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Ian Sample Science editor High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other. The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found. The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient. Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity. “If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 21665 - Posted: 11.28.2015

By Lenny Bernstein BALTIMORE — Deep into a three-day heroin binge at a local hotel, Samantha told the newbie he was shooting too much. He wasn’t accustomed to heroin, she said, and hadn’t waited long enough since his last injection. “But he didn’t listen,” she said. Sure enough, he emerged from a visit to the bathroom, eyes glazed, and collapsed from an overdose. Samantha, who declined to give her last name to avoid trouble with her bosses at a nearby strip club, said she grabbed her naloxone, the fast-acting antidote to opioid overdoses. She was too panicked to place the atomizer on the end of the syringe, but her boyfriend wasn’t. He sprayed the mist into the nose of the unconscious drug user, who awoke minutes later. “I always have it because I’m scared to death,” said Samantha, who said she has been shooting heroin for 22 years. “I don’t want to be helpless.” As the opioid epidemic has exploded in small towns and suburbs in recent years, officials have scrambled to put naloxone in the hands of drug users’ families and friends, and to make it more widely available by equipping police officers with the drug. At the same time, thousands of lives are being saved by giving the antidote to drug users. More than 80 percent of overdose victims revived by “laypeople” were rescued by other users, most of them in the past few years, according to one national survey published in June.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21654 - Posted: 11.24.2015

by Bethany Brookshire Many people perceive cocaine as one of the most intense stimulant drugs available: It’s illegal, highly addictive and dangerous. Caffeine, in contrast, is the kinder, cuddlier stimulant. It’s legal, has mild effects and in forms such as coffee, it might even be good for your health. But caffeine in combination with cocaine is another story. In South America, drug distributors have started “cutting” their cocaine with caffeine. This cheaper substitute might, at first glance, seem to make the cocaine less potent. After all, there’s less of the drug there. But new data shows that when combined, cocaine and caffeine make a heck of a drug. Coca paste is a popular form of cocaine in South American countries. A smoked form of cocaine, coca paste is the intermediate product in the extraction process used to get pure cocaine out of coca leaves. Because it is smoked, the cocaine in the coca paste hits the brain very quickly, making the drug highly addictive, explains Jose Prieto, a neurochemist at the Biological Research Institute Clemente Stable in Montevideo, Uruguay. Much of the time, Coca paste isn’t acting alone, however. In a 2011 study published in Behavioral Brain Research, Prieto and his colleagues examined the contents of coca paste from police seizures. “Nearly 80 percent of the coca paste samples” were adulterated, Prieto says, “most with caffeine.” Caffeine adulteration ranged from 1 to 15 percent of the drug volume. © Society for Science & the Public 2000 - 2015.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21643 - Posted: 11.18.2015

by Teresa Shipley Feldhausen The benefits of drinking coffee continue to filter in. An analysis of more than 200,000 medical professionals followed for nearly 30 years finds that drinking up to five cups of coffee a day is associated with reduced risk of dying early from heart and brain diseases as well as suicide. The study’s results were adjusted for factors like smoking, weight and diet. Benefits were more pronounced for those who had never smoked, an international team of researchers report November 16 in Circulation. Both caffeinated and decaf java had positive effects, leading the researchers to speculate that coffee’s potency as a health elixir may stem from chemical compounds in the bean such as diterpenes and chlorogenic acids. © Society for Science & the Public 2000 - 2015.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21634 - Posted: 11.17.2015

By Jason G. Goldman When a monkey has the sniffles or a headache, it doesn't have the luxury of popping a few painkillers from the medicine cabinet. So how does it deal with the common colds and coughs of the wildlife world? University of Georgia ecologist Ria R. Ghai and her colleagues observed a troop of more than 100 red colobus monkeys in Uganda's Kibale National Park for four years to figure out whether the rain forest provides a Tylenol equivalent. Monkeys infected with a whipworm parasite were found to spend more time resting and less time moving, grooming and having sex. The infected monkeys also ate twice as much tree bark as their healthy counterparts even though they kept the same feeding schedules. The findings were published in September in the journal Proceedings of the Royal Society B. The fibrous snack could help literally sweep the intestinal intruder out of the simians' gastrointestinal tracts, but Ghai suspects a more convincing reason. Seven of the nine species of trees and shrubs preferred by sick monkeys have known pharmacological properties, such as antisepsis and analgesia. Thus, the monkeys could have been self-medicating, although she cannot rule out other possibilities. The sick individuals were, however, using the very same plants that local people use to treat illnesses, including infection by whipworm parasites. And that “just doesn't seem like a coincidence,” Ghai says. © 2015 Scientific American,

