By Bernardo Kastrup, Edward F. Kelly A long-awaited resurgence in psychedelic research is now under way and some of its early results have been startling. Whereas most scientists expected the mind-boggling experiences of psychedelic states to correlate with increased brain activity,a landmark study from 2012 found the opposite to be the case. Writing in this magazine, neuroscientist Christof Koch expressed the community’s collective surprise. These unexpected findings have since been repeatedly confirmed with a variety of psychedelic agents and measures of brain activity (2013,2015,2016, 2017). Under the mainstream physicalist view that brain activity is, or somehow generates, the mind, the findings certainly seem counterintuitive: How can the richness of experience go up when brain activity goes down? Understandably, therefore, researchers have subsequently endeavored to find something in patterns of brain activity that reliably increases in psychedelic states. Alternatives include brain activity variability, functional coupling between different brain areas and, most recently, a property of brain activity variously labeled as “complexity,” “diversity,” “entropy” or “randomness”—terms viewed as approximately synonymous. The problem is that modern brain imaging techniques do detect clear spikes in raw brain activity when sleeping subjects dream even of dull things such as staring at a statue or clenching a hand. So why are only decreasesin brain activity conclusively seen when subjects undergo psychedelic experiences, instead of dreams? Given how difficult it is to find one biological basis for consciousness, how plausible is it that two fundamentally different mechanisms underlie conscious experience in the otherwise analogous psychedelic and dreaming states? © 2018 Scientific American

Keyword: Depression; Drug Abuse
Link ID: 25414 - Posted: 09.04.2018

By Austin Frakt and Aaron E. Carroll The United States receives tremendous benefits from public health spending — with far more value per dollar than with most other types of health care spending. We reviewed those benefits in a recent article, suggesting that more such spending should be considered. Then Upshot readers weighed in with their choices of what public health campaigns they’d like to see. Those included more help for mothers and babies (the Nurse-Family Partnership), and a greater focus on diabetes, nutrition, gun deaths (including suicide), loneliness and the harms of sharing hypodermic needles. We asked some experts — officials who run public health departments, academics and leaders of funding organizations — what they think we should be doing in public health, and a few themes emerged. Overrating doctors and hospitals Although we spend huge sums on health care, it’s not always on the right things. “The key to better health isn’t always to build more hospitals and train more specialists,” said Vivek Murthy, the former surgeon general. “In fact, it usually is not.” That’s where public health comes in. Consider antismoking commercials late in the last century, for example. Or as Richard Besser, the president and chief executive of the Robert Wood Johnson Foundation, put it, public health has kept us safe “from infectious diseases through immunizations, information, mosquito control and food safety.” “It ensures that our water is safe to drink and our pools and lakes are safe for swimming,” he added. “It provides screening for cancer and works to prevent injuries.” Karen DeSalvo, a former New Orleans health commissioner, said: “Of the $1 trillion in federal spending, only 1 percent is on public health — an infrastructure that saves lives” and that can “reduce suffering and improve community well-being and vitality.” © 2018 The New York Times Company

Keyword: Drug Abuse; Neurotoxins
Link ID: 25413 - Posted: 09.04.2018

By Ben Guarino A blight of bad eyesight plagues urban centers in China and other East Asian countries. In Hong Kong and Singapore, the rate of myopia, or nearsightedness, is as high as 90 percent in young adults. Though things aren't as blurry in the United States — about a third of the population has trouble seeing distant objects — rates have doubled since the 1970s. If current trends continue, half of the world could be myopic by 2050. China blames video games for the eyeglass epidemic and recently took them to task. The state-run Xinhua News Agency wrote this week that the "vision health of our country’s young people has always been of great concern" to Xi Jinping, the Communist Party general secretary and China's president. Chinese media distributors, the New York Times reported Friday, will limit the number of new games approved for sale. By singling out video games, China has taken a somewhat "extreme stance," according to Aaron M. Miller, a pediatric ophthalmologist and a clinical spokesman for the American Academy of Ophthalmology. "There's not a direct correlation or a clear relationship between video games, screen time and nearsightedness development." The scientific literature can offer only a fuzzy picture of myopia's causes. Diet and genes influence myopia; myopic parents are more likely to have myopic children. Behaviors can play a role, too. Some ophthalmologists look to activities lumped together under a term called "near-work" — any prolonged focus on a nearby object, as when reading, checking phones, studying and, yes, watching screens. Researchers have observed higher rates of myopia in college students, post-literate societies and, in one study, people who frequently use microscopes. © 1996-2018 The Washington Post

