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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

Hannah Devlin Science correspondent Widely used antidepressants cause “emotional blunting”, according to research that offers new insights into how the drugs may work and their possible side-effects. The study found that healthy volunteers became less responsive to positive and negative feedback after taking a selective serotonin reuptake inhibitor (SSRI) drug for three weeks. The “blunting” of negative emotions could be part of how the drugs help people recover from depression, but could also explain a common side-effect. The work’s senior author, Prof Barbara Sahakian of the University of Cambridge, said: “In a way, this may be in part how they work. They take away some of the emotional pain that people who experience depression feel, but unfortunately it seems that they also take away some of the enjoyment.” The findings could help patients make better informed choices about their medication, she said, but added “there is no doubt that antidepressants are beneficial” for many patients. According to the NHS more than 8.3 million patients in England received an antidepressant drug in 2021-22. SSRIs are among the most widely used, and are effective for the majority of, although not all, patients. Some people on the medication report feeling emotionally dull or no longer finding things as pleasurable, with one study suggesting this applied to 40-60% of people taking the drug. However, it has been unclear whether this symptom is a drug side-effect or a symptom of depression. The latest work suggests that the drug alone can produce emotional blunting. In the study, published in the journal Neuropsychopharmacology, 66 volunteers were given either the SSRI drug, escitalopram, or a placebo for at least 21 days before doing a set of cognitive tests. © 2023 Guardian News & Media 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: 28641 - Posted: 01.25.2023

By Sandra G. Boodman The 23-year-old patient arrived in the back of a police car and was in four point restraints — hands and feet strapped to a gurney — when emergency physician Elizabeth Mitchell saw her at a Los Angeles hospital early on March 17. Chloe R. Kral was being held on a 5150, shorthand in California for an emergency psychiatric order that allows people deemed dangerous to themselves or others to be involuntarily confined for 72 hours. She had spent the previous six months at a private treatment center receiving care for bipolar disorder and depression. Chloe had improved and was set to move to transitional housing when she suddenly became combative and threatened to harm staff and kill herself. Police had taken her to the emergency room at Cedars-Sinai Marina del Rey Hospital before a planned transfer to a mental hospital. Chloe, Mitchell recalled, was “mumbling about Rosa Parks” when they met. She managed to tell the doctor that she hadn’t used drugs or alcohol, but was otherwise incoherent. “We get a lot of psychiatric patients, and they’re just waiting for placement,” Mitchell said. But something indefinable — Mitchell characterized it as “maybe gut instinct” honed by nearly two decades of practice — prompted her to order a CT scan of Chloe’s head to better assess her mental status. When she pulled up the image, Mitchell gasped. “I had never seen anything like it,” she said. She rounded up her colleagues and “made everyone in the whole ER come look.” “I was speechless,” she said. “All I could think was ‘How did no one figure this out?’ ”

Related chapters from BN: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory and Learning; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 28603 - Posted: 12.21.2022

Hannah Devlin Science correspondent Scientists claim to have found the first direct evidence that people with depression have a reduced capacity for releasing serotonin in the brain. The findings from a brain-imaging study reignite a debate within psychiatry over the so-called serotonin hypothesis of depression and challenge the conclusions of an influential review published in July that found “no clear evidence” that low serotonin levels are responsible. The latest work, led by scientists at Imperial College London, suggested that people with depression have a decreased serotonin response. “This is the first direct evidence that the release of serotonin is blunted in the brains of people with depression,” said Prof Oliver Howes, a consultant psychiatrist based at Imperial College and King’s College London, and a co-author. “People have been debating this question for 60 years, but it’s all been based on indirect measures. So this is a really important step.” The serotonin hypothesis arose from evidence from postmortem brains and blood samples that suggested a serotonin deficit could be involved in depression. The theory provides a plausible biological mechanism for how the main class of antidepressant drugs, selective serotonin reuptake inhibitors (SSRIs), are effective, and is why the brain chemical is sometimes referred to as a “happy hormone”. However, there is not yet conclusive evidence that serotonin abnormalities are the underlying cause of depression and resolving this question is seen as crucial to providing better treatments. The latest paper adds weight to the view that serotonin plays a role and demonstrates a new brain imaging technique that could pave the way to a better understanding of why SSRI drugs fail to help an estimated 10% to 30% of patients. “It’s the closest anyone has been able to get so far,” said Howes. “It’s hard to measure these transmitters in the brains of living people. We can’t put a pipette in there and take a sample. This is the closest we’re likely to come.” © 2022 Guardian News & Media Limited o

