Links for Keyword: Obesity

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Susan Gaidos Most people would be happy to get rid of excess body fat. Even better: Trade the spare tire for something useful — say, better-functioning knees or hips, or a fix for an ailing heart or a broken bone. The idea is not far-fetched, some scientists say. Researchers worldwide are repurposing discarded fat to repair body parts damaged by injury, disease or age. Recent studies in lab animals and humans show that the much-maligned material can be a source of cells useful for treating a wide range of ills. At the University of Pittsburgh, bioengineer Rocky Tuan and colleagues extract buckets full of yellow fat from volunteers’ bellies and thighs and turn the liposuctioned material into tissue that resembles shock-absorbing cartilage. If the cartilage works as well in people as it has in animals, Tuan’s approach might someday offer a kind of self-repair for osteoarthritis, the painful degeneration of cartilage in the joints. He’s also using fat cells to grow replacement parts for the tendons and ligaments that support the joints. Foremost among fat’s virtues is its richness of stem cells, which have the ability to divide and grow into a wide variety of tissue types. Fat stem cells — also known as adipose-derived stem cells — can be coerced to grow into bone, cartilage, muscle tissue or, of course, more fat. Cells from fat are being tested to mend tissues found in damaged joints, hearts and muscle, and to regrow bone and heal wounds. © Society for Science & the Public 2000 - 2016

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: 21972 - Posted: 03.10.2016

By Anahad O'Connor Mark Mattson, a neuroscientist at the National Institute on Aging in Maryland, has not had breakfast in 35 years. Most days he practices a form of fasting — skipping lunch, taking a midafternoon run, and then eating all of his daily calories (about 2,000) in a six-hour window starting in the afternoon. “Once you get used to it, it’s not a big deal,” said Dr. Mattson, chief of the institute’s laboratory of neurosciences. “I’m not hungry at all in the morning, and this is other people’s experience as well. It’s just a matter of getting adapted to it.” In a culture in which it’s customary to eat three large meals a day while snacking from morning to midnight, the idea of regularly skipping meals may sound extreme. But in recent years intermittent fasting has been gaining popular attention and scientific endorsement. It has been promoted in best-selling books and endorsed by celebrities like the actors Hugh Jackman and Benedict Cumberbatch. The late-night talk show host Jimmy Kimmel claims that for the past two years he has followed an intermittent fasting program known as the 5:2 diet, which entails normal eating for five days and fasting for two — a practice Mr. Kimmel credits for his significant weight loss. Fasting to improve health dates back thousands of years, with Hippocrates and Plato among its earliest proponents. Dr. Mattson argues that humans are well suited for it: For much of human history, sporadic access to food was likely the norm, especially for hunter-gatherers. As a result, we’ve evolved with livers and muscles that store quickly accessible carbohydrates in the form of glycogen, and our fat tissue holds long-lasting energy reserves that can sustain the body for weeks when food is not available. “From an evolutionary perspective, it’s pretty clear that our ancestors did not eat three meals a day plus snacks,” Dr. Mattson said. © 2016 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: 21969 - Posted: 03.09.2016

By Roberto A. Ferdman In the mid 1970s, psychologist Merrill Elias began tracking the cognitive abilities of more than a thousand people in the state of New York. The goal was fairly specific: to observe the relationship between people's blood pressure and brain performance. And for decades he did just that, eventually expanding the Maine-Syracuse Longitudinal Study (MSLS) to observe other cardiovascular risk factors, including diabetes, obesity, and smoking. There was never an inkling that his research would lead to any sort of discovery about chocolate. And yet, 40 years later, it seems to have done just that. Late in the study, Elias and his team had an idea. Why not ask the participants what they were eating too? It wasn't unreasonable to wonder if what someone ate might add to the discussion. Diets, after all, had been shown to affect the risk factors Elias was already monitoring. Plus, they had this large pool of participants at their disposal, a perfect chance to learn a bit more about the decisions people were making about food. The researchers incorporated a new questionnaire into the sixth wave of their data collection, which spanned the five years between 2001 and 2006 (there have been seven waves in all, each conducted in five year intervals). The questionnaire gathered all sorts of information about the dietary habits of the participants. And the dietary habits of the participants revealed an interesting pattern. "We found that people who eat chocolate at least once a week tend to perform better cognitively," said Elias. "It's significant—it touches a number of cognitive domains." © 1996-2016 The Washington Post

