Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By Nathan Seppa High blood glucose levels appear to be associated with an increased risk of dementia in older people, a new study finds. Paul Crane at the University of Washington in Seattle and his colleagues recorded blood glucose levels in 2,067 people an average of 76 years old who initially had no signs of dementia. After five years, roughly one-fourth of the participants developed some form of dementia. Among people without diabetes, the risk of developing dementia was 18 percent greater in those with high blood glucose levels than in those with low levels. In people with diabetes, the risk of dementia was 40 percent higher in the high-glucose group, the scientists report in the Aug. 8 New England Journal of Medicine. The researchers took into account differences in age, gender, education, heart disease, blood pressure, smoking history and exercise level. While the study doesn’t establish a biological link between high blood glucose and dementia, the researchers speculate that the association could be explained by either glucose-related damage to tiny blood vessels in the central nervous system or insulin resistance – in which cells lose the ability to efficiently process sugar. © Society for Science & the Public 2000 - 2013
Link ID: 18476 - Posted: 08.08.2013
By ANAHAD O'CONNOR Losing sleep tends to make people eat more and gain weight, and now a new study suggests that one reason may be the impact that sleep deprivation has on the brain. The research showed that depriving people of sleep for one night created pronounced changes in the way their brains responded to high-calorie junk foods. On days when the subjects had not had proper sleep, fattening foods like potato chips and sweets stimulated stronger responses in a part of the brain that helps govern the motivation to eat. But at the same time, the subjects experienced a sharp reduction in activity in the frontal cortex, a higher-level part of the brain where consequences are weighed and rational decisions are made. The findings suggested that one unfortunate result of sleep loss is this “double hit” in brain activity, said Matthew P. Walker, an author of the study and a professor of psychology and neuroscience at the University of California, Berkeley. A sleepy brain appears to not only respond more strongly to junk food, but also has less ability to rein that impulse in. Some experts have theorized that in a sleep-deprived state, people eat more food simply to make up for all the calories they expend as they burn the midnight oil. But the new study showed that the changes in brain activity were evident even when the subjects were fed extra food and not experiencing any increased sensations in hunger. “Their hunger was no different when they were sleep deprived and when they had a normal night of sleep,” Dr. Walker said. “That’s important because it suggests that the changes we’re seeing are caused by sleep deprivation itself, rather than simply being perhaps more metabolically impaired when you’re sleep deprived.” Copyright 2013 The New York Times Company
By Scicurious I’ve got a terrible sweet tooth. And I am kind of proud of it, in a way. Yeah, I CAN eat that whole chocolate cake. I’d even LIKE it. Honeycomb dipped in chocolate? YES PLEASE. There are very few sweet things that I’d refuse. But should I really be ok with my sweet tooth? Could my sweet tooth correlate with something more sinister…a preference for alcohol? I can blame my sweet tooth on my parents, probably. Studies have shown that variability in preference for sweet things (though, to a greater or lesser extent, we all like sweet things), has a genetic basis. But the sweet tooth doesn’t go alone. In animals (mice especially), a preference for sugar in their water correlates with preference for alcohol as well. When you breed mice to make sure they drink alcohol (this is done to study alcoholism, for example), they also tend to really prefer sweet things, above and beyond mice that aren’t so into martinis. There is a correlation in humans, too. Humans who are more into sweet things are slightly more likely to abuse alcohol. But what is the basis? The authors of this study wanted to look at the reward related systems of humans, and see how sweet taste might compare to alcohol drinking. They took 16 people, put them in an fMRI scanner, and then carefully sprayed their tongues with sugar water. fMRI looks at the blood oxygen levels in various areas of the brain. Higher blood oxygen levels are thought to correlate with increased “activity” of the brain (the idea being that more neurons in use means the area needs more oxygen). An example of this would be that your visual cortex will show increased blood oxygen levels when you are looking at something. © 2013 Scientific American
