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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

David Cox In June 2021, 32-year-old actor Kate Hyatt travelled to a farmhouse near Great Malvern in Worcerstershire for a plant medicine retreat that she hoped would improve her mental health after a difficult time during the pandemic lockdowns. While there, she is believed to have taken a substance called wachuma, or San Pedro cactus, a powerful hallucinogen used by Indigenous people in the Andes for thousands of years. But Hyatt did not experience relief; instead, her mental health worsened. Three months later, she described being in “some sort of psychotic break” and feeling as if her brain was going to explode. Later that autumn she took her own life. At the subsequent inquest, the coroner’s report linked her worsening symptoms to the hallucinogens she had consumed. Such tragedies represent the darker side of the psychedelics renaissance. These cases are often forgotten amid the feverish anticipation surrounding the therapeutic potential of these drugs, combined with exhaustive media coverage, the rapid rise of a billion-dollar industry – ranging from venture capital-backed startups to wellness retreats – and the hype around last year’s Netflix series How to Change Your Mind (based on Michael Pollan’s bestselling book). Yet without careful monitoring and scrutiny of who receives them, this class of drugs – which includes LSD, MDMA (commonly known as ecstasy or molly) and psilocybin (the active ingredient of magic mushrooms) – can be dangerous. There is evidence that they can destabilise vulnerable individuals who have experienced a previous psychotic episode or have a family history of psychosis. The substances are illegal to distribute and possess in the UK, although they are often obtained on the hidden market. Scientific researchers and biotechnology companies are able to use them in clinical trials only after obtaining a Home Office licence and applying extensive security arrangements. © 2023 Guardian News & Media Limited

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: 28873 - Posted: 08.19.2023

By Pam Belluck The Food and Drug Administration on Friday approved the first pill for postpartum depression, a milestone considered likely to increase recognition and treatment of a debilitating condition that afflicts about a half-million women in the United States every year. Clinical trial data show the pill works quickly, beginning to ease depression in as little as three days, significantly faster than general antidepressants, which can take two weeks or longer to have an effect. That — along with the fact that it is taken for just two weeks, not for months — may encourage more patients to accept treatment, maternal mental health experts said. The most significant aspect of the approval may not be the features of the drug, but that it is explicitly designated for postpartum depression. Several doctors and other experts said that while there were other antidepressants that are effective in treating the condition, the availability of one specifically shown to address it could help reduce the stigma of postpartum depression by underscoring that it has biological underpinnings and is not something women should blame themselves for. The hope is that it will encourage more women to seek help and prompt more obstetricians and family doctors to screen for symptoms and suggest counseling or treatment. “This is a patient population that just so often falls through the cracks,” said Dr. Ruta Nunacs, a psychiatrist with the Center for Women’s Mental Health at Massachusetts General Hospital. “When women are told, ‘You have postpartum depression,’ it’s embarrassing, it is demeaning, it makes them feel like a bad mom.” She added, “There’s also a lot of stigma about taking antidepressant medication, so that might make this treatment more appealing because it’s really a treatment specific for postpartum depression.” © 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: 28867 - Posted: 08.05.2023

by Brendan Borrell The New York State Psychiatric Institute in New York City is undergoing an audit and a change in leadership following a suicide that occurred during one of its clinical trials. Autism researcher Jeremy Veenstra-VanderWeele has abruptly taken the helm as the interim executive director of the institute and chair of the Columbia University psychiatry department, replacing Helen Blair Simpson, Spectrum has learned. The New York State Psychiatric Institute is part of the New York State Office of Mental Health, but it shares buildings and staff with Columbia University and the university’s hospital. The Office of Mental Health is currently conducting an audit of the institute, according to Carla Cantor, the institute’s director of communications. The audit and turnover in leadership comes after the halting of a series of clinical trials conducted by Columbia psychiatrist Bret Rutherford, which tested whether the drug levodopa — typically used to treat Parkinson’s disease — could improve mood and mobility in adults with depression. During a double-blind study that began in 2019, a participant in the placebo group died by suicide. That study was suspended prior to completion, according to an update posted on ClinicalTrials.gov in 2022. Two published reports based on Rutherford’s pilot studies have since been retracted, as Spectrum has previously reported. The National Institute of Mental Health has terminated Rutherford’s trials and did not renew funding of his research grant or K24 Midcareer Award. Former members of Rutherford’s laboratory describe it as a high-pressure environment that often put publications ahead of study participants. “Research is important, but not more so than the lives of those who participate in it,” says Kaleigh O’Boyle, who served as clinical research coordinator there from 2018 to 2020. © 2023 Simons Foundation

