95% CI: 0.48–0.94). A two-point increase in the MDS was also related to lower risk of CVD (multivariable HR = 0.85; 95% CI: 0.73–0.99; Figure 2). The association of the MD with CHD or stroke risk reflected a similar protective trend but results did not reach statistical significance (Table 2).
Table 2 Adherence to the traditional MD Two-point increase in MDS Poor (0–3) Average (4–5) High (≥6) N of subjects 5812 8361 4818 - CHD + Stroke (n = 256) N of events/rate 79 (1.36%) 109 (1.30%) 68 (1.41%) Person-years 24189 36319 22210 Model 1 (HR; 95% CI) -1‐ 0.78 (0.58–1.04) 0.70 (0.50–0.97) 0.87 (0.74–1.01) Model 2 (HR; 95% CI) ‐1‐ 0.75 (0.56–1.01) 0.67 (0.48–0.94) 0.85 (0.73–0.99) CHD (n = 207) N of events/rate 61 (1.05%) 90 (1.08%) 56 (1.16%) Person-years 24218 36344 22225 Model 1 (HR; 95% CI) ‐1‐ 0.83 (0.60–1.16) 0.75 (0.55–1.08) 0.89 (0.75–1.06) Model 2 (HR; 95% CI) ‐1‐ 0.80 (0.58–1.12) 0.71 (0.49–1.04) 0.87 (0.73–1.04) Stroke (n = 49) N of events/rate 18 (0.31%) 19 (0.23%) 12 (0.25%) Person-years 24303 36502 22309 Model 1 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.13) 0.54 (0.25–1.14) 0.78 (0.55–1.10) Model 2 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.14) 0.54 (0.25–1.16) 0.77 (0.54–1.11) Adherence to the traditional MD Two-point increase in MDS Poor (0–3) Average (4–5) High (≥6) N of subjects 5812 8361 4818 - CHD + Stroke (n = 256) N of events/rate 79 (1.36%) 109 (1.30%) 68 (1.41%) Person-years 24189 36319 22210 Model 1 (HR; 95% CI) -1‐ 0.78 (0.58–1.04) 0.70 (0.50–0.97) 0.87 (0.74–1.01) Model 2 (HR; 95% CI) ‐1‐ 0.75 (0.56–1.01) 0.67 (0.48–0.94) 0.85 (0.73–0.99) CHD (n = 207) N of events/rate 61 (1.05%) 90 (1.08%) 56 (1.16%) Person-years 24218 36344 22225 Model 1 (HR; 95% CI) ‐1‐ 0.83 (0.60–1.16) 0.75 (0.55–1.08) 0.89 (0.75–1.06) Model 2 (HR; 95% CI) ‐1‐ 0.80 (0.58–1.12) 0.71 (0.49–1.04) 0.87 (0.73–1.04) Stroke (n = 49) N of events/rate 18 (0.31%) 19 (0.23%) 12 (0.25%) Person-years 24303 36502 22309 Model 1 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.13) 0.54 (0.25–1.14) 0.78 (0.55–1.10) Model 2 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.14) 0.54 (0.25–1.16) 0.77 (0.54–1.11)
Table 2 Adherence to the traditional MD Two-point increase in MDS Poor (0–3) Average (4–5) High (≥6) N of subjects 5812 8361 4818 - CHD + Stroke (n = 256) N of events/rate 79 (1.36%) 109 (1.30%) 68 (1.41%) Person-years 24189 36319 22210 Model 1 (HR; 95% CI) -1‐ 0.78 (0.58–1.04) 0.70 (0.50–0.97) 0.87 (0.74–1.01) Model 2 (HR; 95% CI) ‐1‐ 0.75 (0.56–1.01) 0.67 (0.48–0.94) 0.85 (0.73–0.99) CHD (n = 207) N of events/rate 61 (1.05%) 90 (1.08%) 56 (1.16%) Person-years 24218 36344 22225 Model 1 (HR; 95% CI) ‐1‐ 0.83 (0.60–1.16) 0.75 (0.55–1.08) 0.89 (0.75–1.06) Model 2 (HR; 95% CI) ‐1‐ 0.80 (0.58–1.12) 0.71 (0.49–1.04) 0.87 (0.73–1.04) Stroke (n = 49) N of events/rate 18 (0.31%) 19 (0.23%) 12 (0.25%) Person-years 24303 36502 22309 Model 1 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.13) 0.54 (0.25–1.14) 0.78 (0.55–1.10) Model 2 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.14) 0.54 (0.25–1.16) 0.77 (0.54–1.11) Adherence to the traditional MD Two-point increase in MDS Poor (0–3) Average (4–5) High (≥6) N of subjects 5812 8361 4818 - CHD + Stroke (n = 256) N of events/rate 79 (1.36%) 109 (1.30%) 68 (1.41%) Person-years 24189 36319 22210 Model 1 (HR; 95% CI) -1‐ 0.78 (0.58–1.04) 0.70 (0.50–0.97) 0.87 (0.74–1.01) Model 2 (HR; 95% CI) ‐1‐ 0.75 (0.56–1.01) 0.67 (0.48–0.94) 0.85 (0.73–0.99) CHD (n = 207) N of events/rate 61 (1.05%) 90 (1.08%) 56 (1.16%) Person-years 24218 36344 22225 Model 1 (HR; 95% CI) ‐1‐ 0.83 (0.60–1.16) 0.75 (0.55–1.08) 0.89 (0.75–1.06) Model 2 (HR; 95% CI) ‐1‐ 0.80 (0.58–1.12) 0.71 (0.49–1.04) 0.87 (0.73–1.04) Stroke (n = 49) N of events/rate 18 (0.31%) 19 (0.23%) 12 (0.25%) Person-years 24303 36502 22309 Model 1 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.13) 0.54 (0.25–1.14) 0.78 (0.55–1.10) Model 2 (HR; 95% CI) ‐1‐ 0.59 (0.31–1.14) 0.54 (0.25–1.16) 0.77 (0.54–1.11)
Figure 2 View largeDownload slide Cardiovascular risk (hazard ratio with 95% confidence intervals) associated with two-point increment in the MDS in the whole study population and across educational and household income groups.
Figure 2 View largeDownload slide Cardiovascular risk (hazard ratio with 95% confidence intervals) associated with two-point increment in the MDS in the whole study population and across educational and household income groups.
