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Janet Raloff WASHINGTON ― Many people have turned to electronic cigarettes in hopes of avoiding the heart and cancer risks associated with smoking conventional tobacco products. But vaping appears far from benign, a trio of toxicologists reported February 11 and 12 at the American Association for the Advancement of Science annual meeting. If used as a means to totally wean people off of tobacco products, then e-cigarettes might have value, concedes Ilona Jaspers of the University of North Carolina at Chapel Hill. But she’s not sure. Unpublished data that she and the others presented at the meeting link e-cig products to a host of new risks. So vaping may not eliminate risks associated with conventional smoking, Jaspers maintains ― “and may actually be introducing new ones.” Her group examined scraped cells from the noses of otherwise healthy people who had a history of smoking, vaping or doing neither. The researchers then measured the activity levels in these cells of 594 genes associated with the body’s ability to fight infections. Among smokers, the activity of 53 genes was substantially diminished, compared with people who neither smoked nor vaped. Among vapers, those same 53 genes showed significantly diminished activity, Jaspers reported, as did 305 more. The normal role of these genes would suggest that the lung tissue as well as nasal tissue of smokers ― and especially vapers ―“may be more susceptible to any kind of infection.” © Society for Science & the Public 2000 - 2016.

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: 21889 - Posted: 02.13.2016

By Dwayne Godwin, Jorge Cham Drugs and other stimuli hijack dopamine signaling in the brain, causing changes that can lead to addiction © 2016 Scientific America

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: 21845 - Posted: 02.02.2016

Jim Pfaus Self-labeled sex addicts often speak about their identities very clinically, as if they’re paralyzed by a scientific condition that functions the same way as drug and alcohol addiction. But sex and porn “addiction” are NOT the same as alcoholism or a cocaine habit. In fact, hypersexuality and porn obsessions are not addictions at all. They’re not included in the Diagnostic and Statistical Manual of Mental Disorders (DSM), and by definition, they don’t constitute what most researchers understand to be addiction. Here’s why: addicts withdraw. When you lock a dope fiend in a room without any dope, the lack of drugs will cause an immediate physiological response — some of which is visible, some of which we can only track from within the body. During withdrawal, the brains of addicts create junctions between nerve cells containing the neurotransmitter GABA. This process more or less inhibits the brain systems usually excited by drug-related cues — something we never see in the brains of so-called sex and porn addicts. A sex addict without sex is much more like a teenager without their smartphone. Imagine a kid playing Angry Birds. He seems obsessed, but once the game is off and it’s time for dinner, he unplugs. He might wish he was still playing, but he doesn’t get the shakes at the dinner table. There’s nothing going on in his brain that creates an uncontrollable imbalance.

Related chapters from BP7e: Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21827 - Posted: 01.27.2016

By Emily Underwood In 2008, in El Cajon, California, 30-year-old John Nicholas Gunther bludgeoned his mother to death with a metal pipe, and then stole $1378 in cash, her credit cards, a DVD/VCR player, and some prescription painkillers. At trial, Gunther admitted to the killing, but argued that his conviction should be reduced to second-degree murder because he had not acted with premeditation. A clinical psychologist and neuropsychologist testified that two previous head traumas—one the result of an assault, the other from a drug overdose—had damaged his brain’s frontal lobes, potentially reducing Gunther’s ability to plan the murder, and causing him to act impulsively. The jury didn’t buy Gunther’s defense, however; based on other evidence, such as the fact that Gunther had previously talked about killing his mother with friends, the court concluded that he was guilty of first-degree murder, and gave him a 25-years-to-life prison sentence. Gunther’s case represents a growing trend, a new analysis suggests. Between 2005 and 2012, more than 1585 U.S. published judicial opinions describe the use of neurobiological evidence by criminal defendants to shore up their defense, according to a study published last week in the Journal of Law and the Biosciences by legal scholar Nita Farahany of Duke University in Durham, North Carolina, and colleagues. In 2012 alone, for example, more than 250 opinions cited defendants’ arguments that their “brains made them do it”—more than double the number of similar claims made in 2007. © 2016 American Association for the Advancement of Science

Related chapters from BP7e: Chapter 1: Biological Psychology: Scope and Outlook; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 21816 - Posted: 01.23.2016

