Links for Keyword: Drug Abuse

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 21 - 40 of 1329

Aaron E. Carroll When I was a kid, my parents refused to let me drink coffee because they believed it would “stunt my growth.” It turns out, of course, that this is a myth. Studies have failed, again and again, to show that coffee or caffeine consumption are related to reduced bone mass or how tall people are. Coffee has long had a reputation as being unhealthy. But in almost every single respect that reputation is backward. The potential health benefits are surprisingly large. When I set out to look at the research on coffee and health, I thought I’d see it being associated with some good outcomes and some bad ones, mirroring the contradictory reports you can often find in the news media. This didn’t turn out to be the case. Just last year, a systematic review and meta-analysis of studies looking at long-term consumption of coffee and the risk of cardiovascular disease was published. The researchers found 36 studies involving more than 1,270,000 participants. The combined data showed that those who consumed a moderate amount of coffee, about three to five cups a day, were at the lowest risk for problems. Those who consumed five or more cups a day had no higher risk than those who consumed none. Of course, everything I’m saying here concerns coffee — black coffee. I am not talking about the mostly milk and sugar coffee-based beverages that lots of people consume. These could include, but aren’t limited to, things like a McDonald’s large mocha (500 calories, 17 grams of fat, 72 grams of carbohydrates), a Starbucks Venti White Chocolate Mocha (580 calories, 22 grams of fat, 79 grams of carbs), and a Large Dunkin’ Donuts frozen caramel coffee Coolatta (670 calories, 8 grams of fat, 144 grams of carbs). I won’t even mention the Cold Stone Creamery Gotta-Have-It-Sized Lotta Caramel Latte (1,790 calories, 90 grams of fat, 223 grams of carbs). Regular brewed coffee has 5 or fewer calories and no fat or carbohydrates. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20908 - Posted: 05.12.2015

by Clare Wilson IT IS considered a soft drug, but increasing numbers of people are seeking help for cannabis addiction – and there's growing interest in finding ways to treat them. Paradoxically, the most promising treatment may be an extract of cannabis. Last month, researchers at the British Neuroscience Association meeting in Edinburgh, UK, described how the compound, called cannabidiol, helped one person who was severely addicted. A clinical trial is underway. Unlike most forms of drug addiction, there are no medical treatments to help people reduce their cannabis use. "Cannabis dependence is a huge unmet need with no pharmacological treatments," says Tom Freeman of University College London, who is involved in the trial. "It's vital we get one." A possible connection between smoking pot and schizophrenia is fairly well known, but the link is controversial and it affects only a small minority of users. Addiction seems to be a more common problem – yet is often overlooked. There is no universal definition of addiction or dependence. Someone is usually deemed to be addicted to a drug if they want to stop but cannot, or if it has a negative impact on their life. They would probably be experiencing withdrawal symptoms that make it hard to give up. In the case of heavy cannabis use, these can include anxiety and insomnia.

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: 20900 - Posted: 05.08.2015

By ANDREW HIGGINS OSLO — In a country so wary of drug abuse that it limits the sale of aspirin, Pal-Orjan Johansen, a Norwegian researcher, is pushing what would seem a doomed cause: the rehabilitation of LSD. It matters little to him that the psychedelic drug has been banned here and around the world for more than 40 years. Mr. Johansen pitches his effort not as a throwback to the hippie hedonism of the 1960s, but as a battle for human rights and good health. In fact, he also wants to manufacture MDMA and psilocybin, the active ingredients in two other prohibited substances, Ecstasy and so-called magic mushrooms. All of that might seem quixotic at best, if only Mr. Johansen and EmmaSofia, the psychedelics advocacy group he founded with his American-born wife and fellow scientist, Teri Krebs, had not already won some unlikely supporters, including a retired Norwegian Supreme Court judge who serves as their legal adviser. The group, whose name derives from street slang for MDMA and the Greek word for wisdom, stands in the vanguard of a global movement now pushing to revise drug policies set in the 1970s. That it has gained traction in a country so committed to controlling drug use shows how much old orthodoxies have crumbled. The Norwegian group wants not only to stir discussion about prohibited drugs, but also to manufacture them, in part, it argues, to guarantee that they are safe. It recently began an online campaign to raise money so that it can, in cooperation with a Norwegian pharmaceuticals company, start quality-controlled production of psilocybin and MDMA, drugs that Mr. Johansen says saved and transformed his life. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20886 - Posted: 05.05.2015

