Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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By Elizabeth Pennisi It’s not such a stretch to think that humans can catch the Ebola virus from monkeys and the flu virus from pigs. After all, they are all mammals with fundamentally similar physiologies. But now researchers have discovered that even a virus found in the lowly algae can make mammals its home. The invader doesn’t make people or mice sick, but it does seem to slow specific brain activities. The virus, called ATCV-1, showed up in human brain tissue several years ago, but at the time researchers could not be sure whether it had entered the tissue before or after the people died. Then, it showed up again in a survey of microbes and viruses in the throats of people with psychiatric disease. Pediatric infectious disease expert Robert Yolken from Johns Hopkins University School of Medicine in Baltimore, Maryland, and his colleagues were trying to see if pathogens play a role in these conditions. At first, they didn't know what ATCV-1 was, but a database search revealed its identity as a virus that typically infects a species of green algae found in lakes and rivers. The researchers wanted to find out if the virus was in healthy people as well as sick people. They checked for it in 92 healthy people participating in a study of cognitive function and found it in 43% of them. What’s more, those infected with the virus performed 10% worse than uninfected people on tests requiring visual processing. They were slower in drawing a line connecting a sequence of numbers randomly placed on a page, for example. And they seemed to have shorter attention spans, the researchers report online today in the Proceedings of the National Academy of Sciences. The effects were modest, but significant. © 2014 American Association for the Advancement of Science
Link ID: 20258 - Posted: 10.29.2014
By ABIGAIL SULLIVAN MOORE The gray matter of the nucleus accumbens, the walnut-shaped pleasure center of the brain, was glowing like a flame, showing a notable increase in density. “It could mean that there’s some sort of drug learning taking place,” speculated Jodi Gilman, at her computer screen at the Massachusetts General Hospital-Harvard Center for Addiction Medicine. Was the brain adapting to marijuana exposure, rewiring the reward system to demand the drug? Dr. Gilman was reviewing a composite scan of the brains of 20 pot smokers, ages 18 to 25. What she and fellow researchers at Harvard and Northwestern University found within those scans surprised them. Even in the seven participants who smoked only once or twice a week, there was evidence of structural differences in two significant regions of the brain. The more the subjects smoked, the greater the differences. Moderate marijuana use by healthy adults seems to pose little risk, and there are potential medical benefits, including easing nausea and pain. But it has long been known that, with the brain developing into the mid-20s, young people who smoke early and often are more likely to have learning and mental health problems. Now researchers suggest existing studies are no longer sufficient. Much of what’s known is based on studies conducted years ago with much less powerful pot. Marijuana samples seized by the federal Drug Enforcement Agency show the concentration of THC, the drug’s psychoactive compound, rising from a mean of 3.75 percent in 1995 to 13 percent in 2013. Potency seesaws depending on the strain and form. Fresh Baked, which sells recreational marijuana in Boulder, Colo., offers “Green Crack,” with a THC content of about 21 percent, and “Phnom Pen,” with about 8 percent. The level in a concentrate called “Bubble Hash” is about 70 percent; cartridges for vaporizers, much like e-cigarettes, range from 15 to 30 percent THC. © 2014 The New York Times Company
