By Molly Glick Not long after upending federal diet guidelines in order to prioritize “real food” on our plates, United States Health and Human Services Secretary Robert F. Kennedy Jr. has offered a new piece of questionable advice. During a tour to promote these dietary recommendations, Kennedy recently claimed that a keto diet can cure schizophrenia—an assertion that experts have quickly thrown cold water on. The ketogenic diet promotes fat-rich meals and low amounts of carbohydrates. While keto eating has skyrocketed in popularity in recent years—it ranked the most Googled diet in the U.S. in 2020—it was initially designed in the early 20th century for patients with epilepsy. More recent studies have confirmed that the diet is effective for certain types of epilepsy because it can control seizures. Meanwhile, we have much less evidence for its impacts on symptoms of schizophrenia. So far, small studies have offered some early evidence that ketogenic diets may help people with the condition. “There is currently no credible evidence that ketogenic diets cure schizophrenia,” Mark Olfson, a psychiatrist at Columbia University, told The New York Times. Kennedy also proclaimed that the diet can essentially cure bipolar disorder, according to studies he recently read. But as with schizophrenia, keto’s impacts on bipolar disorder have only been examined in limited numbers of patients so far. Preliminary findings have also hinted that a keto diet could ease symptoms of depression. It may offer “small antidepressant benefits” for people who don’t respond to medication, according to a recently published JAMA Psychiatry paper. But this work is in the early stages as well and remains far from conclusive. © 2026 NautilusNext Inc.

Keyword: Schizophrenia; Depression
Link ID: 30109 - Posted: 02.07.2026

By Ellen Barry A new analysis of birth cohorts in the Canadian province of Ontario has found a striking rise in the incidence of psychotic disorders among young people, a finding that its authors said could reflect teens’ increasing use of substances like cannabis, stimulants and hallucinogens. The study, published on Monday in The Canadian Medical Association Journal, found that the rate of new diagnoses of psychotic disorders among people ages 14 to 20 increased by 60 percent between 1997 and 2023, while new diagnoses at older ages plateaued or declined. Compared with people born in the late 1970s, those born in the early 2000s were about twice as likely to have been diagnosed with a psychotic disorder by age 20. The researchers included 12 million people born in Ontario between 1960 and 2009, of which 0.9 percent were diagnosed with a psychotic disorder during the study period. The study was epidemiological and did not try to identify a cause for the rising prevalence. There are a number of possible explanations, among them older paternal age, the stress of migration, neonatal health problems and early intervention programs that now regularly identify the disorders at younger ages, the authors note. But Dr. Daniel Myran, one of the study’s authors, said he undertook the study, in part, to follow up on concerns that the legalization of cannabis might increase population-level rates of schizophrenia and other psychotic disorders. “I was expecting to see some increases in these younger folks, but I was quite surprised by the scale,” said Dr. Myran, a family physician and research chair at North York General Hospital. He said the results suggested a need for more research into the impact of expanding cannabis use by young people. © 2026 The New York Times Company

Keyword: Schizophrenia; Drug Abuse
Link ID: 30106 - Posted: 02.04.2026

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

Keyword: Depression; Hormones & Behavior
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

Keyword: Depression; Drug Abuse
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

