Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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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
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
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
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
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.
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
Link ID: 21757 - Posted: 01.07.2016
By Nicholas Bakalar Psychotherapy is effective in easing the symptoms of irritable bowel syndrome, researchers have found, even after therapy has ended. Irritable bowel syndrome can cause diarrhea, cramping, fever and sometimes rectal bleeding. The chronic ailment affects up to 11 percent of the population, and there is no cure or completely effective treatment. The study, in Clinical Gastroenterology and Hepatology, used data from 41 clinical trials that included 1,183 people assigned to psychotherapy and 1,107 controls. The approach was usually cognitive therapy, but some studies tested hypnotherapy, mindfulness, behavioral therapy or dynamic psychotherapy. The studies all used questionnaires at the start and end of the treatment, asking about severity and frequency of symptoms. Over all, the researchers found that 12 months after the end of treatment, 75 percent of the treatment group had greater symptom relief than the average member of the control group, although the benefits were modest. “I.B.S. is notoriously difficult to treat,” said the lead author, Kelsey T. Laird, a doctoral candidate at Vanderbilt University, “so the fact that these effects are just as strong six to 12 months later is very exciting — a significant effect, which did not decrease over time.” Whether a given individual will benefit from psychotherapy is still unknown, Ms. Laird said. But, she added, “We do know that this seems to be one of the best treatments out there. So I would recommend it.” © 2016 The New York Times Company
Link ID: 21740 - Posted: 01.02.2016
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.
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
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
by Chris Samoray Every fall, blackpoll warblers fly from North America to South America in what’s the longest migration route of any warbler in the Western Hemisphere. But some of the tiny songbirds take a detour before making their epic transoceanic leap. Over 40 years of data from 22,295 birds show that blackpoll warblers (Setophaga striata) living in western North America head east for a pit stop to put on weight, giving the birds the energy stores they need to cross the Atlantic Ocean, researchers report December 9 in the Auk: Ornithological Advances. For birds that breed farther west in places like Alaska, the eastern stopover means a migration distance that’s nearly twice that of their eastern U.S. counterparts, the scientists find. © Society for Science & the Public 2000 - 2015.
Keyword: Animal Migration
Link ID: 21687 - Posted: 12.10.2015
Carl Zimmer In 2013, an obese man went to Hvidovre Hospital in Denmark to have his stomach stapled. All in all, it was ordinary bariatric surgery — with one big exception. A week before the operation, the man provided a sperm sample to Danish scientists. A week after the procedure, he did so again. A year later, he donated a third sample. Scientists were investigating a tantalizing but controversial hypothesis: that a man’s experiences can alter his sperm, and that those changes in turn may alter his children. That idea runs counter to standard thinking about heredity: that parents pass down only genes to their children. People inherit genes that predispose them to obesity, or stress, or cancer — or they don’t. Whether one’s parents actually were obese or constantly anxious doesn’t rewrite those genes. Yet a number of animal experiments in recent years have challenged conventional thinking on heredity, suggesting that something more is at work. In 2010, for example, Dr. Romain Barres of the University of Copenhagen and his colleagues fed male rats a high-fat diet and then mated them with females. Compared with male rats fed a regular diet, those on the high-fat diet fathered offspring that tended to gain more weight, develop more fat and have more trouble regulating insulin levels. Eating high-fat food is just one of several experiences a father can have that can change his offspring. Stress is another. Male rats exposed to stressful experiences — like smelling the odor of a fox — will father pups that have a dampened response to stress. © 2015 The New York Times Company
Laura Sanders Faced with a shortage of the essential nutrient selenium, the brain and the testes duke it out. In selenium-depleted male mice, testes hog the trace element, leaving the brain in the lurch, scientists report in the Nov. 18 Journal of Neuroscience. The results are some of the first to show competition between two organs for trace nutrients, says analytical neurochemist Dominic Hare of the University of Technology Sydney and the Florey Institute of Neuroscience and Mental Health in Melbourne. In addition to uncovering this brain-testes scuffle, the study “highlights that selenium in the brain is something we can’t continue to ignore,” he says. About two dozen proteins in the body contain selenium, a nonmetallic chemical element. Some of these proteins are antioxidants that keep harmful molecules called free radicals from causing trouble. Male mice without enough selenium have brain abnormalities that lead to movement problems and seizures, neuroscientist Matthew Pitts of the University of Hawaii at Manoa and colleagues found. In some experiments, Pitts and his colleagues depleted selenium by interfering with genes. Male mice engineered to lack two genes that produce proteins required for the body to properly use selenium had trouble balancing on a rotating rod and moving in an open field. In their brains, a particular group of nerve cells called parvalbumin interneurons didn’t mature normally. © Society for Science & the Public 2000 - 2015.
