Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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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
Think you’ll always pick chocolate over a bag of chips? Don’t be so sure. Researchers have found that if they can get people to pay more attention to a particular type of junk food, they will begin to prefer it—even weeks or months after the experiment. The finding suggests a new way to manipulate our decisions and perhaps even encourage us to pick healthy foods. “This paper is provocative and very well done,” says Antonio Rangel, a neuroeconomist at the California Institute of Technology in Pasadena, who was not involved in the new study. “It is exciting because it’s a proof of concept that a relatively simple intervention can have this long-lasting effect.” Economists who study decision-making had previously found that, when deciding between multiple items, people tend to let their gaze linger on the things that they end up choosing. This observation has motivated companies to pursue flashy packaging to attract consumers’ eyes. Tom Schonberg, a neuroscientist at the University of Texas, Austin, wondered whether people’s preferences could be changed before being faced with such a decision by training their brains to pay more attention to certain items. His first task was figuring out what kind of junk food people preferred. He and his colleagues recruited more than 200 university students and set up an auction-style program that asked them how much they were willing to pay for 60 different kinds of snacks, from M&M’s to Fritos. Then, the participants went through a 30- to 50-minute computer training program that showed photos of foods that the participants had already rated. When some treats appeared on the screen, a short tone would play and signal the subject to press a button as fast as possible. When other treats popped up, the computer remained silent and the subject refrained from pressing the button. © 2014 American Association for the Advancement of Science
By Debra Weiner An active lifestyle improves brain health, scientists have long believed. The studies bear this out: physical, intellectual and social activity—or “environmental enrichment,” in the parlance—enhances learning and memory and protects against aging and neurological disease. Recent research suggests one benefit of environmental enrichment at the cellular level: it repairs brain myelin, the protective insulation surrounding axons, or nerve fibers, which can be lost because of aging, injury or diseases such as multiple sclerosis. But how does an enriched environment trigger myelin repair in the first place? The answer appears to involve naturally occurring membrane-wrapped packets called exosomes. A number of different cell types release these little sacs of proteins and genetic material into the body's fluids. Loaded with signaling molecules, exosomes spread through the body “like messages in a bottle,” says R. Douglas Fields, a neurobiologist at the National Institutes of Health. They target particular cells and change their behavior. In animal studies, exosomes secreted by immune cells during environmental enrichment caused cells in the brain to start myelin repair. Researchers think exosomes might find use as biomarkers for diagnosing diseases or as vehicles to deliver cancer drugs or other therapeutic agents. The exosomes produced during environmental enrichment carry microRNAs—small pieces of genetic material—which appear to instruct immature cells in the brain to develop into myelin-making cells called oligodendrocytes. When researchers at the University of Chicago withdrew exosomes from the blood of rats and administered them to aging animals, the older rats' myelin levels rose by 62 percent, the team reported in February in Glia. © 2014 Scientific American
By GRETCHEN REYNOLDS Obesity may have harmful effects on the brain, and exercise may counteract many of those negative effects, according to sophisticated new neurological experiments with mice, even when the animals do not lose much weight. While it’s impossible to know if human brains respond in precisely the same way to fat and physical activity, the findings offer one more reason to get out and exercise. It’s been known for some time that obesity can alter cognition in animals. Past experiments with lab rodents, for instance, have shown that obese animals display poor memory and learning skills compared to their normal-weight peers. They don’t recognize familiar objects or recall the location of the exit in mazes that they’ve negotiated multiple times. But scientists hadn’t understood how excess weight affects the brain. Fat cells, they knew, manufacture and release substances into the bloodstream that flow to other parts of the body, including the heart and muscles. There, these substances jump-start biochemical processes that produce severe inflammation and other conditions that can lead to poor health. Many thought the brain, though, should be insulated from those harmful effects. It contains no fat cells and sits behind the protective blood-brain barrier that usually blocks the entry of undesirable molecules. However, recent disquieting studies in animals indicate that obesity weakens that barrier, leaving it leaky and permeable. In obese animals, substances released by fat cells can ooze past the barrier and into the brain. The consequences of that seepage became the subject of new neurological experiments conducted by researchers at Georgia Regents University in Augusta and published last month in The Journal of Neuroscience. © 2014 The New York Times Company
Link ID: 19323 - Posted: 03.05.2014
