Datasets:

Query-of-CC
/

Knowledge_Pile

Dataset card Data Studio Files Files and versions Community

Split (1)

train · 1.07M rows

content stringlengths 71 484k	url stringlengths 13 5.97k
The source of the English word Aryan comes from the Sanskrit word ārya, which is the self-designation used by the Vedic... The Indus Written by Andrew Robinson and published by Reaktion Books in 2015, The Indus is an introduction to the Indus Valley Civilization... Indus Script The Indus Script is the writing system developed by the Indus Valley Civilization and it is the earliest form of writing... Religious Developments in Ancient India For well over 1,000 years, sacred stories and heroic epics have made up the mythology of Hinduism. Nothing in these complex... Initiation of religions in India The religious practices of the early Indo-Aryans, known as the Vedic religion (1500 BCE to 500 BCE) were written down... Ancient India India is a country in South Asia whose name comes from the Indus River. The name `Bharata’ is used as a designation... Brahmi Script The Brahmi script is the earliest writing system developed in India after the Indus script. It is one of the most influential... The History of Ancient India The earliest imprints of human activities in India go back to the Paleolithic Age, roughly between 400,000 and 200,000... Mohenjo-daro the Ancient Indus Valley City in Photographs Mohenjo Daro, or "Mound of the Dead" is an ancient Indus Valley Civilization city that flourished between 2600 and 1900... Banner at the North Gate of Dholavira The 10 Harappan alphabets/signs found at the Northern Gate of the ancient Indus Valley Civilization city of Dholavira... Indus Valley Seals Seals with Indus Script from Indus Valley Civilizations. Harappa: An Overview of Harappan Architecture and Town Planning Introduction Harappa is a large village presently in the province of Punjab in Pakistan. The modern town...	https://www.ancient.eu/related/1-10070/1/
The religious studies program offers an opportunity to study religion from an academic, multicultural, and global point of view. The interdisciplinary courses will expand students' knowledge beyond Western, monotheistic religions to include Eastern, African, and Native American faith traditions. Students who enroll in this minor explore the nature of religious beliefs and the role of language, metaphor, culture, and social institutions in establishing these views. The program's curriculum emphasizes the history of religious practices and how they have changed over time. Program Requirements The minor in religious studies is available to students in any major who are in good standing at the University. To obtain the minor, students must successfully complete 18 credits as designated below: 1. REL 100 Religion and Human Culture (3 credits) - All students are required to complete this course or the REL Ethical Inquiry Core course with a grade of C or better. 2. Multiple Religious Systems (6 credits) Select any two of the following courses: PHI 230 Philosophy of Religion PSY 399 Psychology of Religion SOC 334 Sociology of Religion HTY 309 Religious Violence and Persecution in Early Western History REL 200 Humanity's Spiritual Heritage 3. Non-Western Religious Systems (3 credits) Select one of the following: HTY 377 Chinese Thought: Confucianism, Daoism and Zen Buddhism PHI 315 Eastern Philosophy HTY 390 Traditional Japan: Court and Warriors 4. Western/Monotheistic Religious Systems (3 credits) Select one of the following: HTY 307 Judaism, Christianity, and Islam HTY 366 History of Religion in America HTY 308 Polytheists, Jews and Christians in the Roman Empire 5. Electives (3 credits) Select one additional course from any of the above categories or from those listed below: ARH 322 Medieval Art ARH 323 Renaissance Art ARH 329 Asian Art COR 122 Introduction to Islamic Civilization CLA 285 Classical Mythology ENG 316 The Bible ENG 317 Studies in Ancient and Biblical Literature and Culture HTY 152 The Islamic Near East HTY 305 The Historical Jesus HTY 312 Renaissance and Reformation HTY 334 The Holocaust: Policy, Practice, Response HTY 308 Polytheism, Judaism, and Christianity in the Roman Empire HTY 309 Religious Violence and Persecution in Early Western History Course Descriptions REL 100 Religion and Human Culture This course is an analytical survey of topics central to religious thought and practice. It considers religion as a worldwide human phenomenon, attempts to extract data about religion from multiple sources and contexts, and focuses upon the common functions of religion from a global perspective. The course also aims to develop sensitivity to topics and issues of a sacred and secular nature as they impact the daily lives of people in a variety of social, cultural, and religious settings. Cr 3. REL 101 The Language of Spiritual Texts: Answering the Problem of Violence Close reading of texts with explicitly spiritual content from world traditions, include the Bible, the Tao te Ching, the Koran, and others, ancient and modern. Inquiry as to whether or not such texts offer answers to the problem of violence. Theory and practice of contemplative as well as critical approaches to language that expresses spiritual experience will be explored. REL 200 Humanity's Spiritual Heritage This course uses a textual, chronological, and interfaith approach to trace the historical development, practices, and principles of the world's religions and spiritual traditions. Using the world's scriptures as primary texts, each faith community speaks for itself, allowing an exploration of the richness underlying the diversity of sacred expressions. Special emphasis is placed upon recognizing differences as well as the similarities in humanity's belief systems.	https://usm.maine.edu/catalogs/2013-14/minor-religious-studies
Please note: This is NOT the most current catalog. Ancient Studies http://wp.stolaf.edu/classics/ Director, 2014-15: Anne H. Groton, Greek and Roman drama Founded by the Department of Classics in 1971, ancient studies is one of St. Olaf’s oldest interdisciplinary programs. In scope it spans the more than two millennia between Greece’s Bronze Age and the fall of the Roman Empire. Combining art, history, language, literature, philosophy, and religion, it encourages students to take a broad look at classical culture, examining it from multiple perspectives. The ancient studies program has no courses of its own; instead it relies on courses offered by individual departments. Students who major in ancient studies choose electives from among the various departmental courses that deal primarily or entirely with the world of ancient Greece and Rome. Many of these courses also satisfy general education requirements. The required courses in Greek or Latin can simultaneously fulfill the college’s foreign language requirement. It is common for St. Olaf students to combine an ancient studies major with a B.A. major like art history, English, history, philosophy, political science, or religion. Even mathematics or natural science majors often complete a second major in ancient studies. The major provides a useful background in the humanities for students interested in virtually any career. OVERVIEW OF THE MAJOR The objectives of the major are competence in ancient Greek or Latin at the intermediate level, familiarity with ancient Greek and Roman civilization, and in-depth knowledge of one subject area within the major. Any student interested in an ancient studies major should draw up a contract with the program’s director. The contract may be changed at any time up to second semester of the senior year. INTENDED LEARNING OUTCOMES FOR THE MAJOR REQUIREMENTS FOR THE MAJOR Students majoring in ancient studies must complete the fourth semester (or higher) of ancient Greek or Latin, one ancient history course, a classics course, four electives chosen from various departments, and an independent research. The following courses have been approved for the major (seminars and topics courses are acceptable only when they focus on the ancient world): Art 275: Topics in Art History Classics 241: Greek and Roman Myth Classics 243: The Golden Age of Greece Classics 244: The Golden Age of Rome Great Conversation 113: The Tradition Beginning: The Greeks and the Hebrews Greek 253: New Testament Greek (or any other Greek course beyond 231) History 101: Ancient Warfare History 190: Europe from the Ancients to the Renaissance History 201: Major Seminar: Ancient History History 203: Ancient: Greece History 204: Ancient: Rome History 205: Ancient: Near East History 299: Topics in History History 302: Greek Civilization History 303: Roman Civilization Latin 252: Vergil and Latin Epic (or any other Latin course beyond 231) Philosophy 235: Ancient Western Philosophy Philosophy 374: Seminar in the History of Philosophy Political Science 299: Topics in Political Science Religion 221: Jesus in Scripture and Tradition Religion 222: The Biblical God Religion 223: Paul: His Letters, His Gospel Religion 273: Hebrew Prophets in History and Christian Tradition Religion 276: Ethics of Jesus Religion 302: History of Christian Thought I Religion 320: Top: Interpreting Sacred Texts Religion 391: Biblical Seminar Religion 392: Sem: Studies in Religion Seminar Religion 399: Thematic Seminar Theater 270: History of Theater up to 1700 298: Independent Study 398: Independent Research Those who fulfill the major's language requirement with Latin may use one Greek course as an elective; those who fulfill the major's language requirement with Greek may use one Latin course as an elective. Interim or summer courses such as: Classics 121: "Western" Greeks and Eastern "Barbarians" in Antiquity Classics 126: Ancient Comedy: A Funny Thing Happened Classics 128: The Fall of the Roman Empire and the Rise of Christianity Classics 129: The Neverending Myth: Ovid's Metamorphoses Classics 251: Classical Studies in Greece (abroad) Great Conversation 115: The Tradition Continuing: The Romans and the Christians History 202: Mediterranean Archaeology Field School Religion 271: Bible in Context: History, Geography, and Culture in Israel and Palestine (abroad) Religion 272: Sacred Places in Greece and Turkey and other courses offered occasionally or only once (including courses at Carleton College) may also be used as electives. See the director for information on courses offered in a particular year. To attain distinction in ancient studies, a student must demonstrate talent with ancient Greek or Latin, skill in conducting research on an ancient topic, and broad knowledge of ancient Western civilization. Specific guidelines are available from the director of ancient studies. Ancient studies majors who wish to pursue distinction should notify the director of the program no later than January 1 of their senior year.	https://www.stolaf.edu/catalog/1415/academicprogram/ancient-studies.html
Brendan has been a high school social studies teacher and author in the Eastern United States since 2015. He has shared his passion for history with students through teaching American, African American, and Modern World History at several schools. At different points in his life he has lived and studied in Ireland, Australia, and South Africa in addition to the US. Ancient Origins has been quoted by: At Ancient Origins, we believe that one of the most important fields of knowledge we can pursue as human beings is our beginnings. And while some people may seem content with the story as it stands, our view is that there exist countless mysteries, scientific anomalies and surprising artifacts that have yet to be discovered and explained. The goal of Ancient Origins is to highlight recent archaeological discoveries, peer-reviewed academic research and evidence, as well as offering alternative viewpoints and explanations of science, archaeology, mythology, religion and history around the globe. We’re the only Pop Archaeology site combining scientific research with out-of-the-box perspectives. By bringing together top experts and authors, this archaeology website explores lost civilizations, examines sacred writings, tours ancient places, investigates ancient discoveries and questions mysterious happenings. Our open community is dedicated to digging into the origins of our species on planet earth, and question wherever the discoveries might take us. We seek to retell the story of our beginnings.	https://www.ancient-origins.net/users/brendan-beatty
To Western eyes, China is one of the most mysterious and intriguing of all civilizations. The legacy of its long dynastic rule, extending back more than 3,000 years, includes fascinating contributions to philosophy, religion, art, science, and mythology that continue to influence the modern world. China explores the ideas and achievements of this unique culture through a combination of authoritative, accessible scholarship and magnificent imagery. Drawing on the most recent discoveries and theories, the book presents China's history, society, and beliefs from the legends of prehistory to the end of imperial power in 1912. It investigates the key cultural, spiritual, and artistic traditions of this vast civilization and describes the country's major scientific and technological innovations, such as gunpowder, printing, and the compass. An investigation of trading routes, both by land and sea, challenges the conventional view of China as an isolated, insular civilization, stressing instead the impact of its sophisticated society upon the world. A final section discusses the continuing legacy of the imperial period through the turbulent years of the twentieth century up to the present day. A wealth of color photography and imaginative artwork, together with a lively and authoritative text, vividly evokes the pinnacles of Chinese civilization as well as the realities of everyday life, from life in the Imperial court to the most rural villages. Title: China: Empire and Civilization Categories: Asia,	https://www.pioneerbook.com/product/28005/China-Empire-and-Civilization-Edward-L-Shaughnessy
Today on the Art 4 All People airwaves we will be chatting with Leigh McCloskey about Art, transformation and healing. We will also delve into the realms of archetype, personal mythology, and the MUSE. Which is our (Art 4 All People's) Arts and Healing exhibition MUSE: The Art of Transformation and Healing. at Commonweal in Bolinas, CA. About Leigh: In many ways Leigh J. McCloskey is a modern Renaissance Man. His interest, knowledge, study and learning ranges from art, music, history, religion, mythology, philo-Sophia and esotericism to string theory, quantum physics and the multidimensional nature of consciousness. He has deeply studied Hermeticism, Alchemy and Kabbalah and has hosted twice weekly philosophical salons at his home, Olandar, for over thirty years. He has written, illustrated and published six books. He lectures both nationally and internationally and has given numerous talks and presentations of his holographic art and visual philosophy. Leigh has contributed numerous essays on topics ranging from William Blake and the Heroic Imagination, the Archetypal Tarot & the Kabbalah, to Jacob Boehme and Theosophical Thought. Leigh is also an accomplished actor whose professional career has spanned four decades. His life and works reveal remarkable artistry, vision and discipline and are a reminder that we are far more interesting than we have lead ourselves to believe. He founded Olandar Foundation for Emerging Renaissance (OFFER) as a seed idea meant to awaken our deepest knowing and to stimulate the emerging waters of imaginative renaissance & rebirth.	https://www.blogtalkradio.com/art4allpeople/2014/09/03/the-flowering-of-creation-interview-with-leigh-mccloskey
Nothing in this complex and colorful mythology is fixed and firm. Although there is an emphasis on personal spirituality, Hinduism's history is closely linked with social and political developments, such as the rise and fall of different kingdoms and empires. Hinduism - Hinduism - The history of Hinduism: The history of Hinduism in India can be traced to about 1500 bce. The Monkeys and the Mango Tree: Teaching Stories of the Saints and Sadhus of India Harish Johari. Hinduism for Kids > Stories With A Moral. Stories from Hinduism (Hardcover). Hinduism is believed to be the oldest religion in the world with its traditions dating back over 4,000 years. Hinduism is the oldest and one of the most complex of all religious systems. January 2021. About the Author… This website has been conceived and being developed by C.V.Rajan. Mahatma Gandhi's killer venerated as Hindu nationalism resurges in India. The soul is immortal, and when a person dies, it takes another body just like how we wear new clothes. Hinduism is the oldest religion in the world. According to the BBC, the Vedic Period, when the Vedas were primarily being written, was circa 1500 – 500 BCE, whereas the Indus Valley Civilisation existed before 2000 BCE. In Hinduism, the body is only a form of container. One day when a disciple offered him sweets, Ganesha accepted the treats and spent the rest of the day hoarding them. Known as the destroyer, Shiva is also the Lord of mercy and compassion who can remove ignorance, evil and grant wisdom. Hinduism is also known as Sanātana Dharma (a Sanskrit phrase which means "the Lord Ganesha, who was the son of Lord Shiva and the goddess Parvati, loved sweets. Historical Facts about Hinduism. Paperback. That night, when it was time to go home, he carried all the sweets along, but when he tripped on a stone and stumbled, all the sweets scattered onto the ground. Draupadi, one of the heroines of the Mahabharata, accepted the role of a faithful wife and at the same time was an influential, assertive, and discerning woman. Hinduism . The rebirth, however, is on the basis of one’s karma. ... get into some mythological explanations for the natural phenomenon of no moon and know some facts about Amavasya in Hinduism… The latest breaking news, comment and features from The Independent. He is a retired Engineer and an ex-design consultant, now living with his wife in Ashram at Amritapuri, Kerala, spending his retired life in quest of spirituality under the holy feet of Amma, Satguru Mata Amritanandamayi. The True Story about Hinduism! It is difficult to provide adequate history of Hinduism because it has no specific founder or theology. The religion of Hinduism is not only the oldest religion in the world but also the most complex. Once upon a time, a king and a merchant were very good friends. Discover smart, unique perspectives on Hinduism and the topics that matter most to you like india, spirituality, religion, bhagavad gita, and yoga. $12.95 #42. However, all Hindus worship one supreme being who created a bunch of gods to be his helpers. Rantidev, The King \| Satsang Stories \| Hindu Stories \| Moral Stories \|Satsang Stories \| Hindu Stories \| Moral Stories\| Hinduism is the predominant and indigenous spiritual custom of South Asia. Click here to sign up for more stories about Hinduism. The history of Hinduism covers a wide variety of related religious traditions native to the Indian subcontinent. Well there are lot of interesting stories running about it. The Best Documentaries about Hinduism:. BAPS Kids - Story Time. With so many deities and traditions forming part of it, it also makes for one of … The story of Hinduism is somewhat elusive. Originally, the Vedas depicted a more subdued and subtle creation story, one that I personally find much more interesting: SEE ALSO: The 10 Most Popular Hindu Deities. 4.4 out of 5 stars 13. Markita Richards. And did you know Hindus don’t believe in millions of gods? Here are few Interesting Facts about Hinduism. The development of this religion was influenced when light-skinned nomadic Aryan Indo-European tribes invaded Northern India BC from Russia and Central Asia attacking the Harappan people who lived there in 1500. Evidence of Hinduism’s early antecedents is derived from archaeology, comparative philology, and comparative religion. Across the mystical lands of India, there is a seemingly endless variety of worship rituals and spiritual practices that differentiate one another. Once, it so happened that the merchant was unable to sell any of his sandalwood logs for 2 to 3 years. You can incarnate as birds, animals or humans or other forms as per your karma. You can find out killing animals, killing women, corruption, polygamy, wishful thinking of hell, heaven, non-sense rites and caste-ism. Story of Early Hinduism and Trimurti Posted on June 13, 2015 by Temple Purohit The most revered values of Hinduism weren’t just the first of all religious findings but also had an impeccable way of reaching the remote of people. For instance, Hinduism is not technically a religion. Hinduism is the world’s oldest known religion and originally known as Sanatana Dharma, with its roots going back to 10,000 years and Hindu scriptures dating back to 7000 BC.. Although Hinduism assigns specific roles to women, it in no way condones their exploitation. The merchant was a trader of sandalwood logs. Hinduism Clothing Girls Clothing:) Boys Clothing:( Girls were scarfs and dress's Boys were long shirts scarfs and pants Texts/Books Hindus book is the bible because it talks about our God and what he has created.Hindus text is Be mindful of negative thoughts. Here we have collected few of interesting stories: The birth of Lord Shiva source Its history overlaps or coincides with the development of religion in the Indian subcontinent since the Iron Age , with some of its traditions tracing back to prehistoric religions such as those of the Bronze Age Indus Valley Civilization . For well over 3,000 years, it has been accumulating the sacred stories and heroic epics that make up the mythology of Hinduism. News about Hinduism, including commentary and archival articles published in The New York Times. If you get good knowledge of Sanskrit, you can interpret the Vedas. A selection of exciting stories from different faiths, illustrated with vibrant artwork. Hinduism (21st Century Skills Library: Global Citizens: World Religions) Katie Marsico. Explore more than 359 'Hinduism Stories' resources for teachers, parents, and students. For example mediating figure that resembles Lord Shiva, a discovery of swastika, mother goddess seal … $7.64 #41. With lesson plans, informative slides, activity ideas, differentiated worksheets and more, these Hindu story lessons provide everything you need to teach your class about Hindu beliefs. Hinduism, which has millions of followers in India and around the world today, is one of the world's oldest religions. Then even nothingness was not, nor existence, There was no air then, nor the heavens beyond it. It is like clothes. Even the term “Hinduism” as we know it today is the result of the British attempt, during colonial times, to group India’s numerous indigenous religions into a single, overarching tradition. The earliest documents on Hinduism date back to 5,500 BCE. The first lesson in this series provides your children with a brief overview of what Hinduism is and where it is prevalent today. With that in mind, here are twenty interesting facts about Hinduism. Various seals and artifacts found at Indus Valley Civilization (Harappa Civilization) prove that the practices of Harappa people were similar to that of Hinduism today. No one knows – or cares to know – who started Hinduism. #Lesson1OneGodManyForms. Short Stories featuring Hinduism Here are the top short stories, fanfiction, poetry, and posts about Hinduism on Commaful, including topics like "horror", "thriller", and more. Kindle Edition. It’s rather simplistic compared to the deeper belief held by many in Hinduism. Pretty Melanin Me! Hinduism is the world's oldest living religion and the third largest, ... Adalaj Stepwell is a five-story stepwell dating back to 1499. The main essence is the soul. Read the Medium top stories about Hinduism written in 2018. Perhaps no other faith glorifies the idea of love between the sexes as Hinduism.This is evident from the amazing variety of mythical love stories that abound in Sanskrit literature, which is undoubtedly one of the richest treasure hoards of exciting love tales. There is no definitive starting point, no founder, no single holy text in the history of Hinduism. Hinduism is a religion of many gods. Hinduism is based on the Vedas, the sacred texts and teachings of the Aryans, the ancient people who settled in India around 1500 BCE. Hinduism is the oldest religion in the world.Its origin can be dated back to 10,000 BCE. Whole Hinduism sucks. Hinduism is a complicated religion to understand, unless one has grown up being a Hindu. Amasya is the Indian name for a new moon. Read stories about Hinduism on Medium. Follow With that, his stories can be relevant tell kids. Here are some Stories about Amavasya. We are Twins! There are abundant stories related to the Supreme, powerful God Lord Shiva. Some stories illustrate how traditional values can clash with contemporary ideals. The world’s 3rd largest religion closely following Christianity and Islam is Hinduism. Art Supplies Under $10, Hilton East Midlands To Alton Towers, Ash River Fishing Report, Balisong Chords The Juans, Homeless Living In Storage Units,	https://coalagroup.com/dqoytk0/15ad4a-stories-about-hinduism
There’s no doubt that without language our world would be a totally different place since most of us agree that language and the written word are the building blocks of human expression. The list of things that would not exist without writing is almost endless: there would be no books, no recorded history, no songs, no newspapers, no magazines, no films, no television programs, no comics, no Internet, and so on. Additionally, before the advent of the telephone people wouldn’t have been able to communicate over long distances through letters if there were no writing systems. Without language and writing we would not be able to fully express our thoughts and feelings, passions and desires. To make a long story short, writing systems are vital to a society and without them no civilization could ever be complete or remembered. However, throughout the years many writing systems have been discovered that we still can’t understand or interpret. The difficulty in deciphering these usually arises from the lack of known language descendants, from the languages being entirely isolated, from insufficient examples of discovered texts, or from whether the glyphs found actually constitute a writing system at all. These are 25 Undeciphered Writing Systems That We Might Never Figure Out. The Singapore Stone The Singapore Stone is a fragment of a large sandstone slab that originally stood at the mouth of the Singapore River. The slab, which is believed to date back to at least the thirteenth century and possibly as early as the tenth or eleventh century, bears an undeciphered inscription. Recent theories suggest the inscription is either in Old Javanese or Sanskrit. It is likely that the person who commissioned it was Sumatran though no scholar can be sure about anything surrounding the mysterious stone. Rongorongo Rongorongo is a system of glyphs discovered in the nineteenth century on Easter Island that appears to be writing or proto-writing. Although some calendrical and what might prove to be genealogical information has been identified, not even these glyphs can actually be read. Tujia Script The Tujia have historically been known as an ethnic minority (in China) without a written language. However, a succession of ancient undeciphered books with glosses presented in Chinese characters has been found in the Youyang Tujia habitation straddling the borders of Hunan, Hubei, Guizhou Province, and Chongqing City. Khitan Scripts The Khitan scripts were the writing systems of the now-extinct para-Mongolian Khitan language used from the tenth to twelfth centuries by the Khitan people who established the Liao dynasty in northeast China. There were two scripts, large and small. Many experts agree that the scripts have not been fully deciphered and that more research and further discoveries are required to proficiently understand them. Issyk Writing The Issyk inscription is not yet certainly deciphered, and is probably in a Scythian dialect, constituting one of very few indigenous epigraphic traces of the language. Lists Going Viral Right Now The Alekanovo inscription The Alekanovo inscription is a group of undeciphered characters found in the fall of 1897 in the Russian village of Alekanovo by Russian archaeologist Vasily Gorodtsov. The characters were inscribed on a small clay pot fifteen centimeters high found at a Slavic burial site. Although the inscription has been authenticated, we’re not quite sure if this is an organized writing system people actually used or something else, perhaps art. The Quipu “writing” system Even though there is still much to be learned about the Inca and their forebears, without a doubt one of the most intriguing mysteries is their writing system, or the apparent lack thereof. The quipu “writing” system is the only thing we inherited from them but have failed to interpret. Mixtec writing Mixtec writing is classified as logographic, meaning the characters and pictures used represent complete words and ideas instead of syllables or sounds. In Mixtec the relationships among pictorial elements denote the text’s meaning, whereas in other Mesoamerican writing the pictorial representations are not incorporated into the text. The characters used in Mixtec can be sorted into three types: pictographic, ideographic, and phonetic. The origin and accurate interpretation of the Mixtec writing system, however, remains unknown. Zapotec Writing Rising in the late preclassic era after the decline of the Olmec civilization, the Zapotecs of present-day Oaxaca built an empire around Monte Alban. On a few monuments at this site archaeologists have found extended text in a glyphic script. Some signs can be recognized as calendric information but the script as such remains undeciphered. The Isthmian script The Isthmian script, also known as the La Mojarra script, is a very early Mesoamerican writing system that was in use around the Isthmus of Tehuantepec from 500 BCE to 500 CE, although there is disagreement concerning these dates. Isthmian script is similar in structure to the Maya script, and like the Maya uses one set of characters to represent logograms (word units) and a second to represent syllables. The Cascajal Block Made of serpentinite, the Cascajal Block is a tablet-sized writing slab in Mexico that has been dated to the early first millennium BCE, incised with unknown characters that may represent the earliest writing system in the New World. According to archaeologist Stephen Houston of Brown University, this discovery helps link the Olmec civilization to literacy, record an unsuspected writing system, and reveal a new layer to the Olmec civilization, even though we have yet to fully comprehend it. Talking about undeciphered writing systems, have you taken a look at the world’s most difficult languages to learn? Sitovo Inscription The Sitovo inscription is an inscription that has yet to be satisfactorily translated or interpreted. An archaeological expedition, led by Alexander Peev, discovered it on the wall of Sitovo Cave in 1928, close to Plovdiv, Bulgaria. It is believed to have most likely been inscribed around 1200 BCE. Southwest Paleohispanic Script The Southwest or Southwestern script, also known as Tartessian or South Lusitanian, is a Paleohispanic script used to write an unknown language usually identified as Tartessian. Southwest inscriptions have been found mainly in the southwestern quadrant of the Iberian Peninsula, in southern Portugal, but also in Spain, in southern Extremadura and western Andalucia. Cypro-Minoan Syllabary The Cypro-Minoan syllabary (CM) is an undeciphered syllabic script used on the Greek island of Cyprus during the Late Bronze Age. Sir Arthur Evans coined the term in 1909 based on its visual similarity to Linear A on Minoan Crete, from which CM is thought to have been derived. Approximately 250 objects, including clay balls, cylinders, tablets, and votive stands, which bear Cypro-Minoan inscriptions, have been found. Byblos Syllabary The Byblos syllabary is an undeciphered writing system known from ten inscriptions found in Byblos (in Lebanon). The inscriptions are engraved on bronze plates and spatulas and carved in stone. They were excavated by Maurice Dunand, from 1928 to 1932, and published in 1945 in his text Byblia Grammata. The inscriptions are conventionally dated to the second millennium BCE, probably between the eighteenth and fifteenth centuries. Proto-Sinaitic Script Proto-Sinaitic was the first consonantal alphabet. Even a cursory glance at its inventory of signs makes it clear that the script is Egyptian in origin. Originally it was thought that at around 1700 BCE Sinai was conquered by Egypt, and that the local West Semitic population was influenced by Egyptian culture, adopting a small number of hieroglyphs (about thirty) to write their own language. However, recent discoveries in Egypt have complicated this perspective. Inscriptions dating to 1900 BCE written in what appears to be proto-Sinaitic were found in Upper Egypt, and nearby Egyptian texts speak of the presence of Semitic-speaking people living in Egypt. Cretan Hieroglyphs Cretan hieroglyphs are undeciphered hieroglyphs found on artifacts of Early Bronze Age Crete, during the Minoan period. It predates Linear A by about a century, but continued to be used alongside it for most of their history. Linear A Linear A is one of two currently undeciphered writing systems used in ancient Greece. This writing system was the primary script used in palace and religious writings of the Minoan civilization. It was discovered by archaeologist Sir Arthur Evans. It is the origin of Linear B, which was largely deciphered in the 1950s and found to encode an early form of Greek. Although the two systems share many symbols, this has not led to a subsequent decipherment of Linear A. Linear Elamite Linear Elamite is a Bronze Age writing system used in Elam, known only from a few monumental inscriptions. It was used contemporaneously with Elamite cuneiform and likely records the Elamite language. It was in use for a brief time during the last quarter of the third millennium BCE. It is often claimed that Linear Elamite is a syllabic writing system derived from the older proto-Elamite system, although this has not been proven. In spite of several attempts, most notably by Walther Hinz and Piero Meriggi, Linear Elamite has not yet been deciphered. Proto-Elamite Script The proto-Elamite script is an Early Bronze Age writing system that was briefly in use before the introduction of Elamite cuneiform. It is uncertain whether the proto-Elamite script was the direct predecessor of Linear Elamite. Both scripts remain largely undeciphered, and it is mere speculation to posit a relationship between the two. Banpo Symbols The Banpo symbols were discovered in China between 1954 and 1957 and are relatively numerous, with twenty-two different symbols on 113 potsherds. Some scholars have concluded that they are meaningful symbols, like clan emblems or signatures, that have some of the traits of writing, perhaps being primitive characters, while others have concluded based on comparisons to oracle bone script that some marks are numerals. Still others feel they may be ownership or potter’s marks, but no one knows for sure. Dispilio Tablet George Xourmouziadis, a professor of prehistoric archaeology, discovered the Dispilio tablet in 1993 in a Neolithic lake settlement in northern Greece near the city of Kastoria. A group of inhabitants used to occupy the settlement seven thousand to eight thousand years ago. Although the Dispilio tablet was one of many artifacts found there, it is of great importance because it has an unknown written text on it that reaches back to before 5000 BCE. Using the C12 method the wooden tablet was dated to 5260 BCE, making it older than the writing system used by the Sumerians. Vinča Symbols The Vinča symbols, also known as “Old European script,” are a set of symbols found on Neolithic-era (sixth to fifth millennia BCE) artifacts found during the 1875 archaeological excavations led by the Hungarian archaeologist Zsófia Torma at Tordos (Turdaș, Romania). The importance of these findings resides in the fact that the bulk of the symbols was created between 4500 and 4000 BCE, with the ones on the Tărtăria clay tablets dating further back, to around 5300 BCE. This means that the Vinča finds predate the proto-Sumerian pictographic script from Uruk (in modern Iraq), which was previously considered the oldest known script. Jiahu Symbols Jiahu symbols refer to the sixteen distinct markings on prehistoric artifacts found in Jiahu, a Neolithic Peiligang culture site in Henan, China, excavated in 1999. A 2003 report in Antiquity interpreted them “not as writing itself, but as features of a lengthy period of sign-use which led eventually to a fully fledged system of writing.” Phaistos Disc Arguably the most famous format of undeciphered writing system in the world, the Phaistos Disc—a disc of fired clay from the Minoan palace of Phaistos on Crete (Greece)—is considered one of the biggest mysteries in history. Experts have been trying to read the pictorial signs for over a century and even though many interpretations have been given, none are widely accepted in linguistic and archaeological circles. Many scholars refer to it as the first “CD-ROM” in history, but in reality the four-thousand-year-old disc still holds many secrets, as it is generally agreed that there is not enough context available for a meaningful analysis.	https://list25.com/25-undeciphered-writing-systems-that-we-might-never-figure-out/?view=all
WEDNESDAY, Jan. 5, 2022 (HealthDay News) – Scientists have known for 100 years that insulin is the body’s main control mechanism blood sugar levels, but researchers have now found that another hormone does the same job a little differently – and says it could be a new target for treatment diabetes. The hormone, called FGF1, is produced in the body fat tissue. As insulin, quickly lowers blood sugar levels, but researchers have found in mice that it acts independently of insulin and a different mechanism. Type 2 diabetes occurs when the body becomes resistant to insulin, which leads to chronically high levels of glucose (sugar) in the blood. Over time, this can affect the body’s arteries and nerves, leading to complications such as heart and kidney disease, stroke, vision problems and permanent nerve damage. In a new study, scientists found that FGF1 suppresses the breakdown of adipose tissue, which reduces the liver’s ability to excrete glucose. Insulin also does these things, but FGF1 accomplishes this through a different “signaling pathway” in the body. And in laboratory mice with insulin resistance, injections of FGF1 significantly lower blood sugar. “This mechanism is basically a second loop, with all the benefits of a parallel path,” said study author Gencer Sancar, a postdoctoral researcher at the Salk Institute in La Jolla, California. “IN insulin resistance, insulin signaling is disrupted, “Sancar said in a statement from the institute.” However, with a different signaling cascade, if one doesn’t work, the other can. That way you still have control over it [fat breakdown] and blood glucose regulation. “ However, whether it is found on animals will ultimately translate to humans s type 2 diabetes remains to be seen. One question is whether people who are insulin resistant will also be resistant to FGF1, noted Dr. Emily Gallagher, endocrinologist who was not included in the study. She said it is also possible that targeting FGF1 could be effective in some people with type 2 diabetes, but not in others. “Type 2 diabetes is a complex condition in which different people have different metabolic profiles,” explained Gallagher, an assistant professor in the Department of Endocrinology, Diabetes and Bone Diseases at the Icahn School of Medicine in Mount Sinai, New York. Scientists knew something about the work of FGF1. In previous studies, researchers from Salka found that it lowers blood sugar in laboratory mice, and when given continuously, it reduces insulin resistance in animals. A new study, published Jan. 4 in the journal Cell metabolism, immersed in exactly how the hormone works. Researchers have found that, similar to insulin, FGF1 suppresses fat breakdown, which in turn helps control blood sugar. But its mode of operation is different: insulin acts through an enzyme called PDE3B, which triggers a chain of events called the signaling pathway. FGF1 uses a different enzyme – called PDE4. “Now that we have a new path, we can understand its role in energy homeostasis in the body and how to manipulate it,” said senior study author Michael Downes, an employee of Salk. Gallagher said it was “very interesting” that FGF1 could have insulin-like effects in adipose tissue. But much remains to be learned. More laboratory research, she said, is needed to understand the long-term effects of FGF1 on insulin signaling and insulin resistance. “And in humans,” Gallagher said, “it would be important to understand more about the systemic effects of FGF1 administration, since FGF1 affects many organ systems – including the inflammatory system – and can also alter tumor growth.” Whether manipulating the hormone or proteins it regulates would be appropriate in people with type 2 diabetes remains to be determined, Gallagher said. More information The U.S. National Institute on Diabetes and Digestive and Kidney Diseases has more on that type 2 diabetes.	https://www.exgujaratnews.com/insulin-is-not-the-only-regulator-of-blood-sugar/
A: Diabetes is a disabling condition in which blood glucose levels are above normal. The majority of food that we consume is converted into glucose, or sugar, for use by our body for energy. When a person has the disabling condition of diabetes, either the body doesn’t produce enough insulin or the insulin produced by the body is not used as well as it should. This causes the level of sugar in your blood to build up. Q: What are the health effects of diabetes? A: There are serious health complications which can be caused by diabetes including heart disease, blindness, kidney failure, and lower-extremity amputations. Diabetes is also the sixth leading cause of death in the U.S. Q: What are the symptoms of diabetes? A: Some of the more prominent symptoms of diabetes are frequent urination, excessive thirst, unexplained weight loss, extreme hunger, sudden loss of vision, and a feeling of fatigue. Q: What are the types of diabetes? A: There are three prominent types of diabetes. - Type 1, or juvenile-onset, diabetes takes place when the body’s immune system attacks the cells in the pancreas which create insulin, leaving patients reliant on synthesized insulin for the remainder of their lives. - Type 2, or adult-onset, diabetes takes place when the body becomes resistant to insulin and eventually ceases production of a suitable amount. - Gestational diabetes is a temporary condition which takes place during pregnancy. Though temporary, if it goes untreated, it can lead to problems for mothers and babies. It will typically disappear after pregnancy. A: For Type 1, healthy eating, physical activity, and insulin injections are the basic therapies. Those who suffer from type 1 diabetes must closely monitor their blood glucose levels through frequent testing of the blood glucose. For Type 2, healthy eating, physical activity, and blood glucose testing are the basic treatments. Many people who suffer from type 2 diabetes also require oral medication, insulin, or both in order to control their blood glucose levels.	https://www.brentadams.com/blog/diabetes-facts.cfm
Diabetes is a serious, chronic disease characterized by chronic elevation of blood glucose and disturbance of carbohydrate, fat and protein metabolism that occurs either when the pancreas does not produce enough insulin or when the body cannot effectively use the insulin it produces. Raised blood glucose, a common effect of uncontrolled diabetes, may, over time, lead to serious damage to the heart, blood vessels, eyes, kidneys and nerves. Diabetes is not only a disease in itself, but also an intermediate stage for many other conditions. Diabetes is one of the leading causes of blindness, heart attacks, strokes, renal failure and lower limb amputations worldwide. What is pre-diabetes? Pre-diabetes means that the blood sugar levels are higher than normal, but not to the levels to diagnose diabetes. Pre-diabetes is the term used for individuals with IFG and/or IGT and/or HbA1c 5.7-6.4% (39-47 mmol/mol). People with pre-diabetes are more likely to develop diabetes within 10 years and there is also an increased risk for cardiovascular disease. Main Types of Diabetes Diabetes can be classified into the following general categories: 1. Type 1 diabetes (T1D) (due to autoimmune β-cell destruction, usually leading to absolute insulin deficiency). T1D was previously 2. Type 2 diabetes (T2D) (due to a progressive loss of β-cell insulin secretion frequently on the background of insulin resistance) 3. Gestational diabetes mellitus (GDM) (diabetes diagnosed in the second or third trimester of pregnancy that was not clearly overt diabetes prior to gestation) 4. Specific types of diabetes due to other causes, e.g., monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset diabetes of the young [MODY]), diseases of the exocrine pancreas (such as cystic fibrosis), and drug- or chemical-induced diabetes (such as with glucocorticoid use, in the treatment of HIV/AIDS, or after organ transplantation) Type 1 Diabetes T1D is caused by an autoimmune reaction, in which the body´s defense system attacks the insulin –producing beta cells in the pancreas. As a result, the body can no longer produce the insulin it needs. The disease can affect people of any age, but onset usually occurs in children and young adults. Type 1 diabetics need insulin every day in order to control the levels of glucose in their blood. Without insulin the person would die. Diabetes type 1 develops suddenly and has following symptoms: • Abnormal thirst and a very dry mouth • Frequent urination • Lack of energy, extreme tiredness • Constant hunger • Sudden weight loss • Blurred vision Diabetes type 1 is diagnosed by an elevated blood glucose level in the presence of the symptoms above. This type of diabetes is increasing. Not clear why, but it may be due to changes in environmental risk factors and/or viral infections. Type 2 Diabetes Type 2 diabetes is the most common type of diabetes. Usually occurs in adults but is increasingly seen in children and adolescents. The body is able to produce insulin but becomes resistant so that the insulin is ineffective. Over time, insulin levels may become insufficient. Insulin resistance and deficiency lead to high blood glucose levels. Symptoms of type 2 diabetes include • Frequent urination • Excessive thirst • Weight loss • Blurred vision The symptoms for T2D are usually less obvious so people with type 2 diabetes remain unaware of their condition for a long time and it may take years to be diagnosed. However, during this time the body is already being damaged by excess blood glucose. The most important risk factors are excess body weight, physical inactivity, and poor nutrition. Other factors which play a role are ethnicity, family history of diabetes, past history of gestational diabetes and advancing age. T2D do not require daily insulin treatment to survive. Adopting a healthy diet, increased physical activity and maintenance of a normal body weight are some of the cornerstones of treatment. Oral medications are available to control blood glucose levels and if the levels continue to rise insulin might be necessary. The number of people with type 2 diabetes is growing rapidly worldwide and is associated with ageing populations, the economic development, increasing urbanization, less healthy diets and reduced physical activity. Gestational diabetes Gestational diabetes is a temporary condition that occurs in pregnancy and carries longterm risk of type 2 diabetes. Hyperglycameia that is first detected at any time during pregnancy is classified as either: • Gestational diabetes mellitus • Diabetes mellitus in pregnancy Slightly elevated blood glucose levels during pregnancy are classified as gestational diabetes. Substantially elevated blood glucose are classified as diabetes mellitus in pregnancy. Symptoms may include increased thirst and frequent urination. It is recommended to screen using oral glucose tolerance test early in pregnancy for high risk women and between the 24th and 28th week of pregnancy in all other women. Women with hyperglycaemia during pregnancy can control their blood glucose levels through a healthy diet, gentle exercise and blood glucose monitoring. In some cases, insulin or oral medication may also be prescribed. Even if gestational diabetes normally disappear after birth, women who have been previously diagnosed are at higher risk of developing type 2 diabetes later in life. Impaired glucose tolerance and impaired fasting glucose Raised blood glucose levels that are not high enough for diabetes diagnosis are sometimes called pre-diabetes. Impaired glucose tolerance (IGT) or impaired fasting glucose (IFG) are intermediate conditions in the transition between normal blood glucose levels and diabetes, especially type 2 diabetes. People with impaired glucose tolerance are at increased risk of developing type 2 diabetes. Lifestyle interventions such as healthy diet and physical exercise can prevent the progression to diabetes. Which tests are used to diagnose diabetes and pre-diabetes? There are three types of tests routinely performed to diagnose pre-diabetes and diabetes. • Fasting Plasma Glucose Test (FPG) Just prior to having this test run, the patient must fast (nothing to eat or drink except water) for eight hours. The health care provider draws blood from the patient. Then the plasma (the fluid part of the blood) is combined with other substances to determine the amount of glucose in the plasma, as measured in mg/dL. The chart below contains the FPG test's blood glucose ranges for prediabetes and diabetes and describes what each diagnosis means. • HbA1C (A1C or glycosylated hemoglobin test) The A1C test can be used for the diagnosis of both prediabetes and diabetes. The average blood glucose for the past 2 to 3 months is measured with HbA1c. This test is more convenient because no fasting is required. An A1C of 5.7% to 6.4% means that there is a high risk for the development of diabetes and that the patient has pre-diabetes. Diabetes is diagnosed when the A1C is 6.5% or higher. • Oral Glucose Tolerance Test (OGTT) The test measures how well the body handles a standard amount of glucose. The health care provider draws the patient's blood before and two hours after the patient drinks a large, premeasured beverage containing glucose. Then, the doctor can compare the before-and-after glucose levels contained in the person's plasma to see how well the body processed the sugar. These levels are measured in mg/dL. The chart below contains the OGTT's blood glucose ranges for prediabetes and diabetes and describes what each diagnosis means. How can diabetes be monitored? Except the home monitoring, performed by the patient at home, the most common test for type 2 diabetes is the HbA1c. The HbA1c (A1C or glycosylated hemoglobin) test provides a picture of the average blood sugar control for the past two to three months. Blood sugar is measured by the amount of glycosylated hemoglobin (A1C) in the blood. What is glycated hemoglobin (HbA1c)? Glucose binds to a specific part of hemoglobin and HbA1c (Hemoglobin A1c), glycated hemoglobin is formed. Initially, the reaction between glucose and hemoglobin is reversible (labile HbA1c), but ultimately an irreversible and stable HbA1c is formed. The average life span of red blood cells is 2-3 months. HbA1c reflects the average blood sugar control for the past two to three months. For a given HbA1c level, the preceding 30 days contribute substantially more (50%) to the HbA1c level, than glucose levels 90-120 days earlier (10%). It does not take 120 days to detect a clinically meaningful change. ~94% of total hemoglobin is non-glycated while ~6% is glycated, ~5% of glycated hemoglobin is HbA1c. How can HbA1c measurement aid diabetes management? It can improve diabetes decision making, patient compliance and outcomes. HbA1c is widely used as the most important marker for routine monitoring of long-term glycemic status in patients with diabetes. HbA1c is used as measure of future risk for the development of diabetes complications. HbA1c or Fasting Plasma Glucose (FPG) is measured for diagnosing diabetes.	https://www.hemocue.co.za/en-za/health-areas/diabetes/what-is-diabetes-faq
Diabetes is a group of metabolic conditions in which the body either doesn’t produce enough of the hormone insulin or the body has become resistant to the effects of insulin (insulin resistance). Insulin is a hormone produced by the Beta islet cells in the pancreas, and it converts sugar, starches and other foods into energy. Type 1 diabetes is an autoimmune disease in which the immune system destroys the pancreatic cells that produce insulin. Thus, the pancreas cannot produce insulin. Type 1 diabetes is typically diagnosed in children and young adults . In Type 2 diabetes, the body becomes resistant to the normal effects of insulin and/or gradually loses the capacity to produce enough insulin in the pancreas. Glucose accumulates and cause damage to vascular and other tissues . Type 2 diabetes represents 85-90% of all diabetes cases and usually develops in adults over 45 years, though increasingly it is occurring in younger people including children . Diabetes affects the large blood vessels leading to cardiovascular disease, including hypertension, atherosclerosis, heart attack, stroke and circulation problems in the lower limbs (peripheral arterial disease). It also affects the microvasculature of the body leading to problems in the eyes, kidneys, feet and nerves. Nerve problems include peripheral neuropathy and autonomic neuropathy. It also affects other parts of the body including skin, teeth and gums . According to the World Health Organization, the number of people worldwide with diabetes has increased from 108 million in 1980 to 422 million in 2014, with the global prevalence of diabetes among adults over 18 years of age having risen from 4.7% in 1980 to 8.5% in 2014. Nearly half of all deaths due to high blood glucose occur before 70b years of age. It is estimated that diabetes is the seventh leading cause of death in 2016 . In 2015 the prevalence of diabetes in adults in the US was 30.3 million or 9.4% of the population. Of the 30.3 million adults with diabetes, 23.1 million were diagnosed and 7.2 million undiagnosed. In addition, in 2015 there were 84.1 million persons in the US aged 18 or older with prediabetes. In 2017 the estimated cost of diabetes in the US was $327 billion . In Australia, the prevalence of diabetes is around 1.7 million (includes all types of diabetes including undiagnosed type 2 diabetes). In 2015, it was estimated that more than 100,000 Australians developed diabetes in the previous year. The total annual cost of diabetes in Australia is estimated at $14.6 billion .	https://ghiaustralia.org.au/diabetes-info/
- What Are the Main Symptoms of Insulin Resistance? - How Is Insulin Resistance Diagnosed? - Should You Be Tested for Insulin Resistance? - Can Insulin Resistance Be Prevented or Reversed? - How to Change Your Lifestyle and Diet to Prevent, Manage, or Help Reverse Insulin Resistance - How do I know if I am Insulin Resistant? - Insulin Resistance Syndrome in the Elderly - CONCLUSIONS— - Insulin Resistance: Dealing With the Diagnosis - What is insulin resistance? - Symptoms of insulin resistance - Causes of insulin resistance - Can insulin resistance be reduced or reversed? - What Is Insulin Resistance? - How Are Insulin Resistance and PCOS Connected? - How Do I Know If I Have Insulin Resistance? - 1. You Have Severe Hangry Attacks - 2. You Store Weight Around Your Belly - 3. No Matter How Many Spin Classes, Miles Run, and Salads Ate, You Can’t Lose Weight - 4. You’ve Developed Dark Velvety Patches in the Folds of Your Skin - 5. You’ve Got Skin Tags - Summary of Insulin Resistance and PCOS - What does insulin do in the body? - What does it mean to be insulin resistant? - What causes insulin resistance? - What are the symptoms of insulin resistance? - What are the complications of insulin resistance? - Is there an insulin resistance test? - Can you reverse insulin resistance? Insulin Resistance and Type 2 Diabetes For well over half a century, the link between insulin resistance and type 2 diabetes has been recognized. Insulin resistance is important. Not only is it the most powerful predictor of future development of type 2 diabetes, it is also a therapeutic target once hyperglycemia is present. In this issue of Diabetes, Morino et al. (1) report a series of studies that provide evidence of a genetic mechanism linking expression of lipoprotein lipase (LPL) to peroxisome proliferator–activated receptor (PPAR)-δ expression and mitochondrial function. This is likely to contribute to the muscle insulin resistance that predisposes to type 2 diabetes. Observation of abnormal mitochondrial function in vitro in type 2 diabetes (2) was soon followed by in vivo demonstration of this abnormality in insulin-resistant, first-degree relatives of people with type 2 diabetes (3). Further reports of a modest defect in muscle mitochondrial function in type 2 diabetes were published shortly thereafter (4,5). These studies raised the question of whether type 2 diabetes could be a primary disorder of the mitochondria. However, the study of first-degree relatives tended to be misinterpreted as having shown a major defect in mitochondrial function in type 2 diabetes, although it had studied nondiabetic groups from the opposite ends of the insulin resistance–sensitivity spectrum. Indeed, other studies showed no defect in mitochondrial function in type 2 diabetes (6,7), which led to further confusion. Mitochondrial function was then shown to be acutely modifiable by changing fatty acid availability (8) and that it was affected by ambient blood glucose concentration (9). When ambient blood glucose levels were near normal in diabetes, no defect in mitochondrial function was apparent. But if mitochondrial function in well-controlled type 2 diabetes is not abnormal, is a defect in insulin-resistant, first-degree relatives clinically relevant? The answer is provided in Fig. 1, which shows population distributions of insulin sensitivity for normoglycemia, impaired glucose tolerance, and type 2 diabetes. The wide range of insulin sensitivity in the normoglycemic population fully encompasses the range observed in type 2 diabetes. Even though mean insulin sensitivity in diabetes is lower than that of matched control subjects, values are drawn from the same distribution and, with matching for body weight and physical activity, differences will be relatively small. Differences in insulin sensitivity will be particularly evident when making comparisons between groups selected from the extreme ends of the population distribution (Fig. 1). When parameters directly linked to muscle insulin resistance are compared between groups selected in this way, any linked difference will be maximized, making this strategy entirely appropriate to investigate the pathophysiology of muscle insulin resistance. FIG. 1. Distribution curves of insulin sensitivity as measured by the euglycemic-hyperinsulinemic clamp showing that people with type 2 diabetes sit within the range of the nondiabetic distribution, but toward the lower range. Identification of factors underlying muscle insulin resistance itself can be investigated by comparing groups drawn from the extremes of the total population distribution. Such factors may not be clearly discernible when type 2 diabetic individuals are compared with normoglycemic control subjects matched for weight and physical activity. The data are from previously published population studies of normal glucose tolerance (n = 256), impaired glucose tolerance (n = 119), and type 2 diabetes (n = 194) (20,21). Muscle insulin resistance as determined by the euglycemic-hyperinsulinemic clamp is clearly a risk factor for development of type 2 diabetes (10). However, the pathophysiology of hyperglycemia in established diabetes relates to hepatic not muscle insulin resistance. This distinction has been elegantly demonstrated in studies of moderate calorie restriction in type 2 diabetes, which resulted in a fall in liver fat, normalization of hepatic insulin sensitivity, and fasting plasma glucose, but no change in muscle insulin resistance (11). More recent work employing severe calorie restriction confirmed previous findings and also demonstrated a longer-term return of normal insulin secretion as intrapancreatic fat content fell (12). The fact that fasting and postprandial normoglycemia can be restored in type 2 diabetes without change in muscle insulin resistance should not be surprising. Mice totally lacking in skeletal muscle insulin receptors do not develop diabetes (13). People with inactive muscle glycogen synthase are not necessarily hyperglycemic (14), and many normoglycemic individuals maintain normal blood glucose with a degree of muscle insulin resistance identical to that among people who develop type 2 diabetes (Fig. 1). The relevance of muscle insulin resistance for development of type 2 diabetes is more subtle. Over many years and only in the presence of chronic calorie excess, hyperinsulinemia steadily brings about hepatic fat accumulation and hepatic insulin resistance. Onset of hyperglycemia is ultimately determined by failure of nutrient-stimulated insulin secretion (15). This new understanding is described by the twin cycle hypothesis (16). So what actually determines this critical primary insulin resistance in muscle? Morino et al. (1) report analyses of mRNA in muscle biopsies to compare expression of genes involved in mitochondrial fatty acid oxidation. Their experiments compare data for subjects at opposite extremes of the insulin resistance spectrum. Findings were confirmed in independent groups selected in the same way and two genes were found to be consistently lower in expression. Using knock down of expression by appropriate inhibitory RNA, Western blotting showed that LPL was the important gene product. In both human rhabdomyosarcoma cells and L6 myocytes, such knock down of LPL induced a decrease in mitochondrial density. The function of LPL is to release fatty acids from triglyceride for direct cellular uptake. The biological relevance of the link between decreased mitochondrial numbers and RNA interference (RNAi) inhibition of LPL was confirmed by observing that the effect was only seen if fat was present in the extracellular media. To test the hypothesis that fatty acid flux into cells regulates mitochondrial biogenesis by a PPAR-dependent process, knock down of PPAR-δ was also shown to decrease mitochondrial density. Furthermore, limitation of fatty acid uptake by directly inhibiting the transmembrane fatty transporter CD36 was shown to achieve the same effect. Overall, these studies suggest that insulin resistance is related to decreased mitochondrial content in muscle due, at least in part, to reductions in LPL expression and consequent decreased PPAR-δ activation. This important article establishes a biological mechanism whereby insulin resistance in muscle is causally linked to genetic influences that are measurable in the general population. It focuses on insulin resistance by comparing extremes of the distribution of this characteristic in the normal population. But does insulin resistance cause mitochondrial dysfunction, or vice versa? The former appears more likely on the basis of current evidence. Exercise can reduce insulin resistance and ameliorate mitochondrial dysfunction (17), whereas established mitochondrial dysfunction does not necessarily produce insulin resistance in animal models or in humans (18,19). Understanding the nature of common insulin resistance in muscle and its relationship to type 2 diabetes is long overdue. Future work should determine whether specific therapeutic manipulation can offset the effect of identifiable genetic influences and interrupt the long run-in to type 2 diabetes. ACKNOWLEDGMENTS No potential conflicts of interest relevant to this article were reported. The author is grateful to Leif Groop of Lund University for permission to use combined data from the Botnia Study and the Malmö Prospective Study in Fig. 1 and to Jasmina Kravic of Lund University for replotting the data. Footnotes - See accompanying original article, p. 877. - © 2012 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details. - ↵ - Morino K, - Petersen KF, - Sono S, - et al . Regulation of mitochondrial biogenesis by lipoprotein lipase in muscle of insulin-resistant offspring of parents with type 2 diabetes. Diabetes 2012;61:877–887 - ↵ - Kelley DE, - He J, - Menshikova EV, - Ritov VB . Dysfunction of mitochondria in human skeletal muscle in type 2 diabetes. Diabetes 2002;51:2944–2950pmid:12351431 - ↵ - Petersen KF, - Dufour S, - Befroy D, - Garcia R, - Shulman GI . Impaired mitochondrial activity in the insulin-resistant offspring of patients with type 2 diabetes. N Engl J Med 2004;350:664–671pmid:14960743 - ↵ - Szendroedi J, - Schmid AI, - Chmelik M, - et al . Muscle mitochondrial ATP synthesis and glucose transport/phosphorylation in type 2 diabetes. PLoS Med 2007;4:e154pmid:17472434 - ↵ - Phielix E, - Schrauwen-Hinderling VB, - Mensink M, - et al . Lower intrinsic ADP-stimulated mitochondrial respiration underlies in vivo mitochondrial dysfunction in muscle of male type 2 diabetic patients. Diabetes 2008;57:2943–2949pmid:18678616 - ↵ - De Feyter HM, - van den Broek NM, - Praet SF, - Nicolay K, - van Loon LJ, - Prompers JJ . Early or advanced stage type 2 diabetes is not accompanied by in vivo skeletal muscle mitochondrial dysfunction. Eur J Endocrinol 2008;158:643–653pmid:18426822 - ↵ - Lim EL, - Hollingsworth KG, - Smith FE, - Thelwall PE, - Taylor R . Effects of raising muscle glycogen synthesis rate on skeletal muscle ATP turnover rate in type 2 diabetes. Am J Physiol Endocrinol Metab 2011;301:E1155–E1162pmid:21917633 - ↵ - Lim EL, - Hollingsworth KG, - Smith FE, - Thelwall PE, - Taylor R . Inhibition of lipolysis in Type 2 diabetes normalizes glucose disposal without change in muscle glycogen synthesis rates. Clin Sci (Lond) 2011;121:169–177pmid:21388348 - ↵ - Schrauwen-Hinderling VB, - Kooi ME, - Hesselink MK, - et al . Impaired in vivo mitochondrial function but similar intramyocellular lipid content in patients with type 2 diabetes mellitus and BMI-matched control subjects. Diabetologia 2007;50:113–120pmid:17093944 - ↵ - Lillioja S, - Mott DM, - Spraul M, - et al . Insulin resistance and insulin secretory dysfunction as precursors of non-insulin-dependent diabetes mellitus. Prospective studies of Pima Indians. N Engl J Med 1993;329:1988–1992pmid:8247074 - ↵ - Petersen KF, - Dufour S, - Befroy D, - Lehrke M, - Hendler RE, - Shulman GI . Reversal of nonalcoholic hepatic steatosis, hepatic insulin resistance, and hyperglycemia by moderate weight reduction in patients with type 2 diabetes. Diabetes 2005;54:603–608pmid:15734833 - ↵ - Lim EL, - Hollingsworth KG, - Aribisala BS, - Chen MJ, - Mathers JC, - Taylor R . Reversal of type 2 diabetes: normalisation of beta cell function in association with decreased pancreas and liver triacylglycerol. Diabetologia 2011;54:2506–2514pmid:21656330 - ↵ - Brüning JC, - Michael MD, - Winnay JN, - et al . A muscle-specific insulin receptor knockout exhibits features of the metabolic syndrome of NIDDM without altering glucose tolerance. Mol Cell 1998;2:559–569pmid:9844629 - ↵ - Savage DB, - Zhai L, - Ravikumar B, - et al . A prevalent variant in PPP1R3A impairs glycogen synthesis and reduces muscle glycogen content in humans and mice. PLoS Med 2008;5:e27pmid:18232732 - ↵ - Ferrannini E, - Nannipieri M, - Williams K, - Gonzales C, - Haffner SM, - Stern MP . Mode of onset of type 2 diabetes from normal or impaired glucose tolerance. Diabetes 2004;53:160–165pmid:14693710 - ↵ - Taylor R . Pathogenesis of type 2 diabetes: tracing the reverse route from cure to cause. Diabetologia 2008;51:1781–1789pmid:18726585 - ↵ - Ritov VB, - Menshikova EV, - Azuma K, - et al . Deficiency of electron transport chain in human skeletal muscle mitochondria in type 2 diabetes mellitus and obesity. Am J Physiol Endocrinol Metab 2010;298:E49–E58pmid:19887598 - ↵ - Zechner C, - Lai L, - Zechner JF, - et al . Total skeletal muscle PGC-1 deficiency uncouples mitochondrial derangements from fiber type determination and insulin sensitivity. Cell Metab 2010;12:633–642pmid:21109195 - ↵ - Maassen JA, - ‘t Hart LM, - van Essen E, - et al . Mitochondrial diabetes: molecular mechanisms and clinical presentation. Diabetes 2004;53(Suppl. 