Chapter 12. Psychopathology: The Biology of Behavioral Disorders
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By Diana Kwon A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being Credit: Thomas Koehler/Getty Images Life in the city can be taxing. City dwellers often face higher rates of crime, pollution, social isolation and other environmental stressors than those living in rural areas. For years studies have consistently linked the risk of developing schizophrenia to urban environments—but researchers are only beginning to understand why this association exists. Addressing the link is increasingly urgent: According to a recent U.N. report, the proportion of people living in cities will rise from 54 percent of the world’s population in 2014 to 66 percent by 2050. Researchers first suggested in the 1930s that urban living might increase schizophrenia risk. Since then many large epidemiological studies have reported an association between the two, primarily in European countries such as Sweden and Denmark. Converging evidence has revealed that growing up in the city doubles the risk of developing psychosis later in life. Studies have also begun to find that urban environments may heighten the risk of other mental health issues such as depression and anxiety. A number of factors, including elements of the social environment (such as inequality and isolation) and physical stressors (such as pollution and noise) could explain how the city erodes well-being. Conversely, people predisposed to mental illness may simply be more likely to move into urban environments. Two studies published this month shed new light on these effects and suggest both scenarios could be involved. © 2016 Scientific American, a Division
Zoe Cormier A hallucinogenic drug derived from magic mushrooms could be useful in treating depression, the first safety study of this approach has concluded. Researchers from Imperial College London gave 12 people psilocybin, the active component in magic mushrooms. All had been clinically depressed for a significant amount of time — on average 17.8 years. None of the patients had responded to standard medications, such as selective serotonin re-uptake inhibitors (SSRIs), or had electroconvulsive therapy. One week after receiving an oral dose of psilocybin, all patients experienced a marked improvement in their symptoms. Three months on, five patients were in complete remission. “That is pretty remarkable in the context of currently available treatments,” says Robin Carhart-Harris, a neuropsychopharmacologist at Imperial College London and first author of the latest study, which is published in The Lancet Psychiatry1. The equivalent remission rate for SSRIs is around 20%. The study's authors are not suggesting that psilocybin should be a treatment of last resort for depressed patients. “Our conclusion is more sober than that — we are simply saying that this is doable,” says Carhart-Harris. “We can give psilocybin to depressed patients, they can tolerate it, and it is safe. This gives us an initial impression of the effectiveness of the treatment.” © 2016 Nature Publishing Group
By CLYDE HABERMAN At respected research centers in the United States and other countries, scientists have spent much of their professional lives in drug rehabilitation. It is not because they themselves struggle with addiction. What they are trying to rehabilitate are the drugs. Their focus is on mind-altering compounds that fell far from grace nearly half a century ago, LSD prominent among them. Along with other psychedelics, it was outlawed by the federal government, damned as bearing a high potential for abuse and offering no accepted medical benefit. But in recent years, researchers have sought to rescue hallucinogens from exile by examining their efficacy in treating certain disorders of the mind, and perhaps even in understanding the nature of consciousness and spirituality. The work of these scientists now draws the attention of Retro Report, a series of video documentaries that examine major news stories of the past and their enduring significance. Psychoactive substances, often derived from mushrooms, have been part of human cultures from Central and South America to the Sahara for thousands of years. But there is no need to look that far back; 1938 will do. That was when Albert Hofmann, a Swiss chemist searching for a drug to combat circulatory ailments, happened to synthesize lysergic acid diethylamide: LSD or, more familiarly, acid. Five years later, Dr. Hofmann, who died in 2008 at age 102, accidentally ingested a small dose of his creation and discovered its mind-blowing potential as he embarked on the first known acid trip. Many more such journeys would follow, for him and for countless others. © 2016 The New York Times Company