Mediterranean diet and CVD risk in socioeconomic strata
A likely different association of the MD, expressed as two-point increase in the MDS, with CVD risk across SES strata was tested by including two separate terms of interaction (educationMDS or incomeMDS) in the multivariable model further controlled for education or income; the P-value for interaction for education was 0.042 and for household income was 0.0098 (Figure 2). A two-point increment in the MDS was associated with lower CVD risk only in the group with a post-secondary education, in a model further controlled for income levels (HR = 0.43; 95% CI: 0.25–0.72), and no relationship was found for those with lower education (HR = 0.94; 95% CI: 0.78–1.14; Table 3). Similarly, the protection from an MD was only evident in the group with higher household income (HR = 0.39; 95% CI: 0.23–0.66 vs HR = 1.01; 95% CI: 0.79–1.29 of the lowest household income group; Table 3).
Table 3 Educational level Up to lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Postgraduate-higher (>13 years) P for interaction N of CVD events/n of subjects 170/9457 63/6926 23/2608 0.042 Event rate (%) 1.80 0.92 0.88 CVD risk (HR; 95% CIa 0.94 (0.78–1.14) 0.80 (0.58–1.10) 0.43 (0.25–0.72) Household income groups (€/year)b <25 000 25 000–40 000 >40 000 P for interaction N of CVD events/n of subjects 101/6730 47/4080 27/2416 0.0098 Event rate (%) 1.50 1.15 1.10 CVD risk (HR; 95% CI)a 1.01 (0.79–1.29) 1.00 (0.69–1.46) 0.39 (0.23–0.66) Educational level Up to lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Postgraduate-higher (>13 years) P for interaction N of CVD events/n of subjects 170/9457 63/6926 23/2608 0.042 Event rate (%) 1.80 0.92 0.88 CVD risk (HR; 95% CIa 0.94 (0.78–1.14) 0.80 (0.58–1.10) 0.43 (0.25–0.72) Household income groups (€/year)b <25 000 25 000–40 000 >40 000 P for interaction N of CVD events/n of subjects 101/6730 47/4080 27/2416 0.0098 Event rate (%) 1.50 1.15 1.10 CVD risk (HR; 95% CI)a 1.01 (0.79–1.29) 1.00 (0.69–1.46) 0.39 (0.23–0.66)
Table 3 Educational level Up to lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Postgraduate-higher (>13 years) P for interaction N of CVD events/n of subjects 170/9457 63/6926 23/2608 0.042 Event rate (%) 1.80 0.92 0.88 CVD risk (HR; 95% CIa 0.94 (0.78–1.14) 0.80 (0.58–1.10) 0.43 (0.25–0.72) Household income groups (€/year)b <25 000 25 000–40 000 >40 000 P for interaction N of CVD events/n of subjects 101/6730 47/4080 27/2416 0.0098 Event rate (%) 1.50 1.15 1.10 CVD risk (HR; 95% CI)a 1.01 (0.79–1.29) 1.00 (0.69–1.46) 0.39 (0.23–0.66) Educational level Up to lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Postgraduate-higher (>13 years) P for interaction N of CVD events/n of subjects 170/9457 63/6926 23/2608 0.042 Event rate (%) 1.80 0.92 0.88 CVD risk (HR; 95% CIa 0.94 (0.78–1.14) 0.80 (0.58–1.10) 0.43 (0.25–0.72) Household income groups (€/year)b <25 000 25 000–40 000 >40 000 P for interaction N of CVD events/n of subjects 101/6730 47/4080 27/2416 0.0098 Event rate (%) 1.50 1.15 1.10 CVD risk (HR; 95% CI)a 1.01 (0.79–1.29) 1.00 (0.69–1.46) 0.39 (0.23–0.66)
Indices of diet quality and diet-related behaviours across SES groups
In order to understand why CVD protection was confined to high-SES individuals, we examined possible gaps (as measured by additional indicators of diet quality or dietary behaviours) still persisting among SES groups sharing similar adherence to the MD (MDS ≥ 6). In the multivariable model additionally controlled for the MDS, educational groups still differed for some diet-related indicators such as diet variety for vegetables and vegetable subgroups that were all higher in highly educated as compared with less educated subjects (Table 4; Figure 1a). Subjects with post-secondary education also reported increased intake of organic vegetables and whole-grain bread as well as higher daily intake of mono-unsaturated and saturated fatty acids, vitamin D, calcium and fibre (Figure 1a). No difference was recorded for any of the indicators used to assess dietary antioxidant or polyphenol content or total antioxidant capacity of the diet, and disparities in cooking methods were limited to vegetable preparation that was healthier in those with higher education (Table 4). In addition, highly educated subjects were more likely to report higher fish intake and low meat/meat products consumption but less likely to report low intake of dairy products (Supplementary Table 5A, available as Supplementary data at IJE online). Dietary intake of polyphenols, antioxidants, fibre and indicators of TAC were all increased in the higher income group as compared with the lowest. Greater income was also associated with increased prevalence of whole-grain bread consumption, and the diversity in vegetable and fruit intake was slightly higher in the lowest income group along with daily intake of MUFAs and PUFAs (Table 4; Figure 1b). Differences in cooking procedures were identified for healthier methods in preparing vegetables but more hazardous procedures for meat (Table 4). Individuals with greater income reported higher consumption of fruits and nuts and fish, and lower intake of meat and meat products (Supplementary table 5B).
