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By Sheila Kaplan, Andrew Jacobs and Choe Sang-Hun In January 2019, the chairman of Altria, Howard A. Willard III, flew to Silicon Valley to speak to senior executives of Juul Labs, fresh off signing a deal for the tobacco giant to pay nearly $13 billion for a 35 percent stake in the popular e-cigarette company. With public fury growing over Juul’s contribution to the epidemic of teenage vaping, he laid out his vision for the company to continue to thrive. “I believe that in five years, 50 percent of Juul’s revenue will be international,” Mr. Willard told the 200 executives gathered at the Four Seasons in East Palo Alto. Kevin Burns, Juul’s chief executive at the time, interrupted: “I told the team to accomplish that in one year!” Many people in audience chuckled, but a year later, nobody is laughing. When the big American tobacco companies started feeling pressure decades ago, they found new markets and friendlier regulation abroad. Juul’s efforts to follow the same playbook have been stunningly unsuccessful. The company has been met with ferocious anti-vaping sentiment and a barrage of newly enacted e-cigarette restrictions, or outright bans, in country after country. As a result, its ambitious overseas plans have collapsed. Juul was kicked off the market in China last fall after just four days. The company has had to abandon plans for India after the government there banned all electronic cigarettes. Thailand, Singapore, Cambodia and Laos have also closed the door to e-cigarettes. In the Philippines, President Rodrigo Duterte ordered the arrest of anyone caught vaping outside designated smoking areas. Juul has postponed its launch in the Netherlands and has pulled out of Israel. In South Korea, the number of Juul customers has plummeted after the government issued dire health warnings about e-cigarettes, and the company has scaled back its distribution there. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27153 - Posted: 03.31.2020

Deborah Becker Alcoholics Anonymous may be just as good or better than scientifically proven treatments to help people quit drinking, according to a new review. But AA still doesn't work for everyone. AILSA CHANG, HOST: Alcoholics Anonymous, or AA, has been around for almost 85 years. But up until this week, medical researchers weren't quite sure just how well AA worked. Well, now a new review published by the Cochrane Collaboration has found that AA may lead to longer breaks from alcohol compared to other evidence-based treatments. Deborah Becker has been following all of this. She's a senior correspondent and host at WBUR and joins us now. Hey, Deborah. DEBORAH BECKER, BYLINE: Hi. CHANG: So for quite some time now, people weren't sure how effective AA was, and now they are. So what's changed? BECKER: Well, what they say has changed is that they have more and better studies about AA and professional programs that are based on AA principles. So the researchers here looked at 27 studies of AA programs involving more than 10,000 people. And the most striking finding of looking at all of this research was that the folks who were in AA or AA-based programs tended to stay away from alcohol longer. CHANG: OK. So can you just very briefly explain the mechanism by which AA is supposed to work? BECKER: Well, AA is primarily a social support network for people, so they can discuss how they are trying to achieve recovery and what they're doing to stay in recovery. And AA is based on what are known as the 12 steps. And these are 12 steps that folks take to guide them to recovery. CHANG: And this leaning into social networks, is that something that's unique to AA? BECKER: Well, I don't know if it's unique to AA, but certainly the support network theory of alcoholism and even addiction treatment is something that's widely used. And one of the lead authors of this Cochrane review is Dr. John Kelly at Massachusetts General Hospital. And he says what this review shows is that AA helps people shift their social networks away from heavy drinkers and toward people in recovery. And he says that's what professional therapy tries to do, but this - AA - does it in a more accessible and obviously less expensive way. © 2020 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27115 - Posted: 03.14.2020

By Jillian Kramer One of the strongest predictors of becoming an alcoholic is family history: the offspring of people with the disorder are four times more likely than others to develop it, according to the National Institute on Alcohol Abuse and Alcoholism (NIAAA). But new research shows a family history of alcoholism (FHA) affects more than your desire to drink. It also changes how your brain transitions from one task to the next—going, say, from cooking breakfast to thinking about a work deadline. A whole line of research has found that having an alcoholic in the family can affect one’s mental processes. But these studies have not fully explored what is called executive function—planning, restraint and other behaviors that are impaired with FHA. To delve further, Enrico Amico, now at the Swiss Federal Institute of Technology in Lausanne, and his colleagues decided to focus on how the brain processes competing cognitive demands—the switching of neural activity from one brain network to another, which is critical to executive functioning. Prior studies acquired “snapshots” of network activity when subjects were either performing a task or resting quietly. But this approach does not provide a continuous record of what is happening in the brain to capture the dynamic transitions from active to resting states that occur constantly throughout the day. So Amico, then at Purdue University, and a team of researchers at Purdue and Indiana University set out to answer how the brain makes these transitions. © 2020 Scientific American