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: 28541 - Posted: 11.05.2022

By Leo Sands Psilocybin, the active hallucinogen found in psychedelic mushrooms — also known as “magic mushrooms” — can effectively alleviate a severe bout of depression when administered in a single dose and combined with talk therapy, a new clinical study found. Adults with depression who were administered a single 25-miligram dose of psilocybin were more likely to experience significant improvements in their mental health — both immediately and for up to three months — than others who were randomly assigned smaller doses of the same drug, said the peer-reviewed study, which was published Wednesday in the New England Journal of Medicine. “There’s something about the psychedelic experience that leads to a rapid resolution of depression symptoms,” said James Rucker, a consultant psychiatrist at King’s College London who worked on the trial. “We don’t really know what that is at the moment, but it’s very different to standard antidepressants.” The trial’s findings could be an encouraging sign for the 16 million Americans estimated each year by the Centers for Disease Control and Prevention to have depression, many of whom struggle to find treatments that work for them. Its authors hope the study — which was relatively small, with just 79 participants receiving the 25 mg dose — will pave the way for eventual regulatory approval of psilocybin by the Food and Drug Administration for use as a drug against depression. The new study randomly assigned 233 adults with depression three doses of psilocybin — 25 mg, 10 mg and 1 mg — across 22 sites in 10 countries. The authors found that the group given the largest dose recorded the most significant improvements in their depression, both immediately and for several weeks after.

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: 28540 - Posted: 11.05.2022

Jon Hamilton Computer games designed to boost self-esteem appear to prolong the antidepressant benefits of the mind-bending anesthetic ketamine. A recent study of 154 people found that those who played games featuring smiling faces and positive messages remained free of depression up to three months after a ketamine infusion, a team reports in the American Journal of Psychiatry. People who got ketamine alone tended to relapse after a week or two. The results are important because "we need new approaches that help people get feeling better faster and help them stay feeling better," says Rebecca Price, an author of the study and an associate professor of psychiatry and psychology at the University of Pittsburgh. Established drugs like Prozac and Zoloft can take weeks to ease depression, and don't work for every patient. Ketamine can offer immediate relief, but the effects often fade after a few days or weeks. "And then returning for infusions over and over to keep that relief going can end up being really burdensome and costly," Price says, "and just isn't accessible to all patients." So Price and a team of researchers wanted to find a way to make ketamine's antidepressant effects last longer. They decided to focus on a common symptom of depression: low self-esteem and self-loathing. The team drew on research suggesting that ketamine temporarily causes certain brain areas to enter a state in which they form lots of new connections. During this period, the brain seems to be more receptive to learning and change. "So we tried to use that window of opportunity just after ketamine to strengthen associations specifically between the idea of me, myself, and positive information and attributes," Price says. © 2022 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: 28535 - Posted: 11.02.2022

