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By Maia Szalavitz Both the FDA and the CDC have recently taken steps to address an epidemic of opioid overdose and addiction, which is now killing some 29,000 Americans each year. But these regulatory efforts will fail unless we acknowledge that the problem is actually driven by illicit—not medical—drug use. You’ve probably read that 80 percent of heroin users started with prescription medications—and you may have seen billboards that compare giving pain medication to children to giving them heroin. You have probably also heard and seen media stories of people with addiction who blame their problem on medical use. But the simple reality is this: According to the large, annually repeated and representative National Survey on Drug Use and Health, 75 percent of all opioid misuse starts with people using medication that wasn’t prescribed for them—obtained from a friend, family member or dealer. And 90 percent of all addictions—no matter what the drug—start in the adolescent and young adult years. Typically, young people who misuse prescription opioids are heavy users of alcohol and other drugs. This type of drug use, not medical treatment with opioids, is by far the greatest risk factor for opioid addiction, according to a study by Richard Miech of the University of Michigan and his colleagues. For this research, the authors analyzed data from the nationally representative Monitoring the Future survey, which includes thousands of students. While medical use of opioids among students who were strongly opposed to alcohol and other drugs did raise later risk for misuse, the overall risk for this group remained small and their actual misuse occurred less than five times a year. In other words, it wasn’t actually addiction. Given that these teens had generally rejected experimenting with drugs, an increased risk of misuse associated with medical care makes sense since they’d otherwise have no source of exposure. © 2016 Scientific American

Keyword: Drug Abuse
Link ID: 22202 - Posted: 05.11.2016

Aaron E. Carroll People get hooked on cigarettes, and enjoy them for that matter, because of the nicotine buzz. The nicotine doesn’t give them cancer and lung disease, though. It’s the tar and other chemicals that do the real harm. A robust debate is going on among public health officials over whether electronic cigarettes, or e-cigarettes, can alleviate the harms of smoking tobacco, or whether they should be treated as negatively as conventional cigarettes. In other countries, such as Britain, officials are more in favor of e-cigarettes, encouraging smokers to switch from conventional to electronic. Last week, the Food and Drug Administration issued new rules on e-cigarettes, banning their sale to anyone under 18 and requiring that adults under the age of 26 show a photo identification to buy them. Electronic cigarettes carry the promise of delivering the nicotine without the dangerous additives. The use of e-cigarettes by youth has increased sharply in recent years. In 2011, about 1.5 percent of high school students reported using them in the last month. In 2014, more than 12 percent of students did. That means that nearly 2.5 million American middle and high school students used them in the past month. The problem is that nicotine is generally considered less safe for children and adolescents than for adults. Poisoning is possible. It’s thought that nicotine may interfere with brain development. Most worrisome, it’s believed that becoming addicted to nicotine in any form makes smoking more likely later in life. E-cigarettes are perceived to be less harmful than conventional cigarettes, and they are thought to be useful aids to quitting. These perceptions, however, are not always fully grounded in evidence. © 2016 The New York Times Company

Keyword: Drug Abuse
Link ID: 22201 - Posted: 05.11.2016

Nancy Shute A body mass index under 25 is deemed normal and healthy, and a higher BMI that's "overweight" or "obese" is not. But that might be changing, at least when it comes to risk of death. The body mass index, or BMI, associated with the lowest risk of death has increased since the 1970s, a study finds, from 23.7, in the "normal" weight category, to 27, which is deemed "overweight." That means a person who is 5-foot-8 could weigh 180 pounds and be in that epidemiological sweet spot, according to the NIH's online BMI calculator. The results were published Tuesday in JAMA, the journal of the American Medical Association. The researchers came to that conclusion by looking at data from three studies of people in Copenhagen, one from the 1970s, one from the 1990s and one from 2003-2013. More than 100,000 people were involved. Because Denmark has an excellent national health registry, they were able to pinpoint the cause of death for every single one of those people. The risk of death for people who are obese, with a BMI of 30 or greater, also declined, to the point that it was on a par with some people of so-called "normal" weight. So being fatter, at least a bit, may be healthier. "I was surprised as a scientist to see how clear the result was," Borge Nordestgaard, a clinical professor and chief physician at Copenhagen University Hospital and senior author of the study, told Shots. So he and his colleagues sliced and diced the data to see what could account for the shift. They looked at age, sex, smoking, cancer and heart disease. The most relevant was the decline in smoking since the 1970s. But when they looked at the mortality rates in nonsmokers who had never had cancer or heart disease, it also became associated with a higher BMI over time. © 2016 npr