By Lisa Damour Parents of teenagers face a confounding crosscurrent. While the legalization of marijuana in several American states now bolsters the common belief among adolescents that the drug is safe for recreational use, research documenting marijuana’s diffuse and possibly permanent harm to the teenage brain continues to pile up. Normally developing teenagers question authority and are likely to be skeptical of adults bearing bad news about a widely used party drug. So how do we have successful conversations about the hazards of marijuana use? An open-ended exchange that credits the adolescent’s own observations may do more good than a single sit-down or lecture. Beyond that, we might consider how the facts are often received by adolescents. With all the talk about cannabis legalization, parents may feel compelled to remind their teenagers that recreational marijuana is still banned for most American adults and for anyone under 21. Adolescents who use marijuana risk immediate legal consequences and, in districts with zero-tolerance policies, may be barred from organized school activities, suspended or expelled. They may also face long-term penalties affecting some jobs, internships, colleges and travel visas. But the repercussions of being caught with marijuana don’t faze all teenagers. Most adolescents can name celebrities, famous athletes and classmates who use marijuana regularly, even flagrantly, without running into trouble. Teenagers tend to bristle at rules that seem arbitrary, such as the state-by-state regulations for marijuana and the fact that alcohol, which has a lot in common with pot, is legal. Further, adolescents can be understandably cynical about laws that aren’t applied evenly to everyone: While African-Americans and whites use the drug at similar rates, African-Americans are nearly four times as likely to be arrested for marijuana possession. However real and lasting the penalties for pot use may be, parents often run into resistance when trying to make this case to teenagers. © 2016 The New York Times Company
Laura Sanders Ketamine, a drug that has shown promise in quickly easing depression, doesn’t actually do the job itself. Instead, depression relief comes from one of the drug’s breakdown products, a new study in mice suggests. The results, published May 4 in Nature, identify a potential depression-fighting drug that works quickly but without ketamine’s serious side effects or potential for abuse. The discovery “could be a major turning point,” says neuroscientist Roberto Malinow of the University of California, San Diego. “I’m sure that drug companies will look at this very closely.” Depression is a pernicious problem with few good treatments. Traditional antidepressants don’t work for everyone, and when the drugs do work, they can take weeks to kick in. Ketamine, developed in the 1960s as a sedative for people and now used commonly by veterinarians to knock out animals, can ease depression in minutes, not weeks, small studies show. But the new study suggests that a metabolite of ketamine — not the drug itself — fights depression. Inside the body, ketamine gets converted into a slew of related molecules. One of these breakdown molecules, a chemical called (2R,6R)-hydroxynorketamine, is behind the benefits, neuropharmacologist Todd Gould of the University of Maryland School of Medicine in Baltimore and colleagues found. On its own, a single dose of (2R,6R)-HNK reduced signs of depression in mice, restoring their drive to search for a hidden platform in water, to try to escape a shock and to choose sweet water over plain. A type of ketamine that couldn’t be broken down easily into HNKs didn’t ease signs of depression in mice. Finding that a breakdown product, and not ketamine itself, was behind the results was a big surprise, Gould says. © Society for Science & the Public 2000 - 2016
