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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
Sara Reardon Every time something poked its foot, the mouse jumped in pain. Researchers at Circuit Therapeutics, a start-up company in Menlo Park, California, had made the animal hypersensitive to touch by tying off a nerve in its leg. But when they shone a yellow light on its foot while poking it, the mouse did not react. The treatment is one of several nearing clinical use that draw on optogenetics — a technique in which light is used to control genes and neuron firing. In March, RetroSense Therapeutics of Ann Arbor, Michigan, began the first clinical-safety trial of an optogenetic therapy to treat the vision disorder retinitis pigmentosa. Many scientists are waiting to see how the trial turns out before they decide how to move forward with their own research on a number of different applications. “I think it will embolden people if there’s good news,” says Robert Gereau, a pain researcher at Washington University in St Louis, Missouri. “It opens up a whole new range of possiblilities for how to treat neurological diseases.” Retinitis pigmentosa destroys photoreceptors in the eye. RetroSense’s treatment seeks to compensate for this loss by conferring light sensitivity to retinal ganglion cells, which normally help to pass visual signals from photoreceptors to the brain. The therapy involves injecting patients who are blind or mostly blind with viruses carrying genes that encode light-sensitive proteins called opsins. The cells fire when stimulated with blue light, passing the visual information to the brain. Chief executive Sean Ainsworth says that the company has injected several individuals in the United States with the treatment, and plans to enroll a total of 15 blind patients in its trial. RetroSense will follow them for two years, but may release some preliminary data later this year. © 2016 Nature Publishing Group
Link ID: 22235 - Posted: 05.21.2016
By Diana Kwon A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being Credit: Thomas Koehler/Getty Images Life in the city can be taxing. City dwellers often face higher rates of crime, pollution, social isolation and other environmental stressors than those living in rural areas. For years studies have consistently linked the risk of developing schizophrenia to urban environments—but researchers are only beginning to understand why this association exists. Addressing the link is increasingly urgent: According to a recent U.N. report, the proportion of people living in cities will rise from 54 percent of the world’s population in 2014 to 66 percent by 2050. Researchers first suggested in the 1930s that urban living might increase schizophrenia risk. Since then many large epidemiological studies have reported an association between the two, primarily in European countries such as Sweden and Denmark. Converging evidence has revealed that growing up in the city doubles the risk of developing psychosis later in life. Studies have also begun to find that urban environments may heighten the risk of other mental health issues such as depression and anxiety. A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being. Conversely, people predisposed to mental illness may simply be more likely to move into urban environments. Two studies published this month shed new light on these effects and suggest both scenarios could be involved. © 2016 Scientific American, a Division
Bret Stetka We've all been caught in that hazy tug of war between wakefulness and sleep. But the biology behind how our brains drive us to sleep when we're sleep-deprived hasn't been entirely clear. For the first time scientists have identified the neurons in the brain that appear to control sleep drive, or the growing pressure we feel to sleep after being up for an extended period of time. The findings, published online Thursday by the journal Cell, could lead to better understanding of sleep disorders in humans. And perhaps, one day, if the work all pans out, better treatments for chronic insomnia could be developed. To explore which brain areas might be involved in sleep drive, Johns Hopkins neuroscientist Dr. Mark Wu and his colleagues turned to fruit flies, that long tinkered-with subject of scientific inquiry. Despite our rather obvious physical distinctions, humans and fruit flies – or Drosophila – have a good deal in common when it comes to genes, brain architecture and even behaviors. Included in the study were over 500 strains of fly, each with unique brain activation profiles (meaning certain circuits are more active in certain flies). By employing a genetic engineering technique in which specific groups of neurons can be activated with heat, the researchers were able to monitor the firing of nearly all the major circuits in the fruit fly brain and monitor the resulting effects on sleep. Moreover, the neurons of interest were engineered to glow green when activated allowing specific cells to be identified with fluorescent microscopy. Wu found that activating a group of cells called R2 neurons, which are found in a brain region known as the ellipsoid body, put fruit flies to sleep, even for hours after the neurons were "turned off." © 2016 npr
