Jon Hamilton Root extracts from the African shrub iboga have long been used in traditional healing rituals and more recently as an experimental treatment for depression and to reduce drug cravings in addiction. Scientists now are working on a version of the extract that doesn't cause heart attacks or hallucinations as side effects. Steeve Jordan/AFP via Getty Images A chemically tweaked version of the psychedelic drug ibogaine appears to relieve depression and addiction symptoms without producing hallucinations or other dangerous side effects. The results of a study in rodents suggest it may be possible to make psychedelic drugs safe enough to become mainstream treatments for psychiatric disorders, the authors report Wednesday in the journal Nature. "What we need is a medicine that is so safe that you can take it home and put it in your medicine cabinet just like you would aspirin," says David Olson, the paper's senior author and an assistant professor at the University of California, Davis. "And that's really what we were trying to achieve." The success with ibogaine is "a promising first step," says Gabriela Manzano, a postdoctoral fellow at Weill Cornell Medicine in New York and a co-author of a commentary on the study. "This provides a road map on how we could start tweaking these chemical compounds to make them very useful in the clinic," she says. "Keep the good parts, get rid of the bad parts." For decades, psychedelic drugs, including ketamine and psilocybin, have shown promise in treating people with mental health problems including addiction, depression and post-traumatic stress disorder. But doctors and researchers have been wary of using the drugs because of their side effects. © 2020 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 0: ; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27621 - Posted: 12.12.2020

By Abby Goodnough PHILADELPHIA — Steven Kelty had been addicted to crack cocaine for 32 years when he tried a different kind of treatment last year, one so basic in concept that he was skeptical. He would come to a clinic twice a week to provide a urine sample, and if it was free of drugs, he would get to draw a slip of paper out of a fishbowl. Half contained encouraging messages — typically, “Good job!” — but the other half were vouchers for prizes worth between $1 and $100. “I’ve been to a lot of rehabs, and there were no incentives except for the idea of being clean after you finished,” said Mr. Kelty, 61, of Winfield, Pa. “Some of us need something to motivate us — even if it’s a small thing — to live a better life.” The treatment is called contingency management, because the rewards are contingent on staying abstinent. A number of clinical trials have found it highly effective in getting people addicted to stimulants like cocaine and methamphetamine to stay in treatment and to stop using the drugs. But outside the research arena and the Department of Veterans Affairs, where Mr. Kelty is a patient, it is nearly impossible to find programs that offer such treatment — even as overdose deaths involving meth, in particular, have soared. There were more than 16,500 such deaths last year, according to preliminary data, more than twice as many as in 2016. Early data suggests that overdoses have increased even more during the coronavirus pandemic, which has forced most treatment programs to move online. Researchers say that one of the biggest obstacles to contingency management is a moral objection to the idea of rewarding someone for staying off drugs. That is one reason publicly funded programs like Medicaid, which provides health coverage for the poor, do not cover the treatment. Some treatment providers are also wary of giving prizes that they say patients could sell or trade for drugs. Greg Delaney, a pastor and the outreach coordinator at Woodhaven, a residential treatment center in Ohio, said, “Until you’re at the point where you can say, ‘I can make a good decision with this $50,’ it’s counterproductive.” © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 0: ; Chapter 13: Memory and Learning
Link ID: 27556 - Posted: 10.28.2020

