Chapter 9. Homeostasis: Active Regulation of the Internal Environment
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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
By Tulip Mazumdar Most people suffering with eating disorders in Japan are not receiving any medical or psychological support, according to doctors. The Japan Society for Eating Disorders claims the health system is failing hundreds of thousands of sufferers. It also says the pressure on girls, in particular, to be thin has "gone too far". The government says it's trying to set up more services and has tried to discover the extent of the problem. "I hated being chubby when I was a kid," says Motoko - who is using a different name to hide her identity. "The other kids bullied me so I always wanted to change." Motoko was 16 years old when her eating disorder started. She would severely limit how much she ate and then started exercising excessively. By the time she was 19, Motoko was dangerously underweight. She says her parents didn't know how to help her. "They were negative about my illness," she says. "When I tried to see my doctor, they told me not to. "My mother felt responsible, perhaps my father blamed her too." Fear of 'wasting food' Motoko's story is a familiar one. Stigma around eating disorders - for both sufferers and their families - prevent many people from coming forward. "They see actions such as binging on food and then vomiting (bulimia) as shameful," says clinical psychiatrist Dr Aya Nishizono-Maher, a member of The Japan Society for Eating Disorders. "They feel they have to hide it. Parents may think they are wasting food so that might stop them seeking help." After more than 10 years, Motoko finally started getting the help she needed and she now attends one of the few eating disorder community support groups which receives money from the government. © 2016 BBC.
Keyword: Anorexia & Bulimia
Link ID: 22137 - Posted: 04.25.2016
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
By Lisa Sanders, M.D. On Thursday we challenged Well readers to take on the case of a 59-year-old woman who had not been able to stop gaining weight. I presented the case as it was presented to the doctor who made the diagnosis and asked for the final piece of data provided by the patient as well as the correct cause of her symptoms. I thought the tough part of this case was something that few of my readers would have to contend with – that her complaints and past medical history were quite ordinary. Like many of us, she was overweight and she came to the doctor because she had difficulty losing weight. In the background she also had high blood pressure, obstructive sleep apnea and low back pain, knee pain and leg swelling. These are some of the most common reasons patients seek medical attention. Although her problems were run of the mill, the cause was not. And many of you had no difficulty spotting this zebra. The correct diagnosis was… Acromegaly The last piece of data, provided by the patient, was a photograph taken several years before. It was only by seeing the changes in the patient’s face that had occurred over the past few years that the doctor recognized that this patient’s problem was unusual. The first person to make this diagnosis was Dr. Clare O’Connor, a physician in the second year of her training in internal medicine. She plans to subspecialize in endocrinology. She says it was the swollen legs that didn’t compress that gave her the first clue. Well done. Acromegaly is a rare disease caused by an excess of growth hormone, usually due to a tumor in the pituitary gland of the brain. The disease’s name, from the Greek, serves as a fitting description of the most obvious symptoms: great (mega) extremity (akron). The tumor secretes a protein called growth hormone that signals the liver to produce a substance called insulin-like growth factor 1, or IGF 1, which in turn tells cells throughout the body to start proliferating. © 2016 The New York Times Company
By DAN BILEFSKY LONDON — The model in the Gucci ad is young and waiflike, her frail body draped in a geometric-pattern dress as she leans back in front of a wall painted with a tree branch that appears to mimic the angle of her silhouette. On Wednesday, the Advertising Standards Authority of Britain ruled that the ad was “irresponsible” and that the model looked “unhealthily thin,” fanning a perennial debate in the fashion industry over when thin is too thin. The regulator said that the way the woman in the image had posed elongated her torso and accentuated her waist, so that it appeared to be very small. It said her “somber facial expression and dark makeup, particularly around her eyes, made her face look gaunt.” It said the offending image — a still photograph of the model that appeared in an online video posted on the website of The Times of London in December — should not appear again in its current form. The specific image was removed from the video on Gucci’s YouTube channel, though the model still appears in the ad directed by Glen Luchford. The image deemed "irresponsible" by the Advertising Standards Authority of Britain appeared at the end of this online video, but has been taken out. Video by Gucci The Italian fashion brand, for its part, had defended the ad, saying it was part of a video that portrayed a dance party and that was aimed at an older and sophisticated audience. Nowhere in the ads were any models’ bones visible, it said, and they were all “toned and slim.” It noted that “it was, to some extent, a subjective issue as to whether a model looked unhealthily thin,” according to the authority. The decision by the advertising authority, an independent industry regulatory group, barred Gucci from using the image in advertisements in Britain. The ruling comes amid a longstanding debate on both sides of the Atlantic about the perils of overly thin models projecting an unhealthy body image for women. As when critics lashed out against idealized images of “heroin chic” in the early 1990s, some have voiced concern that fashion houses are encouraging potentially hazardous behaviors by glamorizing models who are rail-thin. © 2016 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 22080 - Posted: 04.07.2016
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
