Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Emotional and behavioral problems show up even with low exposure to lead, and as blood lead levels increase in children, so do the problems, according to research funded by the National Institute of Environmental Health Sciences (NIEHS), part of the National Institutes of Health. The results were published online June 30 in the journal JAMA Pediatrics. “This research focused on lower blood lead levels than most other studies and adds more evidence that there is no safe lead level,” explained NIEHS Health Scientist Administrator Kimberly Gray, Ph.D. “It is important to continue to study lead exposure in children around the world, and to fully understand short-term and long-term behavioral changes across developmental milestones. It is well-documented that lead exposure lowers the IQ of children.” Blood lead concentrations measured in more than 1,300 preschool children in China were associated with increased risk of behavioral and emotional problems, such as being anxious, depressed, or aggressive. The average blood lead level in the children was 6.4 micrograms per deciliter. While many studies to date have examined health effects at or above 10 micrograms per deciliter, this study focused on lower levels. The CDC now uses a reference level of 5 micrograms per deciliter, to identify children with blood lead levels that are much higher than normal, and recommends educating parents on reducing sources of lead in their environment and continued monitoring of blood lead levels.
|By Lindsey Konkel and Environmental Health News Babies whose moms lived within a mile of crops treated with widely used pesticides were more likely to develop autism, according to new research. The study of 970 children, born in farm-rich areas of Northern California, is part of the largest project to date that is exploring links between autism and environmental exposures. The University of California, Davis research – which used women’s addresses to determine their proximity to insecticide-treated fields – is the third project to link prenatal pesticide exposures to autism and related disorders. “The weight of evidence is beginning to suggest that mothers’ exposures during pregnancy may play a role in the development of autism spectrum disorders,” said Kim Harley, an environmental health researcher at the University of California, Berkeley who was not involved in the new study. One in every 68 U.S. children has been identified with an autism spectrum disorder—a group of neurodevelopmental disorders characterized by difficulties with social interactions, according to the Centers for Disease Control and Prevention. “This study does not show that pesticides are likely to cause autism, though it suggests that exposure to farming chemicals during pregnancy is probably not a good thing,” said Dr. Bennett Leventhal, a child psychiatrist at University of California, San Francisco who studies autistic children. He did not participate in the new study. The biggest known contributor to autism risk is having a family member with it. Siblings of a child with autism are 35 times more likely to develop it than those without an autistic brother or sister, according to the National Institutes of Health. © 2014 Scientific American
Heidi Ledford If shown to be possible in humans, addiction to the Sun could help explain why some tanners continue to seek out sunlight despite being well aware of the risks. The lure of a sunny day at the beach may be more than merely the promise of fun and relaxation. A study published today reports that mice exposed to ultraviolet (UV) rays exhibit behaviours akin to addiction. The researchers found that mice exposed repeatedly to UV light produced an opioid called β-endorphin, which numbs pain and is associated with addiction to drugs. When they were given a drug that blocks the effect of opioids, the mice also showed signs of withdrawal — including shaky paws and chattering teeth. If the results hold true in humans, they would suggest an explanation for why many tanners continue to seek out sunlight, despite the risks — and, in some cases, even after being diagnosed with skin cancer. “This offers a clear potential mechanism for how UV radiation can be rewarding and, in turn, potentially addictive,” says Bryon Adinoff, an addiction psychiatrist at the University of Texas Southwestern Medical Center in Dallas, who was not involved with the study. “That’s a big deal.” Oncologist David Fisher of the Massachusetts General Hospital in Boston and his colleagues became interested in sunlight addiction after studying the molecular mechanisms of pigment production in the skin after UV light exposure. In the new study published today in Cell1, they show that in mice, some skin cells also synthesize β-endorphin in response to chronic, low doses of UV light. © 2014 Nature Publishing Group
Keyword: Drug Abuse
Link ID: 19752 - Posted: 06.21.2014
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
By Elizabeth Norton A single dose of a century-old drug has eliminated autism symptoms in adult mice with an experimental form of the disorder. Originally developed to treat African sleeping sickness, the compound, called suramin, quells a heightened stress response in neurons that researchers believe may underlie some traits of autism. The finding raises the hope that some hallmarks of the disorder may not be permanent, but could be correctable even in adulthood. That hope is bolstered by reports from parents who describe their autistic children as being caught behind a veil. "Sometimes the veil parts, and the children are able to speak and play more normally and use words that didn't seem to be there before, if only for a short time during a fever or other stress" says Robert Naviaux, a geneticist at the University of California, San Diego, who specializes in metabolic disorders. Research also shows that the veil can be parted. In 2007, scientists found that 83% of children with autism disorders showed temporary improvement during a high fever. The timing of a fever is crucial, however: A fever in the mother can confer a higher risk for the disorder in the unborn child. As a specialist in the cell's life-sustaining metabolic processes, Naviaux was intrigued. Autism is generally thought to result from scrambled signals at synapses, the points of contact between nerve cells. But given the specific effects of something as general as a fever, Naviaux wondered if the problem lay "higher up" in the cell's metabolism. © 2014 American Association for the Advancement of Science.