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory and Learning
Link ID: 27086 - Posted: 03.03.2020

By Erin Blakemore Drug overdoses were once spoken about in whispers. Social stigma cast a dark shadow over them because they were seen as the natural, even deserved, consequence of illicit drug use. So why are they spoken about so openly today? Science historian Nancy D. Campbell has an answer: naloxone. The miraculous-seeming drug, which reverses opioid overdoses, was first approved in 1971. In “OD: Naloxone and the Politics of Overdose,” Campbell tracks how it helped turn overdose from an unmentionable affliction to an experience that is now seen as both common and preventable. In the days before overdose reversal, ODs were understudied and barely reported. Drug users faced harsh punishments. Heroin and other opioid overdoses were cast as a problem that mostly affected people of color, even though the majority of opioid users were white, Campbell says, and “overdose deaths occurred at or beyond the margins of respectability.” But armed with naloxone and a vision of a world without overdoses, scientists, health-care workers and community advocates began to push for more data, treatment and prevention. Campbell’s deeply researched book is driven by her desire to understand why it took so long for naloxone, and overdose prevention, to hit the mainstream. She discovered a group of varied protagonists — drug users, advocates, scientists and others — whose stories illustrate how naloxone, scientific progress and advocacy slowly shifted social attitudes.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27085 - Posted: 03.03.2020

David Nutt I was a scientific adviser to the UK government from 2000 to 2009. During this time, it became clear to me that drugs policy was being formed, not based on evidence, but on the political expediency of winning votes and pandering to the hysteria whipped up by a media more concerned with increased sales than decreased drug harms. When I was sacked, I wrote Drugs Without the Hot Air and used the proceeds to set up a charity, DrugScience.org.uk, dedicated to researching the truth about drugs. The book is set for its upcoming US release in a revised and updated second edition.The first research funded by DrugScience, published in The Lancet in 2010, quantified the overall harm of 20 drugs in the UK. The scores, which were derived from a powerful new technique called multi-criteria decision analysis, tabulated both the harms done to the users of these drugs and harms done to others. Alcohol topped this list with a score of 72, heroin scored 55, tobacco 26, cannabis in eighth place with 20, and LSD had a score of 7. Another European study in 2013 and Australian research published in 2019 showed strikingly similar patterns. There is evidence in the scientific literature that psychedelics could be helpful in treating depression, alcoholism, and cluster headaches. Similarly, researchers have shown MDMA (ecstasy) to be useful in the treatment of PTSD and alcoholism. Ketamine, a version of which was just FDA approved, is another illegal recreational drug that has shown great promise in treating depression. Is it not utterly inhumane that legal restrictions drive sufferers to be criminals to get the treatment they need? © 1986–2020 The Scientist.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27072 - Posted: 02.26.2020

By Aimee Cunningham The stories that Judith Feinberg hears from people with substance use disorder are riddled with loss: of jobs, opportunity, security, dignity. “People really are struggling to see that they have a viable future,” Feinberg says. “Then you take a drug … and you don’t care until you need the drug again.” For years, that drug was very likely an opioid. But Feinberg, a physician at West Virginia University School of Medicine in Morgantown who studies infectious diseases and injection drug use, recently has seen shifts in the addictive substances used. And it’s occurring not just in West Virginia — which has the highest rate of drug overdose deaths in the nation, at 51.5 deaths per 100,000 people — but across the country, the U.S. Centers for Disease Control and Prevention reported January 30. Fueled by a plentiful supply, people have increasingly been turning to such stimulants as cocaine and methamphetamine — so much so that the rates of overdose deaths for those drugs each surpassed that of prescription opioids in 2018. There’s a small bit of hope: After two decades of rising numbers, around 3,000 fewer people overall died of a drug overdose in 2018 than in 2017. But with 67,367 deaths, 2018 ranks as the second-worst year for drug overdoses in U.S. history. It’s too soon to say whether the nudge downward is a blip or the start of a meaningful drop. In part, that may depend upon whether the rise in stimulant use over much of the last decade continues. In 2018, the rate of overdose deaths involving cocaine was 4.5 per 100,000, more than triple what it was in 2012; for methamphetamine and similar drugs, the rate jumped from 0.8 to 3.9 per 100,000 during that period. Each now surpasses the death rate from prescription opioids, and cocaine’s rate is just shy of heroin’s. © Society for Science & the Public 2000–2020