By John Horgan I had to ask Anthony Bossis about bad trips. Bossis, a psychologist at New York University, belongs to an intrepid cadre of scientists reviving research into psychedelics’ therapeutic potential. I say “reviving” because research on psychedelics thrived in the 1950s and 1960s before being crushed by a wave of anti-psychedelic hostility and legislation. Psychedelics such as LSD, psilocybin and mescaline are still illegal in the U.S. But over the past two decades, researchers have gradually gained permission from federal and other authorities to carry out experiments with the drugs. Together with physicians Stephen Ross and Jeffrey Guss, Bossis has tested the potential of psilocybin—the primary active ingredient of “magic mushrooms”--to alleviate anxiety and depression in cancer patients. Journalist Michael Pollan described the work of Bossis and others in The New Yorker last year. Pollan said researchers at NYU and Johns Hopkins had overseen 500 psilocybin sessions and observed “no serious adverse effects.” Many subjects underwent mystical experiences, which consist of "feelings of unity, sacredness, ineffability, peace and joy," as well as the conviction that you have discovered "an objective truth about reality." Pollan’s report was so upbeat that I felt obliged to push back a bit, pointing out that not all psychedelic experiences—or mystical ones--are consoling. In The Varieties of Religious Experience, William James emphasized that some mystics have “melancholic” or “diabolical” visions, in which ultimate reality appears terrifyingly alien and uncaring. Taking psychedelics in a supervised research setting doesn’t entirely eliminate the risk of a bad trip. That lesson emerged from a study in the early 1990s by psychiatrist Rick Strassman, who injected dimethyltryptamine, DMT, into human volunteers. © 2016 Scientific American
Symptoms of depression that steadily increase over time in older age could indicate early signs of dementia, scientists have said. Other patterns of symptoms, such as chronic depression, appear not to be linked, a study found. Dutch researchers looked at different ways depression in older adults progressed over time and how this related to any risk. They concluded worsening depression may signal the condition is taking hold. The research, published in The Lancet Psychiatry, followed more than 3,000 adults aged 55 and over living in the Netherlands. All had depression but no symptoms of dementia at the start of the study. Dr M Arfan Ikram of the Erasmus University Medical Center in Rotterdam said depressive symptoms that gradually increase over time appear to be a better predictor of dementia later in life than other paths of depression. "There are a number of potential explanations, including that depression and dementia may both be symptoms of a common underlying cause, or that increasing depressive symptoms are on the starting end of a dementia continuum in older adults," he said. Only the group whose symptoms of depression increased over time were found to be at increased risk of dementia - about one in five of people (55 out of 255) in this group developed dementia. Others who had symptoms that waxed and waned or stayed the same were not at increased risk. For example, in those who experienced low but stable levels of depression, around 10% went on to develop dementia. The exact nature of depression on dementia risk remains unknown. © 2016 BBC
People who've recovered from depression stave off relapses with mindfulness therapy as well as with antidepressants, a new review finds. Mindfulness-based cognitive therapy (MBCT) is an eight-week group program that helps people become better observers of their own thoughts and emotions and to learn to distance themselves before ruminations spiral downwards. An international team of psychiatry researchers combined data from nine randomized trials of 1,258 patients total with recurrent depression to compare the mindfulness therapy to placebo, treatment as usual and other active treatments including antidepressants. People suffering from depression who received the mindfulness therapy were 31 per cent less likely to suffer a relapse during the next 60 weeks compared with those who did not receive it, Willem Kuyken of the University of Oxford, in England and his co-authors reported in a meta-analysis review in Wednesday's issue of the journal JAMA Psychiatry. "If you compare MBCT against antidepressant medication it basically holds its own, which means it provides protection on par with what people would get from continuing to take to take medications for one, two or three years after they've recovered from depression," said co-author Dr. Zindel Segal, a professor of psychology at the University of Toronto Scarborough. No one reported side-effects associated with participating in the therapy. ©2016 CBC/Radio-Canada.