Link ID: 19749 - Posted: 06.19.2014
by Helen Thomson KULLERVO HYNYNEN is preparing to cross neuroscience's final frontier. In July he will work with a team of doctors in the first attempt to open the blood-brain barrier in humans – the protective layer around blood vessels that shields our most precious organ against threats from the outside world. If successful, the method would be a huge step in the treatment of pernicious brain diseases such as cancer, Parkinson's and Alzheimer's, by allowing drugs to pass into the brain. The blood-brain barrier (BBB) keeps toxins in the bloodstream away from the brain. It consists of a tightly packed layer of endothelial cells that wrap around every blood vessel throughout the brain. It prevents viruses, bacteria and any other toxins passing into the brain, while simultaneously ushering in vital molecules such as glucose via specialised transport mechanisms. The downside of this is that the BBB also completely blocks the vast majority of drugs. Exceptions include some classes of fat and lipid-soluble chemicals, but these aren't much help as such drugs penetrate every cell in the body – resulting in major side effects. "Opening the barrier is really of huge importance. It is probably the major limitation for innovative drug development for neurosciences," says Bart De Strooper, co-director of the Leuven Institute for Neuroscience and Disease in Belgium. © Copyright Reed Business Information Ltd.
Link ID: 19748 - Posted: 06.19.2014
By Denali Tietjen Caffeine isn’t healthy, but that’s no news. The withdrawal headaches, jitteriness and dehydration kind of gave that one way. What is news, however, is that starting at puberty, it’s worse for boys than girls. Girls and boys have the same cardiovascular reactions to caffeine in childhood, but begin to react differently in adolescence, finds a new study conducted by researchers from The University of Buffalo. In the double-blind study published in the June issue of Pediatrics, researchers examined the cardiovascular reactions of 52 pre-pubescent (ages eight to nine) and 49 post-pubescent (ages 15 to 17) children to varying levels of caffeine. Participants consumed either the placebo, 1 mg/kg or 2 mg/kg caffeinated sodas, and then had their heart rates and blood pressures taken. The results found that pre-pubescent children had the same reaction to caffeine regardless of gender, while post-pubescent boys had much stronger cardiovascular reactions to caffeine than girls. The study also examined post-pubescent girls’ reactions to caffeine at various phases of their menstrual cycles. At different stages of the cycle, the girls metabolized caffeine differently. “We found differences in responses to caffeine across the menstrual cycle in post-pubertal girls, with decreases in heart rate that were greater in the mid-luteal phase and blood pressure increases that were greater in the mid-follicular phase of the menstrual cycle,” Dr. Jennifer Temple, one of the researchers who conducted the study said in a University at Buffalo press release announcing the study.