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27065 - Posted: 02.24.2020

Rachel Patton McCord, Rebecca A. Prosser Have you ever slipped when trying to avoid sugar, quit smoking, or break another habit or addiction? Usually that one piece of cake or one cigarette won’t ruin your whole plan, but for people struggling with cocaine addiction, one slip can undo months of hard work. Cocaine consumption is increasing, with 2.2 million people in the U.S. admitting to recent cocaine use in 2017. In 2014, the National Survey on Drug Use and Health estimated that nearly 1 million Americans were addicted to cocaine. The effect of cocaine on the brain and body is so powerful that, even after state-of-the-art treatments, many people trying to quit cocaine relapse within a year. What if cocaine could be made less euphoric, so that a single use by a recovering addict doesn’t result in a full-blown relapse? Scientists at the Mayo Clinic recently published progress toward making this idea a reality – a gene therapy that would treat cocaine addiction by making cocaine less rewarding. We are a molecular biologist and a neurobiologist who are interested in understanding and treating human disease, including neurological disorders such as cocaine addiction. As University of Tennessee faculty members leading basic biomedical research, we have worked for years on how genes are turned on and off in people and the effects of cocaine on mice, respectively. So, we were excited to see a promising convergence of novel gene therapy and cocaine addiction therapy. Beginning more than 20 years ago, scientists have worked to engineer a new version of a human protein that could break down cocaine so quickly that it doesn’t produce an addictive high. We all have the normal human protein BChE that helps regulate neurotransmitters, and which can slowly break down cocaine. Targeted mutations in BChE can turn it into a super-CocH – a protein that can quickly break down cocaine. When this CocH is injected into the bloodstream, it breaks down cocaine very fast – before the user can experience the pleasurable effects – so a dose of cocaine is less rewarding. Being less rewarding means it is easier to stop using cocaine. © 2010–2020, The Conversation US, Inc.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27033 - Posted: 02.11.2020

Liz Fuller-Wright, Office of Communications Barry L. Jacobs, an emeritus professor of psychology and neuroscience who became internationally known for his research on serotonin, sleep and depression, died Friday, Jan. 10, in Princeton. He was 77 years old. Jacobs joined the Princeton faculty in 1972 and transferred to emeritus status in 2017. Among his roles at the University, he served as director of the neuroscience graduate program from 1988 to 2000. “Barry Jacobs was a truly wonderful colleague — brilliant, knowledgeable, interesting, generous, and always upbeat and friendly,” said Ronald Comer, an emeritus member of Princeton’s psychology faculty. “Deeply committed to his work and to all of neuroscience, he was just as interested in and curious about the work of his other psychology colleagues, including those of us in social and clinical psychology. As a result of his special accomplishments in neuroscience, multiple interests, extraordinary skills as a teacher and communicator, and contagious passion for science, Barry was able to develop and teach, for decades, one of the University’s most successful and popular courses, ‘The Brain: A User’s Guide’ — a course that brought the wonders of neuroscience to life for University students of all concentrations and interests.” Jacobs was born Feb. 26, 1942, in Chicago. He received his B.S. in economics from the University of Illinois-Chicago, in 1966, and his doctorate in psychology from the University of California-Los Angeles in 1971. He was a postdoctoral fellow in the psychiatry department at Stanford University Medical School before coming to Princeton. © 2020 The Trustees of Princeton University

