by Bethany Brookshire Cheese is a delicious invention. But if you saw the news last week, you might think it’s on its way to being classified as a Schedule II drug. Headlines proclaimed “Say cheese? All the time? Maybe you have an addiction,” “Cheese really is crack” and “Your cheese addiction is real.” Under the headlines, the stories referred to a study examining the addictive properties of various foods. Pizza was at the top. The reason? The addictive properties of cheese, which the articles claim contains “dangerous” opiate-like chemicals called casomorphins. But you can’t explain away your affinity for cheese by saying you’re addicted. The study in those stories, published earlier this year in PLOS ONE, did investigate which foods are most associated with addictive-like eating behaviors. Pizza did come out on top in one experiment. But the scientists who did the research say this has little to do with the delicious dairy products involved. Instead, they argue, the foods we crave the most are those processed to have high levels of sugars and fat, and it’s these ingredients that leave us coming back for another slice. The cheese? “I was horrified by the misstatements and the oversimplifications … and the statements about how it’s an excuse to overeat,” says Ashley Gearhardt of the University of Michigan in Ann Arbor, who led the study. “Liking is not the same as addiction. We like lots of things. I like hip-hop music and sunshine and my wiener dog, but I’m not addicted to her. I eat cheese every day. That’s doesn’t mean you’re addicted or it has addictive potential.” © Society for Science & the Public 2000 - 2015

Keyword: Drug Abuse
Link ID: 21592 - Posted: 11.02.2015

By Simon Makin Most people have felt depressed or anxious, even if those feelings have never become debilitating. And how many times have you heard someone say, “I'm a little OCD”? Clearly, people intuitively think that most mental illnesses have a spectrum, ranging from mild to severe. Yet most people do not know what it feels like to hallucinate—to see or hear things that are not really there—or to have delusions, persistent notions that do not match reality. You're psychotic, or you're not, according to conventional wisdom. Evidence is growing, however, that there may be no clear dividing line. Psychiatrists have long debated whether psychosis exists on a spectrum, and researchers have been investigating the question for more than a decade now. A 2013 meta-analysis, combining much of the existing data, by Jim van Os of Maastricht University in the Netherlands and Richard Linscott of the University of Otago in New Zealand, found the prevalence of hallucinations and delusions in the general population was 7.2 percent—much higher than the 0.4 percent prevalence of schizophrenia diagnoses found in recent studies. Now the most comprehensive epidemiological study of psychotic experiences to date, published in July in JAMA Psychiatry, has given researchers the most detailed picture yet of how many people have these experiences and how frequently. The results strongly imply a spectrum—and suggest that the standard treatment for a psychotic episode might be due for an overhaul. After ruling out experiences caused by drugs or sleep, the researchers determined that 5.8 percent of the respondents had psychotic experiences. Two thirds of these people had had only one type of episode, with hallucinations being four times more common than delusions. © 2015 Scientific American

Keyword: Schizophrenia
Link ID: 21591 - Posted: 11.02.2015

By Jennie Baird Last week’s news that Sesame Street was introducing the first autistic Muppet was met in my house with a resounding, “Huh?” “But there already is an autistic Muppet,” my high-functioning 14-year-old said. “Fozzie Bear.” I had never thought of Fozzie that way, but my son had a point. Fozzie is not good at taking social cues; he doesn’t read a room well and he tends to monologue and perseverate (to repeat himself long after the need has passed). He interprets figurative language as literal — remember that fork in the road in “The Muppet Movie?” He has a verbal tic he falls back on, “wokka-wokka.” And he hates to be separated from his hat for no obvious reason. I’ve tested this theory on friends and have seen the light bulb of recognition go off every time. Of course Fozzie has autism! One friend, a mother whose son is also on the spectrum even told me her family had the exact same conversation. Sesame Street hopes children will identify with their new character Julia, described as a “friend who has autism,” and appearing, for now, only in the book “We’re Amazing 1-2-3!” There is no question, the mere presence of Julia is a positive development. But she also introduces a rarely discussed complication of autism. Let’s call it the Fozzie Conundrum. I’m particularly sensitive to the Fozzie Conundrum now that my son attends regular honors classes in a regular public high school. Naturally sociable and charismatic — and with eight years of support and interventions from a team of terrific teachers and therapists at specialized schools — he can easily “pass” as a regular, funny, quirky teenager. © 2015 The New York Times Company

