Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By Christie Wilcox There’s a lot to be said for smarts—at least we humans, with some of the biggest brains in relation to our bodies in the animal kingdom, certainly seem to think so. The size of animal brains is extravagantly well-studied, as scientists have long sought to understand why our ancestors developed such complex and energetically costly neural circuitry. One of the most interesting evolutionary hypotheses about brain size is The Expensive Tissue Hypothesis. Back in the early 1990s, scientists were looking to explain how brain size evolves. Brains are exceedingly useful organs; more brain cells allows for more behavioral flexibility, better control of larger bodies, and, of course, intelligence. But if bigger brains were always better, every animal would have them. Thus, scientists reasoned, there must be a downside. The hypothesis suggests that while brains are great and all, their extreme energetic cost limits their size and tempers their growth. When it comes to humans, for example, though our brains are only 2% of our bodies, they take up a whopping 20% of our energy requirements. And you have to wonder: with all that energy being used by our brains, what body parts have paid the price? The hypothesis suggested our guts took the hit, but that intelligence made for more efficient foraging and hunting, thus overcoming the obstacle. This makes sense, but despite over a century of research on the evolution of brain size, there is still controversy, largely stemming from the fact that evidence for the expensive tissue hypothesis is based entirely on between species comparisons and correlations, with no empirical tests. © 2013 Scientific American
Analysis by Sheila Eldred This spring, it's likely there will be a new diet pill on the market. Belviq (lorcaserin) won approval from the FDA last spring, making it the first weight-loss drug approved in 13 years, and the DEA proposed this week that the drug be classified as a Schedule IV controlled substance. Belviq is an appetite suppressant. The new chemical entity works by activating the brain's response to serotonin. Serotonin is a neuro-transmitter known for evoking happy moods; some anti-depressants work by keeping serotonin levels elevated. Belviq works specifically with the serotonin receptors involved with appetite, according to Time. In trial, patients who took Belviq lost 3 to 3.7 percent more weight than those taking a placebo; after taking it for one or two years, 47 percent lost at least 5 percent of their body weight (compared to 23 percent of those who took a placebo), WebMD reports. Another new weight loss drug, Qsymia, is already on the market, although sales have been slow. Belviq is approved for obese people and overweight people who have another weight-related disease or risk factor. Side effects include headache, dizziness, fatigue, nausea, dry mouth and constipation; in patients with diabetes, additional side effects include low blood sugar, back pain, and coughing. © 2012 Discovery Communications, LLC.
Link ID: 17630 - Posted: 12.22.2012
By Kate Clancy I tend to go to bed freezing, especially so in the winter, so I pile our flannel sheet, blanket, and down comforter over me when I settle in to sleep. A few times each menstrual cycle, clustered together in the luteal phase between ovulation and menses, I wake up from sleep completely soaked in my own sweat – not a delightful sight or experience. Usually I get up, change pajamas, and try to find a dry spot on the bed to go back to sleep (I promise the sheets eventually get washed, but I’m not about to wake my husband – and sometimes daughter – to change the bed at 3am). These night sweats started when I was still intensively breastfeeding my daughter and was marathon training, when she was under a year old. At first, I thought it was because we were co-sleeping and we slept next to each other. But I never experienced them next to my husband before that point, and he is a six foot four heat generating machine. When the marathon was over and I returned to less strenuous activity, breastfeeding frequency was also starting to decline. I didn’t get any night sweats again for quite some time. Then there was roller derby. At first, roller derby was a pastime, a recreational activity where I got to learn something totally new and hang out with women I respected. But of course, being the competitive person I am, it became an obsession, and in addition to roller derby practices I was working out quite a lot on my own time. Over the last year I’ve made additional nutritional adjustments to further improve my performance, and I’ve increased the intensity of my off-skates workouts. I work out a minimum of five hours a week, but in the middle of the season it is usually a minimum of nine hours per week. © 2012 Scientific American
Keyword: Hormones & Behavior
Link ID: 17609 - Posted: 12.17.2012
