Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Kill, Fido! Docile ants become aggressive guard dogs after a secret signal from their caterpillar overlord. The idea turns on its head the assumption that the two species exchange favours in an even-handed relationship. The caterpillars of the Japanese oakblue butterfly (Narathura japonica) grow up wrapped inside leaves on oak trees. To protect themselves against predators like spiders and wasps, they attract ant bodyguards, Pristomyrmex punctatus, with an offering of sugar droplets. The relationships was thought to be a fair exchange of services in which both parties benefit. But Masaru Hojo from Kobe University in Japan noticed something peculiar: the caterpillars were always attended by the same ant individuals. “It also seemed that the ants never moved away or returned to their nests,” he says. They seemed to abandon searching for food, and were just standing around guarding the caterpillar. Intrigued, Hojo and his colleagues conducted lab experiments in which they allowed some ants to interact with the caterpillars and feed on the secretions, and kept others separate. Ants that ate the caterpillar’s secretions remained close to the caterpillar. They didn’t return to their nest. And whenever the caterpillar everted its tentacles – flipped them so they turned inside out – the ants moved around rapidly, acting aggressively. © Copyright Reed Business Information Ltd.
By Christie Wilcox Venomous cone snails have been a gift to biomedical researchers. Over the past 50 years, scientists have isolated compounds from these predatory marine animals that do everything from stop pain to protect cells during a heart attack. Now, researchers have isolated a cone snail compound that does something unexpected: It puts mice to sleep. All of these compounds belong to a group of ion channels modifiers known as conotoxins. In the wild, the snails use these toxins for capturing prey, and typically when researchers inject them into mice, the rodents either have no response or become paralyzed. In the new study, published this month in Toxicon, researchers isolated and sequenced 14 novel peptide toxins from the venom of the cobweb cone, Conus araneosus (pictured above with its dissected venom gland). When they injected five of them into mice, one put the rodents to sleep for several hours, whereas the others had no effect. The team says the discovery expands the range of therapeutic uses for conotoxins, and could lead to drugs to treat sleep disorders. © 2015 American Association for the Advancement of Science
By BENEDICT CAREY Bill Cosby stands accused of committing date rape long before drugs like GHB or Rohypnol were widely used for that purpose. Many of Mr. Cosby’s accusers believed they had been drugged — but with what? And how? In a recently obtained legal deposition, Mr. Cosby acknowledged giving quaaludes to some women with whom he had sex, but said consumption of the drug was consensual, “the same as a person would say, ‘Have a drink.’ ” In a transcript of the deposition, reported on Sunday in The New York Times, the comedian told lawyers had had obtained seven prescriptions for quaaludes. Originally approved and marketed as a “safer” sleeping pill, less addictive than barbiturates, the drug (known generically as methaqualone) was both sedating and hypnotic. Recreational use was common, but the federal government withdrew them from the market in 1982. “It was inevitable that it would be tried by people looking for a ‘better high,’ ” Dr. David Smith, medical director of the Haight-Ashbury Free Clinic, and Dr. Donald Wesson noted in The Journal of Psychedelic Drugs. Intoxication with quaaludes “soon developed a reputation for being especially pleasant.” Young people in the 1970s used quaaludes as they would a strong drink: to loosen up, to relax, to socialize. The pills also won a reputation for inducing periods of euphoria, as well as sexual arousal — “heroin for lovers,” some called it. By the middle of the decade, quaaludes were a staple of the club scene, often taken with alcohol. So embedded were quaaludes in the cultural scene that even years later the Dead Kennedys and Billy Idol were singing about the drug’s captivating effects. But reckless users risked overdose, especially when combining the pills with alcohol, which could lead to coma, convulsions and sometimes death. In a 1973 review of 252 hospital admissions for drug overdose, doctors in Edinburgh found that the third most common cause of “self-poisoning,” after barbiturates and LSD, was Mandrax — the British version of quaaludes, widely abused in South Africa as well. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21198 - Posted: 07.22.2015
Don’t do drugs, kids. Especially if you’re female. Women dependent on stimulants like cocaine and methamphetamine appear to have less grey matter, even after they stop using them. Weirdly, men’s brains don’t show this difference. The brain regions most affected are those involved in reward, emotion and learning – although it isn’t clear yet whether the smaller than average size of these brain areas could be a cause or effect of addiction. Jody Tanabe, at the University of Colorado Hospital in Aurora, hopes these results will help lead to a better understanding of sex differences in substance abuse, and better, more distinct treatments for women. Tanabe’s team used MRI scans to measure the brain volumes of 59 people previously dependent on stimulants and compared them with people who have never been dependent on these kinds of drugs. On average, the 28 women who had formerly been dependent on a stimulant drug had a smaller volume of grey matter in their prefrontal cortices, temporal lobes, insulae and other regions. This effect was not seen in men. Shrinking brains The women who had been addicted also differed in their personalities – on average, they were more impulsive and more reward-driven. We already know that women respond differently to stimulants: they start taking the drugs earlier, use larger quantities and may have more difficulty quitting. It’s possible that this pattern of female addiction could be linked to the brain size difference. However, it’s unclear whether less grey matter causes female addictive behaviours, or if addiction might shrink these brain regions. “The question of causality is complex. There is evidence for both pre-existing and post-drug changes in brain structure and function,” says Tanabe.