By Jyoti Madhusoodanan Q: I recently started taking an S.S.R.I. antidepressant, but I have been confused about whether it’s safe to drink alcohol. Some internet sources say it’s fine, others say to avoid drinking completely. Help! For many health care providers who treat anxiety and depression, the concern about whether it’s safe — or even advised — to drink alcohol while taking an antidepressant is a common one. “Patients tell me all the time, ‘I’m going to be drinking with friends tonight, so I skipped a dose,’” said Dr. Sarah Ramsay Andrews, a psychiatrist at the Johns Hopkins University School of Medicine. But skipping a dose is never a good idea, said Dr. Jody Glance, an addiction medicine specialist at the University of Pittsburgh Medical Center Western Behavioral Health — even if you’re going out for cocktails with friends. “When people stop taking their medicines for a day or two, they often don’t resume, and that can lead to a relapse of anxiety or depression.” Besides, she added, how safe it is to drink while on antidepressants depends on the kind of antidepressant you’re taking — and for most people taking selective serotonin reuptake inhibitors (or S.S.R.I.s), an occasional drink likely won’t do much harm. There are, however, caveats to keep in mind. S.S.R.I. medications — which include citalopram (Celexa), sertraline (Zoloft) and escitalopram (Lexapro) — are the most commonly prescribed class of antidepressants. They are typically used to help treat depression, and can also be effective for other conditions like anxiety, obsessive compulsive disorder, certain phobias and even premenstrual dysphoric disorder. They work by increasing the levels of the brain chemical serotonin — which is thought to influence your mood and emotions, among other things — by blocking its removal after it carries messages in the brain. But unlike many other medications used to treat mood disorders — like the anxiety medication alprazolam (Xanax) or the tricyclic antidepressant amitriptyline (Elavil) — S.S.R.I.s are less likely to interact with alcohol than other kinds of drugs, Dr. Glance said. © 2022 The New York Times Company

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: 28517 - Posted: 10.19.2022

Jon Hamilton Drugs like magic mushrooms and LSD can act as powerful and long-lasting antidepressants. But they also tend to produce mind-bending side-effects that limit their use. Now, scientists report in the journal Nature that they have created drugs based on LSD that seem to relieve anxiety and depression – in mice – without inducing the usual hallucinations. "We found our compounds had essentially the same antidepressant activity as psychedelic drugs," says Dr. Bryan Roth, an author of the study and a professor of pharmacology at UNC Chapel Hill School of Medicine. But, he says, "they had no psychedelic drug-like actions at all." The discovery could eventually lead to medications for depression and anxiety that work better, work faster, have fewer side effects, and last longer. The success is just the latest involving tripless versions of psychedelic drugs. One previous effort created a hallucination-free variant of ibogaine, which is made from the root bark of a shrubby plant native to Central Africa known as the iboga tree. "It's very encouraging to see multiple groups approach this problem in different ways and come up with very similar solutions," says David E. Olson, a chemical neuroscientist at the University of California, Davis, who led the ibogaine project. The new drug comes from a large team of scientists who did not start out looking for an antidepressant. They had been building a virtual library of 75 million molecules that include an unusual structure found in a number of drugs, including the psychedelics psilocybin and LSD, a migraine drug (ergotamine), and cancer drugs including vincristine. The team decided to focus on molecules that affect the brain's serotonin system, which is involved in regulating a person's mood. But they still weren't looking for an antidepressant. Roth recalls that during one meeting, someone asked, "What are we looking for here anyway? And I said, well, if nothing else, we'll have the world's greatest psychedelic drugs." © 2022 npr

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: 28502 - Posted: 10.05.2022

Daniel Merino & Josjan Zijlmans As research into psychedelics and their medical uses makes a comeback, scientists are having to deal with the legacy – both scientific and social – of a 40-year nearly total freeze on psychedelics research. In this episode of “The Conversation Weekly” podcast, we speak with three experts about the early rise and fall of psychedelics in Western science and culture, how the mystical and often vague language of the ‘60s and '70s still pervades research today and what it’s like to actually run clinical trials using psilocybin. According to a poll done in the summer of 2022, nearly 30% of U.S. residents have tried at least one psychedelic drug in their lifetime. Whether from personal experience, hearing about the experiences of friends or widespread depictions in the media, many people will have either tried to describe a psychedelic trip or heard someone else describe one. The language commonly used in these descriptions is, for lack of a better word, often quite trippy. “A key function of the ego is to identify differentiation,” says Robin Carhart-Harris, a neurologist and psychologist at the University of California, San Francisco, and one of the world’s leading psychedelics researchers. “And when that function breaks down, it’s replaced with a sense of de-differentiation, a sense of unity, like everything is interconnected in a web of relationships. That’s not nothingness, it’s sort of everythingness.” Many psychedelics researchers use an approach called “the mystical framework” to assess psychedelic experiences. Researchers who use this framework give participants in psychedelics studies a survey as a way to define and categorize the experience. The survey asks participants to rate how strongly they felt certain phenomena during their trip, including feelings like the “certainty of encounter with ultimate reality (in the sense of being able to 'know’ and ‘see’ what is really real at some point during your experience).” © 2010–2022, The Conversation US, Inc.

