By Mo Costandi The controversy began about 10 years ago, when it emerged that the National Football League had first tried to cover up evidence linking repetitive head injuries in players to chronic traumatic encephalopathy (CTE), a progressive neurodegenerative disorder, and then to discredit the scientists doing the work. Since then evidence supporting this link has grown as an increasing number of players have come forward to report that they are suffering from depression, and some have committed suicide. And yet, exactly how repetitive head injuries are linked to CTE development and the psychiatric symptoms associated with it is still a matter of debate. The largest-ever study of its kind has now given the most compelling evidence yet linking repetitive head impacts in football players to CTE. The study, published recently in JAMA The Journal of the American Medical Association, has notable limitations, however. It has also sparked calls for more research to measure the impact of head blows on players over the course of a lifetime. The new work builds on findings from 2013: neuropathologist Ann McKee of Boston University and her colleagues published a postmortem report of 68 male athletes and military veterans with CTE, in which they described a spectrum of pathological signatures associated with the condition. McKee and colleagues observed two distinct sets of clinical symptoms: one involving disturbances in mood and behavior, which was seen in the younger subjects, and the other including cognitive impairments, which developed at an older age. © 2017 Scientific American

Keyword: Brain Injury/Concussion
Link ID: 23920 - Posted: 08.05.2017

Daniel Trotta NEW YORK (Reuters) - While President Donald Trump has thrust transgender people back into the conflict between conservative and liberal values in the United States, geneticists are quietly working on a major research effort to unlock the secrets of gender identity. A consortium of five research institutions in Europe and the United States, including Vanderbilt University Medical Center, George Washington University and Boston Children's Hospital, is looking to the genome, a person's complete set of DNA, for clues about whether transgender people are born that way. Two decades of brain research have provided hints of a biological origin to being transgender, but no irrefutable conclusions. Now scientists in the consortium have embarked on what they call the largest-ever study of its kind, searching for a genetic component to explain why people assigned one gender at birth so persistently identify as the other, often from very early childhood. (reut.rs/2w3Ozg9) Researchers have extracted DNA from the blood samples of 10,000 people, 3,000 of them transgender and the rest non-transgender, or cisgender. The project is awaiting grant funding to begin the next phase: testing about 3 million markers, or variations, across the genome for all of the samples.

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 23919 - Posted: 08.05.2017

Nicola Davis A drug commonly used to treat diabetes could help those living with Parkinson’s disease, research has revealed. By 2020 it is predicted that 162,000 individuals in the UK will be living with the condition. While existing drugs help to control its symptoms, there are currently none available which slow or halt its progression. But now scientists say they have found that a drug commonly used to treat type 2 diabetes appears to improve movement-related issues. The benefit persisted even when the drug had not been taken for 12 weeks, suggesting it might be helping to slow the progression of the disease. “It is not ready for us to say ‘well, everyone needs to start this drug’,” said Thomas Foltynie, professor of neurology at University College London and co-author of the study. “[But] if we can replicate these findings in a multicentre trial, especially with longer follow-up, then this can change the face of our approach to treating Parkinson’s.” Writing in the Lancet, Foltynie and colleagues in the UK and US describe how they tested the impact of the drug, known as exenatide. With recent studies suggesting problems with insulin signalling in the brain could be linked to neurodegenerative disorders, hopes have been raised that diabetes drugs could also be used to tackle Parkinson’s, with previous research – including in cell cultures and animals, as well as a recent pilot study on humans by Foltynie and colleagues – backing up the notion.. But the latest study is the first robust clinical trial of the drug, randomly allocating 60 people with Parkinson’s to one of two treatments – either receiving injections of exenatide or a placebo once a week. © 2017 Guardian News and Media Limited

