Chapter 13. Homeostasis: Active Regulation of the Internal Environment
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By Jessica Hamzelou As any weight-watcher knows, carb cravings can be hard to resist. Now there’s evidence that carbohydrate-rich foods may elicit a unique taste too, suggesting that “starchy” could be a flavour in its own right. It has long been thought that our tongues register a small number of primary tastes: salty, sweet, sour and bitter. Umami – the savoury taste often associated with monosodium glutamate – was added to this list seven years ago, but there’s been no change since then. However, this list misses a major component of our diets, says Juyun Lim at Oregon State University in Corvallis. “Every culture has a major source of complex carbohydrate. The idea that we can’t taste what we’re eating doesn’t make sense,” she says. Complex carbohydrates such as starch are made of chains of sugar molecules and are an important source of energy in our diets. However, food scientists have tended to ignore the idea that we might be able to specifically taste them, says Lim. Because enzymes in our saliva break starch down into shorter chains and simple sugars, many have assumed we detect starch by tasting these sweet molecules. Her team tested this by giving a range of different carbohydrate solutions to volunteers – who it turned out were able to detect a starch-like taste in solutions that contained long or shorter carbohydrate chains. “They called the taste ‘starchy’,” says Lim. “Asians would say it was rice-like, while Caucasians described it as bread-like or pasta-like. It’s like eating flour.” © Copyright Reed Business Information Ltd.
Hannah Devlin Science correspondent Babies born by caesarean section are more likely to be obese as adults, according to a study that suggests the way we are born could have a lasting impact on health. Birth by caesarean was linked to a 15% higher risk of obesity in children compared with vaginal birth. The scientists involved believe that babies born by caesarean miss out on exposure to bacteria in the birth canal that colonise the baby’s gut and may ultimately change the body’s metabolic rate - and even how hungry we feel. Audrey Gaskins, an epidemiologist at Harvard University and co-author of the new study, said: “Children born via C-section harbour less diverse gut bacteria and these patterns of less diversity have been linked to increased capacity for energy harvest by the gut microbiota. You can think of it as a slower metabolism.” Previous studies have found the same link, but were less able to rule out other factors, such as the mother’s weight or health. The latest research, which included 22,068 children born to 15,271 women, suggests that the link is not simply explained by overweight women or those with pregnancy complications such as high blood pressure being more likely to deliver by caesarean. The link remained after maternal weight was taken into account, and was more striking when siblings who had different types of births were compared. Within families, children born by caesarean were 64% more likely to be obese than their siblings born by vaginal delivery. “With siblings, they have the same mother and home environment so the genetics, the feeding environment, are all controlled for,” said Dr Gaskins. © 2016 Guardian News and Media Limited
By Alison F. Takemura | In mice, severely restricting caloric intake promotes the transformation of white fat into brown fat, which contains cells that burn energy faster, according to a study published today (August 25) in Cell Metabolism. The innate immune system, researchers from the University of Geneva, Switzerland, and their colleagues reported, mediates this fat cell-transforming effect. “The paper nicely characterizes this phenomenon,” said Ajay Chawla of the University of California, San Francisco, who was not involved in the work. “And it mechanistically seems to identify a pathway that we had identified.” Whereas the present study found diet induced a “beiging” phenotype—in which white adipose tissue starts to express more energy-expending brown fat cells—Chawla and colleagues had previously shown that cold temperatures, another extreme condition, can produce the same effect. Scientists are keenly interested in learning how to generate brown fat cells. A treatment could help stem the obesity epidemic. “Finding some mechanism to activate this response—ideally, in obese or diabetic individuals—is really attractive,” said postdoctoral researcher Salvatore Fabbiano of the University of Geneva who led the present study. Several conditions are already known to make white fat tissue more brown—cold temperatures, microbe loss, and gastric bypass surgery among them. Fabbiano and colleagues hypothesized that the common feature of all these experiences was an increased expenditure of calories compared to intake. © 1986-2016 The Scientist
Link ID: 22615 - Posted: 08.31.2016
