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Toronto Mayor Rob Ford said Tuesday that he had smoked crack cocaine, probably "in one of my drunken stupors," about a year ago. Here’s a look at the drug that can rapidly produce a high, some of the ways it can affect an individual’s behaviour and health, its legal status and other instances of high-profile use. What is crack cocaine? Crack cocaine is a chemically processed form of cocaine, a stimulant drug made into a white powder from leaves of coca bushes growing in the Andes Mountains of South America. To make crack, the white crystalline cocaine powder — cocaine hydrochloride — is dissolved and boiled in a mixture of water and ammonia or baking soda. When that cools into a solid substance, small pieces, often called "rocks," are formed, according to a 2009 RCMP report on "The Illicit Drug Situation in Canada." How is it used? Cocaine is injected or snorted. Crack cocaine is usually smoked, often in a glass pipe, although it can also be injected. The word "crack" comes from the distinctive sound heard when the substance heats up. When crack is heated and inhaled, the vapours are absorbed through the lungs and into the bloodstream, according to the U.S. National Institute on Drug Abuse. A high from smoking crack could last five to 10 minutes, says the institute, compared to 15 to 30 minutes for a high from snorting cocaine. © CBC 2013

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: 18876 - Posted: 11.06.2013

By Ferris Jabr When Shirley was in her mid-20s she and some friends road-tripped to Las Vegas on a lark. That was the first time she gambled. Around a decade later, while working as an attorney on the East Coast, she would occasionally sojourn in Atlantic City. By her late 40s, however, she was skipping work four times a week to visit newly opened casinos in Connecticut. She played blackjack almost exclusively, often risking thousands of dollars each round—then scrounging under her car seat for 35 cents to pay the toll on the way home. Ultimately, Shirley bet every dime she earned and maxed out multiple credit cards. “I wanted to gamble all the time,” she says. “I loved it—I loved that high I felt.” In 2001 the law intervened. Shirley was convicted of stealing a great deal of money from her clients and spent two years in prison. Along the way she started attending Gamblers Anonymous meetings, seeing a therapist and remaking her life. “I realized I had become addicted,” she says. “It took me a long time to say I was an addict, but I was, just like any other.” Ten years ago the idea that someone could become addicted to a habit like gambling the way a person gets hooked on a drug was controversial. Back then, Shirley's counselors never told her she was an addict; she decided that for herself. Now researchers agree that in some cases gambling is a true addiction. In the past, the psychiatric community generally regarded pathological gambling as more of a compulsion than an addiction—a behavior primarily motivated by the need to relieve anxiety rather than a craving for intense pleasure. In the 1980s, while updating the Diagnostic and Statistical Manual of Mental Disorders (DSM), the American Psychiatric Association (APA) officially classified pathological gambling as an impulse-control disorder—a fuzzy label for a group of somewhat related illnesses that, at the time, included kleptomania, pyromania and trichotillomania (hairpulling). In what has come to be regarded as a landmark decision, the association moved pathological gambling to the addictions chapter in the manual's latest edition, the DSM-5, published this past May. © 2013 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: 18875 - Posted: 11.06.2013

By Bradley E. Alger, Ph.D. Cannabis, derived from a plant and one of the oldest known drugs, has remained a source of controversy throughout its history. From debates on its medicinal value and legalization to concerns about dependency and schizophrenia, cannabis (marijuana, pot, hashish, bhang, etc.) is a hot button for politicians and pundits alike. Fundamental to understanding these discussions is how cannabis affects the mind and body, as well as the body’s cells and systems. How can something that stimulates appetite also be great for relieving pain, nausea, seizures, and anxiety? Whether its leaves and buds are smoked, baked into pastries, processed into pills, or steeped as tea and sipped, cannabis affects us in ways that are sometimes hard to define. Not only are its many facets an intrinsically fascinating topic, but because they touch on so many parts of the brain and the body, their medical, ethical, and legal ramifications are vast. The intercellular signaling molecules, their receptors, and synthetic and degradative enzymes from which cannabis gets its powers had been in place for millions of years by the time humans began burning the plants and inhaling the smoke. Despite records going back 4,700 years that document medicinal uses of cannabis, no one knew how it worked until 1964. That was when Yechiel Gaoni and Raphael Mechoulam1 reported that the main active component of cannabis is tetrahydrocannabinol (THC). THC, referred to as a “cannabinoid” (like the dozens of other unique constituents of cannabis), acts on the brain by muscling in on the intrinsic neuronal signaling system, mimicking a key natural player, and basically hijacking it for reasons best known to the plants. Since the time when exogenous cannabinoids revealed their existence, the entire natural complex came to be called the “endogenous cannabinoid system,” or “endocannabinoid system” (ECS). Copyright 2013 The Dana Foundation

