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By Robert Dudley When we think about the origins of agriculture and crop domestication, alcohol isn’t necessarily the first thing that comes to mind. But our forebears may well have been intentionally fermenting fruits and grains in parallel with the first Neolithic experiments in plant cultivation. Ethyl alcohol, the product of fermentation, is an attractive and psychoactively powerful inebriant, but fermentation is also a useful means of preserving food and of enhancing its digestibility. The presence of alcohol prolongs the edibility window of fruits and gruels, and can thus serve as a means of short-term storage for various starchy products. And if the right kinds of bacteria are also present, fermentation will stabilize certain foodstuffs (think cheese, yogurt, sauerkraut, and kimchi, for example). Whoever first came up with the idea of controlling the natural yeast-based process of fermentation was clearly on to a good thing. Using spectroscopic analysis of chemical residues found in ceramic vessels unearthed by archaeologists, scientists know that the earliest evidence for intentional fermentation dates to about 7000 BCE. But if we look deeper into our evolutionary past, alcohol was a component of our ancestral primate diet for millions of years. In my new book, The Drunken Monkey, I suggest that alcohol vapors and the flavors produced by fermentation stimulate modern humans because of our ancient tendencies to seek out and consume ripe, sugar-rich, and alcohol-containing fruits. Alcohol is present because of particular strains of yeasts that ferment sugars, and this process is most common in the tropics where fruit-eating primates originated and today remain most diverse. © 1986-2014 The Scientist

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: 19751 - Posted: 06.21.2014

By Brian Palmer Maureen Dowd, a 62-year-old Pulitzer Prize–winning columnist for the New York Times, had a bad marijuana trip earlier this year. As part of her research into the legalization of recreational cannabis in Colorado, she ate a few too many bites of a pot-infused candy bar, entered a “hallucinatory state,” and spent eight paranoid hours curled up on her hotel room bed. Dowd used the experience as a jumping-off point to discuss the risks of overdosing on edible marijuana, which has become a major issue in pot-friendly states. It’s also possible, however, that Dowd just doesn’t handle cannabis very well. While pot mellows most people out, everyone has heard of someone who barricaded himself or herself in a dorm room after a few bongs hits in college. (Or maybe that someone is you.) Why do people react so differently to the same drug? The question itself may be something of a fallacy. Cannabis is not a single drug—it contains dozens of compounds, and they appear to have varying, and sometimes opposing, effects on the brain. Tetrahydrocannabinol, or THC, and cannabidiol, or CBD, have been the subject of some intriguing research. In 2010, researchers showed that pretreating people with a dose of CBD can protect against the less pleasant effects of THC, such as paranoia. In a similar 2012 study, participants took pills that contained only one of the two chemicals, rather than the combination that you receive in cannabis. The subjects who took THC pills were more likely to suffer paranoia and delusion than those who took CBD. The researchers went one step further to investigate which specific cognitive effects of THC are likely to lead to paranoia and other symptoms of psychosis. After taking either THC or CBD, participants watched a series of arrows appear on a screen and responded by indicating which direction the arrows were pointing. Most of the arrows pointed directly left or right, but occasionally a tilted arrow appeared. (Researchers called the tilted arrows “oddballs.”) Subjects who took the CBD had a heightened brain activity response to the oddballs. That’s the way a nondrugged person typically reacts—repetitions of the same stimulus don’t interest us, but a sudden change grabs our attention. The THC-takers had an abnormal response: They found the left and right arrows, which constituted the overwhelming majority of the images, more noteworthy than the oddballs. © 2014 The Slate Group LLC

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: 19734 - Posted: 06.16.2014