Link ID: 21640 - Posted: 11.18.2015
Sarah Schwartz With outposts in nearly every organ and a direct line into the brain stem, the vagus nerve is the nervous system’s superhighway. About 80 percent of its nerve fibers — or four of its five “lanes” — drive information from the body to the brain. Its fifth lane runs in the opposite direction, shuttling signals from the brain throughout the body. Doctors have long exploited the nerve’s influence on the brain to combat epilepsy and depression. Electrical stimulation of the vagus through a surgically implanted device has already been approved by the U.S. Food and Drug Administration as a therapy for patients who don’t get relief from existing treatments. Now, researchers are taking a closer look at the nerve to see if stimulating its fibers can improve treatments for rheumatoid arthritis,heart failure, diabetes and even intractable hiccups. In one recent study, vagus stimulation made damaged hearts beat more regularly and pump blood more efficiently. Researchers are now testing new tools to replace implants with external zappers that stimulate the nerve through the skin. But there’s a lot left to learn. While studies continue to explore its broad potential, much about the vagus remains a mystery. In some cases, it’s not yet clear exactly how the nerve exerts its influence. And researchers are still figuring out where and how to best apply electricity. © Society for Science & the Public 2000 - 2015.
Link ID: 21633 - Posted: 11.14.2015
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.”
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, 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,
Link ID: 21584 - Posted: 10.31.2015
By Jan Hoffman As the first semester of the school year reaches the halfway mark, countless college freshmen are becoming aware that their clothes are feeling rather snug. While the so-called freshman 15 may be hyperbole, studies confirm that many students do put on five to 10 pounds during that first year away from home. Now new research suggests that an underlying cause for the weight gain may be the students’ widely vacillating patterns of sleep. A study in the journal Behavioral Sleep Medicine looked at the sleep habits of first-semester freshmen. Researchers followed 132 first-year students at Brown University who kept daily sleep diaries. After nine weeks, more than half of them had gained nearly six pounds. There are many poor sleep habits that might have exacerbated their weight gains, a growing body of research indicates. Was it abbreviated sleep? Optimally, experts say, teenagers need about nine hours and 15 minutes a night. These freshmen averaged about seven hours and 15 minutes. In a study earlier this year, in the journal PLOS One, researchers found that when teenagers are sleep-deprived, they more readily reach for candy and desserts. Or were the Brown students’ late bedtimes the scale-tipping factor? On average, they went to bed around 1:30 a.m. A study this month in the journal Sleep that followed teenagers into adulthood found that each hour later bedtime was pushed during the school or workweek was associated with about a two-point increase in body mass index. While both the amount of sleep and the lateness of bedtime may have played a role, the researchers in the Brown study identified a new sleep factor for predicting weight gain: variability, or the extent to which a student’s bedtime and waking time changed daily. © 2015 The New York Times Company
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
By Carrie Arnold Most of the anorexia patients Dr. Joanna Steinglass sees in the inpatient eating-disorders unit at the New York State Psychiatric Institute have been to treatment before. While in the hospital or a residential treatment center, they generally gained weight and began to eat a wider variety of foods. But after they left, their old anorexic habits returned. They began skipping meals again or returning to their extreme exercise routines. All too soon, it seemed, the gains made in treatment and the hope for recovery that went along with it began to evaporate. According to the conventional wisdom around eating disorders, these relapses were really a misguided search for control. Or maybe the patients just weren’t ready for recovery yet. Or perhaps these were signs of self-control gone awry, spurred on by friends who marvel at their seemingly endless willpower. Interesting theories, and yet Steinglass disagreed. “Even when people show up at our hospital and want to make changes, they find it tough,” she said. Now a new study in Nature Neuroscience — which Steinglass co-authored — reveals why people with anorexia often struggle so much to integrate new ways of eating into their lives. In the brain, the behaviors associated with anorexia act a lot like habits, those daily decisions we make without thinking. And habits, according to both the scientific evidence and the colloquial wisdom, are phenomenally difficult to break. This new finding helps explain why anorexia has historically been so hard to treat: Anorexic patients are essentially fighting their own brains in an uphill battle for wellness. But more important, the new research may also point toward new and better ways to help those with the eating disorder overcome it. © 2015, New York Media LLC.
Keyword: Anorexia & Bulimia
Link ID: 21560 - Posted: 10.24.2015
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