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: 28496 - Posted: 10.01.2022

Perspective by Steven Petrow A few weeks ago, I mentioned to a friend that I was interested in learning more about psychedelics, especially how they might help me with depression and anxiety. That’s a broad category of plant medicines including psilocybin (“magic”) mushrooms, MDMA (ecstasy), DMT (Dimitri or the Businessman’s Trip), ketamine (“special K”) and some others. I’d been hesitant to be open about my search, because I’m old enough to remember the warnings about “bad trips” that scramble your brain. Imagine my surprise when my friend told me he’d recently taken his first “trip,” which he described as life-changing. I asked him — a real estate developer living in Northern California, married with kids — why he decided to try a psychedelic substance. “My work felt increasingly stale and meaningless,” he explained to me over a beer. “Despite a massive amount of reflection and coaching around how to break the rut, I felt as though I was still off track.” He and the others who have used these medicines spoke on the condition of anonymity because most of these psychedelics are Schedule I substances, meaning they are illegal to manufacture, buy, possess or distribute. When I confided my interest in psychedelics to a few other friends, several said they had tried the drugs and experienced several benefits: from easing anxiety to finding spiritual insights to combating depression and, among some with cancer, helping to reduce the fear of dying. They are hardly outliers. According to a new YouGovAmerica study, “one in four Americans say they’ve tried at least one psychedelic drug,” amounting to some 72 million U.S. adults. (The study included the medicines mentioned earlier, plus LSD, mescaline and salvia.) Was I missing a beat by not getting onboard?

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: 28463 - Posted: 09.07.2022

Adam Miller · CBC News · A new analysis of the cause of depression has seemingly upended what we know about this common condition and challenged the use of antidepressants. But it may also leave patients with more questions than answers as the science evolves. A systematic umbrella review of 17 studies published in Molecular Psychology on July 20 looked at the decades-old theory that depression is caused by low serotonin, and found there was "no consistent evidence" of "an association between serotonin and depression." The theory that depression is caused by a chemical imbalance in the brain has been around since the 1960s. But for years, many experts have doubted this, feeling it oversimplified a complex condition. "The serotonin theory is very old and has been very popular since the '90s, when the pharmaceutical industry started promoting it," said Dr. Joanna Moncrieff, a psychiatry professor at University College London and lead author of the study. "But since about 2005, probably a bit before then, there's been sort of rumours that actually the evidence isn't very strong, or it's inconsistent. Some studies are positive, some studies are negative, but no one's really got that evidence together anywhere." Moncrieff and her team set out to challenge the serotonin theory in a systematic review of available research. They also went a step further in their conclusion by suggesting that antidepressants are ineffective at treating depression — and have largely worked as a placebo. ©2022 CBC/Radio-Canada.

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: 28434 - Posted: 08.13.2022

By Sarah Wild In 2015, psychiatrist Mark Horowitz tried to come off his antidepressants. He reduced his dosage by a set proportion over the course of several months, which is much longer than what the United Kingdom’s guidelines recommended. But in the process of tapering, he experienced a storm of new symptoms, including anxiety, dizziness, and bouts of insomnia. “I’d wake in the morning, feeling like I was being chased by an animal on the edge of a cliff,” he says. Ultimately, he felt he had no choice but to go back on his medication. As it happened, Horowitz had recently completed a Ph.D. on the neurobiology of antidepressants. During his training, he recalls, his professors had told him that stopping antidepressants was fairly easy. Their view was supported by the scientific literature, which had found that any withdrawal symptoms were minor and faded quickly. Experiences such as Horowitz’s were considered an anomaly. But a series of widely reported studies published over the past seven years suggest that discontinuation symptoms are common and can be severe, including everything from panic attacks and flu-like symptoms to electric shock sensations in the head. The longer people remain on antidepressants and the higher their dose, the more likely they are to experience withdrawal symptoms. Each year, millions of people begin taking antidepressants. They have been shown to help anxiety sufferers feel calmer and lift the moods of those with severe depression and balance their emotions. For many, the intervention is lifesaving. Yet even today, few physicians inform their patients about the potential difficulties of coming off the medication. Most national guidelines suggest a slow taper, but there is little to no guidance on precisely how to do this. Patients who experience intense withdrawal symptoms may end up remaining on antidepressants or turning to online peer support groups for help.

