Helen Shen For Frank Donobedian, sitting still is a challenge. But on this day in early January, he has been asked to do just that for three minutes. Perched on a chair in a laboratory at Stanford University in California, he presses his hands to his sides, plants his feet on the floor and tries with limited success to lock down the trembling in his limbs — a symptom of his Parkinson's disease. Only after the full 180 seconds does he relax. Other requests follow: stand still, lie still on the floor, walk across the room. Each poses a similar struggle, and all are watched closely by Helen Bronte-Stewart, the neuroscientist who runs the lab. “You're making history,” she reassures her patient. “Everybody keeps saying that,” replies the 73-year-old Donobedian, a retired schoolteacher, with a laugh. “But I'm not doing anything.” “Well, your brain is,” says Bronte-Stewart. Like thousands of people with Parkinson's before him, Donobedian is being treated with deep brain stimulation (DBS), in which an implant quiets his tremors by sending pulses of electricity into motor areas of his brain. Last October, a team of surgeons at Stanford threaded the device's two thin wires, each with four electrode contacts, through his cortex into a deep-seated brain region known as the subthalamic nucleus (STN). But Donobedian's particular device is something new. Released to researchers in August 2013 by Medtronic, a health-technology firm in Minneapolis, Minnesota, it is among the first of an advanced generation of neurostimulators that not only send electricity into the brain, but can also read out neural signals generated by it. On this day, Bronte-Stewart and her team have temporarily turned off the stimulating current and are using some of the device's eight electrical contacts to record abnormal neural patterns that might correlate with the tremors, slowness of movement and freezing that are hallmarks of Parkinson's disease. © 2014 Nature Publishing Group,

Keyword: Parkinsons; Robotics
Link ID: 19387 - Posted: 03.20.2014

by Ashley Yeager Owl monkeys don't sleep around, genetic tests show. That could be a result of the amount of care males provide for their young, a new study suggests. Infidelity appears to be common in mammals that live in pairs. But new genetic tests suggest that Azara's owl monkeys are unusually faithful. Scientists studied 35 infants born to 17 owl monkey pairs and found that in all cases the youngsters were being raised by their biological parents. Data from the owl monkeys and 14 other species showed that the more involved the males were in raising an infant, the more likely the males were to be faithful, the team reports March 18 in Proceedings of the Royal Society B. Owl monkeys are the only primates and one of five mammal species, including coyotes and California mice, that don’t seem to cheat, according to genetic studies. The evolution of animals’ sexual fidelity is probably linked to the intensity of male care, the researchers suggest. © Society for Science & the Public 2000 - 2013.

Keyword: Sexual Behavior
Link ID: 19386 - Posted: 03.20.2014

By Lenny Bernstein When your name is Leonard Bernstein, and you can’t play or sing a note, people are, understandably, a bit prone to noting this little irony. But now I have an explanation: My lack of musical aptitude is mostly genetic. Finnish researchers say they have found genes responsible for auditory response and neuro-cognitive processing that partially explain musical aptitude. They note “several genes mostly related to the auditory pathway, not only specifically to inner ear function, but also to neurocognitive processes.” The study was published in the March 11 issue of the journal “Molecular Psychiatry.” In an e-mail, one of the researchers, Irma Jarvela, of the University of Helsinki’s department of medical genetics, said heredity explains 60 percent of the musical ability passed down through families like Bach’s. The rest can be attributed to environment and training. Genes most likely are responsible for “better perception skills of different sounds,” Jarvela said. Feel free to cite this research at your next karaoke night. © 1996-2014 The Washington Post

Keyword: Hearing; Genes & Behavior
Link ID: 19385 - Posted: 03.20.2014

Sara Reardon The US brain-research programme aims to create tools to image and control brain activity, while its European counterpart hopes to create a working computational model of the organ. It seems a natural pairing, almost like the hemispheres of a human brain: two controversial and ambitious projects that seek to decipher the body's control center are poised to join forces. The European Union’s €1-billion (US$1.3-billion) Human Brain Project (HBP) and the United States’ $1-billion Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative will launch a collaboration later this year, according to government officials involved in both projects. Representative Chaka Fattah (Democrat, Pennslyvania) hinted at the plan in a speech on 12 March. The brain, he says, ”is something that has defied understanding. You can't imagine a more important scientific cooperation”, says Fattah, the highest-ranking Democratic member of a House of Representatives panel that oversees funding for several US science agencies. Details about how closely the US and European programmes will coordinate are still nebulous, but US government officials say that the effort will include all of the BRAIN Initiative's government partners — the US National Institutes of Health (NIH), the National Science Foundation and Defense Advanced Research Projects Agency. Henry Markram, a neuroscientist at the Swiss Federal Institute of Technology in Lausanne (EPFL), who directs the HBP, says that Israel's brain initiative will also be involved. © 2014 Nature Publishing Group

