Chapter 13. Homeostasis: Active Regulation of the Internal Environment
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Carl Zimmer All animals do the same thing to the food they eat — they break it down to extract fuel and building blocks for growing new tissue. But the metabolism of one species may be profoundly different from another’s. A sloth will generate just enough energy to hang from a tree, for example, while some birds can convert their food into a flight from Alaska to New Zealand. For decades, scientists have wondered how our metabolism compares to that of other species. It’s been a hard question to tackle, because metabolism is complicated — something that anyone who’s stared at a textbook diagram knows all too well. As we break down our food, we produce thousands of small molecules, some of which we flush out of our bodies and some of which we depend on for our survival. An international team of researchers has now carried out a detailed comparison of metabolism in humans and other mammals. As they report in the journal PLOS Biology, both our brains and our muscles turn out to be unusual, metabolically speaking. And it’s possible that their odd metabolism was part of what made us uniquely human. When scientists first began to study metabolism, they could measure it only in simple ways. They might estimate how many calories an animal burned in a day, for example. If they were feeling particularly ambitious, they might try to estimate how many calories each organ in the animal’s body burned. Those tactics were enough to reveal some striking things about metabolism. Compared with other animals, we humans have ravenous brains. Twenty percent of the calories we take in each day are consumed by our neurons as they send signals to one another. Ten years ago, Philipp Khaitovich of the Max Planck Institute of Evolutionary Anthropology and his colleagues began to study human metabolism in a more detailed way. They started making a catalog of the many molecules produced as we break down food. “We wanted to get as much data as possible, just to see what happened,” said Dr. Khaitovich. To do so, the scientists obtained brain, muscle and kidney tissues from organ donors. They then extracted metabolic compounds like glucose from the samples and measured their concentrations. All told, they measured the levels of over 10,000 different molecules. © 2014 The New York Times Company
Link ID: 19670 - Posted: 05.28.2014
By JANE E. BRODY Bowels, especially those that don’t function properly, are not a popular topic of conversation. Most of the 1.4 million Americans with inflammatory bowel disease — Crohn’s disease or ulcerative colitis — suffer in silence. But scientists are making exciting progress in understanding the causes of these conditions and in developing more effective therapies. And affected individuals have begun to speak up to let others know that they are not alone. Abby Searfoss, 21, who just graduated from the University of Connecticut, shared her story not in a support group, but online. She was a high school senior in Ridgefield, Conn., when she became ill. After she researched her symptoms on the Internet, she realized that, like her father, she had developed Crohn’s disease. Her father had been very ill, losing 40 pounds, spending weeks in the hospital and undergoing surgery. Soon after Ms. Searfoss’s own diagnosis, her two younger sisters learned that they, too, had the condition. In Crohn’s disease, the immune system attacks cells in the digestive tract, most often the end of the small intestine and first part of the colon, or large intestine. Sufferers may experience bouts of abdominal pain, cramps and diarrhea, often accompanied by poor appetite, fatigue and anxiety. “You don’t go anywhere without checking where the bathroom is and how many stalls it has,” said Dr. R. Balfour Sartor, a gastroenterologist at the University of North Carolina School of Medicine and a patient himself. “The fear of incontinence is huge.” Neither Crohn’s disease nor its less common relative ulcerative colitis, which affects only the large intestine, is curable (except, in the latter instance, by removing the entire colon). But research into what predisposes people to develop these conditions has resulted in more effective treatments and has suggested new ways to prevent the diseases in people who are genetically susceptible. © 2014 The New York Times Company
By ANAHAD O'CONNOR Americans have long been told that the cure for obesity is simple: Eat fewer calories and exercise more. But a new documentary challenges that notion, making the case that Americans have been misled by the idea that we get fat simply because we consume more calories than we expend. The film explores what it sees as some of the more insidious corporate and political forces behind the rise of childhood obesity, and it examines whether increasing levels of sugar consumption have played an outsized role in the epidemic. The film, called “Fed Up,” has as executive producers Katie Couric, the former anchor of “The CBS Evening News,” and Laurie David, who was also a producer of the global warming documentary “An Inconvenient Truth.” Ms. Couric, who narrates the film, said she came up with the idea after years of covering the obesity epidemic left her with more questions than answers. “What