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

Andrew Gregory Health editor Doing more than an hour of moderate intensity exercise each week may reduce the severity of “baby blues” and almost halve the risk of new mothers developing major clinical depression, the largest analysis of evidence suggests. However, researchers behind the study acknowledged that finding the time amid so many new responsibilities and challenges would not be easy, and recovery from childbirth should be prioritised. New mothers could restart exercise with “gentle” walks, which they could do with their babies, and then increase to “moderate” activity when they were ready, they added. This moderate physical activity could include brisk walking, water aerobics, stationary cycling or resistance training, according to the team of academics in Canada. Maternal depression and anxiety are relatively common after giving birth and associated with reduced self-care and compromised infant caregiving and bonding, which could in turn affect the child’s cognitive, emotional and social development, the researchers said. Conventional treatments for depression and anxiety in the first weeks and months after giving birth mostly involve drugs and counselling, which are often associated with, respectively, side-effects and poor adherence, and lack of timely access and expense. Research has previously shown that physical activity is an effective treatment for depression and anxiety in general. But until now it has not been known whether it could reduce the severity of the baby blues in the first few weeks after giving birth or lower the risk of major postpartum depression several months later. © 2024 Guardian News & Media Limited

Keyword: Depression; Hormones & Behavior
Link ID: 29548 - Posted: 11.09.2024

By Claire Murashima What do you think of when you hear the term “OCD”? In pop culture, people with obsessive-compulsive disorder are often portrayed as meticulous to an extreme degree. They’re highly organized, perfectionistic, or germophobic — like Jack Nicholson’s character in the film As Good As It Gets, who tosses out bars of soap after using them once. Depictions like that aren’t inaccurate, but they’re not the whole story. Research shows that 1 in 40 American adults have OCD or will develop it at some point in their lives, according to the International OCD Foundation. Although the term “OCD” is often used casually, the disorder must be diagnosed by a medical professional. We wanted to take a closer look at how people with OCD cope with it every day as OCD Awareness Month wraps up. I live with OCD, and it impacts just about every aspect of my life. Growing up, I had to say a prayer before I ate anything, because I thought I’d vomit if I didn’t. Later in life, I struggled with flying, because I feared that I might vomit on the plane, or that someone might vomit near me. The fear of vomiting is called emetophobia, and it’s a common symptom of OCD — though it’s not talked about as often. People with OCD can experience very specific intrusive thoughts known as obsessions, and then engage in compulsions, which are ritualized behaviors to address them, according to the International OCD Foundation. Anxiety can be the underlying emotion of OCD — but unlike generalized anxiety disorder, the underlying emotion could also be a sense of disgust, wrongness or incompleteness, according to Dr. Christopher Pittenger, the director of the Yale School of Medicine OCD Research Clinic. © 2024 npr

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 29536 - Posted: 11.02.2024

PA Media Digital characters – avatars – could help people with psychosis hear voices less often and reduce the distress caused, research suggests. The therapy involves a series of guided sessions during which patients are able to have a conversation with an animated digital representation of their distressing voice. Often in psychosis, as in other conditions, the voices people hear can be abusive or bullying and affect people’s day-to-day life. The voices can be experienced as powerful and almost omniscient, seeming to know what the person is thinking and feeling, and preventing them from taking the steps they want to every day. According to the research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, the avatar therapy using computer-generated animations is an effective way of helping people with psychosis who hear voices. Philippa Garety, professor emerita of clinical psychology at King’s IoPPN and the study’s lead author, said: “To our knowledge, this is the first therapeutic intervention that has a direct and sustained impact upon the frequency with which people hear voices. “This is an extremely important finding, as it is a clear priority for voice-hearers, and hearing fewer voices, less often, or voices going away altogether can have a hugely positive impact on their day-to-day lives. “People who hear voices rarely only hear one. In an interesting development, the extended version of the therapy proved effective at reducing voice frequency in total, despite participants only creating one avatar for one voice.” © 2024 Guardian News & Media Limited

