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By Abby Phillip Most long-time, pack-a-day smokers who took part in a small study were able to quit smoking after six months, and researchers believe the hallucinogenic substance found in "magic mushrooms" could be the reason why. The study of the 15 participants, published this week in the Journal of Psychopharmacology, is the first to look at the feasibility of using the psychedelic drug psilocybin to aid in a smoking cessation treatment program. Existing treatments, from quitting cold turkey to prescription medications like Varenicline (Chantix), work for some people, but not the majority of smokers. With Varenicline, which mimics the effect of nicotine in the body, only about 35 percent of participants in a clinical trial were still abstaining from smoking six months later. Nearly half of all adult smokers reported that they tried to quit in 2010, according to the Centers for Disease Control and Prevention, yet 480,000 deaths are attributed to the addiction every year. Researchers at Johns Hopkins University recruited a group of long-time, heavy smokers — an average of 19 cigarettes a day for an average of 31 years — to participate in the study. They were treated with cognitive behavioral therapy for 15 weeks, and they were given a dose of the hallucinogen psilocybin at the five-week mark, when they had agreed to stop smoking. Although it was a small study, the results were promising. Twelve of the participants had quit smoking six months after being treated with the drug.

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: 20076 - Posted: 09.15.2014

by Michael Slezak "Cannabis catastrophic for young brains" screamed the headline on an Australian medical news website this week. The article, and others like it, were reporting on a study linking teenage cannabis use with school dropouts, addiction and suicide, published in the The Lancet Psychiatry. Echoing the research findings, the articles declared that if teenagers smoke cannabis daily, it makes them seven times more likely to commit suicide compared with non-users. Indeed, "there is no safe level of use", most reported. They also urged caution to legislators around the world that are gingerly taking steps towards weakening prohibition of cannabis, lest young people get easier access to it. So does smoking pot cause suicide? The Lancet authors say it probably does. Their study combined data from three previous longitudinal studies which together tracked cannabis use in more than 3000 people in Australia and New Zealand over many years. The authors looked for associations between the frequency of cannabis use before the age of 17 and outcomes, such as high school completion, until the people reached the age of 30. They found that those who smoked cannabis daily before they were 17 had lower odds of finishing high school and getting a degree than people who had never used cannabis. Larger increased odds were associated with cannabis dependence later in life, trying other illicit drugs and suicide attempts. But longitudinal studies only show correlation, not causation. The difficulty is that people take drugs for a reason, and that reason could be what's causing the outcome. In the case of school dropout, suicide and daily pot smoking, it is not hard to imagine what else could be going on in someone's life to engender these behaviours. © Copyright Reed Business Information Ltd

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20071 - Posted: 09.13.2014

|By Amy Nordrum If you were one of millions of children who completed the Drug Abuse Resistance Education program, or D.A.R.E., between 1983 and 2009, you may be surprised to learn that scientists have repeatedly shown that the program did not work. Despite being the nation’s most popular substance-abuse prevention program, D.A.R.E. did not make you less likely to become a drug addict or even to refuse that first beer from your friends. But over the past few years prevention scientists have helped D.A.R.E. America, the nonprofit organization that administers the program, replace the old curriculum with a course based on a few concepts that should make the training more effective for today’s students. The new course, called keepin’ it REAL, differs in both form and content from the former D.A.R.E.—replacing long, drug-fact laden lectures with interactive lessons that present stories meant to help kids make smart decisions. Beginning in 2009 D.A.R.E. administrators required middle schools across the country that teach the program to switch over to the 10-week, researcher-designed curriculum for seventh graders. By 2013, they had ordered elementary schools to start teaching a version of those lessons to fifth and sixth graders, too. "It's not an antidrug program," says Michelle Miller-Day, co-developer of the new curriculum and a communications researcher at Chapman University. “It's about things like being honest and safe and responsible." Even so, keepin’ it REAL has reduced substance abuse and maintained antidrug attitudes over time among students in early trials—an achievement that largely eluded the former iteration of the program. D.A.R.E.’s original curriculum was not shaped by prevention specialists but by police officers and teachers in Los Angeles. They started D.A.R.E. in 1983 to curb the use of drugs, alcohol and tobacco among teens and to improve community–police relations. Fueled by word of mouth, the program quickly spread to 75 percent of U.S. schools. © 2014 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: 20060 - Posted: 09.11.2014

