Links for Keyword: Obesity

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 916

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22582 - Posted: 08.22.2016

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,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22578 - Posted: 08.20.2016

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,

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22522 - Posted: 08.06.2016

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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22512 - Posted: 08.04.2016

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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 22455 - Posted: 07.19.2016

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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22454 - Posted: 07.19.2016

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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 22421 - Posted: 07.11.2016

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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 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

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22298 - Posted: 06.08.2016

By Anahad O'Connor The federal government’s decision to update food labels last month marked a sea change for consumers: For the first time, beginning in 2018, nutrition labels will be required to list a breakdown of both the total sugars and the added sugars in packaged foods. But is sugar really that bad for you? And is the sugar added to foods really more harmful than the sugars found naturally in foods? We spoke with some top scientists who study sugar and its effects on metabolic health to help answer some common questions about sugar. Here’s what they had to say. Why are food labels being revised? The shift came after years of urging by many nutrition experts, who say that excess sugar is a primary cause of obesity and heart disease, the leading killer of Americans. Many in the food industry opposed the emphasis on added sugars, arguing that the focus should be on calories rather than sugar. They say that highlighting added sugar on labels is unscientific, and that the sugar that occurs naturally in foods like fruits and vegetables is essentially no different than the sugar commonly added to packaged foods. But scientists say it is not that simple. So, is added sugar different from the naturally occurring sugar in food? It depends. Most sugars are essentially combinations of two molecules, glucose and fructose, in different ratios. The sugar in a fresh apple, for instance, is generally the same as the table sugar that might be added to homemade apple pie. Both are known technically as sucrose, and they are broken down in the intestine into glucose and fructose. Glucose can be metabolized by any cell in the body. But fructose is handled almost exclusively by the liver. “Once you get to that point, the liver doesn’t know whether it came from fruit or not,” said Kimber Stanhope, a researcher at the University of California, Davis, who studies the effects of sugar on health. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 9: Hearing, Vestibular Perception, Taste, and Smell
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 6: Hearing, Balance, Taste, and Smell
Link ID: 22297 - Posted: 06.08.2016

What do large tables, large breakfasts, and large servers have in common? They all affect how much you eat. This week on Hidden Brain, we look at the hidden forces that drive our diets. First we hear from Adam Brumberg at Cornell University's Food and Brand Lab about how to make healthier choices more easily (hint: good habits and pack your lunch!). Then, Senior (Svelte) Stopwatch Correspondent Daniel Pink returns for another round of Stopwatch Science to tell you about those tables, breakfasts, and servers. If you don't like spoilers, stop reading and go listen to the episode! Here are the studies: You may have heard that smaller portions can help you eat fewer calories. That's true. But what about larger tables? Researchers Brennan Davis, Collin Payne, and My Bui hypothesized that one of the ways smaller food units lead us to eat less is by playing with our perception. They tested this with pizza and found that while study participants tended to eat more small slices, they consumed fewer calories overall because it seemed like they were eating more. The researchers tried to distort people's perception even further by making the smaller slices seem bigger by putting them on a bigger table. What they found is that even hungry college students at fewer calories of (free) pizza when it was chopped into tiny slices and put on a big table. What about who's around that big table? That seems to matter, too. Researchers found both men and women order more food when they eat with women but choose smaller portions when they eat in the company of men. They say breakfast is the most important meal of the day. Well, it may also be the most slimming. When researchers assigned two groups of overweight women to eat a limited number of calories each day, they found those who ate more at breakfast and less at dinner shed about twice as many pounds as the other group. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22266 - Posted: 05.31.2016

Dean Burnett A recent report by the National Obesity Forum stated that official advice about low-fat diets is wrong. As ever, there’s now heated debate over how valid/accurate this claim is. But let’s step back a moment and ask a revealing question: why do official government dietary guidelines even exist? Why are they necessary? From an entirely logical position, eating food fulfils several requirements. It provides the energy to do things, helps us build up stores of energy for when needed, and provides the materials required to build and maintain our bodies. Therefore, the human body requires a regular intake of nutrients, vitamins and calories to maintain day-to-day functioning. As a result, the human body has developed an intricate digestive system to monitor and regulate our food intake. The digestive system is quite cool. It has a sophisticated nervous system that can operate pretty much independently, so is often regarded as separate from the main one, leading some to describe it as a “second brain”, there to encourage, monitor and process the consumption and digestion of food. It also utilises hormones, namely leptin and ghrelin, which decrease and increase appetite respectively depending on how much food the body has/needs. It’s a painstakingly complex and precise system that’s evolved over aeons to make sure we eat what and when we need to, and get the most out of our food. However, at some point the human brain got involved, then everything went to hell. This is why we can now be presented with foodstuffs we’re repeatedly told are unhealthy, even dangerous, and say “Thanks. Extra chilli sauce on mine, please”.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Attention and Consciousness
Link ID: 22247 - Posted: 05.25.2016

