Chapter 12. Psychopathology: The Biology of Behavioral Disorders

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By April Dembosky Every year, an estimated 100,000 young adults or adolescents in the U.S. experience a psychotic episode. Only 10-20% of them gain access to the holistic treatment approach recommended by the National Institute of Mental Health as the gold standard of care for early psychosis, due to lack of space or because insurance won't cover it. Illustration by Anna Vignet/KQED After M graduated from high school in California, she got a job at a fast food restaurant making burgers. Her coworkers were chatting over the fryer one day when M got a weird feeling, like somehow they knew what she was thinking. It was like her coworkers could read her mind and were discussing her thoughts with each other. "I was like, are they talking about burgers or are they talking about me?" says M, now 21. NPR has agreed to identify M by her middle initial because she fears the stigma around her mental illness could disrupt her career path. There was one coworker in particular, a guy she had a crush on, and she was pretty sure he was watching her. She suspected he hacked into her phone so he could listen to her conversations, find out where she was and follow her around. If she was walking down the street, or hanging out in the park, she saw him. Her mom remembers M wanted to sleep with the lights on, repeatedly asking her through the night, "Mom, is someone here?" One day, her mom said M got so paranoid, so scared, she locked herself in the bathroom and just screamed and screamed and screamed. Her mom wanted to call for help. But she didn't have a job at the time. This was about a year into the pandemic, and the hotel where M's mom worked had been closed since the first lockdown. When she lost her job, she lost her family's health benefits, too. "My husband was like, 'What is that going to cost?'" her mom remembers. © 2024 npr

Keyword: Schizophrenia
Link ID: 29076 - Posted: 01.03.2024

By Elizabeth Svoboda Esther Oladejo knew she'd crossed an invisible boundary when she started forgetting to eat for entire days at a time. A gifted rugby player, Oladejo had once thrived on her jam-packed school schedule. But after she entered her teenage years, her teachers started piling on assignments and quizzes to prepare students for high-stakes testing that would help them to qualify for university. As she devoted hours on hours to cram sessions, Oladejo's resolve began to fray. Every time she got a low grade, her mood tanked—and with it, her resolve to study hard for the next test. “Teachers [were] saying, ‘Oh, you can do much better than this,’” says Oladejo, now 18, who lives in Merseyside, England. “But you're thinking, ‘Can I? I tried my best on that. Can I do any more than what I've done before?’” One morning, as Oladejo steeled herself for another endless day, her homeroom teacher passed out a questionnaire to the students, explaining that it would help assess their moods and well-being. Oladejo filled it out, her mind ticking forward to her upcoming classes. Soon after that, someone called to tell her she'd been slotted into a new school course called the Blues Program. Developed by Oregon Research Institute psychologist Paul Rohde and his colleagues at Stanford University, the program—a six-week series of hour-long group sessions—teaches students skills for managing their emotions and stress. The goal is to head off depression in vulnerable teens. Although Oladejo didn't know it at the time, her course was one in an expanding series of depression prevention programs for young people, including Vanderbilt University's Teens Achieving Mastery Over Stress (TEAMS); the University of Pennsylvania's Penn Resiliency Program; Happy Lessons, developed by Dutch social scientists; and Spain's Smile Program. The growing global interest in depression prevention is helping to establish the efficacy of a range of programs in diverse settings. © 2023 SCIENTIFIC AMERICAN,

Keyword: Depression; Development of the Brain
Link ID: 29066 - Posted: 12.27.2023

Ian Sample Science editor Human tears carry a substance that dampens down aggression, according to researchers, who believe the drops may have evolved over time to protect wailing babies from harm. Sniffing emotional tears from women reduced male aggression by more than 40% in computerised tests, and prompted corresponding changes in the brain, though the scientists behind the study think all human tears would have a similar effect. “The reduction in aggression was impressive to us, it seems real,” said Noam Sobel, a professor of neurobiology at the Weizmann Institute of Science in Israel. “Whatever is in tears actually lowers aggression.” Charles Darwin puzzled over the point of weeping. Writing in The Expression of Emotions in Man and Animals in 1872, the great naturalist declared sobbing as “purposeless as the secretion of tears from a blow outside the eye”. But in the 150 years since, researchers have proposed all manner of roles, from signalling vulnerability and helplessness to clearing bacteria from the eyes. Previous work at Sobel’s lab found that sniffing women’s tears reduced male testosterone but it was unclear whether this affected behaviour. In animals, the picture is clearer: subordinate mole rats, for example, cover themselves in tears to protect themselves from aggressors. For the latest study, Dr Shani Agron and others in Sobel’s lab collected tears rolling down women’s faces as they watched sad movies. The researchers did not specifically advertise for female tear donors but nearly all who came forward were women, of whom six were selected because they produced tears in such quantities. The experiments involved 31 men who sniffed either saline or women’s tears before having swabs dabbed with the droplets stuck to their upper lip. The men then took part in a computerised game used in psychology to provoke aggressive behaviour by unfairly deducting players’ points. © 2023 Guardian News & Media Limited

