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by Scott Alexander The first thing you notice at the American Psychiatric Association meeting is its size. By conservative estimates, a quarter of the psychiatrists in the United States are packed into a single giant San Francisco convention center, more than 15,000 people. Being in a crowd of 15,000 psychiatrists is a weird experience. You realize that all psychiatrists look alike in an indefinable way. The men all look balding, yet dignified. The women all look maternal, yet stylish. Sometimes you will see a knot of foreign-looking people huddled together, their nametags announcing them as the delegation from the Nigerian Psychiatric Association or the Nepalese Psychiatric Association or somewhere else very far away. But however exotic, something about them remains ineffably psychiatrist. The second thing you notice at the American Psychiatric Association meeting is that the staircase is shaming you for not knowing enough about Vraylar®. Seems kind of weird. Maybe I’ll just take the escalator… …no, the escalator is advertising Latuda®, the “number one branded atypical antipsychotic”. Aaaaaah! Maybe I should just sit down for a second and figure out what to do next… AAAAH, CAN’T SIT DOWN, VRAYLAR® HAS GOTTEN TO THE BENCHES TOO! Surely there’s a non-Vraylar bench somewhere in this 15,000 person convention center! …whatever, close enough. You know how drug companies pay six or seven figures for thirty-second television ads just on the off chance that someone with the relevant condition might be watching? You know how they employ drug reps to flatter, cajole, and even seduce doctors who might prescribe their drug? Well, it turns out that having 15,000 psychiatrists in one building sparks a drug company feeding frenzy that makes piranhas look sedate by comparison. Every flat surface is covered in drug advertisements.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26270 - Posted: 05.28.2019

Ed Yong In 1996, a group of European researchers found that a certain gene, called SLC6A4, might influence a person’s risk of depression. It was a blockbuster discovery at the time. The team found that a less active version of the gene was more common among 454 people who had mood disorders than in 570 who did not. In theory, anyone who had this particular gene variant could be at higher risk for depression, and that finding, they said, might help in diagnosing such disorders, assessing suicidal behavior, or even predicting a person’s response to antidepressants. Back then, tools for sequencing DNA weren’t as cheap or powerful as they are today. When researchers wanted to work out which genes might affect a disease or trait, they made educated guesses, and picked likely “candidate genes.” For depression, SLC6A4 seemed like a great candidate: It’s responsible for getting a chemical called serotonin into brain cells, and serotonin had already been linked to mood and depression. Over two decades, this one gene inspired at least 450 research papers. But a new study—the biggest and most comprehensive of its kind yet—shows that this seemingly sturdy mountain of research is actually a house of cards, built on nonexistent foundations. Richard Border of the University of Colorado at Boulder and his colleagues picked the 18 candidate genes that have been most commonly linked to depression—SLC6A4 chief among them. Using data from large groups of volunteers, ranging from 62,000 to 443,000 people, the team checked whether any versions of these genes were more common among people with depression. “We didn’t find a smidge of evidence,” says Matthew Keller, who led the project. (c) 2019 by The Atlantic Monthly Group.

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 26261 - Posted: 05.22.2019

By Neuroskeptic | A paper in PNAS got some attention on Twitter recently. It’s called Childhood trauma history is linked to abnormal brain connectivity in major depression and in it, the authors Yu et al. report finding (as per the Significance Statement) A dramatic primary association of brain resting-state network (RSN) connectivity abnormalities with a history of childhood trauma in major depressive disorder (MDD). The authors go on to note that even though “the brain imaging took place decades after trauma occurrence, the scar of prior trauma was evident in functional dysconnectivity.” Now, I think that this talk of dramatic scarring is overblown, but in this case there’s also a wider issue with the use of a statistical method which easily lends itself to misleading interpretations – canonical correlation analysis (CCA). First, we’ll look at what Yu et al. did. In a sample of 189 unmedicated patients with depression, Yu et al. measured the resting-state functional connectivity of the brain using fMRI. They then analyzed this to give a total of 55 connection strengths for each individual. Each of these 55 measures reflects the functional coupling between two brain networks. For each patient, Yu et al. also administered questionnaires measuring personality, depression and anxiety symptoms, and history of trauma. These measures were then compressed into 4 clinical clusters, (i) anxious misery (ii) positive traits (iii) physical and emotional neglect or abuse, and (iv) sexual abuse.