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 18874 - Posted: 11.06.2013

The generic anticonvulsant medication gabapentin shows promise as an effective treatment for alcohol dependence, based on the results of a 150-patient clinical trial of the medication. Conducted by scientists supported by the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of the National Institutes of Health, the study found that alcohol dependent patients using gabapentin were more likely to stop drinking or refrain from heavy drinking than those taking placebo. Gabapentin is already widely prescribed to treat pain conditions and epilepsy. “Gabapentin adds to the list of existing medications that have shown promise in treating alcohol dependence,” said Kenneth R. Warren, Ph.D., acting director of the NIAAA. “We will continue to pursue research to expand the menu of treatment options available for alcoholism in the hopes of reaching more people.” A report of the study, led by Barbara J. Mason, Ph.D., of The Scripps Research Institute (TSRI) in La Jolla, Calif., appears in the Nov. 4, 2013 edition of JAMA Internal Medicine. Dr. Mason and her colleagues randomly assigned alcohol dependent patients to receive a moderate or high dose of gabapentin (900 milligrams or 1,800 milligrams) or a placebo. Over the 12-week treatment, patients receiving the 1,800-milligram dose were twice as likely to refrain from heavy drinking (45 percent vs. 23 percent) and four times as likely to stop drinking altogether (17 percent vs. 4 percent), compared to placebo. Participants receiving gabapentin also reported improved sleep and mood and fewer alcohol cravings. The medication appeared to be well tolerated with few side effects.

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: 18873 - Posted: 11.05.2013

By JANE E. BRODY Marijuana has been used medically, recreationally and spiritually for about 5,000 years. Known botanically as cannabis, it has been called a “crude drug”: marijuana contains more than 400 chemicals from 18 chemical families. More than 2,000 compounds are released when it is smoked, and as with tobacco, there are dangers in smoking it. Medical marijuana clinics operate in 20 states and the District of Columbia, and its recreational use is now legal in Colorado and Washington. A Gallup poll conducted last month found that 58 percent of Americans support the legalization of marijuana. Yet researchers have been able to do relatively little to test its most promising ingredients for biological activity, safety and side effects. The main reason is marijuana’s classification by Congress in 1970 as an illegal Schedule I drug, defined as having a potential for abuse and addiction and no medical value. American scientists seeking clarification of marijuana’s medical usefulness have long been stymied by this draconian classification, usually reserved for street drugs like heroin with a high potential for abuse. Dr. J. Michael Bostwick, a psychiatrist at the Mayo Clinic in Rochester, Minn., said the classification was primarily political and ignored more than 40 years of scientific research, which has shown that cellular receptors for marijuana’s active ingredients are present throughout the body. Natural substances called cannabinoids bind to them to influence a wide range of body processes. In a lengthy report entitled “Blurred Boundaries: The Therapeutics and Politics of Medical Marijuana,” published last year in Mayo Clinic Proceedings, Dr. Bostwick noted that the so-called endocannabinoid system has an impact on the “autonomic nervous system, immune system, gastrointestinal tract, reproductive system, cardiovascular system and endocrine network.” Copyright 2013 The New York Times Company

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: 18866 - Posted: 11.04.2013

Melissa Dahl TODAY You know smoking doesn’t do any favors for your face – or your lungs, or your heart, or just about any other part of your body, for that matter! – but a new study of twins hints at the ways the habit makes you look older than you really are. In what is perhaps the best detail of the study, researchers used the annual Twins Days Festival in Twinsburg, Ohio (the "Largest Annual Gathering of Twins in the World!") to round up the 79 identical pairs they include in the report. A panel of three plastic surgery residents compared the faces of the twins, one of which had been smoking for at least five years longer than the other. They identified a few major areas of accelerated aging in the faces of the smoking twins: The smokers' upper eyelids drooped while the lower lids sagged, and they had more wrinkles around the mouth. The smokers were also more likely to have jowls, according to the study, which was published today in the journal Plastic and Reconstructive Surgery. Smoking reduces oxygen to the skin, which also decreases blood circulation, and that can result in weathered, wrinkled, older-looking skin, explains Dr. Bahman Guyuron, a plastic surgeon in Cleveland, Ohio, and the lead author of the study. The logic of research like this and others like it is this: If threats of cancer, heart and lung disease, or the dangers of second- and third-hand smoke aren’t enough to get people to stop smoking, or to never start in the first place, then why not try appealing to people’s vanity? (The same tactic has been used in an attempt to warn young people away from tanning.)

