Links for Keyword: Depression

Follow us on Facebook or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 1328

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

By Ellen Barry After more than a decade of argument, psychiatry’s most powerful body in the United States added a new disorder this week to its diagnostic manual: prolonged grief. The decision marks an end to a long debate within the field of mental health, steering researchers and clinicians to view intense grief as a target for medical treatment, at a moment when many Americans are overwhelmed by loss. The new diagnosis, prolonged grief disorder, was designed to apply to a narrow slice of the population who are incapacitated, pining and ruminating a year after a loss, and unable to return to previous activities. Its inclusion in the Diagnostic and Statistical Manual of Mental Disorders means that clinicians can now bill insurance companies for treating people for the condition. It will most likely open a stream of funding for research into treatments — naltrexone, a drug used to help treat addiction, is currently in clinical trials as a form of grief therapy — and set off a competition for approval of medicines by the Food and Drug Administration. Since the 1990s, a number of researchers have argued that intense forms of grief should be classified as a mental illness, saying that society tends to accept the suffering of bereaved people as natural and that it fails to steer them toward treatment that could help. A diagnosis, they hope, will allow clinicians to aid a part of the population that has, throughout history, withdrawn into isolation after terrible losses. “They were the widows who wore black for the rest of their lives, who withdrew from social contacts and lived the rest of their lives in memory of the husband or wife who they had lost,” said Dr. Paul S. Appelbaum, who is chair of the steering committee overseeing revisions to the fifth edition of the D.S.M. © 2022 The New York Times Company

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: 28247 - Posted: 03.19.2022

By Linda Searing Depression affects about 280 million people worldwide, including about 5 percent of all adults, according to data from the World Health Organization and a report from the World Psychiatric Association Commission, an international research group. The commission describes depression as “one of the leading causes of avoidable suffering and premature mortality in the world” and labels it a neglected global health crisis. FAQ: What to know about the omicron variant of the coronavirus In the United States, an estimated 21 million adults, or about 8 percent of those 18 and older, are living with depression, according to the National Institute of Mental Health. In addition, the Centers for Disease Control and Prevention note that roughly 11 percent of all physician office visits and emergency department visits are related to depression. Though most everyone feels sad or gloomy from time to time, depression — what the medical world refers to as depressive disorder or major depression — goes beyond simple mood fluctuations. Rather, such feelings as sadness, hopelessness or low self-worth, loss of interest in usual activities, sleep problems and lack of energy persist for two weeks or more, interfering with a person’s everyday life. Genetics, chemical changes in the brain and stressful events are among factors believed to be responsible for depressive episodes. Left untreated, depression can have devastating effects. But treatment — which may include such approaches as talk therapy, medication, exercise, light therapy or acupuncture — can ease symptoms and help prevent a recurrence. However, the World Psychiatric Association Commission report, published in the Lancet, notes that about half of people suffering from depression in high-income countries are not diagnosed or treated, a number that increases to as much as 90 percent of those with depression who live in low- and middle-income countries. © 1996-2022 The Washington Post

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: 28224 - Posted: 03.02.2022

By Ellen Barry A new book by Dr. Thomas P. Insel, who for 13 years ran the United States’ foremost mental health research institution, begins with a sort of confession. During his tenure as the “nation’s psychiatrist,” he helped allocate $20 billion in federal funds and sharply shifted the focus of the National Institute of Mental Health away from behavioral research and toward neuroscience and genetics. “I should have been able to help us bend the curves for death and disability,” Dr. Insel writes. “But I didn’t.” Dr. Insel, 70, who left N.I.M.H. in 2015, calls the advances in neuroscience of the last 20 years “spectacular” — but in the very first pages of his new book, he says that, for the most part, they haven’t yet benefited patients. His book, “Healing: Our Path From Mental Illness to Mental Health,” is not an indictment of the science to which he devoted much of his adult life. Instead, it chronicles failures in virtually every other element of our mental health system, including the ineffective delivery of care, the gutting of community health services and the reliance on police and jails for crisis services. It also calls out a paradox: that the United States, a country that leads the world in spending on medical research, also stands out for its dismal outcomes in people with mental illnesses. Indeed, over the last three decades, even as the government invested billions of dollars in better understanding the brain, by some measures, those outcomes have deteriorated. The country’s long spell without breakthrough treatments can be attributed, in part, to the complexity of the brain. Dr. Insel rose through the ranks at a time of optimism that advances in neurobiology would lead to new treatments, and as head of N.I.M.H., as he put it, he “bet big on genomics.” But 20 years later, he said the role that genes play in schizophrenia and bipolar disorder has proven to be extraordinarily complex. “Each of those variants that have been discovered just account for a tiny, tiny amount of risk, so in aggregate, they’re probably significant, but you have to put a hundred of them together,” he said. “So we started doing bigger and bigger studies to find smaller and smaller effects.” © 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: 28214 - Posted: 02.23.2022