By SOMINI SENGUPTA A coalition of political figures from around the world, including Kofi Annan, the former United Nations secretary general, and several former European and Latin American presidents, is urging governments to decriminalize a variety of illegal drugs and set up regulated drug markets within their own countries. The proposal by the group, the Global Commission on Drug Policy, goes beyond its previous call to abandon the nearly half-century-old American-led war on drugs. As part of a report scheduled to be released on Tuesday, the group goes much further than its 2011 recommendation to legalize cannabis. The former Brazilian president Fernando Henrique Cardoso, a member of the commission, said the group was calling for the legal regulation of “as many of the drugs that are currently illegal as possible, with the understanding that some drugs may remain too dangerous to decriminalize.” The proposal comes at a time when several countries pummeled by drug violence, particularly in Latin America, are rewriting their own drug laws, and when even the United States is allowing state legislatures to gingerly regulate cannabis use. The United Nations is scheduled to hold a summit meeting in 2016 to evaluate global drug laws. The commission includes former presidents like Mr. Cardoso of Brazil, Ernesto Zedillo of Mexico and Ruth Dreifuss of Switzerland, along with George P. Shultz, a former secretary of state in the Reagan administration, among others. The group stops short of calling on countries to legalize all drugs right away. It calls instead for countries to continue to pursue violent criminal gangs, to stop incarcerating users and to offer treatment for addicts. © 2014 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: 20052 - Posted: 09.10.2014

Ewen Callaway Caffeine's buzz is so nice it evolved twice. The coffee genome has now been published, and it reveals that the coffee plant makes caffeine using a different set of genes from those found in tea, cacao and other perk-you-up plants. Coffee plants are grown across some 11 million hectares of land, with more than two billion cups of the beverage drunk every day. It is brewed from the fermented, roasted and ground berries of Coffea canephora and Coffea arabica, known as robusta and arabica, respectively. An international team of scientists has now identified more than 25,000 protein-making genes in the robusta coffee genome. The species accounts for about one-third of the coffee produced, much of it for instant-coffee brands such as Nescafe. Arabica contains less caffeine, but its lower acidity and bitterness make it more flavourful to many coffee drinkers. However, the robusta species was selected for sequencing because its genome is simpler than arabica’s. Caffeine evolved long before sleep-deprived humans became addicted to it, probably to defend the coffee plant against predators and for other benefits. For example, coffee leaves contain the highest levels of caffeine of any part of the plant, and when they fall on the soil they stop other plants from growing nearby. “Caffeine also habituates pollinators and makes them want to come back for more, which is what it does to us, too,” says Victor Albert, a genome scientist at the University of Buffalo in New York, who co-led the sequencing effort. The results were published on 4 September in Science1. © 2014 Nature Publishing Group

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20040 - Posted: 09.06.2014

On 5th May, 1953, the novelist Aldous Huxley dissolved four-tenths of a gram of mescaline in a glass of water, drank it, then sat back and waited for the drug to take effect. Huxley took the drug in his California home under the direct supervision of psychiatrist Humphry Osmond, to whom Huxley had volunteered himself as “a willing and eager guinea pig”. Osmond was one of a small group of psychiatrists who pioneered the use of LSD as a treatment for alcoholism and various mental disorders in the early 1950s. He coined the term psychedelic, meaning ‘mind manifesting’ and although his research into the therapeutic potential of LSD produced promising initial results, it was halted during the 1960s for social and political reasons. Born in Surrey in 1917, Osmond studied medicine at Guy’s Hospital, London. He served in the navy as a ship’s psychiatrist during World War II, and afterwards worked in the psychiatric unit at St. George’s Hospital, London, where he became a senior registrar. While at St. George’s, Osmond and his colleague John Smythies learned about Albert Hoffman’s discovery of LSD at the Sandoz Pharmaceutical Company in Bazel, Switzerland. Osmond and Smythies started their own investigation into the properties of hallucinogens and observed that mescaline produced effects similar to the symptoms of schizophrenia, and that its chemical structure was very similar to that of the hormone and neurotransmitter adrenaline. This led them to postulate that schizophrenia was caused by a chemical imbalance in the brain, but these ideas were not favourably received by their colleagues. In 1951 Osmond took a post as deputy director of psychiatry at the Weyburn Mental Hospital in Saskatchewan, Canada and moved there with his family. Within a year, he began collaborating on experiments using LSD with Abram Hoffer. Osmond tried LSD himself and concluded that the drug could produce profound changes in consciousness. Osmond and Hoffer also recruited volunteers to take LSD and theorised that the drug was capable of inducing a new level of self-awareness which may have enormous therapeutic potential. © 2014 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 20036 - Posted: 09.04.2014