Keyword: Vision
Link ID: 25412 - Posted: 09.04.2018

Laura Sanders Skulls seem solid, but the thick bones are actually riddled with tiny tunnels. Microscopic channels cut through the skull bones of people and mice, scientists found. In mice, inflammatory immune cells use these previously hidden channels to travel from the bone marrow of the skull to the brain, the team reports August 27 in Nature Neuroscience. It’s not yet known whether immune cells travel these paths through people’s skulls. If so, these tunnels represent a newfound way for immune cells to reach — and possibly inflame — the brain. Along with other blood cells, immune cells are made in bones including those in the arm, leg, pelvis and skull. Researchers injected tracking dyes into bone marrow in the skull and other bones of mice, marking immune cells called neutrophils that originated in each locale. After a stroke, neutrophils flocked to the brain. Instead of coming equally from all sources of bone marrow, as some scientists had thought, most of these responding cells came from skull marrow, study coauthor Matthias Nahrendorf of Massachusetts General Hospital and Harvard Medical School and colleagues found. Curious about cells’ journeys from skull marrow to the brain, the researchers used powerful microscopes to look where skull meets brain. Tiny rivulets through the skull bone connected bone marrow inside the skull to the outer covering of the brain. In mice, neutrophils used these channels, which averaged about 22 micrometers across, as shortcuts to reach the brain. |© Society for Science & the Public 2000 - 2018

Keyword: Neuroimmunology
Link ID: 25411 - Posted: 09.04.2018

By William J. Broad During the Cold War, Washington feared that Moscow was seeking to turn microwave radiation into covert weapons of mind control. More recently, the American military itself sought to develop microwave arms that could invisibly beam painfully loud booms and even spoken words into people’s heads. The aims were to disable attackers and wage psychological warfare. Now, doctors and scientists say such unconventional weapons may have caused the baffling symptoms and ailments that, starting in late 2016, hit more than three dozen American diplomats and family members in Cuba and China. The Cuban incidents resulted in a diplomatic rupture between Havana and Washington. The medical team that examined 21 affected diplomats from Cuba made no mention of microwaves in its detailed report published in JAMA in March. But Douglas H. Smith, the study’s lead author and director of the Center for Brain Injury and Repair at the University of Pennsylvania, said in a recent interview that microwaves were now considered a main suspect and that the team was increasingly sure the diplomats had suffered brain injury. “Everybody was relatively skeptical at first,” he said, “and everyone now agrees there’s something there.” Dr. Smith remarked that the diplomats and doctors jokingly refer to the trauma as the immaculate concussion. Strikes with microwaves, some experts now argue, more plausibly explain reports of painful sounds, ills and traumas than do other possible culprits — sonic attacks, viral infections and contagious anxiety. In particular, a growing number of analysts cite an eerie phenomenon known as the Frey effect, named after Allan H. Frey, an American scientist. Long ago, he found that microwaves can trick the brain into perceiving what seem to be ordinary sounds. The false sensations, the experts say, may account for a defining symptom of the diplomatic incidents — the perception of loud noises, including ringing, buzzing and grinding. Initially, experts cited those symptoms as evidence of stealthy attacks with sonic weapons. © 2018 The New York Times Company

Keyword: Brain Injury/Concussion; Hearing
Link ID: 25410 - Posted: 09.01.2018

By Bahar Gholipour Milena Canning can see steam rising from a coffee cup but not the cup. She can see her daughter’s ponytail swing from side to side, but she can’t see her daughter. Canning is blind, yet moving objects somehow find a way into her perception. Scientists studying her condition say it could reveal secrets about how humans process vision in general. Canning was 29 when a stroke destroyed her entire occipital lobe, the brain region housing the visual system. The event left her sightless, but one day she saw a flash of light from a metallic gift bag next to her. Her doctors told her she was hallucinating. Nevertheless, “I thought there must be something happening within my brain [allowing me to see],” she says. She went from doctor to doctor until she met Gordon Dutton, an ophthalmologist in Glasgow, Scotland. Dutton had encountered this mystery before—in a 1917 paper by neurologist George Riddoch describing brain-injured World War I soldiers. To help enhance Canning’s motion-based vision, Dutton prescribed her a rocking chair. Canning is one of a handful of people who have been diagnosed with the “Riddoch phenomenon,” the ability to perceive motion while blind to other visual stimuli. Jody Culham, a neuroscientist at Western University in Ontario, and her colleagues launched a 10-year investigation into Canning’s remarkable vision and published the results online in May in Neuropsychologia. The team confirmed that Canning was able to detect motion and its direction. She could see a hand moving toward her, but she could not tell a thumbs-up from a thumbs-down. She was also able to navigate around obstacles, reach and grasp, and catch a ball thrown at her. © 2018 Scientific American