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28861 - Posted: 08.02.2023

By Stephanie Pappas Have you felt butterflies in your stomach or hunger pangs? Those “gut feelings” happen thanks to the vagus nerve, which is a superhighway that connects the brain and the gut. In recent years the vagus nerve has become an intriguing target for researchers looking to cure disorders of both the brain and the body. Vagus nerve stimulation—usually achieved with an electrode implanted in the neck to deliver electrical pulses directly to the nerve—is an approved treatment for epilepsy and some forms of depression. Scientists are now studying vagus nerve stimulation (VNS) for disorders such as rheumatoid arthritis and the inflammatory bowel disease Crohn’s. What gives this nerve such widespread impact? The vagus nerve is the longest of the cranial nerves, which emerge directly from the brain rather than traveling through the spinal cord. It begins at an opening at the base of the skull and runs down the neck and into the abdomen, where it collects signals from the viscera and helps regulate the automatic processes of the body, from digestion to sleep to inflammation. About 80 percent of its signals are sensory ones that travel from the inner organs up to the brain, while the other 20 percent travel from the brain to the body and regulate things such as intestinal contractions and heart rate. The vagus nerve is the key player in the parasympathetic nervous system, which is the “rest and digest” system that calms the body during times of low stress. “If you are relaxed, if you are sleeping, if you are in a restorative phase, it’s the vagus nerve dominating,” says Gregor Hasler, a psychiatrist at the University of Fribourg in Switzerland, who has written about the gut-brain connection.

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: 28843 - Posted: 07.06.2023

By Sujata Gupta Teenagers in the United States are in crisis. That news got hammered home earlier this year following the release of a nationally representative survey showing that over half of high school girls reported persistent feelings of “sadness or hopelessness” — common words used to screen for depression. Almost a third of teenage boys reported those same feelings. “No one is doing well,” says psychologist Kathleen Ethier. She heads the U.S. Centers for Disease Control and Prevention’s Division of Adolescent and School Health, which has overseen this biennial Youth Risk Behavior Survey since 1991. During the latest round of data collection, in fall 2021, over 17,000 students from 31 states responded to roughly 100 questions related to mental health, suicidal thoughts and behaviors, sexual behavior, substance use and experiences of violence. One chart in particular garnered considerable media attention. From 2011 to 2021, persistent sadness or hopelessness in boys went up 8 percentage points, from 21 to 29 percent. In girls, it rose a whopping 21 percentage points, from 36 to 57 percent. Some of that disparity may arise from the fact that girls in the United States face unique stressors, researchers say. Compared with boys, girls seem more prone to experiencing mental distress from social media use, are more likely to experience sexual violence and are dealing with a political climate that is often hostile to women’s rights (SN: 7/16/22 & 7/30/22, p. 6). But the gap between boys and girls might not be as wide as the numbers indicate. Depression manifests differently in boys and men than in girls and women, mounting evidence suggests. Girls are more likely to internalize feelings, while boys are more likely to externalize them. Rather than crying when feeling down, for instance, boys may act irritated or lash out. Or they may engage in risky, impulsive or even violent acts. Inward-directed terms like “sadness” and “hopelessness” miss those more typically male tendencies. And masculine norms that equate sadness with weakness may make males who are experiencing those emotions less willing to admit it, even on an anonymous survey. © Society for Science & the Public 2000–2023

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: 28841 - Posted: 07.01.2023