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21619 - Posted: 11.10.2015

by Bethany Brookshire Cheese is a delicious invention. But if you saw the news last week, you might think it’s on its way to being classified as a Schedule II drug. Headlines proclaimed “Say cheese? All the time? Maybe you have an addiction,” “Cheese really is crack” and “Your cheese addiction is real.” Under the headlines, the stories referred to a study examining the addictive properties of various foods. Pizza was at the top. The reason? The addictive properties of cheese, which the articles claim contains “dangerous” opiate-like chemicals called casomorphins. But you can’t explain away your affinity for cheese by saying you’re addicted. The study in those stories, published earlier this year in PLOS ONE, did investigate which foods are most associated with addictive-like eating behaviors. Pizza did come out on top in one experiment. But the scientists who did the research say this has little to do with the delicious dairy products involved. Instead, they argue, the foods we crave the most are those processed to have high levels of sugars and fat, and it’s these ingredients that leave us coming back for another slice. The cheese? “I was horrified by the misstatements and the oversimplifications … and the statements about how it’s an excuse to overeat,” says Ashley Gearhardt of the University of Michigan in Ann Arbor, who led the study. “Liking is not the same as addiction. We like lots of things. I like hip-hop music and sunshine and my wiener dog, but I’m not addicted to her. I eat cheese every day. That’s doesn’t mean you’re addicted or it has addictive potential.” © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21592 - Posted: 11.02.2015

By KATHARINE Q. SEELYE NEWTON, N.H. — When Courtney Griffin was using heroin, she lied, disappeared, and stole from her parents to support her $400-a-day habit. Her family paid her debts, never filed a police report and kept her addiction secret — until she was found dead last year of an overdose. At Courtney’s funeral, they decided to acknowledge the reality that redefined their lives: Their bright, beautiful daughter, just 20, who played the French horn in high school and dreamed of living in Hawaii, had been kicked out of the Marines for drugs. Eventually, she overdosed at her boyfriend’s grandmother’s house, where she died alone. “When I was a kid, junkies were the worst,” Doug Griffin, 63, Courtney’s father, recalled in their comfortable home here in southeastern New Hampshire. “I used to have an office in New York City. I saw them.” When the nation’s long-running war against drugs was defined by the crack epidemic and based in poor, predominantly black urban areas, the public response was defined by zero tolerance and stiff prison sentences. But today’s heroin crisis is different. While heroin use has climbed among all demographic groups, it has skyrocketed among whites; nearly 90 percent of those who tried heroin for the first time in the last decade were white. And the growing army of families of those lost to heroin — many of them in the suburbs and small towns — are now using their influence, anger and grief to cushion the country’s approach to drugs, from altering the language around addiction to prodding government to treat it not as a crime, but as a disease. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21583 - Posted: 10.31.2015

By Dina Fine Maron When powerful street drugs collectively known as synthetic pot are smoked, the resulting high mimics the effects of marijuana. Yet these man-made cannabinoids are not marijuana at all. The drugs, more commonly called spice, fake weed or K2, are made up of any number of dried, shredded plants sprayed with chemicals that live in a murky legality zone. They are highly dangerous—and their use is on the rise. Synthetic pot, which first hit the market in the early 2000s, has especially caught the attention of public health officials in the past couple of years, stemming from a surge in hospitalizations and violent episodes. Although the drugs act on the same brain pathway as weed's active ingredient, they can trigger harsher reactions, including heart attacks, strokes, kidney damage and delusions. Between June and early August usage of these drugs led to roughly 2,300 emergency room visits in New York State alone. Nationwide more than 6,000 incidents involving spice have been reported to U.S. poison-control centers this year—about double the number of calls in 2013. Ever changing recipes make it possible for spice sellers to elude the authorities. Each time an ingredient is banned, producers swap in another compound. The drugs are then sold on the Internet or at gas stations and convenience stores at prices lower than genuine marijuana. The changing formulations also pose a challenge for researchers trying to match the chemicals with their side effects or to develop tests to identify them in a user's system. “The drugs are present in blood for only a short period, so it's very difficult to detect them,” says Marilyn Huestis, chief of the Chemistry and Drug Metabolism Section at the National Institute on Drug Abuse. © 2015 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21570 - Posted: 10.27.2015

