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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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: 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 BN8e: 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 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26891 - Posted: 12.12.2019

By Anna Schaverien and Allison McCann LONDON — Homeless drug users in Scotland will be allowed to inject pharmaceutical-grade heroin twice a day under the supervision of medical officials as part of a new program intended to reduce drug deaths and H.I.V. infection. From 9 a.m. to 5 p.m. seven days a week, a $1.5 million facility in Glasgow that opened on Tuesday will allow a handful of drug users to receive doses of the drug alongside other treatment for their physical and psychological health, according to Glasgow City Council. The pilot project, known as heroin-assisted treatment, is the first such licensed operation in Scotland, a country that has been called the “drug death capital of the world.” It has struggled to cope with high rates of fatal drug overdoses and its worst H.I.V. outbreak in decades. The program will target those with the “most severe, longstanding and complex addiction issues,” the City Council said. It aims to reduce the risk of overdoses and the spread of viruses such as H.I.V. by prescribing diamorphine — the clinical name for pharmaceutical-grade heroin — for patients to inject in a secure clinical room under the supervision of trained medics. The clinic opened in Glasgow, Scotland’s largest city, after Britain’s Home Office granted it a license, and follows a similar initiative that began in Middlesbrough, England, last month. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26862 - Posted: 12.02.2019

Merrit Kennedy A newly published study from University College London suggests that a single dose of ketamine could help dramatically reduce the alcohol intake of heavy drinkers. Bruce Forster/Getty Images What if a single dose of ketamine could make a heavy drinker dramatically cut back on booze? A team at University College London thinks that ketamine may be able to "rewrite" memories that shape a person's relationship with alcohol. Scientists say that participants who were given ketamine as part of an experimental study dramatically reduced their average alcohol intake for months after the initial dose. Their research was published Tuesday in Nature Communications. Ketamine — sometimes known as a club drug called Special K that can produce hallucinations — has been shown to be a powerful and fast-acting treatment for depression. Researchers also are looking into whether ketamine can help patients with post-traumatic stress disorder. The U.K. findings may signal yet another use for the drug for hard-to-treat conditions. In general, the treatment options for alcoholism "aren't particularly effective for the majority of people, particularly over the long term," says Ravi Das, a UCL psychopharmacologist and the study's lead researcher. Das thinks part of the problem is that current remedies don't necessarily help patients deal with positive memories of drinking that could make them want to drink again. "When people become addicted, they're learning that kind of behavior in response to things in their environment," he says. "Those memories, those associative trigger memories, can be really long lasting and really kind of ingrained. And current treatments don't target those." © 2019 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26858 - Posted: 11.29.2019

By Julie Creswell and Sheila Kaplan SAN FRANCISCO — In the face of mounting investigations, subpoenas and lawsuits, Juul Labs has insisted that it never marketed or knowingly sold its trendy e-cigarettes and flavored nicotine pods to teenagers. As youth vaping soared and “juuling” became a high school craze, the company’s top executives have stood firm in their assertion that Juul’s mission has always been to give adult smokers a safer alternative to cigarettes, which play a role in the deaths of 480,000 people in the United States each year. “We never wanted any non-nicotine user and certainly nobody underage to ever use Juul products,” James Monsees, a co-founder of the company, testified at a congressional hearing in July. But in reality, the company was never just about helping adult smokers, according to interviews with former executives, employees and investors, along with reviews of legal filings and social media archives. Juul’s remarkable rise to resurrect and dominate the e-cigarette business came after it began targeting consumers in their 20s and early 30s, a generation with historically low smoking rates, in a furious effort to reward investors and capture market share before the government tightened regulations on vaping. As recently as 2017, as evidence grew that high school students were flocking to its sleek devices and flavored nicotine pods, the company refused to sign a pledge not to market to teenagers as part of a lawsuit settlement. It wasn’t until the summer of 2018, when the Food and Drug Administration required it to do so, that the company put a nicotine warning label on its packaging. Though some former employees recalled Mr. Monsees wearing a T-shirt at the office that used an expletive to refer to Big Tobacco, the start-up’s early pitches to potential investors listed selling the business to a big tobacco company as one of the potential ways to cash out. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26846 - Posted: 11.23.2019

