/ 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

By JANE E. BRODY Putting carboxymethylcellulose sodium in one’s eyes two, three or more times a day may not sound like a great experience. But I can assure you that it can be. Drops of this chemical, called a topical lubricant, help to keep my eyes from burning, avoiding bright lights, becoming red and itchy, and generally feeling miserable. Like tens of millions of Americans, especially women older than 50, I have dry eye disease, medically known as keratoconjunctivitis sicca. Fortunately, my problem is not severe, certainly not as bad as that of an elderly woman I know who has to use a nightly ointment of mineral oil and Vaseline, which minimizes the dryness but temporarily blurs her vision. The drops I use, an over-the-counter preservative-free product called Refresh Plus (also sold as generic store brands) that I carry with me at all times, are a crucial measure I take to keep my eyes from becoming overly dry and chronically irritated — but not the only one. To minimize the drying effect of wind when driving, cycling or sitting in a room cooled by a fan or air-conditioning, I wear wraparound glasses even when I don’t need them to see clearly. Watertight goggles are de rigueur when swimming, even in fresh water. And I refresh my eyes with drops when I watch a movie, work long hours at the computer, or do any activity that depresses the frequency of blinking, which moistens the eyes. Dry eye is sometimes referred to as “a nuisance complaint — it’s not the sexiest of eye problems,” Dr. Rachel Bishop, chief consulting ophthalmologist at the National Eye Institute, told me. Nonetheless, she said, “Dry eye disease deserves serious professional — and personal — attention. It can be very debilitating and seriously diminish a person’s quality of life.” Tears serve a variety of functions, which accounts for the kinds of complications their deficiency can cause. They lubricate the eye, supply it with nutrients and oxygen, and help to focus images and clear the eye of debris. © 2017 The New York Times Company

Keyword: Vision
Link ID: 23900 - Posted: 08.01.2017

By Leslie Nemo, Liz Tormes Gray, white and wet, an image of the brain by itself can repulse more often than inspire. But when researchers and artists look past its outward appearance, they can reveal thrilling images of the organ that the rest of us would otherwise never see. Though many of these images resulted from lab work and research into how our nervous system functions, they easily stand alone as art—clearly a neuroscience degree is not necessary to appreciate the brain’s intricacies. For the seventh year in a row, the Art of Neuroscience competition out of the Netherlands Institute for Neuroscience in Amsterdam asked researchers and artists to submit their paintings, renderings, magnifications and videos of animal brains. The committee’s winning entry and honorable mentions are presented below, along with a selection of Scientific American editors’ favorites. © 2017 Scientific American

Keyword: Brain imaging
Link ID: 23899 - Posted: 08.01.2017

By Harrison Smith Marian Diamond, a pathbreaking neuroscientist whose research — including a study of Albert Einstein’s preserved brain — showed that the body’s three-pound seat of consciousness was a dynamic structure of beautiful complexity, capable of development even in old age, died July 25 at an assisted-living community in Oakland, Calif. She was 90. A daughter, Ann Diamond, confirmed her death but did not know the cause. Dr. Diamond, a professor emerita of integrative biology at the University of California at Berkeley, was for decades known on campus as the woman with the hat box. Inside the container, decorated on the outside with a floral print and carried by a bright blue string, was a preserved human brain. It was the crucial prop for a lesson she spent a half century teaching: that the brain was, as she once wrote, “the most complex mass of protoplasm on this earth and, perhaps, in our galaxy.” Dr. Diamond was considered a foundational figure in modern neuroscience. Crucially, she provided the first hard evidence demonstrating the brain’s plasticity — its ability to develop, to grow, even in adulthood. “In doing so,” her colleague George Brooks said in a statement, “she shattered the old paradigm of understanding the brain as a static and unchangeable entity that simply degenerated as we age.” Her breakthrough occurred in the early 1960s, when — building on the work of psychologist Donald O. Hebb — she began studying the brains of lab rats. Rats that were raised alone, in small and desolate cages, had more trouble navigating a maze than did rats that were raised in “enriched” cages, with toys and rat playmates. © 1996-2017 The Washington Post

Keyword: Learning & Memory
Link ID: 23898 - Posted: 08.01.2017

By CADE METZ SAN FRANCISCO — Dawn Jewell recently treated a patient haunted by a car crash. The patient had developed acute anxiety over the cross streets where the crash occurred, unable to drive a route that carried so many painful memories. So Dr. Jewell, a psychologist in Colorado, treated the patient through a technique called exposure therapy, providing emotional guidance as they revisited the intersection together. But they did not physically return to the site. They revisited it through virtual reality. Dr. Jewell is among a handful of psychologists testing a new service from a Silicon Valley start-up called Limbix that offers exposure therapy through Daydream View, the Google headset that works in tandem with a smartphone. “It provides exposure in a way that patients feel safe,” she said. “We can go to a location together, and the patient can tell me what they’re feeling and what they’re thinking.” The service recreates outdoor locations by tapping into another Google product, Street View, a vast online database of photos that delivers panoramic scenes of roadways and other locations around the world. Using these virtual street scenes, Dr. Jewell has treated a second patient who struggled with anxiety after being injured by another person outside a local building. The service is also designed to provide treatment in other ways, like taking patients to the top of a virtual skyscraper so they can face a fear of heights or to a virtual bar so they can address an alcohol addiction. Backed by the venture capital firm Sequoia Capital, Limbix is less than a year old. The creators of its new service, including its chief executive and co-founder, Benjamin Lewis, worked in the seminal virtual reality efforts at Google and Facebook. © 2017 The New York Times Company

