Links for Keyword: Obesity

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By Mitch Leslie Scientists once had high hopes that inhibiting a hormone named ghrelin would be the key to preventing obesity. Ghrelin didn’t turn out to be a weight loss panacea. But now, the discovery of the first molecule naturally made by the body that blocks ghrelin’s effects may open up new avenues for treating other conditions, including diabetes and anorexia. The finding may also explain some of the benefits of bariatric surgery, which shrinks or reroutes the stomach to control weight. “It’s a very impressive piece of research,” says bariatric physician Carel le Roux of University College Dublin, who wasn’t connected to the study. “I think it will have significant clinical impact.” When researchers discovered ghrelin about 20 years ago, they dubbed it the “hunger hormone” because early results suggested it ramped up our appetite. But studies soon found that thwarting the molecule didn’t curtail food consumption or promote weight loss in mice. Still, the hormone induces a variety of other positive changes in our metabolism. For example, ghrelin may bolster muscle strength, spurring scientists to test whether drugs that mimic the hormone can counteract the muscle deterioration and weakness often suffered by cancer patients. The new study didn’t start as a hunt for ghrelin-blocking compounds. Instead, a team headed by researchers at NGM Biopharmaceuticals in South San Francisco, California, was investigating how bariatric surgery overhauls metabolism. The scientists operated on obese mice, performing a type of bariatric surgery called vertical sleeve gastrectomy that involves removing most of the stomach. They then examined which genes became more or less active after the procedure. As they report online today in Cell Metabolism, the rodents’ downsized stomachs produced 52 times more of a protein named LEAP2 than normal. © 2017 American Association for the Advancement of Science

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 24407 - Posted: 12.08.2017

Jessica Brown Sugar’s demise from childhood staple to public enemy can be seen everywhere. Chocolate bars are shrinking, sugary drinks are set to be taxed and our recommended daily sugar intake has been slashed in half. But the battle against sugar might have begun sooner if the industry hadn’t kept secrets to protect its commercial interests, according to new findings. In 1967, when scientists were arguing over the link between sugar consumption and increased risk of heart disease, researchers now claim that the International Sugar Research Foundation (ISRF) withheld findings that rats that were fed a high-sugar diet had higher levels of triglycerides (a fat found in the blood) than those fed starch. In a move researchers from the University of California at San Francisco have compared to the tobacco industry’s self-preservation tactics, the foundation stopped funding the project. Cristin Kearns, one of the researchers who analysed ISRF documents, says, “ISRF’s research was designed to cast doubt on the importance of elevated triglycerides in the blood as a heart disease risk factor. It is now commonly accepted that triglycerides are a risk factor, but this was controversial for decades. I think the scientific community would have come to consensus about elevated triglycerides being a risk factor for heart disease much sooner [if the research been published].” A year later the foundation funded Project 259, looking into the effects of sucrose consumption in the intestinal tracts of rats. It found a possible link between sugar consumption and increased risk of bladder cancer, and described the findings as “one of the first demonstrations of a biological difference between sucrose and starch fed rats”. But the ISRF terminated the project’s funding before the experiments were finished, despite the study having already lasted 27 months, and requiring only three more months. © 2017 Guardian News and Media Limited

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24365 - Posted: 11.27.2017

By Diana Kwon | Most of us are familiar with the role of smell in our dining habits—that basket of freshly baked cookies is usually much harder to resist than a plate of odorless carrot sticks, and the taste of food is strongly tied to its aroma. But animals’ sense of smell is even more intricately linked with eating and metabolism. Prior studies have shown that, in humans, fasting enhances olfactory sensitivity, while satiety reduces it. And a new study, published today (July 5) in Cell Metabolism, suggests that, at least in mice, this link may go even further—animals engineered to lack a sense of smell gained less weight and burned more fat than their unaltered counterparts. This difference in weight gain was almost entirely due to alterations in body fat composition. “The major thing was that [the mice lacking smell] weren’t gaining fat,” coauthor Andrew Dillin, a biology professor at the University of California, Berkeley, tells The Scientist. “Somehow, the olfactory system is engaging the major control circuit in the brain that controls peripheral metabolism . . . and that is turning on a program to burn fat.” Dillin says his team was interested in knowing whether simply eating fattening food led to weight gain, or if it was how the olfactory system “perceived” those calories that matters. To assess this link between olfaction and metabolism, scientists genetically engineered mice that expressed a gene for a diphtheria toxin receptor on olfactory sensory neurons. Once the animals were around seven weeks old, the researchers injected the toxin to kill off these nerve cells and found that these animals had lost their sense of smell. Control animals generated without this receptor retained all their smell neurons after receiving the toxin. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 24352 - Posted: 11.24.2017