Daniel Cressey In many respects, the modern electronic cigarette is not so different from its leaf-and-paper predecessor. Take a drag from the mouthpiece and you get a genuine nicotine fix — albeit from a fluid wicked into the chamber of a battery-powered atomizer and vaporized by a heating element. Users exhale a half-convincing cloud of ‘smoke’, and many e-cigarettes even sport an LED at the tip that glows blue, green or classic red to better simulate the experience romanticized by countless writers and film-makers. The only things missing are the dozens of cancer-causing chemicals found in this digital wonder’s analogue forebears. E-cigarettes — also known as personal vaporizers or electronic nicotine-delivery systems among other names — are perhaps the most disruptive devices that public-health researchers working on tobacco control have ever faced. To some, they promise to snuff out a behaviour responsible for around 100 million deaths in the twentieth century. Others fear that they could perpetuate the habit, and undo decades of work. Now, a group once united against a common enemy is divided. “These devices have really polarized the tobacco-control community,” says Michael Siegel, a physician and tobacco researcher at Boston University School of Public Health in Massachusetts. “You now have two completely opposite extremes with almost no common ground between them.” Evidence is in short supply on both sides. Even when studies do appear, they are often furiously debated. And it is not just researchers who are attempting to catch up with the products now pouring out of Chinese factories: conventional tobacco companies are pushing into the nascent industry, and regulators are scrambling to work out what to do. © 2014 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: 20000 - Posted: 08.27.2014

By Chelsea Rice Opioid-related overdose deaths are a bleak public health issue in this country. The percentage of patients who receive opioid prescriptions to treat noncancer pain has almost doubled in the past decade, but the number of overdose-related deaths for women have increased five times as much, according to the Centers for Disease Control and Prevention. To put the nationwide stats in perspective, more women have died each year from drug overdoses than from motor vehicle-related injuries since 2007. For men in the past decade, the rate of opioid overdose deaths has increased three-fold. According to the CDC, women in particular are more likely to be prescribed opioid pain relievers than men, more likely to use them chronically, and more likely to be prescribed them in higher doses. But what if medical marijuana, another option for treating chronic pain, could have an impact on these staggering statistics? Research published today in JAMA Internal Medicine found that states with medical marijuana laws before 2010 had 24.8 percent lower annual opioid overdose deaths on average when compared to states where medical marijuana was illegal. Medical cannabis laws were associated in the study with lower overdose mortality rates that generally strengthened over time. In 2010, for instance, researchers noticed there were 1,729 fewer deaths in states where medical marijuana was legal. The research team, lead by Dr. Marcus A. Bachhuber at the Philadelphia Veterans Affairs Medical Center, examined state medical marijuana laws and opioid overdose deaths using death certificate data from 1999 to 2010.

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: 19993 - Posted: 08.26.2014

By DAVE PHILIPPS WRAY, Colo. — Behind a tall curtain of corn that hides their real cash crop from prying eyes, the Stanley family is undertaking an audacious effort to expand their medical marijuana business to a national market. For years, the five Stanley brothers, who sell a nonintoxicating strain of cannabis that has gained national attention as a treatment for epilepsy, have grown medical marijuana in greenhouses, under tight state and federal regulations. But this year, they are not only growing marijuana outdoors by the acre, they also plan to ship an oil extracted from their plants to other states. The plan would seem to defy a federal prohibition on the sale of marijuana products across state lines. But the Stanleys have justified it with a simple semantic swap: They now call their crop industrial hemp, based on its low levels of THC, the psychoactive ingredient in pot. “The jump to industrial hemp means we can serve thousands of people instead of hundreds,” said Jared Stanley, 27, who wore muddy Carhartts and a rainbow friendship bracelet as he knelt down to prune his plants. Colorado, which has legalized the sale of marijuana for recreational and medical use, has accepted the new designation. But the real question is whether the federal government will go along. If it does, the impact would be significant, opening the door to interstate sales not just by the Stanleys, but possibly by scores of other medical cannabis growers across the country. But if it does not, the Stanley brothers could be shut down by federal agents. So far, the Drug Enforcement Administration is offering few clues, insisting in public statements that while it is willing to allow marijuana sales in states that have legalized the drug, it might step in if growers try to sell beyond state borders. © 2014 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: 19990 - Posted: 08.25.2014

