Links for Keyword: Obesity

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By Clare Wilson Pass the sick bag. A device that allows people to empty a portion of their stomach contents into a toilet after a meal has just got the go-ahead from the US Food and Drug Administration. The device is approved for use by people who are severely obese, defined as having a body mass index of over 35 kg/m2. The stomach-churning device, which is already available in some European countries, involves a tube being placed into the stomach in a short surgical procedure. The end of the tube contains a valve that lies flush against the skin. Normally it is kept closed, but after meals, the person can connect the valve to another tube to drain about a third of their partially digested food into the toilet. It cannot remove more food than this, because the end of the internal tube is positioned higher than most of the stomach’s contents. Manufacturer Aspire Bariatrics, based in Pennsylvania, says users need to chew their food well and eat more slowly to stop the 6 millimetre tube from getting blocked, and that this in itself helps reduce overeating. “You get some solid chunks,” says Kathy Crothall, head of Aspire Bariatrics. “If a patient doesn’t chew their food very carefully they won’t get anything out of this device.” The device, called AspireAssist, has a safety feature within the valve that means it can only be used three times a day for up to six weeks. After this time it stops working and part of the device must be replaced. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22327 - Posted: 06.16.2016

Tina Hesman Saey Gut microbes cause obesity by sending messages via the vagus nerve to pack on pounds, new research in rodents suggests. Bacteria in the intestines produce a molecule called acetate, which works through the brain and nervous system to make rats and mice fat, researchers report in the June 9 Nature. If the results hold up in humans, scientists would understand one mechanism by which gut microbes induce obesity: First, the microbes convert fats in food to a short-chain fatty acid called acetate. Acetate in the blood somehow makes its way to the brain. The brain sends a signal through the vagus nerve to the pancreas to increase insulin production. Insulin tells fat cells to store more energy. Fat builds up, leading to obesity. Acetate also increases levels of a hunger hormone called ghrelin, which could lead animals and people to eat even more, says Yale University endocrinologist Gerald Shulman, who led the study. “This is a tour-de-force paper,” says biochemist Jonathan Schertzer of McMaster University in Hamilton, Canada. Most studies that examine the health effects of intestinal microbes just list which bacteria, viruses, fungi and other microorganisms make up the gut microbiome, Schertzer says. But a catalog of differences between lean and obese individuals doesn’t address what those microbes do, he says. “What’s in name?” he asks. “When you find a factor that actually influences metabolism, that’s important.” © Society for Science & the Public 2000 - 2016.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22305 - Posted: 06.09.2016

Jean Fain When Sandra Aamodt talks about dieting, people listen ... or, they stick their fingers in their ears and go la, la, la. Aamodt's neuroscientific take on why diets backfire is that divisive. Aamodt is a neuroscientist, book author and former editor of a leading brain research journal. She also has become a prominent evangelist of the message that traditional diets just don't work and often leave the dieter worse off than before. And she's an enthusiastic proponent of mindful eating. "I define it as eating with attention and joy, without judgment," Aamodt said in an interview. "That includes attention to hunger and fullness, to the experience of eating and to its effects on our bodies." Even if you've never heard of her, you likely will soon. Her new book, Why Diets Make Us Fat, is bound to change the weight-loss conversation, if not dismantle Biggest Loser-sized dreams. I am a therapist specializing in eating issues, and among my clients, Aamodt has already shifted the focus from weight loss to self-care. Most clients are reluctant to accept her central argument: That our body weight tends to settle at "set points" — that 10- to 15-pound range the brain maintains despite repeated efforts to lower it. However, once they see how the set-point theory reflects their dieting experience, they realize that although they don't have the final say on their weight (their brain does), they do have real influence — through exercise and other health-affirming activities — over their health and well-being. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22298 - Posted: 06.08.2016