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 21962 - Posted: 03.07.2016

Heidi Ledford Obese mice — like obese humans — are at increased risk of colon cancer, and a study published today in Nature finally suggests why. Overweight mice fed a high-fat diet showed an increase in intestinal stem cells due to activation of a protein called PPAR-δ that regulates metabolism1. If the results hold true in humans, they could explain a phenomenon seen in epidemiological studies. “For quite some time there’s been an understanding that obesity leads to an increase in cancer in many tissues,” says Ömer Yilmaz, a cancer biologist at the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology (MIT) in Cambridge, and one of the leaders of the study. “We really wanted to understand the mechanism behind this.” Those molecular details could be important, says cell biologist P. Kay Lund who works at the University of North Carolina in Chapel Hill and the National Institutes of Health in Bethesda, Maryland. Tissue samples from people who have undergone colonoscopies could be tested to see if the same patterns hold true. Ultimately, the the increase in PPAR-δ activity could yield a useful indicator of cancer risk. “It could provide an opportunity to give those patients an earlier intervention,” says Lund, who was not involved in the obesity work. Yilmaz teamed up with David Sabatini, who studies metabolism at MIT and the Whitehead Institute, also in Cambridge, to learn more about the link between cancer and obesity. Their teams fed mice high-fat, high-calorie chow for about a year, and then tested the effects of the diet on the number and function of stem cells in their intestines. © 2016 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: 21952 - Posted: 03.03.2016

Mo Costandi Most of us are well aware of the health risks associated with obesity. Being overweight or obese is associated with an increased risk of numerous other conditions, from high blood pressure, heart disease and stroke, to diabetes, gout and some forms of cancer. Self-control saps memory resources Read more Research published over the past few years shows that obesity also has neurological consequences – it is associated with altered function in, and shrinkage of, certain parts of the brain, particularly the frontal lobes, which are the seat of intelligence, and the hippocampus, which is critical for memory formation. A new study now shows that this in turn is associated with impaired memory function. Lucy Cheke of the University of Cambridge and her colleagues recruited 50 volunteers aged between 18 and 35, with Body Mass Indexes (BMIs) ranging from 18 (underweight) to 51 (extremely obese), and asked them to perform a computerised memory test called the “Treasure Hunt Task”. This involved moving food items around around complex scenes, such as a desert with palm trees, hiding them in various locations, and indicating afterwards where they had hidden them. The participants were then shown various locations from the computerised scenes, and some of the food items, and asked if they had hidden something in each of the locations, or where they had hidden each of the items. Finally, they were shown pairs of the food items they had seen, and asked to indicate which of each pair they had hidden first. © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 21951 - Posted: 03.03.2016

By James Gallagher Health editor, BBC News website People who are obese have a worse memory than their thinner friends, a small study shows. Tests on 50 people showed being overweight was linked to worse "episodic memory" or the ability to remember past experiences. The study in the Quarterly Journal of Experimental Psychology argues that a less vivid memory of recent meals may lead to overeating. However, other aspects of memory - such as general knowledge - were unaffected. Tests on rats have previously shown that with burgeoning waistlines come poorer performances in memory tests, but the evidence in humans has been mixed. The latest experiments looked at episodic memory - the video tape in your mind - that remembers the smell of a cup of coffee or the feel of holding someone's hand. Fifty people with a Body Mass Index (BMI) ranging from 18 (healthy) to 51 (very obese) took part in a memory test - a bit like doing a treasure hunt on your own. They had to "hide" objects at different times and on different scenes displayed on a computer screen. They were later asked to recall what they had hidden, when and where. The results showed obese people's scores were 15% lower than thinner people. Dr Lucy Cheke, from the University of Cambridge, told the BBC News website: "The suggestion we're making is that a higher BMI is having some reduction on the vividness of memory, but they're not drawing blanks and having amnesia. "But if they have a less strong memory of a recent meal, with a less strong impact in the mind, then they may have less ability to regulate how much they eat later on." Hunger hormones play a huge role in how much we eat, but it is already recognised that our minds have a key role too. © 2016 BBC