Keyword: Obesity
Link ID: 22200 - Posted: 05.11.2016

By Geraldine Dawson There’s a popular saying in the autism community: “If you’ve met one person with autism, you’ve met one person with autism.” Although this phrase is meant to convey the remarkable variation in abilities and disabilities among people with autism spectrum disorder (ASD), we’re learning that it also applies to the extraordinary variability in how ASD develops. When I first began doing research on autism decades ago, we thought of it as one condition and aimed to discover its “cause.” Now we know ASD is actually a group of lifelong conditions that can arise from a complex combination of multiple genetic and environmental factors. In the same way that each person with ASD has a unique personality and profile of talents and disabilities, each also has a distinct developmental history shaped by a specific combination of genetic and environmental factors. More evidence of this extraordinary variety will be presented this week in Baltimore, where nearly 2,000 of the world’s leading autism researchers will gather for the International Meeting for Autism Research (IMFAR). As president of the International Society for Autism Research, which sponsors the conference, I am more impressed than ever with the progress we are making. New findings being presented at the conference will highlight the importance of the prenatal period in understanding how various environmental factors such as exposure to alcohol, smoking and certain chemical compounds can increase risk for ASD. The impact of many environmental factors depends, however, on an individual’s genetic background and the timing of the exposure. Other research links inflammation—detected in blood spot tests taken at birth—with a higher likelihood of an ASD diagnosis later on. Researchers suggest that certain factors such as maternal infection and other factors during pregnancy may influence an infant’s immune system and contribute to risk. As our knowledge of these risk factors grows, so do the opportunities for promoting healthy pregnancies and better outcomes. © 2016 Scientific American

Keyword: Autism; Neuroimmunology
Link ID: 22199 - Posted: 05.10.2016

By Dan Kiefer I’m on the heavy bag, throwing left jabs, ignoring the relentless blare of Kanye’s “Drive Slow, Homie” played at a volume that would raise the dead. I punch to a one-two count: left jab, right cross. I’m working as hard as I’ve ever worked, and even in this unheated gym I sweat as if it’s a sauna. Finally, the bell rings. It feels as if I’ve been at it for an hour; actually, three minutes have passed. The ensuing one-minute break seems to last four seconds. Let’s be clear: Boxing, even when the opponent is only a heavy bag, is a brutal sport. But brutality is needed, even welcome, when you’re facing a progressive, incurable neurological disease. I have Parkinson’s disease, and it causes my body to just freeze up. Weirdly enough, boxing helps me get unstuck. All 12 of us in this class bear the unmistakable signs of Parkinson’s disease. I spot a dapper, cheerful white-haired fellow shaking like a leaf (tremor). Next, a balding, heavyset guy stumbling forward awkwardly on his toes (dystonia, or muscle cramping). Then I see myself in a mirror: a man in a white T-shirt, khaki shorts and Nike running shoes, standing still, seemingly paralyzed. I’m in the midst of a Parkinson’s freeze (an extreme form of bradykinesia, or slow movement). Although Parkinson’s is generally thought of as an old-person’s disease, I was diagnosed with a young-onset version 18 years ago, at age 35. Since then, I’ve taken every sort of medication known to science. I’ve had brain surgery — two tiny electrodes were implanted deep in my brain to stimulate an area affected by Parkinson’s — which unquestionably have helped treat some of my symptoms. But medicine and surgery have not cured my freezing and falling, my gait and balance issues that worsen as my disease progresses: When walking across a busy street, I may suddenly, inexplicably come to a full stop as the light is about to change. Even the slightest downhill slope of a path causes me to fall forward.