Laura Sanders Scientists have identified the “refrigerator” nerve cells that hum along in the brains of mice and keep the body cool. These cells kick on to drastically cool mice’s bodies and may prevent high fevers, scientists report online August 25 in Science. The results “are totally new and very important,” says physiologist Andrej Romanovsky of the Barrow Neurological Institute in Phoenix. "The implications are far-reaching." By illuminating how bodies stay at the right temperature, the discovery may offer insights into the relationship between body temperature and metabolism. Scientists had good reasons to think that nerve cells controlling body temperature are tucked into the hypothalamus, a small patch of neural tissue in the middle of the brain. Temperature fluctuations in a part of the hypothalamus called the preoptic area prompt the body to get back to baseline by conserving or throwing off heat. But the actual identify of the heat sensors remained mysterious. The new study reveals the cells to be those that possess a protein called TRPM2. “Overall, this is a major discovery in the field of thermoregulation,” says Shaun Morrison of Oregon Health & Science University in Portland. Jan Siemens, a neurobiologist at the University of Heidelberg in Germany, and colleagues tested an array of molecules called TRP channels, proteins that sit on cell membranes and help sense a variety of stimuli, including painful tear gas and cool menthol. In tests of nerve cells in lab dishes, one candidate, the protein TRPM2, seemed to respond to heat. |© Society for Science & the Public 2000 - 201
Keyword: Pain & Touch
Link ID: 22605 - Posted: 08.27.2016
Laura Sanders Fractions of a second after food hits the mouth, a specialized group of energizing nerve cells in mice shuts down. After the eating stops, the nerve cells spring back into action, scientists report August 18 in Current Biology. This quick response to eating offers researchers new clues about how the brain drives appetite and may also provide insight into narcolepsy. These nerve cells have intrigued scientists for years. They produce a molecule called orexin (also known as hypocretin), thought to have a role in appetite. But their bigger claim to fame came when scientists found that these cells were largely missing from the brains of people with narcolepsy. People with narcolepsy are more likely to be overweight than other people, and this new study may help explain why, says neuroscientist Jerome Siegel of UCLA. These cells may have more subtle roles in regulating food intake in people without narcolepsy, he adds. Results from earlier studies hinted that orexin-producing nerve cells are appetite stimulators. But the new results suggest the opposite. These cells actually work to keep extra weight off. “Orexin cells are a natural obesity defense mechanism,” says study coauthor Denis Burdakov of the Francis Crick Institute in London. “If they are lost, animals and humans gain weight.” Mice were allowed to eat normally while researchers eavesdropped on the behavior of their orexin nerve cells. Within milliseconds of eating, orexin nerve cells shut down and stopped sending signals. |© Society for Science & the Public 2000 - 2016
Link ID: 22583 - Posted: 08.22.2016
By KATHERINE KINZLER You may not be surprised to learn that food preference is a social matter. What we choose to eat depends on more than just what tastes good or is healthful. People in different cultures eat different things, and within a culture, what you eat can signal something about who you are. More surprising is that the sociality of food selection, it turns out, runs deep in human nature. In research published this month in the Proceedings of the National Academy of Sciences, my colleagues and I showed that even 1-year-old babies understand that people’s food preferences depend on their social or cultural group. Interestingly, we found that babies’ thinking about food preferences isn’t really about food per se. It’s more about the people eating foods, and the relationship between food choice and social groups. While it’s hard to know what babies think before they can talk, developmental psychologists have long capitalized on the fact that babies’ visual gaze is guided by their interest. Babies tend to look longer at something that is novel or surprising. Do something bizarre the next time you meet a baby, and you’ll notice her looking intently. Using this method, the psychologists Zoe Liberman, Amanda Woodward, Kathleen Sullivan and I conducted a series of studies. Led by Professor Liberman, we brought more than 200 1-year-olds (and their parents) into a developmental psychology lab, and showed them videos of people visibly expressing like or dislike of foods. For instance, one group of babies saw a video of a person who ate a food and expressed that she loved it. Next they saw a video of a second person who tried the same food and also loved it. This second event was not terribly surprising to the babies: The two people agreed, after all. Accordingly, the babies did not look for very long at this second video; it was what they expected. © 2016 The New York Times Company
