By Clare Wilson A patient-led movement is helping people taking psychiatric medicines to hack their dosing regimens so they can wean themselves off the drugs without any side effects. Now a Dutch website that sells kits to help people do this is about to launch an English-language site, triggering safety concerns among UK regulators and doctors. Some people find it impossible to stop taking certain antidepressants and anti-anxiety medicines such as valium because, unless the dose is reduced very gradually, they get severe mental and physical side-effects. The problem is these medicines aren’t sold in small enough tablets to allow for tapering. This has prompted some people to flout mainstream medical advice and use DIY methods for reducing their doses, such as grinding up tablets and dissolving them in water, or breaking open capsules of tiny beads and counting them out. The UK mental health charity Mind advises people who want to stop taking antidepressants of some techniques to try, but recommends they get advice from their doctor or pharmacist first. To help people taper their dose more easily, a Dutch medical charity, called Cinderella Therapeutics, creates personalised “tapering kits”, with precisely weighed out tablets in labelled packets that gradually reduce over several months. The website recommends people do this under medical supervision and must first receive a doctor’s prescription. © Copyright New Scientist Ltd.

Keyword: Depression
Link ID: 23817 - Posted: 07.09.2017

Robin McKie Observer science editor Scientists at Cambridge University have co-opted an unusual ally in their battle to find treatments for an incurable degenerative ailment that affects thousands of people in the UK. They have taken charge of a flock of merino sheep that have been genetically modified to carry the gene for Huntington’s disease. The research, led by neuroscientist Professor Jenny Morton, aims to understand how to pinpoint early symptoms of the brain condition, which affects more than 6,700 people in the UK. The gene responsible for Huntington’s was isolated more then 30 years ago but scientists have yet to develop drugs that might halt or even slow its development in patients. The brain’s complexity has defied attempts to understand how the condition develops. “Until now, much of our effort has been based on research on mice or rats,” said Morton. “But sheep should make better research subjects. Not only do they live much longer than rodents, their brains are larger and closer in size and structure to humans.” Huntington’s disease, which affects men and women equally, is an inherited neurological condition whose symptoms manifest themselves in adulthood, usually between 35 and 55. Initially mood, personality, coordination and memory are affected but, as the disease progresses, speech, swallowing and motor function deteriorate until death occurs 10 to 25 years after symptoms first appear. There is no known cure for Huntington’s disease although there are treatments to manage symptoms. © 2017 Guardian News and Media Limited

Keyword: Huntingtons
Link ID: 23816 - Posted: 07.09.2017

By Abby Olena For more than 50 years, scientists have taken for granted that all snakes share a ZW sex determination system, in which males have two Z chromosomes and females have one Z and one W. But a study, published today (July 6) in Current Biology, reveals that the Central American boa (Boa imperator) and the Burmese python (Python bivittatus) use an XY sex determination system, which evolved independently in the two species. “This work is a culmination of a lot of questions that we’ve had about pythons and boas for a long time,” says Jenny Marshall Graves, a geneticist at La Trobe Univeristy in Melbourne, Australia, who did not participate in the study. Some of these questions came up for Warren Booth, a geneticist and ecologist at the University of Tulsa, as he studied parthenogenesis—the growth and development of offspring in the absence of fertilization. He noticed a pattern for organisms undergoing parthenogenesis: animal species that use a ZW system have only male (ZZ) offspring, and the organisms that use an XY system have only female (XX) offspring. Except this pattern doesn’t hold true for boas and pythons, who consistently produce female offspring by parthenogenesis. Booth contacted Tony Gamble, a geneticist at Marquette University in Milwaukee, Wisconsin, who studies sex chromosomes, to begin a collaboration to investigate whether boas and pythons might actually have X and Y chromosomes. Spurred by Booth’s questions, “I went back and reread some of the early papers” on snake sex chromosomes, says Gamble. “What became clear is that they didn’t show that boas and pythons had a ZW sex chromosome system. They just said it without any evidence.” © 1986-2017 The Scientist

