Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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By Diana Kwon Charlene Sunkel was 19 when she started hearing voices and strange thoughts began filling her head. People wanted to infiltrate her mind, to poison her, to rat her out to the police. She stopped making eye contact, convinced that it would enable others to steal her thoughts. Once sociable and outgoing, Sunkel withdrew from friends and family, worried that they were conspiring against her. On her way to work, she had visions of men in hoods from the corner of her eye. As the illness progressed, she lost the ability to understand what people were saying, and when she spoke, the words would not come out right. About a year after her symptoms started, Sunkel was diagnosed with schizophrenia. Delusions, hallucinations and disordered thinking are collectively known as psychosis. These “positive” symptoms are among the most widely recognized aspects of schizophrenia. For about two thirds of patients with schizophrenia—which affects approximately 23 million people around the world—traditional antipsychotic drugs are often highly effective at treating psychosis. But these drugs frequently come with problematic side effects. And they do little to help with the so-called negative symptoms of schizophrenia, such as emotional flatness and social withdrawal, or with other issues involving thinking and memory referred to as cognitive problems. Until quite recently, all antipsychotics worked in essentially the same way. They blocked the activity of dopamine, a chemical messenger in the brain involved in motivation, learning, habit formation, and other processes. The successful treatment of psychosis with dopamine blockers led many clinicians to believe that they understood schizophrenia and that its underlying cause was an imbalance in dopamine. When a particular antipsychotic did not work in a patient, all doctors needed to do, they thought, was up the dosage or try another dopamine-targeting drug. But the arrival last September of a new drug, KarXT, supports an emerging awareness among clinicians that schizophrenia is more complex than most of them had realized. KarXT is the first antipsychotic to target a molecule other than dopamine. © 2024 SCIENTIFIC AMERICAN,

Keyword: Schizophrenia
Link ID: 29711 - Posted: 03.19.2025

By Ellen Barry On a recent Friday morning, Daniel, a lawyer in his early 40s, was in a Zoom counseling session describing tapering off lithium. Earlier that week he had awakened with racing thoughts, so anxious that he could not read, and he counted the hours before sunrise. At those moments, Daniel doubted his decision to wean off the cocktail of psychiatric medications which had been part of his life since his senior year in high school, when he was diagnosed with bipolar disorder. Was this his body adjusting to the lower dosage? Was it a reaction to the taco seasoning he had eaten the night before? Or was it what his psychiatrist would have called it: a relapse? “It still does go to the place of — what if the doctors are right?” said Daniel. On his screen, Laura Delano nodded sympathetically. Ms. Delano is not a doctor; her main qualification, she likes to say, is having been “a professional psychiatric patient between the ages of 13 and 27.” During those years, when she attended Harvard and was a nationally ranked squash player, she was prescribed 19 psychiatric medications, often in combinations of three or four at a time. Then Ms. Delano decided to walk away from psychiatric care altogether, a journey she detailed in a new memoir, “Unshrunk: A Story of Psychiatric Treatment Resistance.” Fourteen years after taking her last psychotropic drug, Ms. Delano projects a radiant good health that also serves as her argument — living proof that, all along, her psychiatrists were wrong. Since then, to the alarm of some physicians, an online DIY subculture focused on quitting psychiatric medications has expanded and begun to mature into a service industry. © 2025 The New York Times Company

Keyword: Schizophrenia
Link ID: 29710 - Posted: 03.19.2025

By Meghan Rosen and Laura Sanders Millions of Americans take antidepressants to help manage everything from depression and anxiety to post-traumatic stress disorder. Now, the Trump administration has announced that these drugs, which have been in use for decades and gone through rigorous testing, will be subject to new scrutiny. Invoking a burden of chronic disease, including in children, the administration has pledged to, in its words, “assess the prevalence of and threat posed by” certain commonly prescribed medications. In the coming months, its “Make America Healthy Again” commission plans to review a slew of existing medications, including SSRIs, or selective serotonin reuptake inhibitors. More than 10 percent of U.S. adults took antidepressants over the previous 30 days, data from 2015 to 2018 show. And SSRIs are among the most widely prescribed of those drugs. U.S. Health and Human Services Secretary Robert F. Kennedy Jr. has long questioned the safety of antidepressants and other psychiatric medicines, making misleading and unsubstantiated claims about the drugs. For instance, as recently as his January confirmation hearings, he likened taking SSRIs to having a heroin addiction. He also has suggested — without evidence — that SSRIs play a role in school shootings. With the executive order and statements like these, “it’s implied there is something nefarious or harmful” about antidepressants and related medications, says Lisa Fortuna, chair of the American Psychiatric Association’s Council on Children, Adolescents and Their Families. “People may think that they’re dangerous drugs.” © Society for Science & the Public 2000–2025