Keyword: Parkinsons
Link ID: 23918 - Posted: 08.05.2017

By JOHN SCHWARTZ The studio for what is arguably the world’s most successful online course is tucked into a corner of Barb and Phil Oakley’s basement, a converted TV room that smells faintly of cat urine. (At the end of every video session, the Oakleys pin up the green fabric that serves as the backdrop so Fluffy doesn’t ruin it.) This is where they put together “Learning How to Learn,” taken by more than 1.8 million students from 200 countries, the most ever on Coursera. The course provides practical advice on tackling daunting subjects and on beating procrastination, and the lessons engagingly blend neuroscience and common sense. Dr. Oakley, an engineering professor at Oakland University in Rochester, Mich., created the class with Terrence Sejnowski, a neuroscientist at the Salk Institute for Biological Studies, and with the University of California, San Diego. Prestigious universities have spent millions and employ hundreds of professionally trained videographers, editors and producers to create their massive open online courses, known as MOOCs. The Oakleys put together their studio with equipment that cost $5,000. They figured out what to buy by Googling “how to set up a green screen studio” and “how to set up studio lighting.” Mr. Oakley runs the camera and teleprompter. She does most of the editing. The course is free ($49 for a certificate of completion — Coursera won’t divulge how many finish). “It’s actually not rocket science,” said Dr. Oakley — but she’s careful where she says that these days. When she spoke at Harvard in 2015, she said, “the hackles went up”; she crossed her arms sternly by way of grim illustration. This is home-brew, not Harvard. And it has worked. Spectacularly. The Oakleys never could have predicted their success. Many of the early sessions had to be trashed. “I looked like a deer in the headlights,” Dr. Oakley said. She would flub her lines and moan, “I just can’t do this.” Her husband would say, “Come on. We’re going to have lunch, and we’re going to come right back to this.” But he confessed to having had doubts, too. “We were in the basement, worrying, ‘Is anybody even going to look at this?’” © 2017 The New York Times Company

Keyword: Learning & Memory
Link ID: 23917 - Posted: 08.05.2017

By Francine Russo Survivors of sexual assault who come forward often confront doubt on the part of others. Did you fight back? they are asked. Did you scream? Just as painful for them, if not more so, can be a sense of guilt and shame. Why did I not resist? they may ask themselves. Is it my fault? And to make matters worse, although the laws are in flux in various jurisdictions, active resistance can be seen as necessary for a legal or even “common sense” definition of rape. Unless it is clearly too dangerous, as when the rapist is armed, resisting is generally thought to be the “normal” reaction to sexual assault. But new research adds to the evidence debunking this common belief. According to a recent study, a majority of female rape survivors who visited the Emergency Clinic for Rape Victims in Stockholm reported they did not fight back. Many also did not yell for help. During the assault they experienced a kind of temporary paralysis called tonic immobility. And those who experienced extreme tonic immobility were twice as likely to suffer post-traumatic stress disorder (PTSD) and three times more likely to suffer severe depression in the months after the attack than women who did not have this response. Tonic immobility (TI) describes a state of involuntary paralysis in which individuals cannot move or, in many cases, even speak. In animals this reaction is considered an evolutionary adaptive defense to an attack by a predator when other forms of defense are not possible. Much less is known about this phenomenon in humans, although it has been observed in soldiers in battle as well as in survivors of sexual assault. A study from 2005, for example, found 52 percent of female undergraduates who reported childhood sexual abuse said they experienced this paralysis. © 2017 Scientific American

Keyword: Stress
Link ID: 23916 - Posted: 08.05.2017

Eojin Choi It seems simple enough: Your task is to trace lines with your computer mouse while listening to soothing music, drawing the branches of a neuron. You can rotate the block where the spidery neuron is embedded, and zoom in to see the details. It’s fascinating stuff, if you think about how you’re piecing together the parts and wires of your brain. But as you follow faint signals consisting of blurry white dots, you realize that this game is less connect-the-dots, more hide-and-seek -- it’s often about guessing where the branches lead and erasing mistakes in the process, wondering if your work is even remotely correct. Even if you feel like you’re failing, though, you keep trying for one heartening reason: you’re helping advance brain science. And you're at the forefront of a 21st century trend: "citizen science" initiatives that use data from game players to further ongoing research, including brain research. This neuron-tracing game is called "Mozak," the Serbo-Croatian word for brain, and is among the latest entries in this category. Created by the Allen Institute for Brain Science and the Center for Game Science, the free online game has attracted around 2,500 players since its release last November. They're helping to fill a major scientific gap: We still don't really understand how neuron circuits in our brain are structured or how they work. From images of 3-D neurons inside living brain tissue, players can trace and reconstruct shapes of human and mouse neurons, which can then be classified and studied. This information may eventually help scientists understand and develop cures for brain diseases like Alzheimer’s. © Copyright WBUR 2017