Keyword: Schizophrenia
Link ID: 29531 - Posted: 10.30.2024

By Joshua Cohen The contagious nature of bacterial or viral infections like strep throat or influenza is well understood. You’re at risk of catching the flu, for example, if someone near you has it, as the virus can be spread by way of droplets in the air, among other modes of transmission. But what about a person’s mental health? Can depression be contagious? A JAMA Psychiatry paper published earlier this year seemed to suggest so. Researchers reported finding “an association between having peers diagnosed with a mental disorder during adolescence and an increased risk of receiving a mental disorder diagnosis later in life.” They suggested that, among adolescents, mental health disorders could be “socially transmitted,” though their observational study could not establish any direct cause. It makes some intuitive sense. Psychologists have studied how moods and emotions can spread from person to person. Someone howling with laughter might be contagious in the sense that it makes you laugh, too. Similarly, seeing a friend in emotional pain can evoke feelings of despair — a phenomenon termed emotional contagion. For more than three decades, researchers have investigated whether mental health disorders, too, may be induced by our social environment. Studies have found mixed results on the extent to which friends’, peers’, and families’ mental health can impact an individual’s mental health in turn. The JAMA Psychiatry study — conducted by researchers at the University of Helsinki and other institutions — analyzed nationwide registry data on 713,809 Finnish citizens born between 1985 to 1997. The research team identified individuals from schools across Finland who had been diagnosed with a mental disorder by the time they were in ninth grade. They followed the rest of the cohort to record later diagnoses, up until the end of 2019.

Keyword: Depression
Link ID: 29520 - Posted: 10.16.2024

By Brendan Borrell, Ellie Kincaid A psychiatry researcher who received a warning letter from the U.S. Food and Drug Administration earlier this year committed research misconduct, another federal watchdog found. Bret Rutherford, formerly a research psychiatrist at the New York State Psychiatric Institute and Columbia University, “engaged in research misconduct by recklessly falsely reporting that all human research subjects met the inclusion/exclusion criteria for late-life depression studies,” according to a case summary from the U.S. Office of Research Integrity (ORI) published today. As The Transmitter previously reported, a suicide that occurred during one of Rutherford’s trials in 2021 was followed by a suspension of his research a few months later. The U.S. Office of Human Research Protections subsequently halted all federally funded research involving human participants at the institute in June 2023 and launched a review of its research practices. The ORI’s findings detail how in five published papers, Rutherford reported that 45 research participants were eligible for clinical studies, when in fact they were taking antidepressants or other medications that should have excluded them from participation. Rutherford also included 15 participants who took medications during a 28-day washout period before the trial when they were not supposed to be taking the medications, and he reported full washout periods for 8 participants who underwent shorter periods. The false reporting affected “the reported clinical research methods and results” of the five articles, the ORI’s finding stated. Three of the articles have been retracted, and the other two have been corrected. The Transmitter previously reported on the corrections and two of the retractions, which reference protocol violations in a clinical trial of whether levodopa, a drug for Parkinson’s disease, could help older adults with depression. © 2024 Simons Foundation

Keyword: Depression
Link ID: 29509 - Posted: 10.09.2024

By Christina Caron It’s not uncommon for our minds to unleash a torrent of difficult feelings under the cover of darkness: sadness and negative thoughts may surface at night, making sleep hard to come by. On social media and elsewhere people often refer to this as “nighttime depression.” But is that really a thing? And if so, why do some people get blue at night? Feeling down after dusk doesn’t necessarily mean that you have a mental health condition, experts said. Understanding why it happens can help you take steps to feel better. What is nighttime depression? Nighttime depression is a colloquial term for depressive symptoms that either appear or worsen late at night. It is not itself a diagnosis. While anxiety can also ramp up at night, and tends to make people feel agitated, tense and restless, nighttime depression is best characterized as a low mood. “It’s a sense of sadness,” said Dr. Theresa Miskimen Rivera, a clinical professor of psychiatry at Rutgers University and president-elect of the American Psychiatric Association. “It’s that feeling of: There’s no joy. My life is so blah.” Nighttime depression can also feel uncomfortable — “not only in your mind, but in your body,” Dr. Rivera added, especially if these feelings interfere with getting enough sleep. © 2024 The New York Times Company

