Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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


Links 81 - 100 of 1261

By Tori Rodriguez The digestive tract and the brain are crucially linked, according to mounting evidence showing that diet and gut bacteria are able to influence our behavior, thoughts and mood. Now researchers have found evidence of bacterial translocation, or “leaky gut,” among people with depression. Normally the digestive system is surrounded by an impermeable wall of cells. Certain behaviors and medical conditions can compromise this wall, allowing toxic substances and bacteria to enter the bloodstream. In a study published in the May issue of Acta Psychiatrica Scandinavica, approximately 35 percent of depressed participants showed signs of leaky gut, based on blood tests. The scientists do not yet know how leaky gut relates to depression, although earlier work offers some hints. Displaced bacteria can activate autoimmune responses and inflammation, which are known to be associated with the onset of depression, lower mood and fatigue. “Leaky gut may maintain increased inflammation in depressed patients,” which could exacerbate the symptoms of depression if not treated, says Michael Maes, a research psychiatrist with affiliations in Australia and Thailand and an author of the paper. Currently leaky gut is treated with a combination of glutamine, N-acetylcysteine and zinc—believed to have anti-inflammatory or antioxidant properties—when behavioral and dietary modifications fail. © 2013 Scientific American

Keyword: Obesity
Link ID: 18830 - Posted: 10.24.2013

Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.

Keyword: Drug Abuse; Aggression
Link ID: 18794 - Posted: 10.16.2013

By GINA KOLATA William Howard Taft, the only massively obese man ever to be president of the United States, struggled mightily to control his weight a century ago, worrying about his health and image, and endured humiliation from cartoonists who delighted in his corpulent figure. But new research has found that his weight-loss program was startlingly contemporary, and his difficulties keeping the pounds off would be familiar to many Americans today. On the advice of his doctor, a famed weight-loss guru and author of popular diet books, he went on a low-fat, low-calorie diet. He avoided snacks. He kept a careful diary of what he ate and weighed himself daily. He hired a personal trainer and rode a horse for exercise. And he wrote his doctor, Nathaniel E. Yorke-Davies, with updates on his progress, often twice a week. In a way, he was ahead of his time. Obesity became a medical issue by the middle of the 20th century, around the time the term “obesity” rather than “corpulence” came into vogue, said Abigail C. Saguy, a sociologist at the University of California, Los Angeles, who specializes in the study of obesity. Taft’s story shows that “at least in some cases, corpulence was already treated as a medical problem early in the century,” she added. Like many dieters today, Taft, 6 feet 2 inches tall, lost weight and regained it, fluctuating from more than 350 to 255 pounds. He was 48 when he first contacted Dr. Yorke-Davies, and spent the remaining 25 years of his life corresponding with the doctor and consulting other physicians in a quest to control his weight. Taft’s struggles are recounted by Deborah Levine, a medical historian at Providence College in Rhode Island. She discovered the extensive correspondence between Taft and the diet doctor, including Taft’s diet program, his food diary, and a log of his weight. Her findings were published Monday in The Annals of Internal Medicine. His story, Dr. Levine said, “sheds a lot of light on what we are going through now.” © 2013 The New York Times Company

Keyword: Obesity
Link ID: 18788 - Posted: 10.15.2013

by Erika Engelhaupt Could I interest you in eating the partially digested stomach contents of a porcupine? No? Maybe a spot of reindeer stomach, then. Still no? Well, that’s curious. The Western aversion to these dishes is odd, because people around the world have long partaken of — even delighted in — the delicacy known to medical science as chyme. That’s what becomes of food after it’s chewed, swallowed and mushed around in the stomach for a while with a healthy dose of hydrochloric acid. And, researchers now suggest, Neandertals were no exception. Eating chyme may even explain the presence of some puzzling plant matter found in Neandertal’s tartar-crusted teeth. Neandertals didn’t have great dental care, and in the last few years anthropologists have begun to take advantage of monstrous tartar buildup on fossilized teeth to figure out what the hominids ate. Various chemical signatures, starch grains and even tiny plant fossils called phytoliths get preserved in the tartar, also known as calculus. Just what Neandertals ate has been more of a puzzle than paleo dieters might have you believe. Isotope analyses of fossilized bones and teeth suggest Neandertals ate very high on the food chain, with high-protein diets akin to those of wolves or hyenas. But wear marks on their teeth suggest the Neandertal diet consisted of more animals in colder high-latitude areas, and more of a mix of plants and animals in warmer areas. Tartar analyses support the idea that Neandertals ate their veggies, and have also suggested the presence of plants considered inedible, or at least unpalatable and non-nutritious. These include some plants like yarrow and chamomile with medicinal value, so one team suggested Neandertals self-medicated. © Society for Science & the Public 2000 - 2013