Keyword: Aggression; Chemical Senses (Smell & Taste)
Link ID: 29063 - Posted: 12.22.2023

Perspective by Michael Varnum and Ian Hohm A growing body of research in psychology and related fields suggests that winter brings some profound changes in how people think, feel and behave. The natural and cultural changes that come with winter often occur simultaneously, making it challenging to tease apart the causes underlying these seasonal swings. Live well every day with tips and guidance on food, fitness and mental health, delivered to your inbox every Thursday. We recently conducted an extensive survey of these findings with research colleagues Alexandra Wormley, a social psychologist at Arizona State University, and Mark Schaller, a psychologist at the University of British Columbia. Wintertime blues and a long winter’s nap Do you find yourself feeling down in the winter months? You’re not alone. As the days grow shorter, the American Psychiatric Association estimates that about 5 percent of Americans will experience a form of depression known as seasonal affective disorder, or SAD. People experiencing SAD tend to have feelings of hopelessness, decreased motivation to take part in activities they generally enjoy, and lethargy. Even those who don’t meet the clinical threshold for this disorder may see increases in anxiety and depressive symptoms. Scientists link SAD and more general increases in depression in the winter to decreased exposure to sunlight, which leads to lower levels of the neurotransmitter serotonin. Consistent with the idea that sunlight plays a key role, SAD tends to be more common in more northern regions of the world, such as Scandinavia and Alaska, where the days are shortest and the winters longest. Humans, special as we may be, are not unique in showing some of these seasonally linked changes. For instance, our primate relative the Rhesus macaque shows seasonal declines in mood.

Keyword: Biological Rhythms; Depression
Link ID: 29043 - Posted: 12.13.2023

By Anil Oza Krista Lisdahl has been studying cannabis use among adolescents for two decades, and what she sees makes her worried for her teenage son. “I see the data coming in, I know that he is going to come across it,” she says. As a clinical neuropsychologist at the University of Wisconsin–Milwaukee, she sees plenty of young people who have come into contact with the drug to varying degrees, from trying it once at a party to using potent preparations of it daily. The encounters have become more frequent as efforts to legalize cannabis for recreational use intensify around the world. In some of her studies, around one-third of adolescents who regularly use cannabis show signs of a cannabis use disorder — that is, they can’t stop using the drug despite negative impacts on their lives. But she wants more conclusive evidence when it comes to talking about the drug and its risks to young people, including her son. Deciding what to say is difficult, however. Anti-drug messaging campaigns have dwindled, and young people are forced to consider sometimes-conflicting messages on risks in a culture that increasingly paints cannabis and other formerly illicit drugs as harmless or potentially therapeutic. “Teenagers are pretty smart, and they see that adults use cannabis,” Lisdahl says. That makes blanket warnings and prohibitions practically useless. It’s now a decade since the drug was officially legalized for recreational use by adults aged 18 and older in Uruguay, and aged 21 and older in the states of Colorado and Washington. Many other states and countries have followed, and researchers are desperately trying to get a handle on how usage patterns are changing as a result; how the drug impacts brain development; and how cannabis use correlates with mental-health conditions such as depression, anxiety and schizophrenia. The data so far don’t tell clear stories: young people don’t seem to be using in greater numbers than before legalization, but there seem to be trends towards more problematic use. © 2023 Springer Nature Limited