Keyword: Brain imaging
Link ID: 23915 - Posted: 08.05.2017

Shirley S. Wang Efforts to develop a treatment that stalls the memory-robbing devastation of Alzheimer's disease have so far been unsuccessful, but scientists are making strides in another important area: the development of better tests to tell who has the condition. Their aim is to develop more accurate, cheaper and less invasive tests to detect the biological markers of Alzheimer's-induced changes in the brain. At the recent Alzheimer's Association International Conference in London, scientists presented early but promising data on a new blood test and a novel brain imaging technique. They also unveiled preliminary data on a study to investigate the potential clinical usefulness of a test that's already on the market but isn't widely reimbursed by insurance. Alzheimer's is characterized by changes to the brain involving clumping of a protein called amyloid and another called tau — pathologies that until the last decade or so could only be seen upon autopsy. The biomarker tests available to date focus primarily on detecting amyloid. These tests are generally used only for research purposes because they can be expensive or require special technology. They are meant to be used for ruling out Alzheimer's in patients who already have memory problems. Less invasive, easier to use and cheaper technologies may mean that more people could have access to testing. For public health, this could mean being able to more broadly screen the population to identify people who are at high-risk for getting the illness and then focusing more expensive, involved efforts for testing, prevention and treatment on them. © 2017 npr

Keyword: Alzheimers
Link ID: 23914 - Posted: 08.05.2017

By Knvul Sheikh The brain has evolved to recognize and remember many different faces. We can instantly identify a friend's countenance among dozens in a crowded restaurant or on a busy street. And a brief glance tells us whether that person is excited or angry, happy or sad. Brain-imaging studies have revealed that several blueberry-size regions in the temporal lobe—the area under the temple—specialize in responding to faces. Neuroscientists call these areas “face patches.” But neither brain scans nor clinical studies of patients with implanted electrodes explained exactly how the cells in these patches work. Now, using a combination of brain imaging and single-neuron recording in macaques, biologist Doris Tsao and her colleagues at the California Institute of Technology appear to have finally cracked the neural code for primate face recognition. The researchers found the firing rate of each face patch cell corresponds to a separate facial feature. Like a set of dials, the cells can be fine-tuned to respond to bits of information, which they can then combine in various ways to create an image of every face the animal encounters. “This was mind-blowing,” Tsao says. “The values of each dial are so predictable that we can re-create the face that a monkey sees by simply tracking the electrical activity of its face cells.” Previous studies had hinted at the specificity of these brain areas for encoding faces. In the early 2000s, when Tsao was a postdoctoral researcher at Harvard Medical School, she and electrophysiologist Winrich Freiwald showed that neurons in a monkey's face patches would fire electrical signals every time the animal saw pictures of a face. But the same brain cells showed little or no response to other objects, such as images of vegetables, radios or nonfacial body parts. Other experiments indicated that neurons in these regions could also distinguish among individual faces, even if they were cartoons. © 2017 Scientific American

Keyword: Attention
Link ID: 23913 - Posted: 08.03.2017

/ By Deborah Blum I’m hesitating over this one question I want to ask the scientist on the phone, a federal researcher studying the health effects of soy formula on infants. I worry that it’s going to sound slightly Dr. Frankenstein-esque. Finally, I spill it out anyway: “Are we talking about a kind of accidental experiment in altering child development?” The line goes briefly silent. “I’m a little worried about the word ‘experiment,’” replies Jack Taylor, a senior investigator at the National Institute of Environmental Health Sciences, a division of the National Institutes of Health. Taylor and his colleagues in North Carolina have been comparing developmental changes in babies fed soy formula, cow-milk formula, and breastmilk. His group’s most recent paper, “Soy Formula and Epigenetic Modifications,” reported that soy-fed infant girls show some distinct genetic changes in vaginal cells, possibly “associated with decreased expression of an estrogen-responsive gene.” But his first reaction is that my phrasing would, incorrectly, “make it sound like we were giving children a bad drug on purpose.” The research group, he emphasizes, is merely comparing the health of infants after their parents independently choose a preferred feeding method. No one is forcing soy formula on innocent infants. “No, no, that’s not what I meant,” I explain with some hurry. “I wasn’t suggesting that you were experimenting on children.” Rather, I was wondering whether we as a culture, with our fondness for all things soy, have created a kind of inadvertent national study. Soy accounts for about 12 percent of the U.S. formula market and I’ve become increasingly curious about what this means. Because the science does seem to suggest that we are rather casually testing the effect of plant hormones on human development, most effectively by feeding infants a constant diet of a food rich in such compounds. Copyright 2017 Undark

