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By Matt Richtel Growing numbers of children and adolescents are being prescribed multiple psychiatric drugs to take simultaneously, according to a new study by researchers at the University of Maryland. The phenomenon is increasing despite warnings that psychotropic drug combinations in young people have not been tested for safety or studied for their impact on the developing brain. The study, published Friday in JAMA Open Network, looked at the prescribing patterns among patients 17 or younger enrolled in Medicaid from 2015 to 2020 in a single U.S. state that the researchers declined to name. In this group, there was a 9.5 percent increase in the prevalence of “polypharmacy,” which the study defined as taking three or more different classes of psychiatric medications, including antidepressants, mood-stabilizing anticonvulsants, sedatives and drugs for A.D.H.D. and anxiety drugs. The study looked at only one state, but state data have been used in the past to explore this issue, in part because of the relative ease of gathering data from Medicaid, the health insurance program administered by states. At the same time, some research using nationally weighted samples have revealed the increasing prevalence of polypharmacy among young people. One recent paper drew data from the National Ambulatory Medical Care Survey and found that in 2015, 40.7 percent of people aged 2 to 24 in the United States who took a medication for A.D.H.D. also took a second psychiatric drug. That figure had risen from 26 percent in 2006. The latest data from the University of Maryland researchers show that, at least in one state, the practice continues to grow and “was significantly more likely among youths who were disabled or in foster care,” the new study noted. Mental health experts said that psychotropic medications can prove very helpful and that doctors have discretion to prescribe what they see fit. A concern among some experts is that many drugs used in frequently prescribed cocktails have not been approved for use in young people. And it is unclear how the simultaneous use of multiple psychotropic medications affects brain development long-term. © 2024 The New York Times Company

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: 29152 - Posted: 02.20.2024

Dawn Megli In late 2022, Sarah Gutilla's treatment-resistant depression had grown so severe that she was actively contemplating suicide. Raised in foster care, the 34-year-old's childhood was marked by physical violence, sexual abuse and drug use, leaving her with life-threatening mental scars. Out of desperation, her husband scraped together $600 for the first of six rounds of intravenous ketamine therapy at Ketamine Clinics Los Angeles, which administers the generic anesthetic for off-label uses such as treating depression. When Gutilla got into an Uber for the 75-mile ride to Los Angeles, it was the first time she had left her home in Llano, Calif., in two years. The results, she says, were instant. "The amount of relief I felt after the first treatment was what I think 'normal' is supposed to feel like," she says. "I've never felt so OK and so at peace." For-profit ketamine clinics have proliferated over the past few years, offering infusions for a wide array of mental health issues, including obsessive-compulsive disorder, depression and anxiety. Although the off-label use of ketamine hydrochloride, a Schedule III drug approved by the Food and Drug Administration as an anesthetic in 1970, was considered radical just a decade ago, now between 500 and 750 ketamine clinics have cropped up across the United States. Market analysis firm Grand View Research pegged industry revenues at $3.1 billion in 2022, and it projects them to more than double to $6.9 billion by 2030. Most insurance doesn't cover ketamine for mental health, so patients must pay out-of-pocket. While it's legal for doctors to prescribe ketamine, the FDA hasn't approved it for mental health treatment, which means that individual practitioners develop their own treatment protocols. The result is wide variability among providers, with some favoring gradual, low-dosage treatments while others advocate larger amounts that can induce hallucinations, as the drug is a psychedelic at the right doses. "Ketamine is the Wild West," says Dustin Robinson, the managing principal of Iter Investments, a venture capital firm specializing in hallucinogenic drug treatments. © 2024 npr

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: 29129 - Posted: 02.03.2024

Ian Sample Science editor From Cain and Abel and the Brothers Karamazov to Cinderella, the warmth and support provided by siblings has hardly been taken for granted. Now, researchers have found that children who moan about their brothers and sisters may have good reason to complain: the more siblings teenagers have, the more it hits their happiness, they claim. A study of secondary schoolchildren in the US and China found that those from larger families had slightly poorer mental health than those from smaller families. The greatest impact was seen in families with multiple children born less than a year apart. Doug Downey, a professor of sociology at Ohio State University, said previous work in the field had revealed a mixed picture of positives and negatives for children with more siblings, adding that the latest results “were not a given”. The researchers asked 9,100 eighth graders in the US and 9,400 in China, with an average age of 14, a range of questions about their mental health, though the specific questions varied between the countries. In China, the teenagers with no siblings fared best for mental health. In the US, children who had no siblings or only one were found to have similar mental health. Overall, mental health was worse the more siblings the teenagers had, with greater impacts seen for teenagers with older siblings, and when brothers and sisters were closely spaced in age. Writing in the Journal of Family Issues, Downey and his colleagues argue that the findings are in line with the “resource dilution” explanation, the driving force behind the unwritten formula that states that the number of balls dropped rises, sometimes dramatically, with the number of siblings born. © 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: 29101 - Posted: 01.16.2024