Scott Hensley When patients brought to the ER have uncontrolled blood pressure, neglected asthma or diabetes that hasn't been dealt with, doctors often start treatment right then and there. But what happens when the patient turns out to be addicted to opioids, such as oxycodone or heroin? In case of an overdose, the medical team can take action to rescue the patient. The underlying addiction is something else, though. Like asthma or diabetes, opioid addiction is a chronic condition. Could starting treatment for addiction in the ER get someone on right road faster? Doctors at Yale University thought it was possible. "You can normalize this chronic disease like any other chronic disease," says Dr. Gail D'Onofrio, chief of emergency medicine at Yale's med school. A kit with naloxone, also known by its brand name Narcan, is displayed at the South Jersey AIDS Alliance in Atlantic City. Naloxone counters an overdose with heroin or certain prescription painkillers by blocking the receptors these opioids bind to in the brain. She and her colleagues at Yale-New Haven Hospital in Connecticut tested whether prescribing medicine to ease withdrawal symptoms in combination with a brief counseling intervention and a focused referral for help would improve the chances a person would get into addiction treatment. It worked pretty well, according to results of a study published Tuesday in JAMA, the journal of the American Medical Association. © 2015 NPR

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20862 - Posted: 04.30.2015

By ALAN SCHWARZ A sharp rise in visits to emergency rooms and calls to poison control centers nationwide has some health officials fearing that more potent and dangerous variations of a popular drug known as spice have reached the nation’s streets, resulting in several deaths. In the first three weeks of April, state poison control centers received about 1,000 reports of adverse reactions to spice — the street name for a family of synthetic substances that mimic the effects of marijuana — more than doubling the total from January through March, according to the American Association of Poison Control Centers. The cases, which can involve spice alone or in combination with other substances, have appeared four times as often this year as in 2014, the organization said. On Thursday alone there were 172 reports, by far the most in one day this year. Health departments in Alabama, Mississippi and New York have issued alerts this month about more spice users being rushed to hospitals experiencing extreme anxiety, violent behavior and delusions, with some of the cases resulting in death. Similar increases have occurred in Arizona, Florida, New Jersey and Texas. The total number of fatalities nationwide this year is not available, health officials said. One person in Louisiana died Wednesday and two others were in intensive care, said Mark Ryan, the director of the Louisiana Poison Center. “We had one hospital in the Baton Rouge area that saw over 110 cases in February. That’s a huge spike,” Dr. Ryan said. “There’s a large amount of use going on. When one of these new ingredients — something that’s more potent and gives a bigger high — is released and gets into distribution, it can cause these more extreme effects.” © 2015 The New York Times Compan

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: 20848 - Posted: 04.25.2015

By ALAN SCHWARZ Fading fast at 11 p.m., Elizabeth texted her dealer and waited just 30 minutes for him to reach her third-floor New York apartment. She handed him a wad of twenties and fifties, received a tattered envelope of pills, and returned to her computer. Her PowerPoint needed another four hours. Investors in her health-technology start-up wanted re-crunched numbers, a presentation begged for bullet points and emails from global developers would keep arriving well past midnight. She gulped down one pill — pale orange, like baby aspirin — and then, reconsidering, took one of the pinks, too. “O.K., now I can work,” Elizabeth exhaled. Several minutes later, she felt her brain snap to attention. She pushed her glasses up her nose and churned until 7 a.m. Only then did she sleep for 90 minutes, before arriving at her office at 9. The pills were versions of the drug Adderall, an amphetamine-based stimulant prescribed for attention deficit hyperactivity disorder that many college students have long used illicitly while studying. Now, experts say, stimulant abuse is graduating into the work force. But in interviews, dozens of people in a wide spectrum of professions said they and co-workers misused stimulants like Adderall, Vyvanse and Concerta to improve work performance. Most spoke on the condition of anonymity for fear of losing their jobs or access to the medication. Doctors and medical ethicists expressed concern for misusers’ health, as stimulants can cause anxiety, addiction and hallucinations when taken in high doses. But they also worried about added pressure in the workplace — where the use by some pressures more to join the trend. © 2015 The New York Times Company

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: 20821 - Posted: 04.20.2015