By Anahad O'Connor The federal government’s decision to update food labels last month marked a sea change for consumers: For the first time, beginning in 2018, nutrition labels will be required to list a breakdown of both the total sugars and the added sugars in packaged foods. But is sugar really that bad for you? And is the sugar added to foods really more harmful than the sugars found naturally in foods? We spoke with some top scientists who study sugar and its effects on metabolic health to help answer some common questions about sugar. Here’s what they had to say. Why are food labels being revised? The shift came after years of urging by many nutrition experts, who say that excess sugar is a primary cause of obesity and heart disease, the leading killer of Americans. Many in the food industry opposed the emphasis on added sugars, arguing that the focus should be on calories rather than sugar. They say that highlighting added sugar on labels is unscientific, and that the sugar that occurs naturally in foods like fruits and vegetables is essentially no different than the sugar commonly added to packaged foods. But scientists say it is not that simple. So, is added sugar different from the naturally occurring sugar in food? It depends. Most sugars are essentially combinations of two molecules, glucose and fructose, in different ratios. The sugar in a fresh apple, for instance, is generally the same as the table sugar that might be added to homemade apple pie. Both are known technically as sucrose, and they are broken down in the intestine into glucose and fructose. Glucose can be metabolized by any cell in the body. But fructose is handled almost exclusively by the liver. “Once you get to that point, the liver doesn’t know whether it came from fruit or not,” said Kimber Stanhope, a researcher at the University of California, Davis, who studies the effects of sugar on health. © 2016 The New York Times Company

Related chapters from BP7e: 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: 22297 - Posted: 06.08.2016

What do large tables, large breakfasts, and large servers have in common? They all affect how much you eat. This week on Hidden Brain, we look at the hidden forces that drive our diets. First we hear from Adam Brumberg at Cornell University's Food and Brand Lab about how to make healthier choices more easily (hint: good habits and pack your lunch!). Then, Senior (Svelte) Stopwatch Correspondent Daniel Pink returns for another round of Stopwatch Science to tell you about those tables, breakfasts, and servers. If you don't like spoilers, stop reading and go listen to the episode! Here are the studies: You may have heard that smaller portions can help you eat fewer calories. That's true. But what about larger tables? Researchers Brennan Davis, Collin Payne, and My Bui hypothesized that one of the ways smaller food units lead us to eat less is by playing with our perception. They tested this with pizza and found that while study participants tended to eat more small slices, they consumed fewer calories overall because it seemed like they were eating more. The researchers tried to distort people's perception even further by making the smaller slices seem bigger by putting them on a bigger table. What they found is that even hungry college students at fewer calories of (free) pizza when it was chopped into tiny slices and put on a big table. What about who's around that big table? That seems to matter, too. Researchers found both men and women order more food when they eat with women but choose smaller portions when they eat in the company of men. They say breakfast is the most important meal of the day. Well, it may also be the most slimming. When researchers assigned two groups of overweight women to eat a limited number of calories each day, they found those who ate more at breakfast and less at dinner shed about twice as many pounds as the other group. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22266 - Posted: 05.31.2016

Dean Burnett A recent report by the National Obesity Forum stated that official advice about low-fat diets is wrong. As ever, there’s now heated debate over how valid/accurate this claim is. But let’s step back a moment and ask a revealing question: why do official government dietary guidelines even exist? Why are they necessary? From an entirely logical position, eating food fulfils several requirements. It provides the energy to do things, helps us build up stores of energy for when needed, and provides the materials required to build and maintain our bodies. Therefore, the human body requires a regular intake of nutrients, vitamins and calories to maintain day-to-day functioning. As a result, the human body has developed an intricate digestive system to monitor and regulate our food intake. The digestive system is quite cool. It has a sophisticated nervous system that can operate pretty much independently, so is often regarded as separate from the main one, leading some to describe it as a “second brain”, there to encourage, monitor and process the consumption and digestion of food. It also utilises hormones, namely leptin and ghrelin, which decrease and increase appetite respectively depending on how much food the body has/needs. It’s a painstakingly complex and precise system that’s evolved over aeons to make sure we eat what and when we need to, and get the most out of our food. However, at some point the human brain got involved, then everything went to hell. This is why we can now be presented with foodstuffs we’re repeatedly told are unhealthy, even dangerous, and say “Thanks. Extra chilli sauce on mine, please”.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 22247 - Posted: 05.25.2016