By Elissa Welle Many of the physicians who worked on the current diagnostic and treatment guidelines for psychiatric conditions in the United States have financial ties to pharmaceutical companies, according to a study published today in The BMJ. Nearly 60 percent of the 92 U.S.-based physicians who shepherded the Diagnostic and Statistical Manual of Mental Disorders, fifth edition, text revision (DSM-5-TR) accepted industry payments totaling $14.2 million during the three years prior to working on the manual, the study shows. The results raise questions about systemic “economies of influence” over a document used by public health officials, health insurance plans and drug regulators, says lead investigator Lisa Cosgrove, professor of counseling and school psychology and a faculty fellow at the Applied Ethics Center at the University of Massachusetts, Boston. “Financial conflicts of interest, industry ties don’t point to wrongdoing — we’re not saying that people did anything wrong consciously,” Cosgrove says. “It’s just implicit bias.” DSM-5-TR decision-makers were not allowed to receive more than $5,000 from industry, according to a statement to The Transmitter by a spokesperson for the American Psychiatric Association (APA), which published the DSM-5-TR in March 2022. And an independent committee reviewed financial and non-financial disclosures for all other contributors to the revision. The text revision centered on literature searches to incorporate new scientific findings since the publication of the DSM-5 in 2013, the spokesperson wrote. “Any rare, minor instances of content that connected a diagnosis to a therapy were omitted from DSM-5-TR,” the spokesperson wrote. “No content was found in the submitted text that related to a specific treatment for which industry funding may have been provided for related research.” © 2023 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: 29096 - Posted: 01.13.2024

By Tim Vernimmen It is increasingly well understood that the countless microbes in our guts help us to digest our food, to absorb and produce essential nutrients, and to prevent harmful organisms from settling in. Less intuitive — perhaps even outlandish — is the idea that those microbes may also affect our mood, our mental health and how we perform on cognitive tests. But there is mounting evidence that they do. For nearly two decades, neuroscientist John Cryan of University College Cork in Ireland has been uncovering ways in which intestinal microbes affect the brain and behavior of humans and other animals. To his surprise, many of the effects he’s seen in rodents appear to be mirrored in our own species. Most remarkably, research by Cryan and others has shown that transplanting microbes from the guts of people with psychiatric disorders like depression to the guts of rodents can cause comparable symptoms in the animals. These effects may occur in several ways — through the vagus nerve connecting the gut to the brain, through the influence of gut bacteria on our immune systems, or by microbes synthesizing molecules that our nerve cells use to communicate. Cryan and coauthors summarize the science in a set of articles including “Man and the Microbiome: A New Theory of Everything?,” published in the Annual Review of Clinical Psychology. Cryan told Knowable Magazine that even though it will take much more research to pin down the mechanisms and figure out how to apply the insights, there are some things we can do already. This conversation has been edited for length and clarity.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 29091 - Posted: 01.11.2024

Pam Belluck A research team analyzed records of nearly a million women in Sweden’s national medical registries from 2001 through 2017, comparing 86,551 women who had perinatal depression with 865,510 women who did not. The groups were matched by age and year they gave birth. In two studies, the team found that depression that begins in pregnancy or soon after can have troubling implications for as long as 18 years. One study, published on Tuesday in JAMA Network Open, found that women with perinatal depression had three times the risk of suicidal behavior, defined as attempted or completed suicide, than women who did not experience perinatal depression. Risks were greatest in the year following their diagnosis, but, while they lessened over time, years later the risks were still twice as high compared with women without the disorder. The other study, published on Wednesday in BMJ, found that women with perinatal depression were more than six times at risk of dying by suicide as those without that diagnosis. The number of suicides was small, but it accounted for a large share of the deaths of women diagnosed with perinatal depression: 149 of the 522 deaths in that group, or 28.5 percent. For women without perinatal depression, there were 117 suicides out of 1,568 deaths or 7.5 percent. Suicide was a major reason women with perinatal depression were twice as likely to die from any cause over the 18-year period of the study compared with women without the disorder. The researchers also compared more than 20,000 women with perinatal depression to their biological sisters who gave birth during the same time frame and did not have the disorder. The risk of suicidal behavior for the sisters with perinatal depression was nearly three times that of their sisters without the diagnosis — almost as high as the difference between women with the illness and those without it to whom they were not related. That suggests depression plays a greater role in these outcomes than genetics or childhood environment, the researchers wrote. © 2024 The New York Times Company

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: 29089 - Posted: 01.11.2024