Link ID: 22059 - Posted: 04.01.2016
By Jordana Cepelewicz The bacteria that inhabit our guts have become key players for neuroscientists. A growing body of research links them to a wide array of mental and neurological disorders—from anxiety and depression to schizophrenia and Alzheimer’s disease. Now a study in mice published this week in Nature Medicine suggests that striking the right microbial balance could cause changes in the immune system that significantly reduce brain damage after a stroke—the second leading cause of both death and disability for people around the globe. (Scientific American is part of Springer Nature.) Experts have known for some time that stroke severity is influenced by the presence of two types of cell, found abundantly within the intestine, that calibrate immune responses: Regulatory T cells have a beneficial inflammatory effect, protecting an individual from stroke. But gamma delta T cells produce a cytokine that causes harmful inflammation after a stroke. A team of researchers at Weill Cornell Medical College and Memorial Sloan Kettering Cancer Center set about investigating whether they could tilt the balance of these cells in the favor of beneficial cells by tinkering with the body’s bacterial residents. To do so, they bred two colonies of mice: One group’s intestinal flora was resistant to antibiotics whereas the other’s gut bacteria was vulnerable to treatment. As a result, when given a combination of antibiotics over the course of two weeks, only the latter’s microbiota underwent change. The researchers then obstructed the cerebral arteries of the mice, inducing an ischemic stroke (the most common type). They found that subsequent brain damage was 60 percent smaller in the drug-susceptible mice than it was in the other group. © 2016 Scientific American,
Link ID: 22054 - Posted: 03.31.2016
Laura Sanders The 22 men took the same pill for four weeks. When interviewed, they said they felt less daily stress and their memories were sharper. The brain benefits were subtle, but the results, reported at last year’s annual meeting of the Society for Neuroscience, got attention. That’s because the pills were not a precise chemical formula synthesized by the pharmaceutical industry. The capsules were brimming with bacteria. In the ultimate PR turnaround, once-dreaded bacteria are being welcomed as health heroes. People gobble them up in probiotic yogurts, swallow pills packed with billions of bugs and recoil from hand sanitizers. Helping us nurture the microbial gardens in and on our bodies has become big business, judging by grocery store shelves. These bacteria are possibly working at more than just keeping our bodies healthy: They may be changing our minds. Recent studies have begun turning up tantalizing hints about how the bacteria living in the gut can alter the way the brain works. These findings raise a question with profound implications for mental health: Can we soothe our brains by cultivating our bacteria? By tinkering with the gut’s bacterial residents, scientists have changed the behavior of lab animals and small numbers of people. Microbial meddling has turned anxious mice bold and shy mice social. Rats inoculated with bacteria from depressed people develop signs of depression themselves. And small studies of people suggest that eating specific kinds of bacteria may change brain activity and ease anxiety. Because gut bacteria can make the very chemicals that brain cells use to communicate, the idea makes a certain amount of sense. © Society for Science & the Public 2000 - 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
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
By ERICA GOODE Their websites show peaceful scenes — young women relaxing by the ocean or caring for horses in emerald pastures — and boast of their chefs and other amenities. One center sends out invitations to a reception with cocktails and hors d’oeuvres. Another offers doctors and therapists all-expense-paid trips to visit and experience their offerings, including yoga classes. Several employ staff who call mental health professionals, saying they would love to have lunch. The marketing efforts by these for-profit residential care centers are aimed at patients with eating disorders and the clinicians who treat them. The programs have proliferated in recent years, with some companies expanding across the country. The rapid growth of the industry — there are more than 75 centers, compared with 22 a decade ago, according to one count — has been propelled by the Affordable Care Act and other changes in health insurance laws that have increased coverage for mental disorders, as well as by investments from private equity firms. The residential programs, their directors say, fill a dire need, serving patients from areas where no adequate treatment is available. “Only 15 to 30 percent of people have access to specialized care for eating disorders, which means there are a lot of people out there who have zippo,” said Doug Bunnell, the chief clinical officer for Monte Nido, a program that began in Malibu, Calif., and now operates centers in five states. But the advertising and the profusion of centers, which typically cost $1,000 a day but can run much higher, is raising concerns among some eating disorders experts, who worry that some programs may be taking advantage of vulnerable patients and their families. In the companies’ rush to expand, they argue, quality of treatment may be sacrificed for profit. And they question whether the spalike atmosphere of some programs is so comfortable that it fosters dependency. © 2016 The New York Times Company
Keyword: Anorexia & Bulimia
Link ID: 21990 - Posted: 03.15.2016