Keyword: Parkinsons
Link ID: 22198 - Posted: 05.10.2016

Chris Woolston A story about epigenetics in the 2 May issue of The New Yorker has been sharply criticized for inaccurately describing how genes are regulated. The article by Siddhartha Mukherjee — a physician, cancer researcher and award-winning author at Columbia University in New York — examines how environmental factors can change the activity of genes without altering the DNA sequence. Jerry Coyne, an evolutionary ecologist at the University of Chicago in Illinois, posted two widely discussed blog posts calling the piece “superficial and misleading”, largely because it ignored key aspects of gene regulation. Other researchers quoted in the blog posts called the piece “horribly damaging” and “a truly painful read”. Mukherjee responded by publishing a point-by-point rebuttal online. Speaking to Nature, he says he now realizes that he erred by omitting key areas of the science, but that he didn’t mean to mislead. “I sincerely thought that I had done it justice,” he says. Mukherjee’s article, ‘Same But Different’, takes a personal view of epigenetics — a term whose definition is highly contentious in the field. The story features his mother and aunt, identical twins who have distinct personalities. Mukherjee, who won a Pulitzer Prize in 2011 for his best-selling book The Emperor of All Maladies: A Biography of Cancer (Scribner, 2010), writes that identical twins differ because: “Chance events — injuries, infections, infatuations; the haunting trill of that particular nocturne — impinge on one twin and not on the other. Genes are turned on and off in response to these events, as epigenetic marks are gradually layered above genes, etching the genome with its own scars, calluses, and freckles.” The article is drawn from a book by Mukherjee that is due out later this month, called The Gene: An Intimate History (Scribner, 2016). © 2016 Nature Publishing Group

Keyword: Epigenetics; Genes & Behavior
Link ID: 22197 - Posted: 05.10.2016

by Julia Belluz and Javier Zarracina "I'm going to make you work hard," a blonde and perfectly muscled fitness instructor screamed at me in a recent spinning class, "so you can have that second drink at happy hour!" At the end of the 45-minute workout, my body was dripping with sweat. I felt like I had worked really, really hard. And according to my bike, I had burned more than 700 calories. Surely I had earned an extra margarita. The spinning instructor was echoing a message we've been getting for years: As long as you get on that bike or treadmill, you can keep indulging — and still lose weight. It's been reinforced by fitness gurus, celebrities, food and beverage companies like PepsiCo and Coca-Cola, and even public-health officials, doctors, and the first lady of the United States. Countless gym memberships, fitness tracking devices, sports drinks, and workout videos have been sold on this promise. There's just one problem: This message is not only wrong, it's leading us astray in our fight against obesity. To find out why, I read through more than 60 studies on exercise and weight loss. I also spoke to nine leading exercise, nutrition, and obesity researchers. Here's what I learned. 1) An evolutionary clue to how our bodies burn calories When anthropologist Herman Pontzer set off from Hunter College in New York to Tanzania to study one of the few remaining hunter-gatherer tribes on the planet, he expected to find a group of calorie burning machines. Unlike Westerners, who increasingly spend their waking hours glued to chairs, the Hadza are on the move most of the time. Men typically go off and hunt — chasing and killing animals, climbing trees in search of wild honey. Women forage for plants, dig up tubers, and comb bushes for berries. "They're on the high end of physical activity for any population that's been looked at ever," Pontzer said. © 2016 Vox Media, Inc