struck me was that the more I reported on childhood obesity and the longer I was in this business, the worse the problem seemed to be getting,” Ms. Couric said in an interview. “I felt like we were never really giving people a handle on what was causing this and why the rates were skyrocketing the way they were.” The film draws on commentary from obesity experts and nutrition scientists, and it tells the stories of several obese children around the country who struggle to lose weight despite strict dieting and in some cases hours of daily exercise. But at the heart of the film is a question that is widely debated among scientists: Are all calories equal? Dr. David Ludwig, the director of the obesity program at Boston Children’s Hospital, argues in the film that they are not. In recent studies, Dr. Ludwig has shown that high-carbohydrate diets appear to slow metabolic rates compared to diets higher in fat and protein, so that people expend less energy even when consuming the same number of calories. Dr. Ludwig has found that unlike calories from so-called low glycemic foods (like beans, nuts and non-starchy vegetables), those from high glycemic foods (such as sugar, bread and potatoes) spike blood sugar and stimulate hunger and cravings, which can drive people to overeat. © 2014 The New York Times Company
Link ID: 19596 - Posted: 05.10.2014
Brian Owens Surveys of people's eating habits have suggested a link between fibre intake and weight loss, but exactly how fibre helps to regulate weight has been unclear. A study of mouse metabolism suggests that a product of fibre fermentation may be directly affecting the hypothalamus, a region of the brain involved in regulating appetite. People have long been told that a diet high in fibre can help to fight obesity, but how it does so has been unclear. “There has been lots of epidemiological information showing a relationship between fibre and obesity, but no one has been able to connect the epidemiological results with actual mechanisms,” says Jimmy Bell, a biochemist at Imperial College London who worked on the research, published today in Nature Communications1. Until now, a high-fibre diet was thought to help keep weight down by stimulating the release of appetite-suppressing hormones in the gut2, says Bell, but humans do not seem to show the same increase in these hormones that mice do. So Bell and his colleagues decided to look elsewhere. An obvious candidate, they thought, might be one of the products of fibre fermentation in the gut. In particular they focused on the short-chain fatty acid acetate, because it is the most abundant and is known to circulate throughout the bloodstream. They fed mice fibre labelled with carbon-13, which has an additional neutron from the more common carbon-12 that gives its nuclei a magnetic spin and therefore makes it easy to track as it progresses through the body's chemical reactions. The fibre was fermented as usual into acetate, which turned up not only in the gut, but also in the hypothalamus, a part of the brain known to be involved in regulating appetite. There, the researchers found, it was metabolized through the glutamine-glutamate cycle, which is involved in controlling the release of neurotransmitters associated with appetite control. The same model has been proposed for acetate metabolism after drinking alcohol. © 2014 Nature Publishing Group,
Link ID: 19557 - Posted: 04.30.2014
By Lenny Bernstein FILE - In this Oct. 7, 2013 file photo, workers collect red grapes in the vineyards of the famed Chateau Haut Brion, a Premier Grand Cru des Graves, during the grape harvest in Pessac-Leognan, near Bordeaux, southwestern France. Global warming makes feeding the world harder and more expensive, a United Nations scientific panel said. A warmer world will push food prices higher, trigger Red wine gets all the good press for the cardiovascular benefits of the flavonoids it contains, but U.S. Department of Agriculture researchers are reporting that one white wine grape has the reds beat when it comes to slowing weight gain and lowering cholesterol, at least in laboratory animals. The researchers put hamsters on a high-fat diet supplemented by flour made from the seeds of grapes used for chardonnay, syrah and cabernet sauvignon wines. They found that the white grapes easily beat the reds in slowing the hamsters’ weight gain and limiting production of cholesterol. They believe the higher levels of flavonoids in the chardonnay grape seeds altered the work of genes related to fat metabolism. They also had an anti-inflammatory effect, according to a study the USDA scientists published in the Journal of Agricultural and Food Chemistry in February. In part, the researchers say in another paper yet to be published, the anti-oxidant compounds in the chardonnay grape seeds may work with bacteria in the gut to produce beneficial effects. The flour production also provides grape-growers a way to use seeds that currently are discarded and dumped during the chardonnay production. The Mayo Clinic has begun human trials to determine whether the same results can be achieved, said Wally Yokoyama, a research chemist for the USDA in Albany, Calif., and one of the authors of the two studies. The innovation is one of many in a new USDA report released this week. © 1996-2014 The Washington Post