Keyword: Brain imaging
Link ID: 19384 - Posted: 03.19.2014

By Michelle Roberts Health editor, BBC News online Statins may be useful in treating advanced multiple sclerosis (MS), say UK researchers. Early trial results in The Lancet show the cholesterol-lowering pills slow brain shrinkage in people with MS. The University College London (UCL) scientists say large trials can now begin. These will check whether statins benefit MS patients by slowing progression of the disease and easing their symptoms. MS is a major cause of disability, affecting nerves in the brain and spinal cord, which causes problems with muscle movement, balance and vision. Currently there is no cure, although there are treatments that can help in the early stages of the disease. Usually, after around 10 years, around half of people with MS will go on to develop more advanced disease - known as secondary progressive MS. It is this later stage disease that Dr Jeremy Chataway and colleagues at UCL hope to treat with low cost statins. To date, no licensed drugs have shown a convincing impact on this later stage of the disease. For their phase two trial, which is published in the Lancet, Dr Chataway's team randomly assigned 140 people with secondary progressive MS to receive either 80mg of a statin called simvastatin or a placebo for two years. The high, daily dose of simvastatin was well tolerated and slowed brain shrinkage by 43% over two years compared with the placebo. Dr Chataway said: "Caution should be taken regarding over-interpretation of our brain imaging findings, because these might not necessarily translate into clinical benefit. However, our promising results warrant further investigation in larger phase three disability-driven trials." BBC © 2014

Keyword: Multiple Sclerosis
Link ID: 19383 - Posted: 03.19.2014

By Helen Briggs BBC News Sleep loss may be more serious than previously thought, causing a permanent loss of brain cells, research suggests. In mice, prolonged lack of sleep led to 25% of certain brain cells dying, according to a study in The Journal of Neuroscience. If the same is true in humans, it may be futile to try to catch up on missed sleep, say US scientists. They think it may one day be possible to develop a drug to protect the brain from the side-effects of lost sleep. The study, published in The Journal of Neuroscience, looked at lab mice that were kept awake to replicate the kind of sleep loss common in modern life, through night shifts or long hours in the office. A team at the University of Pennsylvania School of Medicine studied certain brain cells which are involved in keeping the brain alert. After several days of sleep patterns similar to those followed by night workers - three days of night shifts with only four to five hours sleep in 24 hours - the mice lost 25% of the brain cells, known as locus coeruleus (LC) neurons. The researchers say this is the first evidence that sleep loss can lead to a loss of brain cells. But they add that more work needs to be done to find out if people who miss out on sleep might also be at risk of permanent damage. Prof Sigrid Veasey of the Center for Sleep and Circadian Neurobiology, told BBC News: "We now have evidence that sleep loss can lead to irreversible injury. "This might be in a simple animal but this suggests to us that we are going to have to look very carefully in humans." BBC © 2014

Keyword: Sleep
Link ID: 19382 - Posted: 03.19.2014

By Maggie Fox and Erika Edwards Women are carrying the bigger burden of Alzheimer’s disease in the U.S., according to a new report — making up not only most of the cases, but paying more of the cost of caring for the growing population of people with the mind-destroying illness. The new report from the Alzheimer’s Association paints Alzheimer’s as a disease that disproportionately affects women, both as patients and as caregivers. It points out that women in their 60s are about twice as likely to develop Alzheimer’s over the rest of their lives as they are to develop breast cancer. “So women are at the epicenter of Alzheimer's disease today, not only by being most likely to be diagnosed with Alzheimer's, but also by being the caregiver most of the time,” said Maria Carrillo, vice president of the advocacy group. Alzheimer’s affects more than 5 million Americans, a number projected to soar to 13 million over the next 35 years. A study published earlier this year suggested it’s a big killer, taking down more than 500,000 Americans every year. Three out of five of those living with Alzheimer’s are women, the report finds. “The surprising statistic we pulled out of this report actually is that women over 65 have a one in six chance of developing Alzheimer's disease, in comparison to one out of 11 in men,” Carrillo said. And that compares to a one in eight lifetime risk for developing breast cancer.