Table 4 Educational level Household income groups (€/year) Lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Post-secondary/ higher (>13 years) P for trend <25 000 25 000– 40 000 >40 000 P for trend N of subjects 2340 1773 705 1706 1118 706 Food antioxidant content (score) 33 (39) 34 (38) 35 (38) 0.69 33 (40) 35 (37) 37 (38) 0.015 Polyphenols intake (score) 8.4 (10.7) 9.1 (10.7) 9.4 (10.7) 0.12 8 (11) 8 (10) 10 (11) 0.031 TEAC 6.6 (2.7) 6.7 (2.5) 6.8 (2.3) 0.38 6.6 (2.6) 6.7 (2.5) 7.0 (2.5) 0.054 TRAP 9.4 (4.1) 9.6 (4.0) 9.7 (3.5) 0.47 9.5 (4.1) 9.7 (3.9) 10.1 (4.0) 0.033 FRAP 19.7 (8.0) 20.2 (7.8) 20.4 (6.8) 0.25 20.0 (8.0) 20.2 (7.6) 21.1 (7.7) 0.030 MUFAs 39.9 (10.7) 40.0 (10.4) 40.2 (10.7) 0.034 8.9 (2.4) 8.9 (2.3) 8.8 (2.3) 0.99 PUFAs 8.7 (2.4) 8.7 (2.3) 8.7 (2.3) 0.38 40.6 (11.0) 40.9 (10.5) 39.8 (10.2) 0.13 SFAs 26.2 (8.6) 26.8 (8.8) 27.0 (8.9) <.0001 8.9 (2.5) 8.8 (2.3) 8.7 (2.2) 0.040 Dietary vitamin D 2.47 (0.98) 2.61 (1.00) 2.64 (1.06) <.0001 26.7 (8.7) 27.2 (8.8) 26.3 (8.9) 0.46 Dietary calcium 901 (290) 945 (311) 960 (317) <.0001 2.51 (0.99) 2.61 (1.02) 2.61 (1.02) 0.25 Dietary fibre 24.3 (6.7) 24.8 (6.8) 25.1 (7.1) 0.12 924 (297) 954 (307) 953 (322) 0.38 Diet diversity fruits (score) 8.9 (2.4) 8.8 (2.4) 8.8 (2.4) 0.15 24.5 (7.1) 24.6 (6.7) 25.9 (7.1) 0.0008 Diet diversity vegetables (score) 7.1 (2.4) 7.2 (2.5) 7.2 (2.5) 0.0005 7.3 (2.4) 7.2 (2.5) 6.9 (2.5) < 0.0001 Diet diversity vegetables subgroup (score) 4.20 (1.05) 4.20 (1.08) 4.23 (1.08) 0.016 4.2 (1.1) 4.2 (1.1) 4.2 (1.1) 0.34 Diet diversity fruit and veg (score) 16 (3.6) 15.9 (3.7) 15.9 (3.6) 0.15 16.2 (3.7) 16.1 (3.6) 15.7 (3.7) 0.0068 Organic vegetables consumers (%) 1.9 2.7 5.1 0.0047 2.2 2.3 4.7 0.08 Whole-grain bread consumers (%) 13.4 18.7 25.4 <.0001 13.8 19.0 21.8 0.018 Educational level Household income groups (€/year) Lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Post-secondary/ higher (>13 years) P for trend <25 000 25 000– 40 000 >40 000 P for trend N of subjects 2340 1773 705 1706 1118 706 Food antioxidant content (score) 33 (39) 34 (38) 35 (38) 0.69 33 (40) 35 (37) 37 (38) 0.015 Polyphenols intake (score) 8.4 (10.7) 9.1 (10.7) 9.4 (10.7) 0.12 8 (11) 8 (10) 10 (11) 0.031 TEAC 6.6 (2.7) 6.7 (2.5) 6.8 (2.3) 0.38 6.6 (2.6) 6.7 (2.5) 7.0 (2.5) 0.054 TRAP 9.4 (4.1) 9.6 (4.0) 9.7 (3.5) 0.47 9.5 (4.1) 9.7 (3.9) 10.1 (4.0) 0.033 FRAP 19.7 (8.0) 20.2 (7.8) 20.4 (6.8) 0.25 20.0 (8.0) 20.2 (7.6) 21.1 (7.7) 0.030 MUFAs 39.9 (10.7) 40.0 (10.4) 40.2 (10.7) 0.034 8.9 (2.4) 8.9 (2.3) 8.8 (2.3) 0.99 PUFAs 8.7 (2.4) 8.7 (2.3) 8.7 (2.3) 0.38 40.6 (11.0) 40.9 (10.5) 39.8 (10.2) 0.13 SFAs 26.2 (8.6) 26.8 (8.8) 27.0 (8.9) <.0001 8.9 (2.5) 8.8 (2.3) 8.7 (2.2) 0.040 Dietary vitamin D 2.47 (0.98) 2.61 (1.00) 2.64 (1.06) <.0001 26.7 (8.7) 27.2 (8.8) 26.3 (8.9) 0.46 Dietary calcium 901 (290) 945 (311) 960 (317) <.0001 2.51 (0.99) 2.61 (1.02) 2.61 (1.02) 0.25 Dietary fibre 24.3 (6.7) 24.8 (6.8) 25.1 (7.1) 0.12 924 (297) 954 (307) 953 (322) 0.38 Diet diversity fruits (score) 8.9 (2.4) 8.8 (2.4) 8.8 (2.4) 0.15 24.5 (7.1) 24.6 (6.7) 25.9 (7.1) 0.0008 Diet diversity vegetables (score) 7.1 (2.4) 7.2 (2.5) 7.2 (2.5) 0.0005 7.3 (2.4) 7.2 (2.5) 6.9 (2.5) < 0.0001 Diet diversity vegetables subgroup (score) 4.20 (1.05) 4.20 (1.08) 4.23 (1.08) 0.016 4.2 (1.1) 4.2 (1.1) 4.2 (1.1) 0.34 Diet diversity fruit and veg (score) 16 (3.6) 15.9 (3.7) 15.9 (3.6) 0.15 16.2 (3.7) 16.1 (3.6) 15.7 (3.7) 0.0068 Organic vegetables consumers (%) 1.9 2.7 5.1 0.0047 2.2 2.3 4.7 0.08 Whole-grain bread consumers (%) 13.4 18.7 25.4 <.0001 13.8 19.0 21.8 0.018