Gary Taubes. “It is better to know nothing,” wrote French physiologist Claude Bernard in An Introduction to the Study of Experimental Medicine (1865), “than to keep in mind fixed ideas based on theories whose confirmation we constantly seek.” Embracing a fixed idea is one of the main dangers in the evolution of any scientific discipline. Ideally, errors will be uncovered in the trial-by-fire of rigorous testing and the science will right itself. In rare cases, however, an entire discipline can be based on a fundamental flaw. As a science journalist turned science historian, I have written at length about how and why this may have happened in obesity research. I have suggested that the discipline may be a house of cards — as, by extension, may much research into the chronic diseases associated with obesity, such as diabetes. Before the Second World War, European investigators believed that obesity was a hormonal or regulatory disorder. Gustav von Bergmann, a German authority on internal medicine, proposed this hypothesis in the early 1900s. The theory evaporated with the war. After the lingua franca of science switched from German to English, the German-language literature on obesity was rarely cited. (Imagine the world today if physicists had chosen to ignore the thinking that emerged from Germany and Austria before the war.) Instead, physicians embraced the ideas of the University of Michigan physician Louis Newburgh, who argued that obese individuals had a “perverted appetite” that failed to match the calories that they consumed with their bodies' metabolic needs. “All obese persons are alike in one fundamental respect,” Newburgh insisted, “they literally overeat.” This paradigm of energy balance/overeating/gluttony/sloth became the conventional, unquestioned explanation for why we get fat. It is, as Bernard would say, the fixed idea. © 2012 Nature Publishing Group
Link ID: 17603 - Posted: 12.13.2012
Analysis by Emily Sohn Older people who remembered going hungry as children were slower to lose their mental sharpness as they reached old age. The new finding was only true for African-Americans, suggesting that the study hit on a particularly resilient group of people who thrived despite extreme childhood adversity. Even so, the study offers insight into how the experiences we have at very young ages can affect our health much later in life. "We know that the social experiences of African-Americans and Caucasians in this country have been very different, at least for people over age 65," said Lisa Barnes, a cognitive neuropsychologist at Rush University Medical Center in Chicago. "We wanted to measure that and see if it had any effect at all." In an effort to add to a growing interest in the long-term health influence of childhood adversity, Barnes and colleagues started by interviewing about 6,100 people who lived in Chicago and were enrolled in a study of Alzheimer's. All participants were at least 65 years old when the study began. The average starting age was 75. In the first interview, seniors answered questions about their childhoods, including details about health, the financial situations of their families and how often someone read books to them. They also took a cognitive exam that included tests of memory. © 2012 Discovery Communications, LLC.
By SABRINA TAVERNISE PHILADELPHIA — After decades of rising childhood obesity rates, several American cities are reporting their first declines. The trend has emerged in big cities like New York and Los Angeles, as well as smaller places like Anchorage, Alaska, and Kearney, Neb. The state of Mississippi has also registered a drop, but only among white students. “It’s been nothing but bad news for 30 years, so the fact that we have any good news is a big story,” said Dr. Thomas Farley, the health commissioner in New York City, which reported a 5.5 percent decline in the number of obese schoolchildren from 2007 to 2011. The drops are small, just 5 percent here in Philadelphia and 3 percent in Los Angeles. But experts say they are significant because they offer the first indication that the obesity epidemic, one of the nation’s most intractable health problems, may actually be reversing course. The first dips — noted in a September report by the Robert Wood Johnson Foundation — were so surprising that some researchers did not believe them. Deanna M. Hoelscher, a researcher at the University of Texas, who in 2010 recorded one of the earliest declines — among mostly poor Hispanic fourth graders in the El Paso area — did a double-take. “We reran the numbers a couple of times,” she said. “I kept saying, ‘Will you please check that again for me?’ ” © 2012 The New York Times Company
Link ID: 17595 - Posted: 12.11.2012
by Julia Brown Forget dieting; just cut down a little on the fat in what you eat and you'll lose weight. The confirmation that you can lose weight without eating less comes from a review of studies involving nearly 75,000 people – none of whom were trying to lose weight. The pounds fell off when they changed to a diet containing less fat. The work was commissioned by the World Health Organization to find out what our optimal intake of fat should be. Lee Hooper at the University of East Anglia in Norwich, UK, and her colleagues reviewed 43 studies carried out in developed countries in which volunteers reduced the overall fat content of their diet, compared with controls who ate either their usual diet or a more healthy one. In all studies, volunteers had to maintain their eating plan for at least six months, with the median time about six years. The studies varied in how volunteers reduced their fat intake and by how much. For example, in one, volunteers simply replaced normal food with low-fat equivalents. In others, participants could change their diet in various ways to reduce their daily fat intake by about 7 per cent on average. In all but one study, the low-fat groups saw a greater weight reduction than the controls, with people losing on average about 1.6 kilograms. "I've never seen quite such a consistent set of results," Hooper says. © Copyright Reed Business Information Ltd.
