Links for Keyword: Obesity

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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,

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

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19538 - Posted: 04.26.2014

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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 19524 - Posted: 04.23.2014

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

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 19486 - Posted: 04.15.2014

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19439 - Posted: 04.02.2014

|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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 19365 - Posted: 03.15.2014

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19362 - Posted: 03.13.2014

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 19338 - Posted: 03.10.2014

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 19324 - Posted: 03.05.2014

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

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19292 - Posted: 02.26.2014

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

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 19187 - Posted: 01.30.2014

By Eric Niiler, It may come as a surprise that Finland — one of the least polluted, wealthiest countries, where average life expectancy is among the world’s highest — has the highest rate of Type 1 diabetes. Each year, there are about 58 cases diagnosed per 100,000 children; in the United States there are 24 cases per 100,000, according to the International Diabetes Federation. Some researchers suspect there may be a connection between Finland’s cleanliness and the incidence of the disease there. They are investigating whether the lack of exposure to a specific group of bacteria found in the intestine may be causing weaker immune systems in Finnish children, making them more susceptible to Type 1 diabetes. This so-called hygiene hypothesis — that cleaner living can result in a weaker immune system — has also been linked to ailments such as asthma, allergies and other autoimmune diseases. “We are working along the idea that we have a trigger which most likely is an infectious agent,” said Mikael Knip, a professor of pediatrics at the University of Helsinki who has been studying diabetes for 30 years. “There is an association between such infections and appearance of antibodies.” Just as there are microbes that trigger the disease, Knip says there are also some bacterial or viral infections that, if they occur at an early age, can protect a young child from developing Type 1 diabetes. Type 1 diabetes, which affects approximately 37 million people worldwide, is an autoimmune disease in which the body does not produce sufficient insulin, a hormone needed to break down sugars. Typically diagnosed in children, teens and young adults, the disease can eventually damage the eyes and organs such as the kidneys, and it increases the likelihood of stroke and heart failure. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19160 - Posted: 01.22.2014

Overweight and obese adults who drink diet pop also tend to eat more calories each day from food, a finding that hints at how relying on diet beverages for weight loss could be a mistake. In this week’s issue of the American Journal of Public Health, researchers from Johns Hopkins Bloomberg School of Public Health in Baltimore analyzed U.S. survey data for 24,000 people from 1999 to 2010. They looked for patterns in beverage consumption and calories. The sweet taste of beverages, whether from sugar or artificial sweeteners, seems to enhance our appetite and encourage cravings for sugar. (Rob Carr/Associated Press) Overweight consumers of diet beverages took in 1,965 in food calories a day compared with 1,874 calories among those in the same weight class who drank beverages sweetened with sugar, such as non-diet soda, sports drinks, fruit drinks and sweetened tea. As people increasingly switch to diet beverages, the focus on reducing sugar from drinks might not be enough to lose weight in the long term, the researchers concluded. "The switch from a sugary beverage to a diet beverage should be coupled with other changes in the diet, particularly reducing snacks," suggested lead author Sara Bleich. In the study, snacking patterns were generally the same between diet and sugary beverage drinkers. The researchers said the finding is consistent with evidence that the sweet taste of beverages, whether from sugar or artificial sweeteners, enhances our appetite and encourage cravings for sugar. © CBC 2014