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 21936 - Posted: 02.27.2016

By Roberto A. Ferdman Poverty has a way of rearing its ugly head, slipping into the cracks in people's lives when they're young and then re-emerging later in life. Sometimes it happens in ways that are easily observable—what poor babies are fed, for instance, has been shown to alter what they crave as adults, creating life-long affinities for foods that might be better left uneaten. But sometimes the influences are hidden, and all the more insidious as a result. A team of researchers, led by Sarah Hill, who teaches psychology at Texas Christian University, believe they have uncovered evidence of one such lingering effect. Specifically, Hill and her colleagues found that people who grow up poor seem to have a significantly harder time regulating their food intake, even when they aren't hungry. "We found that they eat comparably high amounts regardless of their need," said Hill. The researchers, interested in exploring why obesity is more prevalent in poorer populations, devised three separate experiments, which tested how people from different socioeconomic backgrounds behaved in front of food. In the first, they invited 31 female participants into their lab, who were asked how long it had been since they had eaten, and how hungry they were. They were then given snacks (cookies and pretzels), which they were free to eat or leave be, as they pleased. When they were finished, Hill and her team measured the number of calories each consumed. The discrepancy between how the participants ate was alarming.

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: 21920 - Posted: 02.22.2016

By Roni Caryn Rabin Does long-term use of artificial sweeteners cause weight gain or contribute to metabolic syndrome? Scientists are still scratching their heads over this question. Artificial, or nonnutritive, sweeteners have no calories and are often used as diet aids. But while some well-designed trials have found that those randomly assigned to drink artificially sweetened beverages gained less weight than those given sugar-sweetened drinks, large population studies suggest that frequent consumption of artificial sweeteners may be linked with unanticipated consequences, including weight gain. A large study that followed a diverse group of 6,814 Americans ages 45 to 84 for at least five years found that those who drank diet soda at least once a day were at 67 percent greater risk of developing Type 2 diabetes than those who didn’t consume diet drinks, regardless of whether they gained weight or not, and at 36 percent greater risk of metabolic syndrome, which can be a precursor to heart disease, stroke and diabetes. Another large study that followed thousands of residents of San Antonio, Tex., for 10 years found those who drank more than 21 servings of diet drinks a week were at twice the risk of becoming overweight or obese, and the more diet soda people drank, the greater the risk. These large observational trials do not prove cause and effect, however, and may reflect the fact that people who are gaining weight may be most likely to drink a lot of diet soda. Dr. John Fernstrom, a University of Pittsburgh professor who is also a paid consultant to Ajinomoto, a maker of aspartame, reviewed the evidence on nonnutritive sweeteners and concluded that the evidence linking them to metabolic problems was “not compelling.” © 2016 The New York Times Company

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: 21913 - Posted: 02.19.2016

Ice cream lovers, look away now. Studies on a simulated human gut have added further evidence that emulsifiers, found in most processed foods, might be linked to obesity, diabetes and inflammatory bowel disorders. Emulsifiers are used to improve a food’s texture and to prevent mixtures from separating, particularly in ice cream. Last year, Benoit Chassaing of Georgia State University showed that mice that drank water containing one of two emulsifiers underwent changes in gut bacteria and inflammation of the gut – changes that led to obesity and diabetes in these animals. However, mice that didn’t have any gut bacteria because they had been raised in a sterile environment didn’t become ill when given the same additives, suggesting that it is the emulsifiers’ effect on the microbiome that is to blame. When the ill mice stopped consuming emulsifiers, their gut bacteria gradually returned to normal. The question is whether the same might be true for humans. The growing use of emulsifiers has coincided with a rise in obesity and diabetes, says Chassaing, while these conditions aren’t as common in countries where less processed food is consumed. Now Chassaing has supported his findings in mice using a simulation of the human gut. Working with a team in Belgium, he looked at two emulsifiers: carboxymethylcellulose (E566 on EU labels) and polysorbate-80 (E433). When added to a series of flasks that mimic the conditions of the human digestive tract, each caused an increase in the levels of a bacterial protein called flagellin, known to cause inflammation at high concentrations. Chassaing presented the results at a recent meeting at the Royal Society in London. © Copyright Reed Business Information Ltd.

