Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Founded by two men in Akron, Ohio, in 1935, Alcoholics Anonymous has since spread around the world as a leading community-based method of overcoming alcohol dependence and abuse. Many people swear by the 12-step method, which has become the basis of programs to treat the abuse of drugs, gambling, eating disorders and other compulsive behaviors. But not everyone's a fan. In a recent critique of AA, author Gabrielle Glaser writes in the April issue of The Atlantic that, "Nowhere in the field of medicine is treatment less grounded in modern science." Glaser, whose 2013 book, Her Best-Kept Secret, explores what she calls "the epidemic of female drinking" in the U.S., says recent research on the brain suggests that the abstinence advocated by AA isn't the only solution — or even the best for many people. Cognitive therapy combined with the medication naltrexone, Glaser says, can help ease cravings and has been shown in some studies to help some problem drinkers learn to drink moderately without quitting. Glaser's magazine story has drawn fire from defenders of AA, including Huffington Post writer Tommy Rosen, who calls himself "a person in long-term recovery (23 years) who overcame severe drug addiction and alcoholism in great part due to the 12 Steps." Glaser's article, Rosen writes, is "painfully one-sided." Therapist and psychology reporter Robi Ludwig told Glaser and the host of MSNBC's program All in With Chris Hayes last week that she thinks it's "very dangerous to put out the idea that AA doesn't work. Does it work for everybody? No. There's not going to be one form of treatment that works for everybody." © 2015 NPR
Keyword: Drug Abuse
Link ID: 20729 - Posted: 03.28.2015
Claudia Dreifus Twenty-three states and the District of Columbia have legalized medical marijuana, but scientific research into its appropriate uses has lagged. Dr. Mark Ware would like to change that. Dr. Ware, 50, is the director of the Canadian Consortium for the Investigation of Cannabinoids and the director of clinical research of the Alan Edwards Pain Management Unit of McGill University Health Center. Medical marijuana has been legal in Canada for 16 years, and Dr. Ware, a practicing physician, studies how his patients take the drug and under what conditions it is effective. We spoke for two hours at the recent meeting of the American Association for the Advancement of Science and later by telephone. Our interviews have been condensed and edited for space. Q. How did you become interested in the medical possibilities of cannabis? A. In the late 1990s, I was working in Kingston, Jamaica, at a clinic treating people with sickle cell anemia. My British father and Guyanese mother had raised me in Jamaica, and I’d attended medical school there. One day, an elderly Rastafarian came for his annual checkup. I asked him, “What are your choices of medicines?” He leaned over the table and said, “You must study the herb.” That night, I went back to my office and looked up “cannabis and pain.” What I found were countless anecdotes from patients who’d obtained marijuana either legally or not and who claimed good effect with a variety of pain-related conditions. There were also the eye-opening studies showing that the nervous system had specific receptors for cannabinoids and that these receptors were located in areas related to pain. Everything ended with, “More studies are needed.” So I thought, “This is what I should be doing; let’s go!” © 2015 The New York Times Company
By Brian Handwerk In the U.S., legal hurdles have long hampered research into marijuana. But as more states approve medical and even recreational marijuana, scientific inquiries have spiked, especially studies aimed at finding out what exactly is in today's weed—and what it does to our bodies. In Colorado, which made marijuana legal in November 2012, the latest results show that the pot lining store shelves is much more potent than the weed of 30 years ago. But the boost in power comes at a cost—modern marijuana mostly lacks the components touted as beneficial by medical marijuana advocates, and it is often contaminated with fungi, pesticides and heavy metals. “There's a stereotype, a hippy kind of mentality, that leads people to assume that growers are using natural cultivation methods and growing organically," says Andy LaFrate, founder of Charas Scientific, one of eight Colorado labs certified to test cannabis. "That's not necessarily the case at all." LaFrate presented his results this week at a meeting of the American Chemical Society (ACS) in Denver. LaFrate says he's been surprised at just how strong most of today's marijuana has become. His group has tested more than 600 strains of marijuana from dozens of producers. Potency tests, the only ones Colorado currently requires, looked at tetrahydrocannabinol (THC), the psychoactive compound that produces the plant's famous high. They found that modern weed contains THC levels of 18 to 30 percent—double to triple the levels that were common in buds from the 1980s. That's because growers have cross-bred plants over the years to create more powerful strains, which today tout colorful names like Bruce Banner, Skunkberry and Blue Cookies.