Keyword: Drug Abuse; Schizophrenia
Link ID: 29041 - Posted: 12.13.2023

Sydney E. Smith When most people hear about electroconvulsive therapy, or ECT, it typically conjures terrifying images of cruel, outdated and pseudo-medical procedures. Formerly known as electroshock therapy, this perception of ECT as dangerous and ineffective has been reinforced in pop culture for decades – think the 1962 novel-turned-Oscar-winning film “One Flew Over the Cuckoo’s Nest,” where an unruly patient is subjected to ECT as punishment by a tyrannical nurse. Despite this stigma, ECT is a highly effective treatment for depression – up to 80% of patients experience at least a 50% reduction in symptom severity. For one of the most disabling illnesses around the world, I think it’s surprising that ECT is rarely used to treat depression. Contributing to the stigma around ECT, psychiatrists still don’t know exactly how it heals a depressed person’s brain. ECT involves using highly controlled doses of electricity to induce a brief seizure under anesthesia. Often, the best description you’ll hear from a physician on why that brief seizure can alleviate depression symptoms is that ECT “resets” the brain – an answer that can be fuzzy and unsettling to some. As a data-obsessed neuroscientist, I was also dissatisfied with this explanation. In our newly published research, my colleagues and I in the lab of Bradley Voytek at UC San Diego discovered that ECT might work by resetting the brain’s electrical background noise. To study how ECT treats depression, my team and I used a device called an electroencephalogram, or EEG. It measures the brain’s electrical activity – or brain waves – via electrodes placed on the scalp. You can think of brain waves as music played by an orchestra. Orchestral music is the sum of many instruments together, much like EEG readings are the sum of the electrical activity of millions of brain cells. © 2010–2023, The Conversation US, Inc.

Keyword: Depression
Link ID: 29036 - Posted: 12.09.2023

By Taylor Beck One sunny day this fall, I caught a glimpse of the new psychiatry. At a mental hospital near Yale University, a depressed patient was being injected with ketamine. For 40 minutes, the drug flowed into her arm, bound for cells in her brain. If it acts as expected, ketamine will become the first drug to quickly stop suicidal drive, with the potential to save many lives. Other studies of ketamine are evaluating its effect as a vaccination against depression and post-traumatic stress. Between them, the goal is nothing less than to redefine our understanding of mental illness itself. Depression is the most common mental illness in the United States, affecting 30 percent of Americans at some point in their lives. But despite half a century of research, ubiquitous advertising, and blockbuster sales, antidepressant drugs just don’t work very well. They treat depression as if it were caused by a chemical imbalance: Pump in more of one key ingredient, or sop up another, and you will have fixed the problem. But the correspondence between these chemicals (like serotonin) and depression is relatively weak. An emerging competitive theory, inspired in part by ketamine’s effectiveness, has it that psychiatric disease is less about chemical imbalance than structural changes in the brain—and that a main cause of these changes is psychological stress. “I really do think stress is to mental illness as cigarettes are to heart disease,” says Gerard Sanacora, the psychiatry professor running the ketamine trial at Yale. The theory describes stress grinding down individual neurons gradually, as storms do roof shingles. This, in turn, changes the nature of their connections to one another and the structure of the brain. Ketamine, along with some similar molecules, acts to strengthen the neuron against that damage, affecting not just the chemistry of the brain but also its structure. © 2023 NautilusNext Inc.,

Keyword: Depression; Stress
Link ID: 29027 - Posted: 12.02.2023

By John Krakauer & Tamar Makin The human brain’s ability to adapt and change, known as neuroplasticity, has long captivated both the scientific community and the public imagination. It’s a concept that brings hope and fascination, especially when we hear extraordinary stories of, for example, blind individuals developing heightened senses that enable them to navigate through a cluttered room purely based on echolocation or stroke survivors miraculously regaining motor abilities once thought lost. For years, the notion that neurological challenges such as blindness, deafness, amputation or stroke lead to dramatic and significant changes in brain function has been widely accepted. These narratives paint a picture of a highly malleable brain that is capable of dramatic reorganization to compensate for lost functions. It’s an appealing notion: the brain, in response to injury or deficit, unlocks untapped potentials, rewires itself to achieve new capabilities and self-repurposes its regions to achieve new functions. This idea can also be linked with the widespread, though inherently false, myth that we only use 10 percent of our brain, suggesting that we have extensive neural reserves to lean on in times of need. But how accurate is this portrayal of the brain’s adaptive abilities to reorganize? Are we truly able to tap into reserves of unused brain potential following an injury, or have these captivating stories led to a misunderstanding of the brain’s true plastic nature? In a paper we wrote for the journal eLife, we delved into the heart of these questions, analyzing classical studies and reevaluating long-held beliefs about cortical reorganization and neuroplasticity. What we found offers a compelling new perspective on how the brain adapts to change and challenges some of the popularized notions about its flexible capacity for recovery. The roots of this fascination can be traced back to neuroscientist Michael Merzenich’s pioneering work, and it was popularized through books such as Norman Doidge’s The Brain That Changes Itself. Merzenich’s insights were built on the influential studies of Nobel Prize–winning neuroscientists David Hubel and Torsten Wiesel, who explored ocular dominance in kittens. © 2023 SCIENTIFIC AMERICAN,