By Meghan Rosen In a spacious hotel room not far from the beach in La Jolla, Calif., Kelsey Heenan gripped her fiancé’s hand. Heenan, a 20-year-old anorexic woman, couldn’t believe what she was hearing. Walter Kaye, director of the eating disorders program at the University of California, San Diego, was telling a handful of rapt patients and their family members what the latest brain imaging research suggested about their disorder. It’s not your fault, he told them. Heenan had always assumed that she was to blame for her illness. Kaye’s data told a different story. He handed out a pile of black-and-white brain scans — some showed the brains of healthy people, others were from people with anorexia nervosa. The scans didn’t look the same. “People were shocked,” Heenan says. But above all, she remembers, the group seemed to sigh in relief, breathing out years of buried guilt about the disorder. “It’s something in the way I was wired — it’s something I didn’t choose to do,” Heenan says. “It was pretty freeing to know that there could be something else going on.” Years of psychological and behavioral research have helped scientists better understand some signs and triggers of anorexia. But that knowledge hasn’t straightened out the disorder’s tangled roots, or pointed scientists to a therapy that works for everyone. “Anorexia has a high death rate, it’s expensive to treat and people are chronically ill,” says Kaye. © Society for Science & the Public 2000 - 2013
Keyword: Anorexia & Bulimia
Link ID: 18413 - Posted: 07.27.2013
Heidi Ledford A procedure increasingly used to treat obesity by reducing the size of the stomach also reprogrammes the intestines, making them burn sugar faster, a study in diabetic and obese rats has shown. If the results, published today in Science1, hold true in humans, they could explain how gastric bypass surgery improves sugar control in people with diabetes. They could also lead to less invasive ways to produce the same effects. “This opens up the idea that we could take the most effective therapy we have for obesity and diabetes and come up with ways to do it without a scalpel,” says Randy Seeley, an obesity researcher at the University of Cincinnati in Ohio, who was not involved in the work. As rates of obesity and diabetes skyrocket in many countries, physicians and patients are turning to operations that reconfigure the digestive tract so that only a small part of the stomach is used. Such procedures are intended to allow people to feel full after smaller meals, reducing the drive to consume extra calories. But clinical trials in recent years have shown that they can also reduce blood sugar levels in diabetics, even before weight is lost2, 3. “We have to think about this surgery differently,” says Seeley. “It’s not just changing the plumbing, it’s altering how the gut handles glucose.” © 2013 Nature Publishing Group,
Link ID: 18412 - Posted: 07.27.2013
Avoiding temptation works better than relying on willpower alone, a study of brain activity finds. "Struggles with self-control pervade daily life and characterize an array of dysfunctional behaviours, including addiction, overeating, overspending and procrastination," Molly Crockett, a postdoctoral fellow at University College London, and her co-authors said in today's issue of the journal Neuron. "Our research suggests that the most effective way to beat temptations is to avoid facing them in the first place," she said in a release. In the experiment, researchers studied 58 healthy heterosexual males in Cambridge and 20 in Amsterdam. Investigators used functional MRI as part of the study of self-control to explore the neural mechanisms involved. At the beginning of the trial, participants were shown a series of 400 images of women in lingerie or swimwear and were asked to rank them on a scale of zero to 10 on how enjoyable they were. Each man's preferences were then used to present small, short-term rewards or a large reward after a delay. Small rewards were mildly enjoyable erotic pictures and large rewards were extremely enjoyable ones. (The scientists said they could not use money, for example, since subjects could only reap the rewards of money once they left the lab. Food rewards like juice could interfere with the MRI readings.) © CBC 2013
By Scicurious We all know we should get more sleep, we’re just not very good at it. In fact, we’re so BAD at it that 28.3% of us (as of 2007, anyway) got less than 6 hours of sleep per night. Really, are we surprised? After all, there are kids that wake up in the night, stress that keeps us awake, always more things to do, multiple jobs, and only so many hours in the day. But that lack of sleep can have some not so great effects on our bodies. It decreases things like cognitive performance, increases anxiety, and…it’s not good for our waistlines. Sleep loss is associated with higher caloric intake, when you can’t sleep you eat. But does this increased caloric intake translate to weight gain? The biggest positive point of this study on sleep restriction was how LARGE it was. When doing human studies that are not large scale surveys (which usually involve phone calls or mail in or online and therefore are less expensive) it costs a LOT of money to bring some people in to the lab to do nothing but hang out and sleep for a week, especially if you are watching for things like food intake (and controlling what they eat). I’m very pleased that they got these numbers, 225 people! The authors took these 225 people, and brought them into the lab. They got two baseline nights (to see how much they naturally slept), 5 sleep restriction nights, and then another 2 recovery nights. But unfortunately, they did not balance the control and sleep restriction, where they were restricted down to FOUR HOURS a night of sleep (ick). They only had 27 controls out of all of these (people allowed to sleep fully all the nights of the study), the rest were sleep restriction. I have to wonder why they did it this way. While the two original nights and the two recovery nights could in theory serve as a partial control, I don’t think that those would work. After all, if most people are slightly sleep restricted, the original two nights will be recovery as well, and both sets of recovery nights may not be representative of optimal sleep. © 2013 Scientific American
