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Ian Sample Science editor A single dose of psilocybin, the active ingredient in magic mushrooms, can induce anatomical changes in the brain, according to research among people who took the psychedelic compound for the first time. Scientists spotted apparent changes in the brain’s structure which were still apparent a month after healthy volunteers took the drug. If confirmed, they may help explain the therapeutic effects that psychedelics can have on anxiety, depression and addiction, researchers said. Evidence for the changes came from specialised scans that measured the diffusion of water along nerve bundles in the brain. They suggested that some nerve tracts had become denser and more robust after the drug was taken. While the findings are preliminary, the scientists said the opposite was seen in ageing and dementia. “It’s remarkable to see potential anatomical brain changes one month after a single dose of any drug,” said Prof Robin Carhart-Harris, a neurologist at the University of California, San Francisco, and senior author on the study. “We don’t yet know what these changes mean, but we do note that overall, people showed positive psychological changes in this study, including improved wellbeing and mental flexibility.” Scientists have long sought to understand how psychedelics affect the brain and the work has gained fresh impetus in the wake of trials and studies that suggest the compounds could be used to treat a range of mental health disorders. The drugs are thought to help by boosting flexible thinking and allowing people to escape destructive cognitive ruts. © 2026 Guardian News & Media Limited
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: 30237 - Posted: 05.06.2026
By Ellen Barry As Health Secretary Robert F. Kennedy Jr. sets out to rein in the use of psychiatric medications, a group of prominent psychiatrists are developing guidance for helping patients to stop taking them, noting that providers sometimes “park” patients on medications that are no longer necessary or effective. The experts, whose first recommendations appeared in JAMA Network Open and the British Journal of Psychiatry, identify structural problems that may lead to overprescribing: There are few clinical trials showing when it is advisable to stop a medication; many providers do not regularly review whether a prescription is still needed; and psychiatry residents receive more training in starting drug prescriptions than stopping them. “We have not really taught our trainees to think about, what is the logical endpoint?” said Dr. Joseph F. Goldberg, a past president of the American Society of Clinical Psychopharmacology, which convened a group of 45 psychiatrists to agree on basic principles for “deprescribing,” as supervised drug tapering is sometimes called. “You’ll see a patient in consultation who has been parked on a medication which seems to be ineffective for years, and you’ll ask, ‘Why are you still on this medicine?’” he said. “We’ve got a bugaboo going about passive re-prescribing, and I hope we’ll see much less of that.” The new recommendations come amid rising pressure from Mr. Kennedy and his allies in the Make America Healthy Again movement, who have long made the case that Americans overuse psychiatric medications. The Department of Health and Human Services will convene expert panels on deprescribing the main class of medication used to treat depression — selective serotonin reuptake inhibitors, or S.S.R.I.s — this summer, with an eye toward developing official guidance. © 2026 The New York Times Company
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: 30228 - Posted: 05.02.2026
By Rachel E. Gross The first question Sophie Davies had was: Will it affect my memory? In the three weeks since giving birth, Ms. Davies had been in a downward spiral. She checked herself into the mother-and-baby unit of her hospital in East Anglia, England, where doctors ratcheted up the dose of Prozac she took to manage her obsessive-compulsive disorder. But every morning she woke up in tears, and every time she looked at her baby boy, she felt hollow with guilt. “I’m never going to be able to be a mom,” she recalled thinking, “or if I am, I’m not going to be able to be a good one.” A month in, a hospital worker suggested she try a headset that used an electric current to treat depression. The word “electric” gave Ms. Davies, then 34, pause. It sounded like electroconvulsive therapy, or ECT, the scary-sounding treatment that triggers seizures and can result in memory loss. This therapy was different. Transcranial direct-current stimulation, or tDCS, uses a weak electric current to shock the brain and does not produce seizures. “This is as far from ECT as a jet engine is from my bicycle,” Dr. Mark George, of the Medical University of South Carolina, where he is a leading expert in neuromodulation, a term that encompasses all therapies that use electricity to modify brain function. Ms. Davies did an internet search and confirmed that the side effects of tDCS — ringing in the ears, headaches and mild burns or irritation where the electrode pads touched the forehead — were generally transient and didn’t include amnesia. She decided to give it a try. In England, the brain stimulation device has been approved for treating depression since 2019. It can be prescribed by a doctor or purchased over the counter, where it sells for around $530. © 2026 The New York Times Company
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 30225 - Posted: 04.29.2026