By Christina Jewett and Benjamin Mueller In early 2020, the Food and Drug Administration responded to decades of escalating concerns about a commonly prescribed drug for asthma and allergies by deploying one of its most potent tools: a stark warning on the drug’s label that it could cause aggression, agitation and even suicidal thoughts. The agency’s label, which was primarily aimed at doctors, was supposed to sound an alert about the 25-year-old medication, Singulair, also known by its generic name, montelukast. But it barely dented use: The drug was still prescribed to 12 million people in the United States in 2022. Children face the greatest risks of the drug’s ill effects, and while usage by minors did decline, it was still taken by 1.6 million of them — including Nicole Sims’s son. Ms. Sims had no idea why, at 6, her son started having nightmares and hallucinations of a woman in the window. When he told her that he wanted to die, Ms. Sims went online, desperate for answers. Only then did she learn about the F.D.A. warning. She also found a Facebook support group with 20,000 members for people who had experienced side effects of the drug. Members of the group recounted a haunting toll that they linked to the drug with the help of peers, not their doctors. “It’s a mental health crisis that nobody is recognizing,” said Anna Maria Rosenberg, an administrator of the group. The F.D.A.’s handling of Singulair illustrates systemic gaps in the agency’s approach to addressing troubling side effects from medicines approved long ago — and to warning the public and doctors when serious issues arise. The agency had flagged the 2020 warning label, known as a “boxed warning,” to physicians’ groups, but it had not required that doctors be educated about the drug’s side effects. Federal regulators in 1998 initially dismissed evidence that emerged during the approval process about the drug’s potential to affect the brain and did not revise their assessment until two decades later. The F.D.A. was slow to alert the public as reports of psychiatric problems surfaced, highlighting deficiencies of a drug-monitoring system that puts the onus on drugmakers to report problems. © 2024 The New York Times Company

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: 29087 - Posted: 01.09.2024

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,

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: 29066 - Posted: 12.27.2023

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.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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.,

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: 29027 - Posted: 12.02.2023

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

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: 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

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: 28986 - Posted: 11.04.2023

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

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: 28952 - Posted: 10.10.2023

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

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: 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

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 28932 - 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.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 28924 - Posted: 09.23.2023

By Phil Jaekl In the mid-1970s, a British researcher named Anthony Barker wanted to measure the speed at which electrical signals travel down the long, slender nerves that can carry signals from the brain to muscles like those in the hand, triggering movement. To find out, he needed a way to stimulate nerves in people. Researchers had already used electrodes placed on the skin to generate a magnetic field that penetrated human tissue — this produced an electric current that activated the peripheral nerves in the limbs. But the technique was painful, burning the skin. Barker, at the University of Sheffield in England, and his colleagues started to work on a better method. In 1985, with promising results under their belts, they tried positioning the coil-shaped magnetic device they’d developed on participants’ heads. The coil emitted rapidly alternating magnetic pulses over the brain region that controls movement, generating weak electrical currents in the brain tissue and activating neurons that control muscles in the hand. After about 20 milliseconds, the participants’ fingers twitched. The technique, now called transcranial magnetic stimulation (TMS), has proved a vital tool for investigating how the human brain works. When targeted to specific brain regions, TMS can temporarily inhibit or enhance various functions – blocking the ability to speak, for instance, or making it easier to commit a series of numbers to memory. And when brain imaging technologies such as functional magnetic resonance imaging (fMRI) emerged in the 1990s, researchers could now “see” inside people’s brains as they received TMS stimulation. They could also observe how neural pathways respond differently to stimulation in psychiatric illnesses like schizophrenia and depression. In recent decades, this fundamental research has yielded new treatments that alter brain activity, with TMS therapies for depression at the fore. In 2008, the US Food and Drug Administration approved NeuroStar, the nation’s first TMS depression device, and many other countries have since sanctioned the approach. Yet even though TMS is now a widely available depression treatment, many questions remain about the method. It’s not clear how long the benefits of TMS can last, for example, or why it appears to work for some people with depression but not others. Another challenge is disentangling the effects of TMS from the placebo effect — when someone believes that they will benefit from treatment and gets better even though they’re receiving a “sham” form of stimulation. © 2023 Annual Reviews