By GINA KOLATA The mice were eating their usual chow and exercising normally, but they were getting fat anyway. The reason: researchers had deleted a gene that acts in the brain and controls how quickly calories are burned. Even though they were consuming exactly the same number of calories as lean mice, they were gaining weight. So far, only one person — a severely obese child — has been found to have a disabling mutation in the same gene. But the discovery of the same effect in mice and in the child — a finding published Wednesday in the journal Science — may help explain why some people put on weight easily while others eat all they want and seem never to gain an ounce. It may also offer clues to a puzzle in the field of obesity: Why do studies find that people gain different amounts of weight while overeating by the same amount? Scientists have long thought explanations for why some people get fat might lie in their genes. They knew body weight was strongly inherited. Years ago, for example, they found that twins reared apart tended to have similar weights and adoptees tended to have weights like their biological parents, not the ones who reared them. As researchers developed tools to look for the actual genes, they found evidence that many — maybe even hundreds — of genes may be involved, stoking appetites, making people voraciously hungry. This rare gene-disabling mutation, though, is intriguing because it seems to explain something different, a propensity to pile on pounds even while eating what should be a normal amount of food. Investigators are now searching for other mutations of the same gene in fat people that may have a similar, but less extreme effect. The hope is that in the long term, understanding how this gene affects weight gain might lead to treatments for obesity that alter the rate at which calories are burned. © 2013 The New York Times Company
By GRETCHEN REYNOLDS Two newly published studies investigate the enticing possibility that we might one day be able to gain the benefits of exercise by downing a pill, rather than by actually sweating. But while some of the research holds out promise for an effective workout pill, there remains the question of whether such a move is wise. The more encouraging of the new studies, which appears this week in Nature Medicine, expands on a major study published last year in Nature. In that study, researchers at the Scripps Research Institute in Jupiter, Fla., reported that a compound they had created and injected into obese mice increased activation of a protein called REV-ERB, which is known to partially control animals’ circadian rhythms and internal biological clocks. The injected animals lost weight, even on a high-fat diet, and improved their cholesterol profiles. Unexpectedly, the treated mice also began using more oxygen throughout the day and expending about 5 percent more energy than untreated mice, even though they were not moving about more than the other animals. In fact, in most cases, they were more physically lazy and inactive than they had been before the injections. The drug, it seemed, was providing them with a workout, minus the effort. Intrigued, the Scripps scientists, in conjunction with researchers from the Pasteur Institute in France and other institutions, set out to see what their compound might be doing inside muscles to provide this ersatz exercise. They knew that their drug increased the potency of the REV-ERB protein, but no one yet knew what REV-ERB actually does in muscles. So they began by developing a strain of mice that could not express very much of the protein in their muscle cells. Copyright 2013 The New York Times Company
Link ID: 18384 - Posted: 07.18.2013
By Sue Shellenbarger It’s easy to be offended when a colleague yawns while you’re talking. But that yawn may not mean what you think. A growing number of researchers believe the purpose of this little-understood behavior is to cool the brain, says a research review published earlier this year in Frontiers in Neuroscience. Changes in climate affect how often people yawn. Researchers in an earlier study asked two groups of pedestrians in Tucson, Ariz., one in early summer and one in the winter. People were asked to look at pictures of people yawning and talk about their own yawning behavior. The participants were nearly twice as likely to yawn when they were surveyed during the winter, when they could inhale cool air to reduce the temperature of the brain, says the study, published in 2011 in Frontiers in Evolutionary Neuroscience. Participants yawned less when surveyed in the early summer, when temperatures outdoors were about the same as the human body. Other studies show yawning increases after people experience heat stress or have a heat pack placed on their foreheads. Yawning also may build empathy within groups. Yawns are seen as contagious, but “catching” a yawn depends on a person’s ability to feel empathy and closeness with the yawner, says a 2013 research review in the International Journal of Applied Basic Medical Research. ©2013 Dow Jones & Company, Inc.
