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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 A paper from the UN Office on Drugs and Crime (UNODC) has been withdrawn after pressure from at least one country.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

By Janet Davison, CBC News Maddy Huggins would binge drink as a teenager and black out, just like other kids at her high school in Kelowna, B.C. When she went backpacking during her gap year, there were more alcoholic overloads and "really risky" moments when something bad could have transpired. "Nothing too terrible happened, but there was the potential for that," says Huggins, 22, who's just about to start fourth year at the University of Saskatchewan. As she settled into university, however, Huggins did some serious thinking about alcohol in her life. "It was just a gradual progression where I was like, 'OK, enough of this.'" These days, Huggins knows her low-risk alcoholic limits and won't hesitate to order water even if her friends are going for something stronger. But other young Canadian women haven't stepped back like that. Reports suggest the percentage of young women binge drinking — defined now as having at least four drinks per occasion at least once a month — is on the rise and encompasses nearly one in four Canadian women between 20 and 34. Indeed, the trend has become so pronounced that the Paris-based Organization of Economic Co-operation and Development warned in May that binge drinking by young people, including in Canada, has become a "major public health and social concern." Looming problems It's a concern that goes beyond the headline issues like date rape and campus horrors to where health scientists are warning that because of physiology — women generally weigh less than men, have a higher percentage of body fat and smaller livers — excessive drinking by young women is setting them up for a series of health problems down the road. ©2015 CBC/Radio-Canada

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Brain Asymmetry, Spatial Cognition, and Language
Link ID: 21282 - Posted: 08.10.2015

RACHEL MARTIN, HOST: Every day, according to the Centers for Disease Control, 44 Americans die because they have overdosed on prescription painkillers. The CDC calls it an epidemic, and drug companies are responding by trying to develop versions of the most addictive painkillers, opioids, that will diminish a user's physical craving for the medicine. Now, to do this, to create these less addictive drugs, pharmaceutical companies are recruiting thousands of self-identified drug users to test their products. David Crow is a reporter for the Financial Times. He's just published a big report on this, and he joins me now to talk more about it. Thanks so much for being with us. Opioids, as we mentioned, are the worst in terms of their addictive quality. These companies are trying to come up with drugs that will achieve the same painkilling effect without the addictiveness. So this is actually possible? CROW: What they're trying to do is develop a new generation of opioid painkillers that have features that make them harder to abuse. Some of the strategies that have been pursued include hard shells that make it harder to crush up the pill so that you can snort it or gumming agents that make it harder to put into a syringe so that you can inject it. And some companies are experimenting with putting different chemicals in the center of the pill that will remain dormant. But if it's tampered with, that chemical would be released, and it would counteract the effect of the opioid. They're testing these drugs on recreational drug users. And the participants go through a screening process where they have to wash out, where they don't have any opioid in their system, and also where they're given a drug called naloxone, which cuts off the effects of opioids. And at that point, if you were addicted or physically dependent, your body would show signs of withdrawal. And that is the screening process. © 2015 NPR

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: 21253 - Posted: 08.02.2015

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

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: 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.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 21168 - Posted: 07.14.2015

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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 21163 - Posted: 07.13.2015

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

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: 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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21159 - Posted: 07.11.2015

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

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 21158 - Posted: 07.11.2015

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

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: 21150 - Posted: 07.09.2015