Keyword: Alzheimers; Sexual Behavior
Link ID: 19381 - Posted: 03.19.2014

by Andy Coghlan Burmese pythons can find their way home even if they are taken dozens of kilometres away. It is the first demonstration that big snakes can navigate at all, and far exceeds the distances known to have been travelled by any other snake. At over 3 metres long, Burmese pythons (Python molurus bivitattus) are among the world's largest snakes. For the last two decades they have been eating their way through native species of Florida's Everglades National Park, having been abandoned to the wild by former owners. "Adult Burmese pythons were able to navigate back to their capture locations after having been displaced by between 21 and 36 kilometres," says Shannon Pittman of Davidson College in North Carolina. Pittman and her colleagues caught 12 pythons and fitted them with radiofrequency tags (see video). She released half of them where they were caught, as controls, and transported the other six to distant locations before releasing them. Five pythons made it back to within 5 kilometres of their capture location, and the sixth at least moved in the right direction. The displaced snakes made progress towards their destination most days and seldom strayed more than 22 degrees from the correct path. They kept this up for 94 to 296 days. By contrast, the control snakes moved randomly. On average, displaced snakes travelled 300 metres each day, while control snakes averaged just 100 metres per day. © Copyright Reed Business Information Ltd.

Keyword: Animal Migration
Link ID: 19380 - Posted: 03.19.2014

|By Nathan Collins A car detects when a driver starts to nod off and gently pulls over. A tablet or laptop senses its user is confused and offers assistance. Such interventions seem futuristic, but in fact they may not require any technological breakthroughs: a recent study suggests that with the aid of a standard camera, a simple computer program can learn to read people's eye movements to determine what they are doing and perhaps how they are feeling. Psychologists at the University of South Carolina were curious if a computer could figure out what a person was up to based on their eye movements. They first had 12 people engage in four tasks, including reading lines of text and searching photographs for a specific printed letter. Each person repeated the tasks 35 to 50 times while a camera recorded how their eyes moved. Using a subset of those data, the team trained a simple computer program, called a naive Bayes classifier, to identify which of the four tasks each person was doing. In the remaining trials, the classifier correctly determined which task the person was working on 75 percent of the time, well above the 25 percent expected by chance. Because the computer program is based on a flexible algorithm that is simple but powerful, this set-up could most likely be used to identify emotions or mental states such as confusion or fatigue, the researchers suggest in the paper, which appeared in September 2013 in PLOS ONE. With only a brief training period, a car's onboard computer—existing models are more than powerful enough—could learn how a driver's gaze changed as he or she became more exhausted. Further work, the authors suggest, could lead to devices capable of identifying and aiding people in need of assistance in a variety of situations. © 2014 Scientific American

Keyword: Attention; Vision
Link ID: 19379 - Posted: 03.19.2014

The cancer gene BRCA1, which keeps tumors in the breast and ovaries at bay by producing proteins that repair damaged DNA, may also regulate brain size. Mice carrying a mutated copy of the gene have 10-fold fewer neurons and other brain abnormalities, a new study suggests. Such dramatic effects on brain size and function are unlikely in human carriers of BRCA1 mutations, the authors of the study note, but they propose the findings could shed light on the gene's role in brain evolution. Scientists have known for a long time that the BRCA1 gene is an important sentinel against DNA damage that can lead to ovarian and breast cancers. More than half of women with a mutated copy of the BRCA1 gene will develop breast cancer, a statistic that has led some who carry the mutation to get preventative mastectomies. But its roles outside the breast and ovaries are less clear, says Inder Verma, a geneticist and molecular biologist at the Salk Institute for Biological Studies in San Diego, California, who headed the new study. Mice bred without BRCA1 die soon after birth, so it’s clear that the gene is necessary to sustain life, but scientists are just starting to unravel its many functions, he says. Several years ago, one of the students in Verma’s lab noticed that BRCA1 is very active in the neuroectoderm, a sliver of embryonic tissue containing neural stem cells that divide and differentiate into the brain’s vast assortment of cell types and structures. Verma and his colleagues wondered why the gene was expressed at such high levels in that region, and what would happen if it were eliminated. They created a strain of mice in which BRCA1 was knocked out only in neural stem cells. As the mice developed, Verma’s team found that the rodents’ brains were only a third of their normal size, with particularly striking reductions in brain areas involved in learning and memory. The grown mice also had a wobbly, drunken gait—a telltale symptom of ataxia, a neurological disorder that affects muscle control and balance, the researchers report online today in the Proceedings of the National Academy of Sciences. © 2014 American Association for the Advancement of Science.