Keyword: Obesity
Link ID: 22196 - Posted: 05.09.2016

By DAN BARRY IDIOT. Imbecile. Cretin. Feebleminded. Moron. Retarded. Offensive now but once quite acceptable, these terms figured in the research for a lengthy article I wrote in 2014 about 32 men who spent decades eviscerating turkeys in a meat-processing plant in Iowa — all for $65 a month, along with food and lodging in an ancient former schoolhouse on a hill. These were men with intellectual disability, which meant they had significant limitations in reasoning, learning and problem solving, as well as in adaptive behavior. But even though “intellectual disability” has been the preferred term for more than a decade, it gave my editors and me pause. We wondered whether readers would instantly understand what the phrase meant. What’s more, advocates and academicians were recommending that I suppress my journalistic instinct to tighten the language. I was told that it was improper to call these men “intellectually disabled,” instead of “men with intellectual disability.” Their disability does not define them; they are human beings with a disability. This linguistic preference is part of society’s long struggle to find the proper terminology for people with intellectual disability, and reflects the discomfort the subject creates among many in the so-called non-disabled world. It speaks to a continuing sense of otherness; to perceptions of what is normal, and not. “It often doesn’t matter what the word is,” said Michael Wehmeyer, the director and senior scientist at the Beach Center on Disability at the University of Kansas. “It’s that people associate that word with what their perceptions of these people are — as broken, or as defective, or as something else.” For many years, the preferred term was, simply, idiot. When Massachusetts established a commission on idiocy in the mid-1840s, it appointed Dr. Samuel G. Howe, an abolitionist and early disability rights advocate, as its chairman. The commission argued for the establishment of schools to help this segment of society, but made clear that it regarded idiocy “as an outward sign of an inward malady.” © 2016 The New York Times Company

Keyword: Development of the Brain
Link ID: 22195 - Posted: 05.09.2016

By Aleszu Bajak In its May 2 issue, The New Yorker magazine published a report titled “Same But Different,” with the subhead: “How epigenetics can blur the line between nature and nurture.” The piece was written by Siddhartha Mukherjee, a physician and author of the Pulitzer prize-winning book “The Emperor of all Maladies: A Biography of Cancer.” In his New Yorker story, Mukherjee, with deft language and colorful anecdotes, examines a topic that is very much du jour in science writing: Epigenetics. Google defines epigenetics as “the study of changes in organisms caused by modification of gene expression, rather than alteration of the genetic code itself.” Merriam Webster’s definition is similar — but not exactly the same: “The study of heritable changes in gene function that do not involve changes in DNA sequence.” The slight variation in definition is telling in itself — and it’s really that “heritable” part that has sparked intense interest not just among scientists, but in the popular mind. Steven Henikoff, a molecular biologist at the Fred Hutchinson Cancer Research Center in Seattle, called Siddhartha Mukherjee’s lyrical take on epigenetics “baloney.” It’s the idea that external factors like diet, or stress or even lifestyle choices can impact not just your own genes, but the genetic information you pass down to all of your descendants. Spend your life smoking cigarettes and eating fatty foods, the thinking goes, and you’ll not just make yourself sick, you’ll predispose your offspring — and their offspring, and their offspring — to associated diseases as well. It’s heady stuff, but much of it remains speculative and poorly supported, which is where Mukherjee may have run into trouble. The publication of his story — an excerpt from his forthcoming book “The Gene: An Intimate History” — was met with swift criticism from biologists working in epigenetics and the broader field of gene regulation. They argue that Mukherjee played fast and loose with his description of epigenetic processes and misled readers by casting aside decades of research into how genes are regulated during development. Copyright 2016 Undark

Keyword: Epigenetics
Link ID: 22194 - Posted: 05.09.2016

By John Horgan Scientists trying to explain consciousness are entitled to be difficult, but what’s philosophers’ excuse? Don’t they have a moral duty to be comprehensible to non-specialists? I recently attended “The Science of Consciousness,” the legendary inquest held every two years in Tucson, Arizona. I reported on the first meeting in 1994 and wanted to see how it’s evolved since then. This year’s shindig lasted from April 26 to April 30 and featured hundreds of presenters, eminent and obscure. I arrived on the afternoon of April 27 and stayed through the closing “End-of-Consciousness Party.” The only event I regret missing is a chat between philosopher David Chalmers, who loosed his “hard problem of consciousness” meme here in Tucson in 1994, and Deepak Chopra, the New Age mogul and a sponsor of this year’s meeting. I feel obliged to post something fast, because conference organizer and quantum-consciousness advocate Stuart Hameroff complained that most reporters “come for free, drink our booze and don’t write anything.” Hameroff also generously allowed me to give a talk, “The Quest to Solve Consciousness: A Skeptic’s View,” even though I teased him in my 1994 article for Scientific American, calling him an “aging hipster.” What follows is a highly subjective account of my first day at the meeting. I’d call this a “stream-of-consciousness report on consciousness,” but that would be pretentious. I'm just trying to answer this question: What is it like to be a skeptical journalist at a consciousness conference? I’ll post on the rest of the meeting soon. -- John Horgan DAY 1, WEDNESDAY, APRIL 27. THE HOROR A bullet-headed former New York fireman picks me up at the Tucson airport. Driving to the Loews Ventana Canyon Resort, he argues strenuously that President Trump will make us great again. As we approach the resort, he back-peddles a bit, no doubt worried about his tip. I tip him well, to show how tolerant I am. Everyone’s entitled to an irrational belief or two. © 2016 Scientific American

