By Sara Kiley Watson Humans started brewing alcohol for consumption thousands of years ago, and researchers have suggested that our ability to break down booze in our bodies has evolutionary roots dating back millions of years. Alcohol, known to scientists as ethanol, occurs naturally throughout nature, when microbes like bacteria and yeast break down sugars. This process of fermentation, harnessed by humans since ancient times, has given us the gifts of cheese, pickles, and wine, among other delights.* Nautilus Members enjoy an ad-free experience. Log in or Join now . But humans are far from the only creatures that imbibe—aye ayes, a species of lemur, will seek out nectar with a higher alcohol content, and spider monkey urine has been found to contain secondary metabolites of alcohol. Wild chimps, with whom humans share over 95 percent of our DNA, were caught on film snacking on fermenting fruit with their buddies earlier this year. Now, for the first time, researchers have discovered just how much alcohol some chimps are getting out of their fermented fruit snacks. In a new paper published in Science Advances, a team of scientists from the United States and the Ivory Coast reported that, in the course of a day, the wild chimps in their study consumed about 14 grams of pure ethanol. That’s about the equivalent, adjusting for body mass, of a human imbibing more than one standard drink a day, says University of California, Berkeley graduate student and study author Aleksey Maro. “We can say, pretty officially, that animals are chronically ingesting ethanol, especially our chimpanzee relatives,” Maro says. Maro and his colleagues made their discovery by following around wild chimps at two national parks in Africa—Kibale in Uganda and Taï in Ivory Coast—and scooping up test samples of 20 species of ripe fruits that the chimps typically like to eat. What they found is that these fruits have an average alcohol content of around 0.26 percent by weight. That might not sound like much, but primatologists at these locations estimate that chimps eat a whopping 10 pounds—or some 7 to 14 percent of their body weight—of fruit a day. The apes tended to prefer a fig called the Ficus mucuso at Kibale and the plum-esque fruit from Parinari excelsa trees at Taï. These treats were among the fruits with the highest alcohol content. © 2025 NautilusNext Inc.,

Keyword: Drug Abuse; Evolution
Link ID: 29937 - Posted: 09.20.2025

By Sofia Caetano Avritzer When Canada legalized cannabis in 2018, its effects on human health were all over the news. Cyntia Duval, a women’s health researcher at the University of Toronto at the time, wondered how its consumption might affect female fertility. To her surprise, there was almost no information on the subject — though there was plenty of data on marijuana’s effects on pregnancy and male fertility. Chemicals in cannabis may push eggs to become ready for fertilization. But this may come at a cost: more eggs with the wrong number of chromosomes, Duval and colleagues now report in a study published September 9 in Nature Communications. Delta-9-tetrahydrocannabinol, or THC, is the main psychoactive chemical in marijuana. It binds to cannabinoid receptors in the brain. But these receptors are all over our bodies, including in our reproductive organs. The receptors usually bind endocannabinoids, molecules naturally produced by the body and essential for normal bodily functions like the production of eggs and sperm. Consuming THC can affect cannabinoid receptors in the reproductive system. Many studies report that using cannabis decreases sperm count and motility. Men are usually told to avoid cannabis for at least three months before trying to conceive, Duval says. But what about women? © Society for Science & the Public 2000–2025.

Keyword: Drug Abuse; Sexual Behavior
Link ID: 29922 - Posted: 09.10.2025

Jon Hamilton A rigorous new study finds that a single dose of LSD can ease anxiety and depression for months. The study involved 198 adults with generalized anxiety disorder, or GAD, a disabling form of anxiety that affects about 1 in 10 people over the course of a year. Participants who got lower doses of LSD (25 or 50 micrograms) did no better than those who got a placebo. But people who received higher doses (100 or 200 micrograms) responded quickly, a team reports in the Journal of the American Medical Association. "By the next day, they were showing strong improvements," says Dr. David Feifel of Kadima Neuropsychiatry Institute in San Diego, one of the 22 centers that participated in the study. "And those improvements held out all the way to the end of the study, which was 12 weeks." But it's unclear whether some of the improvement was related to non-drug factors like the sensory environment in which people were treated, says Robin Carhart-Harris, a psychedelics researcher at the University of California, San Francisco who was not involved in the study. "The safety looks good, the tolerability looks good," he says, "but where is the depth of information about the way you delivered this product?" Carhart-Harris, like many scientists who study psychedelics, believes that successful treatment is more likely if a person has the right mindset when beginning a trip and if the trip occurs in a place with the right sensory environment. "It's characterized by continuous worry, inability to relax, and all the physical manifestations, racing heart rates and sweatiness," Feifel says. It's also frequently accompanied by depression. Current antidepressant and antianxiety drugs are inadequate for about half of people diagnosed with GAD. © 2025 npr