Keyword: Development of the Brain
Link ID: 19378 - Posted: 03.18.2014

|By Shannon Firth A dog will do anything for a biscuit—over and over again. Most people will, too, because when sugar touches the taste buds it excites reward regions in the brain. A new study shows that people with eating disorders do not react to sweet flavors the way healthy people do, however, lending evidence to the hypothesis that brain differences predispose people toward bulimia and anorexia. A team of psychiatrists at U.C. San Diego studied 14 recovered anorexic women, 14 recovered bulimic women (who used to binge and purge) and 14 women who had never had an eating disorder, matched by age and weight. None of the women had had any pathological eating-related behaviors in the 12 months preceding the study. After fasting overnight, subjects received a modest breakfast to ensure similar levels of satiety. They were then fed small tastes of sugar every 20 seconds through a syringe pump while their brains were scanned. The women who had recovered from anorexia—those who formerly starved themselves—showed less activity than the healthy women in a reward center in the brain known as the primary gustatory cortex. The participants who were no longer bulimic showed more activity than the healthy women did. The results were published in October 2013 in the American Journal of Psychiatry. The researchers believe these abnormal responses to sugar predispose people to eating disorders, adding to a growing body of work suggesting that genetic and biological risk factors underlie most cases, according to study co-author Walter Kaye, director of U.C.S.D.'s Eating Disorders Research and Treatment Program. © 2014 Scientific American

Keyword: Anorexia & Bulimia
Link ID: 19377 - Posted: 03.18.2014

by Laura Sanders Candy and sweets make your kid hyper, the common lore goes. But science says that's not true. 1. Sugar makes kids hyper. Lots of parents swear that a single hit of birthday cake holds the power to morph their well-behaved, polite youngster into a sticky hot mess that careens around a room while emitting eardrum-piercing shrieks. Anyone who has had the pleasure to attend a 5-year-old’s birthday party knows that the hypothesis sounds reasonable, except that science has found that it’s not true. Sugar doesn’t change kids’ behavior, a double-blind research study found way back in 1994. A sugary diet didn’t affect behavior or cognitive skills, the researchers report. Sugar does change one important thing, though: parents’ expectations. After hearing that their children had just consumed a big sugar fix, parents were more likely to say their child was hyperactive, even when the big sugar fix was a placebo, another study found. Of course, there are plenty of good reasons not to feed your kids a bunch of sugar, but fear of a little crazed sugar monster isn’t one of them. © Society for Science & the Public 2000 - 2013.

Keyword: Development of the Brain
Link ID: 19376 - Posted: 03.18.2014

by Tania Lombrozo St. Patrick's Day is my excuse to present you with the following illusion in green, courtesy of , a psychology professor at Ritsumeikan University in Japan. In this perceptual illusion, the two spirals appear to be different shades of green. In fact, they are the same. In this perceptual illusion, the two spirals appear to be different shades of green. In fact, they are the same. This image includes two spirals in different shades of green, one a yellowish light green and the other a darker turquoise green. Right? Wrong. At least, that's not what the pixel color values on your monitor will tell you, or what you'd find if you used a photometer to measure the distribution of lightwaves bouncing back from the green-looking regions of either spiral. In fact, the two spirals are the very same shade of green. If you don't believe me, here's a trick to make the illusion go away: replace the yellow and blue surrounding the green segments with a uniform background. Here I've replaced the blue with black: And here the yellow is gone, too: Tada! The very same green. The fact that the illusion disappears when the surrounding colors are replaced with a uniform background illustrates an important feature of color perception. Our experience of color for a given region of space isn't just a consequence of the wavelengths of light reaching our retinas from that region. Instead, the context matters a lot! ©2014 NPR

Keyword: Vision
Link ID: 19375 - Posted: 03.18.2014

By Ella Davies Reporter, BBC Nature The whales are known for their tusks which can reach 2.6m (9ft) in length, earning them comparisons with mythological unicorns. The tusk is an exaggerated front tooth and scientists have discovered that it helps the animals sense changes in their environment. Dr Martin Nweeia from the Harvard School of Dental Medicine, US, undertook the study alongside an international team of colleagues. Through the years, many theories have tried to explain the function of the narwhal's impressive tusk. "People have said it's everything from an ice pick to an acoustic probe, but this is the first time that someone has discovered sensory function and has the science to show it," said Dr Nweeia. More recently, experts have agreed that the tusk is a sexual characteristic because it is more often exhibited by males and they appear to use them during fights to assert their social hierarchy. But because the animals are rarely seen, the exact function of the tusk has remained a mystery. Previous studies have revealed that the animals have no enamel on their tusk - the external layer of the tooth that provides a barrier in most mammal teeth. Dr Nweeia and the team's analysis revealed that the outer cementum layer of the tusk is porous and the inner dentin layer has microscopic tubes that channel in towards the centre. In the middle of the tusk lies the pulp, where nerve endings which connect to the narwhal's brain are found. BBC © 2014

