Chapter 13. Homeostasis: Active Regulation of the Internal Environment
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by Bethany Brookshire “You are what you eat.” We’ve all heard that one. What we eat can affect our growth, life span and whether we develop disease. These days, we know that we also are what our mother eats. Or rather, what our mothers ate while we were in the womb. But are we also what our father eats? A new study shows that in mice, a dietary deficiency in dad can be a big downer for baby. The dietary staple in the study was folic acid, or folate. Folate is one of the B vitamins and is found in dark leafy greens (eat your kale!) and has even been added to some foods like cereals. It is particularly essential to get in the diet because we cannot synthesize it on our own. And it plays roles in DNA repair and DNA synthesis, as well as methylation of DNA. It’s particularly important during development. Without adequate folate, developing fetuses are prone to neural tube disorders, such as spina bifida. Some of the neural tube disorders caused by folate deficiency could result from breaks in the DNA itself. But folic acid is also important in the epigenome. Epigenetics is a mechanism that allows cells to change how genes are used without changing the genes themselves. Instead of altering the DNA itself, epigenetic alterations put chemical “marks” or “notes” —methyl or acetyl groups — on the DNA and the proteins associated with it. The marks can either make a gene more accessible (acetylation) or less accessible (methylation), making it more or less likely to be made into a protein. This means that each cell type can have a different epigenome, allowing a neuron to function differently than a muscle cell, even though they contain the same DNA. Folate affects DNA synthesis, but it can also affect DNA methylation. In fact, DNA methylation requires the presence of folate. So low folate could affect whether genes are turned off or on and by how much. In a developing fetus, that could contribute to developmental problems. © Society for Science & the Public 2000 - 2013.
Many physicians and parents report that their autistic children have unusually severe gastrointestinal problems, such as chronic constipation or diarrhea. These observations have led some researchers to speculate that an ailing gut contributes to the disorder in some cases, but scientific data has been lacking. Now, a provocative study claims that a probiotic treatment for gastrointestinal issues can reduce autismlike symptoms in mice and suggests that this treatment could work for humans, too. The reported incidence of gut maladies in people with autism varies wildly between published studies—from zero to more than 80%—making it difficult to establish just how commonly the two conditions go together, says principal investigator Sarkis Mazmanian, a microbiologist at the California Institute of Technology (Caltech) in Pasadena. Overall, however, the evidence seems to point toward a connection. Last year, for example, a Centers for Disease Control and Prevention study of thousands of children with developmental disabilities found that kids with autism were twice as likely as children with other types of disorders to have frequent diarrhea or colitis, an inflammation of the large intestine. For many years, Mazmanian and his and colleagues have been studying the effects of a nontoxic strain of the bacterium Bacteroides fragilis on diseases such as Crohn's disease, which causes intestinal inflammation and allows potentially harmful substances that should pass out of the body to leak through junctions between cells that are normally tight. Although the researchers don’t understand the mechanism, the bacterium appears to restore the damaged gut, possibly by helping close these gaps. © 2013 American Association for the Advancement of Science.
Link ID: 19009 - Posted: 12.06.2013
By NICHOLAS BAKALAR A high body mass and a large waist are both associated with self-reported hearing loss, a new study has found. Researchers used data from a 20-year prospective study of 68,421 women who were25 to 42 years old at the start. After controlling for age, smoking, diabetes, hypertension and other factors, they found that the higher the body mass index, the greater the risk for hearing loss. Compared with women with a B.M.I. under 25, those with an index of 25 to 29 had an 8 percent increased risk. The numbers kept going up in tandem: 11 percent for 30 to 34, 16 percent for 35 to 39 and 19 percent for those above 40. The increasing risk associated with larger waist circumference followed a similar pattern. The study, published in the December issue of The American Journal of Medicine, found that moderate physical activity — as little as four hours of walking a week — also reduced the risk for hearing loss. Researchers found no further advantage in more vigorous exercise. The lead author, Dr. Sharon G. Curhan, a clinical researcher at Brigham and Women’s Hospital in Boston, suggested that obesity might compromise blood flow to the inner ear, and that exercise might improve it, which could explain the associations. “Hearing loss may not be an inevitable part of growing older,” she said. “There may be things we can do to prevent it.” Copyright 2013 The New York Times Company
