Links for Keyword: Obesity

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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

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

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: 22178 - Posted: 05.04.2016

By Helen Briggs BBC News The Labrador retriever, known as one of the greediest breeds of dog, is hard-wired to overeat, research suggests. The dog is more likely to become obese than other breeds partly because of its genes, scientists at Cambridge University say. The gene affected is thought to be important in controlling how the brain recognises hunger and the feeling of being full after eating. The research could help in the understanding of human obesity. "About a quarter of pet Labradors carry this gene [difference]," lead researcher Dr Eleanor Raffan told the BBC. "Although obesity is the consequence of eating more than you need and more than you burn off in exercise, actually there's some real hard-wired biology behind our drive to eat," she added. Lifestyle factors Canine obesity mirrors the human obesity epidemic, with lifestyle factors such as lack of exercise and high-calorie food both implicated - as well as genetics. As many as two in three dogs (34-59%) in rich countries are now overweight. The Labrador has the highest levels of obesity and has been shown to be more obsessed with food than other breeds. Researchers screened more than 300 Labradors kept as pets or assistance dogs for known obesity genes in the study, published in the journal Cell Metabolism. The international team found that a change in a gene known as POMC was strongly linked with weight, obesity and appetite in Labradors and Flat-Coated retrievers. In both breeds, for each copy of the gene carried, the dog was on average 2kg heavier. Other breeds of dog - from the Shih Tzu to the Great Dane - were also screened, but the genetic difference was not found. However, the variation was more common in Labradors working as assistance dogs, which the researchers say might be because these dogs are easier to train by rewarding with food. © 2016 BBC.

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: 22177 - Posted: 05.04.2016

By GINA KOLATA Danny Cahill stood, slightly dazed, in a blizzard of confetti as the audience screamed and his family ran on stage. He had won Season 8 of NBC’s reality television show “The Biggest Loser,” shedding more weight than anyone ever had on the program — an astonishing 239 pounds in seven months. When he got on the scale for all to see that evening, Dec. 8, 2009, he weighed just 191 pounds, down from 430. Dressed in a T-shirt and knee-length shorts, he was lean, athletic and as handsome as a model. “I’ve got my life back,” he declared. “I mean, I feel like a million bucks.” Mr. Cahill left the show’s stage in Hollywood and flew directly to New York to start a triumphal tour of the talk shows, chatting with Jay Leno, Regis Philbin and Joy Behar. As he heard from fans all over the world, his elation knew no bounds. But in the years since, more than 100 pounds have crept back onto his 5-foot-11 frame despite his best efforts. In fact, most of that season’s 16 contestants have regained much if not all the weight they lost so arduously. Some are even heavier now. Yet their experiences, while a bitter personal disappointment, have been a gift to science. A study of Season 8’s contestants has yielded surprising new discoveries about the physiology of obesity that help explain why so many people struggle unsuccessfully to keep off the weight they lose. Kevin Hall, a scientist at a federal research center who admits to a weakness for reality TV, had the idea to follow the “Biggest Loser” contestants for six years after that victorious night. The project was the first to measure what happened to people over as long as six years after they had lost large amounts of weight with intensive dieting and exercise. © 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: 22168 - Posted: 05.02.2016

By Jordana Cepelewicz Everyone is familiar with the complaints of a hungry stomach. For years, scientists attributed the gnawing increase in appetite before a meal to ghrelin, a hormone which is secreted in the gut and circulates in the blood, playing a role in food intake and storage. Researchers have found that levels of ghrelin, dubbed the “hunger hormone,” peak before meals and recede after eating. Given its association with appetite, ghrelin is a tempting drug target for potential obesity treatments—but findings thus far have not lived up to expectations. Experiments that knock out the genes coding for ghrelin and its single receptor, GHSR (growth hormone secretagogue receptor), have been inconclusive: Remove the hormone or receptor, and rodents used in the experiments do not necessarily lose their drive to eat. Now a team of researchers at the French Institute of Health and Medical Research (INSERM) in Paris believe that scientists have had it wrong all along. In a study published this week in Science Signaling, they report that ghrelin does not enhance appetite in rats but rather increases weight gain and fat buildup. Unlike in earlier work, in the new study the researchers used a novel genetic method that kept the ghrelin receptor functional but modified it to have greater signaling in response to ghrelin—in other words, the receptor would enhance the hormone’s effects. The team then performed a series of experiments, first in isolated cells and then in rats. As expected, exposing ghrelin to modified receptors prompted a more potent response compared with the unaltered GHSR. © 2016 Scientific American

