Chapter 3. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.

Links 61 - 80 of 2739

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

Keyword: Drug Abuse
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

Keyword: Drug Abuse
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

Keyword: Drug Abuse; 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

Keyword: Drug Abuse; Pain & Touch
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

Keyword: Drug Abuse
Link ID: 27153 - Posted: 03.31.2020

By Joshua Sokol The city of Minamata, Japan, is dotted with monuments commemorating victims of an industrial mass poisoning decades ago. High in the hills, a small stone memorial honors other deaths—of cats sacrificed in secret to science. Now, after restudying the remains of one of those cats, a team of scientists is arguing, controversially, that the long-standing explanation for the tragedy is wrong. No one questions the root cause of the disaster, which at minimum poisoned more than 2000 people: mercury in a chemical factory’s wastewater that was dumped into Minamata Bay and taken up by seafood eaten by fishermen and their families. At first, the chemical form of the mercury, which ultimately killed many of its victims and left many babies with severe neurological disorders, was unknown. But in 1968, the Japanese government blamed methylmercury, a common byproduct of mercury pollution. Many studies supported that conclusion, finding methylmercury spikes in shellfish, bay sludge, and even hundreds of umbilical cords from babies delivered during the time. But methylmercury is not the culprit, says Ingrid Pickering, an x-ray spectroscopist at the University of Saskatchewan. “Our work is indicating that it’s something else”: an unusual mercury compound that may say little about the broader threat of mercury pollution. Minamata has long been a vivid case study of mercury’s dangers. The metal is toxic on its own, but it becomes far more dangerous when bacteria in natural environments convert it into methylmercury, an organic compound, readily absorbed by living tissues, that can be concentrated and passed up food chains. Since the 1990s, scientists have argued that the Chisso chemical factory in Minamata produced methylmercury and dumped it directly into the bay. © 2020 American Association for the Advancement of Science.

Keyword: Neurotoxins
Link ID: 27140 - Posted: 03.25.2020

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

Keyword: Drug Abuse
Link ID: 27115 - Posted: 03.14.2020

By Alex Gatenby Victoria Derbyshire programme The mental health charity Mind says it is signposting people to street drug charities to help them withdraw from antidepressants because of the lack of alternatives available. Those affected can experience debilitating symptoms. "Within a couple of days of coming off, it was overwhelming - agitation, anxiety, akathisia [restlessness], just restlessness, can't sleep, suicidal ideations, all that stuff going on very quickly," Stuart Bryan tells the BBC's Victoria Derbyshire programme. The 48-year-old has been taking anti-depressants on and off for more than two decades. "The withdrawals are far worse than the original depression, for me and so many other people." Stuart has tried to stop more than 10 times, but has struggled with what he calls his withdrawal "hell" - and has now had to stop working. He says doctors have advised him to take anything between "a few weeks" to three months to slowly stop using the drugs. But he believes people coming off anti-depressants are being "abandoned by the system". Image caption Mind's Stephen Buckley says it is not fully understood how difficult a process coming off anti-depressants can be While antidepressants are not addictive, just over half of those who stop or reduce their dosage experience withdrawal symptoms, according to one review of 24 studies last year. The mental health charity Mind's head of information Stephen Buckley says it is having to signpost patients to street-drug charities, even though they have been prescribed the drugs on the NHS. Street-drug charities usually help those misusing alcohol and illegally-obtained drugs. © 2020 BBC

Keyword: Depression
Link ID: 27112 - Posted: 03.12.2020

By Nicholas Bakalar Moderate alcohol consumption is associated with reduced levels of beta amyloid, the protein that forms the brain plaques of Alzheimer’s disease, a new study suggests. Korean researchers studied 414 men and women, average age 71, who were free of dementia or alcohol-related disorders. All underwent physical exams, tests of mental acuity, and PET and M.R.I. scans. They were carefully interviewed about their drinking habits. The study, in PLOS Medicine, measured drinking in “standard drinks” — 12 ounces of beer, five ounces of wine, or one-and-a-half ounces of hard liquor. Compared with abstainers, those who drank one to 13 standard drinks a week had a 66 percent lower rate of beta amyloid deposits in their brains. The results applied only to those who drank moderately for decades, and not to those who recently began drinking moderately or drank more than 13 drinks a week. The study controlled for age, sex, education, socioeconomic status, body mass index, vascular health and many other factors. Dr. Dong Young Lee, the senior author and a professor of psychiatry at Seoul National University College of Medicine, cautioned that this was an observational study that looked at people at one point in time, and does not prove cause and effect. Still, he said, “In people without dementia and without alcohol abuse or dependency, moderate drinking appears to be helpful as far as brain health is concerned.” © 2020 The New York Times Company