By Emily Underwood Roughly half of Americans use marijuana at some point in their lives, and many start as teenagers. Although some studies suggest the drug could harm the maturing adolescent brain, the true risk is controversial. Now, in the first study of its kind, scientists have analyzed long-term marijuana use in teens, comparing IQ changes in twin siblings who either used or abstained from marijuana for 10 years. After taking environmental factors into account, the scientists found no measurable link between marijuana use and lower IQ. “This is a very well-conducted study … and a welcome addition to the literature,” says Valerie Curran, a psychopharmacologist at the University College London. She and her colleagues reached “broadly the same conclusions” in a separate, nontwin study of more than2000 British teenagers, published earlier this month in the Journal of Psychopharmacology, she says. But, warning that the study has important limitations, George Patton, a psychiatric epidemiologist at the University of Melbourne in Australia, adds that it in no way proves that marijuana—particularly heavy, or chronic use —is safe for teenagers. Most studies that linked marijuana to cognitive deficits, such as memory loss and low IQ, looked at a single “snapshot” in time, says statistician Nicholas Jackson of the University of Southern California in Los Angeles, lead author of the new work. That makes it impossible to tell which came first: drug use or poor cognitive performance. “It's a classic chicken-egg scenario,” he says. © 2016 American Association for the Advancement of Science.

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: 21800 - Posted: 01.19.2016

By Melinda Beck Here’s a sobering thought for the holidays: Chronic heavy drinking can cause insidious damage to the brain, even in people who never seem intoxicated or obviously addicted. Experts say alcohol-related brain damage is underdiagnosed and often confused with Alzheimer’s disease, other forms of dementia or just getting older. Now, brain imaging is revealing how long-term alcohol abuse can change the structure of the brain, shrinking gray-matter cells in areas that govern learning, memory, decision-making and social behavior, as well as damaging white-matter fibers that connect one part of the brain with others. “As we get older, we all lose a little gray-matter volume and white-matter integrity, but in alcoholics, those areas break down more quickly. It looks like accelerated aging,” says Edith Sullivan, a professor of psychiatry and behavioral science at Stanford University, who has studied alcohol’s effects for years. Long-term alcohol abuse also changes how the brain regulates emotion and anxiety and disrupts sleep systems, creating wide-ranging effects on the body. Increasingly, clinicians are diagnosing “alcohol-induced neurocognitive disorder” and “alcohol-related dementia.” How much is too much and over what period of time? ©2016 Dow Jones & Company, 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: 21794 - Posted: 01.18.2016

Angus Chen A new method of delivering medication for opioid addicts gained approval from a Food and Drug Administration advisory panel this week. It's a matchstick-like insert designed to slip under the skin and release a drug over a period of months. Some physicians say the implant will be a useful addition to the currently short lineup of medication-assisted treatment options. The rod is called Probuphine, developed by the companies Braeburn Pharmaceuticals and Titan Pharmaceuticals. It contains a medication called buprenorphine which the FDA approved for opioid addiction in 2002 and is currently widely in use. The FDA typically follows the advice of its advisory panels on approvals. This molecule binds to opioid receptors in the body, but doesn't hit them as hard as something like heroin or morphine would. So it can reduce cravings without giving a full high. It's often taken in combination with a medication called naloxone, which negates the effect of any additional opiates and acts as an antidote for overdoses. Right now, patients must hold a tablet or a film under their tongue or in their cheek until it dissolves every day. This gives a long-lasting implant a few advantages over oral daily doses. Probuphine lasts up to six months. So unless patients want to dig underneath their skin to tear the thing out, there's no deviating from the treatment. "With the Suboxone [a daily combination of buprenorphine and naloxone], you can go on these drug holidays," says Patrick Kennedy, a former congressman and former opiate addict who urged the panel to approve Probuphine. "If I knew I had access to another drug, OxyContin, I would just stop taking the Suboxone and — you know." © 2016 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: 21790 - Posted: 01.16.2016

