Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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Richard A. Friedman Psychedelics, the fabled enlightenment drugs of the ’60s, are making a comeback — this time as medical treatment. A recent study claimed that psilocybin, a mushroom-derived hallucinogenic, relieves anxiety and depression in people with life-threatening cancer. Anecdotal reports have said similar things about so-called microdoses of LSD. The allure is understandable, given the limits of our treatments for depression and anxiety. About a third of patients with major depression don’t get better, even after several trials of different antidepressants. But I fear that in our desire to combat suffering, we will ignore the potential risks of these drugs, or be seduced by preliminary research that seems promising. This appears to be the case with the new psilocybin study, which has some serious design flaws that cast doubt on the results (and which the authors mention briefly). The study, done at New York University School of Medicine, examined a very small number of people with cancer in a “crossover” design in which each subject served as her own control, sequentially receiving doses of psilocybin and the control drug niacin, in random order. (Another recent study of psilocybin, done at Johns Hopkins University, used a similar crossover design.) Psilocybin, being a hallucinogen, has immediately recognizable mental effects, so subjects would almost certainly know when they were getting it compared with niacin, a vitamin that causes flushing but has no discernible effect on mood or thinking. This makes it hard to know if subjects got better because of the psilocybin, or because of a placebo effect. The design also means that subjects who got psilocybin first could have had a “carry-over effect” from the drug when they received niacin. In other words, they might still have been under the influence, contaminating the control condition. © 2017 The New York Times Company
By Abigail Zuger, M.D. It was in 2011 that the Centers for Disease Control first drew public attention to the ongoing nationwide opioid crisis. Much earnest commentary has explored the roots of this new killer epidemic since then, focusing on the broad highway between heroin and pain pills, and the online pharmacies, pill mills, and bad-apple doctors who fueled the two-way traffic and enabled catastrophe. Forgive me for rolling my eyes. Anyone with a prescription pad and a shred of common sense saw this whole thing coming down the pike decades ago, a speeding 18-wheeler, tires squealing, no brakes. Furthermore, it has long been clear that while the bad medical apples certainly did their share of damage, there is not a health policy guru or medical school dean in the country whose sins of omission and commission are not also partly responsible. Call it an epidemic of unconscious collusion or, as Dr. Anna Lembke bluntly states, a nation’s doctors “trapped in a system gone mad.” In less than 200 pages, this may be the most important medical book of the decade for finally getting the story of the opioid epidemic exactly right. As far as I am concerned, “Drug Dealer, M.D.,” in less than 200 unassuming, readable, and carefully referenced pages, may be the most important medical book of the decade for finally getting the story of this epidemic exactly right. And it’s not the medical bad apples Lembke is talking about in her title — it’s every doctor in the country. Copyright 2017 Undark
By KATHARINE Q. SEELYE and ABBY GOODNOUGH MANCHESTER, N.H. — Chad Diaz began using heroin when he was 12. Now 36 and newly covered by Medicaid under the Affordable Care Act, he is on Suboxone, a substitute opioid that eases withdrawal symptoms and cravings, and he is slowly pulling himself together. “This is the best my life has gone in many, many years,” Mr. Diaz, a big man wearing camouflage, said as he sat in a community health center here. If Congress and President Trump succeed in dismantling the Affordable Care Act, he will have no insurance to pay for his medication or counseling, and he fears he will slide back to heroin. “If this gets taken from me, it’s right back to Square 1,” he said. “And that’s not a good place. I’m scary when I’m using. I don’t care who I hurt.” As the debate over the fate of the health law intensifies, proponents have focused on the lifesaving care it has brought to people with cancer, diabetes and other physical illnesses. But the law has also had a profound, though perhaps less heralded, effect on mental health and addiction treatment, vastly expanding access to those services by designating them as “essential benefits” that must be covered through the A.C.A. marketplaces and expanded Medicaid. The Center on Budget and Policy Priorities, a left-leaning research group, calculates that 2.8 million people with substance use disorders, including 220,000 with opioid disorders, have coverage under the A.C.A. As the opioid epidemic continues to devastate communities nationwide, public health officials say the law has begun to make a critical difference in their ability to treat and rehabilitate people. © 2017 The New York Times Company