Keyword: Evolution
Link ID: 18776 - Posted: 10.12.2013

By ANAHAD O'CONNOR They are a mystery to researchers: people who are significantly overweight and yet show none of the usual metabolic red flags. Despite their obesity, they have normal cholesterol levels, healthy blood pressure levels and no apparent signs of impending diabetes. Researchers call them the metabolically healthy obese, and by some estimates they represent as many as a third of all obese adults. Scientists have known very little about them, but new research may shed some light on the cause of their unusual metabolic profile. A study in the journal Diabetologia has found that compared with their healthier counterparts, people who are obese but metabolically unhealthy have impaired mitochondria, the cellular powerhouses that harvest energy from food, as well as a reduced ability to generate new fat cells. Unlike fat tissue in healthy obese people, which generates new cells to help store fat as it accumulates, the fat cells of the unhealthy obese swell to their breaking point, straining the cellular machinery and ultimately dying off. This is accompanied by inflammation, and it leads to ectopic fat accumulation — the shuttling of fat into organs where it does not belong, like the liver, heart and skeletal muscle. A fatty liver frequently coincides with metabolic abnormalities, and studies suggest that it may be one of the causes of insulin resistance, the fundamental defect in Type 2 diabetes. In the healthy obese, however, the fat tends to remain in the subcutaneous padding just beneath the skin, where it appears to be fairly innocuous. “The group that doesn’t gain fat in the liver as they get obese seems to avoid inflammation and maintain their metabolic health,” said Dr. Jussi Naukkarinen, a research scientist specializing in internal medicine at the University of Helsinki. “There is a complete difference in how they react to obesity.” Copyright 2013 The New York Times Company

Keyword: Obesity
Link ID: 18771 - Posted: 10.10.2013

By ABBY ELLIN When binge eating disorder gained legitimacy as a full-fledged mental condition in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders in May, many people in the eating disorders and obesity communities wondered: Will this inspire us to finally get along? It was a good question, since historically, the two groups have been at odds. Unlike people with anorexia or bulimia, who tend to be excessively thin, many binge eaters are overweight or obese. And much of the focus of anti-obesity efforts — listing calories at restaurants, banning cupcakes in schools, sending students home with body mass index “report cards” — are decried by eating disorder activists, who say such measures can encourage anorexia or bulimia. Anti-obesity activists, in turn, worry that the eating disorder community minimizes the medical risks of obesity, which the American Medical Association classified as a disease in June, and plays down the discrimination many obese people face. “They come out of different traditions,” said Kelly Brownell, dean of the Sanford School of Public Policy at Duke University. “Obesity was mainly dealt with in medical professions, and eating disorders were dealt with more in psychology professions.” But binge eating disorder, symptoms of which include consuming enormous amounts of food in a two-hour window without purging at least once a week for three months, could bridge the gap between the two worlds, while also reducing the stereotype that only thin people suffer from eating disorders. Copyright 2013 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 18770 - Posted: 10.10.2013

by Linda Geddes They are identical in almost every way, except one twin is fat and the other is thin. Now a study of this rare group is shedding light on a medical mystery: how some people can be obese and perfectly healthy. Obesity usually goes hand in hand with metabolic syndrome – high blood pressure, high cholesterol and type 2 diabetes – but a minority of obese people escape this fate. To probe the fit fat phenomenon, Jussi Naukkarinen at the University of Helsinki in Finland and his colleagues turned to a registry of identical twins, picking 16 pairs whose body weight differed by 17 kilograms on average. They are a perfect model for studying such differences because they are genetically identical and have usually been raised in very similar environments. Naukkarinen's team started by looking at the siblings' body fat distribution and quickly saw that the fat twins fell into two groups: those that tended to accumulate fat within their livers, and those whose liver fat resembled that of their thin twin. Suppressed activity Next, they looked at other markers of ill-health, including insulin resistance, cholesterol, inflammation and blood pressure. These measures also divided the group. "Basically all the hallmarks of the metabolic syndrome were lacking in the group where there was no liver fat," Naukkarinen says. Researchers also compared samples of the twins' abdominal fat, or adipose tissue. In unhealthy obese twins, genes involved in inflammation were activated – genes that were not activated in their thin twin. The activity of cellular powerhouses called mitochondria seemed to be suppressed as well. But in healthy obese twins, gene expression was similar to that of the thin twin. © Copyright Reed Business Information Ltd.