Keyword: Autism
Link ID: 21590 - Posted: 11.02.2015

? Joanne Silberner Each year, nearly three times as many Americans die from suicide as from homicide. More Americans kill themselves than die from breast cancer. As Thomas Insel, longtime head of the National Institute of Mental Health, prepared to step down from his job in October, he cited the lack of progress in reducing the number of suicides as his biggest disappointment. While the homicide rate in the US has dropped 50 percent since the early 1990s, the suicide rate is higher than it was a decade ago. "That to me is unacceptable," Insel says. It hasn't been for lack of trying. The US has a national suicide hotline and there are suicide prevention programs in every state. There's screening, educational programs, and midnight walks to raise awareness. Yet over the last decade or so, the national suicide rate has increased. In 2003, the suicide rate was 10.8 per 100,000 people. In 2013, it was 12.6. An effort that began in Detroit in 2001 to treat depression, the most common cause of suicide, is offering hope. With a relentless focus on finding and treating people with depression, the Henry Ford Health System has cut the suicide rate among the people in its insurance plan dramatically. The story of the health system's success is a story of persistence, confidence, hope and a strict adherence to a very specific approach. © 2015 npr

Keyword: Depression
Link ID: 21589 - Posted: 11.02.2015

By Hanae Armitage Fake fingerprints might sound like just another ploy to fool the feds. But the world’s first artificial prints—reported today—have even cooler applications. The electronic material, which mimics the swirling designs imprinted on every finger, can sense pressure, temperature, and even sound. Though the technology has yet to be tested outside the lab, researchers say it could be key to adding sensation to artificial limbs or even enhancing the senses we already have. “It’s an interesting piece of work,” says John Rogers, materials scientist at the University of Illinois, Urbana-Champaign, who was not involved in the study. “It really adds to the toolbox of sensor types that can be integrated with the skin.” Electronic skins, known as e-skins, have been in development for years. There are several technologies used to mimic the sensations of real human skin, including sensors that can monitor health factors like pulse or temperature. But previous e-skins have been able to “feel” only two sensations: temperature and pressure. And there are additional challenges when it comes to replicating fingertips, especially when it comes to mimicking their ability to sense even miniscule changes in texture, says Hyunhyub Ko, a chemical engineer at Ulsan National Institute of Science and Technology in South Korea. So in the new study, Ko and colleagues started with a thin, flexible material with ridges and grooves much like natural fingerprints. This allowed them to create what they call a “microstructured ferroelectric skin” The e-skin’s perception of pressure, texture, and temperature all come from a highly sensitive structure called an interlocked microdome array—the tiny domes sandwiched in the bottom two layers of the e-skin, also shown in the figure below. © 2015 American Association for the Advancement of Science