ByElizabeth Pennisi The trillions of bacteria in and on our bodies can bolster our health and contribute to disease, but just which microbes are the key actors has been elusive. Now, a study involving thousands of people in Finland has identified a potential microbial culprit in some cases of depression. The finding, which emerged from a study of how genetics and diet affect the microbiome, “is really solid proof that this association could have major clinical importance,” says Jack Gilbert, a microbial ecologist at the University of California, San Diego, who was not involved with the work. Researchers are finding ever more links between brain conditions and gut microbes. People with autism and mood disorders, for example, have deficits of certain key bacteria in their guts. Whether those microbial deficits actually help cause the disorders is unclear, but the findings have spawned a rush to harness gut microbes and the substances they produce as possible treatments for a variety of brain disorders. Indeed, researchers recently reported in Frontiers in Psychiatry that fecal transplants improved symptoms in two depressed patients. Guillaume Méric didn’t set out to find microbes that cause depression. A microbial bioinformatician at the Baker Heart & Diabetes Institute, he and his colleagues were analyzing data from a large health and lifestyle study from Finland. Part of a 40-year effort to track down underlying causes of chronic disease in Finnish people, the 2002 study assessed the genetic makeup of 6000 participants, identified their gut microbes, and compiled extensive data about their diets, lifestyles, prescription drug use, and health. Researchers tracked the health of participants until 2018. Méric and his colleagues combed the data for clues to how a person’s diet and genetics affect the microbiome. “There have been very few studies that have examined [all these factors] in such detail,” Gilbert says. Two sections of the human genome seemed to strongly influence which microbes are present in the gut, the researchers report this week in Nature Genetics. One contains the gene for digesting the milk sugar lactose, and the other helps specify blood type. (A second study, also published today in Nature Genetics, identified the same genetic loci by analyzing the relationship between the genomes and gut microbes of 7700 people in the Netherlands.) © 2022 American Association for the Advancement of Science.

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: 28188 - Posted: 02.05.2022

ByRobert F. Service More than 50 years after the Summer of Love, psychedelics are again the rage. This time the love comes from doctors beginning to embrace psychedelics such as LSD and psilocybin to treat depression, substance abuse, and other serious mental health conditions. But because the drugs cause hallucinations, their medical use requires intensive monitoring by clinicians. That drives up treatment costs, making psychedelics impractical for widespread therapeutic use. In recent years, researchers have begun to tweak psychedelics’ chemical structures, aiming to make analogs that retain medical usefulness but don’t cause hallucinations. Now, researchers report in Science they’ve teased apart the molecular interactions responsible for psychedelics’ antidepressive effects from those that cause hallucinations. They used that knowledge to make new compounds that appear to activate brain cellular circuits that help relieve depression without triggering a closely related pathway involved in hallucinations. So far, the compounds have only been studied in mice. But if such psychedelic analogs work in humans, they could spawn new families of pharmaceuticals. “This work is going to generate a lot of interest,” says Bryan Roth, a pharmacologist at the University of North Carolina School of Medicine, whose lab is also seeking nonhallucinogenic psychedelic analogs. The need is profound. Mental or neurological disorders are estimated to affect roughly one-quarter of U.S. adults every year, and therapies often don’t work. LSD, psilocybin (the main ingredient in magic mushrooms), and other psychedelics might do better. Studies have shown a single dose of psilocybin can offer relief from depression for months at a time, and last year, a clinical trial of 3,4-methylenedioxymethamphetamine, or ecstasy, showed it can alleviate posttraumatic stress disorder. © 2022 American Association for the Advancement of Science.