By R. Douglas Fields “Why can’t you stop drinking?” This week at the Annual Meeting of the Society for Neuroscience in Chicago, researchers from the University of Chicago announced a new finding that provides a fresh answer to this persistent question that plagues people addicted to alcohol. The discovery offers an entirely new approach to treatment. Neuroscientist, Amy Lasek, at the Department of Psychiatry at the University of Illinois, Chicago, and colleagues, report that after binge drinking, neurons in brain circuits responsible for alcohol addiction become encased in a protein material, called a perineuronal net. The impenetrable coating cements neurons involved in alcohol addiction into a circuit that is extremely difficult to break. Current drugs for treating alcohol dependence work by modifying neurotransmitter signaling between neurons, but for many people these treatments cannot break the overwhelming compulsion to drink. Drugs that can break down the glue-like cement in perineuronal nets could offer a new approach to treatment. Lasek’s unusual approach into addiction research stems from her background as a molecular and cell biologist working in the field of cancer research. The root of cancer is changes in specific genes. Small molecules designed to target these aberrant genes is the approach used in cancer therapy. Lasek’s background made her think of finding molecularly targeted therapies for psychiatric disorders. Lasek and her colleagues began by studying fruit flies to search for gene variations that altered the fly’s behavior toward alcohol. She found several genes that had this effect, including an obscure one called ALK (anaplastic lymphoma kinase). Then she suppressed these genes in mice to see if the animal’s response to alcohol was altered. “I got hooked,” she says, “because to me the fact that you can manipulate a single gene in a single brain region and change behavior—like drinking or cocaine reward—was fascinating from a biological point of view!” © 2015 Scientific America

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21561 - Posted: 10.24.2015

Olivia Maynard It has been described as a ‘disruptive technology’ potentially capable of breaking our fatal relationship with tobacco. So the setting for a public debate on e-cigarettes - a museum part-funded by the tobacco industry, in a city home to the global headquarters of one of the largest tobacco manufacturers - was perhaps ironic. Yet on Wednesday evening, I found myself at the M-Shed in Bristol, watching just that: a debate about whether e-cigarettes could be part of the solution to the tobacco epidemic. To mark the launch of a new Integrative Cancer Epidemiology Programme, linked to the Medical Research Centre Integrative Epidemiology Unit at the University of Bristol, Professor Marcus Munafò (Professor of Biological Psychology at the University of Bristol) and Professor Linda Bauld (Professor of Health Policy at the University of Stirling), both collaborators of mine, discussed e-cigarettes. Professor Gabriel Scally (Public Health Doctor and former Regional Director of Public Health for the South West of England) chaired the discussion. Billed as a debate about whether e-cigarettes might be ‘the key to reducing smoking’, some in the audience may have expected a heated discussion. However, with this line-up of academics, influential in the fields of public health, tobacco and addiction, the discussion was evidence-based and measured. As for the motion of the debate, the panel was unanimous: e-cigarettes may not be the key to reducing smoking, but they are certainly an important part of the solution. © 2015 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21556 - Posted: 10.24.2015

Mark Easton Home editor An attempt by UN officials to get countries to decriminalise the possession and use of all drugs has been foiled, the BBC can reveal. A paper from the UN Office on Drugs and Crime (UNODC) has been withdrawn after pressure from at least one country. The document, which was leaked, recommends that UN members consider "decriminalising drug and possession for personal consumption". It argued "arrest and incarceration are disproportionate measures". The document was drawn up by Dr Monica Beg, chief of the HIV/AIDs section of the UNODC in Vienna. It was prepared for an international harm reduction conference currently being held in Kuala Lumpur. The UNODC oversees international drugs conventions and offers guidance on compliance. Sources within the UNODC have told the BBC the document was never sanctioned by the organisation as policy. One senior figure within the agency described Dr Beg as "a middle-ranking official" who was offering a professional viewpoint. The document, on headed agency notepaper, claims it "clarifies the position of UNODC to inform country responses to promote a health and human-rights approach to drug policy". "Treating drug use for non-medical purposes and possession for personal consumption as criminal offences has contributed to public health problems and induced negative consequences for safety, security, and human rights," the document states. © 2015 BBC.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21535 - Posted: 10.21.2015