By Karen Weintraub There are case reports of people with no previously known risks having a heart attack after a nightmare, though they appear to be quite rare. No studies have been done to determine just how rare nightmare-induced heart attacks might be, and experts do not know whether they may result from the pulse-racing effects of the frightening dream itself. Nightmares are more commonly seen in the rapid eye movement, or REM, phase of sleep, which gets longer as the night progresses. Therefore, nightmares are more likely to occur in the early morning hours. Heart attacks, too, are most common in the early morning hours, when internal body clocks start secreting stress hormones and blood pressure tends to rise, said Dr. Mary Ann McLaughlin, a cardiologist at the Icahn School of Medicine at Mount Sinai in New York. If someone is at risk for a heart attack — because of high blood pressure, diabetes, sleep apnea, smoking or other factors — that attack is more likely to occur in the early morning. But “it’s rare for an otherwise healthy person to have a nightmare that causes a heart attack,” said Dr. McLaughlin. Nightmares can be triggered by alcohol, lack of sleep and medications, including some antidepressants and blood pressure medications, she said. Anxiety and depression have also been linked to increased risk of nightmares. On the flip side, patients with heart disease often have sleep apnea, a form of disordered breathing that can lead to fragmented sleep, and potentially more nightmares, said Dr. Neomi Shah, a sleep specialist, also at Mount Sinai. One 2013 study found that apnea patients with regular nightmares woke up more often than those who didn’t. Nightmares disappeared in more than 90 percent of the patients who used a continuous positive airway pressure, or CPAP, machine to treat their apnea. © 2016 The New York Times Company
Link ID: 22232 - Posted: 05.21.2016
Laura Sanders In mice, a long course of antibiotics that wiped out gut bacteria slowed the birth of new brain cells and impaired memory, scientists write May 19 in Cell Reports. The results reinforce evidence for a powerful connection between bacteria in the gut and the brain (SN: 4/2/16, p. 23). After seven weeks of drinking water spiked with a cocktail of antibiotics, mice had fewer newborn nerve cells in a part of the hippocampus, a brain structure important for memory. The mice’s ability to remember previously seen objects also suffered. Further experiments revealed one way bacteria can influence brain cell growth and memory. Injections of immune cells called Ly6Chi monocytes boosted the number of new nerve cells. Themonocytes appear to carry messages from gut to brain, Susanne Wolf of the Max Delbrück Center for Molecular Medicine in Berlin and colleagues found. Exercise and probiotic treatment with eight types of live bacteria also increased the number of newborn nerve cells and improved memory in mice treated with antibiotics. The results help clarify the toll of prolonged antibiotic treatment, and hint at ways to fight back, the authors write. L. Möhle et al. Ly6Chi monocytes provide a link between antibiotic-induced changes in gut microbiota and adult hippocampal neurogenesis. Cell Reports. Vol. 15, May 31, 2016. doi: 10.1016/j.celrep.2016.04.074. © Society for Science & the Public 2000 - 2016
By D. T. Max When a spinal cord is damaged, location is destiny: the higher the injury, the more severe the effects. The spine has thirty-three vertebrae, which are divided into five regions—the coccygeal, the sacral, the lumbar, the thoracic, and the cervical. The nerve-rich cord traverses nearly the entire length of the spine. The nerves at the bottom of the cord are well buried, and sometimes you can walk away from damage to these areas. In between are insults to the long middle region of the spine, which begins at the shoulders and ends at the midriff. These are the thoracic injuries. Although they don’t affect the upper body, they can still take away the ability to walk or feel below the waist, including autonomic function (bowel, bladder, and sexual control). Injuries to the cord in the cervical area—what is called “breaking your neck”—can be lethal or leave you paralyzed and unable to breathe without a ventilator. Doctors who treat spinal-cord-injury patients use a letter-and-number combination to identify the site of the damage. They talk of C3s (the cord as it passes through the third cervical vertebra) or T8s (the eighth thoracic vertebra). These morbid bingo-like codes help doctors instantly gauge the severity of a patient’s injury. Darek Fidyka, who is forty-one years old, is a T9. He was born and raised in Pradzew, a small farming town in central Poland, not far from Lodz. ... Several of the wounds punctured his lungs, and one nearly cut his spinal cord in half. As Fidyka lay on the ground, he felt his body change. “I can remember very vividly losing feeling in my legs, bit by bit,” he says. “It started in the upper part of the spine and was moving down slowly while I lay waiting for the ambulance to arrive.”
