Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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by Jennifer Couzin-Frankel Publish your data, or else we will—that's the stark warning to drug companies in a new proposal released today. Peter Doshi (shown right), a postdoctoral fellow at Johns Hopkins University in Baltimore, Maryland, and his colleagues are fed up that only about half of all clinical trials are published. They want to change that, by convincing researchers and journals to print data that have been publicly released through other means, such as litigation and Freedom of Information Act requests, but, practically speaking, are sitting dormant in the filing cabinets or computers of individual scientists. The unusual proposal is called RIAT, for Restoring Invisible and Abandoned Trials. It was published today in BMJ and also endorsed by PLOS Medicine. Doshi, who studies comparative effectiveness research, came up with the idea when his colleague, Swaroop Vedula, was analyzing reporting biases involving the drug gabapentin. Gabapentin's maker Pfizer had been sued for the way in which they marketed the drug for unapproved indications. During litigation, Pfizer had released thousands of pages involving gabapentin trials, and Vedula was poring through them. (One of the authors of the RIAT paper, Kay Dickersin, served as an expert witness against Pfizer in gabapentin litigation.) Pfizer had published only 12 of its 20 trials in gabapentin. But Doshi's center at Hopkins had the clinical study reports detailing the results of the other eight. At the time, "it just hits me," Doshi says. "Why are we still referring to these as unpublished trials? Why aren't we publishing them ourselves?" © 2010 American Association for the Advancement of Science
By LIZ ALDERMAN PARIS — On a recent day in the shadow of the Arc de Triomphe, a line of 20 people spilled onto the sidewalk of a trendy new boutique, eager to get a taste of its latest gourmet offerings. A sign in the window promoted piña colada as the store’s flavor of the month. A woman wearing a Chanel jacket said she wanted to try peach. But this was no temple of gastronomy. It was one of scores of electronic cigarette shops that have been springing up by the week in Paris as well as in numerous cities across Europe and the United States. Inside the ClopiNette boutique, shoppers can choose from among more than 60 flavors of nicotine liquid — including Marlboro and Lucky Strike flavors — all in varying strengths and arranged in color-coded rows. (ClopiNette is a play on “clope,” French slang for a cigarette.) “It’s like visiting a Nespresso store,” said Anne Stephan, a lawyer specializing in health issues at a nearby law firm. What’s driving her into the store is a desire shared by many: they want to give up smoking tobacco but don’t want to kick the smoking habit. After smoking 20 cigarettes daily for 25 years and failing to quit, Ms. Stephan said she had cut down to one a day in the three months since she began puffing on a so-called e-cig. Using technology that turns nicotine-infused propylene glycol into an inhalable vapor, e-cigarettes smoke almost like the real thing, without the ashtray odor. © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18270 - Posted: 06.13.2013
by Satoshi Kanazawa in The Scientific Fundamentalist Drinking alcohol is evolutionarily novel, so the Hypothesis would predict that more intelligent people drink more alcohol than less intelligent people. The human consumption of alcohol probably originates from frugivory (consumption of fruits). Fermentation of sugars by yeast naturally present in overripe and decaying fruits produces ethanol, known to intoxicate birds and mammals. However, the amount of ethanol alcohol in such fruits ranges from trace to 5%, roughly comparable to light beer. (And you can't really get drunk on light beer.) It is nothing compared to the amount of alcohol present in regular beer (4-6%), wine (12-15%), and distilled spirits (20-95%). Human consumption of alcohol, however, was unintentional, accidental, and haphazard until about 10,000 years ago. The intentional fermentation of fruits and grain to yield ethanol arose only recently in human history. The production of beer, which relies on a large amount of grain, and that of wine, which similarly requires a large amount of grapes, could not have taken place before the advent of agriculture around 8,000 BC and the consequent agricultural surplus. Archeological evidence dates the production of beer and wine to Mesopotamia at about 6,000 BC. The origin of distilled spirits is far more recent, and is traced to Middle East or China at about 700 AD. The word alcohol - al kohl - is Arabic in origin, like many other words that begin with "al," like algebra, algorithm, alchemy, and Al Gore. Human experience with concentrations of ethanol higher than 5% that is attained by decaying fruits is therefore very recent. © Copyright 2002-2013 Sussex Directories, Inc.
