Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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By ANDREW POLLACK A study of an obesity drug has ended after the manufacturer released early and ultimately misleading data, researchers said on Tuesday. The company, Orexigen Therapeutics, disclosed in March that early results from a clinical trial of its drug Contrave had shown a 41 percent reduction in the risk of heart attacks, strokes and death from cardiovascular causes. Orexigen’s stock shot up, and the information no doubt helped lift sales of Contrave. But the academic researchers who oversaw the study said on Tuesday that Orexigen had violated an agreement that the early results were not going to be shared widely, even within the company. Moreover, as participants in the trial were followed for a longer period of time, the benefit of the drug in reducing cardiovascular risks vanished. The researchers, in a news release issued by the Cleveland Clinic, said they took the unusual step of terminating the study and releasing the more updated results. “We felt it was unacceptable to allow misleading interim data to be in the public domain and be acted upon by patients and providers,” Dr. Steven Nissen, chairman of cardiovascular medicine at the Cleveland Clinic and head of the trial’s steering committee, said in an interview. He said Orexigen had “acted improperly and unethically in violating the data access agreement” and the premature release of data had made it difficult to continue the study. It’s unlikley that patients would want to stay in the trial and risk getting a placebo if they thought the drug, which is already available on the market, could reduce their risk of heart attacks. © 2015 The New York Times Company
Link ID: 20921 - Posted: 05.13.2015
By David Shultz We no longer live in a world governed by the sun. Artificial light lets millions of people stay up late, or work in the predawn hours. But the price many of us pay for this extra illumination is a disrupted internal clock—and, growing evidence suggests, obesity. Now, a study of mice suggests that excessive light exposure causes the rodents to burn less fat, a finding that if confirmed could lead to new paths to weight loss in humans. Many mammals have two types of tissues that store fat: brown fat and white fat. Both store energy, but white fat releases its energy stores to power other cells, while brown fat produces heat from metabolizing its contents. For years, scientists have been trying to coax brown fat into action as a way to stimulate weight loss. They’ve identified a protein called β3 adrenergic receptor that, when activated, encourages brown fat cells to burn off more fat and produce more heat. To test the relationship between light exposure and brown fat activity, researchers exposed groups of mice to artificial light for 12, 16, or 24 hours per day and monitored their levels of β3 adrenergic receptor activity. The team also monitored the rate at which energy molecules such as glucose and fatty acids were absorbed from the bloodstream by brown fat tissue to test whether the tissue was using less energy to begin with. Both metrics showed the same trend: Brown fat in mice exposed to prolonged periods of light, 16 or 24 hours compared with a normal 12, absorbed less nutrients from the blood and burned less fat as a result of reduced β3 adrenergic receptor activity. In essence, their furnaces were using less fuel and burning less intensely. To compound the problem, the fatty molecules left in the blood stream were absorbed elsewhere—often in white adipose tissue that makes up the classical body fat that causes obesity, says team leader Patrick Rensen, a biochemist at Leiden University Medical Center in the Netherlands. © 2015 American Association for the Advancement of Science.
