Chapter 4. The Chemistry of Behavior: Neurotransmitters and Neuropharmacology

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By Maria Cramer Quarantinis. Zoom happy hours. Easy front-door liquor delivery. The boredom of staying home and the intense anxiety produced by the pandemic have given rise to Twitter jokes about drinking before noon as alcohol sales have spiked. But addiction experts say they are worried it could also trigger more serious drinking problems and even create new ones for people who have never struggled with alcohol dependency before. “I expect we’re going to see pretty significant increases in what I call unhealthy alcohol use, which means drinking above recommended limits,” said Dr. Sarah Wakeman, an addiction medicine doctor at Massachusetts General Hospital in Boston. “It will be pretty unlikely for someone who has never tried alcohol before to start drinking for the first time and immediately develop an alcohol use disorder,” Dr. Wakeman said. “I would see this as a risk more in people who are already drinking and then their alcohol use escalates.” Before the pandemic, Mhairi McFarlane, a 44-year-old novelist in Nottingham, England, had been thinking of cutting back. But the first weekend she was in quarantine, she said, she was “cheerfully” having three or four drinks a night, usually gin and tonics or “very cold bottles of cava.” “It was very much not my style of drinking,” she said. “I’ve always associated drink with going out and being social. I was never really one for opening a bottle of wine in front of the television.” Drinking alone worried her. Then she woke up one Thursday with a headache and a sense that her body was unhappy with what she was doing. She decided to give herself a two-night break from drinking. To her surprise, she wanted to keep going. It has been two months since she had a drink. © 2020 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 27265 - Posted: 05.28.2020

By Rachel Nuwer Humans are not the only animals that get drunk. Birds that gorge on fermented berries and sap are known to fall out of trees and crash into windows. Elk that overdo it with rotting apples get stuck in trees. Moose wasted on overripe crab apples get tangled in swing sets, hammocks and even Christmas lights. Elephants, though, are the animal kingdom’s most well-known boozers. One scientific paper describes elephant trainers rewarding animals with beer and other alcoholic beverages, with one elephant in the 18th century said to have drunk 30 bottles of port a day. In 1974, a herd of 150 elephants in West Bengal, India, became intoxicated after breaking into a brewery, then went on a rampage that destroyed buildings and killed five people. Despite these widespread reports, scientists have questioned whether animals — especially large ones such as elephants and elk — actually become inebriated. In 2006, researchers calculated that based on the amount of alcohol it takes to get a human drunk, a 6,600-pound elephant on a bender would have to quickly consume up to 27 liters of seven percent ethanol, the key ingredient in alcohol. Such a quantity of booze is unlikely to be obtained in the wild. Intoxicated wild elephants, the researchers concluded, must be a myth. As the lead author said at the time, “People just want to believe in drunken elephants.” If you are one who wanted to believe, a study published in April in Biology Letters might serve as your vindication. A team of scientists say that the earlier myth-busting researchers made a common mistake: They assumed that elephants would have to consume as much alcohol to get drunk as humans do. In fact, elephants are likely exceptional lightweights because they — and many other mammals — lack a key enzyme that quickly metabolizes ethanol. The findings highlight the need to consider species on an individual basis. © 2020 The New York Times Company