By Abby Olena Two people with a rare genetic disorder have helped shed light on the fundamental neuroscience of appetite and, scientists say, opened up a new target for potential obesity treatments. Neonatal progeroid syndrome (NPS) affects only a handful of people worldwide. The most telling features of the condition are an aged appearance due to an absence of the fat layer under the skin and extreme thinness. Researchers report in in Nature Medicine today (November 6) that a glucose-releasing hormone involved in the disease crosses the blood-brain barrier and homes in on neurons that regulate appetite in mice. The study suggests it might be possible to target the hormone, asprosin, in the treatment of diabetes and obesity. “Rare diseases with extreme phenotypes like this are very valuable to learn important things that then apply to more common diseases,” says coauthor and medical geneticist Atul Chopra of Baylor College of Medicine in Houston, Texas. Chopra and colleagues showed in a previous study that patients with NPS have mutations near the end of a gene called FBN1, which encodes profibrillin. It was already known that profibrillin is processed to form fibrillin 1, an extracellular matrix protein. The 140-amino-acid chunk cleaved from the end of profibrillin, which Chopra’s group named asprosin, is secreted by adipose tissue and functions as a hormone that causes the liver to make glucose. They determined that two individuals with NPS are heterozygous for FBN1 mutations and have greatly reduced levels of circulating asprosin. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24351 - Posted: 11.24.2017

By Bob Grant In 1971, a 27-year-old, 456-pound man went to the University of Dundee’s department of medicine in Scotland looking for help. Patient A.B., as doctors referred to him, needed to lose weight. His physicians recommended a short but drastic course of action: stop eating altogether. The patient responded so well to a brief stint without food that he decided to prolong the deprivation—for more than a year. “[H]is fast was continued into what is presently the longest recorded fast (Guinness Book of Records, 1971),” the clinicians wrote in a 1973 case report, claiming A.B. suffered little or no untoward effects on his health.1 And at the end of his 382-day dietary abstinence, during which he had ingested only vitamin supplements, yeast, and noncaloric fluids, A.B. had lost a remarkable 276 pounds. When doctors checked back in on A.B. five years later, their patient reported gaining back only about 15 pounds. Although aspects of this published report seem almost unbelievable, and the period of fasting is obviously extreme, the case highlights some of the metabolic dynamics that result when bodies are deprived of food. For example, when external calories stop fueling an animal’s metabolism, stores of triglycerides in fat cells are mobilized, and levels of ketones—chemicals that result from the burning of fat for fuel—rise. Decreases in body weight follow. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24350 - Posted: 11.24.2017

By Stephani Sutherland When we experience something painful, our brain produces natural painkillers that are chemically similar to potent drugs such as morphine. Now research suggests these endogenous opioids also play another role: helping regulate the body's energy balance. Lauri Nummenmaa, a brain-imaging scientist at the University of Turku in Finland, and his colleagues measured endogenous opioid release in the brains of 10 healthy men. The subjects were injected with a radioactive substance that binds to opioid receptors, making it possible to visualize the receptors' activity using positron-emission tomography. The study found evidence of natural painkillers in the men's brains after they ate a palatable meal of pizza. Surprisingly, their brains released even more of the endogenous opioids after they ate a far less enticing—but nutritionally similar—liquid meal of what Nummenmaa called “nutritional goo.” Although the subjects rated the pizza as tastier than the goo, opioid release did not appear to relate to their enjoyment of the meal, the researchers reported earlier this year in the Journal of Neuroscience. Advertisement “I would've expected the opposite result,” says Paul Burghardt, an investigator at Wayne State University, who was not involved in the work. After all, previous human and animal studies led researchers to believe that endogenous opioids helped to convey the pleasure of eating. Nummenmaa, too, was surprised. His group's earlier research showed that obese people's brains had fewer opioid receptors—but that receptor levels recover with weight loss. “Maybe when people overeat, endogenous opioids released in the brain constantly bombard the receptors, so they [decrease in number],” he says. © 2017 Scientific American

