Chapter 13. Homeostasis: Active Regulation of the Internal Environment

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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 Now withdrawn, the article lists five authors who are all supposedly from the School of Health Sciences at the University of Thessaly in Trikala, Greece, and is entitled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

By Caitlin Shure The newest chemical under investigation for managing Alzheimer’s disease (AD) is actually not new at all. Insulin, the therapeutic hormone all-too familiar to individuals with diabetes, has been around for decades. In fact December will mark 90 years since its discoverers earned the Nobel Prize in Physiology or Medicine for the extraction of insulin for clinical use. Yet to say that insulin has been under our noses all these years wouldn’t exactly be correct. Because if it had been under our noses, we might have sensed its neurologic benefits sooner. The latest insulin therapy is not delivered via injection like its diabetes-treating counterparts, nor does it come in the form of a pill or a patch like the cholinesterase inhibitors often prescribed to patients with AD. Instead this novel therapeutic enters the body through the nose—the only entry point that gives insulin a chance of reaching the brain. A large peptide molecule, insulin from the blood cannot float easily into the brain because the blood brain barrier (BBB), a sort of neuroprotective moat, prevents its transport. Fortified by cellular guards called tight junctions, the BBB rejects many pharmacologic hopefuls, allowing entrance only to certain types of substances. Namely small or lipophilic molecules can be administered orally (or via injection, or through the skin) and as long as the relevant chemicals end up in the blood stream, they can casually saunter across the BBB and act on the brain. Large and cumbersome, insulin does not have this luxury and must therefore take a more creative route across the moat. © 2013 Scientific American

Keyword: Alzheimers; Aggression
Link ID: 18546 - Posted: 08.22.2013

By Jessica Shugart People who need sugary snacks to stay sharp throughout the day could be prisoners of their own beliefs. The brain works just fine without regular shots of sugar in people who believe their willpower is unlimited, a new study shows. “There's a dominant theory in psychology that willpower is limited, and whenever you exert yourself to do a hard task or to resist a temptation, you deplete this limited resource,” says psychologist Carol Dweck from Stanford University. Previous studies have shown that mental exertion diminishes blood glucose levels and that a person’s willpower can be rejuvenated by ingesting a sugary drink. But Dweck’s earlier work led her to suspect that people’s attitudes about willpower may be responsible for that effect. In the new study, published online August 19 in the Proceedings of the National Academy of Sciences, Dweck, along with colleagues at the University of Zurich in Switzerland, focused on how attitudes about willpower may shape a person’s sugar dependence in the face of a challenge. The scientists also tested whether altering these beliefs might liberate a person from such a calorie-rich requirement. In the first of three experiments, the researchers asked students about their attitudes on willpower, then gave them lemonade sweetened with either sugar or a sugar substitute. Ten minutes after downing the sweet beverage, the students took tests of self-control and mental acuity. The students who subscribed to a self-generating belief about unlimited willpower scored equally well whether their drinks contained sugar or not. But the students who felt willpower was limited needed sugar to perform as well as the other group did. © Society for Science & the Public 2000 - 2013

Keyword: Attention; Aggression
Link ID: 18537 - Posted: 08.20.2013

By Cristy Gelling Repairing a faulty communication line between the gut and the brain can quell the urge to overeat, an experiment that cured chubby mice of their junk food addiction indicates. A similar strategy might be used to treat compulsive eating in people. Some scientists have proposed that, in both mice and humans, overeating can resemble drug addiction; the more food a person consumes, the less responsive the brain becomes to the pleasure of eating. By restoring normal communication between the gut and brain, researchers were able to resensitize overfed rodents to the pleasures of both fatty and healthy foods. "The therapeutic implications are huge,” says neuroscientist Paul Kenny of the Scripps Research Institute in Jupiter, Fla., who was not involved in the study. In the brain, a chemical called dopamine surges in response to pleasurable experiences like eating, sex and taking drugs. But brain-scanning studies suggest that obese individuals have muted dopamine reponses to food. These changes could lead overeaters to seek more and more food to satisfy their cravings, suggests study leader Ivan de Araujo of Yale University. De Araujo and his colleagues looked for ways to restore the dopamine response of overfed mice by studying the signals sent by their guts. In previous work, the researchers found that mice get a dopamine rush when fat is introduced directly into the small intestine via catheters. This shows that the gut communicates with the brain’s reward center even when the mouse can’t taste food. © Society for Science & the Public 2000 - 2013

Keyword: Obesity; Aggression
Link ID: 18522 - Posted: 08.17.2013

Drinking several servings of soda a day is associated with behaviour problems such as aggression, a new study of preschoolers suggests. When researchers looked at 2,929 children in the U.S., they found 43 per cent of parents said their child had at least one serving of soda a day and four per cent had four or more servings daily. Four per cent of parents in the study reported their children had four or more servings of pop a day. Sugar and caffeine are potential triggers for behaviour, but parenting practices and home environment are also an influence.Four per cent of parents in the study reported their children had four or more servings of pop a day. Sugar and caffeine are potential triggers for behaviour, but parenting practices and home environment are also an influence. (Reuters) "In this large sample of five-year-old urban U.S. children, we found strong and consistent relationships between soda consumption and a range of problem behaviours, consistent with the findings of previous studies in adolescents," Shakira Suglia of Columbia University's Mailman School of Public Health in New York and her coauthors concluded in Friday's issue of the Journal of Pediatrics. Children who consumed four or more servings of soda per day were more than twice as likely to destroy things belonging to others, to get into fights and to physically attack people compared with children who drank no soda. Drinking four servings of soft drinks was associated with increased aggressive behaviour, even after accounting for factors such as TV viewing, candy consumption, maternal depression and intimate partner violence. © CBC 2013

Keyword: Aggression; Aggression
Link ID: 18521 - Posted: 08.17.2013

Brian Owens Too much sugar is bad for you, but how much, exactly, is too much? A study in mice has found that the animals' health and ability to compete can be harmed by a diet that has sugar levels equivalent to what many people in the United States currently consume. High-sugar diets are associated not only with obesity and diabetes, but also with other human conditions such as coronary heart disease. However, the exact causal links for many of these has not been established. When studies are done in mice to evaluate health effects of sugar, the doses given are often so high, and outside the range of equivalent human consumption, that it is hard to tell conclusively whether the results are relevant to people. “Nobody has been able to show adverse effects at human-relevant levels,” says Wayne Potts, an evolutionary biologist at the University of Utah in Salt Lake City. But in a study published today in Nature Communications1, Potts and his colleagues looked at what happens under conditions comparable to the lifestyles of a substantial number of people in the United States. The researchers bred a pair of wild mice captured by Potts in a bakery, and fed offspring a diet in which 25% of the calories came from sugar. This is the maximum 'safe' level recommended by the US National Academies and by the US Department of Agriculture, and such a diet is consumed by around 13–25% of the US population. The safe level is roughly equivalent to drinking three cans of sugary drinks a day but having an otherwise sugar-free diet. © 2013 Nature Publishing Group

Keyword: Obesity
Link ID: 18509 - Posted: 08.14.2013