Link ID: 19545 - Posted: 04.29.2014
By LAWRENCE K. ALTMAN Douglas L. Coleman, a Canadian-born scientist who upset scientific dogma by discovering that genes — not willpower, eating habits or other behaviors — could cause obesity in some people, died on April 16 at his home in Lamoine, Me. He was 82. The cause was aggressive basal cell cancer, said a spokeswoman for the Jackson Laboratory in Bar Harbor, Me., where Dr. Coleman spent his entire research career. Beginning in the 1960s, Dr. Coleman’s research showed that a blood-borne substance could curb hunger. In the 1990s, his findings led Dr. Jeffrey M. Friedman’s team at the Rockefeller University in Manhattan to identify the gene that produces the appetite suppressant leptin, which is released by fat cells. For their work, Dr. Coleman and Dr. Friedman shared the prestigious Lasker Award for basic medical research in 2010. Their discoveries upended the conventional wisdom that fat cells are simply energy storage bins, and demonstrated that fat tissue is an endocrine organ required for normal development. Scientists have learned from their research and others’ that fat produces a variety of hormones, cytokines and other chemicals in the body’s natural weight-control system. Douglas Leonard Coleman was born on Oct. 6, 1931, in Stratford, Ontario. Influenced by his father, Leonard, who repaired radios and refrigerators for a living, Douglas spent much of his youth investigating how things worked by taking them apart. He earned a chemistry degree from McMaster University in Hamilton, Ontario, and a doctorate in biochemistry from the University of Wisconsin. In 1958, facing poor employment prospects in academia or industry in Canada, he became a research scientist at the Jackson Laboratory, which studies mouse genetics to learn about human disease. He intended to spend a year or two there to gain experience in genetics and immunology, but stayed until he retired in 1991. After retiring, he turned a tract of land he owned into a nature preserve. © 2014 The New York Times Company
Victoria Colliver, Erin Allday Women who gain too much or too little weight during pregnancy can greatly increase their baby's risk of being overweight or obese as a young child, according to a study by Kaiser Permanente researchers. Researchers examined the health records from 4,145 Northern California Kaiser members who filled out a health survey between 2007 and 2009 and subsequently gave birth. They found that women who exceeded the Institute of Medicine's revised 2009 guidelines for weight gain during pregnancy were 46 percent more likely than women who met the guidelines to have an obese or overweight child between the ages of 2 and 5 years old. Under the new guidelines, women who are obese - defined as those with a body mass index, or BMI, of 30 or higher - should gain 11 to 20 pounds. Overweight women - with BMIs between 25 and 29 - can gain 15 to 25 pounds. And normal-weight women are recommended to gain between 25 and 35 pounds. Those who are underweight - with BMIs under 18.5 - are to gain 28 to 40 pounds. Women who had a healthy BMI before their pregnancy but gained less weight than recommended were 63 percent more likely than those who met the guidelines to have an obese or overweight child. Meanwhile, healthy-weight women who exceeded the guidelines were 79 percent more likely to have an overweight child. Researchers suggested gaining too little or too much weight may permanently affect the body's mechanisms that manage energy balance and metabolism. The study, which is considered the largest to examine the new guidelines in relationship to childhood obesity, was published April 14 in the American Journal of Obstetrics and Gynecology. © 2014 Hearst Communications, Inc.
by Bethany Brookshire Many of us have experienced that depressing sight: The bottom of the ice cream pint. You get to the end of your favorite movie and suddenly realize the ice cream is gone — and you’re far too full for comfort. We’re left wondering why we did it. But when it comes to forgetting ourselves and bingeing on the pint, the power of habit can be strong. It could be that our previous eating experiences make us helpless to our habits. A new study in rats, published April 2 in the Journal of Neuroscience, shows that long-term exposure to bursts of sweet, fatty foods produces animals that appear to seek food not out of hunger, but out of habit. And neural changes associated with habit formation accompany the behavioral changes. The results suggest that repeated binges on sugar and fat could tilt the neural balance from taking a few scoops of Cherry Garcia toward mindlessly reaching the bottom of the bowl. But while the results show us the power of habit, bad habits don’t necessarily make us food addicts. Teri Furlong and her colleagues at the University of Sydney in Australia were interested in how animals control behaviors. Some behaviors are goal-directed, while others are more efficiently taken care of with habits. Furlong describes habits as “behaviors where we are not thinking about the consequences as we do them.” Many habits can be useful things to develop — eating breakfast daily or brushing your teeth, for example. But other habits can become maladaptive, such as drug abuse — or binge eating. © Society for Science & the Public 2000 - 2013.