Keyword: Stress; Drug Abuse
Link ID: 29917 - Posted: 09.06.2025

By Danielle Ivory. Julie Tate and Megan Twohey Amy Enochs was texting with other parents, all wondering why their central Ohio elementary school had gone into lockdown, when the school called. Several fourth graders, including Ms. Enochs’s daughter, had eaten marijuana gummies and were being taken to the hospital with racing pulses, nausea and hallucinations. A classmate had found the gummies at home and mistaken them for Easter candy. Ms. Enochs recalled hyperventilating that spring day three years ago. “I was scared to death,” she said, her voice breaking. “It was shock and panic.” As legalization and commercialization of cannabis have spread across the United States, making marijuana edibles more readily available, the number of cannabis-related incidents reported to poison control centers has sharply increased: from about 930 cases in 2009 to more than 22,000 last year, data from America’s Poison Centers shows. Of those, more than 13,000 caused documented negative effects and were classified by the organization as nonlethal poisonings. These numbers are almost certainly an undercount, public health officials say, because hospitals are not required to report such cases. More than 75 percent of the poisonings last year involved children or teenagers. In most instances of cannabis exposure, the physical effects were not severe, according to the poison control data. But a growing number of poisonings have led to breathing problems or other life-threatening consequences. In 2009, just 10 such cases were reported to poison centers; last year, there were more than 620 — a vast majority of them children or teens. More than 100 required ventilators. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29884 - Posted: 08.13.2025

By Shoshana Walter In 2005, J. was a young pharmacist, in the middle of a divorce, when he decided he needed a change. He was outgoing, a former rugby player, and he had begun to feel out of place among his quiet co-workers. “Does a pharmacist ever come over to you and chitchat?” he says. “They’re very mousy and very introverted.” For his new job, J. — who asked to be referred to by his first initial to protect his privacy — had in mind something a little more glamorous: pharmaceutical sales. He found a contract position at Reckitt Benckiser Pharmaceuticals, a U.S. subsidiary of a household-goods company based in Britain that was best known for Lysol and French’s mustard. The company had recently introduced Suboxone, a groundbreaking new medication in the United States that treats opioid addiction. Much like nicotine gum, Suboxone worked as a substitute, binding to the same receptors in the brain as illicit opioids, taking away withdrawal symptoms, quelling cravings and making it hard to continue misusing drugs. At other companies — like Purdue Pharma, the maker of OxyContin — sales reps regularly trawled doctors’ offices and used company credit cards to treat physicians to expensive meals and lavish trips. At Reckitt, sales reps were told they had a different mandate. “You weren’t a credit card on legs,” says Chris Hassan, who oversaw Reckitt’s sales force at the time. Reps held the title “clinical liaisons,” and their job was not only to sell Suboxone but also to convince doctors that addiction was a disease, not a moral failing, and that it could be treated with medication instead of prison sentences. Reckitt hired people of all backgrounds — counselors and behavioral-health clinicians as well as traditional salespeople, including ones they recruited from Purdue Pharma. Those who had sold OxyContin, Hassan notes, seemed especially motivated to sell the solution to the problem they had helped cause. “The people that had mirrors in their home and had to look at themselves, they didn’t like what they saw,” he says. “Purdue was a great source of hires for us.” Almost right away, however, it became clear that most doctors were not lining up to care for addicted patients. Some were the same physicians who were driving the opioid crisis by overprescribing painkillers. Others felt ill equipped to treat substance users or dismissed such patients as untrustworthy. An addicted patient was “a liar or crook,” says George Agapios, an Indiana doctor who initially resisted offering treatment. He describes many physicians’ feelings in that era as: “The people associated with it were not exactly the cream of the crop — so let’s not waste our time.” Several doctors turned Reckitt reps away from their offices. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29880 - Posted: 08.09.2025

