Links for Keyword: Obesity

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By Meghan Rosen Skinniness could be contagious. Gut bacteria from thin people can invade the intestines of mice carrying microbes from obese people. And these invaders can keep mice from getting tubby, researchers report in the Sept. 6 Science. “It’s very surprising,” says molecular microbiologist Andreas Schwiertz of the University of Giessen in Germany, who was not involved in the work. “It’s like a beneficial infection.” But the benefits come with a catch. The invading microbes drop in and get to work only when mice eat healthy food. Even fat-blocking bacteria can’t fight a bad diet, suggests study leader Jeffrey Gordon, a microbiologist at Washington University in St. Louis. In recent years, researchers have collected clues that suggest that gut microbes can tweak people’s metabolism. Fat and thin people have different microbes teeming in their intestines, for example. And normal-weight mice given microbes from obese mice pack on extra fat, says coauthor Vanessa Ridaura, also of Washington University. These and other hints have led researchers to experiment with fecal transplants to flush out bad gut microbes and dump in good ones. The transplants can clear up diarrhea and may even help some obese people regain insulin sensitivity. But feces can house dangerous microbes as well as friendly ones. “We want to make therapies that are more standardized — and more appealing,” says gastroenterologist Josbert Keller of the Haga Teaching Hospital in The Hague, Netherlands. © Society for Science & the Public 2000 - 2013

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: 18616 - Posted: 09.07.2013

By Tamar Haspel, American eaters love a good villain. Diets that focus on one clear bad guy have gotten traction even as the bad guy has changed: fat, carbohydrates, animal products, cooked food, gluten. And now Robert Lustig, a pediatric endocrinologist at the University of California at San Francisco, is adding sugar to the list. His book “ Fat Chance: Beating the Odds Against Sugar, Processed Food, Obesity, and Disease ” makes the case that sugar is almost single-handedly responsible for Americans’ excess weight and the illnesses that go with it. “Sugar is the biggest perpetrator of our current health crisis,” says Lustig, blaming it for not just obesity and diabetes but also for insulin resistance, cardiovascular disease, stroke, even cancer. “Sugar is a toxin,” he says. “Pure and simple.” His target is one particular sugar: fructose, familiar for its role in making fruit sweet. Fruit, though, is not the problem; the natural sugar in whole foods, which generally comes in small quantities, is blameless. The fructose in question is in sweeteners — table sugar, high-fructose corn syrup, maple syrup, honey and others — which are all composed of the simple sugars fructose and glucose, in about equal proportions. Although glucose can be metabolized by every cell in the body, fructose is metabolized almost entirely by the liver. There it can result in the generation of free radicals ( damaged cells that can damage other cells) and uric acid ( which can lead to kidney disease or gout ), and it can kick off a process called de novo lipogenesis, which generates fats that can find their way into the bloodstream or be deposited on the liver itself. These byproducts are linked to obesity, insulin resistance and the group of risk factors linked to diabetes, heart disease and stroke. (Lustig gives a detailed explanation of fructose metabolism in a well-viewed YouTube video called “Sugar: The Bitter Truth.”) © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 18615 - Posted: 09.07.2013

By Stephen L. Macknik A new study in the Journal of Neuroscience suggests that a part of the brain critical to motivation, the substantia nigra, which is famous for its role as a primary culprit in Parkinson’s Disease, is central to the relationship between feeding and drug seeking behavior. Neuroscientists have known for some time that acquisition of drug seeking behavior is higher in people whose food supply is restricted. But nobody knew why. Neuroscientist Sarah Branch and her colleagues at the University of Texas Health Science Center in San Antonio have now discovered a critical neural mechanism that links food restriction to enhanced drug efficacy. They mildly restricted the diet of mice and found that it caused certain neurons in the substantia nigra burst in activity. These neurons, called dopamine neurons, are implicated in the feeling of pleasure felt with drugs of abuse. It’s as if the neurons are preparing to reward their owner the moment that food is found, perhaps to reinforce food acquisition. When the mice were given cocaine as well, the bursty effect in food restricted mice was enhanced even further, which leads to increased drug seeking behavior too. Interestingly, they found that the effects could persist up to ten days after the food restriction ended. The results suggest that there may be a way to enhance drug efficacy in patients with chronic pain. But it also serves as a cogent reminder that the substantia nigra is central to how the brain generates motivational behavior. When the substantia nigra dies, you get Parkinson’s, and you find it difficult to motivate yourself to even pass through a doorway. © 2013 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18578 - Posted: 08.29.2013