Table 4 Educational level Household income groups (€/year) Lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Post-secondary/ higher (>13 years) P for trend <25 000 25 000– 40 000 >40 000 P for trend N of subjects 2340 1773 705 1706 1118 706 Food antioxidant content (score) 33 (39) 34 (38) 35 (38) 0.69 33 (40) 35 (37) 37 (38) 0.015 Polyphenols intake (score) 8.4 (10.7) 9.1 (10.7) 9.4 (10.7) 0.12 8 (11) 8 (10) 10 (11) 0.031 TEAC 6.6 (2.7) 6.7 (2.5) 6.8 (2.3) 0.38 6.6 (2.6) 6.7 (2.5) 7.0 (2.5) 0.054 TRAP 9.4 (4.1) 9.6 (4.0) 9.7 (3.5) 0.47 9.5 (4.1) 9.7 (3.9) 10.1 (4.0) 0.033 FRAP 19.7 (8.0) 20.2 (7.8) 20.4 (6.8) 0.25 20.0 (8.0) 20.2 (7.6) 21.1 (7.7) 0.030 MUFAs 39.9 (10.7) 40.0 (10.4) 40.2 (10.7) 0.034 8.9 (2.4) 8.9 (2.3) 8.8 (2.3) 0.99 PUFAs 8.7 (2.4) 8.7 (2.3) 8.7 (2.3) 0.38 40.6 (11.0) 40.9 (10.5) 39.8 (10.2) 0.13 SFAs 26.2 (8.6) 26.8 (8.8) 27.0 (8.9) <.0001 8.9 (2.5) 8.8 (2.3) 8.7 (2.2) 0.040 Dietary vitamin D 2.47 (0.98) 2.61 (1.00) 2.64 (1.06) <.0001 26.7 (8.7) 27.2 (8.8) 26.3 (8.9) 0.46 Dietary calcium 901 (290) 945 (311) 960 (317) <.0001 2.51 (0.99) 2.61 (1.02) 2.61 (1.02) 0.25 Dietary fibre 24.3 (6.7) 24.8 (6.8) 25.1 (7.1) 0.12 924 (297) 954 (307) 953 (322) 0.38 Diet diversity fruits (score) 8.9 (2.4) 8.8 (2.4) 8.8 (2.4) 0.15 24.5 (7.1) 24.6 (6.7) 25.9 (7.1) 0.0008 Diet diversity vegetables (score) 7.1 (2.4) 7.2 (2.5) 7.2 (2.5) 0.0005 7.3 (2.4) 7.2 (2.5) 6.9 (2.5) < 0.0001 Diet diversity vegetables subgroup (score) 4.20 (1.05) 4.20 (1.08) 4.23 (1.08) 0.016 4.2 (1.1) 4.2 (1.1) 4.2 (1.1) 0.34 Diet diversity fruit and veg (score) 16 (3.6) 15.9 (3.7) 15.9 (3.6) 0.15 16.2 (3.7) 16.1 (3.6) 15.7 (3.7) 0.0068 Organic vegetables consumers (%) 1.9 2.7 5.1 0.0047 2.2 2.3 4.7 0.08 Whole-grain bread consumers (%) 13.4 18.7 25.4 <.0001 13.8 19.0 21.8 0.018 Educational level Household income groups (€/year) Lower secondary (≤8 years) Upper secondary (>8 ≤ 13 years) Post-secondary/ higher (>13 years) P for trend <25 000 25 000– 40 000 >40 000 P for trend N of subjects 2340 1773 705 1706 1118 706 Food antioxidant content (score) 33 (39) 34 (38) 35 (38) 0.69 33 (40) 35 (37) 37 (38) 0.015 Polyphenols intake (score) 8.4 (10.7) 9.1 (10.7) 9.4 (10.7) 0.12 8 (11) 8 (10) 10 (11) 0.031 TEAC 6.6 (2.7) 6.7 (2.5) 6.8 (2.3) 0.38 6.6 (2.6) 6.7 (2.5) 7.0 (2.5) 0.054 TRAP 9.4 (4.1) 9.6 (4.0) 9.7 (3.5) 0.47 9.5 (4.1) 9.7 (3.9) 10.1 (4.0) 0.033 FRAP 19.7 (8.0) 20.2 (7.8) 20.4 (6.8) 0.25 20.0 (8.0) 20.2 (7.6) 21.1 (7.7) 0.030 MUFAs 39.9 (10.7) 40.0 (10.4) 40.2 (10.7) 0.034 8.9 (2.4) 8.9 (2.3) 8.8 (2.3) 0.99 PUFAs 8.7 (2.4) 8.7 (2.3) 8.7 (2.3) 0.38 40.6 (11.0) 40.9 (10.5) 39.8 (10.2) 0.13 SFAs 26.2 (8.6) 26.8 (8.8) 27.0 (8.9) <.0001 8.9 (2.5) 8.8 (2.3) 8.7 (2.2) 0.040 Dietary vitamin D 2.47 (0.98) 2.61 (1.00) 2.64 (1.06) <.0001 26.7 (8.7) 27.2 (8.8) 26.3 (8.9) 0.46 Dietary calcium 901 (290) 945 (311) 960 (317) <.0001 2.51 (0.99) 2.61 (1.02) 2.61 (1.02) 0.25 Dietary fibre 24.3 (6.7) 24.8 (6.8) 25.1 (7.1) 0.12 924 (297) 954 (307) 953 (322) 0.38 Diet diversity fruits (score) 8.9 (2.4) 8.8 (2.4) 8.8 (2.4) 0.15 24.5 (7.1) 24.6 (6.7) 25.9 (7.1) 0.0008 Diet diversity vegetables (score) 7.1 (2.4) 7.2 (2.5) 7.2 (2.5) 0.0005 7.3 (2.4) 7.2 (2.5) 6.9 (2.5) < 0.0001 Diet diversity vegetables subgroup (score) 4.20 (1.05) 4.20 (1.08) 4.23 (1.08) 0.016 4.2 (1.1) 4.2 (1.1) 4.2 (1.1) 0.34 Diet diversity fruit and veg (score) 16 (3.6) 15.9 (3.7) 15.9 (3.6) 0.15 16.2 (3.7) 16.1 (3.6) 15.7 (3.7) 0.0068 Organic vegetables consumers (%) 1.9 2.7 5.1 0.0047 2.2 2.3 4.7 0.08 Whole-grain bread consumers (%) 13.4 18.7 25.4 <.0001 13.8 19.0 21.8 0.018
Discussion
In this large community-based Mediterranean population, higher adherence to MD was associated with lower risk of CVD in line with previous evidence.2,3,24 However, this relationship was confined in fact to high-SES groups. Specifically, a two-point increase in the MDS was associated with 57% lower risk of CVD for subjects with post-secondary education, or 61% lower risk in the highest category of household income, whereas no relationship was found for less educated groups or in the lower income categories.
To the best of our knowledge, this is the first study to show that the association between Mediterranean diet and CVD risk differs across SES groups.
Socioeconomic disparities in the composition of similar MDS
Given a comparable score of adherence to MD, both higher educational and higher income groups were more frequently found to consume higher intake of fish and lower amounts of meat. Many studies have documented the important role of the above-mentioned food groups in promoting favourable health effects25 and reducing main CVD risk factors.26 However, whether higher fish consumption and limited meat intake may contribute to the different CVD risk reduction across SES groups remain to be ascertained.
