Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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By Sara Solovitch It was November 2012 when Dennis Hartman, a Seattle business executive, managed to pull himself out of bed, force himself to shower for the first time in days and board a plane that would carry him across the country to a clinical trial at the National Institute of Mental Health (NIMH) in Bethesda. After a lifetime of profound depression, 25 years of therapy and cycling through 18 antidepressants and mood stabilizers, Hartman, then 46, had settled on a date and a plan to end it all. This clinical trial would be his last stab at salvation. For 40 minutes, he sat in a hospital room as an IV drip delivered ketamine through his system. Several more hours passed before it occurred to him that all his thoughts of suicide had evaporated. “My life will always be divided into the time before that first infusion and the time after,” Hartman says today. “That sense of suffering and pain draining away. I was bewildered by the absence of pain.” Ketamine, popularly known as the psychedelic club drug Special K, has been around since the early 1960s. It is a staple anesthetic in emergency rooms, regularly used for children when they come in with broken bones and dislocated shoulders. It’s an important tool in burn centers and veterinary medicine, as well as a notorious date-rape drug, known for its power to quickly numb and render someone immobile.
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
Keyword: Drug Abuse
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.
by Graham McDougall, Jr., behavioral scientist at U. of Alabama Chemo brain is a mental cloudiness reported by about 30 percent of cancer patients who receive chemotherapy. Symptoms typically include impairments in attention, concentration, executive function, memory and visuospatial skills. Since the 1990s researchers have tried to understand this phenomenon, particularly in breast cancer patients. But the exact cause of chemo brain remains unclear. Some studies indicate that chemotherapy may trigger a variety of related neurological symptoms. One study, which examined the effects of chemotherapy in 42 breast cancer patients who underwent a neuropsychological evaluation before and after treatment, found that almost three times more patients displayed signs of cognitive dysfunction after treatment as compared with before (21 versus 61 percent). A 2012 review of 17 studies considering 807 breast cancer patients found that cognitive changes after chemotherapy were pervasive. Other research indicates that the degree of mental fogginess that a patient experiences may be directly related to how much chemotherapy that person receives: higher doses lead to greater dysfunction. There are several possible mechanisms to explain the cognitive changes associated with chemotherapy treatments. The drugs may have direct neurotoxic effects on the brain or may indirectly trigger immunological responses that may cause an inflammatory reaction in the brain. Chemotherapy, however, is not the only possible culprit. Research also shows that cancer itself may cause changes to the brain. In addition, it is possible that the observed cognitive decline may simply be part of the natural aging process, especially considering that many cancer patients are older than 50 years. © 2016 Scientific American,
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
Keyword: Drug Abuse
Link ID: 21816 - Posted: 01.23.2016
By Diana Kwon Stories of cannabis’s abilities to alleviate seizures have been around for about 150 years but interest in medical marijuana has increased sharply in the last decade with the help of legalization campaigns. Credit: ©iStock Charlotte Figi, an eight-year-old girl from Colorado with Dravet syndrome, a rare and debilitating form of epilepsy, came into the public eye in 2013 when news broke that medical marijuana was able to do what other drugs could not: dramatically reduce her seizures. Now, new scientific research provides evidence that cannabis may be an effective treatment for a third of epilepsy patients who, like Charlotte, have a treatment-resistant form of the disease. Last month Orrin Devinsky, a neurologist at New York University Langone Medical Center, and his colleagues across multiple research centers published the results from the largest study to date of a cannabis-based drug for treatment-resistant epilepsy in The Lancet Neurology. The researchers treated 162 patients with an extract of 99 percent cannabidiol (CBD), a nonpsychoactive chemical in marijuana, and monitored them for 12 weeks. This treatment was given as an add-on to the patients’ existing medications and the trial was open-label (everyone knew what they were getting). The researchers reported the intervention reduced motor seizures at a rate similar to existing drugs (a median of 36.5 percent) and 2 percent of patients became completely seizure free. Additionally, 79 percent of patients reported adverse effects such as sleepiness, diarrhea and fatigue, although only 3 percent dropped out of the study due to adverse events. “I was a little surprised that the overall number of side effects was quite high but it seems like most of them were not enough that the patients had to come off the medication,” says Kevin Chapman, a neurology and pediatric professor at the University of Colorado School of Medicine who was not involved in the study. “I think that [this study] provides some good data to show that it's relatively safe—the adverse effects were mostly mild and [although] there were serious adverse effects, it's always hard to know in such a refractory population whether that would have occurred anyway.” © 2016 Scientific American,