Keyword: Drug Abuse
Link ID: 20712 - Posted: 03.24.2015
By Camilla Turner It is one of life’s most enduring mysteries. A question that music, poetry, myth and legend has, for thousands of years, tried but failed to answer. However, we may now be a step closer to discovering what love is, thanks to a scientific study that has obtained the first empirical evidence of love-related alterations in the brain. A team of researchers from universities in China and New York used MRI scans to track the physical effects of love on the brain and has pieced together a “love map” of the human mind. The study found that several areas of the brain showed increased activity in those who were in love, including in the parts of the brain linked to reward and motivation. The researchers said their results shed light on the “underlying mechanisms of romantic love” and would pave the way for a brain scan that could act as a “love test”. Scientists recruited 100 students from Southwest University in Chongqing, China, who were divided into three groups according to their relationship status: an “in-love” group, comprised of those who were in love at the time; an “ended-love” group, who had recently ended loving relationships; and a “single” group, who had never been in love. Participants were told not to think of anything while their brains were scanned, so that researchers could monitor the differences between the brains of students in all three groups. © Copyright of Telegraph Media Group Limited 2015
Keyword: Sexual Behavior
Link ID: 20692 - Posted: 03.17.2015
By John Horgan In 1990 The New York Times published a front-page article by Lawrence Altman, a reporter with a medical degree, announcing that scientists had discovered “a link between alcoholism and a specific gene.” The evidence for the "feel-good gene," which supposedly reduces anxiety, is flimsy, just like the evidence linking specific genes to high intelligence, violent aggression, homosexuality, bipolar disorder and countless other complex human traits and ailments. That was merely one in a string of reports in which the Times and other major media hyped what turned out to be erroneous claims linking complex traits and disorders—from homosexuality and high intelligence to schizophrenia and bipolar disorder—to specific genes. I thought those days were over, and that scientists and the media have learned to doubt extremely reductionist genetic accounts of complex traits and behaviors. I was wrong. Last Sunday, the “Opinion” section of the Times published an essay, “The Feel-Good Gene,” which states: “For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide–the so-called bliss molecule and our natural marijuana–in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character.” This article, like the one touting the alcoholism gene 25 years ago, was written by a physician, Richard Friedman, professor of psychiatry at Weill Cornell Medical College. I emphasize this fact because scientific hype is often blamed on supposedly ignorant journalists like me rather than on physicians and other so-called experts. © 2015 Scientific American
By Maggie Fox Teenagers who use marijuana heavily grow up to have poor memories and also have brain abnormalities, a new study shows. The study cannot say which came first — the brain structure differences or the pot use. But it suggests there could be long-term effects of heavy marijuana use. A team at Northwestern University looked at 97 volunteers with and without mental illness. The dope smokers said they'd used marijuana daily starting at age 16 or 17, and said they had not used other drugs. The daily marijuana users had an abnormally shaped hippocampus and performed about 18 percent more poorly on long-term memory tasks, the researchers reported in the journal Hippocampus. The hippocampus is a part of the brain used in storing long-term memory. "The memory processes that appear to be affected by cannabis are ones that we use every day to solve common problems and to sustain our relationships with friends and family," said Dr. John Csernansky, who worked on the study. Previous research by the same Northwestern team showed heavy pot smokers had poor short-term and working memory and abnormally shaped brain structures including the striatum, globus pallidus and thalamus. "It is possible that the abnormal brain structures reveal a pre-existing vulnerability to marijuana abuse," Matthew Smith, who led the study, said in a statement.