Keyword: Alzheimers; Drug Abuse
Link ID: 27096 - Posted: 03.06.2020

By David H. Freedman Two levels below ground, under a small, drab building at the University of Bonn, is a wall of cages containing mice that, according to standard tests, are extraordinarily average. They learn and remember how to run mazes no better nor worse than other mice. It takes them a typical amount of time to figure out how to extricate themselves from a tank of water with hidden exit steps. There’s nothing out of line about how they interact with other mice, nor their willingness to explore open spaces. And yet these mice are the center of attention at the lab of Andreas Zimmer. That’s because their boringly average minds may well hold the key to beating Alzheimer’s and elderly dementia. Many of the mice are 18 months old, roughly equivalent to a 70-year-old human. Mice normally start to show mental decline at around a year old, and by 18 months, struggle with mazes and other mental tasks, as well as with socializing. But not these rodent seniors. “You can’t tell the difference between them and two-month-old mice,” says Zimmer. Even more surprising is what Zimmer has done to get these elderly mice remembering and behaving like younger ones. It’s not special genes, a particular training regimen, nor an unusual diet. They don’t get any approved memory drug, nor a new investigational procedure. Basically, Zimmer keeps them very slightly stoned. A longtime U.S. National Institutes of Health (NIH) researcher who is now one of Germany’s most respected neuroscientists, Zimmer has been on a long journey to answer a question that few researchers had thought to ask: Is it possible that weed, long seen as the stuff of slackers, might actually contain the secret to sharpening the aging brain? © 2020 Kalmbach Media Co.

Keyword: Alzheimers; Drug Abuse
Link ID: 27094 - Posted: 03.05.2020

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

Keyword: Drug Abuse; Genes & Behavior
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.

Keyword: Drug Abuse
Link ID: 27085 - Posted: 03.03.2020

By Kelly Servick The dark side of opioids’ ability to deaden pain is the risk that they might kill their user. The same brain receptors that blunt pain when drugs such as morphine or oxycodone bind to them can also signal breathing to slow down. It’s this respiratory suppression that causes most overdose deaths. So scientists have hoped to design opioids that are “biased” toward activating painkilling signals while leaving respiratory signaling alone. Several companies have cropped up to develop and test biased opioids. But two new studies in mice contest a key hypothesis underlying these efforts—that a signaling protein called beta-arrestin2 is fundamental to opioids’ effect on breathing. “It seems like the premise was wrong,” says Gaspard Montandon, a neuroscientist and respiratory physiologist at the University of Toronto. He and others doubt that the good and bad effects of opioids can be disentangled. Hopes first arose in the late 1990s and early 2000s, as neuroscientist Laura Bohn, biochemist Robert Lefkowitz, and colleagues at Duke University explored the cascades of signals triggered when a drug binds to muopioid receptors on a neuron. This binding changes the receptor’s structure and its interactions with two types of proteins inside the cell—signaling molecules known as G-proteins, and beta-arrestins, which, among other effects, inhibit G-protein signaling. It’s still not clear how the resulting signal cascades influence cells or brain circuits. But the researchers reported in 1999 that mice engineered to lack the gene for beta-arrestin2 got stronger and longer lasting pain relief from morphine. And in 2005, Bohn and her colleagues at Ohio State University found that two morphine-induced side effects, constipation and slowed breathing, were dramatically reduced in these “knockout” mice. The findings suggested that a drug able to nudge the mu-opioid receptors toward G-protein signaling and away from beta-arrestin2 signaling would prompt more pain relief with fewer risks. © 2020 American Association for the Advancement of Science

Keyword: Pain & Touch; Drug Abuse
Link ID: 27083 - Posted: 02.28.2020

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,, 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.

Keyword: Drug Abuse
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

Keyword: Drug Abuse
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.