Keyword: Obesity; Aggression
Link ID: 18754 - Posted: 10.07.2013

by Ed Yong I’ve just arrived home from 14 hours of flying. The clocks on my phone and laptop have been ticking away the whole time, and it takes a few seconds to reset them to British time. The clocks in my body are more difficult. We run on a daily 24-hour body clock, which controls everything from our blood pressure to our temperature to how hungry we feel. It runs on proteins rather than gears. Once they’re built, these proteins stop their own manufacture after a slight delay, meaning that their levels rise and fall with a regular rhythm. These timers tick away inside almost all of our cells, and they’re synchronised by a tiny collection of 10,000 neurons at the bottom of our brain. It’s called the suprachiasmatic nucleus (SCN). It’s the master clock. It’s the conductor that keeps the orchestra in sync. The SCN is also sensitive to light. It gets signals from our eyes, which allows it to synchronise its ticking with the 24-hour cycle of day and night outside. The SCN is what connects the rhythms of our bodies with those of the planet. But when we travel far and fast, and suddenly land in a new time zone, the SCN becomes misaligned with the environment. It takes time to re-adjust, typically one day for every time zone crossed. In the meantime, our sleep is disrupted and our physiology goes weird. In other words: jet lag. But at Kyoto University, Yoshiaki Yamaguchi and Toru Suzuki have engineered mice that break this rule. They are, with apologies for the awful word, unjetlaggable. If you change the light in their cages to mimic an 8-hour time difference, they readjust almost immediately. Put them on a red-eye flight from San Francisco to London and they’d be fine.

Keyword: Biological Rhythms; Aggression
Link ID: 18745 - Posted: 10.05.2013

By Shelly Fan Disclaimer: First things first. Please note that I am in no way endorsing nutritional ketosis as a supplement to, or a replacement for medication. As you’ll see below, data exploring the potential neuroprotective effects of ketosis are still scarce, and we don’t yet know the side effects of a long-term ketogenic diet. This post talks about the SCIENCE behind ketosis, and is not meant in any way as medical advice. The ketogenic diet is a nutritionist’s nightmare. High in saturated fat and VERY low in carbohydrates, “keto” is adopted by a growing population to paradoxically promote weight loss and mental well-being. Drinking coffee with butter? Eating a block of cream cheese? Little to no fruit? To the uninitiated, keto defies all common sense, inviting skeptics to wave it off as an unnatural “bacon-and-steak” fad diet. Yet versions of the ketogenic diet have been used to successfully treat drug-resistant epilepsy in children since the 1920s – potentially even back in the biblical ages. Emerging evidence from animal models and clinical trials suggest keto may be therapeutically used in many other neurological disorders, including head ache, neurodegenerative diseases, sleep disorders, bipolar disorder, autism and brain cancer. With no apparent side effects. Sound too good to be true? I feel ya! Where are these neuroprotective effects coming from? What’s going on in the brain on a ketogenic diet? In essence, a ketogenic diet mimics starvation, allowing the body to go into a metabolic state called ketosis (key-tow-sis). © 2013 Scientific American

Keyword: Obesity
Link ID: 18732 - Posted: 10.02.2013

By Julianne Wyrick Some people are drawn to the thick smell of bacon, sizzling and crackling in the skillet on a Saturday morning. For others, it’s the aroma of freshly baked cookies on a Friday night or the smell of McDonald’s fries creeping in through the car window. At this time of year, I find the scent of freshly baked pumpkin muffins irresistible. Of course, I’d like to think I’m not a slave to my nose, at least not when I’m nice and full from dinner. If I were a fruit fly, my outlook might not be so good. Already-fed fruit fly larvae exposed to certain food-related odors ate more food than larvae that didn’t experience the smells, according to research published by scientists at the University of Georgia last spring. “They’re not hungry, but they will get an extra kick in terms of appetite, so they will eat, for example, 30 percent extra,” said Ping Shen, lead author on the study. The scents, which included the sweet odor of bananas or the sharper smell of balsamic vinegar, served as “cues” or triggers that the flies associated with food. The triggers motivated the fly larvae to eat, even when they’d already had dinner. That doesn’t bode so well for flies trying to watch their weight. For the fly to feel this urge to eat, the smell has to be transported from sensory receptors in the nose to the part of the brain that regulates appetite—the brain’s “feeding center”—via a series of neurons. Part of this signal transfer involves dopamine, a neurotransmitter associated with behavior motivated by a cue or hint of something to come, like smells associated with food. © 2013 Scientific American