The Chamorro people of the Pacific island of Guam know it as lytigo-bodig. For decades, they have been struck down by a mysterious illness that resembles the muscle-wasting disease amyotrophic lateral sclerosis (ALS), Parkinson’s disease and Alzheimer’s-like dementia. It now looks like we have a clue that could point to a way of slowing its development. Lytigo-bodig is a progressive disease. ALS symptoms arrive when people are in their mid-40s and early 50s. By the time they reach their 60s, they also have the shaking and lack of coordination that characterises Parkinson’s, before the cognitive problems associated with dementia also set in. “Initially they stumble a bit, but as their muscles wither, they need help with eating and going to the toilet, as well as having difficulty swallowing and breathing,” says Paul Cox of the Institute for Ethnomedicine in Wyoming. For a long time, a chemical called BMAA, found in the cycad seeds that the Chamorro grind up to make flour, has been suspected as the cause of the disease. The toxin builds up in the cyanobacteria that grow in the roots of cycad plants. It also accumulates in the tissue of seed-eating flying foxes, which the Chamorro hunt and eat. To see if they could confirm BMAA as the culprit, Cox fed fruit spiked with the toxin to vervet monkeys for 140 days. They estimated this was equivalent to the dose a typical islander might get over a lifetime. Although they didn’t show cognitive problems, the animals did develop brain abnormalities called tau tangles and deposits of amyloid plaque. The density and placement of these abnormalities were similar to those seen in the islanders. “The structure of the pathology is almost identical,” says Cox. “We were stunned.” © Copyright Reed Business Information Ltd.
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.
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
Keyword: Drug Abuse
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
Keyword: Drug Abuse
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
Keyword: Drug Abuse
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.' "
Keyword: Drug Abuse
Link ID: 21773 - Posted: 01.11.2016
By Veronique Greenwood Last year a new sleep drug called Belsomra came on the market, featuring a mechanism unlike any other pill: it mimics narcolepsy. That might sound odd, but the potential users are many. More than 8.5 million Americans take prescription sleep aids, and many others use snooze-inducing over-the-counter medications. All these pills, including Belsomra, do one of two things: they enhance the effects of the neurotransmitter GABA, known for quieting brain activity, or they arrest the actions of neurotransmitters that keep the brain aroused. Yet it's not quite as simple as flipping a switch; the drugs have a range of side effects, including daytime drowsiness, hallucinations and sleep-eating. Here's an overview of the sleeping pills currently available in the U.S.—plus a look at cognitive-behavior therapy for insomnia, which may be more successful than drugs alone. It requires a lot more work than popping a pill, but cognitive-behavior therapy for insomnia (CBT-I) has been shown to successfully alleviate sleep problems. Aimed at developing healthy habits, CBT-I comes with a lot of homework—between weekly or so visits with a specialist, a patient keeps track of hours spent in bed and hours sleeping and uses the bed only for sleep and sex. The patient must stay up until an established bedtime and get up on awakening, generating a sleep deficit that makes it easier to fall asleep at the right time. Avoiding caffeine and alcohol after 4 P.M. and timing exercise so that it doesn't interfere with drowsiness are also part of the system. © 2016 Scientific American
Link ID: 21770 - 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
Keyword: Drug Abuse
Link ID: 21747 - Posted: 01.04.2016
By Elizabeth Pennisi Imagine trying to train wild sea lions—without them ever seeing you. That was Peter Cook's challenge 8 years ago when he was trying to figure out whether poisonous algae were irrevocably damaging the animals’ brains. With a lot of patience and some luck, the comparative neuroscientist from Emory University in Atlanta has succeeded, and the news isn't good. Toxins from the algae mangle a key memory center, likely making it difficult for sick animals to hunt or navigate effectively, Cook and his colleagues report today. "Sea lions can be seen as sentinels of human health," says Kathi Lefebvre, a research biologist at the Northwest Fisheries Science Center in Seattle, Washington, who was not involved with the work. As oceans warm, toxic algae proliferate and cause so-called red tides because the water looks reddish. So "understanding these toxins in wild animals is going to become more important," she says. Red tides are produced by algae called diatoms. They make a toxin called domoic acid, which is consumed by other plankton that in turn become food for fish and other organisms. Predators such as anchovies, sardines, and other schooling fish accumulate this toxin in their bodies. So when algal populations explode, say, because of warming water, domoic acid concentrations increase in these animals to a point that they affect the sea lions that feast on them. Scientists first recognized this problem in 1998, after hundreds of sea lions were found stranded or disoriented along California's coast. Since then, researchers have studied sick and dead sea lions and documented that the toxin causes seizures and damages the brain, sometimes killing the animal. © 2015 American Association for the Advancement of Science.