Link ID: 17580 - Posted: 12.08.2012
Children who are obese may be more vulnerable to food advertising, a brain scanning study suggests. Food and beverage companies market to children to establish brand recognition, brand preference and loyalty. Previous studies found preschoolers said foods tasted better wrapped in branded packaging than plain packaging and kids were more likely to try to influence their parents' purchases when exposed to ads. Researchers in the U.S. suspected that children who are obese would show greater activation to food logos in the "drive" regions of the brain compared with healthy weight children. Amanda Bruce of the psychology department at the University of Missouri-Kansas City and her colleagues looked at 10 healthy children and 10 obese children aged 10 to 14 using questionnaires measuring self-control and functional magnetic resonance imaging of brain activity. Other corporate logos and blurred images were also tested. Obese children showed more activation in some reward regions of the brain than the healthy weight children when shown food logos. But that wasn't the case for the control regions of the brain. "When shown food logos, obese children showed significantly less brain activation than the healthy weight children in regions association with cognitive control," the study's authors concluded in Friday's issue of The Journal of Pediatrics. "This provides initial neuroimaging evidence that obese children may be more vulnerable to the effects of food advertising." © CBC 2012
By Melissa Hogenboom BBC News Researchers say a baby's chance of being obese in childhood can be predicted at birth using a simple formula. The formula combines several known factors to estimate the risk of obesity. The authors of the study, published in PLos One, hope it will be used to identify babies at risk. Childhood obesity can lead to many health problems, including Type 2 diabetes and heart disease. Researchers from Imperial College London looked at 4,032 Finnish children born in 1986 and at data from two further studies of 1,503 Italian children and 1,032 US children. They found that looking at a few simple measurements, such as a child's birthweight and whether the mother smoked, was enough to predict obesity. Previously it had been thought that genetic factors would give bigger clues to later weight problems, but only about one in 10 cases of obesity is the result of a rare gene mutation that affects appetite. Obesity in children is rising, with the NHS estimating that 17% of boys and 15% of girls in England are now obese. BBC © 2012
By ANAHAD O'CONNOR Weight loss surgery, which in recent years has been seen as an increasingly attractive option for treating Type 2 diabetes, may not be as effective against the disease as it was initially thought to be, according to a new report. The study found that many obese Type 2 diabetics who undergo gastric bypass surgery do not experience a remission of their disease, and of those that do, about a third redevelop diabetes within five years of their operation. The findings contrast with the growing perception that surgery is essentially a cure for Type II diabetes. Earlier this year, two widely publicized studies reported that surgery worked better than drugs, diet and exercise in causing a remission of Type 2 diabetes in overweight people whose blood sugar was out of control, leading some experts to call for greater use of surgery in treating the disease. But the studies were small and relatively short, lasting under two years. The latest study, published in the journal Obesity Surgery, tracked thousands of diabetics who had gastric bypass surgery for more than a decade. It found that many people whose diabetes at first went away were likely to have it return. While weight regain is a common problem among those who undergo bariatric surgery, regaining lost weight did not appear to be the cause of diabetes relapse. Instead, the study found that people whose diabetes was most severe or in its later stages when they had surgery were more likely to have a relapse, regardless of whether they regained weight. Copyright 2012 The New York Times Company
Link ID: 17552 - Posted: 11.29.2012
A substance made by the body when it uses fat as fuel could provide a new way of treating epilepsy, experts hope. Researchers in London who have been carrying out preliminary tests of the fatty acid treatment, report their findings in Neuropharmacology journal. They came up with the idea because of a special diet used by some children with severe, drug resistant epilepsy to help manage their condition. The ketogenic diet is high in fat and low in carbohydrate. The high fat, low carbohydrate diet is thought to mimic aspects of starvation by forcing the body to burn fats rather than carbohydrates. Although often effective, the diet has attracted criticism, as side-effects can be significant and potentially lead to constipation, hypoglycaemia, retarded growth and bone fractures. By pinpointing fatty acids in the ketogenic diet that are effective in controlling epilepsy, researchers hope they can develop a pill for children and adults that could provide similar epilepsy control without the side-effects. In early trials, the scientists, from Royal Holloway and University College London, say they have identified fatty acids that look like good candidates for the job. They found that not only did some of the fatty acids outperform a regular epilepsy medication called valproate in controlling seizures in animals, they also had fewer side-effects. BBC © 2012