By Nicholas Bakalar The type of sugar you eat may affect your cravings for high-calorie foods, researchers report. An experiment with 24 healthy volunteers found that compared with consuming glucose, consuming fructose — the sugar found in fruits, honey and corn syrup — resulted in more activity in the brain’s reward regions, increased responses to images of food and a tendency to choose eating a high-calorie food over a future monetary reward. The volunteers drank a 10-ounce glass of cherry-flavored liquid that contained two and a half ounces of fructose or glucose. (Table sugar, or sucrose, extracted from sugar cane or sugar beets, is a compound of glucose and fructose.) Researchers also took blood samples to measure levels of glucose, fructose and insulin, and of leptin and ghrelin, enzymes involved in controlling hunger and feelings of fullness. Before having their drinks, the participants rated their desire to eat on a one-to-10 scale from “not at all” to “very much.” Then they drank the liquids and had functional magnetic resonance imaging brain scans while looking at images of food and of neutral objects like buildings or baskets. As they did so, they rated their hunger using the scale. The volunteers were then presented with images of high-calorie foods and asked whether they would like to have the food now, or a monetary award a month later instead. The study, published in the journal PNAS, found that compared with glucose, consuming fructose produced greater responses to food cues in the orbital frontal cortex of the brain, a region that plays an important role in reward processing. The fructose drink also produced greater activity in the visual cortex when volunteers looked at images of food, a finding that suggests increased craving compared with glucose. © 2015 The New York Times Company
Link ID: 20883 - Posted: 05.05.2015
By Nicholas Bakalar Many people consume sweets in response to stress. Now researchers may have discovered why. Sugar reduces levels of cortisol, the stress hormone. Scientists recruited 19 female volunteers. For 12 days, eight of them consumed beverages sweetened with aspartame, an artificial sweetener. The rest drank an identical beverage containing 25 percent sucrose, or table sugar. Before and after the experiment, researchers measured the volunteers’ saliva cortisol levels and performed functional M.R.I. scans while they took arithmetic tests designed to be just beyond their abilities — a procedure known to increase cortisol levels. The study, in the Journal of Clinical Endocrinology and Metabolism, found no differences in the tests between the two groups before the 12-day diet. But in tests afterward, cortisol levels were lower in the sugar consumers and higher in the aspartame group. The post-diet M.R.I. showed increased activity in the areas of the brain controlling fear and stress in the sugar group. The aspartame group showed decreased activity in those areas. The senior author, Kevin D. Laugero, a nutritionist with the federal Department of Agriculture, said no one should conclude that sugar should be used as a stress reducer. But, he said, “the finding is intriguing because it suggests that there is a metabolic pathway sensitive to sugar outside the brain that may expose new targets for treating neurobehavioral and stress-related conditions.” © 2015 The New York Times Company
Physical activity has little role in tackling obesity - and instead public health messages should squarely focus on unhealthy eating, doctors say. In an editorial in the British Journal of Sports Medicine, three international experts said it was time to "bust the myth" about exercise. They said while activity was a key part of staving off diseases such as diabetes, heart disease and dementia, its impact on obesity was minimal. Instead excess sugar and carbohydrates were key. The experts, including London cardiologist Dr Aseem Malhotra, blamed the food industry for encouraging the belief that exercise could counteract the impact of unhealthy eating. They even likened their tactics as "chillingly similar" to those of Big Tobacco on smoking and said celebratory endorsements of sugary drinks and the association of junk food and sport must end. They said there was evidence that up to 40% of those within a normal weight range will still harbour harmful metabolic abnormalities typically associated with obesity. But despite this public health messaging had "unhelpfully" focused on maintaining a healthy weight through calorie counting when it was the source of calories that mattered most - research has shown that diabetes increases 11-fold for every 150 additional sugar calories consumed compared to fat calories. And they pointed to evidence from the Lancet global burden of disease programme which shows that unhealthy eating was linked to more ill health than physical activity, alcohol and smoking combined. © 2015 BBC