Aaron E. Carroll I don’t eat breakfast. It’s not that I dislike what’s offered. Given the choice of breakfast food or lunch food, I’d almost always choose eggs or waffles. It’s just that I’m not hungry at 7:30 a.m., when I leave for work. In fact, I’m rarely hungry until about lunchtime. So, other than a morning cup of coffee, I don’t eat much before noon. This habit has forced me to be subjected to more lectures on how I’m hurting myself, my diet, my work and my health than almost any other. Only a fool would skip the most important meal of the day, right? As with many other nutritional pieces of advice, our belief in the power of breakfast is based on misinterpreted research and biased studies. It does not take much of an effort to find research that shows an association between skipping breakfast and poor health. A 2013 study published in the journal Circulation found that men who skipped breakfast had a significantly higher risk of coronary heart disease than men who ate breakfast. But, like almost all studies of breakfast, this is an association, not causation. More than most other domains, this topic is one that suffers from publication bias. In a paper published in The American Journal of Clinical Nutrition in 2013, researchers reviewed the literature on the effect of breakfast on obesity to look specifically at this issue. They first noted that nutrition researchers love to publish results showing a correlation between skipping breakfast and obesity. They love to do so again and again. At some point, there’s no reason to keep publishing on this. However, they also found major flaws in the reporting of findings. People were consistently biased in interpreting their results in favor of a relationship between skipping breakfast and obesity. They improperly used causal language to describe their results. They misleadingly cited others’ results. And they also improperly used causal language in citing others’ results. People believe, and want you to believe, that skipping breakfast is bad. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22238 - Posted: 05.23.2016

Laura Sanders In mice, a long course of antibiotics that wiped out gut bacteria slowed the birth of new brain cells and impaired memory, scientists write May 19 in Cell Reports. The results reinforce evidence for a powerful connection between bacteria in the gut and the brain (SN: 4/2/16, p. 23). After seven weeks of drinking water spiked with a cocktail of antibiotics, mice had fewer newborn nerve cells in a part of the hippocampus, a brain structure important for memory. The mice’s ability to remember previously seen objects also suffered. Further experiments revealed one way bacteria can influence brain cell growth and memory. Injections of immune cells called Ly6Chi monocytes boosted the number of new nerve cells. Themonocytes appear to carry messages from gut to brain, Susanne Wolf of the Max Delbrück Center for Molecular Medicine in Berlin and colleagues found. Exercise and probiotic treatment with eight types of live bacteria also increased the number of newborn nerve cells and improved memory in mice treated with antibiotics. The results help clarify the toll of prolonged antibiotic treatment, and hint at ways to fight back, the authors write. L. Möhle et al. Ly6Chi monocytes provide a link between antibiotic-induced changes in gut microbiota and adult hippocampal neurogenesis. Cell Reports. Vol. 15, May 31, 2016. doi: 10.1016/j.celrep.2016.04.074. © Society for Science & the Public 2000 - 2016

Related chapters from BP7e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory, Learning, and Development
Link ID: 22231 - Posted: 05.21.2016

Nancy Shute A body mass index under 25 is deemed normal and healthy, and a higher BMI that's "overweight" or "obese" is not. But that might be changing, at least when it comes to risk of death. The body mass index, or BMI, associated with the lowest risk of death has increased since the 1970s, a study finds, from 23.7, in the "normal" weight category, to 27, which is deemed "overweight." That means a person who is 5-foot-8 could weigh 180 pounds and be in that epidemiological sweet spot, according to the NIH's online BMI calculator. The results were published Tuesday in JAMA, the journal of the American Medical Association. The researchers came to that conclusion by looking at data from three studies of people in Copenhagen, one from the 1970s, one from the 1990s and one from 2003-2013. More than 100,000 people were involved. Because Denmark has an excellent national health registry, they were able to pinpoint the cause of death for every single one of those people. The risk of death for people who are obese, with a BMI of 30 or greater, also declined, to the point that it was on a par with some people of so-called "normal" weight. So being fatter, at least a bit, may be healthier. "I was surprised as a scientist to see how clear the result was," Borge Nordestgaard, a clinical professor and chief physician at Copenhagen University Hospital and senior author of the study, told Shots. So he and his colleagues sliced and diced the data to see what could account for the shift. They looked at age, sex, smoking, cancer and heart disease. The most relevant was the decline in smoking since the 1970s. But when they looked at the mortality rates in nonsmokers who had never had cancer or heart disease, it also became associated with a higher BMI over time. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22200 - Posted: 05.11.2016