By Melinda Wenner Moyer Few phenomena have created as divisive a rift recently among health professionals as the so-called “obesity paradox,” the repeated finding that obese people with certain health conditions live longer than slender people with the same ailments. And when a January meta-analysis involving nearly three million research subjects suggested that overweight people in the general population also live longer than their slimmer counterparts, the head of Harvard University’s nutrition department, Walter Willett, called the work “a pile of rubbish.” A few new studies suggest that these paradoxes may largely be artifacts of flawed research designs, but some experts disagree, accusing the new studies of being inaccurate. Among the biggest questions raised by this new research is the impact of age: whether obesity becomes more or less deadly as people get older and why. The January meta-analysis, led by U.S. Centers for Disease Control and Prevention senior scientist Katherine Flegal, pooled data from 97 studies of the general global population and reported that, in sum, overweight individuals—those with a body mass index of 25 to 29.9—were 6 percent less likely to die over various short time periods than people of normal weight (with a BMI 18.5 to 24.9) were. For people over the age of 65, however, being overweight conferred a 10 percent survival advantage. Flegals' findings also suggest that obesity, which has always been considered a major health risk, is not always dangerous and that it becomes less so with age: Adults with grade 1 obesity (BMIs of 30 to 34.9), she found, were no more likely to die than were normal weight adults; for grade 2 obesity (BMI of 35 to 39.9), the increased death risk for adults of all ages was 29 percent, but restricting the analysis to adults over the age of 65, the increased death risk associated with grade 2 obesity was not statistically significant.. The older a person is, the analysis seemed to say, the safer extra pounds become. © 2013 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: 18553 - Posted: 08.24.2013

By Cristy Gelling Repairing a faulty communication line between the gut and the brain can quell the urge to overeat, an experiment that cured chubby mice of their junk food addiction indicates. A similar strategy might be used to treat compulsive eating in people. Some scientists have proposed that, in both mice and humans, overeating can resemble drug addiction; the more food a person consumes, the less responsive the brain becomes to the pleasure of eating. By restoring normal communication between the gut and brain, researchers were able to resensitize overfed rodents to the pleasures of both fatty and healthy foods. "The therapeutic implications are huge,” says neuroscientist Paul Kenny of the Scripps Research Institute in Jupiter, Fla., who was not involved in the study. In the brain, a chemical called dopamine surges in response to pleasurable experiences like eating, sex and taking drugs. But brain-scanning studies suggest that obese individuals have muted dopamine reponses to food. These changes could lead overeaters to seek more and more food to satisfy their cravings, suggests study leader Ivan de Araujo of Yale University. De Araujo and his colleagues looked for ways to restore the dopamine response of overfed mice by studying the signals sent by their guts. In previous work, the researchers found that mice get a dopamine rush when fat is introduced directly into the small intestine via catheters. This shows that the gut communicates with the brain’s reward center even when the mouse can’t taste food. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18522 - Posted: 08.17.2013