Sara Reardon Psychedelic drugs are promising treatments for many mental-health conditions, but researchers don’t fully understand why they have such powerful therapeutic effects. Now, a study in mice suggests that psychedelics all work in the same way: they reset the brain to a youthful state in which it can easily absorb new information and form crucial connections between neurons1. The findings raise the prospect that psychedelic drugs could allow long-term changes in many types of behavioural, learning and sensory system that are disrupted in mental-health conditions. But scientists caution that more research needs to be done to establish how the drugs remodel brain connections. The study was published on 14 June in Nature. Psychedelics such as MDMA (also known as ecstasy), ketamine and psilocybin — the active ingredient in magic mushrooms — are known for producing mind-altering effects, including hallucinations in some cases. But each compound affects a different biochemical pathway in the brain during the short-term ‘trip’, leaving scientists to wonder why so many of these drugs share the ability to relieve depression2, addiction and other difficult-to-treat conditions in the long term. Gül Dölen, a neuroscientist at Johns Hopkins University in Baltimore, Maryland, and her colleagues sought answers by studying how psychedelics affect social behaviour in mice. Mice can learn to associate socializing with positive feelings, but only during an adolescent ‘critical period’, which closes as they become adults. The scientists trained mice to associate one ‘bedroom’ in their enclosure with mousy friends and another room with solitude. They could then examine how psychedelics affected the rodents’ room choices — a proxy for whether the drug affects the critical period. © 2023 Springer Nature Limited

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: 28825 - Posted: 06.17.2023

By Christina Caron A new study suggests that, for some patients, the anesthetic ketamine is a promising alternative to electroconvulsive therapy, or ECT, currently one of the quickest and most effective therapies for patients with difficult-to-treat depression. The study is the largest head-to-head comparison of the two treatments. Patients who don’t respond to at least two antidepressants — about one-third of clinically depressed patients — have a condition that clinicians refer to as “treatment-resistant.” Their options for relief are limited. Doctors typically recommend up to 12 sessions of ECT, which has a long-established efficacy, but is tainted by the stigma of historical misuse and frightening Hollywood images of people strapped to tables, writhing in agony. Today’s ECT is much safer and done under general anesthesia, but the procedure remains underutilized. The study, published on Wednesday in The New England Journal of Medicine, found that ketamine, when administered intravenously, was at least as effective as ECT in patients with treatment-resistant depression who do not have psychosis. (For people with psychosis, ketamine, even in very low doses, can worsen psychosis-like symptoms.) “The results were very surprising to us,” said Dr. Amit Anand, lead author of the study and a professor of psychiatry at Harvard Medical School who studies mood disorders at Mass General Brigham. His team had initially hypothesized that ketamine would be nearly as effective as ECT. Instead, Dr. Anand said, they found that ketamine performed even better than that. This is significant in part because some patients are uncomfortable with ECT’s potential side effects, such as temporary memory loss, muscle pain or weakness. (In rare cases it can result in permanent gaps in memory.) © 2023 The New York Times Company

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: 28806 - Posted: 05.31.2023

By Claudia Lopez Lloreda Ketamine is a powerful anesthetic and sometimes recreational drug that causes people to feel dissociated from their own bodies. Recent studies suggest the drug may help treat people with depression who have tried more conventional treatments without success. But there are major questions about what makes it work. Is it the weird dissociative experience? Some molecular effect on the brain? Or just the experience of being in a clinical trial? In a new study that is yet to be peer reviewed, researchers attempted to find the answer in a unique way: They gave volunteers ketamine while they were under general anesthesia, theoretically preventing the participants from going on a trip. The approach alleviated the subjects’ depression, but not any better than a placebo did. The authors interpret this as evidence that ketamine’s effects on depression are strongly tied to a patient’s experience of being seen by medical professionals. But other experts say the study’s implications may be more complicated. Ketamine causes “dissociative” effects such as out-of-body experiences. Patients sometimes also report visual and auditory hallucinations—the voices of friends and family members who aren’t there, for example. The dissociative effects of ketamine have been linked to a stronger antidepressant response, possibly by helping patients reframe their experience from an outside perspective. But it’s a problem for researchers running double-blinded clinical trials, as participants can usually tell whether they have received ketamine or a placebo. To disentangle the subjective experience of ketamine from the biochemical effects of the drug, researchers at Stanford University recruited 40 participants who were preparing to undergo general surgery and who also had mild to moderate depression. The scientists gave the volunteers ketamine or saline as placebo right after they were put under anesthesia, but before their surgery, essentially blinding them to any psychedelic or dissociative effects. Then, for the next 3 days, the researchers surveyed the participants on their depression symptoms, scoring them on such factors as sadness, loss of appetite, and lack of sleep.