Keyword: Consciousness
Link ID: 22193 - Posted: 05.09.2016

By Jane E. Brody Truth to tell, sometimes I don’t follow my own advice, and when I suffer the consequences, I rediscover why I offer it. I’ve long recommended drinking plenty of water, perhaps a glass with every meal and another glass or two between meals. If not plain water, which is best, then coffee or tea without sugar (but not alcoholic or sugary drinks) will do. I dined out recently after an especially active day that included about five miles of walking, 40 minutes of lap swimming and a 90-minute museum visit. I drank only half a glass of water and no other beverage with my meal. It did seem odd that I had no need to use the facilities afterward, not even after a long trip home. But I didn’t focus on why until the next day when, after a fitful night, I awoke exhausted, did another long walk and swim, and cycled to an appointment four miles away. I arrived parched, begging for water. After downing about 12 ounces, I was a new person. I no longer felt like a lead balloon. It seems mild dehydration was my problem, and the experience prompted me to take a closer look at the body’s need for water under a variety of circumstances. Although millions of Americans carry water bottles wherever they go and beverage companies like Coke and Pepsi would have you believe that every life can be improved by the drinks they sell, the truth is serious dehydration is not common among ordinary healthy people. But there are exceptions, and they include people like me in the Medicare generation, athletes who participate in particularly challenging events like marathons, and infants and small children with serious diarrhea. Let’s start with some facts. Water is the single most important substance we consume. You can survive for about two months without food, but you would die in about seven days without water. Water makes up about 75 percent of an infant’s weight and 55 percent of an older person’s weight. © 2016 The New York Times Company

Keyword: Miscellaneous
Link ID: 22192 - Posted: 05.09.2016

By JAN HOFFMAN The pop superstar Prince may have lived an outsize life, but emerging details about his long struggle with pain and reliance on opioids will resonate with thousands of patients who have stumbled down that well-trod path. It is a remarkably common narrative in the unfolding story of the nation’s opioid epidemic. Many details have yet to be confirmed about Prince’s case, but a typical trajectory can go something like this. A patient undergoes a procedure to address a medical issue — extracted wisdom teeth for example, or, as Prince did, orthopedic surgery. To help the patient get through recovery, a dentist or surgeon writes a prescription for opioid painkillers, like Percocet or Vicodin. Procedure over, problem addressed. But that prescription may not be written judiciously. “Opioids may be required after a procedure for a few days, but sometimes, physicians practice sloppy prescribing habits and they give patients much more than they need,” said Dr. Patrick G. O’Connor, a professor of medicine at Yale School of Medicine and a past president of the American Board of Addiction Medicine. “And the more patients take, the more likely they are to become dependent.” After a follow-up visit or two, the specialist who did the procedure has no reason to continue seeing the patient. (That doctor could also be an emergency room physician who treated kidney stones, sciatica or any number of other conditions involving stabbing pain.) Yet the patient’s pain may persist, demanding to be tamed. The patient, who now knows just how effective these drugs are, wants to refill the prescription. “The default approach is you go to your primary care provider, and they’ll take care of it,” said Dr. Jonathan H. Chen, an instructor at the Stanford University School of Medicine, who has researched the distribution of opioid prescriptions. As he spoke during a break in his shift in a same-day urgent care clinic, he had just attended to a patient who had recently had shoulder surgery but said she was still in pain. © 2016 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 22191 - Posted: 05.07.2016

