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by Viviane Callier It's a fresh problem. People who smoke menthol cigarettes often smoke more frequently and can be less likely to quit – and it could be because fresh-tasting menthol is changing their brains to more sensitive to nicotine. How menthol enhances nicotine addiction has been something of a mystery. Now, Brandon Henderson at the California Institute of Technology in Pasadena and his colleagues have shown that exposing mice to menthol alone causes them to develop more nicotinic receptors, the parts of the brain that are targeted by nicotine. Menthol can be used medically to relieve minor throat irritations, and menthol-flavoured cigarettes were first introduced in the 1920s. But smokers of menthol cigarettes can be less likely to quit. In one study of giving up smoking, 50 per cent of unflavoured-cigarette smokers were able to quit, while menthol smokers showed quitting rates as low as 23 per cent, depending on ethnicity. Over time, smokers of both menthol and unflavoured cigarettes acquire more receptors for nicotine, particularly in neurons involved in the body's neural pathways for reward and motivation. And research last year showed that smokers of menthol cigarettes develop even more of these receptors than smokers of unflavoured cigarettes. To understand how menthol may be altering the brain, Henderson's team exposed mice to either menthol with nicotine, or menthol alone. They found that, even without nicotine, menthol increased the numbers of brain nicotinic receptors. They saw a 78 per cent increase in one particular brain region – the ventral tegmental area – which is involved in the dopamine signalling pathway that mediates in addiction. © 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: 20395 - Posted: 12.06.2014

By Sarah C. P. Williams Craving a stiff drink after the holiday weekend? Your desire to consume alcohol, as well as your body’s ability to break down the ethanol that makes you tipsy, dates back about 10 million years, researchers have discovered. The new finding not only helps shed light on the behavior of our primate ancestors, but also might explain why alcoholism—or even the craving for a single drink—exists in the first place. “The fact that they could put together all this evolutionary history was really fascinating,” says Brenda Benefit, an anthropologist at New Mexico State University, Las Cruces, who was not involved in the study. Scientists knew that the human ability to metabolize ethanol—allowing people to consume moderate amounts of alcohol without getting sick—relies on a set of proteins including the alcohol dehydrogenase enzyme ADH4. Although all primates have ADH4, which performs the crucial first step in breaking down ethanol, not all can metabolize alcohol; lemurs and baboons, for instance, have a version of ADH4 that’s less effective than the human one. Researchers didn’t know how long ago people evolved the more active form of the enzyme. Some scientists suspected it didn’t arise until humans started fermenting foods about 9000 years ago. Matthew Carrigan, a biologist at Santa Fe College in Gainesville, Florida, and colleagues sequenced ADH4 proteins from 19 modern primates and then worked backward to determine the sequence of the protein at different points in primate history. Then they created copies of the ancient proteins coded for by the different gene versions to test how efficiently each metabolized ethanol. They showed that the most ancient forms of ADH4—found in primates as far back as 50 million years ago—only broke down small amounts of ethanol very slowly. But about 10 million years ago, the team reports online today in the Proceedings of the National Academy of Sciences, a common ancestor of humans, chimpanzees, and gorillas evolved a version of the protein that was 40 times more efficient at ethanol metabolism. © 2014 American Association for the Advancement of Science.

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: 20378 - Posted: 12.02.2014

By Tara Parker-Pope Most people who drink to get drunk are not alcoholics, suggesting that more can be done to help heavy drinkers cut back, a new government report concludes. The finding, from a government survey of 138,100 adults, counters the conventional wisdom that every “falling-down drunk” must be addicted to alcohol. Instead, the results from the National Survey on Drug Use and Health show that nine out of 10 people who drink too much are not addicts, and can change their behavior with a little — or perhaps a lot of — prompting. “Many people tend to equate excessive drinking with alcohol dependence,’’ sad Dr. Robert Brewer, who leads the alcohol program at the Centers for Disease Control and Prevention. “We need to think about other strategies to address these people who are drinking too much but who are not addicted to alcohol.” Excessive drinking is viewed as a major public health problem that results in 88,000 deaths a year, from causes that include alcohol poisoning and liver disease, to car accidents and other accidental deaths. Excessive drinking is defined as drinking too much at one time or over the course of a week. For men, it’s having five or more drinks in one sitting or 15 drinks or more during a week. For women, it’s four drinks on one occasion or eight drinks over the course of a week. Underage drinkers and women who drink any amount while pregnant also are defined as “excessive drinkers.” Surprisingly, about 29 percent of the population meets the definition for excessive drinking, but 90 percent of them do not meet the definition of alcoholism. That’s good news because it means excessive drinking may be an easier problem to solve than previously believed. © 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: 20342 - Posted: 11.21.2014