Keyword: Pain & Touch; Robotics
Link ID: 21588 - Posted: 10.31.2015

Laura Sanders A fly tickling your arm hair can spark a maddening itch. Now, scientists have spotted nerve cells in mice that curb this light twiddling sensation. If humans possess similar itch-busters, the results, published in the Oct. 30 Science, could lead to treatments for the millions of people who suffer from intractable, chronic itch. For many of these people, there are currently no good options. “This is a major problem,” says clinician Gil Yosipovitch of Temple University School of Medicine in Philadelphia and director of the Temple Itch Center. The new study shows that mice handle an itch caused by a fluttery touch differently than other kinds of itch. This distinction “seems to have clinical applications that clearly open our field,” Yosipovitch says. In recent years, scientists have made progress teasing apart the pathways that carry itchy signals from skin to spinal cord to brain (SN: 11/22/2008, p. 16). But those itch signals often originate from chemicals, such as those delivered by mosquitoes. All that’s needed to spark a different sort of itch, called mechanical itch, is a light touch on the skin. The existence of this kind of itch is no surprise, Yosipovitch says. Mechanical itch may help explain why clothes or even dry, scaly skin can be itchy. The new finding came from itchy mice engineered to lack a type of nerve cell in their spinal cords. Without prompting, these mice scratched so often that they developed sore bald patches on their skin. © Society for Science & the Public 2000 - 2015

Keyword: Pain & Touch
Link ID: 21587 - Posted: 10.31.2015

Adam Cole Watch a scary movie and your skin crawls. Goose bumps have become so associated with fear that the word is synonymous with thrills and chills. But what on earth does scary have do to with chicken-skin bumps? For a long time, it wasn't well understood. Physiologically, it's fairly simple. Adrenaline stimulates tiny muscles to pull on the roots of our hairs, making them stand out from our skin. That distorts the skin, causing bumps to form. Call it horripilation, and you'll be right — bristling from cold or fear. Charles Darwin once investigated goose bumps by scaring zoo animals with a stuffed snake. He argued for the now accepted theory that goose bumps are a vestige of humanity's ancient past. Our ancestors were hairy. Goose bumps would have fluffed up their hair. When they were scared, that would have made them look bigger — and more intimidating to attackers. When they were cold, that would have trapped an insulating layer of air to keep them warm. We modern humans still get goose bumps when we're scared or cold, even though we've lost the advantage of looking scarier or staying warmer ourselves. And researchers have found that listening to classical music (or Phil Collins), seeing pictures of children or drinking a sour drink can also inspire goose bumps. There's clearly a link with emotion and reward, too. © 2015 npr

Keyword: Pain & Touch; Emotions
Link ID: 21586 - Posted: 10.31.2015

A single variation in the gene for brain-derived neurotropic factor (BDNF) may influence obesity in children and adults, according to a new study funded by the National Institutes of Health. The study suggests that a less common version of the BDNF gene may predispose people to obesity by producing lower levels of BDNF protein, a regulator of appetite, in the brain. The authors propose that boosting BDNF protein levels may offer a therapeutic strategy for people with the genetic variation, which tends to occur more frequently in African Americans and Hispanics, than in non-Hispanic Caucasians. The study is published in the journal Cell Reports. Obesity in children and adults is a serious issue in the United States, contributing to health conditions such as heart disease, stroke and type 2 diabetes. Importantly, genetic factors can predispose a person to obesity, as well as influence the effectiveness of weight-loss strategies. The body relies on cells to process and store energy, and changes in genes that regulate these functions can cause an imbalance that leads to excessive energy storage and weight gain. “The BDNF gene has previously been linked to obesity, and scientists have been working for several years to understand how changes in this particular gene may predispose people to obesity,” said Jack A. Yanovski, M.D., Ph.D., one of the study authors and an investigator at NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD). “This study explains how a single genetic change in BDNF influences obesity and may affect BDNF protein levels. Finding people with specific causes of obesity may allow us to evaluate effective, more-personalized treatments.”