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 8: Hormones and Sex
Link ID: 22146 - Posted: 04.26.2016

By Nicholas Bakalar Eating a high-fat diet may lead to daytime sleepiness, a new study concludes. Australian researchers studied 1,800 men who had filled out food-frequency questionnaires and reported on how sleepy they felt during the day. They were also electronically monitored for obstructive sleep apnea, which causes people to wake up many times during the night. After adjusting for factors that could influence sleep — smoking, alcohol intake, waist circumference, physical activity, medications, depression and others — they found that compared with those in the lowest one-quarter for fat intake, those in the highest one-quarter were 78 percent more likely to suffer daytime sleepiness and almost three times as likely to have sleep apnea. The connection of fat intake to apnea was apparent most clearly in people with a high body mass index, but the positive association of fat intake with daytime sleepiness persisted strongly in all subjects, regardless of B.M.I. Thestudy is in the journal Nutrients. “The possible mechanism could be meal timing, but we didn’t have that information,” said the lead author, Yingting Cao, a doctoral candidate at the University of Adelaide. “But we have reason to believe that circadian rhythm, hormones and diet all work together to create these effects. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 10: Biological Rhythms and Sleep
Link ID: 22135 - Posted: 04.25.2016

Meghan Rosen Despite massive public health campaigns, the rise in worldwide obesity rates continues to hurtle along like a freight train on greased tracks. In 2014, more than 640 million men and women were obese (measured as a body mass index of 30 or higher). That’s up from 105 million in 1975, researchers estimate in the April 2 Lancet. The researchers analyzed four decades of height and weight data for more than 19 million adults, and then calculated global rates based on population data. On average, people worldwide are gaining about 1.5 kilograms per decade — roughly the weight of a half-gallon of ice cream. But the road isn’t entirely rocky. During the same time period, average life expectancy also jumped: from less than 59 years to more than 71 years, George Davey Smith points out in a comment accompanying the new study. Smith, an epidemiologist at the University of Bristol in England, boils the data down to a single, seemingly paradoxical sentence: “The world is at once fatter and healthier.” © 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: 22059 - Posted: 04.01.2016

Tracie McMillan When it comes to school breakfasts, two is better than none, says a new report released Thursday in the journal Pediatric Obesity. Researchers tracked nearly 600 middle-school students from fifth to seventh grade, looking to see if students ate no breakfast; ate breakfast at home or school; or ate both — and whether that affected obesity rates. The result: Weight gain among students who ate "double-breakfast" was no different than that seen among all other students. Meanwhile, the risk of obesity doubled among students who skipped breakfast or ate it inconsistently. "It seems it's a bigger problem to have kids skipping breakfast than to have these kids eating two breakfasts," says Marlene Schwartz of the Rudd Center for Food Policy and Obesity and one of the study's authors. "This study ... debunks an important misconception that school breakfast contributes to childhood obesity," says Duke Storen from Share Our Strength, a national group that runs anti-hunger and nutrition programs for children. While direct opposition to free school breakfast is unusual, says Storen, officials sometimes balk at implementing "alternative breakfast models" designed to encourage use of the program — such as offering breakfast in grab-and-go bags or in classrooms, rather than traditional sit-down meals in a cafeteria. That's a concern, say hunger advocates, because while eligibility rules for free and reduced-price breakfast are the same as for lunch, only about half as many children get subsidized breakfast as receive lunch, according to the Food Research and Action Center, an advocacy group. Indeed, the study was inspired in part by real-world concerns that school breakfast programs might promote obesity, says Schwartz. © 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: 22005 - Posted: 03.19.2016