Sarah Boseley, health editor A record haul of “smart” drugs, sold to students to enhance their memory and thought processes, stay awake and improve concentration, has been seized from a UK website by the medicines regulator, which is alarmed about the recent rise of such sites. The seizure, worth £200,000, illustrates the increasing internet trade in cognitive enhancement drugs and suggests people who want to stay focused and sharp are moving on from black coffee and legally available caffeine tablets. Most of the seized drugs are medicines that should only be available on a doctor’s prescription. One, Sunifiram, is entirely experimental and has never been tested on humans in clinical trials. Investigators from the Medicines and Healthcare Products Regulatory Authority (MHRA) are worried at what they see as a new phenomenon – the polished, plausible, commercial website targeting students and others who are looking for a mental edge over the competition. In addition to Ritalin, the drug that helps young people with attention deficit disorder (ADD) focus in class and while writing essays, and Modafinil (sold as Provigil), licensed in the US for people with narcolepsy, they are also offering experimental drugs and research chemicals. MHRA head of enforcement, Alastair Jeffrey, said the increase in people buying cognitive-enhancing drugs or “nootropics” is recent and very worrying. “The idea that people are willing to put their overall health at risk in order to attempt to get an intellectual edge over others is deeply troubling,” he said. © 2014 Guardian News and Media Limited
A drug being studied as a fast-acting mood-lifter restored pleasure-seeking behavior independent of — and ahead of — its other antidepressant effects, in a National Institutes of Health trial. Within 40 minutes after a single infusion of ketamine, treatment-resistant depressed bipolar disorder patients experienced a reversal of a key symptom — loss of interest in pleasurable activities — which lasted up to 14 days. Brain scans traced the agent’s action to boosted activity in areas at the front and deep in the right hemisphere of the brain. “Our findings help to deconstruct what has traditionally been lumped together as depression,” explained Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health. “We break out a component that responds uniquely to a treatment that works through different brain systems than conventional antidepressants — and link that response to different circuitry than other depression symptoms.” This approach is consistent with the NIMH’s Research Domain Criteria project, which calls for the study of functions – such as the ability to seek out and experience rewards – and their related brain systems that may identify subgroups of patients in one or multiple disorder categories. Zarate and colleagues reported on their findings Oct. 14, 2014 in the journal Translational Psychiatry. Although it’s considered one of two cardinal symptoms of both depression and bipolar disorder, effective treatments have been lacking for loss of the ability to look forward to pleasurable activities, or anhedonia. Long used as an anesthetic and sometimes club drug, ketamine and its mechanism-of-action have lately been the focus of research into a potential new class of rapid-acting antidepressants that can lift mood within hours instead of weeks.
Posted by Rachel Dolhun, MD, The ability to quit smoking, especially “cold turkey” or on the first attempt, has been heralded as a marker of strong willpower and determination. But could the ease with which one eschews cigarettes also serve as an early sign of Parkinson’s disease (PD)? This is the conclusion drawn by Beate Ritz, MD, PhD, and colleagues from the University of California, Los Angeles in a recent study published in Neurology. Researchers compared lifelong tobacco use, use of nicotine substitutes, and individual’s rating of their difficulty in trying to quit tobacco among 1,808 Danish people with PD and 1,876 control volunteers. They found that those with PD were less inclined to ever pick up the smoking habit, but, even if they did, they were less likely to need nicotine replacement therapies and able to more effortlessly stop smoking cigarettes. Therefore, ease of quitting smoking may be a sign of early PD. This joins a short list of other symptoms — smell loss, constipation and REM sleep behavior disorder — that usually predate diagnosis and are strongly associated with PD. Physicians rely heavily on such information to help confirm the diagnosis of Parkinson’s, given that biomarkers, objective measurements of disease, are currently lacking. Research led by The Michael J. Fox Foundation is ongoing to identify biological markers of PD, which could help diagnose and treat people earlier. In the meantime, doctors must look for symptoms and behaviors to help identify Parkinson’s. Researchers have long known that tobacco use was linked to a lower risk of PD. An ongoing Foundation-funded study is investigating whether nicotine might guard against or slow the progression of PD.