Keyword: Depression; Sexual Behavior
Link ID: 29701 - Posted: 03.12.2025

By Pam Belluck Postpartum depression affects about one in every seven women who give birth, but little is known about what happens in the brains of pregnant women who experience it. A new study begins to shed some light. Researchers scanned the brains of dozens of women in the weeks before and after childbirth and found that two brain areas involved in the processing and control of emotions increased in size in women who developed symptoms of postpartum depression. The results, published Wednesday in the journal Science Advances, constitute some of the first evidence that postpartum depression is associated with changes in the brain during pregnancy. Researchers found that women with symptoms of depression in the first month after giving birth also had increases in the volume of their amygdala, a brain area that plays a key role in emotional processing. Women who rated their childbirth experience as difficult or stressful — a perception that is often associated with postpartum depression — also showed increases in the volume of the hippocampus, a brain area that helps regulate emotions. “This is really the first step in trying to understand how does the brain change in people who have a normal course of pregnancy and then those who experience perinatal depression, and what can we do about it,” said Dr. Sheila Shanmugan, an assistant professor of psychiatry, obstetrics-gynecology and radiology at the University of Pennsylvania who was not involved in the study. “The big takeaways are about how there are these really profound brain changes during pregnancy and how now we’re seeing it in depression circuitry specifically,” she said. The study was conducted in Madrid by a team that has led efforts to document the effects of pregnancy on the brain. It is part of a growing body of research that has found that certain brain networks, especially those involved in social and emotional processing, shrink during pregnancy, possibly undergoing a fine-tuning process in preparation for parenting. Such changes correspond with surges in pregnancy hormones, especially estrogen, and some last at least two years after childbirth, researchers have found. © 2025 The New York Times Company

Keyword: Hormones & Behavior; Depression
Link ID: 29699 - Posted: 03.08.2025

By Sydney Wyatt Numerous actions by the Trump administration over the past month have caused confusion and fear throughout the U.S. scientific community. In response, a group called Stand Up for Science, which says it opposes attacks on science and on efforts to improve diversity, equity and inclusion (DEI) in research, has planned rallies on 7 March in Washington, D.C., and across the United States. “The biggest thing for us is that science is for everyone, in that it benefits every person,” says rally co-organizer Colette Delawalla, a graduate student in clinical psychology at Emory University. “It doesn’t matter who you voted for. It doesn’t even matter if you voted or not.” The event is reminiscent of the 2017 March for Science, which drew more than 1 million attendees in 600 cites around the world to show support for scientific research and protest proposed budget cuts to the U.S. National Institutes of Health and other federal agencies during Donald Trump’s first term as president. Scientists were divided in their views about that march, with some criticizing it for a lack of concrete goals and others saying it engaged more people with science and policy than ever before. This year is no different. Some scientists say protests do little to change minds, whereas others say it can raise awareness. The effectiveness of a protest depends on several factors, including the clarity of its goals, the scope of the target audience, the tactics used and whether the movement continues after the initial event, says Susan Olzak, professor emerita of sociology at Stanford University. “Temporary, fleeting protests are not likely to have much of an effect on anything, but if you have a sustained campaign, then you’re more likely to have some kind of impact, even if it’s just on public opinion,” Olzak says. © 2025 Simons Foundation

