Chapter 9. Homeostasis: Active Regulation of the Internal Environment

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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.; 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

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

Keyword: Obesity; Aggression
Link ID: 18615 - Posted: 09.07.2013

By Caitlin Kirkwood Do NOT EAT the chemicals. It is the #1 laboratory safety rule young scientists learn to never break and for good reason; it keeps lab citizens alive and unscathed. However, if it hadn’t been for the careless, rule-breaking habits of a few rowdy scientists ingesting their experiments, many artificial sweeteners may never have been discovered. Perhaps the strangest anecdote for artificial sweetener discovery, among tales of inadvertent finger-licking and smoking, is that of graduate student Shashikant Phadnis who misheard instructions from his advisor to ‘test’ a compound and instead tasted it. Rather than keeling over, he identified the sweet taste of sucralose, the artificial sweetener commonly known today as Splenda. Artificial sweeteners like Splenda, Sweet’N Low, and Equal provide a sweet taste without the calories. Around World War II, in response to a sugar shortage and evolving cultural views of beauty, the target consumer group for noncaloric sweetener manufacturers shifted from primarily diabetics to anyone in the general public wishing to reduce sugar intake and lose weight. Foods containing artificial sweeteners changed their labels. Instead of cautioning ‘only for consumption by those who must restrict sugar intake’, they read for those who ‘desire to restrict’ sugar. Today, the country is in the middle of a massive debate about the health implications of artificial sweeteners and whether they could be linked to obesity, cancer, and Alzheimer disease. It’s a good conversation to have because noncaloric sweeteners are consumed regularly in chewing gums, frozen dinners, yogurts, vitamins, baby food, and particularly in diet sodas. © 2013 Scientific American

Keyword: Chemical Senses (Smell & Taste); Aggression
Link ID: 18614 - Posted: 09.07.2013

By Laura Sanders Rats spent hours in a state of chilly suspended animation after researchers injected a compound into the animals in a cold room. The animals’ heart rates slowed, brain activity became sluggish and body temperature plummeted. The research joins a small number of studies that attempt to induce the metabolically lethargic state known as torpor in animals that can’t normally slow their metabolism. “It’s a breakthrough” in understanding aspects of torpor, says neuroscientist Kelly Drew of the University of Alaska Fairbanks. Lowering the body temperature of a nonhibernating mammal is really hard, says Domenico Tupone of Oregon Health & Science University in Portland. As temperatures inside the body fall, several failsafe systems spring into action. Blood vessels near the skin squeeze tight to hold warmth in, the body starts to shiver and brown fat, a tissue that’s especially plentiful in newborns, starts to produce heat. But Tupone and colleagues bypassed the rats’ defenses against the cold with a compound that’s similar to adenosine, a molecule in the body that signals sleepiness. After about an hour in a room chilled to 15° Celsius, the rats grew lethargic. Their brain waves slowed, their blood pressure dropped and their heart grew sluggish, occasionally skipping beats. The rats’ core temperature dropped from about 38° to about 30° C, or 80° Fahrenheit, the authors report in the Sept. 4 Journal of Neuroscience. Tupone and his colleagues measured even lower temperatures in further experiments — rats’ core body temperature reached 15° C or about 57° F. “That is a pretty amazing temperature. No one has done this before,” he says. © Society for Science & the Public 2000 - 2013

Keyword: Miscellaneous
Link ID: 18609 - Posted: 09.05.2013

By Scicurious For my food week post, I’m going at it a little differently. We spend a lot of time talking about food, thinking about whether it’s good for us, bad for us, which aspects of it are good or bad for us. We talk about why we crave some foods vs others, and we talk about why some foods taste disgusting. We talk about whether you’d want to replace your entire diet with a chalky fluid substance. Foodies spend a lot of time taking pictures of it, diet mags spend a lot of time talking about how to eat less of it. Food is surrounded by a culture that permeates almost everything we put in our mouths. But food is more than what we like or don’t like. Food is more than a relationship between our stomach and our tongues and noses. There is a very strong relationship between food and your brain, and when it goes wrong, the results can be devastating. There is anorexia, where there is distorted body perception, huge fear of weight gain, and food restriction so severe it can kill. On the opposite end, there is binge eating, uncontrollable eating that people are unable to stop, despite health consequences and social stigma. Critical to both of these problems are issues with “reward”. Food needs to be rewarding, it needs to make you crave it, want more of it, seek it out, work to obtain it. We need to crave food because if we didn’t, we’d all starve to death due to lack of motivation. In binge eating, though, that craving becomes an obsession. And it’s a dangerous one. People who binge eat severely are at risk for obesity, heart problems, diabetes, and other health problems. There is also a lot of anxiety, depression, guilt, and other mental distress that goes along with binge eating. This is more than just a need for portion control or more exercise. It’s a serious compulsion and mental illness, and it shouldn’t be taken lightly. © 2013 Scientific American

Keyword: Anorexia & Bulimia; Aggression
Link ID: 18601 - Posted: 09.03.2013

By Felicity Muth In my previous post, I talked about how crickets were influenced by who was watching them when they performed a victory dance after winning a fight. Although this is a unique finding, it fits into a larger picture of many animals (including insects) being affected by their social context. At the animal behaviour conference I went to in Colorado (where I heard both about the cricket research and about the study I’m going to write about today), you could see how people were affected by what others were doing around them. When one person sneaked out before the end of a talk to go to a talk in a different room, a load of other people would follow. When chatting with a friend, a person would modify what they were saying depending on who else was in the vicinity. Whether we are aware of it all of the time or not, we constantly modify our behaviour depending on the social context we’re in. Well, in addition to crickets, it turns out that honeybees are affected by social context too. This isn’t surprising, given that these bees are highly social animals, but quite how they are affected is rather interesting. Honeybees live in colonies of up to 40, 000 – 80, 000 individuals, almost all females. Like humans, honeybees like to keep their dwelling at constant temperature, not least to make sure that their brood can develop. Unlike humans however, bees think around 36°C (96.8°F) is a great temperature to have their home at. In the winter, honeybees shiver to produce heat, pressing their abdomens against their brood (stored in cells) to distribute the heat more evenly. In the summer however, it can get pretty hot, and so the bees use some strategies to cool down that are not dissimilar to our own. They collect water that can evaporate in the colony and cool it down. They also fan to circulate air around the colony. However, until recently it was not clear how bees decide to start fanning, and whether this might be influenced by what others are doing. © 2013 Scientific American

Keyword: Miscellaneous
Link ID: 18586 - Posted: 08.31.2013

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

Keyword: Obesity; Aggression
Link ID: 18578 - Posted: 08.29.2013

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

Keyword: Obesity
Link ID: 18553 - Posted: 08.24.2013