By KRISTIN WARTMAN THE solution to one of America’s most vexing problems — our soaring rates of obesity and diet-related diseases — may have its roots in early childhood, and even in utero. Researchers at the Monell Chemical Senses Center, a nonprofit research organization in Philadelphia, have found that babies born to mothers who eat a diverse and varied diet while pregnant and breast-feeding are more open to a wide range of flavors. They’ve also found that babies who follow that diet after weaning carry those preferences into childhood and adulthood. Researchers believe that the taste preferences that develop at crucial periods in infancy have lasting effects for life. In fact, changing food preferences beyond toddlerhood appears to be extremely difficult. “What’s really interesting about children is, the preferences they form during the first years of life actually predict what they’ll eat later,” said Julie Mennella, a biopsychologist and researcher at the Monell Center. “Dietary patterns track from early to later childhood but once they are formed, once they get older, it’s really difficult to change — witness how hard it is to change the adult. You can, but it’s just harder. Where you start, is where you end up.” This may have profound implications for the future health of Americans. With some 70 percent of the United States population now overweight or obese and chronic diseases skyrocketing, many parents who are eating a diet high in processed, refined foods are feeding their babies as they feed themselves, and could be setting their children up for a lifetime of preferences for a narrow range of flavors. The Monell researchers have identified several sensitive periods for taste preference development. One is before three and a half months of age, which makes what the mother eats while pregnant and breast-feeding so important. “It’s our fundamental belief that during evolution, we as humans are exposed to flavors both in utero and via mother’s milk that are signals of things that will be in our diets as we grow up and learn about what flavors are acceptable based on those experiences,” said Gary Beauchamp, the director of the Monell Center. © 2013 The New York Times Company
by Jessica Griggs HAVING type 2 diabetes may mean you are already on the path to Alzheimer's. This startling claim comes from a study linking the two diseases more intimately than ever before. There is some good news: the same research also offers a way to reverse memory problems associated with diabetes – albeit in rats – which may hint at a new treatment for Alzheimer's. "Perhaps you should use Alzheimer's drugs at the diabetes stage to prevent cognitive impairment in the first place," says Ewan McNay from the University at Albany in New York. Alzheimer's cost the US $130 billion in 2011 alone. One of the biggest risk factors is having type 2 diabetes. This kind of diabetes occurs when liver, muscle and fat cells stop responding efficiently to insulin, the hormone that tells them to absorb glucose from the blood. The illness is usually triggered by eating too many sugary and high-fat foods that cause insulin to spike, desensitising cells to its presence. As well as causing obesity, insulin resistance can also lead to cognitive problems such as memory loss and confusion. In 2005, a study by Susanne de la Monte's group at Brown University in Providence, Rhode Island, identified a reason why people with type 2 diabetes had a higher risk of developing Alzheimer's. In this kind of dementia, the hippocampus, a part of the brain involved in learning and memory, seemed to be insensitive to insulin. Not only could your liver, muscle and fat cells be "diabetic" but so it seemed, could your brain. © Copyright Reed Business Information Ltd.
By Sandra G. Boodman, Dorsey Davidge felt her thrumming anxiety burst into barely controlled panic as she watched her 14-year-old daughter Cate Chapin struggle to get from her bedroom to the bathroom. During the last week of January, the eighth-grader contracted what appeared to be a bad case of the flu. After a week, a doctor decided she had pneumonia, a diagnosis that was later changed to a possible infectious disease. Davidge, a single mother who lives in McLean, had maintained her equanimity during the early days of Cate’s illness. But when she saw that her older daughter was unable to walk 10 feet without stopping midway to rest, she was shocked by how cadaverous-looking Cate had become in a matter of weeks. “I was really scared for the first time,” Davidge said. “She was incredibly weak, and I thought, “ ‘Oh, my God, my child is just wasting away.’ ” By then, the 5-foot-2 Cate, a skinny 95 pounds before she got sick, had shriveled to a little over 80 pounds. She had no appetite, was barely drinking anything and seemed unable to consume more than a quarter of a bagel at a sitting. “That day was the last straw,” Davidge recalled. She telephoned Cate’s pediatrician, who agreed that the girl needed to be admitted immediately to a Northern Virginia hospital. It would take another harrowing month — which included the insertion of a feeding tube to help restore Cate’s weight, consultations with a bevy of specialists and numerous tests — before doctors figured out what was actually wrong, a diagnosis made possible after Cate developed a seemingly unrelated condition that sent her to an ophthalmologist. © 1996-2013 The Washington Post
Keyword: Anorexia & Bulimia
Link ID: 18943 - Posted: 11.19.2013
by Jessica Griggs, San Diego Glugging lots of sugary drinks won't just make you fat, it might also lead to changes in the brain that have been linked to cancer and Alzheimer's – at least in rats. This finding comes from the first analysis of how sugary drinks affect proteins in the brain. It showed that 20 per cent of the proteins produced in a brain region related to decision-making were altered in rats that drank sugary drinks compared with those given water. It is well established that drinking sugar-sweetened drinks is linked to obesity and diabetes, as well as increasing the risk of cardiovascular problems. A recent estimate put the number of deaths associated with soft drinks at 184,000 a year globally. But the effects of sugar-rich drinks on the brain have received much less attention. "For many people around the world, soft drinks are their sole source of liquid, or at least they provide a very high proportion of their daily calories", says Jane Franklin at the behavioural neuropharmacology lab at Macquarie University in Sydney, Australia, who carried out the study. "We know that soft drinks are bad for the body, so it's reasonable to assume that they aren't doing anything good for your brain either". To find out, Franklin and her colleague Jennifer Cornish gave 24 adult rats either water or a solution of water containing 10 per cent sugar – about the proportion you would find in an average can of soft drink – for 26 days. © Copyright Reed Business Information Ltd.