by Helen Thompson It's no secret that some plants lace their nectar with caffeine in an effort to attract more pollinators, and that buzz sticks around in a bee's memory. These caffeinated flowers lure naive honeybees to return over and over again — and bring their friends, researchers report October 15 in Current Biology. When feeding off caffeinated nectar (versus noncaffeinated nectar), honeybees increased their foraging activity and performed four times as many waggle dances to alert other workers to food sources. Though bees might be more persistent foragers while under the influence of caffeine, they focused mainly on caffeinated sources instead casting a broad search. Plants may also substitute caffeine for sugar, the researchers note, duping bees into gathering nectar that's less valuable for honey production. © Society for Science & the Public 2000 - 2015.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21515 - Posted: 10.16.2015

By CATHERINE SAINT LOUIS Ever since the Food and Drug Administration approved the use of the narcotic painkiller OxyContin for certain children in August, it has faced unabated criticism from lawmakers and public officials who are wrestling with devastating rates of prescription opioid abuse in their communities. Last week, Hillary Rodham Clinton brought the issue to the presidential race, calling the agency’s action “absolutely incomprehensible.” The crux of the issue is whether the agency’s approval will lead to more prescriptions for OxyContin in young patients. For years, the powerful long-acting drug has been prescribed off-label to very sick children in severe pain from cancer or spinal-fusion surgery. (Doctors can prescribe an approved drug to anyone and for any use they see fit regardless of specifications on the label.) The agency’s approval means those doctors will finally have “information about how to do it appropriately,” like dosage recommendations, said Dr. Stephen Ostroff, the agency’s acting commissioner, in an interview. “We recognize this is a very nuanced issue,” said Dr. Ostroff, when asked about Mrs. Clinton’s recent comments. “It needs to be understood in the context of why this was done.” Dr. Kathleen A. Neville, a pediatric oncologist at Arkansas Children’s Hospital, routinely treats children with unremitting pain caused by cancer or sickle cell anemia. Her patients are the kind the F.D.A. envisioned would benefit from OxyContin, despite its “risks of addictions, abuse and misuse” as a warning on the new label says. Dr. Neville, who said she had no financial ties to makers of painkillers, applauded the agency’s approval. “Just because OxyContin has been abused or prescribed inappropriately doesn’t mean we should deprive the children who need the drug,” she said, adding it is “our obligation to have the best level of evidence for its use in children.” © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 21491 - Posted: 10.09.2015

By Gretchen Reynolds We’ve probably all heard someone exclaim, “Ah, my endorphins are kicking in!” at the end of a good run. Endorphins are famous for supposedly producing “runner’s high,” that fleeting sense of calm and euphoria that engulfs many of us after a satisfying workout. But in fact, endorphins may be unfairly hogging the credit for making workouts enjoyable, according to an enlightening new experiment with animals. The findings suggest that endorphins have little to do with runner’s high. Instead, that euphoric feeling may be the product of a completely different but oddly familiar substance — the body’s own endocannabinoids, the chemicals that, like the cannabinoids in marijuana, lighten mood. Endorphins first became a household word in the 1980s, when researchers found that blood levels increased after prolonged exercise. This finding made sense. Exercise can cause discomfort or pain, and endorphins are the body’s self-produced opiates, with pain-relieving properties much like morphine. From that discovery, it was a short step to believing that endorphins must also produce the pleasurable mental sensations that many people feel after exercise. But there is a substantial problem with that idea, and it involves the substantial-ness of endorphins. They are large molecules, too big to pass through the blood-brain barrier. They might staunch pain in the muscles, but they wouldn’t have effects directly inside the brain, where any high would originate. So for the past decade or so, scientists have been looking for other substances that might be involved in making exercisers feel high, which led them, perhaps unsurprisingly, to endocannabinoids. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21488 - Posted: 10.08.2015

