Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By Nicholas Bakalar Women with sleeping difficulties are at increased risk for Type 2 diabetes, researchers report. Scientists used data from 133,353 women who were generally healthy at the start of the study. During 10 years of follow-up, they found 6,407 cases of Type 2 diabetes. The researchers looked at four sleep problems: self-reported difficulty falling or staying asleep, frequent snoring, sleep duration of less than six hours, and either sleep apnea or rotating shift work. The study is in Diabetologia. Self-reported difficulty sleeping was associated with higher B.M.I., less physical activity, and more hypertension and depression. But even after adjusting for these and other health and behavioral characteristics, sleeping difficulty was still associated with a 22 percent increased risk for Type 2 diabetes. Compared to women with no sleep problems, those with two of the sleep conditions studied had double the risk, and those with all four had almost four times the risk of developing the illness. The senior author, Dr. Frank B. Hu, a professor of nutrition and epidemiology at Harvard, said that sleep problems are associated with excess secretion of two hormones: ghrelin, which increases appetite, and cortisol, which increases stress and insulin resistance. Both are linked to metabolic problems that increase the risk for diabetes. “And,” he added, “it’s not just quantity of sleep, but quality as well” that is associated with these health risks. © 2016 The New York Times Company
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
By Roni Caryn Rabin The first time she skipped an insulin dose, the 22-year-old said, it wasn’t planned. She was visiting her grandparents over a summer break from college and indulged in bags of potato chips and fistfuls of candy, but forgot to take the extra insulin that people with Type 1 diabetes, like her, require to keep their blood sugar levels in a normal range. She was already underweight after months of extreme dieting, but when she stepped on the scale the next day, she saw she had dropped several pounds overnight. “I put two and two together,” said the young woman, who lives in Boston and wished to remain anonymous. She soon developed a dangerous habit that she used to drive her weight down: She would binge, often consuming an entire pint of Ben & Jerry’s peanut butter cup ice cream, and then would deliberately skip the insulin supplements she needed. People with Type 1 diabetes, who don’t produce their own insulin, require continuous treatments with the hormone in order to get glucose from the bloodstream into the cells. When they skip or restrict their insulin, either by failing to take shots or manipulating an insulin pump, it causes sugars — and calories — to spill into the urine, causing rapid weight loss. But the consequences can be fatal. “I knew I was playing with fire, but I wasn’t thinking about my life, just my weight,” said the young woman, who was treated at The Renfrew Center of Boston, which specializes in treating eating disorders, and is in recovery. “I got used to my blood sugars running high all the time. I would get so nauseous I would throw up, which I knew was a serious sign that I should go to the hospital. It was very scary.” © 2016 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 21847 - Posted: 02.02.2016
By Lisa Rapaport Mothers who are obese during pregnancy have almost twice the odds of having a child with autism as women who weigh less, a U.S. study suggests. When women are both obese and have diabetes, the autism risk for their child is at least quadrupled, researchers reported online January 29 in Pediatrics. "In terms of absolute risk, compared to common pediatric diseases such as obesity and asthma, the rate of autism spectrum disorder (ASD) in the U.S. population is relatively low, however, the personal, family and societal impact of ASD is enormous," said senior study author Dr. Xiaobin Wang, a public health and pediatrics researcher at Johns Hopkins University in Baltimore. About one in 68 children have ASD, according to the U.S. Centers for Disease Control and Prevention, or about 1.5 percent of U.S. children. The study findings suggest the risk rises closer to about 3 percent of babies born to women who are obese or have diabetes, and approaches 5 percent to 6 percent when mothers have the combination of obesity and diabetes. Wang and colleagues analyzed data on 2,734 mother-child pairs followed at Boston Medical Center between 1998 and 2014. Most of the children, 64 percent, weren't diagnosed with any other development disorders, but there were 102 kids who did receive an ASD diagnosis. © 2016 Scientific American
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
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
Link ID: 21837 - Posted: 01.30.2016
by Emily Reynolds We know more about what the brain does when it's active than we do when it's at rest. It makes sense -- much neuroscientific research has looked to understand particular (and active) processes. James Kozloski, a researcher at IBM, has investigated what the brain does when it's resting -- what he calls 'the Grand Loop'. "The brain consumes a great amount of energy doing nothing. It's a great mystery of neuroscience," Kozloski told PopSci. He argued that around 90 percent of the energy used by the brain remained "unaccounted for". He believes that the brain is constantly 'looping signals', retracing neural pathways over and over again. It's a "closed loop", according to Kozloski, meaning it isn't reliant on external inputs as much of the brain's activity is. Kozloski tested his theory by running his model through IBM's neural tissue simulator and found that it could potentially account for genetic mutations such as Huntington's. He argued that information created by one mutated gene could, through the 'Grand Loop', affect an entire neural pathway. So what happens when our brain is at work? And how does expending energy affect our neural processes? Much historic research into anxiety has found that people tend to exert more energy or force when they're being watched -- something that leads to slip-ups or mistakes under pressure.
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