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: 28414 - Posted: 07.30.2022

Ismaeel Yunusa Taking oxycodone at the same time as certain selective serotonin reuptake inhibitors (SSRIs), a commonly prescribed class of antidepressant, can increase the risk of opioid overdose, according to a study my colleagues and I published. Doctors prescribe the opioid oxycodone to treat moderate to severe pain after surgeries and injuries or certain conditions like cancer. Opioids are also a common drug of abuse. In the U.S., over 70% of drug overdose deaths in 2019 involved an opioid. Because many patients with depression also experience chronic pain, opioids are often coprescribed with antidepressants like SSRIs. Prior research has shown that certain SSRIs, namely fluoxetine (Prozac or Sarafem) and paroxetine (Paxil, Pexeva or Brisdelle), can strongly inhibit a liver enzyme crucial to the proper breakdown of drugs in the body, including oxycodone. The resulting increased concentration of oxycodone in the blood may lead to accidental overdose. To see whether different types of SSRIs might affect a patient’s risk of overdosing on oxycodone, my colleagues and I examined data from three large U.S. health insurance claims databases. We included over 2 million adults who began taking oxycodone while using SSRIs between 2000 and 2020. The average age of the group was around 50, and a little over 72% were women. A little over 30% were taking the SSRIs paroxetine and fluoxetine. We found that patients taking paroxetine or fluoxetine had a 23% higher risk of overdosing on oxycodone than those using other SSRIs. © 2010–2022, The Conversation US, Inc.

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: 28413 - Posted: 07.30.2022

By Christina Caron In recent years, the vagus nerve has become an object of fascination, especially on social media. The vagal nerve fibers, which run from the brain to the abdomen, have been anointed by some influencers as the key to reducing anxiety, regulating the nervous system and helping the body to relax. TikTok videos with the hashtag “#vagusnerve” have been viewed more than 64 million times and there are nearly 70,000 posts with the hashtag on Instagram. Some of the most popular ones feature simple hacks to “tone” or “reset” the vagus nerve, in which people plunge their faces into ice water baths or lie on their backs with ice packs on their chests. There are also neck and ear massages, eye exercises and deep-breathing techniques. Now, wellness companies have capitalized on the trend, offering products like “vagus massage oil,” vibrating bracelets and pillow mists, that claim to stimulate the nerve, but that have not been endorsed by the scientific community. Researchers who study the vagus nerve say that stimulating it with electrodes can potentially help improve mood and alleviate symptoms in those who suffer from treatment-resistant depression, among other ailments. But are there other ways to activate the vagus nerve? Who would benefit most from doing so? And what exactly is the vagus nerve, anyway? Here’s a look at what we know so far. The term “vagus nerve” is actually shorthand for thousands of fibers. They are organized into two bundles that run from the brain stem down through each side of the neck and into the torso, branching outward to touch our internal organs, said Dr. Kevin J. Tracey, a neurosurgeon and president of the Feinstein Institutes for Medical Research, Northwell Health’s research center in New York. Imagine something akin to a tree, whose limbs interact with nearly every organ system in the body. (The word “vagus” means “wandering” in Latin.) The vagus nerve picks up information about how the organs are functioning and also sends information from the brain stem back to the body, helping to control digestion, heart rate, voice, mood and the immune system. For those reasons, the vagus nerve — the longest of the 12 cranial nerves — is sometimes referred to as an “information superhighway.” Dr. Tracey compared it to a trans-Atlantic cable. “It’s not a mishmash of signals,” he said. “Every signal has a specific job.” © 2022 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Cells and Structure of the Nervous System
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 2: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 28361 - Posted: 06.09.2022