By J. DAVID GOODMAN and ANEMONA HARTOCOLLIS Amid the weeknight bustle of a Walmart parking lot in Centereach, N.Y., a young woman in a pickup truck had lost consciousness and was turning blue. Her companion called 911. Possible drug overdose; come fast. A Suffolk County police officer, Matthew Siesto, who had been patrolling the lot, was the first to arrive. Needles were visible in the center console; the woman was breathing irregularly, and her pupils had narrowed to pinpoints. It seemed clear, Officer Siesto recalled of the October 2012 episode, that the woman had overdosed on heroin. He went back to his squad car and retrieved a small kit of naloxone, an anti-overdose medication he had only recently been trained to use in such circumstances. He prepared the dose, placed the atomizer in her nostril and sprayed. “Within a minute,” the officer said, “she came back.” Once the exclusive purview of paramedics and emergency room doctors, administering lifesaving medication to drug users in the throes of an overdose is quickly becoming an everyday part of police work amid a national epidemic of heroin and opioid pill abuse. On Wednesday, Gov. Andrew M. Cuomo committed state money to get naloxone into the hands of emergency medical workers across New York, saying the heroin epidemic in the state was worse than that seen in the 1970s, and the problem is growing. Last month, the New York police commissioner, William J. Bratton, announced that the city’s entire patrol force would soon be trained and equipped with naloxone. “Officers like it because it puts them in a lifesaving opportunity,” Mr. Bratton said, suggesting that beat officers would carry it on their belts. © 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: 19728 - Posted: 06.14.2014

​Nathan Greenslit A recent neuroscience study from Harvard Medical School claims to have discovered brain differences between people who smoke marijuana and people who do not. Such well-intentioned and seemingly objective science is actually a new chapter in a politicized and bigoted history of drug science in the United States. The study in question compared magnetic resonance imaging (MRI) scans of 20 “young adult recreational marijuana users” (defined as individuals 18 to 25 who smoke at least once a week but who are not “dependent”), to 20 “non-using controls” (age-matched individuals who have smoked marijuana less than five times in their lives). The researchers reported differences in density, volume, and shape between the nucleus accumbens and amygdala regions of the two groups’ brains—areas hypothesized to affect a wide range of emotions from happiness to fear, which could influence basic decision-making. Researchers did not make any claims about how marijuana affected actual emotions, cognition, or behavior in these groups; instead; the study merely tried to establish that the aggregated brain scans of the two groups look different. So, who cares? Different-looking brains tell us literally nothing about who these people are, what their lives are like, why they do or do not use marijuana, or what effects marijuana has had on them. Neither can we use such brain scans to predict who these people will become, or what their lives will be like in the future. Nonetheless the study invented two new categories of person: the “young casual marijuana user” and the young non-marijuana user. This is the latest example of turning to brain imaging to make something seem objective. Establishing brain differences among certain groups highlights the uniquely ignoble political history surrounding the criminalization of a plant. © 2014 by The Atlantic Monthly 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: 19725 - Posted: 06.14.2014

A moderate dose of MDMA. commonly known as Ecstasy or Molly, that is typically nonfatal in cool, quiet environments can be lethal in rats exposed to conditions that mimic the hot, crowded, social settings where the drug is often used by people, a study finds. Scientists have identified the therapeutically-relevant cooling mechanism to enable effective interventions when faced with MDMA-induced hyperthermia. The study, publishing tomorrow in the Journal of Neuroscience, was conducted by researchers at the National Institute on Drug Abuse’s Intramural Research Program (NIDA IRP). NIDA is a part of the National Institutes of Health. While MDMA can have a range of adverse health effects, previous studies have shown that high doses of MDMA increase body temperature, while results with moderate doses were inconsistent. This has led some people to assume that the drug is harmless if taken in moderation. However, this study shows that in rats even moderate doses of MDMA in certain environments can be dangerous because it interferes with the body’s ability to regulate temperature. “We know that high doses of MDMA can sharply increase body temperature to potentially lead to organ failure or even death,” said NIDA Director Dr. Nora D. Volkow. “However, this current study opens the possibility that even moderate doses could be deadly in certain conditions.” It is impossible to predict who will have an adverse reaction even to a low dose of MDMA. However, in this study scientists gave the rats low to moderate doses that have been shown in past studies to not be fatal. They monitored the rats to determine drug-induced changes in brain and body temperature and in the body’s ability to cool itself through blood vessel dilation. When rats were alone and in a room-temperature environment, a moderate dose of MDMA modestly increased brain and body temperature and moderately diminished the rats’ ability to eliminate excessive heat. However, when researchers injected the same dose in rats that were either in a warmer environment or in the presence of another rat in the cage, brain temperature increased, causing death in some rats. These fatal temperature increases were because the drug interfered with the body’s ability to eliminate heat.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19695 - Posted: 06.05.2014

