Links for Keyword: Obesity

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The Brain: Our Food-Traffic Controller By KATHLEEN A. PAGE and ROBERT S. SHERWIN IMAGINE that, instead of this article, you were staring at a plate of freshly baked chocolate chip cookies. The mere sight and smell of them would likely make your mouth water. The first bite would be enough to wake up brain areas that control reward, pleasure and emotion — and perhaps trigger memories of when you tasted cookies like these as a child. That first bite would also stimulate hormones signaling your brain that fuel was available. The brain would integrate these diverse messages with information from your surroundings and make a decision as to what to do next: keep on chewing, gobble down the cookie and grab another, or walk away. Studying the complex brain response to such sweet temptations has offered clues as to how we might one day control a profound health problem in the country: the obesity epidemic. The answer may partly lie in a primitive brain region called the hypothalamus. The hypothalamus, which monitors the body’s available energy supply, is at the center of the brain’s snack-food signal processing. It keeps track of how much long-term energy is stored in fat by detecting levels of the fat-derived hormone leptin — and it also monitors the body’s levels of blood glucose, minute-to-minute, along with other metabolic fuels and hormones that influence satiety. When you eat a cookie, the hypothalamus sends out signals that make you less hungry. Conversely, when food is restricted, the hypothalamus sends signals that increase your desire to ingest high-calorie foods. The hypothalamus is also wired to other brain areas that control taste, reward, memory, emotion and higher-level decision making. These brain regions form an integrated circuit that was designed to control the drive to eat. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 18087 - Posted: 04.28.2013

By Stephen L. Macknik Why, oh why, would I order a plastic fork, costing $89 (on-sale), 5 months before its scheduled release? Because it promises to help me control my eating speed, which, I am now convinced, is indeed critical to controlling obesity and diabetes. The fork is essentially a Bluetooth device that communicates to your smartphone and counts how many bites you take each meal. More importantly, I believe it counts the amount of time between each bite and if you go too fast, it vibrates. [Insert vibrator to mouth joke here. Yes, I'm blonde.] The reason I think it will help me goes back to my gastric bypass two months ago. Before and after the surgery, patients of Dr. Robin Blackmore at the Scottsdale Healthcare Bariatric Surgery Unit must take a series of courses aimed at preparing patients for life after surgery. One of the main lessons is that patients must now eat each meal over a 20 minute period. No more, no less. As you might surmise, for patients like me, “no more” is ready to achieve, but “no less” than 20 minutes is surprisingly difficult. And they are well aware of how hard it is, demanding that you practice ahead of time. I don’t know about my fellow patients, but I didn’t practice at all and have paid the price numerous times since my surgery for eating too fast: let’s just say it sometimes leads to a temporary obstruction and leave it at that. Because the details are unbelievably disgusting. © 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: 18068 - Posted: 04.24.2013

By CATHERINE SAINT LOUIS Laura Ward, 41, had always attributed her excess pounds to the drugs she takes for major depression. So Ms. Ward, who is 5-foot-6 and once weighed 220 pounds, didn’t try to slim down or avoid dietary pitfalls like fried chicken. But in a clinical trial, Ms. Ward managed to lose more than 30 pounds doing low-impact aerobics three times a week. During the 18-month experiment, she was introduced to cauliflower and post-workout soreness for the first time. She and the other participants attended counseling sessions where they practiced refusing junk food and choosing smaller portions. She drank two liters of Diet Dr Pepper daily instead of eight. Eventually, Ms. Ward, who lives in Baltimore, realized her waistline wasn’t simply a drug side effect. “If it was only the medications, I would have never lost all that weight,” she said. People with serious mental illnesses, like schizophrenia, bipolar disorder or major depression, are at least 50 percent more likely to be overweight or obese than the general population. They die earlier, too, with the primary cause heart disease. Yet diet and exercise usually take a back seat to the treatment of their illnesses. The drugs used, like antidepressants and antipsychotics, can increase appetite and weight. It has been a difficult issue for mental health experts. A 2012 review of health promotion programs for those with serious mental illness by Dartmouth researchers concluded that of 24 well-designed studies, most achieved statistically significant weight loss, but very few achieved “clinically significant weight loss.” Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18042 - Posted: 04.16.2013