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: 28789 - Posted: 05.21.2023

Hannah Devlin Daniela da Silva is feeling good. Lying cocooned under fleece blankets inside a medical scanner, her eyes are closed and her mind is focused and remarkably unperturbed by negative thoughts. Three hours earlier, the 39-year-old yoga teacher and neuroscience student was given a dose of the stimulant drug dextroamphetamine, which is often used to treat ADHD. “I’m having a serotonin increase. Oh definitely,” she predicts before entering the PET scanner. Da Silva is a healthy volunteer in a trial using a pioneering brain imaging technique designed to measure serotonin changes in the brains of living people. Last year, scientists used the scan to obtain what they claimed to be the first direct evidence that serotonin release is blunted in the brains of people with depression. The findings added fuel to a fiercely fought debate over the role of the brain chemical – if any – in depression. Just months earlier, a high-profile scientific review caused a stir when it reached the opposite conclusion that “after a vast amount of research, conducted over several decades, there is no convincing evidence” for the idea that depression is caused by a chemical imbalance in the brain. To many, it was news that the case for serotonin being implicated in depression was not already watertight. The idea of a chemical imbalance is embedded in public consciousness and has shaped the way we view mental illness. The main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are widely assumed to work by boosting serotonin levels. So the suggestion that the way we discuss, and treat, mental illness might be based on shaky foundations was disconcerting. But it also served as a wake-up call that this view of depression has failed to provide effective treatments for a substantial proportion of those affected. Serotonin is sometimes referred to as the “happy hormone”, conjuring up the image of a substance that swooshes through the brain leaving a warm glow of contentment in its wake. In reality, its biological role is complex and extends to basic functions like the regulation of sleep, intestinal activity and the formation of blood clots. In the brain, serotonin acts as a chemical messenger between neurons, but also as a form of volume control that alternately increases or decreases the level of communication between other neurons. “Put another way, serotonin fine-tunes the working of the brain, regulating how different parts of the brain communicate with each other,” says Dr James Rucker, a consultant psychiatrist at South London and Maudsley NHS foundation trust, whose research focuses on developing new treatments for depression. © 2023 Guardian News & Media Limited

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: 28703 - Posted: 03.15.2023

By Sheryl Gay Stolberg and Ellen Barry Lynn Rivers, a Democrat from Michigan, opened up about her diagnosis with bipolar disorder during a radio call-in show when she first ran for Congress. Her opponents had been hinting she had mental health problems. She decided, spur of the moment, to let it out. “Finally, I just said, ‘Are you asking me if I have depression? Yes, and so do thousands and millions of other people,’” she recalled. “I was like, ‘OK, here we go. The ball is thrown at you, just hit it.’ And so I did.” That was 1994. Ms. Rivers was elected, despite a Republican tidal wave, and served four terms. Now another Democrat, Senator John Fetterman of Pennsylvania, has announced that he has entered a hospital to be treated for clinical depression. Politicians of both parties are praising him for his openness. Mental health experts say he is a powerful symbol — especially for men, who are less likely to seek treatment for depression and suffer higher rates of suicide. Yet the stigma around mental illness remains strong — especially in politics, where questions about temperament can determine a candidate’s electability. Mr. Fetterman and others face a continuing challenge: How much do they really want to say? “We’ve come a long way; people are willing to say they have a diagnosis or that they’re going to therapy,” said Patrick J. Kennedy, a scion of the political Kennedy family, who disclosed his treatment for bipolar disorder and drug abuse when he was a congressman from Rhode Island. “But we’re still not in a place where people are comfortable saying any more than that. And really the question with Senator Fetterman is: How much is he going to disclose?” Clinical depression, also called major depression, is a severe form of the disease. Symptoms may include feelings of sadness, hopelessness or guilt; angry outbursts; loss of pleasure in ordinary activities; fatigue; anxiety; reduced appetite; and thoughts of suicide. In recent years, there have been great strides in treatment. © 2023 The New York Times Company

Related chapters from BN: Chapter 19: Language and Lateralization; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 15: Language and Lateralization; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28671 - Posted: 02.18.2023