Link ID: 18932 - Posted: 11.16.2013
By SENDHIL MULLAINATHAN Why is obesity soaring? The answer seems pretty clear. In 1955, a standard soda at McDonald’s was only seven ounces. Today, a medium is three times as large, and even a child’s-size version is 12 ounces. It’s a widely held view that obesity is a consequence of our behaviors, and that behavioral economics thus plays a central role in understanding it — with markets, preferences and choices taking center stage. As a behavioral economist, I subscribed to that view — until recently, when I began to question my thinking. For many health problems, of course, behavior plays some role but biology is often a major villain. “Biology” here is my catchall term for the myriad bodily mechanics that are only weakly connected to our choices. A few studies have led me to wonder whether the same is true with obesity. Have I been the proverbial owner of a (behavioral) hammer, looking for (behavioral) nails everywhere? Have I failed to appreciate the role of biology? A first warning sign comes from looking at other animals. Our pets have been getting fatter along with us. In 2012, some 58.3 percent of cats were, literally, fat cats. That is taken from a survey by the Association for Pet Obesity Prevention. (The very existence of this organization is telling.) Pet obesity, however, can easily be tied to human behavior: a culture that eats more probably feeds its animals more, too. And yet, a study by a group of biostatisticians in the Proceedings of the Royal Society challenges this interpretation. They collected data from animals raised in captivity: macaques, marmosets, chimpanzees, vervets, lab rats and mice. The data came from labs and centers and spanned several decades. These captive animals are also becoming fatter: weight gain for female lab mice, for example, came out to 11.8 percent a decade from 1982 to 2003. But this weight gain is harder to explain. Captive animals are fed carefully controlled diets, which the researchers argue have not changed for decades. Animal obesity cannot be explained through eating behavior alone. We must look to some other — biological — driver. © 2013 The New York Times Company
Link ID: 18905 - Posted: 11.10.2013
By NICHOLAS BAKALAR Children who do not sleep enough may be increasing their risk for obesity, according to a new study. Researchers randomly divided 37 children aged 8 to 11 into two groups. Each group increased their habitual time in bed by an hour and a half per night for one week, then decreased their time by the same amount the next week. They wore electronic devices to measure sleep time, were assessed for daily food intake three times a week, and had blood tests to measure leptin, a hormone that affects hunger, and high levels of which correlate with fat tissue accumulations. Children consumed 134 calories fewer each day during the increased sleep week than the during the week with less sleep. Fasting leptin levels were lower when the children slept more and, over all, the children’s weight averaged about a half pound less at the end of long sleep weeks than short ones. The study was published online in Pediatrics. The lead author, Chantelle N. Hart, an associate professor of public health at Temple University who was at Brown University when she did the study, cautioned that it was small, and looked only at acute changes in sleep and their effect on eating behaviors. Still, she said, “I think these findings suggest that getting a good night’s sleep in childhood could have important benefits for weight regulation through decreased food intake.” Copyright 2013 The New York Times Company
Guest post by Bruce Bower Among 16- to 22-year-old U.S. males, 7.6 percent report taking various potentially dangerous substances at least monthly to counteract what they regard as an alarming lack of muscularity. Young men whose insecurities inspire them to use growth hormones, steroids and other body-altering chemicals represent the male counterpart of females whose idealization of thinness prompts them to induce vomiting and otherwise purge their bodies of food, proposes a team led by epidemiologist Alison Field of Boston Children’s Hospital. Purging and other eating disorders occur mainly in girls and women. Boys and men so obsessed with muscles that they take substances prohibited in competitive sports are more numerous than researchers and clinicians realized, and have been overlooked, Field and her colleagues conclude November 4 in JAMA Pediatrics. The researchers examined questionnaires that each of 5,527 males completed eight times between 1999 — at ages 12 to 18 — and 2010. Most participants were white and from middle-class families. No information on sports team participation was available. © Society for Science & the Public 2000 - 2013.