Keyword: Attention; Vision
Link ID: 25409 - Posted: 09.01.2018

Abby Olena Mice with faulty circadian clocks are prone to obesity and diabetes. So are mice fed a diet high in fat. Remarkably, animals that have both of these obesity-driving conditions can stay lean and metabolically healthy by simply limiting the time of day when they eat. In a study published today (August 30) in Cell Metabolism, researchers report that restricting feeding times to mice’s active hours can overcome both defective clock genes and an unhealthy diet, a finding that may have an impact in the clinic. The work corroborates previous research showing how powerful restricted feeding can be to improve clock function, says Kristin Eckel-Mahan, a circadian biologist at the University of Texas Health Science Center at Houston who did not participate in the study. Over the last 20 years, biologists have found circadian clocks keeping physiologic time in almost every organ. They have also shown that mice with disrupted clocks often develop metabolic diseases, such as obesity, and that circadian clock proteins physically bind to the promoters of many metabolic regulators and instruct them when to turn on and off. For Satchidananda Panda of the Salk Institute, these lines of evidence came together in 2009, when his group published a study showing that in mice without the clock component Cryptochrome, feeding and fasting could drive the expression of some, but not all, of the metabolic regulators throughout the body. Other groups have also confirmed that even in the absence of the clock it is still possible to drive some genetic rhythms. In this latest study, he and colleagues wanted to look more closely at how the cycling of clock and metabolic transcripts induced by time-restricted feeding, rather than normal genetic rhythms, influences the health of mice. © 1986 - 2018 The Scientist

Keyword: Obesity
Link ID: 25408 - Posted: 09.01.2018

Sarah Boseley Health editor Erica Avey, 27, microdosed on LSD for eight months, using an analogue that was legal in Germany, where she was living. “I started microdosing essentially because I was in a really depressed stage of my life. It was for mental health reasons – mood balancing, mood management. It was hard for me to leave my apartment and do normal things as a human being,” she said. Depression or sadness are very common reasons for starting; Avey was unusual only in that she could be open about it. Her workplace knew and thought it was fine. “As long as I wasn’t out of control or permanently high at work they were quite OK.” She took about 15 micrograms (a whole tab is 100 micrograms). “That was a good amount for me. Some people take as little as six,” she said. She adopted a popular protocol – one day on, three days off. It worked for her. “It definitely had the effect I wanted,” she said. “It lifted me out of a pretty deep depression. I’m still trying to wrap my head around what it has done to me in the long-term. I think it has changed me.” She had been “pretty negative”, she said, mindlessly going through social media, plagued with obsessive thoughts. “I’m able to be more mindful of my emotions. If I’m feeling sad, that’s OK. I don’t obsess anymore. I don’t dwell on it. I don’t get worked up about it.” © 2018 Guardian News and Media Limited