|By Anne Skomorowsky On a Saturday night last month, 12 students at Wesleyan University in Connecticut were poisoned by “Molly,” a hallucinogenic drug they had taken to enhance a campus party. Ambulances and helicopters transported the stricken to nearby hospitals, some in critical condition. Molly—the street name for the amphetamine MDMA—can cause extremely high fevers, liver failure, muscle breakdown, and cardiac arrest. Given the risks associated with Molly, why would anybody take it? The obvious answer—to get high—is only partly true. Like many drugs of abuse, Molly causes euphoria. But Molly is remarkable for its “prosocial” effects. Molly makes users feel friendly, loving, and strongly connected to one another. Molly is most commonly used in settings where communion with others is highly valued, such as raves, music festivals, and college parties. Recently, psychiatrists have taken an interest in its potential to enhance psychotherapy; this has led to new research into the mechanisms by which MDMA makes people feel closer. It appears that MDMA works by shifting the user’s attention towards positive experiences while minimizing the impact of negative feelings. To investigate this, a 2012 study by Cedric Hysek and colleagues used the Reading the Mind in the Eyes Test (RMET), which was developed to evaluate people with autism. In the RMET, participants are shown 36 pictures of the eye region of faces. Their task is to describe what the person in the picture is feeling. Volunteers taking MDMA, under carefully controlled conditions, improved in their recognition of positive emotions; but their performance in recognizing negative emotions declined. In other words, they incorrectly attributed positive or neutral feelings to images that were actually negative in emotional tone. They mistook negative and threat-related images for friendly ones. © 2015 Scientific American
Keyword: Drug Abuse
Link ID: 20678 - Posted: 03.12.2015
By RICHARD A. FRIEDMAN CHANCES are that everyone on this planet has experienced anxiety, that distinct sense of unease and foreboding. Most of us probably assume that anxiety always has a psychological trigger. Yet clinicians have long known that there are plenty of people who experience anxiety in the absence of any danger or stress and haven’t a clue why they feel distressed. Despite years of psychotherapy, many experience little or no relief. It’s as if they suffer from a mental state that has no psychological origin or meaning, a notion that would seem heretical to many therapists, particularly psychoanalysts. Recent neuroscience research explains why, in part, this may be the case. For the first time, scientists have demonstrated that a genetic variation in the brain makes some people inherently less anxious, and more able to forget fearful and unpleasant experiences. This lucky genetic mutation produces higher levels of anandamide — the so-called bliss molecule and our own natural marijuana — in our brains. In short, some people are prone to be less anxious simply because they won the genetic sweepstakes and randomly got a genetic mutation that has nothing at all to do with strength of character. About 20 percent of adult Americans have this mutation. Those who do may also be less likely to become addicted to marijuana and, possibly, other drugs — presumably because they don’t need the calming effects that marijuana provides. One patient of mine, a man in his late 40s, came to see me because he was depressed and lethargic. He told me at our first meeting that he had been using cannabis almost daily for at least the past 15 years. “It became a way of life,” he explained. “Things are more interesting, and I can tolerate disappointments without getting too upset.” © 2015 The New York Times Company
Hannah Devlin, science correspondent Psychedelic drugs could prove to be highly effective treatments for depression and alcoholism, according to a study which has obtained the first brain scans of people under the influence of LSD. Early results from the trial, involving 20 people, are said to be “very promising” and add to existing evidence that psychoactive drugs could help reverse entrenched patterns of addictive or negative thinking. However, Prof David Nutt, who led the study, warned that patients are missing out on the potential benefits of such treatments due to prohibitive regulations on research into recreational drugs. Speaking at a briefing in London, the government’s former chief drugs adviser, said the restrictions amounted to “the worst censorship in the history of science”. After failing to secure conventional funding to complete the analysis of the latest study on LSD, Nutt and colleagues at Imperial College London, are now attempting to raise £25,000 through the crowd-funding site Walacea.com. “These drugs offer the greatest opportunity we have in mental health,” he said. “There’s little else on the horizon.” There has been a resurgence of medical interest in LSD and psilocybin, the active ingredient in magic mushrooms, after several recent trials produced encouraging results for conditions ranging from depression in cancer patients to post-traumatic stress disorder. © 2015 Guardian News and Media Limited