By Laura Sanders You’d be forgiven for thinking that depression has a simple explanation. The same mantra — that the mood disorder comes from a chemical imbalance in the brain — is repeated in doctors’ offices, medical textbooks and pharmaceutical advertisements. Those ads tell us that depression can be eased by tweaking the chemicals that are off-kilter in the brain. The only problem — and it’s a big one — is that this explanation isn’t true. The phrase “chemical imbalance” is too vague to be true or false; it doesn’t mean much of anything when it comes to the brain and all its complexity. Serotonin, the chemical messenger often tied to depression, is not the one key thing that explains depression. The same goes for other brain chemicals. The hard truth is that despite decades of sophisticated research, we still don’t understand what depression is. There are no clear descriptions of it, and no obvious signs of it in the brain or blood. The reasons we’re in this position are as complex as the disease itself. Commonly used measures of depression, created decades ago, neglect some important symptoms and overemphasize others, particularly among certain groups of people. Even if depression could be measured perfectly, the disorder exists amid myriad levels of complexity, from biological confluences of minuscule molecules in the brain all the way out to the influences of the world at large. Countless combinations of genetics, personality, history and life circumstances may all conspire to create the disorder in any one person. No wonder the science is stuck. So here, up front, is your fair warning: There will be no satisfying wrap-up at the end of this story. You will not come away with a scientific explanation for depression, because one does not exist. But there is a way forward for depression researchers, Aftab says. It requires grappling with nuances, complexity and imperfect data. © Society for Science & the Public 2000–2023.

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: 28670 - Posted: 02.15.2023

By Joanna Thompson People often think they know what causes chronic depression. Surveys indicate that more than 80% of the public blames a “chemical imbalance” in the brain. That idea is widespread in pop psychology and cited in research papers and medical textbooks. Listening to Prozac, a book that describes the life-changing value of treating depression with medications that aim to correct this imbalance, spent months on the New York Times bestseller list. The unbalanced brain chemical in question is serotonin, an important neurotransmitter with fabled “feel-good” effects. Serotonin helps regulate systems in the brain that control everything from body temperature and sleep to sex drive and hunger. For decades, it has also been touted as the pharmaceutical MVP for fighting depression. Widely prescribed medications like Prozac (fluoxetine) are designed to treat chronic depression by raising serotonin levels. Yet the causes of depression go far beyond serotonin deficiency. Clinical studies have repeatedly concluded that the role of serotonin in depression has been overstated. Indeed, the entire premise of the chemical-imbalance theory may be wrong, despite the relief that Prozac seems to bring to many patients. If you were still of the opinion that it was simply a chemical imbalance of serotonin, then yeah, it’s pretty damning. A literature review that appeared in Molecular Psychiatry in July was the latest and perhaps loudest death knell for the serotonin hypothesis, at least in its simplest form. An international team of scientists led by Joanna Moncrieff of University College London screened 361 papers from six areas of research and carefully evaluated 17 of them. They found no convincing evidence that lower levels of serotonin caused or were even associated with depression. People with depression didn’t reliably seem to have less serotonin activity than people without the disorder. Experiments in which researchers artificially lowered the serotonin levels of volunteers didn’t consistently cause depression. Genetic studies also seemed to rule out any connection between genes affecting serotonin levels and depression, even when the researchers tried to consider stress as a possible cofactor. All Rights Reserved © 2023

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: 28647 - Posted: 01.27.2023

Liam Drew The emergence of disease-causing bacteria that are resistant to antibiotics is often attributed to the overuse of antibiotics in people and livestock. But researchers have homed in on another potential driver of resistance: antidepressants. By studying bacteria grown in the laboratory, a team has now tracked how antidepressants can trigger drug resistance1. “Even after a few days exposure, bacteria develop drug resistance, not only against one but multiple antibiotics,” says senior author Jianhua Guo, who works at the Australian Centre for Water and Environmental Biotechnology at the University of Queensland in Brisbane. This is both interesting and scary, he says. Globally, antibiotic resistance is a significant public-health threat. An estimated 1.2 million people died as a direct result of it in 20192, and that number is predicted to climb. Early clues Guo became interested in the possible contributions of non-antibiotic drugs to antibiotic resistance in 2014, after work by his lab found more antibiotic-resistance genes circulating in domestic wastewater samples than in samples of wastewater from hospitals, where antibiotic use is higher. Guo’s group and other teams also observed that antidepressants — which are among the most widely prescribed medicines in the world — killed or stunted the growth of certain bacteria. They provoke “an SOS response”, Guo explains, triggering cellular defence mechanisms that, in turn, make the bacteria better able to survive subsequent antibiotic treatment. © 2023 Springer Nature Limited

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: 28645 - Posted: 01.27.2023