By TARA PARKER-POPE When the antidrug educator Tim Ryan talks to students, he often asks them what they know about marijuana. “It’s a plant,” is a common response. But more recently, the answer has changed. Now they reply, “It’s legal in Colorado.” These are confusing times for middle and high school students, who for most of their young lives have been lectured about the perils of substance abuse, particularly marijuana. Now it seems that the adults in their lives have done an about-face. Recreational marijuana is legal in Colorado and in Washington, and many other states have approved it for medical use. Lawmakers, the news media and even parents are debating the merits of full-scale legalization. “They are growing up in a generation where marijuana used to be bad, and maybe now it’s not bad,” said Mr. Ryan, a senior prevention specialist with FCD Educational Services, an antidrug group that works with students in the classroom. “Their parents are telling them not to do it, but they may be supporting legalization of it at the same time.” Antidrug advocates say efforts to legalize marijuana have created new challenges as they work to educate teenagers and their parents about the unique risks that alcohol, marijuana and other drugs pose to the developing teenage brain. These educators say their goal is not to vilify marijuana or take a stand on legalization; instead, they say their role is to convince young people and their parents that the use of drugs is not just a moral or legal issue, but a significant health issue. “The health risks are real,” said Steve Pasierb, the chief executive of the Partnership for Drug-Free Kids. “Every passing year, science unearths more health risks about why any form of substance use is unhealthy for young people.” © 2014 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: 19976 - Posted: 08.19.2014

By SERGE F. KOVALESKI Nearly four years ago, Dr. Sue Sisley, a psychiatrist at the University of Arizona, sought federal approval to study marijuana’s effectiveness in treating military veterans with post-traumatic stress disorder. She had no idea how difficult it would be. The proposal, which has the support of veterans groups, was hung up at several regulatory stages, requiring the research’s private sponsor to resubmit multiple times. After the proposed study received final approval in March from federal health officials, the lone federal supplier of research marijuana said it did not have the strains the study needed and would have to grow more — potentially delaying the project until at least early next year. Then, in June, the university fired Dr. Sisley, later citing funding and reorganization issues. But Dr. Sisley is convinced the real reason was her outspoken support for marijuana research. “They could never get comfortable with the idea of this controversial, high-profile research happening on campus,” she said. Dr. Sisley’s case is an extreme example of the obstacles and frustrations scientists face in trying to study the medical uses of marijuana. Dating back to 1999, the Department of Health and Human Services has indicated it does not see much potential for developing marijuana in smoked form into an approved prescription drug. In guidelines issued that year for research on medical marijuana, the agency quoted from an accompanying report that stated, “If there is any future for marijuana as a medicine, it lies in its isolated components, the cannabinoids and their synthetic derivatives.” Scientists say this position has had a chilling effect on marijuana research. © 2014 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: 19933 - Posted: 08.11.2014

by Bethany Brookshire Every day sees a new research article on addiction, be it cocaine, heroin, food or porn. Each one takes a specific angle on how addiction works in the brain. Perhaps it’s a disorder of reward, with drugs hijacking a natural system that is meant to respond to food, sex and friendship. Possibly addiction is a disorder of learning, where our brains learn bad habits and responses. Maybe we should think of addiction as a combination of an environmental stimulus and vulnerable genes. Or perhaps it’s an inappropriate response to stress, where bad days trigger a relapse to the cigarette, syringe or bottle. None of these views are wrong. But none of them are complete, either. Addiction is a disorder of reward, a disorder of learning. It has genetic, epigenetic and environmental influences. It is all of that and more. Addiction is a display of the brain’s astounding ability to change — a feature called plasticity — and it showcases what we know and don’t yet know about how brains adapt to all that we throw at them. “A lot of people think addiction is what happens when someone finds a drug to be the most rewarding thing they’ve ever experienced,” says neuroscientist George Koob, director of the National Institute on Alcohol Abuse and Alcoholism in Bethesda, Md. “But drug abuse is not just feeling good about drugs. Your brain is changed when you misuse drugs. It is changed in ways that perpetuate the problem.” The changes associated with drug use affect how addicts respond to drug cues, like the smell of a cigarette or the sight of a shot of vodka. Drug abuse also changes how other rewards, such as money or food are processed, decreasing their relative value. © Society for Science & the Public 2000 - 2013