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 23912 - Posted: 08.03.2017

By Stefania De Vito, Sergio Della Sala On Saturday, December 4, 1926, a green Morris Cowley stood abandoned in a roadside ditch near the city of Guildford, England. The car belonged to the renowned author Agatha Christie, who had apparently disappeared without a trace. But 11 days later she turned up in a hotel in Harrogate, a spa town in Yorkshire about 240 miles north of Guildford. Christie was unable to explain what had transpired during the intervening time period; nor is this mysterious episode mentioned in her autobiography. Unlike those in her many books, this mystery remains unsolved. Is it possible that Christie suffered from what is called retrograde amnesia as a result of an automobile accident, and was no longer capable of remembering the event? Was she, by disappearing, perhaps exacting revenge on her unfaithful husband? Or was this just a clever public relations ploy aimed at promoting her latest novel? The drama began in April 1926, when Christie’s mother died. According to Christie’s biographer Janet Morgan, the death hit her very hard. At the time her husband, Col. Archibald Christie, known as Archie, was on a business trip to Spain. On returning, he informed his psychologically fragile wife that he had fallen in love with a woman named Nancy Neele. For awhile the Christies stayed together for their daughter’s sake, even moving together to Styles, her house in Sunningdale, Berkshire. All the while, however, Archie maintained his affair with Nancy. © 2017 Scientific American

Keyword: Learning & Memory
Link ID: 23911 - Posted: 08.03.2017

By Mitch Leslie Prions are insidious proteins that spread like infectious agents and trigger fatal conditions such as mad cow disease. A protein implicated in diabetes, a new study suggests, shares some similarities with these villains. Researchers transmitted diabetes from one mouse to another just by injecting the animals with this protein. The results don’t indicate that diabetes is contagious like a cold, but blood transfusions, or even food, may spread the disease. The work is “very exciting” and “well-documented” for showing that the protein has some prionlike behavior, says prion biologist Witold Surewicz of Case Western Reserve University in Cleveland, Ohio, who wasn’t connected to the research. However, he cautions against jumping to the conclusion that diabetes spreads from person to person. The study raises that possibility, he says, but “it remains to be determined.” Prions are misfolded proteins that can cause normally folded versions of the same protein to misfold themselves. When this conversion occurs in the brain, the distorted proteins bunch up inside cells and kill them. Although prion diseases are rare in people, they share some similarities with more common illnesses. In Alzheimer’s disease, for instance, globs of a misshapen protein known as β amyloid build up in the brain. Parkinson’s disease and Huntington disease, two other brain maladies, also feature aggregates, or lumps of misfolded proteins. © 2017 American Association for the Advancement of Science.

Keyword: Obesity; Prions
Link ID: 23910 - Posted: 08.02.2017

Obese people aren’t able to regulate the way body fat is stored or burned because a “switch” in their brain stays on all the time, a new study by Australian researchers has shown. Specialised fat cells called adipocytes are switched back and forth from brown cells, which are energy burning, to white, which store energy. The study, published on Wednesday in Cell Metabolism, showed that after a meal the brain responds to insulin when sugars spike by sending signals to promote the browning of fat to expend energy. Then, after a fast, the brain instructs these browned cells to convert back to white adipocytes, again storing energy. The brain’s ability to sense insulin and coordinate feeding with burning energy is controlled by a switch-like mechanism, researchers from the metabolic disease and obesity program at Monash University say. “What happens in the context of obesity is that the switch stays on all the time – it doesn’t turn on off during feeding,” said the lead researcher, Prof Tony Tiganis. “As a consequence, browning is turned off all the time and energy expenditure is decreased all the time, so when you eat, you don’t see a commensurate increase in energy expenditure – and that promotes weight gain.” Researchers are exploring the possibility of inhibiting the switch to aid weight loss but they say any therapy is “a long way off”. © 2017 Guardian News and Media Limited

