By Jan Hoffman To treat their pain, anxiety and sleep problems, millions of Americans turn to cannabis, which is now legal in 40 states for medical use. But a new review of 15 years of research concludes that the evidence of its benefits is often weak or inconclusive, and that nearly 30 percent of medical cannabis patients meet criteria for cannabis use disorder. “The evidence does not support the use of cannabis or cannabinoids at this point for most of the indications that folks are using it for,” said Dr. Michael Hsu, an addiction psychiatrist and clinical instructor at the University of California, Los Angeles, and the lead author of the review, which was published last month in the medical journal JAMA. (Cannabis refers to the entire plant; cannabinoids are its many compounds.) The analysis arrives amid a surging acceptance and normalization of cannabis products, a $32 billion industry. For the review, addiction experts at academic medical centers across the country studied more than 2,500 clinical trials, guidelines and surveys conducted mostly in the United States and Canada. They found a wide gulf between the health purposes for which the public seeks out cannabis and what gold-standard science shows about its effectiveness. The researchers distinguished between medical cannabis, sold at dispensaries, and pharmaceutical-grade cannabinoids — the handful of medicines approved by the Food and Drug Administration with formulations containing either low-grade THC, a psychoactive compound, or CBD, a nonintoxicating compound. Those medicines, including Marinol, Syndros and Cesamet, are available by prescription at conventional pharmacies and have had good results in easing chemotherapy-related nausea, stimulating the appetite of patients with debilitating illnesses like H.I.V./AIDS, and easing some pediatric seizure disorders. © 2025 The New York Times Company

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 10: Biological Rhythms and Sleep
Link ID: 30045 - Posted: 12.13.2025

By Siddhant Pusdekar A single dose of psilocybin leads to widespread network-specific changes to cortical circuitry in mice, according to a new study published today in Cell. The results help explain how psilocybin can bring about lasting changes in behavior, and they pinpoint “the neurons that are most affected,” says Andrea Gomez, assistant professor of molecular and cellular biology at the University of California, Berkeley, who was not involved in the study. Specifically, the psychedelic strengthens cortical inputs from sensory brain areas and weakens inputs into cortico-cortical recurrent loops. Overall, these network changes suggest that psychedelics reroute information in a way that enhances responses to the outside world and reduces rumination, says study investigator Alex Kwan, professor of biomedical engineering at Cornell University. “This study provides some more mechanistic insight for why the drug may be a good antidepressant.” And the rewiring itself is not static, Kwan adds: “It can be influenced by manipulating neural activity” during psychedelic treatment. With this locus of psychedelic-induced changes identified, researchers can unpack how these neuronal ensembles coordinate “to create particular percepts or particular cognitions,” Gomez says. Kwan’s team focused on the mouse dorsal medial prefrontal cortex (dmPFC), which includes the anterior cingulate cortex—an important hub for the serotonin receptors that psilocybin targets. One dose of psilocybin increases dendritic spine growth in the medial prefrontal cortex of mice, an effect that lasts for at least a month, according to a 2021 study by Kwan’s team. And the treatment reduces the animals’ learned stress-related behaviors, but only if pyramidal tract neurons—one of the major types of excitatory neurons in the dmPFC—are active, Kwan’s group reported in April. © 2025 Simons Foundation

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 4: Development of the Brain; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 30042 - Posted: 12.06.2025

Elie Dolgin Last April, neuroscientist Sue Grigson received an e-mail from a man detailing his years-long struggle to kick addiction — first to opioids, and then to the very medication meant to help him quit. The man had stumbled on research by Grigson, suggesting that certain anti-obesity medications could help to reduce rats’ addiction to drugs such as heroin and fentanyl. He decided to try quitting again, this time while taking semaglutide, the blockbuster GLP-1 drug better known as Ozempic. “That’s when he wrote to me,” says Grigson, who works at Pennsylvania State University College of Medicine in Hershey. “He said that he was drug- and alcohol-free for the first time in his adult life.” Stories like this have been spreading fast in the past few years, through online forums, weight-loss clinics and news headlines. They describe people taking diabetes and weight-loss drugs such as semaglutide (also marketed as Wegovy) and tirzepatide (sold as Mounjaro or Zepbound) who find themselves suddenly able to shake long-standing addictions to cigarettes, alcohol and other drugs. And now, clinical data are starting to back them up. Earlier this year, a team led by Christian Hendershot, a psychologist now at the University of Southern California in Los Angeles, reported in a landmark randomized trial that weekly injections of semaglutide cut alcohol consumption1 — a key demonstration that GLP-1 drugs can alter addictive behaviour in people with a substance-use disorder. More than a dozen randomized clinical studies testing GLP-1 drugs for addiction are now under way worldwide, with some results expected in the next few months. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 30036 - Posted: 12.03.2025