By Bridget Alex More than 10 million years ago, ancestral apes in Africa rummaged through leaf litter for tasty morsels: fallen, fermenting fruit. Tapping this resource may have given some apes a nutritional boost, an advantage that could have paved the way for the evolution of our own alcohol tolerance. A study out today in BioScience adds support to this so-called “drunken monkey” hypothesis by examining just how often living apes indulge in fallen—presumably boozy—fruits. The research also gives this behavior a much-needed name: “scrumping.” The work provides “a fresh and useful perspective on the importance of fallen fruit,” says Amanda Melin, a biological anthropologist at the University of Calgary who was not involved with the research. She adds that scrumping “is an efficient and evocative way to describe this behavior” that she will use in the future. The form of alcohol we imbibe, ethanol, occurs naturally when yeast grows in fruits, saps, or nectars. Many animals, from elephants to songbirds, can get buzzed off these wild taps. Meanwhile, most human societies have invented ways to ferment food and drink. Biomolecular traces on artifacts show that by at least 8000 years ago, people in the Caucasus region were brewing alcoholic beverages from grapes, while people in China were sipping on boozy drinks made from many ingredients, including millet, rice, ginger, and yam. These beverages’ arrival coincides roughly with the start of farming. In fact, some scholars think cereals may have been domesticated for beer rather than bread. The idea that our species’ ability to consume alcohol arose in our distant primate ancestors was formulated by evolutionary biologist Robert Dudley 25 years ago as he was studying monkeys—hence the name of the hypothesis—rather than the chimps and other apes analyzed in the new study. Rank, fermenting fruit is easy to sniff out, the idea goes, so being able to eat it would have given ancient apes an additional resource that other animals avoided.

Keyword: Drug Abuse; Evolution
Link ID: 29876 - Posted: 08.06.2025

By Diana Kwon A new sensor makes it possible for the first time to simultaneously track dopamine and up to two additional molecules in the brains of living animals. The sensor, dubbed HaloDA1.0, uses a novel dopamine-tagging system that emits light at the far-red end of the color spectrum, according to the team behind the work. “There’s a real need to monitor multiple relevant molecules, as they’re doing here,” says Nicolas Tritsch, assistant professor of neuroscience at McGill University, who was not involved in the study. Because dopamine is involved in a range of key brain functions, when studying its effects on a cell it’s important to consider other neuromodulators that are released at the same time, as well as the signaling cascades these molecules may trigger, Tritsch says. Most dopamine-tracking strategies genetically encode a naturally occurring fluorescent protein into dopamine receptors; when dopamine attaches to the modified receptors, the fluorescent protein changes shape and emits light. But naturally occurring fluorescent proteins have a limited color palette, which has made it difficult to develop sensors that can go beyond two-color imaging, says study investigator Yulong Li, professor of life sciences at Peking University. Instead of genetically encoding a fluorescent protein, HaloDA1.0 attaches a synthetic molecule called HaloTag to dopamine receptors. This tag binds tightly to previously developed artificial dyes that change shape and fluoresce in the far-red spectrum when dopamine binds to its receptors. Because the dyes fluoresce at the far end of the red spectrum, it leaves room for other sensors to glow at different wavelengths. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29868 - Posted: 07.26.2025