by Julia Belluz and Javier Zarracina "I'm going to make you work hard," a blonde and perfectly muscled fitness instructor screamed at me in a recent spinning class, "so you can have that second drink at happy hour!" At the end of the 45-minute workout, my body was dripping with sweat. I felt like I had worked really, really hard. And according to my bike, I had burned more than 700 calories. Surely I had earned an extra margarita. The spinning instructor was echoing a message we've been getting for years: As long as you get on that bike or treadmill, you can keep indulging — and still lose weight. It's been reinforced by fitness gurus, celebrities, food and beverage companies like PepsiCo and Coca-Cola, and even public-health officials, doctors, and the first lady of the United States. Countless gym memberships, fitness tracking devices, sports drinks, and workout videos have been sold on this promise. There's just one problem: This message is not only wrong, it's leading us astray in our fight against obesity. To find out why, I read through more than 60 studies on exercise and weight loss. I also spoke to nine leading exercise, nutrition, and obesity researchers. Here's what I learned. 1) An evolutionary clue to how our bodies burn calories When anthropologist Herman Pontzer set off from Hunter College in New York to Tanzania to study one of the few remaining hunter-gatherer tribes on the planet, he expected to find a group of calorie burning machines. Unlike Westerners, who increasingly spend their waking hours glued to chairs, the Hadza are on the move most of the time. Men typically go off and hunt — chasing and killing animals, climbing trees in search of wild honey. Women forage for plants, dig up tubers, and comb bushes for berries. "They're on the high end of physical activity for any population that's been looked at ever," Pontzer said. © 2016 Vox Media, Inc

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22196 - Posted: 05.09.2016

Why You Can’t Lose Weight on a Diet By SANDRA AAMODT SIX years after dropping an average of 129 pounds on the TV program “The Biggest Loser,” a new study reports, the participants were burning about 500 fewer calories a day than other people their age and size. This helps explain why they had regained 70 percent of their lost weight since the show’s finale. The diet industry reacted defensively, arguing that the participants had lost weight too fast or ate the wrong kinds of food — that diets do work, if you pick the right one. But this study is just the latest example of research showing that in the long run dieting is rarely effective, doesn’t reliably improve health and does more harm than good. There is a better way to eat. The root of the problem is not willpower but neuroscience. Metabolic suppression is one of several powerful tools that the brain uses to keep the body within a certain weight range, called the set point. The range, which varies from person to person, is determined by genes and life experience. When dieters’ weight drops below it, they not only burn fewer calories but also produce more hunger-inducing hormones and find eating more rewarding. The brain’s weight-regulation system considers your set point to be the correct weight for you, whether or not your doctor agrees. If someone starts at 120 pounds and drops to 80, her brain rightfully declares a starvation state of emergency, using every method available to get that weight back up to normal. The same thing happens to someone who starts at 300 pounds and diets down to 200, as the “Biggest Loser” participants discovered. This coordinated brain response is a major reason that dieters find weight loss so hard to achieve and maintain. For example, men with severe obesity have only one chance in 1,290 of reaching the normal weight range within a year; severely obese women have one chance in 677. A vast majority of those who beat the odds are likely to end up gaining the weight back over the next five years. In private, even the diet industry agrees that weight loss is rarely sustained. A report for members of the industry stated: “In 2002, 231 million Europeans attempted some form of diet. Of these only 1 percent will achieve permanent weight loss.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22188 - Posted: 05.07.2016