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: 19921 - Posted: 08.06.2014

By PHILIP M. BOFFEY For Michele Leonhart, the administrator of the Drug Enforcement Administration, there is no difference between the health effects of marijuana and those of any other illegal drug. “All illegal drugs are bad for people,” she told Congress in 2012, refusing to say whether crack, methamphetamines or prescription painkillers are more addictive or physically harmful than marijuana. Her testimony neatly illustrates the vast gap between antiquated federal law enforcement policies and the clear consensus of science that marijuana is far less harmful to human health than most other banned drugs and is less dangerous than the highly addictive but perfectly legal substances known as alcohol and tobacco. Marijuana cannot lead to a fatal overdose. There is little evidence that it causes cancer. Its addictive properties, while present, are low, and the myth that it leads users to more powerful drugs has long since been disproved. That doesn’t mean marijuana is harmless; in fact, the potency of current strains may shock those who haven’t tried it for decades, particularly when ingested as food. It can produce a serious dependency, and constant use would interfere with job and school performance. It needs to be kept out of the hands of minors. But, on balance, its downsides are not reasons to impose criminal penalties on its possession, particularly not in a society that permits nicotine use and celebrates drinking. Marijuana’s negative health effects are arguments for the same strong regulation that has been effective in curbing abuse of legal substances. Science and government have learned a great deal, for example, about how to keep alcohol out of the hands of minors. Mandatory underage drinking laws and effective marketing campaigns have reduced underage alcohol use to 24.8 percent in 2011, compared with 33.4 percent in 1991. Cigarette use among high school students is at its lowest point ever, largely thanks to tobacco taxes and growing municipal smoking limits. There is already some early evidence that regulation would also help combat teen marijuana use, which fell after Colorado began broadly regulating medical marijuana in 2010. © 2014 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: 19909 - Posted: 08.02.2014

By BRENT STAPLES The federal law that makes possession of marijuana a crime has its origins in legislation that was passed in an atmosphere of hysteria during the 1930s and that was firmly rooted in prejudices against Mexican immigrants and African-Americans, who were associated with marijuana use at the time. This racially freighted history lives on in current federal policy, which is so driven by myth and propaganda that it is almost impervious to reason. The cannabis plant, also known as hemp, was widely grown in the United States for use in fabric during the mid-19th century. The practice of smoking it appeared in Texas border towns around 1900, brought by Mexican immigrants who cultivated cannabis as an intoxicant and for medicinal purposes as they had done at home. Within 15 years or so, it was plentiful along the Texas border and was advertised openly at grocery markets and drugstores, some of which shipped small packets by mail to customers in other states. The law enforcement view of marijuana was indelibly shaped by the fact that it was initially connected to brown people from Mexico and subsequently with black and poor communities in this country. Police in Texas border towns demonized the plant in racial terms as the drug of “immoral” populations who were promptly labeled “fiends.” As the legal scholars Richard Bonnie and Charles Whitebread explain in their authoritative history, “The Marihuana Conviction,” the drug’s popularity among minorities and other groups practically ensured that it would be classified as a “narcotic,” attributed with addictive qualities it did not have, and set alongside far more dangerous drugs like heroin and morphine. © 2014 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: 19903 - Posted: 07.31.2014