Related chapters from BN8e: 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: 26248 - Posted: 05.20.2019

By Daniel Barron It’s 3 P.M. on a Saturday in March, and I’m working at Silver Hill Hospital. As the on-duty doctor, my job is to admit new patients and to work with the other staff to make sure that everything goes smoothly. I’m about to see a young patient I’ll call Adrian* I glance in the glass-paned waiting room and notice Adrian sitting on the sofa. Their parents are also in the room (I’m using gender-neutral names pronouns for the patients in this essay, as the author’s note at the bottom explains), standing with concerned looks on their faces. A few minutes later, I meet with Adrian, who turns out to be a pleasant college student. They’ve been feeling anxious and depressed and, in addition to worsening paranoid thoughts, is thinking about suicide. Each patient is uniquely complex. I have never seen two identical patients: even within the same family, even among twins, patients are unique. Each patient’s history and symptoms, brain and genes, hopes and fears differ, which is one reason why psychiatry is so difficult. I need to figure out how to help Adrian. To do this, I need to reduce their complexity into something cognitively manageable, into something I can understand. The way I (and all clinicians) do this is to look for patterns: common symptoms and trends that help me understand what’s going on and suggest a type of treatment. © 2019 Scientific American

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26220 - Posted: 05.09.2019

Hattie Garlick Rosie has just returned from the school run. She drops a bag of groceries on to her kitchen table, and reaches for a clear plastic cup, covered by a white hanky and sealed with a hairband. Inside is a grey powder; her finely ground homegrown magic mushrooms. “I’ll take a very small dose, every three or four days,” she says, weighing out a thumbnail of powder on digital jewellery scales, purchased for their precision. “People take well over a gram recreationally. I weigh out about 0.12g and then just swallow it, like any food. It gives me an alertness, an assurance. I move from a place of anxiety to a normal state of confidence, not overconfidence.” Over the last 12 months, I have been hearing the same story from a small but increasing number of women. At parties and even at the school gates, they have told me about a new secret weapon that is boosting their productivity at work, improving their parenting and enhancing their relationships. Not clean-eating or mindfulness but microdosing – taking doses of psychedelic drugs so tiny they are considered to be “subperceptual”. In other words, says Rosie: “You don’t feel high, just… better.” It’s a trend that first emerged in San Francisco less than a decade ago. Unlike the hippies who flocked to the city in the 60s, these new evangelists of psychedelic drugs were not seeking oblivion. Quite the opposite. While a “full” tripping dose of LSD is about 100 micrograms, online forums began to buzz with ambitious tech workers from Silicon Valley eulogising the effect of taking 10 to 20 micrograms every few days. Others used magic mushrooms. While both drugs are illegal in the US and the UK, increasing numbers claimed that tiny amounts were making them more focused, creative and productive. © 2019 Guardian News & Media Limited

Related chapters from BN8e: 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: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26210 - Posted: 05.04.2019