Keyword: Learning & Memory; Regeneration
Link ID: 29019 - Posted: 11.22.2023

by Grace Huckins In 1961, the late psychiatrist Daniel Freedman made what would become one of the most replicated — and most mysterious — discoveries in the history of autism research. Comparing blood levels of the neurotransmitter serotonin in 4 non-autistic and 23 autistic children, he found significantly higher levels among the latter group. Since then, researchers have repeatedly identified this trait, called hyperserotonemia, in about a third of autistic people tested. It’s not difficult to theorize how hyperserotonemia might be linked to a range of autism traits. Neurons that release serotonin extend into practically every part of the brain, where they modulate signals sent among other neurons. Selective serotonin reuptake inhibitors (SSRIs), drugs that raise levels of serotonin in the brain’s synapses, treat psychiatric conditions, such as anxiety and obsessive-compulsive disorder, that can co-occur with autism. And serotonin prompts the gut to contract and facilitate digestion, which is often impaired in autistic people. So when Edwin Cook, professor of psychiatry at the University of Illinois at Chicago, began to study the biology of autism in the 1980s, hyperserotonemia seemed like an obvious place to start. “We didn’t have much [else],” he says. “There were plenty of mothers of older patients I saw who had been labeled refrigerator mothers,” a term that refers to the discredited idea that unaffectionate mothers cause autism. The serotonin finding offered a tangible, biological clue. Even today, with decades more autism research to look back on, the hyperserotonemia result stands out. “It’s one of the few robust biological clues that we’ve had in autism,” says Jeremy Veenstra-VanderWeele, professor of psychiatry at Columbia University and a former advisee of Cook’s. But so far, it has escaped explanation. Nor have researchers been able to definitively link hyperserotonemia to specific genetic, anatomical or behavioral traits in autistic people. This apparent lack of progress has led some to disregard work on the neurotransmitter, according to serotonin researcher Georgianna Gould, associate professor of physiology at the University of Texas Health Science Center at San Antonio. “I’ve actually seen reviews come back that say that serotonin has nothing to do with autism,” she says. © 2023 Simons Foundation

Keyword: Autism; Obesity
Link ID: 28998 - Posted: 11.11.2023

By Azeen Ghorayshi Doctors and patients have long known that antidepressants can cause sexual problems. No libido. Pleasureless orgasms. Numb genitals. Well over half of people taking the drugs report such side effects. Now, a small but vocal group of patients is speaking out about severe sexual problems that have endured even long after they stopped taking selective serotonin reuptake inhibitors, the most popular type of antidepressants. The drugs’ effects have been devastating, they said, leaving them unable to enjoy sex or sustain romantic relationships. “My clitoris feels like a knuckle,” said Emily Grey, a 27-year-old in Vancouver, British Columbia, who took one such drug, Celexa, for depression from age 17 to 23. “It’s not a normal thing to have to come to terms with.” The safety label on Prozac, one of the most widely prescribed S.S.R.I.s, warns that sexual problems may persist after the drug is discontinued. And health authorities in Europe and Canada recently acknowledged that the medications can lead to lasting sexual issues. But researchers are only just beginning to quantify how many people have these long-term problems, known as post-S.S.R.I. sexual dysfunction. And the chronic condition remains contested among some psychiatrists, who point out that depression itself can curb sexual desire. Clinical trials have not followed people after they stop the drugs to determine whether such sexual problems stem from the medications. “I think it’s depression recurring. Until proven otherwise, that’s what it is,” said Dr. Anita Clayton, the chief of psychiatry at the University of Virginia School of Medicine and a leader of an expert group that will meet in Spain next year to formally define the condition. Dr. Clayton published some of the earliest research showing that S.S.R.I.s come with widespread sexual side effects. © 2023 The New York Times Company