Keyword: Depression; Drug Abuse
Link ID: 25407 - Posted: 09.01.2018

By Raymond Zhong BEIJING — It started this week with a call to action from China’s leader, Xi Jinping. Too many of the country’s children need glasses, he said, and the government was going to do something about it. It ended on Friday with billions of dollars being wiped from the market value of the world’s largest video game company. New controls on online games were among Chinese authorities’ recommendations for reducing adolescent nearsightedness on Thursday, sending shares in the country’s leading game publisher, Tencent, tumbling the next day. Shares of Japanese game makers like Capcom, Konami and Bandai Namco also fell on Friday, a sign of the size and importance of the Chinese market. The sell-off is the latest in a series of government-related stumbles for Tencent, one of the world’s largest technology companies. Chinese state media has blamed video games for causing young people to become addicted, lowering their grades and worse. An incident last year, in which a 17-year-old in the southern city of Guangzhou died after playing a smartphone game for 40 hours straight, received wide attention. As the biggest game distributor in the world’s biggest game market, Tencent has grown fantastically rich in recent years. It has bought up game developers around the world, including the makers of influential titles such as League of Legends and Clash of Clans. It owns a stake in Epic Games, creator of the international blockbuster Fortnite. Back at home, Tencent also operates China’s most popular messaging app, WeChat, and processes a big chunk of the smartphone payments that are now used to make transactions of all kinds in the country. But over the last year, Tencent's hugely profitable game business has come under fire as Beijing takes a more forceful approach to guiding Chinese culture — a reminder of the state’s growing role in deciding the fortunes of the country’s largest and most innovative private companies. © 2018 The New York Times Company

Keyword: Vision
Link ID: 25406 - Posted: 08.31.2018

By Meredith Wadman Controversy is exploding around a paper published earlier this month in PLOS ONE by a public health expert at Brown University describing reports by parents that their children suddenly experienced unease with the gender they were assigned at birth; the paper calls the condition “rapid onset gender dysphoria” (ROGD). The paper, by physician-scientist Lisa Littman, is drawing fierce criticism from transgender advocates, who call it antitransgender because it suggests that some cases of gender dysphoria may be “socially contagious.” They say the paper has serious methodological flaws, noting that Littman interviewed only parents, not the young people themselves, and recruited from websites frequented by parents who were concerned about their children’s apparently sudden gender transitions. Meanwhile, the reactions of Brown and the journal are being assailed by critics who accuse them of caving to political pressure. On Monday, PLOS ONE announced it is conducting a postpublication investigation of the study’s methodology and analysis. “This is not about suppressing academic freedom or scientific research. This is about the scientific content itself—whether there is anything that needs to be looked into or corrected,” PLOS ONE Editor-in-Chief Joerg Heber in San Francisco, California, told ScienceInsider in an interview yesterday. Also on Monday, Brown officials removed the university’s press release highlighting the paper from its website. On Tuesday, Bess Marcus, dean of Brown’s School of Public Health, wrote in an open statement that the university acted “in light of questions raised about research design and data collection related to the study.” She added that people in the Brown community have raised concerns that the study’s conclusions “could be used to discredit efforts to support transgender youth and invalidate the perspectives of members of the transgender community.” © 2018 American Association for the Advancement of Science

Keyword: Sexual Behavior
Link ID: 25405 - Posted: 08.31.2018

By Emily Willingham In 1995 the late actor Christopher Reeve, who most famously played Superman, became paralyzed from the neck down after a horseback-riding accident. The impact from the fall left him with a complete spinal cord injury at the neck, preventing his brain from communicating with anything below it. Cases like Reeve’s are generally considered intractable injuries, absent any way to bridge the gap to restore disrupted communication lines. When Reeve died in 2004 a means of reconnection had yet to be built. Now, 14 years later, researchers have coaxed nerve cells to span the divide of a complete spinal cord injury. Their findings, described August 29 in Nature, are specific to only one kind of nerve cell and much work remains before a means of reconnection reaches patients, but the results make an impression. “From the scientific perspective, this is pretty significant,” says Yu-Shang Lee, an assistant professor of medicine at Cleveland Clinic’s Lerner Research Institute, who was not involved in the study. “As far as scientific impact, it is a good leap.” That leap across a completely compromised spinal cord relied on studies in rats and mice. The research team knew a certain type of nerve cell sometimes helps restore signaling from the spinal cord in partial spinal cord injury. Even when all direct connections to the brain are ruined, these cells can help sustain limited walking function, says Michael Sofroniew, professor of neurobiology at the University of California, Los Angeles, one of the senior authors on the study. He and his colleagues banked on the idea these cells, propriospinal neurons, might do the same if they could grow into an area of complete injury in their experimental animals. So they tried to get these cells to extend their electrical conduction fibers, the axons, into the spinal breach. © 2018 Scientific American