Keyword: Sexual Behavior; Evolution
Link ID: 23815 - Posted: 07.09.2017

Hannah Devlin A Catholic priest, a Rabbi and a Buddhist walk into a bar and order some magic mushrooms. It may sound like the first line of a bad joke, but this scenario is playing out in one of the first scientific investigations into the effects of psychedelic drugs on religious experience – albeit in a laboratory rather than a bar. Scientists at Johns Hopkins University in Baltimore have enlisted two dozen religious leaders from a wide range of denominations, to participate in a study in which they will be given two powerful doses of psilocybin, the active ingredient in magic mushrooms. Dr William Richards, a psychologist at Johns Hopkins University in Baltimore, Maryland who is involved in the work, said: “With psilocybin these profound mystical experiences are quite common. It seemed like a no-brainer that they might be of interest, if not valuable, to clergy.” The experiment, which is currently under way, aims to assess whether a transcendental experience makes the leaders more effective and confident in their work and how it alters their religious thinking. Despite most organised religions frowning on the use of illicit substances, Catholic, Orthodox and Presbyterian priests, a Zen Buddhist and several rabbis were recruited. The team has yet to persuade a Muslim imam or Hindu priest to take part, but “just about all the other bases are covered,” according to Richards. After preliminary screening, including medical and psychological tests, the participants have been given two powerful doses of psilocybin in two sessions, one month apart. © 2017 Guardian News and Media Limited

Keyword: Drug Abuse; Attention
Link ID: 23814 - Posted: 07.09.2017

By Michael Price Male baboons that harass and assault females are more likely to mate with them, according to a new study, adding evidence that sexual intimidation may be a common mating strategy among promiscuous mammals. The study’s authors even argue that the findings could shed light on the evolutionary origins of our own species’ behavior, although others aren’t convinced the results imply anything about people. “I think the data and analyses in this study are first-rate,” says Susan Alberts, a biologist who studies primate behavior at Duke University in Durham, North Carolina. “[But] I also think it’s a big stretch to infer something about the origins of human male aggression towards women.” To conduct the research, Elise Huchard, a zoologist at the National Center for Scientific Research in Montpellier, France, and colleagues examined a group of chacma baboons (Papio ursinus) living in Tsaobis Nature Park in Namibia over a 9-year period. These brownish, dog-sized primates live in troops of dozens of males and females. Females will mate with multiple males throughout the year. The male chacma are about twice the size of females and aggressively fight one another and engage in howling competitions to establish dominance. The more dominant a male is, the more likely he is both to succeed in finding a mate and to sire offspring. Males rarely force females to mate, but after years spent observing the animals in the wild, Huchard noticed that a subtler form of sexual coercion appeared to be going on. “Males often chase and attack some females of their own group when meeting another group, and they generally target sexually receptive females on such occasions,” she says. “I spent a great deal of time studying female mate choice, and my main impression … was that females don't have much room to express any preference.” © 2017 American Association for the Advancement of Science

Keyword: Sexual Behavior; Aggression
Link ID: 23813 - Posted: 07.07.2017

Ewen Callaway For 18 months in the early 1980s, John Sulston spent his days watching worms grow. Working in twin 4-hour shifts each day, Sulston would train a light microscope on a single Caenorhabditis elegans embryo and sketch what he saw at 5-minute intervals, as a fertilized egg morphed into two cells, then four, eight and so on. He worked alone and in silence in a tiny room at the Medical Research Council Laboratory of Molecular Biology in Cambridge, UK, solving a Rubik's cube between turns at the microscope. “I did find myself little distractions,” the retired Nobel prize-winning biologist once recalled. His hundreds of drawings revealed the rigid choreography of early worm development, encompassing the births of precisely 671 cells, and the deaths of 111 (or 113, depending on the worm’s sex). Every cell could be traced to its immediate forebear and then to the one before that in a series of invariant steps. From these maps and others, Sulston and his collaborators were able to draw up the first, and so far the only, complete ‘cell-lineage tree’ of a multicellular organism1. Although the desire to record an organism’s development in such exquisite detail preceded Sulston by at least a century, the ability to do so in more-complex animals has been limited. No one could ever track the fates of billions of cells in a mouse or a human with just a microscope and a Rubik’s cube to pass the time. But there are other ways. Revolutions in biologists’ ability to edit genomes and sequence them at the level of a single cell have sparked a renaissance in cell-lineage tracing. © 2017 Macmillan Publishers Limited