Nathan Seppa For a historically mistrusted drink, coffee is proving to be a healthy addiction. Scientific findings in support of coffee’s nutritional attributes have been arriving at a steady drip since the 1980s, when Norwegian researchers reported that coffee seemed to fend off liver disease. Since then, the dark brown beverage has shown value against liver cancer, too, as well as type 2 diabetes, heart disease and stroke. Coffee even appears to protect against depression, Parkinson’s and Alzheimer’s diseases. Taken as a whole, these results might explain the most astonishing finding of all. People who drink two or more cups of coffee a day live longer than those who don’t, after accounting for behavioral differences, U.S. researchers reported in 2012. Studies in Japan, Scotland and Finland agree. Talk about a twofer. Coffee not only picks you up, it might put off the day they lower you down. Yet coffee has had trouble shaking its bad-for-you reputation. It may be one of the most widely consumed drinks in the world, but people have long assumed that, at least in its energizing caffeinated version, coffee comes with a catch. “People notice the caffeine,” says cardiologist Arthur Klatsky, who has researched coffee for decades at the Kaiser Permanente Northern California Division of Research in Oakland. “And there is this general feeling that anything that has some effect on the nervous system has to have something bad about it.” It doesn’t help that caffeine is mildly addictive.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 21420 - Posted: 09.20.2015

A particular region of the brain may drive smoking addiction, say scientists who found stroke survivors with damage to their insular cortex more easily kicked the habit. They studied 156 stroke patients with different patterns of brain injury. More of those with insular cortex damage successfully gave up smoking and reported fewer withdrawal symptoms than the other stroke patients. Experts say targeting this brain area may help other smokers quit. Most stop smoking medicines currently on the market work by blocking the brain's reward pathways in response to nicotine. And patches and gums aim to lessen cravings by supplying a controlled dose of nicotine as the person weans themselves off tobacco. But post-graduate researcher Amir Abdolahi and colleagues believe the insular cortex could be a valuable new target for quit smoking aids. Therapies that could hone in on this area of the brain and disrupt its role in addiction, potentially with new drugs or other techniques such as deep brain stimulation or transcranial magnetic stimulation, should be explored, they say. "Much more research is needed in order for us to more fully understand the underlying mechanism and specific role of the insular cortex, but it is clear that something is going on in this part of the brain that is influencing addiction," Mr Abdolahi said. The research findings are published in two medical journals - Addiction and Addictive Behaviors. The patients in the study were smokers who had been admitted to hospital because of a stroke. Medical scans revealed that 38 of them had suffered damage to the insular cortex, while the remaining 118 had damage to other parts of the brain. All of the patients were encouraged by their doctor to quit smoking. © 2015 BBC.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21385 - Posted: 09.08.2015

Raiding the fridge or downing glasses of water after a night of heavy drinking won't improve your sore head the next day, Dutch research suggests. Instead, a study concluded, the only way to prevent a hangover is to drink less alcohol. More than 800 students were asked how they tried to relieve hangover symptoms, but neither food nor water was found to have any positive effect. The findings are being presented at a conference in Amsterdam. A team of international researchers from the Netherlands and Canada surveyed students' drinking habits to find out whether hangovers could be eased or if some people were immune to them. Among 826 Dutch students, 54% ate food after drinking alcohol, including fatty food and heavy breakfasts, in the hope of staving off a hangover. With the same aim, more than two-thirds drank water while drinking alcohol and more than half drank water before going to bed. Although these groups showed a slight improvement in how they felt compared with those who hadn't drunk water, there was no real difference in the severity of their hangovers. Previous research suggests that about 25% of drinkers claim never to get hangovers. So the researchers questioned 789 Canadian students about their drinking in the previous month and the hangovers they experienced, finding that those who didn't get a hangover simply consumed "too little alcohol to develop a hangover in the first place". Of those students who drank heavily, with an estimated blood alcohol concentration of more than 0.2%, almost no-one was immune to hangovers. © 2015 BBC.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21356 - Posted: 08.29.2015