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 24347 - Posted: 11.22.2017

By JANE E. BRODY I hope you’re not chomping on a bagel or, worse, a doughnut while you read about what is probably the most serious public health irony of the last half century in this country: As one major killer — smoking — declined, another rose precipitously to take its place: obesity. Many cancer deaths were averted after millions quit lighting up, but they are now rising because even greater numbers are unable to keep their waistlines in check. Today, obesity and smoking remain the two leading causes of preventable deaths in this country. Reviewing more than 1,000 studies, the International Agency for Research on Cancer and the Centers for Disease Control and Prevention linked the risk of developing 13 kinds of cancer to overweight and obesity, especially cancers that are now being diagnosed in increasing numbers among younger people. Included are cancers of the esophagus, liver, gallbladder, colon and rectum, upper stomach, pancreas, uterus, ovary, kidney and thyroid; breast cancer in postmenopausal women; meningioma and multiple myeloma. Only for colorectal cancers has the overall incidence declined, primarily the result of increased screening and removal of precancerous polyps. In most cases, the studies revealed, cancer risk rose in direct proportion to the degree of excess weight. In other words, the heavier you are, the more likely you will be to develop one of these often fatal cancers. From 2005 to 2014, the C.D.C. reported in October, there was a 1.4 percent annual increase in cancers related to overweight and obesity among people aged 20 to 49, and a 0.4 percent rise in these cancers among people 50 to 64. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24322 - Posted: 11.13.2017

By JANE E. BRODY Modern technology is making it possible for medical scientists to analyze inhabitants of our innards that most people probably would rather not know about. But the resulting information could one day save your health or even your life. I’m referring to the trillions of bacteria, viruses and fungi that inhabit virtually every body part, including those tissues once thought to be sterile. Together, they make up the human microbiome and represent what is perhaps the most promising yet challenging task of modern medicine: Determining the normal microscopic inhabitants of every organ and knowing how to restore the proper balance of organisms when it is disrupted. Proof of principle, as scientists call it, has already been established for a sometimes devastating intestinal infection by the bacterium Clostridium difficile. This infection, popularly called C. diff, often occurs when potent antibiotics wipe out the normal bacterial inhabitants of the gut that otherwise keep it in check. When all else fails to clear up a recurrent C. diff infection, the Food and Drug Administration has approved treatment with a fecal transplant from a healthy gut presumed to contain bacteria that can suppress C. diff activity. The treatment is highly effective, with a cure rate in excess of 90 percent. Under the auspices of the National Institutes of Health, a large team of scientists is now engaged in creating a “normal” microbiological road map for the following tissues: gastrointestinal tract, oral cavity, skin, airways, urogenital tract, blood and eye. The effort, called the Human Microbiome Project, takes advantage of new technology that can rapidly analyze large samples of genetic material, making it possible to identify the organisms present in these tissues. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24294 - Posted: 11.06.2017

