Links for Keyword: Obesity

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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

Tina Hesman Saey SAN DIEGO — New research may help explain why chronic stress, sleep deprivation and other disruptions in the body’s daily rhythms are linked to obesity. Chronic exposure to stress hormones stimulates growth of fat cells, Mary Teruel of Stanford University reported December 16 at the annual meeting of the American Society for Cell Biology. Normally, stress hormones, such as cortisol, are released during waking hours in regular bursts that follow daily, or circadian, rhythms. Those regular pulses don’t cause fat growth, Teruel and colleagues discovered. But extended periods of exposure to the hormones, caused by such things as too little sleep, break up that rhythm and lead to more fat cells. Even though only about 10 percent of fat cells are replaced each year, the body maintains a pool of prefat cells that are poised to turn into fat. “If they all differentiated at once, you’d be drowning in fat,” Teruel said. Previous studies have shown that a protein called PPAR-gamma controls the development of fat cells and that stress hormones turn on production of PPAR-gamma. Teruel’s team discovered that prefat cells with levels of PPAR-gamma below a certain threshold don’t transform into fat in laboratory tests. Steady hormone exposure eventually allowed the precursor cells to build up enough PPAR-gamma to cross the threshold into fat making. But in cells given the same total amount of stress hormone in short pulses, PPAR-gamma levels rose and fell. © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 21709 - Posted: 12.19.2015

A single variation in the gene for brain-derived neurotropic factor (BDNF) may influence obesity in children and adults, according to a new study funded by the National Institutes of Health. The study suggests that a less common version of the BDNF gene may predispose people to obesity by producing lower levels of BDNF protein, a regulator of appetite, in the brain. The authors propose that boosting BDNF protein levels may offer a therapeutic strategy for people with the genetic variation, which tends to occur more frequently in African Americans and Hispanics, than in non-Hispanic Caucasians. The study is published in the journal Cell Reports. Obesity in children and adults is a serious issue in the United States, contributing to health conditions such as heart disease, stroke and type 2 diabetes. Importantly, genetic factors can predispose a person to obesity, as well as influence the effectiveness of weight-loss strategies. The body relies on cells to process and store energy, and changes in genes that regulate these functions can cause an imbalance that leads to excessive energy storage and weight gain. “The BDNF gene has previously been linked to obesity, and scientists have been working for several years to understand how changes in this particular gene may predispose people to obesity,” said Jack A. Yanovski, M.D., Ph.D., one of the study authors and an investigator at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “This study explains how a single genetic change in BDNF influences obesity and may affect BDNF protein levels. Finding people with specific causes of obesity may allow us to evaluate effective, more-personalized treatments.”

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: 21585 - Posted: 10.31.2015

Heidi Ledford An analysis of 53 weight-loss studies that included more than 68,000 people has concluded that, despite their popularity, low-fat diets are no more effective than higher-fat diets for long-term weight loss. And overall, neither type of diet works particularly well. A year after their diets started, participants in the 53 studies were, on average, only about 5 kilograms (11 pounds) lighter. “That’s not that impressive,” says Kevin Hall, a physiologist at the US National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland. “All of these prescriptions for dieting seem to be relatively ineffective in the long term.” The study, published in The Lancet Diabetes and Endocrinology[1], runs counter to decades' worth of medical advice and adds to a growing consensus that the widespread push for low-fat diets was misguided. Nature looks at why low-fat diets were so popular and what diet doctors might prescribe next. Are the new findings a surprise? The advantages of low-fat diets have long been in question. “For decades we’ve been touting low-fat diets as the way to lose weight, but obesity has gone up,” says Deirdre Tobias, lead author of the study and an epidemiologist at Brigham and Women’s Hospital in Boston, Massachusetts. “It seemed evident that low-fat diets may not be the way to go.” © 2015 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: 21584 - Posted: 10.31.2015