By Benedict Carey Ever since its premiere, on March 31, 2017, the Netflix series “13 Reasons Why,” about a teenage girl’s suicide, has alarmed many health experts, who believe it glamorizes the topic for some young people. The show also has impressed critics, along with viewers young and old, who see it as an honest portrayal of adolescent distress. Now, a new study finds that suicide rates spiked in the month after the release of the series among boys aged 10 to 17. That month, April 2017, had the highest overall suicide rate for this age group in the past five years, the study found; the rate subsequently dropped back into line with recent trends, but remained elevated for the year. Suicide rates for girls aged 10 to 17 — the demographic expected to identify most strongly with the show’s protagonist — did not increase significantly. The study, posted Monday by the Journal of Child and Adolescent Psychiatry, is likely to fuel further debate about the merits of “13 Reasons Why,” the third season of which is in production. “Suicide is a problem worldwide, and it’s so hard to knock these rates down,” said Lisa M. Horowitz, a staff scientist in the National Institute of Mental Health’s Intramural Research Program, and an author of the paper. “The last thing we need is something that increases them.” In a statement, a Netflix spokesperson said: “We’ve just seen this study and are looking into the research, which conflicts with last week’s study from the University of Pennsylvania,” which focused on young adults. “This is a critically important topic and we have worked hard to ensure that we handle this sensitive issue responsibly.” © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 26186 - Posted: 04.30.2019

By Amy Barnhorst SACRAMENTO — If suicide is preventable, why are so many people dying from it? Suicide is the 10th leading cause of death in the United States, and suicide rates just keep rising. A few years ago, I treated a patient, a flight attendant, whose brother had brought her in to the psychiatric crisis unit after noticing her unusual behavior at a wedding. After the ceremony, she quietly handed out gifts and heartfelt letters to her family members. When her brother took her home, he noticed many of her furnishings and paintings were missing. In her bathroom he found three unopened bottles of prescription sleep medication. He confronted her, and she admitted that she had donated her possessions to charity. She had also cashed out her retirement account and used the money to pay off her mortgage, her car loan and all of her bills. When I interviewed her, she said that for the last four months, doing anything — eating, cleaning her house, talking to her neighbors — had taken colossal effort, and brought her no joy. She felt exhausted by having to live through each day, and the thought of sustaining this for years to come was an intolerable torment. After evaluating her, I told her that I thought she was experiencing an episode of bipolar depression, and needed to be committed to the hospital while we started treatment. She shrugged and gave me her most troubling response yet: “I don’t care.” One of the reasons I remember this woman so well is that, of all the patients I have evaluated for suicide risk, she was an anomaly. She had a sustained and thought-out commitment to ending her life. Fortunately, that allowed her to be discovered, and her family was able to quickly get her into emergency care. She responded well to lithium, one of only two psychiatric medications shown to reduce suicide (the other is an antipsychotic, clozapine). Her depression lifted slowly and she began to remember the things that made her life worth living. © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26179 - Posted: 04.29.2019

Sarah Boseley Antidepressants can save lives. At best, they work. At worst, they are a sticking plaster, hopefully enabling people to hold it all together until they get other help in the form of talking therapies. Either way, they are not supposed to be long-term medication. But whether depression is now better diagnosed or we live in sad times, more and more people are taking the pills and the weeks extend into months and years. In some cases, the users find they can’t stop. “I am currently trying to wean myself off,” one told researchers, “which honestly is the most awful thing I have ever done. I have horrible dizzy spells and nausea whenever I lower my dose.” “The withdrawal effects if I forget to take my pill,” another reported, “are severe shakes, suicidal thoughts, a feeling of too much caffeine in my brain, electric shocks, hallucinations, insane mood swings … Kinda stuck on them now cos I’m too scared to come off.” “While there is no doubt I am better on this medication,” said a third, “the adverse effects have been devastating when I have tried to withdraw – with ‘head zaps’, agitation, insomnia and mood changes. This means that I do not have the option of managing the depression any other way.” These anonymised accounts come from scientific studies cited in a report last year to the all-party parliamentary group for prescribed drug dependence and published in the journal Addictive Behaviors. They give a flavour of the reality of dependence on modern antidepressants, the SSRIs (selective serotonin reuptake inhibitors). The most famous is Prozac, AKA fluoxetine, once portrayed as a wonder drug that would make the world rosy and shiny again for all of us, without the dangerous dark side of Valium and the rest of the benzodiazepines. Not only was it harder to overdose on SSRIs than on “benzos”, the experts said; it was also easier to come off them. © 2019 Guardian News & Media Limited