OLIVER SACHGAU Marc Lewis spends a lot of his time thinking about addiction. He has good reason to: In his 20s he struggled with his own addiction to opiates. He was eventually able to quit, and began researching addiction and neuroscience. Mr. Lewis became a professor of developmental psychology at the University of Toronto in 1989, and moved to Radboud University in the Netherlands in 2010. His new book, The Biology of Desire: Why Addiction is Not a Disease, looks at the neuroscience of addiction, mixing personal narratives with scientific data. The book will be released in Canada on Aug. 4. You argue addiction is not a disease, but an example of very normal brain activity. What do you mean? [It’s] an exaggerated form of learning. Let’s put it that way. People in neuroscience agree that addiction corresponds with brain changes, and that’s the basis of the disease argument: That addiction changes the brain, or hijacks the brain, as they say. As though it were a pathology or disease process. Whereas I argue that all learning changes – the brain is designed to change – but when you have highly motivated learning, especially something that gets repeated over and over, then the learning curve rises extremely rapidly, and you have a kind of exaggerated learning phenomenon, where the learning is deep and specialized, and blots out other available habits or other available perceptions. You chose to mix hard scientific data with these anecdotal stories. How come? I love that way of writing. It seems to me so amazing that brain changes are going on at the same time as lived experiences: The moment-to-moment changes of thoughts and feelings are completely yoked to changes and activity in your brain, but it’s almost impossible to tell both stories at the same time, because one is under the skin, in terms of cell firings and electrochemical impulses and stuff, and the other one is in terms of behavior and human values and norms and so forth. © Copyright 2015 The Globe and Mail Inc
Rebecca Hersher and Carla Javier In a community center just south of Los Angeles, upwards of 50 people pack into a room to offer each other words of comfort. Most of them are moms, and they've been through a lot. At Solace, a support group for family members of those suffering from addiction, many of the attendees have watched a child under 30 die of a fatal drug overdose — heroin, or opioids like Oxycontin or Vicodin that are considered gateway drugs to heroin. And they're not alone. This week, a new report from the Centers for Disease Control and Prevention offered some startling numbers: Heroin deaths have quadrupled since 2002. Many of those deaths are young people, whose families have suffered alongside them — and who are left behind to cope with the loss. The family members at Solace begin their meetings by introducing themselves. On this night, it takes them about an hour to make their way around the table and complete the introductions. Among them is Jenny Maraletos. She came to the support group to talk about her son, Dimitri Zarate. He has overdosed on heroin at least 10 times. "He fought addiction for several years, multiple overdoses, multiple deaths," Maraletos begins. "And I'm glad to say that he's in recovery today, and he's here." Zarate, 37, sits across the room from his mother. The support group is open to anyone who has been touched by addiction, including current addicts; as a recovering addict himself, Zarate brings some hope to the others there. "You know what, I have a warm bed and a shower," he says to the group. "I was homeless, and my life today is absolutely amazing." © 2015 NPR
Keyword: Drug Abuse
Link ID: 21162 - Posted: 07.13.2015
By James Gallagher Health editor, BBC News website Smoking could play a direct role in the development of schizophrenia and needs to be investigated, researchers say. The team at King's College London say smokers are more likely to develop the disorder and at a younger age. Published in the Lancet Psychiatry, their analysis of 61 separate studies suggests nicotine in cigarette smoke may be altering the brain. Experts said it was a "pretty strong case" but needed more research. Smoking has long been associated with psychosis, but it has often been believed that schizophrenia patients are more likely to smoke because they use cigarettes as a form of self-medication to ease the distress of hearing voices or having hallucinations. The team at King's looked at data involving 14,555 smokers and 273,162 non-smokers. It indicated: 57% of people with psychosis were already smokers when they had their first psychotic episode Daily smokers were twice as likely to develop schizophrenia as non-smokers Smokers