|By Brian Bienkowski and Environmental Health News Babies born to mothers with high levels of perchlorate during their first trimester are more likely to have lower IQs later in life, according to a new study. The research is the first to link pregnant women's perchlorate levels to their babies’ brain development. It adds to evidence that the drinking water contaminant may disrupt thyroid hormones that are crucial for proper brain development. Perchlorate, which is both naturally occurring and manmade, is used in rocket fuel, fireworks and fertilizers. It has been found in 4 percent of U.S. public water systems serving an estimated 5 to 17 million people, largely near military bases and defense contractors in the U.S. West, particularly around Las Vegas and in Southern California. “We would not recommend action on perchlorate levels from this study alone, although our report highlights a pressing need for larger studies of perchlorate levels from the general pregnant population and those with undetected hypothyroidism,” the authors from the United Kingdom, Italy and Boston wrote in the study published in The Journal of Clinical Endocrinology & Metabolism. The Environmental Protection Agency for decades has debated setting a national drinking water standard for perchlorate. The agency in 2011 announced it would start developing a standard, reversing an earlier decision. In the meantime, two states, California and Massachusetts, have set their own standards. © 2014 Scientific American
By Jennifer Cutraro and Michael Gonchar Marijuana is illegal in the United States. Yet 35 states and the District of Columbia permit some form of marijuana consumption for medical purposes, and, as of this year, two states now allow its recreational use. As national policy evolves on this issue, the New York Times editorial board this summer published a six-part series calling for legalization. In this lesson, we pull together those opinion pieces as well as many other Times articles, graphics and videos to offer starting points for science, social studies and English teachers aiming to use the debate as an opportunity for learning, research and discussion. Like other crops, marijuana is largely cultivated — legally and illegally — in greenhouse-type “grow houses” and on farms. And like other crops, marijuana comes from a plant — cannabis, originally found in the wild and cultivated over thousands of years. Have students research the history of cannabis, from its origins in South and Central Asia to its introduction to the Americas. How have people used the different parts of the plant throughout history? Then, have students work in groups to annotate a map of the world, tracing the history of marijuana cultivation. Marijuana is best known for its psychoactive properties. But how does marijuana bring about these sensations and how else does it behave in the body? To answer these questions, students might research how the active compounds in marijuana affect the body at the level of the cell, and draw parallels with how other drugs act in the body. As is the case with many other drugs — from legal, over-the-counter medications to illegal street drugs, like heroin — the active compounds interact with locations on the surfaces of cells called receptors. Cell surface receptors provide a means for cells to receive information and input from the environment; when a molecule attaches, or binds, to a cell surface receptor, it triggers a series of events inside the cell, like the release of hormones, neurotransmitters or other molecules. A discussion about marijuana’s effects on the body might dovetail nicely with a broader class discussion or review of cell biology, the makeup and function of the cell membrane, and the function of neurotransmitters. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 20118 - Posted: 09.27.2014
|By Simon Makin The Claim Casual cannabis use harms young people's brains. The Facts A study found differences in the brains of users and nonusers, but it did not establish that marijuana use caused the variations or that they had any functional significance. The Details Researchers at Northwestern University and Harvard Medical School conducted MRI scans of two groups of 20 young adults ages 18 to 25. One group reported using marijuana at least once a week, smoking 11 joints a week on average, whereas the other had used it less than five times total and not at all during the last year. Neither group had any psychiatric disorders, and the users were psychiatrically assessed as not dependent on the drug. The study focused on two brain regions involved in processing rewards, the nucleus accumbens and the amygdala. These areas create pleasurable experiences of things such as food and sex, as well as the high associated with drugs, and have been shown to change in animals given THC, the main psychoactive component of cannabis. The researchers found that cannabis users had more gray matter density in the left nucleus accumbens and left amygdala, as well as differences in the shape of the left nucleus accumbens and right amygdala. The left nucleus accumbens also tended to be slightly larger in users. They concluded that recreational cannabis use might be associated with abnormalities in the brain's reward system. News reports have proclaimed that scientists have shown that even casual cannabis use harms young people's brains. The Caveats The most obvious problem with leaping to that conclusion is that the scans were conducted at only one point. © 2014 Scientific American