1):S103–S109pmid:16703328 - ↵ - Groop L, - Forsblom C, - Lehtovirta M, - et al . Metabolic consequences of a family history of NIDDM (the Botnia study): evidence for sex-specific parental effects. Diabetes 1996;45:1585–1593pmid:8866565 - ↵ - Tripathy D, - Eriksson KF, - Orho-Melander M, - Fredriksson J, - Ahlqvist G, - Groop L . Parallel manifestation of insulin resistance and beta cell decompensation is compatible with a common defect in Type 2 diabetes. Diabetologia 2004;47:782–793pmid:15114470 What Is Insulin Resistance? Everything You Ever Wanted to Know Having insulin resistance may increase the risk of prediabetes, type 2 diabetes, and metabolic syndrome. But changing your diet and lifestyle can help reverse this health state. The hormone insulin helps keep blood sugar levels steady, but when insulin resistance occurs, glucose accumulates in the blood, either leading to or exacerbating prediabetes and type 2 diabetes. Thinkstock Carbohydrates — sugars and starches found in many foods — are a main source of fuel for your body. Your digestive system breaks down carbs into glucose, or sugar, which is then released into your bloodstream. And with the help of insulin, glucose can absorb into the cells of your body to be used for energy or storage. (1) But if you have insulin resistance, your cells will have trouble absorbing this glucose, and your body will require more insulin to function properly. (2) It is possible to overcome insulin resistance. But before you can deal with this problem, you must understand what insulin is, and how insulin affects control of blood glucose. (2) Defining Insulin: How the Hormone Helps Regulate Blood Sugar Insulin is a hormone produced by your pancreas, and it plays an important role in metabolism. Your pancreas secretes insulin into your bloodstream after you eat a meal. Insulin allows sugar in your bloodstream to enter into muscles, cells, and fat. (2) This hormone is also important because it stops sugar from accumulating in your bloodstream. The more you eat, the more insulin your body releases to regulate your blood sugar and keep it within a healthy range. (3) RELATED: Everything You Need to Know About Insulin if You Have Type 2 Diabetes Understanding Insulin Resistance and Its Effect on Blood Sugar Control Although the production and release of insulin is a natural metabolic response after eating, some people don’t use insulin properly. To receive energy, your cells, fat, and muscles must be able to absorb the glucose in your bloodstream. If your body doesn’t respond well to insulin, glucose can build up in your blood and raise your blood sugar level. To help you maintain a normal blood sugar level, your pancreas compensates for this resistance by releasing more insulin. (3) The effects of insulin resistance on the body vary from person to person. Sometimes, the increased production of insulin by the pancreas is enough to overcome insulin resistance and normalize blood sugar levels. But other times, the pancreas is unable to produce sufficient amounts of insulin to overcome the resistance. This triggers high blood sugar (hyperglycemia) and other health problems. (3) RELATED: How to Stabilize Your Blood Sugar Although insulin resistance can exist on its own without another diagnosis, it relates to certain health conditions, too. Here are a few: Prediabetes If your pancreas struggles to produce enough insulin to handle the glucose in your body, your blood sugar level can become mildly elevated and you may develop prediabetes. This means your blood sugar is higher than normal but not high enough to be diagnosed with diabetes. This condition — which affects about 84.1 million people — is a precursor to type 2 diabetes. Having prediabetes also is associated with an increased risk for heart disease, stroke, eye problems, neuropathy (nerve damage), and kidney disease. Type 2 Diabetes In the case of prediabetes, your pancreas works overtime to secrete enough insulin to regulate your blood sugar. But if your pancreas can’t keep up with the demand, insulin resistance can progress from prediabetes to type 2 diabetes. Most people diagnosed with prediabetes end up with type 2 diabetes within 10 years. (3) Metabolic Syndrome Metabolic syndrome is also closely related to insulin resistance. Interestingly, metabolic syndrome isn’t a condition in itself but rather a collection of metabolic risk factors that can set the stage for type 2 diabetes and heart disease. Insulin resistance is included among these risk factors, along with high blood pressure, abnormal cholesterol levels, high triglycerides (a form of fat storage often related to lifestyle factors), and a large waist circumference. RELATED: 10 Things Your Doctor Won’t Tell You About Metabolic Syndrome The Potential Causes of Insulin Resistance Although the exact cause of insulin resistance is unknown, certain factors have been linked with this condition. These include: (4) - Obesity (defined as having a certain body mass index, or BMI) - Eating a high-calorie, high-sugar diet - Lack of physical activity - Taking high doses of a steroid - Chronic stress - Having polycystic ovary syndrome (PCOS) or Cushing’s disease Some people are also at higher risk for developing insulin resistance. These include people: (3) - With a family history of type 2 diabetes - With a personal history of gestational diabetes - Over the age of 45 - Who are Hispanic, African-American, Native American, or Asian-American - With a waist circumference larger than 40 inches (men) or larger than 35 inches (women) - With a history of high blood pressure (hypertension) or high triglycerides The risk factors for insulin resistance are similar to the risk factors for prediabetes and type 2 diabetes. But lifestyle changes can help your body use insulin properly, which can reduce your risk of diabetes. RELATED: 10 Bad Habits That Raise Your Diabetes Risk What Are the Main Symptoms of Insulin Resistance? Insulin resistance may not cause any noticeable symptoms, so you can have insulin resistance and not know it. Symptoms don’t usually occur until you develop prediabetes or type 2 diabetes. If your blood sugar level becomes elevated and you have prediabetes, symptoms may include increased thirst and hunger, tiredness, and blurry vision. Insulin resistance can also cause the formation of dark patches on the neck, groin, and armpits called acanthosis nigricans. (5) When insulin resistance progresses to type 2 diabetes, you may also have tingling sensations in your hands or feet. (6) How Is Insulin Resistance Diagnosed? Although insulin resistance doesn’t usually have symptoms, your doctor may recommend testing your blood sugar if you have risk factors for this condition, such as obesity, a sedentary lifestyle, or high blood pressure. This involves a series of tests, which are the same for diagnosing prediabetes and type 2 diabetes. (7) Hemoglobin A1C Test This blood test measures your average blood glucose level over a period of two to three months. This test can determine your blood sugar level, and help your doctor assess how well you’re managing the diabetes. A normal A1C test result is under 5.7 percent; results between 5.7 percent and 6.4 percent is prediabetes; and results equal to or above 6.5 percent is type 2 diabetes. (7) You’ll repeat testing at different intervals over three months to confirm an initial diagnosis. RELATED: 5 Ways to Lower Your A1C Fasting Plasma Glucose (FPG) You will not consume food or liquids for at least eight hours, and then your doctor will draw blood to measure your blood sugar level after fasting. If you have an elevated blood sugar, you’ll return a few days later to repeat the test. A repeatedly high level can indicate either prediabetes or diabetes. A number under 100 milligrams per decliliter (mg/dL) is normal; a number between 100 to 125 mg/dL signals prediabetes; and a number greater than 125 mg/dL signals type 2 diabetes. (7) Glucose Tolerance Testing (OGTT) Your doctor measures your blood glucose level, gives you a sugary liquid to drink, and then repeats the test two hours after you drink the liquid. If after two hours your blood sugar level is less than 140 mg/dL, your blood glucose level is considered normal. A number between 140 mg/dL and 199 mg/dL is considered prediabetes, and a number 200 mg/dL or higher signals type 2 diabetes. (7) Should You Be Tested for Insulin Resistance? You should be tested for insulin resistance if you’re showing signs of having a high blood sugar level. (3) Again, there’s no specific test to confirm insulin resistance. But if you’re experiencing fatigue, brain fog, or increased hunger, see your doctor. Getting tested may reveal an elevated blood sugar or prediabetes. With an early diagnosis, you can take steps to help reverse the condition and avoid full-blown type 2 diabetes. RELATED: 7 Blood Sugar Testing Mistakes to Avoid If you see your doctor for symptoms, your doctor can perform a random blood sugar test. This may happen if you’re having obvious symptoms of diabetes, and you have risk factors for insulin resistance and diabetes, like obesity, high cholesterol, or high blood pressure. A random blood sugar test can be completed anytime of the day. Results over 200 mg/dL may confirm diabetes. (7) Can Insulin Resistance Be Prevented or Reversed? This metabolic condition doesn’t have to progress to prediabetes or type 2 diabetes. Making lifestyle changes can help reverse insulin resistance so that your body can respond properly to insulin. (4) Lose weight. One study found that losing weight combined with getting regular exercise could improve insulin sensitivity in obese older individuals. (8) Reduce your fat and calorie intake and get physically active. Do a moderate-intensity exercise, like biking or speed-walking, five days a week at minimum. (9) RELATED: Reversing Diabetes Is Possible Through Weight Loss, Study Finds Choose activities that you find enjoyable, such as walking, biking, swimming, or playing sports. Losing as little as 10 to 15 pounds may help reverse and prevent insulin resistance. (7) Eat a low-carb diet. Reducing your intake of carbohydrates may also improve glucose metabolism and reduce insulin resistance. Other research found that eating three low-carb meals in a 24-hour period could reduce post-meal insulin resistance by more than 30 percent. Study participants limited their carbohydrate intake to no more than 30 percent per meal. (10) Although more research is needed to confirm these results, eating a balanced diet that consists of moderate portions of carbohydrates and sugars may improve how your body uses insulin and reverse insulin resistance. RELATED: 10 Foods That Can Help With Blood Sugar Control Change your medication with doctor supervision. You may have insulin resistance if you take steroid medication to treat pain and inflammation. (11) These drugs prompt the liver to release extra glucose, increasing the risk for steroid-induced diabetes. Lowering your dosage or slowly weaning yourself off steroids may improve insulin sensitivity. Speak with your doctor before modifying your medication. Quit smoking. Giving up cigarettes may also reverse insulin resistance. Nicotine can cause your body to produce extra glucose, which makes it harder to control your blood sugar level. (12) Get plenty of sleep. Aim for seven to nine hours of sleep a night for optimal health. (13) Not getting enough sleep may increase your risk for diabetes or make it harder to control. (14) Speak with your doctor if you’re having trouble sleeping. This may indicate a sleep disorder. Manage stress well. When you’re under stress, your body produces higher amounts of cortisol, which is a stress hormone. (15) This hormone can make your muscles and cells resistant to insulin, resulting in higher blood sugar. As a result, chronic stress may increase your risk for prediabetes and type 2 diabetes. (16) How to Change Your Lifestyle and Diet to Prevent, Manage, or Help Reverse Insulin Resistance Having insulin resistance doesn’t mean that you’ll develop prediabetes or type 2 diabetes, but this can happen if you don’t make changes to your diet and lifestyle habits. RELATED: What Makes for a Good Type 2 Diabetes Diet? Consuming carbohydrates in moderation, prioritizing fitness, and giving up bad habits like smoking not only may help you avoid diabetes but also all the health complications related to the disease, including heart disease, stroke, nerve damage, and vision problems. (17) How do I know if I am Insulin Resistant? And should I care? Well yes you should care. A lot. You are likely pre-diabetic… Who cares? You’d care because being insulin resistance combined with a moderate to high carbohydrate diet makes you “hyperinsulinemic” – you have high insulin all the time. This means you are now metabolically dysregulated meaning your body: - turns fat burning off - promotes fat storage - dials down your physical activity (feel lethargic and lazy) - disrupts the hunger control mechanisms in the brain - has all the physiological factors in play (reactive oxygen species, inflammation, IGF-1 etc) which eventually result in the range of metabolic diseases which will kill most of us with a reduced quality of life for a decade before we die – diabetes, cancer, heart disease and dementia. Understanding how your own body reacts to different types of food, stress, and other environmental factors is absolutely key to long term health, especially weight control. That’s why we care about insulin resistance and maybe you should too…..read on What is insulin? Insulin is a protein produced by the pancreas. It helps in the regulation of nutrients and energy around the body. It is best known for helping move glucose (carbs) into cells so it can be used for energy. That’s a pretty crucial function; without insulin you will die. Type 1 diabetes is a failure of the pancreas to produce insulin, so Type 1 diabetics can inject synthetic insulin. But insulin is way more interesting than just that. It is part of a complex hormonal and neural system that affects all parts of our body. That system controls energy storage and energy use. That system controls: - Fat burning – elevated insulin turns off fat burning - Fat storage – elevated insulin promotes nutrients (both carbs and fat) to be stored away in fat cells - Physical activity – elevated insulin dials down (your brain suppresses your body) energy output - Hunger – a more complex interaction with insulin, leptin and ghrelin (other hunger hormones), the hypothalamus (hunger centre in the brain), inflammation and other anabolic (growth) promoting agents switch hunger off and on. We are still learning exactly how this might work, but insulin in short spikes might switch off hunger, but when chronically high (longer term) keeps the “I’m still hungry” switch on. People are said to be insulin resistant when they have trouble getting glucose into their cells. One way to think about it is that the cells become “resistant” to insulin trying to open them up and get glucose in. This can be temporary – for example when we starve ourselves our body wants to divert any glucose away from most cells in the body and have it used by some cells which require more glucose (eg, brain cells, red blood cells). In the meantime the rest of the body runs off fat. The same is true when we eat excessive amounts of carbohydrates. We can become temporarily insulin resistant, helping us pack away that extra energy into fat for a famine in the future. When the body is properly regulated, the whole metabolic machine works perfectly. We produce insulin when we need to, become insulin resistant to help us when we are starving, and store extra energy when we are in times of plenty. In an evolutionary sense, this is a system designed to work across feast and famine. Unfortunately the whole system can become “uncoupled” by modern life. Stress, lack of famine and constant feast, too little exercise, poor quality foods and much more all make you insulin resistant. Modern human life promotes insulin resistance. In fact, my colleagues at Otago University have shown that in older New Zealanders, pre-diabetes may affect as much as 50% of the populaiton. I’d say that this condition called “pre-diabetes” really indicates the start of “end stage” failure of the body. This is because pre-diabetes is the point where people start to be unable to get glucose into their cells, regardless of how much insulin they produce OR their pancreas has started to fail because of having to produce so much insulin for so long (it’s burnt out), then we can be almost certain that the majority of the older and other higher risk groups (Maori and Pacific people in New Zealand) are insulin resistant. We need to identify insulin resistance way before you start to fail the tests your doctor currently uses. We’ll look at that now. How can you tell if you are insulin resistant? The main reason I wrote this post was because I am often asked how you tell if you are insulin resistant. That’s a great question and hard to answer, but very very important to your health. Read on. The health system has some serious diagnostics which will show you if you are insulin resistant. I’ve listed everything below. You’ll know some of these already . Diagnostics - High fasting blood sugar - 110 to 125 mg/dL (6.1 mM to 6.9 mM) – WHO criteria - 100 to 125 mg/dL (5.6 mM to 6.9 mM) – ADA criteria - High HbA1C (glycated Haemoglobin) between 5.7 and 6.4 percent. - Oral glucose tolerance testing: High and prolonged levels of glucose to carbohydrates ingested (usually administered as 75g of pure glucose drink). Diagnosed with a blood sugar level of 140 to 199 mg/dL (7.8 to 11.0 mM) after two hours. So these are the techniques your doctor will use to screen you to understand whether you have Type 2 diabetes or pre-diabetes. All of these by definition indicate moderate to severe insulin resistance, which has probably been persistent for decades. But it’s not the end of the story. The problem is that you can pass any one of these tests fine but still have insulin resistance and all the problems described above. Why? Because current medical testing looks at our inability to get glucose into cells, rather than how much insulin we are producing. Many people can move glucose into their cells at an acceptable rate but need to do so with massive amounts of insulin. Therein lies the biggest unnoticed problem in modern medicine. We have a large part of the population told they are metabolically healthy when they are not. We send them away, tell them all is good, and it is only when they show “end stage” symptoms that we act. Do you see a problem? Bottom line 1: High and prolonged levels of insulin because of carbohydrates ingested, even with normal blood glucose responses, is dangerous to your health. There is a better way – that is measuring both insulin and glucose response in the oral glucose tolerance test. That way we can see if you have this condition called “hyperinsulinemia” even with good glucose disposal. The trouble is that would cost you nearly $1000 in New Zealand, if you could find someone willing to do it and interpret the results. It’s costly, time consuming (a few hours in a lab) and messy and painful (lots of blood samples). You could measure fasting insulin – but I’m not convinced that most insulin resistant people show problems here. But can you observe symptoms yourself without a clinical diagnosis? I think if you have a few of the symptoms below then it is likely you have insulin resistance. A checklist - I’ve had trouble controlling my weight my whole life - I have a high waist circumference (I’ve got a fat gut) – more than 100 cm men, 85 cm women - I always feel hungry - I feel like something sweet after dinner to stop my hunger - Fatigue, exhaustion, depression - High blood pressure - Frequent hypoglycemia (low blood sugars) - You are over 50 years old BTW – if you have failed one of the glucose tests then don’t bother with the checklist, you are already insulin resistant. Bottom line 2: If you have some of these symptoms, the easy “try it yourself” work around is to severely restrict the amount of carbohydrate you eat for a couple of weeks and see how you feel. I’d say if you are insulin resistant, then the carb restriction is the method which can best help you reset your metabolism. Insulin Resistance Syndrome in the Elderly CONCLUSIONS— IRS is increasingly recognized as a harbinger of classical disease states, including diabetes and metabolic syndrome X. It has been postulated that insulin resistance, diabetes, and metabolic syndrome X are all associated with a proinflammatory state, but it has been difficult to determine whether the proinflammatory state is a cause or effect of these conditions. Furthermore, it is unclear what proinflammatory cytokines are most likely to be elevated early in the course of these conditions, especially in insulin resistance. All these conditions also become increasingly common with aging. Here, we examined functional, chemical, metabolic, and inflammatory status in a relatively healthy and uniform population of elderly women. We excluded any person taking diabetes medications and used strict criteria for euglycemia (i.e., fasting glucose <110 mg/dl). These residents had significant impairments in their abilities to care for themselves, requiring nursing home placement. They were, however, the healthiest members of the nursing home population, having on average mild to moderate cognitive and functional impairments. Mean insulin levels were 280 pmol/l in the IR group and 58.4 pmol/l in the NIR group. It is significant that the majority of recruited residents did not have IRS, fasting hyperglycemia, or frank diabetes, as it is generally assumed that residents this debilitated would have near-universal insulin resistance (13). Those with IR did not differ from the NIR group in age, height, weight, smoking history, drinking history, or nutritional risk, as measured by the mini–nutritional assessment tool. Importantly, the two groups did not differ in BMI, although the IR group had a BMI that was ∼6% greater (P = 0.09). The groups did not differ on measures of severe illness as measured by the comorbidity scale of Charlson, a medical record–based inventory of 19 conditions associated with in-patient mortality. Functional status did not differ between the two groups, as measured by four different measures: the functional index measure, the activities of daily living, the 6-m walk, and the 6-min walk. This lack of difference suggests that the muscle wasting, sarcopenia, and frailty associated with insulin resistance (13) is confounded by aging and other associated factors and is more likely a later association with IRS. Levels of depression, as measured by the geriatric depression scale, or dementia, as measured by the mini–mental status examination, were similar between the groups. Balance and risk of falls as measured by the timed get-up-and-go test was also similar. This lack of difference shows that any deleterious effects of insulin resistance had not yet manifested themselves in common indexes of health status. These groups did not differ in the indicators of general inflammation, including C-reactive protein, prealbumin, albumin, transferrin, or immune cell levels, or in hemoglobin or hematocrit. They also did not differ in cholesterol levels. Hyperlipidemia is a hallmark of metabolic syndrome X, whereas low cholesterol (<160 mg/dl) is used in geriatrics as an index of malnutrition. Overall, therefore, insulin resistance had little impact on immediate general health, giving us the opportunity to examine an early stage of IRS. Although the study included only those with a fasting blood glucose of <110 mg/dl, glucose was higher (P < 0.05) in the IR (94.2 mg/dl) versus the NIR group (87.9 mg/dl). The IR group fasting glucose was well within normal limits and only 7% higher than in the NIR group. Nevertheless, it is a clear indication that even this early stage of IRS is associated with impairments in glucose handling. In contrast to the lack of differences in routine laboratories, several hormone levels were elevated in the IR group. As expected, insulin C-peptide was elevated but only by ∼15%. Interestingly, the insulin/C-peptide level was about fivefold higher in the IR group, suggesting that insulin or C-peptide clearance or degradation was affected more than secretion. Any difference in insulin clearance cannot be ascribed to renal failure, as serum creatinine did not differ between the IR and NIR groups. Amylin, cosecreted with insulin in a 1:1 molar ratio from the pancreas, was also elevated over fourfold in the IR population. The ratio of insulin and amylin did not differ between the two groups, suggesting that the two peptides were cleared and secreted in a similar fashion. Serum insulin levels were highly correlated with serum leptin levels, consistent with insulin resistance being associated with obesity. As expected from numerous other studies, leptin also correlated positively with BMI and inversely with adiponectin. Leptin was increased ∼70% in the IR population (P < 0.01). This was unexpected, given that the average BMI for the IR group was only marginally (6%), and not significantly, higher than in the NIR group. However, BMI is a cruder measure of adiposity than serum leptin, as BMI does not distinguish between lean and adipose tissue. The leptin-to-BMI ratio was also ∼70% higher in the IR group in comparison with the NIR group (P < 0.005). This suggests that either those in the IR group were hypersecreting leptin per unit of fat mass or that a greater percent of their body weight was adipose tissue. The latter seems more likely, considering the recent description of the sarcopenic obese. These residents, despite having a normal or high BMI, have decreased muscle mass, and so a greater proportion of their BMI is adipose tissue. Such residents are at an increased risk for mortality and morbidity. The current findings suggest that insulin resistance could be an early component of sacropenic obesity. The strong associations of leptin and leptin/BMI with serum insulin and their segregation between the NIR and IR groups suggest a strong association between obesity and insulin resistance. However, BMI only showed a trend toward association with insulin (P = 0.06), whereas the leptin-to-BMI ratio correlated better with serum insulin than did leptin alone. This again suggests that serum levels of leptin are much more sensitive at inventorying the metabolic parameters associated with insulin resistance than is BMI. This is further suggested by the finding that the leptin-to-insulin ratio did not differ between the IR and NIR groups, even though each of these components alone were very different. Thus, leptin and insulin overlap to some degree in their abilities to distinguish the IR and NIR groups but likely retain independent predictive abilities. In contrast, serum adiponectin levels correlated even more strongly with leptin than did insulin. Adiponectin is secreted from fat and can reverse insulin resistance and hyperglycemia, possibly through its ability to regulate proinflammatory cytokines (14–17). However, adiponectin did not distinguish insulin resistance from non–insulin resistance, being decreased in the IR group by ∼25% (P = 0.08). Evidence for a proinflammatory state was most clearly revealed by a significant (P < 0.01) elevation in TNF. TNF levels were 50% higher in IR compared with NIR residents. Arithmetic increases that did not reach statistical significance were evident in every other proinflammatory and anti-inflammatory cytokine measured with the exceptions of MIP-1α and RANTES. The lack of statistical significance in the elevations of some of the cytokines may have been caused in part by the large variance within groups. To further assess a global trend of cytokine elevation and to negate variance, we computed two proinflammatory indexes, both of which included TNF that assessed elevations on nonparametric scoring. However, neither of these summations was different between the two populations. This suggests that even with the power of including a statistically significant component (TNF), there is no evidence for a statistically meaningful global cytokine increase. This supports TNF as being the primary cytokine whose elevation is relevant in early insulin resistance. The role of serum TNF is further supported by a strong correlation with serum insulin levels. This correlation between TNF and insulin was even stronger than that between leptin and insulin. One source of serum TNF could be from adipose tissue. However, serum TNF levels did not correlate with serum leptin levels. In some studies, TNF and leptin levels correlate, presumably because both can be secreted from fat. However, TNF has sources in addition to adipose tissue, whereas adipose tissue is essentially the sole source of serum leptin. Therefore, the lack of correlation between leptin and TNF suggests that the source of elevated TNF was not adipose tissue. Further supporting this were the findings that the TNF-to-BMI ratio did not distinguish between IR and NIR groups the way leptin-to-BMI ratio did, and the TNF-to-insulin ratio, unlike the leptin-to-insulin ratio, still distinguished the IR and NIR groups. Therefore, TNF and leptin behaved very differently, making it unlikely that adipose tissue was the source of the elevation in TNF. TNF did show a statistical trend with C-reactive protein (P = 0.07), suggesting that it might have arisen from a generalized proinflammatory condition. In conclusion, we examined early insulin resistance in a population of elderly women living in a long-term care facility before debility ascribable to insulin resistance had arisen. Although no functional impairments were found between the IR and NIR groups, we found that other parameters were already changing. Despite exclusion of any person with a serum fasting glucose ≥110, a slight, statistically significant increase in serum glucose of 7% demonstrated an early glucose intolerance in the IR group. Differences in C-peptide and the insulin–to–C-peptide ratio suggested an increased insulin secretion and a decreased insulin clearance in the IR group. Increased leptin and leptin-to-BMI ratios in the absence of differences in BMI suggest that the IR group had a higher percent of body fat mass and that IR could be related to sarcopenia of obesity. TNF was the one proinflammatory cytokine statistically elevated in the IR group. The lack of correlation of TNF with BMI or leptin suggests that the TNF did not originate from fat. Thus, early insulin resistance is associated with elevations of leptin, even after correction of BMI and a proinflammatory state, as evidenced by elevated levels of serum TNF. If you have insulin resistance, following a healthy lifestyle can reduce your chances of developing Type II diabetes. Studies have shown that combining: - Healthy eating - Weight loss - Regular physical activity can all help reduce your risk of Type II diabetes in the years to come. These lifestyle changes were shown to be at least as effective as a common medication used to treat insulin resistance. Smart eating tips for improving insulin resistance - If you are overweight, losing some weight will improve insulin resistance. Eating smaller portion sizes, being more physically active and eating less energy dense foods (‘extra’ foods) can assist with weight reduction. - Physical activity is not only beneficial for weight management but can also independently assist with improving insulin resistance. Include 30 minutes of physical activity on most days of the week. - Resistance training (e.g. hand weights) can also help with insulin resistance. Also try to increase your incidental activity. Examples of incidental activity include gardening, housework and walking around the shops. Healthy eating tips - Eat at least five serves of vegetables and two pieces of fruit each day. - Eat wholegrain foods everyday such as high fibre breakfast cereals, multigrain bread, oats, barley and cracked wheat. - Enjoy legumes (dried peas, beans and lentils) on a regular basis. - Include low glycaemic index (GI) foods. Low GI foods can help by slowing the rate of absorption of glucose into the blood stream, so not as much insulin is required. - Reduce the amount of saturated fat in your diet. Limit commercial cakes and biscuits, fried take-away foods, butter, lard, cream and trim the visible fat off meat. An Accredited Practising Dietitian (APD) can help you plan and implement these lifestyle changes. Insulin Resistance: Dealing With the Diagnosis When my daughter was a pre-teen, her routine blood glucose test came back a little high. Her pediatrician had her undergo a special test called a fasting blood glucose test, which was followed by a series of other tests. The results prompted her doctor to come back with a chilling diagnosis: insulin resistance. As a pediatric nurse, I was familiar with the topic of diabetes and insulin resistance, but this was a frightening diagnosis. My daughter was very upset, thinking she now had a terrible disease. And both my husband and daughter turned to me for ways to deal with this new diagnosis. What is insulin resistance? It’s a condition in which the hormone, insulin, becomes less effective at managing sugar levels in the blood glucose after eating or drinking anything that contains a simple sugar. Insulin is produced by the pancreas and acts to open the doors of the cells, taking glucose out of the bloodstream and putting it into the cells for energy. When cells don’t respond enough to insulin, blood glucose levels rise as a result. How serious is insulin resistance? The presence of insulin resistance typically precedes the diagnosis of type 2 diabetes, previously known as adult onset diabetes. When an individual has diabetes, his or her pancreas does not make enough insulin to keep blood sugars level. This is a chronic disease which can result in a number of side effects and disabilities. How do I know if my child has insulin resistance? The signs and symptoms can vary with each person, but some are very noticeable. In my nursing career, I have taken care of children who seem to have a dark ring around their necks that looks like oily dirt. This is not dirt and can’t be washed away. It also can occur under the arms or in the groin area. This ring is called acanthosis nigricans and is a sign of insulin resistance. Other signs of insulin resistance include: - Brain fogginess or inability to focus, - Depression, - Fatigue, - High blood sugar, - Higher blood pressure, - Increased hunger, - Intestinal bloating, - Sleepiness, especially after meals. If your child is exhibiting these symptoms, make an appointment with their pediatrician and be sure to let his or her doctor know exactly what signs your child has been displaying. At Children’s Hospital Los Angeles, the Division of Endocrinology and Metabolism provides clinical care and research focused on childhood diabetes, growth, weight management, endocrinology and bone metabolism. For more information, visit their webpage. Diet and Exercise to Avoid Diabetes As we researched more on the subject of insulin resistance, what became clear to my family was that this condition was something we could treat and correct, and if we did so early enough, it didn’t have to mean “diabetes” for my child. There are some medications available, but what else could we do? The answer was, two things: - Exercise - Healthy eating Everything we read indicated that insulin resistance and diabetes have a relation to nutrition. I knew that from nursing school and also had some tools to work with because I have a long on-and-off relationship with Weight Watchers! The Family Plan So, as a family, we came up with a plan to make meaningful changes in our lifestyle, but none so drastic or difficult to maintain that we couldn’t stick to them. - My daughter remembers some of the basics: - No more fast food, - No excessively sugary drinks (including juice), - Lots of fruits and vegetables, - Reading food labels, - My Food Pyramid Website (Website is interactive for adults and children) And, sadly, we also had to stop Dad from making his wonderful buttery and cheesy sauces, except as a rare treat! Balance and variety were important. So what to choose? - Fresh, colorful vegetables and fruits, - Whole grains, - Healthy fats, not trans fats, - Avoid heavily processed foods, high fructose corn syrup and excessively-sugared beverages. Many weight-loss programs are low in carbohydrates (carbs), but some are needed in the diet so as not to starve the cells of energy, which can otherwise upset the body’s blood sugar balance. The carbs that do this well come from whole grains, fruits and vegetables. It’s best to avoid refined sugars (or carbohydrates) and grains. My daughter’s doctor prescribed Vitamin D for her, as this is often deficient in those with insulin resistance. However, your child’s doctor may or may not prescribe something different, depending on your child’s needs. What Works at Our House To be a better role model for my daughter, I went back to Weight Watchers and my daughter came with me for a few months. We joined a gym and made a promise to the dog to walk her more often. We stopped going to fast food places, except as a rare treat. And we gave up sodas. Thankfully, I had given my daughter broccoli as a baby, so she already had one vegetable she liked. From there, we explored and tasted to integrate more vegetables and fruits into our diet. We steamed them or ate them raw to avoid adding any additional oil when possible. I tried out “lighter” recipes from books and magazines to introduce variety and make these changes into a lifestyle and not a diet. My daughter discovered that she loved to eat couscous, a whole grain, with vegetables. There are healthier choices for snacks in every grocery store these days, but we read the labels to find the best ones. Insulin Resistance Success Story My daughter’s blood sugar levels are now normal and she no longer has insulin resistance. Knowing that once you are insulin resistant, you continue to be at risk for insulin resistance and hyperglycemia, however, it can be controlled with diet and exercise. Because she made some simple life changes and stuck with them, she was able to successfully lower her risk of developing diabetes later in life. Insulin resistance is the name given to when cells of the body don’t respond properly to the hormone insulin. Insulin resistance is the driving factor that leads to type 2 diabetes, gestational diabetes and prediabetes Insulin resistance is closely associated with obesity; however, it is possible to be insulin resistant without being overweight or obese. Modern research has shown that insulin resistance can be combatted by treatment methods that reduce how much insulin the body is producing or taking via insulin injections or insulin pumps. Reducing insulin resistance can be achieved by following low-carbohydrate and ketogenic diets. What is insulin resistance? The role of insulin is to allow cells of the body to take in glucose to be used as fuel or stored as body fat. It also means that glucose is more likely to build up in the blood and this can lead to too high blood sugar levels When the body becomes resistant to insulin, it tries to cope by producing more insulin. People with insulin resistance are often producing too more insulin than healthy people. Producing too much insulin is known as hyperinsulinemia Symptoms of insulin resistance Initially, insulin resistance presents no symptoms. The symptoms only start to appear once it leads to secondary effects such as higher blood sugar levels. When this happens, the symptoms may include: - Lethargy (tiredness) - Hunger - Difficulty concentrating (brain fog) Other signs that often appear in people with insulin resistance include: - Weight gain around the middle (belly fat) - High blood pressure - High cholesterol levels If insulin resistance develops into prediabetes or type 2 diabetes, the symptoms will include increased blood glucose levels and more of the classic symptoms of type 2 diabetes Causes of insulin resistance Whilst the exact cause of insulin resistance is still not fully understood, it is well-known which factors can lead to insulin resistance developing. Insulin resistance can commonly develop if one or more of the following factors apply: - If you are overweight or obese - Having a high-calorie diet, high-carbohydrate or high-sugar diet - Sedentary lifestyle – taking little physical activity - Taking high doses of steroids over an extended period of time - Having chronic stress - Having Cushing’s disease or polycystic ovary disease In terms of what is happening inside the body that causes insulin resistance, researchers have observed that insulin resistance occurs in people that have: - High levels of insulin circulating in their blood - Excessive fat stored in the liver and pancreas - High levels of inflammation Transcript Insulin resistance is a state where the body does not respond to insulin as well as it should. It’s almost like a lack of communication between insulin and the cells of the body. Insulin resistance is a key feature of type 2 diabetes. Insulin resistance is a problem because it affects the body in a number of ways. Resistance to insulin causes the body to produce more insulin which leads to increased hunger higher blood pressure and weight gain. It is still not fully understood what causes insulin resistance. There does seems to be a strong link between weight gain and insulin resistance. Studies have shown that significantly reducing calorific intake can improve the body’s sensitivity to insulin. Download a FREE blood glucose chart for your phone, desktop or as a printout. Can insulin resistance be reduced or reversed? It is certainly possible to reduce the effects of insulin resistance and there are a number of effective ways to do this. Effective methods include: - Low-carbohydrate and ketogenic diets - Very-low-calorie diets - Weight loss surgery - Taking a lot of exercise in combination with a healthy diet These methods share a similar way of working in that they all help to reduce the body’s need for insulin and help people to lose weight. Read more on reversing the effects of diabetes What Is Insulin Resistance? Insulin resistance and PCOS. You may have been diagnosed with the latter, but are not sure whether you also have the former. An insulin resistance test should be one of the first that your doctor does after diagnosing PCOS. Unfortunately, that’s not always the case… In this article I’ll outline some classic signs and symptoms to help inform you of whether you should be pushing for further testing. Of course, you’re smart women, you know this is not a diagnosis. I’m not a doctor, I’m a degree-qualified nutritionist. Even if I was a doctor, I could not diagnose you via a blog. You need to get a blood test done to know for sure. So, book one as soon as you can. Insulin is our storage hormone. When we eat, our body detects a rise in blood sugar (glucose). Our body doesn’t like blood sugar to be high. This is because cells can be damaged if it’s high for prolonged periods of time. These cells include those in the brain, liver, pancreas, heart, and eyes. Therefore, in response to high blood sugar, the body stores excess glucose in muscle and liver cells for later use. Insulin is the hormone that allows this to happen. It tells the cells to open up and let the glucose in. Insulin is excreted by the pancreas. It binds to a receptor on the cell and tells it to open up. This process is similar to the way a key opens a door. Insulin resistance occurs when insulin no longer works effectively due to chronic low grade inflammation. The key has been used too much, the lock gets worn and the key no longer fits. As a result, the blood glucose level stays high. The brain believes that more insulin is required. It sends a message to the pancreas to get it to make even more. However, the ‘lock’ is still worn so the extra insulin doesn’t help. If this process continues over a long period of time, the pancreas becomes so fatigued that it’s unable to produce enough insulin. This is called Type 2 diabetes. How Are Insulin Resistance and PCOS Connected? 70% of women with PCOS have insulin resistance. Studies have shown that improving insulin resistance can reduce: – Testosterone levels – Body weight and improve: – Ovulation Metformin is a drug that you may already know about. It’s often prescribed to help with fertility – you may have even been prescribed it yourself! Metformin is a drug that improves insulin sensitivity. However, it’s not thing that improves insulin sensitivity. In fact, it’s not even effective for many women. Studies have shown that a very low carbohydrate (ketogenic) diet can be very successful alternative. It can improve insulin resistance, help weight control, and reduce testosterone levels. Reducing testosterone levels is especially important if ovulation is to happen. How Do I Know If I Have Insulin Resistance? The stats say that insulin resistance and PCOS often go hand in hand. A blood test can tell you whether you have insulin resistance. This should measure fasting blood glucose, fasting insulin, and HbA1c (long-term blood glucose performance). It’s important that you don’t just accept them telling you that your levels are normal. Make sure that you ask for the actual results. The ‘normal’ range for fasting blood glucose is 3.61-5.50 mmol/L. Your level could be deemed ‘normal’ even when it’s 5.49mmol/L. Get the actual figure and then make an informed decision about how normal it actually is. Here are some more indicators that you should get your levels checked: 1. You Have Severe Hangry Attacks I know you know what I’m talking about! One minute you’re not even hungry, and the next you must eat everything in sight. No food? No problem! The closest boyfriend’s, friend’s, or colleague’s head will suffice. If no food’s available, then you might even start to feel shaky, jittery, and faint. You’re experiencing severe blood sugar crashes. These show that your blood glucose isn’t stable and is not doing what it should be. 2. You Store Weight Around Your Belly This is true even if you’re not overweight, or ‘Lean PCOS.’ If you put on weight, where does it go? If the answer is your stomach, then that’s a really good sign that you’ve got some insulin resistance going on. Studies that have looked at both overweight and normal weight women have shown that weight gain around the stomach is a significant sign you have insulin resistance. 3. No Matter How Many Spin Classes, Miles Run, and Salads Ate, You Can’t Lose Weight Feel like you’re doing everything ‘right’ and still not losing weight? Insulin resistance might be playing a factor in this. Studies have shown that insulin resistance impacts the ability to burn fat. In fact, one study showed that the muscles of people with insulin resistance are geared towards fat storage, not fat burning. No wonder it’s hard to lose weight! 4. You’ve Developed Dark Velvety Patches in the Folds of Your Skin These could be under your arms or on the back of your neck. The proper name for them is acanthosis nigricans. It’s caused when insulin-like growth factor (increased by insulin resistance) stimulates the cells in the skin to produce more keratin and dermal fibroblasts. Studies have shown that insulin resistance is not the only reason that these patches develop. However, they are still a potential indicator of it. 5. You’ve Got Skin Tags Skin tags are little bits of skin that hang off. I know what you’re thinking, “Oh is that what they’re called?” Yes, I admit, until recently I didn’t know either. Studies have shown that multiple skin tags are a really good indicator of insulin resistance, so if you have them then go and get them checked out. Summary of Insulin Resistance and PCOS Insulin resistance and PCOS often go hand in hand. Insulin resistance causes excess androgens, which causes a lot of the horrible PCOS symptoms. Longer term, insulin resistance can develop into Type 2 diabetes and put us at risk for all manner of nasty metabolic diseases. But it is reversible, so you need to address it now. It needs to be diagnosed by blood tests from your doctor, but some signs that you may be insulin resistant include: – Blood sugar crashes (aka hangry attacks) – Putting on weight around your belly – Struggling to lose weight – Dark velvety patches on your skin – Skin tags by Dr. Will Cole A staggering 50 percent of us are now either prediabetic or have full-blown type 2 diabetes. No, that is not a typo; one out of two of us have some serious blood sugar problems, making a condition that was once a rarity completely commonplace. Much of the blood sugar problems we see today are due to one thing: insulin resistance. Insulin is a hormone that directs blood sugar into cells to create energy in the form of ATP, but when you become resistant to its effects, your cell receptor sites are blunted and you’re left with a backup of insulin and blood sugar, which is no bueno. If this condition goes on for too long without intervention, you could get diabetes, which is one of the leading causes of heart attacks and strokes! Know the signs of blood sugar imbalance If more than one of these is true for you, I suggest getting your blood sugar levels checked stat. - You crave sweets or breads and pastries….a lot! - Eating sweets doesn’t relieve your sugar cravings and even increases them. - You become irritable and “hangry” if you miss a meal. - You find yourself needing caffeine to get through the day. - You become lightheaded if you miss a meal. - Eating makes you exhausted and in need of a nap. - It’s difficult for you to lose weight. - You feel weak, shaky, or jittery pretty frequently. - You have to pee a lot. - You get agitated, easily upset, or nervous, out of proportion to the reason for these feelings. - Your memory is not what it used to be. - Your vision is blurry. - Your waist measurement is equal to or larger than your hip measurements. - You have an atypically low sex drive. - You’re always thirsty. Natural ways to improve blood sugar balance You don’t have to settle for a future of diabetes. Intervene now with these tips for restoring a healthy blood sugar/insulin balance. 1. Find your baseline. The labs I run on my patients to assess their blood sugar balance and check for insulin resistance are: 2. Sip on matcha. EGCG is a compound in green tea, EGCG has demonstrated a stabilizing effect on blood sugar levels. Drinking the whole green tea leaf in the form of matcha powder is a great way to up your ECGC intake. 3. Try alpha-lipoic acid. In several studies, alpha-lipoic acid supplements helped balance blood sugar levels and improved insulin resistance. This antioxidant also strengthens immunity, improves energy production in cells, protects brain cells against excitotoxicity, and helps the body remove excess toxic metals. For blood sugar control, take 200 milligrams three times a day. 4. Take magnesium. According to research published in the medical journal Circulation, in a group of nearly 5,000 people, those who took higher levels of magnesium over a period of 15 years had a decreased risk of metabolic syndrome, a condition that is often a precursor to diabetes. A similar study, published in the American Journal of Epidemiology, followed more than 1,000 healthy adults for five years and found that greater magnesium intake improved insulin sensitivity. Other studies have shown that magnesium improves triglycerides and high blood pressure – two other hallmarks of metabolic syndrome and diabetes. 5. Add chromium. When chromium levels are low, good cholesterol tends to drop and the risk of insulin resistance, as well as triglyceride levels, go up. Chromium supplementation has been shown to improve blood sugar receptor function. The best food sources of chromium include onions, tomatoes, potatoes, and sea vegetables. 6. Increase Nrf-2. The protein Nrf-2 plays a role in regulating antioxidant gene induction by turning on genes that are responsible for antioxidant and detox pathways. When Nrf-2 is activated, inflammation tends to subside. There are many antioxidant rich foods that tend to activate Nrf-2, including: - EGCG from green tea - Quercetin from apples - Curcumin from turmeric - Resveratrol from grapes - Rosmarinic acid from rosemary - L-sulforaphane from broccoli - Thiosulfonateallicin from garlic 7. Bring in vitamin E. This fat-soluble tocopherol has been shown to support insulin sensitivity. Standard doses range between 600 and 900 milligrams. 8. Sprinkle cinnamon. Proanthocyanidin, a bioflavonoid found in cinnamon, may alter the insulin-signaling activity in fat cells, making it a potential diabetes buster. The spice has also been shown to significantly reduce blood sugar levels and triglycerides in people with type 2 diabetes. 9. Seal and heal the gut. Your gut health and blood sugar balance are inextricably connected – one study found that transplanting the microbiome of diabetic mice into healthy mice made the recipients diabetic! Among the culprits are advanced glycation end products (AGE) – harmful compounds that have the potential to cause leaky gut. A high sugar diet can also tip your microbiome in the wrong direction, causing candida overgrowth, which is also linked to blood sugar problems. What’s good for your gut is good for your blood sugar, and vice versa. 10. Get more sun. Most people have low vitamin D levels, which can cause a host of problems, but in one study, supplementing with vitamin D for 12 weeks decreased body fat by 7 percent, and lower weight correlates with better blood sugar control. Low D levels have also been linked to metabolic syndrome. Aim for 60 to 80 ng/mL per day. 11. Eat more healthy fats. One study found that higher blood sugar in non-diabetics decreased function in areas of the brain affected by Alzheimer’s disease (AD). This is one reason why Alzheimer’s is often referred to in the medical literature as “type 3 diabetes.” On the other hand, a ketogenic diet – where fat, not sugar, is your primary source of energy – has been shown to do some remarkable things for your brain health. Healthy fats provide a slow, sustainable form of energy, subverting the more drastic ups and downs that can happen with sugar burning. Humans were meant to rely more on fat and less on sugar – for example, babies primarily use the fat in breast milk for brain development and energy. From a biological and evolutionary perspective, the most sustainable form of energy for optimal brain health as well as blood sugar control is healthy natural fat. 12. Take B-vitamins for the win. Methylation is a complex process that supports many crucial function in the body, including healthy blood sugar balance. Activated B vitamins – like B9 L-Methylfolate (L-5-MTHF) and B6 Pyridoxyl-5-Phosphate (P5P) – are a great way to support methylation pathways. Food medicines to focus on are spinach, okra, and turnip greens, and meats like chicken liver or grass-fed beef liver, which have the highest levels of bioavailable B vitamins. 13. Activate your PPARs. Studies suggest that PPARs, or peroxisome proliferator-activated receptors, may help improve inflammatory conditions such as atherosclerosis, asthma, colitis, MS, and other autoimmune conditions. Some PPAR activators for you to bring into your life: wild-caught fish, green tea, astragalus, ginger, and sea buckthorn. 14. Get your omega-3s on. You’ve probably heard that omega-3 fatty acids can lower the risk of stroke and heart attacks, but these healthy fats most prevalent in fish oil also convert the potentially harmful very low-density lipoproteins (VLDL), which are linked to diabetes, into less dangerous low-density lipoproteins (LDL). 15. Never forget adaptogens! Adaptogens are awesome at balancing out hormones and inflammation. A study found the adaptogen American ginseng berry juice could significantly improve glucose tolerance and normal bloods sugar levels after just 10 days. If you want to learn more about your own health case please check out our free health evaluation. We offer in person as well as phone and webcam consultations for people across the country and around the world. Photo: iStock The information on this website has not been evaluated by the Food & Drug Administration or any other medical body. We do not aim to diagnose, treat, cure or prevent any illness or disease. Information is shared for educational purposes only. You must consult your doctor before acting on any content on this website, especially if you are pregnant, nursing, taking medication, or have a medical condition. Our articles may include products that have been independently chosen and recommended by Dr. Will Cole and our editors. If you purchase something mentioned in this article, we may earn a small commission. Your body naturally produces the hormone, insulin, to help keep your blood sugar at healthy levels, but sometimes your body doesn’t respond to insulin the way it should. When this happens, it’s called insulin resistance. Here, we’ll discuss what insulin resistance is, how it can cause complications like type 2 diabetes, and what you can do to prevent it. What does insulin do in the body? Insulin is a hormone that helps regulate your blood sugar and is made by an organ known as the pancreas that sits behind your stomach. Your pancreas sends insulin into your bloodstream after you eat or if it detects that your blood sugar levels are high. Once insulin enters your blood, it has 2 major jobs: 1) Insulin takes sugar out of your blood and sends it into your cells to be used for energy. When you eat a meal with carbohydrates (also called carbs or sugars), you often get a burst of energy. Well, your cells get energy from sugar too, but how does the sugar get into the cells? That’s where insulin comes in. Most of the cells in your body contain insulin receptors. Think of an insulin receptor like a lock and the insulin hormone like a key. When the key opens the lock—or when insulin binds to the insulin receptor—the cell opens to let sugar in. By attaching to insulin receptors, insulin helps take sugar out of the blood and sends it into cells to be put to good use. As a result, your blood sugar levels should return to normal. 2) Insulin takes sugar out of your blood and stores it in muscles, fat cells, and the liver for later use. Even though it’s helpful for your cells to take in blood sugar for energy, they don’t need immediate access to that sugar all the time. In fact, insulin will take any extra blood sugar that your cells can’t use right away and send it to your muscle cells, fat cells, and liver to be stored for later use. When it’s stored, the original form of sugar, glucose, becomes another form of sugar known as glycogen. What does it mean to be insulin resistant? Both of insulin’s primary jobs require your cells—specifically, the insulin receptors on your cells—to respond to insulin. But for several reasons, your cells may stop responding to insulin as well as they should. In other words, instead of being sensitive to the effects of insulin, they become resistant to the effects of insulin—hence, the name insulin resistance. When cells become insulin resistant, sugar stays in your bloodstream, which can lead to high blood sugar. What causes insulin resistance? There are numerous potential causes of insulin resistance. Some of the most common causes include: - Polycystic ovary syndrome (PCOS). PCOS is a condition that affects a woman’s reproductive health but also causes high levels of insulin, which can lead to insulin resistance over time. - High doses of steroids taken for longer than a few weeks. When taken for extended periods of time, steroids can cause continuously high blood sugar, which can lead to insulin resistance. - Chronic stress. Persistent stress can have the same effects as high doses of steroids, since stress causes your body to release its own stress steroids like cortisol. - Being overweight or obese. Although scientists don’t know exactly how, being overweight or obese contributes to poor insulin sensitivity. - Sedentary lifestyle. Living an inactive lifestyle can lead to insulin sensitivity, but the opposite—living an active lifestyle—can actually improve insulin sensitivity. - Poor diet (high-carbohydrate or high-sugar diet). Any diet that is high in carbs or sugars will increase blood sugar levels, which can lead to insulin resistance over time. There are also some unchangeable factors that can increase your risk of developing insulin resistance—for example, having a family history of insulin resistance or diabetes or belonging to Black, Asian, and/or Hispanic ethnic groups. What are the symptoms of insulin resistance? At first, your pancreas tries to fight the effects of insulin resistance by releasing more insulin. Even though your cells are not responding to insulin as well as they should, the fact that there is more insulin in your bloodstream helps keep your blood sugar levels normal. Therefore, you may not have any noticeable symptoms of insulin resistance initially. Over time, as insulin resistance gets worse, even more insulin won’t be able to make up for your cells’ weak response to insulin. At this point, high blood sugar levels often become the first key sign of insulin resistance. As high blood sugar persists, you may begin to notice symptoms like excessive thirst, frequent urination, and headaches. What are the complications of insulin resistance? High blood sugar levels can contribute to several complications associated with insulin resistance. One of the most severe complications is a condition called metabolic syndrome, also known as insulin resistance syndrome. This chronic condition involves a combination of: - high cholesterol - high blood pressure - high blood sugar (which can lead to prediabetes and type 2 diabetes) - excess body fat around the waist Insulin resistance can also lead to each of the symptoms of metabolic syndrome individually. Metabolic syndrome, prediabetes, and type 2 diabetes are the most common complications of insulin resistance. Prediabetes and type 2 diabetes result from high blood sugar levels that may have to be controlled with medications if changing your diet and exercising aren’t enough. These complications are especially serious because they increase your risk of heart disease, heart attacks, and strokes. Is there an insulin resistance test? Unfortunately, there is no insulin resistance test that is commonly used in medicine. Your doctor can use a blood glucose test or hemoglobin A1C test to evaluate your blood sugar levels. But remember that in the early stages of insulin resistance, your blood sugar levels may still appear normal, so a blood glucose or A1C test is not always a reliable test of insulin resistance. Can you reverse insulin resistance? On the bright side, there are ways you can help improve insulin sensitivity and reverse insulin resistance: - Engage in at least 30 minutes of physical activity most days of the week. Exercise is one of the fastest and most effective ways to reverse insulin resistance. - Lose weight, especially around the middle. Losing weight around the abdomen not only improves insulin sensitivity but also lowers your risk of heart disease. - Adopt a high-protein, low-sugar diet. Protein helps keep your body’s blood sugar levels stable, whereas high-sugar diets can cause spikes in blood sugar that only make insulin resistance worse. Even though being insulin resistant doesn’t necessarily mean you have diabetes, following a meal plan recommended by the American Diabetes Association can help improve insulin sensitivity. Put drug prices & coupons in your pocket! We’ll text you a link to download our free Android or iPhone app Get GoodRx Mobile App Your link is on the way! We’ve sent a link to download the GoodRx mobile app to your phone. Something went wrong We were unable to send a link to your phone.	https://clique2click.com/am-i-insulin-resistant/
Jump up ^ Kyu HH, Bachman VF, Alexander LT, Mumford JE, Afshin A, Estep K, Veerman JL, Delwiche K, Iannarone ML, Moyer ML, Cercy K, Vos T, Murray CJ, Forouzanfar MH (August 2016). "Physical activity and risk of breast cancer, colon cancer, diabetes, ischemic heart disease, and ischemic stroke events: systematic review and dose-response meta-analysis for the Global Burden of Disease Study 2013". BMJ. 354: i3857. doi:10.1136/bmj.i3857. PMC 4979358. PMID 27510511. Being overweight is a risk factor for developing diabetes, but other risk factors such as how much physical activity you get, family history, ethnicity, and age also play a role. Unfortunately, many people think that weight is the only risk factor for type 2 diabetes, but many people with type 2 diabetes are at a normal weight or only moderately overweight. Diabetes mellitus is a group of metabolic diseases characterized by high blood sugar (glucose) levels that result from defects in insulin secretion, or its action, or both. Diabetes mellitus, commonly referred to as diabetes (as it will be in this article) was first identified as a disease associated with "sweet urine," and excessive muscle loss in the ancient world. Elevated levels of blood glucose (hyperglycemia) lead to spillage of glucose into the urine, hence the term sweet urine. Diabetes mellitus is a condition in which the body does not produce enough of the hormone insulin, resulting in high levels of sugar in the bloodstream. There are many different types of diabetes; the most common are type 1 and type 2 diabetes, which are covered in this article. Gestational diabetes occurs during the second half of pregnancy and is covered in a separate article. Diabetes can also be caused by disease or damage to the pancreas, Cushing's syndrome, acromegaly and there are also some rare genetic forms. When diabetes occurs in women during pregnancy, it is called gestational diabetes. It usually is diagnosed between the 24th and 28th weeks of pregnancy. Like in type 1 and type 2 diabetes, blood sugar levels become too high. When women are pregnant, more glucose is needed to nourish the developing baby. The body needs more insulin, which is produced by the pancreas. In some women, the body does not produce enough insulin to meet this need, and blood sugar levels rise, resulting in gestational diabetes. People with type 1 diabetes sometimes receive transplantation of an entire pancreas or of only the insulin-producing cells from a donor pancreas. This procedure may allow people with type 1 diabetes mellitus to maintain normal glucose levels. However, because immunosuppressant drugs must be given to prevent the body from rejecting the transplanted cells, pancreas transplantation is usually done only in people who have serious complications due to diabetes or who are receiving another transplanted organ (such as a kidney) and will require immunosuppressant drugs anyway. Childhood obesity rates are rising, and so are the rates of type 2 diabetes in youth. More than 75% of children with type 2 diabetes have a close relative who has it, too. But it’s not always because family members are related; it can also be because they share certain habits that can increase their risk. Parents can help prevent or delay type 2 diabetes by developing a plan for the whole family: Progression toward type 2 diabetes may even be self-perpetuating. Once a person begins to become insulin resistant, for whatever reason, things may snowball from there. The increased levels of circulating insulin required to compensate for resistance encourage the body to pack on pounds. That extra weight will in turn make the body more insulin resistant. Furthermore, the heavier a person is, the more difficult it can be to exercise, continuing the slide toward diabetes. Diabetes is one of the first diseases described with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine." The first described cases are believed to be of type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or honey urine noting that the urine would attract ants. The term "diabetes" or "to pass through" was first used in 230 BCE by the Greek Apollonius Of Memphis. The disease was rare during the time of the Roman empire with Galen commenting that he had only seen two cases during his career. Home blood sugar (glucose) testing is an important part of controlling blood sugar. One important goal of diabetes treatment is to keep the blood glucose levels near the normal range of 70 to 120 mg/dl before meals and under 140 mg/dl at two hours after eating. Blood glucose levels are usually tested before and after meals, and at bedtime. The blood sugar level is typically determined by pricking a fingertip with a lancing device and applying the blood to a glucose meter, which reads the value. There are many meters on the market, for example, Accu-Check Advantage, One Touch Ultra, Sure Step and Freestyle. Each meter has its own advantages and disadvantages (some use less blood, some have a larger digital readout, some take a shorter time to give you results, etc.). The test results are then used to help patients make adjustments in medications, diets, and physical activities. If you’re getting a good night’s rest but still find yourself so tired you can barely function, it’s definitely worth mentioning to your doctor. Diabetes often wreaks havoc on a person’s normal blood sugar levels, causing fatigue in the process. In later stages, the tissue death associated with untreated diabetes can also limit circulation, meaning oxygenated blood isn’t being effectively transported to your vital organs, making your body work harder and tiring you out along the way. The classic symptoms of diabetes such as polyuria, polydypsia and polyphagia occur commonly in type 1 diabetes, which has a rapid development of severe hyperglycaemia and also in type 2 diabetes with very high levels of hyperglycaemia. Severe weight loss is common only in type 1 diabetes or if type 2 diabetes remains undetected for a long period. Unexplained weight loss, fatigue and restlessness and body pain are also common signs of undetected diabetes. Symptoms that are mild or have gradual development could also remain unnoticed. The ADA recommends using patient age as one consideration in the establishment of glycemic goals, with different targets for preprandial, bedtime/overnight, and hemoglobin A1c (HbA1c) levels in patients aged 0-6, 6-12, and 13-19 years. Benefits of tight glycemic control include not only continued reductions in the rates of microvascular complications but also significant differences in cardiovascular events and overall mortality. Insulin is the hormone responsible for reducing blood sugar. In order for insulin to work, our tissues have to be sensitive to its action; otherwise, tissues become resistant and insulin struggles to clear out sugar from the blood. As insulin resistance sets in, the first organ to stop responding to insulin is the liver, followed by the muscles and eventually fat. How does insulin resistance begin? The root of the problem is our diet. Creatinine is a chemical waste molecule that is generated from muscle metabolism. Creatinine is produced from creatine, a molecule of major importance for energy production in muscles. Creatinine has been found to be a fairly reliable indicator of kidney function. As the kidneys become impaired the creatinine level in the blood will rise. Normal levels of creatinine in the blood vary from gender and age of the individual. In type 2 diabetes (formerly called non– insulin-dependent diabetes or adult-onset diabetes), the pancreas often continues to produce insulin, sometimes even at higher-than-normal levels, especially early in the disease. However, the body develops resistance to the effects of insulin, so there is not enough insulin to meet the body’s needs. As type 2 diabetes progresses, the insulin-producing ability of the pancreas decreases. Another dipstick test can determine the presence of protein or albumin in the urine. Protein in the urine can indicate problems with kidney function and can be used to track the development of renal failure. A more sensitive test for urine protein uses radioactively tagged chemicals to detect microalbuminuria, small amounts of protein in the urine, that may not show up on dipstick tests. While poor vision is hardly uncommon—more than 60 percent of the American population wears glasses or contacts, after all—sudden changes in your vision, especially blurriness, need to be addressed by your doctor. Blurry vision is often a symptom of diabetes, as high blood sugar levels can cause swelling in the lenses of your eye, distorting your sight in the process. Fortunately, for many people, the effect is temporary and goes away when their blood sugar is being managed. Type 2 diabetes is believed to have a strong genetic link, meaning that it tends to run in families. Several genes are being studied that may be related to the cause of type 2 diabetes. If you have any of the following type 2 diabetes risk factors, it’s important to ask your doctor about a diabetes test. With a proper diabetes diet and healthy lifestyle habits, along with diabetes medication, if necessary, you can manage type 2 diabetes just like you manage other areas of your life. Be sure to continue seeking the latest information on type 2 diabetes as you become your own health advocate. So what determines where fat is stored, and thus a person's propensity for insulin resistance and type 2 diabetes? Well, just having more fat in the body increases the risk that some of it will get misplaced. But exercise may also have a role in fat placement. Exercise is known to reduce insulin resistance; one way it may do this is by burning fat out of the muscle. Because of this, getting enough exercise may stave off type 2 in some cases. Genes may also help orchestrate the distribution of fat in the body, which illustrates how lifestyle and genetics interact. Progression toward type 2 diabetes may even be self-perpetuating. Once a person begins to become insulin resistant, for whatever reason, things may snowball from there. The increased levels of circulating insulin required to compensate for resistance encourage the body to pack on pounds. That extra weight will in turn make the body more insulin resistant. Furthermore, the heavier a person is, the more difficult it can be to exercise, continuing the slide toward diabetes. About 84 million adults in the US (more than 1 out of 3) have prediabetes, and about 90% do not know they have it until a routine blood test is ordered, or symptoms of type 2 diabetes develop. For example, excessive thirst, frequent urination, and unexplained weight loss. If you have prediabetes also it puts you at risk for heart attack, stroke, and type 2 diabetes. Doctors, pharmacists, and other health-care professionals use abbreviations, acronyms, and other terminology for instructions and information in regard to a patient's health condition, prescription drugs they are to take, or medical procedures that have been ordered. There is no approved this list of common medical abbreviations, acronyms, and terminology used by doctors and other health- care professionals. You can use this list of medical abbreviations and acronyms written by our doctors the next time you can't understand what is on your prescription package, blood test results, or medical procedure orders. Examples include: Your risk for Type 2 diabetes increases as you get older. It also increases if you smoke. Although smoking doesn't cause diabetes per se, the negative effects on your health are enough to make it more likely that Type 2 diabetes will occur if you have the other risk factors. "We try to be aggressive with smoking cessation, in particular in patients with diabetes," says Dr. Asha M. Thomas, an endocrinologist with Sinai Hospital of Baltimore. The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly. Learning about the disease and actively participating in the treatment is important, since complications are far less common and less severe in people who have well-managed blood sugar levels. The goal of treatment is an HbA1C level of 6.5%, but should not be lower than that, and may be set higher. Attention is also paid to other health problems that may accelerate the negative effects of diabetes. These include smoking, elevated cholesterol levels, obesity, high blood pressure, and lack of regular exercise. Specialized footwear is widely used to reduce the risk of ulceration, or re-ulceration, in at-risk diabetic feet. Evidence for the efficacy of this remains equivocal, however. The causes of diabetes mellitus are unclear, however, there seem to be both hereditary (genetic factors passed on in families) and environmental factors involved. Research has shown that some people who develop diabetes have common genetic markers. In Type I diabetes, the immune system, the body's defense system against infection, is believed to be triggered by a virus or another microorganism that destroys cells in the pancreas that produce insulin. In Type II diabetes, age, obesity, and family history of diabetes play a role. Cataracts and glaucoma are also more common among diabetics. It is also important to note that since the lens of the eye lets water through, if blood sugar concentrations vary a lot, the lens of the eye will shrink and swell with fluid accordingly. As a result, blurry vision is very common in poorly controlled diabetes. Patients are usually discouraged from getting a new eyeglass prescription until their blood sugar is controlled. This allows for a more accurate assessment of what kind of glasses prescription is required. Diabetes was one of the first diseases described, with an Egyptian manuscript from c. 1500 BCE mentioning "too great emptying of the urine". The Ebers papyrus includes a recommendation for a drink to be taken in such cases. The first described cases are believed to be of type 1 diabetes. Indian physicians around the same time identified the disease and classified it as madhumeha or "honey urine", noting the urine would attract ants. In type 2 diabetes (adult onset diabetes), the pancreas makes insulin, but it either doesn't produce enough, or the insulin does not work properly. Nine out of 10 people with diabetes have type 2. This type occurs most often in people who are over 40 years old but can occur even in childhood if there are risk factors present. Type 2 diabetes may sometimes be controlled with a combination of diet, weight management and exercise. However, treatment also may include oral glucose-lowering medications (taken by mouth) or insulin injections (shots). Certain genetic markers have been shown to increase the risk of developing Type 1 diabetes. Type 2 diabetes is strongly familial, but it is only recently that some genes have been consistently associated with increased risk for Type 2 diabetes in certain populations. Both types of diabetes are complex diseases caused by mutations in more than one gene, as well as by environmental factors. Sources of processed or added sugar, including condiments, honey, and especially sugary drinks, are just a few of the potential culprits for weight gain, Grieger says, and it’s when they’re consumed in excess that they can contribute to diabetes risk. “The largest source of added sugar comes from sweetened beverages. They run the gamut of soda, sweetened tea, juices with added sugar, sports drinks — it’s a plethora. Just about everything we drink has added sugar in it, except for water,” she explains. Dr. Erica Oberg, ND, MPH, received a BA in anthropology from the University of Colorado, her doctorate of naturopathic medicine (ND) from Bastyr University, and a masters of public health (MPH) in health services research from the University of Washington. She completed her residency at the Bastyr Center for Natural Health in ambulatory primary care and fellowship training at the Health Promotion Research Center at the University of Washington. People with glucose levels between normal and diabetic have impaired glucose tolerance (IGT) or insulin resistance. People with impaired glucose tolerance do not have diabetes, but are at high risk for progressing to diabetes. Each year, 1% to 5% of people whose test results show impaired glucose tolerance actually eventually develop diabetes. Weight loss and exercise may help people with impaired glucose tolerance return their glucose levels to normal. In addition, some physicians advocate the use of medications, such as metformin (Glucophage), to help prevent/delay the onset of overt diabetes. In people with type 1 diabetes, the symptoms often begin abruptly and dramatically. A serious condition called diabetic ketoacidosis, a complication in which the body produces excess acid, may quickly develop. In addition to the usual diabetes symptoms of excessive thirst and urination, the initial symptoms of diabetic ketoacidosis also include nausea, vomiting, fatigue, and—particularly in children—abdominal pain. Breathing tends to become deep and rapid as the body attempts to correct the blood’s acidity (see Acidosis), and the breath smells fruity and like nail polish remover. Without treatment, diabetic ketoacidosis can progress to coma and death, sometimes very quickly. Insulin is a hormone that is produced by specialized cells (beta cells) of the pancreas. (The pancreas is a deep-seated organ in the abdomen located behind the stomach.) In addition to helping glucose enter the cells, insulin is also important in tightly regulating the level of glucose in the blood. After a meal, the blood glucose level rises. In response to the increased glucose level, the pancreas normally releases more insulin into the bloodstream to help glucose enter the cells and lower blood glucose levels after a meal. When the blood glucose levels are lowered, the insulin release from the pancreas is turned down. It is important to note that even in the fasting state there is a low steady release of insulin than fluctuates a bit and helps to maintain a steady blood sugar level during fasting. In normal individuals, such a regulatory system helps to keep blood glucose levels in a tightly controlled range. As outlined above, in patients with diabetes, the insulin is either absent, relatively insufficient for the body's needs, or not used properly by the body. All of these factors cause elevated levels of blood glucose (hyperglycemia). Recently, battery-operated insulin pumps have been developed that can be programmed to mimic normal insulin secretion more closely. A person wearing an insulin pump still must monitor blood sugar several times a day and adjust the dosage, and not all diabetic patients are motivated or suited to such vigilance. It is hoped that in the future an implantable or external pump system may be perfected, containing a glucose sensor. In response to data from the sensor the pump will automatically deliver insulin according to changing levels of blood glucose.	http://diabeteshelpcare.com/diabetes-sugar-levels-diabetes-cookbook.html
Diabetes mellitus is a disease in dogs that occurs when the body is unable to produce or utilize insulin effectively. Insulin is a hormone that regulates blood sugar levels by allowing glucose to enter cells, where it can be used as fuel. In diabetes mellitus, the pancreas produces too little insulin or the body’s cells do not respond properly to insulin. The most common symptoms of diabetes mellitus in dogs include: - Urinating more often than usual (polyuria) - Increased thirst (polydipsia) - Weight loss despite normal or increased appetite (anorexia) Other symptoms include increased weight loss without other signs of illness (such as vomiting), lethargy or weakness due to low blood sugar levels (hypoglycemia), pale gums (called “mucous membranes”), and slow growth rate in puppies. Dogs may also have recurrent infections due to low blood sugar levels (which makes them more susceptible). Two Types of Diabetes in Dogs There are two types of diabetes in dogs: type 1 and type 2. Type 1 diabetes is typically caused by an autoimmune disorder that destroys the ability of the pancreas to make insulin. This type is also called juvenile diabetes because it usually affects younger dogs. Type 2 diabetes occurs when your dog’s body becomes resistant to insulin and doesn’t respond as well as it should.	https://dogcancerfoundation.org/glossary/diabetes-mellitus/
Diabetes \| sugar \| Causes \|How Type 2 diabetes is caused Diabetes is a disease in which your blood glucose, or blood sugar, levels are too high. Glucose comes from the foods you eat. Insulin is a hormone that helps the glucose get into your cells to give them energy. With type 1 diabetes, your body does not make insulin. Type 2 diabetes develops when the body becomes resistant to insulin or when the pancreas stops producing enough insulin. Exactly why this happens is unknown, although genetics and environmental factors, such as excess weight and inactivity, seem to be contributing factors. source Leave a Reply Be the First to Comment!	http://www.healerdiabetes.com/diabetes-sugar-causes-how-type-2-diabetes-is-caused/
Set up agonist/antagonist stations so you are able to move quickly between exercises. Perform a set of the first exercise and then go directly to the second movement. Rest for approximately 30 seconds, and then perform two additional supersets. Once you finish, quickly proceed to the next agonist/antagonist pairing (and so on) until all muscle groups have been worked. This could be considered the "corollary" to #2. Doing a set of 100 barbell snatches is absurd, as technique breaks down, and the amount of weight an athlete can use is almost too trivial to even call it metabolic RESISTANCE training. Plus, it would likely take about 2-3 minutes to complete, which means that you're getting much more aerobic, even if an athlete is "working hard." My feeling is that you use your work bouts to challenge anaerobic systems, and your recovery period to condition the aerobic energy system. Let's be honest: most strength training enthusiasts care more about the aerobic system for recovery than actual aerobic exercise performance, anyway. ^ Aronow WS, Fleg JL, Pepine CJ, Artinian NT, Bakris G, Brown AS, Ferdinand KC, Ann Forciea M, Frishman WH, Jaigobin C, Kostis JB, Mancia G, Oparil S, Ortiz E, Reisin E, Rich MW, Schocken DD, Weber MA, Wesley DJ, Harrington RA, Bates ER, Bhatt DL, Bridges CR, Eisenberg MJ, Ferrari VA, Fisher JD, Gardner TJ, Gentile F, Gilson MF, Hlatky MA, Jacobs AK, Kaul S, Moliterno DJ, Mukherjee D, Rosenson RS, Stein JH, Weitz HH, Wesley DJ (2011). "ACCF/AHA 2011 expert consensus document on hypertension in the elderly: a report of the American College of Cardiology Foundation Task Force on Clinical Expert Consensus Documents developed in collaboration with the American Academy of Neurology, American Geriatrics Society, American Society for Preventive Cardiology, American Society of Hypertension, American Society of Nephrology, Association of Black Cardiologists, and European Society of Hypertension". J Am Soc Hypertens. 5 (4): 259–352. doi:10.1016/j.jash.2011.06.001. PMID 21771565. The primary problem in metabolic syndrome is insulin resistance. In the body's attempt to compensate for insulin resistance, extra insulin is produced, leading to elevated insulin levels. The elevated insulin levels can lead, directly or indirectly, to the characteristic metabolic abnormalities seen in these patients. Frequently, the insulin resistance will progress to overt type 2 diabetes, which further increases the risk of cardiovascular complications. Gary Edward Sander, MD, PhD, FACC, FAHA, FACP, FASH is a member of the following medical societies: Alpha Omega Alpha, American Chemical Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American Federation for Clinical Research, American Federation for Medical Research, American Heart Association, American Society for Pharmacology and Experimental Therapeutics, American Society of Hypertension, American Thoracic Society, Heart Failure Society of America, National Lipid Association, Southern Society for Clinical Investigation Blood pressure goals are generally set lower than 130/80. Some blood pressure medications offer more benefits than simply lowering blood pressure. For example, a class of blood pressure drugs called ACE inhibitors has been found to also reduce the levels of insulin resistance and actually deter the development of type 2 diabetes. This is an important consideration when discussing the choice blood pressure drugs in the metabolic syndrome. https://i.ytimg.com/vi/xQRE2ht3elA/maxresdefault.jpg What you need to know about beta-blockers Beta-blockers are drugs that are used to slow down a person's heart rate. Doctors may prescribe them for a range of reasons, including angina and high blood pressure. There are many types and brands of beta-blockers, some of which affect other parts of the body. Learn about side effects, cautions, and interactions. Read now When you have type 2 diabetes, your cells don't get enough glucose, which may cause you to lose weight. Also, if you are urinating more frequently because of uncontrolled diabetes, you may lose more calories and water, resulting in weight loss, says Daniel Einhorn, MD, medical director of the Scripps Whittier Diabetes Institute and clinical professor of medicine at the University of California in San Diego. Insulin is a fat storage hormone, it works to shuttle the sugar from your blood stream into your fat cells to store for later. Insulin has a number of other reproductive functions and has effects on skin health, cravings and the like. Insulin levels naturally increase after eating a meal that contains carbohydrates, dairy or protein. If you are insulin resistant then you can have an elevated level of insulin when you are fasting, or you can experience too much insulin release in response to those foods. This can trap your body in fat storage mode and inhibit fat loss. Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity. Your doctor may have handed you an info sheet on the foods you should be avoiding, but you might make more progress by adding certain foods to your diet. Focus on incorporating foods rich in soluble fiber, like oats and beans, into your meals. Insoluble fibers like whole grains can provide a "moving experience" by transporting foods through your gastrointestinal tract while keeping you feeling satisfied. Fill at least half your plate with veggies and fruits, and choose whole-grain carbs to make less room on your plate (and in your stomach) for less-beneficial choices. In patients with type 2 diabetes, stress, infection, and medications (such as corticosteroids) can also lead to severely elevated blood sugar levels. Accompanied by dehydration, severe blood sugar elevation in patients with type 2 diabetes can lead to an increase in blood osmolality (hyperosmolar state). This condition can worsen and lead to coma (hyperosmolar coma). A hyperosmolar coma usually occurs in elderly patients with type 2 diabetes. Like diabetic ketoacidosis, a hyperosmolar coma is a medical emergency. Immediate treatment with intravenous fluid and insulin is important in reversing the hyperosmolar state. Unlike patients with type 1 diabetes, patients with type 2 diabetes do not generally develop ketoacidosis solely on the basis of their diabetes. Since in general, type 2 diabetes occurs in an older population, concomitant medical conditions are more likely to be present, and these patients may actually be sicker overall. The complication and death rates from hyperosmolar coma is thus higher than in diabetic ketoacidosis. ^ Grundy SM, Cleeman JI, Daniels SR, Donato KA, Eckel RH, Franklin BA, Gordon DJ, Krauss RM, Savage PJ, Smith SC, Spertus JA, Costa F (October 2005). "Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement". Circulation. 112 (17): 2735–52. doi:10.1161/CIRCULATIONAHA.105.169404. PMID 16157765. Metabolic syndrome is a cluster of metabolic risk factors that come together in a single individual. These metabolic factors include insulin resistance, hypertension (high blood pressure), cholesterol abnormalities, and an increased risk for blood clotting. Affected individuals are most often overweight or obese. An association between certain metabolic disorders and cardiovascular disease has been known since the 1940s.	http://lovinglifewithdiabetes.com/endocrinology-metabolic-syndrome-journal-impact-factor--metabolic-syndrome-symptoms-.html