Linda Geddes The health effects of a bad diet can carry over to offspring through eggs and sperm cells without DNA mutations, researchers have found. The mouse study, published in Nature Genetics1, provides some of the strongest evidence yet for the non-genetic inheritance of traits acquired during an organism’s lifetime. And although previous work has suggested that sperm cells can carry 'epigenetic' factors, this is the first time that such an effect has been observed with egg cells. Researchers have suspected for some time that parents' lifestyle and behaviour choices can affect their children's health through epigenetics. These are chemical modifications to DNA or the proteins in chromosomes that affect how genes are expressed, but that do not alter the gene sequences themselves. Whether those changes can be inherited is still controversial. In particular, there have been suggestions that parental eating habits might shape the offspring's risk of obesity and diabetes. However, it has been difficult to disentangle the possibility that the parents’ behaviour during pregnancy or during the offspring's early childhood was to blame, rather than epigenetic changes that had occurred before conception. To get around this issue, endocrinologist Peter Huypens at the German Research Center for Environmental Health in Neuherberg, Germany, and his colleagues gave genetically identical mice one of three diets — high fat, low fat or standard laboratory chow — for six weeks. As expected, those fed the high-fat diet became obese and had impaired tolerance to glucose, an early sign of type 2 diabetes. © 2016 Nature Publishing Group

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: 21991 - Posted: 03.15.2016

Susan Gaidos Most people would be happy to get rid of excess body fat. Even better: Trade the spare tire for something useful — say, better-functioning knees or hips, or a fix for an ailing heart or a broken bone. The idea is not far-fetched, some scientists say. Researchers worldwide are repurposing discarded fat to repair body parts damaged by injury, disease or age. Recent studies in lab animals and humans show that the much-maligned material can be a source of cells useful for treating a wide range of ills. At the University of Pittsburgh, bioengineer Rocky Tuan and colleagues extract buckets full of yellow fat from volunteers’ bellies and thighs and turn the liposuctioned material into tissue that resembles shock-absorbing cartilage. If the cartilage works as well in people as it has in animals, Tuan’s approach might someday offer a kind of self-repair for osteoarthritis, the painful degeneration of cartilage in the joints. He’s also using fat cells to grow replacement parts for the tendons and ligaments that support the joints. Foremost among fat’s virtues is its richness of stem cells, which have the ability to divide and grow into a wide variety of tissue types. Fat stem cells — also known as adipose-derived stem cells — can be coerced to grow into bone, cartilage, muscle tissue or, of course, more fat. Cells from fat are being tested to mend tissues found in damaged joints, hearts and muscle, and to regrow bone and heal wounds. © Society for Science & the Public 2000 - 2016

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: 21972 - Posted: 03.10.2016

By Anahad O'Connor Mark Mattson, a neuroscientist at the National Institute on Aging in Maryland, has not had breakfast in 35 years. Most days he practices a form of fasting — skipping lunch, taking a midafternoon run, and then eating all of his daily calories (about 2,000) in a six-hour window starting in the afternoon. “Once you get used to it, it’s not a big deal,” said Dr. Mattson, chief of the institute’s laboratory of neurosciences. “I’m not hungry at all in the morning, and this is other people’s experience as well. It’s just a matter of getting adapted to it.” In a culture in which it’s customary to eat three large meals a day while snacking from morning to midnight, the idea of regularly skipping meals may sound extreme. But in recent years intermittent fasting has been gaining popular attention and scientific endorsement. It has been promoted in best-selling books and endorsed by celebrities like the actors Hugh Jackman and Benedict Cumberbatch. The late-night talk show host Jimmy Kimmel claims that for the past two years he has followed an intermittent fasting program known as the 5:2 diet, which entails normal eating for five days and fasting for two — a practice Mr. Kimmel credits for his significant weight loss. Fasting to improve health dates back thousands of years, with Hippocrates and Plato among its earliest proponents. Dr. Mattson argues that humans are well suited for it: For much of human history, sporadic access to food was likely the norm, especially for hunter-gatherers. As a result, we’ve evolved with livers and muscles that store quickly accessible carbohydrates in the form of glycogen, and our fat tissue holds long-lasting energy reserves that can sustain the body for weeks when food is not available. “From an evolutionary perspective, it’s pretty clear that our ancestors did not eat three meals a day plus snacks,” Dr. Mattson said. © 2016 The New York Times Company