developed schizophrenia a year earlier on average The argument is that if there is a higher rate of smoking before schizophrenia is diagnosed, then smoking is not simply a case of self-medication. Dr James MacCabe, from the Institute of Psychiatry, Psychology and Neuroscience at King's, said: "It's very difficult to establish causation [with this style of study], what we're hoping that this does is really open our eyes to the possibility that tobacco could be a causative agent in psychosis, and we hope this will then lead to other research and clinical trials that would help to provide firmer evidence." Clearly most smokers do not develop schizophrenia, but the researchers believe it is increasing the risk. The overall incidence of the condition is one in every 100 people normally, which may be increased to two per 100 by smoking. © 2015 BBC
Zoë Corbyn Jesper Noehr, 30, reels off the ingredients in the chemical cocktail he’s been taking every day before work for the past six months. It’s a mixture of exotic dietary supplements and research chemicals that he says gives him an edge in his job without ill effects: better memory, more clarity and focus and enhanced problem-solving abilities. “I can keep a lot of things on my mind at once,” says Noehr, who is chief technology officer for a San Francisco startup. The chemicals he takes, dubbed nootropics from the Greek “noos” for “mind”, are intended to safely improve cognitive functioning. They must not be harmful, have significant side-effects or be addictive. That means well-known “smart drugs” such as the prescription-only stimulants Adderall and Ritalin, popular with swotting university students, are out. What’s left under the nootropic umbrella is a dizzying array of over-the-counter supplements, prescription drugs and unclassified research chemicals, some of which are being trialled in older people with fading cognition. There is no official data on their usage, but nootropics as well as other smart drugs appear popular in the Silicon Valley. “I would say that most tech companies will have at least one person on something,” says Noehr. It is a hotbed of interest because it is a mentally competitive environment, says Jesse Lawler, a LA based software developer and nootropics enthusiast who produces the podcast Smart Drug Smarts. “They really see this as translating into dollars.” But Silicon Valley types also do care about safely enhancing their most prized asset – their brains – which can give nootropics an added appeal, he says. © 2015 Guardian News and Media Limited
By STEVE FEATHERSTONE One evening in April, Ethan Darbee, a 24-year-old paramedic in Syracuse, responded to a call on the city’s south side: unknown man down. Rolling up to the scene, he saw a figure lying motionless on the sidewalk. Darbee raked his knuckles across the man’s sternum to assess his level of consciousness. His eyelids fluttered. Inside the ambulance, Darbee hooked him up to a heart monitor, and he jerked involuntarily. The odd reaction puzzled Darbee. Why would the guy recoil from an electrode sticker but not a sternal rub? The driver started for the hospital. Darbee sat in the captain’s chair in the back of the rig, typing on a laptop. Then he heard a sound no paramedic ever wants to hear: the click of a patient’s shoulder harness unlatching. Swiveling around, he found himself eyeball to eyeball with his patient, who was now crouched on all fours on top of the stretcher, growling. That same evening, Heather Drake, a 29-year-old paramedic, responded to a call at an apartment complex on the west side. When she arrived, four firefighters were grappling with a 120-pound woman who was flailing and flinging vomit at anyone who came near her. A bystander shouted that the woman was high on ‘‘spike’’ — the prevailing local term for synthetic marijuana, which is more commonly known around the country as spice. But Drake didn’t believe it. Spike didn’t turn people into violent lunatics. Phencyclidine (PCP) or synthetic cathinones (‘‘bath salts’’) could do that, maybe even a joint soaked in formaldehyde — but not spike. Drake sprayed a sedative up the woman’s nose and loaded her into the ambulance. A mayday call from another crew came over the radio. In the background static of the transmission, Drake could hear Ethan Darbee yelling. Darbee’s patient had sprung off the stretcher and knocked him to the floor of the ambulance, punching him repeatedly in the face. Darbee grasped the side-door handle and tumbled into the street. Within moments, the police arrived and quickly subdued the man. Two days later, 19 more spike overdoses would swamp local emergency rooms, more in one day in Syracuse than the number of overdoses reported statewide in most states for all of April. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21150 - Posted: 07.09.2015