Keyword: Drug Abuse
Link ID: 23215 - Posted: 02.11.2017
By Catherine Offord As an undergraduate at Auburn University in the early 2000s, Jeremy Day was thinking of becoming an architect. But an opportunity to work on a research project investigating reward learning in rodents changed the course of his career. “It really hooked me,” he says. “It made me immediately wonder what mechanisms were underlying that behavior in the animal’s brain.” It’s a question Day has pursued ever since. In 2004, he enrolled in a PhD program at the University of North Carolina at Chapel Hill and began studying neural reward signaling under the mentorship of neuroscientist Regina Carelli. “He was a stellar student by all accounts,” Carelli recalls. “He was very clear on the type of work he wanted to do, even that early on in his career.” Focusing on the nucleus accumbens, a brain region involved in associative learning, Day measured dopamine levels in rats undergoing stimulus-reward experiments. Although a rat’s brain released dopamine on receipt of a reward early in training, Day found that, as the rodent became accustomed to specific cues predicting those rewards, this dopamine spike shifted to accompany the cues instead, indicating a changing role for the chemical during learning.1 Day completed his PhD in 2009, but realized that to better understand dopamine signaling and errors in the brain’s reward system that lead to addiction, he would need a broader skill set. “I had a strong background in systems neuroscience, but my training in molecular neuroscience was not as strong,” he explains. So he settled on “a field that I knew almost nothing about?”—epigenetics—and joined David Sweatt’s lab at the University of Alabama at Birmingham (UAB) as a postdoc. For someone used to a field where “data come in as it’s happening,” Day says, “transitioning to a molecular lab where you might do an assay and you don’t get an answer for a week or two was a culture shock.” © 1986-2017 The Scientist
By SHARON LERNER IN the fall, I began to research an article that I gave the working title “The Last Days of Chlorpyrifos.” A widely used pesticide, chlorpyrifos affects humans as well as the bugs it kills. Back in the halcyon days before the election, the optimism of the title seemed warranted. After years of study, the Environmental Protection Agency had announced in October 2015 that it could no longer vouch for the safety of chlorpyrifos on food. The agency had acknowledged for decades that chlorpyrifos can cause acute poisoning and in the early 2000s it had prohibited its use in most home products and reduced the amounts that could be used on some crops. But the 2015 announcement stemmed from the agency’s recognition of mounting evidence that prenatal exposure to chlorpyrifos could have lasting effects on children’s brains. Though the process of re-evaluating the safety of the pesticide had stretched on for years, at long last, chlorpyrifos seemed to be going down. Another report was expected to provide all the ammunition necessary to stop its use on fruits and vegetables, and I was eager to document its demise. For a reporter who covers the environment, this was going to be the rare happy story. The election of President Trump has thrown that outcome — indeed, the fate of many of the E.P.A.’s public health protections — into question. On Monday, Mr. Trump signed an executive order requiring federal agencies to scrap two regulations for every one they institute on small businesses. In its first week, his administration suspended 30 environmental regulations issued under President Barack Obama. And Myron Ebell, who oversaw the agency’s transition team, suggested recently that the E.P.A.’s staff may soon be reduced by as much as two-thirds. How will the agency’s mission “to protect human health and the environment” fare under this assault? What happens with chlorpyrifos may be our best indication. “I think it’ll be a very early test of their commitment to environmental protection,” Jim Jones, who oversaw the evaluation of chlorpyrifos as the E.P.A.’s assistant administrator for chemical safety and pollution prevention, told me, not long after he stepped down on Inauguration Day. © 2017 The New York Times Company