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: 21880 - Posted: 02.10.2016

By Sarah Knapton, Science Editor For women, shedding the pounds can feel like a unending struggle of dieting and exercise with little results. But a new study suggests that there could be a reason why females find it more difficult to lose weight than men. Researchers say hormones responsible for regulating appetite, physical activity and energy expenditure work differently in the sexes. "This could have broad implications for medications used to combat obesity, which at present largely ignore the sex of the individual." Professor Lora Heisler, University of Aberdeen The discovery could change the way obesity is tackled through targeted medication, experts at the University of Aberdeen believe. Working with teams from the University of Cambridge and the University of Michigan, they used a mouse model to study how weight gain differs in each sex depending on physical activity and energy expenditure. During the study, researchers were able to transform obese male into lean, healthy mice, but the same transformation did not occur in the female mice. Current obesity medications stimulate the production of POMC peptides in the brain which regulate appetite, increase energy expenditure through heat and encourage movement. But researchers found in female mice the hormones only regulated appetite - they did not have the extra benefits. © Copyright of Telegraph Media Group Limited 2016

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: 21851 - Posted: 02.03.2016

By Mitch Leslie Identical twins may be alike in everything from their eye color to their favorite foods, but they can diverge in one important characteristic: their weight. A new study uncovers a molecular mechanism for obesity that might explain why one twin can be extremely overweight even while the other is thin. Heredity influences whether we become obese, but the genes researchers have linked to the condition don’t explain many of the differences in weight among people. Identical twins with nonidentical weights are a prime example. So what accounts for the variation? Changes in the intestinal microbiome—the collection of bacteria living in the gut—are one possibility. Another is epigenetic changes, or alterations in gene activity. These changes occur when molecules latch on to DNA or the proteins it wraps around, turning sets of genes “on” or “off.” Triggered by factors in the environment, epigenetic modifications can be passed down from one generation to the next. This type of transmission happened during the Hunger Winter, a famine that occurred when the Germans cut off food supplies to parts of the Netherlands in the final months of World War II. Mothers who were pregnant during the famine gave birth to children who were prone to obesity decades later, suggesting that the mothers’ diets had a lasting impact on their kids’ metabolism. However, which epigenetic changes in people promote obesity remains unclear. © 2016 American Association for the Advancement of Science

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: 21838 - Posted: 01.30.2016

Haroon Siddique Exercise alone is not enough to lose weight because our bodies reach a plateau where working out more does not necessarily burn extra calories, researchers have found. The team are the latest to challenge obesity prevention strategies that recommend increasing daily physical activity as a way to shed the pounds. In a study, published in Current Biology on Thursday, they suggest that there might be a physical activity “sweet spot”, whereby too little can make one unhealthy but too much drives the body to make big adjustments to adapt, thus constraining total energy expenditure. If true, it would go some way to explaining an apparent contradiction between two types of study carried out by researchers. On the one hand, there are studies which show that increasing exercise levels tends to lead to people expending more energy and on the other, there are ecological studies in humans and animals showing that more active populations (for example hunter-gatherers in Africa) do not have higher total energy expenditure. Prof Herman Pontzer of City University of New York (CUNY), one of the new study’s authors, said: “Exercise is really important for your health. That’s the first thing I mention to anyone asking about the implications of this work for exercise. There is tons of evidence that exercise is important for keeping our bodies and minds healthy, and this work does nothing to change that message. What our work adds is that we also need to focus on diet, particularly when it comes to managing our weight and preventing or reversing unhealthy weight gain.” © 2016 Guardian News and Media Limited