Keyword: Miscellaneous
Link ID: 29693 - Posted: 03.05.2025

By Jennifer Couzin-Frankel Sign up for a clinical trial of a psychedelic drug and you’re agreeing to a potentially bizarre experience. “All of a sudden, your dead grandma or Satan is in front of you,” says psychiatrist Charles Raison of the University of Wisconsin–Madison. Some think this consciousness-altering “trip” underlies the potential benefits of drugs such as psilocybin and LSD, which are under study to treat depression, trauma, chronic pain, and more. But the trip can also be a roadblock to assessing the drugs’ effects, making it near-impossible to conceal who is getting an active substance and who’s been assigned to placebo—a trial strategy called blinding that aims to keep participants’ expectations from skewing their response to a drug. This “functional unblinding” is not unique to psychedelics, but it’s especially pronounced in this drug class. The U.S. Food and Drug Administration (FDA) has expressed concern about the issue in psychedelic trials. And it was among the critiques FDA advisers leveled at Lykos Therapeutics, whose application for MDMA to treat post-traumatic stress disorder (PTSD) FDA rejected last summer. Now, scientists and companies are experimenting with trial designs meant to shield participants from recognizing what they’re getting, or to separate expectations from the drug’s impact on health. These include incorporating a range of doses; giving the drug, with permission, to people who are asleep; and misleading participants about how a trial is set up. Companies running large-scale psychedelic trials mostly view unblinding as inevitable. Participants “are going to feel” the drug, “that’s just how it is,” says Rob Barrow, CEO of MindMed, which has late-stage trials underway to test LSD’s ability to ease anxiety. But he believes there are ways to parse a drug’s efficacy even if people know they’re getting it. In one recent trial, MindMed recruited 198 people with anxiety, giving some a placebo and the others LSD at one of four doses. Virtually all who received active drug correctly guessed that they’d gotten it. But those on the two higher doses saw clinically meaningful reduced anxiety, whereas those on the lower doses didn’t. That split means the benefit “has to be due to something other than thinking you’re getting drug,” Barrow says. MindMed is using a lower, nontherapeutic dose as well as a higher dose in an ongoing phase 3 trial, and hopes to report results next year.

Keyword: Depression; Drug Abuse
Link ID: 29691 - Posted: 03.05.2025

By Ellen Barry The Food and Drug Administration has taken a crucial step toward expanding access to the antipsychotic medication clozapine, the only drug approved for treatment-resistant schizophrenia, among the most devastating of mental illnesses. The agency announced on Monday that it was eliminating a requirement that patients submit blood tests before their prescriptions can be filled. Clozapine, which was approved in 1989, is regarded by many physicians as the most effective available treatment for schizophrenia, and research shows that the drug significantly reduces suicidal behavior. Clozapine is also associated with a rare side effect called neutropenia, a drop in white blood cell counts that, in its most severe form, can be life-threatening. In 2015, federal regulators imposed a regimen known as risk evaluation and mitigation strategies, or REMS, that required patients to submit to weekly, biweekly and monthly blood tests that had to be uploaded onto a database and verified by pharmacists. Physicians have long complained that, as a result, clozapine is grossly underutilized. Dr. Frederick C. Nucifora, director of the Adult Schizophrenia Clinic at the Johns Hopkins School of Medicine, said he believed that around 30 percent of patients with schizophrenia would benefit from clozapine — far more than the 4 percent who currently take it. “I have had many patients who were doing terribly, who struggled to function outside the hospital, and cycled through many medications,” he said. “If they go on clozapine, they really tend to not be hospitalized again. I’ve had people go on to finish college and work. It’s quite remarkable.” © 2025 The New York Times Company