Ian Sample Science editor People with major depressive disorder can see a rapid and lasting improvement after a single dose of the psychedelic drug dimethyltryptamine (DMT) when it is combined with psychotherapy, doctors have said. A small clinical trial involving 34 people found that psychedelic-assisted therapy prompted a swift reduction in depressive symptoms that endured long after the drug had worn off, with some still feeling the benefits six months later. “There is an immediate antidepressant effect that is significantly sustained over a three-month period and that’s exciting because this is one session with a drug, embedded in psychological support,” said Dr David Erritzoe, a psychiatrist at Imperial College London and lead investigator on the trial. Although preliminary, the results add to a growing body of evidence that psychedelic drugs, when coupled with psychotherapy, could help to alleviate depression in the millions of people worldwide who do not respond to existing antidepressants or therapies. An estimated 100 million people worldwide have treatment-resistant depression, defined as a major depressive disorder that has not responded to at least two antidepressants. About half are unable to perform routine daily tasks. The trial, reported in Nature Medicine, focused on people with moderate to severe treatment-resistant depression. One half received a single 21.5mg dose of DMT infused into a vein over 10 minutes. The other half received a placebo infused the same way. All of the participants had psychotherapy and follow-up assessments. © 2026 Guardian News & Media Limited
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: 30126 - Posted: 02.18.2026
By Ellen Barry and Pam Belluck Emily Sliwinski got home from the hospital after giving birth to her first child three years ago, and almost immediately began spiraling. Her thoughts raced; she was unable to sleep; she began hallucinating that her dog was speaking to her. She became obsessed with solving the national shortage of infant formula, covering a corkboard with notes and ideas. About a week later, Ms. Sliwinski, of Greensboro, N.C., went to a hospital emergency room, thinking she would be given medication to help her sleep, she said. She had no history of mental health issues. When doctors decided to commit her for inpatient psychiatric treatment, she became so agitated and fearful that she slapped her mother and her husband. She spent 11 days in the psychiatric hospital, but it didn’t help. “Every day I was trying to figure out where I was and what was happening,” Ms. Sliwinski, 33, recalled. Doctors there did not connect her symptoms to childbirth, she said, and diagnosed her with schizophrenia. It was only when her family got her transferred to a specialized perinatal psychiatric unit at the University of North Carolina at Chapel Hill that doctors zeroed in on the right diagnosis: postpartum psychosis. Ms. Sliwinski’s delayed diagnosis reflects an issue simmering in the highest echelons of American psychiatry. For more than five years, a group of women’s health specialists have been pushing for postpartum psychosis to be listed as a distinct diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, the thousand-page guidebook that influences research funding, medical training and clinical care. But two committees at the apex of the D.S.M. have been split over whether to add it. “Psychiatry’s Bible,” as it is sometimes known, has raised the evidentiary bar for including new diagnoses — only one, prolonged grief syndrome, has been added since 2013. © 2026 The New York Times Company
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 30087 - Posted: 01.21.2026
By Andrew Jacobs In the billion-dollar race to commercialize psychedelic medicine, psilocybin, a naturally occurring hallucinogen better known as magic mushrooms, or “shrooms,” has decisively pulled ahead of the pack. The Food and Drug Administration in November said it would move up its review of a psilocybin treatment for severe depression by nine to 12 months, according to the applicant, Compass Pathways. It hopes to receive the agency’s approval for the therapy before the end of the year. The news is among the first concrete signs that the Trump administration is recognizing psychedelic medicine as a potential therapy tool. The moves have injected a fresh dose of optimism into a nascent field, which was rattled by the F.D.A.’s rejection in 2024 of MDMA-assisted therapy, the first psychedelic to reach a formal review by federal regulators. “Between research results and policy changes, it’s a watershed moment for psychedelic health care, and psilocybin is the star,” said Nate Howard, director of operations at InnerTrek, a psilocybin clinic in Portland, Ore. Mr. Howard was a driving force behind a successful ballot measure in 2023 that created Oregon’s psilocybin program. State lawmakers, however, are not waiting for regulators in the nation’s capital. Last year, New Mexico joined Colorado and Oregon in offering legal psilocybin therapy to adults. Lawmakers in a dozen states, including North Carolina, Maryland, Georgia and California, are considering easing restrictions on the drug using public funds to research the potential benefits of psilocybin therapy. © 2026 The New York Times Company
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: 30081 - Posted: 01.14.2026