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: 21837 - Posted: 01.30.2016

by Bethany Brookshire The high fiber refrain never seems to stop. We all know that we’re supposed to eat more fiber and focus on whole grains, fresh fruits and vegetables. But when forced to choose between chewy, crumbly, flavorless oat bran and delicious white buttered toast for breakfast, it’s easy to tune out. But that fiber isn’t for you. It fuels and sustains your gut microbes — and those in your kids, and grandkids and great-grandkids, too, a study in mice finds. The results suggest that when we pass our genes on to our children, we also pass on a gut ecosystem that reflects our previous dietary choices. (No pressure.) The Food and Drug Administration recommends that Americans eat about 25 grams of dietary fiber per day. But most people don’t hit that mark. “The average American gets 10 to 15 grams of dietary fiber,” says Erica Sonnenburg, a microbiologist at Stanford University. If that doesn’t make you feel ashamed, compare your diet to the Hadza, hunter-gatherers who live in Tanzania. “The tubers they’re eating are so fibrous [that people] chew for a while and spit it out,” Sonnenburg says. It’s hard to calculate exactly how much fiber the Hadza get from the tubers, but Sonnenburg says that some some speculate it’s between 100 and 150 grams per day at certain times of year. That high level of fiber is reflected in their guts. “What all the studies have found is that these populations who are living a more traditional lifestyle are the best approximation for our ancient microbiota. They all harbor microbiota that’s much more diverse.” © Society for Science & the Public 2000 - 2016. A

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: 21791 - Posted: 01.16.2016

By Dina Fine Maron We may be able to keep our gut in check after all. That’s the tantalizing finding from a new study published today that reveals a way that mice—and potentially humans—can control the makeup and behavior of their gut microbiome. Such a prospect upends the popular notion that the complex ecosystem of germs residing in our guts essentially acts as our puppet master, altering brain biochemistry even as it tends to our immune system, wards off infection and helps us break down our supersized burger and fries. In a series of elaborate experiments researchers from Harvard Medical School and Brigham and Women’s Hospital discovered that mouse poop is chock full of tiny, noncoding RNAs called microRNAs from their gastrointestinal (GI) tracts and that these biomolecules appear to shape and regulate the microbiome. “We’ve known about how microbes can influence your health for a few years now and in a way we’ve always suspected it’s a two-way process, but never really pinned it down that well,” says Tim Spector, a professor of genetic epidemiology at King’s College London, not involved with the new study. “This [new work] explains quite nicely the two-way interaction between microbes and us, and it shows the relationship going the other way—which is fascinating,” says Spector, author of The Diet Myth: Why the Secret to Health and Weight Loss Is Already in Your Gut. What’s more, human feces share 17 types of microRNAs with the mice, which may portend similar mechanisms in humans, the researchers found. It could also potentially open new treatment approaches involving microRNA transplantations. “Obviously that raises the immediate question: ‘Where do the microRNAs come from and why are they there?,’” says senior author Howard Weiner, a neurologist at both Harvard and Brigham. The work was published in the journal Cell Host & Microbe. © 2016 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: 21789 - Posted: 01.14.2016

By Anahad O'Connor For much of his life, Dr. Vincent Pedre, an internist in New York City, suffered from digestive problems that left him feeling weak and sick to his stomach. As an adult he learned he had irritable bowel syndrome, or I.B.S., a chronic gut disorder that affects up to 10 percent of Americans. Through the process of elimination, Dr. Pedre discovered that his diet was the source of many of his problems. Cutting out dairy and gluten reversed many of his symptoms. Replacing processed foods with organic meats, fresh vegetables and fermented foods gave him more energy and settled his sensitive stomach. Dr. Pedre, a clinical instructor in medicine at the Mount Sinai School of Medicine, began to encourage many of his patients who were struggling with digestive disorders to do the same, helping them to identify food allergens and food sensitivities that could act as triggers. He also urged his patients to try yoga and meditation to alleviate chronic stress, which can worsen digestive problems. Dr. Pedre now has a medical practice specializing in gastrointestinal disorders and is the author of a new book called “Happy Gut.” In the book, Dr. Pedre argues that chronic health problems can in some cases be traced to a dysfunctional digestive system, which can be quelled through a variety of lifestyle behaviors that nurture the microbiota, the internal garden of microbes that resides in the gut. Recently, we caught up with Dr. Pedre to talk about what makes a “happy gut,” how you can avoid some common triggers of digestive problems, and why fermented foods like kombucha and kimchi should be part of your diet. Here are edited excerpts from our conversation. © 2016 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: 21788 - Posted: 01.14.2016