By GINA KOLATA It is a question that plagues all who struggle with weight: Why do some of us manage to keep off lost pounds, while others regain them? Now, a study of 14 participants from the “Biggest Loser” television show provides an answer: physical activity — and much more of it than public health guidelines suggest. On average, those who managed to maintain a significant weight loss had 80 minutes a day of moderate activity, like walking, or 35 minutes a day of vigorous exercise, like running. The researchers conducting the new study did not distinguish between purposeful exercise, like going to the gym and working out, and exercise done over the course of the day, like walking to work or taking the stairs. Guidelines from the Centers for Disease Control and Prevention, by comparison, call for at least 150 minutes a week of moderate exercise, or 75 minutes a week of vigorous exercise for healthy adults. The study was published on Tuesday in the journal Obesity. The lead author, Kevin Hall, chief of the Integrative Physiology Section at the National Institute of Diabetes and Digestive and Kidney Diseases, and his colleagues also presented their work at the Obesity Society’s annual meeting. Although the study is very small and must be replicated, Dr. Hall said, it is the first to assess obese people years after they lost weight with state-of-the-art methods to measure the calories they had consumed and the amount of exercise they had done. The researchers did their measurements when the contestants were chosen, and again at six weeks, thirty weeks and six years after the contest began. “The findings here are important,” said Rena Wing, a psychiatry professor at Brown University and a founder of the National Weight Control Registry, which includes more than 10,000 people. The food eaten “is the key determinant of initial weight loss. And physical activity is the key to maintenance,” she said. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24267 - Posted: 10.31.2017

By RONI CARYN RABIN Can you be fit and healthy, even if you’re overweight? And will working out, despite the extra pounds, reduce your risk of a heart attack? The idea that you can be “fat but fit” has long been controversial. While health experts endorse physical activity as beneficial, many doctors view the concept of being “fat but fit” with suspicion. Now a new study, believed to be the largest of its kind, suggests that even when overweight or obese people are free of health complications, they are still more likely to develop heart disease than their peers who aren’t overweight. It didn’t matter whether obese people were free from diabetes, high blood pressure or high cholesterol, a condition sometimes referred to as “metabolically healthy obesity.” As long as they were obese, they were at modestly higher risk for having a stroke, at nearly 50 percent greater risk of coronary heart disease and had nearly double the risk of developing heart failure than people who were not overweight and in similar metabolic health. People who were metabolically healthy but considered merely overweight were at a 30 percent greater risk of coronary heart disease compared to their normal weight and metabolically healthy peers. “The bottom line is that metabolically healthy obesity doesn’t exist,” said Dr. Rishi Caleyachetty, of the College of Medical and Dental Sciences at the University of Birmingham in England, who was the lead author of the paper, published in the Journal of the American College of Cardiology. “Obesity is not a benign condition.” © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24250 - Posted: 10.27.2017

Aaron E. Carroll Changing your diet is hard. So is helping our children make healthy choices. When a solution comes along that seems simple and gets everyone to eat better, we all want to believe it works. That’s one reason a study by Cornell researchers got a lot of attention in 2012. It reported that you could induce more 8-to-11-year-olds to choose an apple over cookies if you just put a sticker of a popular character on it. That and similar work helped burnish the career of the lead author, Brian Wansink, director of the Cornell Food and Brand Lab. Unfortunately, we now know the 2012 study actually underscores a maxim: Nutrition research is rarely simple. Last week the study, which was published in a prestigious medical journal, JAMA Pediatrics, was formally retracted, and doubts have been cast about other papers involving Mr. Wansink. When first published, the study seemed like an enticing example of behavioral economics, nudging children to make better choices. Before the study period, about 20 percent of the children chose an apple, and 80 percent the cookie. But when researchers put an Elmo sticker on the apple, more than a third chose it. That’s a significant result, and from a cheap, easily replicated intervention. While the intervention seems simple, any study like this is anything but. For many reasons, doing research in nutrition is very, very hard. First, the researchers have to fund their work, which can take years. Then the work has to be vetted and approved by an Institutional Review Board, which safeguards subjects from potential harm. I.R.B.s are especially vigilant when studies involve children, a vulnerable group. Even if the research is of minimal risk, this process can take months. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24233 - Posted: 10.24.2017