JoNel Aleccia NBC News Obesity may be a factor in early puberty in U.S. girls, a new study finds. About 17 percent of American kids ages 2 to 17 are obese, according to the CDC. There’s yet another reason to worry about the obesity epidemic among America’s kids: Extra weight may be sending U.S. girls into puberty earlier than ever. Researchers have found that girls with higher body mass index, a ratio of height and weight, may start developing breasts more than a year before their thinner friends — perhaps as early as second grade. The change is spawning a whole new market of child-sized sanitary pads — decorated with hearts and stars — and deodorants aimed at 8- to 10-year-olds, according to a new study and an editorial published Monday in the journal Pediatrics. “The girls who are obese are clearly maturing earlier,” said Dr. Frank Biro, a pediatrics professor at Cincinnati Children’s Hospital Medical Center. “BMI is, we found, the biggest single factor for the onset of puberty.” In addition, white girls are maturing about four months earlier than in a landmark 1997 study that shocked parents with the news that their daughters who played with My Little Pony could be entering puberty. Biro’s team followed more than 1,200 girls ages 6 to 8 in three cities — San Francisco, Cincinnati and New York — from 2004 to 2011, carefully documenting their BMI and their maturation process.
by Tina Hesman Saey BOSTON— Siberians may use genes to stay warm, a new study shows. As part of an effort to catalog genetic diversity in Siberia, Alexia Cardona of the University of Cambridge and collaborators sampled DNA from 200 Siberians representing 10 native groups. The team looked for genes that have more changes in Siberians than would be expected by chance — a sign that the genes evolved rapidly in the 24,000 years since people settled the frigid land. Rapid changes suggest that a gene is important for adapting to an environment. Several of the Siberians’ genes have variants that may help keep Arctic dwellers warm during the long winters, Cardona reported October 24 at the annual meeting of the American Society of Human Genetics. Among the candidates for genetic heaters are genes involved in metabolizing fats. Some Siberian groups eat mostly meat, so genes that help convert animal fat to energy are important for creating heat. Another gene with variants unique to Siberians is called PRKG1; it helps regulate body heat by controlling muscle contraction and the constriction and dilation of blood vessels. Muscle contractions are an important part of shivering, which can raise body temperature. The researchers also identified variants in genes involved in thyroid function, which plays a role in temperature regulation. A. Cardona et al. Genome-wide analysis of cold adaption in indigenous Siberian populations. American Society of Human Genetics annual meeting, Boston, October 24, 2013. © Society for Science & the Public 2000 - 2013
By James Gallagher Health and science reporter, BBC News The mocked "obesity excuse" of being born with a slow metabolism is actually true for some people, say researchers. A team at the University of Cambridge has found the first proof that mutated DNA does indeed slow metabolism. The researchers say fewer than one in 100 people are affected and are often severely obese by early childhood. The findings, published in the journal Cell, may lead to new obesity treatments even for people without the mutation. Scientists at the Institute of Metabolic Science, in Cambridge, knew that mice born without a section of DNA, a gene called KSR2, gained weight more easily. But they did not know what effect it may be having in people, so they analysed the DNA of 2,101 severely obese patients. Some had mutated versions of KSR2. It had a twin effect of increasing their appetite while their slowing metabolism. "You would be hungry and wanting to eat a lot, you would not want to move because of a slower metabolism and would probably also develop type 2 diabetes at a young age," lead researcher Prof Sadaf Farooqi told the BBC. She added: "It slows the ability to burn calories and that's important as it's a new explanation for obesity." BBC © 2013
By Tori Rodriguez The digestive tract and the brain are crucially linked, according to mounting evidence showing that diet and gut bacteria are able to influence our behavior, thoughts and mood. Now researchers have found evidence of bacterial translocation, or “leaky gut,” among people with depression. Normally the digestive system is surrounded by an impermeable wall of cells. Certain behaviors and medical conditions can compromise this wall, allowing toxic substances and bacteria to enter the bloodstream. In a study published in the May issue of Acta Psychiatrica Scandinavica, approximately 35 percent of depressed participants showed signs of leaky gut, based on blood tests. The scientists do not yet know how leaky gut relates to depression, although earlier work offers some hints. Displaced bacteria can activate autoimmune responses and inflammation, which are known to be associated with the onset of depression, lower mood and fatigue. “Leaky gut may maintain increased inflammation in depressed patients,” which could exacerbate the symptoms of depression if not treated, says Michael Maes, a research psychiatrist with affiliations in Australia and Thailand and an author of the paper. Currently leaky gut is treated with a combination of glutamine, N-acetylcysteine and zinc—believed to have anti-inflammatory or antioxidant properties—when behavioral and dietary modifications fail. © 2013 Scientific American
Link ID: 18830 - Posted: 10.24.2013
Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.