By Tara Haelle New evidence is confirming that the environment kids live in has a greater impact than factors such as genetics, insufficient physical activity or other elements in efforts to control child obesity. Three new studies, published in the April 8 Pediatrics, land on the import of the 'nurture' side of the equation and focus on specific circumstances in children's or teen's lives that potentially contribute to unhealthy bulk. In three decades child and adolescent obesity has tripled in the U.S., and estimates from 2010 classify more than a third of children and teens as overweight or obese. Obesity puts these kids at higher risk for type 2 diabetes, cardiovascular disease, sleep apnea, and bone or joint problems. The variables responsible are thought to range from too little exercise to too many soft drinks. Now it seems that blaming Pepsi or too little PE might neglect the bigger picture. "We are raising our children in a world that is vastly different than it was 40 or 50 years ago," says Yoni Freedhoff, an obesity doctor and assistant professor of medicine at the University of Ottawa. "Childhood obesity is a disease of the environment. It's a natural consequence of normal kids with normal genes being raised in unhealthy, abnormal environments." The environmental factors in these studies range from the seemingly minor, such as kids' plate sizes, to bigger challenges, such as school schedules that may keep teens from getting sufficient sleep. But they are part of an even longer list: the ubiquity of fast food, changes in technology, fewer home-cooked meals, more food advertising, an explosion of low-cost processed foods and increasing sugary drink serving sizes (pdf) as well as easy access to unhealthy snacks in vending machines, at sports games and in nearly every setting children inhabit—these are just a handful of environmental factors research has linked to increasing obesity, and researchers are starting to pick apart which among them play bigger or lesser roles in making kids supersized. © 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: 18009 - Posted: 04.10.2013

Scientists have identified a group of brain cells which have the power to control appetite and could be a major cause of eating disorders such as obesity. In experiments in rodents, cells called tanycytes were found to produce neurons which specifically regulate appetite. The University of East Anglia researchers say their find means appetite is not fixed at birth. Their study is published in the Journal of Neuroscience. It was previously thought that nerve cells in the brain associated with appetite regulation were generated entirely during an embryo's development in the womb and could not be altered. But the UEA study's discovery of these tanycytes, which act like stem cells, in the brains of young and adult rodents shows that appetite can be modified. Researchers looked in detail at the hypothalamus section of the brain, which is known to regulate sleep, energy expenditure, appetite, thirst and many other critical biological functions. They studied the nerve cells that regulate appetite using a 'genetic fate mapping' technique and found that some cells added neurons to the appetite-regulating circuitry of the mouse brain after birth and into adulthood. BBC © 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: 17998 - Posted: 04.08.2013

Steve Connor The rise in the number of overweight children in Britain may be as much to do with their genes as their diet and exercise levels, according to a study that has identified a handful of genetic mutations linked with childhood obesity. Scientists have discovered that children with the most severe kinds of obesity are more likely than other children to have one or more of four genetic variations in their DNA, which could influence such things as appetite and food metabolism. The discovery is part of a wider search for the genes involved in increasing a person’s risk of becoming overweight when exposed to an “obesogenic environment” of high-calorie food and inactivity – which is known to affect some people more than others. The study looked at 1,000 children with the most severe form of early-onset obesity, which is highly likely to result in obesity in adulthood. Some of the 10-year-olds in the study weighed between 80kg and 100kg (12.5st-15.7st). Some of the genetic variations revealed by the study were rare but others are relatively common, suggesting an interaction between genetics and environment, which could explain why certain children become obese while others do not even when they share a similar upbringing. Obesity among British children aged between two and ten has risen since 1995 from 10.1 per cent to 13.9 per cent in 2011. This rise cannot be due to a change in genes alone, because it takes many generations to alter the frequency of genetic mutations in the population. © independent.co.uk

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: 17997 - Posted: 04.08.2013

By Neil Bowdler BBC News UK-based scientists have designed an 'intelligent' microchip which they claim can suppress appetite. Animal trials of the electronic implant are about to begin and its makers say it could provide a more effective alternative to weight-loss surgery. The chip is attached to the vagus nerve which plays a role in appetite as well as a host of other functions within the body. Human trials of the implant could begin within three years, say its makers. The work is being led by Prof Chris Toumazou and Prof Sir Stephen Bloom of Imperial College London. It involves an 'intelligent implantable modulator', just a few millimetres across, which is attached using cuff electrodes to the vagus nerve within the peritoneal cavity found in the abdomen. The chip and cuffs are designed to read and process electrical and chemical signatures of appetite within the nerve. The chip can then act upon these readings and send electrical signals to the brain reducing or stopping the urge to eat. The researchers say identifying chemicals rather than electrical impulses will make for a more selective, precise instrument. The project has just received over 7m euros (£5.9m; $9m) in funding from the European Research Council. A similar device designed by the Imperial team has already been developed to reduce epileptic seizures by targeting the same vagus nerve. "This is a really small microchip and on this chip we've got the intelligence which can actually model the neural signals responsible for appetite control," Prof Toumazou told the BBC. BBC © 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: 17965 - Posted: 03.30.2013