Link ID: 22230 - Posted: 05.19.2016
By Christie Aschwanden When concussions make the news, it’s usually about football. But head injuries happen in other sports too, and not just to men. During a congressional hearing on concussions in youth sports on Friday, Dawn Comstock, an epidemiologist who studies sports injuries, told a House Energy and Commerce subcommittee that in sports like soccer and basketball in which girls and boys play by the same rules, with the same equipment and the same facilities, “girls have higher concussion rates than boys.” Comstock, a researcher at the Colorado School of Public Health, is the first author of a 2015 study published in JAMA Pediatrics that quantified concussions in high school soccer and found that they were about one and a half times more common in girls than in boys. When U.S. Rep. Diana DeGette, D-Colo., asked whether more data was needed to show that girls have higher concussion rates, Comstock replied, “We already have the data that’s consistently shown this gender difference.” What we don’t have, she said, is a proven explanation for the discrepancy. Some researchers have wondered whether women and girls are simply more likely to report their symptoms than men and boys are. “It’s a sexist way to say that they’re not as tough,” said Katherine Price Snedaker, executive director of Pink Concussions,1 an organization that is seeking answers to how concussions affect women and girls. The group recently held a summit on female concussion and traumatic brain injuries at Georgetown University, and one of the speakers was Shannon Bauman, a sports physician who presented data from 207 athletes — both male and female — who’d been evaluated at her specialty concussion clinic in Barrie, Ontario, between September 2014 and January 2016.
Stephen Cave For centuries, philosophers and theologians have almost unanimously held that civilization as we know it depends on a widespread belief in free will—and that losing this belief could be calamitous. Our codes of ethics, for example, assume that we can freely choose between right and wrong. In the Christian tradition, this is known as “moral liberty”—the capacity to discern and pursue the good, instead of merely being compelled by appetites and desires. The great Enlightenment philosopher Immanuel Kant reaffirmed this link between freedom and goodness. If we are not free to choose, he argued, then it would make no sense to say we ought to choose the path of righteousness. Today, the assumption of free will runs through every aspect of American politics, from welfare provision to criminal law. It permeates the popular culture and underpins the American dream—the belief that anyone can make something of themselves no matter what their start in life. As Barack Obama wrote in The Audacity of Hope, American “values are rooted in a basic optimism about life and a faith in free will.” So what happens if this faith erodes? The sciences have grown steadily bolder in their claim that all human behavior can be explained through the clockwork laws of cause and effect. This shift in perception is the continuation of an intellectual revolution that began about 150 years ago, when Charles Darwin first published On the Origin of Species. Shortly after Darwin put forth his theory of evolution, his cousin Sir Francis Galton began to draw out the implications: If we have evolved, then mental faculties like intelligence must be hereditary. But we use those faculties—which some people have to a greater degree than others—to make decisions. So our ability to choose our fate is not free, but depends on our biological inheritance. © 2016 by The Atlantic Monthly Group.
Link ID: 22228 - Posted: 05.18.2016
George Johnson At the Science of Consciousness conference last month in Tucson, I was faced with a quandary: Which of eight simultaneous sessions should I attend? In one room, scientists and philosophers were discussing the physiology of brain cells and how they might generate the thinking mind. In another, the subject was free will — real or an illusion? Next door was a session on panpsychism, the controversial (to say the least) idea that everything — animal, vegetable and mineral — is imbued at its subatomic roots with mindlike qualities. Running on parallel tracks were sessions titled “Phenomenal Consciousness,” the “Neural Correlates of Consciousness” and the “Extended Mind.” For much of the 20th century, the science of consciousness was widely dismissed as an impenetrable mystery, a morass of a problem that could be safely pursued only by older professors as they thought deep thoughts in their endowed chairs. Beginning in the 1990s, the field slowly became more respectable. There is, after all, a gaping hole in science. The human mind has plumbed the universe, concluding that it is precisely 13.8 billion years old. With particle accelerators like the Large Hadron Collider at CERN, scientists have discovered the vanishingly tiny particles, like the Higgs boson, that underpin reality. But there is no scientific explanation for consciousness — without which none of these discoveries could have been made. © 2016 The New York Times Company
Link ID: 22227 - Posted: 05.18.2016