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: 18851 - Posted: 10.30.2013

By ADAM NAGOURNEY and RICK LYMAN LOS ANGELES — In the heart of Northern California’s marijuana growing region, the sheriff’s office is inundated each fall with complaints about the stench of marijuana plots or the latest expropriation of public land by growers. Its tranquil communities have been altered by the emergence of a wealthy class of marijuana entrepreneurs, while nearly 500 miles away in Los Angeles, officials have struggled to regulate an explosion of medical marijuana shops. But at a time when polls show widening public support for legalization — recreational marijuana is about to become legal in Colorado and Washington, and voter initiatives are in the pipeline in at least three other states — California’s 17-year experience as the first state to legalize medical marijuana offers surprising lessons, experts say. Warnings voiced against partial legalization — of civic disorder, increased lawlessness and a drastic rise in other drug use — have proved unfounded. Instead, research suggests both that marijuana has become an alcohol substitute for younger people here and in other states that have legalized medical marijuana, and that while driving under the influence of any intoxicant is dangerous, driving after smoking marijuana is less dangerous than after drinking alcohol. Although marijuana is legal here only for medical use, it is widely available. There is no evidence that its use by teenagers has risen since the 1996 legalization, though it is an open question whether outright legalization would make the drug that much easier for young people to get, and thus contribute to increased use. And though Los Angeles has struggled to regulate marijuana dispensaries, with neighborhoods upset at their sheer number, the threat of unsavory street traffic and the stigma of marijuana shops on the corner, communities that imposed early and strict regulations on their operations have not experienced such disruption. © 2013 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: 18840 - Posted: 10.28.2013

Doug Greene, WVIT and NBC News staff NBC News Oreos are as addictive as cocaine, at least for lab rats, and just like us, they like the creamy center best. Eating the sugary treats activates more neurons in the brain’s “pleasure center” than drugs such as cocaine, the team at Connecticut College found. “Our research supports the theory that high-fat/ high-sugar foods stimulate the brain in the same way that drugs do,” neuroscience assistant professor Joseph Schroeder says. “That may be one reason people have trouble staying away from them and it may be contributing to the obesity epidemic.” Schroeder’s neuroscience students put hungry rats into a maze. On one side went rice cakes. “Just like humans, rats don’t seem to get much pleasure out of eating them,” Schroeder said. On the other side went Oreos. Then the rats got the option of hanging out where they liked. They compared the results to a different test. In that on, rats on one side if the maze got an injection of saline while those on the other side got injections of cocaine or morphine. Rats seems to like the cookies about as much as they liked the addictive drugs. When allowed to wander freely, they’d congregate on the Oreo side for about as much time as they would on the drug side. Oh, and just like most people - the rats eat the creamy center first.

Related chapters from BP7e: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18794 - Posted: 10.16.2013

By Larry Greenemeier The leaves of the herb kratom (Mitragyna speciosa), a native of Southeast Asia in the coffee family, are used to relieve pain and improve mood as an opiate substitute and stimulant. The herb is also combined with cough syrup to make a popular beverage in Thailand called “4x100.” Because of its psychoactive properties, however, kratom is illegal in Thailand, Australia, Myanmar (Burma) and Malaysia. The U.S. Drug Enforcement Administration lists kratom as a “drug of concern” because of its abuse potential, stating it has no legitimate medical use. The state of Indiana has banned kratom consumption outright. Now, looking to control its population’s growing dependence on methamphetamines, Thailand is attempting to legalize kratom, which it had originally banned 70 years ago. At the same time, researchers are studying kratom’s ability to help wean addicts from much stronger drugs, such as heroin and cocaine. Studies show that a compound found in the plant could even serve as the basis for an alternative to methadone in treating addictions to opioids. The moves are just the latest step in kratom’s strange journey from home-brewed stimulant to illegal painkiller to, possibly, a withdrawal-free treatment for opioid abuse. With kratom’s legal status under review in Thailand and U.S. researchers delving into the substance’s potential to help drug addicts, Scientific American spoke with Edward Boyer, a professor of emergency medicine and director of medical toxicology at the University of Massachusetts Medical School. Boyer has worked with Chris McCurdy, a University of Mississippi professor of medicinal chemistry and pharmacology, and others for the past several years to better understand whether kratom use should be stigmatized or celebrated. © 2013 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: 18726 - Posted: 10.01.2013