By Scicurious When I am stressed (and I’m stressed a lot of the time, as I bet a lot of you are as well), I turn to coffee. Not just to keep me going through the time when I need to get things done, but also for relaxation. For me, the smell and taste of coffee brings me thoughts of relaxing conversations with friends and other fun times. But what if the memories weren’t all the relaxing the caffeine was doing for me? What if the chronic caffeine consumption was keeping my stressful life at bay? It’s time to look at adenosine 2A receptors in the hippocampus. Don’t worry, the coffee will be back. First let’s talk about stress. Specifically, childhood stress. In small doses, stress exposure can actually be good for you, but in large, or prolonged, doses, it’s definitely not. There are effects immediately after stress, as well as long term ones. when you suffer strong stressors in development, you can end up with changes all the way into adulthood, from cognitive deficits to predisposition to psychiatric disorders. Why is stress in development so important? During development, our brains are developing too, particularly our hippocampus. While the hippocampus is best known for its role in memory and spatial navigation, it’s also extremely important in emotional responses. Neuronal growth in the hippocampus can come from enriched environments or chronic antidepressants, and death of those neurons can come from chronic stress. Chronic stress also disrupts the hypothalamic-pituitary-adrenal axis (the HPA axis) And that’s just in adults! During development, animals are very susceptible to stress, and the hippocampus is still developing its connections. And we’re still figuring out what changes occur during early life stress and how they relate to behaviors in adulthood. © 2013 Scientific American
By GRETCHEN REYNOLDS For thousands of years, coffee has been one of the two or three most popular beverages on earth. But it’s only recently that scientists are figuring out that the drink has notable health benefits. In one large-scale epidemiological study from last year, researchers primarily at the National Cancer Institute parsed health information from more than 400,000 volunteers, ages 50 to 71, who were free of major diseases at the study’s start in 1995. By 2008, more than 50,000 of the participants had died. But men who reported drinking two or three cups of coffee a day were 10 percent less likely to have died than those who didn’t drink coffee, while women drinking the same amount had 13 percent less risk of dying during the study. It’s not clear exactly what coffee had to do with their longevity, but the correlation is striking. Other recent studies have linked moderate coffee drinking — the equivalent of three or four 5-ounce cups of coffee a day or a single venti-size Starbucks — with more specific advantages: a reduction in the risk of developing Type 2 diabetes, basal cell carcinoma (the most common skin cancer), prostate cancer, oral cancer and breast cancer recurrence. Perhaps most consequential, animal experiments show that caffeine may reshape the biochemical environment inside our brains in ways that could stave off dementia. In a 2012 experiment at the University of Illinois at Urbana-Champaign, mice were briefly starved of oxygen, causing them to lose the ability to form memories. Half of the mice received a dose of caffeine that was the equivalent of several cups of coffee. After they were reoxygenated, the caffeinated mice regained their ability to form new memories 33 percent faster than the uncaffeinated. Close examination of the animals’ brain tissue showed that the caffeine disrupted the action of adenosine, a substance inside cells that usually provides energy, but can become destructive if it leaks out when the cells are injured or under stress. The escaped adenosine can jump-start a biochemical cascade leading to inflammation, which can disrupt the function of neurons, and potentially contribute to neurodegeneration or, in other words, dementia. Copyright 2013 The New York Times Company
By Stuart McMillen A classic experiment into drug addiction science. Would rats choose to take drugs if given a stimulating environment and social company?
Sally Satel From the recent announcement of President Obama's BRAIN Initiative to the Technicolor brain scans ("This is your brain on God/love/envy etc") on magazine covers all around, neuroscience has captured the public imagination like never before. Understanding the brain is of course essential to developing treatments for devastating illnesses like schizophrenia and Parkinson's. More abstract but no less compelling, the functioning of the brain is intimately tied to our sense of self, our identity, our memories and aspirations. But the excitement to explore the brain has spawned a new fixation that my colleague Scott Lilienfeld and I call neurocentrism -- the view that human behavior can be best explained by looking solely or primarily at the brain. The critical question, though, is whether this neural disruption proves that the addict's behavior is involuntary, and that he is incapable of self-control. It does not. Sometimes the neural level of explanation is appropriate. When scientists develop diagnostic tests or a medications for, say, Alzheimer's disease, they investigate the hallmarks of the condition: amyloid plaques that disrupt communication between neurons, and neurofibrillary tangles that degrade them. Other times, a neural explanation can lead us astray. In my own field of addiction psychiatry, neurocentrism is ascendant -- and not for the better. Thanks to heavy promotion by the National Institute on Drug Abuse, part of the National Institutes of Health, addiction has been labeled a "brain disease." © 2013 by The Atlantic Monthly Group.