Keyword: Schizophrenia
Link ID: 29683 - Posted: 02.26.2025

By Laura Sanders Depression can affect not just the mind, but the body, too. Inner experiences of mental struggles are private. But in this episode, Jon Nelson and another volunteer, Amanda, let listeners in. Woven into their stories is a brief history of deep brain stimulation, the experimental treatment that involves permanent brain implants. You’ll hear how that research — with its ups and downs — carried the experiments to where they are today. Laura Sanders: This episode deals with mental illness, depression, and suicide. Please listen with care. Previously on The Deep End: Support Science Today. Barbara: He would be up in bed with the lights out or watching like endless hours of television and it was very unpredictable and then there’s a whole life going on downstairs. Jon: That isolation, there’s a little bit of lying involved because you just wanna get out of things, right? Mayberg: I think part of why this kind of treatment resistant depression is so painful and so associated with high rates of suicide, is that you’re suffering. You know exactly what you’re trying to get away from and you can’t move. And if you do move, it follows you. There’s no relief. Jon: I’d be the one standing up in front of everybody leading the champagne toast, and then I’d be driving home and wanting to slam my car into a tree. Sanders: Today we’re going to get into some heavy stuff, but there’s light at the end, I promise. We’re going to pull back the curtain on what depression can do to the body and to the brain. Maybe you know that feeling firsthand. If you don’t, you probably know somebody who does. You’ll also hear the backstory of some people who volunteered for the experiment and the backstory of the science itself. I’m Laura Sanders. Welcome to The Deep End. © Society for Science & the Public 2000–2025.

Keyword: Depression
Link ID: 29676 - Posted: 02.19.2025

By Georgia E. Hodes Psychiatric conditions have long been regarded as issues of “mental health,” a term that inherently ties our understanding of these disorders to the brain. But the brain does not exist in a vacuum. Growing evidence over the past 10 years highlights a link between the body and what we think of as mental health. Many studies, for example, report that the peripheral immune system is altered in people who experience neurological and psychiatric conditions, including mood disorders, anxiety and schizophrenia. Researchers traditionally assumed that peripheral inflammation was a downstream effect of these conditions, but basic research is now revealing that the immune system, the gut microbiome and peripheral inflammation are not just bystanders or results of psychiatric conditions—they are active participants and may hold the key to new treatments. Scientists are beginning to uncover the mechanisms by which the body influences the brain, challenging the notion that mental health is solely a matter of brain chemistry and reshaping ideas on the etiology of psychiatric disorders. Like other neuroscience groups, we started our work in this area with the “brain-first” perspective: the idea that immune changes in the brain trigger stress-induced changes in behavior and peripheral inflammation. Our earliest studies supported this idea, demonstrating that directly infusing an inflammatory molecule, the cytokine interleukin 6 (IL6), into an area of the brain associated with reward behavior made male mice more likely to avoid others. Our later work, however, found that the source of IL6 in the brain is actually peripheral immune cells. Either stopping the immune cells from producing this molecule or just blocking it from entering the brain made the animals resilient to social stress. These studies offered some of the first evidence that treating the body with a compound that does not cross the blood brain-barrier could prevent a brain-mediated behavior. Before this, blood markers were considered only indirect indicators of brain changes—and not direct mediators or potential targets for treatment. © 2025 Simons Foundation

Keyword: Depression; Stress
Link ID: 29670 - Posted: 02.12.2025

By Laura Sanders Meet Jon Nelson. He’s a dad, a husband, a coach and a professional who works in marketing. But underneath it all, he suffered – for years – from severe depression. His suffering was so great that he volunteered for an experimental treatment called deep brain stimulation, in which electrodes are permanently implanted in his brain. In this episode, you’ll hear from Jon about his life before the surgery, and you’ll be introduced to the neuroscience designed to save him. Laura Sanders: This podcast touches on mental illness, depression, and suicide. There are moments of darkness. There are moments of lightness, too. Please keep that in mind before you listen. Jon Nelson is a guy who’s probably a lot like a guy you know. He lives in Newtown, a picturesque small town northeast of Philadelphia. He has three kids, a loving wife, a dog, a cat, and a bearded dragon named Lizzie. He works in marketing. He coaches his kids in softball and hockey, and he’s a ride-or-die Steelers fan. The Nelsons are, in fact, so perfect that they’re almost a caricature, like a sitcom family with a zany dad who’s fond of the phrase, “I’m going to give you some life advice.” Jon Nelson: You know, we try to do the standard sit down and cook together and have meals together. We’re the messy house in the neighborhood with basketballs outside and, you know, we’re constantly playing and doing stuff like that. But, you know, truly we like to spend time together. Sanders: But the view from the outside was a lot different than what Jon felt on the inside. On the outside, Jon lived a charmed life, but inside, he had been fighting with everything he had to stay alive for years. Jon: I would literally read a newspaper article about a plane wreck and I would have instantaneous, like, “Oh, like why couldn’t I have been on that?” Right? Or, you know, you, somebody died in a car wreck, like, “Why couldn’t that have been me?” © Society for Science & the Public 2000–2025