by Laura Sanders Some people think marijuana is nature’s gift to humankind: a nonaddictive drug, safe at any dose, that opens the mind, lifts the spirit and transports the user to a more profound reality. “The illegality of cannabis is outrageous, an impediment to full utilization of a drug which helps produce the serenity and insight, sensitivity and fellowship so desperately needed in this increasingly mad and dangerous world,” a user named Mr. X wrote in the 1971 book Marihuana Reconsidered. Close to 30 years later, Mr. X was revealed to be the legendary science communicator and astronomer Carl Sagan. His message still reverberates with many Americans, whose support for legalizing marijuana has tripled since 1989 — from 16 percent to 54 percent today. In Colorado and Washington state, voters legalized recreational marijuana use in November 2012. That formal embrace of marijuana may signal a growing shift in acceptance. Today, 21 states and the District of Columbia sanction medical use (up from 16 in 2010) and 17 have curbed punishments for possession of small amounts of recreational cannabis. Marijuana as medicine is gaining support in studies, both to tamp down nausea and pain and to directly counter insidious diseases such as epilepsy, cancer and multiple sclerosis (SN: 6/19/10, p. 16). But what about for healthy people? Is marijuana really a safe way to rise above the tumult and distress of daily life? Michele Leonhart, the head of the U.S. Drug Enforcement Administration, says no. In congressional testimony in 2012, she portrayed marijuana as a dangerous addictive drug on par with methamphetamines or heroin. Like other drugs cordoned off by her agency to a list called Schedule I, she said, marijuana has no medical use and a high potential for abuse. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19676 - Posted: 05.31.2014

By IAN AUSTEN Hershey stopped producing chocolate in Smiths Falls, Ontario, six years ago. The work went to Mexico, but the factory remains, along with reminders of the glory days: A sign that once directed school buses delivering children for tours. A fading, theme-park-style entrance that marks what used to be the big attraction — a “Chocolate Shoppe” that sold about $4 million of broken candy and bulk bars a year. The once ever-present sweet smell of chocolate is gone, too. In the high-ceilinged warehouse, where stacks of Hershey’s bars and Reese’s Peanut Butter Cups once awaited shipment, the nose now picks up a different odor: the woody, herbal aroma of 50,000 marijuana plants. Clinical, climate-controlled rooms with artificial sunlight house rows upon rows of plants at various stages of growth. In the “mother room,” horticulturalists use cuttings to start new plants. The “flowering rooms” are flooded with intense light 12 hours a day to nurture nearly grown plants in strains with vaguely aristocratic names like Argyle, Houndstooth and Twilling. The new owner of this factory, at 1 Hershey Drive, is Tweed Marijuana. It is one of about 20 companies officially licensed to grow medical marijuana in Canada. A court ordered the government to make marijuana available for medicinal purposes in 2000, but the first system for doing so created havoc. The government sold directly to approved consumers, but individuals were also permitted to grow for their own purposes or to turn over their growing to small operations. The free-for-all approach prompted a flood of complaints from police and local governments. So the Canadian government decided to create an extensive, heavily regulated system for growing and selling marijuana. The new rules allow users with prescriptions to buy only from one of the approved, large-scale, profit-seeking producers like Tweed, a move intended to shut down the thousands of informal growing operations scattered across the country. © 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: 19657 - Posted: 05.25.2014