Hannah Devlin Science correspondent It sounds like torment for the smoker attempting to quit: handling packets of cigarettes and watching footage of people smoking, without being allowed to light up. However, scientists believe that lengthy exposure to environmental triggers for cravings could be precisely what smokers need to help them quit. The technique, known as extinction therapy, targets the harmful Pavlovian associations that drive addiction with the aim of rapidly “unlearning” them. The latest study, by scientists at the Medical University of South Carolina, found that after two one-hour sessions people smoked significantly fewer cigarettes one month after treatment compared to a control group. The study was not an unqualified success – many participants still relapsed after treatment – but the authors believe the work could pave the way for new approaches to treating addiction. Michael Saladin, the psychologist who led the work, said: “When I initially saw the results from this study it was pretty eye-opening.” In smokers, environmental triggers have typically been reinforced thousands of times so that the sight of a lighter, for instance, becomes inextricably linked to the rush of nicotine that the brain has learned will shortly follow. After quitting an addictive substance, these associations fade slowly over time, but people often flounder in the first days and weeks when cravings are most powerful. Saladin and others believe it is possible to fast-track this process in carefully designed training sessions, to help people over the initial hurdle. © 2017 Guardian News and Media Limited
By CATHERINE SAINT LOUIS During her pregnancy, she never drank alcohol or had a cigarette. But nearly every day, Stacey, then 24, smoked marijuana. With her fiancé’s blessing, she began taking a few puffs in her first trimester to quell morning sickness before going to work at a sandwich shop. When sciatica made it unbearable to stand during her 12-hour shifts, she discreetly vaped marijuana oil on her lunch break. “I wouldn’t necessarily say, ‘Go smoke a pound of pot when you’re pregnant,’” said Stacey, now a stay-at-home mother in Deltona, Fla., who asked that her full name be withheld because street-bought marijuana is illegal in Florida. “In moderation, it’s O.K.” Many pregnant women, particularly younger ones, seem to agree, a recent federal survey shows. As states legalize marijuana or its medical use, expectant mothers are taking it up in increasing numbers — another example of the many ways in which acceptance of marijuana has outstripped scientific understanding of its effects on human health. Often pregnant women presume that cannabis has no consequences for developing infants. But preliminary research suggests otherwise: Marijuana’s main psychoactive ingredient — tetrahydrocannabinol, or THC — can cross the placenta to reach the fetus, experts say, potentially harming brain development, cognition and birth weight. THC can also be present in breast milk. “There is an increased perception of the safety of cannabis use, even in pregnancy, without data to say it’s actually safe,” said Dr. Torri Metz, an obstetrician at Denver Health Medical Center who specializes in high-risk pregnancies. Ten percent of her patients acknowledge recent marijuana use. © 2017 The New York Times Company
Elizabeth Eaton Electronic cigarettes may increase the risk of heart disease, researchers at UCLA report. The team found that two risk factors for heart disease were elevated in 16 e-cigarette users compared with 18 nonsmokers. “The pattern was spot-on” for what has been seen in heart attack patients and those with heart disease and diabetes, says cardiologist Holly Middlekauff, a coauthor of the study published online February 1 in JAMA Cardiology. But because the study only looked at a small number of people, the results are not definitive — just two or three patients can skew results, John Ambrose, a cardiologist with the University of California, San Francisco cautions. Plus, he says, some of the e-cigarette users in the study used to smoke tobacco, which may have influenced the data. Even so, Ambrose called the study interesting, noting that “the medical community just doesn’t have enough information” to figure out if e-cigarettes are dangerous. E-cigarette smokers in the study had heartbeat patterns that indicated high levels of adrenaline — also known as epinephrine — in the heart, a sign of heart disease risk. Researchers also found signs of increased oxidative stress, an imbalance of certain protective molecules that can cause the hardening and narrowing of arteries. © Society for Science & the Public 2000 - 2017.