Feeling peeved at your partner? You may want to check your blood sugar. A new study suggests that low levels of glucose in the blood may increase anger and aggression between spouses. The researchers say their findings suggest a connection between glucose and self-control, but other experts disagree about the study’s implications. Glucose is a source of fuel for the body, and its levels in the blood rise and fall throughout the day, as the body metabolizes meals that include carbohydrates. Researchers have suspected since the 1960s that low glucose or swings in glucose may play a role in human aggression. In two 2010 studies, psychologist Brad Bushman of Ohio State University, Columbus, attempted to figure out just what that role is, first by measuring vengefulness among people with symptoms of type 2 diabetes (a disease in which the body can’t regulate glucose levels properly), and then by providing sweetened drinks to strangers competing on a computerized task. Both studies suggested that higher glucose levels can make strangers less likely to treat each other aggressively. Bushman wondered about the relationship between glucose levels and aggression among romantic couples. So he and colleagues at the University of Kentucky and the University of North Carolina recruited 107 married couples and equipped them with blood glucose meters, voodoo dolls, and 51 pins to record their glucose and anger levels over time. For 21 days, the couples used the meters to measure their glucose levels each morning before breakfast and each evening before bed. They also assessed how angry they were at their spouse at the end of each day, by recording how many of the 51 pins they stuck into their voodoo dolls just before bed when their partner wasn’t looking. After 21 days, the couples were invited into the lab. There, they played a computer game that allowed them to blast their spouse with an unpleasant noise—a mixture of fingernails scratching a chalkboard, ambulance sirens, and dentist drills—as loudly and for as long as he or she wanted, as a proxy for their willingness to act aggressively and make their partner suffer. © 2014 American Association for the Advancement of Science.
By SABRINA TAVERNISE WASHINGTON — Researchers at the University of North Carolina published a paper last week that introduced another wrinkle into the debate about childhood obesity. They disputed recent findings that obesity among young children had fallen since 2004, arguing that a longer view — using data all the way back to 1999 — showed that these youngsters were not really getting any thinner. So which view is correct? The answer seems to be both. Obesity has become a major health problem in the United States, affecting about 17 percent of Americans ages 2 to 19, up from about 5 percent in the early 1970s. The rate rose for years but then leveled off, and the current debate centers on whether obesity has begun to decline in the youngest of these children. The question has drawn considerable attention not just because scientists disagree on the answer, but also because it has a political dimension: The issue has been vigorously championed by Michelle Obama, the first lady. The North Carolina researchers and the federal team that produced the earlier findings both relied on the same data from the National Health and Nutrition Examination Survey. It is considered the gold standard in health research because height and weight are measured by a health professional, not the respondents themselves. But instead of looking only at the past decade of data on children ages 2 to 5, the North Carolina researchers looked at 14 years’ worth. An unusual spike in obesity among these children in 2003 created the false appearance of a later decline, they concluded, so comparing 2012 to 1999 gave a truer view of the trends. © 2014 The New York Times Company
Link ID: 19487 - Posted: 04.15.2014
by Alix Spiegel It was late, almost 9 at night, when Justin Holden pulled the icy pizza box from the refrigerator at the Brookville Supermarket in Washington, D.C. He stood in front of the open door, scanning the nutrition facts label. A close relative had recently had a heart attack, and in the back of his mind there was this idea stalking him: If he put too much salt in his body, it would eventually kill him. For this reason the information in the label wasn't exactly soothing: 1,110 milligrams of sodium seemed like a lot. But there was even worse-sounding stuff at the bottom of the label. Words like "diglyceride," with a string of letters that clearly had no business sitting next to each other. It suggested that something deeply unnatural was sitting inside the box. "Obviously it's not good for me," the 20ish Holden said. "But, hopefully, I can let it slide in." He tucked the pizza under his arm, and headed one aisle over for a sports drink. Who among us has not had a moment like this? That intimate tete-a-tete with the nutrition label, searching out salt, sugar, fat, trying to discern: How will you affect me? Are you good? Or are you bad? Here's the thing you probably haven't stopped to consider: how the label itself is affecting you. "Labels are not just labels; they evoke a set of beliefs," says , a clinical psychologist who does research at the Columbia Business School in New York. A couple of years ago, Crum found herself considering what seems like a pretty strange question. She wanted to know whether the information conveyed by a nutritional label could physically change what happens to you — "whether these labels get under the skin literally," she says, "and actually affect the body's physiological processing of the nutrients that are consumed." ©2014 NPR