Business Insider has an article called, “The 7 Most Important Medical Conditions to Understand and Prevent”. The article focuses on 7 key conditions that are prevalent in our society. 1. Type 2 diabetes (type 2 diabetes is defined as type 1 diabetes, which is characterized by insulin resistance and elevated blood glucose). Type 2 is characterized more by high blood sugar and insulin resistance, but is more often linked to obesity. Type 1 diabetes is not considered a condition by the American Diabetes Association (ADA). Type 1 and type 2 diabetes are also linked to cardiovascular disease, hypertension, type 2 cancers, and certain cancers. Type 3 diabetes is the second most common type of diabetes, followed by type 2. Type 4 is not yet recognized as a serious condition, but it is a significant contributor to the burden of chronic diseases such as type 2 and 3 diabetes. Type 5 is also considered to be a serious disease, but the number of people with it is not high. 2. Coronavirus-related diabetes. Coronal is a condition that occurs when the pancreas produces excess insulin that causes the body to become resistant to insulin. Type 6 and 7 are the most common types of coronal. 3. Acute kidney injury (AKI) is when blood vessels within the kidney rupture causing a large amount of fluid to leak out of the kidney. Type 8 is a more serious form of AKI that is more likely to cause severe bleeding and can lead to death. 4. Endometrial cancer (OGC) is a type of cancer in the lining of the uterus that can affect the uterine lining and the ovaries. 5. Pancreatitis is when the lining around the lining in the stomach becomes inflamed. 6. Prostate cancer (PC) is the most prevalent cancer in men. 7. Cancer of the pancresis is a cancer of the lining that connects the stomach to the small intestine. Type 9 is the third most common cancer of men. Type 10 is the fifth most common. Type 11 is a rare form of PC. Type 12 is a common form of pancreatitis. Type 13 is a very rare form. Type 14 is the sixth most common form. 8. Prostaglandins, prostaglandin-1s (PGS), and prostaglobulin (PGL) are chemical compounds that are found in some foods and drugs that have been linked to the development of type 2 Diabetes. Type 15 is a precursor of these compounds that can be found in certain foods and medicines. The type 15 compound is called prostaglycin. 9. Proteolysis is a process in which the body breaks down fats in the body. Type 16 is a form of this process that occurs in the muscles, and is the primary cause of the production of these chemicals in the muscle tissue. 10. Insulin resistance occurs when insulin is secreted into the blood when blood glucose levels drop. Type 17 is a hormone that causes blood sugar to rise, causing the body’s cells to secrete more glucose. Type 18 is a glucocorticoid hormone that is involved in muscle growth. 11. Heart disease (HD) is an inherited disease that can lead, at times, to death if left untreated. Type 19 is a genetic disease that is caused by mutations in the gene encoding a protein that triggers the production and secretion of insulin. 12. Diabetes is the leading cause of preventable death in the US. 13. Diabetes mellitus is a chronic disease that affects a large proportion of the population, but also has a high mortality rate. 14. Type 20 is a disease that causes more damage than it does cure. Type 21 is a lifelong disease that results in a variety of health problems and is caused primarily by a defect in insulin production. 15. Cardiovascular disease (CVD) is considered the third leading cause to which people are most likely to die. 16. Cancer is the largest and most common chronic disease. 17. Diabetes, high blood pressure, and high cholesterol are the major risk factors for developing type 2Diabetes. 18. Obesity is a major risk factor for developing diabetes. 19. Cancer can also be a precursor to type 2CVD, but there is no evidence that it can be prevented by diabetes treatments. 20. Obesity has been linked with many of the major chronic diseases listed above. Type 23 is a non-cancerous tumor in the pancretophyses that causes excess insulin to be released into the bloodstream. Type 24 is a benign tumor in one of the small blood vessels that supplies blood to the pancreatic cells. Type 25 is a tumor in a different part of the blood vessel, which produces more insulin. 21. Type 26 is a relatively benign tumor that causes less insulin to enter the blood. Type 27 is a large tumor that is often present at the beginning of a disease.	https://localbusinesslistingsites.com/2021/08/how-to-get-the-best-medical-advice-for-your-medical-conditions/
A report from the World Health Organization (WHO) says the prevalence of diabetes is increasing among people of all ages, and many people in developing countries are battling with managing the condition every 20 minutes. Sadly, many Nigerians are living with the condition, with many unaware that they have it while others grapple with pain, hospitalization, and taking medications. However, the world has continued to celebrate World Diabetes Day (WDD) annually on Nov. 14 to raise awareness of the growing burden of the disease, and the theme for 2022 is "Access to Diabetes Education." But has the annual commemoration raised the desired awareness and provided strategies to prevent and manage the condition? Is there hope for people living with the condition? Dr. Uwajeh Raalueke, the President of the Medical Women's Association of Nigeria in Taraba State, gave an overview of the causes of diabetes and the management of the condition. She says diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys, and nerves. Raalueke, who is also the acting Head of the Department of Internal Medicine at Taraba State Specialist Hospital, Jalingo, says a person can be tested for diabetes using tests that measure blood glucose (sugar) levels. "These tests include glycated hemoglobin (HbA1c), fasting blood sugar (FBS), oral glucose tolerance testing (OGTT), and random blood sugar (RBS) tests." "Normal HbA1c is 5.7 percent, while >6.5 percent is indicative of diabetes; normal FBS is 5.5 mmol/L, while 7 mmol/L is indicative of diabetes." "Normal OGTT is 7.8 mmol/L, while 11.1 mmol/L is indicative of diabetes, and an RBS 11.1 mmol/L is indicative of diabetes," she explained. On the health problems of diabetes, she says it can cause acute (immediate) or chronic (long-term) problems if not properly managed. "High sugar levels in your blood over a long period of time can seriously damage your blood vessels." If your blood vessels are not working properly, blood cannot travel to the parts of your body it needs to. "This means your nerves will not work properly and that you will lose feeling in parts of your body." "Once you have damaged blood vessels and nerves in one part of your body, you are more likely to develop similar problems in other parts of your body." "Long-term problems develop gradually, leading to serious damage if they go unchecked and untreated." Raalueke says the cause of most types of diabetes is unknown, but in all cases, sugar builds up in the bloodstream because the pancreas produces little or no insulin or because the body's tissues are resistant to the effects of insulin. She says "insulin is a hormone produced by the pancreas, a gland located behind the stomach, and this hormone helps to regulate blood sugar levels." "Insulin cannot cure diabetes, but it is used to treat type 1 diabetes and manage hyperglycemic states in other types of diabetes." Explaining further the relationship between diabetes and insulin and whether insulin can cure diabetes, she says diabetes occurs when the body doesn't use insulin properly or make enough insulin. "In type 1 diabetes, autoantibodies attack the insulin-producing cells of the pancreas, resulting in little or no insulin production and elevated blood sugar levels." "In type 2 and other types of diabetes, the body is resistant to the effects of insulin, resulting in elevated blood sugar levels." Raalueke listed some of these problems as eye problems (retinopathy), explaining that diabetic retinopathy can result in vitreous hemorrhage, retinal detachment, glaucoma, and, if untreated, blindness. Another issue, she says, is diabetes foot problems, which are serious and can lead to amputation if untreated. Others, she adds, are "nerve damage, which can affect the feeling in your feet, and raised blood sugar, which can damage circulation, making it slower for sores and cuts to heal." "High blood sugar over a long period can damage blood vessels, and this can lead to heart attacks and strokes." "Diabetic kidney disease (nephropathy) and nerve damage (neuropathy) can make it harder for the nerves to carry messages between the brain and every part of the body, so it can affect how we see, hear, feel, and move." She says there is also the issue of gum disease and other mouth problems, as well as sexual problems in both women and men: decreased sensation, vaginal thrush, and urinary tract infections (UTI) in women, and erectile dysfunction in men. "There is an increased risk of developing certain cancers, like pancreatic cancer, and psychiatric problems like depression and dementia." "Acute problems can occur at any time, and these include hypoglycemia, hyperosmolar hyperglycemic state (occurs only in type 2 DM), and diabetic ketoacidosis." Raalueke says these three states require immediate treatment as they are life-threatening conditions. On the types of diabetes a person is at risk for, she explains that it depends on one's age, sex, family history, and medical history, among others, as one can be at increased risk of developing type 1 diabetes, type 2 diabetes, or gestational diabetes. On the treatment of diabetes, she says it depends on the type of diabetes, how well the blood glucose level is managed, and other existing health conditions. She says, "Type 1 diabetes is treated with insulin, a healthy diet, and physical activities." "Treatment for T2DM can include medications (both for diabetes and for conditions that are risk factors for diabetes), insulin, and lifestyle changes such as losing weight, making healthy food choices, and being physically active." "In gestational diabetes, if the blood glucose level is not too high, initial treatment might be modifying the diet and getting regular exercise." "If the target goal is still not met or the glucose level is very high, insulin therapy is usually initiated," she said. The boss of the medical women's association further explains that oral medications and insulin work in one of these ways to treat diabetes: they stimulate the pancreas to make and release more insulin and slow down the release of glucose from the liver. "It blocks the breakdown of carbohydrates in the stomach or intestines so that body tissues are more sensitive and helps to get rid of body glucose through increased urination." "Foot care in diabetic patients is a very important aspect in their management. "Diabetics are advised to inspect their feet daily, wash daily with warm water and mild soap, pat them dry with a clean towel, and moisturise if the feet feel rough or dry, but don't moisturise between the toes." On how to help prevent diabetes, she says Type 1 diabetes is not preventable, but other types of diabetes can be prevented. "To prevent diabetes, we need to know the risk factors that predispose an individual to developing the disease." "These risk factors include family history of diabetes; being black, Hispanic, or Asian; being overweight or obese; having high blood pressure; having low HDL cholesterol; and having high triglyceride levels." "Others are excessive alcohol consumption, being physically inactive, being age 45 or older, having gestational diabetes, having polycystic ovarian syndrome, having a history of heart disease or stroke, and smoking." "We don't have control over risk factors like family history, age, sex, or race, but we can prevent diabetes by eating healthy diets, being physically active, working toward achieving a healthy weight, lowering stress, and limiting alcohol intake." Raalueke advised men to drink no more than two beverages containing alcohol a day, while women should drink no more than one. According to her, getting an adequate amount of sleep (typically 7 to 9 hours), quitting smoking, and taking medications as directed by a healthcare provider to manage existing risk factors for heart disease (like high blood pressure and cholesterol) will reduce the risk of developing Type 2 diabetes. On managing diabetes better, the expert says diabetes affects the whole body, and to best manage it, one needs to take steps to manage the risk factors. The risk factors, she says, include keeping your blood glucose levels as close to normal as possible by following a diet plan, taking prescribed medication, and increasing your activity level. "Maintaining blood cholesterol (HDL and LDL levels) and triglyceride levels as near the normal ranges as possible, and blood pressure of not more than 140/90 mmHg. "You hold the keys to managing your diabetes by taking your diabetes medications as prescribed." taking all other medications to treat any risk factors (high blood pressure, high cholesterol, and other heart-related problems and other health conditions) as directed. "Keeping yourself well-hydrated (water is your best choice). If you smoke, quit. Seeing your doctor regularly to monitor your diabetes and to watch for complications," Raalueke advised. Meanwhile, the Diabetes Association of Nigeria (DAN) has advised families to own glucometers at home to enable them to quickly and easily ascertain their glucose levels. The National Secretary of the association, Mr. Bernard Enya, made the call in Calabar in commemoration of the 2022 World Diabetes Day (WDD). A glucometer is a medical device for ascertaining the approximate concentration of glucose in the blood. A blood glucose test is a blood test that screens for diabetes by measuring the level of glucose (sugar) in a person's blood. Enya, who doubles as the chairman of DAN in Cross River, said Nigerians didn't need to be university graduates to be able to use and understand the results of a glucometer. He added that knowing the result will help them know if their sugar level is high, normal, or low. The chairman also said that Cross River was performing poorly in the care of diabetes and needed to do more. According to him, awareness is poor, and the state lacks desk officers for non-communicable diseases like diabetes to coordinate government interventions against the disease and gather data. "One major problem in Cross River is the unavailability of data, and we all know that without data, a government cannot plan." "Also, the state does not have desk officers for diabetes and other non-communicable diseases, so there is no coordination across the 18 local government areas." "This has led to many non-governmental organizations (NGOs) doing the same thing, which is essentially screening without looking at treatment and effective data collection," he said. He also said some of the few works done on the disease in the state were only done in the Southern Senatorial District where University of Calabar Teaching Hospital (UCTH) is located. Enya added that the situation makes it difficult for patients from the central and northern parts of the state to benefit due to the distance to Calabar. While appealing to Nigerians to cultivate healthy lifestyles to prevent diabetes, he called on the government to have an annual diabetes intervention plan. On her part, Mrs. Felicita Opata, the president of the Lions Club, District 404A2, said the club carried out diabetes awareness activities in collaboration with the Endocrinology, Diabetes, and Metabolism Unit of the UCTH. She added that "we had a walk this morning from the Lions Park to our Diabetes Center in UCTH, and there, we are carrying out free screenings on blood glucose, eye health, blood pressure, hepatitis, and the distribution of some drugs." "However, I urge the state government to also key into this project and support it for us to reach out to more diabetic patients in the state and procure more kits for screening.'' Ms. May Ikokwu, Chief Executive Officer of Save Our Heritage Initiative (SOHI), says early testing and detection are paramount in the management of diabetes for normal living. Ikokwu said this on the occasion of the 2022 World Diabetes Day in Abuja. She explained that the theme for this year's celebration, "Access to Diabetes Education," underpins the larger multi-year theme of "Access to Care." She advocated for preventive interventions, especially dieting, saying that diabetes could be triggered by diets. Ikokwu, who described diabetes as the body's ability or inability to produce the required amount of insulin to control glucose levels in the blood, said there are broadly two types of diabetes. "According to medical experts, type 1 diabetes requires the daily administration of artificial insulin by means of injection or an insulin pump. "Type 2 is more generally managed by a combination of dietary control and medication in the form of tablets," she said. According to her, replacing most of the carbohydrates in a normal diet with vegetables is recommended. She added: "Fonio (Digitaris exilis, a West African cereal), tamarind, moringa, ewedu, bitter leaf, and baobab are types of African superfoods that can effectively reduce blood sugar and fight diabetes." Ikokwu stressed the need for regular monitoring of sugar levels in the body to avert diabetes, saying that the equipment is inexpensive and available at most pharmacies. She advised: "It is important that development work continues to ensure people with the condition can live as normal a life as possible." The SOHI boss said, "Diabetes can affect anyone, irrespective of age, with complications like blindness and so many other issues." The WDD should,therefore, not be a day for rhetoric, but rather, more practical measures must be introduced and implemented all year round by the government, stakeholders, and everyone else so as to raise the desired awareness of what needs to be done, collectively and individually, for better prevention, diagnosis, and management of the condition.	https://www.suprememagazine.news/featuresspotlight/2022-wdd-beyond-rhetoric-any-hope-for-people-suffering-with-illness-357729
Studies have been done on how to reverse type 2 diabetes. It’s clear that achieving remission from prediabetes or Type 2 diabetes requires significant lifestyle changes. Diabetes is a chronic disease that occurs either when your body doesn’t produce enough insulin or when your body is unable to effectively use the insulin it produces. It is a disorder caused by a malfunction in the way you make and/or use insulin. Insulin is a hormone produced by your pancreas. It regulates and lowers your blood sugar by moving it out of your bloodstream and into your body’s cells. Hyperglycemia, or elevated blood sugar, is a common effect of uncontrolled diabetes. Over time, if you don’t treat or manage it well, it may lead to serious damage to many of your body’s systems, especially your nerves and blood vessels. This post may contain affiliate links as explained in my Disclosure Policy. Causes of hyperglycemia - You probably eat more food than your body can convert to energy or you exercise less than you should. - If you have type 1 diabetes, and you didn’t give yourself enough insulin. - You have stress from an illness, such as a cold or flu. - You’re stressed out due to factors such as family conflicts, school, dating or marital problems. - If you have type 2 diabetes, your body may have enough insulin, but the insulin is not as effective as it should be. Diabetes Symptoms The signs and symptoms of hyperglycemia include: - High blood sugar levels - Increased thirst - Frequent urination - High levels of sugar in your urine. To properly manage your diabetes, you should check your blood sugar often. Ask your doctor how often you’ll have to check your sugar levels, and what your readings should be. Checking your blood as often as you should, and treating high blood sugar early will help you reverse type 2 diabetes and avoid problems associated with hyperglycemia. Testing your blood sugar If you are testing your blood sugar at home, you should follow the directions that came with your blood sugar testing meter. However for most meters, the general procedure is as follows: - Wash your hands and place a test strip in your blood sugar meter - Clean the tip of one of your fingers - Prick the side of the finger with a lancet to draw a drop of blood - Place the tip of the test strip on the drop of blood so that the test strip draws up the drop of blood - In a few seconds, the blood sugar meter will give you a reading. Shop for glucometer and test strips After you’ve checked your blood sugar, compare your reading with the ranges below (1): - Normal blood sugar should be less than 100 mg/dL (5.6 mmol/L ) after fasting overnight. It should be up to 140 mg/dL (7.8 mmol/L ) two hours after you’ve had a meal. - You have prediabetes if your blood sugar is between 100-125 mg/dL (5.6-7.0 mmol/L) after fasting overnight - You’re likely to have diabetes if your reading is 126 mg/dL (7.0 mmol/L) or higher after fasting overnight, or higher than 200 mg/dL (11.1 mmol/L) at any time - 13 Tips on Healthy Ways To Lose Your Belly Fat - 15 Ways to Achieve Your Spiritual Health Goals - How To Stay Busy While Social Distancing Keep a log of your readings so that you’ll take them to your doctor on your next visit. A single abnormal blood sugar reading is not sufficient to determine that you’re diabetic. You should be concerned about a diagnosis of diabetes if you have at least two or more readings that are high. You should also keep in mind that the glucometer readings you get at home are not considered accurate enough to make a diagnosis of prediabetes or diabetes. A single abnormal blood sugar reading is not sufficient to determine that you’re diabetic. After you’ve had two or more such readings, consult your doctor. If your blood sugar has been high a couple of times on your glucometer, your doctor will run a simple blood test to confirm the diagnosis. How to treat high blood sugar You can lower your blood sugar level when you exercise. If your blood sugar tends to run high, check your blood sugar before you exercise. If your sugar level is above 240 mg/dl, check your urine for ketones. If you have ketones in your urine, do not exercise (1). Exercising when ketones are present in your urine may make your blood sugar level go even higher. Therefore it is not advisable to exercise whenever you have high blood sugar. If your blood sugar is always high above 240 mg/dl, you’ll need to work with your doctor to find the safest way for you to lower your blood sugar level so that you can exercise. Cutting down on the amount of food you eat is one of the ways to reverse type 2 diabetes. It’s advisable to work with your dietitian to make changes to your meal plan. If changes in your diet and exercise don’t work to reduce your blood sugar, your doctor may change the number or dosage of the medication or insulin that you’re taking. They may also possibly change the timing of when you take them. What if high blood sugar goes untreated or uncontrolled? Hyperglycemia can be a serious problem for you if it goes untreated. Therefore, it’s important to have yourself treated as soon as you detect that your blood sugar levels tend to be high. If you fail to treat hyperglycemia, it will result in a condition called ketoacidosis, also known as diabetic coma. Ketoacidosis occurs when your body doesn’t have enough insulin. Without insulin, your body is unable to use glucose for fuel. When this happens, your body breaks down fats to use for energy, instead of glucose. When your body breaks down fats, it produces waste products called ketones. Your body is not conditioned to tolerate large amounts of ketones, therefore it will try to get rid of them through your urine. Unfortunately, your body is unable to release all the ketone waste products through your urine. The leftover then builds up in your blood, leading to ketoacidosis. Ketoacidosis is a life-threatening condition that requires immediate medical attention. Symptoms of ketoacidosis include: - Fruity smell in your breath - Very dry mouth - Shortness of breath - Nausea and vomiting. How you develop Type 2 diabetes You’ll develop Type 2 diabetes when your body becomes resistant to insulin or when your pancreas is unable to produce enough insulin. It is caused by defects in both the way your pancreas produces and uses insulin. When this occurs and progresses to the point where your pancreas can no longer spontaneously release enough insulin to overcome your body’s resistance to it, your blood sugar levels rise. If there’s too much glucose in your blood, you have a problem. Excess blood sugar can damage your blood vessels. In addition to this, the tissues in your body can not effectively use the glucose in the food you eat for energy. Too much of the glucose stays in your bloodstream, instead of entering your cells for use as energy. Before your blood glucose level becomes consistently high, there must have been some underlying illness that might have been going on for years before your blood sugar starts rising and becoming very high. When insulin-producing beta cells in your body start dying or malfunctioning, your pancreas will react in such a way that too much insulin will be in your blood. At this point, your body is said to be insulin resistant. Your blood sugar becomes high, and you’re diagnosed with type 2 diabetes. If this happens, you should start considering how to reverse type 2 diabetes as quickly as you can. Risks of having too little insulin The problem you have at this stage is that the ability of your pancreas to make insulin gets worse. The insulin that you’re able to make isn’t working very well also. Because insulin is what you need to convert the sugar that you consume into energy, the shortage of insulin results in excess sugar in your blood. A defect in insulin function in your body doesn’t only cause your blood sugar to rise. It results in the progression of your condition to type 2 diabetes, also leading to weight gain. Certain conditions or diseases may cause damage to the insulin-producing cells in your pancreas. Exactly why this happens is not known, but genetics and environmental factors, such as being overweight and inactive may be contributing factors (2). Risk factors for Type 2 Diabetes A number of factors can increase your risk of developing type 2 diabetes. They include (3, 4): - Being overweight or obese – if you’re overweight, this is the main risk factor for type 2 diabetes. However, you don’t have to be overweight to develop the condition. - Eating an unhealthy diet - Physical inactivity – the less active you are, the greater your risk of type 2 diabetes. If you’re physically active, it helps you control your weight. The activity uses up glucose as energy and makes your cells more sensitive to insulin. - Smoking increases your risk of developing Type 2 diabetes. - Family history – having a first-degree relative with type 2 diabetes. The risk increases if your parent or sibling has type 2 diabetes. - High blood pressure or raised cholesterol levels - Fat distribution – if you store fat mainly in your abdominal area. A waist size of 31.5 inches or more (women) or more than 37 inches (men) - Race – it’s unclear why, but people of certain races (including black, Hispanic, American Indian, and Asian-American people) are more likely to develop type 2 diabetes than white people are. - Age – your risk increases as you get older, especially after age 45. However, type 2 diabetes is also increasing now among children, adolescents, and younger adults. Adult-onset diabetes is primarily seen in middle-aged adults over the age of 40. - Gestational diabetes – if you developed gestational diabetes while you were pregnant, your risk of developing type 2 diabetes is high. Also, if you gave birth to a baby weighing more than 9 pounds (4 kilograms), you’re also at risk of developing type 2 diabetes - Areas of darkened skin – this usually occurs in your armpits and neck. If these areas are darkened, you are at risk of developing type 2 diabetes because this condition often indicates insulin resistance. Complications of Type 2 diabetes If you have Type 2 diabetes, you may easily ignore it, especially if it’s in the early stages when you’re feeling fine. However, over time you stand the risk of developing complications. If untreated or poorly treated, type 2 diabetes can affect many major organs in your body. These include your eyes, heart, kidneys, blood vessels, and nerves. If you control your blood sugar levels and reverse type 2 diabetes, it can help prevent complications. The most common complications of type 2 diabetes that you may have include (5, 6): - Heart disease and blood vessel disease including high blood pressure, stroke, and atherosclerosis (narrowing of your blood vessels). - Kidney disease – kidney damage can result from uncontrolled Type 2 diabetes. This can lead to kidney failure. You may require dialysis or a kidney transplant. - Eye disease caused by eye damage such as cataracts and glaucoma. This may damage the blood vessels of the retina in your eyes, potentially causing blindness - Hearing impairment – problems with hearing are more common in people with diabetes. - Nerve damage (neuropathy) which raises the risk of amputation - Skin infections – Type 2 diabetes may leave you more susceptible to skin problems, including bacterial and fungal infections - Slow healing of wounds – if left untreated, your cuts and blisters can become serious infections, leading to poor healing. Severe damage may even require toe, foot or leg amputation - Sleep apnea – you may develop sleep apnea which is common in people with type 2 diabetes. You are at even higher risk if you are obese as well. - Alzheimer’s disease. You stand a higher risk of Alzheimer’s disease, though it’s not clear why. The worse your blood sugar control, the greater the risk appears to be. How you can reverse Type 2 diabetes so you treat the cause of your problem, not just the symptoms? The good news is that modifying your diet and exercising can help decrease your insulin resistance and its associated weight gain. You will ultimately be able to prevent or even reverse type 2 diabetes. Type 2 diabetes pandemic As the incidence of Type 2 diabetes continues to increase worldwide, the fight against the chronic condition continues. There’s been research done that explains not only what triggers type 2 diabetes but also how to reverse the condition. Fortunately, the findings also shed light on what can lead to your remission from type 2 diabetes after its reversal. It was reported that between 1980 and 2014, the number of people living with diabetes across the world had increased from about 108 million to 422 million. About 90% of them have type 2 diabetes. Unfortunately, pharmacological interventions have done little to stop what some have referred to as a diabetes pandemic. Currently, type 2 diabetes is known to generate billions of dollars for pharmaceutical companies. How to reverse Type 2 Diabetes Although there’s no cure for type 2 diabetes, studies have shown that it’s possible for some people to reverse it. Through diet changes and weight loss, you may be able to reach and hold normal blood sugar levels without medication. There is now scientific proof that you can reverse type 2 diabetes without medication. Lifestyle interventions seem to be succeeding where other approaches have failed. You may now use nutritional methods to reverse Type 2 diabetes. Your disease doesn’t have to be progressive and irreversible. If you have type 2 diabetes, you can clearly treat the condition when you use an effective lifestyle intervention. A couple of years ago, results of a clinical trial study showed that you can reverse type 2 diabetes and achieve remission through intensive weight loss programs, without taking any medication. In Japan they target the root cause of health problems, while here in the US and other western countries, symptoms are managed with medication (7). And that’s why in Japan they have far lower levels of diabetes type 2, heart disease, obesity, and cancer. That’s also why they live much longer than us on average. Although there’s no cure, studies have shown that it’s possible for you to reverse type 2 diabetes through diet changes and weight loss. You may be able to reach and hold normal blood sugar levels without medication, by managing the underlying cause of Type 2 diabetes. Medications merely treat your symptoms of the disease. You don’t just have to “manage” your diabetes as it progresses. Instead, you can often lower your blood sugar to normal levels with diet alone. When you do this successfully, you may be able to avoid or discontinue most of the medications that you’re taking (8). Normal blood sugar levels and fewer or no medications likely means there’ll be no progression of your disease and no progression of any complications. You can help reverse type 2 diabetes and be able to live a long, healthy life, with your toes, eyesight, and kidneys intact. If you are not on any medications, you can start your journey back to health today and reverse type 2 diabetes. Many diabetes success stories have revealed proven scientific methods used to reverse type 2 diabetes. The disorder has been reversed in a lot of people, and they are no longer on medication. If you are on medications for diabetes or for other conditions, consult your doctor before beginning any lifestyle change, such as a low-carb diet, so that your medications can be adjusted safely as your blood sugar levels improve. To effectively reverse type 2 diabetes, your goal should be long-term. That goal is clearly achievable by properly managing your diabetes. Diabetes management works to reduce insulin resistance and improve (or preserve) beta-cell function with diet, physical activity, and medication when appropriate.	https://sassydama.com/blog/reverse-type-2-diabetes/
Diabetes is a lifelong condition that is characterized by a raised blood glucose level. Diabetes is a lifelong condition that is characterized by a raised blood glucose level. There are two main types of diabetes: type 1 and type 2. Signs of diabetes include an increased sense of thirst, frequent urination, fatigue, weight and muscle loss, cuts or wounds that heal slowly and blurred vision. It is extremely important for diabetes to be diagnosed as early as possible - if left untreated the condition will get progressively worse. An overview of diabetes types and treatments Diabetes is a condition that impairs the body's ability to process blood glucose, otherwise known as blood sugar. In the United States, the estimated number of people over 18 years of age with diagnosed and undiagnosed diabetes is 30.2 million. The figure represents between 27.9 and 32.7 percent of the population. Without ongoing, careful management, diabetes can lead to a buildup of sugars in the blood, which can increase the risk of dangerous complications, including stroke and heart disease. Different kinds of diabetes can occur, and managing the condition depends on the type. Not all forms of diabetes stem from a person being overweight or leading an inactive lifestyle. In fact, some are present from childhood. Types Three major diabetes types can develop Type 1, type 2, and gestational diabetes. Type I diabetes: Also known as juvenile diabetes, this type occurs when the body fails to produce insulin. People with type I diabetes are insulin-dependent, which means they must take artificial insulin daily to stay alive. Type 2 diabetes: Type 2 diabetes affects the way the body uses insulin. While the body still makes insulin, unlike in type I, the cells in the body do not respond to it as effectively as they once did. This is the most common type of diabetes, according to the National Institute of Diabetes and Digestive and Kidney Diseases, and it has strong links with obesity. Gestational diabetes: This type occurs in women during pregnancy when the body can become less sensitive to insulin. Gestational diabetes does not occur in all women and usually resolves after giving birth. Less common types of diabetes include monogenic diabetes and cystic fibrosis-related diabetes. Click here to learn more about type I diabetes. Prediabetes Doctors refer to some people as having prediabetes or borderline diabetes when blood sugar is usually in the range of 100 to 125 milligrams per deciliter (mg/dL). Normal blood sugar levels sit between 70 and 99 mg/dL, whereas a person with diabetes will have a fasting blood sugar higher than 126 mg/dL. The prediabetes level means that blood glucose is higher than usual but not so high as to constitute diabetes. People with prediabetes are, however, at risk of developing type 2 diabetes, although they do not usually experience the symptoms of full diabetes. The risk factors for prediabetes and type 2 diabetes are similar. They include: If a doctor identifies that a person has prediabetes, they will recommend that the individual makes healthful changes that can ideally stop the progression to type 2 diabetes. Losing weight and having a more healthful diet can often help prevent the disease. How insulin problems develop Doctors do not know the exact causes of type I diabetes. Type 2 diabetes, also known as insulin resistance, has clearer causes. Insulin allows the glucose from a person's food to access the cells in their body to supply energy. Insulin resistance is usually a result of the following cycle: A person has genes or an environment that make it more likely that they are unable to make enough insulin to cover how much glucose they eat. The body tries to make extra insulin to process excess blood glucose. The pancreas cannot keep up with the increased demands, and the excess blood sugar starts to circulate in the blood, causing damage. Over time, insulin becomes less effective at introducing glucose to cells, and blood sugar levels continue to rise. In the case of type 2 diabetes, insulin resistance takes place gradually. This is why doctors often recommend making lifestyle changes in an attempt to slow or reverse this cycle. Using insulin People with type I diabetes and some people with type 2 diabetes may need to inject or inhale insulin to keep their blood sugar levels from becoming too high. Various types of insulin are available, and most are grouped by how long their effect lasts. There are rapid, regular, intermediate, and long-acting insulins. Some people will use a long-acting insulin injection to maintain consistently low blood sugar levels. Some people may use short-acting insulin or a combination of insulin types. Whatever the type, a person will usually check their blood glucose levels using a fingerstick. This method of checking blood sugar levels involves using a special, portable machine called a glucometer. A person with type I diabetes will then use the reading of their blood sugar level to determine how much insulin they need. Self-monitoring is the only way a person can find out their blood sugar levels. Assuming the level from any physical symptoms that occur may be dangerous unless a person suspects extremely low glucose and thinks they need a rapid dose of glucose. How much is too much? Insulin helps people with diabetes live an active lifestyle. However, it can lead to serious side effects, especially if a person administers too much. Excessive insulin can cause hypoglycemia, or extremely low blood sugar, and lead to nausea, sweating, and shaking. It is essential that people measure insulin carefully and eat a consistent diet that balances blood sugar levels as much as possible. Other medications In addition to insulin, other types of medication are available that can help a person to manage their condition. Metformin For type 2 diabetes, a doctor may prescribe metformin in pill or liquid form. It contributes to: It can also help in weight loss. Having a healthy weight can reduce the impact of diabetes. As well as diabetes, a person may also have other health risks, and they may need medication to control these. A doctor will advise the individual about their needs. Jul 4, 2020 \| Category: Apple \| Comments And not just.in the browser.	https://newstargeted.com/news/1304/33/Diabetes-information
Doctor insights on: Which Of The Following Is Associated With Type 2 Diabetes 1 Hi I have type 2 diabetes and have been ill (vomitting) for the past two days. I'm starting to worry? Do not worry: Do not eat or drink for now. Just ice chips. ...Read more Diabetes (Definition) A group of diseases that result in too much sugar in the ...Read more 2 How could I have to type 2 diabetes two months ago and then have my blood taken and it shows I am hyperglycemic now? Diabetes: Do you mean hypo or hyperglycemic? There is a big difference. ...Read more 3 My husband has type 2 diabetes. Yesterday he went on a two mile hike. His night time blood sugar we're high and still elevated this morning. Why? Complicated disease: Diabetes is a complicated disease and often doesn't work the way we expect. You'd think that after exercise, the blood sugar would be good - but he could run a marathon and still have an elevated blood sugar after. It's a combo of how much Insulin he's producing and his muscles' sensitivity to insulin. Over weeks to months of exercise, he will see a change in his fasting sugars, so keep it up! ...Read more 4 For type 2 diabetes, if someone has to choose between whole grain sorghum flour and whole grain wheat flour, which one of the two would b better? Sorghum: It digests slower, slowing the rise of serum glucose, therefore allowing for better control of diabetes. While this benefit is small, sorghum also has the bonus of being gluten-free, and it grows well in drought conditions. ...Read more 5 For a person early 70's, slight blood pressure 130, with type 2 diabetes using insulin before meals, which of the two is better atacand or micardis (telmisartan)? Similar: Both these drugs belong to the same class so the choice boils down to cost and the one you tolerate better. ...Read more 6 Is diabetes genetic? I think I may be diabetic, my mom just got diagnosed with type 2 diabetes and I have two symptoms of it. Should I get tested? Type II diabetes: There is a strong heritable component of diabetes, especially type ii. I don't know what symptoms you are currently experiencing, but the classic ones are polyuria, polydipsia, nocturia, and polyphagia. If you have symptoms, you should be screened with a hemoglobin a1c blood test or fasting plasma glucose test; especially if you are obese, or have additional risk factors besides family history. ...Read more 7 Just diagnosed with type 2 diabetes two days ago. At er blood sugar was 325. they started insulin and discharged. Sugar now 470 but been taking meds? Too high: Yu certainly have DM that is not controlled at this time. Over 400 is too high and if persists, you will need to go to the emergency room. Call your Dr. ASAP and get in for an evaluation and adjustment of medication, dietary counseling, and advice on Therapeutic lifestyle changes. Basically, you need to establish care with a Doctor who will provide you with continuity of care and DM management. ...Read more 8 I really need to be educated on type 2 diabetes. My blood sugar is either too low or high. When should I take. My metformin. 166 two hr after eating. Lose the weight: The first part of treating diabetes is to lose weight. I know how difficult that can be but I'm just saying. Your medicine, metformin, is taken two times a day with food. The most important test which is done by the doctor is called hemoglobin A 1 C and its value should be from 6.7-7.5% It can be lower with great control but its the most important. ...Read more 9 What health problems are associated with type 2 diabetes? Many: It is associated with kidney problems (diabetic nephropathy), eye problems (diabetic retinopathy), nerve problems (diabetic neuropathy), vascular disease (includes heart attacks, strokes, circulation problems) and stomach/intestine problems (gastroparesis). It is also associated with slow wound healing, and with altered glucose (sugar) levels, an extreme example of which is diabetc ketoacidosis. ...Read more 10 What risk factors are associated with type 2 diabetes and what is the age of onset? Obesity, age, genes: The major risk factors for type 2 diabetes are; obesity, especially if it is in the abdomen, advancing age, family history of diabetes, certain meds such as steroids, antipsychotics. It typically occurs in obese adults (over age 40) but can occur in younger people as well. The best prevention is to keep weight down and exercise. ...Read more 11 What short & long term effects are associated with type 2 diabetes? Uncontrolled signs: Short term if out of control: fatigue, frequency of urination, increased thirst, blurred vision, weight loss or gain long term if uncontrolled: chronic kidney disease, peripheral neuropathy, diabetic retinopathy, heart disease, increased risk of stroke. ...Read more 12 What risk are associated with type 2 diabetes pregnancy? Why pregnancy in type 2 diabetes are high risks? With slow metabolism rate. Type 2 diabetes/preg: Type 2 diabetes is accentuated by pregnancy, and poor control of glucose levels can adversely affect the fetus. Type 2 diabetes can also cause retinal problems, cardiovascular compromise, and placental insufficiency. It is critical if pregnant, to see a maternal-fetal medicine expert at a University setting or at King Faisal hospital in Riyadh. ...Read more 13 If having ED due to type 2 diabetes, what are some ways to fix this? ED from Diabetes II: Diabetes can damage small blood vessels and nerves. Optimal treatment of your diabetes could help. Sometimes Alpha lipoic acid can help in my experience. Optimizing your testosterone may help. ED meds like Viagra (sildenafil) may help, too. Work with your doctor. ...Read more 14 What is type 2 diabetes? Insulin resistance: This is the type of diabetes where your body is resistant to the hormone Insulin and therefore your body can't process carbohydrates properly. ...Read more 15 What causes type 2 diabetes? No: In the child diabetic, the general problem is that the pancreas quits producing Insulin so your body can not utilize the available sugar. In the adult diabetic, your cells become resistant to the available insulin. The result is too much sugar in the blood. If you are a diabetic and you eat a lot of sugar, then this can make your diabetes worse, but it is not the cause of diabetes. ...Read more 16 Why did I get type 2 diabetes? Not sure: Diabetes tends to run in families, so ifanyone in your family had diabetes, that's probably why you have it. It is also more common in people who are obese (bmi over 30) and people over the age of 50. ...Read more 17 Is type 2 diabetes sex-linked? No: No even though it can run in families but it is not sex linked recessive disease. ...Read more 18 How do I beat type 2 diabetes? Lifestyle change: If you're on hypoglycemic oral medication, your doctor could possibly, eventually, wean you provided that you develop a healthier lifestyle including weight control, exercise, and good sleep. ...Read more 19 How do you cure type 2 diabetes? There is no cure: Only control (diet, exercise, weight loss, medications, bariatric surgery) but none remove the genes that put one at risk in first place!! ...Read more 20 What exactly is type 2 diabetes? Insulin resistance: Type 2 diabetes is when your body stpos responding to Insulin properly. Insulin is what gives the signal for your cells to take up glucose (sugar) for energy, if the key (insulin) does not fit the lock (in the membrane of the cell). Then glucose is not burned and accumulates in your blood to be spilled by the kidneys. ...Read more 21 How is type 2 diabetes diagnosed? Many options: Symptoms such as excessive thirst and hunger, excessive urination, fatigue can point you to the possibility of diabetes.To diagnose you have 4 ways:1)fasting bs>/=126, 2)oral glucose tolerance test (drinking a high carbohydrate drink)2 hr after the drink with bs>/=200 mmol/dl 3)hba1c>6.5% or 4) random bs>200 mmol/dl with the symptoms described above. You need 2 positive tests to confirm diagnosis. ...Read more 22 What happens with type 2 diabetes? Insulin Resistance: If you have Type2 Diabetese your body does not use insulin properly. This is called Insulin Resistance. At first your Pancreas make extra insulin to make up for it. But over time can not keep up and can not make enough Insulin to keep sugar at normal levels. Your Blood Sugar goes up and you need medicines that work on the insulin resistance along with diet and exrcise. Some may need more than one med ...Read more 23 How do you manage type 2 diabetes? Diet, exercise +meds: The first and best way is to control the diet.This is ideally done with the help of a nutrtionist and diabetes expert. Stability in the diet ie eating 3 meals and 2 snacks a day, keeping carbs stable and lowering calories not only helps with weight loss but also with deciding on med choice. The medications for diabetes are excellent, and your doctor can help find the best choice if diet isn't enough. ...Read more 24 How can a person get type 2 diabetes? Insulin resistance: A big part of the problem is resistance to insulin's normal actions develops. Insulin resistance is affected by body composition, diet, activity. With sedentary lifestyle, more body fat, higher weight/obesity comes more resistance to Insulin and higher blood sugars. Eating healthy, exercising, losing weight, building muscle can all prevent or delay type 2 diabetes from developing. ...Read more 25 What is a diagnosis of type 2 diabetes? See below: Fasting plasma glucose above 126mg% on two occasions, plasma glucose above 200 mg% after a 75 gm glucose load, hemoglobin a1c above 6.5%, inreased thirst, urination, and related clinical picture. See this site for more info. http://shp. Missouri. Edu/vhct/case2600/dx_criteria. Htm. ...Read more 26 Help? I believe I have type 2 diabetes? See below: If fasting for >8 hours. Fasting sugar 100-125 is pre-diabetes and 2-hrs after eating 140-199 is prediabetes. Fasting -126 and higher; and 2 hours after eating, 200 and greater, is diabetes can get home blood glucose testing equipment over the counter in pharmacies if you have either, see md! ...Read more 27 How do I know if I have type 2 diabetes? Lab tests: Either a glucose tolerance test or an A1c will tell if you have dm or prediabetes if you are asymptomatic. ...Read more 28 What kind of disorder is type 2 diabetes? Older patients: Type two diabetes is generally seen in older patients. It is caused by the body becoming resistant to Insulin so initially the Insulin level is high as opposed to juvenile diabetes where there is a lack of insulin. However, eventually the type two diabetic may have low Insulin levels also and require insulin. Both are major risk factors for vascular disease. ...Read more 29 What are the symptoms of type 2 diabetes? See below: Excessive urination, increased thirst, blurred vision, fatigue and weight loss are the key symptoms of uncontrolled diabetes. ...Read more 30 Is there a solution for type 2 diabetes?	https://www.healthtap.com/topics/which-of-the-following-is-associated-with-type-2-diabetes
- Hyperglycemia is when blood sugar levels are 130 mg / dL before a meal or 180 mg / dL two hours after a meal. - Signs and symptoms of hyperglycaemia include increased thirst, more frequent urination and blurred vision. - Hyperglycemia occurs mostly in people with diabetes, although it can also occur as a result of stress or steroid medications. - This article was reviewed by Jason R. McKnight, MD, family physician and clinical assistant at Texas A&M Medical College. - Visit the Insider’s Health reference library for more tips. Hyperglycemia is when you have high blood sugar. Before meals or when you have not eaten for several hours, high blood sugar is defined as 1 By comparison, normal blood sugar levels are usually between 80 mg / dL and 130 mg / dL. Hyperglycemia is most common in people with diabetes and essentially describes the high blood sugars that determine the chronic condition. In some cases, hyperglycaemia may also occur as a result of stress or as a side effect of a steroid medication. Here’s how you can recognize the signs of high blood sugar and lower it quickly. Signs and symptoms The most common symptoms of hyperglycaemia include: - Increased thirst - Drink fluids more often - Urination more often - Blurred vision - Weight loss However, the only way to know for sure if you have hyperglycemia is by taking blood, says Dr. Jordan Mesler, a physician at the Morton Plant Hospitalist group in Clearwater, Florida. This may confirm that your blood sugar levels are elevated and by how much. In fact, the symptoms will often not become severe until the blood sugar rises above 200 mg / dL. If left untreated, hyperglycemia can lead to diabetic ketoacidosis (DKA) within 24 hours in some cases. This condition, most commonly in people with type 1 diabetes, occurs when the body is unable to break down sugar properly for fuel, so it breaks down fat instead, says Mesler. This naturally releases acids into the blood and because the body cannot wash the acid fast enough, it becomes toxic in the blood. DKA is an emergency medical service and people with the following symptoms should visit the emergency department, especially if they have diabetes, says Messler: - Nausea - Fatigue - Shortness of breath - Dry mouth - Stomach ache Reasons Both type 1 and type 2 diabetes can cause hyperglycemia. But there are other potential causes, such as stress or steroid medications. Diabetes People with diabetes are unable to process blood sugar effectively, either because they do not produce insulin, the hormone that breaks down blood sugar (type 1), or because their body does not use insulin effectively (type 2). Because the body cannot break down blood sugar, it builds up in the blood and is more likely to cause high blood glucose levels or hyperglycaemia. Hyperglycemia can also occur from time to time in people being treated for diabetes. These spikes in blood sugar levels can be caused by: - He eats too much - Not exercising enough - You are giving yourself too little insulin or medicine - The phenomenon of dawn or a surge of hormones in the early morning, which can raise blood sugar - Stress or illness Stress Even people without diabetes can get hyperglycemia. For example, stress can cause insulin resistance – a condition in which your body does not use insulin effectively. At the same time, the stress hormone cortisol promotes the release of hepatic glucose or glucose stored in the liver, which further raises blood sugar. This so-called “stress hyperglycemia” can occur during acute medical situations, such as infection or heart attack, says Mesler. Steroids Steroids, such as prednisone and methylprednisolone, can also cause hyperglycemia in up to 46% of patients without diabetes, but this usually goes away when the drug is stopped. Like the effects of stress, these drugs also increase the release of hepatic glucose and increase insulin resistance and can cause hyperglycaemia, even if you do not have diabetes. Treatment The goal of treatment for hyperglycemia is to lower blood sugar. For people with diabetes, this may mean adjusting your insulin dose or following a plan that you and your doctor have set up in advance when you have hyperglycaemia. People who have chronic hyperglycemia caused by diabetes should also work to lower their blood sugar over time, in addition to treating individual episodes of hyperglycemia. “The best way to start lowering your blood sugar for someone with diabetes is through lifestyle changes, such as diet and exercise,” says Mesler. People with type 1 diabetes will need insulin to lower their blood sugar, while type 2 diabetics are often treated with oral medications such as metformin and possibly insulin, Mesler said. However, for people with stress or steroid-induced hyperglycemia, the condition usually resolves on its own as soon as the stress subsides or about four to six hours after stopping treatment. If hyperglycemia persists after coping with the underlying health condition, the patient may be diagnosed with diabetes, Mesler said. Taking Hyperglycemia is a serious condition, especially if left untreated. As it can only be diagnosed by measuring your blood sugar, it is important to talk to your doctor if you are worried about hyperglycaemia. “If you suffer from symptoms of increased thirst and frequent urination with weight loss, then you should discuss with your doctor and check your blood sugar,” says Mesler. He also recommends that people who have risk factors for diabetes – including being overweight, have a family history of diabetes or are over 45 – check their blood sugar levels regularly.	https://hotinfonow.com/hyperglycemia-symptoms-causes-and-treatment/
The pain of diabetic nerve damage may respond to traditional treatments with certain medications such as gabapentin (Neurontin), phenytoin (Dilantin), and carbamazepine (Tegretol) that are traditionally used in the treatment of seizure disorders. Amitriptyline (Elavil, Endep) and desipramine (Norpraminine) are medications that are traditionally used for depression. While many of these medications are not indicated specifically for the treatment of diabetes related nerve pain, they are used by physicians commonly. Your doctor may recommend a 24-hour blood pressure monitoring test called ambulatory blood pressure monitoring to confirm if you have high blood pressure. The device used for this test measures your blood pressure at regular intervals over a 24-hour period and provides a more accurate picture of blood pressure changes over an average day and night. However, these devices aren't available in all medical centers, and they may not be reimbursed. A study published in the Journal of the American College of Nutrition in April 1999 showed this effect. This study looked at a group of obese individuals who were put on a very low calorie diet and assigned to one of two exercise regimes. One group did aerobic exercise (walking, biking, or jogging four times per week) while the second group did resistance training three times per week and no aerobic exercise. Hypertension develops secondary to environmental factors, as well as multiple genes, whose inheritance appears to be complex. [12, 21] Furthermore, obesity, diabetes, and heart disease also have genetic components and contribute to hypertension. Epidemiological studies using twin data and data from Framingham Heart Study families reveal that BP has a substantial heritable component, ranging from 33-57%. [22, 23, 24] ^ Vancampfort D, Correll CU, Wampers M, Sienaert P, Mitchell AJ, De Herdt A, Probst M, Scheewe TW, De Hert M (July 2014). "Metabolic syndrome and metabolic abnormalities in patients with major depressive disorder: a meta-analysis of prevalences and moderating variables". Psychological Medicine. 44 (10): 2017–28. doi:10.1017/S0033291713002778. PMID 24262678. Insulin serves as a “key” to open your cells, to allow the glucose to enter -- and allow you to use the glucose for energy. Without insulin, there is no “key.” So, the sugar stays -- and builds up-- in the blood. The result: the body’s cells starve from the lack of glucose. And, if left untreated, the high level of “blood sugar” can damage eyes, kidneys, nerves, and the heart, and can also lead to coma and death. Consistently high levels of insulin are associated with many harmful changes in the body prior to its manifesting as disease including chronic inflammation and damage to arterial walls, decreased excretion of salt by the kidneys, and thickening of the blood. People with metabolic disease also exhibit elevations in blood pressure and changes in their blood lipids, primarily with triglycerides (elevated) and good cholesterol or high density lipoprotein (HDL) (reduced). Problems associated with metabolic syndrome develop over time and usually worsen if left untreated. When you have diabetes, it’s important to avoid eating many packaged, processed snacks such as cookies, chips, cake, granola bars, and the like, in lieu of fresh, whole foods, like fiber-rich fruits, veggies, and whole grains. (27) Eating foods high in fiber can help keep blood sugar levels steady and fill you up, potentially promoting weight loss and improving insulin sensitivity. (28) Monitoring your caloric intake may be helpful if you’re overweight, but everyone with type 2 diabetes should track how many carbs they’re taking in. That can be tricky because carbs are in many of the common foods you may already eat, but there are both good and bad sources of carbs. Fruits and vegetables, for example, are good sources, while pretzels and cookies are bad sources. (29) [Guideline] Skyler JS, Bergenstal R, Bonow RO, et al. Intensive glycemic control and the prevention of cardiovascular events: implications of the ACCORD, ADVANCE, and VA Diabetes Trials: a position statement of the American Diabetes Association and a Scientific Statement of the American College of Cardiology Foundation and the American Heart Association. J Am Coll Cardiol. 2009 Jan 20. 53(3):298-304. [Medline]. Target organ damage occurs through multiple mechanisms in metabolic syndrome. The individual diseases leading to metabolic syndrome produce adverse clinical consequences. For example, hypertension in metabolic syndrome causes left ventricular hypertrophy, progressive peripheral arterial disease, and renal dysfunction. However, the cumulative risk for metabolic syndrome appears to cause microvascular dysfunction, which further amplifies insulin resistance and promotes hypertension. Perform a set of an exercise, follow it immediately with a short bout of moderate-intensity aerobics, and then repeat for another couple sets. For example, you may perform a set of leg presses, go straight to a 30-second set of jumping jacks, go back to a set of leg presses, then to jumping jacks, etc. Once you perform three sets of an exercise, move to the next exercise as quickly as possible. On the downside, this form of MRT has the greatest potential to lead to overtraining, so use it judiciously! Your doctor may also use a device called an ophthalmoscope to look at the blood vessels in your eyes. Doctors can see if these vessels have thickened, narrowed, or burst, which may be a sign of high blood pressure. Your doctor will also use a stethoscope to listen to your heart and the sound of blood flowing through your arteries. In some cases, a chest x-ray and electrocardiogram may be needed. Ambulatory blood pressure monitoring can be done by using at-home devices that measure your blood pressure at periodic increments throughout a 24-hour or 48-hour time period. This provides your medical team with an average blood pressure reading that is believed to be more accurate than one taken at the doctor's office. Accumulating evidence supports the reliability of this approach. POPs primarily impact the thyroid gland by decreasing its ability to make thyroid hormone, disrupting thyroid hormones once they are made, and causing thyroid hormones to be removed from the body faster. If your metabolism is a large jumbo jetliner, the thyroid gland is one of the engines. POPs appear to work in part by blowing out the thyroid engine. Because some medications, such as over-the-counter cold medicines, pain medications, antidepressants, birth control pills and others, can raise your blood pressure, it might be a good idea to bring a list of medications and supplements you take to your doctor's appointment. Don't stop taking any prescription medications that you think may affect your blood pressure without your doctor's advice. Diabetes is a chronic, metabolic disease characterized by elevated levels of blood glucose (or blood sugar), which leads over time to serious damage to the heart, blood vessels, eyes, kidneys, and nerves. The most common is type 2 diabetes, usually in adults, which occurs when the body becomes resistant to insulin or doesn't make enough insulin. In the past three decades the prevalence of type 2 diabetes has risen dramatically in countries of all income levels. Type 1 diabetes, once known as juvenile diabetes or insulin-dependent diabetes, is a chronic condition in which the pancreas produces little or no insulin by itself. For people living with diabetes, access to affordable treatment, including insulin, is critical to their survival. There is a globally agreed target to halt the rise in diabetes and obesity by 2025. The term "type 1 diabetes" has replaced several former terms, including childhood-onset diabetes, juvenile diabetes, and insulin-dependent diabetes mellitus (IDDM). Likewise, the term "type 2 diabetes" has replaced several former terms, including adult-onset diabetes, obesity-related diabetes, and noninsulin-dependent diabetes mellitus (NIDDM). Beyond these two types, there is no agreed-upon standard nomenclature. As you lose weight your leptin levels drop, signalling to your body that it should probably start to slow things down. In this case you can feel hungry all of the time, but also sluggish and weight loss stops. Some people even see weight gain which can either send you into frustration nation… or alternatively lead you to cut more calories and drive your metabolic rate and gut hormone signalling down even further! Yikes! The primary problem in metabolic syndrome is insulin resistance. In the body's attempt to compensate for insulin resistance, extra insulin is produced, leading to elevated insulin levels. The elevated insulin levels can lead, directly or indirectly, to the characteristic metabolic abnormalities seen in these patients. Frequently, the insulin resistance will progress to overt type 2 diabetes, which further increases the risk of cardiovascular complications. Several other signs and symptoms can mark the onset of diabetes although they are not specific to the disease. In addition to the known ones above, they include blurred vision, headache, fatigue, slow healing of cuts, and itchy skin. Prolonged high blood glucose can cause glucose absorption in the lens of the eye, which leads to changes in its shape, resulting in vision changes. Long-term vision loss can also be caused by diabetic retinopathy. A number of skin rashes that can occur in diabetes are collectively known as diabetic dermadromes. Potassium – as part of the electrolyte panel, which also includes sodium, chloride, and carbon dioxide (CO2); to evaluate and monitor the balance of the body's electrolytes. For example, low potassium can be seen in Cushing syndrome and Conn syndrome, two causes of secondary hypertension. Some high blood pressure medications can upset electrolyte balance by causing excessive loss of potassium or potassium retention. Insulin — the hormone that allows your body to regulate sugar in the blood — is made in your pancreas. Essentially, insulin resistance is a state in which the body’s cells do not use insulin efficiently. As a result, it takes more insulin than normal to transport blood sugar (glucose) into cells, to be used immediately for fuel or stored for later use. A drop in efficiency in getting glucose to cells creates a problem for cell function; glucose is normally the body’s quickest and most readily available source of energy.	http://lovinglifewithdiabetes.com/metabolic-syndrome-update--metabolic-syndrome-research-articles-.html
Diabetes mellitus type II is a chronic metabolic syndrome that affects the body’s sugar metabolism by resisting the stimulation and production of insulin. Symptoms presented by most patients include blurred vision, frequent urge to urinate, excess feeling of thirst and constant hunger. This paper will provide a rationale for the top four differential diagnoses for a type II clinical condition, and identify the priority diagnostic pathophysiology and clinical tests. In addition, therapeutic interventions, care referrals and professional collaborations will be discussed. Finally, a recent journal article will be reviewed, and a follow up plan for future wellness will be provided. Differential Diagnosis Over the last few decades, medical associations have invented diagnosis methods that guide professionals in determining glucose levels in the body. Even so, decisions on methods to be adapted are made on an individual basis. The most used approaches are based on laboratory results from blood and urine samples. The following include the top four differential diagnosis for non-insulin diabetes. Dyslipidemia Hyperlipidemia is a common condition responsible for causing cardiovascular complications in diabetic patients. It is mostly associated with high concentrations of lipids in plasma, a characteristic condition of increased fatty acids caused by insulin resistance. Even though the genesis of diabetic dyslipidemia remains unknown, more evidence suggests that insulin resistance, a characteristic physiology in non-insulin dependent diabetes plays an important role (Mooradian, 2009). Hypertension High blood pressure is a common comorbid condition in patients suffering from diabetes. Studies by the American Diabetes Association reveal high metabolic predominance of the condition in insulin resistance, dyslipidemia and obesity. Hypertension increases risks for both macro and micro vascular problems (American Diabetes Association, 2003). Urine Tests Albuminuria gives an appropriate measure the presence of albumin or protein in the urine, especially in people with high blood sugar. In people with type 2 diabetes, kidneys excrete albumin, and thus, the test mark the presence of diabetes nephropathy (IHS Division of Diabetes Treatment and Prevention 2009). Blood Tests As indicated in the introduction, the main characteristic of diabetes mellitus type 2 is high glucose levels. Based on this, the primary criteria for diagnosis would be laboratory tests to measure and determine amounts of glucose levels circulating in blood plasma. The American Diabetes Association (2010) proposes diagnosis criteria for diabetes mellitus type II based on the following tests: - Random Glucose Test: Blood is drawn randomly regardless of when the patient lastly had a meal. Results revealing 200mg/dl level or higher indicate high levels. - Fasting Plasma Glucose (FPG): Blood is drawn after 8-12 hour fasting period. Results revealing 126 mg/dl level or higher indicate elevated levels. - Hemoglobin AIC test: The test, done anytime of the day, either before or after meals measures average blood sugar levels over the duration of 2 to 3 months. Normal values should be 4 – 5.6 percent. Results revealing 6.5 percent or higher indicate high blood sugar. - Oral Glucose Tolerance Test: Famously known as the OGTT, it involves interrupting blood sugar levels using special glucose solutions. Glucose levels are measured prior to taking the solution, as well as periodically after taking. Results revealing 200mg/dl level or higher after two hours indicate raised blood sugar. Pathophysiology Also known as non-insulin dependent or adult-onset diabetes, the condition is a characteristic of hyperglycemia triggered by excess circulation of glucose in the plasma, and moderate deficiency of insulin, a chemical substance responsible for controlling the amount of sugar in the body. Its origin is related to inadequate secretion and supply of insulin by pancreatic beta cells. Insulin resistance affects physiological processes in cells, leading to activated release of unwanted glucose by liver cells, elevated amounts of lipids, reduced levels of glucose in muscle cells, amplified breakdown of lipids, and resistance to incretin. Induced insulin resistance from increased body lipids triggers elevated glucagon and insulinotropic polypeptide levels, which in turn cause intolerance. However, it is important to note that the process does not alter the glucagonlike peptide response and thus increases the excretion of glucagon (Khardori et al., 2014). Excess production of glucagon subverts the production of insulin-secreting hormones in the beta cell, leading to hyperglucagmenia, that later develops to hyperglycemia due to failure of suppressed gluconeogenesis. In turn, the development of hyperglycemia increases cardiovascular risks, cognitive dysfunction and other health related conditions. Medical studies link the genesis of the disorder mainly to genetic, medical, and lifestyle factors (American Diabetes Association, 2010). It is important to note that some of these factors, such as obesity, lack of physical exercise and, unhealthy diet are controllable through individual interventions. However, other factors among them, aging, genetics, and gender need clinical interventions. Insulin resistance and unstable pancreatic functions may be heritable genes (Khardori et al., 2014). For example, Genetic variations involving incretin, a gastrointestinal hormone, may stimulate insulin secretion. High amino acid concentrations in body metabolism play a significant role in the development of type two diabetes mellitus. These concentrations mostly develop from high carbohydrate diets. Khardori et al. (2014) studied medical reports that led to the conclusion, elevated amino acid concentrations exposed diabetic risk among normoglycemic individuals. In essence, for the disorder to crop up there must be an occurrence of insulin resistance, and inadequate insulin secretion. Even though obesity is related to type two, diabetes does not develop in all cases because, some obese people can sufficiently secrete insulin sufficient for stabilizing their insulin resistance. From the discussion above, it is evident that the pathophysiology of the disorder differs among individuals. Nevertheless, more health complications, including cardiovascular risks, retinopathy, stroke, nephropathy, and neuropathy share the same risks. Therapeutic Interventions Effective treatment depends on introduction of both scientific and non-scientific methods. Pharmacological medications initiate glycemic control and thus reduce long-term complications (Khardori et al., 2014). Nevertheless, it is important to bear in mind an individual’s symptoms and clinical results. In this case, the patient has symptoms that reveal an onset of the disorder. The best-recommended intervention would be a combination of anti-diabetics (biguanides) and insulin medications. Anti-diabetics (biguanides) Just as their name suggests, they fight against diabetes by reducing hyperglycemia. These agents control the effects of hyperglycemia by decreasing hepatic gluconeogenesis, and increasing the peripheral insulin secretion (Khardori et al., 2014). In addition, they have negative effects in elevating insulin levels and obesity. Biguanides do not undergo metabolism and hence are quickly removed by the kidneys. Furthermore, lactic acidosis rarely occurs. Insulin Transitory insulin treatment to patients with initial presentation of diabetes reduces glucose in the blood, and relieves early symptoms such as polydipsia and polyuria (Khardori et al., 2014). The reduction of glucose toxicity reduces secretion of insulin in the beta cells, which in turn worsens resistance. Injectable insulin solutions provide glycemic levels without any unfavorable effects. Since most patients are insulin resistant, induction of insulin using small doses of scientific drugs may be inefficient. Non-Pharmacological Interventions The American Diabetes Association (2013) clinical practice guidelines recommends patients using non-insulin therapies or regular insulin injections to adjust to other non-pharmacological therapies, which include, adjusting to medications, physical activity, and low-calorie diet to reach individualized glycemic goals. The modification of diet is important in management of diabetes. Glycemia can also be controlled by regulating weight and thus medications aimed at inducing weight loss, such as orlisat could be helpful to patients. Referrals and Professional Collaboration Diabetes mellitus 2 has numerous complications that affect the general health of a human person. For effective management, clinicians work with other specialists and make appropriate referrals, which include: - Diet Modifications therapy - Depression screening - Renal screening - Eye Screening Journal Literature Review Rochester, Leon, Dombrowski, & Haines (2012) carried out a study to determine the management of insulin in patients with type two diabetes mellitus using collaborative drug therapy. The study revealed unsatisfactory treatment of glycosylated hemoglobin with oral antihyperglycemic agents alone. After the introduction of an insulin initiation primary care clinic, which was developed to offer required insulin therapy, the use of oral medication decreased within the first three months. As a result, pharmacists were required to follow insulin dosing protocols to guide therapeutic decision making. In addition, patient comprehensive education and training about blood-glucose self monitoring skills, using insulin injection, treating hypoglycemia, and lifestyle modifications was introduced. Patients were then discharged to primary care providers after a duration of six months. The journal sets off a conclusion that planned insulin initiation would improve patients’ glycemic control. Planning for Future Wellness In line with the 2013 American Diabetes Association recommendations, clinicians not only have the duty to educate their patients about self-monitoring and data interpretation, but also they should conduct follow-up routine assessment. In this case, I would recommend the following approaches for preventing complications related to the disorder. - Glycated hemoglobin tests every 3 months to determine the effectiveness of medication, and make necessary changes if required. - Statin therapy to reduce the presence of lipidoproteins in cholesterol - Blood pressure tests every visit to ensure that lipids do not affect cardiovascular processes - Microalbumi checks after 6 months to ensure kidneys do not leak albumin to urine and cause renal complications - Foot checks every visit to detect and survey diabetic neuropathy and peripheral arterial disease. For effective management, the patient should be trained about self-monitoring techniques, interpretation of results, and suitable actions. For effective and accurate results, clinicians should check and recalibrate glucose testing meters every visit. Conclusion In summation, it is important to strike the difference between the diabetes mellitus type 1 and 2 that appear to share symptoms. Diabetes mellitus type 2 is preventable through both natural and pharmacological strategies. Natural methods are acquired through a change of lifestyle that would encourage the maintenance of age-appropriate body weight through engaging in physical activity. This drives away the obesity condition. The observation of a nutritious diet characterized by low fats, regulated fats and more intakes of water, fluids and fruits is also a natural way of regulating the level of insulin and fat in the body. Lastly, medication at early stages can prevent deaths caused by cardiovascular related disorders. References American Diabetes Association (2013). Clinical practice recommendations: 2013. Diabetes Care, 36 (1), 1-110. American Diabetes Association. (2010). Diagnosis and classification of diabetes mellitus. Diabetes Care, 33 (1), 10-62. Web. American Diabetes Association. (2003). Treatment of hypertension in adults with diabetes. Diabetes Care, 26 (1), 80-82. Web. IHS Division of Diabetes Treatment and Prevention. (2009). Urine Albumin Screening and Monitoring in Type 2 DM. Mooradian, A. (2009). Dyslipidemia in type 2 diabetes mellitus. Nature Clinical Practice Endocrinology & Metabolism, 5, 150-159. Web. Rochester, D., Leon, N., Dombrowski, R., & Haines, T. (2012) Collaborative drug therapy management for initiating and adjusting insulin therapy in patients with type 2 diabetes mellitus. American Journal of Health-System Pharmacy, 67 (1), 42-48. Khardori, R., George, G., Howard, B., Barry, B., William, I., Kenneth, L., Anne, P., David, S., Don, S., Erik, S., Francisco, T., & Scott, V. (2014). Type 2 diabetes mellitus medication. Web.	https://nursingbird.com/diabetes-mellitus-type-ii/