Keyword: Learning & Memory; Emotions
Link ID: 23897 - Posted: 07.31.2017

By Robert Sanders, Media relations Marian Cleeves Diamond, one of the founders of modern neuroscience who was the first to show that the brain can change with experience and improve with enrichment, and who discovered evidence of this in the brain of Albert Einstein, died July 25 at the age of 90 in Oakland. A professor emerita of integrative biology at the University of California, Berkeley, Diamond achieved celebrity in 1984 when she examined preserved slices of Einstein’s brain, finding that he had more support cells in the brain than average. Her main claim to fame, however, came from work on rats, in which she showed that an enriched environment — toys and companions — changed the anatomy of the brain. The implication was that the brains of all animals, including humans, benefit from an enriched environment, and that impoverished environments can lower the capacity to learn. “Her research demonstrated the impact of enrichment on brain development — a simple but powerful new understanding that has literally changed the world, from how we think about ourselves to how we raise our children,” said UC Berkeley colleague George Brooks, a professor of integrative biology. “Dr. Diamond showed anatomically, for the first time, what we now call plasticity of the brain. In doing so she shattered the old paradigm of understanding the brain as a static and unchangeable entity that simply degenerated as we age. ” Her results were initially resisted by some neuroscientists. At one meeting, she later recalled, a man stood up after her talk and said loudly, “Young lady, that brain cannot change!” © 2017 UC Regents

Keyword: Learning & Memory
Link ID: 23896 - Posted: 07.31.2017

Jon Hamilton The human brain knows what it knows. And so, it appears, does a rat brain. Rats have shown that they have the ability to monitor the strength of their own memories, researchers from Providence College reported this month in the journal Animal Cognition. Brain scientists call this sort of ability metacognition. It's a concept that became famous in 2002, when then Secretary of Defense Donald Rumsfeld explained to reporters: There are known knowns. There are things we know we know. We also know there are known unknowns; that is to say we know there are some things we do not know. Rumsfeld wasn't talking about rats. But he could have been, says Michael Beran, a comparative psychologist and associate professor at Georgia State University who was not part of the research. The new study of rats offers "consistent and clear evidence that they have these glimmerings of metacognitive monitoring," Beran says. The finding suggests an ancient evolutionary path that eventually led to humans' highly developed ability to monitor their own thoughts. It also suggests that rats could be valuable animal models for studying diseases like Alzheimer's, which erode metacognition. The study focused on a type of metacognition called metamemory. It's something we depend on to get through the day, says Victoria Templer, the study's lead author and an assistant professor in the psychology department at Providence College. © 2017 npr

Keyword: Learning & Memory
Link ID: 23895 - Posted: 07.29.2017

By Helen Thomson Have you recently arrived at work naked or turned up for an exam without revising? If you want to avoid having nightmares like these, it might be best to get less than 9 hours’ sleep a night. People often have nightmares following upsetting events, and research into nightmares has mostly focused on people with conditions like post-traumatic stress disorder (PTSD). But most people get nightmares at some point, prompting Stephanie Rek at the University of Oxford and her colleagues to perform one of the largest ever studies of nightmares in the general population. Discover the new science of sleep and dreaming: Learn more at New Scientist Live in London The team recruited 846 people through media advertisements and databases of people interested in sleep studies, and asked them to complete an online survey. The participants were asked questions such as how many nightmares they had experienced over the past two weeks, and how bad they were. These answers contributed to an overall score on a “nightmare severity scale”. Each volunteer was also assessed for PTSD and asked about other aspects of their life, such as recent divorces or legal trouble, their tendency to worry, how much sleep they get and how much alcohol they drink. © Copyright New Scientist Ltd.

Keyword: Sleep
Link ID: 23894 - Posted: 07.29.2017

By Laurie McGinley and William Wan An electronic cigarette is demonstrated in Chicago. (AP Photo/Nam Y. Huh, File) The Food and Drug Administration said Friday it wants to reduce the nicotine in cigarettes to make them less addictive. The unexpected announcement sent shares of tobacco companies plummeting and sparked praise among some public health advocates. If successful, the effort would be the first time the government has tried to get the Americans to quit cigarettes by reaching beyond warning labels or taxes to attacking the actual addictive substance inside. The FDA rolled out a second major announcement at the same time: It is delaying for several years a key regulation affecting cigars and e-cigarettes, including flavored vaping products that studies show are especially enticing to youth. Specifically, it postponed the requirement that such products be approved by the agency. FDA’s commissioner Scott Gottlieb said both actions are part of a comprehensive plan to eventually wean smokers off conventional cigarettes and steer them toward less harmful alternative forms of nicotine like vaping. “The overwhelming amount of death and disease attributable to tobacco is caused by addiction to cigarettes — the only legal consumer product that, when used as intended, will kill half of all long-term users,” he said. Some health proponents, however, expressed caution, pointing out that the nicotine-reduction proposal could take years to enact and could be derailed by major hurdles, including the significant lobbying power of tobacco industry. © 1996-2017 The Washington Post

Keyword: Drug Abuse
Link ID: 23893 - Posted: 07.29.2017