By Lenny Bernstein Primed by widespread use of prescription opioid pain-killers, heroin addiction and the rate of fatal overdoses have increased rapidly over the past decade, touching parts of society that previously were relatively unscathed, the Centers for Disease Control and Prevention reported Tuesday. The death rate from overdoses nearly quadrupled to 2.7 per 100,000 people between 2002 and 2013, CDC Director Tom Frieden said during a telephone news conference Tuesday. In 60 percent of those cases, the cause of death was attributed to heroin and at least one other drug, often cocaine, according to Chris Jones, lead author of the report and a member of the Food and Drug Administration's Office of Public Health Strategy and Analysis. But it is the highly addictive pain-killing opioids, prescribed and sometimes over-prescribed by physicians who are not highly trained in pain management, that concerns officials most, Frieden said. "A few doses and someone can have a life of addiction, a few too many and someone can die of an overdose," Frieden said. With heroin an estimated five times less expensive than prescription drugs and widely available on the street, people with opioid addictions are turning to the drug in large numbers, he said. The annual rate of heroin use rose from 1.6 per 1,000 people between 2002 and 2004 to 2.6 per 1,000 between 2011 and 2013, according to the report. That includes a doubling among women, a 114 percent increase for whites and a 109 percent rise among people ages 18 to 25, the report shows.
Keyword: Drug Abuse
Link ID: 21146 - Posted: 07.08.2015
By Erika Beras Marijuana is the drug of choice for people who drink alcohol. And people who use both are twice as likely to do so at the same time than to indulge in just one or the other. That’s according to a study in the journal Alcoholism: Clinical and Experimental Research. [Meenakshi S. Subbaraman and William C. Kerr, Simultaneous Versus Concurrent Use of Alcohol and Cannabis in the National Alcohol Survey The data came from self-reported answers that more than 8,600 people provided to what’s called the National Alcohol Surveys, done by phone in 2005 and 2010. People who used pot and alcohol were about twice as likely to drive drunk than those who just drank. And they doubled their chances of what are referred to as negative social consequences, such as arrests, fights and job problems. Meanwhile, another new study finds that if you’re chronically stoned, you’re more likely to remember things differently from how they happened, or not at all. Researchers showed a series of words to people who do not use marijuana and to regular pot users who had not partaken in a month. A few minutes later, all participants were shown the same list of words along with other words. The volunteers were then asked to identify only the original words. The pot smokers thought more of the new words were in the original list than did the nonusers. And brain scans revealed that the regular pot users showed less activity in brain regions associated with memory and cognitive resources than did the nonusers. The study is in the journal Molecular Psychiatry. [J. Riba et al, Telling true from false: cannabis users show increased susceptibility to false memories] © 2015 Scientific American
by Colin Barras Men often lose their sex drive with age – and so, it seems do male Drosophila. Tsai-Feng Fu at the National Chi Nan University in Taiwan and his colleagues suspected that low levels of dopamine in the flies were to blame. Almost 300 neurones in the fruit-fly brain use dopamine. Comparing those linked to sexual function in elderly 40-day-old male flies and sprightly 10-day-old flies, Fu found the older neurones carried 10 times less dopamine. Boosting levels lengthened the time the older flies spent trying to mate. There are obviously big differences between a man's brain and that of a male Drosophila, but Fu says that the new results could provide a useful starting point for in-depth studies that may have clinical implications. For instance, that research might eventually identify ways to fine-tune dopamine levels in humans, perhaps to reverse age-related declines in sexual drive, or even to suppress an overactive libido. We already have therapies for treating male sexual dysfunction – notably the drug viagra. But probing the link between dopamine and sexual dysfunction is still important. For instance, dopamine-replacement therapy is one of the most effective treatments for Parkinson's disease – but the therapy can lead to harmful compulsive sexual behaviour. But Wendi Neckameyer at the Saint Louis University School of Medicine in Missouri isn't sure we should talk about potential implications for men just yet – it's enough to say that the researchers "have begun to tease out an incredibly complex neural circuit", she says. © Copyright Reed Business Information Ltd