Brian Owens Too much sugar is bad for you, but how much, exactly, is too much? A study in mice has found that the animals' health and ability to compete can be harmed by a diet that has sugar levels equivalent to what many people in the United States currently consume. High-sugar diets are associated not only with obesity and diabetes, but also with other human conditions such as coronary heart disease. However, the exact causal links for many of these has not been established. When studies are done in mice to evaluate health effects of sugar, the doses given are often so high, and outside the range of equivalent human consumption, that it is hard to tell conclusively whether the results are relevant to people. “Nobody has been able to show adverse effects at human-relevant levels,” says Wayne Potts, an evolutionary biologist at the University of Utah in Salt Lake City. But in a study published today in Nature Communications1, Potts and his colleagues looked at what happens under conditions comparable to the lifestyles of a substantial number of people in the United States. The researchers bred a pair of wild mice captured by Potts in a bakery, and fed offspring a diet in which 25% of the calories came from sugar. This is the maximum 'safe' level recommended by the US National Academies and by the US Department of Agriculture, and such a diet is consumed by around 13–25% of the US population. The safe level is roughly equivalent to drinking three cans of sugary drinks a day but having an otherwise sugar-free diet. © 2013 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: 18509 - Posted: 08.14.2013

Heidi Ledford A procedure increasingly used to treat obesity by reducing the size of the stomach also reprogrammes the intestines, making them burn sugar faster, a study in diabetic and obese rats has shown. If the results, published today in Science1, hold true in humans, they could explain how gastric bypass surgery improves sugar control in people with diabetes. They could also lead to less invasive ways to produce the same effects. “This opens up the idea that we could take the most effective therapy we have for obesity and diabetes and come up with ways to do it without a scalpel,” says Randy Seeley, an obesity researcher at the University of Cincinnati in Ohio, who was not involved in the work. As rates of obesity and diabetes skyrocket in many countries, physicians and patients are turning to operations that reconfigure the digestive tract so that only a small part of the stomach is used. Such procedures are intended to allow people to feel full after smaller meals, reducing the drive to consume extra calories. But clinical trials in recent years have shown that they can also reduce blood sugar levels in diabetics, even before weight is lost2, 3. “We have to think about this surgery differently,” says Seeley. “It’s not just changing the plumbing, it’s altering how the gut handles glucose.” © 2013 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: 18412 - Posted: 07.27.2013

By GINA KOLATA The mice were eating their usual chow and exercising normally, but they were getting fat anyway. The reason: researchers had deleted a gene that acts in the brain and controls how quickly calories are burned. Even though they were consuming exactly the same number of calories as lean mice, they were gaining weight. So far, only one person — a severely obese child — has been found to have a disabling mutation in the same gene. But the discovery of the same effect in mice and in the child — a finding published Wednesday in the journal Science — may help explain why some people put on weight easily while others eat all they want and seem never to gain an ounce. It may also offer clues to a puzzle in the field of obesity: Why do studies find that people gain different amounts of weight while overeating by the same amount? Scientists have long thought explanations for why some people get fat might lie in their genes. They knew body weight was strongly inherited. Years ago, for example, they found that twins reared apart tended to have similar weights and adoptees tended to have weights like their biological parents, not the ones who reared them. As researchers developed tools to look for the actual genes, they found evidence that many — maybe even hundreds — of genes may be involved, stoking appetites, making people voraciously hungry. This rare gene-disabling mutation, though, is intriguing because it seems to explain something different, a propensity to pile on pounds even while eating what should be a normal amount of food. Investigators are now searching for other mutations of the same gene in fat people that may have a similar, but less extreme effect. The hope is that in the long term, understanding how this gene affects weight gain might lead to treatments for obesity that alter the rate at which calories are burned. © 2013 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: 18394 - Posted: 07.20.2013