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19148 - Posted: 01.18.2014

By ANAHAD O'CONNOR Scientists call it the obesity paradox, the notion that being overweight or moderately obese lowers the risk of an early death. They have documented the phenomenon in large population studies and in groups of patients with chronic diseases like hypertension and Type 2 diabetes. But now a new report, published on Wednesday in The New England Journal of Medicine, is calling the obesity paradox into question, at least for patients with Type 2 diabetes. The study, of nearly 12,000 people with the disease, found that there was no survival advantage for those who had a body mass index that put them in the overweight or obese categories. Instead, the researchers found that the diabetics with the lowest mortality rate were those who were considered normal weight. The study is among the largest to examine the obesity paradox among people with Type 2 diabetes, an illness that afflicts more than 25 million Americans. The authors argue that previous studies showing a protective effect of a high B.M.I. among diabetics were flawed because they were too small or failed to account for factors like smoking or undiagnosed illnesses that can contribute to low body weight but a shorter life span as well. The new study found that when smoking and other factors that can contribute to weight loss were accounted for, people in the highest B.M.I. groups had higher mortality rates. “I think the case is not necessarily closed,” said Deirdre K. Tobias, the lead author of the paper and a research fellow at the Harvard School of Public Health. “But at this point, there is no reason to believe that being overweight or obese would be protective for people with diabetes.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19138 - Posted: 01.16.2014

By ANDREW POLLACK Launch media viewer Kristin Tremblay helps make dinner at home in Gainesville, Fla. She has a disorder that makes her uncontrollably hungry. Rob C. Witzel for The New York Times Lisa Tremblay still recalls in horror the time her daughter Kristin pulled a hot dog crawling with ants from the garbage at a cookout and prepared to swallow it. Kristin has a rare genetic abnormality that gives her an incessant, uncontrollable hunger. Some people with the condition, called Prader-Willi syndrome, will eat until their stomach ruptures and they die. And, not surprisingly, many are obese. “She’s eaten dog food. She’s eaten cat food,” said Ms. Tremblay, who lives in Nokomis, Fla. When Kristin, now 28, was a child, neighbors once called social welfare authorities, thinking Kristin was not being fed because she complained of being hungry so much. Once an obscure and neglected disease, Prader-Willi is starting to attract more attention from scientists and pharmaceutical companies for a simple reason: It may shed some light on the much broader public health problems of overeating and obesity. “These are remarkable human models of severe obesity,” said Dr. Steven B. Heymsfield, a professor and former executive director of the Pennington Biomedical Research Center in Baton Rouge, La. “When we discover the underlying mechanism of these very rare disorders, they will shed light on garden-variety obesity.” One drug being developed to help obese people lose weight has shown some preliminary signs of success in patients with Prader-Willi. The drug, beloranib, is believed to work by reducing fat synthesis and increasing fat use. In a small trial, it reduced weight and body fat and lowered the food-seeking urge, according to the drug’s developer, Zafgen. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 19136 - Posted: 01.15.2014

By Stephen L. Macknik Hypoglycemia occurs when your blood sugar gets dangerously low, resulting in sweating, the feeling of weakness and dysphoria (the “don’t touch me” feeling you have when you’re sick and nauseous, possibly unconscious, as with the flu), and a variety of other symptoms. You basically go into a state similar to shock. The principal problem, however, arises from low blood sugar supply to the brain, resulting in impairment of function. It’s a common problem in diabetic non-compliance (not eating low-carbohydrate foods while diabetic), which is especially prevalent in the poor. SABRINA TAVERNISE, of The New York Times reported on a new study in the journal Health Affairs, by Seligman and colleagues of the University of California, San Francisco, in which they analyzed the prevalence of hypoglycemia in low income populations at risk for hypoglycemia, as a function of time since the patients’ households’ last pay day. They found that hypoglycemia increases at the end of a pay cycle in low-income diabetics. They thus concluded that low-income diabetic patients have low access to food at the end of the month, resulting in frank starvation and thus low blood sugar. I find this to be an unlikely scenario. It’s not that I don’t believe that low-income is tied to diabetes and hypoglycemia at the end of the pay cycle. I do believe it, and the Centers for Disease Control have determined that 8% of the population has diabetes, and that the burden is carried by low-income families. So I think the main effect, increased hypoglycemia in the poor at the end of their pay cycle, is correct (and Ms. Tavernise reports that experts in the field are happy with the methods, so I’m happy with them too as a non-expert in this field). © 2014 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19114 - Posted: 01.09.2014