Keyword: Depression; Sleep
Link ID: 29506 - Posted: 10.05.2024

By Elie Dolgin The first schizophrenia medication in decades with a new mechanism of action won US regulatory approval today. The approval offers the hope of an antipsychotic that would be more effective and better tolerated than current therapies. The drug, known as KarXT, targets proteins in the brain known as muscarinic receptors, which relay neurotransmitter signals between neurons and other cells. Activating these receptors dampens the release of the chemical dopamine, a nervous-system messenger that is central to the hallmark symptoms of schizophrenia, such as hallucinations and delusions. But muscarinic signalling also modulates other brain circuits involved in cognition and emotional processing. This mode of action provides KarXT with a more comprehensive therapeutic effect than other schizophrenia treatments, which mainly blunt dopamine activity alone. In clinical trials, KarXT not only alleviated core symptoms of schizophrenia, but also showed signs of improving cognitive function, all while avoiding many of the burdensome side effects commonly associated with older antipsychotics. “This will be a revolution of the treatment of psychosis, and I’m not saying this lightly,” says Christoph Correll, a psychiatrist at the Zucker School of Medicine at Hofstra/Northwell in Hempstead, New York, who helped to analyse data from the trials. “Now we will now be able to treat people who haven’t been helped with traditional antipsychotics. That’s highly exciting.” KarXT is just the first of many next-generation drug candidates designed to engage muscarinic receptors in the brain. Several follow-on schizophrenia therapies are already in or nearing clinical trials, showing promise for improved tolerability and more convenient dosing schedules. This progress is leading clinicians and drug developers to imagine a future in which schizophrenia treatment becomes more tailored to individual needs — providing an alternative for the many people who don’t benefit from current therapies or abandon them owing to intolerable side effects. © 2024 Springer Nature Limited

Keyword: Schizophrenia
Link ID: 29498 - Posted: 09.28.2024

By Mariana Lenharo There’s a bar in Baltimore, Maryland, that very few people get to enter. It has a cocktail station, beer taps and shelves stacked with spirits. But only scientists or drug-trial volunteers ever visit, because this bar is actually a research laboratory. Here, in a small room at the US National Institutes of Health (NIH), scientists are harnessing the taproom ambience to study whether blockbuster anti-obesity drugs might also curb alcohol cravings. Evidence is mounting that they could. Animal studies and analyses of electronic health records suggest that the latest wave of weight-loss drugs — known as glucagon-like peptide 1 (GLP-1) receptor agonists — cut many kinds of craving or addiction, from alcohol to tobacco use. “We need randomized clinical trials as the next step,” says Lorenzo Leggio, an addiction researcher at the NIH in Baltimore. In the trial he is leading, volunteers sit at the bar and get to see, smell and hold their favourite drinks, while going through tests such as questions about their cravings; separately, participants will have their brains scanned while looking at pictures of alcohol. Some will be given the weight-loss drug semaglutide (marketed as Wegovy) and others will get a placebo. George Koob and Lorenzo Leggio pose for a photograph in a research laboratory designed as a bar inside the National Institutes of Health’s hospital. Curbing addiction isn’t the only potential extra benefit of GLP-1 drugs. Other studies have suggested they can reduce the risk of death, strokes and heart attacks for people with cardiovascular disease1 or chronic kidney ailments2, ease sleep apnoea symptoms3 and even slow the development of Parkinson’s disease4. There are now hundreds of clinical trials testing the drugs for these conditions and others as varied as fatty liver disease, Alzheimer’s disease, cognitive dysfunction and HIV complications (see ‘Diseases that obesity drugs might treat’ at the end of this article). © 2024 Springer Nature Limited

Keyword: Obesity; Drug Abuse
Link ID: 29494 - Posted: 09.25.2024

Natasha May Young people with severe depression experience disruptions in the way regions of their brain communicate with each other which are distinct from those observed in adults, a study has found. The research published on Tuesday in Nature Mental Health could be used to identify potential targets for brain stimulation therapies, extending their existing application from adults to youth. The study analysed the brain scans of 810 young people aged 12-25, of which 440 had major depressive disorder (MDD) and 370 were healthy comparison individuals. The study led by the University of Melbourne found that in those with MDD, some densely connected regions of the brain (known as hubs) showed stronger connectivity and others showed weaker connectivity compared with youth without depression. Young woman running at sunset on Australian beach Nutrition and exercise as good as therapy for mild and moderate depression, study says Prof Andrew Zalesky, the supervising researcher, said they found the connectivity was particularly strong in the part of the brain associated with someone’s internalised thoughts and rumination. “We see that in youth with depression, the default mode is more strongly connected, it’s more activated, which suggests that there is a greater focus on self-thought and self-reflection,” Zalesky said. The study, whose first author was third-year PhD student at the University of Melbourne, Nga (Connie) Yan Tse, also found the extent of these differences could reliably predict how severe a person’s depressive symptoms were. © 2024 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 29491 - Posted: 09.25.2024