By Natasha Gilbert In May of 2018, Tabitha Bird spent a memorable day with her eldest son at a comic book convention in London. Later that evening, after she made sure that her two younger kids were safely tucked up in bed, Bird gathered every sleeping tablet, antidepressant, anti-anxiety med and ibuprofen pill she could find and walked out of the house. She drove to a nearby store where she bought a big bottle of water and some acetaminophen. Then she stopped in an empty industrial park and began to take the lot. Bird woke up from a coma four days later. The 47-year-old, from a town in West Sussex in the UK, now attributes her suicide attempt and the depression leading up to it to perimenopause — the time in most women’s lives when menstrual cycles become irregular and fertility wanes. During this transition, many women experience a suite of changes, including hot flashes, disrupted sleep and mood swings. Some breeze through perimenopause with little difficulty, but many — about 45 percent to 68 percent — experience depression, symptoms of which can include low mood, a loss of interest in things and even thoughts of suicide. Women with a history of depression, like Bird — who also suffered with it while pregnant — are the most vulnerable. During perimenopause, they are twice as likely to experience debilitating full-blown depressive disorder than women who haven’t had past episodes. As researchers probe for reasons why some women fall prey to depression at this time and others don’t, a leading candidate has emerged: widely fluctuating levels of the sex hormone estrogen. Estrogen directs fertility, but mounting research shows that it also holds sway on parts of the brain involved in regulating emotion and stress. © 2022 Annual Reviews

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: 28329 - Posted: 05.18.2022

By Melinda Wenner Moyer The more popular antidepressants become, the more questions they raise. The drugs are one of the most widely prescribed types of medications in the United States, with more than one out of eight Americans over 18 having recently taken them, according to a survey from the Centers for Disease Control and Prevention. Yet we know very little about how well antidepressants work over the long term, and especially how they affect overall quality of life, experts say. Most clinical drug trials have followed people taking antidepressants for only eight to 12 weeks, so it’s unclear what happens when patients take them for longer than that, said Gemma Lewis, a research psychologist at University College London who studies the causes, treatment and prevention of depression and anxiety. “We definitely need longer follow-ups of people who are using or are not using antidepressants, to see what the long-term outcomes are,” Dr. Lewis said. A study published yesterday in the journal PLoS One aimed to close this knowledge gap by comparing, over the course of two years, the changes in quality of life reported by Americans with depression who took antidepressants versus the changes reported by those with the same diagnosis who did not take the medications. The study included people who took all types of antidepressants, including selective serotonin reuptake inhibitors like Prozac, serotonin-norepinephrine reuptake inhibitors like Effexor and older antidepressants such as clomipramine and phenelzine. Researchers assessed both mental and physical quality of life with a survey that asked questions about subjects’ physical health, energy levels, mood, pain and ability to perform daily activities, among other things. The paper found no significant differences in the changes in quality of life reported by the two groups, which suggests that antidepressant drugs may not improve long-term quality of life. Both groups reported slight increases in the mental aspects of quality of life over time, and slight drops in their physical quality of life. But the study is imperfect, researchers say, and it certainly doesn’t settle the debate over the effectiveness of these drugs. © 2022 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: 28301 - Posted: 04.27.2022

