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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

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 29701 - Posted: 03.12.2025

Psychedelic drug studies face a potent source of bias: the ‘trip’

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.

Related chapters from BN: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: Development of the Brain; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29691 - Posted: 03.05.2025

‘It felt like dread.’ Hear what severe depression can do to people

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.

Rethinking mental health: The body’s impact on the brain

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

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 29670 - Posted: 02.12.2025

A man volunteered to get brain implants for depression. Hear his story

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

Welcome to The Deep End, a new podcast about brain implants and depression

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

Brain implant that could boost mood by using ultrasound to go under NHS trial

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

Tiny fish on ketamine may show how drug eases depression

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

Here’s how Antidepressants can affect weight, mood, libido and other functions.

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

More than an hour of exercise a week may help with ‘baby blues'

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

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 29548 - Posted: 11.09.2024

Is Depression Contagious? The Science Is Uncertain.

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.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 29520 - Posted: 10.16.2024

Former Columbia University psychiatrist committed research misconduct

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

Why Depression Symptoms Come on at Night

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

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 29506 - Posted: 10.05.2024

Brain scan study identifies potential targets to treat youths with severe depression

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

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory and Learning
Link ID: 29491 - Posted: 09.25.2024

Ketamine targets lateral habenula, setting off cascade of antidepressant effects

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

Part of brain network much bigger in people with depression

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

The Deeper Issue With Expanding Assisted Dying to Mental Illness

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.

Moving in Childhood Contributes to Depression

By Ellen Barry In recent decades, mental health providers began screening for “adverse childhood experiences” — generally defined as abuse, neglect, violence, family dissolution and poverty — as risk factors for later disorders. But what if other things are just as damaging? Researchers who conducted a large study of adults in Denmark, published on Wednesday in the journal JAMA Psychiatry, found something they had not expected: Adults who moved frequently in childhood have significantly more risk of suffering from depression than their counterparts who stayed put in a community. In fact, the risk of moving frequently in childhood was significantly greater than the risk of living in a poor neighborhood, said Clive Sabel, a professor at the University of Plymouth and the paper’s lead author. “Even if you came from the most income-deprived communities, not moving — being a ‘stayer’ — was protective for your health,” said Dr. Sabel, a geographer who studies the effect of environment on disease. “I’ll flip it around by saying, even if you come from a rich neighborhood, but you moved more than once, that your chances of depression were higher than if you hadn’t moved and come from the poorest quantile neighborhoods,” he added. The study, a collaboration by Aarhus University, the University of Manchester and the University of Plymouth, included all Danes born between 1982 and 2003, more than a million people. Of those, 35,098, or around 2.3 percent, received diagnoses of depression from a psychiatric hospital. Are you concerned for your teen? If you worry that your teen might be experiencing depression or suicidal thoughts, there are a few things you can do to help. Dr. Christine Moutier, the chief medical officer of the American Foundation for Suicide © 2024 The New York Times Company

Depression, schizophrenia and bipolar disorder linked with ancient viral DNA in our genome

Rodrigo Duarte Around 8% of human DNA is made up of genetic sequences acquired from ancient viruses. These sequences, known as human endogenous retroviruses (or Hervs), date back hundreds of thousands to millions of years – with some even predating the emergence of Homo sapiens. Our latest research suggests that some ancient viral DNA sequences in the human genome play a role in susceptibility to psychiatric disorders such as schizophrenia, bipolar disorder and major depressive disorder. Hervs represent the remnants of these infections with ancient retroviruses. Retroviruses are viruses that insert a copy of their genetic material into the DNA of the cells they infect. Retroviruses probably infected us on multiple occasions during our evolutionary past. When these infections occurred in sperm or egg cells that generated offspring, the genetic material from these retroviruses was passed on to subsequent generations, becoming a permanent part of our lineage. Initially, scientists considered Hervs to be “junk DNA” – parts of our genome with no discernible function. But as our understanding of the human genome has advanced, it’s become evident that this so-called junk DNA is responsible for more functions than originally hypothesised. First, researchers found that Hervs can regulate the expression of other human genes. A genetic feature is said to be “expressed” if its DNA segment is used to produce RNA (ribonucleic acid) molecules. These RNA molecules can then serve as intermediaries leading to the production of specific proteins, or help to regulate other parts of the genome. Initial research suggested that Hervs regulate the expression of neighbouring genes with important biological functions. One example of this is a Herv that regulates the expression of a gene involved in modifying connections between brain cells. © 2010–2024, The Conversation US, Inc.

What Happens in the Brain to Cause Depression?

By Steven Strogatz For decades, the best drug therapies for treating depression, like SSRIs, have been based on the idea that depressed brains don’t have enough of the neurotransmitter serotonin. Yet for almost as long, it’s been clear that simplistic theory is wrong. Recent research into the true causes of depression is finding clues in other neurotransmitters and the realization that the brain is much more adaptable than scientists once imagined. Treatments for depression are being reinvented by drugs like ketamine that can help regrow synapses, which can in turn restore the right brain chemistry and improve whole body health. In this episode, John Krystal, a neuropharmacologist at the Yale School of Medicine, shares the new findings in mental health research that are revolutionizing psychiatric medication. STEVEN STROGATZ: According to the World Health Organization, 280 million people worldwide suffer from depression. For decades, people with chronic depression have been told their problem lies with a chemical imbalance in the brain, specifically a deficit in a neurotransmitter called serotonin. And based on this theory, many have been prescribed antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, to correct this chemical imbalance. This theory has become the common narrative, yet almost from the beginning, researchers have questioned the role of serotonin in depression, even though SSRIs do seem to bring a lot of relief to many people. So, if bad brain chemistry isn’t at the root of chronic depression, what is? If the thinking behind SSRIs is wrong, why do they seem to help? And is it possible that as we get closer to the true cause of depression, we may find better treatments for other conditions as well? © 2024 the Simons Foundation.

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