Carl Zimmer Scientists recently turned Harvard’s Skeletal Biology Laboratory into a pop-up restaurant. It would have fared very badly on Yelp. Katherine D. Zink, then a graduate student, acted as chef and waitress. First, she attached electrodes to the jaws of diners to record the activity in the muscles they use to chew food. Then she brought out the victuals. Some volunteers received a three-course vegetarian meal of carrots, yams or beets. In one course, the vegetables were cooked; in the second, they were raw and sliced; in the last course, Dr. Zink simply served raw chunks of plant matter. Other patrons got three courses of meat (goat, in this case). Dr. Zink grilled the meat in the first course, but offered it raw and sliced in the second. In the third course, her volunteers received an uncooked lump of goat flesh. In some of the trials, the volunteers chewed the food until it was ready to swallow and then spat it out. Dr. Zink painstakingly picked apart those food bits and measured their size. Every week, we'll bring you stories that capture the wonders of the human body, nature and the cosmos. “If that was all my dissertation was, I would have quit graduate school,” Dr. Zink said. “It was as lovely as it sounds.” Dr. Zink persevered, however, because she was exploring a profound question about our origins: How did our ancestors evolve from small-brained, big-jawed apes into large-brained, small-jawed humans? Scientists studying the fossil record have long puzzled over this transition, which happened around two million years ago. Before then, early human relatives — known as hominins — were typically about the size of chimpanzees, with massive teeth and a brain only a third the size of humans’ current brains. © 2016 The New York Times Company
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
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
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
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
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
Ian Sample Science editor Too little sleep may bring on a form of the marijuana “munchies”, say scientists who found that sleep-deprived people craved crisps, sweets and biscuits far more than healthier foods. The US researchers believe that skimping on sleep alters brain chemicals in much the same way as the hunger-boosting ingredient in cannabis, which has long propped up snack sales at 24-hour convenience stores. After several nights of poor sleep, healthy volunteers who took part in the study reached for snacks containing more calories - and nearly twice as much fat - than ones they favoured after sleeping well for the same period, the scientists say. When sleepy, the participants had terrible trouble resisting the snacks, even when they were full, said Erin Hanlon, who led the study at the University of Chicago. Research has shown time and again that sleep loss raises the risk of obesity, but the reasons are complex and unclear. Insufficient sleep disrupts hormones that govern appetite and satiety. But those who sleep less have more time to eat, and may be too tired to exercise. To muddy the waters further, obesity can lead to breathing problems that themselves disrupt sleep patterns. In a small study published in the journal Sleep, Hanlon invited 14 men and women in their twenties to spend two four-day sessions at the university’s clinical research centre. The volunteers’ time in bed was controlled, so that on one visit they averaged 7.5 hours of sleep a night, but on the other only 4 hours 11 minutes a night. During their stays, the volunteers ate identical meals, dished out at 9am, 2pm and 7pm.
By James Gallagher Health editor, BBC News website People who are obese have a worse memory than their thinner friends, a small study shows. Tests on 50 people showed being overweight was linked to worse "episodic memory" or the ability to remember past experiences. The study in the Quarterly Journal of Experimental Psychology argues that a less vivid memory of recent meals may lead to overeating. However, other aspects of memory - such as general knowledge - were unaffected. Tests on rats have previously shown that with burgeoning waistlines come poorer performances in memory tests, but the evidence in humans has been mixed. The latest experiments looked at episodic memory - the video tape in your mind - that remembers the smell of a cup of coffee or the feel of holding someone's hand. Fifty people with a Body Mass Index (BMI) ranging from 18 (healthy) to 51 (very obese) took part in a memory test - a bit like doing a treasure hunt on your own. They had to "hide" objects at different times and on different scenes displayed on a computer screen. They were later asked to recall what they had hidden, when and where. The results showed obese people's scores were 15% lower than thinner people. Dr Lucy Cheke, from the University of Cambridge, told the BBC News website: "The suggestion we're making is that a higher BMI is having some reduction on the vividness of memory, but they're not drawing blanks and having amnesia. "But if they have a less strong memory of a recent meal, with a less strong impact in the mind, then they may have less ability to regulate how much they eat later on." Hunger hormones play a huge role in how much we eat, but it is already recognised that our minds have a key role too. © 2016 BBC
By Roberto A. Ferdman Poverty has a way of rearing its ugly head, slipping into the cracks in people's lives when they're young and then re-emerging later in life. Sometimes it happens in ways that are easily observable—what poor babies are fed, for instance, has been shown to alter what they crave as adults, creating life-long affinities for foods that might be better left uneaten. But sometimes the influences are hidden, and all the more insidious as a result. A team of researchers, led by Sarah Hill, who teaches psychology at Texas Christian University, believe they have uncovered evidence of one such lingering effect. Specifically, Hill and her colleagues found that people who grow up poor seem to have a significantly harder time regulating their food intake, even when they aren't hungry. "We found that they eat comparably high amounts regardless of their need," said Hill. The researchers, interested in exploring why obesity is more prevalent in poorer populations, devised three separate experiments, which tested how people from different socioeconomic backgrounds behaved in front of food. In the first, they invited 31 female participants into their lab, who were asked how long it had been since they had eaten, and how hungry they were. They were then given snacks (cookies and pretzels), which they were free to eat or leave be, as they pleased. When they were finished, Hill and her team measured the number of calories each consumed. The discrepancy between how the participants ate was alarming.