Sara Reardon A technique that makes mouse brains transparent shows how the entire brain responds to cocaine addiction and fear. The findings could uncover new brain circuits involved in drug response. In the technique, known as CLARITY, brains are infused with acrylamide, which forms a matrix in the cells and preserves their structure along with the DNA and proteins inside them. The organs are then treated with a detergent that dissolves opaque lipids, leaving the cells completely clear. To test whether CLARITY could be used to show how brains react to stimuli, neuroscientists Li Ye and Karl Deisseroth of Stanford University in California engineered mice so that their neurons would make a fluorescent protein when they fired. (The system is activated by the injection of a drug.) The researchers then trained four of these mice to expect a painful foot shock when placed in a particular box; another set of mice placed in the box received cocaine, rather than shocks. Once the mice had learned to associate the box with either pain or an addictive reward, the researchers tested how the animals' brains responded to the stimuli. They injected the mice with the drug that activated the fluorescent protein system, placed them in the box and waited for one hour to give their neurons time to fire. The next step was to remove the animals' brains, treat them with CLARITY, and image them using a system that could count each fluorescent cell across the entire brain (see video). A computer combined these images into a model of a three-dimensional brain, which showed the pathways that lit up when mice were afraid or were anticipating cocaine. © 2014 Nature Publishing Group

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: 20337 - Posted: 11.20.2014

Details of the role of glutamate, the brain’s excitatory chemical, in a drug reward pathway have been identified for the first time. This discovery in rodents — published today in Nature Communications — shows that stimulation of glutamate neurons in a specific brain region (the dorsal raphe nucleus) leads to activation of dopamine-containing neurons in the brain’s reward circuit (dopamine reward system). Dopamine is a neurotransmitter present in regions of the brain that regulate movement, emotion, motivation, and feelings of pleasure. Glutamate is a neurotransmitter whose receptors are important for neural communication, memory formation, and learning. The research was conducted at the Intramural Research Program (IRP) of the National Institute on Drug Abuse (NIDA), which is part of the National Institutes of Health. The research focused on the dorsal raphe nucleus, which has long been a brain region of interest to drug abuse researchers, since nerve cells in this area connect to part of the dopamine reward system. Many of the pathways are rich in serotonin, a neurotransmitter linked to mood regulation. Even though electrical stimulation of the dorsal raphe nucleus promotes reward-related behaviors, drugs that increase serotonin have low abuse potential. As a result, this region of the brain has always presented a seeming contradiction, since it is involved in drug reward but is also abundant in serotonin - a chemical not known for a role in drug reinforcement. This has led researchers to theorize that another neurotransmitter may be responsible for the role that the dorsal raphe nucleus plays in reward.

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: 20308 - Posted: 11.13.2014