Related chapters from BN8e: 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: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26169 - Posted: 04.24.2019

James Hamblin The past two weeks have been frenetic for Bre Hushaw, who is now known to millions of people as the girl in the depression helmet. Hushaw has been hearing from people all around the world who want to try it, or at least want to know how it works. Her life as a meme began when she agreed to an on-camera interview with the local-news site AZfamily.com for a story headlined “Helmet Approved by FDA to Treat Depression Available in Arizona.” The feel-good tale of Hushaw’s miraculous recovery from severe depression was tossed into the decontextualizing maw of the internet and distilled down to a screenshot of a young woman looking like a listless Stormtrooper. Jokes poured in. Some of the most popular, each with more than 100,000 likes on Twitter, include: “If u see me with this ugly ass helmet mind ur business.” “Friend: hey everything alright? Me, wearing depression helmet: yeah I’m just tired.” “The depression helmet STAYS ON during sex.” Hushaw has been tracking the virality, sometimes cringing and sometimes laughing. She replies to as many serious inquiries as she can, while finishing up her senior year at Northern Arizona University before starting a job in marketing. A year ago, she didn’t think she was going to live to graduation. When she was 10 years old, her mother died. Her depression symptoms waxed and waned from then on, and they waxed especially when she heard the gunshots on her campus during a shooting at the school in 2015. She’s tried many medications over the years—14, by her count. (c) 2019 by The Atlantic Monthly Group.

Related chapters from BN8e: 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: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26163 - Posted: 04.22.2019

By Sam Rose You’ve probably heard about microdosing, the “productivity hack” popular among Silicon Valley engineers and business leaders. Microdosers take regular small doses of LSD or magic mushrooms. At these doses, they don’t experience mind-bending, hallucinatory trips, but they say they get a jolt in creativity and focus that can elevate work performance, help relationships, and generally improve a stressful and demanding daily life. If its proponents are to be believed, microdosing offers the cure for an era dominated by digital distractions and existential anxiety—a cup of coffee with a little Tony Robbins stirred in. So far, though, it’s been impossible to separate truth from hype. That’s because, until recently, microdoses haven’t been tested in placebo-controlled trials. Late last year, the first placebo-controlled microdose trial was published. The study concluded that microdoses of LSD appreciably altered subjects’ sense of time, allowing them to more accurately reproduce lapsed spans of time. While it doesn’t prove that microdoses act as a novel cognitive enhancer, the study starts to piece together a compelling story on how LSD alters the brain’s perceptive and cognitive systems in a way that could lead to more creativity and focus. The idea behind microdosing traces its roots back decades. In the 1950s, a handful of psychedelic therapists at a mental health facility in Saskatchewan wanted to help alcoholics get clean. They guided the patients through a high dose, ego-dissolving, LSD experience. When they came out the other side, over half of the patients reported complete recovery from alcoholism. The Canadian government was intrigued and ordered more rigorous trials, this time with placebo controls, and without the experienced “trip guides” offering suggestions on what patients should feel. These trials were a bust. In the fall-out, many viewed psychedelic therapy as more shamanism than science. The mindset of the user and suggestion from the therapist (termed “set and setting” to LSD proponents) are just as important as the drug itself. In other words, LSD’s effects had as much to do with goings on outside the brain as inside it. To LSD proponents, though, this was part of how it worked. “Set and setting” guard against a bad trip (with large doses), and give the user an idea of what they should experience. © 2019 Scientific American