Keyword: Drug Abuse; Evolution
Link ID: 27261 - Posted: 05.21.2020

By Ellen Ruppel Shell My first day in Mexico City was tough. The smog was so thick that I gasped for breath while climbing the stairs to my hotel room. I had braced for headaches from the high altitude and thin air, but I was not prepared for how dirty that air was or for the bloodshot eyes and burning lungs. Declared the world's most polluted metropolis by the United Nations in 1992, greater Mexico City has worked hard to clean up its act. To some degree it has: the city is rightfully proud of its miles of bike paths and lush parks. Yet a casual glance at the smudged horizon shows that those efforts are not enough. Most days the area has levels of airborne sooty particles that greatly exceed standards set by the World Health Organization, as well as elevated amounts of other pollutants. Clogged with more than 9.6 million vehicles and an estimated 50,000 smokestacks, Mexico City stews in a toxic brew known to corrode human lungs and hearts. Now many scientists agree that this pollution also damages the brain. In 2018 a study found lesions known to be hallmarks of Alzheimer's disease in the brains of Mexico City residents in their 30s and 40s—decades before signs of the disease normally can be detected—and tied this damage to exposure to the city's bad air. The researchers who did that work, who are from institutions in Mexico and the U.S., have also found early forms of this frightening damage in infants and young children. And Mexico City is not the only place where bad air has been linked to Alzheimer's. Just a few years ago a team of Harvard scientists released data from a large study of 10 million Medicare recipients ages 65 and older living in 50 different cities in the northeastern U.S. The researchers reported a strong correlation between exposure to specific air pollutants and a number of neurodegenerative disorders, including Alzheimer's. © 2020 Scientific American

Keyword: Alzheimers; Neurotoxins
Link ID: 27247 - Posted: 05.14.2020

Amy Schleunes When Lilian Kloft stumbled across a 2015 study showing a connection between cannabis use and susceptibility to false memories, she found herself wondering about the legal implications of the results. The study had discovered that heavy users of cannabis were more likely than controls to form false memories—recollections of events that never occurred, for example, or warped memories of events that did—even when they were not at the moment “high.” This kind of false remembering can pose difficulties for people gathering reliable testimony in the event of a crime, says Kloft, a PhD student in psychopharmacology and forensic psychology at Maastricht University in the Netherlands. Consequently, the growing acceptance of cannabis worldwide raises questions not only about how the drug affects memory, but also about how law enforcement officials should conduct interviews with suspects, victims, and witnesses who may be under the influence or regular users of the drug. In order to further investigate the connection between cannabis and false memory formation, Kloft and collaborators recruited 64 volunteers for a series of experiments. Participants, who were occasional cannabis users, were given a vaporizer containing either cannabis or a hemp placebo and then told to inhale deeply and hold their breath for 10 seconds. After that, the researchers tested them in three different tasks designed to induce false memories. © 1986–2020 The Scientist.

Keyword: Drug Abuse; Learning & Memory
Link ID: 27244 - Posted: 05.12.2020

By Godfrey Pearlson Around the world, about 188 million people use marijuana every year. The drug has been legalized for recreational use in 11 U.S. states, and it may eventually become legal at the federal level. In a Gallup survey conducted last summer, 12 percent of American adults reported that they smoked marijuana, including 22 percent of 18- to 29-year-olds. Those are the stats. The consequences remain a mystery. As access to marijuana increases—and while acceptance of the drug grows and perception of its harmfulness diminishes—it is important to consider the potential for long-term ill effects, especially in users who start young. One of marijuana’s best-documented consequences is short-lived interference with memory. The substance makes it harder to get information into memory and, subsequently, to access it, with larger doses causing progressively more problems. Much less documented, however, is whether the drug has lasting effects on cognitive abilities. Finding the answer to that question is essential. Depending on the severity of any such effects and their persistence, marijuana use could have significant downstream impacts on education, employment, job performance and income. There are plausible reasons why the teenage brain may be especially vulnerable to the effects of marijuana use. Natural cannabinoids play an essential role in brain cell migration and development from fetal life onward. And adolescence is a crucial age for finalizing brain sculpting and white matter proliferation. The hippocampi, paired structures in the temporal lobe that are crucial in the formation of new memories, are studded with cannabinoid receptors. THC, the main ingredient behind marijuana’s “high,” acts on the brain’s cannabinoid receptors to mimic some of the effects of the body’s endogenous cannabinoids, such as anandamide. The compound’s effects are more persistent and nonphysiological, however. It may be throwing important natural processes out of balance. © 2020 Scientific American,