Mark Brown Sophisticated and deadly “brain weapons” that can attack or alter human consciousness, perception, memory or behaviour are no longer the stuff of science fiction, two British academics argue. Michael Crowley and Malcolm Dando, of Bradford University, are about to publish a book that they believe should be a wake-up call to the world. They are this weekend travelling to The Hague for a key meeting of states, arguing that the human mind is a new frontier in warfare and there needs to be urgent global action to prevent the weaponisation of neuroscience. “It does sound like science fiction,” said Crowley. “The danger is that it becomes science fact.” The book, published by the Royal Society of Chemistry, explores how advances in neuroscience, pharmacology and artificial intelligence are coming together to create a new threat. “We are entering an era where the brain itself could become a battlefield,” said Crowley. “The tools to manipulate the central nervous system – to sedate, confuse or even coerce – are becoming more precise, more accessible and more attractive to states.” The book traces the fascinating, if appalling, history of state-sponsored research into central nervous system (CNS)-acting chemicals. During the cold war and after, the US, Soviet Union and China all “actively sought” to develop CNS-acting weapons, said Crowley. Their purpose was to cause prolonged incapacitation to people, including “loss of consciousness or sedation or hallucination or incoherence or paralysis and disorientation”. © 2025 Guardian News & Media Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 11: Emotions, Aggression, and Stress
Link ID: 30023 - Posted: 11.22.2025

By Nima Sadrian In the popular narrative, cannabidiol, or CBD, is portrayed as a natural, non-intoxicating cure for a host of ailments — and sometimes that extends to the anxieties of modern adolescence. CBD is everywhere, infused in products such as gummy candies, vapes, skincare serums, and even fizzy seltzers. Usually derived from the hemp plant, CBD is pitched as a calming remedy with none of the stigma of marijuana. Even a 2018 World Health Organization report noted that CBD shows no signs of abuse or dependence potential. But as a physician and neuroscientist who studies how CBD affects the developing brain, I have to offer a different, more troubling answer: We simply don’t know if it’s safe for teens. And early evidence suggests potential for real, lasting harm. The comforting story our culture tells itself about CBD — that it offers harmless, botanical relief for stress and sleep problems — is dangerously out of step with the science. While we have been sold a simple wellness narrative, my own work and that of other scientists reveal a far more complex and cautionary tale — one that challenges the very foundation of the multibillion-dollar CBD industry. How did a compound that the Food and Drug Administration has only approved as a potent prescription drug for severe childhood epilepsy become a common additive? The answer lies in a catastrophic regulatory failure. The 2018 farm bill legalized hemp, but the legislation and its extensions created no framework to ensure that the products made from it were safe, effective, or accurately labeled, nor did the bill set an age limit for it. The result is a market that operates like the Wild West, a gold rush where consumer safety is an afterthought. The FDA-approved CBD medicine, Epidiolex, comes with a long list of documented risks, including liver damage and suicidal ideation, and requires careful medical supervision. Yet numerous consumer products containing CBD are sold without such warnings, mandatory testing, or oversight.

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29991 - Posted: 11.01.2025

By Rachel Nuwer No one knows why magic mushrooms evolved to produce psilocybin, a powerful psychedelic molecule. But this trait was apparently so beneficial for fungi that it independently evolved in two distantly related types of mushrooms. An even greater surprise to biologists was that rather than arriving at the same solution for producing psilocybin, the two groups pursued completely different biochemical pathways, according to a study published last month in the journal Angewandte Chemie International Edition. “This finding reminds us that nature finds more than one way to make important molecules,” said Dirk Hoffmeister, a pharmaceutical microbiologist at Friedrich Schiller University Jena in Germany and an author of the study. He added that it was also evidence that mushrooms were “brilliant chemists.” Practically speaking, Dr. Hoffmeister said, the research also suggested a possible new path for synthesizing psilocybin for use in scientific research and therapies. “We can expand our toolbox,” he said. Psilocybe and Inocybe mushrooms occur in some of the same habitats, but they follow different lifestyles. Psilocybe, the group that includes what are traditionally called magic mushrooms, thrives on decaying material such as decomposing organic matter or cow dung. Inocybe, commonly known as fiber caps, are symbiotic organisms that form intimate, mutually beneficial relationships with trees. In 1958, Albert Hofmann, the Swiss chemist who discovered LSD, became the first researcher to isolate psilocybin from Psilocybe mushrooms. Some scientists later suspected that a few Inocybe mushrooms also produced the compound. Since then, psilocybin has been identified in around half a dozen Inocybe species. (The other species tend to produce a potent neurotoxin.) © 2025 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 4: Development of the Brain
Link ID: 29985 - Posted: 10.25.2025