By Linda Searing Already known to help ease depression, regular exercise may also help prevent it, with people who exercised just half the recommended weekly amount lowering their risk for depression by 18 percent, according to research published in the journal JAMA Psychiatry. However, those who were more active, meeting at least the minimum recommended physical activity level, reduced their risk for depression by 25 percent, compared with inactive people. The findings stem from the analysis of data from 15 studies, involving 191,130 adults who were tracked for at least three years. Those who met activity guidelines did at least 150 minutes a week of moderate-intensity activity, such as brisk walking, as recommended in the Physical Activity Guidelines for Americans. Mental health experts note that nearly 10 percent of American adults struggle with some form of depression each year. Antidepressant medication and talk therapy are commonly prescribed treatments, but exercise is also considered an effective treatment. Exercise sparks the brain’s release of endorphins, sometimes referred to as feel-good hormones. It can also quiet the mind, quelling the cycle of negative thoughts that often accompany depression, and can help reduce stress, improve sleep and boost self-esteem. Urging doctors to encourage their patients to increase their physical activity, the researchers wrote that the study’s findings suggest “significant mental health benefits from being physically active, even at levels below the public health recommendations.” If less-active participants in the study had exercised more, they say, 11.5 percent of depression cases could have been prevented.

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: 28300 - Posted: 04.27.2022

By Andrew Jacobs Psychedelic compounds like LSD, Ecstasy and psilocybin mushrooms have shown significant promise in treating a range of mental health disorders, with participants in clinical studies often describing tremendous progress taming the demons of post-traumatic stress disorder, or finding unexpected calm and clarity as they face a terminal illness. But exactly how psychedelics might therapeutically rewire the mind remains an enigma. A group of neuroscientists in London thought advanced neuroimaging technology that peered deep into the brain might provide some answers. They included 43 people with severe depression in a study sponsored by Imperial College London, and gave them either psilocybin, the active ingredient in magic mushrooms, or a conventional antidepressant; the participants were not told which one they would receive. Functional magnetic resonance imaging, which captures metabolic function, took two snapshots of their brain activity — the day before receiving the first dose and then roughly three weeks after the final one. What they found, according to a study published Monday in the journal Nature Medicine, was illuminating, both figuratively and literally. Over the course of three weeks, participants who had been given the antidepressant escitalopram reported mild improvement in their symptoms, and the scans continued to suggest the stubborn, telltale signs of a mind hobbled by major depressive disorder. Neural activity was constrained within certain regions of the brain, a reflection of the rigid thought patterns that can trap those with depression in a negative feedback loop of pessimism and despair. By contrast, the participants given psilocybin therapy reported a rapid and sustained improvement in their depression, and the scans showed flourishes of neural activity across large swaths of the brain that persisted for the three weeks. That heightened connectivity, they said, resembled the cognitive agility of a healthy brain that, for example, can toggle between a morning bout of melancholia, a stressful day at work and an evening of unencumbered revelry with friends. © 2022 The New York Times Company

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: 28283 - Posted: 04.13.2022

By Ingrid K. Williams This article is part of a limited series on artificial intelligence’s potential to solve everyday problems. Imagine a test as quick and easy as having your temperature taken or your blood pressure measured that could reliably identify an anxiety disorder or predict an impending depressive relapse. Health care providers have many tools to gauge a patient’s physical condition, yet no reliable biomarkers — objective indicators of medical states observed from outside the patient — for assessing mental health. But some artificial intelligence researchers now believe that the sound of your voice might be the key to understanding your mental state — and A.I. is perfectly suited to detect such changes, which are difficult, if not impossible, to perceive otherwise. The result is a set of apps and online tools designed to track your mental status, as well as programs that deliver real-time mental health assessments to telehealth and call-center providers. Psychologists have long known that certain mental health issues can be detected by listening not only to what a person says but how they say it, said Maria Espinola, a psychologist and assistant professor at the University of Cincinnati College of Medicine. With depressed patients, Dr. Espinola said, “their speech is generally more monotone, flatter and softer. They also have a reduced pitch range and lower volume. They take more pauses. They stop more often.” Patients with anxiety feel more tension in their bodies, which can also change the way their voice sounds, she said. “They tend to speak faster. They have more difficulty breathing.” Today, these types of vocal features are being leveraged by machine learning researchers to predict depression and anxiety, as well as other mental illnesses like schizophrenia and post-traumatic stress disorder. The use of deep-learning algorithms can uncover additional patterns and characteristics, as captured in short voice recordings, that might not be evident even to trained experts. © 2022 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 19: Language and Lateralization
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 15: Language and Lateralization
Link ID: 28271 - Posted: 04.06.2022