Keyword: Drug Abuse; Learning & Memory
Link ID: 27237 - Posted: 05.08.2020

By Amanda Heidt Koalas begging firefighters for water have become emblematic of Australia’s recent wildfire woes. But aside from these unusual interactions, scientists have never been quite sure how koalas drink. Now, a new study has documented the first evidence of the clever way they stay hydrated: by licking water from the smooth bark of gum trees as it rains. Past research has suggested that because koalas spend the vast majority of their time in trees, they likely get most of their water from the eucalyptus leaves they eat. But over the course of 13 years—from 2006 to 2019—citizen scientists, ecologists, and land owners reported 46 sightings of tree-licking behavior (above) in wild koalas. Researchers reviewed video and photographic evidence, and they found that even when puddles or lakes were nearby, koalas were more likely to drink the water running down trees, they report this month in Ethology. Koalas face a number of threats, and dwindling access to water is high on the list. Australia is now experiencing its driest period on record, with higher average temperatures and fewer days of rain. If tree licking provides a significant proportion of koalas’ water needs, researchers hope their results can identify areas where water should be supplemented as the rain dries up. © 2020 American Association for the Advancement of Science.

Keyword: Drug Abuse; Evolution
Link ID: 27233 - Posted: 05.06.2020

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

Keyword: Drug Abuse; Evolution
Link ID: 27230 - Posted: 05.05.2020

Ruth Williams Scientists have created a light-responsive opsin so sensitive that even when engineered into cells deep within tissue it can respond to an external light stimulus, according to a report in Neuron yesterday (April 30). Experiments in mice and macaques showed that shining blue light on the surface of the skull or brain was sufficient to activate opsin-expressing neurons six millimeters deep. “I was pretty blown away that this was even possible,” says Gregory Corder, who studies the neurological basis of pain and addiction at the University of Pennsylvania and who was not involved with the work. At that sort of depth, he continues, “essentially no part of the rodent brain is off-limits now for doing this non-invasive [technique]. . . . It’s pretty impressive.” “This development will help to extend the use of optogenetics in non-human primate models, and bring the techniques closer to clinical application in humans,” adds neurological disease expert Adriana Galvan of Yerkes National Primate Research Center in an email to The Scientist. Galvan was not a member of the research team. Optogenetics is a technique whereby excitable cells, such as neurons, can be controlled at will by light. To do this, cells are genetically engineered to produce ion channels called opsins that sit in the cells’ membranes and open in response to a certain wavelength of light. Switching on the light, then, floods the cells with ions, causing them to fire. Because light doesn’t penetrate tissue easily, to activate opsin-producing neurons deep in the brain of a living animal, researchers insert fiber optic cables. This is “highly invasive,” says Galvan, explaining that “the brain tissue can be damaged.” © 1986–2020 The Scientist.

Keyword: Brain imaging
Link ID: 27226 - Posted: 05.02.2020

By Austin Frakt OxyContin, and the aggressive, misleading way that Purdue Pharma marketed it, might have been even more damaging than was previously understood. Recent research shows how the company focused its marketing in states with lighter prescription regulation — to devastating effect. Also, a new version of OxyContin introduced a decade ago — which was meant to reduce harm — had unintended consequences. Besides contributing to heroin overdoses, it led to hepatitis C and other infections. Careful studies are only now starting to reveal the extent of the damage. OxyContin is an opioid painkiller that Purdue Pharma first brought to the U.S. market in 1996. Its chief innovation was its 12-hour timed release of oxycodone. This made it ripe for abuse, since by crushing or dissolving OxyContin pills, abusers of the drug could ingest the entire dose at once. Several studies have pointed to Purdue’s aggressive marketing of OxyContin as a significant contributor to the opioid epidemic. The marketing took various forms, including calling and visiting doctors; paying them for meals and travel; providing gifts; and funding pain treatment groups that urged liberalization of opioid prescribing. Some of the company’s marketing messages minimized the potential for OxyContin to lead to addiction, for which it paid over $600 million in fines in 2007. A National Bureau of Economic Research working paper published last fall sheds light on Purdue’s role. The researchers, economists from the University of Pennsylvania, the University of Notre Dame and the RAND Corporation, looked at variations in prescribing regulations that led Purdue to market OxyContin more aggressively in some states than in others. © 2020 The New York Times Company

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