Keyword: Regeneration; Movement Disorders
Link ID: 25404 - Posted: 08.31.2018

Laurel Hamers Gene editing can reverse muscular dystrophy in dogs. Using CRISPR/Cas9 in beagle puppies, scientists have fixed a genetic mutation that causes muscle weakness and degeneration, researchers report online August 30 in Science. Corrections to the gene responsible for muscular dystrophy have been made before in mice and human muscle cells in dishes, but never in a larger mammal. The results, though preliminary, bring scientists one step closer to making such treatments a reality for humans, says study coauthor Eric Olson, a molecular biologist at the University of Texas Southwestern Medical Center in Dallas. Duchenne muscular dystrophy is a rare but severe, progressive disease that affects mostly boys and men. People with the disease, which is just one of many types of muscular dystrophy, rarely live past their 20s, usually dying of heart failure. An estimated 300,000 people worldwide suffer from the condition. The disease can be caused by any number of mutations to the gene that makes the protein dystrophin, which is essential for muscle structure and function. The mutations, which are often clustered in one particular region of the gene, usually stop production of the protein. Gene editing targeting that region could correct for these mutations’ effects, restoring protein production. Researchers injected two 1-month-old beagle puppies with a mutation in this hot spot with different doses of a virus carrying the gene-editing machinery. The team then measured dystrophin levels in different muscles after eight weeks. |© Society for Science & the Public 2000 - 201

Keyword: Movement Disorders; Muscles
Link ID: 25403 - Posted: 08.31.2018

By Jocelyn Kaiser When molecular biologist Darren Baker was winding up his postdoc studying cancer and aging a few years ago at the Mayo Clinic in Rochester, Minnesota, he faced dispiritingly low odds of winning a National Cancer Institute grant to launch his own lab. A seemingly unlikely area, however, beckoned: Alzheimer's disease. The U.S. government had begun to ramp up research spending on the neurodegenerative condition, which is the sixth-leading cause of death in the United States and will afflict an estimated 14 million people in this country by 2050. "There was an incentive to do some exploratory work," Baker recalls. Baker's postdoc studies had focused on cellular senescence, the cellular version of aging, which had not yet been linked to Alzheimer's. But when he gave a drug that kills senescent cells to mice genetically engineered to develop an Alzheimer's-like illness, the animals suffered less memory loss and fewer of the brain changes that are hallmarks of the disease. Last year, those data helped Baker win his first independent National Institutes of Health (NIH) research grant—not from NIH's National Cancer Institute, which he once expected to rely on, but from the National Institute on Aging (NIA) in Bethesda, Maryland. He now has a six-person lab at the Mayo Clinic, working on senescence and Alzheimer's. Baker is the kind of newcomer NIH hoped to attract with its recent Alzheimer's funding bonanza. For years, patient advocates have pointed to the growing toll and burgeoning costs of Alzheimer's as the U.S. population ages. Spurred by those projections and a controversial national goal to effectively treat the disease by 2025, Congress has over 3 years tripled NIH's annual budget for Alzheimer's and related dementias, to $1.9 billion. The growth spurt isn't over: Two draft 2019 spending bills for NIH would bring the total to $2.3 billion—more than 5% of NIH's overall budget. © 2018 American Association for the Advancement of Science

Keyword: Alzheimers
Link ID: 25402 - Posted: 08.31.2018

Shawna Williams Deciphering the communications of electric fish in their native streams is not for the faint of heart. “Once in a while, there is a thunderstorm ten kilometers away, then at some point the water level of those streams rises by one meter in one hour or so,” says Jan Benda, a computational neuroscientist at the University of Tübingen in Germany. “Then we are in big trouble with our equipment.” Even in the absence of extreme weather, given the normal heat and humidity levels at his team’s research sites in Panama and Columbia, “things break and then you sit there in the field and try to solder a wire back to something late at night,” he says, laughing. “You’re dreaming about your nice lab where everything is so easy.” To reach the study site with their equipment, researchers traveled by boat, and then on foot. Benda was driven from his comfortable lab a few years ago by a gaping hole in the body of scientific knowledge: weakly electric fish, which use electricity to communicate but not to stun prey, are popular subjects for neuroscientists who want to know how vertebrate brains process sensory information, but few if any researchers had ever eavesdropped on the animals zap-chatting in nature. Gaining this type of insight into the behavior of a species studied for decades in the lab is “a massively important undertaking,” says Malcolm MacIver, a neuroscientist and engineer researching animal behavior at Northwestern University in Illinois. © 1986 - 2018 The Scientist