By Jan Hoffman Jamie Mains showed up for her checkup so high that there was no point in pretending otherwise. At least she wasn’t shooting fentanyl again; medication was suppressing those cravings. Now it was methamphetamine that manacled her, keeping her from eating, sleeping, thinking straight. Still, she could not stop injecting. “Give me something that’s going to help me with this,” she begged her doctor. “There is nothing,” the doctor replied. Overcoming meth addiction has become one of the biggest challenges of the national drug crisis. Fentanyl deaths have been dropping, in part because of medications that can reverse overdoses and curb the urge to use opioids. But no such prescriptions exist for meth, which works differently on the brain. In recent years, meth, a highly addictive stimulant, has been spreading aggressively across the country, rattling communities and increasingly involved in overdoses. Lacking a medical treatment, a growing number of clinics are trying a startlingly different strategy: To induce patients to stop using meth, they pay them. The approach has been around for decades, but most clinics were uneasy about adopting it because of its bluntly transactional nature. Patients typically come in twice a week for a urine drug screen. If they test negative, they are immediately handed a small reward: a modest store voucher, a prize or debit card cash. The longer they abstain from use, the greater the rewards, with a typical cumulative value of nearly $600. The programs, which usually last three to six months, operate on the principle of positive reinforcement, with incentives intended to encourage repetition of desired behavior — somewhat like a parent who permits a child to stay up late as a reward for good grades. Research shows that the approach, known in addiction treatment as “contingency management,” or CM, produces better outcomes for stimulant addiction than counseling or cognitive behavioral therapy. Follow-up studies of patients a year after they successfully completed programs show that about half remained stimulant-free. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29854 - Posted: 07.16.2025

By Ellen Barry Few practices in mental health are debated more than the long-term use of antidepressant medications, which are prescribed to roughly one in nine adults in the United States, according to data from the Centers for Disease Control and Prevention. A reassessment began in 2019, when two British researchers published a study that found that 56 percent of patients suffered from withdrawal symptoms when they stopped antidepressant medications and that 46 percent of those described their symptoms as severe. The findings made headlines in Britain and had a powerful ripple effect, forcing changes to psychiatric training and prescribing guidelines. And they fed a growing grass-roots movement calling to rein in the prescription of psychotropic drugs that has, in recent months, gained new influence in the United States with the rise of Robert F. Kennedy Jr. as health secretary. A new study, published on Wednesday in the journal JAMA Psychiatry, makes the case that these warnings were overblown. The authors of the new paper found that a week after quitting antidepressants, patients reported symptoms like dizziness, nausea and vertigo, but that they remained, on average, “below the threshold for clinically significant” withdrawal. Dr. Sameer Jauhar, one of the authors, said the new analysis should reassure both patients and prescribers. “The messaging that came out in 2019 was all antidepressants can cause this and this can happen in this proportion of people, and that just doesn’t survive any scientific scrutiny,” said Dr. Jauhar, a professor of psychiatry at Imperial College London. He criticized the earlier study for including data from online surveys as a quantitative measure, for failing to control for the placebo effect, and for failing to distinguish between various types of antidepressants. These methodologies, he said, led to inflated estimates of withdrawal. © 2025 The New York Times Company

Keyword: Depression
Link ID: 29850 - Posted: 07.12.2025

Sydney Lupkin Jerry Abrams, a 64-year-old marketing strategist in Minneapolis, used to run marathons. But two decades of degenerative spine disease have left him unable to run — and he's grieving. For Abrams, losing running felt like "the loss of a loved one – that friend who's been with you every day you needed him. "You know, having that taken away from you because of pain is the hardest thing of all," he says. The constant pain in his lower back makes running impossible. Sometimes, when the pain isn't under control, he can't get out of bed. Abrams has tried taking opioids. They help, but he feels he has to be careful because they're potentially addictive. He's also worried about building up a tolerance to them "I don't ever want to be in a situation where I need surgery and need to recover and opioid medication no longer does what it needs to do," he explains. The Food and Drug Administration approved a new non-opioid drug earlier this year called Journavx. It's a pill for severe acute pain that works by blocking plain signals from where someone hurts. It's offered hope for the 1 in 5 Americans who suffer from chronic pain, but it's also just out of reach. Journavx is the first new kind of painkiller in more than 20 years, and the medical community is cautiously optimistic that Journavx doesn't have the same addictive potential as opioids do. But the new pills are expensive, and not everyone has been able to access them, thanks to a narrowly-focused FDA approval and limited insurance coverage Abrams' doctor wanted him to be able to try Journavx. But the FDA only approved the medication for short-term use for acute pain, which is usually defined as lasting less than three months, such as right after surgery. Because Abrahm's pain is chronic, his insurance wouldn't cover it. A single Journavx pill costs around $15 without insurance, according to Vertex Pharmaceuticals, the drug's manufacturer. © 2025 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 29849 - Posted: 07.12.2025