Andrea Hsu Scientists and doctors say the case is clear: The best way to tackle the country's opioid epidemic is to get more people on medications that have been proven in studies to reduce relapses and, ultimately, overdoses. Yet, only a fraction of the more than 4 million people believed to abuse prescription painkillers or heroin in the U.S. are being given what's called medication-assisted treatment. One reason is the limited availability of the treatment. But it's also the case that stigma around the addiction drugs has inhibited their use. Methadone and buprenorphine, two of the drugs used for treatment, are themselves opioids. A phrase you often hear about medication-assisted treatment is that it's merely replacing one drug with another. While doctors and scientists strongly disagree with that characterization, it's a view that's widespread in recovery circles. Now, the White House is pushing to change the landscape for people seeking help. In his 2017 budget, President Obama has asked Congress for $1.1 billion in new funding to address the opioid epidemic, with almost all of it geared toward expanding access to medication-assisted treatment. The White House is also highlighting success stories. At the National Prescription Drug Abuse and Heroin Summit held in Atlanta in March, President Obama appeared on stage with Crystal Oertle, a 35-year-old mother of two from Ohio. Oertle spoke of her spiral into addiction, which began with prescription painkillers and progressed to heroin. She tried unsuccessfully to quit on her own several times, before being prescribed buprenorphine a year ago. © 2016 npr
Keyword: Drug Abuse
Link ID: 22226 - Posted: 05.18.2016
By Sarah Kaplan You probably wouldn't be surprised if a scientist told you that your genes influence when you hit puberty, how tall you are, what your BMI will be and whether you're likely to develop male pattern baldness. But what if he said that the same gene could hold sway over all four things? That finding comes from a study published Monday in the journal Nature Genetics. Using data from dozens of genome-wide association studies (big scans of complete sets of DNA from many thousands of people), researchers at the New York Genome Center and the genetic analysis company 23andMe found examples of single "multitasking" genes that influence diverse and sometimes seemingly disparate traits. The scientists say that the links they uncovered could help researchers understand how certain genes work, and figure out better ways of treating some of the health problems they might control. "Most studies tend to go one disease at a time," said Joseph Pickrell, a professor at Columbia University and the New York Genome Center's lead investigator on the project. "But if we can try to make these sorts of connections between what you might think of as unrelated traits ... that gives us another angle of attack to understand the connections between these different diseases." To start, Pickrell and his team sought out genome-wide association studies (GWAS) identifying particular genetic variants associated with 42 different traits. Many had to do with diseases (for example, studies that linked certain genes to the risk of developing Alzheimer's or type 2 diabetes) and other personal health traits (body mass index, blood type, cholesterol levels).
Keyword: Genes & Behavior
Link ID: 22225 - Posted: 05.18.2016
Zoe Cormier A hallucinogenic drug derived from magic mushrooms could be useful in treating depression, the first safety study of this approach has concluded. Researchers from Imperial College London gave 12 people psilocybin, the active component in magic mushrooms. All had been clinically depressed for a significant amount of time — on average 17.8 years. None of the patients had responded to standard medications, such as selective serotonin re-uptake inhibitors (SSRIs), or had electroconvulsive therapy. One week after receiving an oral dose of psilocybin, all patients experienced a marked improvement in their symptoms. Three months on, five patients were in complete remission. “That is pretty remarkable in the context of currently available treatments,” says Robin Carhart-Harris, a neuropsychopharmacologist at Imperial College London and first author of the latest study, which is published in The Lancet Psychiatry1. The equivalent remission rate for SSRIs is around 20%. The study's authors are not suggesting that psilocybin should be a treatment of last resort for depressed patients. “Our conclusion is more sober than that — we are simply saying that this is doable,” says Carhart-Harris. “We can give psilocybin to depressed patients, they can tolerate it, and it is safe. This gives us an initial impression of the effectiveness of the treatment.” © 2016 Nature Publishing Group
By Simon Oxenham The “cuddle chemical”. The “moral molecule”. Oxytocin has quite a reputation – but much of what we thought about the so-called “love hormone” may be wrong. Oxytocin is made by the hypothalamus and acts on the brain, playing a role in bonding, sex and pregnancy. But findings that a sniff of the hormone is enough to make people trust each other more are being called into question after a string of studies failed to replicate classic experiments. Paul Zak at the Centre for Neuroeconomic Studies in Claremont, California, made his moral molecule hypothesis famous in 2011 when he memorably squirted a syringe of the hormone into the air while delivering a TED talk. When people sniff oxytocin before playing a money-lending game, it increases how much they trust each other, he explained. But several teams have been unable to replicate his finding. Last November, Gideon Nave at the California Institute of Technology in Pasadena and his colleagues reviewed studies of oxytocin, and concluded that the effect of nasal squirts of the hormone on trust are not reliably different from zero. Nave’s team aren’t the only ones calling the moral molecule hypothesis into question. In 2012, Moïra Mikolajczak at the Catholic University of Louvain (UCL) in Belgium and her colleagues published their own seminal findings backing a link between trust and oxytocin. They found that when people filled out an anonymous questionnaire about their sex lives and fantasies, they were less likely to seal the envelopes they returned them in if given a nasal dose of oxytocin beforehand. © Copyright Reed Business Information Ltd.