Link ID: 18383 - Posted: 07.18.2013
by Sarah C. P. Williams Researchers think they've hit on why a common obesity gene causes weight gain: Those who carry a version of it don't feel full after eating and take in extra calories. That's because the variant of the FTO gene in question, which one in six individuals carry, leads to higher levels of ghrelin, a hormone involved in mediating appetite and the body's response to food, researchers have discovered. While most studies on FTO have relied on mice, the new work analyzed blood samples and brain scans from humans. "This is a very exciting piece of research," says geneticist Andrew Hattersley of the Peninsula Medical School in Exeter, U.K., who was not involved in the new study. "There is a lot of work that's been done on the mechanism of FTO in animals, but you have to be careful about applying those lessons to people. So it's nice to finally see work done in humans." Hattersley was part of a team that in 2007 reported that people who had one version of the FTO gene, called AA, weighed an average of 3 kilograms more than those with the TT version of the gene. Since then, studies in mice have shown that in everyone, there are high levels of the FTO protein in brain areas that control energy balance. Researchers have also found that animals with the AA version tend to eat more and prefer high-fat food compared with those with the TT version. But why FTO had this effect wasn't known. © 2010 American Association for the Advancement of Science.
Should I stay or should I go? Well, how much food do you have? In some organisms, sexual desire is expressed by leaving, that is, by bidding adieu to a delicious pile of food and wandering off in search of a mate. But not just any mate, a mate with food! Lipton et al., at Albert Einstein College of Medicine, use the “leaving assay” to measure male sexual desire. Their subject is the elegant, rod-like worm, Caenorhabditis elegans.* They start by placing males on their preferred food source; then they measure how often males exit in search of mating partners. You can see the trails they leave in the substrate in this video of C. elegans appropriating Harlem art and culture. How do the researchers know “leaving” is a sex behavior? Context. Leaving a food source occurs only in a sexual context, and the leaving assay is being used to tease apart the threads that control the appetites for food and sex. First, a quick lesson in the fascinating sexuality of C. elegans. Males are not interested in other males, but they search intensely for a mating partner of the other sex. Note that I said “other sex” not “opposite sex.” There are no female C. elegans. Males of this species mate enthusiastically with hermaphrodites. Hermaphrodites can, of course, self-fertilize, but sexual unions between males and hermaphrodites are far more fruitful than selfing. For hermaphrodites, mating with a male will produce more offspring, and for males, hermaphrodites are the only crying game in town.
Keyword: Sexual Behavior
Link ID: 18341 - Posted: 07.03.2013
by Elizabeth Norton Transforming fat cells into calorie-burning machines may sound like the ultimate form of weight control, but the idea is not as far-fetched as it sounds. Unexpectedly, some fat cells directly sense dropping temperatures and release their energy as heat, according to a new study; that ability might be harnessed to treat obesity and diabetes, researchers suggest. Fat is known to help protect animals from the cold—and not only by acting as insulation. In the early 1990s, scientists studying mice discovered that cold temperatures trigger certain fat cells, called brown adipose tissue, to release stored energy in the form of heat—to burn calories, in other words. Researchers have always assumed this mechanism was an indirect response to the physiological stress of cold temperatures, explains cell biologist Bruce Spiegelman of Harvard Medical School, Boston. The activation of brown fat seems to start with sensory neurons throughout the body informing the brain of a drop in temperature. In response the brain sends out norepinephrine, the chief chemical messenger of the sympathetic nervous system, which mobilizes the body to cope with many situations. In experimental animals, stimulating norepinephrine receptors triggered brown adipose tissue to release its energy and generate heat, while animals bred to be missing these receptors were unable to mount the same fat cell response. People also have brown adipose tissue that generates heat when the body is cold. And unlike white fat, which builds up around the abdomen and contributes to many disorders including heart disease and diabetes, this brown fat is found in higher proportions in leaner people and seems to actively protect against diabetes. © 2010 American Association for the Advancement of Science
Link ID: 18334 - Posted: 07.02.2013