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26981 - Posted: 01.23.2020

Merrit Kennedy Smoking can be an easy habit to pick up and a hard one to quit. Here's the good news — there are decades of research on how to drop the habit. And we heard from hundreds of former smokers about how they did it. If you've tried to quit before, and it didn't work out, don't let that discourage you from trying again. It's common for quitting to take multiple attempts. "It's not a one time event. It is a process," says Gary Tedeschi, the clinical director at the California Smokers' Helpline. "And if I could say nothing else, I would say never ever stop trying to quit." We heard about a wide range of methods that helped people quit—and the truth is that no one method will work for everyone. But it's clear that having a roadmap for how you want to quit is going to boost your chances of succeeding. 1. You need a plan "A lot of smokers, when they are thinking about quitting, they sort of dive in without a plan," says Yvonne Prutzman, a scientist from the National Cancer Institute's Tobacco Control Research Branch. "And maybe the plan is to rely on willpower — but that makes it a lot harder for them," she adds. Your plan might be pretty personal. People quit many different ways — and reach the conclusion that they need to quit for very different reasons. For example, for Stacey Moore from Georgia, a serious health scare prompted her decision. "Just a couple of weeks ago I woke up with what I thought was a cancerous lump in my throat," she tells NPR. "It turned out to just be tonsillitis but it scared me enough that I knew I just had to stop, I just can't play this roulette game anymore." Others, like Greg Moulton from South Carolina, spent months or even years preparing to quit, slowly reducing the amount of nicotine they were taking in every day. "You slay the beast slowly and let it bleed to death on its own," he says. © 2020 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26965 - Posted: 01.17.2020

By Matt Richtel The number of women drinking dangerous amounts of alcohol is rising sharply in the United States. That finding was among several troubling conclusions in an analysis of death certificates published Friday by the National Institute on Alcohol Abuse and Alcoholism. The analysis looked at deaths nationwide each year from 1999 through 2017 that were reported as being caused at least partly by alcohol, including acute overdose, its chronic use, or in combination with other drugs. The death rate tied to alcohol rose 51 percent overall in that time period, taking into account population growth. Most noteworthy to researchers was that the rate of deaths among women rose much more sharply, up 85 percent. In sheer numbers, 18,072 women died from alcohol in 2017, according to death certificates, compared with 7,662 in 1999. “More women are drinking and they are drinking more,” said Patricia Powell, deputy director of the alcohol institute, which is a division of the National Institutes of Health. Still, far more men than women die from alcohol-related illnesses, the study showed. In 2017, alcohol played a role in the deaths of 72,558 men, compared to 35,914 in 1999, a 35 percent increase when population growth is factored in. Like much research of its kind, the findings do not alone offer the reasons behind the increase in alcohol deaths. In fact, the data is confounding in some respects, notably because teenage drinking overall has been dropping for years, a shift that researchers have heralded as a sign that alcohol has been successfully demonized as a serious health risk. Experts said that the new findings could partly reflect the fact that baby boomers are aging and the health effects of chronic alcohol use have become more apparent. The increase in deaths might also reflect the increase in opioid-related deaths, which in many cases can involve alcohol as well, and that would be reflected on death certificates. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 26955 - Posted: 01.13.2020

Lesley McClurg Americans know the dangers of drugs such as morphine and heroin. But what about a supplement that acts in the brain a bit like an opiate and is available in many places to kids — even from vending machines. Kratom, an herb that's abundant, legal in most states and potentially dangerous, is the subject of an ongoing debate over its risks and benefits. Usually, the leaf, which comes from a tropical Southeast Asian tree, is chewed, brewed or crushed into a bitter green powder. The chemicals in the herb interact with different types of receptors in the brain — some that respond to opioids, and others to stimulants. Often sold in the U.S. in a processed form — as pills, capsules or extracts — a small amount of kratom can perk you up, while a large dose has a sedative effect. Some people who have struggled with an opioid addiction and switched to kratom swear the substance salvaged their health, livelihood and relationships. But the federal Food and Drug Administration and the Drug Enforcement Administration worry that kratom carries the risk of physical and psychological dependency and, in some people, addiction. The FDA warns consumers not to use kratom, and the DEA threatened to prohibit kratom's sale and use in the U.S. (outside of research) in 2016; advocates and lawmakers subsequently pushed back, and the stricter scheduling of kratom that would have prompted that sort of ban never occurred. These days, the DEA lists it as a drug of concern. © 2020 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26951 - Posted: 01.13.2020