Keyword: Drug Abuse; Neuroimmunology
Link ID: 27033 - Posted: 02.11.2020

By Perri Klass, M.D. Whenever I write about attention deficit hyperactivity disorder — whether I’m writing generally about the struggles facing these children and their families or dealing more specifically with medications — I know that some readers will write in to say that A.D.H.D. is not a real disorder. They say that the rising numbers of children taking stimulant medication to treat attentional problems are all victims, sometimes of modern society and its unfair expectations, sometimes of doctors, and most often of the rapacious pharmaceutical industry. I do believe that A.D.H.D. is a valid diagnosis, though a diagnosis that has to be made with care, and I believe that some children struggle with it mightily. Although medication should be neither the first nor the only treatment used, some children find that the stimulants significantly change their educational experiences, and their lives, for the better. Dr. Mark Bertin, a developmental pediatrician in Pleasantville, N.Y., who is the author of “Mindful Parenting for A.D.H.D.,” said, “On a practical level, we know that correctly diagnosed A.D.H.D. is real, and we know that when they’re used properly, medications can be both safe and effective.” The choice to use medications can be a difficult one for families, he said, and is made even more difficult by “the public perception that they’re not safe, or that they fundamentally change kids.” He worries, he says, that marketing is really effective, and wants to keep it “at arm’s length,” far away from his own clinical decisions, not allowing drug reps in the office, not accepting gifts — but acknowledging, all the same, that it’s probably not possible to avoid the effects of marketing entirely. Still, he said, when it comes to stimulants, “the idea that we’re only using them because of the pharmaceutical industry is totally off base,” and can make it much harder to talk with parents about the potential benefits — and the potential problems — of treating a particular child with a particular medication. “When it comes to A.D.H.D. in particular, it’s a hard enough thing for families to be dealing with without all the fear and judgment added on.” © 2020 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 27030 - Posted: 02.10.2020

A fast acting ketamine-like anti-depressant spray that can lift mood within hours has been rejected by the NHS healthcare watchdog. The National Institute for Health and Care and Excellence (NICE) says there are too many uncertainties about the correlation between the price and clinical benefits of esketamine. It is licensed as a therapy for people with hard-to-treat depression. But it costs about £10,000 per patient for a single course of treatment. Mixed reactions Some people already prescribed it - as part of a trial, for example - will be able to continue on the treatment if their doctor says it is appropriate to do so, the NICE's draft recommendation for England and Wales says. Scotland is yet to issue guidance. Experts have expressed mixed reactions to NICE's decision. Dr Sameer Jauhar, at the Institute of Psychiatry, Psychology and Neuroscience, King's College London, said NICE had made the call because there was not yet enough long-term evidence to support the use of nasal esketamine alongside another anti-depressant. Consultant psychiatrist Dr Paul Keedwell, at Cardiff University, said patients would be disappointed by a decision based largely on cost rather than lack of effectiveness. Marjorie Wallace, chief executive of mental health charity Sane, said: "People with depression are currently relying on medications that are 30 years old. "Although these drugs can be life-saving for some people, they can have unpleasant side-effects and do not work for everyone. "It is therefore deeply disappointing that the first new compound that works in a fundamentally different way on the brain should not have passed this hurdle. "This is especially so because people can take as much as six to eight weeks to feel the full effects of most anti-depressants. "We hope this setback will serve only to inspire pharmaceutical companies, researchers and others to discover new ways of treating serious depression." Recreational misuse Ketamine is used in medicine to numb the body or induce sleep and sometimes prescribed for depression. © 2020 BBC.

Keyword: Depression; Drug Abuse
Link ID: 27004 - Posted: 01.29.2020

By Laura Sanders After taking a compound found in magic mushrooms, people with cancer had less anxiety and depression, even years later, a new study suggests. The evidence isn’t strong enough yet to pin these lasting improvements on the hallucinatory episode itself, as opposed to other life changes. But the findings leave open the possibility that the compound, called psilocybin, may be able to profoundly reshape how people handle distress and fear (SN: 9/26/06). Research published in 2016 suggested that a dose of psilocybin in combination with therapy could quickly ease anxiety and depression in people with cancer. But scientists wanted to know whether these effects lasted. Surveys conducted about three and 4½ years after the psilocybin dose showed that a majority of the 15 people still had fewer signs of anxiety and depression compared with before they took the compound, the team reports January 28 in the Journal of Psychopharmacology. (By the second follow-up, about a third of the participants still had active cancer; the rest were in partial or complete remission.) All the participants said they had “moderate,” “strong” or “extreme” positive changes in their behavior that they attribute to their experience, which many described as one of the most personally meaningful events of their lives. © Society for Science & the Public 2000–2020

Keyword: Depression; Drug Abuse
Link ID: 27003 - Posted: 01.29.2020

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

Keyword: Drug Abuse
Link ID: 26981 - Posted: 01.23.2020