By SABRINA TAVERNISE E-cigarettes have arrived in the life of the American teenager. Use of the devices among middle- and high school students tripled from 2013 to 2014, according to federal data released on Thursday, bringing the share of high school students who use them to 13 percent — more than smoke traditional cigarettes. About a quarter of all high school students and 8 percent of middle school students — 4.6 million young people altogether — used tobacco in some form last year. The sharp rise of e-cigarettes, together with a substantial increase in the use of hookah pipes, led to 400,000 additional young people using a tobacco product in 2014, the first increase in years, though researchers pointed out the percentage of the rise fell within the report’s margin of error. But the report also told another story. From 2011 to 2014, the share of high school students who smoked traditional cigarettes declined substantially, to 9 percent from 16 percent, and use of cigars and pipes ebbed too. The shift suggested that some teenage smokers may be using e-cigarettes to quit. Smoking is still the single-biggest cause of preventable death in the United States, killing more than 480,000 Americans a year, and most scientists agree that e-cigarettes, which deliver the nicotine but not the dangerous tar and other chemicals, are likely to be far less harmful than traditional cigarettes. The numbers came as a surprise and seemed to put policy makers into uncharted territory. The Food and Drug Administration took its first tentative step toward regulating e-cigarettes last year, but the process is slow, and many experts worry that habits are forming far faster than rules are being written. Because e-cigarettes are so new, scientists are still gathering evidence on their long-term health effects, leaving regulators scrambling to gather data. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20811 - Posted: 04.18.2015

By Laura Sanders To drive a rat to drink, make it smoke first. Rats dependent on nicotine escalate their drinking more quickly than rats that haven’t been exposed to nicotine, researchers report in the April 15 Journal of Neuroscience. The results help explain why alcohol and tobacco addictions in people often go hand in hand. After nicotine injections, rats that had previously been exposed to alcohol dosed themselves with more alcohol than rats unexposed to nicotine did. Scientists were able to curb this booziness: Rats injected with a compound that made brain cells ignore nicotine did not boost their intake of alcohol. The double whammy of nicotine and alcohol dependence may be due to a select group of nerve cells throughout the rat brain that respond to this nicotine-aided drinking, Olivier George of the Scripps Research Institute in La Jolla, Calif., and colleagues found. If a similar response happens in humans, studying these particular nerve cells might ultimately lead to better ways to curb both alcohol and tobacco dependencies, the researchers write. R. Leão et al. Chronic nicotine activates stress/reward-related brain regions and facilitates the transition to compulsive alcohol drinking. Journal of Neuroscience. Vol. 35, April 15, 2015. doi:10.1523/JNEUROSCI.3302-14.2015. © Society for Science & the Public 2000 - 2015.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20799 - Posted: 04.15.2015

Leana Wen Every doctor and nurse in our hospital's emergency room knew Jerome. He was one of our regulars. In his 20s, he had back problems that led him to become addicted to prescription painkillers. That habit proved too expensive, and he switched to heroin. Jerome used to come to the ER nearly every week. Often, he just wanted a sandwich and someone to talk to. He had lost his job and his home. Several months ago, he decided he had to quit heroin. We helped him with health insurance so that he could find a primary care doctor. Our social worker connected him with addiction treatment, including medications and mental health counseling. He was also working on rekindling a relationship with his estranged family. One day, paramedics brought Jerome to the ER. They had found him in an abandoned building. He'd relapsed and was shooting heroin. A friend saw him unconscious and called for help. By the time paramedics arrived, he wasn't breathing and his heart had stopped beating. In the ER, we tried to resuscitate him for nearly an hour. We weren't successful. In Baltimore, where I serve as health commissioner, more people die from drug and alcohol overdoses than from homicide. In 2013, there were 246 deaths related to drugs and alcohol, compared with 235 homicides. © 2015 NPR

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20783 - Posted: 04.11.2015

Cari Romm “As humans, we can identify galaxies light-years away. We can study particles smaller than an atom,” President Barack Obama said in April 2013, “But we still haven’t unlocked the mystery of the three pounds of matter that sits between our ears.” The observation was part of the president’s announcement of the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, an effort to fast-track the development of new technology that will help scientists understand the workings of the human brain and its diseases. With progress, though, comes a whole new set of ethical questions. Can drugs used to treat conditions like ADHD, for example, also be used to make healthy people into sharper, more focused versions of themselves—and should they? Can a person with Alzheimer’s truly consent to testing that may help scientists better understand their disease? Can brain scans submitted as courtroom evidence reveal anything about a defendant’s intent? Can a person with Alzheimer’s truly consent to testing that may help scientists better understand their disease? To address these questions, the Presidential Commission for the Study of Bioethical Issues, an independent advisory group, recently released the second volume of a report examining the issues that may arise as neuroscience advances. The commission outlined three areas it deemed particularly fraught: cognitive enhancement, consent, and the use of neuroscience in the legal system. © 2015 by The Atlantic Monthly Group