By DENISE GRADY The bacterial makeup of the intestines may help determine whether people gain weight or lose it, according to two new studies, one in humans and one in mice. The research also suggests that a popular weight-loss operation, gastric bypass, which shrinks the stomach and rearranges the intestines, seems to work in part by shifting the balance of bacteria in the digestive tract. People who have the surgery generally lose 65 percent to 75 percent of their excess weight, but scientists have not fully understood why. Now, the researchers are saying that bacterial changes may account for 20 percent of the weight loss. The findings mean that eventually, treatments that adjust the microbe levels, or “microbiota,” in the gut may be developed to help people lose weight without surgery, said Dr. Lee M. Kaplan, director of the obesity, metabolism and nutrition institute at the Massachusetts General Hospital, and an author of a study published Wednesday in Science Translational Medicine. Not everyone who hopes to lose weight wants or needs surgery to do it, he said. About 80 million people in the United States are obese, but only 200,000 a year have bariatric operations. “There is a need for other therapies,” Dr. Kaplan said. “In no way is manipulating the microbiota going to mimic all the myriad effects of gastric bypass. But if this could produce 20 percent of the effects of surgery, it will still be valuable.” In people, microbial cells outnumber human ones, and the new studies reflect a growing awareness of the crucial role played by the trillions of bacteria and other microorganisms that live in their own ecosystem in the gut. Perturbations there can have profound and sometimes devastating effects. © 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: 17959 - Posted: 03.28.2013

Alternating between periods of eating and fasting is gaining in popularity among dieters and generating criticism in nutritional circles. Intermittent fasting, sometimes known as the 5:2 diet, asks people to eat very little or nothing at times, such as eating normally for five days a week and fasting for the other two. Brad Pilon designed one of the first intermittent fasts that became popular after he published a guide, Eat Stop Eat. Pilon said the diet allows followers to eat the foods they crave most of the time and still lose weight. "In the fasted state your body's set up to burn the calories you stored while eating," said Pilon. "So it's set up specifically for the act of burning body fat." Cutting down on weekly calorie intake is generally recommended. And there's research underway into the hypothesis that restricting calories could extend a healthy lifespan. Critics of intermittent fasting say that besides burning unwanted fat, the body will also burn its building blocks. "So when those energy stores start to drop the body looks for other sources and it goes to the muscles and burns muscle," said Margaret De Melo, a registered dietician at Toronto Western Hospital. © CBC 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: 17954 - Posted: 03.27.2013

By TARA PARKER-POPE The best path to a healthy weight may be a good night’s sleep. For years researchers have known that adults who sleep less than five or six hours a night are at higher risk of being overweight. Among children, sleeping less than 10 hours a night is associated with weight gain. Now a fascinating new study suggests that the link may be even more insidious than previously thought. Losing just a few hours of sleep a few nights in a row can lead to almost immediate weight gain. Sleep researchers from the University of Colorado recruited 16 healthy men and women for a two-week experiment tracking sleep, metabolism and eating habits. Nothing was left to chance: the subjects stayed in a special room that allowed researchers to track their metabolism by measuring the amount of oxygen they used and carbon dioxide they produced. Every bite of food was recorded, and strict sleep schedules were imposed. The goal was to determine how inadequate sleep over just one week — similar to what might occur when students cram for exams or when office workers stay up late to meet a looming deadline — affects a person’s weight, behavior and physiology. During the first week of the study, half the people were allowed to sleep nine hours a night while the other half stayed up until about midnight and then could sleep up to five hours. Everyone was given unlimited access to food. In the second week, the nine-hour sleepers were then restricted to five hours of sleep a night, while the sleep-deprived participants were allowed an extra four hours. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 17918 - Posted: 03.19.2013