Keyword: Obesity
Link ID: 23909 - Posted: 08.02.2017

By DAVID C. ROBERTS Five years ago, I still lived a double life. I was 35, looking out over the Gulf of Thailand and a few weathered beach tenders. Inside, where dark suits filled the conference room, I could feel the eyes of my fellow diplomats. No doubt they were wondering why I was sitting on my briefcase. I joked to no one in particular “My nuclear codes,” trying to deflect awkwardness. The case actually concealed an orthotic sitting cushion that muffled the pain in my lower back; without it, silent shrieking was all I heard. Or maybe they had noticed I was the only one sweating. The air-conditioning tempered the tropical heat, but it was no match for the corset heat wrap that lay discreetly under my tailored suit. Over the previous decade I had become adept at hiding the unexplained pain that racked my back and joints. To all appearances, I was a fit 6-foot-3 man with an easy gait. No one in that conference room knew my suit pants disguised a lace-up ankle brace and a strap velcroed around my left knee. Nor did they know that during breaks I would sneak back to my hotel room where my wife, an artist who moonlighted as my one-person pit crew, waited to press my quadratus lumborum muscle back into submission. I lasted through that meeting as I had through countless others. But in the months that followed, sitting and walking became increasingly difficult. I started to stand during meetings, avoid plane travel, and take motorcycle taxis to go just a couple of buildings’ distance. Eventually, I let the doctors at the embassy in on my secret. They deemed me unfit for work and medevac’ed me from Bangkok back to the United States for treatment. I left quickly, without awkward explanations or goodbyes. © 2017 The New York Times Company

Keyword: Pain & Touch
Link ID: 23908 - Posted: 08.02.2017

by Kate Travis Nearly 5 percent of U.S. adults misused prescription opioids in 2015, a new study shows. Based on the National Survey on Drug Use and Health, an in-person survey of more than 50,000 people, researchers estimated that 91.8 million, or 37.8 percent, of adults used prescription opioids in 2015. Some 11.5 million people misused the painkillers and 1.9 million people reported opioid dependence or abuse, Beth Han of the Substance Abuse and Mental Health Services Administration in Rockville, Md., and colleagues report online August 1 in Annals of Internal Medicine. Among people reporting opioid misuse, nearly 60 percent used the painkillers without a prescription, 22 percent took a bigger dose than prescribed, about 15 percent used them more frequently than directed, and 13 percent of people used them for longer than directed. Relieving pain was the most commonly cited reason for misusing opioids — for 66 percent of people reporting misuse and nearly 49 percent of those with opioid dependence or abuse. These results underscore the urgent need for better approaches to pain management, the authors conclude. As part of the efforts to curb the nation’s opioid epidemic — and pain problem — scientists are searching for safer opioids and opioid alternatives. Misuse motivators Pain relief was the top reason cited for misusing or abusing opioid painkillers. Other reasons included to relax, sleep or get high. B. Han et al/Annals of Internal Medicine 2017 © Society for Science & the Public 2000 - 2017.