Keyword: Drug Abuse
Link ID: 18213 - Posted: 06.01.2013
By ALAN SCHWARZ An analysis published Wednesday by the American Medical Association said children with attention deficit hyperactivity disorder who take stimulant medication do not have a lower risk over all for later substance abuse, contradicting the longstanding and influential message that such medicines tend to deter those with the disorder from abusing other substances. The paper, written by three researchers at the University of California, Los Angeles, examined data from 15 previous studies on the subject and determined that, on average, medications like Adderall and Ritalin had no effect one way or the other on whether children abused alcohol, marijuana, nicotine or cocaine later in life. A 2003 study in the journal Pediatrics had concluded that the introduction of stimulant medication to children with A.D.H.D. reduced the risk of such abuse later in life, a finding that has been repeated by doctors and pharmaceutical companies not only to assuage parents’ fears of medication but also to suggest that the pills would protect their children from later harm. “I always doubted the whole ‘protection’ argument, and I wasn’t the only one, but that message was really out there,” said Liz Jorgensen, an adolescent addiction specialist at Insight Counseling in Ridgefield, Conn. “Hopefully, this message will be heard loud and clear.” The study comes amid growing concern about the persistent rise in A.D.H.D. diagnoses and prescriptions for medication among children. A recent New York Times analysis of data collected by the Centers for Disease Control and Prevention found that 11 percent of all children ages 4 through 17 — 6.4 million over all — had received a diagnosis of A.D.H.D. from a medical professional. The diagnosis rate rose to 19 percent for boys of high school age. © 2013 The New York Times Company
By Scicurious My eye was caught last week by a piece in Scientific American proper asking “is ketamine the next big depression drug?” It’s a good piece, and I appreciate the balance in the article, but I was also kind of surprised that…it took so long. There have been previous media rumblings (and blog) about ketamine through the years, so I’m rather curious as to why the article came out now (maybe there’s another new paper out? I didn’t see any referenced and couldn’t find anything). To be honest, while yes, ketamine has a lot of interesting potential, it’s not really quite as “new” as you might think. The first major clinical reports of ketamine as an effective antidepressant actually date back to 2000. Since then, scientists have been spending a lot of time trying to figure out WHY a drug usually used to knock out horses, or abused for its perception-changing qualities, acts as an antidepressant. And not just any antidepressant, but an almost miracle drug (maybe), helping people who respond to no other treatment, and with effects of a single dose occurring within hours (currently antidepressants take weeks), and lasting for weeks. And for all that…they don’t know how it works. So I saw the article, and I wanted to write a bit of follow-up. Because yes, while we don’t know QUITE how ketamine works…we have some ideas. And here is one of them. Ketamine isn’t like the current drugs used as antidepressants. Current drugs, like Prozac affect chemical neurotransmitters like serotonin. © 2013 Scientific American
Link ID: 18197 - Posted: 05.28.2013
By ABIGAIL ZUGER, M.D. I hadn’t seen Larry in a dozen years when he reappeared in my office a few months ago, grinning. We were both grinning. I always liked Larry, even though he was a bit of a hustler, a little erratic in his appointments, a persistent dabbler in a variety of illegal substances. But he was always careful to avoid the hard stuff; he said he had a bad problem as a teenager and was going to stay out of trouble. It was to stay out of trouble that he left town all those years ago, and now he was back, grayer and thinner but still smiling. Then he pulled out a list of the medications he needed, and we both stopped smiling. According to Larry’s list, he was now taking giant quantities of one of the most addictive painkillers around, an immensely popular black-market drug most doctors automatically avoid prescribing except under the most exceptional circumstances. “I got a bad back now, Doc,” Larry said. Doctors hate pain. Let me count the ways. We hate it because we are (mostly) kindhearted and hate to see people suffer. We hate it because it is invisible, cannot be measured or monitored, and varies wildly and unpredictably from person to person. We hate it because it can drag us closer to the perilous zones of illegal practice than any other complaint. And we hate it most of all because unless we specifically seek out training in how to manage pain, we get virtually none at all, and wind up flying over all kinds of scary territory absolutely solo, without a map or a net. Copyright 2013 The New York Times Company