By Andrew Jacobs and Jacey Fortin News reports detailing Elon Musk’s drug use have prompted renewed attention to ketamine, a powerful anesthetic that has become increasingly popular as a therapy for treatment-resistant depression and other mental health issues. Although Mr. Musk has acknowledged using ketamine in the past to treat depression, he has denied suggestions that he is currently using ketamine — or any other drug. “I am NOT taking drugs!” he wrote last week in a social media post following the publication of an article in The New York Times that described reports of his use of drugs on the campaign trail last year. Those drugs included ketamine and other psychedelic compounds, among them MDMA and psilocybin mushrooms. Mr. Musk left the White House last week. Since then, he and President Trump have traded barbs on social media over the president’s domestic policy bill and have mentioned government contracts with Mr. Musk’s companies and Mr. Musk’s relationship to the White House. Mr. Trump, who was briefed on the article in The Times, has been telling associates in the last day or so that Musk’s “crazy” behavior is linked to his drug use, according to a Times report citing two people with knowledge of Mr. Trump’s private conversations. But later on Friday, Mr. Trump told reporters he did not want to comment on Mr. Musk’s drug use. The very public feud between the two men has once again drawn unflattering attention to ketamine, a drug that has become increasingly available at legal clinics across the country. It is also used recreationally and can be dangerous when misused. What is ketamine, and is it legal? Ketamine is an injectable, short-acting dissociative anesthetic that can have hallucinogenic effects at certain doses. It distorts perceptions of sight and sound and makes users feel detached from pain and their surroundings. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29824 - Posted: 06.07.2025

By Lauren Schenkman Addiction may be known as a disease of “more,” but drug-taking also taps a powerful drive for less that can suppress reward in the brain, even at low doses, according to a new study of nicotine responses in mice. The results suggest that the systems of reward and aversion that regulate addiction are more intertwined than previously thought. “That’s absolutely fascinating, because the field has been dominated by this notion of the go, the drive to get drug, but the drive is moderated by the stop,” says Paul Kenny, professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who was not involved in the work. A faulty “stop” signal could be one of the culprits in addiction, he adds. Recent studies have begun to explore this stop signal. Intravenous nicotine activates nicotinic acetylcholine receptors on dopamine neurons in the midbrain’s ventral tegmental area (VTA), generating a rewarding effect that promotes more drug consumption. And high doses activate a tiny adjacent area, the interpeduncular nucleus (IPN), which drives aversion, previous studies have suggested. But doses too low to excite the VTA also activate the IPN in mice, the new work shows. In another experiment, the team used fluorescent proteins to find where axons from the IPN terminate and to identify the intermediate player connecting the IPN and the VTA: the laterodorsal tegmental nucleus (LDTg). The findings were published in Neuron in April. “This was very thrilling,” says the study’s principal investigator, Alexandre Mourot, research director in brain plasticity at the Institut National de la Santé et de la Recherche Médicale (INSERM). It suggests that at very low doses, the VTA does not respond because the IPN “erases the rewarding properties of the drug,” he says. © 2025 Simons Foundation