By GRETCHEN REYNOLDS Two newly published studies investigate the enticing possibility that we might one day be able to gain the benefits of exercise by downing a pill, rather than by actually sweating. But while some of the research holds out promise for an effective workout pill, there remains the question of whether such a move is wise. The more encouraging of the new studies, which appears this week in Nature Medicine, expands on a major study published last year in Nature. In that study, researchers at the Scripps Research Institute in Jupiter, Fla., reported that a compound they had created and injected into obese mice increased activation of a protein called REV-ERB, which is known to partially control animals’ circadian rhythms and internal biological clocks. The injected animals lost weight, even on a high-fat diet, and improved their cholesterol profiles. Unexpectedly, the treated mice also began using more oxygen throughout the day and expending about 5 percent more energy than untreated mice, even though they were not moving about more than the other animals. In fact, in most cases, they were more physically lazy and inactive than they had been before the injections. The drug, it seemed, was providing them with a workout, minus the effort. Intrigued, the Scripps scientists, in conjunction with researchers from the Pasteur Institute in France and other institutions, set out to see what their compound might be doing inside muscles to provide this ersatz exercise. They knew that their drug increased the potency of the REV-ERB protein, but no one yet knew what REV-ERB actually does in muscles. So they began by developing a strain of mice that could not express very much of the protein in their muscle cells. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 18384 - Posted: 07.18.2013

by Sarah C. P. Williams Researchers think they've hit on why a common obesity gene causes weight gain: Those who carry a version of it don't feel full after eating and take in extra calories. That's because the variant of the FTO gene in question, which one in six individuals carry, leads to higher levels of ghrelin, a hormone involved in mediating appetite and the body's response to food, researchers have discovered. While most studies on FTO have relied on mice, the new work analyzed blood samples and brain scans from humans. "This is a very exciting piece of research," says geneticist Andrew Hattersley of the Peninsula Medical School in Exeter, U.K., who was not involved in the new study. "There is a lot of work that's been done on the mechanism of FTO in animals, but you have to be careful about applying those lessons to people. So it's nice to finally see work done in humans." Hattersley was part of a team that in 2007 reported that people who had one version of the FTO gene, called AA, weighed an average of 3 kilograms more than those with the TT version of the gene. Since then, studies in mice have shown that in everyone, there are high levels of the FTO protein in brain areas that control energy balance. Researchers have also found that animals with the AA version tend to eat more and prefer high-fat food compared with those with the TT version. But why FTO had this effect wasn't known. © 2010 American Association for the Advancement of Science.

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: 18381 - Posted: 07.16.2013

by Elizabeth Norton Transforming fat cells into calorie-burning machines may sound like the ultimate form of weight control, but the idea is not as far-fetched as it sounds. Unexpectedly, some fat cells directly sense dropping temperatures and release their energy as heat, according to a new study; that ability might be harnessed to treat obesity and diabetes, researchers suggest. Fat is known to help protect animals from the cold—and not only by acting as insulation. In the early 1990s, scientists studying mice discovered that cold temperatures trigger certain fat cells, called brown adipose tissue, to release stored energy in the form of heat—to burn calories, in other words. Researchers have always assumed this mechanism was an indirect response to the physiological stress of cold temperatures, explains cell biologist Bruce Spiegelman of Harvard Medical School, Boston. The activation of brown fat seems to start with sensory neurons throughout the body informing the brain of a drop in temperature. In response the brain sends out norepinephrine, the chief chemical messenger of the sympathetic nervous system, which mobilizes the body to cope with many situations. In experimental animals, stimulating norepinephrine receptors triggered brown adipose tissue to release its energy and generate heat, while animals bred to be missing these receptors were unable to mount the same fat cell response. People also have brown adipose tissue that generates heat when the body is cold. And unlike white fat, which builds up around the abdomen and contributes to many disorders including heart disease and diabetes, this brown fat is found in higher proportions in leaner people and seems to actively protect against diabetes. © 2010 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: 18334 - Posted: 07.02.2013