Related chapters from BP7e: Chapter 17: Learning and Memory; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 1: An Introduction to Brain and Behavior
Link ID: 20771 - Posted: 04.08.2015

Do Alcoholics Anonymous participants do better at abstinence than nonparticipants because they are more motivated? Or is it because of something inherent in the A.A. program? How researchers answered these questions in a recent study offers insight into challenges of evidence-based medicine and evidence-informed policy. The study, published in the journal Alcoholism: Clinical and Experimental Research, teased apart a treatment effect (improvement due to A.A. itself) and a selection effect (driven by the type of people who seek help). The investigators found that there is a genuine A.A. treatment effect. Going to an additional two A.A. meetings per week produced at least three more days of alcohol abstinence per month. Separating treatment from selection effects is a longstanding problem in social and medical science. Their entanglement is one of the fundamental ways in which evidence of correlation fails to be a sign of causation. For many years, researchers and clinicians have debated whether the association of A.A. with greater abstinence was caused by treatment or a correlation that arises from the type of people who seek it. Such confounding is often addressed with an experiment in which individuals are randomly assigned to either a treatment or a nontreatment (or control) group in order to remove the possibility of self-selection. The treatment effect is calculated by comparing outcomes obtained by participants in each group. Several studies of A.A. have applied this approach. For instance, Kimberly Walitzer, Kurt Dermen and Christopher Barrick randomized alcoholics to receive treatment that strongly encouraged and supported A.A. participation or a control group. The former exhibited a greater degree of abstinence. In an ideal randomized controlled trial (R.C.T.), everyone selected for treatment receives it and no one in the control group does. The difference in outcomes is the treatment effect, free of bias from selection. That’s the ideal. However, in practice, randomized controlled trials can still suffer selection problems. © 2015 The New York Times Company

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20767 - Posted: 04.08.2015

by Bethany Brookshire A new round of dietary do’s and don’ts accompanied last month’s scientific report on the latest food research, summarizing everything from aspartame to saturated fats. The report puts eggs back on the menu. High dietary cholesterol is no longer linked to blood cholesterol in most healthy people. But what grabbed the headlines? Coffee, of course. Many of us are happy to raise a mug to our legal stimulant of choice, especially with the report’s suggestion that three to five cups of joe get a pass. But where do these numbers come from? What science do nutrition experts take into account to determine whether coffee is harmful or safe? And — perhaps the most important question — what does “three to five cups” really mean? The good news for coffee comes from the 2015 Dietary Guidelines Advisory Committee, a group of experts in nutrition and health appointed by the Department of Health and Human Services and the U.S. Department of Agriculture to review the science behind what Americans should eat. The report, released February 19, is not the be-all-end-all of what should be on our plates and in our cups. Instead, it’s a scientific report intended to help the HHS and USDA make policy decisions for the next edition of the Dietary Guidelines for Americans, due out later this year. This is the first time the U.S. Dietary Guidelines have addressed coffee at all. But now, there is enough science on coffee to make a closer look worthwhile, says Tom Brenna, a food scientist at Cornell University and a member of the Committee. “There was so much evidence out there,” he says. “Instead of just five or six papers on the subject, there’s a huge number.” © Society for Science & the Public 2000 - 2015

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20758 - Posted: 04.06.2015

Founded by two men in Akron, Ohio, in 1935, Alcoholics Anonymous has since spread around the world as a leading community-based method of overcoming alcohol dependence and abuse. Many people swear by the 12-step method, which has become the basis of programs to treat the abuse of drugs, gambling, eating disorders and other compulsive behaviors. But not everyone's a fan. In a recent critique of AA, author Gabrielle Glaser writes in the April issue of The Atlantic that, "Nowhere in the field of medicine is treatment less grounded in modern science." Glaser, whose 2013 book, Her Best-Kept Secret, explores what she calls "the epidemic of female drinking" in the U.S., says recent research on the brain suggests that the abstinence advocated by AA isn't the only solution — or even the best for many people. Cognitive therapy combined with the medication naltrexone, Glaser says, can help ease cravings and has been shown in some studies to help some problem drinkers learn to drink moderately without quitting. Glaser's magazine story has drawn fire from defenders of AA, including Huffington Post writer Tommy Rosen, who calls himself "a person in long-term recovery (23 years) who overcame severe drug addiction and alcoholism in great part due to the 12 Steps." Glaser's article, Rosen writes, is "painfully one-sided." Therapist and psychology reporter Robi Ludwig told Glaser and the host of MSNBC's program All in With Chris Hayes last week that she thinks it's "very dangerous to put out the idea that AA doesn't work. Does it work for everybody? No. There's not going to be one form of treatment that works for everybody." © 2015 NPR

