Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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Erika Check Hayden Nearly 750,000 babies born each year in the United Kingdom are at risk of brain damage because of low oxygen during birth. Cooling babies who are at risk of brain damage provides long-lasting prevention of such injuries, researchers report today in the New England Journal of Medicine1. A team led by Denis Azzopardi, a neonatologist at King’s College London, lowered the body temperature of 145 full-term babies who were born after at least 36 weeks of gestation. All were at risk of brain damage because they had been deprived of oxygen during birth — a problem that is often caused by troubles with the placenta or umbilical cord, and affects nearly 750,000 babies a year in the United Kingdom. The researchers cooled the infants to between 33°C and 34°C for 72 hours, starting within 6 hours of birth. The technique is known to boost the chances that children avoid brain damage until they become toddlers2, but any longer-term benefits have remained unclear. The study finds treated babies had better mental and physical health than untreated infants through to ages 6 or 7: they were 60% more likely to have normal intelligence, hearing and vision. Those who survived to childhood also had fewer disabilities such as difficulty walking and seeing. "The bottom line is that this doubles a child’s chance of normal survival," says David Edwards, a neonatologist at King’s College London and an author of the study. Neonatologist David Rowitch from the University of California, San Francisco, who studies treatments for paediatric brain damage, says the new findings are important because they show sustained improvements. "This study is encouraging, adding to the weight of evidence showing both positive early indicators and also school-age benefits to hypothermia," Rowitch adds. © 2014 Nature Publishing Group,

Keyword: Development of the Brain
Link ID: 19814 - Posted: 07.10.2014

Adults with extreme obesity have increased risks of dying at a young age from cancer and many other causes including heart disease, stroke, diabetes, and kidney and liver diseases, according to results of an analysis of data pooled from 20 large studies of people from three countries. The study, led by researchers from the National Cancer Institute (NCI), part of the National Institutes of Health, found that people with class III (or extreme) obesity had a dramatic reduction in life expectancy compared with people of normal weight. The findings appeared July 8, 2014, in PLOS Medicine. “While once a relatively uncommon condition, the prevalence of class III, or extreme, obesity is on the rise. In the United States, for example, six percent of adults are now classified as extremely obese, which, for a person of average height, is more than 100 pounds over the recommended range for normal weight,” said Cari Kitahara, Ph.D., Division of Cancer Epidemiology and Genetics, NCI, and lead author of the study. “Prior to our study, little had been known about the risk of premature death associated with extreme obesity.” In the study, researchers classified participants according to their body mass index (BMI), which is a measure of total body fat and is calculated by dividing a person’s weight in kilograms by their height in meters squared. The 20 studies that were analyzed included adults from the United States, Sweden and Australia. These groups form a major part of the NCI Cohort Consortium, which is a large-scale partnership that identifies risk factors for cancer death. After excluding individuals who had ever smoked or had a history of certain diseases, the researchers evaluated the risk of premature death overall and the risk of premature death from specific causes in more than 9,500 individuals who were class III obese and 304,000 others who were classified as normal weight.

Keyword: Obesity
Link ID: 19812 - Posted: 07.10.2014

|By Emilie Reas A poor diet can eat away at brain health. Now a study in Neurology helps elucidate why. It suggests that eating a lot of sugar or other carbohydrates can be hazardous to both brain structure and function. Diabetes, which is characterized by chronically high levels of blood glucose, has been linked to an elevated risk of dementia and a smaller hippocampus, a brain region critical for memory. The new study sought to identify whether glucose had an effect on memory even in people without the disease because having it could induce other brain changes that confound the data. In the experiment, researchers at the Charité University Medical Center in Berlin evaluated both short- and long-term glucose markers in 141 healthy, nondiabetic older adults. The participants performed a memory test and underwent imaging to assess the structure of their hippocampus. Higher levels on both glucose measures were associated with worse memory, as well as a smaller hippocampus and compromised hippocampal structure. The researchers also found that the structural changes partially accounted for the statistical link between glucose and memory. According to study co-author Agnes Flöel, a neurologist at Charité, the results “provide further evidence that glucose might directly contribute to hippocampal atrophy,” but she cautions that their data cannot establish a causal relation between sugar and brain health. These findings indicate that even in the absence of diabetes or glucose intolerance, higher blood sugar may harm the brain and disrupt memory function. Future research will need to characterize how glucose exerts these effects and whether dietary or lifestyle interventions might reverse such pathological changes. © 2014 Scientific American