Keyword: Depression
Link ID: 30077 - Posted: 01.14.2026

By Diana Kwon edited by Jeanna Bryner By the time Maggie May, an Arkansas resident in her 30s, was admitted to a psychiatric clinic in 2024, she had been struggling for years with atypical anorexia nervosa, an eating disorder that leads to severe food restriction and profound disturbances in body image. (Her name has been changed for privacy.) She had already tried traditional interventions with a psychotherapist and a dietitian, but they had failed to improve her condition. So when May heard about a trial of a new and unconventional therapy, she jumped at the opportunity. The treatment was unusual in that alongside talk therapy, May underwent several sessions in a sensory-deprivation chamber: a dark, soundproof room where she floated in a shallow pool of water heated to match the temperature of her skin and saturated with Epsom salts to make her more buoyant. The goal was to blunt May’s external senses, enabling her to feel from within—focusing on the steady thudding of her heart, the gentle flow of air in and out of her lungs, and other internal bodily signals. The ability to connect with the body’s inner signals is called interoception. Some people are better at it than others, and one’s aptitude for it may change. Life events can also bolster or damage a person’s interoceptive skills. Sahib Khalsa, a psychiatrist and neuroscientist at the University of California, Los Angeles, and his colleagues think a disrupted interoception system might be one of the driving forces behind anorexia nervosa. So they decided to repurpose a decades-old therapy called flotation-REST (for “reduced environmental stimulation therapy”) and launched a trial with it in 2018. They hypothesized that in people with anorexia and some other disorders, an underreliance on internal signals may lead to an overreliance on external ones, such as how one looks in the mirror, that ultimately causes distorted body image, one of the key factors underlying these conditions. “When they’re in the float environment, they experience internal signals more strongly,” Khalsa says. “And having that experience may then confer a different understanding of the brain-body relationship that they have.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Schizophrenia; Anorexia & Bulimia
Link ID: 30067 - Posted: 01.03.2026

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.,

Keyword: Depression; Drug Abuse
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

Keyword: Depression; Pain & Touch
Link ID: 30051 - Posted: 12.17.2025

David Shariatmadari In 1973, an American psychologist called David Rosenhan published the results of a bold experiment. He’d arranged for eight “pseudo-patients” to attend appointments at psychiatric institutions, where they complained to doctors about hearing voices that said “empty”, “hollow” and “thud”. All were admitted, diagnosed with either schizophrenia or manic-depressive psychosis. They immediately stopped displaying any “symptoms” and started saying they felt fine. The first got out after seven days; the last after 52. Told of these findings, psychiatrists at a major teaching hospital found it hard to believe that they’d make the same mistake, so Rosenhan devised another experiment: over the next three months, he informed them, one or more pseudopatients would go undercover and, at the end, staff would be asked to decide who had been faking it. Of 193 patients admitted, 20% were deemed suspicious. It was then that Rosenhan revealed this had been a ruse as well: no pseudopatients had been sent to the hospital at all. Not only had doctors failed to spot sane people in their midst; they couldn’t reliably recognise the actually insane. Rosenhan’s gambit seized the public imagination. Were the men in white suits just quacks? Was mental illness even real? Two years later, the film One Flew Over the Cuckoo’s Nest added to the sense of reputational meltdown, and the psychiatric establishment responded with a major tightening up of diagnostic criteria, squeezing disparate symptoms into even tighter boxes. A freewheeling challenge to psychiatry ended up provoking a kind of counter-reformation, making the profession more medicalised than it had been for decades. The whole affair is a neat example of the ideological switchbacks Edward Bullmore maps in his fascinating, personally inflected history of psychiatric ideas. It is all the more mind-boggling – pun intended – when you find out Rosenhan’s paper was largely made up. Research by journalist Susannah Cahalan in 2019 concluded that most of the pseudopatients were invented; one colleague remembered the psychologist as a “bullshitter”. © 2025 Guardian News & Media Limited

Keyword: Schizophrenia
Link ID: 30050 - 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

Keyword: Depression
Link ID: 30047 - 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

Keyword: Drug Abuse; Depression
Link ID: 30042 - Posted: 12.06.2025

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

Keyword: Depression; Sexual Behavior
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.

Keyword: Depression
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

Keyword: Depression
Link ID: 29995 - Posted: 11.01.2025

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.

Keyword: Drug Abuse; Development of the Brain
Link ID: 29991 - 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.”

Keyword: Depression; Learning & Memory
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

Keyword: Depression
Link ID: 29983 - Posted: 10.25.2025

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

Keyword: Depression; Genes & Behavior
Link ID: 29958 - Posted: 10.08.2025

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

Keyword: Drug Abuse; Depression
Link ID: 29956 - Posted: 10.04.2025

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