Link ID: 20840 - Posted: 04.23.2015
|By Cari Nierenberg and LiveScience Women who develop gestational diabetes early in their pregnancy have a higher chance of having a child with autism than women who don't develop the condition, a new study suggests. Researchers found that mothers-to-be who developed gestational diabetes — high blood sugar during pregnancy in women who have never had diabetes — by their 26th week of pregnancy were 63 percent more likely to have a child diagnosed with an autism spectrum disorder (ASD) compared with women who did not have gestational diabetes at any point during their pregnancy (and who also did not have type 2 diabetes prior to pregnancy). The finding does not mean that autism is common among children born to women who had gestational diabetes. "Autism is still rare," said study co-author Anny Xiang, a research scientist at Kaiser Permanente Southern California in Pasadena. The findings show that, although the risk of having a child with autism is still low among women who have gestational diabetes early in pregnancy (before 26 weeks), the study did find a relationship between these women and an increased risk that the child would have autism, Xiang said. The study, published today (April 14) in the Journal of the American Medical Association, looked at more than 320,000 children born in Southern California between 1995 and 2009. About 8 percent of the kids were born to mothers who had pregnancy-related diabetes, and 2 percent had mothers with type 2 diabetes. © 2015 Scientific American
By James Gallagher Health editor, BBC News website Those who were overweight had an 18% reduction in dementia, researchers found Being overweight cuts the risk of dementia, according to the largest and most precise investigation into the relationship. The researchers admit they were surprised by the findings, which run contrary to current health advice. The analysis of nearly two million British people, in the Lancet Diabetes & Endocrinology, showed underweight people had the highest risk. Dementia charities still advised not smoking, exercise and a balanced diet. Dementia is one of the most pressing modern health issues. The number of patients globally is expected to treble to 135 million by 2050. There is no cure or treatment, and the mainstay of advice has been to reduce risk by maintaining a healthy lifestyle. Yet it might be misguided. The team at Oxon Epidemiology and the London School of Hygiene and Tropical Medicine analysed medical records from 1,958,191 people aged 55, on average, for up to two decades. Their most conservative analysis showed underweight people had a 39% greater risk of dementia compared with being a healthy weight. But those who were overweight had an 18% reduction in dementia - and the figure was 24% for the obese. "Yes, it is a surprise," said lead researcher Dr Nawab Qizilbash. He told the BBC News website: "The controversial side is the observation that overweight and obese people have a lower risk of dementia than people with a normal, healthy body mass index. "That's contrary to most if not all studies that have been done, but if you collect them all together our study overwhelms them in terms of size and precision." Loss of tissue in a demented brain compared with a healthy one © 2015 BBC
By Rachel Feltman If you give a mouse an eating disorder, you might just figure out how to treat the disease in humans. In a new study published Thursday in Cell Press, researchers created mice who lacked a gene associated with disordered eating in humans. Without it, the mice showed behaviors not unlike those seen in humans with eating disorders: They tended to be obsessive compulsive and have trouble socializing, and they were less interested in eating high-fat food than the control mice. The findings could lead to novel drug treatments for some of the 24 million Americans estimated to suffer from eating disorders. In a 2013 study, the same researchers went looking for genes that might contribute to the risk of an eating disorder. Anorexia nervosa and bulimia nervosa aren't straightforwardly inherited -- there's definitely more to an eating disorder than your genes -- but it does seem like some families might have higher risks than others. Sure enough, the study of two large families, each with several members who had eating disorders, yielded mutations in two interacting genes. In one family, the estrogen-related receptor α (ESRRA) gene was mutated. The other family had a mutation on another gene that seemed to affect how well ESRRA could do its job. So in the latest study, they created mice that didn't have ESRRA in the parts of the brain associated with eating disorders. "You can't go testing this kind of gene expression in a human," lead author and University of Iowa neuorscientist Michael Lutter said. "But in mice, you can manipulate the expression of the gene and then look at how it changes their behavior."