Keyword: Obesity; Genes & Behavior
Link ID: 21585 - Posted: 10.31.2015

Heidi Ledford An analysis of 53 weight-loss studies that included more than 68,000 people has concluded that, despite their popularity, low-fat diets are no more effective than higher-fat diets for long-term weight loss. And overall, neither type of diet works particularly well. A year after their diets started, participants in the 53 studies were, on average, only about 5 kilograms (11 pounds) lighter. “That’s not that impressive,” says Kevin Hall, a physiologist at the US National Institute of Diabetes and Digestive and Kidney Diseases in Bethesda, Maryland. “All of these prescriptions for dieting seem to be relatively ineffective in the long term.” The study, published in The Lancet Diabetes and Endocrinology[1], runs counter to decades' worth of medical advice and adds to a growing consensus that the widespread push for low-fat diets was misguided. Nature looks at why low-fat diets were so popular and what diet doctors might prescribe next. Are the new findings a surprise? The advantages of low-fat diets have long been in question. “For decades we’ve been touting low-fat diets as the way to lose weight, but obesity has gone up,” says Deirdre Tobias, lead author of the study and an epidemiologist at Brigham and Women’s Hospital in Boston, Massachusetts. “It seemed evident that low-fat diets may not be the way to go.” © 2015 Nature Publishing Group,

Keyword: Obesity
Link ID: 21584 - Posted: 10.31.2015

By KATHARINE Q. SEELYE NEWTON, N.H. — When Courtney Griffin was using heroin, she lied, disappeared, and stole from her parents to support her $400-a-day habit. Her family paid her debts, never filed a police report and kept her addiction secret — until she was found dead last year of an overdose. At Courtney’s funeral, they decided to acknowledge the reality that redefined their lives: Their bright, beautiful daughter, just 20, who played the French horn in high school and dreamed of living in Hawaii, had been kicked out of the Marines for drugs. Eventually, she overdosed at her boyfriend’s grandmother’s house, where she died alone. “When I was a kid, junkies were the worst,” Doug Griffin, 63, Courtney’s father, recalled in their comfortable home here in southeastern New Hampshire. “I used to have an office in New York City. I saw them.” When the nation’s long-running war against drugs was defined by the crack epidemic and based in poor, predominantly black urban areas, the public response was defined by zero tolerance and stiff prison sentences. But today’s heroin crisis is different. While heroin use has climbed among all demographic groups, it has skyrocketed among whites; nearly 90 percent of those who tried heroin for the first time in the last decade were white. And the growing army of families of those lost to heroin — many of them in the suburbs and small towns — are now using their influence, anger and grief to cushion the country’s approach to drugs, from altering the language around addiction to prodding government to treat it not as a crime, but as a disease. © 2015 The New York Times Company

Keyword: Drug Abuse
Link ID: 21583 - Posted: 10.31.2015

By Diana Kwon Six years before her husband was diagnosed with Parkinson’s disease, a progressive neurodegenerative disorder marked by tremors and movement difficulties, Joy Milne detected a change in his scent. She later linked the subtle, musky odor to the disease when she joined the charity Parkinson’s UK and met others with the same, distinct smell. Being one of the most common age-related disorders, Parkinson’s affects an estimated seven million to 10 million people worldwide. Although there is currently no definitive diagnostic test, researchers hope that this newly found olfactory signature will lead help create one. Milne, a super-smeller from Perth, Scotland, wanted to share her ability with researchers. So when Tilo Kunath, a neuroscientist at the University of Edinburgh, gave a talk during a Parkinson’s UK event in 2012, she raised her hand during the Q&A session and claimed she was able to smell the disease. “I didn’t take her seriously at first,” Kunath says. “I said, ‘No, I never heard of that, next question please.’” But months later Kunath shared this anecdote with a colleague and received a surprising response. “She told me that that lady wasn’t wrong and that I should find her,” Kunath says. Once the researchers found Milne, they tested her claim by having her sniff 12 T-shirts: six that belonged to people with Parkinson’s and six from healthy individuals. Milne correctly identified 11 out of 12, but miscategorized one of the non-Parkinson’s T-shirts in the disease category. It turned out, however, she was not wrong at all—that person would be diagnosed with Parkinson’s less than a year later. © 2015 Scientific American