Keyword: Pain & Touch; Sexual Behavior
Link ID: 19374 - Posted: 03.18.2014

By FLORENCE WILLIAMS So there’s this baby who has swallowed a .22-caliber bullet. The mother rushes into a drugstore, crying, “What shall I do?” “Give him a bottle of castor oil,” replies the druggist, “but don’t point him at anybody.” Whether you find this joke amusing depends on many more variables than you probably ever realized. It depends on a common cultural understanding of the technical properties of castor oil. It depends, as many funny jokes do and as any fourth grader can attest, on our own squeamishness about bodily functions. Getting less obvious, your sense of humor can also depend on your age, your gender, your I.Q., your political inclinations, how extroverted you are and the health of your dopamine reward circuit. If you think all this analysis sounds a bit, well, unfunny, E. B. White would back you up. He once wrote that picking apart jokes is like dissecting frogs: Few people are interested, and the subject always dies in the end. Fortunately, the cognitive neuroscientist Scott Weems isn’t afraid of being unfunny. Humor is worthy of serious academic study, he argues in his book, “Ha! The Science of When We Laugh and Why,” (Read an excerpt.) because it yields insights into how our brains process a complex world and how that, in turn, makes us who we are. Though animals laugh, humans spend more time laughing than exhibiting any other emotion. But what gives some people a better sense of humor than others? Not surprisingly, extroverts tend to laugh more and produce more jokes; yet in tests measuring the ability to write cartoon captions, people who were more neurotic, assertive, manipulative and dogmatic were actually funnier. As the old saw holds, many of the best comics really are miserable. © 2014 The New York Times Company

Keyword: Emotions
Link ID: 19373 - Posted: 03.18.2014

by Colin Barras Amyloid plaques, a hallmark of diseases like Alzheimer's, are bad news for humans – but they could have been drivers of the earliest life on Earth. A new study shows that these amyloid clusters can behave as catalysts, backing a theory that they helped trigger the reactions that sustain life, long before modern enzymes appeared. Without enzymes, life's metabolic reactions simply wouldn't occur. But making enzymes from scratch isn't easy. They are normally large, complicated proteins folded into a specific three-dimensional shape. It's difficult to see how these large proteins could have popped out of the primordial soup fully formed. Even if they did, nature faced another problem. There are 20 naturally occurring amino acids, which are the building blocks for all proteins, and each enzyme is made up of a unique sequence of at least 100 amino acids. This means there is a mind-bogglingly vast number – 20100 – of possible enzymes, each with a different amino acid sequence and a slightly different 3D structure. But very few of these 3D structures will work effectively as enzymes because they have to be an exact fit for the substrate they react with – in the same way that a lock can only be opened by one particular key. Even with millions of years to work at the problem, says Ivan Korendovych at Syracuse University in New York, nature would have struggled to build and test all possible enzyme molecules to identify the relatively few that catalyse today's metabolic reactions. © Copyright Reed Business Information Ltd.

Keyword: Alzheimers
Link ID: 19372 - Posted: 03.17.2014

By Gary Marcus and Christof Koch What would you give for a retinal chip that let you see in the dark or for a next-generation cochlear implant that let you hear any conversation in a noisy restaurant, no matter how loud? Or for a memory chip, wired directly into your brain's hippocampus, that gave you perfect recall of everything you read? Or for an implanted interface with the Internet that automatically translated a clearly articulated silent thought ("the French sun king") into an online search that digested the relevant Wikipedia page and projected a summary directly into your brain? Science fiction? Perhaps not for very much longer. Brain implants today are where laser eye surgery was several decades ago. They are not risk-free and make sense only for a narrowly defined set of patients—but they are a sign of things to come. Unlike pacemakers, dental crowns or implantable insulin pumps, neuroprosthetics—devices that restore or supplement the mind's capacities with electronics inserted directly into the nervous system—change how we perceive the world and move through it. For better or worse, these devices become part of who we are. Neuroprosthetics aren't new. They have been around commercially for three decades, in the form of the cochlear implants used in the ears (the outer reaches of the nervous system) of more than 300,000 hearing-impaired people around the world. Last year, the Food and Drug Administration approved the first retinal implant, made by the company Second Sight. ©2014 Dow Jones & Company, Inc.