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20729 - Posted: 03.28.2015

Claudia Dreifus Twenty-three states and the District of Columbia have legalized medical marijuana, but scientific research into its appropriate uses has lagged. Dr. Mark Ware would like to change that. Dr. Ware, 50, is the director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research of the Alan Edwards Pain Management Unit of McGill University Health Center. Medical marijuana has been legal in Canada for 16 years, and Dr. Ware, a practicing physician, studies how his patients take the drug and under what conditions it is effective. We spoke for two hours at the recent meeting of the American Association for the Advancement of Science and later by telephone. Our interviews have been condensed and edited for space. Q. How did you become interested in the medical possibilities of cannabis? A. In the late 1990s, I was working in Kingston, Jamaica, at a clinic treating people with sickle cell anemia. My British father and Guyanese mother had raised me in Jamaica, and I’d attended medical school there. One day, an elderly Rastafarian came for his annual checkup. I asked him, “What are your choices of medicines?” He leaned over the table and said, “You must study the herb.” That night, I went back to my office and looked up “cannabis and pain.” What I found were countless anecdotes from patients who’d obtained marijuana either legally or not and who claimed good effect with a variety of pain-related conditions. There were also the eye-opening studies showing that the nervous system had specific receptors for cannabinoids and that these receptors were located in areas related to pain. Everything ended with, “More studies are needed.” So I thought, “This is what I should be doing; let’s go!” © 2015 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: 20713 - Posted: 03.24.2015

By Brian Handwerk In the U.S., legal hurdles have long hampered research into marijuana. But as more states approve medical and even recreational marijuana, scientific inquiries have spiked, especially studies aimed at finding out what exactly is in today's weed—and what it does to our bodies. In Colorado, which made marijuana legal in November 2012, the latest results show that the pot lining store shelves is much more potent than the weed of 30 years ago. But the boost in power comes at a cost—modern marijuana mostly lacks the components touted as beneficial by medical marijuana advocates, and it is often contaminated with fungi, pesticides and heavy metals. “There's a stereotype, a hippy kind of mentality, that leads people to assume that growers are using natural cultivation methods and growing organically," says Andy LaFrate, founder of Charas Scientific, one of eight Colorado labs certified to test cannabis. "That's not necessarily the case at all." LaFrate presented his results this week at a meeting of the American Chemical Society (ACS) in Denver. LaFrate says he's been surprised at just how strong most of today's marijuana has become. His group has tested more than 600 strains of marijuana from dozens of producers. Potency tests, the only ones Colorado currently requires, looked at tetrahydrocannabinol (THC), the psychoactive compound that produces the plant's famous high. They found that modern weed contains THC levels of 18 to 30 percent—double to triple the levels that were common in buds from the 1980s. That's because growers have cross-bred plants over the years to create more powerful strains, which today tout colorful names like Bruce Banner, Skunkberry and Blue Cookies.

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: 20712 - Posted: 03.24.2015

By John Horgan In 1990 The New York Times published a front-page article by Lawrence Altman, a reporter with a medical degree, announcing that scientists had discovered “a link between alcoholism and a specific gene.” The evidence for the "feel-good gene," which supposedly reduces anxiety, is flimsy, just like the evidence linking specific genes to high intelligence, violent aggression, homosexuality, bipolar disorder and countless other complex human traits and ailments. That was merely one in a string of reports in which the Times and other major media hyped what turned out to be erroneous claims linking complex traits and disorders—from homosexuality and high intelligence to schizophrenia and bipolar disorder—to specific genes. I thought those days were over, and that scientists and the media have learned to doubt extremely reductionist genetic accounts of complex traits and behaviors. I was wrong. Last Sunday, the “Opinion” section of the Times published an essay, “The Feel-Good Gene,” which states: “For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide–the so-called bliss molecule and our natural marijuana–in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character.” This article, like the one touting the alcoholism gene 25 years ago, was written by a physician, Richard Friedman, professor of psychiatry at Weill Cornell Medical College. I emphasize this fact because scientific hype is often blamed on supposedly ignorant journalists like me rather than on physicians and other so-called experts. © 2015 Scientific American

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: 20689 - Posted: 03.14.2015

By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.