By ERICA GOODE PORTLAND, Ore. — The 911 caller had reported a man with a samurai sword, lunging at people on the waterfront. It was evening, and when the police arrived, they saw the man pacing the beach and called to him. He responded by throwing a rock at the embankment where they stood. They shouted to him from a sheriff’s boat; he threw another rock. They told him to drop the sword; he said he would kill them. He started to leave the beach, and after warning him, they shot him in the leg with a beanbag gun. He turned back, still carrying the four-foot blade. In another city — or in Portland itself not that long ago — the next step would almost certainly have been a direct confrontation and, had the man not put down the weapon, the use of lethal force. But the Portland Police Bureau, prodded in part by the 2012 findings of a Justice Department investigation, has spent years putting in place an intensive training program and protocols for how officers deal with people with mental illness. At a time when police behavior is under intense scrutiny — a series of fatal shootings by police officers have focused national attention on issues of race and mental illness — Portland’s approach has served as a model for other law enforcement agencies around the country. And on that Sunday last summer, the police here chose a different course. At 2:30 a.m., after spending hours trying to engage the man, the officers decided to “disengage,” and they withdrew, leaving the man on the beach. A search at daylight found no signs of him. People with mental illnesses are overrepresented among civilians involved in police shootings: Twenty-five percent or more of people fatally shot by the police have had a mental disorder, according to various analyses. © 2016 The New York Times Company
Link ID: 22150 - Posted: 04.27.2016
By Bret Stetka The multibillion-dollar supplement industry spews many dubious claims, but a new study suggests that some nutritional supplements, including omega-3 fatty acids and vitamin D, may boost the effectiveness of antidepressants. If so, the supplements might help relieve symptoms for the millions of people who don’t immediately respond to these drugs. The meta-analysis—published Tuesday in the American Journal of Psychiatry—reviewed the results of 40 clinical trials that evaluated the effects of taking nutritional supplements in conjunction with several major classes of antidepressants, including selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants. It revealed that four supplements in particular upped the potency of the medications, compared with a placebo. The researchers, based at Harvard University and the University of Melbourne, found the strongest evidence for an omega-3 fish oil called eicosapentaenoic acid, or EPA. In general, people with depression who took an antidepressant drug and an omega-3 sourced from fish oil experienced a significant reduction in their symptoms as assessed by a the Hamilton Depression Rating Scale, a common measure used by most of the studies in the review. The same was true, although to a lesser extent, for S-adenosylmethionine, methylfolate (a form of the B vitamin folic acid) and Vitamin D. A few isolated studies found some benefit from augmenting treatment with creatine, while adding zinc, vitamin C, the amino acid tryptophan and folic acid produced mixed results. The authors deemed all of these supplements relatively safe. © 2016 Scientific American,
Link ID: 22149 - Posted: 04.27.2016
By Nicholas Bakalar Treating pregnant women for depression may benefit not just themselves but their babies as well. A study, in the May issue of Obstetrics & Gynecology, included 7,267 pregnant women, of whom 831 had symptoms of depression. After controlling for maternal age, race, income, body mass index and other health and behavioral characteristics, the researchers found that depressive symptoms were associated with a 27 percent increased relative risk of preterm birth (less than 37 weeks of gestation), an 82 percent increased risk of very preterm birth (less than 32 weeks of gestation), and a 28 percent increased risk of having a baby small for gestational age. They also found that among those who were treated with antidepressants for depression — about a fifth of those with the diagnosis — there was no association with increased risk for any of these problems. But they acknowledge that this group was quite small, which limits the power to draw conclusions. Still, the lead author, Dr. Kartik K. Venkatesh, a clinical fellow in obstetrics and gynecology at Harvard, said that it was important to screen mothers for depression, not only for their health but for that of their babies. “By screening early in pregnancy, you could identify those at higher risk and counsel them about the importance of treatment,” he said. “Treating these women for depression may have real benefits.” © 2016 The New York Times Company