Keyword: Depression; Sexual Behavior
Link ID: 28996 - Posted: 11.11.2023

Sara Reardon Psychedelic drugs have been undergoing a major makeover in psychiatry, earning mainstream acceptance that has eluded them for decades. In 2019, a variant of ketamine — an animal tranquillizer well known as a club drug — was approved by the US Food and Drug Administration (FDA) for treating post-traumatic stress disorder (PTSD). In May, Oregon opened its first treatment centre for administering psilocybin — the hallucinogenic compound found in magic mushrooms — following the state’s decision to legalize it (psilocybin remains illegal at the federal level). And, after decades of effort, the Multidisciplinary Association for Psychedelic Studies, a non-profit research organization in San Jose, California, formally asked the FDA for approval to market MDMA — also known as molly or ecstasy — as a treatment for PTSD. Most specialists expect the MDMA approval to go through on the weight of clinical evidence and popular support. Two large trials have shown that the drug can reduce the symptoms of PTSD when administered in controlled therapy sessions1,2. And it seems to do so more quickly than other treatments. But how MDMA and other psychedelics work is still largely a mystery, both because the drugs have long been illegal and because psychiatric conditions are difficult to study in animals. Psychedelic drug MDMA moves closer to US approval following success in PTSD trial With the regulatory landscape shifting, legal psychedelic research is becoming easier — and potentially more profitable. Neuroscientists, psychiatrists, pharmacologists, biochemists and others are entering the field, bringing fresh ideas about what the drugs do at a cellular and molecular level and trying to unravel how these mechanisms might help to relieve symptoms of psychiatric conditions. From a clinical perspective, understanding how the drugs work might not matter. “You don’t need to know the mechanism of the drug to have a very effective therapy,” says David Olson, a biochemist at the University of California, Davis. But, understanding more about psychedelics could lead to the development of proprietary drugs that are safer, less hallucinogenic and ultimately more effective. It could also affect the way psychedelics are administered in the clinic — helping providers to tailor treatments to each person. Several key questions are driving the basic research that progresses in the background as MDMA and others march towards the market. © 2023 Springer Nature Limited

Keyword: Depression; Stress
Link ID: 28986 - Posted: 11.04.2023

By Regina G. Barber What your parents didn't tell you about pulling an all-nighter? It might just ease depression for several days. At least, that's what researchers found happened to mice in a study published in the journal Neuron Thursday. Most people who've stayed up all night know the "tired and wired" feeling they get the next day. The body might be exhausted, but the brain feels jittery, hyperactive or even giddy. Even after these changes wear off, sleep loss can have a strong antidepressant effect in people that lasts several days. But researchers hadn't figured out why sleeplessness might have this effect —until this study from neurobiologists at Northwestern University. To study all of this, the team looked at the effects of sleep loss in mice. They induced sleep loss in some of the mice, while the others got a typical night's rest. They found that after this sleepless night, the mice were more excitable, more aggressive, more sexual and less depressed than mice that got a regular amount of sleep. Of course, researchers can't just ask mice whether they feel "less depressed." Instead, they created a depression-like state in all the mice before either disrupting their sleep or allowing them to rest by repeatedly giving them small shocks. In response to these shocks, the mice entered a depressive-like state and eventually stopped trying to escape their cages. Then, they tested the mice's response to shocks again. The ones that had stayed up all night showed a reversed depressive state, indicated by more attempts to escape the shocks. Dopamine is responsible for the brain's reward response. Changes in the brain's dopamine system have also been implicated in conditions like depression and in sleep regulation. And so, to see how the mice's brains responded to their sleepless night, the researchers measured dopamine neuron activity. They saw that sleep-deprived mice showed higher dopamine activity in three regions: the prefrontal cortex, nucleus accumbens and hypothalamus. © 2023 npr

Keyword: Sleep; Depression
Link ID: 28985 - Posted: 11.04.2023

By Mike Baker In a carpeted office suite, Alex Beck settled onto a mattress and, under the watch of a trained guide, began chomping through a handful of “Pumpkin Hillbilly” mushrooms. A Marine Corps veteran who was sexually assaulted during his time in the armed forces, Mr. Beck had long been searching unsuccessfully for a way to put those nightmarish years behind him. Now he was ready for a different kind of journey, a psychedelic trip through the nether regions of his own mind. As he felt his thoughts starting to spin, his “facilitator,” Josh Goldstein, urged him to surrender and let the mushrooms guide him. “It’s like the idea of planting a seed and then letting it go,” he said. Stigmatized in law and medicine for the past half-century, psychedelics are in the midst of a sudden revival, with a growing body of research suggesting that the mind-altering compounds could upend psychiatric care. Governments in several places have cautiously started to open access, and as Oregon voters approved a broad drug decriminalization plan in 2020, they also backed an initiative to allow the use of mushrooms as therapy. This summer, the state debuted a first-of-its-kind legal market for psilocybin mushrooms, more widely known as magic mushrooms. Far from the days of illicit consumption in basements and vans, the program allows people to embark on a therapeutic trip, purchasing mushrooms produced by a state-approved grower and consuming them in a licensed facility under the guidance of a certified facilitator. Mr. Beck, 30, was one of the first clients at a facility in the central Oregon city of Bend that began conducting sessions this summer in a building that on other days of the week offers chiropractic services. In his youth, Mr. Beck had experimented with psychedelics for recreation. But as he struggled with his lingering post-traumatic stress in adulthood, he learned about what seemed to be promising new research into plant-based psychedelics for mental health issues that did not respond to other treatments. He wondered if they could help him clear his head from the horrors of the past. © 2023 The New York Times Company