by Alison George Misguided notions about our sexual appetites are missing the bigger picture and making people unhappy, says Emily Nagoski Why is there no such thing as a sex drive? A drive is a motivational system to deal with life-or-death issues, like hunger or being too cold. You're not going to die if you don't have sex. But biologists might say that if you don't reproduce, that is a form of death Yes. That's the argument that was used when desire was being added to the way sexual dysfunctions were diagnosed in the 1970s, to justify the framing of sexual desire as a drive. But when it comes to sex, there just isn't any physical evidence of a drive mechanism. So what's going on? If sex is a drive then desire should be spontaneous, like a hunger. When you see a sexy person or have a stray sexy thought, it activates an internal craving or urge for sex. That's called "spontaneous desire". It feels like it comes out of the blue. But there is another way of experiencing desire which is also healthy and normal, called "responsive desire", where your interest only emerges in response to arousal. So, your partner comes over and starts kissing your neck and you're like, "oh, right, sex, that's a good idea". Do you think an absence of spontaneous desire is normal? Yes. If our metaphor for desire is hunger, if you are never hungry for food there will be dire consequences and that's clearly a disorder, right? That's a medical problem that needs to be fixed. But not experiencing spontaneous hunger for sex doesn't have dire consequences; it is not a medical disorder. I think the reason we expect everyone to have spontaneous desire is because that's how most men experience it. © Copyright Reed Business Information Ltd
Keyword: Sexual Behavior
Link ID: 20759 - Posted: 04.06.2015
By Harriet Brown If you’re one of the 45 million Americans who plan to go on a diet this year, I’ve got one word of advice for you: Don’t. You’ll likely lose weight in the short term, but your chance of keeping if off for five years or more is about the same as your chance of surviving metastatic lung cancer: 5 percent. And when you do gain back the weight, everyone will blame you. Including you. This isn’t breaking news; doctors know the holy trinity of obesity treatments—diet, exercise, and medication—don’t work. They know yo-yo dieting is linked to heart disease, insulin resistance, higher blood pressure, inflammation, and, ironically, long-term weight gain. Still, they push the same ineffective treatments, insisting they’ll make you not just thinner but healthier. In reality, 97 percent of dieters regain everything they lost and then some within three years. Obesity research fails to reflect this truth because it rarely follows people for more than 18 months. This makes most weight-loss studies disingenuous at best and downright deceptive at worst. One of the principles driving the $61 billion weight-loss industries is the notion that fat is inherently unhealthy and that it’s better, health-wise, to be thin, no matter what you have to do to get there. But a growing body of research is beginning to question this paradigm. Does obesity cause ill health, result from it, both, or neither? Does weight loss lead to a longer, healthier life for most people? Studies from the Centers for Disease Control and Prevention repeatedly find the lowest mortality rates among people whose body mass index puts them in the “overweight” and “mildly obese” categories.
Link ID: 20718 - Posted: 03.25.2015
By RENEE ENGELN ON Tuesday, in the wake of an online petition signed by thousands of people, Facebook announced that it was removing “feeling fat” from its list of status update emoticons. The petition argued that the offending emoticon, with its chubby cheeks and double chin, reinforced negative body images, and Facebook seemed to agree. Is it really such a big deal if you tell everyone how fat you feel? After all, a simple “I’m so fat!” can result in a chorus of empathetic voices, saying, “Me, too!” or “You’re beautiful just the way you are!” And that will help you feel better, and help others feel better, too — right? Wrong. As someone who studies this type of public body self-disparagement, known as “fat talk,” I can say that it probably will make you feel worse. And it may drag down other people with you. Conversational shaming of the body has become practically a ritual of womanhood (though men also engage in it). In a survey that a colleague and I reported in 2011 in the Psychology of Women Quarterly, we found that more than 90 percent of college women reported engaging in fat talk — despite the fact that only 9 percent were actually overweight. In another survey, which we published in December in the Journal of Health Psychology, we canvassed thousands of women ranging in age from 16 to 70. Contrary to the stereotype of fat talk as a young woman’s practice, we found that fat talk was common across all ages and all body sizes. Most important, fat talk is not a harmless social-bonding ritual. According to an analysis of several studies that my colleagues and I published in 2012 in the Psychology of Women Quarterly, fat talk was linked with body shame, body dissatisfaction and eating-disordered behavior. Fat talk does not motivate women to make healthier choices or take care of their bodies; in fact, the feelings of shame it brings about tend to encourage the opposite. © 2015 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 20691 - Posted: 03.17.2015