Allison Aubrey If you feel a lift after exercise, you're in good company. Movement can boost mood, and according to the results of a new study, it can also help relieve symptoms of depression. As part of a review of evidence by the Cochrane collaboration — an independent network of researchers — scientists evaluated 73 randomized controlled trials that included about 5,000 people with depression, many of whom also tried antidepressant medication. "We found that exercise was as effective as pharmacological treatments or psychological therapies as well," says Andrew Clegg, a professor at the University of Lancashire in the U.K. The findings are not a surprise to psychiatrist Dr. Stephen Mateka, medical director of psychiatry at Inspira Health. "This new Cochrane review reinforces the evidence that exercise is one of the most evidence-based tools for improving mood," says Mateka. He explains how it mirrors some of the effects of medication. "Exercise can help improve neurotransmitter function, like serotonin as well as dopamine and endorphins. So there is certainly overlap between exercise and how antidepressants offer relief," Mateka says. And there's another powerful effect too. Exercise can trigger the release of brain growth factors, explains Dr. Nicholas Fabiano of the University of Ottawa. He says depression can decrease neuroplasticity, making it harder for the brain to adapt and change. "The brain in depression is thought to be less plastic. So there's less what we call neurotrophic factors, or BDNF," Fabiano explains. He calls it the Miracle-Gro for the brain. "And we know that exercise can also boost it. So I think exercise is a fundamental pillar we really need to counsel patients on," he says. © 2026 npr
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 30077 - Posted: 01.14.2026
By Calli McMurray For the past two and a half years, a team of five labs in the San Francisco Bay Area have endeavored to nail down how psilocybin affects the way mice behave. Psilocybin and other psychedelic drugs have been shown to improve anxiety and depression symptoms in people, but results in mouse studies are less consistent. Those inconsistencies spell trouble for researchers trying to unpack the drug’s mechanism, because if behavioral changes in mice don’t mirror those in humans, the underlying biological changes might be irrelevant, says team member Boris Heifets, associate professor of anesthesiology, perioperative and pain medicine at Stanford University. So, to establish a behavioral ground truth, the five labs gave about 200 mice the same dose of psilocybin and measured how the drug affected the animals’ performance on a range of simple behavioral assays, including the elevated plus maze and open field, tail suspension and forced swim tests, while taking the drug as well as 24 hours later. While on psilocybin, the mice showed a temporary increase in anxiety-like behaviors, including spending less time than usual exploring new objects and open areas, the team reported in April. But, unlike in people, the drug had no lasting effects once it wore off. The issue, some behavioral neuroscientists argue, is not replication between labs—it’s the assays themselves. “I love the idea of these multisite experiments in animal models, but the models—the behavioral models—still have to be the right ones,” says Jennifer Mitchell, professor of neurology and psychiatry and behavioral sciences at the University of California, San Francisco. “The tests themselves—I’m not sure how much they tell us about what a psychedelic is actually doing.” © 2025 Simons Foundation
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: 30055 - Posted: 12.20.2025
By Mattha Busby Bruce Damer had the audience under his Gandalf spell. He was giving a keynote speech in a grand hall at Breaking Convention, a psychedelic-consciousness conference in Exeter, England, in April 2025. Tall and slender, very much bearded, and sporting two large gold hoop earrings, one on either side, Damer looked exactly like you would expect a sexagenarian psychedelic professor to look. A boyishly enthusiastic speaker, he said a psychedelic trip had transported him through time to face a deep trauma. Nautilus Members enjoy an ad-free experience. Log in or Join now . “If you believe in a ‘mother ayahuasca’ or a healing force, I was allowed to experience my conception and birth and be in my mother’s belly,” Damer said. His birth mother had given him up because she and his father were too poor to raise him. Ayahuasca had released him from the pain. “Being in the belly, I could feel her love, and it healed,” he said. “As a result of the clarity and the opening of the blockage that had been this sort of knot in my belly, my whole system opened wide,” Damer continued. “And I thought for a moment, I could potentially travel through time to a place where I’ve been working on the question of how life began, the birth of us all.” In psychedelic science, a field dominated by scientists who are loath to be pigeon-holed as too woo-woo, Damer, 63, has become a cult figure by wearing his woo on his sleeve. His adoptive mother described him as “in his own world” when his new parents brought him home. And he has been his own thinker ever since. His science cred is sound: a Ph.D. in computer science from University College Dublin in Ireland, former relationships with Xerox and NASA, and papers published in journals like Astrobiology. Currently he is a research associate in the Department of Biomedical Engineering at the University of California, Santa Cruz. © 2025 NautilusNext Inc.,
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: 30052 - Posted: 12.17.2025