By Kate Kelland LONDON (Reuters) - British scientists say they have found the best way yet to analyze the effects of smoking on the brain -- by taking functional magnetic resonance imaging (fMRI) scans of people while they puff on e-cigarettes. In a small pilot study, the researchers used electronic cigarettes, or e-cigarettes, to mimic the behavioral aspects of smoking tobacco cigarettes, and say future studies could help scientists understand why smoking is so addictive. E-cigarettes use battery-powered cartridges to produce a nicotine-laced vapor to inhale -- hence the new term "vaping". Their use has rocketed in recent years, but there is fierce debate about the risks and benefits. Some public health experts say they could help millions quit tobacco cigarettes, while others argue they could "normalize" the habit and lure children into smoking. While that argument rages, tobacco kills some 6 million people a year, and the World Health Organization estimates that could rise beyond 8 million by 2030. Matt Wall, an imaging scientist at Imperial College London who led the study using e-cigarettes, said he was not aiming to pass judgment on their rights or wrongs, but to use them to dig deeper into smoking addiction. The fact that other forms of nicotine replacement therapy, such as patches or gum, have had only limited success in getting hardened smokers to quit suggests they are hooked on more than just nicotine, he noted. © 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: 20307 - Posted: 11.13.2014

By Jia You Like humans, flies are attracted to alcohol. Fruit flies (Drosophila melanogaster, above) prefer to lay their eggs on rotten food that can contain ethanol in as high as 7% concentration. (That’s 14 proof to you bar hoppers.) And just like people, the insects differ in their ability to hold their drinks. Biologists know that compared with flies from tropical Africa, flies from temperate regions such as Europe survive longer when exposed to ethanol vapors of high concentrations, and they know it has something to do with enzymes on the flies’ second chromosomes, which break down alcohol and are more active in European flies. But now, biologist James Fry of the University of Rochester in New York has pinpointed a missing piece of the story: the role played by the flies’ third chromosomes. After studying flies collected from Vienna and Cameroon, Fry found that the Vienna flies break down alcohol much faster than Cameroon ones, as expected. But when he replaced the third chromosomes in Cameroon flies with those from Vienna, the African flies gained much more resistance, Fry reports online today in The Journal of Experimental Biology. In a specialized population of flies that could not detoxify alcohol, however, the genetic engineering made no difference whatsoever. Fry suggests that’s because the third chromosomes in European flies help them tolerate acetic acid, a byproduct of internal alcohol breakdown that also gives vinegar its sour taste. There’s no telling what the acetic acid does to the flies, but previous studies on mice have found that it may be responsible for hangover headaches, Fry says. © 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: 20303 - Posted: 11.13.2014

By Abby Phillip If you're confused about what marijuana use really does to people who use it, you're not alone. For years, the scientific research on health effects of the drug have been all over the map. Earlier this year, one study suggested that even casual marijuana use could cause changes to the brain. Another found that marijuana use was also associated with poor sperm quality, which could lead to infertility in men. But marijuana advocates point to other research indicating that the drug is far less addictive than other drugs, and some studies have found no relationship between IQ and marijuana use in teens. Researchers at the Center for Brain Health at the University of Texas in Dallas sought to clear up some of the confusion with a study that looked at a relatively large group of marijuana users and evaluated their brains for a slew of different indicators. What they found was complex, but the pattern was clear: The brains of marijuana users were different than those of non-marijuana users. The area of the brain responsible for establishing the reward system that helps us survive and also keeps us motivated was smaller in users than in non-marijuana users. But there was also evidence that the brain compensated for this loss of volume by increasing connectivity and the structural integrity of the brain tissue. Those effects were more pronounced for marijuana users who started young. "The orbitofrontal cortex is one of the primary regions in a network of brain areas called the reward system," explained Francesca Filbey, lead author of the study and an associate professor of the neurogenetics of addictive behavior at the University of Texas in Dallas. "

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: 20299 - Posted: 11.11.2014

How Magic Mushrooms Rearrange Your Brain By Brandon Keim A new way of looking at brain activity may give insight into how psychedelic drugs produce their consciousness-altering effects. In recent years, a focus on brain structures and regions has given way to an emphasis on neurological networks: how cells and regions interact, with consciousness shaped not by any given set of brain regions, but by their interplay. Understanding the networks, however, is no easy task, and researchers are developing ever more sophisticated ways of characterizing them. One such approach, described in a new Proceedings of the Royal Society Interface study, involves not simply networks but networks of networks. Perhaps some aspects of consciousness arise from these meta-networks—and to investigate the proposition, the researchers analyzed fMRI scans of 15 people after being injected with psilocybin, the active ingredient in magic mushrooms, and compared them to scans of their brain activity after receiving a placebo. Investigating psychedelia wasn’t the direct purpose of the experiment, said study co-author Giovanni Petri, a mathematician at Italy’s Institute for Scientific Interchange. Rather, psilocybin makes for an ideal test system: It’s a sure-fire way of altering consciousness. “In a normal brain, many things are happening. You don’t know what is going on, or what is responsible for that,” said Petri. “So you try to perturb the state of consciousness a bit, and see what happens.” A representation of that is seen in the image above. Each circle depicts relationships between networks—the dots and colors correspond not to brain regions, but to especially connection-rich networks—with normal-state brains at left, and psilocybin-influenced brains at right. © 2014 Condé Nast.