Keyword: Stress; Depression
Link ID: 28969 - Posted: 10.25.2023

By Matt Richtel Approximately 20 percent of adolescents had symptoms of major depressive disorder in 2021 — the first full calendar year of the pandemic — but less than half who needed treatment received it, according to a new study. The research, published in JAMA Pediatrics, found that treatment was most lacking for minority adolescents, particularly those who are Latino and mixed-race. Major depressive disorder is a chronic condition that surfaces in episodes of depressed mood and loss of joy, with symptoms lasting at least two weeks. It is distinct from persistent depressive disorder, in which symptoms last two years or more. Previous research showed that the prevalence of major depressive disorder among adolescents nearly doubled recently, rising to 15.8 percent in 2019 from 8.1 percent in 2009. The Covid-19 pandemic amplified this trend as it caused isolation, uncertainty, loneliness and fear of illness among family members. The new study on the prevalence of major depressive disorder in 2021 drew from a nationally representative sample of 10,700 adolescents, ages 12 to 17, whose experiences were recorded by the National Survey on Drug Use and Health. The study found some sharp differences in the prevalence of the condition across racial and ethnic groups. About 14.5 percent of Black adolescents, 14.6 percent of Asian adolescents and 20 percent of white adolescents reported symptoms of major depressive disorder. Latino adolescents experienced major depressive disorder at a slightly higher rate, around 23 percent. Though mixed-race and Latino adolescents had the highest rates of major depressive disorder, they had the lowest rates of treatment, the study found. Twenty-one percent of mixed-race adolescents and 29 percent of Latino adolescents with the condition received treatment for it, compared with nearly half of white adolescents. Treatment rates for Asian and Black adolescents fell in between. © 2023 The New York Times Company

Keyword: Depression
Link ID: 28952 - Posted: 10.10.2023

Jon Hamilton A team of researchers has developed a new way to study how genes may cause autism and other neurodevelopmental disorders: by growing tiny brain-like structures in the lab and tweaking their DNA. These "assembloids," described in the journal Nature, could one day help researchers develop targeted treatments for autism spectrum disorder, intellectual disability, schizophrenia, and epilepsy. "This really accelerates our effort to try to understand the biology of psychiatric disorders," says Dr. Sergiu Pașca, a professor of psychiatry and behavioral sciences at Stanford University and an author of the study. The research suggests that someday "we'll be able to predict which pathways we can target to intervene" and prevent these disorders, adds Kristen Brennand, a professor of psychiatry at Yale who was not involved in the work. The study comes after decades of work identifying hundreds of genes that are associated with autism and other neurodevelopmental disorders. But scientists still don't know how problems with these genes alter the brain. "The challenge now is to figure out what they're actually doing, how disruptions in these genes are actually causing disease," Pașca says. "And that has been really difficult." For ethical reasons, scientists can't just edit a person's genes to see what happens. They can experiment on animal brains, but lab animals like rodents don't really develop anything that looks like autism or schizophrenia. So Pașca and a team of scientists tried a different approach, which they detailed in their new paper. The team did a series of experiments using tiny clumps of human brain cells called brain organoids. These clumps will grow for a year or more in the lab, gradually organizing their cells much the way a developing brain would. And by exposing an organoid to certain growth factors, scientists can coax it into resembling tissue found in brain areas including the cortex and hippocampus. © 2023 npr