Daniel Cressey In 2013, Beau Kilmer took on a pretty audacious head count. Citizens in the state of Washington had just voted to legalize marijuana for recreational use, and the state's liquor control board, which would regulate the nascent industry, was anxious to understand how many people were using the drug — and importantly, how much they were consuming. The task was never going to be straightforward. Users of an illicit substance, particularly heavy users, often under-report the amounts they take. So Kilmer, co-director of the RAND Drug Policy Research Center in Santa Monica, California, led a team to develop a web-based survey that would ask people how often they had used cannabis in the past month and year. To help them gauge the amounts, the surveys included scaled pictures showing different quantities of weed. The survey, along with other data the team had collected, revealed a rift between perception and reality. Based on prior data, state officials had estimated use at about 85 tonnes per year; Kilmer's research suggested that it was actually double that, about 175 tonnes1. The take-home message, says Kilmer, was “we're going to have to start collecting more data”. Scientists around the world would echo that statement. Laws designed to legalize cannabis or lessen the penalties associated with it are taking effect around the world. They are sweeping the sale of the drug out of stairwells and shady alleys and into modern shopfronts under full view of the authorities. In 2013, Uruguay became the first nation to legalize marijuana trade. And several countries in Europe — Spain and Italy among them — have moved away from tough penalties for use and possession. Thirty-nine US states plus Washington DC have at least some provisions for medicinal use of the drug. Washington, Colorado, Alaska and Oregon have gone further, legalizing the drug for recreational consumption. A handful of other states including California and Massachusetts are expected to vote on similar recreational-use measures by the end of 2016. © 2015 Nature Publishing Group

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21315 - Posted: 08.19.2015

By Lisa Rapaport (Reuters Health) - U.S. teens who try electronic cigarettes may be more than twice as likely to move on to smoking conventional cigarettes as those who have never tried the devices, report researchers from the University of Southern California. The findings, published August 18 in JAMA, offer some of the best evidence yet at establishing a link between e-cigarettes and smoking, said Dr. Nancy Rigotti, an expert in tobacco research at Massachusetts General Hospital and author of an editorial accompanying the study. "Adolescent brains appear to be especially susceptible to becoming addicted to nicotine when exposed," Rigotti told Reuters Health in an email. About 2 million middle- and high-school students tried e-cigarettes in 2014, triple the number of teen users in 2013, the Centers for Disease Control and Prevention reported in April. The data sparked alarm among tobacco control advocates who fear e-cigarettes will create a new generation of nicotine addicts who may eventually switch to conventional cigarettes. Big tobacco companies, including Altria Group Inc, Lorillard Tobacco Co and Reynolds American Inc, are all developing e-cigarettes. The battery-powered devices feature a glowing tip and a heating element that turns liquid nicotine and other flavorings into a cloud of vapor that users inhale. An international review of published research by the Cochrane Review in December concluded that the devices could help smokers quit but said much of the existing evidence on e-cigarettes was thin. © 2015 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21314 - Posted: 08.19.2015

By Robert F. Service Move over, poppies. In one of the most elaborate feats of synthetic biology to date, a research team has engineered yeast with a medley of plant, bacterial, and rodent genes to turn sugar into thebaine, the key opiate precursor to morphine and other powerful painkilling drugs that have been harvested for thousands of years from poppy plants. The team also showed that with further tweaks, the yeast could make hydrocodone, a widely used painkiller that is now made chemically from thebaine. “This is a major milestone,” says Jens Nielsen, a synthetic biologist at Chalmers University of Technology in Göteborg, Sweden. The work, he adds, demonstrates synthetic biology’s increasing sophistication at transferring complex metabolic pathways into microbes. By tweaking the yeast pathways, medicinal chemists may be able to produce more effective, less addictive versions of opiate painkillers. But some biopolicy experts worry that morphinemaking yeast strains could also allow illicit drugmakers to brew heroin as easily as beer enthusiasts home brew today—the drug is a simple chemical conversion from morphine. That concern is one reason the research team, led by Christina Smolke, a synthetic biologist at Stanford University in Palo Alto, California, stopped short of making a yeast strain with the complete morphine pathway; medicinal drug
makers also primarily use thebaine to make new compounds. Synthetic biologists had previously engineered yeast to produce artemisinin, an antimalarial compound, but that required inserting just a handful of plant genes. To get yeast to make thebaine, © 2015 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 21297 - Posted: 08.15.2015