By Deborah Kotz / Globe Staff Obesity rates plummeted among preschool children in the past decade, from nearly 14 percent to just over 8 percent in 2011-12, according to a new federal government analysis that was hailed by one researcher as a “glimmer of hope.” But the campaign to combat the nation’s obesity epidemic has had no success with adults and older children: Americans remain just as overweight as ever, with two out of three adults at an unhealthy weight and more than one out of three obese in 2011-12, the latest years for which statistics were available. The study, published Tuesday in the Journal of the American Medical Association, examined annual government health and nutrition surveys that sampled more than 9,000 Americans of all ages. Despite the gains for toddlers, the study found that overall among children under age 20, 17 percent were at the extreme obese end of the weight spectrum. Nearly one-third of kids remain either overweight or obese—nearly triple the rate of 50 years ago—which pediatricians blame for the sharp rise in type 2 diabetes, high blood pressure, and high cholesterol levels in children. Rates actually increased in one group: Women over age 60 experienced a rise in obesity from just under 32 percent 10 years ago to over 38 percent in 2011-2012. “Obesity rates haven’t changed for most Americans, but there was a glimmer of hope in preschoolers,” said study leader Cynthia Ogden, an epidemiologist at the federal Centers for Disease Control and Prevention’s National Center for Health Statistics. © 2014 Boston Globe Media Partners, LLC
Link ID: 19292 - Posted: 02.26.2014
Ian Sample, science correspondent, in Chicago A woman's diet in early life has more impact on her baby's birth weight than the food she eats as an adult, researchers say. The surprise finding suggests that you are what your mother ate, and that a woman's diet in her adult life has less influence on her baby's health than previously thought. Prof Christopher Kuzawa at Northwestern University in Illinois said that women's bodies seemed to "buffer" the supply of nutrients to their unborn babies, meaning that foetuses were partly protected from changes in women's diets. Kuzawa advised pregnant women to follow a healthy diet, but said they need not worry about every calorie because their health and diet as a toddler could be more important for their baby. "There is some good news here for expectant mothers. Although there certainly are some harmful things to avoid during pregnancy, and some supplements to take to make sure some important bases are covered, the mother's body seems to do a good job of buffering overall nutritional supply to her growing baby," he said. "Within the bounds of a healthy balanced diet, the overall quantity of food that a mother eats is unlikely to have large effects on her baby's birth weight," he added. The findings emerged from a 30-year study that followed more than 3,000 pregnant women in the Philippines whose children have now begun to have babies of their own. Kuzawa said that while there was good evidence that unborn children benefit from their mothers taking extra folate and that they are harmed by toxins such as lead, mercury, excessive alcohol and bisphenol A, which is used to make some plastics, the picture was less clear on the roles of calories, protein, fat and carbohydrates. © 2014 Guardian News and Media Limited
By CATHERINE SAINT LOUIS Does chocolate really hurt dogs? It can, depending on their weight and how much they eat, so be vigilant this Valentine’s Day. Stimulants in chocolate can lead to vomiting, diarrhea, agitation and life-threatening elevated heart rates or seizures. “Dogs have no off button,” said Dr. Tina Wismer, the medical director of the ASPCA Animal Poison Control Center. “If you or I ate 10 percent of our body weight in chocolate, we’d have the same problems. A 10-pound dog can easily eat a pound of chocolate.” The darker the chocolate, the more toxic it is. For a 20-pound dog, 9 ounces of milk chocolate can cause seizures, but it takes only 1.5 ounces of baker’s chocolate, she said. Signs of chocolate poisoning usually appear six to 12 hours after ingestion, according to The Merck Veterinary Manual. “Seizures due to toxicity don’t stop unless you treat them,” Dr. Wismer said. So head to the emergency clinic or veterinarian if you come home to find your dog vomiting repeatedly and extremely agitated, and certainly if the pet is unconscious and its limbs are shaking. By contrast, dogs who vomit once and fall sleep can be watched at home, she said. Unlike cats, dogs like sweets. So it’s best to keep chocolate stored away and off countertops, which are no match for a motivated climber. © 2014 The New York Times Company
By JENNIFER CONLIN It is the moment “The Biggest Loser” viewers anticipate all season. That episode when the finalists emerge, one by one, to bare all — or rather less — to a waiting audience of millions. But on Tuesday night, when Rachel Frederickson, 24, walked onto the studio stage 155 pounds lighter than at the start of Season 15, the reaction was not one of awe, but shock, apparent even on the trainers’ frozen faces. In the few months since Ms. Frederickson, 5 feet 4 inches tall, had left the ranch for her home, her body had radically changed from the athletic 150 pounds she had weighed upon her departure to a gaunt sliver of herself, obvious despite her shimmering silver dress, strappy sandals and big grin. Ms. Frederickson, as the scale would soon reveal, now weighed 105 pounds, and having lost 59.62 percent of her body weight would also be the competition’s winner, making her $250,000 richer. But as confetti dropped all around her, few were celebrating on Twitter. “I feel like Rachel lost too much,” one woman wrote. “I had to turn away.” Another posted, “There needs to be a red line that disqualifies finalists for too much weight loss.” Kai Hibbard, a finalist on Season 3, was at her home in Alaska when another former contestant, whom she declined to name, sent her a message. “Have you seen tonight’s winner?” it read. “NBC is about to have a public-relations nightmare.” When Ms. Hibbard pulled up Ms. Frederickson’s winning photo, she promptly burst into tears. “Rachel doesn’t know what damage she has done to her body and her mind, and sadly she won’t until the spotlight goes away,” said Ms. Hibbard, 35, who seven years ago lost 118 pounds during her competition but has since spoken out publicly against the show’s extreme dieting and exercise regimen. © 2014 The New York Times Company