Keyword: Development of the Brain
Link ID: 23812 - Posted: 07.07.2017

By Aggie Mika Microglia—the brain’s own macrophages—can prompt excess eating and subsequent weight gain in mice fed high-fat diets, according to a study published today (July 5) in Cell Metabolism. The researchers demonstrate that an appetite-promoting inflammatory cascade driven by these immune cells occurs within the mediobasal region of the hypothalamus, a structure that, according to a news release, “contains key groups of neurons that regulate food intake and energy expenditure.” Prior studies have demonstrated that when mice are fed a diet high in saturated fat, they consume more while expending fewer calories, leading them to gain weight, the news release states. Additionally, previous work in both obese mice and humans has also shown that microglia within the hypothalamus increase following high-fat feeding, prompting inflammation, the authors write in their report. In the current study, the researchers examined whether microglial activity in the mediobasal hypothalamus had anything to do with the increased food consumption and weight gain observed in mice consuming diets high in fat. First, they used a drug to wipe out microglia in this region brain and found that microglia-lacking, high-fat consuming mice gained less weight than their non-drugged, high-fat counterparts. They then genetically manipulated mice so that their microglia weren’t capable of mounting an inflammatory response, and these mice also ate less and gained less weight than normal mice on the high-fat diets. © 1986-2017 The Scientist

Keyword: Obesity; Glia
Link ID: 23811 - Posted: 07.07.2017

By Mitch Leslie When you have a stuffy nose, a slice of freshly baked apple pie tastes like mush. But not being able to smell your food could have a surprising effect on your metabolism, potentially helping you remain thin even when you eat fatty foods, a new study in mice suggests. “This is a very exciting study, and the outcome is quite compelling,” says neuroendocrinologist Tamas Horvath of Yale School of Medicine, who wasn’t connected to the research. To conduct the study, molecular biologist Andrew Dillin of the University of California, Berkeley, and colleagues turned to a variety of genetically altered mice. The scientists gave them regular doses of the diphtheria toxin—which causes a temporary loss of odor-sensing neurons—to suppress their sense of smell. They then fed the rodents either a normal diet or fatty foods—the mouse equivalent of cheesecake and pizza—that usually induce obesity. After more than 3 months of noshing on regular chow, the odor-deprived rodents weighed slightly less than mice whose sense of smell was intact. In the group on the high-fat diet, however, the mice that couldn’t smell weighed 16% less than animals that could, which became obese. Losing the ability to smell also caused a different group of already-obese mice to lose weight, the researchers reveal today in Cell Metabolism. © 2017 American Association for the Advancement of Science.

Keyword: Obesity; Chemical Senses (Smell & Taste)
Link ID: 23810 - Posted: 07.06.2017

Carl Zimmer With fossils and DNA, scientists are piecing together a picture of humanity’s beginnings, an origin story with more twists than anything you would find at the movie theater. The expert consensus now is that Homo sapiens evolved at least 300,000 years ago in Africa. Only much later — roughly 70,000 years ago — did a small group of Africans establish themselves on other continents, giving rise to other populations of people today. To Johannes Krause, the director of the Max Planck Institute for Human History in Germany, that gap seems peculiar. “Why did people not leave Africa before?” he asked in an interview. After all, he observed, the continent is physically linked to the Near East. “You could have just walked out.” In a study published Tuesday in Nature Communications, Dr. Krause and his colleagues report that Africans did indeed walk out — over 270,000 years ago. Based on newly discovered DNA in fossils, the researchers conclude that a wave of early Homo sapiens, or close relatives of our species, made their way from Africa to Europe. There, they interbred with Neanderthals. Then the ancient African migrants disappeared. But some of their DNA endured in later generations of Neanderthals. “This is now a comprehensive picture,” Dr. Krause said. “It brings everything together.” Since the 1800s, paleontologists have struggled to understand how Neanderthals are related to us. Fossils show that they were anatomically distinct, with a heavy brow, a stout body and a number of subtler features that we lack. The oldest bones of Neanderthal-like individuals, found in a Spanish cave called Sima de los Huesos, date back 430,000 years. More recent Neanderthal remains, dating to about 100,000 years ago, can be found across Europe and all the way to southern Siberia. © 2017 The New York Times Company