By ALEX HUTCHINSON WHEN marketing researchers at the University of Pennsylvania’s Wharton School rigged shopping carts at a major East Coast supermarket with motion-tracking radio-frequency tags, they unwittingly stumbled on a metaphor for our path through the aisles of life. Route data from more than 1,000 shoppers, matched to their purchases at checkout, revealed a clear pattern: Drop a bunch of kale into your cart and you’re more likely to head next to the ice cream or beer section. The more “virtuous” products you have in your basket, the stronger your temptation to succumb to vice. Such hedonic balancing acts are neither unpredictable — who, after all, hasn’t rewarded themselves with a piece of cake or an extra beer after a killer workout? — nor inherently bad. But an emerging body of research into what psychologists call the “licensing effect” suggests that this tit-for-tat tendency is deeply wired in us, operating even when we’re not aware of it. And in a world where we’re bombarded by pitches for an endless array of health-boosting products of dubious efficacy, that can be a problem. The key insight underlying the licensing effect, which was first described in 2006 by Uzma Khan, then a professor of marketing at Carnegie Mellon University, and Ravi Dhar of the Yale School of Management, is that our choices are contingent: Since we each have a fairly stable self-concept of how good/bad, healthy/unhealthy or selfish/altruistic we are, when one decision swings too far from this self-concept, we automatically take action to balance it out. © 2015 The New York Times Company

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: 21565 - Posted: 10.26.2015

By Tara Parker-Pope Children who regularly use antibiotics gain weight faster than those who have never taken the drugs, according to new research that suggests childhood antibiotics may have a lasting effect on body weight well into adulthood. The study, published in the International Journal of Obesity, examined the electronic medical records of 163,820 children ages 3 to 18, counting antibiotic prescriptions, body weight and height. The records, which covered pediatric exams from 2001 through 2012, showed that one in five — over 30,000 children — had been prescribed antibiotics seven or more times. By the time those children reached age 15, they weighed, on average, about 3 pounds more than children who had received no antibiotics. While earlier studies have suggested a link between antibiotics and childhood weight gain, they typically have relied on a mother’s memories of her child’s antibiotic use. The new research is significant because it’s based on documented use of antibiotics in a child’s medical record. “Not only did antibiotics contribute to weight gain at all ages, but the contribution of antibiotics to weight gain gets stronger as you get older,” said Dr. Brian S. Schwartz, the first author and a professor in the department of environmental health sciences at the Johns Hopkins Bloomberg School of Public Health. Scientists have known for years that antibiotic use promotes weight gain in livestock, which is why large food producers include low doses of antibiotics in the diets of their animals. © 2015 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: 21544 - Posted: 10.22.2015

Susan Gaidos CHICAGO — Eating a high-fat diet as a youngster can affect learning and memory during adulthood, studies have shown. But new findings suggest such diets may not have long-lasting effects. Rats fed a high-fat diet for nearly a year recovered their ability to navigate their surroundings. University of Texas at Dallas neuroscientist Erica Underwood tested spatial memory for rats fed a high-fat diet for either 12 weeks or 52 weeks, immediately after weaning. After rats placed in a chamber-filled box containing Lego-like toys became familiar with the box, the researchers moved the toys to new chambers. Later, when placed in the box, rats who ate high-fat foods for 12 weeks appeared confused and had difficulty finding the toys. But rats that ate high-fat foods for nearly a year performed as well as those fed a normal diet. Underwood repeated the experiment, posing additional spatial memory tests to new groups of rats. The findings were the same: Over the long-term, rats on high-fat diets recovered their ability to learn and remember. Studies of brain cells revealed that rats on the long-term high-fat diet showed reduced excitability in nerve cells from the hippocampus, the same detrimental effects seen in rats on the short-term high-fat diet. “The physiology that should create a dumber animal is there, but not the behavior,” said Lucien Thompson of UT Dallas, who oversaw the study. Underwood and Thompson speculate that some other part of the brain may be compensating for this reduction in neural response. © Society for Science & the Public 2000 - 2015.