By SABRINA TAVERNISE SILVER SPRING, Md. — A panel of medical experts recommended Tuesday that the Food and Drug Administration approve a new way of treating opioid addicts, using a slender rod implanted into the arm that delivers medicine for months at a time. Some doctors say it could help ease the national epidemic of drug overdoses. The rod is about the size of a small matchstick and delivers daily doses of buprenorphine — one of the most common medical treatments for opioid addicts — for six-month periods. In controlled doses, buprenorphine can help the body withdraw from opioid addiction, but can also itself be addictive. That risk is increased by the fact that the medicine can be taken only by mouth, requiring patients, often ill from addiction, to manage their daily dosages. The advisory panel voted 12 to 5 to recommend approval. The panel concluded that flaws in the evidence the company presented, including missing data in a clinical study, were not fatal, and that the product was roughly as effective as the oral form of the drug. They agreed it would be a useful tool for doctors in the face of a major public health epidemic and could help stem the flow of illicit use of buprenorphine. “I think this will save some folks’ lives,” said Dr. David Pickar, adjunct professor of psychiatry at Johns Hopkins Medical School, who voted to recommend approval. “From a safety point of view I think we’re in good shape.” Dr. Thomas Grieger, a staff psychiatrist at the Maryland Department of Health and Mental Hygiene, said: “There is not evidence of significant risk using this agent, but there is evidence of significant benefit.” © 2016 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: 21783 - Posted: 01.13.2016

When Jack O'Connor was 19, he was so desperate to beat his addictions to alcohol and opioids that he took a really rash step. He joined the Marines. "This will fix me," O'Connor thought as he went to boot camp. "It better fix me or I'm screwed." After 13 weeks of sobriety and exercise and discipline, O'Connor completed basic training, but he started using again immediately. "Same thing," he says. "Percocet, like, off the street. Pills." Percocet is the brand name for acetaminophen and oxycodone. Oxycodone is a powerful opioid. It's one of the most commonly prescribed painkillers, and is a key factor in one of the country's most pressing public health problems — an opioid addiction epidemic. It is a crisis that started, in part, from the over-prescription of painkillers, like Percocet, and then shifted to heroin, as people addicted to prescription drugs looked for a cheaper high. O'Connor is one of an estimated 2.5 million Americans addicted to opioids and heroin, according to the National Institute on Drug Abuse. Over three years, he detoxed from prescription painkillers — and heroin — more than 20 times. Each time, he started using again. So why is it so hard for opioid addicts to quit? You can boil it down to two crucial bits of science: the powerful nature of opioids and the neuroscience behind how addiction hijacks the brain. "The first recording of opioid use was 5,000 years ago," says Dr. Seddon Savage, an addiction and pain specialist at Dartmouth College. It was "a picture of the opium poppy and the words 'the joy plant.' "

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: 21773 - Posted: 01.11.2016

By ALAN SCHWARZ DELRAY BEACH, Fla. — Three shaky months into recovery from heroin addiction, Dariya Pankova found something to ease her withdrawal. A local nonalcoholic bar sold a brewed beverage that soothed her brain and body much as narcotics had. A perfect solution — before it backfired. Ms. Pankova grew addicted to the beverage itself. She drank more and more, awakened her cravings for the stronger high of heroin, and relapsed. Only during another stay in rehab did Ms. Pankova learn that the drink’s primary ingredient, a Southeast Asian leaf called kratom, affects the brain like an opiate and can be addictive, too. “It’s preying on the weak and the broken,” said Ms. Pankova, 23, a Brooklyn native who received treatment in Delray Beach. “It’s a mind-altering substance, so people like me who are addicts and alcoholics, they think just because it’s legal, it’s fine. It’s a huge epidemic down here, and it’s causing a lot of relapses.” Some users embrace kratom as a natural painkiller and benign substitute for more dangerous substances that, in most states, is legal. But its growing popularity and easy availability are raising concerns among substance abuse experts and government officials who say it is being furtively marketed as a way out of addiction, even though it is itself addictive. Worse, some of those experts say, kratom can lead some addicts back to heroin, which is cheaper and stronger. “It’s a fascinating drug, but we need to know a lot more about it,” said Dr. Edward W. Boyer, a professor of emergency medicine at the University of Massachusetts Medical School and a co-author of several scientific articles on kratom. “Recreationally or to self-treat opioid dependence, beware — potentially you’re at just as much risk” as with an opiate. Concern is particularly high in South Florida, where a rising concentration of drug-treatment providers has coincided with the sprouting of kratom bars. But kratom is now available around the country. © 2016 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: 21747 - Posted: 01.04.2016