By Diana Kwon When glial cells were discovered in the 1800s, they were thought to be passive, supporting structures—the “glue”—as their Greek name implies—that holds neurons together in the brain and throughout the nervous system. In recent years, however, neuroscientists have discovered that far from being passive, these small cells play an astonishing variety of roles in both the development and functioning of the brain. Some of the latest discoveries suggest that glia play complex roles in regulating appetite and metabolism, making them a possible target for treating obesity. Signs that glia might play such roles were first identified in the 1980s. Neuroscientist Pierre Magistretti and his colleagues found evidence that neurotransmitters could promote the release of glucose reserves stored in astrocytes, a star-shaped type of glial cell. Other studies revealed that obesity leads to increased activation of glial cells in the hypothalamus—the key area of the brain for controlling metabolic processes. This was despite the fact that, for a long time, “neurons were considered the only players in the control of energy metabolism,” says Cristina García-Cáceres, a neurobiologist at the Helmholtz Diabetes Center in Germany. Two recent studies add new evidence that glia play a key role in metabolism. In one study, published last week in Cell, García-Cáceres, together with Matthias Tschöp, the director of the Helmholtz Diabetes Center and colleagues, reported that insulin acts on astrocytes to regulate sugar intake in the brain. © 2016 Scientific American,
By Roxanne Khamsi, What if controlling the appetite were as easy as flipping a switch? It sounds like the stuff of science fiction, but Jeffrey Friedman of Rockefeller University and his colleagues did exactly this in genetically engineered mice to try to shed light on how the brain influences appetite. Friedman and his colleagues used magnetic stimulation to switch on neurons in a region of the brain called the ventromedial hypothalamus and found that doing so increased the rodents' blood sugar levels and decreased levels of the hormone insulin. Turning on the neurons also caused the mice to eat more than their control counterparts. The ultimate confirmation came when they inhibited these neurons and saw the opposite effects: it drove blood sugar down, elevated insulin levels and suppressed the animals' urge to consume their chow. That the brain influences hunger is not an unexpected finding, but scientists have recently narrowed in on how it has sway on what ends up in the gut—and how the gut talks to the mind. This two-way communication, defined as the 'gut–brain axis', happens not only through nerve connections between the organs, but also through biochemical signals, such as hormones, that circulate in the body. “The idea that there is bidirectional communication between the gastrointestinal tract and brain that affects metabolism traces back more than a century,” Friedman says, referring to the work of the nineteenth-century French scientist Claude Bernard, who made seminal discoveries into how the body maintains physiological equilibrium. “Our new findings that insulin-producing cells in the pancreas can be controlled by certain neurons in the brain that sense blood sugar provides further experimental evidence supporting this notion.” © 2016 Scientific American,
Link ID: 22522 - Posted: 08.06.2016
By Jonathan Webb Science reporter, BBC News Scientists have glimpsed activity deep in the mouse brain which can explain why we get thirsty when we eat, and why cold water is more thirst-quenching. A specific "thirst circuit" was rapidly activated by food and quietened by cooling down the animals' mouths. The same brain cells were already known to stimulate drinking, for example when dehydration concentrates the blood. But the new findings describe a much faster response, which predicts the body's future demand for water. The researchers went looking for this type of system because they were puzzled by the fact that drinking behaviour, in humans as well as animals, seems to be regulated very quickly. "There's this textbook model for homeostatic regulation of thirst, that's been around for almost 100 years, that's based on the blood," said the study's senior author Zachary Knight, from the University of California, San Francisco. "There are these neurons in the brain that… generate thirst when the blood becomes too salty or the blood volume falls too low. But lots of aspects of everyday drinking can't possibly be explained by that homeostatic model because they occur much too quickly." Take the "prandial thirst" that comes while we consume a big, salty meal - or the fact that we feel quenched almost as soon as we take a drink. © 2016 BBC.