|By Victoria Stern Many studies show that teens who use marijuana face a greater risk of later developing schizophrenia or symptoms of it, especially if they have a genetic predisposition. For instance, one 15-year study followed more than 45,000 Swedes who initially had no psychotic symptoms. The researchers determined that subjects who smoked marijuana by age 18 were 2.4 times more likely to be diagnosed with schizophrenia than their nonsmoking peers, and this risk increased with the frequency of cannabis use. The connection still held when researchers accounted for participants' use of other drugs. Yet despite these results and an uptick in marijuana use in the 1970s and 1980s, other researchers have not uncovered an increase in the incidence of schizophrenia in the general Swedish population—suggesting that perhaps people who were going to develop schizophrenia anyway were more likely to use marijuana. Another study, conducted in Australia over a 30-year period, also found no increase in schizophrenia diagnoses among the general population, despite rising rates of teen marijuana use. These authors concluded that although cannabis most likely does not cause schizophrenia, its use might trigger psychosis in vulnerable people or exacerbate an existing condition. © 2014 Scientific American
Elie Dolgin When Carol Steinberg was diagnosed with multiple sclerosis (MS) in 1995, there was only one drug approved by the US Food and Drug Administration to treat the disease. Now there are eleven. Yet none of these agents can help Steinberg. She suffers from progressive MS, a form of the disease that is characterized by steadily worsening neurological function. All eleven approved drugs combat the unpredictable symptom outbreaks that are associated with the relapsing–remitting form of MS. Around 85% of newly diagnosed patients have the relapsing–remitting form; after 10 to 20 years, most of them develop the progressive type. The lack of good treatment options for progressive MS weighs heavily on Steinberg. She uses a wheelchair, but continues to work as a trial lawyer in Newton, Massachusetts. “I’m constantly afraid of my disease getting worse,” she says. A global initiative called the Progressive MS Alliance now hopes to kick-start the development of therapies specifically for Steinberg and the million or so people worldwide living with progressive MS. On 11 September, at a joint meeting of the European and Americas Committees for Treatment and Research in Multiple Sclerosis, the alliance announced an inaugural round of research awards — part of a six-year, €22-million (US$28.5-million) programme that is the first concerted effort to tackle the disease’s less-common form. © 2014 Nature Publishing Group
By ANDREW POLLACK New York State’s attorney general filed an antitrust lawsuit on Monday seeking to stop a pharmaceutical company from forcing patients with Alzheimer’s disease to switch to a new version of a widely used drug. The lawsuit contends that the switch is designed to blunt competition from low-priced generic versions of the medication. Forest Laboratories, now owned by Actavis, announced in February that it would stop selling the existing tablet form of the drug, Namenda, in favor of new extended-release capsules called Namenda XR that can be taken once a day instead of twice. While the company said that patients preferred the newer drug, it has made little secret of its desire to switch all patients to the newer form, which has a longer patent life, before the old tablets face generic competition in July. The strategy would make it much harder for the generics to gain traction. The lawsuit, filed in Federal District Court in Manhattan, says the step is an illegal attempt by Forest to maintain its monopoly even after its patent expires. “A drug company manipulating vulnerable patients and forcing physicians to alter treatment plans unnecessarily, simply to protect corporate profits, is unethical and illegal,” the attorney general, Eric T. Schneiderman, said in a statement. A spokesman for Actavis said the company did not comment on pending litigation as a matter of policy. The company said that the once-a-day drug had “significant advantages” for patients and their caregivers. The lawsuit argues that the benefit of switching is not very great. It says the company decided to force the switch because it feared that not enough patients would switch voluntarily. © 2014 The New York Times Company
Link ID: 20078 - Posted: 09.16.2014
By Abby Phillip Most long-time, pack-a-day smokers who took part in a small study were able to quit smoking after six months, and researchers believe the hallucinogenic substance found in "magic mushrooms" could be the reason why. The study of the 15 participants, published this week in the Journal of Psychopharmacology, is the first to look at the feasibility of using the psychedelic drug psilocybin to aid in a smoking cessation treatment program. Existing treatments, from quitting cold turkey to prescription medications like Varenicline (Chantix), work for some people, but not the majority of smokers. With Varenicline, which mimics the effect of nicotine in the body, only about 35 percent of participants in a clinical trial were still abstaining from smoking six months later. Nearly half of all adult smokers reported that they tried to quit in 2010, according to the Centers for Disease Control and Prevention, yet 480,000 deaths are attributed to the addiction every year. Researchers at Johns Hopkins University recruited a group of long-time, heavy smokers — an average of 19 cigarettes a day for an average of 31 years — to participate in the study. They were treated with cognitive behavioral therapy for 15 weeks, and they were given a dose of the hallucinogen psilocybin at the five-week mark, when they had agreed to stop smoking. Although it was a small study, the results were promising. Twelve of the participants had quit smoking six months after being treated with the drug.