Puffing on a battery-powered, electronic cigarette to satisfy nicotine cravings could help longtime smokers quit their tobacco addiction. The evidence supporting that claim has been thin in the past, but researchers have now reported that adults in England who used the devices were 60% more likely to remain smoke-free than those who turned to nicotine patches or went cold turkey. Some public health researchers, though, still worry that’s not enough to cancel out the negative effects of e-cigarettes, which might keep other smokers hooked on nicotine or prevent them from seeking out more effective ways to quit. “This is an important study because, until now, the data on quitting smoking with e-cigarettes has been mostly anecdotal,” says Neal Benowitz, a physician at the University of California, San Francisco (UCSF), who studies tobacco addiction and was not involved in the work. E-cigarettes produce a nicotine-rich vapor that’s free of many of the toxins and carcinogens that make tobacco cigarettes so unhealthy. Their popularity has skyrocketed since they hit the market in the early 2000s; a 2012 survey found that 30% of adult smokers in the United States had tried e-cigarettes. But studies attempting to establish both the risks and benefits of the devices have had varied conclusions. One recent review of the scientific literature, which included Benowitz as an author, reported that smokers who used e-cigarettes were less likely to quit smoking than those who didn’t use the devices. The results were based on broad surveys of all smokers, however, not just those attempting to quit. Another paper concluded that e-cigarettes are about as effective as nicotine patches at helping people stop smoking. Since 2006, researchers in England have run an ongoing surveillance program, in conjunction with the government’s research bureau, called the Smoking Toolkit Study. Every month, they survey a new sample of 1800 random adults about their smoking behavior. © 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: 19640 - Posted: 05.20.2014

By Venkat Srinivasan In 1995, Ivan Goldberg, a New York psychiatrist, published one of the first diagnostic tests for Internet Addiction Disorder. The criteria appeared on psycom.net, a psychiatry bulletin board, and began with an air of earnest authenticity: “A maladaptive pattern of Internet use, leading to clinically significant impairment or distress as manifested by three (or more) of the following.” The test listed seven symptoms. You might have a problem if you were online “for longer periods of time than was intended,” or if you made “unsuccessful efforts to cut down or control Internet use.” Hundreds of people heard of the diagnostic test, logged on, clicked through and diagnosed themselves as being Internet addicts. Goldberg’s test, however, was a parody of the rigid language in the Diagnostic and Statistical Manual of Mental Disorders (DSM), the American Psychiatric Association (APA)’s psychiatric research manual. In a New Yorker story in January 1997, Goldberg said having an Internet addiction support group made “about as much sense as having a support group for coughers.” I’ve been researching the science and controversy over the last five years and wrote a long story about it last year for The Caravan. Since Goldberg’s prank, about one hundred scientific journals in psychology, sociology, neuroscience, anthropology, healthy policy and computer science have taken up the addiction question in some form. And after two decades of ridicule, research, advocacy and pushbacks, the debate is still about four basic questions. What do you call it? Does the ‘it’ exist? How do we size up such an addiction? Does it matter? © 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: 19621 - Posted: 05.15.2014

A single alcohol binge can cause bacteria to leak from the gut and increase levels of bacterial toxins in the blood, according to a study funded by the National Institutes of Health. Increased levels of these bacterial toxins, called endotoxins, were shown to affect the immune system, with the body producing more immune cells involved in fever, inflammation, and tissue destruction. Binge drinking is defined by NIAAA as a pattern of drinking alcohol that brings blood alcohol concentration (BAC) to 0.08g/dL or above. For a typical adult, this pattern corresponds to consuming five or more drinks for men, or four or more drinks for women, in about two hours. Some individuals will reach a 0.08g/dL BAC sooner depending on body weight. Binge drinking is known to pose health and safety risks, including car crashes and injuries. Over the long term, binge drinking can damage the liver and other organs. “While the negative health effects of chronic drinking are well-documented, this is a key study to show that a single alcohol binge can cause damaging effects such as bacterial leakage from the gut into the blood stream,” said Dr. George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, part of NIH. The study was led by Gyongyi Szabo, M.D., Ph.D., Professor and Vice Chair of Medicine and Associate Dean for Clinical and Translational Sciences at the University of Massachusetts Medical School. The article appears online in PLOS ONE In the study, 11 men and 14 women were given enough alcohol to raise their blood alcohol levels to at least .08 g/dL within an hour. Blood samples were taken every 30 minutes for four hours after the binge and again 24 hours later.