By Ann Gibbons We may not be raring to go on a Monday morning, but humans are the Energizer Bunnies of the primate world. That’s the conclusion of a new study that, for the first time, measures precisely how many calories humans and apes burn each day. Compared with chimpanzees and other apes, our revved-up internal engines burn calories 27% faster, according to a paper in Nature this week. This higher metabolic rate equips us to quickly fuel energy-hungry brain cells, sustaining our bigger brains. And lest we run out of gas when food is short, the study also found that humans are fatter than other primates, giving us energy stores to draw on in lean times. “The brilliant thing here is showing for the first time that we do have a higher metabolic rate, and we do use more energy,” says paleoanthropologist Leslie Aiello, president of the Wenner-Gren Foundation for Anthropological Research in New York City. “Humans during evolution have become more and more hypermetabolic,” says biological anthropologist Carel van Schaik of the University of Zurich in Switzerland. “We turned up the thermostat.” For decades, researchers assumed that “there weren’t any differences in the rate at which different species burned calories,” says biological anthropologist Herman Pontzer of Hunter College in New York City, lead author of the new study. Comparing humans and other primates, they saw little difference in basal metabolic rate, which reflects the total calories used by our organs while we are at rest. © 2016 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 22183 - Posted: 05.05.2016

By Gretchen Reynolds Young rats prone to obesity are much less likely to fulfill that unhappy destiny if they run during adolescence than if they do not, according to a provocative new animal study of exercise and weight. They also were metabolically healthier, and had different gut microbes, than rats that keep the weight off by cutting back on food, the study found. The experiment was done in rodents, not people, but it does raise interesting questions about just what role exercise may play in keeping obesity at bay. For some time, many scientists, dieting gurus and I have been pointing out that exercise by itself tends to be ineffective for weight loss. Study after study has found that if overweight people start working out but do not also reduce their caloric intake, they shed little if any poundage and may gain weight. The problem, most scientists agree, is that exercise increases appetite, especially in people who are overweight, and also can cause compensatory inactivity, meaning that people move less over all on days when they exercise. Consequently, they wind up burning fewer daily calories, while also eating more. You do the math. But those discouraging studies involved weight loss. There has been much less examination of whether exercise might help to prevent weight gain in the first place and, if it does, how it compares to calorie restriction for that purpose. So for the new study, which was published last week in Medicine & Science in Sports & Exercise, researchers at the University of Missouri in Columbia and other schools first gathered rats from a strain that has an inborn tendency to become obese, starting in adolescence. (Adolescence is also when many young people begin to add weight.) © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22178 - Posted: 05.04.2016

By Helen Briggs BBC News The Labrador retriever, known as one of the greediest breeds of dog, is hard-wired to overeat, research suggests. The dog is more likely to become obese than other breeds partly because of its genes, scientists at Cambridge University say. The gene affected is thought to be important in controlling how the brain recognises hunger and the feeling of being full after eating. The research could help in the understanding of human obesity. "About a quarter of pet Labradors carry this gene [difference]," lead researcher Dr Eleanor Raffan told the BBC. "Although obesity is the consequence of eating more than you need and more than you burn off in exercise, actually there's some real hard-wired biology behind our drive to eat," she added. Lifestyle factors Canine obesity mirrors the human obesity epidemic, with lifestyle factors such as lack of exercise and high-calorie food both implicated - as well as genetics. As many as two in three dogs (34-59%) in rich countries are now overweight. The Labrador has the highest levels of obesity and has been shown to be more obsessed with food than other breeds. Researchers screened more than 300 Labradors kept as pets or assistance dogs for known obesity genes in the study, published in the journal Cell Metabolism. The international team found that a change in a gene known as POMC was strongly linked with weight, obesity and appetite in Labradors and Flat-Coated retrievers. In both breeds, for each copy of the gene carried, the dog was on average 2kg heavier. Other breeds of dog - from the Shih Tzu to the Great Dane - were also screened, but the genetic difference was not found. However, the variation was more common in Labradors working as assistance dogs, which the researchers say might be because these dogs are easier to train by rewarding with food. © 2016 BBC.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22177 - Posted: 05.04.2016