Keyword: Evolution
Link ID: 23809 - Posted: 07.06.2017

By Linda Geddes BILLIONS of dollars have been spent in search of treatments for psychiatric conditions and brain disorders, when a cheap and effective drug may have been right under our noses: light. Now hospitals are turning to light to treat depression, strokes and Parkinson’s disease, using it to hit the reset button on our internal clocks. From green light soothing the pain of migraine, to blue light reducing organ damage during surgery, recent small studies have uncovered some intriguing effects of this therapy. But apart from easing seasonal affective disorder, we’ve been slow to embrace light as a serious contender for treating neurological conditions. We’ve known for 15 years that a special kind of receptor in our eyes transmits information directly to the body’s master clock, as well as other brain areas that control mood and alertness. These cells are particularly responsive to bluish light, including sunlight. These receptors enable light to act as a powerful reset switch, keeping the clock in our brain synced to the outside world. But this clock can fall out of sync or weaken as part of ageing or a range of disorders – a problem doctors are now starting to treat with light. Most hospitals have small windows and 24-hour lighting, both of which might exacerbate health problems. To tackle this, several hospitals in Europe and the US are installing dynamic “solid state” lighting, which changes like daylight over the course of a day. Such lights can, for example, shine bright whitish-blue in the morning, grow warmer and dimmer throughout the day, and turn orange or switch off at night. © Copyright New Scientist Ltd.

Keyword: Biological Rhythms; Stroke
Link ID: 23808 - Posted: 07.06.2017

By James Gallagher Abnormal deposits that build up in the brain during Alzheimer's have been pictured in unprecedented detail by UK scientists. The team at the MRC Laboratory of Molecular Biology says its findings "open up a whole new era" in neurodegenerative disease. Their work should make it easier to design drugs to stop brain cells dying. The researchers used brain tissue from a 74-year-old woman who died after having Alzheimer's disease. The form of dementia leads to tangles of a protein called tau spreading throughout the brain. The more tau tangles there are, the worse the symptoms tend to be. Doctors have known this has happened for decades but what has been missing is a detailed understanding of what the tangles look like. The team took advantage of the "resolution revolution" in microscopy to take thousands of highly detailed images of the tau inside the woman's brain tissues. And using computer software, they figured out the tangles look like this: Image copyright LMB It is pretty meaningless to an untrained eye, but to scientists this could be one of the most important recent discoveries in tackling dementia. Attempts to develop a drug to slow the pace of dementia have been met by repeated failure. But it is hard to come up with a drug when you do not know the precise chemical structure of what you are targeting. Dr Sjors Scheres, one of the researchers, told the BBC News website: "It's like shooting in the dark - you can still hit something but you are much more likely to hit if you know what the structure is. "We are excited - it opens up a whole new era in this field, it really does." © 2017 BBC.

Keyword: Alzheimers
Link ID: 23807 - Posted: 07.06.2017

By NICHOLAS BAKALAR Poor sleep may be an indication of increased risk for Alzheimer’s disease, a new study of older people suggests. Researchers studied 101 cognitively normal people, average age 63, who completed well-validated sleep questionnaires. They analyzed their spinal fluid for the presence of indicators of the plaques and tangles that are characteristic of Alzheimer’s. The study is in Neurology. After controlling for age, a family history of Alzheimer’s, the ApoE gene that increases Alzheimer’s risk and other factors, they found that poor sleep quality, sleep problems and daytime sleepiness were associated with increased spinal fluid indicators of Alzheimer’s disease. The reason for the association is unclear, but at least one animal study found that during sleep the brain’s capacity to clear toxins like beta amyloid, the toxic protein that forms plaques in the brains of those with Alzheimer’s, improves. It may be that poor sleep interferes with this process in people, too. “Not everyone with sleep problems is destined to develop Alzheimer’s disease,” said the senior author, Barbara B. Bendlin, an associate professor of medicine at the University of Wisconsin School of Medicine and Public Health. “We’re looking at groups of people, and over the whole group we find the association of poor sleep with the markers of Alzheimer’s. But when you look at individuals, not everyone shows that pattern.” © 2017 The New York Times Company