By Christina Caron Julianna McLeod, 26, had her first psychotic episode while taking Vyvanse for attention deficit hyperactivity disorder last year. Ms. McLeod, who lives in Ontario, Canada, had taken the drug before but paused while pregnant with her first child and didn’t start taking it again until six months postpartum. Although the dose was 40 milligrams, she often forgot when she had last taken a pill. So she took one whenever she remembered — and may have ended up taking more than her prescribed daily dose. The delusions that she experienced made her feel euphoric and highly energetic. “I felt like my brain was exploding with connections,” she said. In her mind, she was a “super detective” who was uncovering the people and organizations that were secretly engaging in child sex trafficking. She even began to believe that someone was drugging her and her baby. Psychosis and mania are each known side effects of stimulant medications, and the Food and Drug Administration has added warnings to the medications’ labels saying that they may cause symptoms like hallucinations, delusional thinking or mania. But these side effects are considered rare — experienced by an estimated 1 in 1,000 patients — and have not been extensively researched. It can take months for someone to fully recover. A new study published on Thursday in The American Journal of Psychiatry suggests that dosage may play a role. It found that among people who took high doses of prescription amphetamines such as Vyvanse and Adderall, there was a fivefold increased risk of developing psychosis or mania for the first time compared with those who weren’t taking stimulants. The researchers defined a high dose as more than 40 milligrams of Adderall, 100 milligrams of Vyvanse or 30 milligrams of dextroamphetamine. The medium dosage (20 to 40 milligrams of Adderall, 50 to 100 milligrams of Vyvanse or 16 to 30 milligrams of dextroamphetamine) was associated with a 3.5 times higher risk of psychosis or mania. There was no increased risk of psychosis or mania among those who used methylphenidate drugs, like Concerta or Ritalin, regardless of the dose. © 2024 The New York Times Company

Keyword: ADHD; Schizophrenia
Link ID: 29478 - Posted: 09.14.2024

By Frieda Klotz For five years, Clare Dolman took lithium to manage her bipolar disorder. The medicine kept her happy and well with few side effects, and she described it as a wonder drug. But when she began to plan for a pregnancy, her psychiatrist advised her to go off the medication to protect the fetus. This was 1988, and it was the standard guidance at the time. While Dolman experienced some stresses during the pregnancy, her mood remained stable. But soon after giving birth, she began to experience mild hallucinations. “I thought, yes, there’s something wrong here,” she recalled. “But I had the insight still to see that I was getting ill, and my husband knew I was getting ill because he had seen me really bad.” She went on to spend five weeks in the hospital. Clare Dolman at the launch of the Bipolar Commission at the U.K. Parliament. Dolman, who has bipolar disorder, stopped taking lithium during her own pregnancies more than 30 years ago. She later became a mental health advocate and has studied the experiences of pregnant women with the illness. Visual: Courtesy of Clare Dolman Bipolar disorder involves extreme fluctuations in mood and is classified into different types according to symptoms and severity. For women with the condition, pregnancy can be a fraught endeavor as they balance the health of their growing fetus with their own mental state. Many, like Dolman, stop taking the medications that keep them well — which can lead to a recurrence of symptoms — and some avoid pregnancy altogether.

Keyword: Schizophrenia; Sexual Behavior
Link ID: 29475 - Posted: 09.11.2024

By Olivia Gieger Unlike traditional antidepressants, ketamine acts quickly to relieve depression symptoms, and its effects last long after the drug has cleared the system. Researchers have puzzled over what ketamine is doing in the brain to achieve these results. For one thing, the drug acts on N-methyl-D-aspartate (NMDA) glutamate receptors, which appear on neurons all over the brain. “Then the question is: Does the drug hit on all these brain regions simultaneously?” says Hailan Hu, professor of brain science at Zhejiang University. Or does it affect one region first, which sets off a series of downstream antidepressant effects? The answer is the latter, Hu and her colleagues report in a new study. Ketamine acts first on neurons in the lateral habenula, they found, in mice with depression-like symptoms. The structure—known as the “anti-reward” center—is hyperactive in people with depression and in mice modeling the condition, previous work has shown. That activity makes it highly susceptible to the drug’s effects, Hu and her colleagues discovered. Ketamine binds the NMDA receptors of cells in the lateral habenula and renders them inactive, which in turn interrupts downstream mechanisms of depression. The findings, published in Science in August, help explain how the known targets of ketamine are involved in such a rapid antidepressant response, explains Christophe Proulx, associate professor of psychiatry and neuroscience at Laval University. Proulx was not involved in the work but co-authored a Perspective article on it. Spotlighting the lateral habenula’s role also represents a new way of thinking about ketamine’s effects on depression—involving a shift away from a focus on weakened circuits and impaired plasticity, says Todd Gould, professor of psychiatry and neurobiology at the University of Maryland School of Medicine, who was not affiliated with the study. “[The work provides] additional strong evidence supporting a different view about how ketamine may be working.” Although ketamine inactivated NMDA receptors in the lateral habenula of the depressive-like mice, it had less impact in the CA1 region of the hippocampus, Hu and her colleagues observed using in-vitro slice electrophysiology and electrode recordings in awake animals. © 2024 Simons Foundation