Keyword: Obesity; Aggression
Link ID: 18730 - Posted: 10.01.2013

By Laura Sanders By hijacking connections between neurons deep within the brain, scientists forced full mice to keep eating and hungry mice to shun food. By identifying precise groups of cells that cause eating and others that curb it, the results begin to clarify the intricate web of checks and balances in the brain that control feeding. “This is a really important missing piece of the puzzle,” says neuroscientist Seth Blackshaw of Johns Hopkins University in Baltimore. “These are cell types that weren’t even predicted to exist.” A deeper understanding of how the brain orchestrates eating behavior could lead to better treatments for disorders such as anorexia and obesity, he says. Scientists led by Joshua Jennings and Garret Stuber of the University of North Carolina at Chapel Hill genetically tweaked mice so that a small group of neurons would respond to light. When a laser shone into the brain, these cells would either fire or, in a different experiment, stay quiet. These neurons reside in a brain locale called the bed nucleus of the stria terminalis, or BNST. Some of the message-sending arms of these neurons reach into the lateral hypothalamus, a brain region known to play a big role in feeding. When a laser activated these BNST neurons, the mice became ravenous, voraciously eating their food, the researchers report in the Sept. 27 Science. “As soon as you turn it on, they start eating and they don’t stop until you turn it off,” Stuber says. The opposite behavior happened when a laser silenced BNST neurons’ messages to the lateral hypothalamus: The mice would not eat, even when hungry. © Society for Science & the Public 2000 - 2013

Keyword: Obesity
Link ID: 18717 - Posted: 09.28.2013

By Tara Haelle A change in the way anorexia is diagnosed may make it easier to help more teens, not just thin ones, with the illness. Previously, overweight or obese teens were more likely to fall through the cracks when they developed anorexic behaviors. Now, the release of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) has broadened the disorder criteria by taking away the weight requirement. The change shifts the focus of the diagnosis from “being thin” to the behaviors of those with the illness. The previous criteria perpetuated the idea that anorexia is a weight disorder—rather than a psychological one. “A lot of people need help even if they don’t narrowly fit the definition of an illness,” says David Hahn, medical director of The Renfrew Center of Philadelphia. “This criteria makes clear that the behaviors, even without a very low weight, are pathologic and need to be addressed. The criteria may very much help pediatricians catch an eating disorder sooner and may teach the public and families to intervene more quickly if it’s understood that anorexia doesn’t only mean underweight.” Anorexia nervosa most often begins in adolescence and affects approximately 0.3 percent of teens. An additional 0.8 percent were found in one large study to have “subthreshold anorexia nervosa”—they showed the symptoms but did not meet all the criteria. Overall, about 6 percent of teens suffer from some kind of eating disorder, such as bulimia, binge-eating and other eating issues previously classified in the DSM-IV as “Eating Disorder—Not Otherwise Specified” (ED-NOS). © 2013 Scientific American

Keyword: Anorexia & Bulimia
Link ID: 18704 - Posted: 09.26.2013

Declan Butler Ghost writing is taking on an altogether different meaning in a mysterious case of alleged scientific fraud. The authors of a paper published in July (A. Vezyraki et al. Biochem. Biophys. Res. Commun. http://doi.org/nxb; 2013), which reported significant findings in obesity research, seem to be phantoms. They are not only unknown at the institution listed on the paper, but no trace of them as researchers can be found. The paper, published in the Elsevier journal Biochemical and Biophysical Research Communications (BBRC), is not the kind of prank that journals have encountered before, in which hoaxsters have submitted dummy papers to highlight weaknesses in the peer-review process. The paper’s reported findings — that overexpression of two novel proteins in fat cells leads to improvements in metabolic processes related to diabetes and obesity in mice — are, in fact, true. Too true, in the opinion of Bruce Spiegelman, a cell biologist at Harvard Medical School’s Dana-Farber Cancer Institute in Boston, Massachusetts. He says that he has presented similar findings at about six research meetings, and is preparing to submit them to a journal. He suspects that the BBRC paper was intended as a spoiler of his own lab’s work. Now withdrawn, the article lists five authors who are all supposedly from the School of Health Sciences at the University of Thessaly in Trikala, Greece, and is entitled ‘Identification of meteorin and metrnl as two novel pro-differentiative adipokines: Possible roles in controlling adipogenesis and insulin sensitivity’. Adipokines are proteins secreted by fat tissue that play an active part in such processes as sugar and fat metabolism, inflammation and obesity-related metabolic disorders, including insulin resistance and diabetes. © 2013 Nature Publishing Group