By ALISSA J. RUBIN PARIS — When a fledgling alternative press published Gabrielle Deydier’s plaintive memoir of growing up fat in France, there was little expectation that the book would attract much notice. Frenchwomen are among the thinnest in Europe, high fashion is big business, and obesity isn’t often discussed. “To be fat in France is to be a loser,” Ms. Deydier said. So no one, least of all Ms. Deydier, expected “On Ne Naît Pas Grosse” (“One Is Not Born Fat”) to become a media sensation. Using her life as a case in point, bolstered by scientific studies, Ms. Deydier exposes in 150 pages the many ways the obese in France face censure, as well as frequent insensitivity from the medical profession. Soon, the 330-pound author was being interviewed by a broad range of news outlets. The coverage provoked a public reaction, and a variety of comments, including empathy and offers of support for those who are overweight, but also statements denigrating them. Some people complained Ms. Deydier was trying to normalize obesity. “To be close to someone obese in a train or a plane haunts me,” Mathieu B. wrote in a comment on Le Monde’s website. “It’s like being close to someone who smells bad. One has a very bad journey, that’s a fact.” In short, Ms. Deydier had touched a nerve. Her small publisher, which ran a limited first printing, has ordered a second. “A book like this had not been done,” said Clara Tellier Savary, Ms. Deydier’s publisher at Éditions Goutte d’Or. “For an obese person to be aware of all the issues and step back is very rare.” Unlike in the United States, where TV regularly features programs urging viewers to take a positive view of their bodies and where a plus-size clothing industry is booming, celebrating one’s girth is almost unheard-of in France. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24228 - Posted: 10.21.2017

By Alice Klein A protein injection that decreases appetite helps obese monkeys to slim down fast and cuts their risk of diabetes. Excitement is growing about a protein called GDF15, which naturally regulates body weight in humans and animals. When extra amounts are injected into mice, they eat less, lose weight and have fewer signs of diabetes. Several research teams have tried developing GDF15 as an obesity treatment, but it breaks down too quickly in the bloodstream to work. Now a team led by Murielle Véniant at pharmaceutical company Amgen has found a way to make GDF15 last longer in the body. The team added an antibody fragment onto GDF15. Antibodies are immune proteins that help recognise foreign molecules in the body. They found that this hybrid protein caused obese monkeys to eat about 40 per cent less. When given weekly injections, the monkeys lost 10 per cent of their body weight over 6 weeks. Their glucose tolerance also improved, making them less likely to develop type 2 diabetes. In comparison, the five obesity medications that are currently approved by the FDA for long-term weight management help patients to lose an average of 7 to 12 per cent of their body weight over the course of a year. Bariatric surgery – the gold standard for weight loss – usually results in 20 to 30 per cent weight loss in obese patients in the first year, but is expensive and can have complications and side-effects. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24213 - Posted: 10.19.2017

Tina Hesman Saey Fungi may affect gut health in unexpected ways, new research suggests. High-fat diets may alter relationships between bacteria and fungi in mice’s intestines, contributing to obesity, researchers report October 11 in mSphere. In independent work, researchers report that a fungus teams up with two types of bacteria to fuel gut inflammation in people with Crohn’s disease. That work was summarized October 4 in Digestive and Liver Disease. Together, the studies are part of a growing body of research indicating that relationships between the bacterial and fungal kingdoms can affect health, says David Andes, a fungal biologist at the University of Wisconsin School of Medicine and Public Health in Madison. Andes wasn’t involved in either study. Scientists have already described links between health issues, including obesity, and gut bacteria — often called the microbiome. But far less is known about the role of the gut’s fungal mix, or mycobiome. “To get the whole picture,” says Andes, “we’re going to need to start looking at the mycobiome in addition to the microbiome.” As part of that picture, fungal biologist and pediatrician Cheryl Gale of the University of Minnesota in Minneapolis wanted to know whether high-fat diets change fungal communities as they do bacterial mixes. |© Society for Science & the Public 2000 - 2017.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24207 - Posted: 10.18.2017

By Jessica Hamzelou For the first time, researchers have shown that being born by C-section can contribute to obesity in mice. This probably happens because the procedure disrupts a newborn’s microbiome. Until fairly recently, babies were thought to be born with sterile guts free from bacteria. But we now know that babies are born with a gutful of microbes, and that at least some of these come from a mother’s vaginal canal during birth. Babies born by C-section are thought to miss out on these bacteria, which could explain why their microbiomes look different. The ecosystem of microbes that live inside us has been implicated in a range of health issues, so this may explain why babies born by C-section are more likely to grow up overweight, and to develop allergies and asthma in later life. To test if C-sections really do lead to heavier babies, Maria Dominguez-Bello at New York University and her colleagues performed C-sections on 34 pregnant mice, and compared the resulting pups to 35 that were born vaginally. By the time the mice had grown into adults 15 weeks later, there were stark difference in body weight between the two groups. The mice born by C-section were, on average, 33 per cent heavier than those born vaginally. Females seemed particularly affected, says Dominguez-Bello. While the C-section males were around 20 per cent heavier than their vaginally-born counterparts, the females were 70 per cent heavier, she says. “We were very surprised to see this,” she says. “We have no idea why it’s happening.” © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 24180 - Posted: 10.12.2017