Keyword: Drug Abuse
Link ID: 20076 - Posted: 09.15.2014
by Michael Slezak "Cannabis catastrophic for young brains" screamed the headline on an Australian medical news website this week. The article, and others like it, were reporting on a study linking teenage cannabis use with school dropouts, addiction and suicide, published in the The Lancet Psychiatry. Echoing the research findings, the articles declared that if teenagers smoke cannabis daily, it makes them seven times more likely to commit suicide compared with non-users. Indeed, "there is no safe level of use", most reported. They also urged caution to legislators around the world that are gingerly taking steps towards weakening prohibition of cannabis, lest young people get easier access to it. So does smoking pot cause suicide? The Lancet authors say it probably does. Their study combined data from three previous longitudinal studies which together tracked cannabis use in more than 3000 people in Australia and New Zealand over many years. The authors looked for associations between the frequency of cannabis use before the age of 17 and outcomes, such as high school completion, until the people reached the age of 30. They found that those who smoked cannabis daily before they were 17 had lower odds of finishing high school and getting a degree than people who had never used cannabis. Larger increased odds were associated with cannabis dependence later in life, trying other illicit drugs and suicide attempts. But longitudinal studies only show correlation, not causation. The difficulty is that people take drugs for a reason, and that reason could be what's causing the outcome. In the case of school dropout, suicide and daily pot smoking, it is not hard to imagine what else could be going on in someone's life to engender these behaviours. © Copyright Reed Business Information Ltd
|By Amy Nordrum If you were one of millions of children who completed the Drug Abuse Resistance Education program, or D.A.R.E., between 1983 and 2009, you may be surprised to learn that scientists have repeatedly shown that the program did not work. Despite being the nation’s most popular substance-abuse prevention program, D.A.R.E. did not make you less likely to become a drug addict or even to refuse that first beer from your friends. But over the past few years prevention scientists have helped D.A.R.E. America, the nonprofit organization that administers the program, replace the old curriculum with a course based on a few concepts that should make the training more effective for today’s students. The new course, called keepin’ it REAL, differs in both form and content from the former D.A.R.E.—replacing long, drug-fact laden lectures with interactive lessons that present stories meant to help kids make smart decisions. Beginning in 2009 D.A.R.E. administrators required middle schools across the country that teach the program to switch over to the 10-week, researcher-designed curriculum for seventh graders. By 2013, they had ordered elementary schools to start teaching a version of those lessons to fifth and sixth graders, too. "It's not an antidrug program," says Michelle Miller-Day, co-developer of the new curriculum and a communications researcher at Chapman University. “It's about things like being honest and safe and responsible." Even so, keepin’ it REAL has reduced substance abuse and maintained antidrug attitudes over time among students in early trials—an achievement that largely eluded the former iteration of the program. D.A.R.E.’s original curriculum was not shaped by prevention specialists but by police officers and teachers in Los Angeles. They started D.A.R.E. in 1983 to curb the use of drugs, alcohol and tobacco among teens and to improve community–police relations. Fueled by word of mouth, the program quickly spread to 75 percent of U.S. schools. © 2014 Scientific American,
Keyword: Drug Abuse
Link ID: 20060 - Posted: 09.11.2014
By SOMINI SENGUPTA A coalition of political figures from around the world, including Kofi Annan, the former United Nations secretary general, and several former European and Latin American presidents, is urging governments to decriminalize a variety of illegal drugs and set up regulated drug markets within their own countries. The proposal by the group, the Global Commission on Drug Policy, goes beyond its previous call to abandon the nearly half-century-old American-led war on drugs. As part of a report scheduled to be released on Tuesday, the group goes much further than its 2011 recommendation to legalize cannabis. The former Brazilian president Fernando Henrique Cardoso, a member of the commission, said the group was calling for the legal regulation of “as many of the drugs that are currently illegal as possible, with the understanding that some drugs may remain too dangerous to decriminalize.” The proposal comes at a time