Keyword: Drug Abuse
Link ID: 23180 - Posted: 02.02.2017
Meghan Rosen New X-ray crystallography images reveal how an LSD molecule gets trapped within a protein that senses serotonin, a key chemical messenger in the brain. The protein, called a serotonin receptor, belongs to a family of proteins involved in everything from perception to mood. The work is the first to decipher the structure of such a receptor bound to LSD, which gets snared in the protein for hours. That could explain why “acid trips” last so long, study coauthor Bryan Roth and colleagues report January 26 in Cell. It’s “the first snapshot of LSD in action,” he says. “Until now, we had no idea how it worked at the molecular level.” But the results might not be that relevant to people, warns Cornell University biophysicist Harel Weinstein. Roth’s group didn’t capture the main target of LSD, a serotonin receptor called 5-HT2A, instead imaging the related receptor 5-HT2B. That receptor is “important in rodents, but not that important in humans,” Weinstein says. Roth’s team has devoted decades to working on 5-HT2A, but the receptor has “thus far been impossible to crystallize,” he says. Predictions of 5-HT2A’s structure, though, are very similar to that of 5-HT2B, he says. LSD, or lysergic acid diethylamide, was first cooked up in a chemist’s lab in 1938. It was popular (and legal) for recreational use in the early 1960s, but the United States later banned the drug (also known as blotter, boomer, Purple Haze and electric Kool-Aid). |© Society for Science & the Public 2000 - 201
Keyword: Drug Abuse
Link ID: 23175 - Posted: 02.01.2017
By Roni Jacobson The psychedelic drug ibogaine is known for two things: its reputation in some circles as a panacea for addiction and the visceral hallucinations it induces. Positive anecdotes abound from people who have sought out the illegal drug at underground clinics. Just one dose, they say, brings near-instant relief from cravings and withdrawal symptoms, a veritable miracle for seemingly intractable addictions. But the side effects of this plant-derived substance can be dangerous or even deadly. Now, with encouraging evidence from animal studies, drugs are being developed to replicate ibogaine's impact on addiction without the side effects. A drug that is chemically related to ibogaine but lacks its hallucinogenic properties is set to begin phase II clinical trials in California early this year. If the results continue to be promising, addiction treatment as we know it could change radically. For decades research on ibogaine has been stymied by its classification as a Schedule I drug, the most tightly regulated category. Yet the results of animal studies have been intriguing. In May 2016 a meta-analysis examining 32 such studies, mostly in mice and rats, found that ibogaine reduced self-administration of cocaine, opioids and alcohol. An earlier study from 2015 found that noribogaine, the substance that ibogaine breaks down to when ingested, reduced self-administration of nicotine in addicted rats by 64 percent. Now Savant HWP, a pharmaceutical company in California, has developed a drug called 18-MC, a compound chemically related to ibogaine, which it hopes will produce the antiaddictive properties without triggering hallucinations. They are betting that the “trip” is not a necessary component of the therapy—an idea shared by some academics. © 2017 Scientific American,
Keyword: Drug Abuse
Link ID: 23170 - Posted: 01.31.2017
By Andrew Joseph, Public health officials on Thursday said they had detected a bizarre cluster of cases in which patients in Massachusetts developed amnesia over the past few years — a highly unusual syndrome that could be connected to opioid use. The officials have identified only 14 cases so far. But officials said it’s possible that clinicians have simply missed other cases. The patients were all relatively young — they ranged in age from 19 to 52. Thirteen of the 14 patients identified had a substance use disorder, and the 14th patient tested positive for opioids and cocaine on a toxicology screen. “What we’re concerned about is maybe a contaminant or something else added to the drug might be triggering this,” said Dr. Alfred DeMaria, the state epidemiologist at the Massachusetts Department of Public Health and an author of the new report. “Traditionally there’s no evidence that the drugs themselves can do this.” The pattern emerged when Dr. Jed Barash, a neurologist at Lahey Hospital and Medical Center in Burlington, Mass., reported four of the amnesia cases to the state’s public health department. The department then sent out an alert to specialists, including neurologists and emergency physicians, asking about similar cases, ultimately identifying 10 more from 2012 to 2016 at hospitals in eastern Massachusetts. (The patients included one person who lived in New Hampshire and one person who was visiting Massachusetts from Washington state.) © 2017 Scientific American,
By Emily Underwood LOS ANGELES, CALIFORNIA—In a barbed wire–enclosed parking lot 100 meters downwind of the Route 110 freeway, an aluminum hose sticks out of a white trailer, its nozzle aimed at an overpass. Every minute, the hose sucks up hundreds of liters of air mixed with exhaust from the roughly 300,000 cars and diesel-burning freight trucks that rumble by each day. Crouched inside the trailer, a young chemical engineer named Arian Saffari lifts the lid off a sooty cylinder attached to the hose, part of a sophisticated filtration system that captures and sorts pollutants by size. Inside is a scientific payload: particles of sulfate, nitrate, ammonium, black carbon, and heavy metal at least 200 times smaller than the width of a human hair. The particles are too fine for many air pollution sensors to accurately measure, says Saffari, who works in a lab led by Constantinos Sioutas at the University of Southern California (USC) here. Typically smaller than 0.2 µm in diameter, these “ultrafine” particles fall within a broader class of air pollutants commonly referred to as PM2.5 because of their size, 2.5 µm or less. When it comes to toxicity, size matters: The smaller the particles that cells are exposed to, Saffari says, the higher their levels of oxidative stress, marked by the production of chemically reactive molecules such as peroxides, which can damage DNA and other cellular structures. © 2017 American Association for the Advancement of Science.