Keyword: Depression
Link ID: 29668 - Posted: 02.12.2025

By Andrew Jacobs and Rachel Nuwer After more than three decades of planning and a $250 million investment, Lykos Therapeutics’ application for the first psychedelic drug to reach federal regulators was expected to be a shoo-in. Lykos, the corporate arm of a nonprofit dedicated to winning mainstream acceptance of psychedelics, had submitted data to the Food and Drug Administration showing that its groundbreaking treatment for post-traumatic stress disorder — MDMA plus talk therapy — was significantly more effective than existing treatments. At a pivotal public hearing last summer, two dozen scientists, doctors and trauma survivors told an F.D.A. advisory panel how MDMA-assisted therapy had brought marked relief from a mental health condition associated with high rates of suicide, especially among veterans. Then came skeptics with disturbing accusations: that Lykos was “a therapy cult,” that practitioners in its clinical trials had engaged in widespread abuse of participants and that the company had concealed a litany of adverse events. “The most significant harms in Lykos’s clinical trials were not caused by MDMA, but by the people who were entrusted to supervise its administration,” Neşe Devenot, one of the speakers opposed to Lykos’s treatment and a writing instructor at Johns Hopkins University, told the committee. Dr. Devenot and six others presented themselves as experts in the field of psychedelics, but none had expertise in medicine or therapy. Nor had the speakers disclosed their connection to Psymposia, a leftist advocacy group whose members oppose the commercialization of psychedelics and had been campaigning against Lykos and its nonprofit parent, the Multidisciplinary Association for Psychedelic Studies, or MAPS. The critics did not provide evidence to back their claims of systematic wrongdoing, but when the votes were counted that day, the panel overwhelmingly rejected Lykos’s application. Before voting, panelists cited a number of concerns, among them MDMA’s potential effects on the heart and liver, and whether trial results were influenced by the fact that most study participants correctly guessed they had received the drug and not a placebo. © 2025 The New York Times Company

Keyword: Drug Abuse; Depression
Link ID: 29659 - Posted: 02.05.2025

By Laura Sanders Brain implants for depression: It sounds like science fiction but it’s real. The Deep End, a new podcast from Science News, will give you a glimpse of what it’s like to live with electrodes in your brain. It might change how you think about mental health, the brain and what makes you you. Transcript Laura Sanders: Inside your brain, there are billions of nerve cells that form trillions of connections. These connections make your thoughts, movements, emotions, and memories. Your first kiss, your favorite song, your dreams. Our brains make us who we are. But sometimes they can betray us. Support Science Today. Thank you for being a subscriber to Science News! Interested in more ways to support STEM? Consider making a gift to our nonprofit publisher, the Society for Science, an organization dedicated to expanding scientific literacy and ensuring that every young person can strive to become an engineer or scientist. Donate Now This is a story about four people whose brains turned against them, plunging their lives into the darkness of severe depression. This is also a story about an experiment designed to pull them back out. Amanda: My initial response was a little bit of skepticism, like, “OK, we’re gonna put a box in you, we’re gonna hook it up to some wires, we’re gonna shove them down in your brain and then electrocute you, and it’s gonna make you feel great.” Like, this doesn’t seem like a, like a safe thing to be doing. Sanders: This experiment sounds like science fiction, but it’s real. This is the Deep End, a new podcast from Science News. I’m Laura Sanders. On this podcast, you’ll hear what led people to sign up for this unconventional experiment and what it was like for them. © Society for Science & the Public 2000–202