Socioeconomic disparities in nutrients and diet-related behaviours
Despite similar score of adherence to MD, post-secondary education was associated with higher diet variety for vegetables and vegetables subgroups, and with preference for whole-grain bread. Such educational gradient in food selection is in agreement with previous evidence indicating that higher SES groups are more likely to get in line with dietary recommendations.27 High education was also related to greater consumption of organic vegetables, which has been previously shown to be strongly determined by SES,13,28 although there is uncertainty on the actual health advantages deriving from organic food consumption.29 Educational disparities emerged also for MUFAs, dietary vitamin D, calcium and fibre, whose higher intake is associated with more favourable cardiovascular health. We also found differences across income groups sharing similar scores of adherence to the MD for dietary polyphenol and antioxidant intake, total antioxidant capacity of the diet, and preference for whole-grain bread.
For both high-education and high-income individuals, disparities in food preparation were limited to healthier cooking methods for vegetables, which are possibly associated with increased overall antioxidant content.14 Of note, high income was also associated with more hazardous cooking methods for beef (frying, roasting, grilling), and such high-temperature cooking techniques are more likely to propagate and accelerate formation of pro-inflammatory compounds associated with increased CVD risk.23,30
There are many studies indicating potential health benefits for each of these diet-related indices that in our study were found to vary consistently among SES groups, net of adherence to the MD. As highlighted in previous research, the nutritional properties of foods are closely dependent on external influences such as food processing and cooking procedures.14 Foods that are not discriminated in epidemiological studies may substantially differ in their bioactive compounds content, with different health outcomes.14 In our study, we also found that higher-SES subjects tend to consume more organic vegetables which can contain higher concentrations of antioxidants, lower concentrations of cadmium and a lower incidence of pesticide residues,29 as compared with conventionally grown foods. We might then speculate that the quality of the bundle of foods that make up the MD actually differs across SES.
Unfortunately, our data derive from self-reported dietary intakes, thus we are not able to unequivocally establish whether, given apparently similar adherence to an MD, high-SES groups actually select foods higher in polyphenols or antioxidants compounds that would result in future health advantages. This hypothesis could be only tested by a direct measure of such natural compounds in biological samples.
On the basis of our results and by accounting for all the limitations inherent to our approach, we suggest that at comparable levels of adherence to the MD, higher SES groups actually select foods with increased nutritional value as those higher in antioxidant content or capacity, and are more keen on reporting a larger variety in fruit and vegetable consumption, thus obtaining more adequate intake of essential nutrients. Such nutritional gaps may partly explain the observed socioeconomic pattern of protection derived from apparently similar scores of adherence to the MD. Of note, the interaction between diet and SES on CVD health outcomes was found both for cultural (education) and financial resources (income), likely indicating that healthier choices are driven either by a good set of knowledge and skills or greater financial resources.
In light of our findings, we speculate that standard dietary scores, although useful and valid parameters to quantify the adherence to the Mediterranean diet, may not fully capture the complexity of this diet, leaving out a number of additional dietary details mainly related to the quality of the products. If so, we would be dealing with a methodological limitation which may be overcome by the use of other tools to better appraise the dietary behaviours of a given population.
Strengths and limitations of this study
Major strengths of the present study include the large sample size, prospective study design, large number of indices of diet quality and diet-related behaviours, and comprehensive information on covariates, thus minimizing sources of bias and confounding.
Some potential limitations include the relatively short follow-up (and the consequent low number of events) and the observational nature of the study, which cannot fully rule out residual confounding. In addition, dietary data were based on self-reported information and therefore may be susceptible to error and bias. Moreover, although we tested a large number of indices for assessing diet beyond the MD, we are aware that several nutritional details may remain unaddressed, i.e. organic foods other than vegetables, and food purchasing behaviours consistent with dietary guideline recommendations. Finally, subjects’ information was collected at baseline only; thus, life course changes possibly occurring during follow-up may influence the strength of the findings.
Conclusions
To the best of our knowledge, this large epidemiological study in a population-based cohort is the first to shed light on SES inequities in the cardiovascular protection associated with a traditional Mediterranean diet. From a public health perspective, these results support the need to adopt more effective strategies aiming to reduce socioeconomic disparities in health, not only by promoting the adoption of healthy eating patterns but also by facilitating access to foods with higher nutritional values likely associated with improved health outcomes.
Supplementary Data
Supplementary data are available at IJE online.
Funding
The enrolment phase of the Moli-sani Study was supported by research grants from the Pfizer Foundation (Rome, Italy), the Italian Ministry of University and Research (MIUR, Rome, Italy)–Programma Triennale di Ricerca, Decreto no.1588 and Instrumentation Laboratory, Milan, Italy. M.B. was supported by a Fondazione Umberto Veronesi Fellowship. The present analyses were partially supported by the Italian Ministry of Health [Grant number GR-2013‐02356060]. Funders had no role in study design; collection, analysis or interpretation of data; the writing of the manuscript; or the decision to submit the article for publication.
Key Messages Adherence to the Mediterranean diet is inversely associated with cardiovascular risk.
Cardiovascular advantages associated with the Mediterranean diet are confined to high socioeconomic status individuals.
In groups sharing similar adherence to the Mediterranean diet, inequities in diet-related behaviours and nutrient intake still persist.
Acknowledgements
The Moli-sani research group thanks the Associazione Cuore Sano Onlus (Campobasso, Italy) for its financial and cultural support.
Author Contributions
M.B., L.I. and A.D.C. contributed to the concept and design of the work and interpretation of data; S.C., M.P. and G.P. managed data collection; M.B. and A.D.C. analysed the data; M.B. wrote the paper; M.B.D., C.C., G.d.G. and L.I. originally inspired the research and critically reviewed the manuscript.
Conflict of interest: None of the authors had a personal or financial conflict of interest. All authors were and are independent from funders.
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Jeff Lagerquist, CTVNews.ca
Choosing a Mediterranean diet has long been linked to a bevy of health benefits, including reduced risk of heart disease and lower rates of cancer. But new research shows if you are going to mimic the eating habits of someone who hails from the region, you had better make sure they are rich and highly educated.
Mainstays of the Mediterranean diet include a high intake of vegetables, legumes, fruits, nuts and unrefined cereals, as well as plenty of olive oil, moderate intake of fish, and low-to-moderate dairy, low red meat and poultry, and moderate wine consumption, according to a 2003 study published in the New England Journal of Medicine.
