Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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Carl Zimmer Scientists recently turned Harvard’s Skeletal Biology Laboratory into a pop-up restaurant. It would have fared very badly on Yelp. Katherine D. Zink, then a graduate student, acted as chef and waitress. First, she attached electrodes to the jaws of diners to record the activity in the muscles they use to chew food. Then she brought out the victuals. Some volunteers received a three-course vegetarian meal of carrots, yams or beets. In one course, the vegetables were cooked; in the second, they were raw and sliced; in the last course, Dr. Zink simply served raw chunks of plant matter. Other patrons got three courses of meat (goat, in this case). Dr. Zink grilled the meat in the first course, but offered it raw and sliced in the second. In the third course, her volunteers received an uncooked lump of goat flesh. In some of the trials, the volunteers chewed the food until it was ready to swallow and then spat it out. Dr. Zink painstakingly picked apart those food bits and measured their size. Every week, we'll bring you stories that capture the wonders of the human body, nature and the cosmos. “If that was all my dissertation was, I would have quit graduate school,” Dr. Zink said. “It was as lovely as it sounds.” Dr. Zink persevered, however, because she was exploring a profound question about our origins: How did our ancestors evolve from small-brained, big-jawed apes into large-brained, small-jawed humans? Scientists studying the fossil record have long puzzled over this transition, which happened around two million years ago. Before then, early human relatives — known as hominins — were typically about the size of chimpanzees, with massive teeth and a brain only a third the size of humans’ current brains. © 2016 The New York Times Company
Susan Gaidos Most people would be happy to get rid of excess body fat. Even better: Trade the spare tire for something useful — say, better-functioning knees or hips, or a fix for an ailing heart or a broken bone. The idea is not far-fetched, some scientists say. Researchers worldwide are repurposing discarded fat to repair body parts damaged by injury, disease or age. Recent studies in lab animals and humans show that the much-maligned material can be a source of cells useful for treating a wide range of ills. At the University of Pittsburgh, bioengineer Rocky Tuan and colleagues extract buckets full of yellow fat from volunteers’ bellies and thighs and turn the liposuctioned material into tissue that resembles shock-absorbing cartilage. If the cartilage works as well in people as it has in animals, Tuan’s approach might someday offer a kind of self-repair for osteoarthritis, the painful degeneration of cartilage in the joints. He’s also using fat cells to grow replacement parts for the tendons and ligaments that support the joints. Foremost among fat’s virtues is its richness of stem cells, which have the ability to divide and grow into a wide variety of tissue types. Fat stem cells — also known as adipose-derived stem cells — can be coerced to grow into bone, cartilage, muscle tissue or, of course, more fat. Cells from fat are being tested to mend tissues found in damaged joints, hearts and muscle, and to regrow bone and heal wounds. © Society for Science & the Public 2000 - 2016
By Anahad O'Connor Mark Mattson, a neuroscientist at the National Institute on Aging in Maryland, has not had breakfast in 35 years. Most days he practices a form of fasting — skipping lunch, taking a midafternoon run, and then eating all of his daily calories (about 2,000) in a six-hour window starting in the afternoon. “Once you get used to it, it’s not a big deal,” said Dr. Mattson, chief of the institute’s laboratory of neurosciences. “I’m not hungry at all in the morning, and this is other people’s experience as well. It’s just a matter of getting adapted to it.” In a culture in which it’s customary to eat three large meals a day while snacking from morning to midnight, the idea of regularly skipping meals may sound extreme. But in recent years intermittent fasting has been gaining popular attention and scientific endorsement. It has been promoted in best-selling books and endorsed by celebrities like the actors Hugh Jackman and Benedict Cumberbatch. The late-night talk show host Jimmy Kimmel claims that for the past two years he has followed an intermittent fasting program known as the 5:2 diet, which entails normal eating for five days and fasting for two — a practice Mr. Kimmel credits for his significant weight loss. Fasting to improve health dates back thousands of years, with Hippocrates and Plato among its earliest proponents. Dr. Mattson argues that humans are well suited for it: For much of human history, sporadic access to food was likely the norm, especially for hunter-gatherers. As a result, we’ve evolved with livers and muscles that store quickly accessible carbohydrates in the form of glycogen, and our fat tissue holds long-lasting energy reserves that can sustain the body for weeks when food is not available. “From an evolutionary perspective, it’s pretty clear that our ancestors did not eat three meals a day plus snacks,” Dr. Mattson said. © 2016 The New York Times Company
Link ID: 21969 - Posted: 03.09.2016
