Chapter 13. Homeostasis: Active Regulation of the Internal Environment
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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
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
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
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”.
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
Link ID: 22238 - Posted: 05.23.2016
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
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
Link ID: 22196 - Posted: 05.09.2016
By Jane E. Brody Truth to tell, sometimes I don’t follow my own advice, and when I suffer the consequences, I rediscover why I offer it. I’ve long recommended drinking plenty of water, perhaps a glass with every meal and another glass or two between meals. If not plain water, which is best, then coffee or tea without sugar (but not alcoholic or sugary drinks) will do. I dined out recently after an especially active day that included about five miles of walking, 40 minutes of lap swimming and a 90-minute museum visit. I drank only half a glass of water and no other beverage with my meal. It did seem odd that I had no need to use the facilities afterward, not even after a long trip home. But I didn’t focus on why until the next day when, after a fitful night, I awoke exhausted, did another long walk and swim, and cycled to an appointment four miles away. I arrived parched, begging for water. After downing about 12 ounces, I was a new person. I no longer felt like a lead balloon. It seems mild dehydration was my problem, and the experience prompted me to take a closer look at the body’s need for water under a variety of circumstances. Although millions of Americans carry water bottles wherever they go and beverage companies like Coke and Pepsi would have you believe that every life can be improved by the drinks they sell, the truth is serious dehydration is not common among ordinary healthy people. But there are exceptions, and they include people like me in the Medicare generation, athletes who participate in particularly challenging events like marathons, and infants and small children with serious diarrhea. Let’s start with some facts. Water is the single most important substance we consume. You can survive for about two months without food, but you would die in about seven days without water. Water makes up about 75 percent of an infant’s weight and 55 percent of an older person’s weight. © 2016 The New York Times Company
Link ID: 22192 - 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
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
By Gretchen Reynolds Young rats prone to obesity are much less likely to fulfill that unhappy destiny if they run during adolescence than if they do not, according to a provocative new animal study of exercise and weight. They also were metabolically healthier, and had different gut microbes, than rats that keep the weight off by cutting back on food, the study found. The experiment was done in rodents, not people, but it does raise interesting questions about just what role exercise may play in keeping obesity at bay. For some time, many scientists, dieting gurus and I have been pointing out that exercise by itself tends to be ineffective for weight loss. Study after study has found that if overweight people start working out but do not also reduce their caloric intake, they shed little if any poundage and may gain weight. The problem, most scientists agree, is that exercise increases appetite, especially in people who are overweight, and also can cause compensatory inactivity, meaning that people move less over all on days when they exercise. Consequently, they wind up burning fewer daily calories, while also eating more. You do the math. But those discouraging studies involved weight loss. There has been much less examination of whether exercise might help to prevent weight gain in the first place and, if it does, how it compares to calorie restriction for that purpose. So for the new study, which was published last week in Medicine & Science in Sports & Exercise, researchers at the University of Missouri in Columbia and other schools first gathered rats from a strain that has an inborn tendency to become obese, starting in adolescence. (Adolescence is also when many young people begin to add weight.) © 2016 The New York Times Company
Link ID: 22178 - Posted: 05.04.2016