Selectively bred strains of laboratory rats that either prefer or avoid alcohol have been a mainstay of alcohol research for decades. So-called alcohol-preferring rats voluntarily consume much greater amounts of alcohol than do non-preferring rats. Scientists at the National Institutes of Health now report that a specific gene plays an important role in the alcohol-consuming tendencies of both types of rats. “This study advances our understanding of the genetics and neurobiology of alcohol consumption in an important animal model of human alcoholism,” says Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH. As reported online in the Proceedings of the National Academy of Sciences, a diverse team of scientists, led by David Goldman, M.D., chief of NIAAA’s Laboratory of Neurogenetics, used exome sequencing, an approach that comprehensively analyzes the DNA that encodes proteins. They found a severely dysfunctional form of the gene for a brain signaling molecule called metabotropic glutamate receptor 2 (Grm2), known as a stop codon, in alcohol-preferring rats but not in non-preferring rats. The researchers then demonstrated that drugs and genetic changes that block Grm2 increased alcohol consumption in normal rats and mice. “We’ve long known that genes play an important role in alcoholism,” says Dr. Goldman. “However, the genes and genetic variants that cause alcoholism have remained largely unknown. This first discovery of a gene accounting for alcohol preference in a mammalian model illustrates that genomic analysis of a model organism is a powerful approach for a complex disease such as alcoholism.”

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: 18724 - Posted: 10.01.2013

The Conservative government is launching a $1.3-billion free market in medical marijuana on Tuesday, eventually providing an expected 450,000 Canadians with quality weed. Health Canada is phasing out an older system on Monday that mostly relied on small-scale, homegrown medical marijuana of varying quality, often diverted illegally to the black market. In its place, large indoor marijuana farms certified by the RCMP and health inspectors will produce, package and distribute a range of standardized weed, all of it sold for whatever price the market will bear. The first sales are expected in the next few weeks, delivered directly by secure courier. "We're fairly confident that we'll have a healthy commercial industry in time," Sophie Galarneau, a senior official with the department, said in an interview. "It's a whole other ball game." The sanctioned birth of large-scale, free-market marijuana production comes as the Conservatives pillory Liberal Leader Justin Trudeau's campaign to legalize recreational marijuana. Health Canada is placing no limits on the number of these new capital-intensive facilities, which will have mandatory vaults and security systems. Private-dwelling production will be banned. Imports from places such as the Netherlands will be allowed. Already 156 firms have applied for lucrative producer and distributor status since June, with the first two receiving licences just last week. © CBC 2013

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: 18721 - Posted: 09.30.2013

By Stuart McMillen A classic experiment into drug addiction science. Would rats choose to take drugs if given a stimulating environment and social 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: 18669 - Posted: 09.19.2013

By JOHN TIERNEY Long before he brought people into his laboratory at Columbia University to smoke crack cocaine, Carl Hart saw its effects firsthand. Growing up in poverty, he watched relatives become crack addicts, living in squalor and stealing from their mothers. Childhood friends ended up in prisons and morgues. Carl Hart, an associate professor of psychology at Columbia, arranged experiments in which drug addicts were offered a choice between a dose of the drug or cash or vouchers. When the dose was smaller, addicts often chose cash or vouchers instead. Those addicts seemed enslaved by crack, like the laboratory rats that couldn’t stop pressing the lever for cocaine even as they were starving to death. The cocaine was providing such powerful dopamine stimulation to the brain’s reward center that the addicts couldn’t resist taking another hit. At least, that was how it looked to Dr. Hart when he started his research career in the 1990s. Like other scientists, he hoped to find a neurological cure to addiction, some mechanism for blocking that dopamine activity in the brain so that people wouldn’t succumb to the otherwise irresistible craving for cocaine, heroin and other powerfully addictive drugs. But then, when he began studying addicts, he saw that drugs weren’t so irresistible after all. “Eighty to 90 percent of people who use crack and methamphetamine don’t get addicted,” said Dr. Hart, an associate professor of psychology. “And the small number who do become addicted are nothing like the popular caricatures.” © 2013 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: 18655 - Posted: 09.17.2013