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: 21969 - Posted: 03.09.2016

By Roberto A. Ferdman In the mid 1970s, psychologist Merrill Elias began tracking the cognitive abilities of more than a thousand people in the state of New York. The goal was fairly specific: to observe the relationship between people's blood pressure and brain performance. And for decades he did just that, eventually expanding the Maine-Syracuse Longitudinal Study (MSLS) to observe other cardiovascular risk factors, including diabetes, obesity, and smoking. There was never an inkling that his research would lead to any sort of discovery about chocolate. And yet, 40 years later, it seems to have done just that. Late in the study, Elias and his team had an idea. Why not ask the participants what they were eating too? It wasn't unreasonable to wonder if what someone ate might add to the discussion. Diets, after all, had been shown to affect the risk factors Elias was already monitoring. Plus, they had this large pool of participants at their disposal, a perfect chance to learn a bit more about the decisions people were making about food. The researchers incorporated a new questionnaire into the sixth wave of their data collection, which spanned the five years between 2001 and 2006 (there have been seven waves in all, each conducted in five year intervals). The questionnaire gathered all sorts of information about the dietary habits of the participants. And the dietary habits of the participants revealed an interesting pattern. "We found that people who eat chocolate at least once a week tend to perform better cognitively," said Elias. "It's significant—it touches a number of cognitive domains." © 1996-2016 The Washington Post

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: 21962 - Posted: 03.07.2016

Heidi Ledford Obese mice — like obese humans — are at increased risk of colon cancer, and a study published today in Nature finally suggests why. Overweight mice fed a high-fat diet showed an increase in intestinal stem cells due to activation of a protein called PPAR-δ that regulates metabolism1. If the results hold true in humans, they could explain a phenomenon seen in epidemiological studies. “For quite some time there’s been an understanding that obesity leads to an increase in cancer in many tissues,” says Ömer Yilmaz, a cancer biologist at the Koch Institute for Integrative Cancer Research at the Massachusetts Institute of Technology (MIT) in Cambridge, and one of the leaders of the study. “We really wanted to understand the mechanism behind this.” Those molecular details could be important, says cell biologist P. Kay Lund who works at the University of North Carolina in Chapel Hill and the National Institutes of Health in Bethesda, Maryland. Tissue samples from people who have undergone colonoscopies could be tested to see if the same patterns hold true. Ultimately, the the increase in PPAR-δ activity could yield a useful indicator of cancer risk. “It could provide an opportunity to give those patients an earlier intervention,” says Lund, who was not involved in the obesity work. Yilmaz teamed up with David Sabatini, who studies metabolism at MIT and the Whitehead Institute, also in Cambridge, to learn more about the link between cancer and obesity. Their teams fed mice high-fat, high-calorie chow for about a year, and then tested the effects of the diet on the number and function of stem cells in their intestines. © 2016 Nature Publishing Group

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: 21952 - Posted: 03.03.2016

Mo Costandi Most of us are well aware of the health risks associated with obesity. Being overweight or obese is associated with an increased risk of numerous other conditions, from high blood pressure, heart disease and stroke, to diabetes, gout and some forms of cancer. Self-control saps memory resources Read more Research published over the past few years shows that obesity also has neurological consequences – it is associated with altered function in, and shrinkage of, certain parts of the brain, particularly the frontal lobes, which are the seat of intelligence, and the hippocampus, which is critical for memory formation. A new study now shows that this in turn is associated with impaired memory function. Lucy Cheke of the University of Cambridge and her colleagues recruited 50 volunteers aged between 18 and 35, with Body Mass Indexes (BMIs) ranging from 18 (underweight) to 51 (extremely obese), and asked them to perform a computerised memory test called the “Treasure Hunt Task”. This involved moving food items around around complex scenes, such as a desert with palm trees, hiding them in various locations, and indicating afterwards where they had hidden them. The participants were then shown various locations from the computerised scenes, and some of the food items, and asked if they had hidden something in each of the locations, or where they had hidden each of the items. Finally, they were shown pairs of the food items they had seen, and asked to indicate which of each pair they had hidden first. © 2016 Guardian News and Media Limited

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: 21951 - Posted: 03.03.2016