A new Italian study led by a team of researchers at IRCCS Neuromed looked at the dietary information of 18,991 southern Italian men and women over 35 between March 2005 and April 2010.
The sample group did not include individuals with a history of cardiovascular disease, diabetes, inordinately high or low calorie intakes, or incomplete personal data.
Socioeconomic information and food intake statistics were collected through questionnaires. The researchers measured factors such as food antioxidant content, variety of fruits and vegetable intake, health of cooking practices (boiling, frying, roasting, grilling), organic food intake, and consumption of whole grain products.
Overall adherence to the Mediterranean diet was given a score measured against the definition outlined by the 2003 New England Journal of Medicine study.
More than 250 cardiovascular disease events were recorded over a median follow-up period of 4.3 years.
Overall, a two-point increase in participants’ Mediterranean diet scores resulted in a 15 per cent decline in cardiovascular disease risk.
But that benefit did not materialize for less educated subjects. Similarly, the cardiovascular disease fighting benefits were confined to the high-income households, compared to lower-earning peers.
“Given a comparable adherence to this eating pattern, the study has shown that the reduction in cardiovascular risk is observed only in people with a higher educational level and/or greater household income. No actual benefits were observed for the less advantaged groups,” said the study’s authors in a release accompanying the study.
The cardiovascular disease findings are even more striking when high education, high income individuals are observed in isolation.
The study notes a two-point increase in the Mediterranean diet score drops cardiovascular disease risk by 57 per cent among those with post-secondary education, and 61 per cent for those in the highest category of household income.
Once again, no such relationship was observed among the less educated and less wealthy.
The difference comes down to “different intakes of antioxidants and polyphenols, fatty acids, micronutrients, dietary antioxidant capacity, dietary diversity, organic vegetables and whole grain bread consumption,” according to the study.
The more highly educated subjects were found to eat a wider variety of vegetables, more organic produce, and whole grain breads. They also opted for higher fish intake versus meat consumption. Greater income was also associated with eating more fruits, nuts and fish, and eating fewer meat products.
The study’s authors admit the limitations of self-reported dietary intake profiles means the research falls short of establishing a direct link between better-heeled groups and the selection of more nutritious food. However, they suggest their findings make a strong case for further investigation of into the role of income and education on diet-based health outcomes.
“Socioeconomic disparities in health are growing, also in access to healthy diets,” wrote IRCCS Department of Epidemiology and Prevention head Giovanni de Gaetano. “We cannot be keeping on saying that the Mediterranean diet is good for health if we are not able to guarantee an equal access to it.”
The findings were based on subjects within the Moli-sani study, which has examined environmental and genetic factors underlying cardiovascular disease, cancer, and degenerative pathologies for the past 12 years.
The research has been published in the International Journal of Epidemiology. ||||| The Mediterranean diet reduces the risk of cardiovascular disease but only if you are rich or highly educated. This is the surprising finding by researchers from the Italian I.R.C.C.S. Neuromed, who performed a study on over 18,000 subjects recruited within the Moli-sani study and published in the International Journal of Epidemiology.
Cardiovascular advantages associated with the Mediterranean diet are well-known but now the Italian study, conducted by a team of researchers at the Department of Epidemiology and Prevention led by Giovanni de Gaetano, reveals that such benefits are strongly influenced by the socioeconomic position of people. Basically, given a comparable adherence to this eating pattern, the study has shown that the reduction in cardiovascular risk is observed only in people with higher educational level and/or greater household income. No actual benefits were observed for the less advantaged groups.
"The cardiovascular benefits associated with the Mediterranean diet in a general population are well known -- says Marialaura Bonaccio, researcher at the Department of Epidemiology and Prevention and first author of the study -- Yet for the first time our study has revealed that the socioeconomic position is able to modulate the health advantages linked to Mediterranean diet. In other words, a person from low socioeconomic status who struggles to follow a Mediterranean model, is unlikely to get the same advantages of a person with higher income, despite the fact that they both similarly adhere to the same healthy diet".
Neuromed researchers went further and tried to unravel the possible mechanisms underlying such disparities.
"Given a comparable adherence to the Mediterranean diet, the most advantaged groups were more likely to report a larger number of indices of high quality diet as opposed to people with low socioeconomic status -- explains Licia Iacoviello, head of the Laboratory of nutritional and molecular Epidemiology at the Department -- For example, within those reporting an optimal adherence to the Mediterranean diet (as measured by a score comprising fruits and nuts, vegetables, legumes, cereals, fish, fats, meat, dairy products and alcohol intake) people with high income or higher educational level consumed products richer in antioxidants and polyphenols, and had a greater diversity in fruit and vegetables choice. We have also found a socioeconomic gradient in the consumption of whole-grain products and in the preferred cooking methods. These substantial differences in consuming products belonging to Mediterranean diet lead us to think that quality of foods may be as important for health as quantity and frequency of intake".
"Our results should promote a serious consideration of socioeconomic scenario of health - comments Giovanni de Gaetano, director of the Department -- Socioeconomic disparities in health are growing also in access to healthy diets. During the very last years, we documented a rapid shifting from the Mediterranean diet in the whole population, but it might also be that the weakest citizens tend to buy 'Mediterranean' food with lower nutritional value. We cannot be keeping on say that the Mediterranean diet is good for health -- de Gaetano concludes -- if we are not able to guarantee an equal access to it".
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The Moli-sani Project
Started in March 2005, it involves about 25,000 citizens living in the Molise region. The aim is to learn about environmental and genetic factors underlying cardiovascular disease, cancer and degenerative pathologies. Moli-sani study, now based in I.R.C.C.S. Neuromed, has transformed an entire Italian region in a large research lab.