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: 19620 - Posted: 05.15.2014

By ANAHAD O’CONNOR Two medications could help tens of thousands of alcoholics quit drinking, yet the drugs are rarely prescribed to patients, researchers reported on Tuesday. The medications, naltrexone and acamprosate, reduce cravings for alcohol by fine-tuning the brain’s chemical reward system. They have been approved for treating alcoholism for over a decade. But questions about their efficacy and a lack of awareness among doctors have resulted in the drugs’ being underused, the researchers said. Less than a third of all people with alcohol problems receive treatment of any kind, and less than 10 percent are prescribed medications. The Affordable Care Act requires that insurers provide coverage for substance abuse treatments and services, and addiction specialists expect to see increases this year in the number of people seeking help for alcoholism. George Koob, the director of the National Institute on Alcohol Abuse and Alcoholism, said the new study should reassure doctors that naltrexone and acamprosate, while not silver bullets, can help many patients. “This is an important paper,” said Dr. Koob, who was not involved in the study. “There are effective medications for the treatment of alcoholism, and it would be great if the world would use them.” In the new study, which was published online on Tuesday in JAMA, the journal of the American Medical Association, a team of researchers based mostly at the University of North Carolina at Chapel Hill compiled findings from the most rigorous trials of medications for alcoholism in the past few decades. Ultimately, they analyzed data on roughly 23,000 people from 122 randomized trials. The researchers focused on a measure known as the “number needed to treat,” an indicator of how many people need to take a pill for one person to be helped. The study found that to prevent one person from returning to drinking, the number needed to treat for acamprosate was 12; for naltrexone, the number was 20. By comparison, large studies of widely used drugs, like the cholesterol-lowering statins, have found that 25 to more than 100 people need treatment to prevent one cardiovascular event. © 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: 19615 - Posted: 05.15.2014

By KATIE THOMAS Almost overnight, a powerful new painkiller has become a $100 million business and a hot Wall Street story. But nearly as quickly, questions are emerging about how the drug is being sold, and to whom. The drug, Subsys, is a form of fentanyl, a narcotic that is often used when painkillers like morphine fail to provide relief. The product was approved in 2012 for a relatively small number of people — cancer patients — but has since become an outsize moneymaker for the obscure company that makes it, Insys Therapeutics. In the last year, the company’s sales have soared and its share price has jumped nearly 270 percent. Behind that business success is an unusual marketing machine that may have pushed Subsys far beyond the use envisioned by the Food and Drug Administration. The F.D.A. approved Subsys only for cancer patients who are already using round-the-clock painkillers, and warned that it should be prescribed only by oncologists and pain specialists. But just 1 percent of prescriptions are written by oncologists, according to data provided by Symphony Health, which analyzes drug trends. About half of the prescriptions were written by pain specialists, and a wide range of doctors prescribed the rest, including general practice physicians, neurologists and even dentists and podiatrists. Interviews with several former Insys sales representatives suggest the company, based in Chandler, Ariz., has aggressively marketed the painkiller, including to physicians who did not treat many cancer patients and by paying its sales force higher commissions for selling higher doses of the drug. Under F.D.A. rules, manufacturers may market prescription drugs only for approved uses. But doctors may prescribe drugs as they see fit. Over the last decade, pharmaceutical companies have paid billions of dollars to settle claims that they encouraged doctors to use drugs for nonapproved treatments, or so-called off-label uses, to increase sales and profits. © 2014 The New York Times Compan

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: 19612 - Posted: 05.15.2014