By Ian Chant Most people make good decisions most of the time. But when drug addiction, disease or brain injury enters the picture, rational thinking can go awry. What if the damaged brain just needed a little reminder of how it feels to choose wisely? Enter the MIMO neural prosthesis, an array of electrodes implanted in the brain that make contact with eight neuron circuits in the prefrontal cor-tex, the brain's command center for decision making. The device can both record the brain activity associated with good choices and stimulate the relevant neurons to get the brain back on track. Although the implant can listen in only on a tiny subset of the neurons in this region, the scientists who developed it, based at Wake Forest Baptist Medical Center, were surprised to discover that they could still pick up signature patterns associated with correct choices, at least in the context of a simple task. The researchers tested the neural prosthesis on monkeys that were trained to move a cursor over a picture on a computer screen to get a food reward. The implant first recorded the brain activity associated with choosing the correct picture. Then the monkeys were given cocaine, and their performance plummeted. But when the implant was switched on to send electric current to the neurons that had earlier been associated with the correct answers, the monkeys immediately started selecting the right pictures again. Some of them did an even better job than they had before receiving cocaine. © 2013 Scientific American,
Ella Pickover A “helpful” new drug which could help problem drinkers reduce the amount of alcohol they consume will today become available to UK patients. If dependent drinkers take the drug nalmefene and undergo counselling they can cut their consumption levels by 61 per cent, manufacturers said. The pill, also known as selincro, has been licensed for use by health officials and will be available for doctors to prescribe to their patients from today. The drug, which is to be taken once a day, has been licensed for "the reduction of alcohol consumption in adult patients with alcohol dependence without physical withdrawal symptoms and who do not require immediate detoxification". While current drugs help patients to become teetotal, nalmefene helps people with drinking problems to cut back on the amount they drink. The drug works by modulating the reward mechanism in the brain. A clinical trial into the drug helped patients cut the amount they consumed from 12.75 units a day to five units a day - a 61 per cent reduction. And patients who underwent counselling as well as taking the drug reduced their "heavy drinking days" from 23 days a month to nine days a month after undergoing the treatment for six months, researchers said. "The people who we saw in the study were not stereotypical alcoholics, most of them had families and jobs," said drug investigator Dr David Collier, of Barts and The London School of Medicine. © independent.co.uk
Keyword: Drug Abuse
Link ID: 18129 - Posted: 05.07.2013
By Gisela Telis, I’ve seen friends fret over the purported link between aluminum and Alzheimer’s disease and have often wondered if their fears are founded on fact. Should they give up aluminum pans or aluminum-containing antiperspirants? I’ve always heard that aluminum’s health dangers are just hype. So what’s the real deal? The connection between aluminum and Alzheimer’s disease is less a myth than a longstanding scientific controversy. It began in 1965, when researchers discovered that injecting rabbits’ brains with aluminum caused them to develop neurofibrillary tangles, the twisted proteins found in brain cells of patients with Alzheimer’s disease, a degenerative brain disorder that destroys memory and cognition. The finding spurred a rush of research. Just eight years later, a Canadian group studying brain tissue from deceased Alzheimer’s patients found that certain parts of their brains had two to three times more aluminum than a normal brain. By 1980, Daniel Perl and Arnold Brody had managed to actually peer inside human tangle-bearing brain cells — and found aluminum there, too. “That really changed the whole complexion of the thing,” recalls Perl, now a professor of pathology in the Uniformed Services University of the Health Sciences in Bethesda. “I was getting called all the time, because there was so much public interest.” Despite the rise in interest, no one could figure out what this meant for human health. Part of the problem was that scientific techniques were — and still are — too imperfect to provide an answer. Whether they were studying brain cells or conducting population-wide epidemiological studies that tracked aluminum exposure and Alzheimer’s risk, researchers lacked the tools to get very precise or conclusive results. © 1996-2013 The Washington Post