Link ID: 22518 - Posted: 08.04.2016
The brains of overweight middle-aged people resemble brains that are a decade older in healthier people. A study of 473 adults has found that people who are overweight have less white matter, which connects different brain areas and enables signaling between them. The volume of white matter in the brains of overweight people at 50 were similar to that seen in the brains of lean people at 60. Human brains naturally shrink with age, but previous research has shown that this seems to happen more quickly in obese people. “As our brains age, they naturally shrink in size, but it isn’t clear why people who are overweight have a greater reduction in the amount of white matter,” says Lisa Ronan, at the University of Cambridge, a member of the research team. “We can only speculate on whether obesity might in some way cause these changes or whether obesity is a consequence of brain changes.” Intriguingly, the difference between lean and overweight people’s brains was only apparent from middle age onwards. It’s possible that this is because we are particularly vulnerable in some way at this time, says team-member Paul Fletcher, also at the University of Cambridge. However, despite this reduction in white matter, cognitive tests did not find any evidence that being overweight was linked to reduced brain function. “We don’t yet know the implications of these changes in brain structure,” says Sadaf Farooqi, at the University of Cambridge, who was also involved in the research. © Copyright Reed Business Information Ltd.
Link ID: 22512 - Posted: 08.04.2016
By James Gallagher Controlling human nerve cells with electricity could treat a range of diseases including arthritis, asthma and diabetes, a new company says. Galvani Bioelectronics hopes to bring a new treatment based on the technique before regulators within seven years. GlaxoSmithKline and Verily, formerly Google, Life Sciences, are behind it. Animal experiments have attached tiny silicone cuffs, containing electrodes, around a nerve and then used a power supply to control the nerve's messages. One set of tests suggested the approach could help treat type-2 diabetes, in which the body ignores the hormone insulin. They focused on a cluster of chemical sensors near the main artery in the neck that check levels of sugar and the hormone insulin. The sensors send their findings back to the brain, via a nerve, so the organ can coordinate the body's response to sugar in the bloodstream. GSK vice-president of bioelectronics Kris Famm told the BBC News website: "The neural signatures in the nerve increase in type 2-diabetes. "By blocking those neural signals in diabetic rats, you see the sensitivity of the body to insulin is restored." And early work suggested it could work in other diseases too. "It isn't just a one-trick-pony, it is something that if we get it right could have a new class of therapies on our hands," Mr Famm said. But he said the field was only "scratching the surface" when it came to understanding which nerve signals have what effect in the body. Both the volume and rhythm of the nerve signals could be having an effect rather than it being a simple case of turning the nerve on or off. © 2016 BBC
Link ID: 22507 - Posted: 08.03.2016
By Alice Klein Blame grandpa. A study in mice shows that the grandsons of obese males are more susceptible to the detrimental health effects of junk food, even if their fathers are lean and healthy. The finding adds to evidence that new traits can be passed down the family line without being permanently recorded in a family’s genes – a phenomenon called transgenerational epigenetics. Last year, a study found that the DNA in the sperm of obese men is modified in thousands of places, and that these sperm also contain short pieces of RNA. These are epigenetic modifications – they don’t affect the precise code of genes, but instead may affect how active particular genes are. Now Catherine Suter at Victor Chang Cardiac Research Institute in Sydney and her team have investigated the longer-term effects of paternal obesity. To do this, they mated obese male mice with lean female mice. They found that, compared with the offspring of lean males, both the sons and grandsons of the obese males were more likely to show the early signs of fatty liver disease and diabetes when given a junk food diet. The same effect wasn’t seen in daughters or granddaughters. Even when the sons of the obese males were fed a healthy diet and kept at a normal weight, their sons still had a greater tendency to develop obesity-related conditions when exposed to a junk diet. © Copyright Reed Business Information Ltd.