Victoria Colliver If all traditional cigarette smokers switched to electronic cigarettes, lives would be saved and overall public health would improve, scientists and doctors say. But UCSF researchers, in a paper published Monday, say a growing body of research shows that people who take up e-cigarettes aren't necessarily giving up conventional cigarettes, and on top of that, the devices are being heavily marketed to young people, creating a potential new market for the nicotine and tobacco industry. "Our bottom line is, at the moment, it doesn't seem like e-cigarettes are having a big impact on the population in terms of quitting," said UCSF's Dr. Neal Benowitz, a leading nicotine researcher and a co-author of the scientific review published in Circulation, a journal of the American Heart Association. E-cigarettes, battery-operated devices that vaporize a nicotine solution, have been sold in the U.S. only since the mid-2000s, but their popularity is exploding, particularly among teenagers. The percentage of U.S. middle and high school students who said they've tried e-cigarettes was 3.3 percent in 2011 but rose to 6.8 percent by the following year, according to a survey by the U.S. Centers for Disease Control and Prevention. Health effects unclear Some manufacturers claim the devices help people stop smoking and some users agree, but researchers in the study say that's unclear. The paper cites studies that show people tend to use e-cigarettes with combustible cigarettes, rather than as an alternative. © 2014 Hearst Communications, Inc.

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: 19605 - Posted: 05.13.2014

By Brian Palmer The Journal of Neuroscience recently published a study linking recreational marijuana use to subtle changes in brain structure. The researchers, led by Jodi Gilman of Massachusetts General Hospital, identified increased gray matter density in the left nucleus accumbens and some bordering areas. The study was fine, but the media coverage was abysmal. Reporters overstated the findings, mischaracterized the study, and failed to mention previous research done on pot smoking and health. Goldfish may not have a three-second memory, but some journalists seem to. When a new paper comes out, it’s often treated as the first ever and final word on the topic. There is a significant body of literature on the neurological and wider health effects of marijuana, and to ignore it when covering new studies seems to me a form of journalistic malpractice. A press release from the Society for Neuroscience trumpeted the Gilman study’s importance because it looked at casual users rather than regular pot smokers, who form the basis of most marijuana studies. That claim is dubious in the extreme. The subjects averaged 3.83 days of smoking and 11.2 total joints per week. Characterizing these people as casual pot smokers was a great media hook, but it defied common sense. Occasional users wondered if they’d done permanent damage, and parents were concerned that their teenagers might face profound neurological changes from experimenting with pot. Any reporter who read the study, however, should have known not to take that bait. Even by the standards of past medical studies, it’s a stretch to call these subjects casual pot smokers. © 2014 The Slate Group LLC.

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: 19559 - Posted: 05.03.2014

By MATTHEW PERRONE WASHINGTON (AP) — The Food and Drug Administration announced Friday it will convene a public meeting in October to review the risks of psychiatric and behavioral side effects with Pfizer’s anti-smoking drug Chantix. The agency said in a federal notice it will convene its panel of psychiatric drug experts to discuss the pill’s risks and how to best manage them. Since 2009 Chantix has carried the government’s strongest safety warning — a ‘‘black box’’ label — because of links to hostility, agitation, depression and suicidal thoughts. The warning was added after the FDA received dozens of reports of suicide and hundreds of reports of suicidal behavior among patients taking the smoking-cessation drug. At that time, the FDA also required Pfizer to conduct additional studies to determine the extent of the side effects. A spokeswoman for Pfizer said Friday that the company recently submitted new data to the FDA comparing the drug’s psychiatric safety to placebo and other anti-smoking techniques. The FDA first began investigating potential side effects with Chantix in 2007, the year after the twice-a-day pill hit the market. The drug’s labeling tells patients to stop taking Chantix immediately if they experience agitation, depressed mood, suicidal thinking and other behavioral changes. Doctors are advised to weigh the drug’s risks against its potential benefits in helping patients quit smoking.