By Dina Fine Maron Almost a decade after manufacturers stopped using certain chemical flame retardants in furniture foam and carpet padding, many of the compounds still lurk in homes. New work to be presented today reaffirms that the chemicals may also still be hurting young children who were exposed before they were born. Researchers investigating the health impacts of prenatal exposure to flame retardants collected blood samples from 309 pregnant women early in their second trimester. Spikes in the levels of one class of flame retardant, polybrominated diphenyl ethers (PBDEs) correlated with behavior and cognition difficulties during early childhood. The researchers tracked children through the first five years of their lives, looking at a battery of tests for IQ and behavior. They found that children of mothers who had high PBDE levels during their second trimester showed cognition deficits when the children were five years old as well as higher rates of hyperactivity at ages two to five. If the mother’s blood had a 10-fold increase in PBDEs, the average five-year-old had about a four-point IQ deficit. “A four-point IQ difference in an individual child may not be perceivable in…ordinary life. However, in a population, if many children are affected, the social and economic impact can be huge due to the shift of IQ distribution and productivity,” says lead author Aimin Chen, an assistant professor of environmental health at the University of Cincinnati College of Medicine. The findings, based on women and children from Cincinnati, will be presented May 6 at the annual meeting of the Pediatric Academic Societies in Washington, D.C. The unpublished results have been submitted to a peer-reviewed journal, but the paper has not yet been accepted. © 2013 Scientific American
The short answer is no. But your question gets to the heart of an important problem that we have in this country: that all medications are approved by the Food and Drug Administration on the basis of relatively short-term studies, even though many are used long-term for medical and psychiatric disorders that are chronic, if not lifelong. The F.D.A. approves antidepressants like selective serotonin re-uptake inhibitors, or S.S.R.I.’s, if the drug beats a placebo in two randomized clinical trials that typically last 4 to 12 weeks and involve a few hundred patients. Longer-term maintenance studies, usually lasting one to two years, indicate that S.S.R.I.’s do not cause any serious harm, though they have plenty of side effects, like weight gain and sexual dysfunction. Once a drug hits the market, we have only a voluntary system of reporting adverse effects in the United States; there are no systematic long-term studies of any drug lasting 10 or more years. Still, S.S.R.I.’s have been used since the late 1980s and given to more than 40 million Americans, so it’s reasonable to say that if these drugs caused any significant toxic effects, we would have seen many such reports. Instead, we have some anecdotal reports claiming a wide range of S.S.R.I.-related toxicity, but one cannot know from these reports whether the symptoms are related to S.S.R.I. use or to medical illnesses that happen to develop over time in people taking these drugs. Copyright 2013 The New York Times Company
Link ID: 18116 - Posted: 05.04.2013
Distinct patterns of brain activity are linked to greater rates of relapse among alcohol dependent patients in early recovery, a study has found. The research, supported by the National Institutes of Health, may give clues about which people in recovery from alcoholism are most likely to return to drinking. "Reducing the high rate of relapse among people treated for alcohol dependence is a fundamental research issue," said Kenneth R. Warren, Ph.D., acting director of the National Institute on Alcohol Abuse and Alcoholism (NIAAA), part of NIH. "Improving our understanding of the neural mechanisms that underlie relapse will help us identify susceptible individuals and could inform the development of other prevention strategies." Using brain scans, researchers found that people in recovery from alcoholism who showed hyperactivity in areas of the prefrontal cortex during a relaxing scenario were eight times as likely to relapse as those showing normal brain patterns or healthy controls. The prefrontal brain plays a role in regulating emotion, the ability to suppress urges, and decision-making. Chronic drinking may damage regions involved in self-control, affecting the ability to regulate cravings and resist relapse. Findings from the study, which was funded by NIAAA, appear online at the JAMA Psychiatry website.
By Scott O. Lilienfeld and Hal Arkowitz A German children's book from 1845 by Heinrich Hoffman featured “Fidgety Philip,” a boy who was so restless he would writhe and tilt wildly in his chair at the dinner table. Once, using the tablecloth as an anchor, he dragged all the dishes onto the floor. Yet it was not until 1902 that a British pediatrician, George Frederic Still, described what we now recognize as attention-deficit hyperactivity disorder (ADHD). Since Still's day, the disorder has gone by a host of names, including organic drivenness, hyperkinetic syndrome, attention-deficit disorder and now ADHD. Despite this lengthy history, the diagnosis and treatment of ADHD in today's children could hardly be more controversial. On his television show in 2004, Phil McGraw (“Dr. Phil”) opined that ADHD is “so overdiagnosed,” and a survey in 2005 by psychologists Jill Norvilitis of the University at Buffalo, S.U.N.Y., and Ping Fang of Capitol Normal University in Beijing revealed that in the U.S., 82 percent of teachers and 68 percent of undergraduates agreed that “ADHD is overdiagnosed today.” According to many critics, such overdiagnosis raises the specter of medicalizing largely normal behavior and relying too heavily on pills rather than skills—such as teaching children better ways of coping with stress. Yet although data point to at least some overdiagnosis, at least in boys, the extent of this problem is unclear. In fact, the evidence, with notable exceptions, appears to be stronger for the undertreatment than overtreatment of ADHD. © 2013 Scientific American,