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: 21533 - Posted: 10.21.2015

Peter Andrey Smith Nearly a year has passed since Rebecca Knickmeyer first met the participants in her latest study on brain development. Knickmeyer, a neuroscientist at the University of North Carolina School of Medicine in Chapel Hill, expects to see how 30 newborns have grown into crawling, inquisitive one-year-olds, using a battery of behavioural and temperament tests. In one test, a child's mother might disappear from the testing suite and then reappear with a stranger. Another ratchets up the weirdness with some Halloween masks. Then, if all goes well, the kids should nap peacefully as a noisy magnetic resonance imaging machine scans their brains. “We try to be prepared for everything,” Knickmeyer says. “We know exactly what to do if kids make a break for the door.” Knickmeyer is excited to see something else from the children — their faecal microbiota, the array of bacteria, viruses and other microbes that inhabit their guts. Her project (affectionately known as 'the poop study') is part of a small but growing effort by neuroscientists to see whether the microbes that colonize the gut in infancy can alter brain development. The project comes at a crucial juncture. A growing body of data, mostly from animals raised in sterile, germ-free conditions, shows that microbes in the gut influence behaviour and can alter brain physiology and neurochemistry. © 2015 Nature Publishing Group

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: 21521 - Posted: 10.16.2015

By Nicholas Bakalar There may be a link between later bedtimes and weight gain, new research suggests. Researchers studied 3,342 adolescents starting in 1996, following them through 2009. At three points over the years, all reported their normal bedtimes, as well as information on fast food consumption, exercise and television time. The scientists calculated body mass index at each interview. After controlling for age, sex, race, ethnicity and socioeconomic status, the researchers found that each hour later bedtime during the school or workweek was associated with about a two-point increase in B.M.I. The effect was apparent even among people who got a full eight hours of sleep, and neither TV time nor exercise contributed to the effect. But fast food consumption did. The study, in the October issue of Sleep, raises questions, said the lead author, Lauren D. Asarnow, a graduate student at the University of California, Berkeley. “First, what is driving this relationship?” she said. “Is it metabolic changes that happen when you stay up late? And second, if we change sleep patterns, can we change eating behavior and the course of weight change?” The scientists acknowledge that their study had limitations. Their sleep data depended on self-reports, and they did not have complete diet information. Also, they had no data on waist circumference, which, unlike B.M.I., can help distinguish between lean muscle and abdominal fat. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 21483 - Posted: 10.07.2015

By Kelly Servick Children born to obese mothers arrive already predisposed to obesity and other health problems themselves. Exactly what happens in the uterus to transmit this risk still isn’t clear, but a new study on mice points to the placenta as a key actor. The study shows that a hormone acting on the placenta can protect the offspring of obese mice from being born overweight. It suggests ways to break the cycle of obesity in humans—although other researchers caution there's a long way to go. Researchers discovered decades ago that conditions in the uterus can “program” a fetus to be more susceptible to certain health problems. People conceived during the 1944 famine in the Netherlands, for example, suffered higher rates of cardiovascular disease, diabetes, cancer, and other problems later in life. Recent animal studies suggest that malnourishment in the womb changes the expression of DNA in ways that can be passed down for generations. But researchers are now increasingly concerned with the opposite problem. Obese women tend to give birth to larger babies with more body fat, and these children are more likely to develop metabolic syndrome—the cluster of conditions including obesity and high blood sugar that can lead to diabetes and heart disease. To probe the roots of fetal “overgrowth,” developmental biologists at the University of Colorado, Denver, looked to the placenta—the whoopee cushion–shaped organ wedged between the fetus and the wall of the uterus, where branching arteries from the umbilical cord take up oxygen and nutrients from the mother’s blood vessels. The placenta “has always been viewed as a passive organ—whatever happens to the mother is translated toward the fetus,” says lead author Irving Aye, now at the University of Cambridge in the United Kingdom. However, recent research has shown that the placenta is less an indiscriminate drainpipe than a subtle gatekeeper. © 2015 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: 21456 - Posted: 09.29.2015