Keyword: Alzheimers; Sleep
Link ID: 23806 - Posted: 07.06.2017

Mike Mariani With its bright colors, anthropomorphic animal motif, and nautical-themed puzzle play mat, Dr. Kimberly Noble’s laboratory at Columbia University looks like your typical day care center—save for the team of cognitive neuroscientists observing kids from behind a large two-way mirror. The Neurocognition, Early Experience, and Development Lab is home to cutting-edge research on how poverty affects young brains, and I’ve come here to learn how Noble and her colleagues could soon definitively prove that growing up poor can keep a child’s brain from developing. Noble, a 40-year-old from outside of Philadelphia who discusses her work with a mix of enthusiasm and clinical restraint, is among the handful of neuroscientists and pediatricians who’ve seen increasing evidence that poverty itself—and not factors like nutrition, language exposure, family stability, or prenatal issues, as previously thought—may diminish the growth of a child’s brain. Now she’s in the middle of planning a five-year, nationwide study that could establish a causal link between poverty and brain development—and, in the process, suggest a path forward for helping our poorest children. It’s the culmination of years of work for Noble, who helped jump-start this fledgling field in the early 2000s when, as a University of Pennsylvania graduate student, she and renowned cognitive neuroscientist Martha Farah began exploring the observation that poor kids tended to perform worse academically than their better-off peers. They wanted to investigate the neurocognitive underpinnings of this relationship—to trace the long-standing correlation between socioeconomic status and academic performance back to specific parts of the brain. “There have been decades of work from social scientists, looking at socioeconomic disparities in broad cognitive outcomes—things like IQ or high school graduation rate,” she says. “But there’s no high school graduation part of the brain.” ©2017 Mother Jones and the Foundation for National Progress.

Keyword: Development of the Brain; Stress
Link ID: 23805 - Posted: 07.04.2017

Blood samples from infants who died of Sudden Infant Death Syndrome (SIDS) had high levels of serotonin, a chemical that carries signals along and between nerves, according to a study funded in part by the National Institutes of Health. The finding raises the possibility that a test could be developed to distinguish SIDS cases from other causes of sleep-related, unexpected infant death. The study, led by Robin L. Haynes, Ph.D., of Boston Children’s Hospital and Harvard Medical School, appears in the Proceedings of the National Academy of Sciences. NIH’s Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) provided funding for the work. SIDS is the sudden death of an infant under one year of age that remains unexplained after a complete autopsy and death scene investigation. In the current study, researchers reported that 31 percent of SIDS infants (19 of 61) had elevated blood levels of serotonin. In previous studies, the researchers reported multiple serotonin-related brain abnormalities in SIDS cases, including a decrease in serotonin in regions involved in breathing, heart rate patterns, blood pressure, temperature regulation, and arousal during sleep. Taken together, the researchers wrote, the findings suggest that an abnormality in serotonin metabolism could indicate an underlying vulnerability that increases SIDS risk and that testing blood samples for serotonin could distinguish certain SIDS cases from other infant deaths. However, they caution that more research is needed. NICHD’s Safe to Sleep campaign provides information on ways to reduce the risk of SIDS and other sleep-related causes of infant death.