By Scicurious Effective treatments for drug addiction have been hard to come by. There’s behavioral interventions, methadone maintenance for heroin users, nicotine patches for smokers, antabuse for acoholics, but while all of these are effective in a minority of users, they aren’t effective in all. Many require repeat behaviors that are difficult for addicts. As examples: getting to the methadone center every day can be difficult if you have bad transportation. Alcoholics often need to go to AA meetings several times a week if not several times a day. Antabuse make you feel like crap when you drink…and all you have to do is NOT take it. Nicotine patches don’t tend to scratch the smoking itch in the same way. In the case of cocaine, where is there no drug intervention option at all, when you have someone who is in serious danger of overdose, you need something to take away the effects of the cocaine. Something to work immediately. Enter the idea of a vaccine against cocaine. For those used to thinking about vaccines as things that fight chicken pox and whooping cough, the idea of a vaccine against a drug can seem a little foreign. But it’s a concept that’s been in development for some time. Not so much in the context of vaccinating against potential cocaine use, but as a way to help people get off the drug. But the question still remains: will it work? The idea is to use a vaccine made of a drug that is very close to cocaine (norcocaine), combined with an inactivated virus. The presence of the virus causes the body’s immune system to try and fight it off, creating antibodies to different parts of the molecule, both the cocaine part and the virus part. The antibodies serve as a signal for other immune cells to come along and gobble up the cocaine. After the original vaccine is gone, the antibodies stay circulating in your blood, ready to attack is they see the cocaine signal again. © 2013 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18628 - Posted: 09.10.2013

by Andy Coghlan Smokers keen to quit are just as likely to be successful if they use electronic cigarettes as they are with nicotine patches, the "gold standard" quitting aid. The findings come ahead of a critical debate in the European Parliament on 8 October to decide whether e-cigarettes should be regulated as medicinal products, which would drastically reduce their availability. When smokers attempt to quit, it is the cutting out of nicotine – the addictive component of tobacco – that triggers withdrawal symptoms. E-cigarettes, which physically resemble real cigarettes, provide a compensatory nicotine hit, without the toxic brew of carcinogenic compounds. Previous studies conducted on e-cigarettes alone have shown that they help smokers quit, but no one knew if they performed as well as nicotine patches. To find out, the New Zealand government funded a head-to-head comparison study. Chris Bullen and his colleagues at the National Institute for Health Innovation in Auckland gave e-cigarettes to 289 smokers who were trying to quit. A separate group of 295 people were given nicotine patches, while 73 received dummy nicotine-free e-cigarettes. Six months later, the team asked participants if their attempts to quit had been a success. Those who had used the nicotine e-cigarettes had the highest success rate: 7.3 per cent had managed to stay away from tobacco. Of the nicotine patch users, 5.8 per cent had quit. And of those taking the placebo around 4 per cent were successful. © Copyright Reed Business Information Ltd.

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: 18618 - Posted: 09.09.2013

By STUART ELLIOTT Electronic cigarettes may be a creation of the early 21st century, but critics of the devices say manufacturers are increasingly borrowing marketing tactics that are more reminiscent of the heady days of tobacco in the mid-1900s. With American smokers buying e-cigarettes at a record pace — annual sales are expected to reach $1.7 billion by year’s end — e-cigarette makers are opening their wallets wide, spending growing sums on television commercials with celebrities, catchy slogans and sports sponsorships. Those tactics can no longer be used to sell tobacco cigarettes, but are readily available to the industry because it is not covered by the laws or regulations that affect the tobacco cigarette industry. The e-cigarette industry is also spending lavishly on marketing methods that are also still available to their tobacco brethren, including promotions, events, sample giveaways and print ads. The Blu eCigs brand — which recently added the actress Jenny McCarthy to its roster of star endorsers, joining the actor Stephen Dorff — spent $12.4 million on ads in major media for the first quarter of this year compared with $992,000 in the same period a year ago, according to the Kantar Media unit of WPP. And ad spending in a category that Kantar Media calls smoking materials and accessories, which includes products like pipes and lighters in addition to e-cigarettes, has skyrocketed: from $2.7 million in 2010 to $7.2 million in 2011 to $20.8 million last year. In the first quarter of 2013, Kantar Media reported, category ad spending soared again, reaching $15.7 million, compared with $2 million in the same period a year ago. In fact, that $15.7 million total exceeded the spending for ads in major media for tobacco cigarettes, at $13.9 million, according to Kantar Media. © 2013 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: 18598 - Posted: 09.03.2013

