Most Recent Links
Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.
By GINA KOLATA Could it be that Alzheimer’s disease stems from the toxic remnants of the brain’s attempt to fight off infection? Provocative new research by a team of investigators at Harvard leads to this startling hypothesis, which could explain the origins of plaque, the mysterious hard little balls that pockmark the brains of people with Alzheimer’s. It is still early days, but Alzheimer’s experts not associated with the work are captivated by the idea that infections, including ones that are too mild to elicit symptoms, may produce a fierce reaction that leaves debris in the brain, causing Alzheimer’s. The idea is surprising, but it makes sense, and the Harvard group’s data, published Wednesday in the journal Science Translational Medicine, supports it. If it holds up, the hypothesis has major implications for preventing and treating this degenerative brain disease. The Harvard researchers report a scenario seemingly out of science fiction. A virus, fungus or bacterium gets into the brain, passing through a membrane — the blood-brain barrier — that becomes leaky as people age. The brain’s defense system rushes in to stop the invader by making a sticky cage out of proteins, called beta amyloid. The microbe, like a fly in a spider web, becomes trapped in the cage and dies. What is left behind is the cage — a plaque that is the hallmark of Alzheimer’s. So far, the group has confirmed this hypothesis in neurons growing in petri dishes as well as in yeast, roundworms, fruit flies and mice. There is much more work to be done to determine if a similar sequence happens in humans, but plans — and funding — are in place to start those studies, involving a multicenter project that will examine human brains. “It’s interesting and provocative,” said Dr. Michael W. Weiner, a radiology professor at the University of California, San Francisco, and a principal investigator of the Alzheimer’s Disease Neuroimaging Initiative, a large national effort to track the progression of the disease and look for biomarkers like blood proteins and brain imaging to signal the disease’s presence. © 2016 The New York Times Company
Ronald Crystal The goal of antiaddiction vaccines is to prevent addictive molecules from reaching the brain, where they produce their effects and can create chemical dependencies. Vaccines can accomplish this task, in theory, by generating antibodies—proteins produced by the immune system—that bind to addictive particles and essentially stop them in their tracks. But challenges remain. Among them, addictive molecules are often too small to be spotted by the human immune system. Thus, they can circulate in the body undetected. Researchers have developed two basic strategies for overcoming this problem. One invokes so-called active immunity by tethering an addictive molecule to a larger molecule, such as the proteins that encase a common cold virus. This viral shell does not make people sick but does prompt the immune system to produce high levels of antibodies against it and whatever is attached to it. In our laboratory, we have tested this method in animal models and successfully blocked chemical forms of cocaine or nicotine from reaching the brain. Another approach researchers are testing generates what is known as passive immunity against addictive molecules in the body. They have cultured monoclonal antibodies that can bind selectively to addictive molecules. The hurdle with this particular method is that monoclonal antibodies are expensive to produce and need to be administrated frequently to be effective. © 2016 Scientific American
By RUSSELL GOLDMAN There’s an elephant at a zoo outside Seoul that speaks Korean. — You mean, it understands some Korean commands, the way a dog can be trained to understand “sit” or “stay”? No, I mean it can actually say Korean words out loud. — Pics or it didn’t happen. Here, watch the video. To be fair, the elephant, a 26-year-old Asian male named Koshik, doesn’t really speak Korean, any more than a parrot can speak Korean (or English or Klingon). But parrots are supposed to, well, parrot — and elephants are not. And Koshik knows how to say at least five Korean words, which are about five more than I do. The really amazing part is how he does it. Koshik places his trunk