By GINA KOLATA Danny Cahill stood, slightly dazed, in a blizzard of confetti as the audience screamed and his family ran on stage. He had won Season 8 of NBC’s reality television show “The Biggest Loser,” shedding more weight than anyone ever had on the program — an astonishing 239 pounds in seven months. When he got on the scale for all to see that evening, Dec. 8, 2009, he weighed just 191 pounds, down from 430. Dressed in a T-shirt and knee-length shorts, he was lean, athletic and as handsome as a model. “I’ve got my life back,” he declared. “I mean, I feel like a million bucks.” Mr. Cahill left the show’s stage in Hollywood and flew directly to New York to start a triumphal tour of the talk shows, chatting with Jay Leno, Regis Philbin and Joy Behar. As he heard from fans all over the world, his elation knew no bounds. But in the years since, more than 100 pounds have crept back onto his 5-foot-11 frame despite his best efforts. In fact, most of that season’s 16 contestants have regained much if not all the weight they lost so arduously. Some are even heavier now. Yet their experiences, while a bitter personal disappointment, have been a gift to science. A study of Season 8’s contestants has yielded surprising new discoveries about the physiology of obesity that help explain why so many people struggle unsuccessfully to keep off the weight they lose. Kevin Hall, a scientist at a federal research center who admits to a weakness for reality TV, had the idea to follow the “Biggest Loser” contestants for six years after that victorious night. The project was the first to measure what happened to people over as long as six years after they had lost large amounts of weight with intensive dieting and exercise. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22168 - Posted: 05.02.2016

By Jordana Cepelewicz Everyone is familiar with the complaints of a hungry stomach. For years, scientists attributed the gnawing increase in appetite before a meal to ghrelin, a hormone which is secreted in the gut and circulates in the blood, playing a role in food intake and storage. Researchers have found that levels of ghrelin, dubbed the “hunger hormone,” peak before meals and recede after eating. Given its association with appetite, ghrelin is a tempting drug target for potential obesity treatments—but findings thus far have not lived up to expectations. Experiments that knock out the genes coding for ghrelin and its single receptor, GHSR (growth hormone secretagogue receptor), have been inconclusive: Remove the hormone or receptor, and rodents used in the experiments do not necessarily lose their drive to eat. Now a team of researchers at the French Institute of Health and Medical Research (INSERM) in Paris believe that scientists have had it wrong all along. In a study published this week in Science Signaling, they report that ghrelin does not enhance appetite in rats but rather increases weight gain and fat buildup. Unlike in earlier work, in the new study the researchers used a novel genetic method that kept the ghrelin receptor functional but modified it to have greater signaling in response to ghrelin—in other words, the receptor would enhance the hormone’s effects. The team then performed a series of experiments, first in isolated cells and then in rats. As expected, exposing ghrelin to modified receptors prompted a more potent response compared with the unaltered GHSR. © 2016 Scientific American

Related chapters from BP7e: 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: 22146 - Posted: 04.26.2016

By Nicholas Bakalar Eating a high-fat diet may lead to daytime sleepiness, a new study concludes. Australian researchers studied 1,800 men who had filled out food-frequency questionnaires and reported on how sleepy they felt during the day. They were also electronically monitored for obstructive sleep apnea, which causes people to wake up many times during the night. After adjusting for factors that could influence sleep — smoking, alcohol intake, waist circumference, physical activity, medications, depression and others — they found that compared with those in the lowest one-quarter for fat intake, those in the highest one-quarter were 78 percent more likely to suffer daytime sleepiness and almost three times as likely to have sleep apnea. The connection of fat intake to apnea was apparent most clearly in people with a high body mass index, but the positive association of fat intake with daytime sleepiness persisted strongly in all subjects, regardless of B.M.I. Thestudy is in the journal Nutrients. “The possible mechanism could be meal timing, but we didn’t have that information,” said the lead author, Yingting Cao, a doctoral candidate at the University of Adelaide. “But we have reason to believe that circadian rhythm, hormones and diet all work together to create these effects. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 22135 - Posted: 04.25.2016