The search for genes predisposing people to depression has taken an unexpected twist, according to Canadian researchers who found a clue in an obesity gene. Studies on families and twins suggest depression has a genetic component, but for 15 years, scientists haven't been able to find genes associated with the illness. Researchers at McMaster University in Hamilton, Ont., took a different approach by testing how obesity genes may be linked with depression. "We found the first gene predisposing to depression with consistent results," said David Meyre, an associate professor in clinical epidemiology and biostatistics at McMaster and a Canada Research Chair in genetic epidemiology. In Monday's issue of the journal Molecular Psychiatry, Meyre and his co-authors reported that a variant of the FTO gene may be associated with a lower risk of depression independent of the gene's effect on obesity. The common perception is that obese people become depressed because of their appearance and poor self-esteem or discrimination. Another common thought is that those who are depressed are less likely to be physically active or follow healthy eating habits. Taking antidepressants can also lead to weight gain. But the genetic findings challenge that thinking, Meyre said, since those with the genetic mutation predisposing to obesity were protected from depression. "This suggests that the FTO gene may have a broader role than initially thought with an effect on depression and other common psychiatric disorders," the researchers wrote. © CBC 2012
By Lindsey Emery, Men’s Health When most people finish a hard workout, they want a reward — possibly a sandwich, or some pancakes, or maybe even a burger and fries. What they don’t want? To not eat anything. And yet, a few recent studies found that moderate intensity aerobic training could actually decrease your appetite or increase your feelings of fullness or satiety. Strange, right? Previous research has shown that people who exercise often reward themselves with food, increasing overall calorie consumption, and often sabotaging their weight loss goals. So, what gives? “Exercise can definitely suppress hunger,” says Barry Braun, director of the Energy Metabolism Laboratory at the University of Massachusetts, Amherst, who has co-authored multiple studies on the subject. How, why, and for how long afterward is something researchers are still working out. They do know that workouts trigger changes in the hunger hormone ghrelin and the satiety hormones, PYY and GLP-1 — though research has yet to establish the exact relationship. A recent study published in the journal Metabolism found that perceived fullness — both while fasting and after eating — was higher among participants after 12 weeks of aerobic training, but not after resistance training for the same amount of time. And another study out of Brigham Young University revealed that women appeared to be less interested in food on mornings when they walked on a treadmill for 45 minutes than on days they didn’t. © 2012 NBCNews.com
Link ID: 17473 - Posted: 11.10.2012
By GRETCHEN REYNOLDS In recent years, some research has suggested that a high-fat diet may be bad for the brain, at least in lab animals. Can exercise protect against such damage? That question may have particular relevance now, with the butter-and cream-laden holidays fast approaching. And it has prompted several new and important studies. The most captivating of these, presented last month at the annual meeting of the Society for Neuroscience in New Orleans, began with scientists at the University of Minnesota teaching a group of rats to scamper from one chamber to another when they heard a musical tone, an accepted measure of the animals’ ability to learn and remember. For the next four months, half of the rats ate normal chow. The others happily consumed a much greasier diet, consisting of at least 40 percent fat. Total calories were the same in both diets. After four months, the animals repeated the memory test. Those on a normal diet performed about the same as they had before; their cognitive ability was the same. The high-fat eaters, though, did much worse. Then, half of the animals in each group were given access to running wheels. Their diets didn’t change. So, some of the rats on the high-fat diet were now exercising. Some were not. Ditto for the animals eating the normal diet. For the next seven weeks, the memory test was repeated weekly in all of the groups. During that time, the performance of the rats eating a high-fat diet continued to decline so long as they didn’t exercise. Copyright 2012 The New York Times Company
