Chapter 3. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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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

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

Keyword: Drug Abuse
Link ID: 26965 - Posted: 01.17.2020

By Brooke N. Dulka Glutamate, arguably the most important chemical in your nervous system, is older than the brain itself. From a single cell bacterium, to mushrooms and plants, to you—every living thing on this planet relies on this tiny molecule for cellular communication. It is absolutely critical for everything we do. “The function of most, if not all, of the trillions of cells in the brain are regulated by glutamate,” neuroscientist David Baker explains to me. On November 1, 2019, neuroscientists gathered at the Harley-Davidson Museum in Milwaukee, WI to share their science. The chrome-laden motorcycle in the corner of the room was hard to ignore, but it was the presentation of Baker, a professor at Marquette University, that really caught my attention. Baker has dedicated his career to understanding how glutamate can treat disorders of the brain. Specifically, his hopes for targeting glutamate lie in a mechanism called system xc-. Glutamate is often called the “major excitatory neurotransmitter” within the brain. It is the brain’s “go” signal. Baker notes that glutamate receptors are found in every kind of brain cell, which means it is doing more than regulating the activity of neurons, it is regulating the brain’s support cells too. Glutamate is that widespread and important! But being almost everywhere increases the chances that something, somewhere, could go wrong. Thus, most disorders of the brain involve some degree of glutamate dysfunction. This includes disorders such as schizophrenia, depression, obsessive-compulsive disorder, Alzheimer’s disease and more. While one might think that this awareness provides neuroscientists with critical insights into treating disorders of the brain, actually the opposite has occurred. In fact, most psychiatric drugs weren’t even discovered through systematic drug development, as one might expect. More often than not, the drugs we commonly use today were serendipitous findings or accidental discoveries. Baker notes that almost none of the most commonly prescribed drugs for psychiatric disorders target glutamate. Given the importance of glutamate to nearly every brain function, there is a genuine, and well-reasoned, concern among both neuroscientists and psychiatrists that glutamatergic therapeutics will produce widespread impairments in the brain. © 2020 Scientific American

Keyword: Schizophrenia
Link ID: 26957 - Posted: 01.14.2020

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

Keyword: Drug Abuse; Sexual Behavior
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

Keyword: Drug Abuse
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.

Keyword: Drug Abuse; Development of the Brain
Link ID: 26943 - Posted: 01.09.2020