The I.R.C.C.S. Neuromed
The Institute for Research, Hospitalization and Health Care (I.R.C.C.S.) Neuromed in Pozzilli (Italy) is a landmark, at Italian and international level, for research and therapy in the field of nervous system diseases. A center in which doctors, researchers, staff and the patients themselves form an alliance aimed at ensuring the best level of service and cutting-edge treatments, guided by the most advanced scientific developments. ||||| | – Despite its many purported advantages, the Mediterranean diet might not be all it's cracked up to be. According to a new study in the International Journal of Epidemiology, its effects depend largely on socioeconomic status. Researchers surveyed 19,000 people ages 35 and over in Italy, giving each a score based on how closely they followed the Mediterranean diet, ranging from 1 on the low end up to 6 or more. After just over four years, they found a two-point increase in score meant a 15% reduced risk of cardiovascular disease overall—but not for participants with low incomes and minimal education. While a two-point increase meant a reduced risk of 61% for those with a household income of at least $47,000, and 57% for those with post-secondary education, "no actual benefits were observed for the less advantaged groups," per a release. Despite similar adherence to the diet, that remained the case after researchers accounted for healthy habits common among the rich, like getting plenty of exercise, avoiding smoking, and making regular visits to the doctor, per HealthDay News. Researchers suspect that's because people with higher education or income tended to eat a greater variety of foods, as well as more whole grains, organic produce, and fish, which can be expensive, per CTV News. They also prepared vegetables in healthier ways. Together, this means they benefited from a "more adequate intake of essential nutrients," says study author Giovanni de Gaetano. He suggests experts should stop promoting the diet "if we are not able to guarantee an equal access to it." (Read about its brain benefits here.) | multi_news_1_0_0 |
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Carbohydrates, long blamed for fuelling obesity, have now been linked to lung cancer.
A new study has revealed a 49 per cent increase in risk among people consuming a diet with a high glycemic index.
The index measures how quickly blood sugar levels are raised after a meal, and foods with a high GI include white bread or bagels, corn flakes and puffed rice.
However, diets high in fruits and vegetables were found to decrease the risk.
Lead study author Dr Stephanie Melkonian, of University of Texas MD Anderson Cancer Center, said: "We observed a 49 per cent increased risk of lung cancer among subjects with the highest daily GI compared to those with the lowest daily GI.
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"Diets high in glycemic index result in higher levels of blood glucose and insulin, which promote perturbations in the insulin-like growth factors (IGFs).
"Previous research suggests increased levels of IGFs are associated with increased lung cancer risk.
"However, the association between glycemic index and lung cancer risk was unclear."
In the UK, there are around 45,525 new cases of the disease diagnosed each year, while 35,371 people lose their life to the disease annually, according to Cancer Research UK.
Photo: Alamy
In the US, lung cancer is the second most common cancer in both men and women.
Five cancer red flags to never ignore
The study, published in the journal Cancer Epidemiology, Biomarkers & Prevention, is the largest ever to investigate the potential link between glycemic index and lung cancer.
Scientists surveyed 1,905 patients newly diagnosed with lung cancer and compared the results with 2,413 healthy individuals.
Senior study author Dr Xifeng Wu said: "The associations were more pronounced among subjects who were never smokers, diagnosed with squamous cell carcinoma or had less than 12 years of education.
"This suggests that it is the average quality, instead of quantity, of carbohydrates consumed that may modulate lung cancer risk."
Photo: Alamy
Dr Wu added: "The results from this study suggest that, besides maintaining healthy lifestyles, such as avoiding tobacco, limiting alcohol consumption and being physically active, reducing the consumption of foods and beverages with high glycemic index may serve as a means to lower the risk of lung cancer."
• Lung cancer victims lack sympathy ||||| Scientists from the University of Texas MD Anderson Cancer Center have found that people who eat a diet full of high glycemic index foods—think processed white bread, bagels, white rice, baguettes—had a 49% higher risk of developing lung cancer, even if they’ve never smoked a single cigarette.
The study, which was published in Cancer Epidemiology, Biomarkers & Prevention this week, is the largest ever to investigate the potential links between glycemic index and lung cancer, according to the authors. A glycemic index is a measurement of how rapidly carbohydrates elevate blood sugar levels in the body. The higher the glycemic index, the more rapidly blood sugar levels rise after a meal which results in elevated levels of blood glucose and insulin. That in turns raises what’s called insulin-like growth factors, which are linked to an increased lung cancer risk, according to the scientists.
Scientists at MD Anderson surveyed 1,905 patients newly diagnosed with lung cancer and another 2,413 healthy individuals, all non-Hispanic whites. Those subjects reported their past dietary habits and health histories, and they were then divided into groups based on their associated glycemic index and glycemic load, a measure of carbohydrate quantity.
“We observed a 49% increased risk of lung cancer among subjects with the highest daily glycemic index compared to those with the lowest daily glycemic index,” said Xifeng Wu, professor of epidemiology and senior author of the study. “The associates were more pronounced among subjects who were never smokers.”
Interestingly, there was no link between the glycemic load—i.e. the quantity of carbohydrates consumed—and lung cancer, which suggests that it’s the quality, not the amount of carbohydrates, that has the biggest effect on lung cancer risk, said Wu.
Lung cancer is the second most common cancer among both men and women in the U.S. It’s also the leading cause of cancer mortality, with over 150,000 deaths from lung cancer expected in the U.S. this year alone, according to the American Cancer Society. Smoking and tobacco use is still the leading cause, though it doesn’t account for all cases. Researchers had long suspected a link between a high-glycemic index diet and lung cancer risk, but the link between the two was unclear until now.
Among non-smokers in the study, those within the highest glycemic index group were more than twice as likely to develop lung cancer as those in the lowest group. For smokers, the difference was elevated by 31% between the two groups.
“The results from this study suggest that, besides maintaining healthy lifestyles, such as avoiding tobacco, limiting alcohol consumption, and being physically active, reducing the consumption of foods and beverages with high glycemic index may serve as a means to lower the risk of lung cancer,” said Wu.
Low glycemic index foods include things like 100% stone-ground whole wheat bread, rolled or steel-cut oatmeal, most fruits, and non-starchy vegetables. ||||| Breaking News Emails Get breaking news alerts and special reports. The news and stories that matter, delivered weekday mornings. SUBSCRIBE
People who eat a sugary, starchy diet may be raising their risk of lung cancer, even if they don’t smoke, researchers say.
They found that people who recall eating more foods that have a high glycemic index also were more likely to develop lung cancer. Glycemic index is a term that’s familiar to people with diabetes. It describes food that raises blood sugar and stimulates production of insulin — think bagels, white rice and some fruits such as melon and pineapple.
It’s not the first study to link glycemic index with cancer risk, but it’s rare to link it with lung cancer. That may be mostly because lung cancer is so overwhelmingly caused by smoking.
The team at MD Anderson Cancer Center in Houston studied 1,905 people who had just been diagnosed with lung cancer and compared them to 2,415 people without cancer. They quizzed them about their eating habits, smoking, income and other factors.