inside his mouth and uses it to modulate the tone and pitch of the sounds his voice makes, a bit like a person putting his fingers in his mouth to whistle. In this way, Koshik is able to emulate human speech “in such detail that Korean native speakers can readily understand and transcribe the imitations,” according to the journal Current Biology. What’s in his vocabulary? Things he hears all the time from his keepers: the Korean words for hello, sit down, lie down, good and no. Elephant Speaks Korean | Video Video by LiveScienceVideos Lest you think this is just another circus trick that any Jumbo, Dumbo or Babar could pull off, the team of international scientists who wrote the journal article say Koshik’s skills represent “a wholly novel method of vocal production and formant control in this or any other species.” Like many innovations, Koshik’s may have been born of sad necessity. Researchers say he started to imitate his keepers’s sounds only after he was separated from other elephants at the age of 5 — and that his desire to speak like a human arose from sheer loneliness. © 2016 The New York Times Company
By Teal Burrell In neuroscience, neurons get all the glory. Or rather, they used to. Researchers are beginning to discover the importance of something outside the neurons—a structure called the perineuronal net. This net might reveal how memories are stored and how various diseases ravage the brain. The realization of important roles for structures outside neurons serves as a reminder that the brain is a lot more complicated than we thought. Or, it’s exactly as complicated as neuroscientists thought it was 130 years ago. In 1882, Italian physician and scientist Camillo Golgi described a structure that enveloped cells in the brain in a thin layer. He later named it the pericellular net. His word choice was deliberate; he carefully avoided the word “neuron” since he was engaged in a battle with another neuroscience luminary, Santiago Ramón y Cajal, over whether the nervous system was a continuous meshwork of cells that were fused together—Golgi’s take—or a collection of discrete cells, called neurons—Ramón y Cajal’s view. Ramón y Cajal wasn’t having it. He argued Golgi was wrong about the existence of such a net, blaming the findings on Golgi’s eponymous staining technique, which, incidentally, is still used today. Ramón y Cajal’s influence was enough to shut down the debate. While some Golgi supporters labored in vain to prove the nets existed, their findings never took hold. Instead, over the next century, neuroscientists focused exclusively on neurons, the discrete cells of the nervous system that relay information between one another, giving rise to movements, perceptions, and emotions. (The two adversaries would begrudgingly share a Nobel Prize in 1906 for their work describing the nervous system.) © 1996-2016 WGBH Educational Foundation
Link ID: 22252 - Posted: 05.26.2016
By Amina Zafar, Tragically Hip frontman Gord Downie's resilience and openness about his terminal glioblastoma and his plans to tour could help to reduce stigma and improve awareness, some cancer experts say. Tuesday's news revealed that the singer has an aggressive form of cancer that originated in his brain. An MRI scan last week showed the tumour has responded well to surgery, radiation and chemotherapy, doctors said. "I was quickly impressed by Gord's resilience and courage," Downie's neuro-oncologist, Dr. James Perry of Sunnybrook Health Sciences Centre, told a news conference. Perry said it's daunting for many of his patients to reveal the diagnosis to their family, children and co-workers. "The news today, while sad, also creates for us in brain tumour research an unprecedented opportunity to create awareness and to create an opportunity for fundraising for research that's desperately needed to improve the odds for all people with this disease," Perry said. Dr. James Perry, head of neurology at Toronto's Sunnybrook Health Sciences Centre, calls Gord Downie's sad news an unprecedented opportunity to fundraise for brain tumour research. (Aaron Vincent Elkaim/Canadian Press) "Gord's courage in coming forward with his diagnosis will be a beacon for all patients with glioblastoma in Canada. They will see a survivor continuing with his craft despite its many challenges." ©2016 CBC/Radio-Canada.