By ALAN SCHWARZ FRESNO, Calif. — Lisa Beach endured two months of testing and paperwork before the student health office at her college approved a diagnosis of attention deficit hyperactivity disorder. Then, to get a prescription for Vyvanse, a standard treatment for A.D.H.D., she had to sign a formal contract — promising to submit to drug testing, to see a mental health professional every month and to not share the pills. “As much as it stunk, it’s nice to know, ‘O.K., this is legit,' ” said Ms. Beach, a senior at California State University, Fresno. The rigorous process, she added, has deterred some peers from using the student health office to obtain A.D.H.D. medications, stimulants long abused on college campuses. “I tell them it takes a couple months,” Ms. Beach said, “and they’re like, ‘Oh, never mind.’ ” Fresno State is one of dozens of colleges tightening the rules on the diagnosis of A.D.H.D. and the subsequent prescription of amphetamine-based medications like Vyvanse and Adderall. Some schools are reconsidering how their student health offices handle A.D.H.D., and even if they should at all. Various studies have estimated that as many as 35 percent of college students illicitly take these stimulants to provide jolts of focus and drive during finals and other periods of heavy stress. Many do not know that it is a federal crime to possess the pills without a prescription and that abuse can lead to anxiety, depression and, occasionally, psychosis. Although few experts dispute that stimulant medications can be safe and successful treatments for many people with a proper A.D.H.D. diagnosis, the growing concern about overuse has led some universities, as one student health director put it, “to get out of the A.D.H.D. business.” © 2013 The New York Times Company
By ABIGAIL ZUGER, M.D. Addiction swallows lives whole, and not only with overdose, illness and concentric cycles of rehab and relapse. A less onerous but still tenacious kind of post-traumatic stress disorder may develop as well, with recovered addicts and their families compulsively reliving the past in private — or, like David Sheff and his son Nic, in public. In the last five years the two have written a small library of memoirs centered on Nic’s battle with substance use, with two by Nic (now 31, and sober) and the 2008 best seller by his father, “Beautiful Boy.” Now comes “Clean,” less memoir than guide for those just entering the terrain Mr. Sheff knows so well. If the book represents a certain redundancy of subject, its likely audience — those who must watch as friends and family spiral away — cannot hear too many sympathetic reiterations of the same truths. In “Clean,” Mr. Sheff changes perspective, writing as advocate and journalist rather than distraught father. Still, his story line recreates that of “Beautiful Boy,” tracing the trajectory of addiction from cradle to rehab and beyond with the same question in mind: How does a promising cleareyed kid from a good family wind up in an inconceivable sea of trouble? His answer, bludgeoned home with the repetitive eloquence of the missionary, is entirely straightforward: The child is ill. Addiction must be considered a disease, as devoid of moral overtones as diabetes or coronary artery disease, just as amenable as they are to scientific analysis, and just as treatable with data-supported interventions, not hope, prayer or hocus-pocus. © 2013 The New York Times Company
Keyword: Drug Abuse
Link ID: 18098 - Posted: 04.30.2013
By Cheryl Knepper Substance abuse and dependence rarely occur in a vacuum. Today’s addict is faced with a multitude of issues that may co-exist and compromise recovery. Co-existing addictions/compulsive behaviors such as drugs and alcohol, pathological gambling, sex, food, work, internet and gaming can become chronic and progressive if left unidentified and untreated. Many of these addictions don’t only coexist, but interact, reinforce and fuse together becoming part of a package known as Addiction Interaction. The term “Addiction Interaction Disorder” was introduced by Patrick Carnes PhD in 2011. Caron Treatment Centers conducted a research study among adult patients with drug and alcohol addictions to determine what percentage may be at risk for sex and love addiction. The 485 participants were given the SAST-R (Sexual Addiction Screening Tool-Revised a 45 item forced choice (Yes/No) instrument): Carnes, Green & Carnes, 2010. The findings of this study indicated that 21 percent of individuals being treated for primary substance dependence scored at risk. Another interesting finding from the study showed a higher percentage of cannabis, cocaine and amphetamine abuse or dependence diagnosis in the individuals that scored at-risk for sexual addiction. In addition, at-risk individuals had higher percentages of mood disorder, PTSD and eating disorder diagnoses. © 2013 Scientific American
Keyword: Drug Abuse
Link ID: 18097 - Posted: 04.30.2013