How Often Should I Check My Blood Sugar Level For those with type 2 diabetes, it is usually recommended to check your blood sugar before meals and just before you go to bed if you take insulin injections. If you use long-acting insulin, you may only need to test at breakfast and bedtime. Those who don’t use insulin and rely on other medications and lifestyle changes may not need to test their blood sugar every day. Your doctor will help you determine how often you should check your blood sugar levels, and they may ask you to write the information in a logbook for your next appointment. How To Prevent High Blood Sugar The best way to treat high blood sugar is to prevent it from happening in the first place. Not only does this help to avoid a potential emergency, but it also reduces the likelihood of experiencing diabetic complications. Patients with diabetes can prevent high blood sugar by taking some of the following measures: References and Sources: What Are Risk Factors For Hyperglycemia Major risk factors for hyperglycemia are: - You have a family history of type 2 diabetes. - You are African American, Native American, Hispanic or Asian American. - You are overweight. - You have high blood pressure or cholesterol. - You have polycystic ovarian syndrome . - You have a history of gestational diabetes. Recommended Reading: How Much Is Insulin At Walmart Causes Related To Lifestyle Physical inactivity Exercising prompts your body to burn more energy than usual, and, as a result, consume more glucose. Maintaining a low level of physical activity, on the other hand, means more glucose will remain in the bloodstream. This raises your overall blood glucose values in the process. Exercise also makes our body more insulin sensitive, which means we will require less insulin for the rest of the day to control glucose levels. Stress Part of the bodyâs fight-or-flight response to stress is to produce additional glucose. Another facet of that response is an increase in the hormone cortisol. High cortisol can reduce the bodyâs sensitivity to insulin. As a result, blood glucose levels may also increase. Poor sleep A lack of quality sleep can inhibit how much insulin your body can release. It can also cause the production of cortisol, which makes it harder for insulin to work. When your bodyâs insulin cannot properly metabolize the glucose in your blood, the glucose remains there and your glucose levels rise. Get better insight into your glucose levels Want to gain a better understanding of how your body responds to glucose? Try monitoring your glucose levels in real time with the Nutrisense Continuous Glucose Health Program. What Is The Test To Check Blood Sugar Levels For Type 2 Diabetes You can check your blood sugar levels several times a day at home with a blood glucose monitor, which uses a drop of blood from your finger. A better measure of how well your diabetes is being managed, however, is a blood test called the A1C. The A1C test involves a blood test that measures the percentage of hemoglobin proteins in your blood that are bound to sugar. In a more practical sense, these tests show how well your blood sugar levels have been managed in the last two to three months. Instead of relying on occasional blood glucose tests that can spike or drop for many reasons, A1C tests provide a more accurate picture of how well your diabetes has been managed on average across the preceding three months. Some people are diagnosed with diabetes using the A1C test, and doctors often recommend that those with prediabetes should get a yearly A1C test. Those with diabetes who don’t use insulin may only need two of these tests per year. People who use insulin, or struggle to keep blood sugar levels within their target range, may get four A1C tests per year. A1C tests don’t require any preparation for fasting beforehand, so you can have this blood test any time of the day, even after eating and drinking normally. Don’t Miss: Grocery Shopping List For Type 2 Diabetes Are Some Canadians At Higher Risk For Elevated Blood Sugar Levels Than Others You may have a higher risk for elevated blood sugars and type 2 diabetes if you: - Are 40 or years of age or older - Have a close relative with diabetes - Are of African, Arab, Asian, Hispanic, Indigenous or South Asian descent - Are overweight - Have been diagnosed with prediabetes Some medical conditions can also increase your risk of type 2 diabetes, such as: - High blood pressure or cholesterol levels - Polycystic ovary syndrome - Psychiatric disorders - Sleep apnea Easy Ways To Lower Blood Sugar Levels Naturally High blood sugar, also known as hyperglycemia, is associated with diabetes and prediabetes. Prediabetes is when your blood sugar is high, but not high enough to be classified as diabetes. Your body usually manages your blood sugar levels by producing insulin, a hormone that allows your cells to use the circulating sugar in your blood. As such, insulin is the most important regulator of blood sugar levels . However, multiple factors can impair blood sugar management and lead to hyperglycemia. Internal causes for high blood sugar include when your liver produces too much glucose, your body makes too little insulin, or your body cant effectively use insulin. The latter is known as insulin resistance ( 2 ). The Centers for Disease Control and Prevention reports that 13% of U.S. adults live with diabetes and that another 34.5% have prediabetes. This means that close to 50% of all U.S. adults have diabetes or prediabetes . Blood sugar management is especially important for people with diabetes, as chronically high blood sugar levels can lead to limb and life threatening complications ( Increased insulin sensitivity means your cells can more effectively use the available sugar in your bloodstream. Exercise also helps your muscles use blood sugar for energy and muscle contraction . Whats more, researchers recommend doing so-called exercise snacks to lower blood sugar and prevent the damage that sitting all day can do . Read Also: Desserts For Type 1 Diabetes You Notice Tingling And Numbness In Your Hands Or Feet As mentioned, uncontrolled blood sugar can cause nerve damage, also known as diabetic neuropathy. What you may notice is a tingling sensation or even numbness in your hands and feet. Some people experience pain in their hands and feet as well. Though neuropathy is most common in people who have had diabetes for a long time, it can occur in anyone with poorly controlled diabetes. Reflect On The Amount Of Sugar In Your Diet Hyperglycemia occurs when there is too much glucose in the blood. Therefore, one way of reducing your blood glucose levels is reflecting on where sugar may be consumed in the diet. Think about any refined and processed foods that may be in your diet as these are often high in sugar. This can be achieved through a low carbohydrate diet. Read Also: Insulin Glargine 300 Units Ml The Ups And Downs Of Blood Sugar Everyone experiences moderate fluctuations in their blood sugar levels. The normal blood glucose range in healthy individuals is between 70 and 125 mg/dl. During times of prolonged physical activity, the glucose level can dip below 50 mg/dl. After carbohydrate-rich meals, it can soar to over 180. That’s normal, according to Dr. Edward Horton of the Joslin Diabetes Center. However, when blood sugar levels remain low or high, symptoms start to appear. - Everyone experiences moderate fluctuations in their blood sugar levels. - During times of prolonged physical activity, the glucose level can dip below 50 mg/dl. Too High Blood Sugar Condition Diabetic Hyperosmolar Syndrome Indiabetics, keeping blood sugar level as normal as possible will be a key partto control the disease and prevent its complications. So its very important tounderstand what the level means! Ifyoure diabetic, ask your doctor about your blood sugar level targets. Becausethe level targets may have a degree of different interpretation for each case!But in general, blood sugar level targets for people with diabetes are asfollows : Actually,there should be nothing to worry when you have diabetes as long as its managedas well. It could be dangerous when it has caused its complications. Uncontrolleddiabetes may cause a condition called diabetic hyperosmolar syndrome, when thebody has an extreme spike in blood sugar level . Diabetichyperosmolar syndrome is serious condition. It is relatively more common intype 2 diabetes, intensive immediate treatment is necessary! When youhave too high blood sugar level, your body works harder to get rid of theexcess glucose in the bloodstream! In such case, this will usually drive you topass more urine to eliminate the excess through urine! Withoutimmediate proper treatment, diabetic coma could be fatal! This is scary situation,but you can take preventive steps to reduce the risk of this complication yes its preventable! Don’t Miss: Men’s Cotton Diabetic Crew Socks Signs That Your Blood Sugar Levels Are Too High Written by 26 May, 2022 Blood sugar, or glucose, is the main source of energy for the cells in the body. This type of sugar is found in flours, honey, carrots, and rice, amongst other foods. While we use need it for daily living, its not good when your blood sugar levels are too high. The specific purpose of this energy is to help you perform important bodily functions, such as digestion. It keeps the heart functioning, the synapses going, and fuels a host of other processes. The sugar found in your blood must be kept between 70 and 110 mg/dL to make the most of its benefits. If it gets too high or low, you may suffer negative health consequences. See Also: Fruits that Can Help Digestion When your blood sugar levels are too high, this condition is called hyperglycemia. It can cause damage to various organs. Even further, when these levels are above 180 mg/dL its diagnosed as diabetes mellitus. Its important to keep this condition under strict medical observation, since it can cause many complications. High Blood Sugar: Causes Complications And How To Lower Blood Sugar Your body breaks down glucose for energy using the insulin produced by the pancreas. This is required for our bodies to function. Illness can have an impact on the way our pancreas functions. Read this to learn how high blood sugar can affect your health. 7 minute read Your body requires energy to function, and this energy comes from food. Specifically, your body breaks down glucose for energy using the insulin produced by the pancreas. Type 1 and type 2 diabetes cause impairment to this breakdown of sugar in the body, causing blood glucose levels to become irregular. When glucose is not broken down into energy, it can build up in the bloodstream and then becomes a health problem. Your pancreas produces insulin, which breaks down glucose. With type 1 diabetes, the cells that produce insulin are mistakenly attacked by your immune system. As a result of this autoimmune condition, blood sugar levels can become dangerously high without intervention. Type 2 diabetes occurs when your body no longer responds to insulin as well as it should and then also causes glucose to accumulate in the blood. Also Check: Type 2 Diabetes Would Be Considered An Prevent Type 2 Diabetes If your test results show you have prediabetes, ask your doctor or nurse if there is a lifestyle change program offered through the CDC-led National Diabetes Prevention Program in your community. You can also search for an online or in-person program. Having prediabetes puts you at greater risk for developing type 2 diabetes, but participating in the program can lower your risk by as much as 58% . Correcting High Blood Sugar Levels With Insulin If you take insulin, one way to reduce blood sugar is to inject insulin. However, be careful as insulin can take 4 hours or longer to be fully absorbed, so you need to make sure you take into account how much insulin you may already have in your body that is yet to be absorbed by the blood. Insulin that is yet to be absorbed by the blood is called active insulin. If you decide to correct with insulin, watch you dont over correct as this can lead to hypoglycemia and can be dangerous, particularly so before bed. Don’t Miss: Is Freshpet Good For Diabetic Dogs What Is The Normal Blood Sugar Level For Adults As we age, our bodies become less able to regulate blood sugar levels as well as they used to. That’s why the ADA recommends that older adults aim for a fasting blood sugar level of less than 100 mg/dL. After eating, it’s ideal that your blood sugar level is below 180 mg/dL. The ADA recommends that most adults with diabetes aim for the following blood sugar goals: - Fasting: Less than 100 mg/dL - Preprandial : 70-130 mg/dL - Postprandial : Less than 180 mg/dL - Bedtime: 100-140 mg/dL If you experience high blood sugar levels or low blood glucose levels compared to this range you should speak to your doctor. You Have Bad Breath And Dry Mouth An unusual smell when you breathe in through your mouth might indicate that something is wrong with the way glucose moves throughout your system. This can cause a buildup in ketone levels within your blood, giving off an unpleasant odor, much like nail polish remover or acetone. Sometimes people mistake this for regular bad breath, but if it happens frequently and seems to have no other cause, it could be a sign that your insulin balance is out of whack, so make sure to see a doctor as soon as possible if you notice this happening. Gum disease is also a frequent problem for people with diabetes, so if you notice that your gums are inflamed or swollen, it might be a sign that blood sugar is starting to rise. The dry mouth associated with this problem can lead to the development of cavities and other dental issues, so make sure you’re drinking enough water throughout the day as well as brushing after meals if necessary. Don’t Miss: What Eye Problems Does Diabetes Cause Are High Levels Of Blood Sugar Dangerous Low blood sugar levels begin at 70 mg/dL or less. - People with diabetes who take too much medication or take their usual amount but then eat less or exercise more than usual can develop hypoglycemia. Although much rarer, hypoglycemia may develop in some people without diabetes when they take someone elses medication, have excessive alcohol consumption, or have hepatitis or a rare tumor of the pancreas . - The treatment for hypoglycemia is oral glucose intake (15.0 grams of sugar, for example, 1 tablespoon of sugar, honey, corn syrup, or IV fluids containing glucose. Rechecking your blood sugar levels in about 15 minutes after the treatment is advised. Things To Know About High Blood Sugar - Low high blood sugar is abnormally high blood levels of insulin in the blood. Hyperglycemia is a hallmark sign of diabetes and prediabetes, and diabetes is the most common cause of it. Severely elevated glucose levels can result in a medical emergency like diabetic ketoacidosis or hyperglycemic hyperosmolar nonketotic syndrome . - The primary symptom of hyperglycemia is excessive amounts of sugar in the urine. Other symptoms and signs of high blood sugar levels in the blood are blurred vision, hunger , and headaches. - Other conditions that can cause high blood sugar are pancreatitis, Cushing’s syndrome, unusual hormone-secreting tumors, pancreatic cancer, certain medications, and severe illnesses. - Insulin is the treatment for people with type 1 diabetes, and life-threatening increases in glucose levels. People with type 2 diabetes may be managed with a combination of different oral and injectable medications. Hyperglycemia due to medical conditions other than diabetes is generally treated by treating the underlying condition responsible for elevated glucose. Don’t Miss: Rite Aid Diabetic Test Strips Recommended Target Blood Glucose Level Ranges The NICE recommended target blood glucose levels are stated below for adults with type 1 diabetes, type 2 diabetes and children with type 1 diabetes. In addition, the International Diabetes Federations target ranges for people without diabetes is stated. The table provides general guidance. An individual target set by your healthcare team is the one you should aim for. \|Target Levels\| *The non-diabetic figures are provided for information but are not part of NICE guidelines. What Is Considered A High Blood Sugar Level If you just received a diabetes diagnosis, you may be wondering what blood sugar levels mean and how you should be creating goals based off of your blood glucose tracking. One of the most important things for you to know is what blood sugar levels are and when theyre considered to be high. Learning what steps to take if you find your levels are too high will help you stay safe. Because diabetes is such an individual condition, the best first step is to consult your doctor about what is a healthy range for your blood sugar. Once youve gotten advice from your medical expert, you can begin to modify your lifestyle and continue to do additional research to improve your health and benefit your diabetes management journey. Before researching online, its important to remember that blood sugar levels are an individual, personal reaction to many factors, and can vary while still being within an acceptable range. Generalized numbers are often not a 100% accurate measure of personal health and there may be other factors that are affecting your blood sugar, resulting in confusing numbers when you check. Make sure that you carefully follow the instructions your doctor has created for you. Diabetes can have negative effects if not managed properly. By understanding healthy blood sugar ranges, you can take steps to reduce or avoid added diabetes complications, and better understand what changes in blood sugar may be reflecting about your bodys health.	https://www.diabetesprohelp.com/what-is-high-blood-sugar-levels/
Written on November 28, 2022 by Theresa Vuskovich, DMD. To give you technically accurate, evidence-based information, content published on the Everlywell blog is reviewed by credentialed professionals with expertise in medical and bioscience fields. Table of contents You know exercise has countless health benefits, but do you know how exercise affects blood sugar levels? If you have diabetes, blood sugar levels are the center of your universe. Exercise can have significant effects on your blood sugar during and after exercise. If you are an adult with type 2 diabetes, here's what you need to know about the effect of exercise on blood sugar. If you have diabetes, exercise is beneficial but can also complicate your blood glucose management. Before we discuss how exercise lowers your blood sugar, let's review the basics of type 2 diabetes. Type 2 diabetics have an inadequate supply of insulin, a hormone responsible for transporting glucose (i.e., sugar) from the blood into cells. Having type 2 diabetes results in insulin resistance, meaning your body no longer responds normally to insulin, and your blood sugar levels rise. High sugar levels can affect your health now and in the future. High sugar levels can cause heart disease, blindness, kidney failure, and nerve problems . Now that we have reviewed the basics of type 2 diabetes, let's explore why exercise lowers your blood glucose levels. When you perform an aerobic exercise (i.e., "cardio"), regardless if you have type 2 diabetes, your body uses the fastest glucose source, the sugar in your blood, to power your muscles during exercise. When you perform cardio, your muscles absorb 5x more glucose than at rest, reducing your blood sugar levels . In contrast to aerobic activity, anaerobic activity (e.g., resistance or strength training) can raise your blood glucose levels . This is often called postexercise hyperglycemia. Increased blood sugar levels are most common following high-intensity interval training (HIIT) or resistance exercise . The rise in blood sugars is due to the release of stress hormones (e.g., adrenaline), which causes your liver to release more sugar into the blood. An aerobic cooldown (e.g., walking) is recommended to minimize elevated blood sugar levels . As a result of exercise, your body is more sensitive to insulin levels, which makes it more efficient at removing sugar from the bloodstream [10, 11]. It is unclear exactly why exercise improves insulin sensitivity, but some research studies have found that the improvement in insulin sensitivity is primarily due to changes in the transcription process, a part of the molecular pathway through which genes make proteins [9,13]. As previously mentioned, your blood sugar levels vary depending on the type of physical exercise and exercise intensity. Aerobic exercise tends to lower blood sugar levels, while anaerobic exercise tends to increase blood sugar levels. Let's explore which exercises are aerobic and anaerobic, as well as the activity recommendations from the American Diabetes Association (ADA) [2,5]. The ADA recommends the following exercise regimen for people with type 2 diabetes [2,5]: You can stay motivated and avoid injury if you practice different exercises. Here are the four types of exercises and recommendations from the ADA [5,7]: These guidelines help control type 2 diabetes blood sugar levels, but there are other factors to consider in addition to these guidelines. A healthy diet and moving throughout the day can also help you control your blood sugar [2,5]. Nutritionists often recommend a Mediterranean diet for individuals with type 2 diabetes . Even though regular exercise is recommended for most adults with type 2 diabetes, it is important to consult a healthcare professional to determine your best exercise regimen.[5,12] Before recommending an exercise regimen, your healthcare professional will review the following information : It is important to discuss changes in your exercise regimen with your healthcare provider when one of these factors changes. Now that we have reviewed many of the short-term effects of exercise on blood sugar, let's explore one of the long-term positive effects of exercise on blood sugar levels. Although blood sugar levels may fluctuate briefly after exercise, exercising can also improve your ability to control your blood sugar levels over time. If you have type 2 diabetes, you know about the A1C or HbA1c test. You use this test to determine the amount of glycated hemoglobin (HbA1c) in your blood. HbA1c is the component of your red blood cells (RBCs) that attaches sugar, so the test tells you how many of your RBCs are sprinkled with sugar. The A1C test measures your blood sugar levels over the past 3 months. Knowing your A1C results is important to ensure you avoid the long-term complications of diabetes, such as heart and nerve problems . Exercise is also an important part of controlling the levels of HbA1c. A meta-analysis, a study of multiple trials, found moderate increases in physical activity reduced HbA1c . Overall, exercise improves blood sugar control and diabetes management. Always check with your healthcare provider before beginning a serious exercise routine. Exercising with type 2 diabetes requires knowing your blood sugar levels. Everlywell offers an at-home HbA1c test to help you check your blood sugar levels over the past 3 months. Visit Everlywell's product page to discover more convenient, at-home wellness tests. HbA1c vs. fasting glucose: understanding the similarities and differences Can stress raise blood sugar levels?	https://www.everlywell.com/blog/hba1c/effect-of-exercise-on-blood-sugar/
I Want To... - Research I Want To... Find Research Faculty Enter the last name, specialty or keyword for your search below. - School of Medicine I Want to... Apply for Admission Johns Hopkins Scientists Identify Third Critical Hormone in Type 2 Diabetes - 04/01/2014 Johns Hopkins Scientists Identify Third Critical Hormone in Type 2 Diabetes Release Date: April 1, 2014 Mehboob Hussain, M.D. Fast Facts: - It is well established that two hormones, glucagon and insulin, must work in perfect unison to maintain healthy blood sugar levels in the body. - Type 2 diabetes typically develops when glucagon, which stimulates sugar secretion, and insulin, which stimulates sugar absorption, are off balance. - Now, scientists at Johns Hopkins have discovered a third critical "player" in the development of type 2 diabetes--a hormone called kisspeptitn-1, which apparently carries out commands issued by glucagon and directly interferes with insulin production in the pancreas. - The discovery may prove to be a long-missing link in the understanding of the origins of the disease. - The researchers are currently designing therapies that block kisspeptin-1 from entering the insulin-producing cells of the pancreas. Working with mice and human blood and liver samples, scientists from the Johns Hopkins Children’s Center have identified a previously unsuspected liver hormone as a critical player in the development of type 2 diabetes, a condition that affects nearly 26 million people in the United States and is a leading cause of heart disease and stroke, as well as kidney, nerve and eye damage. Results of the research, to be published April 1 in the journal Cell Metabolism, show that the hormone, kisspeptin 1, or K1 — up until now known for its regulation of puberty and fertility — also slows down the production of insulin, the sugar-regulating hormone secreted by the pancreas, and in doing so fuels the development of type 2 diabetes. The findings provide what researchers consider a missing link in understanding the origins of type 2 diabetes. Two hormones, glucagon and insulin, must work in synchrony to maintain healthy sugar levels in the bloodstream. Secreted when sugar levels drop, glucagon causes the liver to release its strategic reserves of glucose into the bloodstream. When sugar levels rise, insulin acts as an antidote to glucagon, helping the body lower blood sugar by transporting it out of the bloodstream and into organs and tissues as fuel. In type 2 diabetes, pancreatic cells secrete too little or no insulin at all, leading to a dangerous buildup of sugar in the blood. People with type 2 diabetes and those with early forms of the disease known as pre-diabetes have abnormally high levels of the sugar-boosting hormone glucagon even in the presence of insulin and even when the body doesn’t need more sugar. Researchers have long wondered if abnormal glucagon levels somehow affect the insulin-secreting cells of the pancreas. The prevailing wisdom has been that exposure to chronically elevated glucagon and blood sugar levels take a gradual toll on the pancreas, and its overworked beta cells slowly decrease insulin output until they stop making insulin altogether. The new findings, however, show that the pancreatic cells don’t just get tired; their function is directly suppressed by K1. Specifically, the researchers found that the liver, stimulated by high levels of glucagon, releases K1 into the bloodstream. K1 then homes in on pancreatic beta cells, where it suppresses insulin secretion. “Our findings suggest that glucagon issues the command, but K1 carries out the orders, and in doing, so it appears to be the very cause of the declining insulin secretion seen in type 2 diabetes,” says lead investigator Mehboob Hussain, M.D., an endocrinologist and metabolism expert at the Johns Hopkins Children’s Center. “Glucagon and insulin alone never really made complete sense,” Hussain adds. “There was always something missing and, we feel, kisspeptin 1 is a very good candidate to be that missing part. All our findings point in this direction.” In one set of experiments, the researchers fattened a group of mice by feeding them calorie-rich food. Predictably, the mice developed diabetes, their insulin production declined and K1 levels in their blood shot up, the researchers found. When the investigators chemically altered the livers of the diabetic mice to make them incapable of K1 production, the animals’ insulin levels returned to healthy ranges. Next, the researchers engineered mice whose pancreatic cells were lacking receptors for K1. Those mice, even when they feasted on high-fat food, maintained healthy insulin production and blood sugar levels. In other words, the missing K1 receptor rendered these animals’ insulin-secreting cells immune to the effects of K1. Moreover, the researchers found, K1 levels were notably increased in blood and liver samples obtained from people with type 2 diabetes. Additionally, when researchers exposed mouse pancreatic cells to K1-rich blood plasma obtained from people with type 2 diabetes, the insulin production of these cells dropped. The identification of K1 as a key player in diabetes, the research team says, offers a possible new treatment target that can lead to the development of drugs that restore the function of the insulin-secreting cells. Currently, diabetes therapy is based on injecting synthetic insulin to maintain blood sugar levels. However, restoring natural insulin production could, in theory, cure diabetes, instead of simply mitigating its symptoms. The Johns Hopkins team says it has already identified a hormone-like substance that blocks the K1 receptor in the pancreatic cells of mice. The investigators will next study whether this receptor-blocker can restore the function of human pancreatic cells. The identification of K1 also makes evolutionary sense, Hussain adds, and may explain why diabetes is an ancient disease common across species. Hussain and colleagues believe that K1 may have evolved to play an insulin-blunting role and prevent sharp falls in sugar levels during fight-or-flight situations. “Sugar provides critical fuel when an animal enters combat or is trying to run away from a predator,” Hussain says. “The high levels of insulin after a meal can cause dangerously low levels of blood sugar, which would render the animal weak and vulnerable. So our theory is that K1 is a defense mechanism that halts the sugar-reducing effects of insulin in such life-and-death situations.” Type 2 diabetes, which is closely associated with high-fat and high-sugar diets and sedentary lifestyles, is the predominant form of the disease, accounting for more than 90 percent of all diabetes cases. While previously seen mostly in middle-aged and older adults, type 2 diabetes is now increasingly common in younger people and children, a phenomenon fueled by growing obesity rates, experts say. The study was funded by the National Institute of Diabetes and Digestive and Kidney Diseases, by the National Institute of Child Health and Human Development and by the National Institute of Arthritis and Musculoskeletal and Skin Diseases (grants DK090816, DK084949, DK079637, DK095140, HD066432, HD068777 and AR057759). Additional funding was provided by the Johns Hopkins Dr. Mohan Swami Institute for International Medical Education. Other Johns Hopkins investigators on the study included Woo-Jin Song, Prosenjit Mondal, Andrew Wolfe, Rachel Stamateris, Benny W.T. Ong, Owen C. Lim, Kil S. Yang, Sally Radovick and Horacio J. Novaira. Researchers from other institutions included Emily A. Farber, Charles R. Farber and Stephen Turner, of the School of Medicine at the University of Virginia, and Laura Alonso of the University of Massachusetts Medical School. For the Media Contacts: Ekaterina Pesheva 410-502-9433 [email protected] Helen Jones 410-502-9422 [email protected] Downloads: Photo/video files to accompany this story are available for download. We are providing this photo/video with the understanding that it will be used only to help illustrate the story in the corresponding news release. Please also find appropriate credit information with the files. If there is anything else you need, please email us at [email protected]. Thank you.	https://www.hopkinsmedicine.org/news/media/releases/johns_hopkins_scientists_identify_third_critical_hormone_in_type_2_diabetes
Diabetes mellitus, commonly known as diabetes, is a metabolic disease that causes high blood sugar. The hormone insulin moves sugar from the blood into your cells to be stored or used for energy. With diabetes, your body either doesn’t make enough insulin or can’t effectively use the insulin it does make. Untreated high blood sugar from diabetes can damage your nerves, eyes, kidneys, and other organs. Our formulation is effective against the following types : - Type 2 diabetes when your body becomes resistant to insulin, and sugar builds up in your blood. - Prediabetes when your blood sugar is higher than normal, but it’s not high enough for a diagnosis of type 2 diabetes. - Gestational diabetes is high blood sugar during pregnancy. Insulin-blocking hormones produced by the placenta cause this type of diabetes.	https://kkproductsayurvedic.com/diabetes-medicine/
Machine learning consultancy Digamma.ai and the U.S. Geological Survey announce a new partnership to use machine learning to advance natural hazards research. Digamma.ai is proud to announce a partnership with the U.S. Geological Survey to apply state-of-the-art machine learning algorithms towards the study of landslides and other natural hazards. “The purpose of this project is to produce algorithms that are capable of automatically recognizing hazardous landscape changes through the interpretation of remote sensing, LiDAR, drone imagery, and satellite imagery data,” Vadim Zaliva, Digamma.ai’s CEO, explained. “The algorithms will be trained to identify slow-moving landslides that are active over many years, rapid landslides that result from storms or earthquakes, or landscape deformation associated with earthquakes.” The objective of the partnership is to better understand landscape responses to earthquakes and large storms in addition to finding the location of landslides that are active over long periods of time. This knowledge will assist in response to earthquakes that cause widespread landslides. Historically, mapping these hazards involves hours spent combing over aerial photographs and digital terrain models, interpreting areas affected by landslides and digitizing the outlines of landslide features. However, this repetitive and time-consuming process takes up time USGS investigators could be spending on field investigations, data analysis, experimental design, and other key tasks.	http://aithority.com/machine-learning/digamma-ai-and-the-u-s-geological-survey-announce-machine-learning-research-partnership/
The Global Facility for Disaster Reduction and Recovery (GFDRR), a grant-funding mechanism managed by the World Bank, has released a new report that analyzes how machine learning (ML) can be applied in disaster risk management (DRM) projects. The publication provides a concise, demystifying reference that readers - from project managers to data scientists - can easily use. It includes key definitions, case studies and practical considerations for the use of machine learning in disaster risk management. Machine Learning at a glance A machine learning (ML) algorithm is a type of computer program that learns to perform specific tasks based on various data inputs or rules provided by its designer. In the context of DRM, machine learning applies predominantly to methods used in the classification or categorization of remotely sensed satellite, aerial, drone and even street-level imagery by capitalizing on a large body of work on image recognition and classification. This approach enables actions to be taken on the information gathered from the data; sometimes in near real time, for instance in the form of suggested web search results, and sometimes with longer-term human input. Planning and implementation tips The document also contains a section dedicated to giving the readers a brief overview of the steps to follow to set up an ML project. It describes how to prepare the inputs for the problem and evaluate the quality of the ML algorithm results and also goes into required project resources in more detail. There are several issues that need to be considered when planning an ML project. Following a step-by-step learning approach, the report divides these into subsections and explains them one at a time: - selecting suitable input data - evaluating model output - expertise, time, infrastructure, and costs - ethics: privacy and bias considerations The implementation and use of ML algorithms apply to the Digital Development and the Open Data for Resilience principles, which promote open innovation through the use of open standards, open data, and open-source software. All over the process of ML projects, several aspects can benefit from being documented and shared: the training data, the algorithm, the methodology, and the output data. Practical case studies Finally, the report shows evidence-driven case studies, selected as they provide an overview of how ML can support various aspects of DRM, from the prevention of social and physical exposure and vulnerability of communities to risk and post-disaster mapping, as well as damage prediction and assessment. All the cases study showcased in the document represent different geographical regions, various input datasets, units of analysis and various ML algorithms. An interesting example is the Guatemala City case study, which shows how urban area physical exposure and vulnerability can be addressed and reduced through technology. Generally, detecting seismic vulnerability in urban areas is critical. Identifying high-risk buildings can save lives and help prioritize retrofitting investments. However, sending large teams of surveyors into the field is time-consuming and expensive. Instead, this case study leverages imagery from satellites and drones, and street-view images from 360° street cameras to identify homes that are a high risk for collapse during an earthquake. Digital elevation models from satellite imagery helped identify buildings located on steep slopes, which are at higher risk for mudslides. A combination of satellite and drone imagery helped identify rooftop material, suggesting underlying construction techniques that are more vulnerable to seismic activities. The availability of street-view imagery is unique, as it can be used to identify soft-story constructions which are vulnerable to seismic activities. This case study is a good example of how different physical factors of vulnerability can be extracted from various data sources and the unique capabilities of street-view imagery. The deep learning algorithm trained on the street-view imagery caught 85% of the buildings which were flagged by expert engineers as vulnerable. ML projects can also support activity such as risk mapping and damage prediction. NASA developed the Landslide Hazard Assessment for Situational Awareness (LHASA) model in order to provide landslide hazard data in real time. They trained an algorithm that links landslide susceptibility factors (slope, geology, road networks, fault zones, and forest loss) to historical landslide events. This model is applied to precipitation data from the Global Precipitation Measurement (GPM) mission at three-hour intervals. When rainfall for a given region is extremely high for that region, the landslide susceptibility map is consulted. If a region is also classified as being highly susceptible to a landslide, a nowcast warning is issued. Thus, LHASA provides near-real-time situational awareness of landslide risk on a global scale, presented in an open-source framework. Another relevant use of open-source and space-based data for post-disaster event mapping and damage assessment is the project developed in 2017 by Orbital Insight, which uses Synthetic Aperture Radar (SAR) as an input for an image classification algorithm that allows the categorization of at-risk areas for flooding in Houston, Texas. A combination of optical and SAR imagery (which is capable of “looking” through clouds) helped identify the flooding extent. Digital elevation models (DEMs) allowed natural watersheds to be delimited, and crowdsourced geotagged images were used to confirm the flood extents. All the advancements made in the applications of the learning machine can and are being used to solve bigger issues confronting societies worldwide, from making the most of our land to preparing for and recovering from crises. Read full story: Publishing Date: Country/Region:	https://un-spider.org/news-and-events/news/world-bank-releases-new-practical-guide-machine-learning-disaster-risk
WHAT IS ARTIFICIAL INTELLIGENCE Artificial intelligence (AI) is, as its name suggests, a form of intelligence that mimics the natural, human thought processes, but is displayed by machines, particularly by computer systems. Expressions of this intelligence are, for example, learning, problem solving, & self-correction. Machine learning is an application of AI and refers to a computer’s ability to learn without being explicitly programmed. Deep learning is a class of machine learning algorithms, focusing on processing (big) data to ‘learn’ to identify complex patterns automatically. WHO IS IT FOR AI has a great potential to assist humans in many tasks, both simple and challenging ones. Its applications can, and already are serving, healthcare, transportation, & finance. WHY IS IT NEEDED At 510, we are building up toward using AI to help with disaster preparedness, early warning early action and response. WHAT ARE WE DOING We nowadays have access to multiple digital sources and tools that can inform on what’s happening at a particular location. For example, we can use social media (Facebook, Twitter), websites, maps, satellite images and collaborative maps such as OSM to focus on a specific area. We have been using AI models for the following purposes: 1. To get a better image of the situation on the ground Timeliness is of utmost importance during a disaster. In the event of a disaster or crises an AI model can assist us in two ways: - To identify which buildings are affected - To assess physical damage of those buildings 2. To make better, more informed decisions, faster AI models can return an assessment of damage after a disaster, identifying areas with no visible damage, and areas with partial, complete or extensive damage. We share this data with humanitarian workers on the ground so that they can better organize and prioritize their response. 3. To predict disasters and intervene before the damage is done Data from previous disasters can be used to create machine learning models to predict damage during future such events. Thus, it becomes possible to prepare and reduce the impact of a disaster. We use text mining and natural language processing techniques to extract impact data from humanitarian documents. Within all these categories, any use of data must respect the ethical and practical standards we set in our data responsibility policy. WHAT ELSE CAN WE DO As part of our innovation efforts, we see further applications for AI, such as: - Automated information retrieval from social media - Automated damage assessment from mobile pictures - Automated damage assessment from satellite images - Building material classification from street view images WHEN & WHERE WE STARTED We have been working with AI since 2016, when we began developing a damage assessment tool using deep learning. The blog posts below pertain AI applications so far:	https://www.510.global/510-our-use-of-ai/
Remote sensing and machine learning techniques for improved nearshore wave prediction Scientific background and motivation: About 40% of the world’s population lives within 100 km from the coast. Present-day storm surge (often associated with large waves), aggravated by predicted sea level rise and driven by changes in extreme wave climate due to global warming are serious hazards for coastal communities, ecosystems and infrastructure. To manage and mitigate current and future coastal hazards the characterisation of wave properties in the nearshore region, including the surf and shoaling zones, is essential. A vital part of the prediction and mitigation of coastal hazards are accurate observations of nearshore wave dynamics, however most ‘traditional’ oceanographic techniques require extensive resources to deploy, maintain and analyse. Additionally, the complex nature of nearshore hydrodynamics can be difficult to measure reliably with many in situ techniques, and most available measurements (e.g., wave buoys) are located further offshore. Satellite remote sensing represents an exciting opportunity to leverage internationally funded sensor platforms to understand the global coastal ocean at the spatial and temporal scales necessary to meet the challenge of understanding our changing environment. However, these sensor platforms are not without limitations, being restricted by e.g., local weather, flight orbits and revisit time. Innovative recording and data processing methodologies have arisen in the past decades, such as video imagery of nearshore wave patterns and machine learning [2,3] that present the opportunity to further improve and utilise satellite remote sensing of nearshore waves through hybrid data assimilation techniques: the blending of large amounts of data from multiple sources. The combination of these approaches provides the potential for a powerful tool to produce better estimates of nearshore wave variables, which might be otherwise difficult to monitor and predict. Aim and objectives of the PhD: This PhD will develop a methodology to accurately estimate nearshore wave conditions from available offshore observations; combining in situ measurements, satellite imagery and altimetry data, numerical modelling and potentially shore-based optical imagery in order to improve nearshore wave monitoring and forecasting. The PhD will help reduce uncertainty in the operational prediction of wave conditions and in future wave climate projections. The project will answer the following research questions: - How can remote sensing be combined with in situ measurements and model data to predict nearshore wave parameters accurately and at high resolution using artificial intelligence? - What can this new method tell us about the effects of different marine conditions on nearshore wave transformation? Methodology: The project will develop a methodology to estimate nearshore wave parameters at high resolution from offshore records [4,5] and satellite data , using machine learning techniques , and considering available outputs from numerical models [8,9]. The case study area will be Martinique, an ecologically diverse French island of the Eastern Caribbean, which is exposed to powerful Atlantic swell and hurricane hazard . Convolutional neural networks will be applied to link multispectral satellite imagery (e.g., Sentinel-2 or Landsat 8, used to extract wavelength, direction and wave height estimates , with potential for 2D mapping) and satellite altimetry data (e.g., CFOSAT or Sentinel-1, providing quality wave spectrum products, but only along-track). The results will be related to model outputs and offshore in situ data using other machine learning techniques (e.g., random forests or artificial neural networks for regression) to produce predictions of nearshore wave parameters. Local video imagery from Basse-Pointe (northern Atlantic coast) may be used at later stages of the project to validate the methods and contribute to increased resolution of the final product. The student will be trained on the use and interpretation of in situ and satellite data, numerical model outputs, and machine learning techniques.	https://eo-cdt.org/projects/remote-sensing-and-machine-learning-techniques-for-improved-nearshore-wave-prediction/
FOR IMMEDIATE RELEASE... Vancouver, British Columbia - Indico Resources Ltd. ("Indico" or the "Company") (TSX-V: IDI) is pleased to announce that it has received positive results from its initial exploration program at the Ocaña project, located in the Southern Peru Porphyry Belt, Peru. Mapping has identified two significant areas of outcropping porphyry oxidized copper mineralization with disseminated copper sulphides (chalcopyrite) noted locally. Molybdenite veining, common associated with mineralized porphyry systems, has also been observed as veins. Geochemical analysis from initial Talus Fines sampling has highlighted a large area of copper, gold and molybdenum anomalies over an area measuring approximately 4 kilometres by 2 kilometres. These anomalies are coincident with an area of extensive quartz stockwork porphyry host lithology and associated permissive alteration. Exploration completed in the past three months includes a ground geophysical (magnetic) survey, detailed structural and alteration mapping, geochemical surveys (talus fines, rocks and trenching) and interpretation of satellite imagery. Two targets are essentially drill-ready with drilling planned for Q2 2011, subject to receipt of applicable permits and permissions. The Ocaña Porphyry Project is located on the northern extension of the Southern Peru Porphyry Belt, 80 kilometres north of the Zafranal porphyry discovery. Positive Geochemistry Following detailed geochemical orientation on site, talus fines were identified as the most suitable method to rapidly identify reliable surface anomalies. Results in the core target area are very positive indicating two distinct porphyry targets, which are essentially drill-ready. Copper anomalies range from 35 ppm to 1187 ppm, which is highly anomalous despite the fact that copper would normally be leached at surface in this environment (Figure 1A). Molybdenum (Moly) ranges from 0.7 ppm to 46 ppm (Figure 1B) and gold ranges from below detection to 0.12 g/t (Figure 1C). Positive results are clustered around the Jimena porphyry target in the central portion of the property and the Waka Waka porphyry target to the east. In both cases, the interpretation of a mineralized porphyry system is strongly supported by altered and mineralized rock. Satellite Imagery An interpretation of satellite imagery has been completed to identify areas of most intense clay alteration, typically associated with large porphyry systems. Two areas of anomalies have been identified, coincident with the Jimena and Waka Waka porphyry targets. The existence of continuous porphyry alteration between the targets at depth cannot be ruled out since considerable scree-type cover is observed at surface and would obscure such anomalies. Talus Fines Copper Anomalies at Surface Talus Fines Molybdenum Anomalies at Surface Talus Fines Gold Anomalies at Surface Geological Mapping Geological mapping throughout the 110 square kilometre property has identified multiple intrusive events as would typically be expected in a large porphyry system A schematic cross section is included to explain the pattern of lithology and alteration observed at surface and to provide context for potentially a mineralized porphyry system at depth. The cross section provides a conservative interpretation, indicating two separate porphyry bodies at depth. Drilling, in addition to testing the two porphyry centres observed at surface, will investigate the potential continuity of mineralization at depth and laterally between the targets. Qualified Person EurGeol Keith J. Henderson, P.Geo., Indico's Chief Scientific Officer, a Director, and a qualified person as defined by National Instrument 43-101, has reviewed the scientific and technical information that forms the basis for this news release. Mr. Henderson is not independent of the Company as he is an officer and a shareholder. Stock Options The Company also announces that, pursuant to its 2004 Incentive Stock Option Plan, it has granted incentive stock options to directors, officers, employees and consultants of the Company to purchase up to an aggregate of 1,275,000 common shares in the capital stock of the Company. The options are exercisable on or before May 7, 2012 at a price of $0.53 per share. About Indico Resources Ltd. Indico Resources Ltd. is a Canadian exploration company focussed on porphyry copper exploration in South America. The Ocaña Porphyry Project is the Company's primary exploration project and is currently the main focus of exploration activities. In addition, the Company has reviewed six additional porphyry exploration projects and is in negotiation to acquire interests in additional porphyry exploration projects. The companies senior technical staff have a cumulative 40 years of porphyry exploration and resource definition experience. Management feels it is well qualified and well financed to medium medium-term corporate goals. For further details on the Company, readers are referred to the Canadian regulatory filing on SEDAR at www.sedar.com. ON BEHALF OF THE BOARD OF DIRECTORS INDICO RESOURCES LTD. "Gary Freeman" Gary Freeman, President & CEO Neither TSX Venture Exchange nor its Regulation Services Provider (as that term is defined in the policies of the TSX Venture Exchange) accepts responsibility for the adequacy or accuracy of this release. Cautionary Statement This press release contains "forward-looking statements" within the meaning of the United States Private Securities Litigation Reform Act of 1995 and "forward looking information" within the meaning of the British Columbia Securities Act and the Alberta Securities Act. Generally, the words "expect", "intend", "estimate", "will" and similar expressions identify forward-looking information. By their very nature, forward-looking statements are subject to known and unknown risks and uncertainties that may cause our actual results, performance or achievements, or that of our industry, to differ materially from those expressed or implied in any of our forward looking information. Statements in this press release regarding Indico's business or proposed business, which are not historical facts are forward-looking information that involve risks and uncertainties, such as estimates and statements that describe Indico's future plans, objectives or goals, including words to the effect that Indico or management expects a stated condition or result to occur. Since forward-looking statements address events and conditions, by their very nature, they involve inherent risks and uncertainties. Actual results in each case could differ materially from those currently anticipated in such statements. Investors are cautioned not to place undue reliance on forward-looking statements, which speak only as of the date they are made. All of the Company's Canadian public disclosure filings may be accessed via www.sedar.com and readers are urged to review these materials, including the technical reports filed with respect to the Company's mineral properties. The foregoing commentary is based on the beliefs, expectations and opinions of management on the date the statements are made. The Company disclaims any intention or obligation to update or revise forward-looking information, whether as a result of new information, future events or otherwise. You can view the Next News Releases item: Thu May 19, 2011, Indico Resources Joins OTCQX You can view the Previous News Releases item: Thu Dec 2, 2010, Indico Resources Closes $4,000,000 Private Placement, provides Update on Ocaña Property Option and Appoints New Director You can return to the main News Releases page, or press the Back button on your browser.	http://www.indicoresources.com/s/NewsReleases.asp?ReportID=454116
Data Science is a field of study that involves the collection, analysis, and interpretation of data. It is used in various fields, such as business and engineering. This article discusses the importance of data preparation in Data Science. Why Is Data Preparation Important In Data Science? Data preparation is a critical part of data science and ensures the data is ready to be analyzed. The analysis can be invaluable without proper data pre-processing, and the results may be incorrect. Some of the critical tasks involved in data preparation are cleaning and organizing the data, transforming it into a form that is easy to understand and work with, filling in missing values, and determining the size and structure of the data set. These tasks help ensure that the data is ready for analysis and that any errors in its collection or processing will not significantly impact the results. By taking these steps before beginning an analysis, we can ensure that our data is reliable and valuable for our purposes. The results of an analysis are more likely to be accurate and insightful if the data is prepared appropriately. How To Prepare Your Data For Data Science? When you’re ready to start data science, the first step is typically data preparation. Data preparation can involve various tasks, from cleaning and organizing your data to transforming it into the format you need. If you’re starting, it’s important to remember that data preparation isn’t a one-time event. Instead, it’s a continuous process that you should continue throughout your data science journey. Here are some tips on how to prepare your data for data science: 1. Start By Cleaning And Organizing Your Data: This is probably the most critical step in data preparation because it will help you get the most out of your analysis. Data helps you clean and organize your data automatically. It also provides valuable data analysis features, such as sentiment analysis and classification. 2. Transform Your Raw Data Into The Format You Need: This is often done through transformations such as indexing and normalizing your data. Indexing allows you to quickly find particular values in your dataset, while normalization ensures that each column will have the same number of values. 3. Manipulate Data: Manipulate your data so a machine learning algorithm can analyze it. This step is often done through transformations such as reshaping and data altering. 4. Model Data: Model your data using an appropriate machine learning algorithm. The best way to do this is through a training set where you sample your dataset and run the proper model on the sample data to test how well it performs on the whole dataset (e.g., a regression model). In this step, you’ve trained a model that uses your raw data to predict the class labels of each item in the training set with high accuracy. 5. Test The Data: Test your model on new datasets to measure how accurate it is at predicting (e.g., predicting ‘iPhone’ from the data of the new dataset). In this step, you’ve made your model more general by setting more parameters to a value. You can then use it to make predictions on new datasets. From these predictions, you can see how well the model performs and if any areas need improvement with your model or its parameters to perform better on other datasets. What Does The World’s Largest Database Of 100 Million Images Teach Us? One of the most important aspects of data science is preparing the data for analysis. This involves cleaning the data, transforming it into a format that machine learning algorithms can use, and understanding the patterns that exist in the data. The world’s largest database of 100 million images has been used to study the universe. The database contains images of galaxies, stars, and planets taken by the Hubble Space Telescope. By studying these images, researchers understood how galaxies are formed, how stars are born, and how planets form. They have also been able to identify new planets and galaxies. By cleaning the data, transforming it into a format that machine learning algorithms can use, and understanding the patterns that exist in the data, researchers can study the universe more thoroughly. Models of the universe have been able to make predictions about discoveries in the future. Artificial intelligence is a branch of computer science that allows programs to perform tasks automatically without human intelligence, such as reading and writing. AI also helps in discovering patterns in large data sets. One area of research that involves artificial intelligence is machine learning. The machine learns from the processing of data. Machine learning involves using algorithms and mathematical formulas to process data. As it processes more and more data, it becomes better at making predictions based on previous experiences with similar data. Machine learning can be used for a wide range of applications, including predicting stock prices or finding patterns in images. Machine learning can be used to solve problems in both scientific fields and industry. For example, machine learning can predict which patient is more likely to relapse based on multiple criteria. Machine learning can also analyze large amounts of data for scientific research. It has been used in the pharmaceutical industry to analyze data for a long time. The primary use is an aide for quality control and analysis of drug development processes. Machines can be trained with massive amounts of data about human drug reactions before they’re tested. Conclusion Data science is all about using data to make predictions and improve outcomes. However, without the proper data preparation, this process can be challenging and even impossible. In this article, we have outlined some of the critical steps that you need to take to prepare your data for analysis. By following these steps, you can get the most out of your data and help yourself make better predictions. We at Onpassive Digital are work towards making Data Analytics and Big Data available to all the businesses and help them in achieving their maximum reach and realizing goals.	https://onpassive.digital/the-importance-of-data-preparation-in-data-science/
Machine learning algorithm taps satellite imagery to better map impoverished regions According to the World Bank Group, almost 900 million people around the world live on less than US$1.90 a day. Although such an enormous global issue, there's actually not that much concrete data available on the exact location of the world's impoverished zones. Stanford University researchers have come up with a method that could start to fill in some of the blanks, feeding satellite imagery into a machine learning algorithm to identify poverty-stricken areas across the African continent. For many impoverished regions around the world, such as parts of Africa, there is only very limited, local-level information available on poverty, collected via on-the-ground surveys. While this method is time-consuming, expensive and results in limited data, high-resolution satellite imagery of such regions is collected almost constantly and possibly presents a more efficient way forward. While satellite imagery in its raw form doesn't readily describe poverty distribution, the researchers came up with a way to use it for this purpose. They determined that daylight imagery alone wouldn't provide enough useful information, but by using a specially-designed machine learning algorithm, a mixture of night and daylight images could be used to paint a clearer picture. The night imagery forms a huge part of the equation, because brighter areas tend to represent more economically prosperous regions. By combining this information with images taken during daylight, the machine learning system was able to identify key features associated with economic development, such as roads and urban areas. The researchers were then able to use this information to accurately predict the wealth of an area, as measured in already available survey data. "Without being told what to look for, our machine learning algorithm learned to pick out of the imagery many things that are easily recognizable to humans, things like roads, urban areas and farmland," says the study's lead author, Neal Jean. The researchers used this method to analyze satellite data covering Uganda, Nigeria, Tanzania, Nigeria, Rwanda and Malawi and say that it did a good job of predicting poverty distribution and outperformed existing approaches. "Our paper demonstrates the power of machine learning in this context," says study co-author Stefano Ermon. "And since it's cheap and scalable – requiring only satellite images – it could be used to map poverty around the world in a very low-cost way." The team published its work online in the journal Science. An overview of the Stanford University project can be seen in the video below.	https://newatlas.com/stanford-satellite-imagery-poverty/44997/
For the past three years, we, at UN Global Pulse, have been working with UNOSAT to build a software tool that leverages artificial intelligence to identify and count structures from satellite images. From there, we expanded to a web-based toolkit that can be easily adapted to other remote sensing applications and which allows the incorporation of models created by other users. Today, we officially launched the toolkit at the AAAI conference on artificial intelligence in New York. Every day, millions of images are captured from space by an ever-growing number of satellites. In humanitarian crises or conflict areas, accurate and timely satellite image analysis is key to supporting critical operations on the ground. Use cases include monitoring population displacement, settlement mapping, damage assessment, fire detection associated with human rights violations, damage to transportation networks, flood assessment and identifying the direct impact of earthquakes, volcanoes, cyclones and landslides. Until recently, this type of analysis was done by human analysts who spent hours in front of a map manually counting and classifying structures and other elements. There are now some pay-as-you-go services which also offer automated options although these are often directed towards specific use cases, or do not have the mandate to provide information on critical areas relevant to the UN. PulseSatellite will allow our UN colleagues to get the most out of earth imagery by putting artificial intelligence to work. We already have three models loaded into the system – one that allows users to map structures in refugee settlements; a roof density detection model that can be used for example, to infer the type of neighborhood by looking at the size and proximity of its roofs; and a flood mapping model. Down the road, additional models will be developed to look at other phenomena such as deforestation, fires, or damage assessment. Our web-based toolkit combines cutting edge machine learning algorithms with human expertise to extract the most relevant information. One way it does this, is by giving users without specific data science knowledge the means of improving machine learning models through simple training workflows. It also enables interactive collaboration since dispersed teams can work on the same satellite image at the same time. The tool was tested with UN colleagues and we continue working to make it more user-friendly, and to increase the levels of accuracy the automatic counts provide, which depending on the degree of order with which camps are built, can vary from anywhere around 65% to as high as 98%. As our network of users grows, so will the amount and quality of trained models allowing users to share and gain insights from each others’ work. Our plan is to open PulseSatellite up to as many UN agencies and offices as possible, and ultimately, if we are able to build a reliable toolkit, we hope to open-source some of its functionalities. Check out our PulseSatellite microsite. What do we say? “We wanted to build a web-based tool that is tailored to the needs of UN agencies and that is easy to use. The collaborative nature of the system is what hopefully makes it invaluable, both because it allows teams across time zones and geographies to work on the same project, and because it encourages teams to upload and use their own models, as well as share them with others.”Tomaz Logar, data engineer, UN Global Pulse and lead of the project What does our partner say? “PulseSatellite is an exciting example of a system combining AI and human experience to greatly improve the use of satellite imagery in the UN system. By employing artificial intelligence and a great and intuitive interface, the power of satellite imagery is much more accessible to UN colleagues.”Lars Bromley, geospatial specialist, UNOSAT We wish to thank our donors, the Government of The Netherlands and the Government of Sweden, for their continued support in the development of this tool.	https://www.unglobalpulse.org/2020/02/pulsesatellite-a-collaboration-tool-using-human-ai-interaction-to-analyse-satellite-imagery/
The Connected Drone solution helps capture and analyze data from remote, spread out or hazardous environments by leveraging the ADDS platform in order to generate meaningful business insights which enable efficient, safe, and cost-effective operations and service management. The solution takes advantage of cameras and sensors embedded on drones to gather required field data on which Applied Intelligence such as image/video analytics is used. The image/video analytics leverages computer vision and machine learning algorithms that are trained to learn specific patterns/defects or compute data. The algorithms are created and customized to adapt as per the use case/industries. The Computer Vision is a set of highly trained servers with advanced deep learning capacities that detect all instances of a pattern/object/defect in pictures or videos. The workflow to implement analytics in ADDS is made up of two steps that consist of training the algorithm until it reaches an acceptable threshold of precision and processing all new imagery (pictures/videos) in order to detect patterns learned.	https://www.digiplug.com/adds-connected-drone.html
With the constant increase of multiple molecular data from genome-, proteome- transcriptome-wide studies become urgent the development of analytical tools that help scientists and clinician in the interpretation and practical application of these large amount of information. Thus algorithms that can select and combine multiple species of molecules, possibly derived from blood tests, may be of particular relevance for the near future development of translational research. It becomes evident that Artificial Intelligence assumes a fundamental role for the improvement of techniques and analytical methods that will promote the transformation from the actual “generalized” medicine to personalized medicine. In this context, artificial neural networks, which use thousands of connected nodes to interpret data much like neurons in the brain and form the basis of machine learning, can process vast amounts of data and identify biomarker patterns associated with liver disease. In addition, by definition, machine learning is self-improving, thus as more data are put into the system, more its own algorithm is trained to improve its performances.	https://www.fegato.it/eng/in-futuro-potremmo-predire-linsorgenza-delle-malattie-croniche-di-fegato-tramite-intelligenza-artificiale/
Surficial geology maps contain information on the distribution of surface sediments and landforms (the ground we live upon) and provide insights into their properties, shapes, and origins. The maps accommodate the increasing demand for geological information for infrastructure development, especially in northern Alberta. This work is part of a long-term, regional, surficial mapping program aimed at supporting the mineral exploration and energy industry by providing baseline geological information across Alberta. The program's objective is to complete the surficial geology mapping of Alberta and to complement studies such as thematic mapping, stratigraphic modelling, and reconstructing the long-term landscape evolution of Alberta. A range of technological developments have recently been incorporated into the Surficial Mapping Project that build on traditional airphoto techniques. A major advance has been the heads-up interpretation of high resolution digital elevation models (DEMs) generated from airborne Light Detection and Ranging (LiDAR) data. LiDAR DEMs are becoming increasingly available in Alberta. This technique offers several advantages over previously used airphoto-based methods because - it can penetrate the vegetation canopy to reveal the shape of the bare-earth surface, - the imagery can highlight subtle landforms by varying simulated sun directions in a process called hill shading, - the vertical exaggeration can be varied in hill-shaded, 3-D perspective, and stereographic views, and - it can be used with digital orthophoto drapes or satellite imagery to analyze both vegetation patterns and small-scale relief. Multiple laser pulses reflect from the vegetation and the underlying bare-earth surface. The final return generates the ground surface elevation beneath the vegetation. Recently published surficial geology maps are based on this new mapping technique that allows the geologist to map from multiple layers of remote sensing information to highlight different characteristics of the sediments and their associated landforms. Even in areas in dense vegetation, LiDAR’s ability to detect the land-surface elevation enables the geologist to ‘see through’ the forest canopy and identify landforms that are not visible using traditional methods.	https://ags.aer.ca/research-initiatives/surficial-mapping-program
Community health systems operating in remote areas require accurate information about where people live to efficiently provide services across large regions. We sought to determine whether a machine learning analyses of satellite imagery can be used to map remote communities to facilitate service delivery and planning. This article was published in the following journal. Name: Journal of the American Medical Informatics Association : JAMIA ISSN: 1527-974X Pages: Automated tree detection from 3D lidar images using image processing and machine learning. Trees in 3D images obtained from lidar were automatically extracted in the presence of other objects that were not trees. We proposed a method combining 3D image processing and machine learning techni... Viable and necrotic tumor assessment from whole slide images of osteosarcoma using machine-learning and deep-learning models. Pathological estimation of tumor necrosis after chemotherapy is essential for patients with osteosarcoma. This study reports the first fully automated tool to assess viable and necrotic tumor in osteo... Self-supervised learning for medical image analysis using image context restoration. Machine learning, particularly deep learning has boosted medical image analysis over the past years. Training a good model based on deep learning requires large amount of labelled data. However, it is... Dynamic multi-outcome prediction after injury: Applying adaptive machine learning for precision medicine in trauma. Machine learning techniques have demonstrated superior discrimination compared to conventional statistical approaches in predicting trauma death. The objective of this study is to evaluate whether mac... Machine learning models can detect aneurysm rupture and identify clinical features associated with rupture. Machine learning (ML) has been increasingly used in medicine and neurosurgery. We sought to determine whether ML models can distinguish ruptured from unruptured aneurysms and identify features associa... Improving Cancer Foci Detection in Prostate Cancer Using Multiparametric MRI/MRS The investigators' goal is to develop a non-selective and non-invasive procedure to identify aggressive tumors and simultaneously identify their exact location in Prostate cancer patients ... Machine Learning From Fetal Flow Waveforms to Predict Adverse Perinatal Outcomes The aim of this study is to get a proof of concept for using a computational model of fetal haemodynamics, combined with machine learning based on Doppler patterns of the fetal cardiovascu... Heuristics, Algorithms and Machine Learning: Evaluation & Testing in Radiation Therapy The Hamlet.rt study is a prospective data collection and patient questionnaire study for patients undergoing image-guided radiotherapy with curative intent. The aim of the study is to use... Artificial Intelligence/Machine Learning Modeling on Time to Palliative Care Review in an Inpatient Hospital Population Investigators are testing whether machine learning prediction models integrated into a health care model will accurately identify participants who may benefit from a comprehensive review b... Machine Learning in Myeloma Response Diffusion-weighted Whole Body Magnetic Resonance Imaging (WB-MRI) is a new technique that builds on existing Magnetic Resonance Imaging (MRI) technology. It uses the movement of water mole... Satellite Imagery Composition of images of EARTH or other planets from data collected during SPACE FLIGHT by remote sensing instruments onboard SPACECRAFT. The satellite sensor systems measure and record absorbed, emitted, or reflected energy across the spectra, as well as global position and time. Unsupervised Machine Learning A MACHINE LEARNING paradigm used to make predictions about future instances based on a given set of unlabeled paired input-output training (sample) data. Supervised Machine Learning A MACHINE LEARNING paradigm used to make predictions about future instances based on a given set of labeled paired input-output training (sample) data. Support Vector Machine SUPERVISED MACHINE LEARNING algorithm which learns to assign labels to objects from a set of training examples. Examples are learning to recognize fraudulent credit card activity by examining hundreds or thousands of fraudulent and non-fraudulent credit card activity, or learning to make disease diagnosis or prognosis based on automatic classification of microarray gene expression profiles drawn from hundreds or thousands of samples. Machine Learning A type of ARTIFICIAL INTELLIGENCE that enable COMPUTERS to independently initiate and execute LEARNING when exposed to new data.	https://www.bioportfolio.com/resources/pmarticle/2451712/Satellite-images-and-machine-learning-can-identify-remote-communities-to-facilitate-access.html
Different types of neural network architecture encode different kinds of biases. For example, convolutional neural networks perform local, translation-invariant operations and recurrent neural networks operate on sequential data. One can use these biases in randomly initialized networks as a basis for interesting computations. This is on of the motivation for reservoir computing with echo-state networks, which uses fixed random recurrent neural network and a simple trainable linear transformation to perform complex computations. The intuition behind this is model is that interesting computations may be happening within the random RNN (and they are probably increasingly likely with bigger RNN). The linear layer can select useful computations and filter out the rest to give a result. This paper invastigates something similar to that idea. However, instead of random models they investigate the capacity of pretrained models, more precisely pretrained transformers. In their setup, all the weights of a transformer are frozen except for an input embedding layer, the positional embeddings, the layer norm parameters and a simple output layer. The architecture is shown in the Figure below taken from the paper: This model is tested on a set of tasks: - Bit memory: a task about memorizing bits in a sequence - Bit XOR: a task about being able to XOR bits from two sequences - ListOps: this task is akin to an elementary interpreter which has to perform operations on lists of integers - MNIST: digit classification - CIFAR-10: image classification - CIFAR-10 LRA: a modified version of CIFAR where images are converted to grayscale and fed to the transformer with a token length of 1. - Remote homology detection The paper uses a range of setups to understand which combination of architecture/pretraining/etc. works the best. Comments The part which is most interesting to me is not the main result of that paper but the results from table 3, shown below It is very interesting to see a possible superiority of random transformers over random LSTM, which may also explain why the former is so much better at many tasks. However I couldn’t find information about the number of frozen parameters in that LSTM vs. the tested transformers. Also, because LSTMs don’t have layer normalization or positional embeddings, there have significantly less trainable parameters (80% less for a task like CIFAR according to numbers from the paper). Maybe the authors factored this in by changing the number of parameters in the LSTM model but I couldn’t find that information in the paper. A fairer comparison would have a transformer and LSTM with the same number of parameters. However this would make gradient computation in the LSTM very expensive compared to the transformer — which was partly invented to cope with that problem. I also think that it is nice to find some evidence for a set of primitives being learned by language models and this may pave the way for unsupervised models that keep learning new things and reusing these elementary functions. Bibliography - Kevin Lu, Aditya Grover, Pieter Abbeel, Igor Mordatch. . "Pretrained Transformers as Universal Computation Engines". Arxiv:2103.05247 [cs]. http://arxiv.org/abs/2103.05247.	https://hugocisneros.com/notes/lupretrainedtransformersuniversal2021/