By Roberto A. Ferdman In the mid 1970s, psychologist Merrill Elias began tracking the cognitive abilities of more than a thousand people in the state of New York. The goal was fairly specific: to observe the relationship between people's blood pressure and brain performance. And for decades he did just that, eventually expanding the Maine-Syracuse Longitudinal Study (MSLS) to observe other cardiovascular risk factors, including diabetes, obesity, and smoking. There was never an inkling that his research would lead to any sort of discovery about chocolate. And yet, 40 years later, it seems to have done just that. Late in the study, Elias and his team had an idea. Why not ask the participants what they were eating too? It wasn't unreasonable to wonder if what someone ate might add to the discussion. Diets, after all, had been shown to affect the risk factors Elias was already monitoring. Plus, they had this large pool of participants at their disposal, a perfect chance to learn a bit more about the decisions people were making about food. The researchers incorporated a new questionnaire into the sixth wave of their data collection, which spanned the five years between 2001 and 2006 (there have been seven waves in all, each conducted in five year intervals). The questionnaire gathered all sorts of information about the dietary habits of the participants. And the dietary habits of the participants revealed an interesting pattern. "We found that people who eat chocolate at least once a week tend to perform better cognitively," said Elias. "It's significant—it touches a number of cognitive domains." © 1996-2016 The Washington Post
Heidi Ledford Obese mice — like obese humans — are at increased risk of colon cancer, and a study published today in Nature finally suggests why. Overweight mice fed a high-fat diet showed an increase in intestinal stem cells due to activation of a protein called PPAR-δ that regulates metabolism1. If the results hold true in humans, they could explain a phenomenon seen in epidemiological studies. “For quite some time there’s been an understanding that obesity leads to an increase in cancer in many tissues,” says Ömer Yilmaz, a cancer biologist at the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology (MIT) in Cambridge, and one of the leaders of the study. “We really wanted to understand the mechanism behind this.” Those molecular details could be important, says cell biologist P. Kay Lund who works at the University of North Carolina in Chapel Hill and the National Institutes of Health in Bethesda, Maryland. Tissue samples from people who have undergone colonoscopies could be tested to see if the same patterns hold true. Ultimately, the the increase in PPAR-δ activity could yield a useful indicator of cancer risk. “It could provide an opportunity to give those patients an earlier intervention,” says Lund, who was not involved in the obesity work. Yilmaz teamed up with David Sabatini, who studies metabolism at MIT and the Whitehead Institute, also in Cambridge, to learn more about the link between cancer and obesity. Their teams fed mice high-fat, high-calorie chow for about a year, and then tested the effects of the diet on the number and function of stem cells in their intestines. © 2016 Nature Publishing Group
Link ID: 21952 - Posted: 03.03.2016
Mo Costandi Most of us are well aware of the health risks associated with obesity. Being overweight or obese is associated with an increased risk of numerous other conditions, from high blood pressure, heart disease and stroke, to diabetes, gout and some forms of cancer. Self-control saps memory resources Read more Research published over the past few years shows that obesity also has neurological consequences – it is associated with altered function in, and shrinkage of, certain parts of the brain, particularly the frontal lobes, which are the seat of intelligence, and the hippocampus, which is critical for memory formation. A new study now shows that this in turn is associated with impaired memory function. Lucy Cheke of the University of Cambridge and her colleagues recruited 50 volunteers aged between 18 and 35, with Body Mass Indexes (BMIs) ranging from 18 (underweight) to 51 (extremely obese), and asked them to perform a computerised memory test called the “Treasure Hunt Task”. This involved moving food items around around complex scenes, such as a desert with palm trees, hiding them in various locations, and indicating afterwards where they had hidden them. The participants were then shown various locations from the computerised scenes, and some of the food items, and asked if they had hidden something in each of the locations, or where they had hidden each of the items. Finally, they were shown pairs of the food items they had seen, and asked to indicate which of each pair they had hidden first. © 2016 Guardian News and Media Limited
Ian Sample Science editor Too little sleep may bring on a form of the marijuana “munchies”, say scientists who found that sleep-deprived people craved crisps, sweets and biscuits far more than healthier foods. The US researchers believe that skimping on sleep alters brain chemicals in much the same way as the hunger-boosting ingredient in cannabis, which has long propped up snack sales at 24-hour convenience stores. After several nights of poor sleep, healthy volunteers who took part in the study reached for snacks containing more calories - and nearly twice as much fat - than ones they favoured after sleeping well for the same period, the scientists say. When sleepy, the participants had terrible trouble resisting the snacks, even when they were full, said Erin Hanlon, who led the study at the University of Chicago. Research has shown time and again that sleep loss raises the risk of obesity, but the reasons are complex and unclear. Insufficient sleep disrupts hormones that govern appetite and satiety. But those who sleep less have more time to eat, and may be too tired to exercise. To muddy the waters further, obesity can lead to breathing problems that themselves disrupt sleep patterns. In a small study published in the journal Sleep, Hanlon invited 14 men and women in their twenties to spend two four-day sessions at the university’s clinical research centre. The volunteers’ time in bed was controlled, so that on one visit they averaged 7.5 hours of sleep a night, but on the other only 4 hours 11 minutes a night. During their stays, the volunteers ate identical meals, dished out at 9am, 2pm and 7pm.