Anna Nowogrodzki Prions, the misfolded proteins that are known for causing degenerative illnesses in animals and humans, may have been spotted for the first time in plants. Researchers led by Susan Lindquist, a biologist at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, report that they have found a section of protein in thale cress (Arabidopsis) that behaves like a prion when it is inserted into yeast. In plants, the protein is called Luminidependens (LD), and it is normally involved in responding to daylight and controlling flowering time. When a part of the LD gene is inserted into yeast, it produces a protein that does not fold up normally, and which spreads this misfolded state to proteins around it in a domino effect that causes aggregates or clumps. Later generations of yeast cells inherit the effect: their versions of the protein also misfold. This does not mean that plants definitely have prion-like proteins, adds Lindquist — but she thinks that it is likely. “I’d be surprised if they weren’t there,” she says. To prove it, researchers would need to grind up a plant and see whether they could find a protein such as LD in several different folded states, as well as show that any potential prion caused a misfolding cascade when added to a test-tube of protein. Lindquist adds that because she's not a plant scientist — her focus is on using yeast to investigate prions — she hasn't tried these experiments. The study is reported on 25 April in the Proceedings of the National Academy of Sciences1. © 2016 Nature Publishing Group
Richard A. Friedman DRUG companies are eager to tell you about their newest medicines. Turn on your TV or go online and there’s a new drug — with a hefty price tag — for whatever ails you, from antidepressants to painkillers to remedies for erectile dysfunction. The pharmaceutical industry spends lavishly to get your attention: In 2014, drug makers poured $4.5 billion into so-called direct-to-consumer advertising, a 30 percent increase over two years. Drug makers claim they are educating the public with their ads, providing information that will help you make better choices about your medical care. So in the spirit of education, let’s consider a recent online ad for Latuda, a new antipsychotic medication. A young woman rides a bike off into the sun as we are told that Latuda has been shown to be effective for many people with bipolar depression, followed by that staccato recitation of potential side effects that most viewers tune out. Here’s what a helpful prescription drug label could look like, with facts that are now out of reach. These are question marks because, although many clinical trial results are published, they are difficult to find and compare. Rules should mandate that all studies are accessible. Note the same high cost for a four-fold range of Latuda doses. Often the lowest dose is just as effective; some low-dose consumers realize they can save money by ordering the higher-dose units and splitting them into pieces. The ideal label would have statistics on how many people have serious side effects. Data are not included for these drugs because they may take years to emerge, if ever. Other drugs have well-known side effects. Fair enough. But the ad omits something that most consumers would like to know: There are many older and cheaper treatments that are just as effective. In fact, Latuda is one of 10 “second generation” antipsychotic medications, many available in generic forms, that essentially work the same way. Of course, the goal of drug companies is not to educate, but to sell products. We could ban the ads, as almost every other country does, and which I’d strongly support. But such a campaign in the United States would face fierce legislative and legal challenges. Instead, let’s help the drug companies make their ads truly educational. © 2016 The New York Times Company
It was December 2012 when the country learned about the massacre at Sandy Hook Elementary School, that left 20 children dead at the hands of 20-year-old shooter Adam Lanza. After the shock and the initial grief came questions about how it could have happened and why. Reports that Adam Lanza may have had some form of undiagnosed mental illness surfaced. The tragedy drove Liza Long to write a blog post on that same day, titled "I Am Adam Lanza's Mother." She wasn't Lanza's mom, but she was raising a child with a mental disorder. Her 13-year-old son had violent rages on a regular basis. He was in and out of juvenile detention. He had threatened to kill her. She detailed all this in her essay that took off online. Now, four years later, her son is speaking out too. This week on For The Record: a mother, a son and life on the edge of bipolar disorder. Eric Walton, Liza Long's son, is now a 16-year-old high school sophomore in Boise, Idaho. After a series of misdiagnoses, he's been diagnosed with bipolar disorder. But four years ago, he didn't know much about his condition. "I knew that there were times when I would have rages, didn't like them. I knew that I wanted them to stop," Walton says. Except he felt a loss of control in those moments. He describes the onset of these rages as a "blackout" of sorts. "I would start getting angry," he says. "Then it's like being trapped inside a box inside your own head. It was like a television on the wall that shows you what you're seeing. You can feel everything, but you no longer have the video game controller to control your own body." Walton's mom says when Eric would get into those states, "he would express a lot of suicidal thoughts, and hearing him just say, 'I want to die, I just want to end it.'" Then, two days before the Newtown shooting, Eric Walton had another episode. © 2016 npr