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: 28177 - Posted: 01.29.2022

By Emily Witt In the fall of 1972, a psychiatrist named Salvador Roquet travelled from his home in Mexico City to the Maryland Psychiatric Research Center, an institution largely funded by the United States government, to give a presentation on an ongoing experiment. For several years, Roquet had been running a series of group-therapy sessions: over the course of eight or nine hours, his staff would administer psilocybin mushrooms, morning-glory seeds, peyote cacti, and the herb datura to small groups of patients. He would then orchestrate what he called a “sensory overload show,” with lights, sounds, and images from violent or erotic movies. The idea was to push the patients through an extreme experience to a psycho-spiritual rebirth. One of the participants, an American psychology professor, described the session as a “descent into hell.” But Roquet wanted to give his patients smooth landings, and so, eventually, he added a common hospital anesthetic called ketamine hydrochloride. He found that, given as the other drugs were wearing off, it alleviated the anxiety brought on by these punishing ordeals. Clinicians at the Maryland Psychiatric Research Center had been studying LSD and other psychedelics since the early nineteen-fifties, beginning at a related institution, the Spring Grove Hospital Center. But ketamine was new: it was first synthesized in 1962, by a researcher named Calvin Stevens, who did consulting work for the pharmaceutical company Parke-Davis. (Stevens had been looking for a less volatile alternative to phencyclidine, better known as PCP.) Two years later, a doctor named Edward Domino conducted the first human trials of ketamine, with men incarcerated at Jackson State Prison, in Michigan, serving as his subjects. At higher doses, Domino noticed, ketamine knocked people out, but at lower ones it produced odd psychoactive effects on otherwise lucid patients. Parke-Davis wanted to avoid characterizing the drug as psychedelic, and Domino’s wife suggested the term “dissociative anesthetic” to describe the way it seemed to separate the mind from the body even as the mind retained consciousness. The F.D.A. approved ketamine as an anesthetic in 1970, and Parke-Davis began marketing it under the brand name Ketalar. It was widely used by the U.S. military during the Vietnam War, and remains a standard anesthetic in emergency rooms around the world. © 2021 Condé Nast.

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: 28132 - Posted: 12.31.2021

By Vanessa Barbara JUIZ DE FORA, Brazil — My first encounter with ketamine did not go well. A lifelong depressive — I picked up the habit of despairing sadness in early adulthood, and it remained faithfully with me — I’d turned to a more experimental form of treatment: ketamine infusions, in which a kindly anesthesiologist funnels the drug into a sad person’s veins for around 50 minutes and hopes it perks her up. Forty-five minutes into my first session, I rather anxiously asked my partner, who was in the room with me, if our 3-year-old daughter was fine. He decided it was the perfect time for a joke. Our daughter, he answered, was safe at home — and as a matter of fact, he added, she was already a very independent 15-year-old. I panicked. While under the strong, dissociative effect of the drug, patients sometimes enter what’s called a k-hole, in which their sense of time and space is distorted or eliminated. In that state of oblivion, I found it entirely plausible that my daughter was not a toddler anymore, but a strong-willed teenager. I became very distressed. My heartbeat accelerated. The anesthesiologist hurriedly ended the session as my partner said: “I’m kidding! Sorry! She’s still 3!” It was an inauspicious start, but I was determined to make the best of it. Ketamine, long used as an anesthetic but better known as an illegal party drug and, of course, a horse tranquilizer, has in recent years been gaining traction as an antidepressant. People have written enthusiastic accounts of their experiences, and researchers and psychiatrists, in a cascade of studies, have pointed to its possible benefits, not least the speed with which it can alleviate symptoms. Today, hundreds of clinics around the world provide infusions to people who have found little, if any, improvement with other treatments. That’s where I come in. Over the years, apart from the good old psychotropic medications, I have tried several types of talk therapy, meditation, acupuncture, singing lessons, bungee jumping and transcranial magnetic stimulation. (I still have sweet memories of the woodpecker sounds tapped into my brain.) © 2021 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: 28130 - Posted: 12.29.2021