In this fourth post on neural networks we are going to see how neural networks ‘learn’. Or are ‘trained’. In the first post we looked at the anatomy of a neuron. This includes its: inputs, outputs, weights, a bias and an activation function. The second post took a closer look at non-linear activation functions. In the third instalment we saw how we could link neurons in layers, with the activations of neurons in one layer feeding the neurons in the next layer – all the way until an output layer. The output layer provides the results of the task that the network has been trained to learn. Cost Functions explained In the third post we also suggested that a neural network could be regarded as a function. A crazily complicated function. But a function nonetheless. It has a bunch of inputs and a bunch of outputs. Crucially it has a large number of parameters, named weights and biases. It is these weights and biases in each neuron that we can tweak. This tweaking is what allows the neural network to ‘learn’ a pattern or mapping between inputs and outputs. The Neural Network as a Function Let’s get a little bit more formal with that ‘a neural network could be regarded as a function’ statement. Functions can be written out. So let’s write down what a neural network looks like as a function. To make things a little easier to digest let’s not write out the whole thing in one go. Instead let’s look at the function from layer to layer. From the input layer through hidden layers and finally to the output layer. Vector & Matrix Representation Up to this point we’ve been looking at equations for a single neuron. While we can continue to write out the equations in this form it is more legible and compact to use matrix notation. Vector representation of a neural network If we want to calculate the activations in neurons a1, a2, and a3 we will multiply the activations of the neurons in the previous layer (here h1 through h4) with their associated weights. We then add each neuron’s bias and apply the activation function. Here denoted as ‘f’. We can use vectors to represent each layer. The elements in each vector represent the activation of each neuron in that layer. We can also use a vector to represent the biases of every neuron in that layer. The weights that multiply the activations in the previous layer can be held in a matrix. This vector and matrix notation helps us write out the equations in a way that they will generalise to any shape and size of network. Transforming Inputs to Outputs Let’s represent our inputs as a vector x, and our outputs as a vector y. We’ll call our first hidden layer h1.If we have n inputs and m neurons in our first hidden layer, and if all inputs are connected to every neuron in this first layer then we can describe the weights connecting these neurons as an n x m matrix. Let’s call this matrix W1. every one of the neurons in this hidden layer will have a bias, so we will need a vector for that too. We shall call that b1. Finally we will need an activation function to generate the output of each neuron in the hidden layer. We’ll call that f1() First Hidden Layer That means we can write out the function to calculate all of the activations in our first hidden layer h1 as: The activations of the first hidden layer, calculated from the input layer General Hidden Layer If we want to write the function that generates the activations in the ith hidden layer then we can similarly write it as: Determining the activations of one hidden layer from the previous hidden layer Output Layer Until we reach the output layer, when our output vector will be: Calculating the output layer of a Neural Network Where the subscript ‘final’ denotes the final hidden layer. Written this way we have a recursive set of formulae that generate our output from our input. You can see how you can get to the output y from the input x. This vector representation translates easily to software More importantly you can see that you, or someone you know, could write the code in Java or Python or some other language to calculate y from x. This would mean writing some loops for the matrix multiplication, doing some addition of the bias terms and coding the algorithm of whatever activation function that you chose. But hopefully even the most cynical among you can concede that this is a realistic endeavour. Seen in this way I hope you agree that a neural network is just a function that maps a vector of inputs, x into a vector of outputs, y. Training: 'Supervised Learning' In this post we are going to focus on what is called supervised learning. For this we need a bunch of associated input/output pairs. That is to say some output data (e.g. an option price) and some input data (time series of underlying) that gives rise to this particular output. You cannot have too much data. The more associated pairs of data you have the better your results will be. To effectively 'learn' AI needs a lot of training data The only substitute for training data is even more training data. No shortcuts, no free lunch. Get your hands on as much training data as you possibly can. Key to successful AI projects is ensuring you have enough training samples Lucidate’s three laws of training data: 1. You can never have enough training data 2. The only substitute for training data is more training data 3. No matter how much training data you have, get some more Training your neural network; step-by-step So armed with as much training data as you can you are now ready to train your network. This is essentially a brute-force approach. What we will do is nudge the weights and biases in each neuron in the network so that our AI is able to generalise. That is it is able to come up with sensible outputs for sets of inputs that it has not seen in its training data. It really is no more complicated than: 1. Present inputs and measure the accuracy of the associated outputs 2. Nudge the weights and biases a little 3. Repeat until satisfied We will focus on step 1 for the remainder of this post and leave steps 2 and 3 for the next installment. The 'Cost Function' Explained Now let’s talk about this mysterious ‘cost function’. Actually it is not that mysterious. All it is, is a way of measuring how good, or how bad, the network is at predicting the correct output while the network is learning. The cost function heavily penalises the network for really bad outputs. That is to say the network’s outputs that are a long way from the target output in the training set. As in life high costs are bad, and lower costs are good. For high costs – that is to say large deviations from the correct output – we’ll want to nudge our weights and biases more. For low cost – that is to say outputs that are close to the correct answer, we might only want to tweak the weights and biases a little. Training with the 'Forward Pass' So we can start with a complete random insitialisation of our weights and baises in the network. Then we can present our first input, let the network do its multiplication, bias addition and activation thing and let the outputs from one layer feed into the next. This is referred to as a ‘forward pass’. At the end of this forward pass, with randomly initialised weights and biases you would expect a truly awful output. If this is your expectation you will usually not be disappointed. A network with random weights will be terrible at getting anywhere close to the correct answer. You can subtract the output calculated by the network from the output you expect and get an error. This error tells us how far the network was from the correct answer. You will often hear this error referred to as the ‘loss’. Calculate the Error or 'Loss' You can then repeat this for a bunch of other examples in the training set. This is the sequence: 1. Plug in the input data 2. Let the network calculate the output with a forward pass 3. Compare the calculated output to the output you expect As you continue with this you will get some negative errors (underestimates) as well as positive errors (overestimates). You want all errors to be cumulative, that is to say you don’t want positive errors to cancel out negative errors. A common tactic for dealing with this is to square the error, as a square will always be positive. Or just to take the absolute value of the error by ignoring any signs. The Mean Squared Error - 'MSE' Thus a common choice of cost function is the sum of the squared errors, better still the mean of the sum of the squared errors to normalise the answer. This means at the end of a training run, by showing a whole bunch of input & output data to our network and comparing the outputs we calculate to the outputs we expect we can sum the square of the errors, take the average and get a single number: that quantifies how good (a low cost) or how bad (a high cost) our network is. Remember also that our network is a function, mapping inputs to outputs. If we decide that our cost function is the mean of the squared errors – or ‘MSE’ that becomes: The 'Mean Squared Error' ('MSE') Cost Function Where ytrain is the correct output from out training set and ynetwork is what our network calculated. Each batch of training examples is called an 'Epoch' You will hear these training runs referred to as ‘epochs’ and at the end of every epoch we can calculate the cost. We can use this cost and some fancy calculus to nudge our weights and biases to get a better set of outputs on the next epoch. The Cost Function not only measures how accurate the network is, but as we shall see in the next post, it also helps us determine the optimum weights and biases The whole phrase ‘Cost Function’ neatly sums things up. The cost bit measure how good or bad the network is. The function bit means that it can be differentiated. We’ll see in the next post how we use calculus to get the derivatives of the cost function and use this as a mechanism to update our weights and biases. In summary: We’ve seen how we can represent the neural network as a function We’ve applied a cost function to measure how accurately (or otherwise) the network has learned the mapping between inputs and outputs while training We’ve looked at the mean squared error as a good choice of cost function. This ticks a lot of boxes: it ensures that positive and negative errors are cumulative (rather than cancelling each other out) and it normalizes the error by taking an average.	https://www.lucidate.co.uk/post/introduction-to-neural-networks-pt4-cost-functions
The Neural Tangent Kernel is a way of understanding the training performance of Neural Networks by relating them to Kernel methods. Here we overview the results of the paper [Jacot et al. here]. The paper considers a deep neural network with a fixed amount of data and a fixed depth. The weights applied to neurons are initially independent and normally distributed. We take a limit where the width of each layer tends to infinity. The main observations of the paper are the following: - The function represented by a neural network changes according to a kernel when undergoing gradient descent training. This is called the Neural Tangent Kernel (NTK). - Under a random normally distributed initialization, the NTK is random. However, under an infinite width limit, this kernel is non-random and the output of each neuron an independent gaussian distribution with zero mean and a fixed covariance. - In the limit, these weights and thus this kernel will not change during training. This is called “Lazy training”. - In this limiting regime, the neural network parameter converge quickly to a global minimum with weight parameters that are arbitrarily close to the initialized neural network. These results are significant as they give a way of understanding why Neural networks converge to a optimal solution. (Neural networks are know to be highly non-convex objects and so understanding their convergence under training is highly non-trivial.) What the following argument does not (fully) explain is why neural networks are so expressive, why they generalize well to unseen, or why in practice neural networks outperform kernel methods. Why Lazy Training Helps Convergence. We give a short heuristic explanation as to why Lazy training helps us understand the convergence of neural networks. Suppose that the weights of a neural network remain close to the values of their initial weights. That is Now suppose we wish to solve where here , is our data. Notice under stochastic gradient decent evolves (approximately) according to the o.d.e. where here is the empirical distribution of our data. (I.e. is selected uniformly at random from , .) Therefore, by the chain rule, we expect to evolve as The term in curly brackets defines a kernel: This kernel is the Neural Tangent Kernel; it’s the kernel that you get from the tangent of a neural network, . Under the assumption that training is lazy this kernel should be constant i.e. Now if the Kernel defines a positive definate matrix on the data (I.e. if is a positive definite matrix), then for becomes (*) We can analyze the error between the Neural network’s estimate and the data for which becomes Since is positive definite Now we see that if weights and the Neural Tangent Kernel defined by is (approximately) constant then the neural network trained under converges fast to a state with zero loss. Next we need to argue that weights and the neural tangent kernel remain approximately constant during training. But first we define a bit more notation. Neural Network Model. We consider a dense -layer neural network. Here gives the number of activations on each layer. The activation functions on each layer are given by the same Lipschitz continuous function . We let weights for the -th layer, and we let be the weights applied at each layer. We let . Given the activations for layer , we define the pre-activations and then we define (Notice that above we rescale the weights by a factor of or .) Starting with inputs and defining , we can recursively apply the above equations to get output . We define to be the function that maps inputs to outputs, i.e. for input , we recursively apply the above equations and to output . 1 We recall the definition of the Neural Tangent Kernel as given above Definition [Neural Tangent Kernel] For a neural network with weights , the neural tangent kernel is defined by where here indexes all the weights of our neural network. Neural Networks with Gaussian Weights. The following shows how initializing the Neural Network effects the distribution of its output. We show that in a multi-layer neural network initialized with Gaussian weights at each neuron as an output that is independent and Gaussian distributed when the width of each layer tends to infinity. In this limit, each layer affects the covariance of the next layer in a constant way. We can use this to show that the initial Neural Tangent Kernel (which is random in the prelimit) tends to a non-random Kernel. Proposition 1. In the limit as , the output of converges to a normal distribution where in the limit each component is independent over , has mean zero and covariance which satisfies the recursion The Neural Tangent Kernel is such that converges to zero for , whereas for the NTK converges to a non-random real valued kernel satisfying the recursion where Proof. The result follows by induction on the number of layers . For it is not too hard to check the above conditions since is Gaussian and there is no limit to be taken. Lets assume the induction hypothesis that, in the limit where , the output from level , is independent mean zero Gaussian with the covariance between inputs and given by . Also assume that, with probability , the NTK satisfies where is some deterministic kernel. Knowing what happens layer , let’s consider what happens at layer when . Recall that the output at level is and, if we differentiate a parameter indexed by from layer then (Note that this is just BackPropogation) Let’s analyse . Notice that if we condition of the weights upto layer then the activations are fixed. So then in is Normally distributed where and the outputs are (conditionally) independent over . By the induction hypothesis, the terms in the sum above are i.i.d. as . So the strong law of large numbers applies to the sum as we let where is as stated above. Thus given the deterministic limit for the covariance , the distribution of in has the same limit: it is normally distributed limit with mean zero and covariance and is independent over , as required. Next, let’s analyse the NTK. Given , we can see that there are two cases depending on whether the weights belong to the final layer or not: I.e. the NTK is Given , we deal with the two terms and separately. Notice from , the terms in are all zero unless . If then is exactly , above, and so limits to as given in . For term , by So In the above we note that term in square brackets is the NTK for the depth network. Thus we apply . The only terms that are non-zero after taking this limit are terms where . We are then left with a sum over i.i.d random variables (indexed by ) thus the strong law of large numbers gives convergence to the limit NTK, as stated. This completes the proof. QED. Lazy Weights. We now sketch out why weights remain approximately constant during training. Recall that weights change according to Previously we took for the data . Here we leave this training direction somewhat general. (Though it is important it stays bounded.) In the limit where , it holds that and are (stochastically) bounded and that (Here is the operator norm and is the norm of the empirical distribution over the data.) We give a sketch proof as otherwise we will spend too much time defining norms etc… To make notation a bit shorter we write and for and . Proof Sketch. (see original paper for full proof — https://arxiv.org/abs/1806.07572 ) First we show is bounded. It is not hard to show (using Cauchy-Schwartz) that any matrix satisfies If the components of are i.i.d. of finite variance, then dividing by and applying the strong law of large numbers gives a finite upper bound as . 2 Next we argue that the scaled activations remains bounded. Notice that from Proposition [init] for any input the preactivations are independent identically distributed Gaussian. So is independent over . If we consider an Euclidean norm for any input then we get the strong law of large numbers giving a finite limit to Now let’s analyze the change in . From above We know for backpropogation holds i.e. from recall that and . We can repeatedly apply this to the above expression so that where we inductively define (Already at this point the division by in should make us think that things are not going to grow when we let ) Now it is not hard to check that for any function . Applying this to above (dividing by and applying Cauchy-Schwartz) we get that where is the Lipschitz constant for the in .	https://appliedprobability.blog/2021/03/10/neural-tangent-kernel/
Would you like to receive an alert when new items match your search? Sort by Journal Articles Publisher: Journals Gateway Neural Computation (1996) 8 (3): 583–593. Published: 01 April 1996 AbstractView article PDF Nonlinear time series modeling with a multilayer perceptron network is presented. An important aspect of this modeling is the model selection, i.e., the problem of determining the size as well as the complexity of the model. To overcome this problem we apply the predictive minimum description length (PMDL) principle as a minimization criterion. In the neural network scheme it means minimizing the number of input and hidden units. Three time series modeling experiments are used to examine the usefulness of the PMDL model selection scheme. A comparison with the widely used cross-validation technique is also presented. In our experiments the PMDL scheme and the cross-validation scheme yield similar results in terms of model complexity. However, the PMDL method was found to be two times faster to compute. This is significant improvement since model selection in general is very time consuming. Journal Articles Initializing Weights of a Multilayer Perceptron Network by Using the Orthogonal Least Squares Algorithm Publisher: Journals Gateway Neural Computation (1995) 7 (5): 982–999. Published: 01 September 1995 AbstractView article PDF Usually the training of a multilayer perceptron network starts by initializing the network weights with small random values, and then the weight adjustment is carried out by using an iterative gradient descent-based optimization routine called backpropagation training. If the random initial weights happen to be far from a good solution or they are near a poor local optimum, the training will take a lot of time since many iteration steps are required. Furthermore, it is very possible that the network will not converge to an adequate solution at all. On the other hand, if the initial weights are close to a good solution the training will be much faster and the possibility of obtaining adequate convergence increases. In this paper a new method for initializing the weights is presented. The method is based on the orthogonal least squares algorithm. The simulation results obtained with the proposed initialization method show a considerable improvement in training compared to the randomly initialized networks. In light of practical experiments, the proposed method has proven to be fast and useful for initializing the network weights.	https://direct.mit.edu/neco/search-results?f_Authors=Kimmo+Kaski
Deep neural networks have been shown to be very powerful modeling tools for many supervised learning tasks involving complex input patterns. However, they can also easily overfit to training set biases and label noises. In addition to various regularizers, example reweighting algorithms are popular solutions to these problems, but they require careful tuning of additional hyperparameters, such as example mining schedules and regularization hyperparameters. In contrast to past reweighting methods, which typically consist of functions of the cost value of each example, in this work we propose a novel meta-learning algorithm that learns to assign weights to training examples based on their gradient directions. To determine the example weights, our method performs a meta gradient descent step on the current mini-batch example weights (which are initialized from zero) to minimize the loss on a clean unbiased validation set. Our proposed method can be easily implemented on any type of deep network, does not require any additional hyperparameter tuning, and achieves impressive performance on class imbalance and corrupted label problems where only a small amount of clean validation data is available.	https://icml.cc/Conferences/2018/ScheduleMultitrack?event=1991
If you’re one of those people with a large number of GPU compute nodes in your basement, or if you work for Google, training neural networks in a short time for challenging tasks is probably easy for you. However, if you don’t happen to be one of those lucky ones, you’re probably experiencing trade-offs between model size, training time, and performance. This problem is particularly pronounced on mobile and embedded systems, where computing power is very limited. Luckily, if you have powerful processors to train on and only care about doing inference/prediction on mobile devices, there are some techniques that have you covered. Current approaches One way would be to start with a large network and train it using certain regularizers that encourage many weights to converge to zero over the course of training, thereby effectively pruning the network. Another way would be to train the whole network until convergence and then prune it after training, removing the connections that contribute least to the predictive performance. Ultimately, you can also train a large performant model and then distill its knowledge into a smaller model by using it as a “teacher” for the smaller “student” model. The common thread with all these methods is that you need to start training with a large network, which requires powerful computing architecture. Once the model is trained and pruned or distilled, you can efficiently make predictions on a mobile system. But what do you do if you want to also do the training on the mobile device? Imagine an application where you want to collect user data and build a predictive model from it, but you don’t want to transfer the data to your servers, e.g. for privacy reasons. Naïvely, one could imagine just using the pruned network architectures and training them from scratch on the device. Alas, this doesn’t work well, and it’s tricky to understand why. So how else could we tackle this problem? The Lottery Ticket Hypothesis It turns out that viewing pruning as identifying a sufficient model architecture could be misguided. Instead, we should perhaps view it as identifying a subnetwork that was randomly initialized with a good set of weights for the learning task. This recently published idea is called the “Lottery Ticket Hypothesis.” The hypothesis states that, before training, randomly initializing weights will mostly assign weights that are inefficient for the task at hand. By random chance, some subnetwork will be assigned a slightly better set of weights than the other ones. This subnetwork will therefore converge quicker and will take on most of the responsibility for the actual prediction task over the course of training. After training, it’s highly likely that this subnetwork will be responsible for most of the network’s performance, while the rest of the network might loosely support the task or be effective for some corner cases only. In line with the lottery metaphor, the authors of the paper call this special subnetwork the “winning ticket”. Using the lottery ticket hypothesis, we can now easily explain the observation that large neural networks are more performant than small ones, but that we can still prune them after training without much of a loss in performance. A larger network just contains more different subnetworks with randomly initialized weights. Therefore, the probability of finding a winning ticket at a certain performance level, or respectively the average performance of the network’s winning ticket, is higher. (Note that when we scale the size of all layers in a network linearly, the number of weights grows quadratically, but the number of credit assignment paths or subnetworks grows exponentially due to combinatorics!) Empirical results This is a compelling idea, but in order to know whether it’s actually true, the authors had to conduct a few experiments. In their first experiment, they trained the LeNet architecture on MNIST and pruned it after training up to different degrees (they call this one-shot pruning). They then reinitialized the pruned networks with the exact same weights used in the first training and retrained the so-obtained smaller networks on the same task.	https://prizelottery.co.za/neural-network-lottery-prediction/
In this tutoral we will discuss about mathematical basis of single-layer neural network training methods. Gradient descent method Gradient descent method is a method of finding a local extremum (minimum or maximum) of a function by moving along a gradient of error function. According to gradient descent method the weights and thresholds of neurons calculated by the formulas: (1) (2) Here, is the error function, and is the learning rate of training algorithm. Delta rule Delta rule also called Widrow-Hoff’s learning rule was introduced by Bernard Widrow and Marcian Hoff, to minimize the error over all training patterns. It implies the minimization of the root-mean-square error of the neural network, determined by the formula: , where d- is a target value. Each neuron calculates a weighted sum of its inputs according to the formula: . If the linear activation function is used, then the error functional will be equal to: (3) The derivatives of the error function by weighs ang threshold expressed as : (4) (5) (6) During the training process the weights and the thresholds of the neuron calculated by the formulas: (7) (8) Consider a neural network consisting of one layer with three neurons Here – is input vector and – target vector. In this case, the error function will be equal to and weights and biases of neurons calculated by the formulas: (9) (10) Single-layer neural network training algorithm The sequence of steps for training single-layer neural network by using Widrow-Hoff learning rule: - Specify the learning step α (0 <α <1) and the desired root-mean-square error of the network . - Initialize the weighting coefficients and the threshold values of neurons by random numbers. - Feed vectors from the training sample to the input of the neural network. Calculate the output values of the neurons. - Change the weight coefficients and thresholds of neural elements according to formulas (9,10). - Calculate the total error of the neural network - If , then go to step 3, otherwise stop the execution of algorithm.	https://learn-neural-networks.com/single-layer-neural-network-training/
performs and what those hidden layers of neurons end up actually looking for. As a reminder, our goal here is the classic example of handwritten digit recognition: the Hello World of neural networks. These digits are rendered on a 28-by-28-pixel grid, each pixel with some grayscale value between zero and one. Those are what determine the activations of 784 neurons in the input layer of the network. And then the activation for each neuron in the following layers is based on a weighted sum of all the activations in the previous layer plus some special number called a bias. Then you compose that sum with some other function like the sigmoid squishification or a ReLu, the way that I walked through last video. In total, given the somewhat arbitrary choice of two hidden layers here with 16 neurons each, the network has about 13000 weights and biases that we can adjust. And it’s these values that determine what exactly the network, you know, actually does. Then what we mean when we say that this network classifies a given digit is that the brightest of those 10 neurons in the final layer corresponds to that digit. And remember, the motivation that we had in mind here for the layered structure was that maybe the second layer could pick up on the edges. And the third layer might pick up on patterns like loops and lines. And the last one could just piece together those patterns to recognize digits. So here, we learn how the network learns. What we want is an algorithm, where you can show this network a whole bunch of training data which comes in the form of a bunch of different images of handwritten digits along with labels for what they’re supposed to be. And it’ll adjust those 13000 weights and biases so as to improve its performance on the training data. Hopefully, this layered structure will mean that what it learns generalizes to images beyond that training data. And the way we test that is that after you train the network, you show it more labeled data that it’s never seen before. And you see how accurately it classifies those new images. Fortunately for us, and what makes this such a common example to start with, is that the good people behind the MNIST database have put together a collection of tens of thousands of handwritten digit images, each one labeled with the numbers that they’re supposed to be. And as provocative as it is to describe a machine as learning, once you actually see how it works, it feels a lot less like some crazy sci-fi premise and a lot more like, well, a calculus exercise. I mean, basically it comes down to finding the minimum of a certain function. Remember, conceptually, we’re thinking of each neuron as being connected to all of the neurons in the previous layer. And the weights in the weighted sum defining its activation are kinda like the strengths of those connections. And the bias is some indication of whether that neuron tends to be active or inactive. And to start things off, we’re just gonna initialize all of those weights and biases totally randomly. Needless to say, this network is gonna perform pretty horribly on a given training example, since it’s just doing something random. For example, you feed in this image of a three, and the output layer, it just looks like a mess. So what you do is you define a cost function, a way of telling the computer, “No! Bad computer! That output should have activations which are zero for most neurons, but one for this neuron. What you gave me is utter trash!” To say that a little more mathematically, what you do is add up the squares of the differences between each of those trash output activations and the value that you want them to have. And this is what we’ll call the cost of a single training example. Notice, this sum is small when the network confidently classifies the image correctly. But it’s large when the network seems like it doesn’t really know what it’s doing. So then what you do is consider the average cost over all of the tens of thousands of training examples at your disposal. This average cost is our measure for how lousy the network is and how bad the computer should feel. And that’s a complicated thing. Remember how the network itself was basically a function, one that takes in 784 numbers as inputs, the pixel values, and spits out 10 numbers as its output. And in a sense, it’s parameterized by all these weights and biases. Well, the cost function is a layer of complexity on top of that. It takes as its input those 13000 or so weights and biases. And it spits out a single number describing how bad those weights and biases are. And the way it’s defined depends on the network’s behavior over all the tens of thousands of pieces of training data. That’s a lot to think about! But just telling the computer what a crappy job it’s doing isn’t very helpful. You wanna tell it how to change those weights and biases so that it gets better. To make it easier, rather than struggling to imagine a function with 13000 inputs, just imagine a simple function that has one number as an input and one number as an output. How do you find an input that minimizes the value of this function? Calculus students will know that you can sometimes figure out that minimum explicitly. But that’s not always feasible for really complicated functions, certainly not in the 13000-input version of this situation for our crazy complicated neural network cost function. A more flexible tactic is to start at any old input and figure out which direction you should step to make that output lower. Specifically, if you can figure out the slope of the function where you are, then shift to the left if that slope is positive and shift the input to the right if that slope is negative. If you do this repeatedly, at each point checking the new slope and taking the appropriate step, you’re gonna approach some local minimum of the function. And the image you might have in mind here is a ball rolling down a hill. And notice, even for this really simplified single input function, there are many possible valleys that you might land in, depending on which random input you start at. And there’s no guarantee that the local minimum you land in is gonna be the smallest possible value of the cost function. That’s gonna carry over to our neural network case as well. And I also want you to notice how if you make your step sizes proportional to the slope, then when the slope is flattening out towards the minimum, your steps get smaller and smaller. And that kind of helps you from overshooting. Bumping up the complexity a bit, imagine instead a function with two inputs and one output. You might think of the input space as the 𝑥𝑦-plane and the cost function as being graphed as a surface above it. Now instead of asking about the slope of the function, you have to ask which direction should you step in this input space so as to decrease the output of the function most quickly. In other words, what’s the downhill direction? And again, it’s helpful to think of a ball rolling down that hill. Those of you familiar with multivariable calculus will know that the gradient of a function gives you the direction of steepest ascent. Basically, which direction should you step to increase the function most quickly. Naturally enough, taking the negative of that gradient gives you the direction to step that decreases the function most quickly. And even more than that, the length of this gradient vector is actually an indication for just how steep that steepest slope is. Now if you’re unfamiliar with multivariable calculus and you wanna learn more, check out some of the work that I did for Khan Academy on the topic. Honestly though, all that matters for you and me right now is that in principle, there exists a way to compute this vector. This vector that tells you what the downhill direction is and how steep it is. You’ll be okay if that’s all you know and you’re not rock solid on the details. Because if you can get that, the algorithm from minimizing the function is to compute this gradient direction. Then take a small step downhill and just repeat that over and over. It’s the same basic idea for a function that has 13000 inputs instead of two inputs. Imagine organizing all 13000 weights and biases of our network into a giant column vector. The negative gradient of the cost function is just a vector. It’s some direction inside this insanely huge input space that tells you which nudges to all of those numbers is gonna cause the most rapid decrease to the cost function. And, of course, with our specially designed cost function, changing the weights and biases to decrease it means making the output of the network on each piece of training data look less like a random array of 10 values and more like an actual decision that we want it to make. It’s important to remember, this cost function involves an average over all of the training data. So if you minimize it, it means it’s a better performance on all of those samples. The algorithm for computing this gradient efficiently, which is effectively the heart of how a neural network learns, is called back propagation. And it’s what I’m gonna be talking about next video. There, I really wanna take the time to walk through what exactly happens to each weight and each bias for a given piece of training data, trying to give an intuitive feel for what’s happening beyond the pile of relevant calculus and formulas. Right here, right now, the main thing I want you to know independent of implementation details is that what we mean when we talk about a network learning is that it’s just minimizing a cost function. And notice, one consequence of that is that it’s important for this cost function to have a nice, smooth output so that we can find a local minimum by taking little steps downhill. This is why, by the way, artificial neurons have continuously ranging activations rather than simply being active or inactive in a binary way, the way that biological neurons are. This process of repeatedly nudging an input of a function by some multiple of the negative gradient is called gradient descent. It’s a way to converge towards some local minimum of a cost function, basically, a valley in this graph. I’m still showing the picture of a function with two inputs, of course, because nudges in a 13000-dimensional input space are a little hard to wrap your mind around. But there is actually a nice non-spatial way to think about this. Each component of the negative gradient tells us two things. The sign, of course, tells us whether the corresponding component of the input vector should be nudged up or down. But importantly, the relative magnitudes of all these components kind of tells you which changes matter more. You see, in a network, an adjustment to one of the weights might have a much greater impact on the cost function than the adjustment to some other weight. Some of these connections just matter more for our training data. So a way that you can think about this gradient vector of our mind-warpingly massive cost function is that it encodes the relative importance of each weight and bias. That is, which of these changes is gonna carry the most bang for your buck? This really is just another way of thinking about direction. To take a simpler example, if you have some function with two variables as an input, and you compute that its gradient at some particular point comes out as three, one. Then on the one hand, you can interpret that as saying that when you’re standing at that input, moving along this direction increases the function most quickly. That when you graph the function above the plane of input points, that vector is what’s giving you the straight uphill direction. But another way to read that is to say that changes to this first variable have three times the importance as changes to the second variable. That at least in the neighborhood of the relevant input, nudging the 𝑥-value carries a lot more bang for your buck. Alright, let’s zoom out and sum up where we are so far. The network itself is this function with 784 inputs and 10 outputs, defined in terms of all of these weighted sums. The cost function is a layer of complexity on top of that. It takes the 13000 weights and biases as inputs and spits out a single measure of lousyness based on the training examples. And the gradient of the cost function is one more layer of complexity still. It tells us what nudges to all of these weights and biases cause the fastest change to the value of the cost function, which you might interpret as saying which changes to which weights matter the most. So when you initialize the network with random weights and biases and adjust them many times based on this gradient descent process, how well does it actually perform on images that it’s never seen before? Well the one that I’ve described here, with the two hidden layers of 16 neurons each, chosen mostly for aesthetic reasons, well it’s not bad! It classifies about 96 percent of the new images that it sees correctly. And honestly, if you look at some of the examples that it messes up on. You kinda feel compelled to cut it a little slack. Now if you play around with the hidden layer structure and make a couple tweaks, you can get this up to 98 percent. And that’s pretty good! It’s not the best. You can certainly get better performance by getting more sophisticated than this plain vanilla network. But given how daunting the initial task is, I just think there’s something incredible about any network doing this well on images that it’s never seen before, given that we never specifically told it what patterns to look for. Originally, the way that I motivated this structure was by describing a hope that we might have. That the second layer might pick up on little edges. That the third layer would piece together those edges to recognize loops and longer lines. And that those might be pieced together to recognize digits. So is this what our network is actually doing? Well, for this one at least, not at all! Remember how last video we looked at how the weights of the connections from all of the neurons in the first layer to a given neuron in the second layer can be visualized as a given pixel pattern that that second layer neuron is picking up on? Well, when we actually do that for the weights associated with these transitions from the first layer to the next, instead of picking up on isolated little edges here and there, they look, well, almost random, just about some very loose patterns in the middle there. It would seem that in the unfathomably large 13000 dimensional space of possible weights and biases, our network found itself a happy little local minimum that despite successfully classifying most images doesn’t exactly pick up on the patterns that we might have hoped for. And to really drive this point home, watch what happens when you input a random image. If the system was smart, you might expect it to either feel uncertain, maybe not really activating any of those 10 output neurons, or activating them all evenly. But instead, it confidently gives you some nonsense answer, as if it feels as sure that this random noise is a five as it does that an actual image of a five is a five. Phrased differently, even if this network can recognize digits pretty well, it has no idea how to draw them. A lot of this is because it’s such a tightly constrained training set-up. I mean, put yourself in the network’s shoes here. From its point of view, the entire universe consists of nothing but clearly defined unmoving digits centered in a tiny grid. And its cost function just never gave it any incentive to be anything but utterly confident in its decisions. So if this is the image of what those second layer neurons are really doing, you might wonder why I would introduce this network with the motivation of picking up on edges and patterns. I mean, that’s just not at all what it ends up doing. Well, this is not meant to be our end goal, but instead a starting point. Frankly, this is old technology, the kind researched in the 80s and 90s. And you do need to understand it before you can understand more detailed modern variants. And it clearly is capable of solving some interesting problems. But the more you dig in to what those hidden layers are really doing, the less intelligent it seems. Shifting the focus for a moment from how networks learn to how you learn, that’ll only happen if you engage actively with the material here somehow. One pretty simple thing that I want you to do is just pause right now and think deeply for a moment about what changes you might make to this system and how it perceives images, if you wanted it to better pick up on things like edges and patterns. But better than that, to actually engage with the material, I highly recommend the book by Michael Nielsen on deep learning and neural networks. In it, you can find the code and the data to download and play with for this exact example. And the book will walk you through, step by step, what that code is doing. What’s awesome is that this book is free and publicly available. So if you do get something out of it, consider joining me in making a donation towards Nielsen’s efforts. I’ve also linked a couple other resources that I like a lot in the description, including the phenomenal and beautiful blog post by Chris Ola and the articles in Distill. To close things off here for the last few minutes, I wanna to jump back into a snippet of the interview that I had with Lisha Li. You might remember her from the last video. She did her PhD work in deep learning. And in this little snippet, she talks about two recent papers that really dig in to how some of the more modern image-recognition networks are actually learning. Just to set up where we were in the conversation, the first paper took one of these particularly deep neural networks that’s really good at image recognition. And instead of training it on a properly labeled data set, it shuffled all of the labels around before training. Obviously, the testing accuracy here was gonna be no better than random, since everything’s just randomly labeled. But it was still able to achieve the same training accuracy as you would on a properly labeled dataset. Basically, the millions of weights for this particular network were enough for it to just memorize the random data, which kind of raises the question for whether minimizing this cost function actually corresponds to any sort of structure in the image. Or is it just, you know, memorization? Lisha Li: ... memorize the entire data set of what the correct classification is. And so a couple of, you know, half a year later at ICML this year, there was not exactly rebuttal paper but paper that address some aspects of — like hey. Actually, these networks are doing something a little bit smarter than that. If you look at that accuracy curve, if you were just training on a random data set, that curve sort of went down very, you know, very slowly in almost kind of a linear fashion. So you’re really struggling to find that local minima of possible, you know, the right weights that would get you that accuracy. Whereas if you’re actually training on a structured data set, one that has the right labels, you know, you fiddle around a little bit in the beginning. But then you kind of dropped very fast to get to that accuracy level. And so in some sense, it was easier to find that local maxima. And so what’s also interesting about that is it brings into light another paper from actually a couple of years ago, which has a lot more simplifications about the network layers. But one of the results was saying how if you look at the optimization landscape, the local minima that these networks tend to learn are actually of equal quality. So in some sense, if your data set is structured, you should be able to find that much more easily.	https://www.nagwa.com/en/videos/376142364186/
So for the last week or so I've tried to implement a Feed Forward network with multiple types of layers (Fully Connected, MaxPool, Convolution), multiple types of non-linear functions (tanh, sigmoid, relu), using the gradient descent optimizer and 2 errors types (sum of squared errors and logistic error). It should be noted that I'm really new in the domain, so I might be making some obvious mistakes I'm not even aware of, which is one of the things I'm looking to fix with this post. The implementation can be found here, which is in Python 3, completely unoptmized (not the purpose of the project) and the main function is in main.py. The training is done only on the MNIST dataset (though my plans were to use it for CIFAR-10 as well, but in the current form it's quite obvious I can't do it). The images in the MNIST dataset are 1x32x32 (grayscale and a padding of 2 from their original shape). The pictures I'll be putting are comparing the accuracy and computed error based on an evaluation set that is randomly picked from the training data (while training, random is redone every time, check evaluate function in hw2.py). The error calculation is done on the respective formulas for both kinds of errors, and can be found on error.py file. The weights/biases are initialized using Xavier method (2 / volume size) for both Fully Connected and Convolutional layers (layer.py). All the tests I show below are using the Sum of Squared errors. Regular 2-layered network The architecture is as follows: 0 Linearize (1, 32, 32) -> (1024, 1) 1 FullyConnected (1024, 1) -> (100, 1) (sigmoid) 2 FullyConnected (100, 1) -> (10, 1) The learning rate used: 0.001 (1e-3). This network gives me a pretty good result (inexplicably good, as described even by LeCun, page 3 at the end). Here are the results for the simple 2 layers network, which look really well compared to what I'll show afterwards: The testing phase with this trained network gives me 85-90% accuracy results, which I consider really good (Tensorflow considers this embarrassing in their tutorial :) ). Convolutional network So, as many tutorials/documentation that I read says, adding a Convolutional layer should improve the accuracy of my testing as the layer learns filters specifically for the dataset instead of having 1 weight mapping between each neuron in the 2 layers. Anyway, I've implemented (with a lot of headache) a Convolutional layer (2 implementations: one simply a 6-for translation of the derivatives formula for forward/backpropagation and one slightly vectorized, still very slow, again not the purpose of the project). The implementation is in layer.py. For this implementation I used some unit testing on the inputs and outputs of the forward and backward step (to validate my 6-for implementation with the vectorized one as well as the results themselves). The test called testConvolution is identical to the convolution test done in the implementation of tiny-dnn (a C++ header-only neural network framework which can be found here), more specifically TEST(convolutional, with_stride), which seems the only test that does not check their correctness between vectorized and linear implementation, but the correctness of the outputs w.r.t inputs. For the second network, I used the following architecture: 0 Convolution (1, 32, 32) -> (5, 28, 28) (tanh) 1 Linearize (5, 28, 28) -> (3920, 1) 2 FullyConnected (3920, 1) -> (100, 1) (sigmoid) 3 FullyConnected (100, 1) -> (10, 1) So the convolutional layer has 5 filters of shape 5x5, with a stride of 1. The learning rate I used was 0.0005 (5 * 1e-4). The training was done in 2 epochs (values on X axis after 60000 are from second epoch). The training took about 14 hours. The results are as follows: So, as we can interpret from the plotted results, the error kind of stabilized around the value of 50, while the accuracy is all over the place (sometimes giving me 0.0%, sometimes going to 70%, peaking at 90% with 2 runner ups of 85%). Now these are results I cannot really understand entirely. The network "seems" to be learning something, but in the same time it gives seemingly random results, such as going from 0.1% to 0.7% between two (random) evaluations very often. The error itself stops decreasing after a point and never goes below a certain value, compared to the simple network, where the error always goes downward due to gradient descent. The testing phase of the final model with this network yielded an accuracy of 51%. I'm sure the Tensorflow guys would be stoked. Convolutional network - LeNet-5 Alright, so I trained this network in parallel with the one above, and while the above one finished (14 hours as I said), this one is still going, but I took the preliminary results I have so far which seem concludent of what's going to happen at the end of the training phase. My theory was that perhaps since the network above was giving me some decent results (sometimes evaluating above 70%, while sometimes 0-10%). The network isn't 100% LeNet-5 (I don't make the partial convolution they do in the paper [lecun-98.pdf]): 0 Convolution (1, 32, 32) -> (6, 28, 28) (tanh) 1 MaxPool (6, 28, 28) -> (6, 14, 14) 2 Convolution (6, 14, 14) -> (16, 10, 10) (tanh) 3 MaxPool (16, 10, 10) -> (16, 5, 5) 4 Convolution (16, 5, 5) -> (120, 1, 1) (tanh) 5 Linearize (120, 1, 1) -> (120, 1) 6 FullyConnected (120, 1) -> (86, 1) (tanh or sigmoid, can't remember) 7 FullyConnected (86, 1) -> (10, 1) The learning rate is also 0.0005 (5 * 1e-4). The results are as follows (everything after 60000 on x axis is also from 2nd epoch, which hasn't finished yet): As we can see, the error stabilized around the value of 52-53, while the accuracy itself is all over the place (similar to previous network), but never going above 30-40%. My actual questions Ok, so after writing all the stuff, I guess I am ready to ask you if you can clarify some things for me based on these results. - Are the results I get correct? I'm saying this because tiny-dnn has an example of a network training on MNIST and after 1 epoch their result is ~70-80% using the same network (LeNet-5) and the same optimizer (gradient descent), while for my it's stuck at 20-30% with the error not changing at all. - What could be the reason that the regular network (no convolution) outperforms the convolutional implementation so much ? Could it be a bad implementation on my side and if so, is there any reference implementation I could look at (I'm trying to reverse-understand the tiny-dnn implementation and this seems to be my next step) - Perhaps you may be wondering why I'm using such "precise" learning rates. Well, had I used even slightly bigger ones (1e-3 for convolution), after 30-40 images, my error would look something like this (followed by a nasty error): - Should I normalize my weights? If yes, what do I do? The only place I update my weights/biases are in the backpropagation step, after a batch of images, calling the optimizer ( weights -= learningRate * gradientWeights), where gradientWeights is the accumulation of gradients of a batch (layer.py and optimizer.py). I'm afraid updating the weights in another way might influence the gradient descent algorithm and give me unreliable results. Also, the tiny-dnn (my first impression only), only update the weights (not the biases), but I might be wrong as I didn't dig very deep in their code (optimizers/optimizer.h). - Should I add a regularization term to my errors (see error.py) and if yes, how would I go about that? Do I just update the derivation of the error at the last layer (derive the sum of the weights w.r.t weights and biases as well). What formula do I use for regularization, do I sum all the weights in the network (so the weights of layers 0, 2, 4, 6, 7 in LeNet-5, as only those have trainable parameters) or just the last layer? - What should be my general next steps? If anyone's reading this, thanks.	https://stats.stackexchange.com/questions/276213/unsure-if-my-implementation-of-a-convolutional-layer-doesnt-learn-or-its-the-c
Stochastic Gradient Descent (SGD) is a simple gradient-based optimization algorithm used in machine learning and deep learning for training artificial neural networks. The point of a gradient descent optimization algorithm is to minimize a given cost function, such as the loss function in training an artificial neural network. Improving the performance of a neural network during training is done by slightly adjusting (i.e. tuning or calibrating) its weights and biases, where weights are values that express how important the corresponding inputs are to the output and bias is equivalent to a negative threshold value used to determine the outcome of the training iteration. Each neuron in the network calculates a weighted sum of the inputs and then applies a pre-set activation function to determine whether or not the weighted sum is greater than a threshold value. There are two possible outcomes from this process: - The weighted sum is greater than or equal to the threshold value: the neuron fires (i.e. activates). - The weighted sum is less than the threshold value: the neuron doesn't activate. The loss function tells how well a neural network performs a certain task by producing a value that represents how close the actual output was to the desired output. The gradient descent calculates the slope of the loss function, then shifts the weights and biases according to that slope in order to lower loss in the next iteration. Minimizing loss is done by taking steps in the opposite direction of the gradient until you finally converge on some local minima. This process of minimizing loss is how neural networks learn to better perform specific tasks through training. The term stochastic describes something that has a random probability distribution or pattern which can be analyzed statistically but not predicated precisely. In order for a gradient descent algorithm to be considered stochastic, it should have a batch size equal to 1, where the one example comprising each batch is chosen at random. When batch size is greater than one, the algorithm is called a mini-batch gradient descent algorithm. Timeline Further Resources A Bayesian Perspective on Generalization and Stochastic Gradient Descent Samuel L. Smith, Quoc V. Le Academic paper Fully Distributed and Asynchronized Stochastic Gradient Descent for Networked Systems Ying Zhang Academic paper How do we 'train' neural networks ? - Towards Data Science Vitaly Bushaev Web Stochastic gradient descent algorithms for strongly convex functions at O(1/T) convergence rates Shenghuo Zhu Academic paper Stochastic Gradient Descent with momentum - Towards Data Science Vitaly Bushaev Web References Categories Related Topics - Machine learningA field of computer science enabling computers to learn. - Artificial neural networkAn artificial neural network is a computer system that is modeled after the way the human brain analyzes and processes information. - RMSpropUnpublished but widely-known gradient descent optimization algorithm for mini-batch learning of neural networks. - Deep learningBranch of machine learning based on learning data representations. - Rpropa gradient descent algorithm for supervised learning in feedforward artificial neural networks. - Show More Contributors - 1 Daniel FrumkinMechanical engineering, cryptocurrencies, AI, and travel. - 2 Melanie ManipulaHelping organize knowledge. - 3 Toxic RainCrypto enthusiast - 4 Tianchang HeStanford EE MS, interested in machine learning, front-end and all things tech. - 5 Jude GomilaFounder and CEO of Golden, Entrepreneur. Investor in 200+ companies. Cantabrigian (Gonville and Caius). Interested in the Universe.	https://golden.com/wiki/Stochastic_gradient_descent_(SGD)-JN5J3R
There is a ton of literature (see, for example, a highly cited paper by Huang et al. (2006)) on neural networks with random weights (NNRWs), i.e. neural networks whose weights are random except for those in the output layer, which are determined analytically by solving a linear system. Two recent publications seem to have differing opinions on the universal approximation capability of such networks. According to Weiping Cao et al. (2017): NNRW is easy to implement and its universal approximation capability has been proven in theory. According to Feilong Cao et al. (2016): From approximation theory, it is obvious that such a way to randomly assign the input weights and biases cannot guarantee the universal approximation capability (in the sense of probability one) of the resulting random learner models. Which of these papers has it right?	https://stats.stackexchange.com/questions/303586/universal-approximation-capability-of-neural-networks-with-random-weights
I'm using the fann library for writing an Artificial Neural Network in C++. I trained my network for the task of recognizing faces inside a set of 128x128 .png images, using three different algorithms: - standard Backpropagation - incremental (or stochastic) Backpropagation - resilient Backpropagation (RPROP) The network performs well with all of the algorithms above, using one hidden layer with 10 neurons and outputting just one number between 0 and 1 (~0.9 if the test image contains the face of the person the network was trained to recognize; ~0.1 if not) in the output layer. After training the network, I then read the weights from the input layer to one neuron and encode them to a .png image (for each neuron in the hidden layer). Now, what I get with the RPROP algorithm is 10 (one for each neuron) 128x128 images, each representing some blurred human face, very similar to the face of the target person the network had to recognize. Nice! But what I get with standard and stochastic Backpropagation is just 10 images with random noise. I even tried initializing the weights to zero but all I got was, again, random noise. Can anyone tell me why is there such a difference between RPROP and the other algorithms, when it comes to interpreting the learned weights that go from the input to the hidden layer? I'm just curious. EDIT: The training set consisted of 457 .png pictures; each picture was 128x128 RGB pixels, so I encoded the pictures in 457 text files containing 128x128x3 integers in the range [0,255] (3 is because each RGB pixel is 3 colors: Red, Green, Blue). The input pixels for the ANN were scaled proportionally from [0,255] to [-1,1] (and the back to [0,255] when I encoded the hidden layer neurons to .png's). The training set contains pictures of 6 different persons (but all in the same pose), approximately 70 for each one. The ANN has 1281283 = 49152 input units, one hidden layer with 10 neurons (but it was almost the same with 8 neurons) and only one output neuron (but my problem persisted even with 6 distinct output units). And yes, the network is fully connected; I'll try the sparse-connected option too, maybe with some more hidden layer. With RPROP and standard Backpropagation I set the desired error to 0.006; usually, the number of training epochs was not more than 300 before the network could converge. With every algorithm, the perceptron unit was the sigmoid function and the learning rate was set to 0.7. The weights were randomly initialised between -0.1 and 0.1; I only tried to monitor the weight updates when I initialized them to zero for incremental Backpropagation, but the images I obtained by encoding the hidden layer neurons to .png's were again just random noise.	https://stats.stackexchange.com/questions/175115/interpreting-hidden-layer-representations-in-anns
Abstract: Fully exploiting the learning capacity of neural networks requires overparameterized dense networks. On the other side, directly training sparse neural networks typically results in unsatisfactory performance. Lottery Ticket Hypothesis (LTH) provides a novel view to investigate sparse network training and maintain its capacity. Concretely, it claims there exist winning tickets from a randomly initialized network found by iterative magnitude pruning and preserving promising trainability (or we say being in trainable condition). In this work, we regard the winning ticket from LTH as the subnetwork which is in trainable condition and its performance as our benchmark, then go from a complementary direction to articulate the Dual Lottery Ticket Hypothesis (DLTH): Randomly selected subnetworks from a randomly initialized dense network can be transformed into a trainable condition and achieve admirable performance compared with LTH -- random tickets in a given lottery pool can be transformed into winning tickets. Specifically, by using uniform-randomly selected subnetworks to represent the general cases, we propose a simple sparse network training strategy, Random Sparse Network Transformation (RST), to substantiate our DLTH. Concretely, we introduce a regularization term to borrow learning capacity and realize information extrusion from the weights which will be masked. After finishing the transformation for the randomly selected subnetworks, we conduct the regular finetuning to evaluate the model using fair comparisons with LTH and other strong baselines. Extensive experiments on several public datasets and comparisons with competitive approaches validate our DLTH as well as the effectiveness of the proposed model RST. Our work is expected to pave a way for inspiring new research directions of sparse network training in the future. Our code is available at this https URL. Submission historyFrom: Yue Bai [view email] [v1] Tue, 8 Mar 2022 18:06:26 UTC (638 KB) Full-text links: Download: (license) References & Citations a Loading... Bibliographic and Citation Tools Bibliographic Explorer (What is the Explorer?) Litmaps (What is Litmaps?) scite Smart Citations (What are Smart Citations?) Code and Data Associated with this Article Demos Recommenders and Search Tools Connected Papers (What is Connected Papers?) CORE Recommender (What is CORE?) arXivLabs: experimental projects with community collaborators arXivLabs is a framework that allows collaborators to develop and share new arXiv features directly on our website. Both individuals and organizations that work with arXivLabs have embraced and accepted our values of openness, community, excellence, and user data privacy. arXiv is committed to these values and only works with partners that adhere to them. Have an idea for a project that will add value for arXiv's community? Learn more about arXivLabs and how to get involved.	https://arxiv.org/abs/2203.04248
In a nutshell: I want to understand why a one hidden layer neural network converges to a good minimum more reliably when a larger number of hidden neurons is used. Below a more detailed explanation of my experiment: I am working on a simple 2D XOR-like classification example to understand the effects of neural network initialization better. Here's a visualisation of the data and the desired decision boundary: Each blob consists of 5000 data points. The minimal complexity neural network to solve this problem is a one-hidden layer network with 2 hidden neurons. Since this architecture has the minimum number of parameters possible to solve this problem (with a NN) I would naively expect that this is also the easiest to optimise. However, this is not the case. I found that with random initialization this architecture converges around half of the time, where convergence depends on the signs of the weights. Specifically, I observed the following behaviour: w1 = [[1,-1],[-1,1]], w2 = [1,1] --> converges w1 = [[1,1],[1,1]], w2 = [1,-1] --> converges w1 = [[1,1],[1,1]], w2 = [1,1] --> finds only linear separation w1 = [[1,-1],[-1,1]], w2 = [1,-1] --> finds only linear separation This makes sense to me. In the latter two cases the optimisation gets stuck in suboptimal local minima. However, when increasing the number of hidden neurons to values greater than 2, the network develops a robustness to initialisation and starts to reliably converge for random values of w1 and w2. You can still find pathological examples, but with 4 hidden neurons the chance that one "path way" through the network will have non-pathological weights is larger. But happens to the rest of the network, is it just not used then? Does anybody understand better where this robustness comes from or perhaps can offer some literature discussing this issue? Some more information: this occurs in all training settings/architecture configurations I have investigated. For instance, activations=Relu, final_activation=sigmoid, Optimizer=Adam, learning_rate=0.1, cost_function=cross_entropy, biases were used in both layers.	https://ai.stackexchange.com/questions/5904/why-does-a-one-layer-hidden-network-get-more-robust-to-poor-initialization-with/18695
Sweat releases heat and cools down the body through evaporative cooling. When sweat escapes through the skin, it carries some of the body's energy with it in the form of heat. Evaporation releases this energy, siphoning it away from the body and cooling the skin and blood vessels. This cools the blood passing through the circulatory system, reducing the body's core temperature. One of the reasons humid days feel particularly uncomfortable is that since the air is saturated with moisture, sweat cannot evaporate as efficiently. This reduces the amount of heat that can be lost through the process and simply causes sweat to run off the body rather than evaporate away. Lower humidity, as well as moving air, helps sweat evaporate quickly, producing a cooler, more comfortable feeling. Since sweat contains salt and minerals as well as water, excessive sweating can lead to dehydration as well as a loss of electrolytes. Many sports drinks include added minerals in an attempt to replenish these vital nutrients after an extended workout. Drinking large volumes of pure water to rehydrate may lead to water intoxication, as the sodium levels in the body dip to dangerously low levels. Common side effects of water intoxication include nausea and cramping, while high levels can result in weakness, confusion, paralysis and even death. Learn more about the signs that may reveal you have an Issue that need attention. Here are 15 possible causes of excessive sweating.	https://www.reference.com/science/water-release-heat-humans-sweat-31feaa98af12f876
Prioritize... When you've finished this page, you should be able to describe the processes of evaporation and condensation, as well as how/why these processes impact temperature. In particular, you should be able to explain temperature and dew point changes that often occur with falling precipitation. Read... Since evaporation and condensation are such important phase changes for water, they deserve more of our attention. I briefly defined them in the previous section, but now I want to take a closer look at how these processes actually work, and what their consequences are for some weather variables that we've already talked about -- temperature and dew point. For starters, evaporation is the process by which liquid water molecules break the bonds with neighboring molecules and escape into the air as water vapor, and as I mentioned briefly in the last lesson, evaporation is a cooling process, for a couple of reasons. First, water molecules with the greatest kinetic energy (fastest vibrations) are most likely break the bonds with their neighbors and evaporate, which means the average kinetic energy of the remaining liquid water is reduced (because the most energetic molecules are no longer liquid). A lower kinetic energy of the remaining water means a lower water temperature. Secondly, the breaking of bonds between liquid water molecules requires energy, and that energy comes from the surrounding air. All of water's phase changes actually either use energy from the surrounding air, or release energy to the surrounding air, as illustrated by the "energy staircase" diagram for ice, water, and water vapor below. Although the diagram includes all of water's possible phase changes, we're going to focus on the two of greatest interest to us for now -- evaporation and condensation. If we start with liquid water, a few highly energetic, free-spirited water molecules can eventually break the bonds with surrounding molecules over time and escape to the vapor phase. Energy is required (600 calories per gram, to be exact) to break all the bonds to allow all the water to rather quickly evaporate and enter the gaseous phase of water vapor (the highest energy step), which cools the surrounding air. So, if evaporation is a cooling process, what about its reverse -- condensation (the process by which water vapor changes to liquid)? When water vapor condenses back into water, there's a step down in energy levels, so if you're thinking that condensation is a warming process, you're correct! Indeed, the energy used to evaporate water in the first place is never lost (a consequence of the conservation of energy), so as water vapor condenses into liquid water and bonds form between molecules, energy is released (600 calories per gram -- identical to the amount required for evaporation) to keep the energy books balanced. The release of this energy, called "latent heat of condensation," warms up the surrounding air. So, any time a phase change (such as evaporation) causes water to go "up the energy staircase," energy is required to break bonds between molecules, which cools the surrounding air. Any time a phase change (such as condensation) causes water to go "down the energy staircase," energy is released, which warms up the surrounding air. The warming that occurs with condensation is not easily noticeable to humans, but I bet you've noticed the impacts of evaporational cooling. When you get out of a swimming pool on a hot day, water drops on your skin begin to evaporate, which cools your skin. You've also noticed evaporational cooling in action if you've ever felt a rush of cool air before a shower or thunderstorm arrives. Indeed, temperatures often decrease just before, and after rain arrives. That's because the smallest raindrops evaporate along their descent to the ground, which extracts energy from the surrounding air. To see a real-life example, check out the graph below, which plots surface temperatures and dew points at Louisville, Kentucky on June 11, 2014. I've highlighted a sharp drop in temperature (black line) that occurred in the middle of the afternoon, between 1500 and 1600 local time (between 3 P.M. and 4 P.M.). At 3 P.M. (15:00 on the graph), Louisville reported a temperature of 81 degrees Fahrenheit, but an hour later, the temperature was only 73 degrees Fahrenheit. Why did the temperature fall during this hour? Evaporational cooling! It started to rain between 3 P.M. and 4 P.M., and during that hour, 0.13 inches of rain fell in Louisville, but as precipitation began, evaporation of rain drops cooled the air and temperatures decreased. Also note that dew points increased during the time highlighted in the graph above. Why is that? Well, if liquid raindrops were evaporating into water vapor, that means more water vapor was present in the air, and as you may recall, higher concentrations of water vapor go along with higher dew points. You probably don't realize it, but evaporation and condensation are occurring around you simultaneously all the time! You just can't see the results because they're happening on the molecular level. Obvious phase changes occur when there's "net" condensation, meaning that the condensation rate exceeds the evaporation rate (liquid water droplets form), or if there's "net" evaporation (assuming you have some liquid water to start with), which means that the evaporation rate exceeds the condensation rate. The evaporation of rain drops on their descent to the ground is a great example of net evaporation. Tiny raindrops end up shrinking or disappearing altogether as the rate of evaporation exceeds the rate of condensation. I should point out that the potential for evaporational cooling is greatest when a large difference between temperature and dew point exists because large differences between temperature and dew point allow for the greatest net evaporation. As temperatures and dew points get closer, net evaporation is reduced, which yields less evaporational cooling. To really understand why this is the case, we need to explore what controls the rates of evaporation and condensation. We'll do that in the next section, as well as see why comparing evaporation rates and condensation rates is so important to weather forecasters. Read on!	https://www.e-education.psu.edu/meteo3/l4_p3.html
In a healthy person in , the body temperature of is constant, with slight fluctuations in the morning and evening hours and does not exceed 37 ° C.Such a constant temperature depends on the processes of heat production and heat transfer in the body. The equilibrium between heat generation and heat transfer is established and maintained as a result of heat regulation - a process in which the formation and release of heat of organisms is regulated. Heat generation is basically a chemical process, the source of which is oxidation, that is,combustion of carbohydrates, fats and some proteins in all cells and tissues of the body, primarily in skeletal muscle and liver. Heat output is basically a physical process, about 80% of the heat formed in the body radiates from the surface of the body, about 20% in the evaporation of water during respiration and perspiration, and about 1.5% in urine and feces. Normally, the temperature in children is slightly higher than in adults, as the children have more intensive oxidative processes necessary for growth. In women, the voltage of oxidative processes can change within a month due to the cyclicity of the sexual function. This entails sometimes a temperature increase in the menstrual period by a few tenths of a degree. Daily fluctuations in temperature are directly dependent on fluctuations in oxidative processes associated with work or food intake. In healthy people, the temperature in the morning is a few tenths of a degree lower than in the evening. Temperature indicators depend on the place where it is measured. Thus, the temperature of the mucous membrane of the oral cavity, vagina, rectum is 0.2-0.4 ° C higher than the temperature of the adult skin, measured in the axillary region and inguinal folds. The average adult body temperature, measured in the axillary region, is assumed to be 36.5-37.5 ° C, in children it is 0.5-1 ° C higher( 37-37.5 ° C), and in the elderly it is lower( 35.5-36.5 ° C).Thus, physiological fluctuations in temperature do not exceed 1 ° C. Measuring and monitoring body temperature is a daily and important responsibility for the nurse of separation of any profile. Body temperature is measured by a medical thermometer. The first medical thermometer was proposed by Fahrenheit in 1723. In our country a Celsius thermometer is used, which consists of a glass tube with a capillary, at the end of which there is a reservoir filled with mercury. This tube is attached to a scale on which fissions are deposited - from 34 to 42 ° C.The existing scale scale, expressed in degrees, allows us to call the thermometer a thermometer. The volume of mercury filling the reservoir and a small part of the thermometer's capillary tube increases with heating. The level of the mercury column in the capillary rises. It is not possible to descend independently after stopping heating. You can return mercury to the tank only by shaking it several times. Do this carefully, so as not to drop the thermometer or hit it against nearby objects. To store thermometers, a glass is usually used, at the bottom of which a layer of cotton wool is placed. At 1/3 or 1/2 of the volume, the beaker is filled with 70% alcohol, any disinfectant solution( for example, 0.5% chloramine solution) can be used, strictly keeping the exposure time in accordance with Order No. 408 and OST 42-21-2-15.In order to shake the thermometer out of the hand when shaking, a rubber cap is put on the top of the thermometer. Before measuring the temperature, the thermometer must be thoroughly wiped and, shaking off the mercury to below 35 ° C, give the patient or place the thermometer himself. The axillary basin should first be wiped with a dry towel, since moisture cools the mercury, and the thermometer will show a lower temperature. Between the thermometer and the body should not get underwear, and next to be a warmer or bubble with ice. In places used to measure body temperature, there should be no inflammatory process( redness of the skin, swelling), as there may be a local increase in temperature. Weak patient sick sister holds his hand. The duration of the measurement is at least 10 minutes. In very exhausted and severe patients, body temperature can be measured in the rectum. Contraindications to the measurement of temperature in this way are stool retention, diarrhea, rectum disease. Before entering the rectum, the thermometer should be lubricated with petroleum jelly or any fat, and then inserted half the length into the patient's position on the side. Buttocks should fit snugly against each other. After each measurement of the temperature in the rectum, the thermometer should be thoroughly washed with warm water and disinfected in alcohol or in one of the available disinfectants. To children, the temperature is measured in the inguinal fold. To do this, the child's leg is bent somewhat in the hip joint so that the thermometer is in the formed fold of the skin. Usually body temperature is measured 2 times a day, in the morning and in the evening - at 7-8 hours and 16-17 hours. The thermometer readings are entered in the temperature sheet, where the points denote the morning and evening temperatures. On the markings within a few days, a temperature curve is formed which, in many diseases, has a characteristic appearance. If necessary, an hourly temperature measurement is made and a graph of daily temperature variations is drawn on the points. The normal temperature for measurement in the armpit is 36.4-36.8 ° C.During the day, body temperature can vary: it is the lowest of all between 17 and 21 pm. The difference between morning and evening temperatures in healthy people does not exceed 0.6 ° C.After eating, heavy physical activity and in a hot room, the body temperature increases slightly.	https://womensecr.com/en/articles/8951