Amy Maxmen The acid tests of 1960s San Francisco have morphed into something quite different in today’s Silicon Valley. Mind-altering trips have given way to subtle productivity boosts purportedly caused by tiny amounts of LSD or other psychedelic drugs. Fans claim that this ‘microdosing’ boosts creativity and concentration, but sceptics doubt that ingesting or inhaling one-tenth of the normal dose could have an effect. Science could soon help to settle the matter. Researchers have finally mapped the 3D structure of LSD in its active state — and the details, published today in Cell1, indicate the key to the chemical’s potency1. Another team reports today in Current Biology2 that it has pinpointed the molecular go-between that creates the perception of deep meaning experienced during acid trips — a feeling that the writer Aldous Huxley once described as “solidarity with the Universe”. “This is what we dreamed of doing when I was a graduate student in the seventies,” says Gavril Pasternak, a pharmacologist at Memorial Sloan Kettering Cancer Center in New York City who has spent decades studying the receptor proteins in the brain that mediate the activity of opioids and psychedelic drugs. “Work like this expands our understanding of how these receptors work.” In 1972, researchers revealed LSD’s shape by mapping the arrangement of atoms in its crystallized form3. But in the decades since, they’ve struggled to reveal the crystal structure of a receptor grasping a molecule of LSD or another psychedelic drug. This active configuration is key to understanding how drugs work, because their action depends on how they cling to molecules in the body. © 2017 Macmillan Publishers Limited,
Hannah Devlin Science correspondent Scientists believe that a radical treatment involving the tranquilliser ketamine could help overcome alcohol addiction by “erasing” drink-related memories. Psychologists based at University College London are testing whether a one-off dose of the drug could help hazardous drinkers who are trying to reduce their alcohol intake. Alcohol addiction is notoriously difficult to treat, and there are few effective therapies available. Using a recreational drug to treat addiction may sound counterintuitive, but the researchers say there is a growing body of research suggesting that ketamine can be used to disrupt harmful patterns of behaviour. Ravi Das, one of the lead researchers, said: “There is evidence that it could be useful as a treatment for alcoholism.” Crucially, ketamine can disrupt the formation of memories, and scientists believe that this property could be harnessed to over-write the memories that drive addiction and harmful patterns of behaviour. “Memories that you form can be hijacked by drugs in some people,” said Das. “If you were an alcoholic you might have a strong memory of being in a certain place and wanting to drink. Those memories get continuously triggered by things in the environment that you can’t avoid.” For instance, seeing a glass of beer, hearing the clinking of glasses or even arriving home from work may trigger memories of the rewarding sensation of taking a drink – and might prompt a person to follow this urge. © 2017 Guardian News and Media Limited
Keyword: Drug Abuse
Link ID: 23146 - Posted: 01.25.2017
By Bob Grant More and more Americans are using cannabis both for medicinal and recreational purposes, but scientists still know little about the drug’s effects on human physiology, according to a National Academies report released this month (January 12). Part of this knowledge gap owes to the fact that cannabis is classified as a Schedule I drug under the US Controlled Substances Act. In the eyes of the federal government, marijuana is a dangerous substance—on par with heroin—that “has no currently accepted medical use in treatment in the United States.” But researchers in Canada are not far ahead of their US counterparts, even though cannabis has since 2001 been functionally legal for medicinal use at the federal level there. See “National Academies Detail the State of Weed Science” “I wish I could say that [legalizing medical marijuana] had led to more research” in Canada, said Mark Ware, a McGill University pain management physician who has researched the safety and efficacy of cannabinoids for the past 18 years. “I think there’s certainly a willingness to be able to document real world use of cannabis under a legal framework.” Ware, who served as a reviewer on the National Academies report, added that while there are several public registries that track the legal use of cannabis among Canadians, experimental evidence on the effects of that use are lacking. “The clinical trials, I think for most people that’s an expensive undertaking,” he said. “There are still questions around who owns the intellectual property, who’s going to sponsor the trials. . . . Those remain barriers even in a legal framework as to the cost of that kind of research and the drug development piece of it.” © 1986-2017 The Scientist