By Grigori Guitchounts On a mellow spring night, I gazed at the setting desert sun in Joshua Tree National Park in California. The sun glowed a warm blood-orange and the sky shimmered pink and purple. I had just defended my Ph.D. in neuroscience, and my partner and I had flown west to celebrate and exhale. It was early March 2020, and we were hoping to quiet our minds in the desert. I was also hoping to change mine. I had been curious about psychedelics for years, but it wasn’t until I read How to Change Your Mind by Michael Pollan about the new science of psychedelics, that I felt ready. The book made a compelling case that psychedelics provided a fascinating introspective experience. Still, I was nervous. I’d heard stories about bad trips and flashbacks. I knew enough neuroscience to know these were serious drugs—compounds that could temporarily dismantle how the brain makes sense of reality and potentially change it irreversibly. I also knew I was burned out. My Ph.D. had been hard in the way Ph.D.s often are: thrilling, lonely, disorienting. My advisor had left academia halfway through, and I’d spent years without much supervision, never quite sure whether I was on the right track and if I had a future in academia. But I didn’t take LSD seeking healing or clarity. I just wanted to see what the fuss was about. After years of hunkering down, I was craving a freeing experience. What followed was strange, intense, and beautiful. The wooden floorboards of our cabin turned into a bustling cityscape. The mirror in the bathroom showed my face aged beyond recognition: The natural lines in my skin became deep wrinkles, my eyes sunken, as if time had decided to give me a sneak peak of what would come. Later, absorbed with coloring pencils, I watched the marks I was making dissolve in real time, as if the paper were being erased by invisible rain. © 2025 NautilusNext Inc.,

Related chapters from BN: Chapter 18: Attention and Higher Cognition; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 14: Attention and Higher Cognition; Chapter 4: Development of the Brain
Link ID: 29979 - Posted: 10.22.2025

Mohana Basu The opioid class of drugs includes heroin and morphine. Unlike those drugs, which are derived from naturally occurring opium, nitazenes are synthesized from scratch in a laboratory. The first nitazenes were developed as painkillers in the 1950s, but were never approved for medical use because they carried a high risk of dangerous side effects such loss of consciousness, coma and death. But since 2019, there has been a rise in the reported use of nitazenes, according to the World Drug Report 2025, which was released in June. In 2023, the report states, 20 different nitazenes were seized by authorities across 28 countries and reported to the United Nations Office on Drugs and Crime (UNODC) Early Warning Advisory on New Psychoactive Substances. Nitazenes can be as much as 500 times more potent than opium-derived drugs. For example, butonitazene is 2.5 times more potent than heroin, whereas isotonitazene and etonitazene are 250 and 500 times more potent, respectively. This means that just a tiny amount can be deadly. In the United Kingdom, there were 179 confirmed deaths from nitazene overdoses in the year to 31 May 2024. And reports suggest that thousands of people might have died from nitazene overdoses in the United States since 2019. In Australia, researchers note that the unpredictable presence of nitazenes in various drugs is increasing the risk of overdose in the country. Most nitazene overdoses are unintentional, says Suzanne Nielsen, an addiction researcher at Monash University in Melbourne, Australia. Overdose tends to occur when nitazenes are sold as other drugs, such as heroin, oxycodone and MDMA (also known as ecstasy). Overdoses can be treated with naloxone, a drug that has long been used to treat other opioid overdoses. More awareness of this among drug users and their families could help save lives, Nielsen adds. © 2025 Springer Nature Limited