R. Douglas Fields As I opened my copy of Science at home one night, an unfamiliar word in the title of a new study caught my eye: dopaminylation. The term refers to the brain chemical dopamine’s ability, in addition to transmitting signals across synapses, to enter a cell’s nucleus and control specific genes. As I read the paper, I realized that it completely upends our understanding of genetics and drug addiction. The intense craving for addictive drugs like alcohol and cocaine may be caused by dopamine controlling genes that alter the brain circuitry underlying addiction. Intriguingly, the results also suggest an answer to why drugs that treat major depression must typically be taken for weeks before they’re effective. I was shocked by the dramatic discovery, but to really understand it, I first had to unlearn some things. “Half of what you learned in college is wrong,” my biology professor, David Lange, once said. “Problem is, we don’t know which half.” How right he was. I was taught to scoff at Jean-Baptiste Lamarck and his theory that traits acquired through life experience could be passed on to the next generation. The silly traditional example is the mama giraffe stretching her neck to reach food high in trees, resulting in baby giraffes with extra-long necks. Then biologists discovered we really can inherit traits our parents acquired in life, without any change to the DNA sequence of our genes. It’s all thanks to a process called epigenetics — a form of gene expression that can be inherited but isn’t actually part of the genetic code. This is where it turns out that brain chemicals like dopamine play a role. All genetic information is encoded in the DNA sequence of our genes, and traits are passed on in the random swapping of genes between egg and sperm that sparks a new life. Genetic information and instructions are coded in a sequence of four different molecules (nucleotides abbreviated A, T, G and C) on the long double-helix strand of DNA. The linear code is quite lengthy (about 6 feet long per human cell), so it’s stored neatly wound around protein bobbins, similar to how magnetic tape is wound around spools in cassette tapes. All Rights Reserved © 2020

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 0: ; Chapter 4: Development of the Brain
Link ID: 27555 - Posted: 10.28.2020

By Jane E. Brody Do you have the heart to safely smoke pot? Maybe not, a growing body of medical reports suggests. Currently, increased smoking of marijuana in public, even in cities like New York where recreational use remains illegal (though no longer prosecuted), has reinforced a popular belief that this practice is safe, even health-promoting. “Many people think that they have a free pass to smoke marijuana,” Dr. Salomeh Keyhani, professor of medicine at the University of California, San Francisco, told me. “I even heard a suggestion on public radio that tobacco companies should switch to marijuana because then they’d be selling life instead of selling death.” But if you already are a regular user of recreational marijuana or about to become one, it would be wise to consider medical evidence that contradicts this view, especially for people with underlying cardiovascular diseases. Well: Get the best of Well, with the latest on health, fitness and nutrition. Compared with tobacco, marijuana smoking causes a fivefold greater impairment of the blood’s oxygen-carrying capacity, Dr. Keyhani and colleagues reported. In a review of medical evidence, published in January in the Journal of the American College of Cardiology, researchers described a broad range of risks to the heart and blood vessels associated with the use of marijuana. The authors, led by Dr. Muthiah Vaduganathan, cardiologist at Brigham and Women’s Hospital in Boston, point out that “marijuana is becoming increasingly potent, and smoking marijuana carries many of the same cardiovascular health hazards as smoking tobacco.” Edible forms of marijuana have also been implicated as a possible cause of a heart attack, especially when high doses of the active ingredient THC are consumed. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 0:
Link ID: 27550 - Posted: 10.26.2020

By Eddie Jacobs How would you feel about a new therapy for your chronic pain, which—although far more effective than any available alternative—might also change your religious beliefs? Or a treatment for lymphoma that brings one in three patients into remission, but also made them more likely to vote for your least preferred political party? These seem like idle hypothetical questions about impossible side effects. After all, this is not how medicine works. But a new mental health treatment, set to be licensed next year, poses just this sort of problem. Psychotherapy assisted by psilocybin, the psychedelic compound in “magic mushrooms,” seems to be remarkably effective in treating a wide range of psychopathologies, but also causes a raft of unusual nonclinical changes not seen elsewhere in medicine. Although its precise therapeutic mechanisms remain unclear, clinically relevant doses of psilocybin can induce powerful mystical experiences more commonly associated with extended periods of fasting, prayer or meditation. Arguably, then, it is unsurprising that it can generate long-lasting changes in patients: studies report increased prosociality and aesthetic appreciation, plus robust shifts in personality, values and attitudes to life, even leading some atheists to find God. What’s more, these experiences appear to be a feature, rather than a bug, of psilocybin-assisted psychotherapy, with the intensity of the mystical experience correlating with the extent of clinical benefit. © 2020 Scientific American,

