Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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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

Keyword: Obesity
Link ID: 22238 - Posted: 05.23.2016

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

Keyword: Obesity
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

Keyword: Obesity
Link ID: 22196 - Posted: 05.09.2016

By Jane E. Brody Truth to tell, sometimes I don’t follow my own advice, and when I suffer the consequences, I rediscover why I offer it. I’ve long recommended drinking plenty of water, perhaps a glass with every meal and another glass or two between meals. If not plain water, which is best, then coffee or tea without sugar (but not alcoholic or sugary drinks) will do. I dined out recently after an especially active day that included about five miles of walking, 40 minutes of lap swimming and a 90-minute museum visit. I drank only half a glass of water and no other beverage with my meal. It did seem odd that I had no need to use the facilities afterward, not even after a long trip home. But I didn’t focus on why until the next day when, after a fitful night, I awoke exhausted, did another long walk and swim, and cycled to an appointment four miles away. I arrived parched, begging for water. After downing about 12 ounces, I was a new person. I no longer felt like a lead balloon. It seems mild dehydration was my problem, and the experience prompted me to take a closer look at the body’s need for water under a variety of circumstances. Although millions of Americans carry water bottles wherever they go and beverage companies like Coke and Pepsi would have you believe that every life can be improved by the drinks they sell, the truth is serious dehydration is not common among ordinary healthy people. But there are exceptions, and they include people like me in the Medicare generation, athletes who participate in particularly challenging events like marathons, and infants and small children with serious diarrhea. Let’s start with some facts. Water is the single most important substance we consume. You can survive for about two months without food, but you would die in about seven days without water. Water makes up about 75 percent of an infant’s weight and 55 percent of an older person’s weight. © 2016 The New York Times Company

Keyword: Miscellaneous
Link ID: 22192 - 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

Keyword: Obesity
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

Keyword: Obesity; Evolution
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

Keyword: Obesity
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.

Keyword: Obesity; Genes & Behavior
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

Keyword: Obesity
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

Keyword: Obesity; Hormones & Behavior
Link ID: 22146 - Posted: 04.26.2016

By Tulip Mazumdar Most people suffering with eating disorders in Japan are not receiving any medical or psychological support, according to doctors. The Japan Society for Eating Disorders claims the health system is failing hundreds of thousands of sufferers. It also says the pressure on girls, in particular, to be thin has "gone too far". The government says it's trying to set up more services and has tried to discover the extent of the problem. "I hated being chubby when I was a kid," says Motoko - who is using a different name to hide her identity. "The other kids bullied me so I always wanted to change." Motoko was 16 years old when her eating disorder started. She would severely limit how much she ate and then started exercising excessively. By the time she was 19, Motoko was dangerously underweight. She says her parents didn't know how to help her. "They were negative about my illness," she says. "When I tried to see my doctor, they told me not to. "My mother felt responsible, perhaps my father blamed her too." Fear of 'wasting food' Motoko's story is a familiar one. Stigma around eating disorders - for both sufferers and their families - prevent many people from coming forward. "They see actions such as binging on food and then vomiting (bulimia) as shameful," says clinical psychiatrist Dr Aya Nishizono-Maher, a member of The Japan Society for Eating Disorders. "They feel they have to hide it. Parents may think they are wasting food so that might stop them seeking help." After more than 10 years, Motoko finally started getting the help she needed and she now attends one of the few eating disorder community support groups which receives money from the government. © 2016 BBC.