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 21582 - Posted: 10.31.2015

Susan Milius Electric eels are even more shocking than biologists thought. When prey fights back, eels just — curl their tails. Muscle has evolved “into a battery” independently in two groups of fishes, explains Kenneth Catania of Vanderbilt University in Nashville. Smaller species send out slight tingles of electric current that detect the fish’s surroundings in murky nighttime water. People can handle these small fishes and not feel even a tickle. But touching the bigger Electrophorus electricus (a member of a South American group of battery-included fishes)“is reminiscent of walking into an electric fence on a farm,” Catania says. (He knows, unintentionally, from experience.) The modified muscle that works as an electricity-generating organ in the eel has just on/off power. But eels have a unique way of intensifying the effect, Catania reports October 28 in Current Biology. Catania has tussled with eels using what he calls his electric eel chew toy — a dead fish on a stick with electrodes inside the carcass to measure current. When fighting difficult prey Iike the recalcitrant toy, eels curl their tails toward the fish struggling in their jaws. This bend puts the electrically negative tail-end of the long battery organ closer to the electrically positive front end, effectively concentrating the electric field on the prey. An eel’s tail curl can double the strength of the electric field convulsing the prey. © Society for Science & the Public 2000 - 2015.

Keyword: Animal Communication; Aggression
Link ID: 21581 - Posted: 10.29.2015

By Diana Kwon | In the human form of mad cow disease, called Creutzfeldt-Jakob, a person's brain deteriorates—literally developing holes that cause rapidly progressing dementia. The condition is fatal within one year in 90 percent of cases. The culprits behind the disease are prions—misfolded proteins that can induce normal proteins around them to also misfold and accumulate. Scientists have known that these self-propagating, pathological proteins cause some rare brain disorders, such as kuru in Papua New Guinea. But growing evidence suggests that prions are at play in many, if not all, neurodegenerative disorders, including Alzheimer's, Huntington's and Parkinson's, also marked by aggregations of malformed proteins. Until recently, there was no evidence that the abnormal proteins found in people who suffer from these well-known diseases could be transmitted directly from person to person. The tenor of that discussion suddenly changed this September when newly published research in the journal Nature provided the first hint such human-to-human transmission may be possible. (Scientific American is part of Springer Nature.) For the study, John Collinge, a neurologist at University College London, and his colleagues conducted autopsies on eight patients who died between the ages of 36 and 51 from Creutzfeldt-Jakob. All the subjects had acquired the disease after treatment with growth hormone later found to be contaminated with prions. The surprise came when the researchers discovered that six of the brains also bore telltale signs of Alzheimer's—in the form of clumps of beta-amyloid proteins, diagnostic for the disease—even though the patients should have been too young to exhibit such symptoms. © 2015 Scientific American,

Keyword: Prions; Alzheimers
Link ID: 21580 - Posted: 10.29.2015

By Christian Jarrett Neuroscientists, for obvious reasons, are really interested in finding out what’s different about the brains of people with unpleasant personalities, such as narcissists, or unsavory habits, like porn addiction. Their hope is that by studying these people’s brains we might learn more about the causes of bad character, and ways to helpfully intervene. Now to the list of character flaws that've received the brain-scanner treatment we can apparently add sexism — a new Japanese study published in Scientific Reports claims to have found its neurological imprint. The researchers wanted to know whether there is something different about certain individuals’ brains that potentially predisposes them to sexist beliefs and attitudes (of course, as with so much neuroscience research like this, it’s very hard to disentangle whether any observed brain differences are the cause or consequence of the trait or behavior that’s being studied, a point I’ll come back to). More specifically, they were looking to see if people who publicly endorse gender inequality have brains that are anatomically different from people who believe in gender equality. In short, it seems the answer is yes. Neuroscientist Hikaru Takeuchi at Tohoku University and his colleagues have identified two brain areas where people who hold sexist attitudes have different levels of gray-matter density (basically, a measure of how many brain cells are packed into a given area), as compared with people who profess a belief in gender equality (their study doesn’t speak to any subconsciously held sexist beliefs). What’s more, these neural differences were correlated with psychological characteristics that could help explain some people’s sexist beliefs. © 2015, New York Media LLC.