Keyword: Drug Abuse
Link ID: 23907 - Posted: 08.02.2017

By Ryan Cross Researchers have discovered tell-tale signs of Alzheimer’s disease in 20 elderly chimpanzee brains, rekindling a decades-old debate over whether humans are the only species that develop the debilitating condition. Whether chimps actually succumb to Alzheimer’s or are immune from symptoms despite having the key brain abnormalities is not clear. But either way, the work suggests that chimps could help scientists better understand the disease and how to fight it—if they could get permission to do such studies on these now-endangered animals. A definitive diagnosis of Alzheimer’s includes dementia and two distortions in the brain: amyloid plaques, sticky accumulations of misfolded pieces of protein known as amyloid beta peptides; and neurofibrillary tangles, formed when proteins called tau clump into long filaments that twist around each other like ribbons. Many other primates including rhesus monkeys, baboons, and gorillas also acquire plaques with aging, but tau tangles are either absent in those species or don’t fully resemble those seen in humans. In the new study, researchers led by biological anthropologist Mary Ann Raghanti at Kent State University in Ohio turned to our closest relative, chimpanzees. In 2015, the U.S. Fish and Wildlife Service declared all U.S. chimps endangered, effectively ending all invasive research on them. But thanks to a newly founded center that collects brains from chimps that die at zoos or research centers, the team was able to examine the brains of 20 chimps aged 37 to 62—the oldest recorded age for a chimp, roughly equivalent to a human at the age of 120. Of these chimps, 13 had amyloid plaques, and four also had the neurofibrillary tangles typical of more advanced stages of Alzheimer’s in humans, the team writes [DATE TK] in Neurobiology of Aging. © 2017 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 23906 - Posted: 08.01.2017

Laura Sanders The company mice keep can change their behavior. In some ways, genetically normal littermates behave like mice that carry an autism-related mutation, despite not having the mutation themselves, scientists report. The results, published July 31 in eNeuro, suggest that the social environment influences behavior in complex and important ways, says neuroscientist Alice Luo Clayton of the Simons Foundation Autism Research Initiative in New York City. The finding comes from looking past the mutated mice to their nonmutated littermates, which are usually not a subject of scrutiny. “People almost never look at it from that direction,” says Clayton, who wasn’t involved in the study. Researchers initially planned to investigate the social behavior of mice that carried a mutation found in some people with autism. Studying nonmutated mice wasn’t part of the plan. “We stumbled into this,” says study coauthor Stéphane Baudouin, a neurobiologist at Cardiff University in Wales. Baudouin and colleagues studied groups of mice that had been genetically modified to lack neuroligin-3, a gene that is mutated in some people with autism. Without the gene, the mice didn’t have Neuroligin-3 in their brains, a protein that helps nerve cells communicate. Along with other behavioral quirks, these mice didn’t show interest in sniffing other mice, as expected. But Baudouin noticed that the behavior of the nonmutated control mice who lived with the neuroligin-3 mutants also seemed off. He suspected that the behavior of the mutated mice might be to blame. |© Society for Science & the Public 2000 - 2017.

Keyword: Autism; Genes & Behavior
Link ID: 23905 - Posted: 08.01.2017

Emily Siner The Grand Ole Opry in Nashville, Tenn., is country music's Holy Land. It's home to the weekly radio show that put country music on the national map in 1925. And it's where this summer, 30 people with Williams syndrome eagerly arrived backstage. Williams syndrome is a rare genetic disorder that can cause developmental disabilities. People with the condition are often known for their outgoing personalities and their profound love of music. Scientists are still trying to figure out where this musical affinity comes from and how it can help them overcome their challenges. That's why 12 years ago, researchers at Vanderbilt University set up a summer camp for people with Williams syndrome. For a week every summer, campers come to Nashville to immerse themselves in country music and participate in cutting-edge research. This isn't the only summer camp for people with Williams syndrome, but it is unique in its distinctive country flair. It's organized by the Vanderbilt Kennedy Center, whose faculty and staff focus on developmental disabilities. Eight years ago, the Academy of Country Music's philanthropic arm, ACM Lifting Lives, started funding the program. Campers spend the week meeting musicians and visiting recording studios, even writing an original song. This year, they teamed up with one of country's hottest stars, Dierks Bentley, on that. And they get a backstage tour of the Grand Ole Opry led by Clancey Hopper, who has Williams syndrome herself and attended the Nashville camp for eight years before applying for a job at the Opry. © 2017 npr