Aaron E. Carroll I don’t eat breakfast. It’s not that I dislike what’s offered. Given the choice of breakfast food or lunch food, I’d almost always choose eggs or waffles. It’s just that I’m not hungry at 7:30 a.m., when I leave for work. In fact, I’m rarely hungry until about lunchtime. So, other than a morning cup of coffee, I don’t eat much before noon. This habit has forced me to be subjected to more lectures on how I’m hurting myself, my diet, my work and my health than almost any other. Only a fool would skip the most important meal of the day, right? As with many other nutritional pieces of advice, our belief in the power of breakfast is based on misinterpreted research and biased studies. It does not take much of an effort to find research that shows an association between skipping breakfast and poor health. A 2013 study published in the journal Circulation found that men who skipped breakfast had a significantly higher risk of coronary heart disease than men who ate breakfast. But, like almost all studies of breakfast, this is an association, not causation. More than most other domains, this topic is one that suffers from publication bias. In a paper published in The American Journal of Clinical Nutrition in 2013, researchers reviewed the literature on the effect of breakfast on obesity to look specifically at this issue. They first noted that nutrition researchers love to publish results showing a correlation between skipping breakfast and obesity. They love to do so again and again. At some point, there’s no reason to keep publishing on this. However, they also found major flaws in the reporting of findings. People were consistently biased in interpreting their results in favor of a relationship between skipping breakfast and obesity. They improperly used causal language to describe their results. They misleadingly cited others’ results. And they also improperly used causal language in citing others’ results. People believe, and want you to believe, that skipping breakfast is bad. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22238 - Posted: 05.23.2016

Laura Sanders In mice, a long course of antibiotics that wiped out gut bacteria slowed the birth of new brain cells and impaired memory, scientists write May 19 in Cell Reports. The results reinforce evidence for a powerful connection between bacteria in the gut and the brain (SN: 4/2/16, p. 23). After seven weeks of drinking water spiked with a cocktail of antibiotics, mice had fewer newborn nerve cells in a part of the hippocampus, a brain structure important for memory. The mice’s ability to remember previously seen objects also suffered. Further experiments revealed one way bacteria can influence brain cell growth and memory. Injections of immune cells called Ly6Chi monocytes boosted the number of new nerve cells. Themonocytes appear to carry messages from gut to brain, Susanne Wolf of the Max Delbrück Center for Molecular Medicine in Berlin and colleagues found. Exercise and probiotic treatment with eight types of live bacteria also increased the number of newborn nerve cells and improved memory in mice treated with antibiotics. The results help clarify the toll of prolonged antibiotic treatment, and hint at ways to fight back, the authors write. L. Möhle et al. Ly6Chi monocytes provide a link between antibiotic-induced changes in gut microbiota and adult hippocampal neurogenesis. Cell Reports. Vol. 15, May 31, 2016. doi: 10.1016/j.celrep.2016.04.074. © Society for Science & the Public 2000 - 2016

Related chapters from BP7e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 13: Memory, Learning, and Development
Link ID: 22231 - Posted: 05.21.2016

Nancy Shute A body mass index under 25 is deemed normal and healthy, and a higher BMI that's "overweight" or "obese" is not. But that might be changing, at least when it comes to risk of death. The body mass index, or BMI, associated with the lowest risk of death has increased since the 1970s, a study finds, from 23.7, in the "normal" weight category, to 27, which is deemed "overweight." That means a person who is 5-foot-8 could weigh 180 pounds and be in that epidemiological sweet spot, according to the NIH's online BMI calculator. The results were published Tuesday in JAMA, the journal of the American Medical Association. The researchers came to that conclusion by looking at data from three studies of people in Copenhagen, one from the 1970s, one from the 1990s and one from 2003-2013. More than 100,000 people were involved. Because Denmark has an excellent national health registry, they were able to pinpoint the cause of death for every single one of those people. The risk of death for people who are obese, with a BMI of 30 or greater, also declined, to the point that it was on a par with some people of so-called "normal" weight. So being fatter, at least a bit, may be healthier. "I was surprised as a scientist to see how clear the result was," Borge Nordestgaard, a clinical professor and chief physician at Copenhagen University Hospital and senior author of the study, told Shots. So he and his colleagues sliced and diced the data to see what could account for the shift. They looked at age, sex, smoking, cancer and heart disease. The most relevant was the decline in smoking since the 1970s. But when they looked at the mortality rates in nonsmokers who had never had cancer or heart disease, it also became associated with a higher BMI over time. © 2016 npr