By James Gallagher Health editor, BBC News website People who are obese have a worse memory than their thinner friends, a small study shows. Tests on 50 people showed being overweight was linked to worse "episodic memory" or the ability to remember past experiences. The study in the Quarterly Journal of Experimental Psychology argues that a less vivid memory of recent meals may lead to overeating. However, other aspects of memory - such as general knowledge - were unaffected. Tests on rats have previously shown that with burgeoning waistlines come poorer performances in memory tests, but the evidence in humans has been mixed. The latest experiments looked at episodic memory - the video tape in your mind - that remembers the smell of a cup of coffee or the feel of holding someone's hand. Fifty people with a Body Mass Index (BMI) ranging from 18 (healthy) to 51 (very obese) took part in a memory test - a bit like doing a treasure hunt on your own. They had to "hide" objects at different times and on different scenes displayed on a computer screen. They were later asked to recall what they had hidden, when and where. The results showed obese people's scores were 15% lower than thinner people. Dr Lucy Cheke, from the University of Cambridge, told the BBC News website: "The suggestion we're making is that a higher BMI is having some reduction on the vividness of memory, but they're not drawing blanks and having amnesia. "But if they have a less strong memory of a recent meal, with a less strong impact in the mind, then they may have less ability to regulate how much they eat later on." Hunger hormones play a huge role in how much we eat, but it is already recognised that our minds have a key role too. © 2016 BBC
By Roberto A. Ferdman Poverty has a way of rearing its ugly head, slipping into the cracks in people's lives when they're young and then re-emerging later in life. Sometimes it happens in ways that are easily observable—what poor babies are fed, for instance, has been shown to alter what they crave as adults, creating life-long affinities for foods that might be better left uneaten. But sometimes the influences are hidden, and all the more insidious as a result. A team of researchers, led by Sarah Hill, who teaches psychology at Texas Christian University, believe they have uncovered evidence of one such lingering effect. Specifically, Hill and her colleagues found that people who grow up poor seem to have a significantly harder time regulating their food intake, even when they aren't hungry. "We found that they eat comparably high amounts regardless of their need," said Hill. The researchers, interested in exploring why obesity is more prevalent in poorer populations, devised three separate experiments, which tested how people from different socioeconomic backgrounds behaved in front of food. In the first, they invited 31 female participants into their lab, who were asked how long it had been since they had eaten, and how hungry they were. They were then given snacks (cookies and pretzels), which they were free to eat or leave be, as they pleased. When they were finished, Hill and her team measured the number of calories each consumed. The discrepancy between how the participants ate was alarming.
By Roni Caryn Rabin Does long-term use of artificial sweeteners cause weight gain or contribute to metabolic syndrome? Scientists are still scratching their heads over this question. Artificial, or nonnutritive, sweeteners have no calories and are often used as diet aids. But while some well-designed trials have found that those randomly assigned to drink artificially sweetened beverages gained less weight than those given sugar-sweetened drinks, large population studies suggest that frequent consumption of artificial sweeteners may be linked with unanticipated consequences, including weight gain. A large study that followed a diverse group of 6,814 Americans ages 45 to 84 for at least five years found that those who drank diet soda at least once a day were at 67 percent greater risk of developing Type 2 diabetes than those who didn’t consume diet drinks, regardless of whether they gained weight or not, and at 36 percent greater risk of metabolic syndrome, which can be a precursor to heart disease, stroke and diabetes. Another large study that followed thousands of residents of San Antonio, Tex., for 10 years found those who drank more than 21 servings of diet drinks a week were at twice the risk of becoming overweight or obese, and the more diet soda people drank, the greater the risk. These large observational trials do not prove cause and effect, however, and may reflect the fact that people who are gaining weight may be most likely to drink a lot of diet soda. Dr. John Fernstrom, a University of Pittsburgh professor who is also a paid consultant to Ajinomoto, a maker of aspartame, reviewed the evidence on nonnutritive sweeteners and concluded that the evidence linking them to metabolic problems was “not compelling.” © 2016 The New York Times Company
Ice cream lovers, look away now. Studies on a simulated human gut have added further evidence that emulsifiers, found in most processed foods, might be linked to obesity, diabetes and inflammatory bowel disorders. Emulsifiers are used to improve a food’s texture and to prevent mixtures from separating, particularly in ice cream. Last year, Benoit Chassaing of Georgia State University showed that mice that drank water containing one of two emulsifiers underwent changes in gut bacteria and inflammation of the gut – changes that led to obesity and diabetes in these animals. However, mice that didn’t have any gut bacteria because they had been raised in a sterile environment didn’t become ill when given the same additives, suggesting that it is the emulsifiers’ effect on the microbiome that is to blame. When the ill mice stopped consuming emulsifiers, their gut bacteria gradually returned to normal. The question is whether the same might be true for humans. The growing use of emulsifiers has coincided with a rise in obesity and diabetes, says Chassaing, while these conditions aren’t as common in countries where less processed food is consumed. Now Chassaing has supported his findings in mice using a simulation of the human gut. Working with a team in Belgium, he looked at two emulsifiers: carboxymethylcellulose (E566 on EU labels) and polysorbate-80 (E433). When added to a series of flasks that mimic the conditions of the human digestive tract, each caused an increase in the levels of a bacterial protein called flagellin, known to cause inflammation at high concentrations. Chassaing presented the results at a recent meeting at the Royal Society in London. © Copyright Reed Business Information Ltd.
Link ID: 21880 - Posted: 02.10.2016
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