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: 19535 - Posted: 04.26.2014

By Brady Dennis, The Food and Drug Administration will for the first time regulate the booming market of electronic cigarettes, as well as cigars, pipe tobacco and hookahs, under a proposal to be released Thursday. The move would begin to place restrictions on e-cigarettes, a nearly $2 billion industry that for years has operated outside the reach of federal regulators. If adopted, the government’s plan would force manufacturers to curb sales to minors, stop handing out free samples, place health warning labels on their products and disclose the ingredients. Makers of e-cigarettes also would be banned from making health-related claims without scientific evidence. The FDA’s proposal stops short of broader restrictions sought by many­ ­tobacco-control advocates. Regulators at this point are not seeking to halt online sales of e-cigarettes, curb television advertising, or ban the use of flavorings such as watermelon, grape soda and piña colada — all tactics that critics say are aimed at attracting young smokers and that have been banned for traditional cigarettes. Those restrictions might come eventually, FDA officials said, but not before more rigorous research can establish a scientific basis for tougher rules. “Right now, for something like e-cigarettes, there are far more questions than answers,” said Mitch Zeller, director of the FDA’s Center for Tobacco Products. Thursday’s action is about expanding FDA’s authority to products that have been “rapidly evolving with no regulation whatsoever,” in order to create a foundation for broader regulation in the future, he said. “It creates the framework. We’re calling this the first step. . . . For the first time, there will be a science-based, independent regulatory agency playing a vital gate-keeping function.” © 1996-2014 The Washington Post

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: 19529 - Posted: 04.24.2014

Muscle weakness from long-term alcoholism may stem from an inability of mitochondria, the powerhouses of cells, to self-repair, according to a study funded by the National Institutes of Health. In research conducted with rats, scientists found evidence that chronic heavy alcohol use affects a gene involved in mitochondrial repair and muscle regeneration. “The finding gives insight into why chronic heavy drinking often saps muscle strength and it could also lead to new targets for medication development,” said Dr. George Koob, director of the National Institute on Alcohol Abuse and Alcoholism, the NIH institute that funded the study. The study is available online in the April issue of the Journal of Cell Biology. It was led by Dr. Gyorgy Hajnoczky, M.D., Ph.D., director of Thomas Jefferson University’s MitoCare Center, Philadelphia, and professor in the Department of Pathology, Anatomy and Cell Biology. Mitochondria are cellular structures that generate most of the energy needed by cells. Skeletal muscle constantly relies on mitochondria for power. When mitochondria become damaged, they can repair themselves through a process called mitochondrial fusion — joining with other mitochondria and exchanging material such as DNA. Although well known in many other tissues, the current study is the first to show that mitochondria in skeletal muscle are capable of undergoing fusion as a repair mechanism. It had been thought that this type of mitochondrial self-repair was unlikely in the packed fibers of the skeletal muscle cells, as mitochondria have little opportunity to interact in the narrow space between the thread-like structures called myofilaments that make up muscle.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 5: The Sensorimotor System
Link ID: 19517 - Posted: 04.22.2014

Associated Press NEW YORK -- A small study of casual marijuana smokers has turned up evidence of changes in the brain, a possible sign of trouble ahead, researchers say. The young adults who volunteered for the study were not dependent on pot, nor did they show any marijuana-related problems. "What we think we are seeing here is a very early indication of what becomes a problem later on with prolonged use," things like lack of focus and impaired judgment, said Dr. Hans Breiter, a study author. Longer-term studies will be needed to see if such brain changes cause any symptoms over time, said Breiter, of the Northwestern University Feinberg School of Medicine and Massachusetts General Hospital. Previous studies have shown mixed results in looking for brain changes from marijuana use, perhaps because of differences in the techniques used, he and others noted in Wednesday's issue of the Journal of Neurosciences. The study is among the first to focus on possible brain effects in recreational pot smokers, said Dr. Nora Volkow, director of the National Institute on Drug Abuse. The federal agency helped pay for the work. She called the work important but preliminary. The 20 pot users in the study, ages 18 to 25, said they smoked marijuana an average of about four days a week, for an average total of about 11 joints. Half of them smoked fewer than six joints a week. Researchers scanned their brains and compared the results with those of 20 nonusers who were matched for age, sex and other traits. The results showed differences in two brain areas associated with emotion and motivation - the amygdala and the nucleus accumbens. Users showed higher density than nonusers, as well as differences in shape of those areas. Both differences were more pronounced in those who reported smoking more marijuana. © 2014 Hearst Communications, Inc.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 19491 - Posted: 04.16.2014