By SABRINA TAVERNISE WASHINGTON — Suicide in the United States has surged to the highest levels in nearly 30 years, a federal data analysis has found, with increases in every age group except older adults. The rise was particularly steep for women. It was also substantial among middle-aged Americans, sending a signal of deep anguish from a group whose suicide rates had been stable or falling since the 1950s. The suicide rate for middle-aged women, ages 45 to 64, jumped by 63 percent over the period of the study, while it rose by 43 percent for men in that age range, the sharpest increase for males of any age. The overall suicide rate rose by 24 percent from 1999 to 2014, according to the National Center for Health Statistics, which released the study on Friday. The increases were so widespread that they lifted the nation’s suicide rate to 13 per 100,000 people, the highest since 1986. The rate rose by 2 percent a year starting in 2006, double the annual rise in the earlier period of the study. In all, 42,773 people died from suicide in 2014, compared with 29,199 in 1999. From 1999 to 2014, suicide rates in the United States rose among most age groups. Men and women from 45 to 64 had a sharp increase. Rates fell among those age 75 and older. “It’s really stunning to see such a large increase in suicide rates affecting virtually every age group,” said Katherine Hempstead, senior adviser for health care at the Robert Wood Johnson Foundation, who has identified a link between suicides in middle age and rising rates of distress about jobs and personal finances. Researchers also found an alarming increase among girls 10 to 14, whose suicide rate, while still very low, had tripled. The number of girls who killed themselves rose to 150 in 2014 from 50 in 1999. “This one certainly jumped out,” said Sally Curtin, a statistician at the center and an author of the report. © 2016 The New York Times Company
By Clare Wilson People who develop schizophrenia may have been born with brains with a different structure. The finding adds further support to the idea that genetics can play a key role in schizophrenia, which involves delusions and hallucinations and is often a lifelong condition once it develops. Schizophrenia has been the subject of a fierce nature-versus-nurture debate: childhood abuse is linked with a raised risk of the condition, but 108 genes have been implicated, too. Probing the biology of schizophrenia is difficult because brain tissue sampled from people with the condition is rarely available to study. Kristen Brennand of the Icahn School of Medicine at Mount Sinai in New York and her colleagues got around this by taking skin cells from 14 people with schizophrenia, and reprogramming them into stem cells and then nerve cells. They found that on average these nerve cells had lower levels of a signalling molecule called miR-9 than similar cells developed from people who do not have schizophrenia. A small string of nucleic acids, miR-9 can change the activity of certain genes and is known to play a role in how neurons develop in the fetus. In further experiments, Brennand’s team showed that miR-9 might also affect how neurons migrate from where they form, next to the fetal brain’s central cavities, out to their final resting place in the brain’s outer layers. © Copyright Reed Business Information Ltd.
By Emily Underwood Earlier this month, György Buzsáki of New York University (NYU) in New York City showed a slide that sent a murmur through an audience in the Grand Ballroom of New York’s Midtown Hilton during the annual meeting of the Cognitive Neuroscience Society. It wasn’t just the grisly image of a human cadaver with more than 200 electrodes inserted into its brain that set people whispering; it was what those electrodes detected—or rather, what they failed to detect. When Buzsáki and his colleague, Antal Berényi, of the University of Szeged in Hungary, mimicked an increasingly popular form of brain stimulation by applying alternating electrical current to the outside of the cadaver’s skull, the electrodes inside registered little. Hardly any current entered the brain. On closer study, the pair discovered that up to 90% of the current had been redirected by the skin covering the skull, which acted as a “shunt,” Buzsáki said. For many meeting attendees, the unusual study heightened serious doubts about the mechanism and effectiveness of transcranial direct current stimulation (tDCS), an experimental, noninvasive treatment that uses electrodes to deliver weak current to a person’s forehead, and the related tACS, which uses alternating current. Little is known about how these techniques might influence the brain. Yet many scientific papers have claimed that the techniques can boost mood, alleviate chronic pain, and even make people better at math by directly affecting neuronal activity. This has spawned a cottage industry of do-it-yourself gadgets promising to make people smarter and happier. © 2016 American Association for the Advancement of Science