By Ann Gibbons The insult "You're a Neandertal!" has taken on dramatic new meaning in the past few years, as researchers have begun to identify the genes many of us inherited from our long-extinct relatives. By sequencing a remarkably complete genome from a 50,000-year-old bone fragment of a female Neandertal found in Vindija Cave in Croatia, researchers report online today in Science a new trove of gene variants that living people outside of Africa obtained from Neandertals. Some of this DNA could influence cholesterol levels, the accumulation of belly fat, and the risk of schizophrenia and other diseases. The genome is only the second from a Neandertal sequenced to such high quality that it can reliably reveal when, where, and what DNA was passed from Neandertals to modern humans—and which diseases it may be causing or preventing today. "It's really exciting because it's more than two times better to have two Neandertal genomes," says evolutionary genomicist Tony Capra of Vanderbilt University in Nashville. The first Neandertal genome was a composite drawn from three individuals from Vindija Cave. Then, over the past few years, ancient DNA researchers sequenced two more Neandertal genomes, including another high-quality sequence from an individual that lived 122,000 years ago in the Altai Mountains of Siberia. Together, the genomes showed that living Europeans and Asians carry traces of DNA from Neandertals who mated with members of Homo sapiens soon after our species left Africa. (Most Africans lack Neandertal DNA as a result.) © 2017 American Association for the Advancement of Science.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24156 - Posted: 10.06.2017

By DIONNE SEARCEY and MATT RICHTEL ACCRA, Ghana — After finishing high school a decade ago, Daniel Awaitey enrolled in computer courses, dropped out to work in a hotel, then settled into a well-paying job in the booming oil sector here. He has an apartment, a car, a smartphone and a long-distance girlfriend he met on a dating website. So he had reasons and the means to celebrate his 27th birthday in late July. His boss and co-workers joined him for an evening of laughter and selfies, lingering over dinner at his favorite restaurant: KFC. Mr. Awaitey first learned about the fried chicken chain on Facebook. The “finger lickin’ good” slogan caught his attention and it has lived up to expectations. “The food is just ——” he said, raising his fingertips to his mouth and smacking his lips. “When you taste it you feel good.” Ghana, a coastal African country of more than 28 million still etched with pockets of extreme poverty, has enjoyed unprecedented national prosperity in the last decade, buoyed by offshore oil. Though the economy slowed abruptly not long ago, it is rebounding and the signs of new fortune are evident: millions moving to cities for jobs, shopping malls popping up and fast food roaring in to greet people hungry for a contemporary lifestyle. Chief among the corporate players is KFC, and its parent company, YUM!, which have muscled northward from South Africa — where KFC has about 850 outlets and a powerful brand name — throughout sub-Saharan Africa: to Angola, Tanzania, Nigeria, Uganda, Kenya, Ghana and beyond. The company brings the flavors that have made it popular in the West, seasoned with an intangible: the symbolic association of fast food with rich nations. But KFC’s expansion here comes as obesity and related health problems have been surging. Public health officials see fried chicken, french fries and pizza as spurring and intensifying a global obesity epidemic that has hit hard in Ghana — one of 73 countries where obesity has at least doubled since 1980. In that period, Ghana’s obesity rates have surged more than 650 percent, from less than 2 percent of the population to 13.6 percent, according to the Institute for Health Metrics and Evaluation, an independent research center at the University of Washington. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24133 - Posted: 10.02.2017