Zoe Cormier Data from population surveys in the United States challenge public fears that psychedelic drugs such as LSD can lead to psychosis and other mental-health conditions and to increased risk of suicide, two studies have found1, 2. In the first study, clinical psychologists Pål-Ørjan Johansen and Teri Suzanne Krebs, both at the Norwegian University of Science and Technology in Trondheim, scoured data from the US National Survey on Drug Use and Health (NSDUH), an annual random sample of the general population, and analysed answers from more than 135,000 people who took part in surveys from 2008 to 2011. Of those, 14% described themselves as having used at any point in their lives any of the three ‘classic’ psychedelics: LSD, psilocybin (the active ingredient in so-called magic mushrooms) and mescaline (found in the peyote and San Pedro cacti). The researchers found that individuals in this group were not at increased risk of developing 11 indicators of mental-health problems such as schizophrenia, psychosis, depression, anxiety disorders and suicide attempts. Their paper appears in the March issue of the Journal of Psychopharmacology1. The findings are likely to raise eyebrows. Fears that psychedelics can lead to psychosis date to the 1960s, with widespread reports of “acid casualties” in the mainstream news. But Krebs says that because psychotic disorders are relatively prevalent, affecting about one in 50 people, correlations can often be mistaken for causations. “Psychedelics are psychologically intense, and many people will blame anything that happens for the rest of their lives on a psychedelic experience.” © 2015 Nature Publishing Group,
Children who attend school in heavy traffic areas may show slower cognitive development and lower memory test scores, Spanish researchers have found. About 21,000 premature deaths are attributed to air pollution in Canada each year, according to the Canadian Medical Association. The detrimental effects of air pollution on cardiovascular health and on the lungs are well documented and now researchers are looking at its effects on the brain. To that end, Dr. Jordi Sunyer and his colleagues from the Centre for Research in Environmental Epidemiology in Barcelona measured three aspects of memory and attentiveness in more than 2,700 primary school children every three months over 12 months. "What was surprising for us is among our children, we see very robust, consistent effects," Sunyer said Tuesday from Rome. The associations between slower cognitive development and higher levels of air pollutants remained after the researchers took factors such as parents’ education, commuting time, smoking in the home and green spaces at school into account. The researchers measured air pollutants from traffic twice, in the school courtyard and inside the classroom for schools with high and low traffic-related air pollution. Pollutants from burning fossil fuels, carbon, nitrogen dioxide and ultrafine particles were measured. For example, working memory improved 7.4 per cent among children in highly polluted schools compared with 11.5 per cent among those in less polluted schools. ©2015 CBC/Radio-Canada.
Anti-depressants are the most commonly-prescribed medication in the U.S., with one in 10 Americans currently taking pills like Zoloft and Lexapro to treat depression. But these pharmaceuticals are only fully effective roughly 30 percent of the time, and often come with troublesome side effects. In a controversial new paper published in the journal Neuroscience & Biobehavioral Reviews, psychologist Paul Andrews of McMaster University in Ontario argues that this failure of medication may be based in a misunderstanding of the underlying chemistry related to depression. Andrews surveyed 50 years' worth of research supporting the serotonin theory of depression, which suggests that the disease is caused by low levels of the "happiness" neurotransmitter, serotonin. But Andrews argues that depression may actually be caused by elevated levels of serotonin. And this fundamental misunderstanding may be responsible for inappropriate treatment: The most common form of antidepressants are selective serotonin re-uptake inhibitors (SSRIs), which operate by targeting serotonin receptors in the brain in an effort to amplify serotonin production. Currently, scientists are unable to measure precisely how the brain releases and uses serotonin, because it can't be safely observed in a human brain. But Andrews points to research on animals which suggests that serotonin might work just the opposite from what we've assumed. ©2015 TheHuffingtonPost.com, Inc.
Link ID: 20636 - Posted: 03.02.2015
by Michael Slezak If you want to counteract the effects of getting drunk, a big dose of the so-called "cuddle-chemical" oxytocin might be the answer. Oxytocin has important roles in sexual behaviour and social bonding, and has previously been investigated as a way to help wean alcoholics off drink. While studying this effect in rats, Michael Bowen from the University of Sydney noticed something strange. Rats that had been given oxytocin didn't seem to get drunk. "Those that had the oxytocin were up and moving about as if they hadn't had any alcohol at all, whereas the ones that didn't have oxytocin were quite heavily sedated," Bowen says. This effect was confirmed in a second experiment, in which half the rats were given an injection of oxytocin straight into the brain, at a level about 150,000 times what would normally be found there. They were then given alcohol, after which researchers tested their motor control and reaction times. Oxytocin seemed to completely counteract the effects of the booze – even when a rat had consumed what would be equivalent to about one and a half bottles of wine in humans. "The rats that had received oxytocin, as well as the alcohol, were virtually indistinguishable from the rats that hadn't received any alcohol at all," says Bowen. This could be thanks to the brain's GABA receptors, where alcohol is thought to exert its intoxicating effects. Bowen's team found that oxytocin was binding to two parts of these receptors, blocking alcohol from getting there. "It was actually preventing alcohol affecting these sites in the brain that make you intoxicated." © Copyright Reed Business Information Ltd