Tina Hesman Saey ORLANDO, Fla. — Weight gain may depend on how an individual’s genes react to certain diets, a new study in mice suggests. Four strains of mice fared differently on four different diets, William Barrington of North Carolina State University in Raleigh reported July 15 at the Allied Genetics Conference. One strain, the A/J mouse, was nearly impervious to dietary changes. Those mice didn’t gain much weight or have changes in insulin or cholesterol no matter what they ate: a fat-and-carbohydrate-laden Western diet, traditional Mediterranean or Japanese diet (usually considered healthy) or very low-carbohydrate, fat-rich fare known as the ketogenic diet. In contrast, NOD/ShiLtJ mice gained weight on all but the Japanese diet. Those mice’s blood sugar shot up — a hallmark of diabetes — on a Mediterranean diet, but decreased on the Japanese diet. FVB/NJ mice didn’t get fat on the Western diet, but became obese and developed high cholesterol and other health problems on the ketogenic diet. The opposite was true for C57BL/6J mice. They became obese and developed cholesterol and other problems linked to heart disease and diabetes in people on the Western diet, but not on the ketogenic diet. They also fattened up on the Mediterranean diet. © Society for Science & the Public 2000 - 2016.
Link ID: 22454 - Posted: 07.19.2016
Rachel Ehrenberg When mice have a stroke, their gut reaction can amp up brain damage. A series of new experiments reveals a surprising back-and-forth between the brain and the gut in the aftermath of a stroke. In mice, this dickering includes changes to the gut microbial population that ultimately lead to even more inflammation in the brain. There is much work to be done to determine whether the results apply to humans. But the research, published in the July 13 Journal of Neuroscience, hints that poop pills laden with healthy microbes could one day be part of post-stroke therapy. The work also highlights a connection between gut microbes and brain function that scientists are only just beginning to understand,says Ted Dinan of the Microbiome Institute at the University College Cork, Ireland. There’s growing evidence that gut microbes can influence how people experience stress or depression, for example (SN: 4/2/16, p. 23). “It’s a fascinating study” says Dinan, who was not involved with the work. “It raises almost as many questions as it answers, which is what good studies do.” Following a stroke, the mouse gut becomes temporarily paralyzed, leading to a shift in the microbial community, neurologist Arthur Liesz of the Institute for Stroke and Dementia Research in Munich and colleagues found. This altered, less diverse microbial ecosystem appears to interact with immune system cells called T cells that reside in the gut. These T cells can either dampen inflammation or dial it up, leading to more damage, says Liesz. Whether the T cells further damage the brain after a stroke rather than soothe it seems to be determined by the immune system cells’ interaction with the gut microbes. © Society for Science & the Public 2000 - 2016.