By Alex Kwan Despite decades of basic research, many neurological and psychiatric conditions lack effective treatments, or at least treatments that work for everyone. For that reason, when I talk with colleagues about the value of research, I often hear the same negative refrain: “Basic neuroscience has not produced new drugs.” Their argument carries some weight; many of today’s medications trace their origins to long-standing human use or to chance discoveries. The opium poppy, used for thousands of years to ease pain, paved the way for morphine and other opioids that are widely used as analgesics. Ketamine was designed as an anesthetic but was later unexpectedly revealed to be an antidepressant at low doses. Yet this narrative is incomplete. It overlooks a growing list of medications—including zuranolone for postpartum depression, suzetrigine for pain, and the gepants class of migraine medicines—that exist only because of insights from basic research. These drugs were not stumbled upon or borrowed from traditional remedies. They were born out of a long arc of studies in the lab. These success stories matter, because they demonstrate that neuroscience research can deliver new medicines. Acknowledging and publicizing such successes is especially important now, as public funding for basic research in the United States faces growing cuts and restrictions. The development of zuranolone stemmed from an observation about allopregnanolone, a steroid our bodies naturally produce. It has little interaction with steroid receptors and instead acts on GABA receptors in the brain, making neurons less excitable. In the late 1990s, researchers reported that allopregnanolone levels in the rat brain rise dramatically during pregnancy, reaching concentrations of up to three times higher than normal. Just before giving birth, however, the level drops precipitously. © 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: 30051 - Posted: 12.17.2025
By Christina Caron When Marjorie Isaacson first started taking medication for depression in her late 20s, she considered it lifesaving. At the time, she had been dealing with a rocky marriage and struggling to eat. The drug, she found, helped her gain equilibrium. “I was really grateful just to be able to function,” she said. But recently, Ms. Isaacson, 69, has been considering whether she wants to stay on antidepressants for the rest of her life. Specifically, Ms. Isaacson wonders about the long-term effects of her medication, a serotonin-norepinephrine reuptake inhibitor that is known to raise blood pressure. And she feels unsettled by the emerging backlash against psychiatric drugs that has condemned their side effects and difficult withdrawal symptoms. “As the years have passed, things have changed from ‘Take it and see how it goes, no need now to be concerned’ to ‘Well, it’s turning out things might be kinda complicated,’” she said. “That is worrisome.” Antidepressants are among the most prescribed and easily accessible drugs in the United States, and many people take them for years. But even though modern-day antidepressants have been around for decades — the Food and Drug Administration approved Prozac for depression treatment in 1987 — there is very little information about long-term use. The F.D.A. approved the drugs based on trials that lasted, at most, a few months, and randomized controlled trials of antidepressants have typically spanned only two years or less. Current clinical guidelines do not specify the optimal amount of time they should be taken for. The lack of data can make it hard for people to know when — or whether — to quit. So we asked psychiatrists: How long should someone stay on antidepressants? © 2025 The New York Times Company
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 30047 - Posted: 12.13.2025
By Daniel Bergner Marie began taking fluoxetine, the generic form of Prozac, when she was 15. The drug — an S.S.R.I., a selective serotonin reuptake inhibitor — was part of her treatment in an outpatient program for an eating disorder. It took its toll on her sexuality. “I was in touch with initial sparks of sexual energy relatively young,” she said, remembering crushes as far back as the age of 6 or 7. Shortly before starting on the drug, she was dazzled, from a distance, by a blue-eyed hockey player at school, tall and funny and charismatic. She recalled the fluster and fantasies he stirred. But on the medication, she felt the infatuation vanish swiftly. Listen to this article, read by Eric Jason Martin “And then,” Marie said, “I realized, Oh, I’m not developing new crushes.” She had no clue that the drug might be the cause: “I wasn’t informed about sexual side effects.” Even as the worst of the eating disorder abated, psychiatrists and family doctors told Marie and her parents that she should stay on an antidepressant. She complied, while trying and failing to escape the sexual side effects. She traded fluoxetine for other antidepressants, including Wellbutrin, a different class of antidepressant, which is sometimes prescribed to combat low libido. She’s 38 now and has been off psychiatric medication for six years. But sexual desire remains absent. “For me it’s just an empty dark space,” she said. “There’s nothing there.” Marie told me she has PSSD, post-S.S.R.I. sexual dysfunction, a loss of sexuality that persists after the drug is no longer being taken. It’s a controversial designation, because while the sexual side effects of S.S.R.I.s are well established — depleted or deadened desire, erectile dysfunction for men, elusive arousal for women, delayed and dulled orgasms or the inability to reach orgasm at all — the general assumption is that they subside completely when the drug is no longer in your system. Some psychiatrists suspect that PSSD is actually a result not of repercussions from the drugs but of the problem that led the patient to be medicated in the first place. Depression itself can stymie sexuality. So can anxiety, the other leading reason patients are prescribed S.S.R.I.s. © 2025 The New York Times Company
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 30006 - Posted: 11.12.2025