By GINIA BELLAFANTE Under the category “Summer Rentals That Have Gone Terribly Wrong,” there are perhaps few parallels to the experience of Charles Henry Warren, a Manhattan banker who, in 1906, took a house in Oyster Bay on Long Island’s North Shore. By the end of the season, Mr. Warren’s young daughter had developed typhoid. She was soon followed in illness by Mr. Warren’s wife, a second daughter, two maids and a gardener. At the time, typhoid, a bacterial illness spread through contaminated food and water, was largely a disease of the urban poor. The property’s owner, George Thompson, concerned that the house, on which he relied for rental income, would become associated with tenement filth in the minds of wealthy New Yorkers, invited a sanitary engineer to determine the source of the outbreak. What the medical investigator, George Soper, discovered was that the Warrens’ cook, Mary Mallon, an Irish immigrant, had left an imprint of malady in other quarters of upper-class Manhattan and its summer enclaves. Typhoid, he wrote, had erupted in every household in which Mallon had worked over the previous decade. An asymptomatic carrier of the disease, Ms. Mallon would be known to history as Typhoid Mary and spend most of the remainder of her life quarantined on North Brother Island in the East River, having failed to abide by a promise to cease working in the city’s kitchens. The events supply the narrative of “Fever,” a new novel by Mary Beth Keane, which arrives at a time when we are once again debating the parameters of public health policy’s encroachments on our behaviors. Last week, a State Supreme Court justice in Manhattan used the words “arbitrary and capricious” in striking down the Bloomberg administration’s efforts to limit the size of sugary drinks (which pertained to certain sweetened beverages but not others, and some retail environments but not all). The phrase, though, could have been similarly applied a century ago to the city’s treatment of Ms. Mallon, given that officials were not in the habit of isolating other healthy carriers whom they had identified as ignoring ordinances against the spread of the disease. © 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: 17907 - Posted: 03.18.2013

Diet pop and other artificially sweetened products may cause us to eat and drink even more calories and increase our risk for obesity and Type 2 diabetes, researchers are learning. Former McGill University researcher Dana Small specializes in the neuropsychology of flavour and feeding at Yale University in New Haven, Conn. Small said there's mounting evidence that artificial sweeteners have a couple of problematic effects. Sugar substitutes such as sucralose and aspartame are more intensely sweet than sugar and may rewire taste receptors so less sweet, healthier foods aren't as enjoyable, shifting preferences to higher calorie, sweeter foods, she said. Small and some other researchers believe artificial sweeteners interfere with brain chemistry and hormones that regulate appetite and satiety. For millennia, sweet taste signalled the arrival of calories. But that's no longer the case with artificial sweeteners. "The sweet taste is no longer signalling energy and so the body adapts," Small said in an interview with CBC News. "It's no longer going to release insulin when it senses sweet because sweet now is not such a good predictor of the arrival of energy." Susan Swithers, a psychology professor at Purdue University in West Lafayette, Ind., studies behavioural neuroscience. "Exposure to high-intensity sweeteners could change the way that sweet tastes are processed," she says. © CBC 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: 17825 - Posted: 02.19.2013

By SARAH LYALL IPSWICH, England — Who knows what the worst moment was for Paul Mason — there were so many awful milestones, as he grew fatter and fatter — but a good bet might be when he became too vast to leave his room. To get him to the hospital for a hernia operation, the local fire department had to knock down a wall and extricate him with a forklift. That was nearly a decade ago, when Mr. Mason weighed about 980 pounds, and the spectacle made him the object of fascinated horror, a freak-show exhibit. The British news media, which likes a superlative, appointed him “the world’s fattest man.” Now the narrative has shifted to one of redemption and second chances. Since a gastric bypass operation in 2010, Mr. Mason, 52 years old and 6-foot-4, has lost nearly two-thirds of his body weight, putting him at about 336 pounds — still obese, but within the realm of plausibility. He is talking about starting a jewelry business. “My meals are a lot different now than they used to be,” Mr. Mason said during a recent interview in his one-story apartment in a cheerful public housing complex here. For one thing, he no longer eats around the clock. “Food is a necessity, but now I don’t let it control my life anymore,” he said. But the road to a new life is uphill and paved with sharp objects. When he answered the door, Mr. Mason did not walk; he glided in an electric wheelchair. And though Mr. Mason looks perfectly normal from the chest up, horrible vestiges of his past stick to him, literally, in the form of a huge mass of loose skin choking him like a straitjacket. Folds and folds of it encircle his torso and sit on his lap, like an unwanted package someone has set there; more folds encase his legs. All told, he reckons, the excess weighs more than 100 pounds. © 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: 17772 - Posted: 02.06.2013