Charles F. Zorumski It is indeed possible for a person to get intoxicated and not remember what she or he did. This state is called a “blackout” or, more precisely, a “memory blackout.” During a blackout a person is intoxicated but awake and interacting with the environment in seemingly meaningful ways, such as holding a conversation or driving a car. After the period of intoxication, usually the next day, the person has no or, at best, vague recall for events that occurred while inebriated. At times, being in this state can have disastrous consequences, such as waking up in an unknown or unsafe place, losing personal possessions or participating in risky behaviors. On the neural level, a blackout is a period of anterograde amnesia. That is, a person's ability to form new memories becomes impaired. Although a person does not lose previously learned information, he or she may also find it more difficult to recall certain facts while intoxicated. Yet once a person sobers up, his or her memory and ability to learn new information are not permanently affected. How alcohol, or ethanol, produces a memory blackout is not completely understood. It is clear, however, that alcohol can impair a process in brain cells called long-term potentiation (LTP), a cellular mechanism thought to underlie memory formation, particularly in the hippocampus. © 2015 Scientific American
A dozen university students have been treated at Connecticut hospitals after overdosing on "Molly" or MDMA, a popular synthetic party drug. Police are investigating after the overdoses were reported late Sunday on the campus of Wesleyan University in Middletown, Connecticut. By Monday, eight remained in hospital and two were in critical condition. It was unclear whether the students had been together or where the drugs had come from. Middletown Police Chief William McKenna said that their "first and foremost goal is to obtain information on the batch of Molly that was distributed to the students on the campus," adding, "this information is critical in ensuring the recovery of those students affected." A pure and more powerful form of MDMA often sold as "Molly" can cause liver, kidney, cardiovascular failure, or death. In a campus-wide statement, Wesleyan president Michael S Roth urged students to "please, please stay away from illegal substances, the use of which can put you in extreme danger. One mistake can change your life forever". Dean Michael Whaley, vice president of student affairs at Wesleyan University, sent a letter to the school body on Sunday recommending students to check on their friends. Ten of the 12 people were Wesleyan students. In 2013, Molly-related deaths and illnesses forced the Electric Zoo Festival in New York to shut down early after two young people died and four were confined to hospital.
Keyword: Drug Abuse
Link ID: 20602 - Posted: 02.24.2015
|By Roni Jacobson Several pharmaceutical drugs promise to help addicts quit, and many people embrace the ease of popping a pill. Yet research continues to show that although medication can help, support networks and therapy targeting the underlying behaviors are still the best available ways to kick addiction over the long term. In addition, some of these medications come with scary side effects—hundreds of people have reportedly committed suicide while on the smoking-cessation drug Chantix, for example. Read on for short profiles of the addiction drugs currently on the market, as well as a few compounds that may hit shelves soon. © 2015 Scientific American,
Keyword: Drug Abuse
Link ID: 20601 - Posted: 02.24.2015
Boer Deng Smoking marijuana may stoke a yearning for crisps, but understanding how it affects hunger is relevant not just to those who indulge in it. The drug has yielded a ripe target for scientists who seek to stimulate or suppress appetite: the receptor CB1, found in cells throughout the body. When activated by the anti-nausea drug dronabinol — which is also a component of marijuana (Cannabis sativa) — CB1 prompts the release of hunger-promoting hormones1. And suppressing its activity is thought to aid in weight loss2. But the mechanism by which the receptor kills or kindles appetite is not entirely understood. Now neuroscientist Tamas Horvath, of Yale University in New Haven, and colleagues report in Nature that nerve cells called pro-opiomelanocortin (POMC) neurons play a key role in this process3. POMC had generally been thought to promote satiation, but Horvath's team found that POMC neurons in the brain release not just a hunger-suppressing hormone, but also one that promotes appetite. Which hormone is secreted is regulated by a protein in the cells' mitochondria, structures that regulate energy levels. When the CB1 receptor is activated, this mitochondrial protein induces POMC to switch from secreting the substance that suppresses gorging to one that encourages it. The finding is intriguing, says Uberto Pagotto, a neuroscientist at the University of Bologna who has studied cannabinoids for many years. “It gives us a different starting point to look at CB1 receptors and the mitochondria,” he says. © 2015 Nature Publishing Group