By David Shultz Did you sleep well? The answer may depend on your age, location and gender. A survey of 5000 sleepers from across the world has revealed that women get the most sleep, particularly those under the age of 25. Daniel Forger at the University of Michigan in Ann Arbor and his team were able to get their huge dataset thanks to Entrain, a smartphone app that people use to track their sleep. With their consent, Forger’s team accessed users’ data on their wake time, bed time, time zone and how much light they were exposed to during the day. Analysing this information, they found that middle-aged men sleep the least, while women under the age of 25 sleep the most. As a whole, women appear to sleep on average for 30 minutes longer than men, thanks to going to bed slightly earlier and waking up slightly later. For an individual, the time they woke up had the strongest link to how much sleep they got, suggesting that having a job that starts early every day can mean that you get less sleep than someone who starts work at a later hour. There were also differences between countries. People in Singapore, for example, sleep for an average of 7.5 hours a night, while Australians get 8.1 hours. Late bedtimes seem to be to blame – people in Singapore tended to stay up until after 11.45 pm each night, while people in Australia were likely to hit the hay closer to 10.45 pm. The team found that, in general, national wake-up times were linked more to daylight hours than bedtimes. This could be because bedtimes are more affected by social factors. © Copyright Reed Business Information Ltd.

Keyword: Sleep; Sexual Behavior
Link ID: 22190 - Posted: 05.07.2016

By Jocelyn Kaiser Gene therapy is living up to its promise of halting a rare, deadly brain disease in young boys. In a new study presented in Washington, D.C., yesterday at the annual meeting of the American Society of Gene and Cell Therapy, all but one of 17 boys with adrenoleukodystrophy (ALD) remained relatively healthy for up to 2 years after having an engineered virus deliver into their cells a gene to replenish a missing protein needed by the brain. The results, which expand on an earlier pilot study, bring this ALD therapy one step closer to the clinic. About one in 21,000 boys are born with ALD, which is caused by a flaw in a gene on the X chromosome that prevents cells from making a protein that the cells need to process certain fats—females have a backup copy of the gene on their second X chromosome. Without that protein, the fats build up and gradually destroy myelin sheaths that protect nerves in the brain. In the cerebral form of ALD, which begins in childhood, patients quickly lose vision and mobility, usually dying by age 12. The disease achieved some degree of fame with the 1992 film Lorenzo’s Oil, inspired by a family’s struggle to prolong their son’s life with a homemade remedy. The only currently approved treatment for ALD is a bone marrow transplant -- white blood cells in the marrow go to the brain and turn into glial cells that produce normal ALD proteins. But bone marrow transplants carry many risks, including immune rejection, and matching donors can’t always be found. As an alternative, in the late 2000s, French researchers treated the bone cells of two boys with a modified virus carrying the ALD gene. They reported in Science in 2009 that this halted progression of the disease. © 2016 American Association for the Advancement of Science

Keyword: Development of the Brain; Movement Disorders
Link ID: 22189 - Posted: 05.07.2016