when several countries pummeled by drug violence, particularly in Latin America, are rewriting their own drug laws, and when even the United States is allowing state legislatures to gingerly regulate cannabis use. The United Nations is scheduled to hold a summit meeting in 2016 to evaluate global drug laws. The commission includes former presidents like Mr. Cardoso of Brazil, Ernesto Zedillo of Mexico and Ruth Dreifuss of Switzerland, along with George P. Shultz, a former secretary of state in the Reagan administration, among others. The group stops short of calling on countries to legalize all drugs right away. It calls instead for countries to continue to pursue violent criminal gangs, to stop incarcerating users and to offer treatment for addicts. © 2014 The New York Times Company
Keyword: Drug Abuse
Link ID: 20052 - Posted: 09.10.2014
By C. CLAIBORNE RAY Q. Is there a difference between alcoholic dementia and “regular” dementia in the elderly? A. Dementia refers to the general category of diseases that cause acquired cognitive loss, usually in later life, said Dr. Mark S. Lachs, director of geriatrics for the NewYork-Presbyterian Healthcare System. Such loss has scores of possible causes, he said, but Alzheimer’s disease is the culprit in a vast majority of cases in the developed world. Alzheimer’s and what doctors call alcohol-related dementia affect parts of the brain cortex that control memory, language and the ability to follow motor commands. Because Alzheimer’s and excessive drinking are relatively common in the older population and can occur at the same time, and because many of their clinical features overlap and affect similar parts of the brain, “it is more accurate to say that each condition potentially exacerbates the other,” Dr. Lachs said. Abstinence is the treatment of choice in alcohol-related dementia, with or without concurrent Alzheimer’s disease or another form of dementia. Even in patients with “pure” Alzheimer’s disease or another kind of dementia, Dr. Lachs said, most experts recommend greatly moderating alcohol consumption or eliminating it, as even occasional drinking “can serve as a brain stress test for a patient with impaired cognition from any cause.” © 2014 The New York Times Company
By MICHAEL HEDRICK I can remember the early days of having schizophrenia. I was so afraid of the implications of subtle body language, like a lingering millisecond of eye contact, the way my feet hit the ground when I walked or the way I held my hands to my side. It was a struggle to go into a store or, really, anywhere I was bound to see another living member of the human species. With a simple scratch of the head, someone could be telling me to go forward, or that what I was doing was right or wrong, or that they were acknowledging the symbolic crown on my head that made me a king or a prophet. It’s not hard to imagine that I was having a tough time in the midst of all the anxiety and delusions. Several months after my diagnosis, I took a job at a small town newspaper as a reporter. I sat in on City Council meetings, covering issues related to the lowering water table and interviewing local business owners for small blurbs in the local section, all the while wondering if I was uncovering some vague connections to an international conspiracy. The nights were altogether different. Every day, I would come home to my apartment and smoke pot, then lay on my couch watching television or head out to the bar and get so hammered that I couldn’t walk. It’s hard to admit, but the only time I felt relaxed was when I was drunk. I eventually lost my newspaper job, but that wasn’t the catalyst for change. It all came to a head one night in July. I had been out drinking all night and, in a haze, I decided it would be a good idea to drive the two miles back to my apartment. This is something I had done several times before, but it had never dawned on me that it was a serious deal. I thought I was doing well, not swerving and being only several blocks from my house, when I saw flashing lights behind me. What started as a trip to the bar to unwind ended with me calling my parents to bail me out of jail at 3 a.m. © 2014 The New York Times Company
