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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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18717 - Posted: 09.28.2013

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18701 - 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Emotions, Aggression, and Stress
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 18637 - 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,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 18615 - Posted: 09.07.2013

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18553 - Posted: 08.24.2013

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18522 - 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18509 - Posted: 08.14.2013

Heidi Ledford A procedure increasingly used to treat obesity by reducing the size of the stomach also reprogrammes the intestines, making them burn sugar faster, a study in diabetic and obese rats has shown. If the results, published today in Science1, hold true in humans, they could explain how gastric bypass surgery improves sugar control in people with diabetes. They could also lead to less invasive ways to produce the same effects. “This opens up the idea that we could take the most effective therapy we have for obesity and diabetes and come up with ways to do it without a scalpel,” says Randy Seeley, an obesity researcher at the University of Cincinnati in Ohio, who was not involved in the work. As rates of obesity and diabetes skyrocket in many countries, physicians and patients are turning to operations that reconfigure the digestive tract so that only a small part of the stomach is used. Such procedures are intended to allow people to feel full after smaller meals, reducing the drive to consume extra calories. But clinical trials in recent years have shown that they can also reduce blood sugar levels in diabetics, even before weight is lost2, 3. “We have to think about this surgery differently,” says Seeley. “It’s not just changing the plumbing, it’s altering how the gut handles glucose.” © 2013 Nature Publishing Group,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18412 - Posted: 07.27.2013

By GINA KOLATA The mice were eating their usual chow and exercising normally, but they were getting fat anyway. The reason: researchers had deleted a gene that acts in the brain and controls how quickly calories are burned. Even though they were consuming exactly the same number of calories as lean mice, they were gaining weight. So far, only one person — a severely obese child — has been found to have a disabling mutation in the same gene. But the discovery of the same effect in mice and in the child — a finding published Wednesday in the journal Science — may help explain why some people put on weight easily while others eat all they want and seem never to gain an ounce. It may also offer clues to a puzzle in the field of obesity: Why do studies find that people gain different amounts of weight while overeating by the same amount? Scientists have long thought explanations for why some people get fat might lie in their genes. They knew body weight was strongly inherited. Years ago, for example, they found that twins reared apart tended to have similar weights and adoptees tended to have weights like their biological parents, not the ones who reared them. As researchers developed tools to look for the actual genes, they found evidence that many — maybe even hundreds — of genes may be involved, stoking appetites, making people voraciously hungry. This rare gene-disabling mutation, though, is intriguing because it seems to explain something different, a propensity to pile on pounds even while eating what should be a normal amount of food. Investigators are now searching for other mutations of the same gene in fat people that may have a similar, but less extreme effect. The hope is that in the long term, understanding how this gene affects weight gain might lead to treatments for obesity that alter the rate at which calories are burned. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 18394 - Posted: 07.20.2013

By GRETCHEN REYNOLDS Two newly published studies investigate the enticing possibility that we might one day be able to gain the benefits of exercise by downing a pill, rather than by actually sweating. But while some of the research holds out promise for an effective workout pill, there remains the question of whether such a move is wise. The more encouraging of the new studies, which appears this week in Nature Medicine, expands on a major study published last year in Nature. In that study, researchers at the Scripps Research Institute in Jupiter, Fla., reported that a compound they had created and injected into obese mice increased activation of a protein called REV-ERB, which is known to partially control animals’ circadian rhythms and internal biological clocks. The injected animals lost weight, even on a high-fat diet, and improved their cholesterol profiles. Unexpectedly, the treated mice also began using more oxygen throughout the day and expending about 5 percent more energy than untreated mice, even though they were not moving about more than the other animals. In fact, in most cases, they were more physically lazy and inactive than they had been before the injections. The drug, it seemed, was providing them with a workout, minus the effort. Intrigued, the Scripps scientists, in conjunction with researchers from the Pasteur Institute in France and other institutions, set out to see what their compound might be doing inside muscles to provide this ersatz exercise. They knew that their drug increased the potency of the REV-ERB protein, but no one yet knew what REV-ERB actually does in muscles. So they began by developing a strain of mice that could not express very much of the protein in their muscle cells. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: The Sensorimotor System
Link ID: 18384 - Posted: 07.18.2013