By GINA KOLATA William Howard Taft, the only massively obese man ever to be president of the United States, struggled mightily to control his weight a century ago, worrying about his health and image, and endured humiliation from cartoonists who delighted in his corpulent figure. But new research has found that his weight-loss program was startlingly contemporary, and his difficulties keeping the pounds off would be familiar to many Americans today. On the advice of his doctor, a famed weight-loss guru and author of popular diet books, he went on a low-fat, low-calorie diet. He avoided snacks. He kept a careful diary of what he ate and weighed himself daily. He hired a personal trainer and rode a horse for exercise. And he wrote his doctor, Nathaniel E. Yorke-Davies, with updates on his progress, often twice a week. In a way, he was ahead of his time. Obesity became a medical issue by the middle of the 20th century, around the time the term “obesity” rather than “corpulence” came into vogue, said Abigail C. Saguy, a sociologist at the University of California, Los Angeles, who specializes in the study of obesity. Taft’s story shows that “at least in some cases, corpulence was already treated as a medical problem early in the century,” she added. Like many dieters today, Taft, 6 feet 2 inches tall, lost weight and regained it, fluctuating from more than 350 to 255 pounds. He was 48 when he first contacted Dr. Yorke-Davies, and spent the remaining 25 years of his life corresponding with the doctor and consulting other physicians in a quest to control his weight. Taft’s struggles are recounted by Deborah Levine, a medical historian at Providence College in Rhode Island. She discovered the extensive correspondence between Taft and the diet doctor, including Taft’s diet program, his food diary, and a log of his weight. Her findings were published Monday in The Annals of Internal Medicine. His story, Dr. Levine said, “sheds a lot of light on what we are going through now.” © 2013 The New York Times Company
Link ID: 18788 - Posted: 10.15.2013
by Erika Engelhaupt Could I interest you in eating the partially digested stomach contents of a porcupine? No? Maybe a spot of reindeer stomach, then. Still no? Well, that’s curious. The Western aversion to these dishes is odd, because people around the world have long partaken of — even delighted in — the delicacy known to medical science as chyme. That’s what becomes of food after it’s chewed, swallowed and mushed around in the stomach for a while with a healthy dose of hydrochloric acid. And, researchers now suggest, Neandertals were no exception. Eating chyme may even explain the presence of some puzzling plant matter found in Neandertal’s tartar-crusted teeth. Neandertals didn’t have great dental care, and in the last few years anthropologists have begun to take advantage of monstrous tartar buildup on fossilized teeth to figure out what the hominids ate. Various chemical signatures, starch grains and even tiny plant fossils called phytoliths get preserved in the tartar, also known as calculus. Just what Neandertals ate has been more of a puzzle than paleo dieters might have you believe. Isotope analyses of fossilized bones and teeth suggest Neandertals ate very high on the food chain, with high-protein diets akin to those of wolves or hyenas. But wear marks on their teeth suggest the Neandertal diet consisted of more animals in colder high-latitude areas, and more of a mix of plants and animals in warmer areas. Tartar analyses support the idea that Neandertals ate their veggies, and have also suggested the presence of plants considered inedible, or at least unpalatable and non-nutritious. These include some plants like yarrow and chamomile with medicinal value, so one team suggested Neandertals self-medicated. © Society for Science & the Public 2000 - 2013
Link ID: 18776 - Posted: 10.12.2013
By ANAHAD O'CONNOR They are a mystery to researchers: people who are significantly overweight and yet show none of the usual metabolic red flags. Despite their obesity, they have normal cholesterol levels, healthy blood pressure levels and no apparent signs of impending diabetes. Researchers call them the metabolically healthy obese, and by some estimates they represent as many as a third of all obese adults. Scientists have known very little about them, but new research may shed some light on the cause of their unusual metabolic profile. A study in the journal Diabetologia has found that compared with their healthier counterparts, people who are obese but metabolically unhealthy have impaired mitochondria, the