Why You Can’t Lose Weight on a Diet By SANDRA AAMODT SIX years after dropping an average of 129 pounds on the TV program “The Biggest Loser,” a new study reports, the participants were burning about 500 fewer calories a day than other people their age and size. This helps explain why they had regained 70 percent of their lost weight since the show’s finale. The diet industry reacted defensively, arguing that the participants had lost weight too fast or ate the wrong kinds of food — that diets do work, if you pick the right one. But this study is just the latest example of research showing that in the long run dieting is rarely effective, doesn’t reliably improve health and does more harm than good. There is a better way to eat. The root of the problem is not willpower but neuroscience. Metabolic suppression is one of several powerful tools that the brain uses to keep the body within a certain weight range, called the set point. The range, which varies from person to person, is determined by genes and life experience. When dieters’ weight drops below it, they not only burn fewer calories but also produce more hunger-inducing hormones and find eating more rewarding. The brain’s weight-regulation system considers your set point to be the correct weight for you, whether or not your doctor agrees. If someone starts at 120 pounds and drops to 80, her brain rightfully declares a starvation state of emergency, using every method available to get that weight back up to normal. The same thing happens to someone who starts at 300 pounds and diets down to 200, as the “Biggest Loser” participants discovered. This coordinated brain response is a major reason that dieters find weight loss so hard to achieve and maintain. For example, men with severe obesity have only one chance in 1,290 of reaching the normal weight range within a year; severely obese women have one chance in 677. A vast majority of those who beat the odds are likely to end up gaining the weight back over the next five years. In private, even the diet industry agrees that weight loss is rarely sustained. A report for members of the industry stated: “In 2002, 231 million Europeans attempted some form of diet. Of these only 1 percent will achieve permanent weight loss.” © 2016 The New York Times Company

Keyword: Obesity
Link ID: 22188 - Posted: 05.07.2016

By John Elder Robison Manipulating your brain with magnetic fields sounds like science fiction. But the technique is real, and it’s here. Called transcranial magnetic stimulation (TMS), it is approved as a therapy for depression in the US and UK. More controversially, it is being studied as a way to treat classic symptoms of autism, such as emotional disconnection. With interest and hopes rising, it’s under the spotlight at the International Meeting for Autism Research in Baltimore, Maryland, next week. I can bear witness to the power of TMS, which induces small electrical currents in neurons. As someone with Asperger’s, I tried it for medical research, and described its impact in my book Switched On. After TMS, I could see emotional cues in other people – signals I had always been blind to, but that many non-autistic people pick up with ease. That sounds great, so why the need for debate? Relieving depression isn’t controversial, because there is no question people suffer as a result of it. I too felt that I suffered – from emotional disconnection. But changing “emotional intelligence” to relieve that comes closer to changing the essence of how we think. Yes, emerging brain therapies like TMS have great potential. Several of the volunteers who went into the TMS lab at Harvard Medical School emerged with new self-awareness, and lasting changes. While I can’t speak with certainty for the others, I believe some of us have a degree of emotional insight that we didn’t have before. I certainly feel better able to fit in. As fellow participant Michael Wilcox put it, we have more emotional reactions to things we see or read. © Copyright Reed Business Information Ltd.

Keyword: Autism
Link ID: 22187 - Posted: 05.07.2016

By Matthew Hutson Last week, Nature, the world’s most prestigious science journal, published a beautiful picture of a brain on its cover. The computer-generated image, taken from a paper in the issue, showed the organ’s outer layer almost completely covered with sprinkles of colorful words. The paper presents a “semantic map” revealing which parts of the brain’s cortex—meaning its outer layer, the one responsible for higher thought—respond to various spoken words. The study has generated widespread interest, receiving coverage from newspapers and websites around the world. The paper was also accompanied by an online interactive model that allowed users to explore exactly how words are mapped in our brains. The combination yielded a popular frenzy, one prompting the question: Why are millions of people suddenly so interested in the neuroanatomical distribution of linguistic representations? Have they run out of cat videos? The answer, I think, is largely the same as the answer to why “This Is Your Brain on X” (where X = food, politics, sex, podcasts, whatever) is a staple of news headlines, often residing above an fMRI image of a brain lit up in fascinating, mysterious patterns: People have a fundamental misunderstanding of the field of neuroscience and what it can tell us. But before explaining why people shouldn’t be excited about this research, let’s look at what the research tells us and why we should be excited. Different parts of the brain process different elements of thought, and some regions of the cortex are organized into “maps” such that the distance between different locations corresponds to the physical and/or conceptual distance between what it represents.