Keyword: Obesity
Link ID: 18701 - Posted: 09.25.2013

By Michelle Roberts Health editor, BBC News online People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers. The University of Southampton team looked at available medical studies and found evidence the two were linked. But there was no proof that one necessarily caused the other. It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal. Or the drugs themselves may interfere with blood sugar control. Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk. Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings. And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs. With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say. Prof Holt said: "Some of this may be coincidence but there's a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes. BBC © 2013

Keyword: Depression; Aggression
Link ID: 18697 - Posted: 09.25.2013

By JAN HOFFMAN When Vinnie Richichi started watching the Pittsburgh Steelers’ home opener against the Tennessee Titans last Sunday, he was feeling great. After all, the Steelers had won their first home game six years in a row. Then things indeed went south. “The worse they looked, the more I kept going to the fridge,” recalled Mr. Richichi, a co-host of a sports talk show on KDKA-FM in Pittsburgh. “First a couple of Hot Pockets. By the second quarter I threw in a box of White Castle hamburgers. As the game progressed, I just went through the refrigerator: the more fear, the more emotion, I’m chomping down. But I’m not going near the salad or the yogurt. If it doesn’t have 700 calories, I’m going right past it.” The aftereffect of the Steelers’ ignominious defeat by a score of 16-9 clung to Mr. Richichi on Monday, when he rejected his regular breakfast of yogurt and strawberries in favor of a bagel sandwich with sausage, eggs, cheese, peppers and hot sauce. Then, his mood hardly improved after spending four hours on the air railing and commiserating with Steelers’ fans, he had pizza for lunch. “My weight goes up and down with my teams, “ said Mr. Richichi. “My team does well? I’m 40, 50 pounds lighter.” Mr. Richichi’s eating habits, joined at the waistline with the N.F.L., were reflected in a recent study that investigated whether a football team’s outcome had an effect on what fans ate the day after a game. Although the study did not look at weight fluctuations, researchers found that football fans’ saturated-fat consumption increased by as much as 28 percent following defeats and decreased by 16 percent following victories. The association was particularly pronounced in the eight cities regarded as having the most devoted fans, with Pittsburgh often ranked No. 1. Narrower, nail-biting defeats led to greater consumption of calorie and fat-saturated foods than lopsided ones. Copyright 2013 The New York Times Company

Keyword: Obesity; Aggression
Link ID: 18650 - Posted: 09.16.2013

By GRETCHEN REYNOLDS As readers of this column know, short, intense workouts, usually in the form of intervals that intersperse bursts of hard effort with a short recovery time, have become wildly popular lately, whether the sessions last for four minutes, seven minutes or slightly longer. Studies have found that such intense training, no matter how abbreviated, usually improves aerobic fitness and some markers of health, including blood pressure and insulin sensitivity, as effectively as much longer sessions of moderate exercise. What has not been clear, though, is whether interval training could likewise also aid in weight control. So for a study published online in June in The International Journal of Obesity, researchers at the University of Western Australia in Perth and other institutions set out to compare the effects of easy versus exhausting exercise on people’s subsequent desire to eat. To do so, they recruited 17 overweight but otherwise healthy young men in their 20s or 30s and asked them to show up at the university’s exercise physiology lab on four separate days. One of these sessions was spent idly reading or otherwise resting for 30 minutes, while on another day, the men rode an exercise bike continuously for 30 minutes at a moderate pace (equivalent to 65 percent of their predetermined maximum aerobic capacity). A third session was more demanding, with the men completing 30 minutes of intervals, riding first for one minute at 100 percent of their endurance capacity, then spinning gently for 4 minutes. The final session was the toughest, as the men strained through 15 seconds of pedaling at 170 percent of their normal endurance capacity, then pedaled at barely 30 percent of their maximum capacity for a minute, with the entire sequence repeated over the course of 30 minutes. Copyright 2013 The New York Times Company

