Links for Keyword: Obesity

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 819

Obese women may have a "food learning impairment" that could explain their attitude to food, research from Yale School of Medicine suggests. Tests on groups of obese and healthy-weight people found that the obese women performed worst when asked to remember a sequence of food picture cards. Writing in Current Biology, Yale researchers tested 135 men and women. The findings could lead to new ways to tackle obesity, the study says. Study author Ifat Levy, assistant professor at Yale School of Medicine, said the difference in the performance of the obese women compared with the other groups was "really striking" and "significant". The tests looked at an individual's ability to learn and predict the appearance of pictures of food or money on coloured cards. The participants were told they would be given whatever appeared on these "reward" cards. In the first phase, the reward cards always followed a particular coloured card in a sequence. Later, the order was changed and the reward cards appeared following a different coloured card. During this time, participants were asked to predict the likelihood of a reward card appearing as the cards were shown one by one. The results showed that obese women performed worst because they overestimated how often the pictures of food, including pretzels or chocolate, appeared. Even after researchers had accounted for other factors, there was still a large difference in their learning performance. Prof Levy said: "This is not a general learning impairment, as obese women had no problem learning when the reward was money rather than food. BBC © 2014

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 19850 - Posted: 07.19.2014

By GRETCHEN REYNOLDS Sleep is essential for good health, as we all know. But a new study hints that there may be an easy but unrealized way to augment its virtues: lower the thermostat. Cooler bedrooms could subtly transform a person’s stores of brown fat — what has lately come to be thought of as “good fat” — and consequently alter energy expenditure and metabolic health, even into daylight hours. Until recently, most scientists thought that adults had no brown fat. But in the past few years, scanty deposits — teaspoonfuls, really — of the tissue have been detected in the necks and upper backs in many adults. This is important because brown fat, unlike the more common white stuff, is metabolically active. Experiments with mice have shown that it takes sugar out of the bloodstream to burn calories and maintain core temperature. A similar process seems to take place in humans. For the new study, published in June in Diabetes, researchers affiliated with the National Institutes of Health persuaded five healthy young male volunteers to sleep in climate-controlled chambers at the N.I.H. for four months. The men went about their normal lives during the days, then returned at 8 every evening. All meals, including lunch, were provided, to keep their caloric intakes constant. They slept in hospital scrubs under light sheets. For the first month, the researchers kept the bedrooms at 75 degrees, considered a neutral temperature that would not prompt moderating responses from the body. The next month, the bedrooms were cooled to 66 degrees, a temperature that the researchers expected might stimulate brown-fat activity (but not shivering, which usually begins at more frigid temperatures). The following month, the bedrooms were reset to 75 degrees, to undo any effects from the chillier room, and for the last month, the sleeping temperature was a balmy 81 degrees. Throughout, the subjects’ blood-sugar and insulin levels and daily caloric expenditures were tracked; after each month, the amount of brown fat was measured. © 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: 19844 - Posted: 07.17.2014

by Helen Thomson You are what your grandmother ate, potentially, but maybe not what your great grandmother consumed. A study in mice shows that undernourishment during pregnancy increases the chances that the next two generations will develop obesity and diabetes. But by then the slate is wiped clean. If the same holds true for humans, it may mean that stressful events in our lives affect our grandchildren's health, but not great-grandchildren. Environmental stresses cause chemical changes to DNA that turn genes on and off. Many researchers believe that these changes can be passed down through sperm and eggs – a mechanism known as epigenetic inheritance. Low-calorie diet For example, studies have linked pregnant mothers that were undernourished during the second world war with gene changes in their children that put them at higher risk of becoming obese or getting cancer. But what happens to later generations is not clear. To model this effect, Anne Ferguson-Smith at the University of Cambridge and her colleagues fed pregnant mice a diet containing 50 per cent fewer calories than usual from the 12th day of gestation until the birth, which is normally after about 20 days. Offspring were smaller than average and developed diabetes when fed a healthy diet. When the male pups had offspring, they were also at higher risk of becoming diabetic. The team analysed the sperm of the offspring from the undernourished mothers to see how many genes had had their expression altered by the addition or removal of a methyl group – an epigenetic change. The team found a decrease in methylation in 111 regions of the DNA compared with sperm from mice born to mothers fed a healthy diet. © Copyright Reed Business Information Ltd

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: 19816 - Posted: 07.12.2014

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.

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: 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

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: 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

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: 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

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: 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

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: 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

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: 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.

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: 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

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: 19709 - Posted: 06.07.2014

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

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: 19691 - 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

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: 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

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: 19677 - Posted: 05.31.2014

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

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: 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,

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