By JANE E. BRODY Most people know that obesity can result in serious health problems, yet many of us continue to focus on its cosmetic consequences rather than its risks to health. This distorted view may change now that the American Medical Association has finally labeled obesity a disease, not just a risk factor for other disorders. Last month, the organization recognized that obesity is a verifiable illness that warrants far more attention than physicians, patients and insurers currently give it. The designation may change how aggressively doctors treat obesity, foster the development of new therapies, and lead to better coverage byinsurers. After all, the price of not treating obesity is now in the stratosphere. Obesity-related health conditions cost the nation more than $150 billion and result in an estimated 300,000 premature deaths each year. If the population’s weight gain is not soon capped (or better yet, reversed), experts predict that half of adults in America will be obese by 2040. The A.M.A. has said in effect that it is medicine’s responsibility to provide the knowledge and tools needed to curb this runaway epidemic. On June 19, James Gandolfini, the hefty award-winning actor who portrayed Tony Soprano in “The Sopranos,” died at 51, apparently of a heart attack, while on vacation in Italy. Even if genetics played a role, Mr. Gandolfini’s weight contributed significantly to his risk of sudden cardiac death. Not a week earlier, a 46-year-old member of my family who weighed over 300 pounds died suddenly of what might have been a heart attack while dozing in front of the television. He had long suffered from sleep apnea (a risk factor for sudden death), high blood pressure and severe gout, all results of his extreme weight. Copyright 2013 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: 18330 - Posted: 07.01.2013

By NICHOLAS BAKALAR Obesity in adolescents is associated with a range of cardiovascular and other health risks. Now a new study adds one more: hearing loss. Several studies have demonstrated the association of obesity with hearing loss in adults, but now researchers examining records of a nationwide sample of 1,488 boys and girls ages 12 to 19 have found the same association in teenagers. The study appeared online in The Laryngoscope. The researchers controlled for various factors, including poverty, sex, race and previous exposure to loud noises. They found that being at or above the 95th percentile for body mass index — the definition of obesity in teenagers — was independently associated with poorer hearing over all frequencies, and with almost double the risk of low-frequency hearing loss in one ear. They suggest that this may represent an early stage of injury that will later progress to both ears, as it does in adults. The reason for the connection is not known, but the scientists suggest that inflammation induced by obesity may be a factor in organ damage. “It’s quite possible that early intervention could arrest the progression,” said the lead author, Dr. Anil K. Lalwani, a professor of otolaryngology at Columbia University. “This is another reason to lose weight — but not to lose hope.” Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 18287 - Posted: 06.20.2013

Published by scicurious What do the overconsumption of food and Obsessive-Compulsive Disorder (OCD) have in common? At first, this sounds like a trick question. But deep in the brain, the molecules underlying our behavior may come together for these two conditions. The first is MC4R, a receptor for melanocortin. It binds hormones and affects feeding behavior, mutations in MC4R are associated with severe overcomsumption of high fat, high calorie foods and with obesity. A mouse without an MC4R gene will become severely obese compared to its wildtype counterparts. SAPAP3 is a protein that is associated with synapses, the spaces between neurons. It can regulate things like receptor levels that determine how well a neuron responds to excitatory input. But a knockout of SAPAP3 in mice produces something very different: severe overgrooming, a model of OCD. All rodents groom themselves, it's necessary to keep clean. But SAPAP3 knockouts groom themselves far, far too much, to the point of creating terrible lesions on their skin. This has been proposed as a model of OCD, as many people with OCD become obsessed with cleanliness, and will do things like, say, washing their hands, to the point of severely damaging their skin. So a knockout of MC4R creates obese mice. A knockout of SAPAP3 creates overgrooming mice. You might think that if you combined the two knockouts, you would get severely obese mice that also overgroomed. But you don't. Instead, you get mice that, to all appearances, seem completely normal. No obesity. No overgrooming. Neurotic Physiology Copyright © 2013