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26148 - Posted: 04.17.2019

by Jesse Noakes In August 2016 I went to New York for the first time. On the second evening, as the sun slipped behind the building across the street, I was sitting on a long couch on the top floor of an old church. All around me instruments were scattered on the floor – singing bowls, tuning forks, rainsticks, Tibetan bells. At the foot of a wall carpeted completely in moss, dripping like the jungle in the baking heat, was a large bronze gong. On the table in front of me two small ceramic bowls contained a capsule of 125mg of pure MDMA and a chilli guacamole with three grams of powdered magic mushrooms stirred through it. I eyed them nervously. I was terrified that I was going to lose my mind but I was more scared that nothing would happen at all, that I was too broken for even this radical treatment. I’d left Australia to take psychedelics with a therapist. Almost a decade of regular talk therapies for depression had done little to explain why I still felt so numb, trapped and terrified. A few months earlier I’d tracked down a guy online who said that, while it wasn’t a magic bullet, he might have something that would help. I can’t name him because it’s still completely illegal. He was sitting across from me and after I’d swallowed the contents of both bowls he handed me a padded eye mask and suggested I lie back on the couch. I heard him move across the room in the steamy darkness as I tried to relax and focus on my breathing. Moments later I heard the first strange notes from the gong. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26141 - Posted: 04.15.2019

Jon Hamilton The anesthetic ketamine can relieve depression in hours and keep it at bay for a week or more. Now scientists have found hints about how ketamine works in the brain. In mice, the drug appears to quickly improve the functioning of certain brain circuits involved in mood, an international team reported Thursday in the journal Science. Then, hours later, it begins to restore faulty connections between cells in these circuits. The finding comes after the Food and Drug Administration in March approved Spravato, a nasal spray that is the first antidepressant based on ketamine. The anesthetic version of ketamine has already been used to treat thousands of people with depression. But scientists have known relatively little about how ketamine and similar drugs affect brain circuits. The study offers "a substantial breakthrough" in scientists' understanding, says Anna Beyeler, a neuroscientist at INSERM, the French equivalent of the National Institutes of Health, who wasn't involved in the research. But there are still many remaining questions, she says. Previous research has found evidence that ketamine was creating new synapses, the connections between brain cells. But the new study appears to add important details about how and when these new synapses affect brain circuits, says Ronald Duman, a professor of psychiatry and neuroscience at Yale University. © 2019 npr

Related chapters from BN8e: 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: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 26132 - Posted: 04.12.2019

By Darby Saxbe Perinatal depression—depression that occurs during pregnancy or after the birth of a child—is surprisingly common, affecting about 1 in 7 women. And, although depression is debilitating at any time, it may carry a particularly heavy public health burden during the transition to parenthood. Women with depression are less likely to obtain medical care for themselves and their babies, and may struggle to bond with their infants. It’s no wonder that the children of depressed mothers experience heightened long-term risk of emotional and behavioral problems. Despite this grim picture, a new report from the US Preventive Services Task Force offers some hope. The USPSTF, a nonpartisan body of experts, reviews scientific research and makes recommendations for preventing disease. In the past, they’ve issued guidelines for lung cancer detection, aspirin use to prevent heart disease, and blood pressure screening. In a review recently published in the Journal of the American Medical Association (JAMA), the task force shared what they deemed “convincing evidence” that counseling (talk therapy) interventions can not just treat, but actually prevent, perinatal depression. This is exciting news given the high cost of depression during this time and the fact that, unlike other potential treatments for perinatal depression (like the new drug Zulresso), talk therapy is low-tech, relatively low-cost, and brings few side effects. In their report, the USPSTF reviewed 50 studies that they deemed to be at least “good or fair quality.” Almost all were randomized clinical trials, the gold standard for treatment research, in which a treatment is directly compared to a control group condition. About half of the studies focused on pregnant women, and the rest on postpartum women. Some studies targeted women who already had elevated risk for depression, based on risk factors like a personal or family history of depression, low socioeconomic status, and exposure to life stress or intimate partner violence. © 2019 Scientific American

Related chapters from BN8e: 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: 26109 - Posted: 04.03.2019