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 0: ; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27521 - Posted: 10.12.2020

By Linda Searing U.S. deaths from overdoses of cocaine, a powerfully addictive stimulant, numbered 14,666 in 2018, the most recent year tallied, according to a new report from the Centers for Disease Control and Prevention. The rate of overdose deaths remained stable from 2009 through 2013, the report found, but then headed upward at about 27 percent each year from 2013 through 2018. That rate increase represents about 2½ times more cocaine-related deaths in 2018 than in 2014. Although the report does not address potential causes of the increase in cocaine overdose deaths, the Drug Enforcement Administration has said increased availability of the drug, “in large part due to record levels of coca cultivation and cocaine production in Colombia,” has led to increased usage in the United States. The CDC report says that the rate of overdose deaths from cocaine was higher among men than women and more common among middle-aged people (35 to 44 years old), those living in urban rather than rural areas, and people residing in the Northeast region. In addition, the rate of overdose deaths attributed to cocaine laced with a synthetic opioid such as fentanyl increased faster in recent years than did overdose deaths from purely cocaine. Cocaine overdoses can cause breathing problems, high blood pressure, hallucinations and extreme agitation, as well as seizures, heart attacks and strokes.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 0:
Link ID: 27520 - Posted: 10.12.2020

Ken Solt & Oluwaseun Akeju The state of dissociation is commonly described as feeling detached from reality or having an ‘out of body’ experience. This altered state of consciousness is often reported by people who have psychiatric disorders arising from devastating trauma or abuse. It is also evoked by a class of anaesthetic drug, and can occur in epilepsy. The neurological basis of dissociation has been a mystery, but writing in Nature, Vesuna et al.1 describe a localized brain rhythm that underlies this state. Their findings will have far-reaching implications for neuroscience. The authors first recorded brain-wide neuronal activity in mice using a technique called widefield calcium imaging. They studied changes in these brain rhythms in response to a range of drugs that have sedative, anaesthetic or hallucinogenic properties, including three that induce dissociation — ketamine, phencyclidine (PCP) and dizocilpine (MK801). Only the dissociative drugs produced robust oscillations in neuronal activity in a brain region called the retrosplenial cortex. This region is essential for various cognitive functions, including episodic memory and navigation2. The oscillations occurred at a low frequency, of about 1–3 hertz. By contrast, non-dissociative drugs such as the anaesthetic propofol and the hallucinogen lysergic acid diethylamide (LSD) did not trigger this rhythmic retrosplenial activity. Vesuna et al. examined the active cells in more detail using a high-resolution approach called two-photon imaging. This analysis revealed that the oscillations were restricted to cells in layer 5 of the retrosplenial cortex. The authors then recorded neuronal activity across multiple brain regions. Normally, other parts of the cortex and subcortex are functionally connected to neuronal activity in the retrosplenial cortex; however, ketamine caused a disconnect, such that many of these brain regions no longer communicated with the retrosplenial cortex. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 0: ; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27481 - Posted: 09.19.2020

Jon Hamilton Scientists used light to control the firing of specific cells to artificially create a rhythm in the brain that acted like the drug ketamine enjoynz/Getty Images Out-of-body experiences are all about rhythm, a team reported Wednesday in the journal Nature. In mice and one person, scientists were able to reproduce the altered state often associated with ketamine by inducing certain brain cells to fire together in a slow, rhythmic fashion. "There was a rhythm that appeared, and it was an oscillation that appeared only when the patient was dissociating," says Dr. Karl Deisseroth, a psychiatrist and neuroscientist at Stanford University. Dissociation is a brain state in which a person feels separated from their own thoughts, feelings and body. It is common in people who have some mental illnesses or who have experienced a traumatic event. It can also be induced by certain drugs, including ketamine and PCP (angel dust). The study linking dissociation to brain rhythms represents "a big leap forward in understanding how these drugs produce this unique state," says Dr. Ken Solt, an anesthesiologist at Harvard Medical School and Massachusetts General Hospital. Solt is the co-author of an article that accompanied the study but was not involved in the research. The finding also could be a step toward finding non-drug methods to control states of consciousness, Solt says. Deisseroth's lab made the discovery while studying the brains of mice that had been given ketamine or other drugs that cause dissociation. The team was using technology that allowed them to monitor the activity of cells throughout the brain. © 2020 npr