Cody A. Siciliano Some individuals consume alcohol their entire adult life without developing an alcohol use disorder. Others, however, quickly transition to compulsive and problematic drinking. Can we determine what makes some people vulnerable to addiction? Alcohol drinking is the third leading cause of preventable death in the United States, and is responsible for millions of deaths per year worldwide. If the reasons why some people are susceptible to alcohol use disorder were known, it might be possible to more effectively treat this devastating disease, or even intervene before serious problems emerge. I have spent my career as a neuroscientist and pharmacologist trying to understand how drugs and alcohol act on the brain, and what makes a brain more or less susceptible to substance use disorders. My laboratory at the Vanderbilt Center for Addiction Research develops approaches for studying addictive behaviors in rats and mice. Using electrochemical and optical approaches to measure brain activity, our goal is to determine how patterns of activity in brain cells give rise to these behaviors – and how we may use this information to treat or prevent substance use disorders. In a report published in the Nov. 22 issue of the journal Science, Kay Tye of the Salk Institute and I set out to understand how binge drinking alters the brain and how this can lead to compulsive behaviors in some drinkers. To study this, we designed an experiment in which mice were scored for their propensity to drink alcohol. We measured compulsive drinking by determining how much they drank when we mixed the alcohol with a bitter tasting substance that mice normally avoid. © 2010–2019, The Conversation US, Inc.

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 26844 - Posted: 11.22.2019

Regina Denney's 17-year-old son Brian called her in a panic; he couldn't stop throwing up. It was April 7, 2018 and the Indianapolis teen asked her to take him to the emergency room — but doctors there couldn't figure out what was wrong. He was severely dehydrated and constantly vomiting. "As we're sitting there talking, another doctor happens to walk by our room and she pokes her head in and she says, 'Do you smoke marijuana?'" Denney said. "And he said yes. And she said, 'Does it get better with hot showers or hot baths?' And he said yes." Brian Smith Jr. was diagnosed with a rare condition called cannabinoid hyperemesis syndrome (CHS). When his lab results came back, his mother said the teen's kidneys were shutting down and his liver wasn't functioning properly. "It was just crazy," Denney said. "They were able to rehydrate him. And [the results] improved. So they released him the next day, but didn't give us any information about what CHS was, what causes it, what to look for." He was a heavy cannabis smoker and his mother convinced him to stop, at least until they could see a gastroenterologist 45 days later. Denney said he still had symptoms leading up to that appointment and thought if they were related to his cannabis use, he would have been symptom free. So he started smoking again. What they didn't know was CHS can present symptoms weeks or months after stopping cannabis use. By October, Denney said her son had lost more than 40 pounds. "You could see his bones. He looked sick," she said. "It's torture." ©2019 CBC/Radio-Canada

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26824 - Posted: 11.16.2019

By Denise Grady A form of vitamin E has been identified as a “very strong culprit” in lung injuries related to vaping THC, health officials reported on Friday, a major advance in a frightening outbreak that has killed 40 people and sickened 2,051. Many patients with the mysterious illness have wound up hospitalized in intensive care units, needing ventilators or even more desperate measures to help them breathe. Most are young, male adults or even teenagers. “For the first time, we have detected a potential toxin of concern, vitamin E acetate, from biological samples from patients,” with lung damage linked to vaping, Dr. Anne Schuchat, principal deputy director of the Centers for Disease Control and Prevention, said at a news briefing. The new report, based on samples taken from the lungs of 29 patients, including two who died, she said, “provided evidence of vitamin E acetate at the primary site of injury in the lungs.” She added, “These findings tell us what entered the lungs of some patients with these injuries.” The patients came from 10 states scattered around the country, so the findings are considered broadly applicable and unlikely to have resulted from a single vaping product or supplier. The results mesh with other research that found the vitamin compound in vaping products. But Dr. Schuchat left open the possibility that other chemicals or toxins from vaping fluids or devices could also be causing the severe respiratory ailments. The outbreak has revealed the existence of a vast, unregulated, shadowy marketplace of illicit or bootleg vaping products that are essentially a stew of unknown chemicals concocted, packed and sold by unknown manufacturers and sellers. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26808 - Posted: 11.09.2019

Sean McMinn Three years ago, only about one in ten high school students reported having recently used e-cigarettes. But a study published this week in JAMA shows the proportion of students vaping nicotine has now grown to more than one in four. Researchers from the Food and Drug Administration and Centers for Disease Control and Prevention analyzed data from the 2019 National Youth Tobacco Survey, which is conducted annually. They drilled down on e-cigarette use among high school and middle school students based on data from 19,000 students in the eighth, tenth and twelfth grades. Teen nicotine vaping has become so prevalent in recent years that the Food and Drug Administration has called it an "epidemic." An estimated 5.3 million teens use e-cigarettes, according to the study. It is illegal in all states for people under 18 to purchase e-cigarettes, and some states have raised that age to 21. Despite this and recent efforts to crack down on retailers selling to youth, rates of teen vaping have continued to rise. "For young people, this is of particular concern," the study's authors wrote, "because it could promote ... nicotine dependence, making it easier to initiate and proceed to regular e-cigarette use or transition to cigarette or other combustible tobacco product use." Students who took the survey, however, didn't appear to have moved on to traditional cigarettes yet. Just 6% of high schoolers reported having smoked a cigarette in the last month — a decrease from last year's survey. © 2019 npr

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26801 - Posted: 11.08.2019