By Elizabeth Brico The statistics are heartbreaking. Each year in the U.S., about 32,000 newborns are diagnosed with neonatal abstinence syndrome, a form of withdrawal that can result from in utero exposure to a number of drugs taken by the mother during pregnancy. Opioids — both prescribed and illegal — are among the most common culprits. These medications can be necessary, even life-saving, but that doesn’t make the resultant NAS any easier to watch: Newborns who suffer from the syndrome may exhibit tremors, irritability, hyperactive reflexes, high-pitched crying, and other symptoms. But drugs are not solely to blame for the prolonged suffering many of these infants experience. The way NAS cases are handled also has a profound impact on their severity, and often leads to negative outcomes. Health care providers and law enforcement authorities have historically separated these fragile babies from their mothers, doling out severe punishments to the latter. Although there is a growing awareness that change is needed, many hospitals still use outdated approaches — and child welfare agencies are particularly behind the times in this arena. Recent studies suggest that policies that place blame on mothers only heighten a newborn’s suffering by preventing infants from accessing potent care for reducing withdrawal symptoms: contact with mom. Misperceptions about opioid addiction, dependency, and NAS are woven into the very fabric of U.S. and state law. In order to receive federal funding for child abuse prevention, health care workers are required to report substance-affected newborns to Child Protective Services. Additionally, states can require health care providers to report or test for drug exposure during pregnancy. In many cases, mothers are reported even if the exposure is the result of prescribed methadone or buprenorphine — opioid-based drugs commonly used to treat addiction.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory and Learning
Link ID: 26943 - Posted: 01.09.2020

By Simon Makin For many people battling addictions, seeing drug paraphernalia—or even places associated with past use—can ignite cravings that make relapse more likely. Associating environmental cues with pleasurable experiences is a basic form of learning, but some researchers think such associations can “hijack” behavior, contributing to problems such as addiction and eating disorders. Researchers led by neuroscientist Shelly Flagel of the University of Michigan have found a brain circuit that may control this hijacking; rats that exhibit a type of compulsive behavior show different brain connectivity and activity than those that do not, and manipulation of the circuit altered their behavior. These findings may help researchers understand why some individuals are more susceptible to impulse-control disorders. “This is technically a really excellent study,” says neuroscientist Jeff Dalley of the University of Cambridge, who was not involved in the work. In the study, published last September in eLife, researchers showed rats an inert lever shortly before delivering a tasty treat via a chute, then sorted them into groups based on their responses. All rats learned to associate the lever with the treat, but some—dubbed “goal trackers”—began to approach the food chute directly after seeing the lever, whereas inherent “sign trackers” kept compulsively returning to the lever itself. The team suspected that two brain regions were involved: the paraventricular nucleus of the thalamus (PVT), which drives behavior, and the prelimbic cortex, which is involved in reward learning. The researchers used a technique called chemogenetics to alter neurons in the circuit connecting these regions, which let them turn on or inhibit signals from the prelimbic cortex using drugs. Activating the circuit reduced sign trackers' tendency to approach the lever but did not affect goal trackers. Deactivating it drew goal trackers to the lever (sign-tracking behavior), without affecting preexisting sign trackers. The team also found increased dopamine, a chemical messenger involved in reward processing, in the newly sign-tracking brains. © 2020 Scientific American

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26933 - Posted: 01.04.2020

By Knvul Sheikh When researchers began tinkering with a class of tranquilizer drugs called benzodiazepines in the 1950s, they felt they had uncovered a solution to modern anxiety and insomnia. Benzodiazepines worked quickly and effectively to quell racing heartbeats and dismiss spinning thoughts. The dozen or so different types — including Xanax, Valium, Ativan and Klonopin — became the most frequently prescribed drugs around the world, even as concerns arose about their potential side effects and addictive properties. “Patients themselves, and not the medical profession, were the first to realize that long-term use of benzodiazepines can cause problems,” wrote Dr. Heather Ashton, a British psychopharmacologist. She said that patients who had been on the medications for months or years would come to her with fears that the drugs were making them more ill. Some continued to have symptoms of depression or anxiety. Others had developed muscle weakness, memory lapses, or heart or digestive issues. Dr. Ashton would dedicate much of her career to listening to hundreds of patients’ experiences and rigorously collecting data. The result of her work, in 1999, was “Benzodiazepines: How They Work And How To Withdraw.” Now known simply as “The Ashton Manual,” it has become a cornerstone for those looking to quit the drugs safely. Addiction researchers worldwide still cite it in studies on benzodiazepines. And patient support groups have translated and distributed it in about a dozen languages. Dr. Ashton died on Sept. 15, 2019, at her home in Newcastle upon Tyne, England. She was 90. Her death, which had not been widely reported, was confirmed by her son John. Image“Benzodiazepines: How They Work and How to Withdraw,” better known as “The Ashton Manual,” has become a cornerstone for those looking to quit anxiety drugs safely. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26930 - Posted: 01.04.2020