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 0: ; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27480 - Posted: 09.19.2020

By Nicholas Bakalar The incidence of hip fracture has decreased steadily over the past 40 years, but a new analysis suggests that new osteoporosis drugs have made only a small contribution to the trend. The report, published in JAMA Internal Medicine, included 10,552 men and women and their offspring followed since 1970. Every five years through 2010, the researchers recorded the number of hip fractures in people over 60. They found that the incidence of hip fractures decreased by 67 percent over those years, and rates were lower in people born later. The bone-strengthening bisphosphonates, like Fosamax (introduced in 1995) and Boniva (introduced in 2003), cut the fracture incidence by about 4.8 percent, the researchers estimate. But smoking decreased to 15 percent of participants in 2010, from 38 percent in 1970, and heavy drinking declined to 4.5 percent, from 7 percent. Both are significant risk factors for fracture. Other risk factors, like being underweight and early menopause, were stable over the years. “Smoking cessation accounts for about 90 percent of the decline in the age-adjusted decrease,” said the lead author, Dr. Timothy Bhattacharyya, an orthopedic surgeon with the National Institutes of Health. Other factors that may have played a role included estrogens, which were approved for osteoporosis treatment in 1988, and bone mineral density testing, which first became available in the 1990s. But “we didn’t observe any effect from estrogens or bone mineral density testing,” Dr. Bhattacharyya said. © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27406 - Posted: 08.08.2020

Craig W. Stevens Even as the COVID-19 pandemic cripples the economy and kills hundreds of people each day, there is another epidemic that continues to kill tens of thousands of people each year through opioid drug overdose. Opioid analgesic drugs, like morphine and oxycodone, are the classic double-edged swords. They are the very best drugs to stop severe pain but also the class of drugs most likely to kill the person taking them. In a recent journal article, I outlined how a combination of state-of-the-art molecular techniques, such as CRISPR gene editing and brain microinjection methods, could be used to blunt one edge of the sword and make opioid drugs safer. I am a pharmacologist interested in the way opioid drugs such as morphine and fentanyl can blunt pain. I became fascinated in biology at the time when endorphins – natural opioids made by our bodies – were discovered. I have been intrigued by the way opioid drugs work and their targets in the brain, the opioid receptors, for the last 30 years. In my paper, I propose a way to prevent opioid overdoses by modifying an opioid user’s brain cells using advanced technology. Opioid receptors stop breathing Opioids kill by stopping a person from breathing (respiratory depression). They do so by acting on a specific set of respiratory nerves, or neurons, found in the lower part of the brain that contain opioid receptors. Opioid receptors are proteins that bind morphine, heroin and other opioid drugs. The binding of an opioid to its receptor triggers a reaction in neurons that reduces their activity. Opioid receptors on pain neurons mediate the pain-killing, or analgesic, effects of opioids. When opioids bind to opioid receptors on respiratory neurons, they slow breathing or, in the case of an opioid overdose, stop it entirely. © 2010–2020, The Conversation US, Inc.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27401 - Posted: 08.06.2020