Keyword: Obesity
Link ID: 19798 - Posted: 07.08.2014

Priyanka Pulla Not everyone who is obese is unhealthy. So say some researchers, who note that a small fraction of overweight people have normal blood sugar levels and blood pressure, and are thus “healthy obese.” Now, scientists have identified a single protein that seems to determine whether obesity is harmful or benign. The protein is a new player in our understanding of how obesity leads to disease, says Alan Saltiel, a cell biologist at the University of Michigan, Ann Arbor, who was not involved in the study. It is well known that obesity leads to a wide range of health problems, from diabetes to heart disease to cancer. So established is the link between extra pounds and illness that last year the American Medical Association voted to classify obesity itself as a disease. Although some researchers have suggested that a small number of obese people are healthy, that idea remains controversial. Instead, the emerging consensus is that healthy obesity is a transient phase, says Ravi Retnakaran, an endocrinologist at the Leadership Sinai Centre for Diabetes in Toronto, Canada. Sooner or later, he says, these outliers will develop metabolic syndrome, a condition in which glucose, cholesterol, and lipid levels soar, causing diabetes and heart disease. In fact, so-called healthy obese people may already have early signs of disease, which are too muted to show up on routine tests. In a study of more than 14,000 metabolically healthy Korean people last year, scientists found early plaque buildup in the arteries of obese subjects more often than they did in the lean ones. © 2014 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 19797 - Posted: 07.04.2014

By LISA SANDERS, M.D. On Wednesday, we challenged Well readers to solve the case of a middle-aged woman who suddenly began to have episodes of confusion caused by low blood sugars. Her endocrinologist thought she might have an insulinoma, an insulin-producing tumor of the pancreas, but the testing he did seemed to rule out that diagnosis. Nearly 200 of you took on the challenge of trying to figure out what was causing her life-threatening drops in blood sugar level. The correct diagnosis is… Insulinoma The first respondent to make the diagnosis was Karen Unkel of Kinder, La. She is not a doctor but has a longstanding interest in hypoglycemia that allowed her to recognize the disease even in the face of an apparently negative work-up. Well done, Ms. Unkel. An insulinoma is a rare tumor of pancreatic tissue that makes and secretes insulin independently of blood glucose levels. This results in episodes of hypoglycemia that can be quite severe, even life-threatening. The diagnosis is suspected when a patient fulfills what is known as Whipple’s triad: 1) symptoms of hypoglycemia 2) associated with low measured blood sugar and 3) which improve when blood sugar is raised to the normal range. The diagnosis is made when doctors show that the patient is making too much insulin given his or her blood sugar level. Measuring insulin levels is not always accurate because insulin is processed rapidly in the body and because it is difficult to distinguish between insulin made naturally in the pancreas and any insulin that the patient might be injecting. What is measured instead is something known as C-peptide. Insulin is first made as a larger molecule known as proinsulin. When blood sugar rises, an extra bit is shaved off the molecule; that extra bit is C-peptide, and both the resulting insulin and C-peptide are released into the bloodstream. © 2014 The New York Times Company

Keyword: Obesity; Hormones & Behavior
Link ID: 19791 - Posted: 07.04.2014

By ANDREW POLLACK It is a tantalizingly simple idea for losing weight: Before meals, swallow a capsule that temporarily swells up in the stomach, making you feel full. Now, some early results for such a pill are in. And they are only partly fulfilling. People who took the capsule lost 6.1 percent of their weight after 12 weeks, compared with 4.1 percent for those taking a placebo, according to results presented Sunday at an endocrinology meeting in Chicago. Gelesis, the company developing the capsule, declared the results a triumph and said it would start a larger study next year aimed at winning approval for the product, called Gelesis100. “I’m definitely impressed, absolutely,” Dr. Arne V. Astrup, head of the department of nutrition, exercise and sports at the University of Copenhagen in Denmark and the lead investigator in the study, said in an interview. He said the physical mode of action could make the product safer than many existing diet drugs, which act chemically on the brain to influence appetite. But Dr. Daniel H. Bessesen, an endocrinologist at the University of Colorado who was not involved in the study, said weight loss of 2 percent beyond that provided by a placebo was “very modest.” “It doesn’t look like a game changer,” he said. Gelesis, a privately held company based in Boston, is one of many trying to come up with a product that can provide significant weight loss without bariatric surgery. Two new drugs — Qsymia from Vivus, and Belviq from Arena Pharmaceuticals and Eisai — have had disappointing sales since their approvals in 2012. Reasons include modest effectiveness, safety concerns, lack of insurance reimbursement and a belief among some doctors and overweight people that obesity is not a disease. © 2014 The New York Times Company