The heat index is the measure of the human body to cool itself. Using a combination of temperature and humidity, the heat index is the feels like temperature. Sweating cools the body through evaporation. Higher relative humidity slows the evaporation process which makes it much more difficult to cool itself. Also, if you are in the mid-day sun, the usual practice is to add 10-15 degrees to the heat index. With today's forecast high of 93, the dew point would have to be 69 degrees in order for today to have the highest heat index of the year so far. Click on the arrows in the lower right corner of the chart for a larger view. Here are the highest heat indices for the last few years in Louisville. 2017: 98 2016: 104 2015: 105 2014: 102 2013: 104 2012: 119 2012 was the extreme heat wave with 9 out of 10 days topping 100 degrees and the heat index was well over 100 for a number of days.	https://www.wlky.com/article/today-may-be-the-highest-index-of-the-year-so-far-for-louisville/10296117
\| \| posted on 25 June 2017 Does Drinking Hot Tea In Summer Really Cool You Down? from The Conversation -- this post authored by Steve Faulkner and Katy Griggs, Loughborough University I remember as a child, on the rare warm days that we used to get in Britain, my grandmother telling me to “have a cup of black tea … it will help cool you down". As a seven-year-old, this seemed like a crazy idea, especially when all I wanted was a cold lemonade and another ice cream. But it appears that this old wives’ tale may actually be more Stephen Hawking than Stephen King. Please share this article - Go to very top of page, right hand side for social media buttons. The idea of drinking hot drinks in warm weather goes back hundreds of years. Tea, or “chai" is one of the most popular drinks in India, and many of the leading consumers of tea per capita are in tropical or desert regions. Recently, evidence has begun to emerge that drinking hot drinks may really help to cool you down, too. In 2012, Ollie Jay published the first of a series of papers to see if drinking a warm drink can actually lower the amount of heat stored by the body compared to a cold drink. In this first study, volunteers were asked to cycle at a relatively low intensity for 75 minutes in around 24°C heat, 23% relative humidity, while consuming water at either 1.5˚C, 10˚C, 37˚C or 50˚C. The change in core temperature was slightly greater when 50˚C water was ingested compared to 1.5˚C and 10˚C water. However, when the authors considered the effect of drink temperature on body heat storage, which is a better indicator of total body temperature, the results were very different. Following the ingestion of the warm drink, overall body heat storage was actually lower following exercise than with cooler drinks. The sweat factor An explanation for these findings appears to be related to how sweating may be influenced by drink temperature. Sweating, and more importantly the evaporation of this sweat, is one of the key avenues for modulating body temperature and maintaining heat balance. Due to the increased heat load from drinking a warm drink, there is a compensatory increase in overall sweat output, which outweighs the internal heat gain from the warm drink. Consistently, a 50˚C drink results in a higher whole body sweat loss (around 570ml vs about 465ml for 1.5˚C). In practical terms, this means that more sweat is produced which is evaporated from the skin surface, increasing heat loss from evaporation and reducing body heat storage. Cold water: should he drink it? Shutterstock Importantly, however, this study was conducted under conditions that allowed complete evaporation of sweat - in other words dripping sweat was limited by maintaining a good airflow and keeping humidity low. The results would likely be different in conditions where sweat evaporation is limited, such as in hot and humid conditions. In fact, drinking cold drinks may be more favourable in these circumstances, minimising inefficient sweat losses - dripping sweat - and consequently aiding an individual’s hydration status. Mouth or stomach? In a second study, Jay aimed to establish the effect of drink temperature on local sweat rate, and to determine the location of thermoreceptors that may influence sweating. They demonstrated that with differing drink temperatures, colder drinks (1.5˚C) resulted in reductions in local sweat rate compared to when warm drinks were ingested (50˚C), despite identical changes in core and skin temperature. Interestingly, however, differences in the sweat response were found when fluid was either swilled around the mouth or delivered directly to the stomach via a nasogastric tube. The data showed that only when cold drinks were delivered directly to the stomach did they result in reduced local sweat rate. This data indicates that the sensors responsible for influencing the sweat response, and therefore regulation of body temperature, reside somewhere in the abdominal cavity. In a third study conducted in their lab, the team asked people to consume either 37˚C fluid or ice during exercise. In agreement with their previous work, they showed that there was a reduction in heat loss following ice ingestion compared to fluid at 37˚C, as a result of reduced sweat evaporation from the skin surface. This has implications for endurance performance in the heat. In essence, where changes in body temperature are known to influence performance, ice ingestion could result in an increase in body heat, negatively influencing endurance capability. The ingestion of an iced drink prior to exercise and in hot and humid environments, however, should be beneficial. So, depending on your environmental conditions, maybe reaching for that cup of tea isn’t such a crazy idea after all. Plus the moral of the story: listen to your grandmother’s advice - it’s based on years of experience. Steve Faulkner, Research associate, Loughborough University and Katy Griggs, Research Assistant and PhD student, Loughborough University This article was originally published on The Conversation. Read the original article.	http://econintersect.com/pages/contributors/contributor.php?post=201706252205
What if We Could Make Buildings Sweat? Following up on the previous post “Can We Design Buildings for Heat and Cooling that Mimic the Human Body”, a similar question popped into my head regarding making buildings sweat. The evaporation of water is an endothermic process that cools a surface. Evaporation of sweat from the skin surface has a cooling effect due to this phenomenon. Hence, in hot weather, or when the individual’s muscles heat up due to exertion, more sweat is produced in response to your rising internal thermostat. Why couldn’t this same process be applied to buildings? What if there was a way to take the condensation that often occurs at sunrise, capture it and re-release it as needed. Could we create materials, while not letting moisture intrude into the building, that could capture the moisture that naturally occurs and evaporate it off in the daytime when the sun hit the walls to cool it off? Obviously this would be a benefit in climates where we are using a great deal of cooling. We don’t want this occurring in cold climates for a variety of reasons. That’s a discussion for another day. Are there any ideas out there? When people get hot, they sweat and it cools them off. Is it possible to apply this concept to buildings?	https://blog.certainteed.com/2012/07/what-if-we-could-make-buildings-sweat/
Why is the surface temperature of a roasting meat lower than the temperature of the oven? One of the most obvious explanations is that the air molecules are hotter because they come in direct contact with the oven's heat source or scorching interior walls. Another significant reason is that the meat's colder interior absorbs heat from, and cools, the warmer surface. As the meat's internal temperature increases during cooking, this cooling influence diminishes in importance. A third major factor, evaporation, is less apparent. As the meat cooks by dry heat, some of its internal juices flow to the surface and evaporate. This ongoing process produces a cooling effect. (When water evaporates, it cools the surrounding area because the change from liquid to gas requires heat calories). For this reason - and because animal flesh is a less efficient conductor than metal - you can briefly touch a roasting meat but not the pan in which it sits.	http://www.asianonlinerecipes.com/rss/xml-rss2.php?itemid=1270
LOWELL -- Scorching temperatures expected to last through Tuesday evening have prompted the National Weather Service to issue a heat advisory for cities across the state, including Lowell and Fitchburg. According to the advisory, the heat index (which combines air temperature and relative humidity) during this period will reach up to 103 degrees due to temperatures in the upper 80s to mid 90s, and dew points are in the lower to mid 70s. The heat advisory is in effect until Tuesday at 8 p.m. National Weather Service Meteorologist Bill Simpson said residents to be careful with any outdoor physical activities. "The sweating process is based upon evaporation of your sweat on the skin surface, which cools the skin surface. Once you get very high dew points and high temperatures, that process is not that efficient," Simpson said Monday. "People don't realize that a lot more people die from heat exhaustion than tornadoes and winter storms. It affects a much wider range of people. There's widespread potential danger if you're out working in the sun during the middle of the day. We like to focus on that." According to the weather service, Tuesday in Lowell is expected to have a high temperature near 97 with a slight chance of showers after 3 p.m. Wednesday is forecast to be partly sunny with a high near 90 and a chance of showers and thunderstorms mainly after 1 p.m. On Thursday, the weather service forecasts the area will remain partly sunny with a high near 86. Friday will also be sunny, with a high near 87. "Today and tomorrow is the worst and then we get some minor relief off on Wednesday and Thursday," Simpson said Monday of the combination of temperatures and dew points. In Fitchburg, the weather service is forecasting a sunny Tuesday with a high near 94, as well as a chance of showers and thunderstorms between 2 p.m. and 5 p.m. The chance of showers and thunderstorms will remain until mainly after noon Wednesday. That day the high temperature will be near 87. The forecast for Thursday in Fitchburg is partly sunny with a high near 84 and a chance of showers before 11 a.m. Friday is expected to be mostly sunny with a high near 85.	http://www.sentinelandenterprise.com/news/ci_32054731/take-care-out-there-hot-humid-all-week
Some interesting phenomena happen when convection is accompanied by a phase change . It allows us to cool off by sweating, even if the temperature of the surrounding air exceeds body temperature. Heat from the skin is required for sweat to evaporate from the skin, but without air flow, the air becomes saturated and evaporation stops. Air flow caused by convection replaces the saturated air by dry air and evaporation continues. The average person produces heat at the rate of about 120 W when at rest. At what rate must water evaporate from the body to get rid of all this energy? (This evaporation might occur when a person is sitting in the shade and surrounding temperatures are the same as skin temperature, eliminating heat transfer by other methods.) Strategy Energy is needed for a phase change ( ). Thus, the energy loss per unit time is We divide both sides of the equation by to find that the mass evaporated per unit time is Solution (1) Insert the value of the latent heat from [link] , . This yields Discussion Evaporating about 3 g/min seems reasonable. This would be about 180 g (about 7 oz) per hour. If the air is very dry, the sweat may evaporate without even being noticed. A significant amount of evaporation also takes place in the lungs and breathing passages. Another important example of the combination of phase change and convection occurs when water evaporates from the oceans. Heat is removed from the ocean when water evaporates. If the water vapor condenses in liquid droplets as clouds form, heat is released in the atmosphere. Thus, there is an overall transfer of heat from the ocean to the atmosphere. This process is the driving power behind thunderheads, those great cumulus clouds that rise as much as 20.0 km into the stratosphere. Water vapor carried in by convection condenses, releasing tremendous amounts of energy. This energy causes the air to expand and rise, where it is colder. More condensation occurs in these colder regions, which in turn drives the cloud even higher. Such a mechanism is called positive feedback, since the process reinforces and accelerates itself. These systems sometimes produce violent storms, with lightning and hail, and constitute the mechanism driving hurricanes. Notification Switch Would you like to follow the 'Physics subject knowledge enhancement course (ske)' conversation and receive update notifications?	https://www.jobilize.com/online/course/8-6-convection-7-heat-transfer-methods-by-openstax?qcr=www.quizover.com&page=2
Why are hot metals softer? Why does metal feel colder than wood? A closer look at our perception of warmth shows that our skin is by no means suitable as a thermometer. Because the perceived temperature depends on the material that we are touching. At low temperatures, a metal fence appears much colder than a wooden fence. The fences - regardless of their material - take on the ambient temperature. This phenomenon can also be observed in many other everyday situations: The 21 degrees Celsius warm water in the sea appears significantly cooler than air with the same temperature. And even a wooden floor feels warmer than a tiled floor at room temperature. So the difference is not made by the temperature, but solely by our perception of warmth. Apparently the skin is not a good thermometer. But what makes the metal fence colder and the wooden fence warmer for us, even though both are at the same temperature? The solution lies in the physical definition of “temperature” and “warmth”, which deviates from everyday understanding. Because there we often equate the two terms. Water in various states of aggression In physics, temperature is an objective measure of how warm or cold something is. It is determined by the constant disorderly movement of the atoms or molecules that make up a solid, liquid or gas. In general, the higher the temperature, the more the particles move. In gases, the atoms or molecules whiz around completely detached from one another, in liquids the building blocks of matter are still freely movable, but touch each other almost permanently - and in solid bodies each atom or molecule sits in a fixed place, but can still do a little to and fro, swing and rotate. The countless particles that are in an iron fence, in a glass full of water or in the air move at different speeds - but their kinetic energy fluctuates around a certain average value. The temperature is a measure of the average speed of the atoms or molecules. However, only the disordered, random movement of the particles makes a contribution to this. If all the atoms in the iron fence were to move in one direction, the entire fence would move - and that would have no effect on the temperature. Over time and without any additional external energy supply, a thermal equilibrium is established in every system - whether solid, liquid or gas: the temperature or the average speed of the atoms or molecules takes on the same value everywhere. But if you bring two systems with different temperatures into contact, the equilibrium is suddenly disturbed. Because in the body with the higher temperature, the atoms and molecules move more on average. At the contact surface, these particles therefore transfer part of their kinetic energy to the building blocks of matter in the body with the lower temperature. So energy is transported - and not just on the contact surface: inside the two bodies, the more energetic particles give off their energy to their closest neighbors. As a result, the temperature of the two systems gradually equalizes until it finally has the same value everywhere and a new thermal equilibrium has been established. The transport of energy does not take place at the same speed in all substances - some transmit heat well, some poorly. In an irregularly structured, porous material such as wood, it is relatively difficult for the atoms to pass on their kinetic energy. Wood therefore has a low thermal conductivity. If, on the other hand, the atoms are regularly arranged in a crystal lattice, the energy transport within the material works much better. In electrically conductive materials such as iron or copper, the freely moving electrons can also be pushed by the vibrating atoms and thus transport the heat even faster through the grid. Metals are therefore good conductors of heat. Iron, for example, conducts heat around 400 to 800 times better than wood. Thermal conductivity also determines how warm or cold an object feels to us. The skin temperature is around 30 degrees Celsius. If we now touch a cool object, energy is transported from the warm skin to the cooler material. How quickly heat is withdrawn from our skin depends on the thermal conductivity of the material touched. Compared to wood, for example, metal cools the skin much faster due to its higher thermal conductivity. Special receptors in the skin react to this flow of heat - i.e. register slow or rapid cooling or warming of the skin - but do not record the actual temperature of the touched object. Therefore, the two materials feel differently warm despite the same temperature. Of course, this effect also works the other way round: We burn our fingers on a hot piece of metal, while we can still touch a piece of wood at the same temperature without any problems. It is very similar when we walk into sea water with an air temperature of 21 degrees Celsius: water conducts heat around twenty times better than air. As a result, our skin dissipates heat to the water much faster than it does to the air - and we freeze until a new state of equilibrium is established. If you leave the water, you freeze again. Another effect plays a role here: the water on the skin evaporates, removing heat from our body and the “perceived temperature” drops. The wind accelerates evaporation and thereby the flow of heat, which makes us tremble even more. So the thermoreceptors in our skin can really lead us astray. If we want to determine a temperature, we should rather use a thermometer. - Can play PlayStation 3 DVDs - What are the benefits of CA studies - How can I change my social situation? - What Pets Allowed NSCC - Ventilation of the lawn helps with drainage - What countries are importing from Sudan - How do giant squids fight sharks - Why is misfortune sometimes necessary? - How to do painless permanent tattoos - What's your worst fanboy fangirl experience - Is the stock market a game of chance?	https://philliesbell.com/?post=7184
Evapotranspiration is the term used to describe two processes in the hydrologic cycle (see below); Water loss from the soil–plant system, through soil evaporation and plant transpiration, is the sum of these processes. Temperature is a major factor controlling evaporation and higher temperature mostly speed the rate of evaporation. Other factors that make an impact on the rate include the amount of water already help by air (humidity) and air movement. Furthermore, high wind speed and low humidity accelerate evaporation. Transpiration is the loss of water vapour primarily through the stomata (stomata is microscopic pores in plants’ surface layers) of green plants and leaves. Plants (all above ground have a cover of wax cuticle that helps prevent water loss. This keeps the internal part of the plant almost concentrated with water vapor and is an important element of a process called photosynthesis. In the daytime, the stomata open to take in carbon dioxide. The water inside the leaves transpires, or simply evaporates and escapes the plant. The transpiration cools the plant leaves; allowing the photosynthetic apparatus to produce at optimum level’s energy in form of carbohydrates. Decreasing rates of transpiration that are due to global warming and local drying also affect photosynthesis.	https://buddhajeans.com/encyclopedia/evapotranspiration/
In the Heat of the Moment Heat-related illness not only happens at work but also at home and anyone can become a victim. The Center for Disease Control in Atlanta states in 2016 there were 658 deaths attributed to heat related illnesses and estimates that number to increase in years to come. At this point, we are well into summer, and with the rise of temperature and humidity, the chances of heat illness are much higher. When our proactive measures dealing with the increased heat don’t work, we can end up with heat-related emergencies. Causes of heat emergencies: Heat is absorbed from the environment faster than the body can get rid of it. The body cools typically by perspiring and varying the blood flow to the skin. When the body's primary cooling system is unable to evaporate, the sweat produced by the body becomes overheated. This typically happens when the temperature is equal to or above body temperature, and humidity is high enough to prevent the cooling effect from the evaporation of sweat. Workers at risk: - People with lighter skin - People not acclimatized (usually takes one to two weeks) - Acclimatized people that are ill or are away from work for one week - People exposed to direct sunlight during hottest part of the day (10 AM to 2 PM) - People exposed to heat producing operations (machinery, boilers, tanks, etc.) - Workers over 40 as they have a reduced ability to sweat The three main types of heat emergencies, in progression, are Heat Cramps, Heat Exhaustion and Heat Stroke. Heat Cramps Symptoms: Painful spasms in the larger body muscles (ex. legs, stomach and/or back) this results from a loss of fluids and salt from heavy sweating. First Aid Treatment: Find a cool place to rest while drinking more water and massage cramped muscles. Heat Exhaustion Symptoms: Can include: Moist, clammy skin (may look pale), heavy sweating, rapid breathing, weak pulse, a feeling of weakness or being tired, confused or clumsy, blurred vision and/or fainting. First Aid Treatment: First move the victim to cool place, give cool water only if conscious and coherent, have victim sit or lay down and apply wet towels and cool packs to pressure points. Seek medical attention if improvement is not noted in 30 minutes as heat exhaustion can lead to heat stroke. Heat Stroke Symptoms: At this point the body has used up excess water and salt, sweating stops and body temperature elevates. The skin will be dry and hot to the touch. The person will appear weak, confused possibly upset and irrational. They will likely have a headache and be dizzy, may have loss of consciousness and have convulsions. First aid treatment: Immediately call an ambulance as heat stroke can quickly lead to death. Move the victim to a cool place and remove heavy and excess clothing. Cool the person’s entire body by sponging or spraying cold water, and fan the person to help lower the person's body temperature. Be prepared to care for seizures if necessary. Do not use aspirin or acetaminophen. Most people with heatstroke have an altered level of consciousness and cannot safely be given fluids to drink. If the person is awake and alert enough to swallow, give the person fluids [32 fl oz (1 L) to 64 fl oz (2 L) over 1 to 2 hours] for hydration. Make sure the person is sitting up enough so that he or she does not choke. Lastly, do not send them home or leave them alone no matter how much they protest, unless a physician has approved it.	https://www.wachsservices.com/wachs-weekly/2018/6/11/in-the-heat-of-the-moment
Humidity is the amount of water vapour present in the air or any other gases, and generally, water vapours are invisible to the human eye. Humidity is dependent on the temperature and pressure of the system, which is in consideration. For example, if there's the same amount of water vapour in cool and warm air, then humidity is higher in the cool air as compared to warm air. When air is cooled to that temperature, it becomes saturated with water vapour, which is known as the dew point. When the airborne water vapour is cooled further, it condenses to produce liquid water (dew). When air cools to its dew point due to contact with a colder-than-air surface, water condenses on the surface. If the temperature increases, the amount of water vapour that is needed to bring saturation also increases. In total, there are three main ways in which we can express humidity. The ratio of the actual water vapour pressure to the saturation vapour pressure is relative humidity, which is the quantity of water vapour in the air represented as a percentage of the highest amount that the air could retain at a given temperature. So, in most cases, relative humidity is measured in terms of percentage. A greater percentage indicates a more humid air-water combination. The air is saturated and reaches its dew point when it has a relative humidity of 100 per cent. Only the invisible water vapour is taken into account when calculating relative humidity. The relative humidity of the air is not affected by mists, clouds, fogs, or water aerosols. The whole mass of water vapour present in a particular volume or mass of air is known as absolute humidity. It doesn't take the temperature into account. When the air is saturated at 30 °C, absolute humidity in the atmosphere ranges from near zero to about 30 g per cubic meter. The unit of measurement of absolute humidity is gram per cubic meter. If the volume is not constant, the absolute humidity fluctuates when the air temperature or pressure changes. As a result, it is inappropriate for chemical engineering calculations, such as drying, where temperature varies greatly. Specific humidity is defined as the ratio of the mass of water vapour to the total mass of the water vapour in the air (or moisture content). The mixing ratio, which is defined as the ratio of the mass of water vapour in an air parcel to the mass of dry air in the same parcel, is roughly equivalent to specific humidity. As the temperature drops, so does the amount of water vapour required to attain saturation drops. Generally, it is stated in terms of grammes of vapour per kilogram of air. In order to provide human comfort, and ensure health and safety, while meeting the environmental requirements for the machinery, sensitive materials (historical documents) and technical processes, some methods are employed. These methods also known as climate control refer to the control of temperature and relative humidity in buildings, vehicles and in other closed environments. Humidity is an important abiotic element in defining any ecosystem, including tundra, marshes and the desert, and it is a determining factor that allows animals and plants to survive in a particular area. Through perspiration and evaporation, the human body disperses heat. The main routes of heat transfer from the body are heat convection to the surrounding air and thermal radiation. The rate of perspiration evaporation from the skin reduces under high humidity. In periods of excessive moisture, the atmosphere cannot disperse heat from the body's surface by conducting it to the air if it is thus warm or warmer than the skin. When so much blood reaches the outside surface and the working muscles, the brain and other inside organs get lesser. Physical strength diminishes, and tiredness happens earlier than others. Heatstroke or Hyperthermia can also impact alertness and mental function. Humidity affects the temperature in two prominent ways. First, water vapour includes "latent" energy in the environment. This amount of heat is removed from the surface fluid through transpiration or evaporation, which cools the surface of the earth. It is the most important non-radiative surface cooling effect. The average net radiative warming on the surface is around 70 percent. Second, the most high percentage of all greenhouse gases found in the atmosphere is water vapour. Water vapour allows entry to the most amount of solar energy like other greenhouse gases. But, it absorbs infrared radiation released (radiated) upwards by the surface of the earth, which is why wet zones are not chilly at night at all, whereas dry desert zones are quite cool at night. This is the selective absorption that causes the greenhouse effect.	https://www.aakash.ac.in/important-concepts/physics/unit-of-humidity
Why is the integumentary system important? BRIAN M. · Mandira P. The Integumentary System is our contact point with the world we live in through, protection, communication, senses, touch, pressure and temperature. The Integumentary System or skin is the primary line of defense between our bodies and the environment. The keratinised top layers of skin form a boundary by being dead to keep out bacteria, fungus, viral particles and other pathogens. The skin pigment melanin also protects our body from the effects of ultra-violet radiation. The skin maintains the moisture of the body by holding in water and keeping the muscular and skeletal and organ systems of the body from desiccation, drying out. The skin maintains blood pressure and temperature by dilation and constriction of blood vessels (dilation causes release of heat and constriction helps to conserve heat). The skin cools the body by the secretion of eccrine sweat and the convection of body heat. The skin secretes wastes through apocrine sweat. The skin is involved in communication through coloration and touch. There are receptors present in skin, responsible for sensation of touch, pressure, pain and temperature.	https://socratic.org/questions/why-is-the-integumentary-system-important
The water vapor in the atmosphere is important because it affects our comfort. Except in cold weather, we sweat continuously: the water in the sweat evaporates, draws its latent heat of evaporation from the skin, and so keeps us cool. Beads of sweat appear only when the water cannot evaporate as fast as it reaches the surface of the skin; we then feel uncomfortably hot. On the other hand, if water evaporates from the skin too rapidly, the skin feels parched and hard; around the mucous membranes-at the mouth and nose-it tends to crack. The rate at which water evaporates, from the skin or anywhere else, depends on the pressure of the water vapor surrounding it. If the water vapor above the skin is far from saturated, evaporation is swift. If the vapor is already saturated, water reaching the skin comes immediately into dynamic equilibrium with it; individual molecules are exchanged between liquid and vapor, but no mass of liquid is lost, and water accumulates. The Partial Pressure of Atmospheric Water The atmosphere contains other gases besides water-vapor, such as oxygen and nitrogen. In speaking of the water-vapor, therefore, we must refer to its ‘partial pressure’ as explained. Water-vapor in the atmosphere is also important because it affects the weather. Let us suppose that the atmosphere has a temperature of 1200C- in a warm day and that the water vapor in it has a partial pressure of 12mm mercury. It will have a density of about 12mg per litre. The density of saturated water vapor at 200C is 17.3mg per litre, and its pressure 17.5mm mercury. The water vapor in the atmosphere is therefore not saturated. Now let us suppose that the atmosphere cools to 140C, without changing its composition. The 60C fall in temperature will hardly affect the density of the water vapor, but it will bring the atmosphere to saturation. For the pressure of saturated water vapor at 140C is 12mm mercury, and its density about 12mg per litre. If the atmosphere cools liquid water-that is, of fog or cloud. Relative Humidity The dampness of the atmosphere, besides affecting the weather and our comfort, it important also in storage and manufacture of many substances-tobacco and cotton, for example. From what we have said already, we can see that the important factor is not the actual proportion of water vapor in the atmosphere, but its nearness to saturation. In the above example, the density of the vapor remained almost constant, but we would have felt the atmosphere becoming much damper as it cooled from 200C to 140C. The dampness of the atmosphere is expressed by its relative humidity, R.H., which is defined as follows: In other words, [RH= Density of water – Vapor in atmosphere/ Density of saturated water – Vapor at the same temperature] Because an unsaturated vapor roughly obeys Boyle’s law, its density is roughly proportional to its pressure; the relative humidity as defined above is therefore given by [RH= Partial pressure of water/ S.V.P at temperature of atmosphere] Where S.V.P. stands for ‘saturated vapor pressure’. Before describing the methods of measurement, we must warm the reader against thinking that the atmosphere ‘takes up’ water vapor. The atmosphere is not a sponge. Water-vapor exists in it in it sown right; and our knowledge of vapor makes us feel sure that, if we could live in an atmosphere of water-vapor alone, we would have just the same experiences of humidity as we now have in our happily richer surroundings.	https://gulpmatrix.com/measure-partial-pressure-atmospheric-water/
During the summer months, with rising temperatures, it is no surprise that in the U.S. alone, over 700 people die a year from heat stroke. According to the CDC, studies suggest that, if current emissions hold steady, excess heat-related deaths in the U.S. could climb to between 3,000 and 5,000 per year by 2050. It is important to take the necessary precautions to avoid heat stroke, as well as to be able to recognize when it’s happening to you or others. Get more information about how to avoid and recognize heat stroke with these summer health tips. During heat stroke, a person’s core body temperature rises to about 105 degrees Fahrenheit. The body overheats, putting a strain on the heart. The heart then pumps less blood to vital organs. This affects blood pressure and symptoms such as dizziness and disorientation come into play. At a cellular level, fluid volume and membrane permeability are also thrown for a loop and cells begin to die. To protect you and your loved ones, several precautions should be taken. Do your best to avoid strenuous physical activity outside during the hottest time of the day, between 10 am and 6 pm. If you are an individual who works outside, you should make sure you drink plenty of water every half-hour or so and take breaks in a cool environment, if at all possible. Try wearing lightweight, light-colored clothing and hats to avoid excess sun exposure. A good indicator of whether or not you are hydrated is the color of your urine. If you are drinking enough water, your urine will probably look light in color. A darker color indicates you are not drinking enough water. Those most affected by heat stroke are the elderly and children. Do not leave children, pets, or the elderly out in the car. When parked in the sun, the temperature in your car can rise 20 degrees in just 10 minutes. Even if the windows are cracked or the car is in the shade, it is still very dangerous. Symptoms of heat stroke include: headache, dizziness, light-headedness, a lack of sweating despite the heat, red, hot, or dry skin, muscle weakness or cramps, nausea or vomiting, rapid heartbeat, rapid breathing, behavioral changes such as confusion, disorientation, or staggering, seizures, or any level of unconsciousness. If heat stroke is suspected, seek medical attention immediately. There are several techniques that may be used to resolve heat stroke. The first is through immersion in cold or ice water. Another includes an evaporation technique that involves misting cool water on the skin while warm air fanned over the body causes water to evaporate, which in turn cools the skin. An additional method works by wrapping the body in a special cooling blanket and applying ice packs to the groin, neck, back and armpits to lower temperature. Avoiding heat stroke is easy. The two most important factors are hydration and the avoidance of excessively hot environments. Drink lots of water, take it easy, and utilize resources like air conditioning and fans. Your body will thank you. For more information and health tips for summer, stay tuned to our blog.	https://www.helprx.info/blog/health-tips/the-body-is-a-furnace-avoiding-heat-stroke
What role does temperature play in clouds? Heated by sunshine, the ground heats the air just above it. That warmed air starts to rise because, when warm, it is lighter and less dense than the air around it. As it rises, its pressure and temperature drop causing water vapor to condense. Eventually, enough moisture will condense out of the air to form a cloud. How does temperature affect rain? As average temperatures at the Earth’s surface rise, more evaporation occurs, which, in turn, increases overall precipitation. … In addition, higher temperatures lead to more evaporation, so increased precipitation will not necessarily increase the amount of water available for drinking, irrigation, and industry. How does temperature form cloud formation? In order for clouds to form, the ground must get warm enough to evaporate water into the air. At higher temperatures, there is more evaporation of water at the surface. Evaporation of water at the surface leads to the formation of clouds and sometimes storms. Why all clouds do not bring rain? Clouds produce rain when tiny droplets of liquid water begin to stick together, forming larger and larger drops. … it won’t produce any rain. For example, if there aren’t enough droplets of water in a cloud to collide and form large drops, the tiny droplets will stay suspended in the air and it won’t rain. Where do clouds go if it doesn’t rain Why? Mike Moss: There are a couple of mechanisms by which the clouds may “go away.” One is by a process called advection, meaning simply that the cloud droplets are moving along at roughly the speed of the wind at cloud height, so that the clouds are carried by the wind in the direction toward which the wind is blowing, … How does temperature affect weather? Higher temperatures mean that heat waves are likely to happen more often and last longer, too. … Warmer temperatures can also lead to a chain reaction of other changes around the world. That’s because increasing air temperature also affects the oceans, weather patterns, snow and ice, and plants and animals. Why does temperature drop when it rains? Rain Cools Us: When the droplet reaches us it cools its surroundings. … Increased Humidity Can Make The Air Feel Colder: As the rain water warms it begins to evaporate, increasing the humidity of the air which correspondingly loses its ability to insulate – the air its self begins to feel cooler. What temperature are clouds? Clouds are made of tiny water droplets or ice crystals – often both water and ice are present together when temperatures are between freezing (32 degrees Fahrenheit and -32.8 degrees Fahrenheit (-36 degrees Celsius). If you have ever walked in fog you have walked in a cloud – a cloud that forms at ground level. How do clouds affect the weather? Clouds affect the climate but changes in the climate, in turn, affect the clouds. … Clouds warm or cool Earth’s atmosphere by absorbing heat emitted from the surface and radiating it to space. Clouds warm and dry Earth’s atmosphere and supply water to the surface by forming precipitation. Why was temperature low when the sky was cloudy? During the day, sunlight heats the Earth. If skies are clear, more heat reaches the ground leading to warmer temperatures. On cloudy days, clouds reflect the sun’s light into space, keeping much of the energy away from the surface and leading to cooler temperatures.	https://laradiometeo.org/natural-phenomena/how-does-temperature-affect-clouds-and-rain.html
DIRECTIONS: Each of the numbered items or incomplete statements in this section is followed by answers or by completions of the statement. Select the ONE lettered answer or completion that is BEST in each case. 1. Antipyretics such as aspirin effectively lower core temperature during fever, but they are not used to counteract the increase in core temperature that occurs during exercise. Which of the following best explains why it is inappropriate to use antipyretics for this purpose? (A) The increase in core temperature during exercise stimulates metabolism via the Q10 effect, helping to support the body's increased metabolic energy demands (B) A moderate increase in core temperature during exercise is harmless, so there is no benefit in preventing it (C) Antipyretics are ineffective during exercise because they act on a mechanism that operates during fever, but not to a significant degree during exercise (D) Antipyretics increase skin blood flow so as to dissipate more heat, increasing circulatory strain during exercise (E) The increased heat production during exercise greatly exceeds the ability of antipyretics to stimulate the responses for heat loss 2. A surgical sympathectomy has completely interrupted the sympathetic nerve supply to a patient's arm. How would one expect the thermoregulatory skin blood flow and sweating responses on that arm to be affected? Vasoconstriction Vasodilation in the Cold in the Heat Sweating (A) Abolished Intact Intact (B) Abolished Intact Abolished (C) Abolished Abolished Intact (D) Abolished Abolished Abolished (E) Intact Abolished Abolished 3. A person resting in a constant ambient temperature is tested in the early morning at 4:00 AM, and again in the afternoon at 4:00 PM. Compared to measurements made in the morning, one would expect to find in the afternoon: Threshold for Core Sweating Cutaneous Temperature Threshold Vasodilation (A) Unchanged Higher Lower (B) Unchanged Unchanged Unchanged (C) Higher Higher Higher (D) Higher Unchanged Lower (E) Lower Lower Lower 4. Compared to an unacclimatized person, one who is acclimatized to cold has (A) Higher metabolic rate in the cold, to produce more heat (B) Lower metabolic rate in the cold, to conserve metabolic energy (C) Lower peripheral blood flow in the cold, to retain heat (D) Higher blood flow in the hands and feet in the cold, to preserve their function (E) Various combinations of the above, depending on the environment that produced acclimatization 5. Which statement best describes how the elevated core temperature during fever affects the outcome of most bacterial infections? (A) Fever benefits the patient because most pathogens thrive best at the host's normal body temperature (B) Fever is beneficial because it helps stimulate the immune defenses against infection (C) Fever is harmful because the accompanying protein catabolism reduces the availability of amino acids for the immune defenses (D) Fever is harmful because the patient's higher temperature favors growth of the bacteria responsible for infection (E) Fever has little overall effect either way 6. A manual laborer moves in March from Canada to a hot, tropical country and becomes acclimatized by working outdoors for a month. Compared with his responses on the first few days in the tropical country, for the same activity level after acclimatization one would expect higher (A) Core temperature (B) Heart rate (C) Sweating rate (D) Sweat salt concentration (E) Thermoregulatory set point In questions 7 to 8, assume a 70-kg young man with the following baseline characteristics: total body water (TBW) = 40 L, extracellular fluid (ECF) volume = 15 L, plasma volume = 3 L, body surface area = 1.8 m2, plasma [Na+] = 140 mmol/L. Heat of evaporation of water = 2,425 kJ/kg = 580 kcal/kg. 7. Our subject begins an 8-hour hike in the desert carrying 5 L of water in canteens. During the hike, he sweats at a rate of 1 L/hr, his sweat [Na+] is 50 mmol/L, and he drinks all his water. After the end of his hike he rests and consumes 3 L of water. (For simplicity in calculations, assume that the plasma osmolality equals 2 times the plasma [Na+].) What are his plasma sodium concentration and ECF volume after he has replaced all the water that he lost? Plasma [Na+] 8. Our subject is bicycling on a long road with a slight upward grade. His metabolic rate (M in the heat-balance equation) is 800 W (48 kJ/min). He performs mechanical work (against gravity, friction, and wind resistance) at a rate of 140 W. Air temperature is 20°C and hc, the convective heat transfer coefficient, is 15 W/(m2^°C). Assume that his mean skin temperature is 34°C, all the sweat he secretes is evaporated, respiratory water loss can be ignored, and net heat exchange by radiation is negligible. How rapidly must he sweat to achieve heat balance? (Remember that 1 W = 1 J/sec = 60 J/min.) Tips and Tricks For Boosting Your Metabolism So maybe instead of being a pencil-neck dweeb, youre a bit of a fatty. Well, thats no problem either. Because this bonus will show you exactly how to burn that fat off AS you put on muscle. By boosting your metabolism and working out the way you normally do, you will get rid of all that chub and gain the hard, rippled muscles youve been dreaming of.	https://www.78stepshealth.us/skeletal-muscle-2/review-questions-xaw.html
(1920–58). A British biophysicist, Rosalind Franklin is best known for her contributions to the discovery of the molecular structure of deoxyribonucleic acid (DNA). DNA is the chief substance composing chromosomes and genes, the hereditary material. When Francis Crick, James Watson, and Maurice Wilkins were awarded the 1962 Nobel prize for physiology or medicine for determining the structure of the DNA molecule, many scientists believed that Franklin should have been honored with them. Born in London on July 25, 1920, Rosalind Elsie Franklin won a scholarship to Newnham College, Cambridge. After graduation in 1941 she began research on the physical structure of coals and carbonized coals. Working in Paris from 1947 to 1950, she gained skill in using X-ray diffraction as an analytical technique. (X-ray diffraction is a method of analyzing the crystal structure of materials by passing X-rays through them and observing the diffraction, or scattering, image of the rays.) Franklin used this technique to describe the structure of carbons with more precision than had previously been possible. She also determined that there are two distinct classes of carbons—those that form graphite when they are heated to high temperatures and those that do not. In 1951 Franklin joined the King’s College Medical Research Council biophysics unit. With Raymond Gosling she conducted X-ray diffraction studies of the molecular structure of DNA. Based on these studies, she at first concluded that the structure was helical (having spiral arms). Later research caused her to change her mind, and it was left to Watson and Crick to develop the double-helix model of the molecule that proved to be consistent with DNA’s known properties. Some of the data used by those scientists in their successful effort, however, was first produced by Franklin. From 1953 until her death on April 16, 1958, Franklin worked at the crystallography laboratory of Birkbeck College, London. There she published her earlier work on coals and helped determine the structure of the tobacco mosaic virus.	https://kids.britannica.com/students/article/Rosalind-Franklin/274418
Search this site. She then studied natural sciences at Newnham College, Cambridge , from which she graduated in Earning a research fellowship, she joined the University of Cambridge physical chemistry laboratory under Ronald George Wreyford Norrish , who disappointed her for his lack of enthusiasm. This helped her earn a Ph. Rosalind Franklin and DNA Skip navigation. Franklin took Photo 51 after scientists confirmed that DNA contained genes. Watson and Crick used that image to develop their structural model of DNA. X-ray crystallography, the technique Franklin used to produce Photo 51 of DNA, is a method scientists use to determine the three-dimensional structure of a crystal. Crystals are solids with regular, repeating units of atoms. Some biological macromolecules, such as DNA, can form fibers suitable for analysis using X-ray crystallography because their solid forms consist of atoms arranged in a regular pattern. To perform an X-ray crystallography, scientists mount a purified fiber or crystal in an X-ray tube. The X-ray tube generates X-rays that strike the purified material. X-rays are electromagnetic waves that have a shorter wavelength and higher energy than visible light. Because of their short wavelength, X-rays can pass through a crystal and interact with the electrons of the atoms within the crystal. When X-rays interact with electrons in a crystal the X-rays scatter, or diffract, at angles that indicate the arrangement of atoms in the crystal, or its structure. When the X-rays scatter, they strike a film mounted behind the crystal and leave a pattern of dark marks. The pattern of dark marks on the film gives scientists information about the structure of the crystal. However, at that time scientists generally agreed that DNA merely provided structural support for cells and that protein must be genetic material. When mounting the DNA fibers for viewing, Wilkins and Gosling were able to bundle many of the thin fibers together and pull them tight to provide a larger sample to better diffract X-rays. Furthermore, the two researchers kept the DNA fibers wet with water by keeping them in a humid environment. The resulting X-ray diffraction pattern of DNA was of a higher quality than any patterns collected prior. Before joining the lab, Franklin conducted X-ray diffraction experiments on carbon compounds at a government lab in Paris, France, and published several papers on X-ray crystallography of coal and coal compounds. By improving her methods of collecting DNA X-ray diffraction images, Franklin obtained Photo 51 from an X-ray crystallography experiment she conducted on 6 May First, she minimized how much the X-rays scattered off the air surrounding the crystal by pumping hydrogen gas around the crystal. Because hydrogen only has one electron, it does not scatter X-rays well. She pumped hydrogen gas through a salt solution to maintain the targeted hydration of the DNA fibers. Franklin tuned the salt concentration of the solution and the humidity surrounding the crystal to keep DNA entirely in the B-Form. After exposing the DNA fibers to X-rays for a total of sixty-two hours, Franklin collected the resulting diffraction pattern and labeled it Number 51 that became Photo The outermost edge of the diffraction pattern consists of a black diamond shape. The diamond has rounded corners with the darkest corners situated at the top and bottom of the film. The diamond shape of the DNA diffraction pattern is not made of fine, definite lines, but rather thick, fuzzy boarders that vary in darkness such that the boarders fade on the left and right hand sides of the film. Inside the diamond is a cross shape like the letter "X. Instead, along each line of the X are four horizontal dashes, called spots that become darker moving closer to the center of the film. There is a hole at the center of the film, with dark spots lining the outside of the center hole. Each nucleotide has three key features. Each nucleotide consists of a center sugar ring called deoxyribose. Attached to one end of the deoxyribose ring is a negatively charged phosphate group consisting of phosphorus and oxygen atoms. Attached to the other end of the deoxyribose ring is a molecule called a base consisting of either single or double rings of carbon and nitrogen. There are four types of bases in DNA. The presence of the X shape in the diffraction pattern indicated to Franklin that DNA strands were helical. Each dash of the X shape marks the repetition of atoms, or atomic repeats, in DNA. Therefore, based on the distances between the dashes, Franklin determined the distance between nucleotides, the smallest repeating units in DNA. The angles of the X shape revealed to Franklin the radius of DNA, or half the horizontal distance from one side of the molecule to the other. From the distance between the top and bottom of the outer diamond shape, Franklin found that there are ten nucleotides between each turn of the DNA molecule. Lastly, the lighter nature of the diamond on the top and bottom of the film showed Franklin that the DNA bases face the inside of the helix whereas the phosphate groups face outside. While Franklin obtained Photo 51 in May , she did not complete her analysis of Photo 51 until early From the image, Watson concluded that DNA was helical. From that report, Crick determined that DNA contains two strands, with each strand running in opposite directions. The model they suggested consisted of two helical strands of repeating nucleotides wound around each other making a double helix. The double helix had ten nucleotides between each turn. The phosphate groups faced outside the double helix and the DNA bases faced horizontally inward of the helix. The two strands held together through interactions between the bases of each strand. The DNA strands ran in opposite directions. Their replication mechanism, later called semi-conservative replication, described how to copy the DNA molecule that contained the genes and to pass the genes from cell to cell and from parent to offspring. Watson and Crick proposed that the DNA strands needed to unwind and separate in order to replicate. However, because of the helical nature of DNA, as shown in the X-ray diffraction pattern of Photo 51, some scientists argued that the DNA strands would be too difficult to unwind and separate. Some years passed before scientists accepted semi-conservative replication due to the perceived difficulty of unwinding the helical strands. Franklin also contributed to understanding DNA structure, especially through her collection of Photo The award of the Nobel Prize is never posthumously and Franklin died in before the award of the Nobel Prize. The DNA structure revealed in Photo 51 related the essential functions of a gene how its information is preserved and carried from cells to cell and from parent to offspring. Franklin, Rosalind E. Hamilton, Leonard D. The Eighth Day of Creation. Klug, Aaron. Lucas, Amand A. Lucas, Amand. Maddox, Brenda. London: HarperCollins Publishers, Marsh, Richard E. Sayre, Anne. Rosalind Franklin and DNA. New York: W. Watson, James D. New York: Athenaeum Press, Printer-friendly version PDF version. the double helix analysis Clyde Manwell, C. Carl Leopold's July BioScience — postulate that certain aspects of the social structure of science inhibit creativity is tested by analysis of the various views of the path to the discovery of the double helical structure of DNA. Cognitive dissonance can result in serious distortions in science, including suppression of dissident scientists by personal calumny. Most users should sign in with their email address. If you originally registered with a username please use that to sign in. PDF \| On Nov 28, , Evelyn Fox Keller published Watson's Needle: Rosalind Franklin and DNA, by Anne Sayre \| Find, read and cite all the. Photograph 51, by Rosalind Franklin (1952) The script was written by William Nicholson, and it was produced and directed by Mick Jackson. They barely communicated, and Franklin by herself made slow progress, opening up the strong possibility that the American chemist Linus Pauling would solve the problem first. Watson had very limited contact with Franklin during the time she worked on DNA. This naturally set up a poisonous state of affairs between Franklin and Wilkins. As he later pursued a PhD in biochemistry, he realized, evolutionary decisions? Published by Norton in New York. Written in English. This book is well-written, it provides a very personal and moving perspective of Rosalind Franklin's life. Navigation menu Похоже, в них угадывался страх. Или это ненависть. Они буквально пожирали ее тело. Новая волна паники охватила Сьюзан. Хейл всей тяжестью своего тела придавил ее ноги, холодно следя за каждым ее движением. Какого черта! - подумал. - Что я делаю здесь в пять вечера в субботу. - Чед? - В дверях его кабинета возникла Мидж Милкен, эксперт внутренней безопасности Фонтейна. В свои шестьдесят она была немного тяжеловатой, но все еще весьма привлекательной женщиной, чем не переставала изумлять Бринкерхоффа. Кокетка до мозга костей, трижды разведенная, Мидж двигалась по шестикомнатным директорским апартаментам с вызывающей самоуверенностью. Как старшему криптографу ей полагался терминал с самым лучшим обзором. Он был установлен на задней стороне компьютерного кольца и обращен в сторону шифровалки. Со своего места Сьюзан могла видеть всю комнату, а также сквозь стекло одностороннего обзора ТРАНСТЕКСТ, возвышавшийся в самом центре шифровалки. Он знал, что Фонтейн прав: у них нет иного выбора. Время на исходе. Джабба сел за монитор. - Хорошо. Давайте попробуем. Стратмор провел рукой по вспотевшему лбу. - Этот шифр есть продукт нового типа шифровального алгоритма, с таким нам еще не приходилось сталкиваться. Эти слова повергли Сьюзан в еще большее смятение. Шифровальный алгоритм - это просто набор математических формул для преобразования текста в шифр. Их прикосновение было знакомым, но вызывало отвращение. Б нем не чувствовалось грубой силы Грега Хейла, скорее - жестокость отчаяния, внутренняя бездушная решительность. Сьюзан повернулась. Алчущие хакеры прорывались со всех уголков мира. Их количество удваивалось каждую минуту. Еще немного, и любой обладатель компьютера - иностранные шпионы, радикалы, террористы - получит доступ в хранилище секретной информации американского правительства. Пока техники тщетно старались отключить электропитание, собравшиеся на подиуме пытались понять расшифрованный текст. Дэвид Беккер и два оперативных агента тоже пробовали сделать это, сидя в мини-автобусе в Севилье.	https://tmeastafrica.org/and-pdf/2089-rosalind-franklin-and-dna-anne-sayre-pdf-963-521.php
Rosalind Franklin is one of the most well-known scientists, not only for her work but also for her role in paving the way for future female chemists. Known for pioneering the discovery of the structure of DNA and the use of X-Ray, Franklin left a major mark on the scientific community. At a time when men dominated almost every industry, Franklin also broke down barriers, faced gender biases, and was an inspiration for women in science. Franklin was breaking glass ceilings before we even knew the phrase. Rosalind Franklin’s Early Life Rosalind Franklin was born in Notting Hill, London in 1920 to an affluent Jewish family. As a child, Franklin excelled in science and went to numerous schools to pursue her passion. She attended Cambridge University and earned a Ph.D. in physical chemistry. At Cambridge, she studied crystallography and X-ray diffraction. Early in her career, she got her start at the Laboratoire Central des Services Chimiques de l’Etat in Paris. Here, she worked with Jacques Mering a crystallographer who taught her about X-ray diffraction. Soon, Franklin used X-Rays in her work with crystalized solids to create images. Being a perfectionist, she quickly became a master in this art. Her Career And Legacy By 1951, Franklin was working with John Randall at King’s College in London. It was here, Franklin made the discovery that DNA has two forms, a wet and dry form. Her photo of the wet form became one of the most famous in history as it identified the structure of DNA. It took Franklin 100 hours of X-Ray exposure for her to refine the infamous photo. A competing scientist disclosed Franklin’s photo of DNA without her permission and it was later used for the famous model of DNA created by Francis Crick and James Watson. The two were awarded the Nobel Prize in 1962, taking most of the credit for her findings. The two did include Franklin in a footnote of their findings but it was known that the work was primarily based off of her photo. Franklin had passed away a few years before the Nobel Prize was awarded. Colleagues later noted that it wasn’t in her personality to fight these men or gain attribution. In 1953, Franklin went to Birkbeck College to study the structure of RNA and the tobacco mosaic virus. Here, she was forced to study viruses and structural virology due to her agreement leaving King’s College, not to study DNA. It was at Birkbeck College that the scientific community would learn that Rosalind’s work didn’t just start and end with the study of DNA. Franklin and her colleagues helped start the study of structural virology making major progress in the area. Their work helped pave the way for many scientific achievements in the field, setting the stage for the future of structural virology. A Life Too Short In 1956, Franklin was diagnosed with ovarian cancer. Although she continued to work over the next two years, she had experimental chemotherapy as well as three operations. Franklin entered a 10-month remission but passed away from cancer on April 16, 1958. Franklin remained dedicated and continued to work just a few weeks before her death. It’s believed that Franklin’s continued exposure to X-rays during her years of study and her career possibly led to the development of her ovarian cancer. She spent hundreds of hours developing photos from X-rays during her work. At the peak of her career, Franklin passed when she was just 37 years old. Her Battle With Gender Harassment Cancer wasn’t the only battle Franklin would face in her life. The fact that Franklin’s work was used without her permission in Crick’s and Watson’s famous model of DNA is an unfortunate case of gender harassment. Known as the Matilda Effect, gender harassment, in this case, is when men are given credit for a woman’s work. Women in the 1950s were many times harassed openly, pursued without their consent or discredited as equal colleagues. Some of Franklin’s former colleagues spoke openly about the way she dressed and her moods and blamed them for distracting male co-workers. Her male counterparts made comments about how she didn’t dress feminine enough or wear lipstick. Comments having nothing to do with her work or their relationship as partners. Possibly due to the era in which she lived, it’s been said by colleagues that Franklin was notably reluctant to share and publish her work until she was completely finished. Being a woman, she was afraid to fail or be criticized for her work. Thankfully today, there are many prominent female scientists in significant roles. Although the workplace in the science industry has gotten better for women, this stigmatism still remains in a lot of cases. Today, there are two institutions that honor the work of Rosalind Franklin. The Rosalind Franklin University of Medicine and Science in Chicago and the Rosalind Franklin Institute in the United Kingdom are dedicated in her honor. Although she passed away when she was still a young woman, Rosalind Franklin left a tremendous impact on the scientific and medical communities. Her work and discoveries led to countless breakthroughs in the years that followed her death. Achieving everything she was able to as a woman, was an achievement equal to her important career. Franklin paved the way for other women scientists to come. She worked tirelessly under harsh conditions with male colleagues to further her cause and continue her pursuit of knowledge and discovery.	https://search.science101.com/rosalind-franklin-chemist
Rosalind Franklin: British Chemist and Crystallographer Let’s travel back in time to the year 1952. On that fateful day, something extraordinary happened. It was so groundbreaking, so earth-shattering that it completely changed the face of science! What was it, you may ask? It was none other than a photo. it was called “Photo 51,” to be exact. You may be wondering how a photo could have such a big impact. Well, let’s take it from the beginning. It all started with a young Rosalind Franklin. She grew up in London in a well-to-do family. Rosalind was very clever, but she wasn’t like other girls. at that time, not many girls studied science. Even her father was against it and suggested she become a social worker instead. But Rosalind was not having it. She was a Brainiac when it came to science and was determined to pursue it. She read books on quantum theory, subatomic energy, and group theory. And she conducted her own experiments. Her father eventually saw how passionate she was and allowed Rosalind to go after her dreams. She went on to earn her doctorate in physical chemistry from Cambridge University in 1945. Rosalind devoted her life to science. Her most awesome achievement was her contribution to the discovery of the double-helix structure of DNA. But Rosalind’s discovery wasn’t so simple. There was a bit of drama that went on. Rosalind was working with her peer, Maurice Wilkins. Tension grew between the two and they were no longer able to work together. So Rosalind went off to work with graduate student Raymond gosling for a while. They eventually took Photo 51. At the time, she didn’t realize its significance. Take a look at Photo 51. It may seem like a bunch of random dots and lines, but there’s more to it than that. Rosalind took a series of photos using a technique called X-ray crystallography to examine DNA molecules. She shot an X-ray beam at the DNA molecules. The beams made interesting designs and patterns. These can be measured with complicated mathematics. The X in the middle was a clue showing the double helix present in DNA. Meanwhile, Wilkins decided to work with scientists Francis Crick and James Watson. He somehow got a hold of Rosalind’s Photo 51. He showed it to Crick and Watson behind her back. The men stared at the photo. then, Ka-Boom! Major inspirations struck! The photo was a game-changer. It led Watson and Crick to create their famous DNA model which changed the face of science. the pair published their findings in 1953 and received a Nobel Prize in 1962. What Is DNA? DNA stands for deoxyribonucleic acid. Try saying that 3 times with t getting tongue-tied! DNA is in our bodies. It carries all the information about how we look and function. It determines things like eye color and how our lungs work. These details are carried in different sections of DNA called genes. DNA is a long, thin molecule made up of parts called nucleotides. It has a special shape called a double helix. Although Rosalind never got proper credit during her lifetime, her invaluable contribution is acknowledged today. Her curiosity, hard work, and perseverance guided her discoveries, and nothing can ever take that away from her. Article originally published in Smore issue #4 Mar – Apr 2018. Subscribe to Smore Science Magazine.	https://www.smorescience.com/rosalind-franklin-photo-51/?print=print
Science and everyday life cannot and should not be separated. Science, for me, gives a partial explanation of life. In so far as it goes, it is based on fact, experience and experiment. Kimberley Lim, an accomplished broadcast journalist, interviews the English experimental scientist Rosalind Franklin, exploring her life, discoveries and also the struggles she had to surmount. Rosalind was born in 1920 and is best known for an X-ray diffraction image that she and her student, Raymond Gosling, published in 1953 which was the key to the discovery of the DNA double helix. But even this incredible finding was only a fraction of what she achieved in her short lifetime working across biology, chemistry and physics on research that mattered to society.	https://www.towtonaudio.com/products/interviews-from-history-nobel-women-rosalind-franklin
King’s College – King’s College is a public research university located in London and is the third oldest university in Great Britain. In 1946, John T. Randall, who had trained under the great Nobel Prize winning physicist, William Lawrence Bragg, was appointed Head of Physics at King’s College, London. The study of physics at King’s has a long and distinguished history, producing several Nobel Prize winners, including Charles Barkla, Sir Owen Richardson and Sir Edward Appleton for important work on x-rays, thermionics and atmospheric physics. During the nineteenth century, notable King’s scientists included the famous physicist James Clerk Maxwell, who undertook groundbreaking research on thermodynamics, and Charles Wheatstone, who pioneered the development of the telegraph and stereoscopy, and who was commemorated in the research laboratories that bear his name. Signer DNA – Rudolf Signer was a Swiss biochemist based out of the University of Berne. Through his work, he had developed a way to extract high-quality DNA samples from the thymus glands of calves, which were fresh and easily accessible at the local butcher’s shop. Signer’s DNA samples were unique because they could be spun into thin, uniform filaments, leading to sharper x-ray photographs, making “Signer DNA” the purest DNA samples of the time. In 1950, Signer attended a meeting of the Faraday Society (founded in 1903 for the study of physical chemistry, now the Royal Society of Chemistry) in London and distributed samples of his DNA to those in attendance, including Maurice Wilkins. Before Rosalind Franklin’s arrival at King’s College, Raymond Gosling and Wilkins used the samples in order to provide the first clearly crystalline x-ray diffraction pictures of DNA. X-ray Crystallography – The study of crystals and their structure by means of the diffraction of x-rays by the regularly spaced atoms of crystalline materials. X-ray Diffraction – The scattering of x-rays by the regularly spaced atoms of a crystal, useful in obtaining information about the structure of the crystal. Sir John Turton Randall (1905 – 1984) – Sir John Turton Randall was a British physicist and biophysicist whose early work included the development of the cavity magnetron, which was a type of vacuum tube crucial to improving the performance of radar during World War II. As Wheatstone Professor of Physics at King’s College London, Randall was responsible for setting up the Medical Research Council Biophysics Unit that pioneered x-ray analysis of the DNA molecule under the supervision of Maurice Wilkins. The Biophysics Unit was later renamed the Randall Division of Cell and Molecular Biophysics. Coal Molecules – Through her work at the British Coal Utilization Research Association (BCURA), Rosalind Franklin found that the pores in coal have fine constrictions at the molecular level, which increase with heating and vary according to the carbon content of the coal. These act as “molecular sieves,” successively blocking penetration of substances according to molecular size. Franklin was the first to identify and measure these micro-structures, and this fundamental work made it possible to classify coals and predict their performance to a high degree of accuracy. Her work at BCURA yielded a doctoral thesis, her PhD from Cambridge in 1945, and five scientific papers. Linus Pauling (1901 – 1994) – Linus Pauling was an American chemist and biochemist. Considered one of the most influential chemists in history, he was one of the first scientists to study quantum chemistry and molecular biology. After graduating from Oregon State University in 1922, he was appointed a Teaching Fellow at California Institute of Technology and was a graduate student there until 1925, working under Professors Roscoe G. Dickinson and Richard C. Tolman. In 1925, he was awarded a PhD in Chemistry, with minors in Physics and Mathematics. In 1922, with Professor Dickinson, he began the experimental determination of the structures of some crystals, and also started theoretical work on the nature of the chemical bond. In 1951, Pauling, along with Robert Corey and Herman Branson, correctly proposed the alpha helix and the beta sheet as the primary structural motifs in protein secondary structure, thereby winning the “race” to find the alpha helix structure of proteins. When Lawrence Bragg’s team at the Cavendish learned of this discovery and that Pauling was working on molecular models for the structure of DNA (a proposed triple helix), Bragg allowed Watson and Crick to start work on their own DNA model. Though Pauling did not win “the race for DNA,” he won the Nobel Prize in Chemistry in 1954 and the Nobel Peace Prize in 1962, making him one of four people to win multiple Nobel Prizes and one of two people to win the Nobel Prize in multiple fields, the other being Madame Marie Curie. Sir William Lawrence Bragg (1890 – 1971) – Sir William Lawrence Bragg was an Australian-born physicist and x-ray crystallographer. Known for discovering the Bragg Law of X-ray Diffraction, the work he did with his father on crystallography jointly earned them the Nobel Prize for Physics in 1915, making Bragg at the age of 25 the youngest-ever Nobel laureate. Together with his father he published various scientific papers on crystal structure after their joint publication of X-rays and Crystal Structure (1915), including The Crystalline State (1934), Electricity (1936), and Atomic Structure of Minerals (1937). Bragg, who had been elected Fellow of the Royal Society in 1921, was Director of the National Physical Laboratory from 1937 to 1938 and Cavendish Professor of Experimental Physics, Cambridge, from 1938 to 1953. He was PhD mentor to J.T. Randall, who went on to head the Biophysics Unit at King’s College, and who nominated Wilkins, Watson, and Crick for the 1962 Nobel Prize for Medicine or Physiology. Deoxyribonucleic Acid/B Form – A self-replicating material, which is present in nearly all living organisms as the main constituent of chromosomes. It is the carrier of genetic information. Each molecule of DNA consists of two strands coiled around each other to form a double helix, a structure like a spiral ladder. Each rung of the ladder consists of a pair of chemical groups called bases (of which there are four types), which combine in specific pairs so that the sequence on one strand of the double helix is complementary to that on the other. It is the specific sequence of bases that constitutes the genetic information. A-DNA/A Form – A right-handed double helix fairly similar to the more common and well-known B-DNA form, but with a shorter more compact helical structure. It appears likely that it occurs only in dehydrated samples of DNA, such as those used in crystallographic experiments. Purines – The DNA bases adenine (pairs with thymine) and guanine (pairs with cytosine). Pyrimidines – The DNA bases thymine (pairs with adenine) and cytosine (pairs with guanine). Nucleic Acid – A complex organic substance present in living cells, especially DNA and RNA, whose molecules consist of many nucleotides (the basic building blocks of nucleic acids) linked in a long chain. Protein – Any of a class of nitrogenous organic compounds, which have large molecules composed of one or more long chains of amino acids and are an essential part of all living organisms. Laboratoire Centrale des Services Chimiques de L’Etat – The Laboratoire Centrale in Paris is the laboratory where Dr. Franklin worked for four years. While working there, she learned the x-ray crystallography method that was essential to her work. Helix – An object having a three-dimensional shape like that of a wire wound uniformly in a single layer around a cylinder or cone, as in a corkscrew or spiral staircase. In biochemistry, it is an extended spiral chain of atoms in a protein, nucleic acid or other polymeric molecule. Tobacco Mosaic Virus (TMV) – A virus which causes mosaic disease that attacks tobacco plants. It is often used in biochemical research. TMV was essential to Rosalind Franklin’s studies involving x-ray crystallography at Birkbeck College. Cyclotron – A cyclotron is a machine used to accelerate charged particles to high energies. The first cyclotron was built by Earnest Orlando Lawrence and his graduate student, M. Stanley Livingston, at the University of California, Berkley, in the early 1930s. The Double Helix: A Personal Account of the Discovery of the Structure of DNA – An autobiographical account of the discovery of the double helix structure of DNA, written by James D. Watson and published in 1968. Though it was originally slated to be published by Harvard University Press, Watson’s home university dropped the arrangement after protestations from Francis Crick and Maurice Wilkins, co-discoverers of the structure of DNA, and it was published privately. It has been criticized as being excessively sexist towards Rosalind Franklin. In 1998, the Modern Library placed The Double Helix at number 7 on its list of the 20th century’s best works of non-fiction. Selected definitions from the Oxford English Dictionary.	https://www.centralsquaretheater.org/shows-events/central-conversations/past-central-conversations/photograph-51-glossary-terms/
Rosalind Franklin, eminent mid-century scientist and heroine of Photograph 51, is driven by The Work. It’s a phrase she utters several times throughout the quasi-biographical play, delivered with a gravity that suggests capital letters. Franklin’s capital-W Work was X-ray crystallography, the data collection process (and subsequent analysis) that allowed scientists in 1953 to discern the molecular structure of DNA — and, more importantly, postulate its replicating function. Thus, the seed of a narrative sprouts. Photograph 51, a 90-minute play by Anna Ziegler, tells the story of the race to discover the structure of DNA. It might sound like tedious subject matter for a stage production — and in fact the “race” was all but unacknowledged by its major participant, the aforementioned Franklin, whose fastidious approach to science left no room for chasing glory — but after seeing the Renaissance Theaterworks production of Photograph 51, you’ll wonder why “science biopic” isn’t a more popular narrative genre. The play, like the X-ray image that supplies its title, takes several overlapping shapes: scenes blur into one another, characters appear both in-scene and in the wings as narrators, interlocutors and self-editing pen pals. James Watson and Francis Crick even form a Greek chorus of sorts at first, commenting and spectating before their characters join the fray. The sparse set punches above its weight through the production’s clever staging and use of lighting, which ushers characters from scene to scene in seamless parade. Though Franklin, played assiduously by the commanding and strong-voiced Cassandra Bissell, is the only female cast member, she remains the play’s nucleus, around whom all five male characters bustle. The contested narration that functions as exposition in the play’s opening moments (“It was a particularly cold winter in London, January 1951,” says Maurice Wilkins. And, “Not again, Wilkins. Really?” from James Watson) was not something I’d seen done before: a group of men discussing the motivations and professional movements of a woman. If there’s a reverse Bechdel test, this play would fail — which is a good thing, in light of Renaissance Theaterworks’ mission to improve gender parity in the theater world. Director Suzan Fete coaxes a nuanced taxonomy of masculinity from each of the supporting stars. Particularly delightful is Nick Narcisi’s James Watson, somehow equally believable and utterly villainous without verging on caricature (a level of restraint evident to those familiar with the real James Watson). Josh Krause is charming as Franklin’s graduate assistant Ray Gosling, toggling between comic relief and omniscient narrator. Francis Crick and Don Caspar (Franklin’s collaborator and would-be love interest) are portrayed with subtlety by Trevor Rees and Joe Picchetti, respectively, but it is Neil Brookshire as Maurice Wilkins who has the toughest of the five male roles. Wilkins, Franklin’s labmate and sparring partner, gets a special note in the script from Ziegler, who entreats the actor to be “neither too awkward nor too condescending.” Photograph 51, and in fact, the real story behind the DNA race, shines in gray areas, and Brookshire strikes a balance that brings Wilkins to life and invites the audience to interrogate the “data” the way Franklin might have. Bissell’s Franklin dispenses with the notion of likable in the first half (her character is described in the script as “a Jewish British scientist in her 30s, doesn’t suffer fools”), indicting the audience’s own deep-seated sexism. Yet Franklin’s humanity is in good hands with the thoughtful actress, who displayed her dedicated familiarity with the real Rosalind Franklin during the post-show talkback session. Even as her character’s vulnerabilities are brought forth, Bissell maintains her brusqueness and scientific scruples, refusing to sacrifice character for character development. Franklin’s devotion to The Work is mirrored in the craft and dexterity of the Renaissance Theaterworks cast and crew, who avoid easy answers where they can’t be empirically proven.	https://www.milwaukeemag.com/review-photograph-51-avoids-easy-answers-likability/