Keyword: Drug Abuse
Link ID: 29817 - Posted: 06.04.2025

Alison Abbott Daiza Gordon watched her two younger brothers die when they were adolescents. They had Hunter syndrome, a rare, incurable disease — predominantly affecting boys — in which a gene for an important enzyme is missing. Guilt compounded her grief when her attempts to resuscitate her youngest brother failed. She was just 19 years old. Gordon went on to discover how merciless genetics can be. Her own three sons were all born with the condition. When her two eldest hit their second birthdays, the symptoms started to emerge: a thickening of facial features, loss of language, hearing and movement and other impacts to mental and physical development. But she sees hope for her sons that was denied to her brothers. Her children are enrolled in a clinical trial testing a technology to carry a replacement for the missing enzyme, called iduronate-2-sulfatase (IDS), into the brain. Early results indicate improvement in some of the condition’s cognitive and physical symptoms. Gordon’s eldest sons are no longer deaf and they have started to run around. They are meeting developmental milestones she’d never dared to hope for. Her two-year-old, who started the therapy when he was just three months old, is showing none of the early symptoms. “When I look at them, I realize they have a chance of an actual future,” says Gordon. Regular infusions of replacement IDS has been the standard of care for the past two decades, and it protects important organs such as the liver and kidneys from damage. But without help, the large enzyme can’t make it through the protective barrier that separates the blood from one of the most important organs — the brain. For Gordon’s children, that help comes from an innovative molecular transport system, a chemical tag attached to IDS that shuttles it through the tightly joined cells that make up the blood–brain barrier. Several such shuttles, which take advantage of natural transport systems in the brain, are now being developed. With the ability to move large biological drugs — including antibodies, proteins and the viruses used in gene therapy — these shuttles promise to revolutionize neuropharmacology. And that’s not just for rare diseases such as Hunter syndrome, but also for cancer, Alzheimer’s disease and other common brain disorders. © 2025 Springer Nature Limited

Keyword: Drug Abuse; Alzheimers
Link ID: 29811 - Posted: 05.28.2025

By Frieda Klotz In 2006, a new study on antidepressants was making headlines with its promising results: Two-thirds of participants who tried various antidepressants recovered from their depression symptoms within less than a year. The findings seemed to offer hope to the tens of millions of Americans who suffer from depression. But Henry Edmund “Ed” Pigott, then a psychologist in private practice, wasn’t buying it. After further exploring the study — a major National Institutes of Health trial that enrolled 4,000 patients — he was convinced that the researchers’ methods greatly inflated their results, almost doubling them. In other words, the drugs may work, but not for as many people as the study suggested. Henry Edmund Pigott, now a retired psychologist, began investigating a major National Institutes of Health trial on depression in 2006. Decades later, after many studies based on the landmark trial have been published, he still has questions. “Once I got started on it, it was like, ‘Okay, this really needs to be exposed,’” said Pigott, who is now retired. His suspicion sparked a two-decade quest to correct the record and obtain a retraction from the authors of the NIH study, whose work had received $35 million of federal funding. In 2023, Pigott and colleagues published a reanalysis of the NIH data in BMJ Open, finding that the original study’s remission rates were roughly half of what was reported. Pigott isn’t against antidepressants wholesale — he said he just wants patients to understand the complete risks and benefits. And many experts and clinicians stress that antidepressants are lifesaving medications. David Matuskey, a psychiatrist and associate professor at Yale University, described them as vital tools to help patients in desperate need: “Is it a perfect tool? No, but it’s an important one.”

Keyword: Depression
Link ID: 29806 - Posted: 05.28.2025

By Christina Caron Tasha Hedges took Xanax for 20 years to treat her anxiety and panic attacks, exactly as a psychiatrist had prescribed it. Then in 2022, that doctor unexpectedly died. A general practitioner continued her prescription but retired shortly afterward. The next doctor moved to Canada. Finally, Ms. Hedges found a new psychiatrist. “The first thing he did was start yelling at me that I had been on Xanax too long,” said Ms. Hedges, 41, who lives in Falling Waters, W.Va. “He ripped me off my meds.” Discontinuing the drug typically requires decreasing the dose slowly over months or even years, a process called tapering. Ms. Hedges stopped cold turkey. Debilitating withdrawal symptoms followed: hot flashes, cold sweats, restless legs, the shakes and teeth grinding. “It was a nightmare,” she said. Two years after discontinuing the medication, she is still dealing with the fallout. “My brain has not been the same.” In social media groups and websites such as BenzoBuddies, people like Ms. Hedges say they have become physically dependent on benzodiazepines. Many then get cut off from their medication or taper too quickly, and face dangerous and potentially life-threatening withdrawal symptoms that can linger long after the drugs are discontinued. Some doctors, fearful of the risks and stigma associated with these drugs, refuse to prescribe them at all. “Benzos generate as much anxiety in the prescriber as they do in the patient,” said Dr. Ronald M. Winchel, an assistant clinical professor of psychiatry at Columbia University. “Do I start it? Is it the right context? Is it safe? Is my patient going to abuse it? What will my colleagues think/ © 2025 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 29789 - Posted: 05.17.2025