Keyword: Language; Development of the Brain
Link ID: 23904 - Posted: 08.01.2017

By Ariana Eunjung Cha By now, the connection between sleep and weight gain has been well established. Numerous studies have provided evidence that sleeping too little — less than five hours — messes with your hormones, slows down your metabolism and reprograms your body to eat more. But just how serious are the consequences in terms of numbers? A new study published in PLOS One takes a stab at this question by studying the relationship between sleep duration and a number of quantifiable factors: waist circumference, blood pressure, lipids, glucose, thyroid hormones and other important measures of a person's metabolic profile. The research, led by the Leeds Institute of Cardiovascular and Metabolic Medicine and the School of Food Science and Nutrition, involved 1,615 people ages 19 to 65 in Great Britain. The most striking suggestion was that getting insufficient sleep may make you go up a clothing size. People in the study who were sleeping an average of six hours each night had waist measurements about 1.2 inches (or 3 centimeters) more than those getting nine hours of sleep a night. Those with less sleep also weighed more. The relationship between more sleep and smaller waists and a lower body mass index (BMI) appeared to be almost linear, as shown below. The findings appear to contradict other studies that show that too much sleep — nine hours or more — might have a similar impact on the body as too little sleep. This new study appears to show that waist circumference and BMI are lowest for those with 12 hours of sleep. The theory of why this relationship exists has to do with two hormones that help tell you when to eat and when to stop. Less sleep upsets the balance, making you eat more. Combine that with the slower metabolism that people with lack of sleep appear to have it's no wonder that people are prone to becoming larger and gaining weight. © 1996-2017 The Washington Post

Keyword: Sleep; Obesity
Link ID: 23903 - Posted: 08.01.2017

By Giorgia Guglielmi After a 5-month road trip across Asia in 2010, 22-year-old college graduate Matthew Lazell-Fairman started feeling constantly tired, his muscles sore and head aching. A doctor recommended getting a gym membership, but after the first training session, Lazell-Fairman’s body crashed: He was so exhausted he couldn’t go to work as a paralegal for the Federal Trade Commission in Washington, D.C., for days. Lazell-Fairman has never fully recovered. He can now do a few hours of light activity—cooking, for example—per day but has to spend the rest of his time lying flat in bed. Lazell-Fairman is among the estimated 17 million people worldwide with chronic fatigue syndrome (CFS), a disease whose trigger is unknown and for which there are neither standard diagnostic tools nor effective treatments. In the largest study of its kind, researchers have now found that the blood levels of immune molecules that cause flulike symptoms such as fever and fatigue track the severity of symptoms in people who have received a diagnosis of CFS. The results may provide insight into the cause of the mysterious illness, or at least provide a way of gauging its progress and evaluating treatments. “This work is another strong piece of evidence that there is a biologic dysfunction at the root of the disease,” says Mady Hornig, a physician scientist at Columbia University whose research has also identified potential biomarkers for CFS. © 2017 American Association for the Advancement of Science.

Keyword: Depression; Neuroimmunology
Link ID: 23902 - Posted: 08.01.2017

Ashlie Stevens Ah, the brain freeze — the signature pain of summer experienced by anyone who has eaten an ice cream cone with too much enthusiasm or slurped down a slushie a little too quickly. But have you ever stopped mid-freeze to think about why our bodies react like this? Well, researchers who study pain have, and some, like Dr. Kris Rau of the University of Louisville in Kentucky, say it's a good way to understand the basics of how we process damaging stimuli. But first, a lesson in terminology. "There's a scientific medical term for ice cream headaches which is sphenopalatine ganglion neuralgia," Rau says. Try breaking that out at your next ice cream social. Anyway, to understand how brain freeze happens, it helps to think of your body and brain as a big computer where everything is hooked together. In this case, you see an ice cream truck. You get some ice cream. And then your brain gives you the go-ahead and you dive face-first into a double-scoop of mint chocolate chip. "Now on the roof of your mouth there are a lot of little blood vessels, capillaries," Rau says. "And there's a lot of nerve fibers called nociceptors that detect painful or noxious stimuli." The rush of cold causes those vessels to constrict. "And when that happens, it happens so quickly that all of those little pain fibers in the roof of your mouth — they interpret that as being a painful stimulus," Rau says. A message is then shot up to your brain via the trigeminal nerve, one of the major nerves of the facial area. The brain itself doesn't have any pain sensing fibers, but its covering — called the meninges — does. © 2017 npr

Keyword: Pain & Touch
Link ID: 23901 - Posted: 08.01.2017