Keyword: Depression
Link ID: 29472 - Posted: 09.11.2024

Nicola Davis Science correspondent Researchers have gained new insight into how and why some people experience depression after finding a particular brain network is far bigger in people living with the condition. The surface of the brain is a communication junction box at which different areas talk to each other to carry out particular processes. But there is a finite amount of space for these networks to share. Now researchers say that in people with depression, a larger part of the brain is involved in the network that controls attention to rewards and threats than in those without depression. “It’s taking up more real estate on the brain surface than we see is typical in healthy controls,” said Dr Charles Lynch, a co-author of the research, from Weill Cornell Medicine in New York. He added that expansion meant the size of other – often neighbouring – brain networks were smaller. Writing in the journal Nature, Lynch and colleagues report how they used precision functional mapping, a new approach to brain imaging that analyses a host of fMRI (functional MRI) scans from each individual. The team applied this method to 141 people with depression and 37 people without it, enabling them to measure accurately the size of each participant’s brain networks. They then took the average size for each group. They found that a part of the brain called the frontostriatal salience network was expanded by 73% on average in participants with depression compared with healthy controls. © 2024 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 29468 - Posted: 09.07.2024

By Jessica Silver-Greenberg and Katie Thomas Acadia Healthcare is one of America’s largest chains of psychiatric hospitals. Since the pandemic exacerbated a national mental health crisis, the company’s revenue has soared. Its stock price has more than doubled. But a New York Times investigation found that some of that success was built on a disturbing practice: Acadia has lured patients into its facilities and held them against their will, even when detaining them was not medically necessary. In at least 12 of the 19 states where Acadia operates psychiatric hospitals, dozens of patients, employees and police officers have alerted the authorities that the company was detaining people in ways that violated the law, according to records reviewed by The Times. In some cases, judges have intervened to force Acadia to release patients. Some patients arrived at emergency rooms seeking routine mental health care, only to find themselves sent to Acadia facilities and locked in. A social worker spent six days inside an Acadia hospital in Florida after she tried to get her bipolar medications adjusted. A woman who works at a children’s hospital was held for seven days after she showed up at an Acadia facility in Indiana looking for therapy. And after police officers raided an Acadia hospital in Georgia, 16 patients told investigators that they had been kept there “with no excuses or valid reason,” according to a police report. Acadia held all of them under laws meant for people who pose an imminent threat to themselves or others. But none of the patients appeared to have met that legal standard, according to records and interviews. Most doctors agree that people in the throes of a psychological crisis must sometimes be detained against their will to stabilize them and prevent harm. These can be tough calls, balancing patients’ safety with their civil rights. But at Acadia, patients were often held for financial reasons rather than medical ones, according to more than 50 current and former executives and staff members. © 2024 The New York Times Company

Keyword: Schizophrenia; Depression
Link ID: 29464 - Posted: 09.04.2024

By Elyse Weingarten In 2016, Canada enacted the Medical Assistance in Dying, or MAID, law, allowing individuals with a terminal illness to receive help from a medical professional to end their life. Following a superior court ruling, the legislation was expanded in 2021 to include nearly anyone with a “grievous and irremediable medical condition” causing “enduring physical or psychological suffering that is intolerable to them.” Whether mental illnesses such as depression, schizophrenia, and addiction should be considered “grievous and irremediable” quickly emerged as the subject of intense debate. Initially slated to go into effect in March 2023, a new mental health provision of the law was postponed a year due to public outcry both in Canada and abroad. Then, in February, Health Minister Mark Holland announced it had been delayed again — this time until 2027 — to allow more time for the country’s health care system to prepare. I was horrified by the news of the law’s latest expansion — a reaction that surprised me. Having grown up with a seriously mentally ill family member, I know first-hand how destructive mental illness can be, and I have no illusion that it is always treatable. Additionally, I support assisted suicide in cases of grave and terminal physical illness, so why do I find it so unacceptable to offer it to people who are intractably mentally ill? For nearly half a century, the Western understanding of mental illness has been shaped to adhere to the larger biomedical concepts of disease and wellness. Biological psychiatry, or the biomedical model, views mental illnesses as organically based disorders of the brain, physiologically indistinguishable from other diseases. The Canadian MAID law’s inclusion of mental illness is the culmination of this framework. Yet the widespread condemnation that the amendment received (that the bill’s previous iterations did not) demonstrates that mental and physical illness — though worthy of the same respect — are in no way equivalent, and that we can recognize this intuitively.