By ANN SANNER Associated Press COLUMBUS, Ohio (AP) — A few weeks before their prom king’s death, students at an Ohio high school had attended an assembly on narcotics that warned about the dangers of heroin and prescription painkillers. But it was one of the world’s most widely accepted drugs that killed Logan Stiner — a powdered form of caffeine so potent that as little as a single teaspoon can be fatal. The teen’s sudden death in May has focused attention on the unregulated powder and drawn a warning from federal health authorities urging consumers to avoid it. ‘‘I don’t think any of us really knew that this stuff was out there,’’ said Jay Arbaugh, superintendent of the Keystone Local Schools. The federal Food and Drug Administration said Friday that it’s investigating caffeine powder and will consider taking regulatory action. The agency cautioned parents that young people could be drawn to it. An autopsy found that Stiner had a lethal amount of caffeine in his system when he died May 27 at his home in LaGrange, Ohio, southwest of Cleveland. Stiner, a wrestler, had more than 70 micrograms of caffeine per milliliter of blood in his system, as much as 23 times the amount found in a typical coffee or soda drinker, according to the county coroner. His mother has said she was unaware her son took caffeine powder. He was just days away from graduation and had planned to study at the University of Toledo. Caffeine powder is sold as a dietary supplement, so it’s not subject to the same federal regulations as certain caffeinated foods. Users add it to drinks for a pick-me-up before workouts or to control weight gain. A mere 1/16th of a teaspoon can contain about 200 milligrams of caffeine, roughly the equivalent of two large cups of coffee. That means a heaping teaspoon could kill, said Dr. Robert Glatter, an emergency physician at Lenox Hill ?Hospital in New York.

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: 19857 - Posted: 07.21.2014

By Lizzie Wade This week, a team from the National Institute on Drug Abuse (NIDA) reported that heavy marijuana use may damage the brain's pleasure center. Meanwhile, researchers in the United Kingdom say they’ve figured out why pot makes you paranoid. But does focusing research on cannabis’s “bad side” give the drug short shrift? Science talked to Ian Mitchell, an emergency physician at the University of British Columbia’s Southern Medical Program in Kamloops, Canada, and author of the blog Clinical Cannabis in Context, who says that politics influences research in this controversial field. As a doctor who recommends medical cannabis to patients, he follows research on the drug and often critiques studies he believes are based on outdated information or were performed with an anticannabis bias. This interview has been edited for clarity and brevity. Q: What do you think of the NIDA study? A: They said they gave marijuana abusers Ritalin and nothing happened. One of the ways you could interpret that is, OK, these pleasure centers are damaged. But you could also say, perhaps marijuana decreases the effects of [Ritalin] on people. That would be equally as right an interpretation. Q: Why do we hear more about studies that show negative effects of marijuana? A: NIDA is at the center of cannabis research in America. And their mandate, very plainly, is to study drug abuse. So they overwhelmingly fund studies that look at abuse. In America, if you wanted to run a study that showed a benefit of cannabis, you weren’t allowed to do that because NIDA couldn’t give you samples to use. So there were no trials [on potential medical benefits] being done. For example, there hasn’t been a good trial yet to study marijuana’s potential for treating posttraumatic stress disorder. They couldn’t get it done, due to all these political roadblocks. © 2014 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19843 - Posted: 07.17.2014

By Lizzie Wade It probably won’t come as a surprise that smoking a joint now and then will leave you feeling … pretty good, man. But smoking a lot of marijuana over a long time might do just the opposite. Scientists have found that the brains of pot abusers react less strongly to the chemical dopamine, which is responsible for creating feelings of pleasure and reward. Their blunted dopamine responses could leave heavy marijuana users living in a fog—and not the good kind. After high-profile legalizations in Colorado, Washington, and Uruguay, marijuana is becoming more and more available in many parts of the world. Still, scientific research on the drug has lagged. Pot contains lots of different chemicals, and scientists don’t fully understand how those components interact to produce the unique effects of different strains. Its illicit status in most of the world has also thrown up barriers to research. In the United States, for example, any study involving marijuana requires approval from four different federal agencies, including the Drug Enforcement Administration. One of the unanswered questions about the drug is what, exactly, it does to our brains, both during the high and afterward. Of particular interest to scientists is marijuana’s effect on dopamine, a main ingredient in the brain’s reward system. Pleasurable activities such as eating, sex, and some drugs all trigger bursts of dopamine, essentially telling the brain, “Hey, that was great—let’s do it again soon.” Scientists know that drug abuse can wreak havoc on the dopamine system. Cocaine and alcohol abusers, for example, are known to produce far less dopamine in their brains than people who aren’t addicted to those drugs. But past studies had hinted that the same might not be true for those who abuse marijuana. © 2014 American Association for the Advancement of Science

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: 19832 - Posted: 07.15.2014