Keyword: Obesity
Link ID: 18641 - Posted: 09.14.2013

By GINA KOLATA It is the scourge of many a middle-aged man: he starts getting a pot belly, using lighter weights at the gym and somehow just doesn’t have the sexual desire of his younger years. The obvious culprit is testosterone, since men gradually make less of the male sex hormone as years go by. But a surprising new answer is emerging, one that doctors say could reinvigorate the study of how men’s bodies age. Estrogen, the female sex hormone, turns out to play a much bigger role in men’s bodies than previously thought, and falling levels contribute to their expanding waistlines just as they do in women’s. The discovery of the role of estrogen in men is “a major advance,” said Dr. Peter J. Snyder, a professor of medicine at the University of Pennsylvania, who is leading a big new research project on hormone therapy for men 65 and over. Until recently, testosterone deficiency was considered nearly the sole reason that men undergo the familiar physical complaints of midlife. The new frontier of research involves figuring out which hormone does what in men, and how body functions are affected at different hormone levels. While dwindling testosterone levels are to blame for middle-aged men’s smaller muscles, falling levels of estrogen regulate fat accumulation, according to a study published Wednesday in The New England Journal of Medicine, which provided the most conclusive evidence to date that estrogen is a major factor in male midlife woes. And both hormones are needed for libido. “Some of the symptoms routinely attributed to testosterone deficiency are actually partially or almost exclusively caused by the decline in estrogens,” said Dr. Joel Finkelstein, an endocrinologist at Harvard Medical School and the study’s lead author, in a news release on Wednesday. © 2013 The New York Times Company

Keyword: Obesity; Aggression
Link ID: 18637 - Posted: 09.12.2013

By Susan Milius Mice in the wild have no problem dining where someone else has pooped. Animals with higher standards of hygiene, reported in earlier studies, may not face the same dangers as small, hungry creatures scurrying around the woods. Feeding among feces of your own species raises the risk of catching nasty intestinal parasites, explains behavioral ecologist Patrick T. Walsh of University of Edinburgh. So far most tests of fecal avoidance have focused on hoofed animals. Horses, cows, sheep, reindeer and even wild antelopes tend not to graze in heavily poop-dotted areas. White-footed and deer mice, however, show no such daintiness of manners in a test in the woods, Walsh and his colleagues report in the September Animal Behaviour. Wild mice may have more immediate problems, like starvation or predators that domesticated--or just plain bigger--animals don’t. For the wild mice, Walsh says, fecal avoidance may be “a luxury.” Learning whether and when animals avoid poop helps clarify how parasites spread, an issue important for the health of both wildlife and people. So far no one has tested fecal avoidance for mice feeding in the lab, but research has shown that female lab mice tend to avoid the urine of parasite-infected males. To see whether mice in the wild dodge parasite risks, Amy Pedersen, a coauthor of the study also at Edinburgh, designed an experiment with a long plastic box divided into zones, some of which had mouse droppings in them. In the experiment, researchers tested more than 130 wild Peromyscus mice, of either the leucopus or maniculatus species, held captive for less than a day in the mountains of Virginia. © Society for Science & the Public 2000 - 2013

Keyword: Neuroimmunology; Aggression
Link ID: 18635 - Posted: 09.12.2013

Brian Owens Gut bacteria from lean mice can invade the guts of obesity-prone cage-mates and help their new hosts to fight weight gain. Researchers led by Jeffrey Gordon, a biologist at Washington University in St. Louis, Missouri, set out to find direct evidence that gut bacteria have a role in obesity. The team took gut bacteria from four sets of human twins in which one of each pair was lean and one was obese, and introduced the microbes into mice bred to be germ-free. Mice given bacteria from a lean twin stayed slim, whereas those given bacteria from an obese twin quickly gained weight, even though all the mice ate about the same amount of food. The team wondered whether the gut microbiota of either group of mice would be influenced by mice with one type living in close quarters with animals harbouring the other type. So the scientists took mice with the ‘lean’ microbiota and placed them in a cage with mice with the ‘obese’ type before those mice had a chance to start putting on weight. “We knew the mice would readily exchange their microbes,” Gordon says — that is, eat each other’s faeces. Sure enough, the populations of bacteria in the obese-type mice changed to match those of their lean cage-mates, and their bodies remained lean, the team writes today in Science1. © 2013 Nature Publishing Group,

Keyword: Obesity
Link ID: 18617 - Posted: 09.07.2013

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

Keyword: Obesity
Link ID: 18616 - Posted: 09.07.2013