Link ID: 22251 - Posted: 05.26.2016
Bradley George All sorts of health information is now a few taps away on your smartphone, from how many steps you take — to how well you sleep at night. But what if you could use your phone and a computer to test your vision? A company is doing just that — and eye care professionals are upset. Some states have even banned it. A Chicago-based company called Opternative offers the test. The site asks some questions about your eyes and overall health; it also wants to know your shoe size to make sure you're the right distance from your computer monitor. You keep your smartphone in your hand and use the Web browser to answer questions about what you see on the computer screen. Like a traditional eye test, there are shapes, lines and letters. It takes about 30 minutes. "We're trying to identify how bad your vision is, so we're kind of testing your vision to failure, is the way I would describe it," says Aaron Dallek, CEO of Opternative. Dallek co-founded the company with an optometrist, who was searching for ways to offer eye exams online. "Me being a lifetime glasses and contact wearer, I was like 'Where do we start?' So, that was about 3 1/2 years ago, and we've been working on it ever since," Dallek says. © 2016 npr
Link ID: 22250 - Posted: 05.26.2016
Susan Milius Forget it, peacocks. Nice try, elk. Sure, sexy feathers and antlers are showy, but the sperm of a fruit fly could be the most over-the-top, exaggerated male ornamentation of all. In certain fruit fly species, such as Drosophila bifurca, males measuring just a few millimeters produce sperm with a tail as long as 5.8-centimeters, researchers report May 25 in Nature. Adjusted for body size, the disproportionately supersized sperm outdoes such exuberant body parts as pheasant display feathers, deer antlers, scarab beetle horns and the forward-grasping forceps of earwigs. Fruit flies’ giant sperm have been challenging to explain, says study coauthor Scott Pitnick of Syracuse University in New York. Now he and his colleagues propose that a complex interplay of male and female benefits has accelerated sperm length in a runaway-train scenario. Males with longer sperm deliver fewer sperm, bucking a more-is-better trend. Yet, they still manage to transfer a few dozen to a few hundred per mating. And as newly arrived sperm compete to displace those already waiting in a female’s storage organ, longer is better. Fewer sperm per mating means females tend to mate more often, intensifying the sperm-vs.-sperm competition. Females that have the longest storage organs, which favor the longest sperm, benefit too: Males producing megasperm, the researchers found, tend to be the ones with good genes likely to produce robust offspring. “Sex,” says Pitnick, “is a powerful force.” © Society for Science & the Public 2000 - 2016
Sara Reardon Children from impoverished families are more prone to mental illness, and alterations in DNA structure could be to blame, according to a study published on 24 May in Molecular Psychiatry1. Poverty brings with it a number of different stressors, such as poor nutrition, increased prevalence of smoking and the general struggle of trying to get by. All of these can affect a child’s development, particularly in the brain, where the structure of areas involved in response to stress and decision-making have been linked to low socioeconomic status. Poor children are more prone to mental illnesses such as depression than their peers from wealthier families, but they are also more likely to have cognitive problems. Some of these differences are clearly visible in the brain structure and seem to appear at birth, which suggests that prenatal exposure to these stressors can be involved2. But neurodevelopment does not stop at birth. Neuroscientist Ahmad Hariri of Duke University in Durham, North Carolina, suspected that continual exposure to stressors might affect older children as well. He decided to test this idea by studying chemical tags known as methyl groups, which alter DNA structure to regulate how genes are expressed. There is some evidence that methylation patterns can be passed down through generations, but they are also altered by environmental factors, such as smoking. © 2016 Nature Publishing Group,
Dean Burnett A recent report by the National Obesity Forum stated that official advice about low-fat diets is wrong. As ever, there’s now heated debate over how valid/accurate this claim is. But let’s step back a moment and ask a revealing question: why do official government dietary guidelines even exist? Why are they necessary? From an entirely logical position, eating food fulfils several requirements. It provides the energy to do things, helps us build up stores of energy for when needed, and provides the materials required to build and maintain our bodies. Therefore, the human body requires a regular intake of nutrients, vitamins and calories to maintain day-to-day functioning. As a result, the human body has developed an intricate digestive system to monitor and regulate our food intake. The digestive system is quite cool. It has a sophisticated nervous system that can operate pretty much independently, so is often regarded as separate from the main one, leading some to describe it as a “second brain”, there to encourage, monitor and process the consumption and digestion of food. It also utilises hormones, namely leptin and ghrelin, which decrease and increase appetite respectively depending on how much food the body has/needs. It’s a painstakingly complex and precise system that’s evolved over aeons to make sure we eat what and when we need to, and get the most out of our food. However, at some point the human brain got involved, then everything went to hell. This is why we can now be presented with foodstuffs we’re repeatedly told are unhealthy, even dangerous, and say “Thanks. Extra chilli sauce on mine, please”.