Keyword: Depression; Schizophrenia
Link ID: 29449 - Posted: 08.22.2024

By Sara Reardon Last week’s decision by the US Food and Drug Administration (FDA) to reject MDMA, also known as ecstasy, as a psychiatric treatment surprised many researchers. Lykos Therapeutics, the company that has been testing MDMA, plans to ask the FDA to reconsider the decision, but scientists are now wondering what the agency’s ruling will mean for other potential psychedelic therapies. In a press release posted on 9 August, Lykos, which is based in San Jose, California, said that the FDA had sent a letter requesting that the company undertake another large-scale trial of the drug in people with post-traumatic stress disorder (PTSD) and resubmit its application. “The FDA request for another study is deeply disappointing,” Lykos chief executive Amy Emerson said in the press release, adding that the company plans to work with the agency to “resolve scientific disagreements”. Conducting another study “would take several years”, she said, adding that Lykos has already addressed many of the FDA’s concerns. In an e-mail to Nature, Lykos declined to provide the complete letter detailing the agency’s specific concerns and directed the news team instead to its press release. Experts say that without access to the letter, it’s hard to determine why the FDA reached the decision it did. “We really are going off incomplete information,” says Mason Marks, who studies drug policy at Florida State University in Tallahassee, adding that he was “a little surprised” by the agency’s decision. Trial concerns But Marks points out that the FDA typically follows the advice of its independent advisory committees — and the one that evaluated MDMA in June overwhelmingly voted against approving the drug, citing problems with clinical trial design that the advisers felt made it difficult to determine the drug’s safety and efficacy. One concern was about the difficulty of conducting a true placebo-controlled study with a hallucinogen: around 90% of the participants in Lykos’s trials guessed correctly whether they had received the drug or a placebo, and the expectation that MDMA should have an effect might have coloured their perception of whether it treated their symptoms. © 2024 Springer Nature Limited

Keyword: Drug Abuse; Depression
Link ID: 29433 - Posted: 08.15.2024

By Sara Reardon Stress can make people feel sick, and bacteria in the gut might be to blame, according to a study1 in mice. The research suggests that a stressed brain directly shuts down specific glands in the gut, affecting gut bacteria and the body’s broader immune system. The study “is a technical tour de force”, says neuroscientist John Cryan at University College Cork in Ireland, who reviewed the study. Most work on the gut–brain connection has focused on how bacteria affect the brain, so Cryan welcomes research into how psychological states can exert ‘top-down’ control of bacteria. “It’s a really cool part of the puzzle”, he says. The research was published on 8 August in Cell. Researchers have long known that the gut and brain ‘talk’ to each other. Under stress, the brain spurs the release of hormones that can trigger gut conditions such as inflammatory bowel disease. And certain bacteria in the gut can release chemical signals that affect the brain and behaviour. Your brain could be controlling how sick you get — and how you recover But the neural communication pathways are less well understood. To find out more, neuroscientist Ivan de Araujo at the Max Planck Institute for Biological Cybernetics in Tübingen, Germany, and his colleagues focused on small organs called Brunner’s glands that are found in the walls of the small intestine. Little is known about these glands, other than that they produce mucus and contain numerous neurons. De Araujo’s team found that removing the Brunner’s glands of mice made the animals more susceptible to infection. It also raised markers of inflammation, a flood of immune chemicals and cells that can damage tissues. The team saw a similar effect in humans: people who’d had tumours removed from the part of the gut containing Brunner’s glands had higher levels of white blood cells — a marker of inflammation — than people who’d had tumours removed from other areas. © 2024 Springer Nature Limited

Keyword: Stress; Neuroimmunology
Link ID: 29432 - Posted: 08.13.2024