By Katherine Harmon Here’s another reason to eat your vegetables. Trillions of microbes in the human large intestine—known as the microbiome—depend on dietary fiber to thrive and give us energy. As fiber intake declines, so, too, does the range of bacteria that can survive in the gut. Now, a new study of multiple generations of mice fed a low-fiber diet indicates that this diversity plummets further with each generation, a hint of what might be happening in the human gut as we continue eating a contemporary diet of refined foods. The work might also help explain rises in many Western diseases, such as inflammatory bowel disease and obesity. "This is a seminal study," says microbial ecologist Jens Walter, of the University of Alberta in Canada. "The magnitude by which the low-[fiber] diet depletes the microbiome in the mouse experiments is startling." For much of human history in hunter-gatherer and early agrarian times, daily fiber intake was likely at least three or four times the officially recommended amounts today (something like 100 grams versus 25 grams)—and several times greater than average U.S. consumption now (about 15 grams). The trend has led many researchers, including microbiologist Erica Sonnenburg of Stanford University in Palo Alto, California, to suspect that the well-documented low diversity of gut microbes among people in developed countries—some 30% less diverse than in modern hunter-gatherers—is, in part, a product of drastically reduced fiber intake. © 2016 American Association for the Advancement of Science. A

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: 21787 - Posted: 01.14.2016

Laura Beil When Elinor Sullivan was a postdoctoral fellow at Oregon Health & Science University in Portland, she set out to explore the influence of food and exercise habits on obesity. In one experiment, she and her colleagues fed a troop of macaque monkeys regular chow. Other macaques dined American-style, with a hefty 32 percent of calories from fat and ready access to peanut butter treats. Over time, the second group of monkeys grew noticeably fatter. Then they all had babies. Sullivan, now at the University of Portland, noticed odd behavior in the plump moms’ offspring. At playtime, they often slinked off by themselves. When handled by keepers, the infants tended to vocalize anxiously, and the males became aggressive. They were prone to repetitive habits, like pacing. In their carefully controlled world, the only difference between those monkeys and others at the facility was their mothers’ extra pounds and indulgent diet. The behavior was so striking that Sullivan changed the course of her research. “It made me start thinking about human children,” she says, and the twin epidemics of obesity and behavioral problems such as attention-deficit/hyperactivity disorder. Her research, published in 2010 in the Journal of Neuroscience, was one of the first studies to note that the progeny of female monkeys eating a high-fat diet were more likely to experience altered brain development and suffer anxiety. Not long after, researchers worldwide began compiling evidence linking the heaviness of human mothers to mental health in their children. One headline-grabbing study of more than 1,000 births, reported in 2012, found that autism spectrum disorders showed up more often in children of obese mothers than in normal-weight women (SN: 5/19/12, p. 16). © Society for Science & the Public 2000 - 2015.

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: 21781 - Posted: 01.13.2016