by Bruce Bower For a landmark 1977 paper, psychologist Andrew Meltzoff stuck his tongue out at 2- to 3-week-old babies. Someone had to do it. After watching Meltzoff razz them for 15 seconds, babies often stuck out their own tongues within the next 2½ minutes. Newborns also tended to respond in kind when the young researcher opened his mouth wide, pushed out his lips like a duck and opened and closed the fingers of one hand. Meltzoff, now at the University of Washington in Seattle, and a colleague were the first to report that babies copy adults’ simple physical deeds within weeks of birth. Until then, most scientists assumed that imitation began at around 9 months of age. Newborns don’t care that imitation is the sincerest form of flattery. For them, it may be a key to interacting with (and figuring out) those large, smiley people who come to be known as mommy and daddy. And that’s job number one for tykes hoping to learn how to talk and hang out with a circle of friends. Meltzoff suspected that babies enter the world able to compare their own movements — even those they can feel but not see, such as a projecting tongue — to corresponding adult actions. Meltzoff’s report has inspired dozens of papers on infant imitation. Some have supported his results, some haven’t. A new report, published May 5 in Current Biology, falls in the latter group. The study of 106 Australian babies tracked from 1 to 9 weeks of age concludes that infants don’t imitate anyone. © Society for Science & the Public 2000 - 201
Keyword: Development of the Brain
Link ID: 22246 - Posted: 05.25.2016
By Lisa Rapaport (Reuters Health) - Attention deficit hyperactivity disorder (ADHD), usually diagnosed in children, may show up for the first time in adulthood, two recent studies suggest. And not only can ADHD appear for the first time after childhood, but the symptoms for adult-onset ADHD may be different from symptoms experienced by kids, the researchers found. “Although the nature of symptoms differs somewhat between children and adults, all age groups show impairments in multiple domains – school, family and friendships for kids and school, occupation, marriage and driving for adults,” said Stephen Faraone, a psychiatry researcher at SUNY Upstate Medical University in Syracuse, New York and author of an editorial accompanying the two studies in JAMA Psychiatry. Faraone cautions, however, that some newly diagnosed adults might have had undetected ADHD as children. Support from parents and teachers or high intelligence, for example, might prevent ADHD symptoms from emerging earlier in life. It’s not clear whether study participants “were completely free of psychopathology prior to adulthood,” Faraone said in an email. One of the studies, from Brazil, tracked more than 5,200 people born in 1993 until they were 18 or 19 years old. © 2016 Scientific American
by Helen Thompson In hunting down delicious fish, Flipper may have a secret weapon: snot. Dolphins emit a series of quick, high-frequency sounds — probably by forcing air over tissues in the nasal passage — to find and track potential prey. “It’s kind of like making a raspberry,” says Aaron Thode of the Scripps Institution of Oceanography in San Diego. Thode and colleagues tweaked a human speech modeling technique to reproduce dolphin sounds and discern the intricacies of their unique style of sound production. He presented the results on May 24 in Salt Lake City at the annual meeting of the Acoustical Society of America. Dolphin chirps have two parts: a thump and a ring. Their model worked on the assumption that lumps of tissue bumping together produce the thump, and those tissues pulling apart produce the ring. But to match the high frequencies of live bottlenose dolphins, the researchers had to make the surfaces of those tissues sticky. That suggests that mucus lining the nasal passage tissue is crucial to dolphin sonar. The vocal model also successfully mimicked whistling noises used to communicate with other dolphins and faulty clicks that probably result from inadequate snot. Such techniques could be adapted to study sound production or echolocation in sperm whales and other dolphin relatives. © Society for Science & the Public 2000 - 2016.