By Helen Briggs BBC News Young men with an eating disorder are not getting the help and support they need because of a perceptions about a "women's illness", say researchers. Men are underdiagnosed and undertreated for anorexia and other eating disorders, despite making up about a quarter of cases, a UK study suggests. Frontline health workers have a key role in identifying eating disorders in young men, they report in BMJ Open. Men are under pressure to have the "ideal" body image, says a charity. Researchers from the University of Oxford and University of Glasgow interviewed 39 young people aged 16 to 25, including 10 men, about their experiences of diagnosis, treatment and support for eating disorders. They say young men with eating disorders were "underdiagnosed, undertreated and underresearched". This is partly because the men themselves were unaware of the symptoms, despite purging, not eating for days or obsessive calorie counting, they said. "Our findings suggest that men may experience particular problems in recognising that they may have an eating disorder as a result of the continuing cultural construction of eating disorders as uniquely or predominantly a female problem," said Dr Ulla Raisanen and Dr Kate Hunt. One man said he thought eating disorders only affected "fragile teenage girls"; another said he thought eating disorders were "something girls got"; while one was told by his doctor to "man up". Others said they often had to wait a long time for specialist referral and had sometimes been misdiagnosed. GPs and other professionals such as teachers have a key role in improving the outlook for men with eating disorders by challenging misconceptions, the researchers said. BBC © 2014
Erika Check Hayden Monkeys on a reduced-calorie diet live longer than those that can eat as much as they want, a new study suggests. The findings add to a thread of studies on how a restricted diet prolongs life in a range of species, but they complicate the debate over whether the research applies to animals closely related to humans. In the study, which has been running since 1989 at the Wisconsin National Primate Research Center in Madison, 38 rhesus macaques (Macaca mulatta) that were allowed to eat whatever they wanted were nearly twice as likely to die at any age than were 38 monkeys whose calorie intakes were cut by 30%1. The same study reported2 in 2009 that calorie-restricted monkeys were less likely to die of age-related causes than control monkeys, but had similar overall mortality rates at all ages. “We set out to test the hypothesis: would calorie restriction delay ageing? And I think we've shown that it does,” says Rozalyn Anderson, a biochemist at the University of Wisconsin who led the study, which is published today in Nature Communications. She said it is not surprising that the 2009 paper did not find that the calorie-restricted monkeys lived longer, because at the time too few monkeys had died to prove the point. Eating a very low-calorie diet has been shown3 to prolong the lives of mice, leading to speculation that such a diet triggers a biochemical pathway that promotes survival. But what that pathway might be — and whether humans have it — has been a matter of hot debate. Eat to live In 2012, a study at the US National Institute on Aging (NIA) in Bethesda, Maryland, cast doubt on the idea, reporting4 that monkeys on low-calorie diets did not live longer than those that ate more food. But Anderson says that the Wisconsin findings are good news. © 2014 Nature Publishing Group
Link ID: 19439 - Posted: 04.02.2014
Neandertals and modern Europeans had something in common: They were fatheads of the same ilk. A new genetic analysis reveals that our brawny cousins had a number of distinct genes involved in the buildup of certain types of fat in their brains and other tissues—a trait shared by today’s Europeans, but not Asians. Because two-thirds of our brains are built of fatty acids, or lipids, the differences in fat composition between Europeans and Asians might have functional consequences, perhaps in helping them adapt to colder climates or causing metabolic diseases. “This is the first time we have seen differences in lipid concentrations between populations,” says evolutionary biologist Philipp Khaitovich of the CAS-MPG Partner Institute for Computational Biology in Shanghai, China, and the Max Planck Institute for Evolutionary Anthropology in Leipzig, Germany, lead author of the new study. “How our brains are built differently of lipids might be due to Neandertal DNA.” Ever since researchers at the Max Planck sequenced the genome of Neandertals, including a super high-quality genome of a Neandertal from the Altai Mountains of Siberia in December, researchers have been comparing Neandertal DNA with that of living people. Neandertals, who went extinct 30,000 years ago, interbred with modern humans at least once in the past 60,000 years, probably somewhere in the Middle East. Because the interbreeding happened after moderns left Africa, today’s Africans did not inherit any Neandertal DNA. But living Europeans and Asians have inherited a small amount—1% to 4% on average. So far, scientists have found that different populations of living humans have inherited the Neandertal version of genes that cause diabetes, lupus, and Crohn’s disease; alter immune function; and affect the function of the protein keratin in skin, nails, and hair. © 2014 American Association for the Advancement of Science.