Keyword: Animal Communication
Link ID: 25401 - Posted: 08.31.2018

Results from a clinical trial of more than 250 participants with progressive multiple sclerosis (MS) revealed that ibudilast was better than a placebo in slowing down brain shrinkage. The study also showed that the main side effects of ibudilast were gastrointestinal and headaches. The study was supported by the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and published in the New England Journal of Medicine. “These findings provide a glimmer of hope for people with a form of multiple sclerosis that causes long-term disability but does not have many treatment options,” said Walter J. Koroshetz, M.D., director of the NINDS. Robert J. Fox, M.D., a neurologist at Cleveland Clinic in Ohio, led a team of researchers across 28 clinical sites in a brain imaging study to investigate whether ibudilast was better than placebo in reducing the progression of brain atrophy, or shrinkage, in patients with progressive multiple sclerosis. In the study, 255 patients were randomized to take up to 10 capsules of ibudilast or placebo per day for 96 weeks. Every six months, the participants underwent MRI brain scans. Dr. Fox’s team applied a variety of analysis techniques on the MRI images to assess differences in brain changes between the two groups. The study showed that ibudilast slowed down the rate of brain atrophy compared to placebo. Dr. Fox and his colleagues discovered that there was a difference in brain shrinkage of 0.0009 units of atrophy per year between the two groups, which translates to approximately 2.5 milliliters of brain tissue. In other words, although both groups experienced atrophy, the brains of the patients in the placebo group shrank on average 2.5 milliliters more over two years compared to the ibudilast group. The whole adult human brain has a volume of approximately 1,350 milliliters. However, it is unknown whether that difference had an effect on symptoms or loss of function.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 25400 - Posted: 08.31.2018

Laurel Hamers A draft of the poppy’s genetic instruction book is providing clues to how the plant evolved to produce molecules such as morphine. Scientists pieced together the genome of the opium poppy (Papaver somniferum). Then, they identified a cluster of 15 close-together genes that help the plant synthesize a group of chemically related compounds that includes powerful painkillers like morphine as well as other molecules with potential medical properties (SN: 6/10/17, p. 22). A group of genes that help poppy plants produce some of these molecules, collectively known as benzylisoquinoline alkaloids, have been clustered together for tens of millions of years, researchers report online August 30 in Science. But the plant’s morphine production evolved more recently. Around 7.8 million years ago, the plant copied its entire genome. Some of the resulting surplus genes evolved new roles helping poppies produce morphine, because the plant already had at least one other copy of those genes carrying out their original jobs. It wasn’t a one-step process, though. An even earlier gene duplication event caused two genes to fuse into one. That hybrid gene is responsible for a key shape-shift in alkaloid precursors, directing those molecules down the chemical pathway toward morphinelike compounds instead of other benzylisoquinoline alkaloids (SN Online: 6/25/15). |© Society for Science & the Public 2000 - 2018.

Keyword: Pain & Touch; Drug Abuse
Link ID: 25399 - Posted: 08.31.2018

By Jake Buehler Whether it’s avoiding the slap of a flyswatter or shooting a tongue out at just the right moment to capture prey, fast reflexes can mean the difference between life and death in the animal kingdom. But a new study finds that not all reflexes are created equal: Larger animals are slower on the draw than smaller ones and because of that, they can’t move nearly as fast as they should be able to. When it comes to reflexes, there’s no doubt that bigger animals are a little slower. Big animals have longer neurons, and that means more time for a signal to travel from the spine to a leg muscle, for example. But nerve speed isn’t the only thing that slows down reflexes. So in the new study, researchers decided to look at myriad factors, like how fast muscles can generate force. They combed through data from other studies on electrically stimulated nerves and muscles in animals as small as shrews to as large as elephants. They also looked at the gaits of these mammals to calculate how long their stride and foot-down positions were in relation to their body size, which allowed researchers to look at how relatively quick their reflexes are. As size scales up, so does the total time it takes for muscles to respond, the team reported yesterday in the Proceedings of the Royal Society B. Large mammals experience a delay between nerve firing and muscle movement that is more than 15 times longer than small mammals. But, relative to the speed of their body movements, that delay is only twice as long—which means to compensate for slow signals, they’re moving more slowly. If this didn’t happen, a running 250-kilogram elk would be a cartoonish blur of legs, taking steps far faster than its reflexes could ever respond to. Call it a biological speed limit. © 2018 American Association for the Advancement of Science

