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

Keyword: Obesity; Aggression
Link ID: 18274 - Posted: 06.15.2013

By Rachel Ehrenberg The salad days of human evolution saw a dietary shift toward grasses and probably grass-fed animals, analyses of more than 100 fossilized teeth from eight species of ancient hominids indicate. “These changes in diet have been predicted,” says paleoanthropologist Richard Klein of Stanford University. “But it’s very nice to have some data, and these data support it very strongly.” Changes in the size and shape of jaws and teeth in both ancient hominids and their ape relatives point to changes in diet. The new study adds to these lines of anatomical evidence chemical analyses that look at different forms of carbon in the fossilized teeth. The ratio of two types of carbon in tooth enamel reflects diet, says geochemist Thure Cerling of the University of Utah, who spent weeks in a vault in the National Museum of Kenya collecting milligram-sized samples of tooth enamel for the analyses. Grasses, grasslike sedges and many other plants in hot, arid environments have evolved a trick that helps prevent water loss. The metabolic adjustment results in taking up more of a heavier form of carbon, known as carbon-13, than most trees and shrubs do. The tooth studies, which cover more than 3 million years and include specimens from southern, eastern and central Africa, found greater quantities of this heavier carbon in hominids that are closer to humans on the evolutionary tree. This pattern suggests that, compared with humans’ more ancient relatives, recent ones were eating more grass or more grass-feeding animals, like zebras. The analyses appear June 3 in the Proceedings of the National Academy of Sciences. © Society for Science & the Public 2000 - 2013

Keyword: Evolution; Aggression
Link ID: 18224 - Posted: 06.04.2013

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

Keyword: Obesity; Aggression
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,

Keyword: Obesity
Link ID: 18185 - Posted: 05.23.2013

By Maggie Fox, Senior Writer, NBC News It might seem against all logic, but adding a little olive oil or a handful of nuts to your diet each day may help keep your mind clear, researchers reported on Monday. It’s the same diet that’s also been shown to reduce deaths from heart attacks and strokes. The researchers found that people who ate these healthy fats were less likely to show the early signs of dementia than those who stuck to a more traditional diet. And this was done in Spain -- where people are already eating a so-called Mediterranean diet. “Our findings support increasing evidence on the protective effects of the Mediterranean Diet on cognitive function,” Miguel Martinez-Gonzalez of the University of Navarra in Spain and colleagues reported in the Journal of Neurology, Neurosurgery and Psychiatry. The findings come from a large and well-publicized trial that showed the Mediterranean diet rich in fruits, vegetables, olive oil and a little wine can cut the risk of heart attacks and strokes by 30 percent. Martinez and colleagues took a part data on 500 volunteers from their own study center, who were followed for more than six and a half years after starting the diet. A Mediterranean diet includes lots of salad, fruit, vegetables, nuts, a little fish, a little lean meat, a small amount of cheese and olive oil. Wine is also served at meals. In the main study, 7,400 volunteers got extra counseling, and either a weekly supply of extra-virgin olive oil or mixed nuts -- walnuts, almonds and hazelnuts. © 2013 NBCNews.com

Keyword: Alzheimers
Link ID: 18176 - Posted: 05.21.2013

By Tara Haelle Identification and treatment issues surrounding attention deficit hyperactivity disorder (ADHD) are challenging enough. Now research is shedding light on long-term outcomes for people with ADHD. A recent study in Pediatrics reports that men who had ADHD in childhood are twice as likely to be obese in middle age, even if they no longer exhibit symptoms of ADHD. ADHD is a mental disorder characterized by hyperactivity, impulsivity, inattention and inability to focus. It affects approximately 6.8 percent of U.S. children ages 3 to 17 in any given year, according to a recent report by the CDC. Medications used to treat ADHD, such as Ritalin (methylphenidate) or Adderall (dextroamphetamine and amphetamine), are stimulants that can suppress appetite, however, a couple recent retrospective studies have pointed to a possible increased risk for obesity among adults diagnosed with ADHD as children. The new 33-year prospective study started with 207 healthy middle-class white boys from New York City between 6 and 12 years old, who had been diagnosed with ADHD. When the cohort reached an average age of 18, another 178 healthy boys without ADHD were recruited for comparison. At the most recent follow-up when the participants were an average age of 41, a total of 222 men remained in the study. A troubling pattern emerged: A comparison of the men’s self-reported height and weight revealed that twice as many men with childhood ADHD were obese than those without childhood ADHD. The average body mass index (BMI) of the men with childhood ADHD was 30.1 and 41.4 percent were obese, whereas those without the condition as kids reported an average BMI of 27.6 and an obesity rate of 21.6 percent. The association held even after the researchers controlled for socioeconomic status, depression, anxiety and substance abuse disorders. © 2013 Scientific American

Keyword: ADHD; Aggression
Link ID: 18174 - Posted: 05.20.2013

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

Keyword: Obesity; Aggression
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

Keyword: Obesity; Aggression
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