|By Dina Fine Maron Obesity stems primarily from the overconsumption of food paired with insufficient exercise. But this elementary formula cannot explain how quickly the obesity epidemic has spread globally in the past several decades nor why more than one third of adults in the U.S. are now obese. Many researchers believe that a more complex mix of environmental exposures, lifestyle, genetics and the microbiome’s makeup help explain that phenomenon. And a growing body of work suggests that exposure to certain chemicals—found in nature as well as industry—may play an essential role by driving the body to produce and store surplus fat in its tissues. Evidence of that cause-and-effect relationship in humans is still limited, but in laboratory animals and in petri dishes data linking the chemicals to problematic weight gain are mounting. Moreover, the effects in animals appear to be passed on not just to immediate offspring but also grandchildren and great-grandchildren—potentially accounting for some multigenerational obesity. The murkier picture for humans may become clearer in the next five years, says Jerry Heindel, a health science administrator at the National Institute of Environmental Health Sciences. His agency is now funding 57 grants related to obesity and diabetes, he said on March 2 at a meeting of the Institute of Medicine (IOM). The studies look at how chemicals, including those that appear to alter hormone regulation (such as the plasticizer bisphenol A and the antibacterial chemical triclosan), affect weight gain or insulin resistance. Thirty-two of the ongoing studies are in humans. And 20 of those will help assess the longer-term risks to children by tracking the youngsters' chemical levels in utero or as newborns and beyond. © 2015 Scientific American
Link ID: 20660 - Posted: 03.07.2015
Dr. Lisa Sanders. On Thursday we challenged Well readers to solve the case of a middle-aged woman with arthritis who developed a wasting illness after what looked like a simple cold. Her rheumatologist was worried that the immune suppressing medications the patient took to treat her joint disease had caused the new illness. More than 300 of you took on the challenge, and 17 of you correctly identified this rarity. The correct diagnosis is … Whipple’s disease The first reader to make the diagnosis was Mike Natter, a second-year medical student at the Sidney Kimmel Medical College at Thomas Jefferson University in Philadelphia. Mike said it was an easy case for him because he had been studying for an exam the next day and had just read about the disease. He is a frequent contributor to this column and says that he got the right diagnosis twice before but this was the first time he got it in first. Well done, Mike! The Diagnosis Whipple’s was first identified in 1907 by Dr. George Whipple, who was caring for a fellow physician who had “gradual loss of weight and strength, stools consisting chiefly of neutral fat and fatty acids, indefinite abdominal signs, and a peculiar multiple arthritis.” The patient eventually died. Dr. Whipple suspected an infectious cause because he found bacteria in many of the patient’s affected tissues, but the organism itself wasn’t identified for nearly 80 years. The bug, Tropheryma whipplei, is common and found mostly in soil. And yet the infection is rare. There have been only about 1,000 reported cases of Whipple’s disease in the more than one hundred years since it was first described. Over two-thirds of those were in middle-aged white men. Many of them were farmers or others who had occupational exposure to soil. © 2015 The New York Times Company
Link ID: 20659 - Posted: 03.07.2015
|By Charles Schmidt The notion that the state of our gut governs our state of mind dates back more than 100 years. Many 19th- and early 20th-century scientists believed that accumulating wastes in the colon triggered a state of “auto-intoxication,” whereby poisons emanating from the gut produced infections that were in turn linked with depression, anxiety and psychosis. Patients were treated with colonic purges and even bowel surgeries until these practices were dismissed as quackery. The ongoing exploration of the human microbiome promises to bring the link between the gut and the brain into clearer focus. Scientists are increasingly convinced that the vast assemblage of microfauna in our intestines may have a major impact on our state of mind. The gut-brain axis seems to be bidirectional—the brain acts on gastrointestinal and immune functions that help to shape the gut's microbial makeup, and gut microbes make neuroactive compounds, including neurotransmitters and