By ANDREW POLLACK Allergan said Tuesday that it was looking to divest itself of its Lap-Band, the once-popular weight-loss device that has experienced several years of falling sales, loss of market share and controversies about its safety and effectiveness. The falling sales “do not fit the profile of a high-growth company like Allergan,” David E. I. Pyott, the company’s chief executive, told analysts Tuesday morning on a call announcing the company’s third-quarter financial results. In an interview, Mr. Pyott said Allergan had already hired an investment banking firm, which he would not name, and was sending letters to other medical device companies and private equity firms seeking a buyer for its obesity business, which also includes a balloonlike device that is not approved in the United States but is used in some other countries. The Lap-Band, a silicone ring that is wrapped around the stomach and can be inserted in an outpatient procedure, once appeared to have a bright future as a less drastic, if less effective, alternative to gastric bypass, which involves rerouting the digestive tract. But Allergan’s obesity business sales have fallen from a peak of $296 million in 2008 to an expected $160 million this year. In the third quarter, the sales fell by 25 percent to $37.4 million from a year earlier. The obesity business, while still profitable, represents less than 3 percent of total product sales for Allergan, which is known most for its Botox treatment for wrinkles, migraine headaches and other conditions. © 2012 The New York Times Company
Link ID: 17440 - Posted: 10.31.2012
People often don't know how many calories they're eating, how many they burn off, or what they need, say doctors who are calling for prominent calorie labels at the point of sale. The Canadian Obesity Network, a group of obesity experts, showed people examples of foods and asked them to guess how many calories the items contained. Many people don't know their recommended daily intake of calories.Many people don't know their recommended daily intake of calories. (Lee Jae Won/Reuters) "A lot of Canadians were quite off the mark," said Dr. Arya Sharma, chair in obesity research and management at the University of Alberta in Edmonton. "When we showed people food labels and asked them to calculate how many calories they'd be getting if they consumed say a can of soup, very few Canadians were able to figure out that number." Sharma is concerned about the consequences of caloric illiteracy considering two-thirds of Canadians are carrying extra pounds and a quarter of adults are considered to be medically obese, according to Statistics Canada. "Ultimately calories are the currency of weight management," Sharma said. "If you don't know how many calories you're eating, you don't know what your body's doing with the calories, you don't know where the calories are going. That's like trying to manage your bank account without knowing how much money you make or how much money things cost." © CBC 2012
Link ID: 17431 - Posted: 10.29.2012
By Katherine Harmon Getting seven to eight solid hours of sleep each night might seem an almost impossible luxury to many people. But not getting enough sleep is known to impair mental function and increase the risk for heart disease, among other ill effects. Accumulating evidence also suggests that even short-term, partial sleep deprivation could pave the way for weight gain and other negative metabolic consequences. More than 28 percent of adults in the U.S. report that they get less than six hours of sleep a night, with this cumulative deprivation becoming more common in the past three decades. And now that more than 35 percent of U.S. adults are currently obese, researchers have been searching for potential links between the two conditions, in hopes of reducing the increasing health and economic burden of obesity. Establishing lack of sleep as a risk factor for weight gain could have important clinical and public health effects, possibly allowing people to make simple lifestyle changes to improve their metabolic health. A new report, published online October 24 in the Journal of the Academy of Nutrition and Dietetics, reviews 18 carefully controlled laboratory studies that tested human subjects' physiological and behavioral responses to sleep deprivation as they relate to metabolic health. Reena Mehra, an associate professor of medicine who studies sleep and health at Case Western Reserve University School of Medicine and who was not involved in the new analysis, notes that the new paper is "a well done review of the experimental data." © 2012 Scientific American
by Shaoni Bhattacharya Talk about having your cake and eating it. Fasting might not be the only route to a longer life – a hormone seems to work just as well, for mice at least. We know that some animals can extend their lifespan by consuming fewer calories. Engineered mice can get the same effect by simply pumping out high levels of a hormone normally produced during a fast, according to Steven Kliewer and David Mangelsdorf at the University of Texas Southwestern Medical Center in Dallas. Their team found that mice engineered to make higher levels of the hormone, FGF21, increased their lifespan on average by over a third. "What we are seeing is the benefit of caloric restriction without having to diet," he says. Humans have the hormone too, and Kliewer believes FGF21 has the potential to extend the human "health-span" – the time we live healthy lives. The researchers believe FGF21 may act to prolong life by affecting pathways such as the insulin-like growth factor-1 (IGF-1) pathway implicated in ageing. "It blocks growth hormones promoting pathways which are associated with diseases, including cancers and metabolic diseases, and as a consequence these animals live longer," says Kliewer. © Copyright Reed Business Information Ltd.