By CATHERINE SAINT LOUIS Doctors are prescribing opioid painkillers to pregnant women in astonishing numbers, new research shows, despite the fact that risks to the developing fetus are largely unknown. Of 1.1 million pregnant women enrolled in Medicaid nationally, nearly 23 percent filled an opioid prescription in 2007, up from 18.5 percent in 2000, according to a study published last week in Obstetrics and Gynecology, the largest to date of opioid prescriptions among pregnant women. Medicaid covers the medical expenses for 45 percent of births in the United States. The lead author, Rishi J. Desai, a research fellow at Brigham and Women’s Hospital, said he had expected to “see some increase in trend, but not this magnitude.” “One in five women using opioids during pregnancy is definitely surprising,” he said. In February, a study of 500,000 privately insured women found that 14 percent were dispensed opioid painkillers at least once during pregnancy. From 2005 to 2011, the percentage of pregnant women prescribed opioids decreased slightly, but the figure exceeded 12 percent in any given year, according to Dr. Brian T. Bateman, an anesthesiologist at Massachusetts General Hospital, and his colleagues. Their research was published in Anesthesiology. Dr. Joshua A. Copel, a professor of obstetrics, gynecology and reproductive sciences at Yale School of Medicine in New Haven, Conn., said he was taken aback by the findings, which come even as conscientious mothers-to-be increasingly view pregnancy as a time to skip caffeine, sushi and even cold cuts. “To hear that there’s such a high use of narcotics in pregnancy when I see so many women who worry about a cup of coffee seems incongruous,” he said. In both studies, the opioids most prescribed during pregnancy were codeine and hydrocodone. Oxycodone was among the top four. Women usually took the drugs for a week or less; however, just over 2 percent of women in both studies took them for longer periods. © 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: 19483 - Posted: 04.14.2014

By GRETCHEN REYNOLDS It’s possible that some of us are born not to run. According to an eye-opening new genetics study of lab rats, published in The Journal of Physiology, the motivation to exercise — or not — may be at least partly inherited. For years, scientists have been bedeviled by the question of why so few people regularly exercise when we know that we should. There are obvious reasons, including poor health and jammed schedules. But researchers have begun to speculate that genetics might also play a role, as some recent experiments suggest. In one, published last year, sets of fraternal and identical adult twins wore activity monitors to track their movements. The results indicated that the twins were more alike in their exercise habits than a shared upbringing alone would explain. Their willingness to work out or sit all day depended to a large extent on genetics, the researchers concluded. But which genes might be involved and how any differences in the activity of those genes might play out inside the body were mysteries. So scientists at the University of Missouri recently decided to delve into those issues by creating their own avid- or anti-exercising animals. They accomplished this task by inter-breeding normal rats that had voluntarily run on wheels in the lab. The male rats that had run the most were bred with the female rats that also had run the most; those that had run the least were likewise mated. This scheme continued through many generations, until the scientists had two distinct groups of rats, some of which would willingly spend hours on running wheels, while the others would skitter on them only briefly, if at all. In their first experiments with these rats, the researchers found some intriguing differences in the activity of certain genes in their brains. In normal circumstances, these genes create proteins that tell young cells to grow up and join the working world. But if the genes don’t function normally, the cells don’t receive the necessary chemical messages and remain in a prolonged, feckless cellular adolescence. Such immature cells cannot join the neural network and don’t contribute to healthy brain function. © 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: 19470 - Posted: 04.10.2014