Judith Grisel I used to think addiction was caused by screwy molecules in the brain, and would be cured by neuroscience. I began learning about how the brain works after I ended up in treatment for drug addiction in the mid-1980s, when hopes for neuroscientific cures were as overblown as the hairstyles. My own journey away from the destructive cycle of addiction has been sourced much more by factors outside my brain Like many at the time, I envisioned the brain as executive director of an epic drama – solely responsible for the total picture of what I did, felt and thought. My specific purpose in getting a doctorate in behavioural neuroscience was to discover the neural explanation for my irrational choices around mind-altering chemicals. What was the faulty neural switch that swept away heartfelt promises or strongly held convictions in response to practically every opportunity to twist reality? I made increasingly risky and harebrained decisions, as the possibility of transient bliss in a shot of cocaine, a belly full of booze or a head in the (cannabis) clouds came to outweigh my obligations or common sense. Final exams, “last chances” at work, or loved ones’ funerals, for example, didn’t stand a chance compared to hitching myself to whatever intoxicating ride I could catch. By the time I hit bottom, the choice between facing stark reality or using drugs to escape was no choice at all: cortical regulation had completely given way to subcortical impulses and habits. Globally 35 million people are estimated to suffer from drug use disorders. The causes of this public health disaster are complicated, but it is widely accepted that about half of the contribution comes from inherited risk, and the rest an unfortunate confluence of environmental factors interacting with that biologic vulnerability.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26926 - Posted: 01.02.2020

Stephanie O'Neill For many Americans, hallucinogens still evoke the psychedelic '60s, bringing to mind the sex-and-drugs lifestyle of the hippie counterculture. But that stereotype lags behind reality, by several decades. Today, psychedelic experimentation is more likely to refer to dozens of clinical trials taking place at universities and research facilities. The psychedelics under study range from psilocybin, the active ingredient in psychedelic mushrooms, to MDMA (also known as Ecstasy or Molly), to LSD, among others. Researchers are studying them for their therapeutic potential in treating hard-to-treat conditions such as PTSD, addiction, depression and anxiety. The promise of freedom from cigarettes was what compelled Carine Chen-McLaughlin, 65, to enroll in an experimental study of psilocybin therapy for smokers. She was desperate to break free from her decades-long physical addiction to nicotine. Quitting smoking had felt impossible for so long. "It's basically saying good-bye to a very old friend, and worrying about: Am I going to be OK without this good friend?'" the Baltimore resident says. Like many of the 49 million tobacco users in the U.S., Chen-McLaughlin wanted to quit and had tried various methods: nicotine gum, the nicotine patch and even stopping cold turkey. But nothing worked for more than a couple days. The clinical trial she joined took place in her hometown of Baltimore, at Johns Hopkins School of Medicine. While she was a bit anxious about the experiment, Chen-McLaughlin says she was nevertheless hopeful about trying something totally different. © 2019 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26915 - Posted: 12.26.2019

By Douglas Martin Baba Ram Dass, who epitomized the 1960s of legend by popularizing psychedelic drugs with Timothy Leary, a fellow Harvard academic, before finding spiritual inspiration in India, died on Sunday at his home on Maui, Hawaii. He was 88. His death was announced on his official Instagram account. Having returned from India as a bushy-bearded, barefoot, white-robed guru, Ram Dass, who was born Richard Alpert, became a peripatetic lecturer on New Age possibilities and a popular author of more than a dozen inspirational books. The first of his books, “Be Here Now” (1971), sold more than two million copies and established him as an exuberant exponent of finding salvation through helping others. ImageRam Dass’s book “Be Here Now,” originally published in 1971, has had more than three dozen printings and sold more than two million copies. Ram Dass’s book “Be Here Now,” originally published in 1971, has had more than three dozen printings and sold more than two million copies. He started a foundation to combat blindness in India and Nepal, supported reforestation in Latin America, and developed health education programs for American Indians in South Dakota. He was particularly interested in the dying. He started a foundation to help people use death as a journey of spiritual awakening and spoke of establishing a self-help line, “Dial-a-Death,” for this purpose. A year later, Ram Dass suffered a cerebral hemorrhage that left him partly paralyzed, unable to speak and in a wheelchair. From his home in Maui, he learned to “surf the silence” at first, he said, but over time he painstakingly reacquired a halting form of speech and was able to lecture on the internet and make tapes. © 2019 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26912 - Posted: 12.26.2019