By JANE E. BRODY Most people know that obesity can result in serious health problems, yet many of us continue to focus on its cosmetic consequences rather than its risks to health. This distorted view may change now that the American Medical Association has finally labeled obesity a disease, not just a risk factor for other disorders. Last month, the organization recognized that obesity is a verifiable illness that warrants far more attention than physicians, patients and insurers currently give it. The designation may change how aggressively doctors treat obesity, foster the development of new therapies, and lead to better coverage byinsurers. After all, the price of not treating obesity is now in the stratosphere. Obesity-related health conditions cost the nation more than $150 billion and result in an estimated 300,000 premature deaths each year. If the population’s weight gain is not soon capped (or better yet, reversed), experts predict that half of adults in America will be obese by 2040. The A.M.A. has said in effect that it is medicine’s responsibility to provide the knowledge and tools needed to curb this runaway epidemic. On June 19, James Gandolfini, the hefty award-winning actor who portrayed Tony Soprano in “The Sopranos,” died at 51, apparently of a heart attack, while on vacation in Italy. Even if genetics played a role, Mr. Gandolfini’s weight contributed significantly to his risk of sudden cardiac death. Not a week earlier, a 46-year-old member of my family who weighed over 300 pounds died suddenly of what might have been a heart attack while dozing in front of the television. He had long suffered from sleep apnea (a risk factor for sudden death), high blood pressure and severe gout, all results of his extreme weight. Copyright 2013 The New York Times Company
Link ID: 18330 - Posted: 07.01.2013
by Sue Langthorp Losing sleep doesn't just make us hazy and irritable. It can also lead to cardiovascular disease, type 2 diabetes, and a host of other conditions. But catching up on some shuteye may help combat these problems. According to a new study, sleep-deprived men who dozed an extra 2 to 3 hours on the weekend may reduce their risk of developing type 2 diabetes. Researchers led by Peter Liu, an endocrinologist at the Los Angeles Biomedical Research Institute at the Harbor-University of California, Los Angeles, Medical Center, recruited 19 men in good health who, due to their workload, were poor sleepers. The subjects, age 29 on average, had been clocking about 6 hours of shuteye on weeknights for just over 5 years. However, they made the most of their weekends and slept an extra 2.3 hours a night on Friday and Saturday. When selecting the candidates for the trial, the scientists verified their reported schedules using sleep actigraphs, devices worn like wrist watches that record sleep patterns. The men slept in the lab for three nights. Some were allowed to sleep 10 hours without interruption, catching up on the sleep that they had lost earlier in the week. Others slept 10 hours with frequent interruption, and still others slept 6 hours without interruption. All the subjects ate the same diet, so the researchers could normalize their insulin and sugar levels. © 2010 American Association for the Advancement of Science
By NICHOLAS BAKALAR Obesity in adolescents is associated with a range of cardiovascular and other health risks. Now a new study adds one more: hearing loss. Several studies have demonstrated the association of obesity with hearing loss in adults, but now researchers examining records of a nationwide sample of 1,488 boys and girls ages 12 to 19 have found the same association in teenagers. The study appeared online in The Laryngoscope. The researchers controlled for various factors, including poverty, sex, race and previous exposure to loud noises. They found that being at or above the 95th percentile for body mass index — the definition of obesity in teenagers — was independently associated with poorer hearing over all frequencies, and with almost double the risk of low-frequency hearing loss in one ear. They suggest that this may represent an early stage of injury that will later progress to both ears, as it does in adults. The reason for the connection is not known, but the scientists suggest that inflammation induced by obesity may be a factor in organ damage. “It’s quite possible that early intervention could arrest the progression,” said the lead author, Dr. Anil K. Lalwani, a professor of otolaryngology at Columbia University. “This is another reason to lose weight — but not to lose hope.” Copyright 2013 The New York Times Company
Published by scicurious What do the overconsumption of food and Obsessive-Compulsive Disorder (OCD) have in common? At first, this sounds like a trick question. But deep in the brain, the molecules underlying our behavior may come together for these two conditions. The first is MC4R, a receptor for melanocortin. It binds hormones and affects feeding behavior, mutations in MC4R are associated with severe overcomsumption of high fat, high calorie foods and with obesity. A mouse without an MC4R gene will become severely obese compared to its wildtype counterparts. SAPAP3 is a protein that is associated with synapses, the spaces between neurons. It can regulate things like receptor levels that determine how well a neuron responds to excitatory input. But a knockout of SAPAP3 in mice produces something very different: severe overgrooming, a model of OCD. All rodents groom themselves, it's necessary to keep clean. But SAPAP3 knockouts groom themselves far, far too much, to the point of creating terrible lesions on their skin. This has been proposed as a model of OCD, as many people with OCD become obsessed with cleanliness, and will do things like, say, washing their hands, to the point of severely damaging their skin. So a knockout of MC4R creates obese mice. A knockout of SAPAP3 creates overgrooming mice. You might think that if you combined the two knockouts, you would get severely obese mice that also overgroomed. But you don't. Instead, you get mice that, to all appearances, seem completely normal. No obesity. No overgrooming. Neurotic Physiology Copyright © 2013