By Abigail Zuger, M.D. I had intended to discuss President Obama’s plans for personalized precision medicine with my patient Barbara last week, but she missed her appointment. Or, more accurately, she arrived two hours late, made the usual giant fuss at the reception desk and had to be rescheduled. I was disappointed. Barbara has some insight into the vortex of her own complications, and I thought she might help organize my thoughts. Mr. Obama announced last month that his new budget included $215 million toward the creation of a national databank of medical information, intended to associate specific gene patterns with various diseases and to predict what genetic, lifestyle and environmental factors correlate with successful treatment. Once all those relationships are clarified, the path will open to drugs or other interventions that firm up the good links and interrupt the bad ones. This step up the scientific ladder of medicine has many advocates. Researchers who sequence the genome are enthusiastic, as are those with a financial interest in the technology. Also celebrating are doctors and patients in the cancer community, where genetic data already informs some treatment choices and where the initial thrust of the initiative and much of its funding will be directed. Skeptics point out that genetic medicine, for all its promise, has delivered relatively few clinical benefits. And straightforward analyses of lifestyle and environment effects on health may occasionally lead to clear-cut advice (don’t smoke), but more often sow confusion, as anyone curious about the best way to lose weight or the optimal quantity of dietary salt knows. Without Barbara’s presence, I was left to ponder her medical record, a 20-year saga that might be titled “Genes, Lifestyle and Environment.” and published as a cautionary tale. © 2015 The New York Times Company
By Lizzie Wade SAN JOSE, CALIFORNIA—Humans have been using cannabis for more than 5000 years. So why don’t scientists know more about it? Three experts gathered here at the annual meeting of AAAS (which publishes Science) to discuss what scientists and doctors know about the drug and what they still need to learn. “By the end of this session, you’ll know more about cannabis than your physician does,” said Mark Ware, a family physician at the McGill University Health Center in Montreal, Canada, who organized the talk. How does marijuana work? Our brains are primed to respond to marijuana, because “there are chemicals in our own bodies that act like THC [the psychoactive ingredient in pot]” and other compounds in cannabis called cannabinoids, explained Roger Pertwee, a neuropharmacologist at the University of Aberdeen in the United Kingdom who has studied cannabinoids since the 1960s. Cannabinoids produced by our bodies or ingested through marijuana use react with a series of receptors in our brains called the endocannabinoid system, which is involved in appetite, mood, memory, and pain sensation. Scientists have discovered 104 cannabinoids so far, but “the pharmacology of most of them has yet to be investigated,” Pertwee said. What are the known medical uses of marijuana? Marijuana has been used for decades to stimulate appetite and treat nausea and vomiting, especially in patients undergoing chemotherapy. Its success in easing the symptoms of multiple sclerosis patients led to the development of Sativex, a drug manufactured by GW Pharmaceuticals that includes THC and cannabidiol (CBD), a cannabinoid that isn’t psychoactive. © 2015 American Association for the Advancement of Science
Smoking potent cannabis was linked to 24% of new psychosis cases analysed in a study by King's College London. The research suggests the risk of psychosis is three times higher for users of potent "skunk-like" cannabis than for non-users. The study of 780 people was carried out by KCL's Institute of Psychiatry, Psychology and Neuroscience. A Home Office spokesman said the report underlines the reasons why cannabis is illegal. Scientists found the risk of psychosis was five times higher for those who use it every day compared with non-users. They also concluded the use of hash, a milder form of the drug, was not associated with increased risk of psychosis. Psychosis refers to delusions or hallucinations that can be present in certain psychiatric conditions such as schizophrenia and bipolar disorder. "Compared with those who had never tried cannabis, users of high potency skunk-like cannabis had a threefold increase in risk of psychosis,' said Dr Marta Di Forti, lead author on the research. She added: "The results show that psychosis risk in cannabis users depends on both the frequency of use and cannabis potency." Dr Di Forti told BBC Radio 4's Today programme that the availability of skunk-like cannabis was becoming more widespread. "In London, it's very difficult to find anything else," she said. "There were lots of reports from police across the UK saying we have become a great producer of skunk. And not only do we use it locally but we export, so this is a Made in England product." Someone suffering from psychosis would often be "extremely paranoid and become very suspicious" about the people around them, she added. She has called for "a clear public message" to cannabis users, comparable to medical advice on alcohol and tobacco. © 2015 BBC