I’ve just finished reading an excellent biography of Rosalind Franklin, the scientist who received no credit (at least, not during her lifetime) for her work on the structure of DNA. James Watson and Francis Crick appropriated her data without her knowledge or consent, and used it to construct their double helix model of DNA. When they published their work in Nature in 1953, they mentioned the DNA research being carried out at her lab in King’s College, but falsely claimed that they “were not aware of the details of the results presented there when we revised our structure”. They were awarded the Nobel Prize in 1962, but neglected to mention Rosalind Franklin’s name in their speeches, and Watson’s 1968 book, The Double Helix, portrayed her as a dowdy shrew who couldn’t understand her own data. However, Rosalind Franklin was far more than “the Sylvia Plath of molecular biology, the woman whose gifts were sacrificed to the greater glory of the male”. Brenda Maddox paints a vivid portrait of the woman who “achieved an international reputation in three different fields of scientific research while at the same time nourishing a passion for travel, a gift for friendship, a love of clothes and good food, and a strong political conscience [and who] never flagged in her duties to the distinguished Anglo-Jewish family of which she was a loyal, if combative, member.” Rosalind was an “alarmingly clever” girl, the eldest daughter in a family of philanthropists that had made a fortune from banking and publishing. Her father was politically conservative, but there were a number of left-wing rebels in the family1. The book contains wonderful descriptions, often from Rosalind’s own letters, of her childhood in Notting Hill and of her time at St Paul’s Girls’ School, which was then one of the few schools that prepared girls for a career. She went up to Cambridge in 1938, as bomb shelters were being dug in Hyde Park and her family were taking in Jewish refugees from Austria. By the end of the war, she had a PhD in physical chemistry and was working on war-related research about coal. After a few years in Paris, she returned (reluctantly) to London, where the focus of her research changed to the structure of DNA, and then the structure of viruses. Don’t be put off, thinking this book is filled with Difficult Science. I’m hardly an expert in X-Ray crystallography, but I was able to follow the progress of Rosalind’s research quite easily, thanks to Maddox’s clear descriptions and diagrams. It probably helps to have some interest in DNA, but you can skim the scientific descriptions if you must. What is really fascinating (and infuriating) is Maddox’s account of the experiences of women scientists in the 1940s and 1950s – how they were refused admission to the Royal Society until 19452, missed out on nominations for awards and research positions, were paid less than men for equal work, and were refused admission to university common rooms and research facilities3. Rosalind, who was a perfectionist and was widely regarded as ‘prickly’, often antagonised senior male researchers. For example, Norman Pirie, a specialist in plant viruses, wrote her a patronising letter in 1954, criticising her data that showed tobacco mosaic virus rods were all the same length. As it turned out, she was right and he was wrong. But he was also friends with the head of the council that was funding her research, which subsequently refused to provide any more money, even though her work had the potential to lead to a cure for a range of viral diseases, including polio. Despite her constant battles at work, Rosalind comes across as a woman who embraced life. She was wonderful with children, she loved to cook elaborate dinners for her friends, and her greatest joy was hiking trips into the mountains. She made two journeys across the United States in the 1950s, and her letters about her travels are affectionate and amusing. She died tragically young, at the age of only thirty-seven, of ovarian cancer. The head of her research facility, J.D. Bernal, wrote that it was “a great loss to science”. He praised her “single-minded devotion to scientific research”, noting that “As a scientist Miss Franklin was distinguished by extreme clarity and perfection in everything she undertook. Her photographs are among the most beautiful X-Ray photographs of any substance ever taken.” Despite James Watson’s4 many attempts to belittle Rosalind’s intelligence and personality after her death, the world eventually came to recognise the value of her work. Buildings at St Paul’s Girls’ School, Newnham College and King’s College are now named after her, and her portrait hangs in the National Portrait Gallery in London – below those of Watson and Crick, of course. Highly recommended if you’re interested in science, or feminism, or simply want to read the story of a fascinating, forthright young woman.	https://michellecooper-writer.com/blog/2012/08/rosalind-franklin-the-dark-lady-of-dna-by-brenda-maddox/
Synopsis: Sir Isaac Newton once declared that his momentous discoveries were only made thanks to having ‘stood on the shoulders of giants’. The same might also be said of the scientists James Watson and Francis Crick. Their discovery of the structure of DNA was, without doubt, one of the biggest scientific landmarks in history and, thanks largely to the success of Watson’s best-selling memoir ‘The Double Helix’, there might seem to be little new to say about this story. But much remains to be said about the particular ‘giants’ on whose shoulders Watson and Crick stood. Of these, the crystallographer Rosalind Franklin, whose famous X-ray diffraction photograph known as ‘Photo 51’ provided Watson and Crick with a vital clue, is now well recognised. Far less well known is the physicist William T. Astbury who, working at Leeds in the 1930s on the structure of wool for the local textile industry, pioneered the use of X-ray crystallography to study biological fibres. In so doing, he not only made the very first studies of the structure of DNA culminating in a photo almost identical to Franklin’s ‘Photo 51’, but also founded the new science of ‘molecular biology’. Yet whilst Watson and Crick won the Nobel Prize, Astbury has largely been forgotten. The Man in the Monkeynut Coattells the story of this neglected pioneer, showing not only how it was thanks to him that Watson and Crick were not left empty-handed, but also how his ideas transformed biology leaving a legacy which is still felt today.	https://sciencebookaday.com/2014/10/24/the-man-in-the-monkeynut-coat-william-astbury-and-the-forgotten-road-to-the-double-helix/
DOI: 10.1107/S1600577521003453 Authors: Daniil Kazantsev (University of Manchester) , Ramona Duman (Diamond Light Source) , Armin Wagner (Diamond Light Source) , Vitaliy Mykhaylyk (Diamond Light Source) , Kazimir Wanelik (Diamond Light Source) , Mark Basham (Diamond Light Source; Rosalind Franklin Institute) , Nicola Wadeson (Diamond Light Source) Co-authored by industrial partner: No Type: Journal Paper Journal: Journal Of Synchrotron Radiation , VOL 28 State: Published (Approved) Published: May 2021 Abstract: In this paper a practical solution for the reconstruction and segmentation of low-contrast X-ray tomographic data of protein crystals from the long-wavelength macromolecular crystallography beamline I23 at Diamond Light Source is provided. The resulting segmented data will provide the path lengths through both diffracting and non-diffracting materials as basis for analytical absorption corrections for X-ray diffraction data taken in the same sample environment ahead of the tomography experiment. X-ray tomography data from protein crystals can be difficult to analyse due to very low or absent contrast between the different materials: the crystal, the sample holder and the surrounding mother liquor. The proposed data processing pipeline consists of two major sequential operations: model-based iterative reconstruction to improve contrast and minimize the influence of noise and artefacts, followed by segmentation. The segmentation aims to partition the reconstructed data into four phases: the crystal, mother liquor, loop and vacuum. In this study three different semi-automated segmentation methods are experimented with by using Gaussian mixture models, geodesic distance thresholding and a novel morphological method, RegionGrow, implemented specifically for the task. The complete reconstruction-segmentation pipeline is integrated into the MPI-based data analysis and reconstruction framework Savu, which is used to reduce computation time through parallelization across a computing cluster and makes the developed methods easily accessible. Journal Keywords: long-wavelength X-ray crystallography; absorption correction; segmentation; iterative reconstruction; high-performance computing Subject Areas: Information and Communication Technology Instruments: I23-Long wavelength MX Documents: mo5234.pdf Discipline Tags: Information & Communication Technologies Data processing Technical Tags:	https://publications.diamond.ac.uk/pubman/viewpublication?publicationId=13504
Today is the birthday of Rosalind Franklin, whose pioneering work on X-ray diffraction of DNA was crucial in determining its structure. What is it? DNA is the pieces of code we receive from our parents that makes us all unique, life's master plan or blueprint, the molecules that contain information necessary to make up a living being … Where did the structure come from? The original double helical model so widely known today was published by Watson and Crick in 1953. Like most scientific breakthroughs, their discovery was based on nearly a century of incremental advances in DNA research. Importantly, Rosalind Franklin's beautiful X-ray diffraction images, collected while she was working at King's College, London, were evidence of the helical structure. What does it look like? The famous double helix structure of DNA is now well known and can be widely seen in various stylised ways in everyday life. What about water? Rosalind Franklin also realised the importance of water in the structure of DNA, and showed that different forms of DNA were produced depending on water content … which brings me to an unavoidable plug for neutron scattering. The neutron fibre diffraction work on DNA is a beautiful example of how neutrons can be used to localise water molecules in a structure, as shown below. Fuller W., Forsyth T., Mahendrasingam A., Philos. Trans. R. Soc. Lond. B (2004) 359 1237-1248.	https://www.iycr2014.org/learn/crystallography365/articles/20140725
The British-built Mars rover scheduled to be launched in 2020 has been named after scientist Rosalind Franklin. Franklin, a chemist, used a technique called X-ray crystallography to map the location of atoms in crystals. It’s said that when American scientist James Watson saw Franklin’s X-ray crystallography image of DNA, he immediately realized he and English scientist Francis Crick were right about its double-helix structure and published their findings. Nine years later, in 1962, Watson, Crick and Franklin’s boss, Maurice Wilkins, went on to win the Nobel Prize in Medicine. Franklin never went further with her research. She developed cancer and died at age 37.	https://www.maharlikanews.com/2019/02/07/european-mars-rover-named-after-dna-pioneer-rosalind-franklin/
- Posted On: - Written By: Ashley Rains Repeatedly, research shows that more than 40 percent of all cancers diagnosed and nearly half of all deaths from cancer in the U.S. can be attributed to preventable causes – things like smoking, excess body weight, physical inactivity and excessive exposure to the sun. Just like going to the dentist or getting a check-up, cancer screening tests should be a part of your healthcare routine. These tests are used to find cancer before a person has any symptoms – it’s important to get regular screenings even if you are feeling fine. Age 25–39 Screening recommendations Cervical cancer screening recommended for people with a cervix beginning at age 25. Age 40–49 Screening recommendations Breast cancer screening recommended beginning at age 45, with the option to begin at age 40. Colorectal cancer screening recommended for everyone beginning at age 45. At age 45, African Americans should discuss prostate cancer screening with a doctor. Age 50+ Screening recommendations People who currently smoke or formerly smoked should discuss lung cancer screening with a doctor. Discussing prostate cancer screening with a doctor recommended. Prevention Cancer Primary Prevention Secondary Prevention Breast Weight control, increase physical activity, decrease alcohol consumption Mammography screening Cervix Tobacco control, limit sexual partners, Human Papilloma Virus (HPV) vaccine, excise pre-cancers Pap smear; HPV screening Colorectal Weight control, increase physical activity, tobacco control, excise pre-cancerous polyps Colonoscopy, FIT test, other screening options Endometrium Weight control, dietary change -- Kidney Control tobacco use, weight, and blood pressure -- Larynx Tobacco control, GI reflux control, decrease alcohol consumption, HPV vaccine Laryngoscopic screening of smokers Liver Hepatitis B & C vaccines; tobacco control, limit alcohol consumption, avoid aflatoxins, treat hepatitis -- Lung & bronchus Tobacco control, radon control, asbestos abatement, occupational safeguards Spiral CT scan screening of healthy smokers age > 55 Melanoma of the skin Limit sun exposure, wear sunscreen, remove pre-cancerous moles Screening by dermatologist Oral cavity Tobacco control, avoid chewing betel quid, limit alcohol consumption; HPV vaccine Dentists screen users of tobacco and alcohol Ovary Weight control, avoid hormone treatments -- Pancreas Control tobacco use, weight, alcohol use, control diabetes mellitus -- Prostate (Unclear) Serial PSA testing Urinary bladder Tobacco control, avoid dietary supplements, workplace exposures -- General approaches to the primary prevention of cancer are as follows, with details below: 1. Lifestyle modifications and healthy living through public education or legislation 2. Cancer vaccines to prevent cancers caused by viruses 3. Control of radiation known to cause cancer 4. Regular cancer screening that may reveal pre-cancerous tissue that can be removed Vaccines and cancer Most of us know about vaccines given to healthy people to help prevent infections, such as measles and chicken pox. These vaccines use weakened or killed germs like viruses or bacteria to start an immune response in the body. Most vaccines used to treat cancer work the same way, but they make the person’s immune system attack cancer cells. The goal is to help treat cancer or to help keep it from coming back after other treatments. Some strains of the human papillomavirus (HPV) have been linked to cervical, anal, throat, vaginal, vulvar and penile cancers. In fact, most cervical cancers are caused by infection with HPV. Vaccinating children and certain young adults against HPV helps protect against cervical cancer and the other five cancers HPV can cause. People who have chronic (long-term) infections with the hepatitis B virus (HBV) are at higher risk for liver cancer. Getting the vaccine to help prevent HBV infection may lower some people’s risk of getting liver cancer. These types of vaccines are only useful for cancers known to be caused by infections. But most cancers, including colorectal, lung, prostate and breast cancers, are not thought to be caused by infections. Infirmary Cancer Care stands with our patients through our continuum of care: prevention, early detection, diagnosis, staging, treatment and remission – every step of the way. Call 251-435-CARE (2273) for more information and visit InfirmaryCancerCare.org for more information about prevention, screening and treatment.	https://www.infirmaryhealth.org/news-center/2022/february/february-is-national-cancer-prevention-month/
Potential Causes of Cancer and Cancerous CellsJanuary 18, 2023 Today, I’ll cover some potential cancer causes that you should avoid or limit. My aim is to provide in-depth and credible information that could help you prevent, lessen or cure cancer if these products are eradicated. I suggest you go through the sites linked below and not base your decisions on excerpts that could be taken out of context. Feel free to open them in a new tab as you read. 1. Vegetable/Seed Oils We already know that seed oils especially canola, sunflower, safflower, cottonseed, rapeseed, soybean, and similar are unstable. They go through a long process; the end result is what most people use for cooking. Here’s an excerpt from the National Library of Medicine on the reason why seed oils could possibly be a cause of cancer: Repeated heating of vegetable oils at high temperatures during cooking is a very common cooking practice. Repeatedly heated cooking oils (RCO) can generate varieties of compounds, including polycyclic aromatic hydrocarbons (PAH), some of which have been reported as carcinogenic. RCO is one of the commonly consumed cooking and frying medium. These RCO consumption and inhalation of cooking fumes can pose a serious health hazard. Taking into account exploratory study, the present review aims to provide the consumption of RCO and its fumes cause the high incidence of genotoxic, mutagenic, tumorogenic and various cancers. The information on RCO and its fumes were collected through a library database and electronic search (ScienceDirect, PubMed, and Google Scholar). Remarkable studies demonstrated that the health adverse effects of RCO and its cooking fumes have been often attributed to their detrimental properties and ease to genotoxic, mutagenic and carcinogenic activities. RCO and its cooking fumes were found to enhance the incidence of aberrant cells, including breaks, fragments, exchanges and multiple chromosomal damages and micronuclei in a dose-dependent manner. Furthermore, the large consumption of RCO has been associated with a number of malignancies, including lung, colorectal, breast, and prostate cancers. The present review provides additional insights into the polluting features of PAHs produced various cancers via cooking activities in indoor environments. Seed oils have also been shown to increase cardiovascular disease risk factors. Another excerpt, this time from Independent UK Cooking with vegetable oil releases toxic chemicals linked to cancer and even the degeneration of the brain, according to experts. Lard, butter, coconut and olive oil are all better dietary choices, leading scientists have said - in advice which directly contradicts the NHS . When heated, corn, sunflower, palm and soya bean oils - often called “vegetable” oils - release chemicals called aldehydes which have been linked to various cancers and neurogenerative diseases such as Alzheimer’s. Martin Grootveld, a professor of bioanalytical chemistry and chemical pathology at DeMontfort University,said that a meal fried in vegetable oil such as fish and chips contains 100 to 200 times more aldehydes than the daily limit set by the World Health Organisation (WHO), according to the Daily Telegraph . Using butter, olive and lard in the frying pan, however, was found to produce much lower levels of aldehydes - with coconut oil coming out as healthiest. Yet the NHS has long warned against cooking with butter and lard. The NHS choices website advises : “Try to cut down on foods that are high in saturated fat and have smaller amounts of foods that are rich in unsaturated fat instead. “For a healthy choice, use just a small amount of vegetable oil or reduced fat spread instead of butter, lard or ghee.” Yet vegetable oil has been linked to heart disease, cancer, inflammation, rising blood pressure and deteriorating mental health. And the omega 6 fatty acids present in vegetable oils are pushing out the important omega 3 fatty acids that keep the brain healthy, according to Professor John Stein, emeritus professor of neuroscience at Oxford University. “If you eat too much corn oil or sunflower oil, the brain is absorbing too much omega 6, and that effectively forces out omega 3,” Prof Stein said according to the Daily Telegraph. “I believe the lack of omega 3 is a powerful contributory factor to such problems as increasing mental health issues and other problems such as dyslexia.” The issue had not received enough attention by health organisations or the food industry, experts added. Olive oil, meanwhile, has been repeatedly linked to health benefits. Another excerpt from Jeff Nobbs Meanwhile, as vegetable oil consumption has grown, rates of obesity, cancer, and diabetes–among other chronic illnesses–have surged to unprecedented levels . Six in ten adults in the US have a chronic disease and four in ten adults have two or more [ 2 ]. Excerpt from Kesser Institute Our cell membranes are composed mainly of delicate fatty acids, the composition of which is directly influenced by the types of fats we eat. The consumption of anti-inflammatory omega-3 fatty acids has beneficial effects on cell membrane structure and function. Conversely, the consumption of rancid dietary fats compromises cell membrane health and promotes oxidative damage. The primary sources of rancid fats in the Standard American Diet are industrial vegetable oils. Industrial vegetable oils, including canola, soybean, peanut, and safflower oils, are high in omega-6 polyunsaturated fatty acids (PUFAs). Omega-6 PUFAs are delicate and quite susceptible to damage from factors such as heat and light. Unfortunately, the very process by which industrial vegetable oils are made exposes omega-6 PUFAs to heat, metals, and other chemicals; this process oxidatively damages the fatty acids and produces “rancid” fats. However, the damage doesn’t stop there; vegetable oils are further oxidized when they are heated during the cooking process. The oxidation of unsaturated fats in industrial vegetable oils produces advanced lipid oxidation end products (ALEs), which pose a significant risk to human health. ALEs are absorbed from the gut into the circulatory system, where they activate an inflammatory response that generates cytotoxic and genotoxic compounds. They are also incorporated into cell membranes, where they increase membrane permeability and impair cell function. ( 5 ) To make matters worse, ALEs also co-oxidize vitamins A, C, and E, depleting the body’s antioxidant stores. The combination of inflammation and antioxidant depletion caused by the consumption of industrial vegetable oils propagates a chain reaction of oxidative damage in the body. However, omega-6 in and of itself may not be the problem; it’s the way omega-6 fatty acids are handled during processing and cooking that cause them to become damaged and pro-inflammatory. We needn’t vilify all forms of omega-6 fatty acids. While it is best to avoid industrial vegetable oils entirely, fresh, whole foods high in omega-6, such as poultry, avocados, and nuts, can be part of a healthy diet. For more information on omega-6 fatty acids, see my previous blog post “ An Update on Omega-6 PUFAs .” I’d suggest you switch to Butter, Ghee, Lard, Avocado, and/or Olive oil. One thing I can say about this is, heart disease, cancer, and high blood pressure among other chronic illnesses have been on the rise despite the removal of saturated fats which were initially blamed as the root cause. More and more people have high cholesterol despite most(all) vegetable oils being labeled as heart-friendly with zero cholesterol. Now, I’d like to bring to your attention a scheme in the 1950s where tobacco companies paid medical associations and scientists to cover up the fact that tobacco use caused cancer. My belief is that the same thing is happening now with big food and medical associations. Wheat is being peddled despite the fact that gluten causes inflammation and is one of the causes of cancer. We’ll get to that in a minute. I leave you to make the decision. To learn more about how big oil and big tobacco did this, visit this link: How Big Oil and Big Tobacco get respected scientists to lie for them - Vox 2. Processed Meat According to the World Health Organization (WHO), there is “ convincing evidence” that processed meat causes cancer. Classified as a Group 1 carcinogen, it is connected specifically to colorectal and stomach cancer. Examples of processed meats that have carcinogenic properties include: Frankfurter hotdogs, ham, sausages, corned beef, beef jerky and canned or lunch meat. 3. Environmental Toxins These are mainly toxins that are made in industries or natural occurring toxins or are byproducts of things made in industries. Here’s an excerpt from Kesser Institute The slew of environmental toxins to which we are exposed daily is a significant source of oxidative stress. A patient’s living environment can be a significant source of oxidative stress. Exposure to particulate air pollution in urban areas and mold and biotoxins in water-damaged buildings promotes oxidative stress by depleting antioxidant reserves. ( 11 , 12 ) You can learn more about the harmful health effects of mold and biotoxins by reading my article “ 5 Things You Should Know about Toxic Mold Illness .” Plastics are well known for their endocrine-disrupting effects. However, research suggests that plastics also induce oxidative stress. In the body’s attempts to detoxify BPA, a ubiquitous plastic chemical, free radicals are generated via activation of cytochrome P450 enzymes in the liver. The induction of free radicals and oxidative stress by BPA is believed to contribute significantly to the toxicity and carcinogenicity of this compound. ( 13 ) Pesticides and heavy metals also provoke oxidative stress. Exposure to organophosphate insecticides (OPs), the residues of which can be found on conventionally grown fruits and vegetables, induces oxidative stress by activating cytochrome P450 enzymes and by disturbing the cell redox system, which reduces cellular energy and makes cells unable to neutralize free radicals. ( 14 ) Heavy metals, found in dental amalgams, air and soil, and our water supply, induce oxidative stress by altering the activities of key antioxidant enzymes such as glutathione peroxidase, glutathione-s-transferase, superoxide dismutase, and catalase. ( 15 ) Here’s an excerpt from Scientific America The National Institutes of Health has classified 54 compounds as known human carcinogens based on studies indicating they cause at least one type of cancer in people, according to the nation’s 11th Report on Carcinogens. The highest exposures occur in an occupational setting, but there are environmental exposures as well. For example, benzene , a known cause of human leukemia, is a common pollutant in vehicle exhaust. Radon, a natural radioactive gas found in many homes, raises the risk of lung cancer. Arsenic , linked to skin, liver, bladder and lung cancer, contaminates some drinking water supplies. Other known human carcinogens include asbestos, hexavalent chromium, aflatoxins and vinyl chloride. Now remember, some of these chemicals are in our cosmetics and grooming products. The skin is the largest organ so you can imagine the dangers of putting these things over the long term. I’ve already talk about endocrine & fertility disruptors found in grooming and cosmetic products, find that here: Endocrine(Hormonal) Disruptors in Grooming Products and Cosmetics \| Stephen Ajulu · Entreprenuer, Writer, Designer & Creator Here’s a list of some cancer causing toxins; - Aflatoxins - Aristolochic Acids - Arsenic - Asbestos - Benzene - Benzidine - Beryllium - 1,3-Butadiene - Cadmium - Coal Tar and Coal-Tar Pitch - Coke-Oven Emissions - Crystalline Silica (respirable size) - Erionite - Ethylene Oxide - Formaldehyde - Hexavalent Chromium Compounds - Indoor Emissions from the Household Combustion of Coal - Mineral Oils: Untreated and Mildly Treated - Nickel Compounds - Radon - Secondhand Tobacco Smoke (Environmental Tobacco Smoke) - Soot - Strong Inorganic Acid Mists Containing Sulfuric Acid - Thorium - Trichloroethylene - Vinyl Chloride - Wood Dust There’s a whole article on this, that I’d suggest you read: Environmental exposures and cancer: using the precautionary principle - PMC (nih.gov) 4. Obesity Obesity is linked to 13 types of cancer, including two of the most common—breast and prostate—but only a little more than half of Americans are aware that it’s a risk factor for cancer. In fact, physical inactivity and obesity together account for 25 percent to 30 percent of colorectal, breast, uterine, kidney and esophageal cancers, which are among the most common types. “Obesity has become so important in the field of oncology today that maintaining an appropriate weight is one of the most important ways you can protect yourself from cancer,” says Anthony Perre, MD, Chief of the Division of Outpatient Medicine at Cancer Treatment Centers of America® (CTCA). To help avoid obesity-related cancers, experts recommend you lose excess weight through diet and exercise. Be careful not to lose it too fast otherwise you’ll be releasing tons of toxins that were stored in the fat. 5. Ionizing radiation Ionizing radiation is thought to cause about 1 percent of all cancers. It comes from cosmic rays that enter the Earth’s atmosphere, the radioactive gas radon—found naturally at low levels in soil—and from certain medical procedures, such as X-rays and radiation therapy. When cancer treatments increase your risk of developing another cancer later in life, the decision-making process often involves weighing the risks against the benefits, says Glynis Vashi, MD, Intake Physician and Chief of Medicine at our hospital near Chicago. “It takes years for a cancer to develop,” she says. “So you do what you have to do at the time, and then you take as many preventive steps as possible to improve the chance that you won’t develop another cancer in the future.” 6. Alcohol Research has found that the more alcohol someone drinks—especially regular use over time—the higher the risk of cancer. For example, people who have three-and-a-half drinks or more a day are two to three times more likely to develop head and neck cancer than those who don’t drink. Alcohol consumption also has been linked to liver, esophageal, colorectal and breast cancers. Alcohol increases cancer risk by damaging cell DNA and proteins, as well as the body’s ability to break down nutrients, and by increasing estrogen levels. People who use both alcohol and tobacco have much higher risks of developing head and neck cancer than those who use alcohol or tobacco alone. 7. Tobacco The most significant environmental risk factor for cancer is tobacco, whether they’re using products like cigarettes, pipes, cigars, chewing tobacco, snuff or vaping, or being exposed to secondhand smoke. In fact, tobacco accounts for 80 percent to 90 percent of all cases of lung cancer, which is the second most common cancer in both men and women. To reduce your risk of lung cancer, avoid tobacco altogether—don’t start the habit, and if you have, quit as soon as possible, and steer clear of secondhand smoke. 8. Oxidative Stress A condition that may occur when there are too many unstable molecules called free radicals in the body and not enough antioxidants to get rid of them. This can lead to cell and tissue damage. There are many factors that may lead to oxidative stress, including obesity, poor diet, smoking, drinking alcohol, taking certain medicines, and exposure to environmental factors such as radiation, toxins, air pollution, pesticides, and sunlight. Long-term oxidative stress may play a role in aging and the development of chronic inflammation, cancer, and other diseases. Diets, especially high-fat or high-carbohydrate diets, have been shown to be associated with oxidative stress by elevating the levels of protein carbonylation and lipid peroxidation products while reducing the antioxidant defense status [ 1 ]. In obesity, chronic oxidative stress and associated inflammation are the underlying factors that cause insulin resistance, metabolic dysfunction, diabetes, and cardiovascular disease by disrupting signaling and metabolism [ 4 , 5 ]. Obesity-associated insulin resistance greatly increases oxidative stress and the risk of hypertension, dyslipidemia, type 2 diabetes, atherosclerosis, and nonalcoholic fatty liver disease [ 6 ]. In general oxidative stress is the leading cause of cancer due to byproducts called free radicals. Most of the causes listed above cause oxidative stress which in turn cause free radicals. How do you avoid them? How Can We Prevent Oxidative Damage? There are many dietary and lifestyle strategies we can implement with our patients to help them prevent oxidative damage. Avoid rancid vegetable oils. You should steer clear of processed, packaged foods and toss out any canola, soybean, safflower, sunflower, peanut, or grapeseed oil you may have sitting in your pantries. When eating out at restaurants, where industrial vegetable oils saturate most foods, ask to have your vegetables cooked in butter and your salads dressed with olive oil. Eat anti-inflammatory fats found in extra virgin olive oil, coconut oil, avocados, wild-caught seafood, butter, tallow and sprouted or lightly roasted nuts and seeds. Eat an antioxidant-rich, whole-foods diet. This type of diet supplies the body with the antioxidants and cofactors it needs to combat oxidative stress. Stop smoking. Emphasize the importance of daily stress-reduction practices . Meditation, yoga, spending time in nature, and taking “technology breaks” alleviate chronic stress, which causes oxidative stress when allowed to continue unabated. Strategies to help you reduce your environmental toxin exposure. Stop using pesticides on your lawns and gardens. Buy organic food as often as possible, avoid storing food in plastic containers and handling receipts, safely eliminate sources of heavy metal exposure such as dental amalgams, and filter drinking and bathing water. Emphasize the importance of circadian rhythms and sleep hygiene. Aiming for a regular sleep schedule, avoiding blue light at night, and getting plenty of sunlight during the day helps to sync circadian rhythms. Treat infections. Chronic infections are a significant cause of oxidative stress and must be addressed to halt the free radical cascade. Get regular exercise. Aim for 30 or more minutes of exercise four to five days a week. Also engage in light, intermittent physical activity throughout the workday by alternating sitting with working at a standing desk or by taking time to go for a walk at lunch. Address iron overload. Iron overload is a complex topic, and there are many ways to go about treating this condition. Briefly, curcumin and green tea are two options for attenuating iron overload-induced oxidative damage. ( 27 , 28 ) Try Intermittent Fasting , OMAD or 2MAD . As shown above, frequent eating increases your chance of becoming obese which is then correlated with an increase in cancer.	https://stephenajulu.com/blog/potential-causes-of-cancer-and-cancerous-cells/
Toxins: What are they and what causes them? Many individuals ask this question, and the answer might be unexpected. Toxins can come from a range of sources, both within and outside the body, and can cause a variety of health issues. There are many different types of toxins inside the globe. They’re in the food we eat, the air we breathe, and the water we drink. Some toxins are inevitable, while others are the product of our poor behaviors. Check out this list of the most prevalent sources of toxins in your body if you’re concerned about what’s causing your bothersome health issues. In this blog post, we’ll discuss the most common causes of toxins in your body. 9 common causes of toxins in the body Pollution in the air Air pollution is the most common source of toxins in your body. Since humans need to breathe to survive, airborne toxins are one of the most difficult forms of toxins to avoid. Unfortunately, many places in the world suffer from poor air quality. The emission of hazardous substances into the atmosphere by burning fossil fuels has a significant influence on our health. It is the most common cause of respiratory issues such as asthma and bronchitis. Many people are allergic to air pollution, which can cause a variety of health issues. You may decrease your exposure to airborne pollutants by wearing masks and using air filters. Water contamination Water pollution is the second most common source of toxins in your body. Although humans require water to survive, it may also contain hazardous contaminants. Drinking polluted water can cause gastrointestinal disease, reproductive troubles, and brain impairments, among other things. To fight microorganisms, chemicals like chlorine and fluoride are added to our water supply, but they may also be detrimental to human health. Fluoride has been connected to a variety of health issues, such as cancer and thyroid issues. Many industrial chemicals also wind up in our water supply, and if we are exposed to them over time, they can create major health concerns. The greatest strategy to avoid toxins in your body is to drink filtered or mineral water. Bad sleep Poor sleep patterns can cause toxin accumulation in your body, even if you aren’t aware of it. When you don’t get enough sleep, your body doesn’t have enough time to heal the harm it has sustained throughout the day. This can lead to weight gain, diabetes, and heart disease, among other health issues. Stress may be exacerbated by not getting enough sleep, which can lead to toxin accumulation. To safeguard your health, make sure you receive at least seven hours of sleep every night. Many individuals prefer affordable and comfy mattresses to obtain a good night’s sleep. Needing a good cheap mattress should be at the top of everyone’s priorities list. Tobacco Smoke Another important source of toxins in your body is tobacco smoke. There are about 7000 compounds in cigarette smoke, many of which are harmful. Cigarette smoking is dangerous not just to the smoker, but also to others who are around him or her. Cancer, heart disease, and other respiratory disorders have all been related to secondhand smoking exposure. Toxins may harm almost every organ in your body, and they’re a leading cause of lung cancer. If you smoke cigarettes or are frequently exposed to secondhand smoke, it’s time to change. Excessive alcohol consumption Toxin accumulation can also occur as a result of excessive alcohol use. Alcohol acts as a diuretic, causing your body to lose water. This can induce dehydration, which can lead to a variety of health issues. Too much alcohol can harm your liver, which is in charge of eliminating toxins from your bloodstream. If you drink alcohol, do it in moderation and drink lots of water to remain hydrated. Additionally, if you are taking drugs that may interact with alcohol, avoid consuming it. Furthermore, drinking might impair your body’s ability to absorb nutrients. Cosmetics and personal care products Many of the cosmetics and personal care items we use on a daily basis include toxic ingredients. Many shampoos and conditioners, for example, include sulfates, which can strip your hair of its natural oils and irritate your scalp. Heavy metals like lead and mercury are commonly found in cosmetics, and if used in excessive quantities, they may be dangerous. To avoid exposure to these dangerous pollutants, use cosmetics and personal care items that are branded “organic” or “all-natural.” More and more individuals are becoming aware of the advantages of utilizing natural, organic goods in recent years. Furthermore, a number of businesses have begun to produce such items. Pesticides In agriculture, pesticides are used to protect crops against insects, weeds, and fungus. These substances, on the other hand, can be hazardous to human health. Pesticide exposure has been linked to an increased risk of some cancers, birth abnormalities, and neurological issues, according to studies. If pesticides are a concern, buy organic produce and carefully wash all fruits and vegetables before eating them. Pesticides should not be used in your home or garden. If you’re exposed to it on a frequent basis, it can cause major health concerns. Chlorine Chlorine is a widely used disinfectant in public water systems. It’s also used to eliminate germs and other pathogens in swimming pools. Although chlorine is good at destroying hazardous bacteria, it is poisonous to humans. Chlorine exposure has been linked to an increased risk of cancer, respiratory issues, and skin irritation in studies. Drink filtered water and avoid chlorinated pools if you’re concerned about chlorine exposure. Prescription drugs A drug given by your doctor is the last thing you anticipate to be hazardous to your health. Many prescription medications, on the other hand, come with a broad list of adverse effects. Some of these side effects are dangerous and can even kill you. If the toxins in your prescription are causing you to worry, talk to your doctor about other possibilities. Also, be sure to carefully follow the directions on your prescription label. In addition, many over-the-counter medications include chemicals that are hazardous to your health. Conclusion To conclude, the aforementioned are the sources of toxins in your body. Take care of yourself and stay away from these situations as much as possible.	https://wondafox.com/causes-of-toxins-in-your-body/
Fatty liver, also known as hepatic steatosis, is a common condition caused by the buildup of excess fat in the liver cells. This condition can cause liver inflammation, which can damage the liver and create scarring. In severe cases, this scarring can even lead to liver failure. There are two main types of fatty liver disease: - Non-alcoholic fatty liver: Fat buildup in the liver that is not linked to drinking alcohol. - Alcoholic fatty liver: Fat buildup in the liver as a result of drinking excessive quantities of alcohol. What are the stages of fatty liver disease? Non-alcoholic fatty liver disease (NAFLD) can be broken down into four different stages: - Stage 1: Steatosis (Simple fatty liver) is a stage where there is a largely harmless build-up of fat in the liver cells but not to an extent to cause symptoms to appear. - Stage 2: Non-alcoholic Steatohepatitis (NASH) is a more serious form of NAFLD and occurs if the liver becomes damaged causing it to become inflamed. NASH is more likely to occur in people who are overweight or obese, or who have diabetes. - Stage 3: Fibrosis occurs when persistent inflammation causes scar tissue around the liver and nearby blood vessels, but the liver is still able to function normally. - Stage 4: Cirrhosis, the most severe stage, happens when normal liver tissues are replaced by fibrosis to the extent that the structure and function of the liver is affected and can lead to liver failure and liver cancer. Alcoholic fatty liver occurs in three stages: - Stage 1: Steatosis (Fatty liver) is characterized by an excessive accumulation of fat inside the liver cells. Heavy drinkers usually get to the fatty liver stage in their early years of alcohol abuse. - Stage 2: Alcoholic Hepatitis is characterized by the inflammation of the liver leading to the degeneration of liver cells. Jaundice is the most common symptom in this stage. - Stage 3: Liver Cirrhosis is the last and final stage of Alcoholic Liver Disease where permanent scarring of healthy liver tissue occurs. It is a severe condition and an irreversible one. What are the causes of fatty liver disease? When the body produces excess fat or doesn’t metabolize fat efficiently, it leads to the accumulation of fat in liver cells and causes fatty liver disease. Some of the common causes of fatty liver disease are: - Intake of excess calories causes fat to build up in the liver. - Certain conditions such as overweight or obesity, diabetes or high triglycerides can lead to fatty liver. - Alcohol abuse, malnutrition may also lead to fatty liver. - Chronic viral hepatitis, especially Hepatitis C - Rapid weight loss. - Pregnancy. - Certain genes may also raise the risk of developing fatty liver. What are the symptoms of fatty liver disease? The symptoms of fatty liver disease may include: - Discomfort or pain in the upper right side of the abdomen. - Abdominal pain - Loss of appetite - Nausea - Weakness - Jaundice, yellowing of skin and eyes - Swelling in the abdomen and legs - Confusion and trouble concentrating - Extreme fatigue or tiredness - Weight loss - Enlarged blood vessels just beneath the skin’s surface - Enlarged spleen - Red palms What are the risk factors for fatty liver disease? There are many risk factors for non-alcoholic fatty liver disease, including: - Obesity - Type 2 diabetes - Insulin resistance - High blood pressure - High cholesterol levels - High triglyceride levels - Polycystic ovary syndrome - Underactive thyroid - Family history of fatty liver disease - Metabolic syndrome - Underactive pituitary gland - Age over 50 years - Smoking What are the complications of fatty liver disease? The main complication is cirrhosis which causes scarring of the liver. Scarring can result in: - Fluid buildup in the abdomen - Swollen veins in the esophagus that can rupture and bleed - Confusion, slurred speech, and drowsiness - Liver cancer - End-stage liver failure How is the fatty liver disease diagnosed? Following tests may be used to diagnose the fatty liver disease: - Blood tests to measure global liver function and indicate inflammation. - Liver ultrasound is a simple imaging procedure that looks for irregularities in the shape and consistency of the liver and for problems of the biliary tract, such as gallstones. - Computed tomography (CT) is a method of body imaging that provides a detailed view of the liver. - A liver biopsy may be needed to make a definite diagnosis of fatty liver disease. The test also helps in defining the stage of disease and the severity of liver inflammation. How can the fatty liver disease be prevented? A person can follow below tips to prevent fatty liver disease: - Maintain a healthy weight. - Eat a balanced diet that is high in vegetables, fruits, and good fats. - Limit consumption of refined carbohydrates such as sweets, white rice, white bread. - Limit consumption of saturated fats, trans fats such as red meat, processed snack foods. - Exercise regularly. - Limit or avoid alcohol. - Take medications as prescribed. - Quit smoking Disclaimer: ERemedium blogs are for informational purposes only and should not be construed as advice or as a substitute for consulting a physician. It is not a substitute for medical advice or treatment from a healthcare professional.	https://eremedium.in/fatty-liver-disease/
The impacts of cancer are far-reaching: In the United States, cancer is the second leading cause of death. In 2021, nearly 2 million new cancer cases were estimated to have occured. Thankfully, the cancer death rate has fallen progressively between the years of 1991 and 2018, due largely to improvements in early detection and treatment, underscoring the importance of prevention and screening when it comes to getting optimal care. What is cancer? The term cancer refers to a large group of diseases characterized by the development and presence of cancer cells. Cancer cells are abnormal cells that can divide, multiply, and spread quickly and have the ability to destroy healthy and normal tissues in the body. Cancer is caused by gene mutations that take place within cells. These mutations can cause a formerly healthy cell to grow and divide more rapidly and make mistakes when repairing DNA errors. Gene mutations can be inherited, but most gene mutations take place after you’re born. These mutations can happen as a result of smoking, radiation, viruses, carcinogens (also known as cancer-causing chemicals), chronic inflammation, and other factors. Though anyone can develop cancer, there are some things that can increase your risk: - Age: Cancer is more common in older adults. - Lifestyle: Habits like smoking, drinking, and getting excessive exposure to the sun can increase your risk of developing cancer. - Family history: Though inherited conditions are only responsible for a small percentage of reported cancers, a family history of cancers can increase your risk of developing certain cancers. However, it’s important to note that having a family history of cancer does not definitively mean you will develop cancer. - Certain health conditions: Some chronic conditions, like ulcerative colitis, can increase your risk of developing specific types of cancer. - Environment: Exposure to secondhand smoke and some chemicals can increase your risk of developing cancer. What are the different types of cancer? There are many different types of cancer. Below is a list of the most common cancers in the US: - Bladder Cancer - Breast Cancer - Cervical Cancer - Colorectal (Colon) Cancer - Head and Neck Cancers, including: - Throat Cancer - Brain Cancer - Eye Cancer - Kidney Cancer - Liver Cancer - Lung Cancer - Lymphoma, cancer that starts in the lymphatic system, including: - Hodgkin lymphoma - Non-Hodgkin lymphoma - Mesothelioma (cancer that forms in the thin tissue that lines some internal organs) - Myeloma (cancer of the plasma cells) - Ovarian Cancer - Prostate Cancer - Skin Cancer (Basal Cell Cancer, Squamous Cell Cancer, Melanoma) - Testicular - Thyroid Cancer - Uterine Cancer - Vaginal and Vulvar Cancers What are some common symptoms of having cancer? Unfortunately, not all cancers cause the same symptoms. Symptoms of having cancer can vary depending on the individual, the type of cancer, and which part of the body is affected by cancer. Still, there are some general symptoms associated with having cancer. These symptoms can include: - Fatigue - Weight changes - A lump that forms under the skin - Skin changes - Difficulty swallowing - Persistent cough or trouble breathing - Problems with sexual, bowel, or bladder function - Hoarseness - Indigestion or discomfort after eating - Chronic and unexplained muscle or joint pain - Persistent and unexplained fever or night sweats - Unexplained bleeding or bruising Are there screening tests I can have done? Screening is an important preventive pressure that checks your body for cancer, often before you start to experience symptoms. The recommendations for cancer screening vary depending on the type of cancer being screened for and other factors (age, sex, family history) of the individual being screened. Here are some of the general recommendations for cancer screening: - Breast Cancer: Mammograms help to detect breast cancer early. The US Preventive Task Force (USPSTF) recommends biennial mammograms for women between the ages of 50 and 74. Screening between the ages of 40-49 is an individual decision, though one you and your provider may decide to make depending on your family history of breast cancer. - Cervical Cancer: A Pap test (also known as a Pap smear) looks for abnormal cells in the cervix that can turn into cancer. The USPSTF recommends women between the ages of 21 and 65 screen for cervical cancer every three years. - Colorectal (Colon) Cancer: Colonoscopies screen for precancerous growths in the colon or rectum. Though timing recommendations vary, USPSTF recommends annual screening for adults between the ages of 50-75 (though screening can begin as early as age 45 depending on family history). - Lung Cancer: The USPSTF recommends annual screening for lung cancer only in adults between the ages of 50 and 80 with a smoking history of smoking at least 20 packs a year or for those who have quit smoking within the past 15 years. Screening for lung cancer is generally done with the use of low-dose computed tomography (CT), a procedure that uses a computer connected to an x-ray machine and produces a low dose of radiation. - Prostate Cancer: Unfortunately, there’s not enough data to make universal recommendations for prostate cancer. Instead, prostate cancer screening is based on an individualized discussion between a patient and their provider. What can I do to prevent cancer? Though not all cancers are avoidable, the WHO estimates that 30-50% of cancers are preventable. Decreasing our risk can largely be accomplished by adopting lifestyle medicine practices. Based on decades of evidence, the American Institute for Cancer Research developed a set of "Top 10 Cancer Prevention Recommendations" that included: - Being a healthy weight - Being physically active - Eating a diet rich in whole grains, vegetables, fruits, and beans - Limiting consumption of “fast foods” and other ultra-processed foods that are high in fat, starches, or sugars - Limiting consumption of red and processed meat - Limiting consumption of sugar-sweetened drinks - Limiting alcohol consumption - Not using supplements for cancer prevention - Not smoking and avoiding other exposure to tobacco - Avoiding excess sun According to the CDC, here are some preventive measures you can take to help reduce your risk of cancer: - Don’t smoke tobacco: Cigarette smoking and exposure to secondhand smoke can significantly increase your risk of lung cancer. If you smoke, find the right resources to help you quit. - Protect your skin: Exposure to ultraviolet (UV) rays from the sun and tanning beds can increase your risk of developing skin cancer. In addition to avoiding tanning beds, you can protect your skin by wearing sunscreen, seeking shade when possible, and wearing protective clothing and accessories (like sunglasses and sun hats) when outdoors. - Don’t drink excessive amounts of alcohol: Regular and excessive alcohol drinking can increase your risk of developing certain mouth and throat cancers. - Maintain a lower body weight: According to research from the American Cancer Society, being overweight or obese is thought to be responsible for about 11% of cancers in women and 5% of cancers in men. - Get tested for Hepatitis C: Hepatitis C is the most common type of viral hepatitis in the US. Over time, it can lead to liver cancer. What should I do if specific cancers run in my family? It’s important to talk to your provider about your personal medical history as well as your family history of cancer. Sharing this information can help you both to decide which preventive measures (including screening tests) are best for you. When detected, early treatment is crucial to having the best outcomes possible. If you’re unsure about where to start, Forfend can help. Our whole person wellness exams can help you optimize your approach to whole body wellness and health. Sources 10 Cancer Prevention Recommendations. (2021). CA: A Cancer Journal for Clinicians. (2021). Cancer Prevention Overview. (2021). Does Body Weight Affect Cancer Risk? (2020). How to Prevent Cancer: 10 Recommendations. (2020).	https://forfendhealth.com/blog/what-we-know-about-cancer-prevention/
A number of factors, including rapid urbanization, globalization, and aging of the population all contribute to the growing NCD burden in Kenya, but many NCDs are largely preventable by changing unhealthy behaviors. The four major NCDs mentioned earlier (CVDs, cancers, chronic lung diseases, and diabetes) share four key risk behaviors: tobacco use, harmful use of alcohol, lack of exercise, and an unhealthy diet. These are all behaviors that are typically initiated or solidified during adolescence or young adulthood and set the stage for NCDs later in life. While these risk behaviors are still relatively low among youth in Kenya compared to youth in other regions, their prevalence is increasing. Therefore, a window of opportunity exists for Kenya now to address the four key risk behaviors in its large and growing youth population to reduce the NCD burden in the coming decades. According to the World Health Organization (WHO), 70 percent of premature deaths in adults worldwide are the result of behaviors that begin in adolescence.4 Scaling up proven, cost-effective interventions that discourage unhealthy behaviors and promote healthy ones can significantly shift the trajectory of the costly NCD epidemic in the near future. Doing so now will also help Kenya meet some of the Sustainable Development Goals and improve chances of achieving greater economic growth and development. NCDs Affect People Earlier in Life in Kenya Kenya will see an increasing number of deaths from NCDs relative to other causes of death over the coming decades. More importantly, many of these NCD deaths will affect Kenyans at the height of their productive years, not in old age. Kenyans, like others living in low- and middle-income countries, develop NCDs at younger ages, get sicker, and die prematurely than those in high-income countries. About two-thirds of NCD deaths in Kenya occur prematurely (defined as deaths among people below age 70), compared to only a quarter in high-income countries.5 Premature deaths result from various factors, including greater exposure to risk factors, delayed diagnosis, and insufficient treatment. Further, deaths from NCDs are typically preceded by a period of disability when one’s productivity is compromised, while the need for health care and other support increases. NCDs sometimes even push those burdened by the disease and their families into poverty or keep them impoverished. The increasing prevalence of NCD risk behaviors among youth in Kenya will likely exacerbate the pattern of premature deaths. Kenyan youth are engaging in all four NCD risk behaviors, and there are signs that the levels are increasing. Alcohol Use. A 2012 survey by the National Authority for the Campaign Against Alcohol and Drug Abuse found that about 10 percent of young people ages 18 to 24 currently use alcohol (defined as having any drinks containing alcohol in the past 30 days).6 Alcohol use contributes to CVDs, cancers, and diabetes. Any amount of alcohol use can be harmful to youth whose bodies are still growing. Heavy drinking is also associated with many other health risks, including unprotected sex that can increase chances of contracting HIV and other sexually transmitted infections, violence against women (and violence in general), road traffic accidents, and poor mental health. The risk of developing alcohol dependence substantially increases for those who start drinking in early adolescence, compared to those who start in late adolescence or in their early 20s, even while taking into account family history of alcohol abuse. In Kenya, locally produced, illicit brews that are cheap and highly potent (and sometimes toxic) are also widely available to youth. This alcohol is even harder to regulate than legally manufactured alcohol and it is challenging to enforce the age restriction on sales. Tobacco Use. The 2013 Global Youth Tobacco Survey, a national survey of 13-15-year-old secondary school students, showed that 13 percent of boys and 7 percent of girls currently use any tobacco products (defined as any use in the past 30 days).7 Among these boys and girls, the majority used “smoked” tobacco products, such as cigarettes and shisha (a water pipe), and girls were more likely to use smokeless tobacco products than boys. Exposure to secondhand smoke was also high: one-quarter of students reported being exposed to tobacco smoke at home and about 45 percent to tobacco smoke inside enclosed public spaces. There have been declines in cigarette smoking among this age group from 15 percent to 5 percent between 2001 and 2013, though the trends in the use of other tobacco products have been less clear. Tobacco use contributes to all four of the main NCDs. A worrisome trend has emerged among youth in the increasingly popular use of shisha, especially in urban areas. Some young people may assume that shisha is safe or safer than regular cigarettes. However, the nicotine dose in a typical shisha smoking session is more than one and a half times higher than that contained in one cigarette.8 Furthermore, while the secondhand smoke from any smoked tobacco poses health risks, one hour of exposure to shisha smoke, compared to cigarette smoke, may result in two to 10 times the amount of harmful chemicals in the air, including some that cause cancer.9 As with alcohol, cheaper, locally produced cigarettes that are poorly regulated and are widely available from street vendors and kiosks bolster their accessibility among youth. Marketing of alcohol and tobacco products to youth plays a key role in initiating use of these substances by youth. Such marketing often comes in the form of advertisements, promotions, and sponsorships. For example, alcohol companies often sponsor sporting events that many youth attend. Also, as many as one in 10 students in Kenya reported ever being offered a free tobacco product from a tobacco company, and one in 10 also reported owning some items with a tobacco brand logo on it.10 Despite restrictions on advertisements, young Kenyans are still exposed to them in many places, and exposure to such marketing strategies have generally been shown to increase use of these substances. Unhealthy Diet and Physical Inactivity. Together, unhealthy diets and insufficient physical activity contribute to overweight and obesity, and consequently, to NCDs such as Type 2 diabetes, CVDs, and certain cancers. Demographic and Health Surveys between 1993 and 2014 show a doubling of the percentage of women who are either overweight or obese for both 15-to-19 and 20-to-24 age groups (overweight defined as a Body Mass Index (BMI) of 18 or above, and obesity defined as a BMI of 25 or above).11 Kenya is also undergoing a nutrition transition—it faces the double burden of an emerging epidemic of overweight and obesity and persistent undernutrition. While 13 percent of 15-19-year-old women were overweight or obese in 2014, 17 percent were classified as being thin, including 5 percent who were particularly thin (thin defined as a BMI below 18.5, and “particularly” thin defined as a BMI below 17). Rapid economic and social change, together with urbanization and globalization in Kenya are leading to a shift away from healthier, traditional diets to those filled with sugar, sodium, and saturated fat. Increased availability and consumption of commercially prepared and highly processed foods and sugary beverages contributes to overweight and obesity and to various NCDs. The food industry targets children and youth in an effort to influence their taste preferences and encourage brand loyalty that can continue into adulthood. Aside from poor diets, a lack of sufficient exercise is also increasing the risk for developing NCDs. According to the International Study of Childhood Obesity, Lifestyle and Environment conducted in Nairobi in 2012, among 9-11-year-old students in primary schools, less than 10 percent of girls and less than 20 percent of boys got sufficient levels of physical activity, defined as engaging in at least 60 minutes of moderate-to-vigorous physical activity every day.12 Over half of the students reported using motorized transportation to and from school every day. Rapid urbanization in Kenya has significantly reduced the levels of physical activity required for work or transportation and has also given rise to environmental factors such as heavy traffic, poor air quality, and crime that can make it difficult to be active outside. Lack of access to safe, well-lit sidewalks and parks and other spaces for recreation can also prevent youth from getting enough exercise. Exercise has multiple other benefits including reducing the risk of developing mental health conditions, such as anxiety and depression that are common among young people. Physical activity among youth is also typically associated with lower levels of other NCD risk behaviors such as tobacco and alcohol use. As a priority, Kenya should focus on curbing NCD risk behaviors in youth while levels are still relatively low. For example, programs need to focus on preventing alcohol initiation and not just alcohol cessation. A clear focus on interventions targeting youth risk behaviors is critical to the overall strategy to address a future NCD epidemic in Kenya. Interventions should target youth, as well as those who influence their various decisions, including peers and family members. While recognizing the importance of personal choice, it is also crucial to put in place a range of supportive, reinforcing policies and programs that make unhealthy decisions less likely for youth. For example, it is essential to enforce regulations on alcohol and tobacco sales and marketing to children and youth, though the availability of informal products makes it challenging. The Tobacco Control Act, 2007, the principal law governing tobacco control in Kenya, prohibits sale of tobacco products to anyone under age 18. Such laws can only be effective when systems are put in place to enforce them.13 Implementing higher taxes on cigarettes has been effective in reducing consumption among youth, who are particularly sensitive to price increases. Mandating that schools and other places where young people congregate be smoke- and alcohol-free also helps limit exposure to these substances. Ensuring that youth receive the correct information about the health impacts of their behaviors is also important to help youth make healthy decisions. For example, the Kenyan Ministry of Health launched an anti-tobacco mass media campaign in 2014 titled, “Smoking Kills—Quit Now.14 It broadcast messages on radio and television about the adverse health effects of smoking tobacco, as well as secondhand smoke in Swahili, English, and other local languages. The Ministry also disseminated informational posters in schools, universities, and other public institutions to create awareness. Youth centers and existing health services targeting youth, such as sexual and reproductive health services and HIV/AIDS services, can also incorporate NCD services, such as counseling and screening for NCD risk behaviors, to reach a wider cross section of youth with the services necessary to reduce risk behaviors.15 Schools can also play an important role. For example, the school curriculum in Kenya is currently being revised to increase the level of physical activity children get during school, though a challenge is the tendency of many schools to spend the physical education time on other academic subjects. School-based information programs on the importance of staying away from alcohol and tobacco have also been found successful in some settings. Now is the time for Kenya to implement a full range of prevention strategies that will build positive health behaviors and reduce NCD risk behaviors among youth. Successfully implementing such strategies requires coordination, creative thinking, collaboration across sectors, and involving young people. Also important is filling critical information gaps by regular data collection efforts, and conducting policy and program evaluations to help identify the most-effective interventions for Kenya. Averting the premature onset of NCDs will enable youth to reach their full potential, increase productivity, decrease future healthcare costs, and contribute to further economic growth and development. 1. World Health Organization (WHO), Global Status Report on Noncommunicable Diseases 2014 (Geneva: WHO, 2014). 2. WHO, Global Health Estimates 2015: Deaths by Cause, Age, Sex, by Country and by Region, 2000-2015 (Geneva: WHO, 2016). 3. Kenya Ministry of Health, Division of Non Communicable Diseases, Kenya STEPwise Survey for Non Communicable Diseases Risk Factors 2015 Report (Nairobi: Ministry of Health, 2016). 4. WHO, Global Health Risks: Mortality and Burden of Disease Attributable to Selected Major Risks (Geneva: WHO, 2009). 5. WHO, Global Health Observatory Data: Premature Deaths, accessed at http://www.who.int/gho/ncd/mortality_morbidity/ncd_premature/en/, on July 1, 2017. 6. National Authority for the Campaign Against Alcohol and Drug Abuse (NACADA), Rapid Situation Assessment of the Status of Drug and Substance Abuse in Kenya (Nairobi: NACADA Authority, 2012). 7. Kenya Ministry of Health, WHO, and U.S. Centers for Disease Control and Prevention (CDC), 2013 Kenya Global Youth Tobacco Survey (GYTS), accessed at https://nccd.cdc.gov/GTSSDataSurveyResources/Ancillary/DataReports.aspx?CAID=1, on July 1, 2017. 8. Thomas Eissenberg and Alan Shihadeh, “Waterpipe Tobacco and Cigarette Smoking: Direct Comparison of Toxicant Exposure,” American Journal of Preventive Medicine 37, no. 6 (2009): 518-23. 9. Nancy Daher, et al., “Comparison of Carcinogen, Carbon Monoxide, and Ultrafine Particle Emissions From Narghile Waterpipe and Cigarette Smoking: Sidestream Smoke Measurements and Assessment of Secondhand Smoke Emission Factors,” Atmospheric Environment 44, no. 1 (2010): 8-14. 10. Kenya Ministry of Health, WHO, and CDC, 2013 Kenya Global Youth Tobacco Survey (GYTS). 11. Kenya National Bureau of Statistics, Kenya Demographic and Health Survey (multiple years), accessed at http://dhsprogram.com/, on July 1, 2017. 12. Stella K. Muthuri et al., “Correlates of Objectively Measured Overweight/Obesity and Physical Activity in Kenyan School Children: Results From ISCOLE-Kenya,” BMC Public Health 14, no. 1 (2014): 436. 13. The Tobacco Control Act, 2007, accessed at http://kenyalaw.org/kl/fileadmin/pdfdownloads/LegalNotices/169-Tobacco_Control_Regulations__2014, on July 1, 2017. 14. The International Tobacco Control Policy Evaluation Project, ITC Kenya National Report: Findings From the Wave 1 (2012) Survey (Nairobi: ITC Project, 2015). 15. Toshiko Kaneda and Reshma Naik, Integrating Health Services for Young People: Tackling the Growing Noncommunicable Disease Epidemic (Washington, DC: PRB, 2017).	https://www.prb.org/resources/promoting-healthy-behaviors-among-youth-to-tackle-kenyas-growing-noncommunicable-diseases-epidemic/
This article is excerpted from an article titled ‘Lifestyle and Diet Tips for Healthy Bones’ by Kelly Andrews at Spine-Health.com on March 17, 2017. A healthy diet is not only comprised of a wide range of nutrients, but also involves eliminating poor quality food choices which can interfere with the assimilation of nutrients. Additionally, while certain diet and lifestyle choices can aid in the absorption of bone nutrients, others can cause the body to excrete higher levels of nutrients than normal. In addition to eating well, there are several other aspects of self-care that are important for a healthy back, including the following. #1 – Drink Plenty of Water The human body is comprised of about 60% to 70% water, making hydration a vitally important part of a healthy diet. Drinking plenty of water allows nutrients to travel to the major organs in the body, helps remove waste, and helps maintain function in the joints, organs, or other structures in the spine. Proper hydration is also important specifically for the spine and back. For instance, intervertebral discs consist largely of water—at birth, discs are about 80% percent water, although this usually declines with age. Keeping the body well hydrated is important to maintain the good health of the spinal discs. Drinking enough water also helps with sustaining or reaching an optimal body weight, which can ultimately improve back health. The typical recommendation for a healthy diet includes at least 8 large glasses of water every day. Medically, there is no hard and fast guideline for how much water should be consumed each day, but it is advised that water should account for at least half of a person’s daily fluid intake.2 Additionally, it is important to distribute water consumption throughout the day rather than drink only when thirsty. #2 – Exercise Regularly Getting enough exercise is critical for many reasons. When it comes to the back, exercise provides the double-benefit of helping injuries heal faster and helping prevent a recurrence of back pain. Movement through gentle, controlled exercise stimulates a flow of nutrients within the spinal structures that facilitates the healing process. For example, physical activity causes the intervertebral discs to swell with water and then expel it, a process necessary to allow the exchange of nutrients between the discs and other spinal structures. Movement also stimulates muscle, ligament, and tendon activity to maintain spinal integrity. If physical activity and gentle exercise is lacking, the spinal discs are deprived of the nutrients and movement they need to stay healthy and functional. A focused exercise program—usually guided by a spine health professional—is a critical part of almost any back pain treatment. Most exercise programs include a combination of stretching, strengthening, and low-impact aerobic exercise. For people who do not have back problems, exercise is important in order to reduce the risk of developing back problems in the future. #3 – Avoid Smoking Nicotine intake and tobacco use are harmful in many ways, affecting various structures and functions in the body. Smoking can increase the risk for developing back pain and interfere with the body’s natural healing processes, including tissue and bone formation. #4 – Avoid Cola Consumption Phosphoric acid is unique to colas (both regular and diet colas) and will bind to calcium and magnesium in the digestive tract. Regular consumption of phosphoric is associated with lower bone mass density (BMD). #5 – Avoid Excessive Alcohol Consumption Regular alcohol consumption has been determined as a risk factor for increased bone loss. One study found that women who regularly consumed alcohol had a greater risk on bone loss later in life when women are already at increased risk for osteoporosis. Alcohol lacks nutritional value and adds unneeded sugar to the diet which can contribute to weight gain and obesity, further complicating back problems. It also has negative effects on the internal organs, especially the liver, and should only be consumed in moderation. Additionally, alcohol acts as a depressant, and can contribute to feelings of depression and anxiety that many experience with chronic pain. The relationship between chronic pain and depression is well-documented but not fully understood. Many healthcare professionals recommend that treatment for one should coincide with treatment for the other. More research is needed to establish effective pain and depression management options for patients who experience both. #6 – Reduce Salt Consumption Sodium and chloride, found in table salt, increase urinary calcium excretion before it can be properly absorbed and utilized by the body for strong bones. Unprocessed Himalayan or sea salts contain many trace minerals that play a role in bone health and are a better option. #7 – Temper Caffeine Consumption Caffeine from coffee, tea, and soft drinks may lead to bone loss if the patient does not consume enough calcium. High levels of caffeine intake have been shown to correspond to significant loss of bone density in elderly women, with genetics also being a factor in bone loss. To read the full article, click here: http://www.spine-health.com/wellness/nutrition-diet-weight-loss/lifestyle-and-diet-tips-healthy-bones.	https://www.bonati.com/blog/7-ways-healthier-bones/
Can alcoholism cause pulmonary embolism? Conclusions: Low to moderate alcohol consumption is associated with a decreased risk of deep venous thrombosis and pulmonary embolism in older persons. Can alcoholism cause DVT? Together, DVT and PE form a condition called venous thromboembolism (VTE). Evidence from a 2015 study suggests that excessive alcohol consumption may raise the risk of DVT. What are the first signs of liver damage from alcohol? Generally, symptoms of alcoholic liver disease include abdominal pain and tenderness, dry mouth and increased thirst, fatigue, jaundice (which is yellowing of the skin), loss of appetite, and nausea. Your skin may look abnormally dark or light. Your feet or hands may look red. Is wine good for blood clots? Resveratrol in red wine Resveratrol might help prevent damage to blood vessels, reduce low-density lipoprotein (LDL) cholesterol (the “bad” cholesterol) and prevent blood clots. What can you not drink on blood thinners? Precautions Against Drinking Alcohol While Taking Blood Thinners. You should limit alcohol consumption while taking anticoagulant blood thinners such as Coumadin (warfarin), as alcohol can potentially increase the risk of bleeding with this prescribed drug. Is coffee bad for blood clots? A new study suggests it can raise your risk of blood clots. But do you really need to worry? Taking caffeine during a high-intensity workout can increase the coagulation factor in your blood, making it more likely to form clots, according to a new study in the journal Medicine & Science in Sports & Exercise. How much alcohol can you drink while on blood thinners? Moderate alcohol use is generally safe while taking most blood thinners. For healthy adults, doctors recommend limiting alcohol intake to a maximum of two drinks a day for males and one drink a day for females. Some people should completely avoid drinking alcohol while on blood thinners. Is coffee a blood thinner? It was concluded that caffeine has the capacity to inhibit the metabolism of warfarin and enhance its plasma concentration and hence anticoagulant effects. Thus, patients should be advised to limit the frequent use of caffeine-rich products i.e. tea and coffee during warfarin therapy. Which wine is good for blood clots? Red wine contains a substance called resveratrol, an antioxidant flavonoid that may lower bad cholesterol levels and thereby minimize the potential for blood clots. Antioxidants called polyphenols, of which resveratrol is one, may aid in the protection of the lining of blood vessels within the heart as well. Is Whiskey good for blood clots? Whiskey can reduce the risk of blood clots, decreasing the chances of suffering from a heart attack or stroke. There are also antioxidants found in whiskey that prevent cholesterol from building up in the arteries, and promote the health of good cholesterol that your heart craves.	https://bacodablogs.com/by-topic/are-alcoholics-more-prone-to-blood-clots.html
