Links for Keyword: Obesity

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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

By TARA PARKER-POPE Are doctors nicer to patients who aren’t fat? A provocative new study suggests that they are — that thin patients are treated with more warmth and empathy than those who are overweight or obese. For the study, published in the medical journal Obesity, researchers at Johns Hopkins obtained permission to record discussions between 39 primary care doctors and more than 200 patients who had high blood pressure. Although patients were there to talk about blood pressure, not weight, most fell into the overweight or obese category. Only 28 were of normal weight, meaning they had a body mass index below 25. Of the remaining patients, 120 were obese (B.M.I. of 30 or greater) and 60 were classified as overweight (index of 25 to 30). For the most part, all of the patients were treated about the same; there were no meaningful differences in the amount of time doctors spent with them or the topics discussed. But when researchers analyzed transcripts of the visits, there was one striking difference. Doctors seemed just a bit nicer to their normal-weight patients, showing more empathy and warmth in their conversations. Although the study was relatively small, the findings are statistically significant. “It’s not like the physicians were being overtly negative or harsh,” said the lead author, Dr. Kimberly A. Gudzune, an assistant professor of general internal medicine at the Johns Hopkins School of Medicine. “They were just not engaging patients in that rapport-building or making that emotional connection with the patient.” Copyright 2013 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: 18093 - Posted: 04.30.2013

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