By Ramin Skibba In August, two parents in California filed a lawsuit against OpenAI, claiming that the company was responsible for their teenage son’s suicide. The previous fall, according to Maria and Matthew Raine, their 16-year-old, Adam, had started using the company’s popular AI chatbot ChatGPT as a homework helper. Over the course of several months, the Raines alleged, it shifted to a digital companion and then to a “suicide coach,” advising the teen how to quietly steal vodka from his parent’s liquor cabinet, urging him to keep his suicidal ideations a secret, and then guiding him about the feasibility and load-bearing capacity of a noose. By the time of Adam’s death in April, according to the Raines’ complaint, the chatbot had used the word “suicide” 1,275 times, six times more often than Adam himself. The case of Adam Raines was not an isolated incident, though publicly available data remains limited. And experts worry that more mental health crises, including suicides — the second leading cause of death among people between ages 10 and 24 years — could arise as users increasingly turn to generative AI chatbots for emotional support. Although it is difficult to pinpoint just how many people are relying on chatbots in this way, according to a recent Harvard Business Review survey based primarily on data collected from Reddit forum posts, the practice is common for therapy, companionship, and finding purpose. Researchers have scrambled to understand the trend, including both the potential risks and benefits of the chatbots, most of which were not designed to be used for mental health support. Some users claim that the bots help them, citing their perception that the tools won’t judge or stigmatize them, while others are seeking a substitute for therapy when they can’t access or afford it, experts say. Some users also don’t think of the chatbots as a form of therapy, but rather a kind of mindful journaling as they work through their emotions and problems. According to one example in the Harvard Business Review report, a Reddit user said, “I found a thread where people talked about using AI to analyze their moods, essentially having low-barrier ‘therapy’ sessions.
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29999 - Posted: 11.05.2025
By Ellen Barry One of the most popular mental health innovations of the past decade is therapy via text message, which allows you to dip in and out of treatment in the course of a day. Say you wake up anxious before a presentation: You might text your therapist first thing in the morning to say that you can’t stop visualizing a humiliating failure. Three hours later, her response pops up on your phone. She suggests that you label the thought — “I’m feeling nervous about my presentation” — and then try to reframe it. She tells you to take a deep breath before deciding what is true in the moment. You read her answer between meetings. “I’m pretty sure my boss thinks I’m an idiot,” you type. The therapist responds the next morning. “What evidence do you have that she thinks that?” she asks. She tells you to write a list of the available evidence, pros and cons. Text-based therapy has expanded swiftly over the past decade through digital mental health platforms like BetterHelp and Talkspace, which pair users with licensed therapists and offer both live chat and as-needed texting sessions. A new study published on Thursday in the journal JAMA Network Open provides early evidence that the practice is effective in treating mild to moderate depression, finding outcomes similar to those of video-based therapy. In a clinical trial, 850 adults with mild to moderate depression were randomly assigned to two groups: One group received psychotherapy via a weekly video session; the other received unlimited, as-needed messaging or emailing with a therapist. After 12 weeks, participants in both groups reported similar improvement in depression symptoms. © 2025 The New York Times Company
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29995 - Posted: 11.01.2025
By Sara Talpos As a new Ph.D. student in 2011, Steve Ramirez and his mentor performed a groundbreaking experiment in the field of memory manipulation. They placed a mouse in a small distinctive box and administered a mild electrical shock to its feet. When the rodent was placed in the box a second time, it froze up — anticipating another shock. From there, the young neuroscientists placed the mouse in a different box, one where nothing bad had happened. They then directed pulses of light to a very specific region in the mouse’s brain that had been genetically modified to respond to the light. This caused the mouse to immediately freeze. Ramirez and his mentor, it turned out, had found a way to artificially activate a fear-inducing memory. “How to Change a Memory: One Neuroscientist’s Quest to Alter the Past,” by Steve Ramirez will be available on November 4, 2025 (Princeton University Press, 256 pages). What was the point? A central goal of such science is to learn how memories form and function in the brain and to then apply this knowledge to treat brain disorders, writes Ramirez in his forthcoming book, “How to Change a Memory: One Neuroscientist’s Quest to Alter the Past.” Perhaps one day, he suggests, it will be possible to activate positive memories to curb depression or to retrieve memories that have seemingly been lost to Alzheimer’s disease. In the book, Ramirez explores the fascinating science of memory while tracing his own journey to becoming a successful professor at Boston University. His path was not without challenges, including the sudden death of his mentor and a decade-long struggle with alcohol addiction. “This book,” he writes, “is my attempt to make sense of the enigma of memory — the snippets of remembrances, the brief moments in time, the decisions we make, the blackouts, the imagined, and the dreamt of — all the things the brain does to breathe life into the past so that we can heal and become whole again.”