Link ID: 22244 - Posted: 05.25.2016
By Ian Randall As if you needed another reason to hate the gym, it now turns out that exercise can exhaust not only your muscles, but also your eyes. Fear not, however, for coffee can perk them right up again. During strenuous exercise, our muscles tire as they run out of fuel and build up waste products. Muscle performance can also be affected by a phenomenon called “central fatigue,” in which an imbalance in the body’s chemical messengers prevents the central nervous system from directing muscle movements effectively. It was not known, however, whether central fatigue might also affect motor systems not directly involved in the exercise itself—such as those that move the eyes. To find out, researchers gave 11 volunteers a carbohydrate solution either with a moderate dose of caffeine—which is known to stimulate the central nervous system—or as a placebo without, during 3 hours of vigorous cycling. After exercising, the scientists tested the cyclists with eye-tracking cameras to see how well their brains could still control their visual system. The team found that exercise reduced the speed of rapid eye movements by about 8%, impeding their ability to capture new visual information. The caffeine—the equivalent of two strong cups of coffee—was sufficient to counteract this effect, with some cyclists even displaying increased eye movement speeds, the team reports today in Scientific Reports. So it might be a good idea to get someone else to drive you home after that marathon. © 2016 American Association for the Advancement of Science.
Link ID: 22243 - Posted: 05.25.2016
By Diana Kwon More than one in 10 Americans older than 12 takes antidepressants, according to a 2011 report by the National Center for Health Statistics. A significant but unknown number of children younger than 12 take them, too. Although most such drugs are not approved for young children, doctors have prescribed them off-label for years because they have been thought to have relatively mild side effects. Yet recent reports have revealed that important data about the safety of these drugs—especially their risks for children and adolescents—have been withheld from the medical community and the public. In the latest and most comprehensive analysis, published in January in the BMJ, researchers at the Nordic Cochrane Center in Copenhagen showed that pharmaceutical companies have not been revealing the full extent of serious harm in clinical study reports, which are detailed documents sent to regulatory authorities such as the U.S. Food and Drug Administration and the European Medicines Agency (EMA) when applying for approval of a new drug. The researchers examined reports from 70 double-blind, placebo-controlled trials of two common categories of antidepressants—selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs)—and found that the occurrence of suicidal thoughts and aggressive behavior doubled in children and adolescents who used these drugs. The investigators discovered that some of the most revealing information was buried in appendices where individual patient outcomes are listed. For example, they found clear instances of suicidal thinking that had been passed off as “emotional lability” or “worsening depression” in the report itself. This information, however, was available for only 32 out of the 70 trials. “We found that a lot of the appendices were often only available on request to the authorities, and the authorities had never requested them,” says Tarang Sharma, a Ph.D. student at Cochrane and lead author of the study. “I'm actually kind of scared about how bad the actual situation would be if we had the complete data.” © 2016 Scientific American
By JOHN BRANCH When the N.F.L. agreed in 2012 to donate tens of millions of dollars to concussion research overseen by the National Institutes of Health, it was widely seen as a positive turning point in football’s long history of playing down the long-term effects of brain injuries on players. At the time, the league said that it would have no influence over how the money was used. But the league and its head, neck and spine committee worked to improperly influence the government research, trying to steer the study toward a doctor with ties to the league, according to a study conducted by a congressional committee and released on Monday. “Our investigation has shown that while the N.F.L. had been publicly proclaiming its role as funder and accelerator of important research, it was privately attempting to influence that research,” the study concluded. “The N.F.L. attempted to