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22200 - Posted: 05.11.2016

by Julia Belluz and Javier Zarracina "I'm going to make you work hard," a blonde and perfectly muscled fitness instructor screamed at me in a recent spinning class, "so you can have that second drink at happy hour!" At the end of the 45-minute workout, my body was dripping with sweat. I felt like I had worked really, really hard. And according to my bike, I had burned more than 700 calories. Surely I had earned an extra margarita. The spinning instructor was echoing a message we've been getting for years: As long as you get on that bike or treadmill, you can keep indulging — and still lose weight. It's been reinforced by fitness gurus, celebrities, food and beverage companies like PepsiCo and Coca-Cola, and even public-health officials, doctors, and the first lady of the United States. Countless gym memberships, fitness tracking devices, sports drinks, and workout videos have been sold on this promise. There's just one problem: This message is not only wrong, it's leading us astray in our fight against obesity. To find out why, I read through more than 60 studies on exercise and weight loss. I also spoke to nine leading exercise, nutrition, and obesity researchers. Here's what I learned. 1) An evolutionary clue to how our bodies burn calories When anthropologist Herman Pontzer set off from Hunter College in New York to Tanzania to study one of the few remaining hunter-gatherer tribes on the planet, he expected to find a group of calorie burning machines. Unlike Westerners, who increasingly spend their waking hours glued to chairs, the Hadza are on the move most of the time. Men typically go off and hunt — chasing and killing animals, climbing trees in search of wild honey. Women forage for plants, dig up tubers, and comb bushes for berries. "They're on the high end of physical activity for any population that's been looked at ever," Pontzer said. © 2016 Vox Media, Inc

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22196 - Posted: 05.09.2016

Why You Can’t Lose Weight on a Diet By SANDRA AAMODT SIX years after dropping an average of 129 pounds on the TV program “The Biggest Loser,” a new study reports, the participants were burning about 500 fewer calories a day than other people their age and size. This helps explain why they had regained 70 percent of their lost weight since the show’s finale. The diet industry reacted defensively, arguing that the participants had lost weight too fast or ate the wrong kinds of food — that diets do work, if you pick the right one. But this study is just the latest example of research showing that in the long run dieting is rarely effective, doesn’t reliably improve health and does more harm than good. There is a better way to eat. The root of the problem is not willpower but neuroscience. Metabolic suppression is one of several powerful tools that the brain uses to keep the body within a certain weight range, called the set point. The range, which varies from person to person, is determined by genes and life experience. When dieters’ weight drops below it, they not only burn fewer calories but also produce more hunger-inducing hormones and find eating more rewarding. The brain’s weight-regulation system considers your set point to be the correct weight for you, whether or not your doctor agrees. If someone starts at 120 pounds and drops to 80, her brain rightfully declares a starvation state of emergency, using every method available to get that weight back up to normal. The same thing happens to someone who starts at 300 pounds and diets down to 200, as the “Biggest Loser” participants discovered. This coordinated brain response is a major reason that dieters find weight loss so hard to achieve and maintain. For example, men with severe obesity have only one chance in 1,290 of reaching the normal weight range within a year; severely obese women have one chance in 677. A vast majority of those who beat the odds are likely to end up gaining the weight back over the next five years. In private, even the diet industry agrees that weight loss is rarely sustained. A report for members of the industry stated: “In 2002, 231 million Europeans attempted some form of diet. Of these only 1 percent will achieve permanent weight loss.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 22188 - Posted: 05.07.2016

By Ann Gibbons We may not be raring to go on a Monday morning, but humans are the Energizer Bunnies of the primate world. That’s the conclusion of a new study that, for the first time, measures precisely how many calories humans and apes burn each day. Compared with chimpanzees and other apes, our revved-up internal engines burn calories 27% faster, according to a paper in Nature this week. This higher metabolic rate equips us to quickly fuel energy-hungry brain cells, sustaining our bigger brains. And lest we run out of gas when food is short, the study also found that humans are fatter than other primates, giving us energy stores to draw on in lean times. “The brilliant thing here is showing for the first time that we do have a higher metabolic rate, and we do use more energy,” says paleoanthropologist Leslie Aiello, president of the Wenner-Gren Foundation for Anthropological Research in New York City. “Humans during evolution have become more and more hypermetabolic,” says biological anthropologist Carel van Schaik of the University of Zurich in Switzerland. “We turned up the thermostat.” For decades, researchers assumed that “there weren’t any differences in the rate at which different species burned calories,” says biological anthropologist Herman Pontzer of Hunter College in New York City, lead author of the new study. Comparing humans and other primates, they saw little difference in basal metabolic rate, which reflects the total calories used by our organs while we are at rest. © 2016 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 13: Memory, Learning, and Development
Link ID: 22183 - Posted: 05.05.2016