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory and Learning
Link ID: 29988 - Posted: 10.29.2025
Will Stone Doctors have long known that antidepressants come with side effects for cardiovascular and metabolic health. But a major analysis from a team of researchers in the U.K. has, for the first time, pulled together data from more than 150 clinical trials to compare the physical side effects of dozens of antidepressants. The study, published in the Lancet this week, details how each medication can affect weight, blood pressure, heart rate, cholesterol and other areas of health. The end result is something akin to a "sports league table" for 30 different antidepressants based on their side effect profile, says lead author Dr. Toby Pillinger, a psychiatrist at King's College London. "It's never been done at this scale before and no one's ever put specific numbers to the amount of weight you'll put on, or to the amount that your cholesterol goes up," he says. The findings are based on existing data, mostly from 8-week drug studies, that altogether represent more than 58,000 patients. The most frequently prescribed antidepressants in the U.S. — selective serotonin reuptake inhibitors, or SSRIs, like Zoloft and Prozac — tended to have fewer physical side effects, according to the analysis. Other medications, particularly some of the older drugs, were shown to have more significant impacts. © 2025 npr
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: 29983 - Posted: 10.25.2025
By Michele Cohen Marill Like many first-time mothers, Lisette Lopez-Rose thought childbirth would usher in a time of joy. Instead, she had panic attacks as she imagined that something bad was going to happen to her baby, and she felt weighed down by a sadness that wouldn’t lift. The San Francisco Bay Area mother knew her extreme emotions weren’t normal, but she was afraid to tell her obstetrician. What if they took her baby away? At about six months postpartum, she discovered an online network of women with similar experiences and ultimately opened up to her primary care doctor. “About two months after I started medication, I started to feel like I was coming out of a deep hole and seeing light again,” she says. Today, Lopez-Rose works at Postpartum Support International, coordinating volunteers to help new mothers form online connections. About one in eight US women go through a period of postpartum depression, making it among the most common complications of childbirth. It typically occurs in the first few weeks after delivery, when there’s a sudden drop in the reproductive hormones estrogen and progesterone. As scientists unravel chemical and genetic changes caused by those shifting hormones, they are discovering new ways to diagnose and treat postpartum depression, and even ways to identify who is at risk for it. Graph showing a steady rise in levels of estradiol and progesterone after conception and then a very steep drop-off right after birth. The hormones estradiol (the main form of estrogen) and progesterone rise during pregnancy. In some women, their sudden drop after childbirth triggers the onset of postpartum depression. The first-ever drug for postpartum depression, containing a derivative of progesterone, received US Food and Drug Administration approval in 2019. That marked a new approach to the disorder. This winter, in another major advance, a San Diego-based startup company will launch a blood test that predicts a pregnant woman’s risk of postpartum depression with more than 80 percent accuracy. © 2025 Annual Reviews
Related chapters from BN: Chapter 15: Emotions, Aggression, and Stress; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 8: Hormones and Sex
Link ID: 29972 - Posted: 10.18.2025
Natasha May Health reporter Women carry a higher genetic risk of depression, a new study has found. Claiming to be the largest genetic study to date on sex differences in major depression, the research published on Wednesday in Nature Communications has found 16 genetic variants linked to depression in women and eight in men. The study, led by Australia’s QIMR Berghofer Medical Research Institute, showed a large proportion of the variants associated with depression were shared between sexes, but there was a “higher burden of genetic risk in females which could be due to female-specific variants”. Dr Brittany Mitchell, a senior researcher at QIMR Berghofer’s genetic epidemiology lab, said “we already know that females are twice as likely to suffer from depression in their lifetime than males”. “And we also know that depression looks very different from one person to another. Until now, there hasn’t been much consistent research to explain why depression affects females and males differently, including the possible role of genetics.” The study acknowledged explanations have been put forward spanning behavioural, environmental and biological domains, including men being less likely to seek help leading to under-diagnosis, and environmental exposures such as women being more frequently exposed to sexual abuse and interpersonal violence. The study stated that together these factors highlight the need for a “multifaceted approach” to understanding the underlying mechanisms of depression but proposed that a “key component of the biological mechanisms underlying these disparities could be differences in genetics”. © 2025 Guardian News & Media Limited