Keyword: Sexual Behavior
Link ID: 21115 - Posted: 07.01.2015
By Megan Cartwright Don’t pet the platypus. I know it’s tempting: Given the chance, I’d want to stroke their thick brown fur, tickle those big webbed feet, and pat that funny duck bill. And why not? What harm could come from this cute, egg-laying mammal from eastern Australia? Plenty. As someone who doesn’t enjoy “long lasting excruciating pain that cannot be relieved with conventional painkillers,” I’d really regret petting a platypus. Especially a male platypus, in late winter, when there’s only one thing on his mind and, even worse, something nasty on his feet. When British biologist Sir Everard Home got ahold of some platypus specimens in 1801, he told his fellow nerds at the Royal Society how the male specimen had a half-inch long “strong crooked spur” on the heel of each rear foot. The female, however, was spur-free. Home suggested that it “is probably by means of these spurs or hooks, that the female is kept from withdrawing herself in the act of copulation.” A very reasonable suggestion. But a wrong one. To be fair to Home, he could only study dead platypuses. If Home could have spent a year hanging out with living platypuses in their river homes, he would’ve seen that this “shy, semi-aquatic, mainly nocturnal” mammal is mostly interested in hunting on the river bottom for delicious insect larvae, crayfish, and shrimp. In other words, the platypus is usually an eater, not a lover. © 2014 The Slate Group
Patricia Neighmond A report finds mixed results when it comes to how well medical marijuana works to calm pain and control symptoms. And, an editorial says states legalizing pot for medical use may be jumping the gun. DAVID GREENE, HOST: Twenty-three states plus the District of Columbia have approved pot for medical use. But a new study in the Journal of the American Medical Association is raising questions about its safety and effectiveness. Here's NPR's Patti Neighmond. PATTI NEIGHMOND, BYLINE: Researchers from the University of Bristol in the United Kingdom reviewed findings from 79 different studies looking at the effect of marijuana on symptoms ranging from chronic pain to sleep difficulties and mental illness. At best, they found only moderate evidence indicating that marijuana reduced nerve pain and pain from cancer. When it came to other conditions, like nausea and vomiting due to chemotherapy, difficulties sleeping or weight loss among HIV patients, there was some anecdotal evidence suggesting that people may be helped by marijuana, but it was just that - anecdote. D'SOUZA: Which is really the bulk of the evidence that the states have used in approving medical marijuana. NEIGHMOND: In an editorial accompanying this study, Dr. Deepak Cyril D'Souza says states legalizing marijuana for medical use may be jumping the gun before good quality evidence is in. D'SOUZA: If a pharmaceutical company, for example, wanted to get a drug approved for a medical condition and they only submitted anecdotal data, there's absolutely no chance that that drug would be approved. NEIGHMOND: D'Souza is a psychiatrist with Yale University's School of Medicine. For years, he's studied the impact of marijuana on mental health. And the big question, he says, is how routine daily use - the way one might use marijuana to treat a medical condition - affects the body and the brain over the long term. Concerns have been raised about memory loss, panic, paranoia and other severe disorders. © 2015 NPR
Keyword: Drug Abuse
Link ID: 21089 - Posted: 06.25.2015
By Nicholas Bakalar Exposure to air pollution may hasten brain aging, a new study has found. Researchers studied 1,403 women without dementia who were initially enrolled in a large health study from 1996 to 1998. They measured their brain volume with M.R.I. scans in 2005 and 2006, when the women were 71 to 89 years old. Using residential histories and air pollution data, they estimated their exposure to air pollution from 1999 to 2006. They used data recorded at monitoring sites on exposure to PM 2.5 — tiny particulate matter that easily penetrates the lungs. Each increase of 3.49 micrograms per cubic centimeter cumulative exposure to pollutants was associated with a 6.23 cubic centimeter decrease in white matter, the equivalent of one to two years of brain aging. The