Ewen Callaway Caffeine's buzz is so nice it evolved twice. The coffee genome has now been published, and it reveals that the coffee plant makes caffeine using a different set of genes from those found in tea, cacao and other perk-you-up plants. Coffee plants are grown across some 11 million hectares of land, with more than two billion cups of the beverage drunk every day. It is brewed from the fermented, roasted and ground berries of Coffea canephora and Coffea arabica, known as robusta and arabica, respectively. An international team of scientists has now identified more than 25,000 protein-making genes in the robusta coffee genome. The species accounts for about one-third of the coffee produced, much of it for instant-coffee brands such as Nescafe. Arabica contains less caffeine, but its lower acidity and bitterness make it more flavourful to many coffee drinkers. However, the robusta species was selected for sequencing because its genome is simpler than arabica’s. Caffeine evolved long before sleep-deprived humans became addicted to it, probably to defend the coffee plant against predators and for other benefits. For example, coffee leaves contain the highest levels of caffeine of any part of the plant, and when they fall on the soil they stop other plants from growing nearby. “Caffeine also habituates pollinators and makes them want to come back for more, which is what it does to us, too,” says Victor Albert, a genome scientist at the University of Buffalo in New York, who co-led the sequencing effort. The results were published on 4 September in Science1. © 2014 Nature Publishing Group
On 5th May, 1953, the novelist Aldous Huxley dissolved four-tenths of a gram of mescaline in a glass of water, drank it, then sat back and waited for the drug to take effect. Huxley took the drug in his California home under the direct supervision of psychiatrist Humphry Osmond, to whom Huxley had volunteered himself as “a willing and eager guinea pig”. Osmond was one of a small group of psychiatrists who pioneered the use of LSD as a treatment for alcoholism and various mental disorders in the early 1950s. He coined the term psychedelic, meaning ‘mind manifesting’ and although his research into the therapeutic potential of LSD produced promising initial results, it was halted during the 1960s for social and political reasons. Born in Surrey in 1917, Osmond studied medicine at Guy’s Hospital, London. He served in the navy as a ship’s psychiatrist during World War II, and afterwards worked in the psychiatric unit at St. George’s Hospital, London, where he became a senior registrar. While at St. George’s, Osmond and his colleague John Smythies learned about Albert Hoffman’s discovery of LSD at the Sandoz Pharmaceutical Company in Bazel, Switzerland. Osmond and Smythies started their own investigation into the properties of hallucinogens and observed that mescaline produced effects similar to the symptoms of schizophrenia, and that its chemical structure was very similar to that of the hormone and neurotransmitter adrenaline. This led them to postulate that schizophrenia was caused by a chemical imbalance in the brain, but these ideas were not favourably received by their colleagues. In 1951 Osmond took a post as deputy director of psychiatry at the Weyburn Mental Hospital in Saskatchewan, Canada and moved there with his family. Within a year, he began collaborating on experiments using LSD with Abram Hoffer. Osmond tried LSD himself and concluded that the drug could produce profound changes in consciousness. Osmond and Hoffer also recruited volunteers to take LSD and theorised that the drug was capable of inducing a new level of self-awareness which may have enormous therapeutic potential. © 2014 Guardian News and Media Limited
|By Roni Jacobson Almost immediately after Albert Hofmann discovered the hallucinogenic properties of LSD in the 1940s, research on psychedelic drugs took off. These consciousness-altering drugs showed promise for treating anxiety, depression, post-traumatic stress disorder (PTSD), obsessive-compulsive disorder (OCD) and addiction, but increasing government conservatism caused a research blackout that lasted decades. Lately, however, there has been a resurgence of interest in psychedelics as possible therapeutic agents. This past spring Swiss researchers published results from the first drug trial involving LSD in more than 40 years. Although the freeze on psychedelic research is thawing, scientists say that restrictive drug policies are continuing to hinder their progress. In the U.S., LSD, psilocybin, MDMA, DMT, peyote, cannabis and ibogaine (a hallucinogen derived from an African shrub) are all classified as Schedule I illegal drugs, which the U.S. Drug Enforcement Administration defines as having a high potential for abuse and no currently accepted medical applications—despite extensive scientific evidence to the contrary. In a joint report released in June, the Drug Policy Alliance and the Multidisciplinary Association for Psychedelic Studies catalogue several ways in which they say that the DEA has unfairly obstructed research on psychedelics, including by overruling an internal recommendation in 1986 that MDMA be placed on a less restrictive schedule. The DEA and the U.S. Food and Drug Administration maintain that there is insufficient research to justify recategorization. This stance creates a catch-22 by basing the decision on the need for more research while limiting the ability of scientists to conduct that research. © 2014 Scientific American