by Bethany Brookshire Last weekend, I ran the Navy-Air Force half-marathon. After pounding pavement for an hour or so, my legs began to feel light. Slightly numb. I felt fantastic. I had to remind myself to run, not to stop and dance, and that singing along to my candy-pop workout music — even at mile 10 — is not socially acceptable. It’s the hope of this euphoria — this runner’s high — that keeps me running. We’re not totally sure what’s responsible for this incredible high. Some studies call out our body’s endorphins. Others point to cannabinoids — chemicals related to the active compound in marijuana. A new study suggests that the appetite hormone leptin may play a role in getting us going. And from an evolutionary perspective, it makes good sense. When our dinner might make a quick getaway, it’s important to link our drive to run with our need to feed. But it’s probably not the whole story. Like many other neurobiological events, the exact recipe for runner’s high is complex and hazy. It takes a whole suite of chemicals to help us get started and to make sure we want to go the distance. Those who get runner’s high know it when they feel it. But a clinical definition is a little more slippery. “I remember someone saying the runner’s high was the moment when the body was disconnected from the brain,” says Francis Chaouloff, who studies running and motivation in mice at the French Institute of Health and Medical Research in Bordeaux. This sense of extreme euphoria, he says, is generally limited to people running or exercising for long periods of time, over many miles or hours. © Society for Science & the Public 2000 - 2015.

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: 21452 - Posted: 09.28.2015

By Sarah C. P. Williams When the human body needs extra energy, the brain tells fat cells to release their stores. Now, for the first time, researchers have visualized the nerves that carry those messages from brain to fat tissue. The activation of these nerves in mice, they found, helps the rodents lose weight—an observation that could lead to new slimming treatments for obese people. “The methods used here are really novel and exciting,” says neuroendocrinologist Heike Muenzberg-Gruening of Louisiana State University’s Pennington Biomedical Research Center in Baton Rouge, who was not involved in the new study. “Their work has implications for obesity research and also for studying these nerves in other tissues.” Diagrams of the chatter between the brain and fat tissues have long included two-way arrows: Fat cells produce the hormone leptin, which travels to the brain to lower appetite and boost metabolism. In turn, the brain sends signals to the fat cells when it’s time to break down their deposits of fatty molecules, such as lipids, into energy. Researchers hypothesized that there must be a set of nerve cells that hook up to traditional fat tissue to carry these messages, but they’d never been able to indisputably see or characterize them. Now they have. Thanks to two forms of microscopy, neurobiologist Ana Domingos, of the Instituto Gulbenkian de Ciência in Oeiras, Portugal, produced images showing bundles of nerves clearly enveloping fat cells in mice. She and her colleagues went on to show, using various stains, that the nerves were a type belonging to the sympathetic nervous system that stretches outward from the spinal cord and keeps the body’s systems in balance. © 2015 American Association for the Advancement of Science

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: 21448 - Posted: 09.26.2015

By Sarah C. P. Williams Immune cells are usually described as soldiers fighting invading viruses and bacteria. But they may also be waging another battle: the war against fat. When mice lack a specific type of immune cell, researchers have discovered, they become obese and show signs of high blood pressure, high cholesterol, and diabetes. The findings have yet to be replicated in humans, but they are already helping scientists understand the triggers of metabolic syndrome, a cluster of conditions associated with obesity. The new study “definitely moves the field forward,” says immunologist Vishwa Deep Dixit of the Yale School of Medicine, who was not involved in the work. “The data seem really solid.” Scientists already know that there is a correlation between inflammation—a heightened immune response—and obesity. But because fat cells themselves can produce inflammatory molecules, distinguishing whether the inflammation causes weight gain or is just a side effect has been tricky. When he stumbled on this new cellular link between obesity and the immune system, immunologist Yair Reisner of the Weizmann Institute of Science in Rehovot, Israel, was studying something completely different: autoimmune diseases. An immune molecule called perforin had already been shown to kill diseased cells by boring a hole in their outer membrane. Reisner’s group suspected that dendritic cells containing perforin might also be destroying the body’s own cells in some autoimmune diseases. To test the idea, Reisner and his colleagues engineered mice to lack perforin-wielding dendritic cells, and then waited to see whether they developed any autoimmune conditions. © 2015 American Association for the Advancement of Science

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: 21415 - Posted: 09.16.2015