Keyword: Epilepsy; Autism
Link ID: 28940 - Posted: 10.03.2023

Rachel Hall University students are more at risk of depression and anxiety than their peers who go straight into work, according to a study, suggesting mental health may deteriorate due to the financial strain of higher education. The research is the first to find evidence of slightly higher levels of depression and anxiety among students, and challenges earlier work suggesting that the mental health of students is the same as or better than their peers. The first author of the study, Dr Tayla McCloud, a researcher in the psychiatry department at University College London (UCL), said the fact that the link between university and poor mental health had not been established in earlier studies could mean that it is due to “increased financial pressures and worries about achieving high results in the wider economic and social context”. As well as grappling with rising costs due to inflation, university students this year are facing unprecedented rent rises averaging at 8% and far outstripping the average maintenance loan in many cities. McCloud said she would have ordinarily expected university students to have better mental health as they tend to be from more privileged backgrounds, making the results “particularly concerning” and requiring more research to pinpoint the risks facing students. The lead author, Dr Gemma Lewis, associate professor at UCL’s school of psychiatry, said poorer mental health at university could have repercussions in later life. She said: “The first couple of years of higher education are a crucial time for development, so if we could improve the mental health of young people during this time it could have long-term benefits for their health and wellbeing, as well as for their educational achievement and longer term success.” © 2023 Guardian News & Media Limited

Keyword: Depression
Link ID: 28935 - Posted: 09.29.2023

Max Kozlov Doctors measure blood pressure to track heart disease, and scrutinize insulin levels in people with diabetes. But when it comes to depression, clinicians must rely on people’s self-reported symptoms, making it difficult to objectively measure a treatment’s effects. Now, researchers have used artificial intelligence (AI) to identify a brain signal linked to recovery from depression in people treated with deep-brain stimulation (DBS), a technique that uses electrodes implanted into the brain to deliver electric pulses that alter neural activity. The team reported1 its results on ten people with severe depression, in Nature on 20 September. If replicated in a larger sample, these findings could represent a “game-changer in how we would be able to treat depression”, says Paul Holtzheimer, a neuroscientist at the Geisel School of Medicine at Dartmouth in Hanover, New Hampshire, who was not involved in the research. Efforts to treat depression with DBS have so far had limited success: two randomized-controlled trials2,3 failed to demonstrate a benefit compared with a placebo. One problem, says Helen Mayberg, a neurologist at Icahn School of Medicine at Mount Sinai in New York City, and a co-author of the Nature paper, is that doctors only have access to self-reported data to assess whether a person’s stimulation voltage needs adjustment. With self-reported data, clinicians have a difficult time distinguishing between normal, day-to-day mood fluctuations and pathological depression, says Todd Herrington, director of the DBS programme at Massachusetts General Hospital in Boston, who was not involved in the research. To find a more objective measure of depression recovery, Mayberg and her colleagues developed a DBS device that includes sensors to measure brain activity, as well as the standard electrodes for brain stimulation. They implanted this device into the subcallosal cingulate cortex — an area of the brain that has a role in regulating emotional behaviour — in ten people with depression that resisted all forms of treatment. © 2023 Springer Nature Limited

Keyword: Depression; Brain imaging
Link ID: 28932 - Posted: 09.27.2023

Perspective by Dan O'Brien I was 12 years old when I developed obsessive-compulsive disorder. My older brother had recently tried to kill himself by jumping from our attic window. I was the one who saw him first, as he limped around the side of the house, his back and hair matted with snow. Inside I found his suicide note and showed it to our mother. She collapsed in my arms, crying, and whispered, “This is a secret we must take to our graves.” Live well every day with tips and guidance on food, fitness and mental health, delivered to your inbox every Thursday. Before long, I found myself obsessing about any number of vague yet existential threats, and compulsively taking defensive action against them. I cycled through most of the classic OCD manifestations: avoiding cracks in the sidewalk, flipping light switches three, six, nine times (depending on my mood), checking and rechecking — and rechecking again — that our front and back doors were indeed locked. I had no idea what was happening to me. I simply knew with certainty that if I did not execute these actions correctly, my loved ones and I would suffer. And hypochondria, too: A book titled “Symptoms” lived in the tall bookcase behind the potted plant in the living room; one searched for one’s symptoms in an index up front, then proceeded to the indicated page where one would be provided with the most dire diagnosis imaginable. “Symptoms,” with its heft, its red-linen hardcover and tissue-thin paper, became my Bible. I touched things and people with trepidation and regret. I probed my body for swollen glands. My frequent handwashing desiccated my skin like a riverbed in drought, blood breaking through the cracks. I was forever certain that I was coming down with something catastrophic, like tuberculosis, AIDS, cancer. I was morally scrupulous, in the clinical sense, and prayed three times a day. (I wasn’t particularly religious; I was trying to cover all my bases.) Morning and evening prayer was easy, at home, but lunchtime at school could be tricky; I’d have to abscond to the boy’s room, or a shadowy, chain-link corner of the playground. I grew adept at praying without moving my lips in rote run-on sentences in which I begged God’s forgiveness for everything and anything I had done wrong in the past and would do wrong in the future.