Link ID: 22431 - Posted: 07.13.2016
By Jane E. Brody To stem the current epidemic of obesity, there’s no arguing with the adage that an ounce of prevention is worth a pound of cure. As every overweight adult knows too well, shedding excess pounds and keeping them off is far harder than putting them on in the first place. But assuring a leaner, healthier younger generation may often require starting even before a baby is born. The overwhelming majority of babies are lean at birth, but by the time they reach kindergarten, many have acquired excess body fat that sets the stage for a lifelong weight problem. Recent studies indicate that the reason so many American children become overweight is far more complicated than consuming more calories than they burn, although this is certainly an important factor. Rather, preventing children from acquiring excess body fat may have to start even before their mothers become pregnant. Researchers are tracing the origins of being overweight and obese as far back as the pre-pregnancy weight of a child’s mother and father, and their explanations go beyond simple genetic inheritance. Twenty-three genes are known to increase the risk of becoming obese. These genes can act very early in development to accelerate weight gain in infancy and during middle childhood. In the usual weight trajectory, children are born lean, get chubby during infancy, then become lean again as toddlers when they grow taller and become more active. Then, at or before age 10 or so, body fat increases in preparation for puberty – a phenomenon called adiposity rebound. In children with obesity genes, “adiposity rebound occurs earlier and higher,” said Dr. Daniel W. Belsky, an epidemiologist at Duke University School of Medicine. “They stop getting leaner sooner and start putting on fat earlier and put on more of it.” © 2016 The New York Times Company
By VANESSA FRIEDMAN IT’S been another big month for talking about women’s bodies. Just as the White House hosted the first United States of Women summit meeting, which culminated in Oprah Winfrey’s noting, in conversation with Michelle Obama, “We live in a world where you are constantly being bombarded by images,” across the ocean the new mayor of London was announcing a policy that would ban ads on public transport that might cause women to feel pressured “into unrealistic expectations surrounding their bodies.” Mayor Sadiq Khan’s policy sounds, on the surface, like a big step forward. Down with fat-shaming! But it is, rather, an old idea, and one that reinforces stereotypes instead of grappling with the real issue: How do we change the paradigm altogether? The immediate impetus for the ban, which will be carried out by the London transit authority via a steering committee that will rule on ads case by case, was a 2015 diet pill ad depicting a very tan, very curvy woman (the kind who is a staple of lad mags) in a bright yellow bikini alongside the words, “Are you beach body ready?” The implication was that if you had not achieved the unrealistic proportions of a Barbie, you were not. The public protested (a petition on change.org received more than 70,000 signatures), and Mr. Khan made it part of his election campaign. The regulation follows decisions by the Advertising Standards Authority of Britain to ban certain ads, such as a Gucci shot that depicted what was deemed an “unhealthily thin” young woman. Though often conflated with the movement to protect models, which resulted in legislation in France in 2015 requiring models to produce a doctor’s note attesting to their health, and digital alteration of photographs to be disclosed, banning is a separate issue. It doesn’t involve working conditions (which can and should be legislated), but subjective, and ultimately regressive, assumptions about what constitutes a positive female image. While I have no doubt that Mr. Khan had the best intentions (he made a reference to his desire to protect his daughters), and there is no question that studies have shown that depictions of thin women in idealized or overly airbrushed photographs can be an important factor in eating disorders and other types of body dysmorphia, I do not believe banning is the answer. And I say that as someone with two daughters (and a son) who is acutely aware of the distortions of the fashion world and their dangers. © 2016 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 22363 - Posted: 06.27.2016
By Ruth Williams The offspring of certain mice fed a high-fat diet have altered gut microbiomes and may be prone to autism-like behaviors including social deficits, according to a study published today (June 16) in Cell. But treating these offspring with a specific microbial species they lack can rectify the animals’ social behavior. “There’s growing evidence that the microbiome, particularly early in life, can have long-term effects on brain development and behavior,” said anatomist and neuroscientist John Cryan of University College Cork in Ireland who was not involved in the study. “What this paper does is take advantage of the fact that we get our microbiome from our mums, and looks at what happens if the mum disturbs her microbiome during pregnancy.” According to the US Centers for Disease Control and Prevention, one in 68 U.S. children have autism spectrum disorder (ASD). Recent evidence suggests that the risk of ASD is increased for the offspring of mothers with obesity. In both humans and non-human primates, the offspring of obese mothers have also been shown to have abnormal microbiomes. And some people with ASD have imbalanced gut microbes, or dysbiosis. Baylor College of Medicine’s Mauro Costa-Mattioli and colleagues sought to better understand how maternal obesity, the microbiome, and ASD are interconnected. The team turned to mice for answers. The researchers gave female animals high-fat diets before setting up matings, later finding that a “large proportion” of the offspring exhibited ASD-like behaviors, including reduced social interaction, repetitive behaviors, and anxiety. The team analyzed the microbiomes of these offspring, finding that they differed from those of control animals. © 1986-2016 The Scientist