Keyword: Anorexia & Bulimia
Link ID: 22137 - Posted: 04.25.2016

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

Keyword: Obesity; Sleep
Link ID: 22135 - Posted: 04.25.2016

By Lisa Sanders, M.D. On Thursday we challenged Well readers to take on the case of a 59-year-old woman who had not been able to stop gaining weight. I presented the case as it was presented to the doctor who made the diagnosis and asked for the final piece of data provided by the patient as well as the correct cause of her symptoms. I thought the tough part of this case was something that few of my readers would have to contend with – that her complaints and past medical history were quite ordinary. Like many of us, she was overweight and she came to the doctor because she had difficulty losing weight. In the background she also had high blood pressure, obstructive sleep apnea and low back pain, knee pain and leg swelling. These are some of the most common reasons patients seek medical attention. Although her problems were run of the mill, the cause was not. And many of you had no difficulty spotting this zebra. The correct diagnosis was… Acromegaly The last piece of data, provided by the patient, was a photograph taken several years before. It was only by seeing the changes in the patient’s face that had occurred over the past few years that the doctor recognized that this patient’s problem was unusual. The first person to make this diagnosis was Dr. Clare O’Connor, a physician in the second year of her training in internal medicine. She plans to subspecialize in endocrinology. She says it was the swollen legs that didn’t compress that gave her the first clue. Well done. Acromegaly is a rare disease caused by an excess of growth hormone, usually due to a tumor in the pituitary gland of the brain. The disease’s name, from the Greek, serves as a fitting description of the most obvious symptoms: great (mega) extremity (akron). The tumor secretes a protein called growth hormone that signals the liver to produce a substance called insulin-like growth factor 1, or IGF 1, which in turn tells cells throughout the body to start proliferating. © 2016 The New York Times Company

Keyword: Hormones & Behavior; Obesity
Link ID: 22097 - Posted: 04.12.2016

By DAN BILEFSKY LONDON — The model in the Gucci ad is young and waiflike, her frail body draped in a geometric-pattern dress as she leans back in front of a wall painted with a tree branch that appears to mimic the angle of her silhouette. On Wednesday, the Advertising Standards Authority of Britain ruled that the ad was “irresponsible” and that the model looked “unhealthily thin,” fanning a perennial debate in the fashion industry over when thin is too thin. The regulator said that the way the woman in the image had posed elongated her torso and accentuated her waist, so that it appeared to be very small. It said her “somber facial expression and dark makeup, particularly around her eyes, made her face look gaunt.” It said the offending image — a still photograph of the model that appeared in an online video posted on the website of The Times of London in December — should not appear again in its current form. The specific image was removed from the video on Gucci’s YouTube channel, though the model still appears in the ad directed by Glen Luchford. The image deemed "irresponsible" by the Advertising Standards Authority of Britain appeared at the end of this online video, but has been taken out. Video by Gucci The Italian fashion brand, for its part, had defended the ad, saying it was part of a video that portrayed a dance party and that was aimed at an older and sophisticated audience. Nowhere in the ads were any models’ bones visible, it said, and they were all “toned and slim.” It noted that “it was, to some extent, a subjective issue as to whether a model looked unhealthily thin,” according to the authority. The decision by the advertising authority, an independent industry regulatory group, barred Gucci from using the image in advertisements in Britain. The ruling comes amid a longstanding debate on both sides of the Atlantic about the perils of overly thin models projecting an unhealthy body image for women. As when critics lashed out against idealized images of “heroin chic” in the early 1990s, some have voiced concern that fashion houses are encouraging potentially hazardous behaviors by glamorizing models who are rail-thin. © 2016 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 22080 - Posted: 04.07.2016