By Nicole Kobie Getting drunk could make it harder to enter your password – even if your brainwaves are your login. Brainwave authentication is one of many biometric measures touted as an alternative to passwords. The idea is for a person to authenticate their identity with electroencephalogram (EEG) readings. For example, instead of demanding a passcode, a computer could display a series of words on a screen and measure the user’s response via an EEG headset. EEG signatures are unique and are more complex than a standard password, making them difficult to hack. But while research suggests that EEG readings can authenticate someone’s identity with accuracy rates around 94 per cent, there could be confounding factors – including whether you’ve had a few too many drinks. Tommy Chin, a security researcher at cybersecurity consultancy firm Grimm, and Peter Muller, a graduate student at the Rochester Institute of Technology, decided to test this theory experimentally, by analysing people’s brainwaves before and after drinking shots of Fireball, a cinnamon-flavoured whisky. “Brainwaves can be easily manipulated by external influences such as drugs [like] opioids, caffeine, and alcohol,” Chin says. “This manipulation makes it a significant challenge to verify the authenticity of the user because they drank an immense amount of alcohol or caffeinated drink.” © Copyright Reed Business Information Ltd.
Tina Rosenberg It has been nearly 30 years since the first needle exchange program opened in the United States, in Takoma, Wash., in 1988. It was a health measure to prevent injecting drug users from sharing needles, and therefore spreading H.I.V. and hepatitis. The idea was controversial, to say the least. Many people felt — and still feel — that it enables drug use and sends a message that drug use is O.K. and can be done safely. Today the evidence is overwhelming that needle exchange prevents disease, increases use of drug treatment by winning users’ trust and bringing them into the health system, and does not increase drug use. Its utility has won over some critics. When Vice President-elect Mike Pence was governor of Indiana, he authorized needle exchange programs as an emergency response to an H.I.V. outbreak. “I do not support needle exchange as antidrug policy, but this is a public health emergency,” he said at a news conference in 2015. Needle exchange saved New York City from a generalized H.I.V. epidemic. In 1990, more than half of injecting drug users had H.I.V. Then in 1992, needle exchange began — and by 2001, H.I.V. prevalence had fallen to 13 percent. America has another epidemic now: overdose deaths from opioids, heroin and fentanyl, a synthetic opioid so powerful that a few grains can kill. A thousand people died of overdose in the city last year — three times the number who were killed in homicides. Nationally, drug overdose has passed firearms and car accidents as the leading cause of injury deaths. If there is a way to save people from overdose death without creating harm, we should do it. Yet there is a potent weapon that we’re ignoring: the supervised injection room. According to a report by the London-based group Harm Reduction International, 90 supervised injection sites exist around the world: in Canada, Australia and eight countries in Europe. Scotland and Ireland plan to open sites this year. In the United States, state officials in New York, California and Maryland, and city officials in Seattle (where a task force recommended two sites), San Francisco, New York City, Ithaca, N.Y., and elsewhere, are discussing such facilities. © 2017 The New York Times Company
Keyword: Drug Abuse
Link ID: 23120 - Posted: 01.18.2017