Ewen Callaway A study in mice and rats suggests that an imbalance in chloride ions during a child's development in the womb could be a factor for autism. Children with autism typically begin showing obvious symptoms, such as trouble making eye contact and slow language development, a year or more after birth. A study in mice and rats now hints that prenatal drug treatment could head off these problems. The findings, reported today in Science1, do not suggest that autism spectrum disorders can be prevented in children. But researchers not involved in the study say that they add support to a controversial clinical trial suggesting that some children with autism benefited from taking a common diuretic medication called bumetanide2. In that trial, a team led by neuroscientist Yehezkel Ben-Ari at the Mediterranean Institute of Neurobiology in Marseille gave 60 children bumetanide or a placebo daily for three months. Children who had less severe forms of autism showed mild improvements in social behaviour after taking the drug, and almost no adverse side effects were observed (see 'Diuretic drug improves symptoms of autism'). But autism researchers greeted the results with caution. Many pointed out that the study did not provide a clear biological mechanism that could explain how the drug improved the symptoms of the disorder. The latest study is an attempt to answer such criticisms by identifying a role for the neurotransmitter GABA. Studies in humans and animals have suggested that GABA, which in healthy people typically inhibits the activity in neurons, is altered in autism and instead activates some brain cells. © 2014 Nature Publishing Group,
Link ID: 19225 - Posted: 02.08.2014
By GRETCHEN REYNOLDS This winter’s frigid temperatures could be having one desirable side effect. They may be revving up your metabolism. Shivering in the cold sparks a series of biochemical reactions deep within the body that alters fat cells and bolsters metabolism, much as formal exercise does, according to a fascinating series of new experiments. The findings intimate that exercise and shivering are related in ways not previously suspected. For the new study, which was published Tuesday in Cell Metabolism, scientists affiliated with several branches of the National Institutes of Health recruited 10 healthy adult men and women and invited them to the lab on three separate occasions. There, the researchers drew blood and obtained small samples of muscle and fat cells. During one lab visit, the volunteers completed a short but very intense session of stationary bicycling, riding as hard as they could until they were exhausted. Then, on another day, they rode the bike at a gentle, easily sustained pace for an hour. Throughout these workouts, the laboratory temperature was maintained at a moderate 65 degrees or so. On their final visit, though, the researchers had each volunteer lie in bed, lightly clad, for 30 minutes as the lab’s temperature dropped from about 75 to a chilly 53 degrees. Monitors were placed on their skin to measure skin and muscle reactions, and by the end of the session, the volunteers were noticeably shivering. After each session, the scientists gathered more blood and other samples and started checking for changes. In particular, they wanted to see what was happening with the volunteers’ white and brown fat. © 2014 The New York Times Company
Link ID: 19204 - Posted: 02.05.2014
By GINA KOLATA For many obese adults, the die was cast by the time they were 5 years old. A major new study of more than 7,000 children has found that a third of children who were overweight in kindergarten were obese by eighth grade. And almost every child who was very obese remained that way. Some obese or overweight kindergartners lost their excess weight, and some children of normal weight got fat over the years. But every year, the chances that a child would slide into or out of being overweight or obese diminished. By age 11, there were few additional changes: Those who were obese or overweight stayed that way, and those whose weight was normal did not become fat. “The main message is that obesity is established very early in life, and that it basically tracks through adolescence to adulthood,” said Ruth Loos, a professor of preventive medicine at the Icahn School of Medicine at Mount Sinai in New York, who was not involved in the study. These results, surprising to many experts, arose from a rare study that tracked children’s body weight for years, from kindergarten through eighth grade. Experts say they may reshape approaches to combating the nation’s obesity epidemic, suggesting that efforts must start much earlier and focus more on the children at greatest risk. The findings, to be published Thursday in The New England Journal of Medicine, do not explain why the effect occurs. Researchers say it may be a combination of genetic predispositions to being heavy and environments that encourage overeating in those prone to it. But the results do provide a possible explanation for why efforts to help children lose weight have often had disappointing results. The steps may have aimed too broadly at all schoolchildren, rather than starting before children enrolled in kindergarten and concentrating on those who were already fat at very young ages. © 2014 The New York Times Company