Keyword: Depression
Link ID: 29655 - Posted: 02.05.2025

Hannah Devlin Science correspondent A groundbreaking NHS trial will attempt to boost patients’ mood using a brain-computer-interface that directly alters brain activity using ultrasound. The device, which is designed to be implanted beneath the skull but outside the brain, maps activity and delivers targeted pulses of ultrasound to “switch on” clusters of neurons. Its safety and tolerability will be tested on about 30 patient in the £6.5m trial, funded by the UK’s Advanced Research and Invention Agency (Aria). In future, doctors hope the technology could revolutionise the treatment of conditions such as depression, addiction, OCD and epilepsy by rebalancing disrupted patterns of brain activity. Jacques Carolan, Aria’s programme director, said: “Neurotechnologies can help a much broader range of people than we thought. Helping with treatment resistant depression, epilepsy, addiction, eating disorders, that is the huge opportunity here. We are at a turning point in both the conditions we hope we can treat and the new types of technologies emerging to do that.” The trial follows rapid advances in brain-computer-interface (BCI) technology, with Elon Musk’s company Neuralink launching a clinical trial in paralysis patients last year and another study restoring communication to stroke patients by translating their thoughts directly into speech. However, the technologies raise significant ethical issues around the ownership and privacy of data, the possibility of enhancement and the risk of neuro-discrimination, whereby brain data might be used to judge a person’s suitability for employment or medical insurance. © 2025 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 29637 - Posted: 01.22.2025

By Christina Caron Barrie Miskin was newly pregnant when she noticed her appearance was changing. Dark patches bloomed on her skin like watercolor ink. A “thicket” of hairs sprouted on her upper lip and chin. The outside world was changing, too: In her neighborhood of Astoria, Queens, bright lights enveloped objects in a halo, blurring her vision. Co-workers and even her doctors started to seem like “alien proxies” of themselves, Ms. Miskin, 46, said. “I felt like I was viewing the world through a pane of dirty glass,” she added. Yet Ms. Miskin knew it was all an illusion, so she sought help. Welcome to Psych 101, a new monthly column that explores mental health terms and trends that are worthy of a bigger conversation. If there is a subject you’d like to see covered, please drop us a line at Psych101@nytimes.com. It took more than a year of consulting with mental health specialists before Ms. Miskin finally found an explanation for her symptoms: She was diagnosed with a dissociative condition called depersonalization/derealization disorder, or D.D.D. Before her pregnancy, Ms. Miskin had stopped taking antidepressants. Her new psychiatrist said the symptoms could have been triggered by months of untreated depression that followed. While Ms. Miskin felt alone in her mystery illness, she wasn’t. Tens of thousands of posts on social media reference depersonalization or derealization, with some likening the condition to “living in a movie or a dream” or “observing the world through a fog.” People who experience depersonalization can feel as though they are detached from their mind or body. Derealization, on the other hand, refers to feeling detached from the environment, as though the people and things in the world are unreal. Those who are living with D.D.D. are “painfully aware” that something is amiss, said Elena Bezzubova, a psychoanalyst who specializes in treating the condition. It’s akin to seeing an apple and feeling that it is so strange it doesn’t seem real, even though you know that it is, she added. The disorder is thought to occur in about 1 to 2 percent of the population, but it’s possible for anyone to experience fleeting symptoms. © 2025 The New York Times Company

Keyword: Attention
Link ID: 29623 - Posted: 01.11.2025

Jon Hamilton A single dose of the anesthetic ketamine can provide weeks of relief from severe depression. One reason may be that the drug causes long-term changes to a brain circuit involved in "giving up," a team reports in the journal Neuron. The team found that in zebrafish, ketamine alters this circuit in a way that causes the fish to persevere in the face of adversity rather than becoming passive. This resilience appears linked to brain cells called astrocytes, which play a central role in the "giving up" circuit. "Something happens within those cells that changes their response" to adversity, says Misha Ahrens, an author of the study and a senior group leader at HHMI's Janelia Research Campus. "We don't know what that is yet." But if scientists can figure it out, they might be able to develop more effective versions of ketamine and other psychiatric drugs, Ahrens says. The research involved the larval zebrafish, which is smaller than a grain of rice and looks like a tadpole. "It's transparent, so you can basically see what's going on in the entire brain all at once," says Alex Chen of Harvard University, another member of the team. For the experiment, the fish had to be kept stationary so scientists could monitor its brain. "But we still want it to feel like it's swimming through a virtual world," Chen says. The team did this by projecting images indicating forward movement when the animal swished its tail. Then they switched to images showing no progress, no matter what the fish did. © 2025 npr