by Sarah C. P. Williams Researchers think they've hit on why a common obesity gene causes weight gain: Those who carry a version of it don't feel full after eating and take in extra calories. That's because the variant of the FTO gene in question, which one in six individuals carry, leads to higher levels of ghrelin, a hormone involved in mediating appetite and the body's response to food, researchers have discovered. While most studies on FTO have relied on mice, the new work analyzed blood samples and brain scans from humans. "This is a very exciting piece of research," says geneticist Andrew Hattersley of the Peninsula Medical School in Exeter, U.K., who was not involved in the new study. "There is a lot of work that's been done on the mechanism of FTO in animals, but you have to be careful about applying those lessons to people. So it's nice to finally see work done in humans." Hattersley was part of a team that in 2007 reported that people who had one version of the FTO gene, called AA, weighed an average of 3 kilograms more than those with the TT version of the gene. Since then, studies in mice have shown that in everyone, there are high levels of the FTO protein in brain areas that control energy balance. Researchers have also found that animals with the AA version tend to eat more and prefer high-fat food compared with those with the TT version. But why FTO had this effect wasn't known. © 2010 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 18381 - Posted: 07.16.2013

by Elizabeth Norton Transforming fat cells into calorie-burning machines may sound like the ultimate form of weight control, but the idea is not as far-fetched as it sounds. Unexpectedly, some fat cells directly sense dropping temperatures and release their energy as heat, according to a new study; that ability might be harnessed to treat obesity and diabetes, researchers suggest. Fat is known to help protect animals from the cold—and not only by acting as insulation. In the early 1990s, scientists studying mice discovered that cold temperatures trigger certain fat cells, called brown adipose tissue, to release stored energy in the form of heat—to burn calories, in other words. Researchers have always assumed this mechanism was an indirect response to the physiological stress of cold temperatures, explains cell biologist Bruce Spiegelman of Harvard Medical School, Boston. The activation of brown fat seems to start with sensory neurons throughout the body informing the brain of a drop in temperature. In response the brain sends out norepinephrine, the chief chemical messenger of the sympathetic nervous system, which mobilizes the body to cope with many situations. In experimental animals, stimulating norepinephrine receptors triggered brown adipose tissue to release its energy and generate heat, while animals bred to be missing these receptors were unable to mount the same fat cell response. People also have brown adipose tissue that generates heat when the body is cold. And unlike white fat, which builds up around the abdomen and contributes to many disorders including heart disease and diabetes, this brown fat is found in higher proportions in leaner people and seems to actively protect against diabetes. © 2010 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18334 - Posted: 07.02.2013

By JANE E. BRODY Most people know that obesity can result in serious health problems, yet many of us continue to focus on its cosmetic consequences rather than its risks to health. This distorted view may change now that the American Medical Association has finally labeled obesity a disease, not just a risk factor for other disorders. Last month, the organization recognized that obesity is a verifiable illness that warrants far more attention than physicians, patients and insurers currently give it. The designation may change how aggressively doctors treat obesity, foster the development of new therapies, and lead to better coverage byinsurers. After all, the price of not treating obesity is now in the stratosphere. Obesity-related health conditions cost the nation more than $150 billion and result in an estimated 300,000 premature deaths each year. If the population’s weight gain is not soon capped (or better yet, reversed), experts predict that half of adults in America will be obese by 2040. The A.M.A. has said in effect that it is medicine’s responsibility to provide the knowledge and tools needed to curb this runaway epidemic. On June 19, James Gandolfini, the hefty award-winning actor who portrayed Tony Soprano in “The Sopranos,” died at 51, apparently of a heart attack, while on vacation in Italy. Even if genetics played a role, Mr. Gandolfini’s weight contributed significantly to his risk of sudden cardiac death. Not a week earlier, a 46-year-old member of my family who weighed over 300 pounds died suddenly of what might have been a heart attack while dozing in front of the television. He had long suffered from sleep apnea (a risk factor for sudden death), high blood pressure and severe gout, all results of his extreme weight. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18330 - Posted: 07.01.2013