Laura Sanders People who use especially potent pot show signs of damage in a key part of their brain. The results, reported online November 27 in Psychological Medicine, are limited, though: The small brain scanning study doesn’t show that marijuana caused the brain abnormality — only that the two go hand-in-hand. But the findings suggest that potency matters, says study coauthor Tiago Reis Marques, a psychiatrist at King’s College London. “We are no longer talking about smoking cannabis or not smoking cannabis,” Reis Marques says. Just as vodka packs more of a punch than beer, a high-potency toke delivers much more of the psychoactive substance tetrahydrocannabinol, or THC. A bigger dose of THC may have stronger effects on the brain, Reis Marques says. That’s important because as marijuana plant breeders perfect their products, THC levels have soared. Samples sold in Colorado, for instance, now have about three times as much THC as plants grown 30 years ago, a recent survey found (SN Online: 3/24/15). Reis Marques and his colleagues scanned the brains of 43 healthy people, about half of whom use cannabis. The researchers used a method called diffusion tensor imaging to study the structure of the brain’s white matter, neural highways that carry messages between brain areas. Participants gave a detailed history of their past drug use, including information about how potent their marijuana was. POT HEAD The corpus callosum — white matter that links the left brain to the right — is weaker in people who smoke high-potency cannabis, a new study suggests. © Society for Science & the Public 2000 - 2015.

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: 21679 - Posted: 12.08.2015

Some people may have a get-out clause when it comes to giving up cigarettes. A third of white people who smoke have gene variations that make it harder for them to kick the habit. A gene called ANKK1 regulates the release of dopamine – a chemical involved in the brain’s reward centres. Ming Li and colleagues at the Zhejiang University School of Medicine in Hangzhou, China, wondered whether variations of this gene might affect people’s ability to give up cigarettes. So his team analysed 23 studies that have linked ANKK1 to smoking, involving more than 11,000 participants in total. Across the board, there was no significant link between successful quitting and the gene variants. But when they looked at just the studies that analysed white people, the results were striking. About two-thirds of white smokers carried a variation of the gene called A2/A2. These people were about 22 per cent more likely to be able to quit smoking than those who carried an alternative version of the gene, either A1/A1 or A1/A2. The A1/A1 and A1/A2 gene variations have previously been linked to obesity and drug addiction, which suggests they may predispose people to addictive behaviours. People carrying these versions of ANKK1 may need more aggressive strategies to fight their addiction to cigarettes, says Li. It is not clear whether the gene has the same effect for non-white people, he says. More studies that involve non-white people will be necessary to investigate this. © Copyright Reed Business Information Ltd.

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: 21672 - Posted: 12.03.2015

Ian Sample Science editor High-strength cannabis may damage nerve fibres that handle the flow of messages across the two halves of the brain, scientists claim. Brain scans of people who regularly smoked strong skunk-like cannabis revealed subtle differences in the white matter that connects the left and right hemispheres and carries signals from one side of the brain to the other. The changes were not seen in those who never used cannabis or smoked only the less potent forms of the drug, the researchers found. The study is thought to be the first to look at the effects of cannabis potency on brain structure, and suggests that greater use of skunk may cause more damage to the corpus callosum, making communications across the brain’s hemispheres less efficient. Paola Dazzan, a neurobiologist at the Institute of Psychiatry at King’s College London, said the effects appeared to be linked to the level of active ingredient, tetrahydrocannabinol (THC), in cannabis. While traditional forms of cannabis contain 2 to 4 % THC, the more potent varieties (of which there are about 100), can contain 10 to 14% THC, according to the DrugScope charity. “If you look at the corpus callosum, what we’re seeing is a significant difference in the white matter between those who use high potency cannabis and those who never use the drug, or use the low-potency drug,” said Dazzan. The corpus callosum is rich in cannabinoid receptors, on which the THC chemical acts. © 2015 Guardian News and Media Limited

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: 21665 - Posted: 11.28.2015