use its ‘unrestricted gift’ as leverage to steer funding away from one of its critics.” The N.F.L., in a statement, said it rejected the accusations laid out in the study, which was conducted by Democratic members of the House Committee on Energy and Commerce. “There is no dispute that there were concerns raised about both the nature of the study in question and possible conflicts of interest,” the league said. “These concerns were raised for review and consideration through the appropriate channels.” It is the latest in a long history of instances in which the N.F.L. has been found to mismanage concussion research, dating to the league’s first exploration of the crisis when it used deeply flawed data to produce a series of studies. In this case, some of the characters are the same, including Dr. Elliot Pellman, who led the league’s concussion committee for years before he was discredited for his questionable credentials and his role as a longtime denier of the effects of concussions on players. © 2016 The New York Times Company
Keyword: Brain Injury/Concussion
Link ID: 22241 - Posted: 05.24.2016
By Andy Coghlan It’s a tear-jerker worthy of Hollywood – and one of the first examples of compassionate care and grief in a wild monkey. The alpha male of a group of snub-nosed monkeys and his dying partner spent a final, tender hour together beneath the tree from which she had fallen minutes earlier, cracking her head on a rock. Before she succumbed, he gently touched and groomed her. And after she was dead he remained by her side for 5 minutes, touching her and pulling gently at her hand, as if to try and revive her (for a full account of what happened, see “A monkey tends to his dying mate – as it unfolded”, below). “The case we’ve reported is particularly important because of the exclusively gentle nature of the interactions, and the special treatment of the dying female shown by the adult male,” says James Anderson of Kyoto University, Japan. “The events suggest that in the case of strongly bonded individuals at least, monkeys may show compassionate behaviour to ailing or dying individuals.” Together, the reports add to evidence that humans may not be the only species to display grieving behaviour following bereavement, or to show respect for dead individuals with whom they have forged ties. They also hint that animals have some recognition of the finality of death. “It seems likely that in long-lived species such as many primates, repeated exposure to death within the group leads to an understanding of the irreversibility of death,” says Anderson. “I believe the adult male and other members of his unit understood the dead female was no longer alive.” © Copyright Reed Business Information Ltd.
“I understand how the appearance and texture of food can change the experience,” says food writer and Great British Bake Off finalist Tamal Ray, “but I never really considered how the other senses might have a role to play.” An anaesthetist by day, Ray is best-known for creating spectacular tiered cakes and using a syringe to inject extra, syrupy deliciousness into them. Which is why we introduced him to Oxford psychologist Charles Spence and chef Jozef Youssef – and turned what they taught him about the science of taste into the video above. Part mad professor, part bon vivant, Spence has spent the past 15 years discovering that little of how we experience flavour is to do with our taste buds – smell, vision, touch and even sound dictate how we perceive flavours. Youssef, meanwhile, sharpened his culinary skills at the Fat Duck, the Connaught and the Dorchester, before starting experimental dining outfit Kitchen Theory, where he applies science to meals that play with the multisensory experience of eating. When Spence started studying the sensory science behind flavour perception, it was a deeply unfashionable subject. “There’s some ancient Roman notion that eating and drinking involve lower senses,” he says, “not higher, rational senses like hearing and vision.” Now, the fruits of the research field he calls “gastrophysics” can be seen everywhere from the world’s top restaurants to airline food, via progressive hospital kitchens and multisensory cocktail bars. Spence heads the Crossmodal Research Laboratory at the University of Oxford. “Crossmodal”, in this context, means the investigation of how all the senses interact. Although we’re often unaware of it, when it comes to flavour perception, we all have synaesthesia. That is, our senses intermingle so that our brains combine shapes, textures, colours and even sounds with corresponding tastes.