cellular powerhouses that harvest energy from food, as well as a reduced ability to generate new fat cells. Unlike fat tissue in healthy obese people, which generates new cells to help store fat as it accumulates, the fat cells of the unhealthy obese swell to their breaking point, straining the cellular machinery and ultimately dying off. This is accompanied by inflammation, and it leads to ectopic fat accumulation — the shuttling of fat into organs where it does not belong, like the liver, heart and skeletal muscle. A fatty liver frequently coincides with metabolic abnormalities, and studies suggest that it may be one of the causes of insulin resistance, the fundamental defect in Type 2 diabetes. In the healthy obese, however, the fat tends to remain in the subcutaneous padding just beneath the skin, where it appears to be fairly innocuous. “The group that doesn’t gain fat in the liver as they get obese seems to avoid inflammation and maintain their metabolic health,” said Dr. Jussi Naukkarinen, a research scientist specializing in internal medicine at the University of Helsinki. “There is a complete difference in how they react to obesity.” Copyright 2013 The New York Times Company
Link ID: 18771 - Posted: 10.10.2013
By ABBY ELLIN When binge eating disorder gained legitimacy as a full-fledged mental condition in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders in May, many people in the eating disorders and obesity communities wondered: Will this inspire us to finally get along? It was a good question, since historically, the two groups have been at odds. Unlike people with anorexia or bulimia, who tend to be excessively thin, many binge eaters are overweight or obese. And much of the focus of anti-obesity efforts — listing calories at restaurants, banning cupcakes in schools, sending students home with body mass index “report cards” — are decried by eating disorder activists, who say such measures can encourage anorexia or bulimia. Anti-obesity activists, in turn, worry that the eating disorder community minimizes the medical risks of obesity, which the American Medical Association classified as a disease in June, and plays down the discrimination many obese people face. “They come out of different traditions,” said Kelly Brownell, dean of the Sanford School of Public Policy at Duke University. “Obesity was mainly dealt with in medical professions, and eating disorders were dealt with more in psychology professions.” But binge eating disorder, symptoms of which include consuming enormous amounts of food in a two-hour window without purging at least once a week for three months, could bridge the gap between the two worlds, while also reducing the stereotype that only thin people suffer from eating disorders. Copyright 2013 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 18770 - Posted: 10.10.2013
by Linda Geddes They are identical in almost every way, except one twin is fat and the other is thin. Now a study of this rare group is shedding light on a medical mystery: how some people can be obese and perfectly healthy. Obesity usually goes hand in hand with metabolic syndrome – high blood pressure, high cholesterol and type 2 diabetes – but a minority of obese people escape this fate. To probe the fit fat phenomenon, Jussi Naukkarinen at the University of Helsinki in Finland and his colleagues turned to a registry of identical twins, picking 16 pairs whose body weight differed by 17 kilograms on average. They are a perfect model for studying such differences because they are genetically identical and have usually been raised in very similar environments. Naukkarinen's team started by looking at the siblings' body fat distribution and quickly saw that the fat twins fell into two groups: those that tended to accumulate fat within their livers, and those whose liver fat resembled that of their thin twin. Suppressed activity Next, they looked at other markers of ill-health, including insulin resistance, cholesterol, inflammation and blood pressure. These measures also divided the group. "Basically all the hallmarks of the metabolic syndrome were lacking in the group where there was no liver fat," Naukkarinen says. Researchers also compared samples of the twins' abdominal fat, or adipose tissue. In unhealthy obese twins, genes involved in inflammation were activated – genes that were not activated in their thin twin. The activity of cellular powerhouses called mitochondria seemed to be suppressed as well. But in healthy obese twins, gene expression was similar to that of the thin twin. © Copyright Reed Business Information Ltd.