Keyword: Obesity
Link ID: 19758 - Posted: 06.23.2014

Jennifer Couzin-Frankel What if you could trick your body into thinking you were racing on a treadmill—and burning off calories at a rapid clip—while simply walking down the street? Changing our rate of energy expenditure is still far into the future, but work in mice explores how this might happen. Two teams of scientists suggest that activating immune cells in fat can convert the tissue from a type of fat that stores energy to one that burns it, opening up potential new therapies for obesity and diabetes. There are two types of fat in humans: white adipose tissue, which makes up nearly all the fat in adults, and brown adipose tissue, which is found in babies but disappears as they age. Brown fat protects against the cold (it’s also common in animals that hibernate), and researchers have found that mice exposed to cold show a temporary “browning” of some of their white fat. The same effect occurred in preliminary studies of people, where the browning—which creates a tissue known as beige fat—helps generate heat and burn calories. But cold is “the only stimulus we know that can increase beige fat mass or brown fat mass,” says Ajay Chawla, a physiologist at the University of California (UC), San Francisco. He wanted to better understand how cold caused this change in the tissue and whether there was a way to mimic cold and induce browning some other way. A few years ago, Chawla’s group had reported that cold exposure activated macrophages, a type of immune cell, in white adipose tissue. To further untangle what was going on, Chawla, his postdoc Yifu Qiu, and their colleagues used mice that lacked interleukin-4 (IL-4) and interleukin-13, proteins that help activate macrophages. When they exposed these mice to the cold, the animals developed far fewer beige fat cells than did normal animals, suggesting that macrophages were key to browning of white fat. © 2014 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 19732 - Posted: 06.14.2014

by Lauren Hitchings Being cold can burn calories but no one wants to freeze just to sculpt their muffin-top. Soon we may not have to. Researchers have identified immune molecules triggered by cold temperatures that make obese mice lose weight – without the need for the mercury to drop. Humans and other mammals respond to cold in two ways. On the surface, we shiver to burn energy and produce a quick burst of heat. On a deeper level, as Ajay Chawla at the University of California, San Francisco, and his colleagues recently discovered, cold temperatures send signals to immune molecules called macrophages. They, in turn, release other molecules that convert energy-storing white fat into another type that burns energy. Babies and some hibernating animals have lots of these energy-burning cells – known as brown fat – but it almost all disappears as people age. We now know that cold temperatures can trigger a "browning" of white fat in adults – converting some of their white fat into an intermediate form called beige fat. It may seem counterintuitive for our bodies to use up fat stores when we get cold, but think of the white fat as the wooden walls of a log cabin – having them there is a good way to keep warm generally, but when the cold sets in, you're going to want firewood – brown or beige fat, to burn. Now Chawla's team have identified interleukin-4 and interleukin-13 as the signalling molecules that kick-start the transition of white fat to its darker counterpart. What's more, by injecting mice with interleukin-4 four times over a period of eight days, the team was able to bypass the physical cold stimulus and activate the pathway biochemically. © Copyright Reed Business Information Ltd.

Keyword: Obesity
Link ID: 19719 - Posted: 06.10.2014

Jennifer Couzin-Frankel What if you could trick your body into thinking you were racing on a treadmill—and burning off calories at a rapid clip—while simply walking down the street? Changing our rate of energy expenditure is still far into the future, but work in mice explores how this might happen. Two teams of scientists suggest that activating immune cells in fat can convert the tissue from a type of fat that stores energy to one that burns it, opening up potential new therapies for obesity and diabetes. There are two types of fat in humans: white adipose tissue, which makes up nearly all the fat in adults, and brown adipose tissue, which is found in babies but disappears as they age. Brown fat protects against the cold (it’s also common in animals that hibernate), and researchers have found that mice exposed to cold show a temporary “browning” of some of their white fat. The same effect occurred in preliminary studies of people, where the browning—which creates a tissue known as beige fat—helps generate heat and burn calories. But cold is “the only stimulus we know that can increase beige fat mass or brown fat mass,” says Ajay Chawla, a physiologist at the University of California (UC), San Francisco. He wanted to better understand how cold caused this change in the tissue and whether there was a way to mimic cold and induce browning some other way. A few years ago, Chawla’s group had reported that cold exposure activated macrophages, a type of immune cell, in white adipose tissue. To further untangle what was going on, Chawla, his postdoc Yifu Qiu, and their colleagues used mice that lacked interleukin-4 (IL-4) and interleukin-13, proteins that help activate macrophages. When they exposed these mice to the cold, the animals developed far fewer beige fat cells than did normal animals, suggesting that macrophages were key to browning of white fat. © 2014 American Association for the Advancement of Science