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: 20687 - Posted: 03.14.2015

|By Anne Skomorowsky On a Saturday night last month, 12 students at Wesleyan University in Connecticut were poisoned by “Molly,” a hallucinogenic drug they had taken to enhance a campus party. Ambulances and helicopters transported the stricken to nearby hospitals, some in critical condition. Molly—the street name for the amphetamine MDMA—can cause extremely high fevers, liver failure, muscle breakdown, and cardiac arrest. Given the risks associated with Molly, why would anybody take it? The obvious answer—to get high—is only partly true. Like many drugs of abuse, Molly causes euphoria. But Molly is remarkable for its “prosocial” effects. Molly makes users feel friendly, loving, and strongly connected to one another. Molly is most commonly used in settings where communion with others is highly valued, such as raves, music festivals, and college parties. Recently, psychiatrists have taken an interest in its potential to enhance psychotherapy; this has led to new research into the mechanisms by which MDMA makes people feel closer. It appears that MDMA works by shifting the user’s attention towards positive experiences while minimizing the impact of negative feelings. To investigate this, a 2012 study by Cedric Hysek and colleagues used the Reading the Mind in the Eyes Test (RMET), which was developed to evaluate people with autism. In the RMET, participants are shown 36 pictures of the eye region of faces. Their task is to describe what the person in the picture is feeling. Volunteers taking MDMA, under carefully controlled conditions, improved in their recognition of positive emotions; but their performance in recognizing negative emotions declined. In other words, they incorrectly attributed positive or neutral feelings to images that were actually negative in emotional tone. They mistook negative and threat-related images for friendly ones. © 2015 Scientific American

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20678 - Posted: 03.12.2015

By RICHARD A. FRIEDMAN CHANCES are that everyone on this planet has experienced anxiety, that distinct sense of unease and foreboding. Most of us probably assume that anxiety always has a psychological trigger. Yet clinicians have long known that there are plenty of people who experience anxiety in the absence of any danger or stress and haven’t a clue why they feel distressed. Despite years of psychotherapy, many experience little or no relief. It’s as if they suffer from a mental state that has no psychological origin or meaning, a notion that would seem heretical to many therapists, particularly psychoanalysts. Recent neuroscience research explains why, in part, this may be the case. For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide — the so-called bliss molecule and our own natural marijuana — in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character. About 20 percent of adult Americans have this mutation. Those who do may also be less likely to become addicted to marijuana and, possibly, other drugs — presumably because they don’t need the calming effects that marijuana provides. One patient of mine, a man in his late 40s, came to see me because he was depressed and lethargic. He told me at our first meeting that he had been using cannabis almost daily for at least the past 15 years. “It became a way of life,” he explained. “Things are more interesting, and I can tolerate disappointments without getting too upset.” © 2015 The New York Times Company

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20666 - Posted: 03.09.2015

Zoe Cormier Data from population surveys in the United States challenge public fears that psychedelic drugs such as LSD can lead to psychosis and other mental-health conditions and to increased risk of suicide, two studies have found1, 2. In the first study, clinical psychologists Pål-Ørjan Johansen and Teri Suzanne Krebs, both at the Norwegian University of Science and Technology in Trondheim, scoured data from the US National Survey on Drug Use and Health (NSDUH), an annual random sample of the general population, and analysed answers from more than 135,000 people who took part in surveys from 2008 to 2011. Of those, 14% described themselves as having used at any point in their lives any of the three ‘classic’ psychedelics: LSD, psilocybin (the active ingredient in so-called magic mushrooms) and mescaline (found in the peyote and San Pedro cacti). The researchers found that individuals in this group were not at increased risk of developing 11 indicators of mental-health problems such as schizophrenia, psychosis, depression, anxiety disorders and suicide attempts. Their paper appears in the March issue of the Journal of Psychopharmacology1. The findings are likely to raise eyebrows. Fears that psychedelics can lead to psychosis date to the 1960s, with widespread reports of “acid casualties” in the mainstream news. But Krebs says that because psychotic disorders are relatively prevalent, affecting about one in 50 people, correlations can often be mistaken for causations. “Psychedelics are psychologically intense, and many people will blame anything that happens for the rest of their lives on a psychedelic experience.” © 2015 Nature Publishing Group,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 20655 - Posted: 03.05.2015