association remained after adjusting for many variables, including age, smoking, physical activity, blood pressure, body mass index, education and income. Previous studies have shown that air pollution can cause inflammation and damage to the vascular system, but this study, in The Annals of Neurology, showed damage to the brain itself. “This tells us that the damage air pollution can impart goes beyond the circulatory system,” said the lead author, Dr. Jiu-Chiuan Chen, an associate professor of preventive medicine at the Keck School of Medicine at the University of Southern California. “Particles in the ambient air are an environmental neurotoxin to the aging brain.” © 2015 The New York Times Company
By Nicholas Bakalar A new study has found a simple way to significantly reduce teenage smoking: raise the tobacco sales age to 21. In 2005, Needham, Mass., did just that, while surrounding communities kept their age limit at 18. Researchers surveyed 16,000 high school students in Needham and 16 surrounding communities four times between 2006 and 2012, gathering data on their smoking habits. The study is in Tobacco Control. Over the seven years, the number of children under 18 buying cigarettes in Needham decreased to 11.6 percent from 18.4 percent, while in the surrounding communities it hardly changed — down to 19 percent from 19.4. In 2006, 12.9 percent of students in Needham and 14.8 percent of students in surrounding communities reported having smoked in the past 30 days. By 2010, 6.7 percent of Needham students reported smoking, compared with 12 percent in other towns. At the end of the study in 2012, smoking had declined to 5.5 percent in Needham and 8.5 percent outside. “More than 80 percent of smokers begin before 18,” said the lead author, Shari Kessel Schneider, project director at the Education Development Center in Waltham, Mass. “Our findings provide strong support for initiatives going on all across the country to increase the sales age as a means for decreasing youth access to cigarettes, initiation of smoking, and ultimately addiction.” © 2015 The New York Times Company
Almost half of 346,000 deaths from 12 cancers among U.S. adults in one year are attributed to cigarette smoking, despite 50 years of progress on butting out, new research suggests. Cancer researchers updated the estimate on deaths due to cigarette smoking to reflect changes in smoking patterns and how some data now suggest that the risk of cancer death among smokers can increase over time. Of 345,962 cancer deaths in the U.S. in 2011, 167,805 or 48.5 per cent were attributed to smoking cigarettes, Rebecca Siegel and her co-authors said in a research letter published in Monday's issue of JAMA Internal Medicine. The largest proportions of cancer deaths linked to smoking among those 35 and older were for cancers of the lung, bronchus and trachea (125,799 of 156, 855 deaths or 80 per cent) and larynx (2,856 of 3,728 deaths or nearly 77 per cent). About half of the deaths from cancers of the oral cavity, esophagus and urinary bladder were also attributable to smoking. Smoking was also cited as the cause of many deaths from cancer of the colon, kidney, liver, pancreas, stomach, cervix, and from myeloid leukemia. "Cigarette smoking continues to cause numerous deaths from multiple cancers despite half a century of decreasing prevalence," Rebecca Siegel from the American Cancer Society in Atlanta and her co-authors said. Dr. Norman Edelman, a senior scientific advisor to the American Lung Association, said when people hear about smoking and cancer, their thoughts often turn to lung cancer alone. ©2015 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 21057 - Posted: 06.16.2015
By BENEDICT CAREY Marijuana use did not increase among teenagers in the states in which medical marijuana has become legal, researchers reported Monday. The new analysis is the most comprehensive effort to date to answer a much-debated question: Does decriminalization of marijuana lead more adolescents to begin using it? The study found that states that had legalized medical use had higher prevailing rates of teenage marijuana use before enacting the laws, compared with states where the drug remains illegal. Those higher levels were unaffected by the changes in the law, the study found. The report, published in The Lancet Psychiatry, covered a 24-year period and was based on surveys of more than one million adolescents in 48 states. The research says nothing about the effect of legalizing recreational use, however. A primary concern on both sides of the debate over medical marijuana has been that loosening marijuana restrictions might send the wrong message to young people, and make the drug both more available and more appealing. Teenagers who develop and sustain a heavy, daily habit increase their risk of having cognitive difficulties later on, several studies now suggest. Previous research on usage trends in the wake of the laws has been mixed, some reporting evidence of an increase among adolescents and others — including two recent, multistate studies — finding no difference. The new analysis should carry far more weight, experts said, not only because of its size and scope but also because the funders included the National Institute of Drug Abuse, whose director has been outspoken about the risks of increased use. © 2015 The New York Times Company
