Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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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
By Catherine Caruso If you give a mouse a beer, he’s going to ask for a cookie—and another, and another. If you give a person enough beer, she might find herself wolfing down a plate of greasy nachos. But why does binge drinking make us binge eat as well? The reason may lie not in the stomach but in the brain, recent research suggests. A study published today in Nature Communications found alcohol activated brain cells that control hunger, sending drunk mice scampering for snacks even when they were not really hungry. Researchers from The Francis Crick Institute Mill Hill Laboratory in London got mice drunk, then tagged and recorded the electrical activity in brain cells linked to hunger, uncovering a neural mechanism that could explain why the animals ate significantly more after binge-drinking sessions even though their bodies did not need the calories. Although hunger pangs in our stomach usually alert us that it is time to eat, the impulse to consume food originates in our brains, and brain cells located in the hypothalamus called agouti-related protein (AgRP) neurons play a key role in controlling hunger. A previous study showed that when AgRP neurons are activated, mice almost immediately seek out food and start eating, even if their stomachs are full. By contrast, when AgRP neurons are deactivated, hungry mice will not eat. AgRP neurons play a similar role in human hunger: Under natural conditions they are activated when our bodies need calories, signaling to us that we should find food. Something different happens, however, when alcohol is involved. Although alcohol is second only to fat in caloric density, previous studies have shown drinking causes humans to eat more, a paradox that made lead authors Craig Blomeley and Sarah Cains and colleagues wonder whether the brain could be to blame. © 2017 Scientific American,
By Virginia Smart, CBC News A controversial Canadian program that gives a regulated, hourly dose of wine to alcoholics to help manage their addiction and keep them safe has caught the attention of health care researchers in Australia. The managed alcohol programs (MAPs) that have sparked the international interest have been giving new hope and new lives to many alcoholics struggling with homelessness and troubles with addiction in communities from British Columbia to Ontario. Kate Dolan, a professor at the National Drug and Alcohol Research Centre at the University of New South Wales in Australia, has visited programs in Ottawa and Vancouver and was impressed. "We used to lead the world in harm reduction services," Dolan tells the fifth estate, but "the alcohol field has not progressed as much as the illicit drug use field." Research led Dolan to Ottawa's MAP. She found MAPs to be cost-effective through reductions in spending on health care and emergency services. Participants also significantly reduce their alcohol consumption and learn a sense of community. The Pour Lucia Ali monitors 'The Pour,' the hourly distribution of a prescribed dose of alcohol dictated by the in-house nurse at the Oaks, a residence for stabilized alcoholics in Ottawa. (CBC) When participants arrive at a MAP, Dolan wrote in her study, "it is all about me, myself and I." But as they progress, they lose the "chip on their shoulder and open up." ©2016 CBC/Radio-Canada.
Keyword: Drug Abuse
Link ID: 23061 - Posted: 01.06.2017
By Don Lattin In the fall of 1965, a 33-year-old father of three named Arthur King—a patient on the alcoholics ward at Baltimore’s Spring Grove Hospital—swallowed an LSD pill and laid back on his bed in a special unit called “Cottage Thirteen.” Sanford Unger, the chief of psychosocial research at the Johns Hopkins University School of Medicine, knelt beside King’s bed, holding his hand and reassuring the patient as he started to feel the drug’s mind-altering effects. This was not a normal psychotherapy session. During his 12-hour experience, designed to help stop his destructive drinking habit, King sat on the edge of the bed and looked at the photo of his son that he’d brought. Suddenly, the child became alive in the picture, which initially frightened him. Then King noticed that a lick of his son’s hair was out of place, so he stroked the photo, putting the errant strands back in place. His fear vanished. Later, Unger held out a small vase with a single red rose. King looked at the flower, which seemed to be opening and closing, as though it were breathing. At one point, Unger asked him whether he’d like to go out to a bar and have a few drinks. King didn’t say anything but was shocked when the rose suddenly turned black and dropped dead before his eyes. He never picked up another drink. Arthur King was one of thousands of research subjects who were given LSD, psilocybin, and mescaline as therapeutic tools in the 1950s and 1960s, often with government support and with promising results. But by the time King was enjoying his sobriety, the backlash against psychedelic testing had already begun. By the mid-1970s, the legal exploration of the therapeutic benefits of psychedelic drugs was over.