Keyword: Chemical Senses (Smell & Taste)
Link ID: 22239 - Posted: 05.23.2016
Aaron E. Carroll I don’t eat breakfast. It’s not that I dislike what’s offered. Given the choice of breakfast food or lunch food, I’d almost always choose eggs or waffles. It’s just that I’m not hungry at 7:30 a.m., when I leave for work. In fact, I’m rarely hungry until about lunchtime. So, other than a morning cup of coffee, I don’t eat much before noon. This habit has forced me to be subjected to more lectures on how I’m hurting myself, my diet, my work and my health than almost any other. Only a fool would skip the most important meal of the day, right? As with many other nutritional pieces of advice, our belief in the power of breakfast is based on misinterpreted research and biased studies. It does not take much of an effort to find research that shows an association between skipping breakfast and poor health. A 2013 study published in the journal Circulation found that men who skipped breakfast had a significantly higher risk of coronary heart disease than men who ate breakfast. But, like almost all studies of breakfast, this is an association, not causation. More than most other domains, this topic is one that suffers from publication bias. In a paper published in The American Journal of Clinical Nutrition in 2013, researchers reviewed the literature on the effect of breakfast on obesity to look specifically at this issue. They first noted that nutrition researchers love to publish results showing a correlation between skipping breakfast and obesity. They love to do so again and again. At some point, there’s no reason to keep publishing on this. However, they also found major flaws in the reporting of findings. People were consistently biased in interpreting their results in favor of a relationship between skipping breakfast and obesity. They improperly used causal language to describe their results. They misleadingly cited others’ results. And they also improperly used causal language in citing others’ results. People believe, and want you to believe, that skipping breakfast is bad. © 2016 The New York Times Company
Link ID: 22238 - Posted: 05.23.2016
By Jessica Hamzelou People who experience migraines that are made worse by light might be better off seeing the world in green. While white, blue, red and amber light all increase migraine pain, low-intensity green light seems to reduce it. The team behind the finding hope that specially developed sunglasses that screen out all wavelengths of light except green could help migraineurs. Many people experience sensitivity to light during a migraine. Photophobia, as it is known, can leave migraineurs resorting to sunglasses in well-lit rooms, or seeking the comfort of darkness. The reaction is thought to be due to the brain’s wiring. In a brain region called the thalamus, neurons that transmit sensory information from our retinas cross over with other neurons that signal pain. As a result, during migraine, light can worsen pain and pain can cause visual disturbance, says Rami Burstein at Harvard University. But not all colours of light have the same effect. Six years ago, Burstein and his colleagues studied migraine in sufferers who are blind, either due to the loss of an eye or retina, or because of retinal damage. They found that people who had some remaining retinal cells had worse migraines when they were in brightly lit environments, and that blue light seemed to have the strongest impact. The finding caused a flurry of excitement, and the promotion of sunglasses that filter out blue light. © Copyright Reed Business Information Ltd.
By Lucas Powers, CBC News You're standing on the side of the road, with traffic whizzing past. The police officer who pulled you over suspects you may have smoked the reefer before departing for McDonald's. But she's in a bit of a quagmire, because, really, there's no reliable way to know for sure. Are you high? If you are high, how high are you, really? Or really did you just want those little cheeseburgers (no ketchup and extra pickles)? So she does the most logical thing: a field sobriety test. Tried and true. Walk the line. Touch the tip your nose. Can't do it? That's... suspicious. Maybe a night in the clink? Some Canadian cops also have roadside saliva swabs that can be used to test for the presence of drugs, but they are useless, legally speaking (for now.) Now, had you been quaffing ales before the drive, a breathalyzer — controversial as they can be in terms of accuracy and reliability — would have cleared up the situation pretty quickly. Of course, no such roadside device exists for cannabis and its psychotropic ingredient THC. There's growing evidence that cannabis can impair driving by slowing reaction times and encouraging perplexing moves by drivers, like slowing way down and being reluctant to change lanes. Doctors at Toronto's Centre for Addiction and Mental Health are doing the world's biggest-ever clinical study, asking exactly what causes this behaviour, and how dangerous it is. Either way, an innovation war worth billions to the victor has been declared over developing a cannabis breathalyzer. ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 22236 - Posted: 05.23.2016