By Lizzie Wade As John Rick excavated one of the many underground chambers at the ancient Peruvian site of Chavín de Huántar in 2017 his trowel hit something intriguing, and exceedingly delicate. It was a cigarette-size tube made of animal bone and packed full of sediment. The following year, his team found almost two dozen more. Rick, an archaeologist at Stanford University, suspected these bone tubes were pieces of ancient drug paraphernalia. Now, a chemical analysis of plant material preserved inside the bone tubes confirms ancient people used them to inhale snuffs made of tobacco and a hallucinogenic plant known as vilca. Rick and colleagues say the rituals involving these drugs may have helped the people of Chavín consolidate their power and influence some 2500 years ago, a time when complex social and political hierarchies were first taking shape in Peru. Although researchers have long suspected rituals at Chavín involved hallucinogenic drugs, “What’s exciting about this paper is that, for first time, we have actual evidence,” says José Capriles, an archaeologist at Pennsylvania State University who wasn’t involved in the research but has studied psychoactive drugs used by ancient people. Chavín de Huántar, which was occupied in the first millennium B.C.E., is renowned for its intricate stone carvings, often depicting animal-human hybrids or transformations of human into beast, and an extensive network of underground chambers. It also had a broad cultural reach. The site in Peru’s north-central highlands abounds with seashells and obsidian, neither found locally, and Chavín-style art shows up in many places throughout the Andes and on the Peruvian coast. “Chavín was part of the first big moment in Andean prehistory when people, ideas, and goods were circulating quite extensively,” says Dan Contreras, an archaeologist at the University of Florida and a co-author of the new paper.

Keyword: Drug Abuse
Link ID: 29775 - Posted: 05.07.2025

By Jan Hoffman Fentanyl overdoses have finally begun to decline over the past year, but that good news has obscured a troubling shift in illicit drug use: a nationwide surge in methamphetamine, a powerful, highly addictive stimulant. This isn’t the ’90s club drug or even the blue-white tinged crystals cooked up in “Breaking Bad.” As cartels keep revising lab formulas to make their product more addictive and potent, often using hazardous chemicals, many experts on addiction think that today’s meth is more dangerous than older versions. Here is what to know. What is meth? Meth, short for methamphetamine, is a stimulant, a category of drugs that includes cocaine. Meth is far stronger than coke, with effects that last many hours longer. It comes in pill, powder or paste form and is smoked, snorted, swallowed or injected. Meth jolts the central nervous system and prompts the brain to release exorbitant amounts of reinforcing, feel-good neurotransmitters such as dopamine, which help people experience euphoria and drive them to keep seeking it. Meth is an amphetamine, a category of stimulant drugs perhaps best known to the public as the A.D.H.D. prescription medications Adderall and Vyvanse. Those stimulants are milder and shorter-lasting than meth but, if misused, they too can be addictive. What are meth’s negative side effects? They vary, depending on the tolerance of the person taking it and the means of ingestion. After the drug’s rush has abated, many users keep bingeing it. They forget to drink water and are usually unable to sleep or eat for days. In this phase, known as “tweaking,” users can become hyper-focused on activities such as taking apart bicycles — which they forget to reassemble — or spending hours collecting things like pebbles and shiny gum wrappers. They may become agitated and aggressive. Paranoia, hallucinations and psychosis can set in. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29750 - Posted: 04.19.2025