Linda Bauld January is a time for New Year’s resolutions and if you’re one of the world’s one billion smokers, your resolution may be to stop smoking. For some people, this year’s quit attempt might involve an electronic cigarette, and a recent study in England, published in the BMJ, suggested that these devices helped at least 18,000 smokers to stop in 2015 who would not otherwise have done so. That’s very good news, but will there be as many quit attempts in 2017 as there have been in the past with e-cigarettes? I’m not so sure. Since I last wrote about e-cigarettes in this column one year ago, headlines about the dangers of these devices have continued to appear and show no sign of abating. The result is clear. More people believe today, compared with a year ago, that e-cigarettes are as harmful as smoking. In fact these incorrect perceptions have risen year on year, from fewer than one in ten adults in Great Britain in 2013 to one in four this past summer. Surveys of smokers show similar patterns, with an increasing proportion believing that e-cigarettes are more or equally harmful than tobacco. Yet we know that these harm perceptions are wrong. There is now very strong evidence, from a range of studies, that vaping - inhaling nicotine without the combustion involved in smoking - is far less risky than smoking cigarettes. Just a few months ago this body of evidence was brought together by the Royal College of Physicians who published an authoritative report analysing dozens of studies and concluded that the hazard to health arising from long term vapour inhalation from e-cigarettes is unlikely to exceed 5% of the harm from smoking tobacco. The RCP, and since then other UK doctor’s organisations such as the Royal College of General Practitioners, have made clear that it is important to promote the use of e-cigarettes, along with other non-tobacco nicotine products (like Nicotine Replacement Therapy such as gum or inhalators) to smokers who are trying to quit. The work of these organisations is underpinned by a consensus statement endorsed by many of the main health charities and public health bodies in the UK. They agree that vaping is safer than smoking, and while these products are not risk free and should not be promoted to children or never smokers, they have a legitimate and positive role to play in tobacco control. © 2017 Guardian News and Media Limited
Keyword: Drug Abuse
Link ID: 23046 - Posted: 01.02.2017
By KEVIN DEUTSCH An anesthetic commonly used for surgery has surpassed heroin to become the deadliest drug on Long Island, killing at least 220 people there in 2016, according to medical examiners’ records. The drug, fentanyl, is a synthetic opioid, which can be 100 times more potent than morphine. The numbers from Long Island are part of a national pattern, as fentanyl fatalities have already surpassed those from heroin in other parts of the country, including New England, as its use has skyrocketed. Part of the reason for the increase is economic — because fentanyl can be manufactured in the lab, it is much cheaper and easier than cultivating heroin. In New York City, more than 1,000 people are expected to die from drug overdoses this year — the first recorded four-digit death total in city history, according to statistics compiled by the Department of Health and Mental Hygiene. Nearly half of all unintentional drug overdose deaths in the city since July have involved fentanyl, the health department said. The medical examiners of Long Island’s two counties, Nassau and Suffolk, compiled the new numbers. “Fentanyl has surpassed heroin as the most commonly detected drug in fatal opioid overdoses,” Dr. Michael J. Caplan, the Suffolk County medical examiner, said in a written statement about the statistics, which were obtained by The New York Times ahead of their release. “The influx of illicitly manufactured fentanyl from overseas is a nationwide issue that requires a multidisciplinary intervention from all levels of government.” Nationwide, recorded deaths from opioids surpassed 30,000 in 2015, according to data compiled by the Centers for Disease Control and Prevention. And overdoses caused by synthetic opioids like fentanyl increased by 72.2 percent in 2015 over 2014 — one of the deadliest year-over-year surges for any drug in United States history, the same data shows. © 2016 The New York Times Company
by Bethany Brookshire An opioid epidemic is upon us. Prescription painkillers such as fentanyl and morphine can ease terrible pain, but they can also cause addiction and death. The Centers for Disease Control and Prevention estimates that nearly 2 million Americans are abusing or addicted to prescription opiates. Politicians are attempting to stem the tide at state and national levels, with bills to change and monitor how physicians prescribe painkillers and to increase access to addiction treatment programs. Those efforts may make access to painkillers more difficult for some. But pain comes to everyone eventually, and opioids are one of the best ways to make it go away. Morphine is the king of pain treatment. “For hundreds of years people have used morphine,” says Lakshmi Devi, a pharmacologist at the Ichan School of Medicine Mount Sinai in New York City. “It works, it’s a good drug, that’s why we want it. The problem is the bad stuff.” The “bad stuff” includes tolerance — patients have to take higher and higher doses to relieve their pain. Drugs such as morphine depress breathing, an effect that can prove deadly. They also cause constipation, drowsiness and vomiting. But “for certain types of pain, there are no medications that are as effective,” says Bryan Roth, a pharmacologist and physician at the University of North Carolina at Chapel Hill. The trick is constructing a drug with all the benefits of an opioid painkiller, and few to none of the side effects. Here are three ways that scientists are searching for the next big pain buster, and three of the chemicals they’ve turned up. |© Society for Science & the Public 2000 - 2016