By Aimee Cunningham Heavy drinking is robbing Americans of decades of life. From 2011 to 2015, an average of 93,296 deaths annually could be tied to excessive alcohol use, or 255 deaths per day. Excessive drinking brought death early, typically 29 years sooner than would have been expected. All told, the United States saw 2.7 million years of potential life lost each year, researchers report in the July 31 Mortality and Morbidity Weekly Report. The researchers used a program developed by the U.S. Centers for Disease Control and Prevention that estimates annual deaths and years of potential life lost due to an individual’s own or another’s excessive drinking. The tool takes into account whether the cause of death is fully attributable to alcohol, such as alcoholic liver cirrhosis, or whether excessive drinking can partially contribute to a condition, such as breast cancer. Annually, about 51,000 of the deaths were from chronic conditions. The rest were sudden demises such as poisonings that involved another substance along with alcohol or alcohol-related car crashes. The CDC defines excessive alcohol use as binging — drinking five or more drinks at a time for men, four or more for women — or drinking heavily over the course of the week. Men qualify at 15 or more drinks per week; for women, it’s eight or more. The numbers of deaths and years of life extinguished due to excessive drinking have gone up since the last report. That assessment covered 2006 to 2010 and reported close to 88,000 deaths and 2.5 million lost years annually. Recommendations from the Community Preventive Services Task Force, made up of public health and prevention experts, to stem excessive drinking include raising taxes on alcohol and regulating the number of places that sell alcoholic beverages (SN: 8/9/17). © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27398 - Posted: 08.03.2020

Justin Rowlatt Chief environment correspondent If you have ever doubted whether solar power can be a transformative technology, read on. This is a story about how it has proved its worth in the toughest environment possible. The market I'm talking about is perhaps the purest example of capitalism on the planet. There are no subsidies here. Nobody is thinking about climate change - or any other ethical consideration, for that matter. This is about small-scale entrepreneurs trying to make a profit. It is the story of how Afghan opium growers have switched to solar power, and significantly increased the world supply of heroin. I was in a military helicopter thundering over the lush poppy fields of the Helmand valley in Afghanistan when I spotted the first solar panel. You've heard of Helmand. It is the most dangerous province in Afghanistan. Of the 454 British soldiers who died in the recent conflict in Afghanistan, all but five lost their lives in Helmand. The province is also at the heart of by far the most productive opium growing region on the planet. Most opium will be refined into heroin, one of the most addictive drugs there is. According to the UN body responsible for tracking and tackling illegal drug production, the UNODC, almost 80% of all Afghan opium now comes from the south-west of the country, including Helmand. That means pretty much two-thirds of global supply. So, not the kind of place you would expect to be at the forefront of efforts to decarbonise the economy. But, once I had seen that first solar panel, I saw more. In fact there seemed to be a small array of solar panels in the corner of most farm compounds, and that was back in 2016. It is only now that the scale of the revolution in heroin production I was unwittingly witnessing has been quantified. Because I wasn't the only person to notice that Afghan farmers were taking an interest in low-carbon technologies. © 2020 BBC.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27386 - Posted: 07.27.2020

By Rachel Nuwer In the years leading up to the roaring 2020s, young people were once again dropping acid. Onetime Harvard psychologist Timothy Leary died almost 25 years ago, after which some of his ashes were launched into space. But from 2015 to 2018, the rate of “turning on and tuning in” with LSD, to paraphrase Leary, increased by more than 50 percent in the U.S.—a rise perhaps fueled by a need for chemical escapism. Those results were published in the July issue of Drug and Alcohol Dependence. The authors of the study suspect that many users may be self-medicating with the illegal substance to find relief from depression, anxiety and general stress over the state of the world. “LSD is used primarily to escape. And given that the world’s on fire, people might be using it as a therapeutic mechanism,” says Andrew Yockey, a doctoral candidate in health education at the University of Cincinnati and lead author of the paper. “Now that COVID’s hit, I’d guess that use has probably tripled.” To arrive at their findings, Yockey and his colleagues turned to data collected from more than 168,000 American adults by the National Survey on Drug Use and Health, an annual, nationally representative questionnaire. They analyzed trends since 2015, partly because of the timing of the 2016 presidential election. The researchers found that past-year LSD use increased by 56 percent over three years. The rise was especially pronounced in certain user groups, including people with college degrees (who saw a 70 percent increase) and people aged 26 to 34 (59 percent), 35 to 49 (223 percent) and 50 or older (45 percent). Younger people aged 18 to 25, on the other hand, decreased their use by 24 percent. © 2020 Scientific American