metabolites that also act on the brain. These interactions could occur in various ways: microbial compounds communicate via the vagus nerve, which connects the brain and the digestive tract, and microbially derived metabolites interact with the immune system, which maintains its own communication with the brain. Sven Pettersson, a microbiologist at the Karolinska Institute in Stockholm, has recently shown that gut microbes help to control leakage through both the intestinal lining and the blood-brain barrier, which ordinarily protects the brain from potentially harmful agents. Microbes may have their own evolutionary reasons for communicating with the brain. They need us to be social, says John Cryan, a neuroscientist at University College Cork in Ireland, so that they can spread through the human population. © 2015 Scientific American
By KATIE THOMAS The retired tennis player Monica Seles spent this month making the rounds of television talk shows, appearing on everything from “Good Morning America” to “The Dr. Oz Show” to share her personal struggle with binge eating. “It took a while until I felt comfortable talking about it,” she said in a People magazine interview, explaining that she secretly devoured food for years while she was a professional athlete. “That’s one of the reasons I decided to do this campaign: to raise awareness that binge eating is a real medical condition.” But that is not the only reason. Ms. Seles is a paid spokeswoman for Shire, which late last month won approval to market its top-selling drug, Vyvanse, to treat binge-eating disorder, a condition that once existed in the shadow of better-known disorders like anorexia and bulimia but was officially recognized as its own disorder in 2013 by the American Psychiatric Association. As Shire introduces an ambitious campaign to promote Vyvanse but also to raise awareness about the disorder, some are saying the company is going too far to market a drug, a type of amphetamine, that is classified by the federal government as having a high potential for abuse. Shire’s track record is adding to the worry: The company helped put another once-stigmatized condition — attention deficit hyperactivity disorder — on the medical map and made billions of dollars from the sale of drugs, like Vyvanse and Adderall, to treat it. In recent years, federal officials have cited the company for inappropriately marketing Vyvanse and other A.D.H.D. drugs. In addition, some drug safety experts questioned why the Food and Drug Administration so swiftly approved the drug for binge eating — seeking little outside input — despite the fact that, for decades, amphetamines, which suppress the appetite, were widely abused as a treatment for obesity. © 2015 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 20614 - Posted: 02.25.2015
by Penny Sarchet An injection and a dash of exercise could be the secret to keeping trim. These rainbow mice, imaged in infrared to reveal how much energy they are burning while on a treadmill, are revealing how a shot can boost a muscle's ability to burn calories. Red body parts show where lots of energy is being used. The mouse on the right has a red patch on its left hind leg, which corresponds to the spot where it received an injection of a substance developed by Denice Hodgson-Zingman from the University of Iowa and colleagues. The substance is a type of morpholino, a compound that can be designed to target specific genes, in this case to alter proteins responsible for storing energy. The disruption causes muscles to burn more energy even during mild exercise, such as a gentle trot on a treadmill. In contrast, the untreated mouse on the left, which is doing the same amount of exercise, is using less energy in the same spot, as illustrated by the colder green colour. The researchers hope the injection will help people who want to burn more calories do so through routine everyday activities, eliminating the need for intense exercise. Journal reference: Molecular Therapy, DOI: 10.1038/mt.2015.2141 © Copyright Reed Business Information Ltd.
Link ID: 20610 - Posted: 02.24.2015
By Aleksandra Sagan, CBC News Photos of emaciated women proudly displaying their protruding hips and ribs, as well as thinspirational quotes "fat-shaming" those who dare to eat, continue to thrive on social media, despite the best attempts by sites like Instagram to temper the reach of the pro-eating disorder community. Some girls gain thousands of followers posting pictures of "thigh gaps" and "bikini bridges," as well as underweight celebrities and thinspirational quotes like model Kate Moss's mantra: "nothing tastes as good as skinny feels." "It just provides a lot of positivity for them, just in a very maladaptive way," says Edward Selby, of the more visual outlet that sites like Instagram provide. An assistant professor of clinical psychology at Rutgers University in New Jersey, Selby is the director of a lab there that studies what makes people more likely to develop anorexia (self-starvation), bulimia (binge-eating and purging) and other eating