Thorsten Rudroff An estimated 400,000 Americans are currently living with multiple sclerosis, an autoimmune disease where the body’s immune cells attack a fatty substance called myelin in the nerves. Common symptoms are gait and balance disorders, cognitive dysfunction, fatigue, pain and muscle spasticity. Colorado has the highest proportion of people living with MS in the United States. It is estimated that one in 550 people living in the state has MS, compared to one in 750 nationally. The reason for this is unknown, but could be related to several factors, such as vitamin D deficiency or environment. Currently available therapies do not sufficiently relieve MS symptoms. As a result many people with the condition are trying alternative therapies, like cannabis. Based on several studies, the American Association of Neurology states that there is strong evidence that cannabis is effective for treatment of pain and spasticity. Although there are many anecdotal reports indicating cannabis’ beneficial effects for treatment of MS symptoms such as fatigue, muscle weakness, anxiety and sleep deprivation, they have not been scientifically verified. This is because clinical trials – where patients are given cannabis – are difficult to do because of how the substance is regulated at the federal level. To learn more, my Integrative Neurophysiology Laboratory at Colorado State University is studying people with MS in the state who are already using medical cannabis as a treatment to investigate what MS symptoms the drug can effectively treat. © 2010–2017, The Conversation US, Inc.
Bruce Bower Marijuana’s medical promise deserves closer, better-funded scientific scrutiny, a new state-of-the-science report concludes. The report, released January 12 by the National Academies of Sciences, Engineering and Medicine in Washington, D.C., calls for expanding research on potential medical applications of cannabis and its products, including marijuana and chemical components called cannabinoids. Big gaps in knowledge remain about health effects of cannabis use, for good or ill. Efforts to study these effects are hampered by federal classification of cannabis as a Schedule 1 drug, meaning it has no accepted medical use and a high potential for abuse. Schedule 1 status makes it difficult for researchers to access cannabis. The new report recommends reclassifying the substance to make it easier to study. Recommendations from the 16-member committee that authored the report come at a time of heightened acceptance of marijuana and related substances. Cannabis is a legal medical treatment in 28 states and the District of Columbia. Recreational pot use is legal in eight of those states and the District. “The legalization and commercialization of cannabis has allowed marketing to get ahead of science,” says Raul Gonzalez, a psychologist at Florida International University in Miami who reviewed the report before publication. While the report highlights possible medical benefits, Gonzalez notes that it also underscores negative consequences of regular cannabis use. These include certain respiratory and psychological problems. |© Society for Science & the Public 2000 - 2017.
Sarah Boseley Health editor No new drugs for depression are likely in the next decade, even though those such as Prozac work for little more than half of those treated and there have been concerns over their side-effects, say scientists. Leading psychiatrists, some of whom have been involved in drug development, say criticism of the antidepressants of the Prozac class, called the SSRIs (selective serotonin reuptake inhibitors), is partly responsible for the pharmaceutical industry’s reluctance to invest in new drugs – even though demand is steadily rising. But the main reason, said Guy Goodwin, professor of psychiatry at Oxford University, is that the the NHS and healthcare providers in other countries do not want to pay the bill for new drugs that will have to go through expensive trials. The antidepressants that GPs currently prescribe work for only about 58% of people, but they are cheap because they are out of patent. Why 'big pharma' stopped searching for the next Prozac Pharma giants have cut research on psychiatric medicine by 70% in 10 years, so where will the next ‘wonder drug’ come from? “We are not going to get any more new drugs for depression in the next decade simply because the pharmaceutical industry is not investing in research,” said Goodwin. “It can’t make money on these drugs. It costs approximately $1bn to do all the trials before you launch a new drug. “There is also a failure of the science. It has to get more understanding of how these things work before they can improve them.” © 2017 Guardian News and Media Limited
Link ID: 23086 - Posted: 01.12.2017