Keyword: Depression
Link ID: 29617 - Posted: 01.08.2025

By Ellen Barry Kevin Lopez had just stepped out of his house, on his way to meet his girlfriend for Chinese food, when it happened: He began to hallucinate. It was just a flicker, really. He saw a leaf fall, or the shadow of a leaf, and thought it was the figure of a person running. For a moment, on a clear night last month, this fast-moving darkness seemed to hurtle in his direction and a current of fear ran through him. He climbed into the car, and the door shut and latched behind him with a reassuring thunk. “It’s nothing,” he said. “I don’t know why — I think there’s a person there.” Light had always caused problems for Kevin when symptoms of schizophrenia came on. He thought that the lights were watching him, like an eye or a camera, or that on the other side of the light, something menacing was crouched, ready to attack. But over time, he had found ways to manage these episodes; they passed, like a leg cramp or a migraine. That night, he focused on things that he knew were real, like the vinyl of the car seat and the chill of the winter air. He was dressed for a night out, with fat gemstones in his ears, and had taken a break from his graduate coursework in computer science at Boston University. A “big bearish, handsome nerd” is the way he styled himself at 24. For the past four years, Kevin has been part of a living experiment. Shortly after he began hallucinating, during his junior year at Syracuse University, his doctors recommended him for an intensive, government-funded program called OnTrackNY. It provided him with therapy, family counseling, vocational and educational assistance, medication management and a 24-hour hotline. © 2025 The New York Times Company

Keyword: Schizophrenia; Stress
Link ID: 29614 - Posted: 01.04.2025

By Dave Philipps A van full of U.S. Special Operations veterans crossed the border into Mexico on a sunny day in July to execute a mission that, even to them, sounded pretty far out. Listen to this article with reporter commentary Over a period of 48 hours, they planned to swallow a psychedelic extract from the bark of a West African shrub, fall into a void of dark hallucinations and then have their consciousness shattered by smoking the poison of a desert toad. The objective was to find what they had so far been unable to locate anywhere else: relief from post-traumatic stress disorder and traumatic brain injury symptoms. “It does sound a little extreme, but I’ve tried everything else, and it didn’t work,” said a retired Army Green Beret named Jason, who, like others in the van, asked that his full name not be published because of the stigma associated with using psychedelics. A long combat career exposed to weapons blasts had left him struggling with depression and anger, a frayed memory and addled concentration. He was on the verge of divorce. Recently, he said, he had put a gun to his head. “I don’t know if this will work,” Jason said of psychedelic therapy. “But at this point, I have nothing to lose.” Psychedelic therapy trips like this are increasingly common among military veterans. For years, psychedelic clinics in Mexico were a little-known last-ditch treatment for people struggling with drug addiction. More recently, veterans have found that they also got lasting relief from mental health issues they had struggled with since combat. No one tracks how many veterans seek psychedelic treatment in Mexico. Clinic owners estimate they now treat a few thousand American veterans a year, and say the number is steadily growing. Many of the veterans have free access to the U.S. veterans’ health care system but find standard treatments for combat-related mental health issues to be ineffective. The Department of Veterans Affairs announced this month that, for the first time in more than 50 years, it would fund research into psychedelic therapy. But while the research is conducted, the treatments will remain inaccessible to most veterans, perhaps for years. © 2024 The New York Times Company