Keyword: Drug Abuse
Link ID: 21056 - Posted: 06.16.2015
By Michael Balter Alcoholic beverages are imbibed in nearly every human society across the world—sometimes, alas, to excess. Although recent evidence suggests that tippling might have deep roots in our primate past, nonhuman primates are only rarely spotted in the act of indulgence. A new study of chimpanzees with easy access to palm wine shows that some drink it enthusiastically, fashioning leaves as makeshift cups with which to lap it up. The findings could provide new insights into why humans evolved a craving for alcohol, with all its pleasures and pains. Scientists first hypothesized an evolutionary advantage to humans’ taste for ethanol about 15 years ago, when a biologist at the University of California, Berkeley, proposed what has come to be called the “drunken monkey hypothesis.” Robert Dudley argued that our primate ancestors got an evolutionary benefit from being able to eat previously unpalatable fruit that had fallen to the ground and started to undergo fermentation. The hypothesis received a boost last year, when a team led by Matthew Carrigan—a biologist at Santa Fe College in Gainesville, Florida—found that the key enzyme that helps us metabolize ethanol underwent an important mutation about 10 million years ago. This genetic change, which occurred in the common ancestor of humans, chimps, and gorillas, made ethanol metabolism some 40 times faster than the process in other primates—such as monkeys—that do not have it. According to the hypothesis, the mutation allowed apes to consume fermented fruit without immediately getting drunk or, worse, succumbing to alcohol poisoning. Nevertheless, researchers had turned up little evidence that primates in the wild regularly eat windfall fruit or are attracted to the ethanol that such fruit contains. Now, a team led by Kimberley Hockings, a primatologist at the Center for Research in Anthropology in Lisbon, concludes from a 17-year study of chimps in West Africa that primates can tolerate significant levels of ethanol and may actually crave it, as humans do. © 2015 American Association for the Advancement of Science
By Sue Bailey, The Canadian Press Scientific studies increasingly suggest marijuana may not be the risk-free high that teens — and sometimes their parents — think it is, researchers say. Yet pot is still widely perceived by young smokers as relatively harmless, said Dr. Romina Mizrahi, director of the Focus on Youth Psychosis Prevention clinic and research program at the Centre for Addiction and Mental Health. She cites a growing body of research that warns of significantly higher incidence of hallucinations, paranoia and the triggering of psychotic illness in adolescent users who are most predisposed. "When you look at the studies in general, you can safely say that in those that are vulnerable, it doubles the risk." Such fallout is increasingly evident in the 19-bed crisis monitoring unit at the Children's Hospital of Eastern Ontario in Ottawa. "I see more and more cases of substance-induced psychosis," said Dr. Sinthu Suntharalingam, a child and adolescent psychiatrist. "The most common substance that's abused is cannabis." One or two cases a week are now arriving on average. "They will present with active hallucinations," Suntharalingam said. "Parents will be very scared. They don't know what's going on. "They'll be seeing things, hearing things, sometimes they will try to self-harm or go after other people." Potential effects need to be better understood She and Mizrahi, an associate professor in psychiatry at University of Toronto, are among other front-line professionals who say more must be done to help kids understand potential effects. "They know the hard drugs, what they can do," Suntharalingam said. "Acid, they'll tell us it can cause all these things so they stay away from it. But marijuana? They'll be: 'Oh, everybody does it."' Mizrahi said the message isn't getting through. ©2015 CBC/Radio-Canada.