By Lenny Bernstein BALTIMORE — Deep into a three-day heroin binge at a local hotel, Samantha told the newbie he was shooting too much. He wasn’t accustomed to heroin, she said, and hadn’t waited long enough since his last injection. “But he didn’t listen,” she said. Sure enough, he emerged from a visit to the bathroom, eyes glazed, and collapsed from an overdose. Samantha, who declined to give her last name to avoid trouble with her bosses at a nearby strip club, said she grabbed her naloxone, the fast-acting antidote to opioid overdoses. She was too panicked to place the atomizer on the end of the syringe, but her boyfriend wasn’t. He sprayed the mist into the nose of the unconscious drug user, who awoke minutes later. “I always have it because I’m scared to death,” said Samantha, who said she has been shooting heroin for 22 years. “I don’t want to be helpless.” As the opioid epidemic has exploded in small towns and suburbs in recent years, officials have scrambled to put naloxone in the hands of drug users’ families and friends, and to make it more widely available by equipping police officers with the drug. At the same time, thousands of lives are being saved by giving the antidote to drug users. More than 80 percent of overdose victims revived by “laypeople” were rescued by other users, most of them in the past few years, according to one national survey published in June.

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: 21654 - Posted: 11.24.2015

by Bethany Brookshire Many people perceive cocaine as one of the most intense stimulant drugs available: It’s illegal, highly addictive and dangerous. Caffeine, in contrast, is the kinder, cuddlier stimulant. It’s legal, has mild effects and in forms such as coffee, it might even be good for your health. But caffeine in combination with cocaine is another story. In South America, drug distributors have started “cutting” their cocaine with caffeine. This cheaper substitute might, at first glance, seem to make the cocaine less potent. After all, there’s less of the drug there. But new data shows that when combined, cocaine and caffeine make a heck of a drug. Coca paste is a popular form of cocaine in South American countries. A smoked form of cocaine, coca paste is the intermediate product in the extraction process used to get pure cocaine out of coca leaves. Because it is smoked, the cocaine in the coca paste hits the brain very quickly, making the drug highly addictive, explains Jose Prieto, a neurochemist at the Biological Research Institute Clemente Stable in Montevideo, Uruguay. Much of the time, Coca paste isn’t acting alone, however. In a 2011 study published in Behavioral Brain Research, Prieto and his colleagues examined the contents of coca paste from police seizures. “Nearly 80 percent of the coca paste samples” were adulterated, Prieto says, “most with caffeine.” Caffeine adulteration ranged from 1 to 15 percent of the drug volume. © 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: 21643 - Posted: 11.18.2015

by Teresa Shipley Feldhausen The benefits of drinking coffee continue to filter in. An analysis of more than 200,000 medical professionals followed for nearly 30 years finds that drinking up to five cups of coffee a day is associated with reduced risk of dying early from heart and brain diseases as well as suicide. The study’s results were adjusted for factors like smoking, weight and diet. Benefits were more pronounced for those who had never smoked, an international team of researchers report November 16 in Circulation. Both caffeinated and decaf java had positive effects, leading the researchers to speculate that coffee’s potency as a health elixir may stem from chemical compounds in the bean such as diterpenes and chlorogenic acids. © 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: 21634 - Posted: 11.17.2015

By Jason G. Goldman When a monkey has the sniffles or a headache, it doesn't have the luxury of popping a few painkillers from the medicine cabinet. So how does it deal with the common colds and coughs of the wildlife world? University of Georgia ecologist Ria R. Ghai and her colleagues observed a troop of more than 100 red colobus monkeys in Uganda's Kibale National Park for four years to figure out whether the rain forest provides a Tylenol equivalent. Monkeys infected with a whipworm parasite were found to spend more time resting and less time moving, grooming and having sex. The infected monkeys also ate twice as much tree bark as their healthy counterparts even though they kept the same feeding schedules. The findings were published in September in the journal Proceedings of the Royal Society B. The fibrous snack could help literally sweep the intestinal intruder out of the simians' gastrointestinal tracts, but Ghai suspects a more convincing reason. Seven of the nine species of trees and shrubs preferred by sick monkeys have known pharmacological properties, such as antisepsis and analgesia. Thus, the monkeys could have been self-medicating, although she cannot rule out other possibilities. The sick individuals were, however, using the very same plants that local people use to treat illnesses, including infection by whipworm parasites. And that “just doesn't seem like a coincidence,” Ghai says. © 2015 Scientific American,