Meghan Rosen Despite massive public health campaigns, the rise in worldwide obesity rates continues to hurtle along like a freight train on greased tracks. In 2014, more than 640 million men and women were obese (measured as a body mass index of 30 or higher). That’s up from 105 million in 1975, researchers estimate in the April 2 Lancet. The researchers analyzed four decades of height and weight data for more than 19 million adults, and then calculated global rates based on population data. On average, people worldwide are gaining about 1.5 kilograms per decade — roughly the weight of a half-gallon of ice cream. But the road isn’t entirely rocky. During the same time period, average life expectancy also jumped: from less than 59 years to more than 71 years, George Davey Smith points out in a comment accompanying the new study. Smith, an epidemiologist at the University of Bristol in England, boils the data down to a single, seemingly paradoxical sentence: “The world is at once fatter and healthier.” © Society for Science & the Public 2000 - 2016

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22059 - Posted: 04.01.2016

Tracie McMillan When it comes to school breakfasts, two is better than none, says a new report released Thursday in the journal Pediatric Obesity. Researchers tracked nearly 600 middle-school students from fifth to seventh grade, looking to see if students ate no breakfast; ate breakfast at home or school; or ate both — and whether that affected obesity rates. The result: Weight gain among students who ate "double-breakfast" was no different than that seen among all other students. Meanwhile, the risk of obesity doubled among students who skipped breakfast or ate it inconsistently. "It seems it's a bigger problem to have kids skipping breakfast than to have these kids eating two breakfasts," says Marlene Schwartz of the Rudd Center for Food Policy and Obesity and one of the study's authors. "This study ... debunks an important misconception that school breakfast contributes to childhood obesity," says Duke Storen from Share Our Strength, a national group that runs anti-hunger and nutrition programs for children. While direct opposition to free school breakfast is unusual, says Storen, officials sometimes balk at implementing "alternative breakfast models" designed to encourage use of the program — such as offering breakfast in grab-and-go bags or in classrooms, rather than traditional sit-down meals in a cafeteria. That's a concern, say hunger advocates, because while eligibility rules for free and reduced-price breakfast are the same as for lunch, only about half as many children get subsidized breakfast as receive lunch, according to the Food Research and Action Center, an advocacy group. Indeed, the study was inspired in part by real-world concerns that school breakfast programs might promote obesity, says Schwartz. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22005 - Posted: 03.19.2016

Linda Geddes The health effects of a bad diet can carry over to offspring through eggs and sperm cells without DNA mutations, researchers have found. The mouse study, published in Nature Genetics1, provides some of the strongest evidence yet for the non-genetic inheritance of traits acquired during an organism’s lifetime. And although previous work has suggested that sperm cells can carry 'epigenetic' factors, this is the first time that such an effect has been observed with egg cells. Researchers have suspected for some time that parents' lifestyle and behaviour choices can affect their children's health through epigenetics. These are chemical modifications to DNA or the proteins in chromosomes that affect how genes are expressed, but that do not alter the gene sequences themselves. Whether those changes can be inherited is still controversial. In particular, there have been suggestions that parental eating habits might shape the offspring's risk of obesity and diabetes. However, it has been difficult to disentangle the possibility that the parents’ behaviour during pregnancy or during the offspring's early childhood was to blame, rather than epigenetic changes that had occurred before conception. To get around this issue, endocrinologist Peter Huypens at the German Research Center for Environmental Health in Neuherberg, Germany, and his colleagues gave genetically identical mice one of three diets — high fat, low fat or standard laboratory chow — for six weeks. As expected, those fed the high-fat diet became obese and had impaired tolerance to glucose, an early sign of type 2 diabetes. © 2016 Nature Publishing Group

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 21991 - Posted: 03.15.2016