Link ID: 22126 - Posted: 04.21.2016
Rachel Becker A highly contagious and deadly animal brain disorder has been detected in Europe for the first time. Scientists are now warning that the single case found in a wild reindeer might represent an unrecognized, widespread infection. Chronic wasting disease (CWD) was thought to be restricted to deer, elk (Cervus canadensis) and moose (Alces alces) in North America and South Korea, but on 4 April researchers announced that the disease had been discovered in a free-ranging reindeer (Rangifer tarandus tarandus) in Norway. This is both the first time that CWD has been found in Europe and the first time that it has been found in this species in the wild anywhere in the world. “It’s worrying — of course, especially for animals. It’s a nasty disease,” says Sylvie Benestad, an animal-disease researcher at the Norwegian Veterinary Institute in Oslo who, along with colleague Turid Vikøren, diagnosed the diseased reindeer. A key question now is whether this is a rare — even unique — case, or if the disease is widespread but so far undetected in Europe. “If it’s similar to our prion disease in the United States and Canada, the disease is subtle and it would be easy to miss,” says Christina Sigurdson, a pathologist at the University of California, San Diego, who has shown that reindeer can contract CWD in a laboratory environment1. © 2016 Nature Publishing Group,
Link ID: 22117 - Posted: 04.19.2016
Ian Sample Science editor The risks of heavy cannabis for mental health are serious enough to warrant global public health campaigns, according to international drugs experts who said young people were particularly vulnerable. The warning from scientists in the UK, US, Europe and Australia reflects a growing consensus that frequent use of the drug can increase the risk of psychosis in vulnerable people, and comes as the UN prepares to convene a special session on the global drugs problem for the first time since 1998. The meeting in New York next week aims to unify countries in their efforts to tackle issues around illicit drug use. While the vast majority of people who smoke cannabis will not develop psychotic disorders, those who do can have their lives ruined. Psychosis is defined by hallucinations, delusions and irrational behaviour, and while most patients recover from the episodes, some go on to develop schizophrenia. The risk is higher among patients who continue with heavy cannabis use. Public health warnings over cannabis have been extremely limited because the drug is illegal in most countries, and there are uncertainties over whether it really contributes to mental illness. But many researchers now believe the evidence for harm is strong enough to issue clear warnings. “It’s not sensible to wait for absolute proof that cannabis is a component cause of psychosis,” said Sir Robin Murray, professor of psychiatric research at King’s College London. © 2016 Guardian News and Media Limited
By Amy Ellis Nutt I saw it all: The beginning of Time and the end of Time. Creation and annihilation. Somehow I’d slipped through a seam in the space-time continuum, and from my privileged mental perch I'd peered into the center of the universe. I was exhilarated and drew diagrams of my visions, trying to figure out what it all meant. But when I shared those visions with friends, they were confused and concerned. I was manic, they said, and making no sense. We were at an impasse. Was I sick – or simply in search of myself? Those questions from my own past hovered in the background while I watched two very different documentaries recently. Both explore bipolar illness -- a diagnosis I received more than 25 years ago and one that 5.5 million Americans share. But the films come from very different perspectives. The first, "Ride the Tiger: A Guide Through the Bipolar Brain," was produced by Detroit Public TV and airs on PBS Wednesday. It chronicles the latest in cutting-edge research into bipolar disorder and in doing so firmly plants its flag in the biological camp: The disorder is about misfiring brain circuits, genetic mutations, neurochemical disruptions and other neurological processes not yet delineated. The result is dramatic swings in mood and behavior that affect a person's ability to think clearly. "Ride the Tiger" features appearances by former congressman Patrick Kennedy and the late actress Patty Duke, both of whom talk about their own experiences. The second documentary, "Bipolarized: Re-Thinking Mental Illness," questions the very reality of the disorder -- at least for one former psychiatric patient.
Link ID: 22104 - Posted: 04.14.2016