By JANE E. BRODY I recently met a slender, health-conscious young woman who insisted that the size of sugar-sweetened drinks should not be legislated. “Getting people to drink less of them should be done through education,” she said. It is an opinion shared by many others. Some may be unaware of the role that these beverages are playing in the nation’s burgeoning epidemics of obesity and Type 2 diabetes. Few know the disappointing history of efforts to change human behavior solely through education. The young woman was reacting to a New York City regulation, to take effect on March 12, limiting to 16 ounces the size of sugar-sweetened soft drinks available for purchase at restaurants, street carts, movie theaters and sporting events. The Barclays Center in Brooklyn, the new home of the Nets, has already imposed this limit. Convenience stores, vending machines and some newsstands are exempted from the regulation. Several new studies underscore the public health potential of the restriction. If it succeeds in curbing the consumption of sweet liquid calories, it is likely to be copied elsewhere, because the nation’s love affair with super-size sugary soft drinks is costing cities and states billions of dollars annually in medical care. We are all born with a natural preference for sweetness, which through evolution enabled us to know when fruits and berries were ripe and ready to eat. But as Gary K. Beauchamp, a biopsychologist and director of the Monell Chemical Senses Center in Philadelphia, has put it, “We’ve separated the good taste from the good food.” Our sweet tooth is no longer working to our advantage. Copyright 2012 The New York Times Company
Link ID: 17400 - Posted: 10.22.2012
By Tina Hesman Saey New work suggests that a hormone that makes the body think it’s starving could prolong life about as long as severely cutting calories does but without the denial. A hormone called fibroblast growth factor-21, or FGF21, lengthened the lives of mice that had been genetically engineered to constantly produce large amounts of the protein, researchers at the University of Texas Southwestern Medical Center at Dallas report online October 15 in eLife. The hormone is normally made by the liver during fasting and may tap into some of the same life-extending biochemical processes as does caloric restriction, a proven longevity booster. Caloric restriction — usually defined as cutting calorie intake to 75 to 80 percent of the amount needed to maintain normal body weight, while still maintaining good nutrition — has been shown lengthen life in a wide variety of species, such as fruit flies and dogs. Minimal calorie consumption turns on many different biological processes that slow aging, says Cynthia Kenyon, a developmental biologist at the University of California, San Francisco. The hormone in the study somehow interferes with a chain reaction anchored by insulin-like growth factor-1 (IGF-1), a process that is also shut down by caloric restriction and thought to be responsible for many of its life-extending effects. In the study, researchers led by UT Southwestern’s David Mangelsdorf and Steven Kliewer genetically engineered mice to constantly make five to 10 times as much FGF21 as normal. These engineered mice lived 30 to 40 percent longer than normal mice on a standard diet. Female mice benefitted from the hormone even more than males; about a third of the FGF21-producing female mice still were alive at 44 months old. Average survival for normal mice in the study was about 28 months. © Society for Science & the Public 2000 - 2012