By Anahad O'Connor David Ludwig often uses an analogy when he talks about weight loss: Human beings are not toaster ovens. If we were, then the types of calories we consumed would not matter, and calorie counting would be the most effective way to lose weight. Dr. Ludwig, an obesity expert and professor of nutrition at the Harvard T.H. Chan School of Public Health, argues that weight gain begins when people eat the wrong types of food, which throws their hormones out of whack and sets off a cycle of cravings, hunger and bingeing. In his new book, “Always Hungry?,” he argues that the primary driver of obesity today is not an excess of calories per se, but an excess of high glycemic foods like sugar, refined grains and other processed carbohydrates. Recently, we caught up with Dr. Ludwig to talk about which foods act as “fertilizer for fat cells,” why he thinks the conventional wisdom on weight loss is all wrong, and long-term strategies for weight loss. Here are edited excerpts from our conversation. What is the basic message of your book? The basic premise is that overeating doesn’t make you fat. The process of getting fat makes you overeat. It may sound radical, but there’s literally a century of science to support this point. Simply cutting back on calories as we’ve been told actually makes the situation worse. When we cut back on calories, our body responds by increasing hunger and slowing metabolism. It responds in an effort to save calories. And that makes weight loss progressively more and more difficult on a standard low calorie diet. It creates a battle between mind and metabolism that we’re doomed to lose. But we’ve all been told that obesity is caused by eating too much. Is that not the case? We think of obesity as a state of excess, but it’s really more akin to a state of starvation. If the fat cells are storing too many calories, the brain doesn’t have access to enough to make sure that metabolism runs properly. So the brain makes us hungry in an attempt to solve that problem, and we overeat and feel better temporarily. © 2016 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: 21757 - Posted: 01.07.2016

Love a sugar hit? Your sweet tooth may hail from an unlikely source: your liver. A hormone made by the organ appears to control how much carbohydrate and sugar we want to eat, and helps slow us down when we are overindulging. The hormone, called FGF21, has already been found to help obese mice lose weight and regain their sensitivity to insulin. A modified form is currently in clinical trials to test whether it has the same effect in people with diabetes. Our bodies break down carbohydrates into sugars such as sucrose, glucose and fructose. Recent genetic studies have suggested that people with altered levels of FGF21 consume more carbohydrates. To find out more, a team co-led by Matthew Potthoff at the University of Iowa observed the eating habits of mice with either abnormally high or low levels of the hormone. They found that mice genetically modified to lack the hormone chose to drink much higher levels of sugar-sweetened drinks than normal mice. Those given an extra dose of the hormone, on the other hand, reduced their sugar intake. The team also showed that the hormone is produced in response to high carbohydrate levels; it then enters the bloodstream, where it sends a signal to the brain to suppress our sugar intake. In people, blood levels of FGF21 triple 24 hours after a spike in blood sugar levels. When monkeys were given the synthetic version of the hormone being tested in clinical trials, they also opted for a diet low in sugar, according to a separate study by Steven Kliewer at the University of Texas Southwestern Medical Center at Dallas and colleagues. The team also found that these monkeys consumed less alcohol than those that weren’t given the compound. © Copyright Reed Business Information Ltd.

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: 21732 - Posted: 12.29.2015

By Ferris Jabr Matthew Brien has struggled with overeating for the past 20 years. At age 24, he stood at 5′10′′ and weighed a trim 135 pounds. Today the licensed massage therapist tips the scales at 230 pounds and finds it particularly difficult to resist bread, pasta, soda, cookies and ice cream—especially those dense pints stuffed with almonds and chocolate chunks. He has tried various weight-loss programs that limit food portions, but he can never keep it up for long. “It's almost subconscious,” he says. “Dinner is done? Okay, I am going to have dessert. Maybe someone else can have just two scoops of ice cream, but I am going to have the whole damn [container]. I can't shut those feelings down.” Eating for the sake of pleasure, rather than survival, is nothing new. But only in the past several years have researchers come to understand deeply how certain foods—particularly fats and sweets—actually change brain chemistry in a way that drives some people to overconsume. Scientists have a relatively new name for such cravings: hedonic hunger, a powerful desire for food in the absence of any need for it; the yearning we experience when our stomach is full but our brain is still ravenous. And a growing number of experts now argue that hedonic hunger is one of the primary contributors to surging obesity rates in developed countries worldwide, particularly in the U.S., where scrumptious desserts and mouthwatering junk foods are cheap and plentiful. “Shifting the focus to pleasure” is a new approach to understanding hunger and weight gain, says Michael Lowe, a clinical psychologist at Drexel University who coined the term “hedonic hunger” in 2007. © 2015 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 21722 - Posted: 12.24.2015