Keyword: Obesity
Link ID: 19709 - Posted: 06.07.2014

A moderate dose of MDMA. commonly known as Ecstasy or Molly, that is typically nonfatal in cool, quiet environments can be lethal in rats exposed to conditions that mimic the hot, crowded, social settings where the drug is often used by people, a study finds. Scientists have identified the therapeutically-relevant cooling mechanism to enable effective interventions when faced with MDMA-induced hyperthermia. The study, publishing tomorrow in the Journal of Neuroscience, was conducted by researchers at the National Institute on Drug Abuse’s Intramural Research Program (NIDA IRP). NIDA is a part of the National Institutes of Health. While MDMA can have a range of adverse health effects, previous studies have shown that high doses of MDMA increase body temperature, while results with moderate doses were inconsistent. This has led some people to assume that the drug is harmless if taken in moderation. However, this study shows that in rats even moderate doses of MDMA in certain environments can be dangerous because it interferes with the body’s ability to regulate temperature. “We know that high doses of MDMA can sharply increase body temperature to potentially lead to organ failure or even death,” said NIDA Director Dr. Nora D. Volkow. “However, this current study opens the possibility that even moderate doses could be deadly in certain conditions.” It is impossible to predict who will have an adverse reaction even to a low dose of MDMA. However, in this study scientists gave the rats low to moderate doses that have been shown in past studies to not be fatal. They monitored the rats to determine drug-induced changes in brain and body temperature and in the body’s ability to cool itself through blood vessel dilation. When rats were alone and in a room-temperature environment, a moderate dose of MDMA modestly increased brain and body temperature and moderately diminished the rats’ ability to eliminate excessive heat. However, when researchers injected the same dose in rats that were either in a warmer environment or in the presence of another rat in the cage, brain temperature increased, causing death in some rats. These fatal temperature increases were because the drug interfered with the body’s ability to eliminate heat.

Keyword: Drug Abuse
Link ID: 19695 - Posted: 06.05.2014

By GRETCHEN REYNOLDS If you are aiming to lose weight by revving up your exercise routine, it may be wise to think of your workouts not as exercise, but as playtime. An unconventional new study suggests that people’s attitudes toward physical activity can influence what they eat afterward and, ultimately, whether they drop pounds. For some time, scientists have been puzzled — and exercisers frustrated — by the general ineffectiveness of exercise as a weight-loss strategy. According to multiple studies and anecdotes, most people who start exercising do not lose as much weight as would be expected, given their increased energy expenditure. Some people add pounds despite burning hundreds of calories during workouts. Past studies of this phenomenon have found that exercise can increase the body’s production of appetite hormones, making some people feel ravenous after even a light workout and prone to consume more calories than they expended. But that finding, while intriguing, doesn’t fully explain the wide variability in people’s post-exercise eating habits. So, for the new study, published in the journal Marketing Letters, French and American researchers turned to psychology and the possible effect that calling exercise by any other name might have on people’s subsequent diets. In that pursuit, the researchers first recruited 56 healthy, adult women, the majority of them overweight. The women were given maps detailing the same one-mile outdoor course and told that they would spend the next half-hour walking there, with lunch to follow. Half of the women were told that their walk was meant to be exercise, and they were encouraged to view it as such, monitoring their exertion throughout. The other women were told that their 30-minute outing would be a walk purely for pleasure; they would be listening to music through headphones and rating the sound quality, but mostly the researchers wanted them to enjoy themselves. When the women returned from walking, the researchers asked each to estimate her mileage, mood and calorie expenditure. © 2014 The New York Times Company