"Reducing the consumption of foods and beverages with high glycemic index may serve as a means to lower the risk of lung cancer."
People who ate the most foods with a high glycemic index were about 50 percent more likely to be in the lung cancer group than people who reported they ate the fewest high-glycemic foods, the team reported in the journal Cancer Epidemiology and Biomarkers.
The link was stronger among people who never smoked; non-smokers were more than twice as likely to have lung cancer if they reported eating a high-glycemic diet.
“The results from this study suggest that, besides maintaining healthy lifestyles, reducing the consumption of foods and beverages with high glycemic index may serve as a means to lower the risk of lung cancer,” said Dr. Xifeng Wu, who led the study.
Related: Here's how sugar might fuel the growth of cancer
How can this happen? Doctors aren’t sure, but there’s a theory that high-glycemic foods stimulate the body to make insulin, which in turn affects the growth of cells via compounds called insulin-like growth factors or IGF. Cancer is the uncontrolled proliferation of cells, so it might be that the high-glycemic foods are fueling the growth of tiny tumors.
“IGFs have been shown to play a critical role in regulating cell proliferation and differentiation in cancer and there is evidence to suggest that IGFs are elevated in lung cancer patients,” Wu’s team wrote.
It’s a suspect in several types of cancer.
“Previous studies have investigated the association between glycemic index, and the related measure glycemic load, and a variety of cancers including colorectal, stomach, pancreas, endometrial, ovarian, prostate, and thyroid but these studies are limited and results have been largely inconclusive,” the researchers wrote.
This study is not conclusive, either. For one thing, the researchers asked their volunteers to remember what they ate. For another, it’s an association. People who eat high-glycemic foods may also do something else that also raises their risk of cancer. And this particular study focused only on non-Hispanic white people.
Marji McCullough, an expert in nutritional epidemiology at the American Cancer Society, says it will be important to look at people who don't have cancer now and watch what they eat for years or decades, and see who develops cancer.
Related: Cancer experts are mad about the dietary guidelines
Lung cancer is the No. 1 cancer killer in the U.S., killing more than 150,000 people a year. It causes only vague symptoms at first, so when most people are diagnosed, the cancer has already spread and is then far more likely to be fatal.
Experts know diet and lifestyle can affect cancer. Obesity, lack of exercise, eating red meat and lots of high-fat dairy foods, and eating too few fruits and vegetables can all raise a person’s odds of developing cancer.
This study adds to a growing body of evidence that people can lower their cancer risk not only by staying away from tobacco and exercising more, but by choosing a healthier diet.
"Aside from not smoking, it’s important to follow cancer prevention guidelines that maintain healthy body weight, physical activity, and eating an overall healthy diet rich in vegetables and plant food and lower red and processed meat. Choose foods that help maintain healthy body weight," McCullough said.
According to the American Diabetes Association, low-glycemic foods include:
100 percent stone-ground whole wheat or pumpernickel bread
Oatmeal (rolled or steel-cut), oat bran, muesli
Pasta, converted rice, barley, bulgar
Sweet potato, corn, yam, lima/butter beans, peas, legumes and lentils
Most fruits, non-starchy vegetables and carrots
Medium glycemic index foods include:
Whole wheat, rye and pita bread
Quick oats
Brown, wild or basmati rice, couscous
High glycemic index foods include: ||||| Abstract
Background: Postprandial glucose (PPG) and insulin responses play a role in carcinogenesis. We evaluated the association between dietary glycemic index (GI) and glycemic load (GL), markers of carbohydrate intake and PPG, and lung cancer risk in non-Hispanic whites.
Methods: GL and GI were assessed among 1,905 newly diagnosed lung cancer cases recruited from the University of Texas MD Anderson Cancer Center (Houston, TX) and 2,413 healthy controls recruited at Kelsey-Seybold Clinics (Houston, TX). We assessed associations between quintiles of GI/GL and lung cancer risk and effect modification by various risk factors. ORs and 95% confidence intervals (CI) were estimated using multivariable logistic regression.
Results: We observed a significant association between GI [5th vs. 1st quintile (Q) OR = 1.49; 95% CI, 1.21–1.83; P trend <0.001] and lung cancer risk and GI ac (5th vs. 1st Q OR = 1.48; 95% CI, 1.20–1.81; P trend = 0.001) and lung cancer risk. We observed a more pronounced association between GI and lung cancer risk among never smokers (5th vs. 1st Q OR = 2.25; 95% CI, 1.42–3.57), squamous cell carcinomas (SCC; 5th vs. 1st Q OR = 1.92; 95% CI, 1.30–2.83), and those with less than 12 years of education (5th vs. 1st Q OR = 1.75; 95% CI, 1.19–2.58, P interaction = 0.02).
Conclusion: This study suggests that dietary GI and other lung cancer risk factors may jointly and independently influence lung cancer etiology.
Impact: Understanding the role of GI in lung cancer could inform prevention strategies and elucidate biologic pathways related to lung cancer risk. Cancer Epidemiol Biomarkers Prev; 25(3); 532–9. ©2016 AACR. |||||
What is a one-paragraph summary of the above article? | – That morning bagel, bowl of corn flakes, or packet of instant oatmeal could be increasing your risk of lung cancer, according to a study published this month. NBC News reports researchers in Texas found a link between foods with a high glycemic index and lung cancer, which kills more Americans per year than any other cancer. After comparing the diets of more than 1,900 people with lung cancer and more than 2,400 without it, researchers found a 49% increase in lung cancer risk for those who ate the most high glycemic foods versus those who ate the least, according to the Telegraph. Forbes reports the glycemic index measures how quickly carbs raise blood sugar levels. Foods with a high glycemic index include white bread, many breakfast cereals, white rice, pineapple, melons, popcorn, and more. High glycemic foods have been linked to other cancers in the past, but doctors aren't sure why they would contribute to lung cancer. One possibility is that as foods with a high glycemic index increase insulin levels, they also increase insulin-like growth factors. Those IGFs could play a role in growing small tumors. Another interesting result from the study: nonsmokers who ate a lot of high glycemic foods were more than twice as likely to have lung cancer than nonsmokers who ate the least amount of those foods. While the study isn't conclusive, the doctor who led it says eating foods with a low glycemic index may lower the risk of lung cancer. Those foods include stone-ground whole wheat bread, rolled oatmeal, non-starchy vegetables, and most fruits. (These five states have the most cancer deaths.) | multi_news_1_0_0 |
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