By Nathan Seppa The link between obesity and vitamin D deficiency appears to be a one-way street. A large study of the genetics underpinning both conditions finds that obesity may drive down vitamin D levels, but a predisposition to the vitamin deficiency doesn’t lead to obesity. The findings also suggest that boosting vitamin D levels won’t reverse obesity. An association between the two has been observed for years, but determining cause and effect has been difficult. “I find this very plausible and a correct interpretation of the data,” says Robert Heaney, an endocrinologist at Creighton University in Omaha, Neb. “I think it’s worth reporting.” In the new study, researchers tapped into a huge international database, accessing the genetic profiles of more than 42,000 people. The scientists noted whether a person harbored any of 12 genetic variants associated with being overweight. Not surprisingly, people with these variants were more likely to be obese than those without them. People with these obesity-associated gene variants were also apt to have low vitamin D levels, Elina Hyppönen, an epidemiologist and nutritionist at University College London, and colleagues report online February 5 in PLOS Medicine. When the researchers tested for four genetic variants linked to low vitamin D levels, they found that people with the variants were not necessarily prone to obesity. The researchers checked both findings against a separate database of people and got similar results. © 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: 17767 - Posted: 02.06.2013

When you eat could play an important role in weight loss, a new study suggests. Researchers looked at the role of meal timing in 420 men and women in southeast Spain participating in a 20-week weight-loss treatment following several studies in animals showing a relationship between the timing of feeding and weight regulation. Lunch was the main meal among the Mediterranean population studied.Lunch was the main meal among the Mediterranean population studied. (Eric Gaillard/Reuters) "Our results indicate that late eaters displayed a slower weight-loss rate and lost significantly less weight than early eaters, suggesting that the timing of large meals could be an important factor in a weight loss program," Frank Scheer, director of the medical chronobiology program at Brigham and Women's Hospital in Boston, said in a release. Of the participants, 51 per cent were early eaters who ate their main meal, lunch, before 3 p.m. The other 49 per cent had lunch after three. The researchers found energy and nutrient intake, estimates of calories burned, appetite hormones and hours of sleep were similar between both groups. "Nevertheless, late eaters were more evening types, had less energetic breakfasts and skipped breakfast more frequently than early eaters," Scheer and his co-authors wrote in Tuesday's issue of the International Journal of Obesity. They suggested that new weight loss strategies should incorporate the timing of food as well as the classic look at calorie intake and distribution of carbohydrates, fats and protein. © CBC 2013

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 17728 - Posted: 01.29.2013

Analysis by Sheila Eldred This spring, it's likely there will be a new diet pill on the market. Belviq (lorcaserin) won approval from the FDA last spring, making it the first weight-loss drug approved in 13 years, and the DEA proposed this week that the drug be classified as a Schedule IV controlled substance. Belviq is an appetite suppressant. The new chemical entity works by activating the brain's response to serotonin. Serotonin is a neuro-transmitter known for evoking happy moods; some anti-depressants work by keeping serotonin levels elevated. Belviq works specifically with the serotonin receptors involved with appetite, according to Time. In trial, patients who took Belviq lost 3 to 3.7 percent more weight than those taking a placebo; after taking it for one or two years, 47 percent lost at least 5 percent of their body weight (compared to 23 percent of those who took a placebo), WebMD reports. Another new weight loss drug, Qsymia, is already on the market, although sales have been slow. Belviq is approved for obese people and overweight people who have another weight-related disease or risk factor. Side effects include headache, dizziness, fatigue, nausea, dry mouth and constipation; in patients with diabetes, additional side effects include low blood sugar, back pain, and coughing. © 2012 Discovery Communications, LLC.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 17630 - Posted: 12.22.2012