L. Carol Ritchie U.S. Surgeon General Vivek Murthy has a warning about the mental health of young people. Murthy told Morning Edition that children and young adults were already facing a mental health crisis before the coronavirus pandemic began: One in three high school students reported persistent feelings of sadness or hopelessness, a 40% increase from 2009 to 2019, he said. Suicide rates went up during that time by 57% among youth ages 10 to 24. During the pandemic, rates of anxiety and depression have increased, he said. The pandemic has made the issues behind the mental health crisis only worse, he said. "This is a critical issue that we have to do something about now," he said. "We can't wait until after the pandemic is over." Murthy, who issued an advisory called "Protecting Youth Mental Health," also cites gun violence, the specter of climate change, racism and social conflict as sources of stress. "We also have to recognize that kids increasingly are experiencing bullying, not just in school but online, that they're growing up in a popular culture and a media culture that reminds kids often that they aren't good-looking enough, thin enough, popular enough, rich enough, frankly, just not enough," he said. Article continues after sponsor message "Even to this day, even though I have parents who I know unconditionally loved me, I never felt comfortable telling them about it because I thought that this was my fault. I don't want that to be the reality for my children, who are 4 and 5 and growing up, you know, in this very complicated world." © 2021 npr

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: 28101 - Posted: 12.08.2021

By Laura Sanders Kanu Caplash was lying on a futon in a medical center in Connecticut, wearing an eye mask and listening to music. But his mind was far away, tunneling down through layer upon layer of his experiences. As part of a study of MDMA, a psychedelic drug also known as molly or ecstasy, Caplash was on an inner journey to try to ease his symptoms of post-traumatic stress disorder. On this particular trip, Caplash, now 22, returned to the locked bathroom door of his childhood home. As a kid, he used to lock himself in to escape the yelling adults outside. But now, he was both outside the locked door, knocking, and inside, as his younger, frightened self. He started talking to his younger self. “I open the door, and my big version picks up my younger version of myself, and literally carries me out,” he says. “I carried myself out of there and drove away.” That self-rescue brought Caplash peace. “I got out of there. I’m alive. It’s all right. I’m OK.” For years, Caplash had experienced flashbacks, nightmares and insomnia from childhood trauma. He thought constantly about killing himself, he says. His experiences while on MDMA changed his perspective. “I still have the memory, but that anger and pain is not there anymore.” Caplash’s transcendent experiences, spurred by three therapy sessions on MDMA, happened in 2018 as part of a research project on PTSD. Along with a handful of other studies, that research suggests that when coupled with psychotherapy, mind-altering drugs bring some people immediate, powerful and durable relief. © Society for Science & the Public 2000–2021.

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: 28099 - Posted: 12.04.2021

By Kelly Servick For patients whose depression resists treatment with drugs and electroconvulsive therapy, surgically implanted wires that stimulate the brain might bring relief. But in recent years, two randomized, controlled trials of this approach, known as deep brain stimulation (DBS), were halted after underwhelming results in interim analyses. “It was like the air was let out of the room,” Sameer Sheth, a neurosurgeon at Baylor College of Medicine, says of those results. “It was a big let-down.” Now, researchers are testing more sophisticated, personalized DBS techniques they hope will yield stronger results. The tests to date have involved just one or a few patients, far from proof of effectiveness. But researchers hope they’ll inform larger studies that finally cement the effectiveness of DBS in depression. “With all these irons in the fire … we will hopefully build up enough understanding and evidence,” says Sheth, an author of a case study published this week. DBS is already approved in the United States to treat epilepsy, obsessive compulsive disorder, and movement disorders such as Parkinson’s disease. Could it also shift patterns of abnormal activity in neural circuits that may drive depression symptoms? Early studies without control groups yielded promising results, but two randomized, controlled trials, sponsored by the medical device companies Medtronic and St. Jude Medical, Inc. (which was later acquired by Abbott Laboratories) did not show significant benefits after several months of DBS, teams reported in 2015 and 2017. Long-term follow-up of participants has revived some optimism. For example, many people in the 30-participant Medtronic trial improved over 1 year or more—beyond the timeline of the initial study, says Stanford University psychiatrist Mahendra Bhati, a co-investigator. Last month, he and colleagues published a follow-up study of eight trial patients, most of whom continue to use their implant about 10 years later. About one-half have had at least a 50% improvement over their pretreatment score on a depression scale. © 2021 American Association for the Advancement of Science.

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: 28089 - Posted: 11.24.2021