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27356 - Posted: 07.11.2020

By Nicholas Bakalar Moderate alcohol consumption may lead to slower mental decline in middle-age and older people, a new study found. Some previous studies have suggested that moderate drinking has beneficial cognitive effects; others have found it harmful. In the new study, published in JAMA Network Open, researchers tracked the cognitive abilities of almost 20,000 people for an average of more than nine years. The scientists tested the participants in three domains: mental status, word recall and vocabulary. In all three areas, compared with abstaining, low to moderate drinking (eight drinks a week or fewer for women, and 15 or fewer for men) was associated with a higher mental functioning trajectory and significantly slower decline over the years. Even former drinkers showed slower mental decline than people who never drank. The study adjusted for smoking, marital status, education, chronic disease and body mass index, but the authors acknowledged that it was an observational study so it could not prove cause and effect. They also noted it relied on self-reports of alcohol consumption, which can be unreliable. “Drinking should be limited to moderate levels,” said the lead author, Ruiyuan Zhang, a doctoral student at the University of Georgia. “Heavy drinking makes cognitive function worse.” © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27344 - Posted: 07.06.2020

An epidemic of fatal drug overdoses across Canada is on the rise amid COVID-19 pandemic restrictions that harm-reduction workers and doctors say exacerbates the toxic supply. Overdose prevention sites continue to run but physical distancing guidelines mean fewer people are able to use the services. For example, a site in Toronto that previously averaged more than 100 visits a day now sees fewer than half that. From March 2019 to May 2020, Ontario's coroner reported a 25 per cent increase in fatal overdoses, based on preliminary estimates for all substances. Nick Boyce, director of the Ontario Harm Reduction Network, said the increase is significant. "It matches anecdotally what I've been hearing from the front-line workers we work with around the province," Boyce said. "They're all saying deaths are going up. But to hear that number and to see that number, I was not expecting it to be that high." Last year, fentanyl directly contributed to about 75 per cent of opioid-related deaths in Ontario. More than 14,000 Canadians have been killed by opioids in the last four years, according to federal data. "Laws actually incentivize drug dealers and suppliers to come up with new and different drugs," Boyce said. "We learned this lesson in the 1920s with alcohol prohibition when people switched from drinking beer to toxic moonshine. We're seeing that with the opioid drug supply now." ©2020 CBC/Radio-Canada.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27296 - Posted: 06.10.2020

By Nicholas Bakalar Women who take benzodiazepines, such as Valium or Xanax, before becoming pregnant may be at increased risk for ectopic pregnancy, a new study found. An ectopic, or tubal, pregnancy is one in which a fertilized egg grows outside the uterus, often in a fallopian tube, and it is a life-threatening event. The egg must be removed with medication or surgery. Benzodiazepines, sold by prescription under several brand names, are widely prescribed for anxiety, sleep problems and seizures. The study, in Human Reproduction, used an insurance database of 1,691,366 pregnancies to track prescriptions for benzodiazepines in the 90 days before conception. Almost 18,000 of the of the women had used the drugs, and the scientists calculated that these women were 47 percent more likely to have a tubal pregnancy than those who did not. The study controlled for other risks for tubal pregnancy, including sexually transmitted infections, pelvic infection, use of an intrauterine device, smoking and fertility treatments. “Women planning a pregnancy who are using these drugs should talk to their care provider to see whether a change in treatment is possible, and then slowly change treatment before going off their contraceptive,” said the lead author, Elizabeth Wall-Wieler, a postdoctoral fellow at Stanford University. “Women for whom there is no alternative, or who have an unplanned pregnancy, should let their care provider know, and those pregnancies should be monitored carefully. The key to treating ectopic pregnancy is to treat it early.” © 2020 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 8: Hormones and Sex
Link ID: 27278 - Posted: 06.04.2020

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

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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27261 - Posted: 05.21.2020

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.

Related chapters from BN: Chapter 17: Learning and Memory; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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,

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory and Learning
Link ID: 27237 - Posted: 05.08.2020