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18274 - Posted: 06.15.2013

Obese mothers tend to have kids who become obese. Now provocative research suggests weight-loss surgery may help break that unhealthy cycle in an unexpected way — by affecting how their children's genes behave. In a first-of-a-kind study, Canadian researchers tested children born to obese women, plus their brothers and sisters who were conceived after the mother had obesity surgery. Youngsters born after mom lost lots of weight were slimmer than their siblings. They also had fewer risk factors for diabetes or heart disease later in life. More intriguing, the researchers discovered that numerous genes linked to obesity-related health problems worked differently in the younger siblings than in their older brothers and sisters. Clearly diet and exercise play a huge role in how fit the younger siblings will continue to be, and it's a small study. But the findings suggest the children born after mom's surgery might have an advantage. "The impact on the genes, you will see the impact for the rest of your life," predicted Marie-Claude Vohl of Laval University in Quebec City. She helped lead the work reported Monday in the journal Proceedings of the National Academy of Sciences. Why would there be a difference? It's not that mom passed on different genes, but how those genes operate in her child's body. The idea: Factors inside the womb seem to affect the dimmer switches that develop on a fetus' genes — chemical changes that make genes speed up or slow down or switch on and off. That in turn can greatly influence health. © CBC 2013

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: 18195 - Posted: 05.28.2013

Virginia Hughes Late in the morning on 20 February, more than 200 people packed an auditorium at the Harvard School of Public Health in Boston, Massachusetts. The purpose of the event, according to its organizers, was to explain why a new study about weight and death was absolutely wrong. The report, a meta-analysis of 97 studies including 2.88 million people, had been released on 2 January in the Journal of the American Medical Association (JAMA)1. A team led by Katherine Flegal, an epidemiologist at the National Center for Health Statistics in Hyattsville, Maryland, reported that people deemed 'overweight' by international standards were 6% less likely to die than were those of 'normal' weight over the same time period. The result seemed to counter decades of advice to avoid even modest weight gain, provoking coverage in most major news outlets — and a hostile backlash from some public-health experts. “This study is really a pile of rubbish, and no one should waste their time reading it,” said Walter Willett, a leading nutrition and epidemiology researcher at the Harvard school, in a radio interview. Willett later organized the Harvard symposium — where speakers lined up to critique Flegal's study — to counteract that coverage and highlight what he and his colleagues saw as problems with the paper. “The Flegal paper was so flawed, so misleading and so confusing to so many people, we thought it really would be important to dig down more deeply,” Willett says. © 2013 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: 18185 - Posted: 05.23.2013

By JANE E. BRODY Sugar, and especially the high-fructose corn syrup that sweetens many processed foods and nearly all soft drinks, has been justly demonized for adding nutritionally empty calories to our diet and causing metabolic disruptions linked to a variety of diseases. But a closer look at what and how Americans eat suggests that simply focusing on sugar will do little to quell the rising epidemic of obesity. This is a multifaceted problem with deep historical roots, and we are doing too little about many of its causes. More than a third of American adults and nearly one child in five are now obese, according to the Centers for Disease Control and Prevention. Our failure to curtail this epidemic is certain to exact unprecedented tolls on health and increase the cost of medical care. Effective measures to achieve a turnaround require a clearer understanding of the forces that created the problem and continue to perpetuate it. The increase in obesity began nearly half a century ago with a rise in calories consumed daily and a decline in meals prepared and eaten at home. According to the Department of Agriculture, in 1970 the food supply provided 2,086 calories per person per day, on average. By 2010, this amount had risen to 2,534 calories, an increase of more than 20 percent. Consuming an extra 448 calories each day could add nearly 50 pounds to the average adult in a year. Sugar, it turns out, is a minor player in the rise. More than half of the added calories — 242 a day — have come from fats and oils, and another 167 calories from flour and cereal. Sugar accounts for only 35 of the added daily calories. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 18173 - Posted: 05.20.2013