Link ID: 22336 - Posted: 06.18.2016
By Clare Wilson Pass the sick bag. A device that allows people to empty a portion of their stomach contents into a toilet after a meal has just got the go-ahead from the US Food and Drug Administration. The device is approved for use by people who are severely obese, defined as having a body mass index of over 35 kg/m2. The stomach-churning device, which is already available in some European countries, involves a tube being placed into the stomach in a short surgical procedure. The end of the tube contains a valve that lies flush against the skin. Normally it is kept closed, but after meals, the person can connect the valve to another tube to drain about a third of their partially digested food into the toilet. It cannot remove more food than this, because the end of the internal tube is positioned higher than most of the stomach’s contents. Manufacturer Aspire Bariatrics, based in Pennsylvania, says users need to chew their food well and eat more slowly to stop the 6 millimetre tube from getting blocked, and that this in itself helps reduce overeating. “You get some solid chunks,” says Kathy Crothall, head of Aspire Bariatrics. “If a patient doesn’t chew their food very carefully they won’t get anything out of this device.” The device, called AspireAssist, has a safety feature within the valve that means it can only be used three times a day for up to six weeks. After this time it stops working and part of the device must be replaced. © Copyright Reed Business Information Ltd.
Link ID: 22327 - Posted: 06.16.2016
Tina Hesman Saey Gut microbes cause obesity by sending messages via the vagus nerve to pack on pounds, new research in rodents suggests. Bacteria in the intestines produce a molecule called acetate, which works through the brain and nervous system to make rats and mice fat, researchers report in the June 9 Nature. If the results hold up in humans, scientists would understand one mechanism by which gut microbes induce obesity: First, the microbes convert fats in food to a short-chain fatty acid called acetate. Acetate in the blood somehow makes its way to the brain. The brain sends a signal through the vagus nerve to the pancreas to increase insulin production. Insulin tells fat cells to store more energy. Fat builds up, leading to obesity. Acetate also increases levels of a hunger hormone called ghrelin, which could lead animals and people to eat even more, says Yale University endocrinologist Gerald Shulman, who led the study. “This is a tour-de-force paper,” says biochemist Jonathan Schertzer of McMaster University in Hamilton, Canada. Most studies that examine the health effects of intestinal microbes just list which bacteria, viruses, fungi and other microorganisms make up the gut microbiome, Schertzer says. But a catalog of differences between lean and obese individuals doesn’t address what those microbes do, he says. “What’s in name?” he asks. “When you find a factor that actually influences metabolism, that’s important.” © Society for Science & the Public 2000 - 2016.
Link ID: 22305 - Posted: 06.09.2016
Jean Fain When Sandra Aamodt talks about dieting, people listen ... or, they stick their fingers in their ears and go la, la, la. Aamodt's neuroscientific take on why diets backfire is that divisive. Aamodt is a neuroscientist, book author and former editor of a leading brain research journal. She also has become a prominent evangelist of the message that traditional diets just don't work and often leave the dieter worse off than before. And she's an enthusiastic proponent of mindful eating. "I define it as eating with attention and joy, without judgment," Aamodt said in an interview. "That includes attention to hunger and fullness, to the experience of eating and to its effects on our bodies." Even if you've never heard of her, you likely will soon. Her new book, Why Diets Make Us Fat, is bound to change the weight-loss conversation, if not dismantle Biggest Loser-sized dreams. I am a therapist specializing in eating issues, and among my clients, Aamodt has already shifted the focus from weight loss to self-care. Most clients are reluctant to accept her central argument: That our body weight tends to settle at "set points" — that 10- to 15-pound range the brain maintains despite repeated efforts to lower it. However, once they see how the set-point theory reflects their dieting experience, they realize that although they don't have the final say on their weight (their brain does), they do have real influence — through exercise and other health-affirming activities — over their health and well-being. © 2016 npr
Link ID: 22298 - Posted: 06.08.2016