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
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
Keyword: Drug Abuse
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
Keyword: Drug Abuse
Link ID: 19725 - Posted: 06.14.2014
Claudia M. Gold Tom Insel, director of the National Institute of Mental Health (NIMH,) in his recent blog post "Are Children Overmedicated?" seems to suggest that perhaps more psychiatric medication is in order. Comparing mental illness in children to food allergies, he dismisses the "usual" explanations given for the increase medication prescribing patterns. In his view, these explanations are: Blaming psychiatrists who are too busy to provide therapy, parents who are too busy to provide a stable home environment, drug companies for marketing their products, and schools for lack of recess. By concluding that perhaps the explanation for the increase in prescribing of psychiatric medication to children is a greater number of children with serious psychiatric illness, Insel shows a lack of recognition of the complexity of the situation. When a recent New York Times article, that Insel makes reference to, reported on the rise in prescribing of psychiatric medication for toddlers diagnosed with ADHD, with a disproportionate number coming from families of poverty, one clinician remarked that if this is an attempt to medicate social and economic issues, then we have a huge problem. He was on to something. In conversations with pediatricians (the main prescribers of these medications) and child psychiatrists on the front lines, I find many in a reactive stance. When people feel overwhelmed, they go into survival mode, with their immediate aim just to get through the day. They find themselves prescribing medication because they have no other options.
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.
Keyword: Drug Abuse
Link ID: 19695 - Posted: 06.05.2014
Sarah C. P. Williams This, in all its molecular complexity, is what the bulging end of a single neuron looks like. A whopping 300,000 proteins come together to form the structure, which is less than a micrometer wide, hundreds of times smaller than a grain of sand. This particular synapse is from a rat brain. It’s where chemical signals called neurotransmitters are released into the space between neurons to pass messages from cell to cell. To create a 3D molecular model of the structure, researchers first isolated the synapses of rat neurons and turned to classic biochemistry to identify and quantify the molecules present at every stage of the neurotransmitter release cycle. Then, they used microscopy to pinpoint the location of each protein. Some proteins—like the red patches of SNAP25 visible in the video at 0:14—aid in the release of vesicles, tiny spheres full of neurotransmitters. Others—like the green, purple, and red rods at 0:45—help the synapse maintain its overall structure. Different proteins surround vesicles when they’re inside the synapse—the circles scattered throughout the structure at 0:56—than when the vesicles are forming at the edge of the synapse—as shown at 2:08. Researchers can use the model, described online today in Science, to better understand how neurons function and what goes wrong in brain disorders. (Video credit: Wilhelm et al. 2014, Science) © 2014 American Association for the Advancement of Science.
Keyword: Brain imaging
Link ID: 19678 - Posted: 05.31.2014
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.
Keyword: Drug Abuse
Link ID: 19676 - Posted: 05.31.2014
By C. CLAIBORNE RAY Q. WHY WOULD A PAIN MEDICATION LOSE ITS EFFICACY AFTER WORKING WELL FOR SEVERAL YEARS? A. The mechanism is complex, said Dr. Shakil Ahmed, a pain medicine specialist at NewYork-Presbyterian Hospital/Weill Cornell Medical Center. “It is due to a phenomenon called tolerance,” in which there is a decrease in response over time to repeated exposures of the body to pain medication, he said. “This might be due to alteration in the way the body disposes of the medication,” Dr. Ahmed suggested. Or it could occur because drug interactions or bodily changes add a substance that induces an enzyme responsible for disposing of the drug. Another explanation is that long-term administration of pain medications results in a reduction of the number of target drug receptors or a drop in their responsiveness, and in desensitization to the pain medication in question. There is also an increase in the function of other nervous system receptors, called NMDA receptors , which may lead to the development of the tolerance, Dr. Ahmed said. Dr. Ahmed’s practice and research include several alternatives to conventional drug treatment for pain, including spinal cord stimulation, use of radio frequency to interrupt the nerve pathways of pain, delivery of pain medication with a pump directly to the space around the spinal cord, and non-invasive laser therapy. © 2014 The New York Times Company
Keyword: Pain & Touch
Link ID: 19666 - Posted: 05.28.2014
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
Keyword: Drug Abuse
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.
Keyword: Drug Abuse
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
Keyword: Drug Abuse
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.
Keyword: Drug Abuse
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
Keyword: Drug Abuse
Link ID: 19615 - Posted: 05.15.2014