disorders. About one in 20 young women in Canada has an eating disorder, according to the Toronto-based National Initiative for Eating Disorders. And people suffering from these diseases often feel good after exercising, purging, swallowing a laxative or doing other things that contribute to their illness, Selby says. They get caught in a "cyclic feedback loop," with the positive emotions pushing them to engage more in these risky behaviours. Online pro-anorexia and bulimia communities simply add to that loop by celebrating a person's unhealthy achievements, he says. "Finally under 130! Woohoo!" writes one user with a photo of her feet on a scale. "Yay congrats," reads a response. Another girl posts a screen grab from an app claiming that she's been fasting for more than a day. It receives 32 likes and a "great job" among the comments. ©2015 CBC/Radio-Canada
Keyword: Anorexia & Bulimia
Link ID: 20607 - Posted: 02.24.2015
Boer Deng Smoking marijuana may stoke a yearning for crisps, but understanding how it affects hunger is relevant not just to those who indulge in it. The drug has yielded a ripe target for scientists who seek to stimulate or suppress appetite: the receptor CB1, found in cells throughout the body. When activated by the anti-nausea drug dronabinol — which is also a component of marijuana (Cannabis sativa) — CB1 prompts the release of hunger-promoting hormones1. And suppressing its activity is thought to aid in weight loss2. But the mechanism by which the receptor kills or kindles appetite is not entirely understood. Now neuroscientist Tamas Horvath, of Yale University in New Haven, and colleagues report in Nature that nerve cells called pro-opiomelanocortin (POMC) neurons play a key role in this process3. POMC had generally been thought to promote satiation, but Horvath's team found that POMC neurons in the brain release not just a hunger-suppressing hormone, but also one that promotes appetite. Which hormone is secreted is regulated by a protein in the cells' mitochondria, structures that regulate energy levels. When the CB1 receptor is activated, this mitochondrial protein induces POMC to switch from secreting the substance that suppresses gorging to one that encourages it. The finding is intriguing, says Uberto Pagotto, a neuroscientist at the University of Bologna who has studied cannabinoids for many years. “It gives us a different starting point to look at CB1 receptors and the mitochondria,” he says. © 2015 Nature Publishing Group
Scientists have uncovered more than 90 new gene regions that could help explain why some people are more likely to put on weight than others. The team scoured DNA libraries of more than 300,000 people, constructing the largest-ever genetic map of obesity. Looking for consistent patterns they found a link with genes involved in brain processes, suggesting obesity could partly have a neurological basis. The results are published in the journal Nature. Researchers from the international Giant consortium (Genetic Investigation of Anthropometric Trait), analysed the genetics behind body mass index (a ratio of weight and height ). And in a separate Nature paper they looked specifically at how genetics influence where fat is distributed around the body. Fat around the abdomen for example can cause more health problems than fat carried around the thighs. Some 33 newly pinpointed gene regions were linked to body fat distribution - giving further clues about why some people are pear-shaped while others put on weight more around the tummy. They also identified more than 60 genetic locations that influence body mass index - tripling the number previously known. And some of these regions have links with the nervous system. © 2015 BBC
|By Erika Beras We know junk food can change the way bodies are shaped. Now, a study finds that those irresistible sweet and salty concoctions may also change the way brains are wired—at least in rats. Researchers divided rats into two groups—one labeled Cafeteria, the other called Chow. Both groups got a typical rat food diet, but the Cafeteria rats also got a bonus: meat pies, cakes and cookies. Both rat groups gained weight. But the Cafeteria rats gained significantly more than the Chows did—nearly half a pound more, which is a big body burden for a rat. But more important, over two weeks time the Cafeteria rats seemed to care less and less about even seeking out a balanced diet. This new behavior endured even after the rats were returned to their more healthy fare. The study is in the journal Frontiers in Psychology. [Amy C. Reichelt, Margaret J. Morris and R.F. Westbrook, Cafeteria diet impairs expression of sensory-specific satiety and stimulus-outcome learning] The researchers think junk-food diets cause lasting changes in the rewards circuits part of the brain—which plays a big role in decision-making. So if you’re a regular cookie eater and the next time you mindlessly reach for a cookie you wonder why you can’t help yourself—well, it could be because you’re not in charge, your rewired brain is. © 2015 Scientific American