By Amanda Onion Belly fat can be deadly, and is linked to a host of chronic diseases, including heart disease and type 2 diabetes. But as many of us probably know, it can be hard to lose weight in this area. Now it seems that inflammation of immune cells may be to blame, and we may be able to use drugs to help us burn off our belly flab. Christina Cammel, of the Yale School of Medicine, and her colleagues have been investigating macrophages – immune cells that normally track down and gobble up pathogens in the body. But as we age, there’s evidence that the macrophages in belly fat become inflamed. To see what effect this might have, Cammel’s team isolated macrophages from the fat tissue of young and old mice, and sequenced the DNA from these cells. They found that the genomes of the aged macrophages expressed more genes that hinder a group of molecules that spread signals between nerve cells, called catecholamines. The genes do this by activating an enzyme that suppresses these neurotransmitters. The boosted activity of this enzyme in aged immune cells in the belly fat of older mice effectively block signals telling the body that there is fat there that is available to burn for energy. “We found [that] macrophages in belly fat interfere with signals in a way that’s new to us,” says Cammel. © Copyright New Scientist Ltd.

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 24120 - Posted: 09.28.2017

By GRETCHEN REYNOLDS For most of us, temptations are everywhere, from the dessert buffet to the online shoe boutique. But a new study suggests that exercise might be a simple if unexpected way to increase our willpower and perhaps help us to avoid making impulsive choices that we will later regret. Self-control is one of those concepts that we all recognize and applaud but do not necessarily practice. It requires forgoing things that entice us, which, let’s face it, is not fun. On the other hand, lack of self-control can be consequential for health and well-being, often contributing to problems like weight gain, depression or money woes. Given these impacts, scientists and therapists have been interested in finding ways to increase people’s self-restraint. Various types of behavioral therapies and counseling have shown promise. But such techniques typically require professional assistance and have for the most part been used to treat people with abnormally high levels of impulsiveness. There have been few scientifically validated options available to help those of us who might want to be just a little better at resisting our more devilish urges. So for the new study, which was published recently in Behavior Modification, a group of researchers at the University of Kansas in Lawrence began wondering about exercise. Exercise is known to have considerable psychological effects. It can raise moods, for example, and expand people’s sense of what they are capable of doing. So perhaps, the researchers speculated, exercise might alter how well people can control their impulses. To find out, the scientists decided first to mount a tiny pilot study, involving only four men and women. © 2017 The New York Times Company

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 24119 - Posted: 09.28.2017

By Amy Lewis Stress, anxiety, and depression are emotions we all feel at some point in our lives, some people to a greater degree than others. Part of the human experience, right? “It may seem odd that my research focuses on the gut if I’m interested in the brain,” says John Cryan, a researcher at the APC Microbiome Institute at University College Cork in Ireland. “But when we think of how we express emotion in language, through sayings like ‘butterflies in your tummy’ and ‘gut feeling,’ it isn’t surprising that they’re connected.” In a recent study, Cryan and his colleagues reported a link between the microbiome and fear. By examining mice with and without gut bacteria, they discovered that the germ-free mice had blunted fear responses (Mol Psychiatr, doi:10.1038/mp.2017.100, 2017). Their findings may pave the way for the development of novel treatments for anxiety-related illnesses, including posttraumatic stress disorder. Researchers at Kyushu University in Japan were the first to show, in 2004, that bacteria in the gut can influence stress responses, prompting many subsequent investigations. Yet despite mounting research, scientists remain uncertain about exactly how the gut microbiome affects the brain. While some bacteria influence the brain through the vagus nerve, other strains seem to use different pathways. It is known, however, that the population of the gut microbiome begins in early life, and recent research suggests that disruptions to its normal development may influence future physical and mental health (Nat Commun, 6:7735, 2015). Researchers are finding that this gut-brain connection could have clinical implications, as influencing the gut microbiome through diet may serve to ameliorate some psychiatric disorders. Together with University College Cork colleague Ted Dinan, Cryan coined the term “psychobiotics” in 2013 to describe live organisms that, when ingested, produce health benefits in patients with psychiatric illness. These include foods containing probiotics, live strains of gut-friendly bacteria. © 1986-2017 The Scientist

Related chapters from BN8e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 24108 - Posted: 09.25.2017