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 28926 - Posted: 09.27.2023

By Laura Sanders On a hot, sunny Sunday afternoon in Manhattan, time froze for Jon Nelson. He stood on the sidewalk and said good-bye to his three kids, whose grandfather had come into the city from Long Island to pick them up. Like any parent, Jon is deeply attuned to his children’s quirks. His oldest? Sometimes quiet but bitingly funny. His middle kid? Rates dad a 10 out of 10 on the embarrassment scale and doesn’t need a hug. His 10-year-old son, the baby of the family, is the emotional one. “My youngest son would climb back up into my wife’s womb if he could,” Jon says. “He’s that kid.” An unexpected parade had snarled traffic, so Jon parked illegally along a yellow curb on 36th Street, near where his father-in-law was waiting. It was time to go. His youngest gave the last hug. “He looked up, scared and sad,” Jon says, and asked, “Dad, am I going to see you again?” That question stopped the clock. “I was like, ‘Oh man,’” Jon says. “It was one of those moments where I was living it through his eyes. And I got scared for the first time.” Until that good-bye, Jon hadn’t wanted to live. For years, he had a constant yearning to die — he talks about it like it was an addiction — as he fought deep, debilitating depression. But his son’s question pierced through that heaviness and reached something inside him. “That was the first time I really thought about it. I was like, ‘I kind of hope I don’t die.’ I hadn’t had that feeling in so long.” That hug happened around 5 p.m. on August 21, 2022. Twelve hours later, Jon was wheeled into a surgical suite. There, at Mount Sinai’s hospital just southwest of Central Park, surgery team members screwed Jon’s head into a frame to hold it still. Then they numbed him and drilled two small holes through the top of his skull, one on each side. Through each hole, a surgeon plunged a long, thin wire dotted at the end with electrodes deep into his brain. The wiring, threaded under his skin, snaked around the outside of Jon’s skull and sank down behind his ear. From there, a wire wrapped around to the front, meeting a battery-powered control box that surgeons implanted in his chest, just below his collarbone. © Society for Science & the Public 2000–2023.

Keyword: Depression
Link ID: 28924 - Posted: 09.23.2023

Sara Reardon The psychedelic drug MDMA, also known as ecstasy or molly, has passed another key hurdle on its way to regulatory approval as a treatment for mental illness. A second large clinical trial has found that the drug — in combination with psychotherapy — is effective at treating post-traumatic stress disorder (PTSD). The results allow the trial’s sponsor to now seek approval from the US Food and Drug Administration (FDA) for MDMA’s use as a PTSD treatment for the general public, which might come as soon as next year. “It’s an important study,” says Matthias Liechti, a psychopharmacologist who studies MDMA at the University of Basel in Switzerland, but who was not involved with the trial or its sponsor. “It confirms MDMA works.” In June, Australia became the first country to allow physicians to prescribe MDMA for treating psychiatric conditions. MDMA is illegal in the United States and other countries because of the potential for its misuse. But the Multidisciplinary Association for Psychedelic Studies (MAPS), a non-profit organization in San Jose, California, has long been developing a proprietary protocol for using MDMA as a treatment for PTSD and other disorders. MAPS has been campaigning for its legalization — a move that could encourage other countries to follow suit. In 2021, researchers sponsored by MAPS reported the results of a study1 in which 90 people received a form of psychotherapy developed by the organization alongside either MDMA or a placebo. After three treatment sessions, 67% of those who received MDMA with therapy no longer qualified for a PTSD diagnosis, compared with 32% of those who received therapy and a placebo. The results were widely hailed as promising, but the FDA typically requires two placebo-controlled trials before a drug can be approved. The results of a second trial, involving 104 further individuals with PTSD and published on 14 September in Nature Medicine2, were similar to those of the original: 71% of people who received MDMA alongside therapy lost their PTSD diagnosis, compared with 48% of those who received a placebo and therapy. © 2023 Springer Nature Limited

Keyword: Drug Abuse; Stress
Link ID: 28911 - Posted: 09.16.2023