By Rachel Ehrenberg The salad days of human evolution saw a dietary shift toward grasses and probably grass-fed animals, analyses of more than 100 fossilized teeth from eight species of ancient hominids indicate. “These changes in diet have been predicted,” says paleoanthropologist Richard Klein of Stanford University. “But it’s very nice to have some data, and these data support it very strongly.” Changes in the size and shape of jaws and teeth in both ancient hominids and their ape relatives point to changes in diet. The new study adds to these lines of anatomical evidence chemical analyses that look at different forms of carbon in the fossilized teeth. The ratio of two types of carbon in tooth enamel reflects diet, says geochemist Thure Cerling of the University of Utah, who spent weeks in a vault in the National Museum of Kenya collecting milligram-sized samples of tooth enamel for the analyses. Grasses, grasslike sedges and many other plants in hot, arid environments have evolved a trick that helps prevent water loss. The metabolic adjustment results in taking up more of a heavier form of carbon, known as carbon-13, than most trees and shrubs do. The tooth studies, which cover more than 3 million years and include specimens from southern, eastern and central Africa, found greater quantities of this heavier carbon in hominids that are closer to humans on the evolutionary tree. This pattern suggests that, compared with humans’ more ancient relatives, recent ones were eating more grass or more grass-feeding animals, like zebras. The analyses appear June 3 in the Proceedings of the National Academy of Sciences. © Society for Science & the Public 2000 - 2013
Obese mothers tend to have kids who become obese. Now provocative research suggests weight-loss surgery may help break that unhealthy cycle in an unexpected way — by affecting how their children's genes behave. In a first-of-a-kind study, Canadian researchers tested children born to obese women, plus their brothers and sisters who were conceived after the mother had obesity surgery. Youngsters born after mom lost lots of weight were slimmer than their siblings. They also had fewer risk factors for diabetes or heart disease later in life. More intriguing, the researchers discovered that numerous genes linked to obesity-related health problems worked differently in the younger siblings than in their older brothers and sisters. Clearly diet and exercise play a huge role in how fit the younger siblings will continue to be, and it's a small study. But the findings suggest the children born after mom's surgery might have an advantage. "The impact on the genes, you will see the impact for the rest of your life," predicted Marie-Claude Vohl of Laval University in Quebec City. She helped lead the work reported Monday in the journal Proceedings of the National Academy of Sciences. Why would there be a difference? It's not that mom passed on different genes, but how those genes operate in her child's body. The idea: Factors inside the womb seem to affect the dimmer switches that develop on a fetus' genes — chemical changes that make genes speed up or slow down or switch on and off. That in turn can greatly influence health. © CBC 2013
Virginia Hughes Late in the morning on 20 February, more than 200 people packed an auditorium at the Harvard School of Public Health in Boston, Massachusetts. The purpose of the event, according to its organizers, was to explain why a new study about weight and death was absolutely wrong. The report, a meta-analysis of 97 studies including 2.88 million people, had been released on 2 January in the Journal of the American Medical Association (JAMA)1. A team led by Katherine Flegal, an epidemiologist at the National Center for Health Statistics in Hyattsville, Maryland, reported that people deemed 'overweight' by international standards were 6% less likely to die than were those of 'normal' weight over the same time period. The result seemed to counter decades of advice to avoid even modest weight gain, provoking coverage in most major news outlets — and a hostile backlash from some public-health experts. “This study is really a pile of rubbish, and no one should waste their time reading it,” said Walter Willett, a leading nutrition and epidemiology researcher at the Harvard school, in a radio interview. Willett later organized the Harvard symposium — where speakers lined up to critique Flegal's study — to counteract that coverage and highlight what he and his colleagues saw as problems with the paper. “The Flegal paper was so flawed, so misleading and so confusing to so many people, we thought it really would be important to dig down more deeply,” Willett says. © 2013 Nature Publishing Group,
Link ID: 18185 - Posted: 05.23.2013