By Maia Szalavitz That little zing you get when someone “likes” your picture or sings your praises on Facebook? That’s the reward center in your brain getting a boost. And that response can predict how much time and energy you put into the social media site, according to new research. In one of the first studies to explore the effects of social media on the brain, scientists led by Dar Meshi, a postdoctoral researcher at the Freie Universität in Berlin, imaged the brains of 31 Facebook users while they viewed pictures of either themselves or others that were accompanied by positive captions. The research was published in Frontiers in Human Neuroscience. “We found that we could predict the intensity of people’s Facebook use outside the scanner by looking at their brain’s response to positive social feedback inside the scanner,” says Meshi. Specifically, a region called the nucleus accumbens, which processes rewarding feelings about food, sex, money and social acceptance became more active in response to praise for oneself compared to praise of others. And that activation was associated with more time on the social media site. Social affirmation tends to be one of life’s great joys, whether it occurs online or off, so it’s not surprising that it would light up this area. Few people are immune to the lures of flattery, after all. But do these results suggest that the “likes” on Facebook can become addictive? While all addictive experiences activate the region, such activation alone isn’t sufficient to establish an addiction. © 2013 Time Inc

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: 18594 - Posted: 09.02.2013

As the debate about legalizing marijuana heats up in Canada, a new study suggests the drug might be riskier for teens to consume than had been previously thought. Researchers from the Université de Montréal and New York's Icahn School of Medicine at Mount Sinai Hospital conducted a review of 120 studies examining cannabis and teenage brain development, and concluded there is strong evidence early cannabis use puts some teens at risk of developing addiction and mental health problems as adults. Dr. Didier Jutras-Aswad, with the Université de Montréal's psychiatry department, is a co-author of the review, which was published this month in the journal Neuroparmacology. He says that in adolescence, the brain is still fine-tuning how different areas, such as learning and memory, interact and it appears that marijuana use alters that process. "When you disrupt this, actually, development, during adolescence, notably through cannabis use, you can have very pervasive, very negative effects in the long-term, including on mental health and addiction risk," he told CBC News. Some studies have also found links between early cannabis use and schizophrenia, but Jutras-Aswad says it seems clear there is a wide risk profile that includes genetics and behavioural traits in addition to age. "For me, the question is not about whether cannabis is good or bad, but who is more likely to suffer from problems in cannabis, because we know for most people that will not happen," he said. © CBC 2013

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: 18579 - Posted: 08.29.2013

By James Gallagher Health and science reporter, BBC News Taking cocaine can change the structure of the brain within hours in what could be the first steps of drug addiction, according to US researchers. Animal tests, reported in the journal Nature Neuroscience, showed new structures linked to learning and memory began to grow soon after the drug was taken. Mice with the most brain changes showed a greater preference for cocaine. Experts described it as the brain "learning addiction". The team at University of California, Berkeley and UC San Francisco looked for tiny protrusions from brain cells called dendritic spines. They are heavily implicated in memory formation. The place or environment that drugs are taken plays an important role in addiction. In the experiments, the mice were allowed to explore freely two very different chambers - each with a different smell and surface texture. Once they had picked a favourite they were injected with cocaine in the other chamber. A type of laser microscopy was used to look inside the brains of living mice to hunt for the dendritic spines. More new spines were produced when the mice were injected with cocaine than with water, suggesting new memories being formed around drug use. The difference could be detected two hours after the first dose. BBC © 2013

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: 18561 - Posted: 08.26.2013

I HAVE been struggling with an addiction to opiates for the past three years. It started with prescription painkillers and progressed to full-blown heroin dependence. In an attempt to kick the habit I signed up for a traditional 30-step inpatient treatment that involved individual and group counselling, and which cost about $30,000. That was a year ago, and it didn't work. I felt unable to stay away from heroin. Now I am at a small clinic in Baja California, Mexico, where I am taking part in the first trial to investigate the effectiveness of treating heroin addiction with a single dose of ibogaine – a psychoactive substance derived from the rainforest shrub Tabernanthe iboga. "Ibogaine can take you many places, causing you to experience a range of emotions, memories and visions. If any of these images become too frightening, just open your eyes." I am reassured by the words of the director of the clinic, Jeff Israel, but the drug's history is not all rosy. Several clinical trials have shown that low doses of ibogaine taken over the course of a few weeks can greatly reduce cravings for heroin and other drugs. There was extensive research on it in the 1990s, with good evidence of safety in animals and a handful of studies in humans. The US National Institute on Drug Abuse invested over $1 million, but then abandoned the project in 1995. A study had shown that at high doses, ibogaine caused some brain cell degeneration in rats. Lower doses similar to those used in human addiction trials showed no such effect, however. © Copyright Reed Business Information Ltd.

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: 18552 - Posted: 08.24.2013