Keyword: Obesity
Link ID: 18156 - Posted: 05.14.2013

By Bruce Bower Human ancestors living in East Africa 2 million years ago weren’t a steak-and-potatoes crowd. But they had a serious hankering for gazelle meat and antelope brains, fossils discovered in Kenya indicate. Three sets of butchered animal bones unearthed at Kenya’s Kanjera South site provide the earliest evidence of both long-term hunting and targeted scavenging by a member of the human evolutionary family, anthropologist Joseph Ferraro of Baylor University in Waco, Texas, and his colleagues conclude. An early member of the Homo genus, perhaps Homo erectus, hunted small animals and scavenged predators’ leftovers of larger creatures, researchers report April 25 in PLOS ONE. Along with hunting relatively small game such as gazelles, these hominids scavenged the heads of antelope and wildebeests, apparently to add a side of fatty, nutrient-rich brain tissue to their diets, the scientists say. Those dietary pursuits could have provided the extra energy Homo erectus needed to support large bodies, expanded brains and extensive travel across the landscape, Ferraro says. A few East African sites dating to as early as 3.4 million years ago had previously produced small numbers of animal bones bearing butchery marks made by stone tools. Scientists think those bones indicate occasional meat eating (SN: 9/11/10, p. 8). Now Kanjera South has yielded several thousand complete and partial animal bones, representing at least 81 individual animals. A known reversal of Earth’s magnetic field preserved in an excavated soil layer allowed Ferraro’s team to determine the age of the finds, which accumulated over a few thousand years at most. © Society for Science & the Public 2000 - 2013

Keyword: Evolution; Aggression
Link ID: 18113 - Posted: 05.04.2013

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

Keyword: Obesity; Aggression
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

Keyword: Obesity; Aggression
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

Keyword: Obesity; Aggression
Link ID: 18087 - Posted: 04.28.2013

Published by scicurious under Behavioral Neuro It's late. I've got a lot on my plate. A lot to do. And most of us do. So here I am, burning the midnight oil along with many of my neighbors. I usually count myself lucky to get 7 hours a night, and I AM lucky. For many parents or other caregivers, for example, 7 hours is unheard-of luxury. Is it just me? Probably not. Most of us don't get enough sleep, and those who don't sleep? Snack. But why? And what does this mean for issues like obesity? We know that there has been an increase in obesity in this country. And many people are asking why. There are probably lots of reasons involved: too much sugar, too little exercise, genetics, too much fat. But what about sleep? It turns out that getting less sleep is a risk factor for obesity, but...how are sleep and weight gain related? It turns out that sleep, or lack thereof, can have a lot of influence on how much we need to eat and how much we feel like eating. For example, sleep deprivation changes hunger hormone levels, which can change food intake, and some scientists hypothesize that decreased sleep can change energy expenditure as well. But in order to understand just how lack of sleep influences weight gain, well you need to sleep deprive some people. The authors took 8 men and 8 women who reported getting an average of 8 hours of sleep per night into an inpatient facility. They were taken off caffeine one week before the study and were told to stick to 9 hours of sleep opportunity (stay in bed 9 hours) per night for the first week. They also were put on a diet that was calibrated exactly to maintain their current weight. Copyright © 2013

Keyword: Sleep; Aggression
Link ID: 18074 - Posted: 04.25.2013

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,

Keyword: Obesity
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

Keyword: Obesity; Aggression
Link ID: 18042 - Posted: 04.16.2013

Published by scicurious I love salt. It's just delicious. I wrote this post while noshing on deliciously salty popcorn, after a dinner which I put salt on. I crave salt so much that my parents used to joke about getting me a salt lick. And I'm not alone. Sodium is an incredibly important part of life, which means it's also an important part of what we eat. To make sure we get enough salt, animals have evolved salt-sensing systems, and low levels (below 100 mM of NaCl) of salt are very attractive. But there IS such a thing as too much salt. High levels of salt (>300 mM NaCl) are really aversive (from personal experience, I wonder if Carrabba's restaurant has concentrations of salt in their food over 300 mM). Most animals will quickly turn up their noses at a high salt concentration. You probably know that you have classes of receptors on your tongue for taste (though they are not clustered into areas of your mouth, like front for sweetness, as previously thought). You have sweet, umami (savory), bitter, sour, and salt. In most animals, sweet and umami are always attractive, while bitter and sour are nasty (except where we have overcome the aversion to enjoy things like coffee and beer). Salt, though, is the only one that goes two ways, with low levels being attractive and high levels being aversive. Now we know how low salt works. The salt receptors that are currently known are good for detecting low salt. But high salt, that's more difficult. First of all, our aversion to high salt concentrations is not very selective. While low salt detection is limited to good old NaCl, high salt detection is non-specific, working for many salts including NaCl, but others as well (like KCl). Neurotic Physiology Copyright © 2013

Keyword: Chemical Senses (Smell & Taste)
Link ID: 18025 - Posted: 04.13.2013

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

Keyword: Obesity; Aggression
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

Keyword: Obesity
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

Keyword: Obesity; Aggression
Link ID: 17997 - Posted: 04.08.2013