Keyword: Attention; Emotions
Link ID: 21579 - Posted: 10.29.2015

By Nicholas Bakalar Certain personality traits are often attributed to oldest, middle and youngest children. But a new study found that birth order itself had no effect on character, though it may slightly affect intelligence. Researchers analyzed three large ongoing collections of data including more than 20,000 people: a British study that follows the lives of people who were born in one particular week in 1958, a German study of private households started in 1984 and a continuing study of Americans born between 1980 and 1984. They searched for differences in extroversion, emotional stability, agreeableness, conscientiousness, self-reported intellect, IQ, imagination and openness to experience. They analyzed families with sisters and brothers, large and small age gaps and different numbers of siblings. They even looked to see if being a middle child correlated with any particular trait. But no matter how they spliced the data, they could find no association of birth order with any personality characteristic. The study, in Proceedings of the National Academy of Sciences, did find evidence that older children have a slight advantage in IQ scores, but the difference was apparent only in a large sample, with little significance for any individual. The lead author, Julia M. Rohrer, a graduate student at the University of Leipzig, said that birth order can have an effect — if your older brother bullied you, for example. “But these effects are highly idiosyncratic,” she said. “There is no such thing as a typical older, middle or younger sibling. It’s important to stop believing that you are the way you are because of birth order.” © 2015 The New York Times Company

Keyword: Development of the Brain; Intelligence
Link ID: 21578 - Posted: 10.29.2015

A drug for Alzheimer’s seems to delay the point at which a person with the condition needs to be moved into a nursing home. Donepezil is usually given to people with moderate forms of the disease, but continuing to take the drug once the disease becomes more severe seems to prolong the period of time a person can remain in their own home. Previously, the drug was not thought to benefit people once they had developed more severe forms of Alzheimer’s. But a study that followed 295 people with moderate to severe Alzheimer’s disease found that those who continued to take donepezil were nearly half as likely to end up in a care home within the next year. “It could mean thousands of patients per year not going into care homes,” says Robert Howard of University College London, who led the study. His team found that those who continued to take donepezil had a 20 per cent chance of being moved into a care home within the first year of the trial, compared to 37 per cent in those who stopped taking the drug. However the effect didn’t last. The trial lasted for three years, and after the first year, those who taking donepezil were just as likely to be moved into a home than those who weren’t, suggesting that the drug does not have a longer-term effect on the care needs of those with Alzheimer’s. “For every six patients treated with donepezil for 12 months, you would prevent one moving into a nursing home,” says Howard. “It’s a modest effect, but it’s important if it’s your mother or your wife.” © Copyright Reed Business Information Ltd.

Keyword: Alzheimers
Link ID: 21577 - Posted: 10.28.2015

Looking at brain tissue from mice, monkeys and humans, scientists have found that a molecule known as growth and differentiation factor 10 (GDF10) is a key player in repair mechanisms following stroke. The findings suggest that GDF10 may be a potential therapy for recovery after stroke. The study, published in Nature Neuroscience, was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “These findings help to elucidate the mechanisms of repair following stroke. Identifying this key protein further advances our knowledge of how the brain heals itself from the devastating effects of stroke, and may help to develop new therapeutic strategies to promote recovery,” said Francesca Bosetti, Ph.D., stroke program director at NINDS. Stroke can occur when a brain blood vessel becomes blocked, preventing nearby tissue from getting essential nutrients. When brain tissue is deprived of oxygen and nutrients, it begins to die. Once this occurs, repair mechanisms, such as axonal sprouting, are activated as the brain attempts to overcome the damage. During axonal sprouting, healthy neurons send out new projections (“sprouts”) that re-establish some of the connections lost or damaged during the stroke and form new ones, resulting in partial recovery. Before this study, it was unknown what triggered axonal sprouting. Previous studies suggested that GDF10 was involved in the early stages of axonal sprouting, but its exact role in the process was unclear. S. Thomas Carmichael, M.D., Ph.D., and his colleagues at the David Geffen School of Medicine at the University of California Los Angeles took a closer look at GDF10 to identify how it may contribute to axonal sprouting.