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 28903 - Posted: 09.10.2023

By Astrid Landon In June 2015, Jeffrey Thelen’s parents noticed their son was experiencing problems with his memory. In the subsequent years, he would get lost driving to his childhood home, forget his cat had died, and fail to recognize his brother and sister. His parents wondered: Was electroconvulsive therapy to blame? Thelen had been regularly receiving the treatment to help with symptoms of severe depression, which he’d struggled with since high school. At 34 years old, he had tried medications, but hadn’t had a therapy plan. His primary care physician referred him to get an evaluation for ECT, which was then prescribed by a psychiatrist. Electroconvulsive therapy has been used to treat various mental illnesses since the late 1930s. The technique, which involves passing electrical currents through the brain to trigger a short seizure, has always had a somewhat torturous reputation. Yet it’s still in use, in a modified form of its original version. According to one commonly cited statistic, 100,000 Americans receive ECT annually — most often to ease symptoms of severe depression or bipolar disorder — although exact demographic data is scarce. For Thelen, the treatment appeared to relieve his depression symptoms somewhat, but he reported new headaches and concentration issues, in addition to the memory loss. Those claims are central to a lawsuit Thelen filed in 2020 against Somatics, LLC and Elektrika, Inc., manufacturers and suppliers of ECT devices, alleging that the companies failed to disclose — and even intentionally hid — risks associated with ECT, including “brain damage and permanent neurocognitive injuries.” Thelen’s legal team told Undark that they have since reached a resolution with Elektrika on confidential terms. With regard to Somatics, in June a jury found that the company failed to warn about risks associated with ECT, but could not conclude that there was a legal causation between that and Thelen’s memory loss. The following month, his lawyers filed a motion for a new trial. (In response to a request for comment, Conrad Swartz, one of Somatics’ co-founders, directed Undark to the company’s attorney, Sue Cole. Cole did not respond to multiple emails. Lawyers for Elektrika declined to comment.)

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory and Learning
Link ID: 28899 - Posted: 09.07.2023

By Amanda Holpuch Doctors in Australia had screened, scanned and tested a woman to find out why she was sick after being hospitalized with abdominal pains and diarrhea. They were not prepared for what they found. A three-inch red worm was living in the woman’s brain. The worm was removed last year after doctors spent more than a year trying to find the cause of the woman’s distress. The hunt for the answer, and the alarming discovery, was described this month in Emerging Infectious Diseases, a monthly journal published by the Centers for Disease Control and Prevention. The woman, whom the article identifies as a 64-year-old resident of southeastern New South Wales, Australia, was admitted to a hospital in January 2021 after complaining of diarrhea and abdominal pain for three weeks. She had a dry cough and night sweats. Scientists and doctors from Canberra, Sydney and Melbourne said in the journal article that the woman was initially told she had a rare lung infection, but the cause was unknown. Her symptoms improved with treatment, but weeks later, she was hospitalized again, this time with a fever and cough. Doctors then treated her for a group of blood disorders known as hypereosinophilic syndrome, and the medicine they used suppressed her immune system. Over a three-month period in 2022, she experienced forgetfulness and worsening depression. An MRI showed that she had a brain lesion and, in June 2022, doctors performed a biopsy. Inside the lesion, doctors found a “stringlike structure” and removed it. The structure was a red, live parasitic worm, about 3.15 inches long and .04 inches in diameter. © 2023 The New York Times Company

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: 28892 - Posted: 08.30.2023

Linda Geddes I’ve made a cup of coffee, written my to-do list and now I’m wiring up my ear to a device that will send an electrical message to my brainstem. If the testimonials are to believed, incorporating this stimulating habit into my daily routine could help to reduce stress and anxiety, curb inflammation and digestive issues, and perhaps improve my sleep and concentration by tapping into the “electrical superhighway” that is the vagus nerve. From plunging your face into icy water, to piercing the small flap of cartilage in front of your ear, the internet is awash with tips for hacking this system that carries signals between the brain and chest and abdominal organs. Manufacturers and retailers are also increasingly cashing in on this trend, with Amazon alone offering hundreds of vagus nerve products, ranging from books and vibrating pendants to electrical stimulators similar to the one I’ve been testing. Meanwhile, scientific interest in vagus nerve stimulation is exploding, with studies investigating it as a potential treatment for everything from obesity to depression, arthritis and Covid-related fatigue. So, what exactly is the vagus nerve, and is all this hype warranted? The vagus nerve is, in fact, a pair of nerves that serve as a two-way communication channel between the brain and the heart, lungs and abdominal organs, plus structures such as the oesophagus and voice box, helping to control involuntary processes, including breathing, heart rate, digestion and immune responses. They are also an important part of the parasympathetic nervous system, which governs the “rest and digest” processes, and relaxes the body after periods of stress or danger that activate our sympathetic “fight or flight” responses. In the late 19th century, scientists observed that compressing the main artery in the neck – alongside which the vagus nerves run – could help to prevent or treat epilepsy. This idea was resurrected in the 1980s, when the first electrical stimulators were implanted into the necks of epilepsy patients, helping to calm down the irregular electrical brain activity that triggers seizures. © 2023 Guardian News & Media Limited

Related chapters from BN: Chapter 13: Homeostasis: Active Regulation of the Internal Environment; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 9: Homeostasis: Active Regulation of the Internal Environment; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28886 - Posted: 08.26.2023