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By Susan Milius An elephant, a narwhal and a guinea pig walk into a bar. From there, things could get ugly. All three might get drunk easily, according to a new survey of a gene involved in metabolizing alcohol. They’re among the creatures affected by 10 independent breakdowns of the ADH7 gene during the history of mammal evolution. Inheriting that dysfunctional gene might make it harder for their bodies to break down ethanol, says molecular anthropologist Mareike Janiak of the University of Calgary in Canada. She and colleagues didn’t look at all the genes needed to metabolize ethanol, but the failure of this important one might allow ethanol to build up more easily in these animals’ bloodstreams, Janiak and colleagues report April 29 in Biology Letters. The carnivorous cetaceans, grain- or leaf-eating guinea pigs and most other animals that the study identified as potentially easy drunks probably don’t binge on sugary fruit and nectar that brews ethanol. Elephants, however, will feast on fruit, and the new study reopens a long-running debate over whether elephants truly get tipsy gorging on marula fruit, a relative of mangoes. Descriptions of elephants behaving oddly after binging on overripe fruit go back at least to 1875, Janiak says. Later, a taste test offering the animals troughs of water spiked with ethanol found that elephants willingly drank. Afterward, they swayed more when moving and seemed more aggressive, observers reported. © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27230 - Posted: 05.05.2020

By Austin Frakt OxyContin, and the aggressive, misleading way that Purdue Pharma marketed it, might have been even more damaging than was previously understood. Recent research shows how the company focused its marketing in states with lighter prescription regulation — to devastating effect. Also, a new version of OxyContin introduced a decade ago — which was meant to reduce harm — had unintended consequences. Besides contributing to heroin overdoses, it led to hepatitis C and other infections. Careful studies are only now starting to reveal the extent of the damage. OxyContin is an opioid painkiller that Purdue Pharma first brought to the U.S. market in 1996. Its chief innovation was its 12-hour timed release of oxycodone. This made it ripe for abuse, since by crushing or dissolving OxyContin pills, abusers of the drug could ingest the entire dose at once. Several studies have pointed to Purdue’s aggressive marketing of OxyContin as a significant contributor to the opioid epidemic. The marketing took various forms, including calling and visiting doctors; paying them for meals and travel; providing gifts; and funding pain treatment groups that urged liberalization of opioid prescribing. Some of the company’s marketing messages minimized the potential for OxyContin to lead to addiction, for which it paid over $600 million in fines in 2007. A National Bureau of Economic Research working paper published last fall sheds light on Purdue’s role. The researchers, economists from the University of Pennsylvania, the University of Notre Dame and the RAND Corporation, looked at variations in prescribing regulations that led Purdue to market OxyContin more aggressively in some states than in others. © 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: 27182 - Posted: 04.13.2020

By Jan Hoffman Anxious times — like a pandemic — can lead to unhealthy but self-soothing habits, whether it’s reaching for a bag of potato chips, more chocolate or another glass of wine. But some stress-reducing behaviors are alarming to medical experts right now — namely vaping and smoking of tobacco or marijuana. Because the coronavirus attacks the lungs, this is exactly the moment, they say, when people should be tapering — or better yet, stopping — their use of such products, not escalating them. ”Quitting during this pandemic could not only save your life, but by preventing the need for your treatment in a hospital, you might also save someone else’s life,” said Dr. Jonathan Winickoff, director of pediatric research at the Tobacco Research and Treatment Center at Massachusetts General Hospital. On Thursday, Dr. Winickoff joined the Massachusetts attorney general, Maura Healey, to issue an advisory alerting the public and particularly young people that smoking and vaping can also exacerbate the risks of spreading Covid-19. “You bring this device or cigarette to your mouth to inhale and you do so repeatedly,” explained Dr. Winickoff, who is also a professor at Harvard Medical School. “You touch the cartridge. You put it next to your face. You are spreading whatever is in your hand into your body. At the same time, many of my patients who smoke or vape have increased coughing or expectorating. And that’s a recipe for increased spread.” Studies already amply show that cigarette smoking weakens the immune system and compromises lung function. Research into the health effects of vaping is limited because the devices are relatively new, but studies suggest that e-cigarettes may cause inflammation in the airways and lungs. © 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: 27180 - Posted: 04.10.2020

By Gary Greenberg The retail showroom of INSA, a farm-to-bong cannabis company in western Massachusetts, is a clean industrial space on the first floor of a four-story brick building in the old mill town Easthampton. When I visited recently, before the coronavirus shut down recreational sales and forbade crowds, the crew of eight behind the glass display cases looked a lot like the staff you’d see dispensing lattes at Starbucks or troubleshooting iPads at the Genius Bar: young, racially diverse, smiling. They were all wearing black T-shirts with the INSA motto, “Uncommon Cannabis.” Standing in line with me were a white-haired couple leaning on canes; a 40-something woman in a black pantsuit, who complained that the wait would be longer than her lunch break; a bald man in a tweed jacket; and a pair of women in perms and polyester discussing the virtues of a strain called Green Crack. We were all waiting at a discreet distance from the counter, as you would at the bank, for the next available “budtender.” I got Ben, who described for me the wares that fill the cases like rings and watches in a jewelry store: waxes and dabs and oils and buds and edibles, most of them, he said, processed in a lab and kitchen on the other side of the wall behind him, using weed grown on the upper three floors. He sounded a little apologetic when he told me that while he knew why the bud I was pointing to was called Peyote Critical — “It speaks a little bit to its parentage, Peyote Purple and Critical Kush” — he hadn’t tried it, so he wasn’t entirely sure how it would affect me. Ben took me around a corner to another glass case, this one displaying vaporizers in different shapes and sizes. He pulled a box off a shelf behind him. It was a $35, 350-milligram disposable vape pen loaded with Jack Herer, a strain named for a legendary grower. If I bought this, he said, I should “resist the temptation to take big rips — four seconds at the max, then pull that pen away and inhale to get a nice full set of lungs.” Ben felt more certain about the effects of Jack Herer than Peyote Critical, especially after he took a look at the label. “The primary terpene in here is limonene,” he said, which should make me “energetic and uplifted.” But there were more terpenes at work, Ben said. “You’ve got pinene coming in at 2.83 percent, good for memory retention and alertness, and then myrcene, which should help balance out some of the raciness from the limonene. Myrcene is good for your brain’s absorption of metabolizing THC but also has relaxing, sedating qualities.” © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27173 - Posted: 04.06.2020

Emiliano Rodríguez Mega On a cold Friday night in February 1995, addiction researcher Nora Volkow and her husband got into their car after a long day at Brookhaven National Laboratory in Upton, New York. Ice had covered the trees and the roads, making them sparkle. But as the couple drove down a slope, the tyres lost their grip. The vehicle spun out of control. Volkow curled up to shield herself as an oncoming car crashed into her door. Metal bit into her flesh. The pain was unrelenting. Finally, the fire service arrived to break her free and an ambulance rushed her to the nearest emergency department, where a doctor gave her Demerol, a powerful and highly addictive opioid painkiller also known as pethidine, which is similar to morphine. Volkow had spent countless hours talking to people with addiction and had read hundreds of papers on the mechanisms of drug abuse. Neither prepared her for what happened next. “It was extraordinary, those impressive sensations,” she says. A moment of ecstasy, one she describes as comparable only to long-lasting sexual pleasure, eclipsed all other feelings. She stayed on the medication for another few days and was sent home with more. But she decided not to take it. She was afraid — she knew many of her patients could not stop once they started. She would get through the pain without the help of drugs. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 8: General Principles of Sensory Processing, Touch, and Pain; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27162 - Posted: 04.02.2020

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