|By Shannon Firth A dog will do anything for a biscuit—over and over again. Most people will, too, because when sugar touches the taste buds it excites reward regions in the brain. A new study shows that people with eating disorders do not react to sweet flavors the way healthy people do, however, lending evidence to the hypothesis that brain differences predispose people toward bulimia and anorexia. A team of psychiatrists at U.C. San Diego studied 14 recovered anorexic women, 14 recovered bulimic women (who used to binge and purge) and 14 women who had never had an eating disorder, matched by age and weight. None of the women had had any pathological eating-related behaviors in the 12 months preceding the study. After fasting overnight, subjects received a modest breakfast to ensure similar levels of satiety. They were then fed small tastes of sugar every 20 seconds through a syringe pump while their brains were scanned. The women who had recovered from anorexia—those who formerly starved themselves—showed less activity than the healthy women in a reward center in the brain known as the primary gustatory cortex. The participants who were no longer bulimic showed more activity than the healthy women did. The results were published in October 2013 in the American Journal of Psychiatry. The researchers believe these abnormal responses to sugar predispose people to eating disorders, adding to a growing body of work suggesting that genetic and biological risk factors underlie most cases, according to study co-author Walter Kaye, director of U.C.S.D.'s Eating Disorders Research and Treatment Program. © 2014 Scientific American
Keyword: Anorexia & Bulimia
Link ID: 19377 - Posted: 03.18.2014
by Laura Sanders Candy and sweets make your kid hyper, the common lore goes. But science says that's not true. 1. Sugar makes kids hyper. Lots of parents swear that a single hit of birthday cake holds the power to morph their well-behaved, polite youngster into a sticky hot mess that careens around a room while emitting eardrum-piercing shrieks. Anyone who has had the pleasure to attend a 5-year-old’s birthday party knows that the hypothesis sounds reasonable, except that science has found that it’s not true. Sugar doesn’t change kids’ behavior, a double-blind research study found way back in 1994. A sugary diet didn’t affect behavior or cognitive skills, the researchers report. Sugar does change one important thing, though: parents’ expectations. After hearing that their children had just consumed a big sugar fix, parents were more likely to say their child was hyperactive, even when the big sugar fix was a placebo, another study found. Of course, there are plenty of good reasons not to feed your kids a bunch of sugar, but fear of a little crazed sugar monster isn’t one of them. © Society for Science & the Public 2000 - 2013.
Keyword: Development of the Brain
Link ID: 19376 - Posted: 03.18.2014
Linda Carroll TODAY contributor The stimulants used to treat ADHD might be making kids fat, a new study suggests. A study of more than 160,000 youngsters found that kids with Attention Deficit and Hyperactivity Disorder who received stimulants were at increased risk of becoming obese as they hit their teens. In contrast, kids with ADHD who took non-stimulant medications or got no therapy were very comparable, in terms of weight gain, to kids who didn’t have the disorder. “Our data suggest that stimulant use during childhood might have lifelong effects,” said Dr. Brian Schwartz, the study’s lead author and a professor of environmental health sciences, epidemiology, and medicine at the Johns Hopkins Bloomberg School of Public Health and senior investigator at the Geisinger Center for Health Research. “They might reset all sorts of physical properties and appetite parameters.” The new research may have uncovered a growing public health issue, Schwartz said. “Our data would seem to offer a lot of cause for concern with respect to prescribing stimulants,” he explained. Schwartz and his colleagues started the study because they were perplexed by the apparent paradox of hyperactive kids being prone to obesity. They scrutinized 12 years-worth of medical information from 163,820 Pennsylvania children, 13,427 of whom received an ADHD diagnosis.