Related chapters from BP7e: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 5: The Sensorimotor System
Link ID: 21619 - Posted: 11.10.2015

by Bethany Brookshire Cheese is a delicious invention. But if you saw the news last week, you might think it’s on its way to being classified as a Schedule II drug. Headlines proclaimed “Say cheese? All the time? Maybe you have an addiction,” “Cheese really is crack” and “Your cheese addiction is real.” Under the headlines, the stories referred to a study examining the addictive properties of various foods. Pizza was at the top. The reason? The addictive properties of cheese, which the articles claim contains “dangerous” opiate-like chemicals called casomorphins. But you can’t explain away your affinity for cheese by saying you’re addicted. The study in those stories, published earlier this year in PLOS ONE, did investigate which foods are most associated with addictive-like eating behaviors. Pizza did come out on top in one experiment. But the scientists who did the research say this has little to do with the delicious dairy products involved. Instead, they argue, the foods we crave the most are those processed to have high levels of sugars and fat, and it’s these ingredients that leave us coming back for another slice. The cheese? “I was horrified by the misstatements and the oversimplifications … and the statements about how it’s an excuse to overeat,” says Ashley Gearhardt of the University of Michigan in Ann Arbor, who led the study. “Liking is not the same as addiction. We like lots of things. I like hip-hop music and sunshine and my wiener dog, but I’m not addicted to her. I eat cheese every day. That’s doesn’t mean you’re addicted or it has addictive potential.” © 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: 21592 - Posted: 11.02.2015

By KATHARINE Q. SEELYE NEWTON, N.H. — When Courtney Griffin was using heroin, she lied, disappeared, and stole from her parents to support her $400-a-day habit. Her family paid her debts, never filed a police report and kept her addiction secret — until she was found dead last year of an overdose. At Courtney’s funeral, they decided to acknowledge the reality that redefined their lives: Their bright, beautiful daughter, just 20, who played the French horn in high school and dreamed of living in Hawaii, had been kicked out of the Marines for drugs. Eventually, she overdosed at her boyfriend’s grandmother’s house, where she died alone. “When I was a kid, junkies were the worst,” Doug Griffin, 63, Courtney’s father, recalled in their comfortable home here in southeastern New Hampshire. “I used to have an office in New York City. I saw them.” When the nation’s long-running war against drugs was defined by the crack epidemic and based in poor, predominantly black urban areas, the public response was defined by zero tolerance and stiff prison sentences. But today’s heroin crisis is different. While heroin use has climbed among all demographic groups, it has skyrocketed among whites; nearly 90 percent of those who tried heroin for the first time in the last decade were white. And the growing army of families of those lost to heroin — many of them in the suburbs and small towns — are now using their influence, anger and grief to cushion the country’s approach to drugs, from altering the language around addiction to prodding government to treat it not as a crime, but as a disease. © 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: 21583 - Posted: 10.31.2015

By Dina Fine Maron When powerful street drugs collectively known as synthetic pot are smoked, the resulting high mimics the effects of marijuana. Yet these man-made cannabinoids are not marijuana at all. The drugs, more commonly called spice, fake weed or K2, are made up of any number of dried, shredded plants sprayed with chemicals that live in a murky legality zone. They are highly dangerous—and their use is on the rise. Synthetic pot, which first hit the market in the early 2000s, has especially caught the attention of public health officials in the past couple of years, stemming from a surge in hospitalizations and violent episodes. Although the drugs act on the same brain pathway as weed's active ingredient, they can trigger harsher reactions, including heart attacks, strokes, kidney damage and delusions. Between June and early August usage of these drugs led to roughly 2,300 emergency room visits in New York State alone. Nationwide more than 6,000 incidents involving spice have been reported to U.S. poison-control centers this year—about double the number of calls in 2013. Ever changing recipes make it possible for spice sellers to elude the authorities. Each time an ingredient is banned, producers swap in another compound. The drugs are then sold on the Internet or at gas stations and convenience stores at prices lower than genuine marijuana. The changing formulations also pose a challenge for researchers trying to match the chemicals with their side effects or to develop tests to identify them in a user's system. “The drugs are present in blood for only a short period, so it's very difficult to detect them,” says Marilyn Huestis, chief of the Chemistry and Drug Metabolism Section at the National Institute on Drug Abuse. © 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: 21570 - Posted: 10.27.2015