- Lifestyle risk behaviours, such as smoking, excessive alcohol intake, poor diet and physical inactivity, are important contributors to morbidity and mortality. WHO identified that these behaviours are responsible for 29 per cent of the disease burden in the most industrialised countries (1). - These risk behaviours consistently cluster among certain population subgroups, such as those with lower socioeconomic status. They are unequally distributed in the population and are impacted upon by the wider social determinants of health. - Michael Marmot’s Review of Health Inequalities called for a proportionate universal response whereby actions to prevent ill health are universal, but with a scale and intensity that is proportionate to the level of need. This chapter refers to people who have one or more unhealthy behaviours: - Tobacco smoking - Excessive alcohol intake (above recommended levels) - Insufficient levels of activity (below recommended levels) - Poor diet (less than recommended levels of fruit and vegetable consumption) For further information, see the following JSNA chapters: - Smoking: Long term conditions chapter, Young People, Mental Health, Maternity and breastfeeding/infant feeding - Excessive Alcohol Intake: Substance misuse chapter - Insufficiently Active: Physical Activity chapter - Mental Health: Wellbeing and adult mental health chapter Introduction Visualisation of data used in this chapter Lifestyle risk factors such as whether someone smokes, how much alcohol they drink, what they eat and whether they take regular exercise are widely recognised as affecting their health and risk of dying prematurely. In 2002, the World Health Organisation identified that in the most industrialised countries, alcohol and smoking, low consumption of fruit and vegetables and lack of physical activity were associated with about 29 per cent of the disease burden, estimated by disability-adjusted life years (DALYs) lost (1). These behaviours are also linked to hypertension, high cholesterol, obesity and overweight which are associated with diseases including coronary heart disease, diabetes and cancer and are responsible for a further 15 percent of the disease burden in these countries. Close to half of the burden of illness in developed countries is therefore associated with the four main unhealthy behaviours (2). In England around a quarter of people are engaged in three or four lifestyle risk behaviours, while only 6% engage in none of them. These factors are likely to interact with one another to further increase the risk of premature death (3). Figure 1 shows the relationship between multiple lifestyle risks and mortality (2). Figure 1: The relationship between multiple lifestyle risks and mortality People with multiple lifestyle risk factors are unequally distributed in the population and are associated with wider social determinants of health. For example, people with learning disabilities are more likely to have poorer health due to factors such as poverty, poor housing conditions, unemployment, social disconnectedness and overt discrimination (4). These factors all contribute to poorer health, shorter lives and increased health inequalities among those in greatest need. In order to address wider determinants that will support behaviour change, multiple organisations, across different sectors need coordinated action and approaches to help support people to tackle multiple lifestyle risk factors. Figure 2 shows the causal relationship between different factors, and how they can have both positive and negative influences on people’s lives, and also undermine health and wellbeing, both for individuals and communities. Figure 2: Dahlgren & Whitehead’s (1992) illustration of health determinants Who’s at risk and why? Table 1 shows the priority groups in Surrey for each risk factor. In order to understand who is at risk and why, it is important to understand the root causes and determinants of population health as highlighted in Dahlgren and Whitehead’s model in section 2. Table 1: priority groups in Surrey for each risk factor. \|Smoking\|\|Excessive Alcohol intake\|\|Insufficiently Active\|\|Poor diet\| \|People within socio-economically deprived areas\|\|✔\|\|✔\|\|✔\|\|✔\| \|Routine and manual workers and people on lower social grades\|\|✔\|\|✔\|\|✔\|\|✔\| \|Pregnant women\|\|✔\|\|✔\|\|✔\| \|People with mental health issues\|\|✔\|\|✔\|\|✔\| \|Black, Asian and minority ethnic groups (BAME), including the Gypsy, Roma and Traveller community\|\|✔\|\|✔\|\|✔\|\|✔\| \|Children and young people\|\|✔\|\|✔\|\|✔\|\|✔\| \|Special Education Needs and Disability (SEND)\|\|✔\| \|Physical disability\|\|✔\|\|✔\| \|Hospital patients and people with long term conditions\|\|✔\|\|✔\|\|✔\|\|✔\| \|Victims and perpetrators of domestic abuse\|\|✔\|\|✔\| \|Females (starting from adolescence)\|\|✔\|\|✔\|\|✔\| \|Older adults\|\|✔\|\|✔\|\|✔\|\|✔\| The level of need in the population Multiply lifestyle risks in Surrey Synthetic estimates of numbers of Surrey residents engaging in multiple lifestyle risks suggest that approximately 243,700 adults in Surrey are engaging in 3 or 4 lifestyle risks, this represents 27% of the 16 and over population. Just over 614,700 Surrey residents (67%) are likely to be engaging in 1 or 2 risky lifestyle behaviours. The remaining 55,200 are not engaging in any of the four unhealthy behaviours described. See Tableau Visualisation, It shows that people with no qualifications are most likely to engage in more risky behaviours. Smoking Smoking is the primary cause of preventable illness and premature death. Smoking harms nearly every organ of the body and reduces both quality of life as well as life expectancy and greatly increases the risk of cancer, cardiovascular disease and respiratory disease. Across Surrey, 14% of people aged 18 and over and 6.8% of those aged 15 are smokers (2015) (6). We can compare this to the national averages of 16.9% and 8.2% respectively and this has been gradually declining year on year. Smoking rates are much higher among our more deprived communities, having a significant impact on increasing health inequalities by reducing life expectancy in these groups. The smoking rate amongst Surrey residents in routine and manual occupations is 22.5% (6). People from our most deprived communities are more likely to smoke, have greater levels of dependency and are less likely to quit than more affluent smokers (7). Local smoking prevalence data estimates higher smoking rates in areas of socioeconomic deprivation such as in Walton North, Town, Preston, Westborough, Old Dean, Maybury and Sheerwater, Valley, Stanwell North, Englefield Green West and Godalming Centre and Ockford wards. Recent research from Action on Smoking and Health (ASH) estimates there are about 87,000 households in Surrey with at least one smoker. 21% of households with a smoker fall below the poverty line. If these smokers were to quit, around 6000 households in Surrey would be elevated out of poverty (7). Other priority groups in Surrey: - Black, Asian and Minority Ethnic (BAME) groups Smoking prevalence varies greatly between ethnic groups and between men and women within these groups. Whilst smoking prevalence amongst minority ethnic groups is generally lower than that of the general population, some have higher rates, most notably amongst black Caribbean, Bangladeshi and Chinese men. The use of niche tobacco products (such as shisha and smokeless tobacco) is also higher in certain ethnic groups. Information from the 2012 Integrated Household Survey suggests that adult smoking rates are higher among Gypsies, Roma and Travellers at around 30% although the sample size is small and may not be fully representative (8). - Prisoners Approximately four times as many people in prisons smoke than in the general population, with similarly high levels of smoking found among those in police custody and probation (9). A 2014 survey of smoking in six prisons across Kent, Surry and Sussex reported smoking rates of between 62% and 81%. Currently there is no Surrey specific data available for smoking amongst prisoners, however with five prisons in Surrey, these numbers would be considerable. In 2013 Public Health England, NHS England and the National Offender Management Service (NOMS) published a joint commitment to support the development of smokefree prisons (10) - Pregnant women – see ‘Maternity and infant feeding‘ JSNA chapter - People with Mental Health problems – see ‘Wellbeing and Adult Mental Health‘ JSNA chapter Cost to Society Smoking not only impacts on the health of the local population but also has a negative impact on the local economy, costing an estimated £252.4 million to society in Surrey every year (11). Secondhand smoke Breathing in other people’s cigarette smoke is called passive or secondhand smoke and comprises of sidestream smoke from the burning tip of the cigarette and mainstream smoke which is smoke that has been inhaled and then exhaled by the smoker. In the UK around 2 million children are estimated to be regularly exposed to secondhand smoke in the home and many more are exposed outside the home (12). Tobacco smoke contains over 4000 chemicals including tar, nicotine and benzene. Immediate effects of exposure to secondhand smoke include eye irritation, headache, cough, sore throat, dizziness, nausea and effect on the heart. In the longer term, passive smokers suffer an increased risk of a range of smoking related disease including lung cancer and coronary heart disease (12). An estimated 11,000 people die each year in the UK as a result of passive smoking (13). The 2015 Surrey Health Related Behaviour Survey showed that 21% of primary school pupils and 31% of secondary school pupils responded that their parents/carers smoke. 6% of primary school pupils and 9% of secondary school responded that someone smokes indoors at home in rooms that they use (14). Excessive Alcohol intake Alcohol misuse means drinking excessively or more than the recommended limits for alcohol consumption. In the UK, alcohol use is categorised by level of risk as defined by alcohol units – lower risk, increasing risk and higher risk (table below). Higher risk drinking can be sub-divided into complex and non-complex. An example of a higher risk drinker with complex needs is an individual who has a mental health diagnosis or who is affected by domestic abuse. A small proportion of those drinking at higher risk are alcohol dependent. Drinking above recommended levels increases a range of health risks including hypertension, stroke, heart and liver disease, pancreatitis, depression, anxiety and insomnia. In addition, the most recent review of evidence suggests that the protective effects of alcohol at low levels (ie to heart health) have been overestimated. For information on higher risk drinkers with complex needs and alcohol dependency, please see Substance Misuse JSNA. Table 2: Categories of drinking as defined by Department of Health (15) \|MEN\|\|WOMEN\| \|Lower Risk\|\|Less than 14 units a week \| spread evenly across 3 or more days. \|Less than 14 units a week \| spread evenly across 3 or more days. \|Increasing Risk\|\|15-49 units per week.\|\|15-34 units per week.\| \|Higher Risk\|\|More than 50 units per week (or more than 8 units per day on a regular basis\|\|More than 35 units per week \| (or more than 6 units per day) on a regular basis \|Alcohol Dependence\|\|Drinking behaviour characterised by an inner drive to consume alcohol, continued drinking despite harm and commonly withdrawal symptoms on stopping drinking\| One alcohol unit is equal to 10ml (in volume) or 8g (in weight) of pure alcohol. Local Alcohol Profiles for England (LAPE) It was previously estimated that 21% of adults in Surrey who drink, do so at increasing risk levels and 6% at higher risk levels. Around 2% of higher risk drinkers are alcohol dependent. LAPE estimates for lower risk, increasing and higher risk drinking are now under review by Public Health England. Alcohol-Related Hospital Admissions Alcohol statistics published by the Health and Social Care Information Centre in 2016 indicate that while admissions rates in Surrey remain significantly lower than England, the narrow measure is showing a year-on-year increase in alcohol-related admission episodes locally, with an 11% increase between 2008-09 and 2014-15. In addition, the broad measure indicates that Surrey has statistically significantly higher rates of alcohol-related hospital admissions compared with the South East region. Don’t Bottle It Up Data from Surrey’s Don’t Bottle It Up website for 2015-16 indicates that 22% of people that complete the alcohol assessment drink at lower risk levels, 43% at increasing risk, 14% at higher risk and 21% are possibly dependent. It is recognised that those who are drinking excessively may be more likely to visit the website and complete the alcohol assessment. Insufficiently Active Physical inactivity has been identified as the fourth leading risk factor for global mortality causing an estimated 3.2 million deaths globally (16). It is also the fourth largest cause of disease and disability in the UK accounting for one in six deaths (17, 18). The UK Chief Medical Officers’ Guidelines for Physical Activity (19) recommend that adults (19-64 years) and older adults (65 years plus) do at least 150 minutes of moderate intensity physical activity per week, or 75 minutes of vigorous intensity activity per week (or a combination of the two). All adults should aim to incorporate activity to improve muscle strength on at least 2 days per week and should also minimise the amount of time spent being sedentary for extended periods. For older adults at risk of falls, activity that improves balance and coordination should be incorporated on at least 2 days per week. Physical activity is not only fun and enjoyable, it is essential for good health. Physical activity can prevent or help to manage over 20 conditions and diseases including coronary heart disease, type 2 diabetes, some cancers, stroke, musculoskeletal conditions and obesity. For example, there is strong evidence that being physically active can reduce your risk of type 2 diabetes by 35-40% and your risk of colon cancer by 30-50% (20). It can also help improve people’s mental health as it has a positive effect on wellbeing, mood, sense of achievement, relaxation and release from daily stress (21). Being physically active increases the chance of staying independent in later life as evidence shows it reduces the risk of falling by 30% as well as reducing the risk of the conditions and diseases mentioned above. The Health Impact of Physical Inactivity (HIPI) tool demonstrates how many deaths/cases of certain diseases could be prevented if the 40-79 yrs population was sufficiently active. The data estimates that if 100% of the Surrey population (aged 40-79) were sufficiently active, 637 deaths could be avoided (22). These figures are based on the time period 2009/10. Not only does physical inactivity have an impact on the individual in terms of poorer health outcomes and quality of life, this also has a significant impact on healthcare services and the wider society. Long term conditions like diabetes, cardiovascular and respiratory disease can lead to greater dependency on domiciliary care, residential and ultimately nursing care. This creates avoidable costs for local authorities as well as economic and social pressure on families. The total estimated cost of physical inactivity in Surrey in 2009/10 was £17,959,001 (23). The Active People Survey, commissioned by Sport England, is a large telephone survey that measures physical activity and sport participation in adults aged 16 and over. The data can be broken down by gender, age, ethnicity, disability, education, work status, social grade, faith, sexual orientation, BMI and geography and records activity levels ranging from inactive (less than 30 minutes physical activity per week) to active (at least 150 minutes physical activity per week). Therefore we are able to see how physical activity levels vary between district or borough in Surrey and by demographic group. The Active People Survey (APS9) data 2014-15 for Surrey (24) show the following groups to have lower levels of physical activity: people living in lower income households; females (starting from adolescence); older adults; BME groups and people living with a limiting illness or disability. The data show a clear gender gap with females participating in sport on average 20% less than males. Similarly people with a limiting illness or disability are half as likely to take part in physical activity and sport and their experiences are less positive than non-disabled peers. In addition to the groups mentioned above, all people with sedentary jobs (such as office jobs, driving jobs and any work that requires sitting for long periods) and those undertaking sedentary behaviour in leisure time (such as spending long periods on the sofa, watching TV or sitting at the computer) can be putting their health at risk; this applies even to those who are already undertaking vigorous regular exercise. Prolonged periods of sedentary behaviour can increase the risk of type 2 diabetes, heart disease and lower levels of aerobic fitness. Public Health guidance suggests that workers who are predominantly desk-based should initially aim to achieve 2 hours per day standing/light activity, progressing towards accumulating 4 hours per day during working hours (25). In Surrey 63.1% of the population are meeting the CMO guidelines of 150+ minutes physical activity per week compared to 57% in England. Waverley has the highest number of people meeting the guidelines (69.3%) and Spelthorne has the lowest (55.8%). The latest data (APS9 Jan 2014-Jan 2015) show that physical activity levels decline considerably with age. For example whilst one in five (19.2%) of adults in Elmbridge (aged 16+) were deemed inactive, there was a steep increase in the over 65 population to more than half (51.9%) being deemed inactive. The same data show that in Elmbridge a person living with a disability is 2.5 times more likely to be inactive as a non-disabled person. As mentioned above, physical activity levels also vary according to gender: in Surrey 26.1% of females (16+) are deemed inactive as compared to 17% of males. The gap is particularly marked in Epsom & Ewell where more than a third (34.4%) of females are inactive as compared to 11.7% of males. Using Mosaic segmentation we can estimate how physical activity levels may vary widely between different wards in the same borough. For example in the Borough of Woking, Mosaic data estimates that 34.8% of the 15+ population in Horsell East & Woodham ward are not doing any exercise, as compared to Maybury & Sheerwater ward where it is estimated 49.2% are not doing any exercise. These differences are reflected in the APS9 data where 19.5% of the Surrey population (16+) on upper social grades are deemed inactive whereas 29.7% on lower social grades in Surrey are deemed inactive. Cycling 4.8% of the adult population in Surrey are cycling at least 3 times per week and 17.5% are cycling at least once per month. Woking is the borough with the highest number of people cycling at least 3 times per week (8.5%), followed by Guildford (7.5%) and Tandridge is the lowest (1.5%) (26). Walking 49.8% of adults in Surrey walk at least 5 times per week, which is slightly lower than England (50.6%). The borough with the highest number of people walking at least 5 times per week is Guildford (56.6%) and the lowest is Spelthorne (37.7%). Use of outdoor space for exercise/health reasons The proportion of adults in Surrey who use outdoor space for exercise or health reasons is 24.9% as compared to 20.1% in the South East. Poor Diet The UK ranks 8th for overweight prevalence (including obesity) for men and women combined, out of the 34 OECD (Organisation for Economic Cooperation and Development) countries. According to the PH Outcomes Framework indicators (2015) 61.1% of adults in Surrey are carrying excess weight. Although lower than the national prevalence of 64.6%, it equates to approximately 550,000 adults. Surrey Heath and Reigate and Banstead have the highest prevalence at 65.54% and 63.3% compared to Guildford and Elmbridge who have the lowest at 57.4% and 58.2% respectively. A new PHE-led study published in The Lancet ranks the diseases and risk factors that cause death and disability in England. Diet was identified as a specific risk factor accounting for 10.8% of the total burden of disease. The proportion of adults meeting the recommended “5 a day”, on a usual day is again higher than the national average (52.3%) at 57%, however there is variation between boroughs with Waverley achieving the highest at 61.9% and Spelthorne the lowest at 49.7%. This means that slightly less than half the adult population of Surrey achieves “5 a day”, which is equivalent to approximately 450,000 adults. When we break this down to view the number of fruit or vegetable portions making up the “5 a day” we see a variation. Guildford consumes the most fruit portions with an average of 2.92 while Runnymede at 2.28 portions consumes the least which is significantly lower than the national average. Waverley consumes the most vegetable portions (2.54) and Spelthorne the least although neither of these is significantly different to the national average of 2.25 portions. Nationally fruit and vegetable consumption is higher in women than men and higher consumption is associated with higher income (27). Services in relation to need. One you www.nhs.uk/oneyou Public Health England (PHE) launched the ‘One You’ campaign in 2016 to help adults across the country avoid future diseases caused by modern day life. ‘One You’ aims to encourage adults, particularly those in middle age, to take control of their health to enjoy significant benefits now, and in later life. The campaign targets every day habits and behaviours such as eating too much unhealthy food, drinking more than is recommended, continuing to smoking and not being active enough. ‘One You’ also provides information on how people can reduce their stress levels and sleep better. The Healthy Surrey website was set up by the Surrey Health and Wellbeing Board to act as an online resource for Surrey health and wellbeing information. The website includes information and advice on health issues and provides links to local services across Surrey. Making Every Contact Count (MECC) MECC encourages conversations based on behaviour change methodologies (ranging from brief advice, to more advanced behaviour change techniques), empowering healthier lifestyle choices and exploring the wider social determinants that influence all of our health. In Surrey, a pilot project is being run with Adult Social Care and Public Health. Workplace wellbeing The Workplace Wellbeing Charter is a statement of intent that demonstrates the commitment of employers to the health and wellbeing of their employees. The aim of the Charter is to support employers to maximise the potential of their staff, and to make small changes that impact positively on staff health and wellbeing. The Charter focuses on the three key elements of Leadership, Culture and Communication that can help employers receive maximum benefit and return from employee health and wellbeing. Stop Smoking Service Stop smoking Services provide support across Surrey and offer either one-to-one or group support by trained stop smoking practitioners, delivering evidence based behaviour support and stop smoking medications. Services provide training and support for GPs and Pharmacies who also deliver the stop smoking programme. Service in Surrey: Tobacco Control The Surrey Tobacco Control Strategy 2016-21 sets out why and how Surrey needs to work together to reduce the harmful effects of tobacco. Led by Surrey County Council Public Health this multi-agency approach is owned and delivered by the Smokefree Surrey Alliance. The strategy and alliance ensure effective and coordinated action across the County by a wide variety of partners and agencies to tackle the greatest cause of premature death and health inequalities. The five priority areas are: Tackling health inequalities and helping tobacco users to quit; Helping young people to be tobacco free; Establishing ‘smokefree’ as the norm; Tackling illicit tobacco; Raising the profile of tobacco control. Alcohol Brief Advice Don’t Bottle It Up is an interactive web-based screening tool that allows people to work out the level of risk they are at as a result of their drinking and access personalised advice anonymously online. The website uses the World Health Organisation’s validated Alcohol Use Disorders Identification Tool (AUDIT) to deliver Identification and Brief Advice within the community. Alcohol Scratch Cards are distributed in a wide range of community settings (ie GP surgeries, leisure centres, community events). The scratch cards allow people to work out if they are at risk of alcohol-related health harm and if so, direct people to Surrey Drug and Alcohol Care telephone helpline and Don’t Bottle It Up for further assessment and advice. Hospital Alcohol Liaison Services Alcohol Liaison Nurse (ALN) Services are based in Surrey’s hospitals and deliver alcohol screening to patients and provide brief advice and extended interventions to those drinking at risky levels. They may also support administration of appropriate and safe alcohol detoxification, liaison with community drug and alcohol services and alcohol training/support to the wider hospital workforce. Community Weight Management Services Currently there are no commissioned community weight management services for adults, although a number of commercial options are available for a charge. The NHS Weight Loss Plan, a 12 week adult weight management programme, is available on the NHS Choices website which can be accessed free of charge. Public Health provide healthy eating and weight management information on the Healthy Surrey website. North West Surrey Clinical Commissioning Group (NWSCCG) are lead commissioners for an Adult Tier 3 Weight Management Programme however this is currently under review. Bariatric Surgery Bariatric surgery is available through NHS Specialised commissioning, however before that can be agreed, patients have to meet the strict criteria. Eat Out, Eat Well Surrey leads on the Eat Out Eat Well Award, recently refreshed in partnership with Public Health England and available across Surrey. Many public and commercial organisations have achieved this “healthy catering award”, further development and roll out is planned. Get Active 50+ programme This programme was launched in January 2016 to provide a range of very low cost physical activity opportunities for the 50+ population across Surrey. Activities include swimming, golf, jogging, badminton, bowls, dance & exercise, inclusive multi-sports and walking football. Health professionals and frontline staff are encouraged to signpost people over 50 to this programme, in particular those who are not meeting the CMO guidelines of 150+ minutes per week. For more information visit the Get Active 50+ webpage Exercise on Referral Patients who are insufficiently active and have a health condition (or other factors that put them at increased risk of ill health) can be referred by their GP to an exercise referral programme (which operate in every Surrey borough except for Epsom & Ewell). Many of these also provide specialised classes in Cardiac Rehab, Stroke, COPD, Diabetes Mellitus and Weight Management. Further information is available by contacting the relevant exercise referral coordinator in each borough. Low impact physical activity across Surrey For people who are insufficiently active but do not have a health condition, GPs/allied health professionals and other frontline staff in community/acute settings can signpost to the wide range of low impact activities on offer in each district or borough. Falls Prevention classes Falls prevention classes, focusing on muscle strengthening and balance exercises, are offered in some of the boroughs in Surrey, i.e. Waverley, Reigate & Banstead (via the YMCA), Elmbridge and Woking. Other boroughs may also offer classes aimed at older people which incorporate muscle strengthening and balance exercises (but which are not specific Falls Prevention classes). Healthy Walks There are ‘Walking for Health’ groups in each borough in Surrey, to suit different levels of ability. There are also self-guided walks with maps and directions, as well as iFootpath which enables people to download a walking guide or GPS route for free. For further information on walks in Surrey (including Surrey Ramblers), visit Healthy Surrey https://www.healthysurrey.org.uk/community-health/social-prescribing/green-social-prescribing/local-green-activities or Explore Surrey’s countryside: https://www.surreycc.gov.uk/culture-and-leisure/countryside/what-can-you-do/walking/health-groups Active Travel initiatives The Travel SMART website contains useful information on how to travel sustainably in Surrey, with the aim of reducing one’s carbon footprint. This also has the benefit of increasing physical activity levels. Information includes details of public transport, park & ride schemes, cycle routes, cycle hire schemes, taking bikes on trains, electric bikes and cycle training. Health Checks The NHS Health Check (HC) programme is a national cardiovascular disease (CVD) risk assessment programme. The responsibility for this programme transferred from the NHS to local authorities in March 2013. The HC provides a personal review of the behavioural factors – such as smoking, inactivity, harmful drinking and obesity – that increase the risk of developing a heart attack or stroke, and offers professional advice and referral to lifestyle services to support behaviour change. It also helps to detect undiagnosed serious conditions such as hypertension, diabetes and chronic kidney disease. The programme in Surrey is provided by many GPs and Pharmacy teams and some community based organisations (see Healthy Surrey website). Participating GPs practices will be prioritising eligible patients who have higher risk factors for CVD to improve health outcomes for Surrey residents. Data Surrey records the numbers of Health Checks offered and numbers received. Unmet needs and service gaps Multiple lifestyle risk factors: - Integrated health and wellbeing services. There is no single point of contact for services, inconsistent assessment of risks factors and referral to health and wellbeing services by all frontline staff Smoking: - Implementing a robust electronic referral system for stop smoking referrals in primary and secondary care and organisations having contact with smokers - Mandatory recording of smoking status in primary and secondary care - Developing and implementing mandatory Very Brief Advice (VBA) training for all frontline staff - Developing and implementing mandatory Carbon Monoxide (CO) screening for all pregnant women at booking and ‘opt-out’ referrals in all maternity departments - Implementing in-house stop smoking support in all hospital trusts and provision of stop smoking medications for inpatients Alcohol: - Inconsistent approach to alcohol Identification and Brief Advice in primary care and the community - Provision of Alcohol Liaison Nurse Services in Surrey hospitals in line with best practice - Routine and systematic Public Health input into alcohol licensing and local Statement of Licensing Policies, - Partnership working to maximise collection, sharing and use of alcohol-related health data in order to reduce alcohol-related harm. Physical Activity: - Implementing consistent referral to exercise classes by GPs and other health professionals - Promotion of low impact physical activity within primary & secondary care - Focus on getting inactive people doing 30 mins or more per week - Focus on populations most in need (older people, women, disabled, BME populations) - Provision of falls prevention classes across Surrey Diet: - Increase Surrey population achieving the recommended ‘5 a day’ fruit and vegetables in their diet - Lack of leadership and countywide coordination for nutrition and healthy weight behaviour change initiatives - Implement initiatives to focus on nutrition as well as physical activity - Delivery of a Healthy Weight Strategy for Children, Young People and Families is in development, however this does not include adults outside the family context What works Integrated health and wellbeing services Historically many public health initiatives have been provided on a programme basis. There has been an increase in the emergence of integrating public health services such as weight management, stop smoking and NHS Health Checks into one individually commissioned programme with a single point of access. NHS Confederation and the Faculty of Public Health (2011) argued that ‘Wellness’ services provide support to people to lead healthier lives. The Wellness approach goes beyond looking at a single issue, healthy lifestyle services and a focus on illness, and instead aims to take a whole-person and community approach to improving health (28). However, the Kings Fund argue that due to shortages of academic research evidence on the usefulness and cost-effectiveness of different approaches, commissioners will need to innovate and take risks (2). If integrating health behaviour services, commissioners need to consider the available resources, intervention intensity and delivery, and the target population. All of these factors impact on the effectiveness, and likely cost-effectiveness, of multiple risk behaviour interventions (3). Consideration needs to be given to the impact that integrated wellbeing has on an individual’s health and wellbeing. The Wellness Services Evidence Based Review (29) identifies a number of benefits to people accessing integrated wellbeing services. For example promoting positive health that can empower individuals, enabling them to maintain and improve their own health, and a focus on promoting quality of life not just length of life. Wellness services should take into consideration inequalities in health and where possible actively seek out those individuals that do not usually benefit from mainstream health services (18). The National Centre for Smoking Cessation and Training (NCSCT) undertook a review of the evidence on integrated health behaviour lifestyle services. Based on four risk behaviours studied (tobacco smoking, hazardous alcohol use, poor diet and physical inactivity), the report concluded that only specific risk behaviours cluster together (3). A moderate number of risk behaviours (two to three) targeted together result in the biggest improvements in outcome and that the effectiveness and cost-effectiveness of multiple risk behaviour interventions depend on the behaviour targeted (3). While there is some evidence to support multiple risk behaviour interventions that target poor diet and physical inactivity, there is little evidence that targeting tobacco use in this manner is either effective or more cost-effective than single risk behaviour interventions (3). There are examples across the country of local authorities with integrated models that have begun to evaluate services and outcomes. These outcomes will help provide further evidence and guidance on developing integrated models. Smoking The Department of Health recommends the use of the six internationally recognised strands of tobacco control to combat local tobacco use. Stopping the Promotion of Tobacco Since April 2013 all shops have been required to remove tobacco products from display. By May 2017, all cigarettes and hand rolling tobacco sold in the UK will be in standardised packaging. Making Tobacco Less Affordable The health gain from high-priced tobacco, can be undermined if smokers have access to cheaper, illicit products which are sold illegally. HM Revenue & Customs (mid-range) estimates for 2013/14 were that 10% of cigarettes consumed in the UK were illicit, and the proportion of hand rolled tobacco that was illicit was 39% (30). Effective Regulation of Tobacco Products There has been an introduction of numerous government policies surrounding smokefree public places, workplaces and vehicles, the display of tobacco products and cigarette packaging, the regulation of e-cigarettes and proxy purchasing of tobacco products. It would be expected that these measures will help facilitate a reduction in smoking and smoke related harm. Helping Tobacco Users to Quit Stop Smoking Service Smokers are four times more likely to be successful at quitting if they receive behavioural support than if they quit on their own. Research shows that over-targeting priority smoking groups is the best way to tackle smoking prevalence amongst these demographics. • NICE Guidance (PH10) Stop smoking services • NICE Guidance (PH5) Smoking: workplace interventions • NICE Guidance (PH48) Smoking: acute, maternity and mental health services Provision of Very Brief Advice by Health Care Professionals - NICE Guidance (PH1) Smoking: brief interventions and referrals Mandatory Carbon Monoxide (CO) screening for all pregnant women. - NICE Guidance (PH26) Smoking: stopping in pregnancy and after childbirth Young people - NICE Guidance (PH14) Smoking: preventing uptake in children and young people Harm reduction Although the best way to avoid harm from smoking is to quit entirely, there are other ways of reducing the harm from smoking, even though this may involve continued use of nicotine. - NICE Guidance (PH45) Smoking: harm reduction Electronic cigarettes The large majority of the more than one million users of electronic cigarettes in the UK are current or former smokers. Most users use them to either replace cigarettes in places where smoking is prohibited or discouraged, to cut down on smoking, to reduce harm from smoking, or to quit smoking. Evidence indicates that e-cigarettes can help people quit smoking, with similar or better results than nicotine replacement therapies (31). For more information, see the following guidance: - Public Health England (PHE) E-cigarettes: an evidence update (2015) - Royal College of Physicians – Nicotine without smoke: Tobacco harm reduction (2016) - National Centre for Smoking Cessation and Training (NCSCT) Electronic cigarettes: A briefing for stop smoking services Partnership working Partnership working across organisations and health care professionals has proved to be key in recruiting and retaining smokers to the stop smoking services. Tobacco Control Alliances have been proven effective in countering illicit tobacco activity in local areas. Reducing Exposure to Secondhand Smoke Smokefree laws are proving to be effective and popular. In 2016, Surrey County Council worked in partnership with borough and districts to launch a voluntary smoking ban in children’s play areas. Many Surrey County Council partners are working on smokefree policies by removing designated smoking areas and making their grounds smokefree. Surrey County Council will also be exploring an update to their policy. Effective Communication for Tobacco Control Incorporating communication strategies into the local tobacco control plans can increase the effectiveness of national and local smokefree campaigns. Local stop smoking services should align their campaigns with national materials and campaigns. Excessive Alcohol intake Identification & Brief Advice - Improved early identification and intervention in primary care has been shown to avert both alcohol-related admissions and A&E attendances (32). - Identification, Brief Advice and Extended Brief Interventions (EBIs) have a high degree of efficacy and cost-effectiveness and should be delivered by health and social care professionals in primary care, secondary care and in the community (33, 34, 35, 36). - 1 in 8 people drinking above recommended levels who receive simple alcohol advice will reduce their drinking to within lower risk levels (37). Higher risk and increasing risk drinkers who receive IBA are twice as likely to moderate their drinking 6 to 12 months after an intervention when compared to drinkers receiving no intervention (38). Alcohol Licensing There is strong evidence that local licensing policies are associated with a reduction in alcohol-related hospital admissions in areas with more intense licensing policies (39). As a Responsible Authority, Public Health should: - Work with police, community safety colleagues and other responsible authorities to set up a system of sharing relevant information and data - Facilitate access to health information such as anonymised A&E data, linked to alcohol-related incidents - Contribute relevant public health data and concerns to the development of the Statement of Licensing Policies - Map the proximity of the premises to local family centres, schools, play groups, community youth centres and other venues where children are present - Resources should be made available to prevent under-age sales, sales to people who are intoxicated, proxy sales (that is the illegal purchase of alcohol for someone who is under-age or intoxicated), and non-compliance with any other alcohol licence condition/ illegal imports of alcohol - National Institute for Health and Care Excellence (2010) Alcohol use disorders: preventing harmful drinking. NICE public health guidance 24. - National Institute for Health and Care Excellence (2011) Alcohol-use disorders: diagnosis, assessment and management of harmful drinking and alcohol dependence. NICE clinical guidance CG115. - National Institute for Health and Care Excellence (2015) Alcohol: preventing harmful use in the community. NICE quality standard 83. - National Institute for Health and Care Excellence (2014) Behaviour change: individual approaches. NICE public health guidance 49. Insufficiently Active NICE guidance: - Physical activity in the workplace (PH13) (40) Physical activity programmes at work have been found to reduce absenteeism by up to 20% with physically active workers taking 27% fewer sick days (41). It is recommended that employers encourage and support employees to be more physically active. - Physical activity and the environment (PH8) (42)Planning applications for new developments should always prioritise the need for people to be physically active. When developing or maintaining streets and roads, pedestrians/cyclists and users of other modes of transport involving physical activity should be given the highest priority. - Physical activity: brief advice for adults in primary care (PH44) (43) Brief interventions in primary care are a cost effective way to increase physical activity levels in adults. - Physical activity: exercise referral schemes(PH54) (44) Exercise Referral schemes are recommended for people who are sedentary or inactive and have an existing health condition, or other factors that put them at increased risk of ill health (e.g. being overweight/obese). These schemes are not recommended for people who are sedentary or inactive, but otherwise healthy (for whom brief advice and signposting to local activities would be recommended). - Physical activity: walking and cycling (PH41) (45) As well as increasing physical activity levels, walking and cycling can help reduce car travel leading to reductions in air pollution; reduce road danger; increase the number of people on the streets making public spaces seem more welcoming; and provide an opportunity for people to participate in the outdoor environment. These benefits may be particularly significant for people with disabilities whose participation in other activities may be more restricted. - Preventing excess weight gain (NG7) (46) Recommendations to help maintain a healthy weight and prevent excess weight gain include encouraging people to be more active and reduce sedentary behaviour; encouraging people to build activity into daily life; developing routines and habits that gradually increase the amount and intensity of activity they do. - Falls in older people: assessing risk and prevention (CG161) (47) Multifactorial interventions which include muscle strengthening and balance training should be offered to older people (65+) assessed as being at risk of falling or having had recurrent falls and/or balance/gait deficit. - A lack of regular physical activity along with a sedentary lifestyle increases the risk of dementia. For older adults, there is evidence that physical activity can have beneficial effects on maintaining or improving cognitive function (48). - Being close and having access to green spaces in residential areas is positively associated with increased overall levels of physical activity across age groups. Amongst older people five year survival rates are positively associated with proximity of access to space for walking, nearby parks and tree-lined streets, independent of socioeconomic status (49). - In the UK a correlation has been observed between those living closest to greener areas and reduced levels of mortality, obesity and obesity-related illnesses. This has been linked to higher levels of exercise, but causality has not been demonstrated (50). Poor Diet Excess weight may increase the risk of many co-morbidities including type 2 diabetes and coronary heart disease. NICE Guidance recommends interventions in which weight is not the primary outcome, such as those aimed at preventing cardiovascular disease or type 2 diabetes, improving mental wellbeing or increasing active travel (51). The Foresight Obesity Systems Atlas (52) highlights the need for a whole system approach, where health is taken into account in every policy and decision across local government and private sector with the aim of making the healthy choice, the easy choice. National Institute of Healthcare Excellence (NICE) has a number of guidance documents which provide recommendations to tackle healthy weight, in which they recommend prevention and self-care with additional support for those most at risk, and that activities are integrated into current services taking a local strategic approach to healthy eating and healthy weight. The government launched a “healthy lifestyle” campaign Change4Life (C4L) in 2009. Its aim is to inspire a broad coalition of people, including the NHS, local authorities, businesses, charities, schools, families, community leaders to all play a part in improving the nation’s health and well-being by encouraging everyone to eat well, move more and live longer. A sister brand, Start4Life, introduces healthy habits right from birth and the Public Health England campaign, “One You” is aimed at adults. Recommendations for Commissioning \|Recommendations for:\| \|Smoking\|\|Excessive Alcohol intake\|\|Insufficiently Active\|\|Poor Diet\|\|Integrated H&WB services\| \|Surrey County Council\|\| \|\| \|\| \|\| \|\| \| \|Clinical Commissioning Group (CCG)\|\| \|\| \|\| \|\| \| \|Providers \| Including NHS, community and voluntary sector \| \|\| \|\| \|\| \|\| \| \|Social Care\|\| \|\| \|\| \|\| \|\| \| Key contacts \|Smoking\|\|Rachael Davis \| Public Health Lead [email protected] 07989 663114 \|Alcohol\|\|Gail Hughes \| Public Health Lead [email protected] 07881 328236 \|Diet\|\|Jennifer Smith \| Senior Public Health Lead [email protected] 07813 538430 \|Physical Activity\|\|Jane Semo \| Public Health Development Worker [email protected] 07794 168300 Chapter References (1) World Health Organisation (2002). Reducing Risks, Promoting Healthy Life. Available at: www.who.int/whr/2002/en/ [Accessed 17 October 2016] (2) Buck, D. & Frosini, F The Kings Fund (2012). Clustering of unhealthy behaviours over time. Available at: http://www.kingsfund.org.uk/sites/files/kf/field/field_publication_file/clustering-of-unhealthy-behaviours-over-time-aug-2012.pdf [Accessed 17 October 2016] (3) NCSCT (2016). Integrated health behaviour (lifestyle) services: a review of the evidence, Available at: http://www.ncsct.co.uk/usr/pub/Integrated%20health%20behaviour%20services%20review.pdf [Accessed 17 October 2016] (4) Emerson, E. & Baines, S. (2010). Improving Health and Lives: Learning Disabilities Observatory. Health Inequalities & people with learning disability in the UK: 2010. Available at: https://www.improvinghealthandlives.org.uk/uploads/doc/vid_7479_IHaL2010-3HealthInequality2010.pdf [Accessed 17 October 2016] (5) The Marmot Review (2010). Fair Society, Healthy Lives. Available at: https://www.parliament.uk/globalassets/documents/fair-society-healthy-lives-full-report.pdf [Accessed 17 October 2016] (6) Public Health England. (2016) Tobacco Control Profiles. Available at: www.tobaccoprofiles.info/ [Accessed 17 October 2016] (7) ASH (2016). Estimates of poverty in England adjusted for expenditure on tobacco. Available at: SUPERSEDED BY: https://ash.org.uk/uploads/Smoking-and-poverty-July-2021.pdf [Accessed 17 October 2016] (8) Department of Health. (2014) Equality analysis: Smoking in private vehicles carrying children. Available at: https://www.gov.uk/government/uploads/system/uploads/attachment_data/file/384320/EqA_-_smoking_in_cars.pdf [Accessed 17 October 2016] (9) Public Health England. (2015) Reducing Smoking in Prisons. Available at: https://assets.publishing.service.gov.uk/government/uploads/system/uploads/attachment_data/file/412567/Reducing_smoking_in_prisons.pdf [Accessed 17 October 2016] (10) ASH (2015) Smoking in Prisons. Available at: https://ash.org.uk/uploads/ASH-smokefree-prisons-briefing-26-November-2018.pdf?v=1648144096 [Accessed 17 October 2016] (11) ASH (2016) Ready Reckoner. Available at: https://ash.org.uk/resources/view/ash-ready-reckoner (12) ASH (2015) Secondhand Smoke. Available at: https://ash.org.uk/law/secondhand-smoke (13) ASH (2015) Smoking & Respiratory disease https://ash.org.uk/resources/view/smoking-and-respiratory-disease (14) Surrey Health Related Behaviour survey 2015 (15) Department of Health (2004) Alcohol Needs Assessment Research Project (ANARP). London (16) World Health Organisation (2016) Physical Activity. Available at: http://www.who.int/topics/physical_activity/en/ (17) Murray et al. (2013) UK health performance: findings of the Global Burden of Disease Study 2010. The Lancet 381: 997-1020. (18) Lee I-M et al. (2012) Effect of physical inactivity on major non-communicable diseases worldwide: an analysis of burden of disease and life expectancy. The Lancet 380: 219–229. (19) UK Chief Medical Officers’ Guidelines (2011) Start active, stay active: report on physical activity in the UK. Available at: https://www.gov.uk/government/publications/start-active-stay-active-a-report-on-physical-activity-from-the-four-home-countries-chief-medical-officers (20) Department of Health (2011) Start active, stay active. [Adapted from US Department of Health and Human Services (2008) Physical activity guidelines advisory committee report. Washington DC: US Department of Health and Human Services]. (21) National Institute for Health and Care Excellence (2013) Physical activity: brief advice for adults in primary care (PH44). Available at: https://www.nice.org.uk/guidance/ph44. (22) Public Health England (2013) Health impact of physical inactivity – estimated preventable deaths in persons aged 40-79, all causes. Time period(s): 2009/10. Available at: http://www.apho.org.uk/resource/view.aspx?RID=123459 (23) Local Sport Profile (2013) Health costs of physical inactivity, split by disease type. Time period(s): 2009/10. Latest reports available at: https://www.sportengland.org/research-and-data/tools/local-area-insights/area-reports#/view-report/96d3b1753495466aa107a68c20b80c03/E10000030 (24) Sport England (2013) Active People Interactive. Available at: http://activepeople.sportengland.org/ (25) Buckley JP et al (2015) The sedentary office: a growing case for change towards better health and productivity. British Journal of Sports Medicine 0:1–6. (26) Public Health England (2014/15) Physical Activity. Available at: http://fingertips.phe.org.uk/profile/physical-activity (27) https://files.digital.nhs.uk/publicationimport/pub16xxx/pub16076/hse2013-ch7-fru-veg-com.pdf (28) NHS Confederation (2011). Briefing: From illness to wellness. Achieving efficiencies and improving outcomes. October 2011; issue 224. Available at: www.nhs-chaplaincy-spiritualcare.org.uk/nationalhealthservice/illness_to_wellness_241011.pdf (29) Winters, Armitage, Stansfield, Scott-Samuel and Farrar (2010). Wellness Services – Evidence based review and examples of good practice. November 2010. Observatory Report Series No. 76. (30) ASH (2015) Illicit Trade in Tobacco. Available at: https://ash.org.uk/resources/view/illicit-trade-in-tobacco (31) PHE (2015) E-cigarettes: An evidence review www.gov.uk/government/publications/e-cigarettes-an-evidence-update (32) Godfrey C, Morton V, Coulton S, Parrott S, (2005) Effectiveness of treatment for alcohol problems: findings of the randomised UK alcohol treatment trial (UKATT). British Medical Journal; 331(7516): 541-544 (33) National Institute for Health and Care Excellence (2010) Alcohol use disorders: preventing harmful drinking. NICE public health guidance 24. (34) National Institute for Health and Care Excellence (2011) Alcohol-use disorders: diagnosis, assessment and management of harmful drinking and alcohol dependence. NICE clinical guidance 115. (35) National Institute for Health and Care Excellence (2015) Alcohol: preventing harmful use in the community. NICE quality standard 83. (36) National Institute for Health and Care Excellence (2014) Behaviour change: individual approaches. NICE public health guidance 49. (37) Moyer, A., Finney, J., Swearingen, C. and Vergun, P. (2002) Brief Interventions for alcohol problems: a meta-analytic review of controlled investigations in treatment -seeking and non-treatment seeking populations, Addiction, 97, 279-292. (38) Wilk, A.I., Jensen, N.M. and Havighurst, T.C. (1997) Meta-analysis of randomized control trials addressing brief interventions in heavy alcohol drinkers, Journal of General Internal Medicine, 12, 274-283. (39) Hickman M. et al (2015) Measurable effects of local alcohol licensing policies on population health in England. Journal of Epidemiology and Community Health. doi:10.1136/jech-2015-206040 (40) National Institute for Health and Care Excellence (2008) Physical activity in the workplace (PH13). Available at: https://www.nice.org.uk/guidance/ph13 (41) Health, Work and Wellbeing Programme (2008) Working for a healthier tomorrow. London: The Stationery Office.	https://www.surreyi.gov.uk/jsna/improving-health-behaviours/
Chronic diseases - such as heart disease, stroke, cancer, diabetes, and arthritis - are among the most common, costly, and preventable of all health problems in the U.S. Chronic Diseases are the Leading Causes of Death and Disability in the U.S. - 7 out of 10 deaths among Americans each year are from chronic diseases. Heart disease, cancer and stroke account for more than 50% of all deaths each year. - In 2005, 133 million Americans - almost 1 out of every 2 adults - had at least one chronic illness. - Obesity has become a major health concern. 1 in every 3 adults is obese3 and almost 1 in 5 youth between the ages of 6 and 19 is obese. - About one-fourth of people with chronic conditions have one or more daily activity limitations. - Arthritis is the most common cause of disability, with nearly 19 million Americans reporting activity limitations. - Diabetes continues to be the leading cause of kidney failure, nontraumatic lower-extremity amputations, and blindness among adults, aged 20-74. - Excessive alcohol consumption is the third leading preventable cause of death in the U.S., behind diet and physical activity and tobacco. Four Common Causes of Chronic Disease Four modifiable health risk behaviorslack of physical activity, poor nutrition, tobacco use, and excessive alcohol consumptionare responsible for much of the illness, suffering, and early death related to chronic diseases. - More than one-third of all adults do not meet recommendations for aerobic physical activity based on the 2008 Physical Activity Guidelines for Americans, and 23% report no leisure-time physical activity at all in the preceding month. - In 2007, less than 22% of high school students10 and only 24% of adults11 reported eating 5 or more servings of fruits and vegetables per day. - More than 43 million American adults (approximately 1 in 5) smoke. - In 2007, 20% of high school students in the United States were current cigarette smokers. - Lung cancer is the leading cause of cancer death, and cigarette smoking causes almost all cases. Compared to nonsmokers, men who smoke are about 23 times more likely to develop lung cancer and women who smoke are about 13 times more likely. Smoking causes about 90% of lung cancer deaths in men and almost 80% in women. Smoking also causes cancer of the voicebox (larynx), mouth and throat, esophagus, bladder, kidney, pancreas, cervix, and stomach, and causes acute myeloid leukemia. - Excessive alcohol consumption contributes to over 54 different diseases and injuries, including cancer of the mouth, throat, esophagus, liver, colon, and breast, liver diseases, and other cardiovascular, neurological, psychiatric, and gastrointestinal health problems. - Binge drinking, the most dangerous pattern of drinking (defined as consuming more than 4 drinks on an occasion for women or 5 drinks for men) is reported by 17% of U.S. adults, averaging 8 drinks per binge.	https://www.rxresource.org/news/chronic-diseases-and-health-promotion.html
Theoclear-80 (theophylline) and Alcohol/Food Interactions There are 3 alcohol/food/lifestyle interactions with Theoclear-80 (theophylline) which include: theophylline Caffeine Moderate Drug Interaction Ask your doctor before using theophylline together with caffeine. Using these medications together may increase some of the side effects of theophylline. This can cause nausea, vomiting, insomnia, tremors, restlessness, uneven heartbeats, and seizure (convulsions). Avoid drinks or foods that contain caffeine, such as coffee, tea, cola, and chocolate. You may need a dose adjustment or special test if you use both medications. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor. theophylline food Moderate Food Interaction Both smoking and excessive caffeine consumption can alter the blood levels of theophylline, which may affect the dosing. Tobacco and marijuana smoke (including secondhand exposure) generally reduces, while caffeine increases, blood levels. In addition, caffeine is a stimulant and may add to the side effects of theophylline such as headache, insomnia, and increases in blood pressure and heart rate. It is best to avoid smoking and to limit caffeine consumption during theophylline therapy. Talk to a healthcare professional if you have any questions or concerns. If you start smoking or undergo smoking cessation, your doctor may need to monitor your blood levels more closely to determine if you need a dose adjustment of theophylline. You should stop taking theophylline and seek medical attention if you experience potential signs and symptoms of excessive drug levels such as nausea, vomiting, persistent headache, insomnia, and rapid heartbeat. It is important to tell your doctor about all other medications you use, including vitamins and herbs. Do not stop using any medications without first talking to your doctor. When theophylline is given with enteral (tube) feedings, blood levels may be decreased due to interference with its absorption. This may reduce the effectiveness of the medication. To minimize potential for interaction, you may interrupt the feeding for one hour before and one hour after the theophylline dose. You may need more frequent blood tests to monitor theophylline levels. High Blood Pressure (Hypertension) Moderate Potential Hazard, Moderate plausibility methylxanthines - tachyarrhythmias The use of theophyllines is associated with an increase in heart rate which may progress to supraventricular tachycardia or ventricular arrhythmia at high serum drug concentrations. Appearance of cardiac adverse effects is generally an indication of theophylline toxicity, although patients with a history of tachyarrhythmias may be more susceptible to the chronotropic effect of these drugs. Therapy with theophyllines should be administered cautiously in such patients. Caution is also advised in patients with hypertension, hyperthyroidism, angina pectoris, or recent myocardial infarction, since high dosages of the drugs are associated with positive inotropic as well as chronotropic effects. Clinical monitoring of serum drug concentrations is recommended to prevent toxicity. References - Levine JH, Michael JR, Guarnieri T "Multifocal atrial tachycardia: a toxic effect of theophylline." Lancet 1 (1985): 12-4 - Sessler CN "Theophylline toxicity: clinical features of 116 consecutive cases." Am J Med 88 (1990): 567-76 - Bittar G, Friedman HS "The arrhythmogenicity of theophylline: a multivariate analysis of clinical determinants." Chest 99 (1991): 1415-20 - Albert S "Aminophylline toxicity." Pediatr Clin North Am 34 (1987): 61-73 - Schiff GD, Hegde HK, LaCloche L, Hryhorczuk DO "Inpatient theophylline toxicity: preventable factors." Ann Intern Med 114 (1991): 748-53 - Patel AK, Skatrud JB, Thomsen JH "Cardiac arrhythmias due to oral aminophylline in patients with chronic obstructive pulmonary disease." Chest 80 (1981): 661-5 - Chazan R, Karwat K, Tyminska K, Tadeusiak W, Droszcz W "Cardiac arrhythmias as a result of intravenous infusions of theophylline in patients with airway obstruction." Int J Clin Pharmacol Ther 33 (1995): 170-5 - Taniguchi A, Ohe T, Shimorura K "Theophylline-induced ventricular tachycardia in a patient with chronic lung disease: sensitivity to verapamil." Chest 96 (1989): 958-9 - Hendeles L, Weinberger M, Johnson G "Monitoring serum theophylline levels." Clin Pharmacokinet 3 (1978): 294-312 - Marchlinski FE, Miller JM "Atrial arrhythmias exacerbated by theophylline: response to verapamil and evidence for triggered activity in man." Chest 88 (1985): 931-4 - Mccarthy M "Theophylline, beta-agonists, and cardiovascular death." Lancet 349 (1997): 33 - Milgrom H, Bender B "Current issues in the use of theophylline." Am Rev Respir Dis 147 (1993): s33-9 Theoclear-80 (theophylline) drug interactions There are 270 drug interactions with Theoclear-80 (theophylline) Theoclear-80 (theophylline) disease interactions There are 7 disease interactions with Theoclear-80 (theophylline) which include: More about Theoclear-80 (theophylline) - Side Effects - During Pregnancy or Breastfeeding - Dosage Information - Drug Interactions - Drug class: methylxanthines Related treatment guides Drug Interaction Classification \|Highly clinically significant. Avoid combinations; the risk of the interaction outweighs the benefit.\| \|Moderately clinically significant. Usually avoid combinations; use it only under special circumstances.\| \|Minimally clinically significant. Minimize risk; assess risk and consider an alternative drug, take steps to circumvent the interaction risk and/or institute a monitoring plan.\| \|No interaction information available.\| Further information Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.	https://www.drugs.com/food-interactions/theophylline,theoclear-80.html
Follow Us: By William B. Ershler, MD, INOVA Fairfax Hospital Cancer Center, Fairfax, VA; Director, Institute for Advanced Studies in Aging, Washington, DC. Dr. Ershler reports no financial relationships relevant to this field of study. Synopsis: There has been much written about the salutary effects of moderate alcohol consumption in reference to a number of non-malignant chronic diseases. The effects on cancer in general are less compelling. However, in the current meta-analysis examining alcohol consumption and the development of renal cell carcinoma, a protective effect for light and moderate drinkers is clearly demonstrated. This protective effect is in the 10-20% range. Source: Bellocco R, et al. Alcohol drinking and risk of renal cell carcinoma: Results of a meta-analysis. Ann Oncology 2012;23:2235-2244. There has been a gradual increase in renal cell carcinoma (RCC) in the United States and slightly improved survival, both of which may relate to earlier detection.1,2 There are well-established risk factors for RCC including tobacco smoking,3 obesity,4 and hypertension,5 but there remains some controversy over the role of moderate or excessive alcohol intake in this context. In fact, in a pooled analysis on alcohol intake and RCC based on 12 cohort studies, moderate consumption of alcohol was inversely related to the risk of RCC, and such protection did not seem to be modified by age, body mass index, hypertension, or smoking.6 That analysis, however, did not address the issue of high levels of alcohol intake. To address this, Bellocco and colleagues conducted a comprehensive meta-analysis of published studies on this topic. The investigators were able to find 20 observational studies (four cohort, one pooled, and 15 case-control) published up to November 2010 that reported results on at least three levels of alcohol consumption in the context of RCC incidence. Overall relative risks (RRs) and 95% confidence intervals (CIs) were estimated using random-effects models, and both second-order fractional polynomials and random effect meta-regression models were implemented for the study of dose-risk relation. They found the estimated RRs were 0.85 (95% CI, 0.80-0.92) for any alcohol drinking, 0.90 (95% CI, 0.83-0.97) for light drinking (0.01-12.49 g/day), 0.79 (95% CI, 0.71-0.88) for moderate drinking (12.5-49.9 g/day), and 0.89 (95% CI, 0.58-1.39) for heavy drinking (≥ 50 g/day), respectively. Thus, the current meta-analysis supports the hypothesis of a negative effect of moderate alcohol consumption on the risk of renal cell cancer. In this analysis, special efforts were undertaken to address the interactions of smoking and obesity, both of which are highly associated with excessive alcohol intake. Thus, the protective effect of alcohol on RCC development might be countered by associated factors. Furthermore, heavy drinkers are more likely to have a poor diet, and this too would favor RCC development.7 As such, this report provides epidemiological evidence that light or moderate alcohol consumption is associated with a reduced risk (10-20%) of RCC, and that such is observed independent of tobacco use, body mass index, or presence of hypertension. The mechanism whereby alcohol would confer such an effect is conjectural at this time but, at least for red wine, may relate to the beneficial metabolic effects conferred by resveratrol.8 However, there is now a growing literature supporting the positive effects of low or moderate alcohol intake on such diverse processes as diabetes,9 cardiac disease,10 and Alzheimer's,11 as well as normal aging and overall mortality.12,13 References 1. Jemal A, et al. Annual report to the nation on the status of cancer, 1975-2005, featuring trends in lung cancer, tobacco use, and tobacco control. J Natl Cancer Inst 2008;100:1672-1694. 2. Levi F, et al. The changing pattern of kidney cancer incidence and mortality in Europe. BJU Int 2008;101:949-958. 3. Gandini S, et al. Tobacco smoking and cancer: A meta-analysis. Int J Cancer 2008;122:155-164. 4. Bergstrom A, et al. Obesity and renal cell cancerA quantitative review. Br J Cancer 2001;85:984-990. 5. Grossman E, et al. Is there an association between hypertension and cancer mortality? Am J Med 2002;112:479-486. 6. Lee JE, et al. Alcohol intake and renal cell cancer in a pooled analysis of 12 prospective studies. J Natl Cancer Inst 2007;99:801-810. 7. Bravi F, et al. Food groups and renal cell carcinoma: A case-control study from Italy. Int J Cancer 2007;120:681-685. 8. Vidavalur R, et al. Significance of wine and resveratrol in cardiovascular disease: French paradox revisited. Exp Clin Cardiol 2006;11:217-225. 9. Joosten MM, et al. Changes in alcohol consumption and subsequent risk of type 2 diabetes in men. Diabetes 2011;60:74-79. 10. Lippi G, et al. Moderate red wine consumption and cardiovascular disease risk: Beyond the "French paradox." Semin Thromb Hemost 2010;36:59-70. 11. Garcia AM, et al. Isolated and joint effects of tobacco and alcohol consumption on risk of Alzheimer's disease. J Alzheimers Dis 2010;20:577-586. 12. Carlsson AC, et al. Health factors and longevity in men and women: A 26-year follow-up study. Eur J Epidemiol 2010;25:547-551. 13. Corley J, et al. Alcohol intake and cognitive abilities in old age: The Lothian Birth Cohort 1936 study. Neuropsychology 2011;25:166-175.	https://www.freecme.com/articles/5-moderate-alcohol-consumption-protective-effect-on-renal-cell-cancer-development
This report represents a work in progress. ACSH realizes that research in the areas of health impacts of alcoholic beverages and of tobacco products is continuing, and we will update this paper as new research and insights are received. We welcome input from readers. dose-related health benefits and risks. The risk/benefit profiles of alcoholic beverage and tobacco product use are significantly different. For example, alcoholic beverage consumption can have positive health effects at low to moderate doses, at least in specific populations. The pattern of consumption is apparently as important as the quantity consumed; binge drinking carries definite health risks. The misuse of alcoholic beverages, which is defined as the use of even small amounts of alcohol at inappropriate times, is associated with an increased risk of motor vehicle accidents. Furthermore, use of higher doses of alcohol (doses for which the term "abuse" is appropriate), is also associated with an increased risk of several diseases, violent behavior, suicide, and birth defects. Unlike with alcohol, no important overall health benefits have been established for tobacco product use at any dosage. Any possible health benefit related to smoking involves the alleviation or prevention of diseases that are uncommon or are rarely fatal. Moreover, there is overwhelming evidence that cigarette smoking greatly increases a number of health risks, including the risk of various cancers, chronic obstructive pulmonary disease (COPD), heart disease, and stroke. Certain health risks may also be increased even with light use of cigarettes. The use of cigarettes, pipes, and cigars, as well as smokeless tobacco, poses different health risks. Tobacco smoke puts others at risk through environmental exposure. Use of tobacco products, and the use, misuse, and abuse of alcoholic beverages pose higher risks to special populations, in particular the elderly, children, and adolescents. The use of these products can also pose risks to "passive" consumers, like developing fetuses, children, and other nonusers, through motor-vehicle and other injuries. The significant differences in individual and public health consequences of the use of alcoholic beverages versus those of the use of tobacco products underscore the opinion of the authors that public policy approaches to these substances should differ. By Cheryl K. Olson, M.P.H., Sc.D., Lawrence Kutner, Ph.D.	https://www.acsh.org/news/2000/06/01/a-comparison-of-the-health-effects-of-alcohol-consumption-and-tobacco-use-in-america
It is the swelling and inflammation of the larynx. It can be acute or chronic, although in most cases the condition is temporary and has no serious consequences. The larynx, also known as the voice box , is home to the vocal cords. These are vital for the processes of breathing, swallowing and talking. The vocal cords are two small folds of mucous membrane that cover cartilage and muscles that vibrate to produce sound. Laryngitis is usually not serious and in most cases resolves without treatment in about 7 days. Fast facts on laryngitis - Viral infections such as colds are the most common causes of laryngitis. - Chronic laryngitis is often caused by lifestyle factors, such as continued exposure to irritants. - Children with laryngitis can develop another respiratory disease called croup . - A doctor may recommend additional tests in more severe cases, such as a laryngoscopy. - Acute laryngitis is best treated with self-care and rest measures. - The vocal cords normally open and close to generate the voice with a slow and steady movement. - When a person has laryngitis, their vocal cords are swollen. This changes the way the air moves through the throat. - This change in airflow leads to a distortion of the sounds produced by the vocal cords. People with laryngitis often have a voice that is hoarse, gravelly, or too quiet to hear properly. - In chronic laryngitis, inflammation is ongoing. The vocal cords can become tight and develop growths, such as polyps or nodules. Symptoms Laryngitis can cause a wide range of symptoms in adults, including: - Ronquera. - Difficulty with speech - Throat pain. - Low fever - Persistent cough These symptoms start suddenly and often become more severe over the next 2 to 3 days. If symptoms last longer than 3 weeks, the case has likely become chronic. This suggests a more serious underlying cause that warrants further investigation. Laryngitis is often associated with other diseases. The tonsillitis , a sore throat , cold or flu can occur with a case of laryngitis, so the following symptoms may occur: - Headache. - Swelling in the glands - Runny nose. - Pain when swallowing - Fatigue and general malaise. Symptoms are likely to resolve without treatment before the seventh day of infection. Consult a physician if symptoms persist longer or are severe. Symptoms in children Symptoms of laryngitis in children may differ from symptoms in adults. The condition is often characterized by a hoarse cough, fever, and can also present as croup . Croup is a common contagious respiratory disease among children. Although croup is generally a simple disease to treat, severe cases require medical attention. Medical attention is recommended for children who experience any of the following symptoms: - Difficulty breathing or swallowing. - A fever over 103 ° Fahrenheit or 39.4 ° Celsius. - Babeo. - Loud, high-pitched sounds of breathing when inhaling. These symptoms can also indicate epiglottitis. This is the inflammation of the tissue that surrounds the windpipe. Both adults and children can develop epiglottitis, and the condition can be life-threatening in certain cases. Causes Several conditions can cause laryngitis. Acute and chronic forms of laryngitis are usually the result of different factors. acute laryngitis The most common cause of laryngitis is a viral infection, often similar to those caused by the common cold or flu. Overuse of the voice can also cause inflammation of the larynx. Examples of overuse include loud singing or excessive yelling. In very rare cases, acute laryngitis can be caused by diphtheria, a bacterial infection. Chronic laryngitis Chronic laryngitis is usually caused by the following: - Acid reflux, a condition in which acid from the stomach and contents back up into the throat. - Bacterial, fungal, or parasitic infection. - Chronic sinusitis. - Excessive cough - Exposure to inhaled irritants, such as allergens or toxic fumes. - High alcohol consumption - Habitual misuse or excessive use of the voice. - Smoking, including secondhand smoke. - Use of inhaled steroid medications, such as asthma inhalers . Tests and Diagnosis Doctors usually diagnose laryngitis with a physical exam that evaluates the ears, nose, throat, and voice. In most cases, no additional testing is required. Laryngitis is usually diagnosed after a physical exam. The most common symptom of the condition is hoarseness, so doctors will take care to listen to the voice of the person with laryngitis. They can also ask questions about lifestyle, possible exposure to airborne irritants, and other related illnesses. If a person has chronic hoarseness, a doctor may recommend additional tests to fully examine the vocal cords. Chronic hoarseness can be caused by other conditions, such as cancer in the throat area. This symptom will require follow-up exams to rule out a more serious illness. A laryngoscope can be used to observe the movement of the vocal cords when used and determine the presence of polyps or nodules on the vocal cords. A biopsy may be performed if a suspicious area of tissue requires further evaluation. Anyone with symptoms lasting more than 2 weeks should see their doctor. In some cases, a doctor may refer the person with laryngitis to an otolaryngologist, also known as an otolaryngologist (otolaryngologist). Treatment Often times, cases of acute laryngitis are best treated with rest, home remedies, and self-care measures that can relieve symptoms. Self-management Staying hydrated is important for laryngitis recovery. Doctors usually recommend rest to control the symptoms of laryngitis. For laryngitis, resting means limiting use of the larynx. Avoid talking, singing, or using the voice box. Although whispering may seem like a gentler alternative to speaking at a normal volume, it requires the vocal cords to be well stretched, making it difficult for them to recover. Whispering should also be avoided. Other simple home remedies include: - Avoid decongestants, as these dry out the throat. - Breathe moist air. - Use of paracetamol, acetaminophen, or ibuprofen to control pain. - Avoid inhaling irritants, such as smoking or secondhand smoke. - Drink a lot of liquids. Doctors may prescribe antibiotics in cases where the laryngitis has been caused by a bacterial infection. However, a recent review found that the risks of prescribing antibiotics for acute laryngitis generally outweigh the benefits. Corticosteroids may be prescribed to reduce inflammation of the vocal cords in severe or urgent cases. This can apply to people who use their voices professionally, such as professional singers or people who speak in public. Babies with severe croup can also be treated with corticosteroids. Chronic laryngitis may require more extensive ongoing treatment. The cause of the inflammation will determine this. If the laryngitis is caused by another condition, such as acid reflux or sinusitis, treating the associated condition may also treat the symptoms of laryngitis. Treatment of laryngitis may require lifestyle changes. For example, if singing is considered to be the cause of laryngitis, the patient may need to modify his singing method. Speech training may be recommended in such cases. Avoiding alcohol, tobacco smoke, and irritants can also help. A person may need surgery in cases where the vocal cords have been severely damaged as a result of a growth of polyps or nodules. Prevention People can take a number of steps to limit vocal cord dryness and irritation. The following steps can help reduce the risk of laryngitis: - Avoid clearing your throat. - Take steps to prevent upper respiratory infections, such as practicing good hygiene and avoiding contact with people who have contagious infections. - Stop smoking and avoid secondhand smoke when possible. - Limit or eliminate alcohol and caffeine intake, as they can increase the risk of dehydration. - Laryngitis can be uncomfortable, but it is easy to manage and often short-lived.	https://scopeheal.com/laryngitis/
10 ways to prevent heart disease and be heart healthy Although complete prevention of heart disease isn't a guarantee, you can do certain things to lower the risk of developing it. It is even more important for those who have close family members with heart disease to take care of their own health. Heart disease is the leading cause of death for both men and women in the United States, with coronary heart disease being the most common. From 1999 to 2015, about 630,000 people died from heart disease every year, according to the Centers for Disease Control and Prevention. Several lifestyle changes and actions can decrease the risk factors associated with heart disease. If you need help making any of these changes, consult with a doctor to determine a plan that is best for your specific health and behavior requirements. 1. Diet The proper balance of nutrients is important to maintaining a healthy body, including the heart. Limit your intake of sugar, sodium and saturated fat. Eat plenty of fresh vegetables and fruit, whole-grain starches, low- or no-fat dairy products and fish. If you choose to eat meat, make sure it is lean and skinless. Avoid fried food. 2. Stress Stress can cause high blood pressure and may lead to a heart attack. Stress is unavoidable, but you can manage it a number of ways. Don't bring outside work problems home with you; instead, leave them at the door. Listen to music, read a book, exercise or meditate. Do not drink alcohol or engage in other unhealthy behaviors such as smoking to manage stress. 3. Exercise Exercise is helpful for relieve stress as well as improving blood circulation, strengthening the heart and assisting with weight loss. Each person's body is different, so consult your doctor to determine the best exercise plan. 4. Smoking Smoking – and breathing secondhand smoke – raises blood pressure and increases the risk of a heart attack and stroke. If you smoke, talk to a doctor about quitting; if someone you live with smokes, encourage that person to quit for everyone's health. 5. Annual physical The best way to determine your heart's health is to get an annual physical examination. Knowing what your heart is like year after year makes it easier to discover when something is wrong. This especially is important for those who have a family history of heart disease. 6. Weight Obesity usually goes hand in hand with high cholesterol, diabetes and high blood pressure – all of which factor into heart disease. Maintain a healthy weight. If you are overweight, talk to your doctor about a safe weight-loss plan that includes exercise and diet changes. 7. Sleep If you have difficulty getting the recommended seven to nine hours of sleep per night or sleep too much, contact your doctor. Too little sleep can have a negative impact on blood pressure and increases the risk of diabetes. Sleep apnea also interferes with a good night's sleep. 8. Alcohol Excessive alcohol can raise blood pressure. Drinking too much also can cause weight gain because of the sugar in alcohol. Limit alcoholic beverages to one per day. 9. Blood pressure High blood pressure is a significant risk factor for heart disease. Some individuals naturally have high blood pressure, so medication may be necessary. For others, simple changes in diet (such as reducing sodium and fat) and exercise can help lower blood pressure. 10. Cholesterol Cholesterol can build up and block arteries. Medicine can lower cholesterol levels, but a healthy diet and exercise are vital to keeping high cholesterol at bay. Avoid fried food and food high in saturated fat.	https://opera.news/health/3c14b4d315d86aafd9d29d2c239f8675?news_entry_id=s7287f769200415en_ng

Subsets and Splits

No community queries yet

The top public SQL queries from the community will appear here once available.