Keyword: Sleep; Development of the Brain
Link ID: 23804 - Posted: 07.04.2017

Elana Gordon By the time Elvis Rosado was 25, he was addicted to opioids and serving time in jail for selling drugs to support his habit. "I was like, 'I have to kick this, I have to break this,' " he says. For Rosado, who lives in Philadelphia, drugs had become a way to disassociate from "the reality that was life." He'd wake up physically needing the drugs to function. His decision to finally stop using propelled him into another challenging chapter of his addiction and one of the most intense physical and mental experiences he could have imagined: detoxing. "The symptoms are horrific," Rosado says. There are recovery and treatment centers that can help people quit using drugs — in fact, it's a multi-billion-dollar industry. But this help can be expensive, and waiting lists for state and city-funded programs are often extremely long. So can detoxing on your own be the solution? In most cases, the answer is no. In fact, a growing movement within the field of addiction medicine is challenging the entire notion of detox and the assumption that when people cleanse themselves of chemicals, they're on the road to recovery. Article continues after sponsorship "That's a really pernicious myth, and it has erroneous implications," says Dr. Frederic Baurer, president of the Pennsylvania Society of Addiction Medicine. But at the time, Rosado says, he needed to end his "longtime love affair" with codeine. Like Oxycontin and morphine, it's an opioid. In jail, these drugs were easily available, Rosado recalls, through friends and cell mates. © 2017 npr

Keyword: Drug Abuse
Link ID: 23803 - Posted: 07.04.2017

By Sandrine Ceurstemont Bird or beast? A cuckoo seems to have learned how to mimic the sounds made by the pig-like peccaries it lives alongside, perhaps to ward off predators. The Neomorphus ground cuckoos live in forests in Central and South America, where they often follow herds of wild peccaries so they can feed on the invertebrates that the peccaries disturb as they plough through the leaf litter. Ecologists have noticed that when the cuckoos clap their beaks together they sound a lot like the tooth clacks the peccaries make to deter large predatory cats. To find out whether this is just coincidence or evidence of mimicry, Cibele Biondo at the Federal University of ABC in Brazil and her team analysed the cuckoo and peccary sounds, and compared them with the beak clapping sounds made by roadrunners – close relatives of the ground cuckoos. Logically, the cuckoos should sound most similar to roadrunners, given that the two are closely related. But the analysis suggested otherwise. “The acoustic characteristics are more similar to the teeth clacking of peccaries,” says Biondo. She suspects that cuckoos have something to gain by imitating the peccaries, particularly in the dark, dense forests where predators rely on hearing as much as vision. “Cuckoos may deceive predators by making it appear that peccaries are present when they are not,” says Biondo. © Copyright New Scientist Ltd.

Keyword: Evolution; Animal Communication
Link ID: 23802 - Posted: 07.04.2017

Fergus Walsh Medical correspondent The world's most detailed scan of the brain's internal wiring has been produced by scientists at Cardiff University. The MRI machine reveals the fibres which carry all the brain's thought processes. It's been done in Cardiff, Nottingham, Cambridge and Stockport, as well as London England and London Ontario. Doctors hope it will help increase understanding of a range of neurological disorders and could be used instead of invasive biopsies. I volunteered for the project - not the first time my brain has been scanned. Computer games In 2006, it was a particular honour to be scanned by the late Sir Peter Mansfield, who shared a Nobel prize for his work on developing Magnetic Resonance Imaging, one of the most important breakthroughs in medicine. He scanned me using Nottingham University's powerful new 7 Tesla scanner. When we looked at the crisp, high resolution images, he told me: "I'm a physicist, so don't ask me to tell you to whether there's anything amiss with your brain - you'd need a neurologist for that." I was the first UK Biobank volunteer to have their brain and other organs imaged as part of the world's biggest scanning project. More recently, I had my brain scanned while playing computer games, as part of research into the effects of sleep deprivation on cognition. So my visit to the Cardiff University's Brain Research Imaging Centre (CUBRIC) held no particular concerns. The scan took around 45 minutes and seemed unremarkable. A neurologist was on hand to reassure me my brain looked normal. My family quipped that they were happy that a brain had been found inside my thick skull. But nothing could have prepared me for the spectacular images produced by the team at Cardiff, along with engineers from Siemens in Germany and the United States. © 2017 BBC.