Keyword: Evolution
Link ID: 25398 - Posted: 08.31.2018

Jon Hamilton A new study suggests that ketamine, an increasingly popular treatment for depression, has something in common with drugs like fentanyl and oxycodone. The small study found evidence that ketamine's effectiveness with depression, demonstrated in many small studies over the past decade, comes from its interaction with the brain's opioid system. A Stanford University team reported their findings Wednesday in The American Journal of Psychiatry. "We think ketamine is acting as an opioid," says Alan Schatzberg, one of the study's authors and a professor of psychiatry and behavioral sciences at Stanford. "That's why you're getting these rapid effects." Until now, most researchers have attributed ketamine's success to its effect on the brain's glutamate system, which is involved in learning and memory. The opioid system, in contrast, controls pain, reward, and addictive behaviors. Ketamine is an anesthetic that is frequently given to children in the emergency room. It is also a popular but illicit party drug that can cause an out-of-body experience at high doses. And in the past few years, ketamine has seen increasing use as an off-label treatment that doctors prescribe for patients with severe depression that doesn't respond to other drugs. Unlike conventional antidepressants like Prozac, which can take weeks to work, an infusion or nasal administration of ketamine typically produces results in hours. © 2018 npr

Keyword: Depression; Drug Abuse
Link ID: 25397 - Posted: 08.29.2018

By Ingfei Chen Newtown, Connecticut. Las Vegas. Parkland, Florida. Annapolis, Maryland. And just two days ago, Jacksonville, Florida, where the details are still coming in. With each ghastly mass shooting in a school, workplace, or other public location, journalists scramble to piece together what happened, and speculation runs high as to whether the gunman had mental illness. But critics say the media coverage perpetuates deep-seated, stigmatizing attitudes about diagnoses such as schizophrenia or bipolar disorder. What can journalists do to cover the mental health connection in these mass murders in a responsible way? “Journalism is far too quick to try to guess at the ‘why’ behind these sorts of things, but speculation can have serious consequences.” Earlier this month, police investigators released a final report on the massacre at a Las Vegas concert last October, the deadliest shooting in modern American history. The motives of the 64-year-old gunman — a wealthy high-stakes gambler — remain unclear, they conceded, but he had burned through much of his fortune and shown potential signs of a troubled mind. While some news outlets made only brief reference to suspicions that the shooter may have had mental illness, others blared it. It’s a familiar theme. In recent years, the national conversation about gun violence has boiled down to a narrative — amplified by the media — that essentially blames mental illness as a prominent cause of these cold-blooded public mass shootings. Mental illness has become highly politicized in the gun-control debate, yet the link between psychiatric problems and violence isn’t so straightforward. And mental health advocates say the over-simplistic narrative unfairly labels millions of Americans who have a psychiatric diagnosis with the false stereotype of being dangerous. Copyright 2018 Undark

Keyword: Aggression; Schizophrenia
Link ID: 25396 - Posted: 08.29.2018

By Daniel Victor On posters distributed to medical facilities across Australia, large type over an image of a pregnant woman read: “It’s safest not to drink while pregnant.” Good so far. It was the next line, in smaller type, that alarmed medical professionals: “It’s not known if alcohol is safe to drink when you are pregnant.” Public health groups responded with resounding protests — drinking alcohol while pregnant is very definitively known to be unsafe, they said. Creating doubt around the science could confuse pregnant women and encourage them to ignore warnings, they feared. The organization that made the posters, DrinkWise, describes its focus as promoting “a healthier and safer drinking culture in Australia,” but is funded largely by the alcohol industry. It withdrew the 2,400 posters after hearing complaints and substituted new text. But concerns remained among people working to spread the message that women should stay away from alcohol while pregnant. “It’s more than just erroneous for the alcohol industry to make that statement,” Michael Thorn, chief executive of the Foundation of Alcohol Research and Education, which is based in the Australian capital, Canberra, said in an interview. “The truth is, that’s what they want the public to believe.” In an emailed statement, DrinkWise’s chief executive, Simon Strahan, suggested the flap was more about precise messaging than intent. “It is clear, from the ‘It’s safest not to drink while pregnant’ headline of the posters, that the intent is to encourage abstinence when pregnant, planning a pregnancy or breast-feeding,” he said. © 2018 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 25395 - Posted: 08.29.2018