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: 20262 - Posted: 11.01.2014

By ABIGAIL SULLIVAN MOORE The gray matter of the nucleus accumbens, the walnut-shaped pleasure center of the brain, was glowing like a flame, showing a notable increase in density. “It could mean that there’s some sort of drug learning taking place,” speculated Jodi Gilman, at her computer screen at the Massachusetts General Hospital-Harvard Center for Addiction Medicine. Was the brain adapting to marijuana exposure, rewiring the reward system to demand the drug? Dr. Gilman was reviewing a composite scan of the brains of 20 pot smokers, ages 18 to 25. What she and fellow researchers at Harvard and Northwestern University found within those scans surprised them. Even in the seven participants who smoked only once or twice a week, there was evidence of structural differences in two significant regions of the brain. The more the subjects smoked, the greater the differences. Moderate marijuana use by healthy adults seems to pose little risk, and there are potential medical benefits, including easing nausea and pain. But it has long been known that, with the brain developing into the mid-20s, young people who smoke early and often are more likely to have learning and mental health problems. Now researchers suggest existing studies are no longer sufficient. Much of what’s known is based on studies conducted years ago with much less powerful pot. Marijuana samples seized by the federal Drug Enforcement Agency show the concentration of THC, the drug’s psychoactive compound, rising from a mean of 3.75 percent in 1995 to 13 percent in 2013. Potency seesaws depending on the strain and form. Fresh Baked, which sells recreational marijuana in Boulder, Colo., offers “Green Crack,” with a THC content of about 21 percent, and “Phnom Pen,” with about 8 percent. The level in a concentrate called “Bubble Hash” is about 70 percent; cartridges for vaporizers, much like e-cigarettes, range from 15 to 30 percent THC. © 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: 20257 - Posted: 10.29.2014

Sarah Boseley, health editor A record haul of “smart” drugs, sold to students to enhance their memory and thought processes, stay awake and improve concentration, has been seized from a UK website by the medicines regulator, which is alarmed about the recent rise of such sites. The seizure, worth £200,000, illustrates the increasing internet trade in cognitive enhancement drugs and suggests people who want to stay focused and sharp are moving on from black coffee and legally available caffeine tablets. Most of the seized drugs are medicines that should only be available on a doctor’s prescription. One, Sunifiram, is entirely experimental and has never been tested on humans in clinical trials. Investigators from the Medicines and Healthcare Products Regulatory Authority (MHRA) are worried at what they see as a new phenomenon – the polished, plausible, commercial website targeting students and others who are looking for a mental edge over the competition. In addition to Ritalin, the drug that helps young people with attention deficit disorder (ADD) focus in class and while writing essays, and Modafinil (sold as Provigil), licensed in the US for people with narcolepsy, they are also offering experimental drugs and research chemicals. MHRA head of enforcement, Alastair Jeffrey, said the increase in people buying cognitive-enhancing drugs or “nootropics” is recent and very worrying. “The idea that people are willing to put their overall health at risk in order to attempt to get an intellectual edge over others is deeply troubling,” he said. © 2014 Guardian News and Media Limited

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Attention and Consciousness
Link ID: 20242 - Posted: 10.27.2014