Keyword: Brain imaging; Language
Link ID: 22186 - Posted: 05.07.2016

By Linda Zajac For nearly 65 million years, bats and tiger moths have been locked in an aerial arms race: Bats echolocate to detect and capture tiger moths, and tiger moths evade them with flight maneuvers and their own ultrasonic sounds. Scientists have long wondered why certain species emit these high-frequency clicks that sound like rapid squeaks from a creaky floorboard. Does the sound jam bat sonar or does it warn bats that the moths are toxic? To find out, scientists collected two types of tiger moths: red-headed moths (pictured above) and Martin’s lichen moths. They then removed the soundmaking organs from some of the insects. In a grassy field in Arizona they set up infrared video cameras, ultrasonic microphones, and ultraviolet lights, the last of which they used to attract bats. In darkness, they released one tiger moth at a time and recorded the moth-bat interactions. They found that the moths rarely produced ultrasonic clicks fast enough to jam bat sonar. They also discovered that without sound organs, 64% of the red-headed moths and 94% of the Martin’s lichen moths were captured and spit out. Together, these findings reported late last month in PLOS ONE suggest that instead of jamming sonar like some tiger moths, these species act tough, flexing their soundmaking organs to warn predators of their toxin. © 2016 American Association for the Advancement of Science

Keyword: Hearing; Evolution
Link ID: 22185 - Posted: 05.07.2016

Laura Sanders Ketamine, a drug that has shown promise in quickly easing depression, doesn’t actually do the job itself. Instead, depression relief comes from one of the drug’s breakdown products, a new study in mice suggests. The results, published May 4 in Nature, identify a potential depression-fighting drug that works quickly but without ketamine’s serious side effects or potential for abuse. The discovery “could be a major turning point,” says neuroscientist Roberto Malinow of the University of California, San Diego. “I’m sure that drug companies will look at this very closely.” Depression is a pernicious problem with few good treatments. Traditional antidepressants don’t work for everyone, and when the drugs do work, they can take weeks to kick in. Ketamine, developed in the 1960s as a sedative for people and now used commonly by veterinarians to knock out animals, can ease depression in minutes, not weeks, small studies show. But the new study suggests that a metabolite of ketamine — not the drug itself — fights depression. Inside the body, ketamine gets converted into a slew of related molecules. One of these breakdown molecules, a chemical called (2R,6R)-hydroxynorketamine, is behind the benefits, neuropharmacologist Todd Gould of the University of Maryland School of Medicine in Baltimore and colleagues found. On its own, a single dose of (2R,6R)-HNK reduced signs of depression in mice, restoring their drive to search for a hidden platform in water, to try to escape a shock and to choose sweet water over plain. A type of ketamine that couldn’t be broken down easily into HNKs didn’t ease signs of depression in mice. Finding that a breakdown product, and not ketamine itself, was behind the results was a big surprise, Gould says. © Society for Science & the Public 2000 - 2016

Keyword: Depression; Drug Abuse
Link ID: 22184 - Posted: 05.05.2016

By Ann Gibbons We may not be raring to go on a Monday morning, but humans are the Energizer Bunnies of the primate world. That’s the conclusion of a new study that, for the first time, measures precisely how many calories humans and apes burn each day. Compared with chimpanzees and other apes, our revved-up internal engines burn calories 27% faster, according to a paper in Nature this week. This higher metabolic rate equips us to quickly fuel energy-hungry brain cells, sustaining our bigger brains. And lest we run out of gas when food is short, the study also found that humans are fatter than other primates, giving us energy stores to draw on in lean times. “The brilliant thing here is showing for the first time that we do have a higher metabolic rate, and we do use more energy,” says paleoanthropologist Leslie Aiello, president of the Wenner-Gren Foundation for Anthropological Research in New York City. “Humans during evolution have become more and more hypermetabolic,” says biological anthropologist Carel van Schaik of the University of Zurich in Switzerland. “We turned up the thermostat.” For decades, researchers assumed that “there weren’t any differences in the rate at which different species burned calories,” says biological anthropologist Herman Pontzer of Hunter College in New York City, lead author of the new study. Comparing humans and other primates, they saw little difference in basal metabolic rate, which reflects the total calories used by our organs while we are at rest. © 2016 American Association for the Advancement of Science

Keyword: Obesity; Evolution
Link ID: 22183 - Posted: 05.05.2016