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 29958 - Posted: 10.08.2025
Mohana Basu People with a psychiatric disorder are more likely to marry someone who has the same condition than to partner with someone who doesn’t, according to a massive study1 suggesting that the pattern persists across cultures and generations. Researchers had previously noted this trend in Nordic countries, but the phenomenon has seldom been investigated outside Europe until now. The latest study, published in Nature Human Behaviour today, used data from more than 14.8 million people in Taiwan, Denmark and Sweden. It examined the proportion of people in those couples who had one of nine psychiatric disorders: schizophrenia, bipolar disorder, depression, anxiety, attention-deficit hyperactivity disorder, autism, obsessive–compulsive disorder (OCD), substance-use disorder and anorexia nervosa. Scientists lack a definitive understanding of what causes people to develop psychiatric disorders — but genetics and environmental factors are both thought to play a part. The team found that when one partner was diagnosed with one of the nine conditions, the other was significantly more likely to be diagnosed with the same or another psychiatric condition. Spouses were more likely to have the same conditions than to have different ones, says co-author Chun Chieh Fan, a population and genetics researcher at the Laureate Institute for Brain Research in Tulsa, Oklahoma. “The main result is that the pattern holds across countries, across cultures, and, of course, generations,” Fan says. Even changes in psychiatric care over the past 50 years have not shifted the trend, he notes. Only OCD, bipolar disorder and anorexia nervosa showed different patterns across countries. For instance, in Taiwan, married couples were more likely to share OCD than were couples in Nordic countries. © 2025 Springer Nature Limited
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: 29908 - Posted: 08.30.2025
By Eric Reinhart A recent study in the journal JAMA Psychiatry claims to offer reassuring news to hundreds of millions of people who are taking, or considering taking, antidepressants: Withdrawal from the medications, it said, is usually mild and below the threshold for clinical significance. The analysis, which drew on data from more than 17,000 patients, was quickly picked up by international news outlets. Critics responded just as quickly, calling it misleading and dismissive of real-world suffering. As both a practicing psychiatrist and critic of the harms inadvertently inflicted by my own field, I fear we’re having the wrong debate — again. Conceptual image of an orange seesaw with a pink brain and an oversized pill balancing on it, could illustrate ideas around ssri, anti-depressants, headache pills and other medication for mental and brain health Every few years, another study or media exposé reignites controversy over these drugs: How effective are they really? Are withdrawal symptoms real or imagined? Are antidepressants harming people more than they help? These questions, while important, are stuck inside the narrow terms set by a medication-centric psychiatric industry, even when criticizing it. They flatten the experience of patients and ignore the intersecting role of clinicians, families, institutions, media, culture, and public policy in shaping both suffering and relief, trapping us in circular debates and deflecting attention from other ways of understanding and addressing what ails us. Yes, antidepressant withdrawal is real. Yes, some people suffer greatly while trying to come off these drugs, with withdrawal risk varying among different kinds of antidepressants. I have also seen many patients appear to benefit greatly from such medications. But when we focus only on the biology of response and withdrawal, or treat psychiatric medications as purely pharmacologic agents whose harms and benefits can be definitively measured and settled by clinical trials, we obscure the more complex — and far more consequential — dynamics by which these medications affect self-perception, social relationships, and political life.
Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29897 - Posted: 08.23.2025


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