By Jennifer Cutraro and Michael Gonchar Marijuana is illegal in the United States. Yet 35 states and the District of Columbia permit some form of marijuana consumption for medical purposes, and, as of this year, two states now allow its recreational use. As national policy evolves on this issue, the New York Times editorial board this summer published a six-part series calling for legalization. In this lesson, we pull together those opinion pieces as well as many other Times articles, graphics and videos to offer starting points for science, social studies and English teachers aiming to use the debate as an opportunity for learning, research and discussion. Like other crops, marijuana is largely cultivated — legally and illegally — in greenhouse-type “grow houses” and on farms. And like other crops, marijuana comes from a plant — cannabis, originally found in the wild and cultivated over thousands of years. Have students research the history of cannabis, from its origins in South and Central Asia to its introduction to the Americas. How have people used the different parts of the plant throughout history? Then, have students work in groups to annotate a map of the world, tracing the history of marijuana cultivation. Marijuana is best known for its psychoactive properties. But how does marijuana bring about these sensations and how else does it behave in the body? To answer these questions, students might research how the active compounds in marijuana affect the body at the level of the cell, and draw parallels with how other drugs act in the body. As is the case with many other drugs — from legal, over-the-counter medications to illegal street drugs, like heroin — the active compounds interact with locations on the surfaces of cells called receptors. Cell surface receptors provide a means for cells to receive information and input from the environment; when a molecule attaches, or binds, to a cell surface receptor, it triggers a series of events inside the cell, like the release of hormones, neurotransmitters or other molecules. A discussion about marijuana’s effects on the body might dovetail nicely with a broader class discussion or review of cell biology, the makeup and function of the cell membrane, and the function of neurotransmitters. © 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: 20118 - Posted: 09.27.2014

|By Simon Makin The Claim Casual cannabis use harms young people's brains. The Facts A study found differences in the brains of users and nonusers, but it did not establish that marijuana use caused the variations or that they had any functional significance. The Details Researchers at Northwestern University and Harvard Medical School conducted MRI scans of two groups of 20 young adults ages 18 to 25. One group reported using marijuana at least once a week, smoking 11 joints a week on average, whereas the other had used it less than five times total and not at all during the last year. Neither group had any psychiatric disorders, and the users were psychiatrically assessed as not dependent on the drug. The study focused on two brain regions involved in processing rewards, the nucleus accumbens and the amygdala. These areas create pleasurable experiences of things such as food and sex, as well as the high associated with drugs, and have been shown to change in animals given THC, the main psychoactive component of cannabis. The researchers found that cannabis users had more gray matter density in the left nucleus accumbens and left amygdala, as well as differences in the shape of the left nucleus accumbens and right amygdala. The left nucleus accumbens also tended to be slightly larger in users. They concluded that recreational cannabis use might be associated with abnormalities in the brain's reward system. News reports have proclaimed that scientists have shown that even casual cannabis use harms young people's brains. The Caveats The most obvious problem with leaping to that conclusion is that the scans were conducted at only one point. © 2014 Scientific American

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: 20107 - Posted: 09.24.2014

|By Victoria Stern Many studies show that teens who use marijuana face a greater risk of later developing schizophrenia or symptoms of it, especially if they have a genetic predisposition. For instance, one 15-year study followed more than 45,000 Swedes who initially had no psychotic symptoms. The researchers determined that subjects who smoked marijuana by age 18 were 2.4 times more likely to be diagnosed with schizophrenia than their nonsmoking peers, and this risk increased with the frequency of cannabis use. The connection still held when researchers accounted for participants' use of other drugs. Yet despite these results and an uptick in marijuana use in the 1970s and 1980s, other researchers have not uncovered an increase in the incidence of schizophrenia in the general Swedish population—suggesting that perhaps people who were going to develop schizophrenia anyway were more likely to use marijuana. Another study, conducted in Australia over a 30-year period, also found no increase in schizophrenia diagnoses among the general population, despite rising rates of teen marijuana use. These authors concluded that although cannabis most likely does not cause schizophrenia, its use might trigger psychosis in vulnerable people or exacerbate an existing condition. © 2014 Scientific American

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: 20101 - Posted: 09.22.2014

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