Keyword: Stress; Drug Abuse
Link ID: 29608 - Posted: 12.21.2024

7 Things Everyone Should Know About Antidepressants By Christina Caron Even if you’ve never taken an antidepressant, you’re probably familiar with the criticism and controversy that surrounds these drugs. It’s not uncommon to hear things like: “Those pills are just a placebo.” “You’ll definitely gain weight.” “Once you start, you’ll become dependent on them.” Is any of this true? Some of these statements have “a kernel of truth,” said Dr. Gerard Sanacora, a professor of psychiatry at the Yale School of Medicine. And it’s important to set the record straight because the expectations people have about their treatment — whether good or bad — “really do play a large role in how the treatment actually unfolds,” he added. Dr. Sanacora and other experts addressed some common questions and misconceptions about antidepressants. Will antidepressants change who I am? When an antidepressant starts to work, you may feel like a different person in some ways, said Naomi Torres-Mackie, a clinical psychologist in New York City. “Picture this giant, dark cloud weighing you down — as that lifts, the world is going to look different,” she said, adding: “But as you get used to it, you may see that it actually allows you to have more joy in your life.” On the other hand, up to half of people who take antidepressants may experience some degree of emotional blunting or numbed emotions, and research suggests that the blunting is more likely to happen with a higher medication dosage. When antidepressants are working correctly, patients should still feel a range of emotions, even if the sadness they used to feel every day is gone, said Dr. Laine Young-Walker, chair of the department of psychiatry at the University of Missouri School of Medicine. © 2024 The New York Times Compan

Keyword: Depression
Link ID: 29593 - Posted: 12.11.2024

By Max Kozlov Joylessness triggered by stress creates a distinct brain signature, according to research in mice1. The study also reveals one brain pattern that seems to confer resilience to stress — and another that makes stressed animals less likely to feel pleasure, a core symptom of depression. These findings, published today in Nature, offer clues as to how the brain gives rise to anhedonia, a resistance to enjoyment and pleasure. The results also provide a new avenue for treating the condition — if the findings are validated in humans. “Their approach in this study is spot on,” says Conor Liston, a neuroscientist at Weill Cornell Medicine in New York City, who was not involved in the work. The experiments fill “a big gap”, he says. “Anhedonia is something we don’t understand very well.” More than 70% of people with severe depression experience anhedonia, which is also common in those with schizophrenia, Parkinson’s disease and other neurological and psychiatric conditions. The symptom is notoriously difficult to treat, even in those taking medication, Liston says. “Anhedonia is something that patients care about the most, and feel like it’s least addressed by current treatments,” he says. To understand how the brain gives rise to anhedonia, Mazen Kheirbek, a systems neuroscientist at the University of California, San Francisco, and his colleagues studied mice that had been placed under stress by exposure to larger, more aggressive mice. Typically, mice have a sweet tooth and prefer sugar water over plain water if given the option. But some stressed mice instead preferred plain water — which Kheirbek and his colleagues interpreted as a rodent version of anhedonia. Other mice subjected to the same stress preferred the sugar water. The authors labelled these animals ‘resilient’. © 2024 Springer Nature Limited

Keyword: Stress; Depression
Link ID: 29592 - Posted: 12.07.2024

By Diana Kwon Since a schizophrenia drug, the first in decades with an innovative mechanism of action, gained US regulatory approval in September, some researchers have proclaimed a new era for psychiatric medicine. About half a dozen similar drugs — for schizophrenia, Alzheimer’s disease and other conditions involving the brain — are in various stages of development, most in early-stage clinical trials. But the success of these medicines is not a given. Last week, a trial of a highly anticipated schizophrenia drug reported disappointing results. For decades, schizophrenia drugs worked in essentially the same way. They blunted the activity of dopamine, a chemical involved in the disorder’s hallmark symptoms, such as hallucinations and delusions. The new kid on the block is KarXT, sold as Cobenfy. It targets muscarinic receptors and leads to antipsychotic and cognitive benefits. “I don’t think I’ve ever seen this much buzz and excitement over a new approach in psychiatry in my career,” says Jeffrey Conn, a pharmacologist at Vanderbilt University in Nashville, Tennessee, who was one of the company’s scientific co-founders. KarXT’s success in winning US regulatory approval has revived interest in muscarinic drugs. “Drug discovery is coming back to psychiatry,” says Arthur Christopoulos, a molecular pharmacologist at Monash University in Melbourne, Australia, who was involved in the development of KarXT. But developing new medicines is a hard, long road. On 11 November, Abbvie, a pharmaceutical company in North Chicago, Illinois, announced that its muscarinic drug for schizophrenia, called emraclidine, had failed to outperform a placebo. What this means for other muscarinic drugs in development remains to be seen, Christopoulos says. “It is still early days.” © 2024 Springer Nature Limited

Keyword: Schizophrenia
Link ID: 29574 - Posted: 11.23.2024