By DANNY HAKIM LONDON — Syngenta, the Swiss pesticide giant, claims on its website that data from an influential 2011 study shows that farmers who use the weed killer paraquat are less likely to develop Parkinson’s disease than the general population. However, Syngenta’s claim is at odds with the actual findings of the study, according to two of its authors. The 2011 study, carried out by the National Institutes of Health and researchers from other institutions around the world, found that people who used paraquat or another pesticide, called rotenone, were roughly two and a half times more likely to develop Parkinson’s. The work is known as the Farming and Movement Evaluation, or FAME, study. It drew on a sweeping United States government project called the Agricultural Heath Study, which tracked more than 80,000 farmers and their spouses, as well as other people who applied pesticides, in Iowa and North Carolina. The FAME researchers identified 115 people from the Agricultural Health Study who developed Parkinson’s, and studied 110 of them who provided information on the pesticides they used. The study was influential even among some people who had been skeptics of a connection between the chemicals and the disease. Gary W. Miller, a professor of environmental health at Emory University, referred to a link between Parkinson’s and paraquat as a “red herring” in a 2007 publication. But while Dr. Miller said in a recent email exchange that he had concerns about some previous research making the connection, “the FAME data are strong and should be considered.” He said the study “appears to show a connection between paraquat exposure and Parkinson’s disease.” Because of the prominence of the FAME study, Syngenta addresses it on one of its websites, paraquat.com. Syngenta claims that the study shows that only 115 people had Parkinson’s out of the more than 80,000 people in the broader Agricultural Health Study. Therefore, “the incidence of Parkinson’s disease” in the study “appears to be lower than in the general U.S. population,” Syngenta says. © 2016 The New York Times Company
By STEVEN PETROW “So why did you stop drinking?” my friend Brad asked recently when we were out for dinner. “You never seemed to have a drinking problem.” The question surprised me, coming as it did a full two years after my decision to take a “break” from alcohol. He was scanning the wine list, and I sensed he was hoping I’d share a bottle of French rosé with him. So I decided to tell him the truth. “To get my depression back under control.” In my late 50s, my longstanding depression had started to deepen, albeit imperceptibly at first. I continued drinking moderately, a couple of glasses of wine most days of the week, along with a monthly Manhattan. Then two dark and stormy months really shook me up, leaving me in a black hole of despair as depression closed in. At my first therapy appointment, the psychopharmacologist listened to me attentively, then said bluntly: “Stop drinking for a month.” The shrink wanted to know whether I was in control of my drinking or my drinking was in control of me. He explained that we become more sensitive to the depressant effects of alcohol as we age, especially in midlife, when our body chemistry changes and we’re more likely to be taking various medications that can interact with alcohol and one another. On doctor’s orders, I went cold turkey off alcohol. When I returned a month later and volunteered that I hadn’t touched a drink since our last visit, he was satisfied that I didn’t have “an active alcohol problem” and told me I could drink in what he considered moderation: No more than two glasses of wine a day, and never two days in a row. He also suggested I keep a log. © 2016 The New York Times Company
By Kai Kupferschmidt New York City is known for its strange sights. But on 12 July, even locals were shocked by what they saw: more than 30 people staggering around a Brooklyn block with empty stares, shuffling their arms and feet and occasionally groaning. What sounds like the opening of a horror movie was suspected from the start to be the work of a synthetic cannabinoid. Now, a new analysis, out today in The New England Journal of Medicine, confirms those suspicions. But it has also raised scientific ire over its prolific use of the word “zombie.” Developed by academics and pharma companies to study cannabinoid receptors in the human body, synthetic cannabinoids act on the same receptor on brain cells as cannabis. The compounds, which can be up to 100 times more potent than cannabis, are a rapidly growing class of drugs, usually dissolved in liquid and sprayed on leaves to be smoked. There are hundreds of different compounds, and though they are quickly made illegal in many places, new ones appear every year. To find out what was responsible for the Brooklyn episode, researchers from the University of California, San Francisco (UCSF), started with a foil-wrapped pouch of herbs found on one of the patients, labeled “AK-47 24 Karat Gold.” When they analyzed a sample, they found it contained the substance AMB-FUBINACA, a powerful synthetic cannabinoid similar to a compound first patented by Pfizer in 2009. The researchers also found breakdown products of AMB-FUBINACA in the blood of eight patients. © 2016 American Association for the Advancement of Science
Keyword: Drug Abuse
Link ID: 22991 - Posted: 12.15.2016