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 29963 - Posted: 10.11.2025

By Devin Effinger, Melissa Herman Psychedelics show growing promise as treatments for a variety of psychiatric diseases. Clinical trials have demonstrated rapid and persistent improvements in major depressive disorder, for example, sparking interest among both psychiatrists and neuroscientists. However, the clinical use of psychedelics is challenging; the drugs induce prolonged visual hallucinations and must be administered and monitored by trained staff, which creates barriers in terms of their availability and accessibility. Clinical trials are also challenging. Psychedelics produce profound subjective effects that make it impossible to properly placebo-control or effectively blind participants. And given the widespread cultural fascination with these drugs, it’s difficult to remove expectancy bias—if someone strongly believes a drug will work, that can influence their perception and reporting of their outcome. Moreover, these drugs are typically delivered and tested in combination with psychotherapy. Discerning whether any treatment effects stem from the drug versus the psychotherapy, as well as the role of therapy in clinical response, is a point of debate within the field. To help resolve some of these issues, we need to better understand the neurobiological mechanisms involved. Human imaging studies have shown that some psychedelics, such as psilocybin, produce long-lasting alterations in global connectivity and negative affect. But to design more effective versions of these drugs, we need to uncover their underlying mechanisms of action at greater resolution—something that is possible only through preclinical research at the level of molecular, cellular and systems neuroscience. © 2025 Simons Foundation

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 29956 - Posted: 10.04.2025

By Roni Caryn Rabin Women who are pregnant, planning a pregnancy or breastfeeding should be screened for cannabis use and strongly discouraged from it, the American College of Obstetricians and Gynecologists said in new clinical guidelines published on Friday. Cannabis use during pregnancy has been rising for years. Many women rely on the drug to cope with nausea and other pregnancy symptoms. But the college warned that mounting evidence linked cannabis to preterm births, low birth weights and a greater need for neonatal intensive care, as well as neurocognitive and behavioral problems in children. “Patients are often using cannabis to help with some kind of medical ailment, not recreationally — in their mind, they think it’s a more natural way to deal with a medical problem,” said Dr. Melissa Russo, an author of the new guidance. “But there are lots of natural things that are not safe,” Dr. Russo said. There are no studies demonstrating that cannabis is effective for pregnant or lactating women, she added, “and research now shows there are potential adverse effects.” The college warned against blood or urine tests for cannabis screening. Instead, it urged physicians to talk with women about their habits, and to encourage them to stop using marijuana as soon as possible while offering alternative therapies for medical ailments. The screening should be universal in an effort to avoid bias and racism, the college said. It noted that pregnant Black and Hispanic women are four to five times as likely as white women to be tested for drug use. Black women are almost five times as likely to be reported to child protective services for suspected drug use. The new guidelines say that cannabis should be discouraged among breastfeeding women, but that breastfeeding should continue even with use of the drug because the benefits most likely outweigh the potential risks. © 2025 The New York Times Company

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 4: Development of the Brain; Chapter 13: Memory and Learning
Link ID: 29942 - Posted: 09.24.2025

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.,

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 4: Development of the Brain
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.

Related chapters from BN: Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 8: Hormones and Sex; Chapter 4: Development of the Brain
Link ID: 29922 - Posted: 09.10.2025

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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
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.

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 4: Development of the Brain
Link ID: 29876 - Posted: 08.06.2025

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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
Link ID: 29854 - Posted: 07.16.2025

By Andrew Jacobs When Gov. Greg Abbott of Texas approved legislation this week to spend $50 million in state money researching ibogaine, a powerful psychedelic, he put the spotlight on a promising, still illegal drug that has shown promise in treating opioid addiction, traumatic brain injury and depression. Interest in ibogaine therapy has surged in recent years, driven in large part by veterans who have had to travel to other countries for the treatment. The measure, which passed the Texas Legislature with bipartisan support, seeks to leverage an additional $50 million in private investment to fund clinical trials that supporters hope will provide a pathway for ibogaine therapy to win approval from the Food and Drug Administration, a process that could take years. The legislation directs the state to work with Texas universities and hospitals and tries to ensure that the state retains a financial stake in any revenue from the drug’s development. “You can’t put a price on a human life, but if this is successful and ibogaine becomes commercialized, it will help people all across the country and provide an incredible return on investment for the people of Texas,” said State Senator Tan Parker, a Republican who sponsored the bill. The initiative, one of the largest government investments in psychedelic medicine to date, is a watershed moment for a field that continues to gain mainstream acceptance. Regulated psilocybin clinics have opened in Oregon and Colorado, and ketamine has become widely available across the country as a treatment for depression and anxiety. There have been speed bumps. Last year, the F.D.A. rejected MDMA-assisted therapy for PTSD, the first psychedelic compound to make it through much of the agency’s rigorous drug review process. © 2025 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29833 - Posted: 06.18.2025

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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 4: Development of the Brain
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

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 29811 - Posted: 05.28.2025