By Karen Weintraub Is sleep induced by a benzodiazepine counted as restorative sleep? Researchers hate to admit it, but they don’t know enough about sleep to answer this question. Their best guess, several experts said, is that sleep is sleep. Dr. John Weyl Winkelman, a sleep disorders expert at Massachusetts General Hospital and Harvard Medical School, said if a patient asked him whether medicated sleep was restorative, “I’d say: ‘You tell me.’” There is quite a bit of evidence about the negative health consequences of insomnia, but researchers don’t know precisely what it is in the brain and body that is "restored" by sleep to aid optimal function. And it is unlikely that any specific stage of sleep is uniquely restorative, said Dr. Daniel J. Buysse, a sleep medicine expert and professor of psychiatry at the University of Pittsburgh. More sleep, less interrupted sleep, and sleep at the right time of night are all likely to be important, he said. There are two types of sleep: REM, when people dream, and non-REM, which has light, medium and deep portions. Sleeping pills mainly increase the amount of medium-depth non-REM sleep, Dr. Buysse said. Medications can help people fall asleep faster and reduce nighttime wakefulness, he said, and those changes are usually considered to contribute to restorative sleep. But different people respond differently. “Do you feel more rested, more alert, more able to concentrate, less irritable on medication versus off?" Dr. Buysse said. "If all those things are true then I would say it’s more restorative. If a hypnotic drug leaves you feeling hung over or more anxious, if it causes you to order five hickory smoked turkeys on the Internet without remembering, then it’s probably not good.” © 2015 The New York Times Company
Link ID: 21691 - Posted: 12.12.2015
Angus Chen Parents of children with severe epilepsy have reported incredible recoveries when their children were given cannabidiol, a derivative of marijuana. The drug, a non-psychoactive compound that occurs naturally in cannabis, has been marketed with epithets like Charlotte's Web and Haleigh's Hope. But those parents were taking a risk; there has been no clinical data on cannabidiol's safety of efficacy as an anti-epileptic. This week, doctors are presenting the first studies trying to figure out if cannabidiol actually works. They say the studies' results are promising, but with a grain of salt. The largest study being presented at the American Epilepsy Society meeting in Philadelphia this week was started in 2014 with 313 children from 16 different epilepsy centers around the country. Over the course of the three-month trial, 16 percent of the participants withdrew because the cannabidiol was either ineffective or had adverse side-effects, says Dr. Orrin Devinsky, a neurologist at the New York University Langone Medical Center and lead author on the study. But for the 261 patients that continued taking cannabidiol, the number of convulsive seizures, called grand mal or tonic-clonic seizures, went down by about half on average. Devinsky says that some children continued to experience benefits on cannabidiol after the trial ended. "In the subsequent periods, which are very encouraging, 9 percent of all patients and 13 percent of those with Dravet Syndrome epilepsy were seizure-free. Many have never been seizure-free before," he says. It's one of several [at least four. checking] papers on cannabidiol being presented this week at the American Epilepsy Society meeting in Philadelphia. © 2015 npr
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.
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.
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