Keyword: Stroke; Regeneration
Link ID: 21576 - Posted: 10.28.2015

by Helen Thompson Five, six, seven, eight! All together now, let's spread those jazz hands and get moving, because synchronized dancing improves our tolerance of pain and helps us bond as humans, researchers suggest October 28 in Biology Letters. A team of psychologists at the University of Oxford taught high school students varied dance routines — each requiring different levels of exertion and synchronized movement — and then tested their pain tolerance with the sharp squeeze of a blood pressure cuff. Statistically, routines with more coordinated choreography and full body movement produced higher pain thresholds and sunny attitudes toward others in the group. Coordinated dancing with a group and exerting more energy may independently promote the release of pain-blocking endorphins as well as increase social bonding, the team writes. |© Society for Science & the Public 2000 - 2015

Keyword: Pain & Touch
Link ID: 21575 - Posted: 10.28.2015

When we hear speech, electrical waves in our brain synchronise to the rhythm of the syllables, helping us to understand what’s being said. This happens when we listen to music too, and now we know some brains are better at syncing to the beat than others. Keith Doelling at New York University and his team recorded the brain waves of musicians and non-musicians while listening to music, and found that both groups synchronised two types of low-frequency brain waves, known as delta and theta, to the rhythm of the music. Synchronising our brain waves to music helps us decode it, says Doelling. The electrical waves collect the information from continuous music and break it into smaller chunks that we can process. But for particularly slow music, the non-musicians were less able to synchronise, with some volunteers saying they couldn’t keep track of these slower rhythms. Rather than natural talent, Doelling thinks musicians are more comfortable with slower tempos because of their musical training. As part of his own musical education, he remembers being taught to break down tempo into smaller subdivisions. He suggests that grouping shorter beats together in this way is what helps musicians to process slow music better. One theory is that musicians have heard and played much more music, allowing them to acquire “meta-knowledge”, such as a better understanding of how composers structure pieces. This could help them detect a broader range of tempos, says Usha Goswami of the University of Cambridge. © Copyright Reed Business Information Ltd.

Keyword: Hearing; Learning & Memory
Link ID: 21574 - Posted: 10.27.2015

By Jan Hoffman As the first semester of the school year reaches the halfway mark, countless college freshmen are becoming aware that their clothes are feeling rather snug. While the so-called freshman 15 may be hyperbole, studies confirm that many students do put on five to 10 pounds during that first year away from home. Now new research suggests that an underlying cause for the weight gain may be the students’ widely vacillating patterns of sleep. A study in the journal Behavioral Sleep Medicine looked at the sleep habits of first-semester freshmen. Researchers followed 132 first-year students at Brown University who kept daily sleep diaries. After nine weeks, more than half of them had gained nearly six pounds. There are many poor sleep habits that might have exacerbated their weight gains, a growing body of research indicates. Was it abbreviated sleep? Optimally, experts say, teenagers need about nine hours and 15 minutes a night. These freshmen averaged about seven hours and 15 minutes. In a study earlier this year, in the journal PLOS One, researchers found that when teenagers are sleep-deprived, they more readily reach for candy and desserts. Or were the Brown students’ late bedtimes the scale-tipping factor? On average, they went to bed around 1:30 a.m. A study this month in the journal Sleep that followed teenagers into adulthood found that each hour later bedtime was pushed during the school or workweek was associated with about a two-point increase in body mass index. While both the amount of sleep and the lateness of bedtime may have played a role, the researchers in the Brown study identified a new sleep factor for predicting weight gain: variability, or the extent to which a student’s bedtime and waking time changed daily. © 2015 The New York Times Company

Keyword: Sleep; Obesity
Link ID: 21573 - Posted: 10.27.2015