By JOSHUA A. KRISCH Excessive alcohol consumption, including binge drinking, is responsible for 10 percent of deaths among working-age adults in the United States, according to a recent study from the Centers for Disease Control and Prevention. The researchers used an online tool called the Alcohol-Related Disease Impact application to estimate alcohol-related deaths ranging from car crashes and alcohol poisoning to liver and heart disease. They defined binge drinking as at least five consecutive drinks for men and four consecutive drinks for women. One in six adults from 20 to 65 reported binge drinking at least four times a month; the actual number is likely higher because subjects tend to underreport their drinking habits, the researchers said. The number of Americans who binge drink skyrocketed during the 1990s and leveled off in 2001, but the average frequency of binge drinking episodes is still rising. Excessive drinking is the fourth leading cause of preventable death in the United States, after smoking, poor nutrition and physical inactivity. “It’s a huge public health problem any way you slice it,” said Robert D. Brewer, a co-author of the paper and the director of the alcohol program at the C.D.C.“There are things that we can do about it,” like raising the alcohol tax and encouraging doctors to talk to their patients about alcohol abuse, “but a lot of those strategies tend to be underused.” © 2014 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: 19799 - Posted: 07.08.2014

By GABRIELLE GLASER When their son had to take a medical leave from college, Jack and Wendy knew they — and he — needed help with his binge drinking. Their son’s psychiatrist, along with a few friends, suggested Alcoholics Anonymous. He had a disease, and in order to stay alive, he’d have to attend A.A. meetings and abstain from alcohol for the rest of his life, they said. But the couple, a Manhattan reporter and editor who asked to be identified only by their first names to protect their son’s privacy, resisted that approach. Instead, they turned to a group of psychologists who specialize in treating substance use and other compulsive behaviors at the Center for Motivation and Change. The center, known as the C.M.C., operates out of two floors of a 19th-century building on 30th Street and Fifth Avenue. It is part of a growing wing of addiction treatment that rejects the A.A. model of strict abstinence as the sole form of recovery for alcohol and drug users. Instead, it uses a suite of techniques that provide a hands-on, practical approach to solving emotional and behavioral problems, rather than having abusers forever swear off the substance — a particularly difficult step for young people to take. And unlike programs like Al-Anon, A.A.’s offshoot for family members, the C.M.C.’s approach does not advocate interventions or disengaging from someone who is drinking or using drugs. “The traditional language often sets parents up to feel they have to make extreme choices: Either force them into rehab or detach until they hit rock bottom,” said Carrie Wilkens, a psychologist who helped found the C.M.C. 10 years ago. “Science tells us those formulas don’t work very well.” When parents issue edicts, demanding an immediate end to all substance use, it often lodges the family in a harmful cycle, said Nicole Kosanke, a psychologist at the C.M.C. Tough love might look like an appropriate response, she said, but it often backfires by further damaging the frayed connections to the people to whom the child is closest. © 2014 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: 19794 - Posted: 07.04.2014

Heidi Ledford If shown to be possible in humans, addiction to the Sun could help explain why some tanners continue to seek out sunlight despite being well aware of the risks. The lure of a sunny day at the beach may be more than merely the promise of fun and relaxation. A study published today reports that mice exposed to ultraviolet (UV) rays exhibit behaviours akin to addiction. The researchers found that mice exposed repeatedly to UV light produced an opioid called β-endorphin, which numbs pain and is associated with addiction to drugs. When they were given a drug that blocks the effect of opioids, the mice also showed signs of withdrawal — including shaky paws and chattering teeth. If the results hold true in humans, they would suggest an explanation for why many tanners continue to seek out sunlight, despite the risks — and, in some cases, even after being diagnosed with skin cancer. “This offers a clear potential mechanism for how UV radiation can be rewarding and, in turn, potentially addictive,” says Bryon Adinoff, an addiction psychiatrist at the University of Texas Southwestern Medical Center in Dallas, who was not involved with the study. “That’s a big deal.” Oncologist David Fisher of the Massachusetts General Hospital in Boston and his colleagues became interested in sunlight addiction after studying the molecular mechanisms of pigment production in the skin after UV light exposure. In the new study published today in Cell1, they show that in mice, some skin cells also synthesize β-endorphin in response to chronic, low doses of UV light. © 2014 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: 19752 - Posted: 06.21.2014