Keyword: Brain imaging
Link ID: 23801 - Posted: 07.04.2017

By RONI CARYN RABIN It may be the most palatable advice you will ever get from a doctor: Have a glass of wine, a beer or a cocktail every day, and you just might prevent a heart attack and live longer. But the mantra that moderate drinking is good for the heart has never been put to a rigorous scientific test, and new research has linked even modest alcohol consumption to increases in breast cancer and changes in the brain. That has not stopped the alcoholic beverage industry from promoting the alcohol-is-good-for-you message by supporting scientific meetings and nurturing budding researchers in the field. Now the National Institutes of Health is starting a $100 million clinical trial to test for the first time whether a drink a day really does prevent heart attacks. And guess who is picking up most of the tab? Five companies that are among the world’s largest alcoholic beverage manufacturers — Anheuser-Busch InBev, Heineken, Diageo, Pernod Ricard and Carlsberg — have so far pledged $67.7 million to a foundation that raises money for the National Institutes of Health, said Margaret Murray, the director of the Global Alcohol Research Program at the National Institute on Alcohol Abuse and Alcoholism, which will oversee the study. The decision to let the alcohol industry pay the bulk of the cost has raised concern among researchers who track influence-peddling in science. “Research shows that industry-sponsored research almost invariably favors the interests of the industry sponsor, even when investigators believe they are immune from such influence,” said Marion Nestle, a professor of nutrition and food studies at New York University who is the author of several books on the topic, including “Food Politics: How the Food Industry Influences Nutrition and Health.” © 2017 The New York Times Company

Keyword: Drug Abuse
Link ID: 23800 - Posted: 07.04.2017

By Wallis Snowdon, Ariel Fournier The seizure of a controversial drug in Edmonton is evidence that more research is required on kratom as a possible antidote in Alberta's deadly opioid epidemic, says a leading researcher in the field. "Everything has to be taken with caution, but does that mean you take it off the streets?" said Susruta Majumdar, a chemist who has worked on numerous studies into the drug. "Probably not," said Majumdar, who works in the department of neurology at Sloan Kettering Cancer Center in New York. "It's a little premature to ban it right away and take it out of the public scenario because very little research has been done. It's a weak alkaloid but we need to be cautious about it." In a news release Tuesday, Health Canada said it had seized unauthorized kratom products from two Edmonton head shops. The packets were confiscated from a store called Jupiter on Whyte Avenue and from another called Bogart's Pipes and Papers on 132nd Avenue. Kratom is a coffee-like plant native to southeast Asia. The drug is traditionally consumed by chewing on the leaves, but can also be ingested as a capsule or powder or as a tea. Health Canada said the herbal product has been linked to both "narcotic and stimulant-like effects," and may pose serious health risks including nausea, vomiting, seizures, and liver toxicity. ©2017 CBC/Radio-Canada.

Keyword: Drug Abuse
Link ID: 23799 - Posted: 07.01.2017

ByMaia Szalavitz George Sarlo is throwing cash at research into how drugs like magic mushrooms can help people overcome trauma like his own. Deep in the Mexican jungle, in a village so remote it's only accessible by boat, 74-year-old venture capitalist George Sarlo waited to meet his father. It was the fall of 2012, and Sarlo knew his quest seemed absurd. After all, his father had been dead for decades, and he had no connection to this region of rainforests and beaches and its indigenous peoples. As the financier watched a shaman prepare a ceremonial cup of bitter brown ayahuasca, he couldn't believe that he'd agreed to swallow this nauseating psychedelic brew for a second time. But he had traveled for 12 hours—via plane, boat, and finally on foot—to this primeval place, a newly-built gazebo-like wood platform without walls. He had expressed his intentions in a group therapy session in preparation; he had eaten a special, bland diet and even halted other medications. He also trusted his friend, Dr. Gabor Maté, a fellow Hungarian Holocaust survivor, who led the therapy and had arranged the trip. Maté is perhaps best known for his book, In the Realm of Hungry Ghosts, which explores his work with extremely traumatized injection drug users in Vancouver. He's been offering psychedelic therapy to trauma survivors since learning about the potential of ayahuasca in 2008.

Keyword: Drug Abuse; Stress
Link ID: 23798 - Posted: 07.01.2017