By Erin Blakemore Consuming more than eight alcoholic drinks a week is associated with brain injuries linked to Alzheimer’s disease and cognitive decline, a recent study in the journal Neurology suggests. The analysis looked for links between heavy drinking and brain health. Researchers used autopsy data from the Biobank for Aging Studies at the University of São Paulo Medical School in Brazil collected between 2004 and 2024. The team analyzed data from 1,781 people ages 50 or older at death. The average age at death was 74.9. With the help of surveys of the deceased’s next of kin, researchers gathered information about the deceased’s cognitive function and alcohol consumption in the three months before their death. Among participants, 965 never drank, 319 drank up to seven drinks per week (moderate drinking), and 129 had eight or more drinks per week (heavy drinking). Another 368 were former heavy drinkers who had stopped drinking before their last three months of life. The analysis showed that heavy drinkers and former heavy drinkers, respectively, had 41 percent and 31 percent higher odds of neurofibrillary tangles — clumps of the protein tau that accumulate inside brain neurons and have been associated with Alzheimer’s disease. Moderate, heavy and former heavy drinkers also had a higher risk of hyaline arteriolosclerosis, which thickens the walls of small blood vessels in the brain, impeding blood flow and causing brain damage over time. Though 40 percent of those who never drank had vascular brain lesions, they were more common in moderate (44.6 percent), heavy (44.1 percent) and former heavy drinkers (50.2 percent), the study found.

Keyword: Drug Abuse; Alzheimers
Link ID: 29749 - Posted: 04.19.2025

The devastating stimulant has been hitting Portland, Maine hard, even competing with fentanyl as the street drug of choice. Although a fentanyl overdose can be reversed with Narcan, no medicine can reverse a meth overdose. Nor has any been approved to treat meth addiction. Unlike fentanyl, which sedates users, meth can make people anxious and violent. Its effects can overwhelm not just users but community residents and emergency responders. John once fielded customer complaints for a telecommunications company. Now he usually hangs out with friends in the courtyard of a center offering services to help people who use drugs, hitting his pipe, or as he calls it, “getting methicated.” He usually lives outdoors, though he can sometimes handle a few days at a shelter. By noon, he tries to stop smoking meth, so he can get to sleep later that night. Quitting is not on his radar: meth rules his life. “We cannot ride on the railroad, the railroad rides upon us,” he said, with a nod to Henry David Thoreau. Most weekdays, Bill Burns, an addiction and mental health specialist with the Portland police, walks the Bayside neighborhood, checking in on folks. On Thursdays, he rewards the regulars he drives to addiction treatment clinics with his own homemade jolts of dopamine: sugar-dense, Rice Krispie-style treats. Recently, he encountered a young man in full meth psychosis, wild-eyed, bare-chested and bleeding, flinging himself against concrete barriers in an alley. Mr. Burns slipped between the man and a brick wall and wrapped his arms protectively around him. Even as the man flailed uncontrollably, smacking Mr. Burns and smearing blood on his shirt, he managed to stammer, “Sorry!” Speaking softly, Mr. Burns kept repeating, “You’re going to be safe. You’re OK. We’re here because we just want to make sure you’re safe. No, you’re not in trouble. Nobody wants to hurt you. ” © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29747 - Posted: 04.16.2025

By Roni Caryn Rabin Middle-aged and older adults who sought hospital or emergency room care because of cannabis use were almost twice as likely to develop dementia over the next five years, compared with similar people in the general population, a large Canadian study reported on Monday. When compared with adults who sought care for other reasons, the risk of developing dementia was still 23 percent higher among users of cannabis, the study also found. The study included the medical records of six million people in Ontario from 2008 to 2021. The authors accounted for health and sociodemographic differences between comparison groups, some of which play a role in cognitive decline. The data do not reveal how much cannabis the subjects had been using, and the study does not prove that regular or heavy cannabis use plays a causal role in dementia. But the finding does raise serious concerns that require further exploration, said Dr. Daniel T. Myran, the first author of the study, which was published in JAMA Neurology. “Figuring out whether or not cannabis use or heavy regular chronic use causes dementia is a challenging and complicated question that you don’t answer in one study,” said Dr. Myran, an assistant professor of family medicine at University of Ottawa. “This contributes to the literature and to a sign, or signal, of concern.” Dr. Myran’s previous research has found that patients with cannabis use disorder died at almost three times the rate of individuals without the disorder over a five-year period. He has also reported that more cases of schizophrenia and psychosis in Canada have been linked to cannabis use disorder since the drug was legalized. © 2025 The New York Times Company

Keyword: Alzheimers; Drug Abuse
Link ID: 29745 - Posted: 04.16.2025