People with severe epilepsy will be able to access a cannabis-based medicine on the NHS from early next year after it was fast-tracked for use. NHS England said doctors would be able to prescribe Epidyolex from 6 January. It will be for children from age two, as well as adults, but some campaigners warn it is "too little too late". Clinical trials have shown the oral solution, which contains cannabidiol (CBD), could reduce the number of seizures by up to 40% in some children. The medicine will be used to treat two rare, but severe, forms of childhood epilepsy - Lennox Gastaut syndrome and Dravet syndrome - which can cause multiple seizures a day. Epilepsy Action's chief executive Philip Lee welcomed the announcement, saying it "brings much-needed hope and could be life-changing for some". However, he added that Epidyolex was not "a silver bullet" and there was more work to be done to "collect robust high-quality evidence of the effectiveness of other cannabis-based medicines". Medical cannabis campaigner Peter Carroll said it was "too little, too late" as he urged action towards making medicinal cannabis with CBD and tetrahydrocannabinol (THC) available for families in need. THC is the psycho-active component of cannabis. Speaking to BBC News, he said: "What's shown to have a transforming effect for children in desperate need is a CBD medicine with a little bit of THC, but those are unlicensed in the UK at the moment." Mr Carroll added: "The law was changed in November 2018 so that specialist doctors could write a prescription for medical cannabis with the CBD and THC, even though they are unlicensed. © 2019 BBC

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26906 - Posted: 12.21.2019

By Abby Goodnough TULSA, Okla. — The teenager had pink cheeks from the cold and a matter-of-fact tone as she explained why she had started using methamphetamine after becoming homeless last year. “Having nowhere to sleep, nothing to eat — that’s where meth comes into play,” said the girl, 17, who asked to be identified by her nickname, Rose. “Those things aren’t a problem if you’re using.” She stopped two months ago, she said, after smoking so much meth over a 24-hour period that she hallucinated and nearly jumped off a bridge. Deaths associated with meth use are climbing here in Oklahoma and in many other states, an alarming trend for a nation battered by the opioid epidemic, and one that public health officials are struggling to fully explain. The meth problem has sneaked up on state and national leaders. In Oklahoma, meth and related drugs, including prescription stimulants, now play a role in more deaths than all opioids combined, including painkillers, heroin and fentanyl, according to the Centers for Disease Control and Prevention. The spending package that lawmakers agreed on this week includes legislation from Senators Jeanne Shaheen, Democrat of New Hampshire, and Rob Portman, Republican of Ohio, that would allow states to address the resurgence of meth and cocaine by using some of the billions of dollars that Congress had appropriated to combat opioid addiction. Meth use first ballooned in the United States from the 1990s into the early 2000s, when it was often made in small home labs with pseudoephedrine, the main ingredient in many drugstore cold medicines. But today’s meth, largely imported from Mexico, is far more potent. © 2019 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26897 - Posted: 12.18.2019

By Diana Kwon MDMA, or ecstasy, once had the reputation of exclusively being an illicit party drug popular at raves and dance clubs. That view has changed in recent years. The substance, known for its ability to produce feelings of euphoria and affection for others, has developed a new identity as a promising therapeutic tool. Researchers are currently investigating MDMA-assisted therapy as a potential treatment for post-traumatic stress disorder in late-stage clinical trials. The drug’s capacity to enhance sociability has also led to studies investigating its benefits for other conditions, such as social anxiety in individuals with autism spectrum disorder. Despite the promise of its therapeutic benefits, concern persists among some scientists that MDMA could be abused because its pleasurable effects can make it addictive. “By no means [does the drug] have the addictive liability of methamphetamine or certain opioids,” says Robert Malenka, a professor of psychiatry and behavioral sciences at Stanford University. “But it does have abuse potential.” A new study by Malenka and his team suggests it may be possible to circumvent this risk. The findings, published today in Science Translational Medicine, reveal that MDMA’s sociability-enhancing abilities and its pleasurable properties are controlled by distinct pathways in the brain—at least in mice. That insight opens the possibility of developing a safer version of the drug. Previous research by Malenka’s group and others had revealed that MDMA stimulated the release of both serotonin and dopamine in the brain. The existing evidence suggested the drug’s effects on sociability were linked to serotonin and its addictive potential to dopamine, but the extent to which these pathways were distinct was unknown. “Separating out the prosocial from the addictive effects has tremendous implications for drug development,” says Boris Heifets, an anesthesiologist at Stanford and lead author of the latest study. A key question is, “Can we make something with the same kind of prosocial effect that maybe isn’t as prone to abuse?” © 2019 Scientific American

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26891 - Posted: 12.12.2019