By Laura Beil When chemists Richard Marshall and Earl Kooi started fiddling with cornstarch, the powder made from the dense insides of corn kernels, their intention was to turn glucose, which is easily produced from the starch, into fructose, which is sweeter. The idea wasn’t that far-fetched. The two sugar molecules are cousins, both made from the same atomic parts slightly rearranged. The duo’s experiment, which took place at the Corn Projects Refining Company in Argo, Ill., was a success. Marshall and Kooi discovered that the bacterium Aeromonas hydrophila produced an enzyme that could reconfigure the components of glucose from corn like so many Lego blocks. It was the first leap forward for a food industry dream: a mass-produced glucose-fructose-blend sweetener that would free commercial food manufacturers from the historical volatility of cane sugar crops. The scientists announced their triumph in a short report in Science in 1957. There the discovery sat in quiet obscurity for almost two decades, until a worldwide spike in sugar prices sent manufacturers scrambling. By the end of the 1980s, high fructose corn syrup had replaced cane sugar in soft drinks, and it soon became popular among makers of baked goods, dairy products, sauces and other foods. Few consumers seemed to care until 2004, when Barry Popkin, a nutrition scientist at the University of North Carolina at Chapel Hill, along with George Bray, at the Pennington Biomedical Research Center in Baton Rouge, La., published a commentary in the American Journal of Clinical Nutrition pointing out that the country’s obesity crisis appeared to rise in tandem with the embrace of high fructose corn syrup by food producers. That shift began in the early 1970s — just about the time Japanese researchers, who had noted Marshall and Kooi’s experiment with keen interest, overcame the technical hurdles of industrial production. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 18172 - Posted: 05.20.2013

Brian Owens The gut is home to innumerable different bacteria — a complex ecosystem that has an active role in a variety of bodily functions. In a study published this week in Proceedings of the National Academy of Sciences1, a team of researchers finds that in mice, just one of those bacterial species plays a major part in controlling obesity and metabolic disorders such as type 2 diabetes. The bacterium, Akkermansia muciniphila, digests mucus and makes up 3–5% of the microbes in a healthy mammalian gut. But the intestines of obese humans and mice, and those with type 2 diabetes, have much lower levels. A team led by Patrice Cani, who studies the interaction between gut bacteria and metabolism at the Catholic University of Louvain in Belgium, decided to investigate the link. Mice that were fed a high-fat diet, the researchers found, had 100 times less A. muciniphila in their guts than mice fed normal diets. The researchers were able to restore normal levels of the bacterium by feeding the mice live A. muciniphila, as well as 'prebiotic' foods that encourage the growth of gut microbes. The effects of this treatment were dramatic. Compared with untreated animals, the mice lost weight and had a better ratio of fat to body mass, as well as reduced insulin resistance and a thicker layer of intestinal mucus. They also showed improvements in a host of other indicators related to obesity and metabolic disorders. “We found one specific common factor between all the different parameters that we have been investigating over the past ten years,” says Cani. © 2013 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: 18156 - Posted: 05.14.2013

By NICHOLAS BAKALAR A large new study confirms that sticking to the Mediterranean diet — fish, poultry, vegetables and fruit, with minimal dairy foods and meat — may be good for the brain. Researchers prospectively followed 17,478 mentally healthy men and women 45 and older, gathering data on diet from food questionnaires, and testing mental function with a well-validated six-item screening tool. They ranked their adherence to the Mediterranean diet on a 10-point scale, dividing the group into low adherence and high adherence. The study was published April 30 in the journal Neurology. During a four-year follow-up, 1,248 people became cognitively impaired. But those with high adherence to the diet were 19 percent less likely to be among them. This association persisted even after controlling for almost two dozen demographic, environmental and vascular risk factors, and held true for both African-Americans and whites. The study included 2,913 people with Type 2 diabetes, but for them adherence to the diet had no effect on the likelihood of becoming impaired. The lead author, Dr. Georgios Tsivgoulis, an assistant professor of neurology at the University of Athens, said that this is the largest study of its kind. The Mediterranean diet, he added, “has many benefits — cardiovascular, cancer risk, anti-inflammatory, central nervous system. We’re on the tip of the iceberg, and trying to understand what is below.” Copyright 2013 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: 18100 - Posted: 05.01.2013