|By Meredith Knight Add another credential to oxytocin's impressive resume: the hormone crucial for bonding also reduces the calories people consume when they are snacking for pleasure, making it a possible therapeutic target for obesity. German researchers gave a group of men a dose of oxytocin thought to be roughly the amount released by the brain after breast-feeding or sex, according to lead author Manfred Hallschmid of the University of Tübingen. These men and another group who took a placebo then had a chance to eat as much as they wanted at a breakfast buffet, and later the same day they were offered snacks. Those who took oxytocin ate fewer snack calories, but the hormone did not change how much the men ate during the main meal, suggesting that oxytocin affected pleasure eating without suppressing normal appetite mechanisms. The researchers hypothesize that the hormone diminished reward-seeking behavior initiated in the ventral tegmental area of the brain, a region found to be highly sensitive to oxytocin in rodent studies. The effect may also be stress-related: subjects who took oxytocin saw a drop in their levels of the stress hormone cortisol, according to the paper published in 2013 in the journal Diabetes. More work is needed to understand whether oxytocin could be used to treat obesity, but until then the finding at least hints that it may be possible to curb your cravings by having more sex. © 2014 Scientific American
Brian Owens Scientists studying what they thought was a ‘fat gene’ seem to have been looking in the wrong place, according to research published today in Nature1. It suggests instead that the real culprit is another gene that the suspected obesity gene interacts with. In 2007, several genome studies identified mutations in a gene called FTO that were strongly associated with an increased risk of obesity and type 2 diabetes in humans. Subsequent studies in mice showed a link between the gene and body mass. So researchers, including Marcelo Nóbrega, a geneticist at the University of Chicago, thought that they had found a promising candidate for a gene that helped cause obesity. The mutations were located in non-coding portions of FTO involved in regulating gene expression. But when Nóbrega looked closer, he found that something was amiss. These regulatory regions contained some elements that are specific for the lungs, one of the few tissues in which FTO is not expressed. “This made us pause,” he says. “Why are there regulatory elements that presumably regulate FTO in the tissue where it isn’t expressed?” This was not the first red flag. Previous attempts to find a link between the presence of the obesity-associated mutations and the expression levels of FTO had been a “miserable failure”, he says. When Nóbrega presented his new results at meetings, he adds that many people came to him to say ‘I just knew there was something wrong here’. So Nóbrega’s team cast the net wider, looking for genes in the broader neighbourhood of FTO whose expression matched that of the mutations, and found IRX3, a gene about half a million base pairs away. IRX3 encodes a transcription factor — a type of protein involved in regulating the expression of other genes — and is highly expressed in the brain, consistent with a role in regulating energy metabolism and eating behaviour. © 2014 Nature Publishing Group
A hormone released during childbirth and sex could be used as a treatment for the eating disorder anorexia nervosa, scientists suggest. Small studies by UK and Korean scientists indicated patients were less likely to fixate on food and body image after a dose of oxytocin. About one in every 150 teenage girls in the UK are affected by the condition. The eating disorders charity Beat said the finding was a long way from becoming a useable treatment. Oxytocin is a hormone released naturally during bonding, including sex, childbirth and breastfeeding. It has already been suggested as a treatment for a range of psychiatric disorders, and has been shown to help lower social anxiety in people with autism. And one four-week study in Australia found people given doses of oxytocin had reduced weight and shape concerns. In the first of the most recent studies, published in Psychoneuroendocrinology, 31 patients with anorexia and 33 people who did not have the condition were given either a dose of oxytocin, delivered via nasal spray, or a placebo, or dummy, treatment. They then looked at a series of images to do with a range high and low calorie foods and people of different body shapes and weight. People with anorexia have previously been found to focus for longer on images of overweight people and what they perceive as undesirable body shapes. However after taking oxytocin, patients with anorexia were less likely to focus on such "negative" images of food and fat body parts. The second study, published in PLOS ONE, involved the same people and looked at their reactions to facial expressions, such as anger, disgust or happiness. It has been suggested that anorexia can be linked to a heightened perception of threat, and animal research has shown oxytocin treatment lessened the amount of attention paid to threatening facial expressions. BBC © 2014