Keyword: Obesity; Emotions
Link ID: 19691 - Posted: 06.04.2014

by Catherine de Lange Could your ideal diet be written in your genes? That's the promise of nutrigenomics, which looks for genetic differences in the way people's bodies process food so that diets can be tailored accordingly. The field had a rocky start after companies overhyped its potential, but with advances in genetic sequencing, and a slew of new studies, the concept is in for a reboot. Last week, Nicola Pirastu at the University of Trieste, Italy, and his colleagues told the European Society of Human Genetics meeting in Milan that diets tailored to genes that are related to metabolism can help people lose weight. The team used the results of a genetic test to design specific diets for 100 obese people that also provided them with 600 fewer calories than usual. A control group was placed on a 600-calorie deficit, untailored diet. After two years, both groups had lost weight, but those in the nutrigenetic group lost 33 per cent more. They also took only a year to lose as much weight as the group on the untailored diet lost in two years. If this is shown to work in bigger, randomised trials, it would be fantastic, says Ana Valdes, a genetic epidemiologist at the University of Nottingham, UK. Some preliminary information will soon be available from Europe's Food4Me project. It is a study of 1200 people across several countries who were given either standard nutrition advice, or a similarly genetically tailored diet. "It's testing whether we can get bigger changes in diet using a personalised approach, and part of that is using genetic information," says team member John Mathers, director of the Human Nutrition Research Centre at Newcastle University, UK. © Copyright Reed Business Information Ltd.

Keyword: Chemical Senses (Smell & Taste); Obesity
Link ID: 19690 - Posted: 06.04.2014

By SANFORD E. DeVOE IN recent years we have seen plenty of studies of the impact of fast food on our bodies. But what about our psychological health? It stands to reason that fast food would have an effect on our mental state. From its production to its consumption, fast food both embodies and symbolizes speed and instant gratification. Moreover, through extensive franchising and large advertising budgets, fast-food companies shape many of the cues in our everyday environment. While the ubiquity of fast food is undoubtedly driven by consumer demand for instant gratification, it may also play a role in exacerbating that very impatience — and not just for food, but in many facets of our lives. In a series of recent papers, I joined two of my colleagues at the University of Toronto, Julian House and Chen-Bo Zhong, in examining this question. We began our experiments by prompting participants with reminders of fast food, like pictures of fast-food logos or having them recall recent experiences of eating fast food. We then gave them a number of tasks to complete. Across several studies, we found that thoughts of fast food spurred participants to hurry through reading a paragraph describing their city; express a greater desire for timesaving products; report less happiness from savoring a beautiful opera duet; and save less for tomorrow. These findings — that our associations with fast food can induce greater impatience — are interesting in their own right, but they are especially important because of the pervasiveness of fast food in our modern environment. We also took our investigation a step further, to consider whether the prevalence of fast-food restaurants in our neighborhoods might undercut our well-being. There is a lengthy epidemiology literature demonstrating a link between the number of fast-food restaurants and obesity. While the consequences of fast food for our health seem quite obvious, we wondered what these same methods might reveal regarding impatience. © 2014 The New York Times Company

Keyword: Obesity
Link ID: 19680 - Posted: 06.02.2014

By NICHOLAS BAKALAR Several observational studies have suggested that drinking diet soda may encourage weight gain, but a new randomized trial finds that it is not so. The study, published in the June issue of Obesity and paid for by the American Beverage Association, suggests that diet drinks may be better for weight loss than plain water. The study tested 303 men and women who followed the same diet for 12 weeks. But half were randomly assigned to drink at least 24 ounces of water daily, and the rest the same amount of artificially sweetened drinks. After controlling for age, sex, ethnicity and initial weight and blood pressure, researchers found that those who drank diet drinks lost an average of 14.2 pounds, compared with a 10-pound loss for the water drinkers. The mechanism, the authors write, is unclear, but the group on diet drinks reported slightly lower scores on a questionnaire measuring the degree of feelings of hunger. “There’s no magic in diet soda,” said the lead author, James O. Hill, a professor of health and wellness at the University of Colorado. But the less intense feelings of hunger among the drinkers, he said, may have made it easier for them to adhere to the diet. “From everything we know about diet soda,” he continued, “this result was totally expected. There’s not a single randomized controlled trial that shows the opposite.” © 2014 The New York Times Company

Keyword: Obesity
Link ID: 19677 - Posted: 05.31.2014

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

Keyword: Evolution
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

Keyword: Stress; Neuroimmunology
Link ID: 19655 - Posted: 05.25.2014

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

Keyword: Obesity
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,

Keyword: Obesity
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

Keyword: Obesity
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

Keyword: Obesity; Genes & Behavior
Link ID: 19538 - Posted: 04.26.2014