Keyword: Robotics
Link ID: 19371 - Posted: 03.17.2014

By Neuroskeptic A neuroscience paper published before Christmas drew my eye with the expansive title: “How Thoughts Give Rise to Action“ Subtitled “Conscious Motor Intention Increases the Excitability of Target-Specific Motor Circuits”, the article’s abstract was no less bold, concluding that: These results indicate that conscious intentions govern motor function… until today, it was unclear whether conscious motor intention exists prior to movement, or whether the brain constructs such an intention after movement initiation. The authors, Zschorlich and Köhling of the University of Rostock, Germany, are weighing into a long-standing debate in philosophy, psychology, and neuroscience, concerning the role of consciousness in controlling our actions. To simplify, one school of thought holds that (at least some of the time), our intentions or plans control our actions. Many people would say that this is what common sense teaches us as well. But there’s an alternative view, in which our consciously-experienced intentions are not causes of our actions but are actually products of them, being generated after the action has already begun. This view is certainly counterintuitive, and many find it disturbing as it seems to undermine ‘free will’. That’s the background. Zschorlich and Köhling say that they’ve demonstrated that conscious intentions do exist, prior to motor actions, and that these intentions are accompanied by particular changes in brain activity. They claim to have done this using transcranial magnetic stimulation (TMS), a way of causing a localized modulation of brain electrical activity.

Keyword: Consciousness
Link ID: 19370 - Posted: 03.17.2014

By Christina Ianzito, We get it: Sleep is good for us. The National Sleep Foundation regularly campaigns “to celebrate the health benefits of sleep,” and experts have been boosting sleep’s values as no less important than proper diet and exercise. Insufficient sleep has been linked to stroke, obesity and heart disease. But sleeping too much may also be risky: It, too, is associated with a higher risk of heart disease and obesity, not to mention diabetes and depression. So, how much is too much? And if you’re sleep-deprived during the week, does sleeping 10 or 11 hours on Saturday and Sunday to catch up put you in any jeopardy? Most experts say that a healthy amount of sleep for an adult is a regular seven to nine hours a night. And the operative term here is “regular,” meaning the issue isn’t the college kid who power-sleeps 15 hours on vacation to catch up from too much studying (or partying). When scientists refer to “long sleepers,” they’re referring to people who consistently sleep nine or more hours a night, says Kristen Knutson, a biomedical anthropologist who focuses on sleep research at the University of Chicago’s Department of Medicine. “If you’ve been pulling all-nighters, by all means extend your sleep on the weekend if you can; try to catch up,” Knutson says, “but if you’re sleeping nine or 10 hours night after night after night for months on end . . . then we’ve got to understand why are you sleeping so much.” You might be getting poor-quality sleep, she adds, or are “already on the pathway to illness and your body is reacting by wanting you to sleep more.” © 1996-2014 The Washington Post

Keyword: Sleep
Link ID: 19369 - Posted: 03.17.2014

Linda Carroll TODAY contributor The stimulants used to treat ADHD might be making kids fat, a new study suggests. A study of more than 160,000 youngsters found that kids with Attention Deficit and Hyperactivity Disorder who received stimulants were at increased risk of becoming obese as they hit their teens. In contrast, kids with ADHD who took non-stimulant medications or got no therapy were very comparable, in terms of weight gain, to kids who didn’t have the disorder. “Our data suggest that stimulant use during childhood might have lifelong effects,” said Dr. Brian Schwartz, the study’s lead author and a professor of environmental health sciences, epidemiology, and medicine at the Johns Hopkins Bloomberg School of Public Health and senior investigator at the Geisinger Center for Health Research. “They might reset all sorts of physical properties and appetite parameters.” The new research may have uncovered a growing public health issue, Schwartz said. “Our data would seem to offer a lot of cause for concern with respect to prescribing stimulants,” he explained. Schwartz and his colleagues started the study because they were perplexed by the apparent paradox of hyperactive kids being prone to obesity. They scrutinized 12 years-worth of medical information from 163,820 Pennsylvania children, 13,427 of whom received an ADHD diagnosis.

Keyword: ADHD; Obesity
Link ID: 19368 - Posted: 03.17.2014