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

Keyword: Obesity
Link ID: 22059 - Posted: 04.01.2016

By Jordana Cepelewicz The bacteria that inhabit our guts have become key players for neuroscientists. A growing body of research links them to a wide array of mental and neurological disorders—from anxiety and depression to schizophrenia and Alzheimer’s disease. Now a study in mice published this week in Nature Medicine suggests that striking the right microbial balance could cause changes in the immune system that significantly reduce brain damage after a stroke—the second leading cause of both death and disability for people around the globe. (Scientific American is part of Springer Nature.) Experts have known for some time that stroke severity is influenced by the presence of two types of cell, found abundantly within the intestine, that calibrate immune responses: Regulatory T cells have a beneficial inflammatory effect, protecting an individual from stroke. But gamma delta T cells produce a cytokine that causes harmful inflammation after a stroke. A team of researchers at Weill Cornell Medical College and Memorial Sloan Kettering Cancer Center set about investigating whether they could tilt the balance of these cells in the favor of beneficial cells by tinkering with the body’s bacterial residents. To do so, they bred two colonies of mice: One group’s intestinal flora was resistant to antibiotics whereas the other’s gut bacteria was vulnerable to treatment. As a result, when given a combination of antibiotics over the course of two weeks, only the latter’s microbiota underwent change. The researchers then obstructed the cerebral arteries of the mice, inducing an ischemic stroke (the most common type). They found that subsequent brain damage was 60 percent smaller in the drug-susceptible mice than it was in the other group. © 2016 Scientific American,

Keyword: Stroke
Link ID: 22054 - Posted: 03.31.2016

Laura Sanders The 22 men took the same pill for four weeks. When interviewed, they said they felt less daily stress and their memories were sharper. The brain benefits were subtle, but the results, reported at last year’s annual meeting of the Society for Neuroscience, got attention. That’s because the pills were not a precise chemical formula synthesized by the pharmaceutical industry. The capsules were brimming with bacteria. In the ultimate PR turnaround, once-dreaded bacteria are being welcomed as health heroes. People gobble them up in probiotic yogurts, swallow pills packed with billions of bugs and recoil from hand sanitizers. Helping us nurture the microbial gardens in and on our bodies has become big business, judging by grocery store shelves. These bacteria are possibly working at more than just keeping our bodies healthy: They may be changing our minds. Recent studies have begun turning up tantalizing hints about how the bacteria living in the gut can alter the way the brain works. These findings raise a question with profound implications for mental health: Can we soothe our brains by cultivating our bacteria? By tinkering with the gut’s bacterial residents, scientists have changed the behavior of lab animals and small numbers of people. Microbial meddling has turned anxious mice bold and shy mice social. Rats inoculated with bacteria from depressed people develop signs of depression themselves. And small studies of people suggest that eating specific kinds of bacteria may change brain activity and ease anxiety. Because gut bacteria can make the very chemicals that brain cells use to communicate, the idea makes a certain amount of sense. © Society for Science & the Public 2000 - 2016

Keyword: Learning & Memory; Stress
Link ID: 22029 - Posted: 03.24.2016

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

Keyword: Obesity
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

Keyword: Obesity; Epigenetics
Link ID: 21991 - Posted: 03.15.2016

By ERICA GOODE Their websites show peaceful scenes — young women relaxing by the ocean or caring for horses in emerald pastures — and boast of their chefs and other amenities. One center sends out invitations to a reception with cocktails and hors d’oeuvres. Another offers doctors and therapists all-expense-paid trips to visit and experience their offerings, including yoga classes. Several employ staff who call mental health professionals, saying they would love to have lunch. The marketing efforts by these for-profit residential care centers are aimed at patients with eating disorders and the clinicians who treat them. The programs have proliferated in recent years, with some companies expanding across the country. The rapid growth of the industry — there are more than 75 centers, compared with 22 a decade ago, according to one count — has been propelled by the Affordable Care Act and other changes in health insurance laws that have increased coverage for mental disorders, as well as by investments from private equity firms. The residential programs, their directors say, fill a dire need, serving patients from areas where no adequate treatment is available. “Only 15 to 30 percent of people have access to specialized care for eating disorders, which means there are a lot of people out there who have zippo,” said Doug Bunnell, the chief clinical officer for Monte Nido, a program that began in Malibu, Calif., and now operates centers in five states. But the advertising and the profusion of centers, which typically cost $1,000 a day but can run much higher, is raising concerns among some eating disorders experts, who worry that some programs may be taking advantage of vulnerable patients and their families. In the companies’ rush to expand, they argue, quality of treatment may be sacrificed for profit. And they question whether the spalike atmosphere of some programs is so comfortable that it fosters dependency. © 2016 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 21990 - Posted: 03.15.2016