Gary Taubes. “It is better to know nothing,” wrote French physiologist Claude Bernard in An Introduction to the Study of Experimental Medicine (1865), “than to keep in mind fixed ideas based on theories whose confirmation we constantly seek.” Embracing a fixed idea is one of the main dangers in the evolution of any scientific discipline. Ideally, errors will be uncovered in the trial-by-fire of rigorous testing and the science will right itself. In rare cases, however, an entire discipline can be based on a fundamental flaw. As a science journalist turned science historian, I have written at length about how and why this may have happened in obesity research. I have suggested that the discipline may be a house of cards — as, by extension, may much research into the chronic diseases associated with obesity, such as diabetes. Before the Second World War, European investigators believed that obesity was a hormonal or regulatory disorder. Gustav von Bergmann, a German authority on internal medicine, proposed this hypothesis in the early 1900s. The theory evaporated with the war. After the lingua franca of science switched from German to English, the German-language literature on obesity was rarely cited. (Imagine the world today if physicists had chosen to ignore the thinking that emerged from Germany and Austria before the war.) Instead, physicians embraced the ideas of the University of Michigan physician Louis Newburgh, who argued that obese individuals had a “perverted appetite” that failed to match the calories that they consumed with their bodies' metabolic needs. “All obese persons are alike in one fundamental respect,” Newburgh insisted, “they literally overeat.” This paradigm of energy balance/overeating/gluttony/sloth became the conventional, unquestioned explanation for why we get fat. It is, as Bernard would say, the fixed idea. © 2012 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: 17603 - Posted: 12.13.2012

By SABRINA TAVERNISE PHILADELPHIA — After decades of rising childhood obesity rates, several American cities are reporting their first declines. The trend has emerged in big cities like New York and Los Angeles, as well as smaller places like Anchorage, Alaska, and Kearney, Neb. The state of Mississippi has also registered a drop, but only among white students. “It’s been nothing but bad news for 30 years, so the fact that we have any good news is a big story,” said Dr. Thomas Farley, the health commissioner in New York City, which reported a 5.5 percent decline in the number of obese schoolchildren from 2007 to 2011. The drops are small, just 5 percent here in Philadelphia and 3 percent in Los Angeles. But experts say they are significant because they offer the first indication that the obesity epidemic, one of the nation’s most intractable health problems, may actually be reversing course. The first dips — noted in a September report by the Robert Wood Johnson Foundation — were so surprising that some researchers did not believe them. Deanna M. Hoelscher, a researcher at the University of Texas, who in 2010 recorded one of the earliest declines — among mostly poor Hispanic fourth graders in the El Paso area — did a double-take. “We reran the numbers a couple of times,” she said. “I kept saying, ‘Will you please check that again for me?’ ” © 2012 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: 17595 - Posted: 12.11.2012

by Julia Brown Forget dieting; just cut down a little on the fat in what you eat and you'll lose weight. The confirmation that you can lose weight without eating less comes from a review of studies involving nearly 75,000 people – none of whom were trying to lose weight. The pounds fell off when they changed to a diet containing less fat. The work was commissioned by the World Health Organization to find out what our optimal intake of fat should be. Lee Hooper at the University of East Anglia in Norwich, UK, and her colleagues reviewed 43 studies carried out in developed countries in which volunteers reduced the overall fat content of their diet, compared with controls who ate either their usual diet or a more healthy one. In all studies, volunteers had to maintain their eating plan for at least six months, with the median time about six years. The studies varied in how volunteers reduced their fat intake and by how much. For example, in one, volunteers simply replaced normal food with low-fat equivalents. In others, participants could change their diet in various ways to reduce their daily fat intake by about 7 per cent on average. In all but one study, the low-fat groups saw a greater weight reduction than the controls, with people losing on average about 1.6 kilograms. "I've never seen quite such a consistent set of results," Hooper says. © 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: 17580 - Posted: 12.08.2012

Children who are obese may be more vulnerable to food advertising, a brain scanning study suggests. Food and beverage companies market to children to establish brand recognition, brand preference and loyalty. Previous studies found preschoolers said foods tasted better wrapped in branded packaging than plain packaging and kids were more likely to try to influence their parents' purchases when exposed to ads. Researchers in the U.S. suspected that children who are obese would show greater activation to food logos in the "drive" regions of the brain compared with healthy weight children. Amanda Bruce of the psychology department at the University of Missouri-Kansas City and her colleagues looked at 10 healthy children and 10 obese children aged 10 to 14 using questionnaires measuring self-control and functional magnetic resonance imaging of brain activity. Other corporate logos and blurred images were also tested. Obese children showed more activation in some reward regions of the brain than the healthy weight children when shown food logos. But that wasn't the case for the control regions of the brain. "When shown food logos, obese children showed significantly less brain activation than the healthy weight children in regions association with cognitive control," the study's authors concluded in Friday's issue of The Journal of Pediatrics. "This provides initial neuroimaging evidence that obese children may be more vulnerable to the effects of food advertising." © CBC 2012

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 17559 - Posted: 12.01.2012