By Rachel Aviv Laura Delano recognized that she was “excellent at everything, but it didn’t mean anything,” her doctor wrote. She grew up in Greenwich, Connecticut, one of the wealthiest communities in the country. Her father is related to Franklin Delano Roosevelt, and her mother was introduced to society at a débutante ball at the Waldorf-Astoria. In eighth grade, in 1996, Laura was the class president—she ran on a platform of planting daffodils on the school’s grounds—and among the best squash players in the country. She was one of those rare proportional adolescents with a thriving social life. But she doubted whether she had a “real self underneath.” The oldest of three sisters, Laura felt as if she were living two separate lives, one onstage and the other in the audience, reacting to an exhausting performance. She snapped at her mother, locked herself in her room, and talked about wanting to die. She had friends at school who cut themselves with razors, and she was intrigued by what seemed to be an act of defiance. She tried it, too. “The pain felt so real and raw and mine,” she said. Her parents took her to a family therapist, who, after several months, referred her to a psychiatrist. Laura was given a diagnosis of bipolar disorder, and prescribed Depakote, a mood stabilizer that, the previous year, had been approved for treating bipolar patients. She hid the pills in a jewelry box in her closet and then washed them down the sink. © 2019 Condé Nast

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26104 - Posted: 04.02.2019

Almost 71m prescriptions for antidepressants were given out in England last year – not including drugs dispensed in hospitals outside the NHS. This is a vast number of pills – more than twice the number of prescriptions given for antibiotics; 20m more than for cholesterol-lowering statins. In a decade, the number of antidepressant prescriptions has doubled; it has risen by 3m in a year. Around 7 million adults (16% of the English adult population) are now taking this medicine, and around 330,000 children. The new data can’t say whether more people are depressed than previously – only that more are being medicated. The most recent official survey, in 2016, revealed an increase in rates of the most common mental health conditions among women, particularly teenage girls. Recent reports from a commission assembled by the Lancet medical journal, and the World Health Organization, have warned of a growing global mental health crisis, and called on policymakers and professionals worldwide to make this a priority. While people being ill is bad news, reports of people being treated for illness should, so long as the treatment is appropriate, be welcomed. Some researchers believe mental disorders remain under-treated because they are poorly understood, because doctors and patients share doubts about the remedies, and because of the social stigma that makes people reluctant to report symptoms or seek a diagnosis. But even granting that some people may be taking antidepressants who previously went untreated, there is a debate about whether pills are being overprescribed. © 2019 Guardian News & Media Limited

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26103 - Posted: 04.02.2019

By Ilana Marcus Grit alone got Linda Greene through her husband’s muscular dystrophy, her daughter’s traumatic brain injury, and her own mysterious illness that lasted for three years and left her vomiting daily before doctors identified the cause. But eventually, after too many days sitting at her desk at work crying, she went to see her doctor for help. He prescribed an antidepressant and referred her to a psychiatrist. When the first medication didn’t help, the psychiatrist tried another — and another and another — hoping to find one that made her feel better. Instead, Greene felt like a zombie and sometimes she hallucinated and couldn’t sleep. In the worst moment, she found herself contemplating suicide. “It was horrible,” she said. She never had suicidal thoughts before and was terrified. She went back her primary care doctor. In the past, when Jeremy Bruce, Greene’s physician in Cincinnati, treated patients for depression, he followed the same steps for almost everyone: start the patient on one antidepressant and switch to another until something helped. Sometimes, before they found the right treatment, the patient would leave his practice to find a new doctor. “They would usually be very angry,” Bruce said. But about three years ago, Bruce tried a new approach. Linda Greene and her husband. She tried many antidepressants before her doctor suggested genetic testing to find a medicine that worked for her. Doctors increasingly use information about genes to evaluate potential risk for some diseases and to determine the best drug treatment. But using pharmacogenetics to help treat depression remains controversial. (Family Photo) © 1996-2019 The Washington Post

Related chapters from BN8e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 13: Memory, Learning, and Development
Link ID: 26099 - Posted: 04.01.2019

Alix Spiegel Our thoughts and fears, movements and sensations all arise from the electrical blips of billions of neurons in our brain. Streams of electricity flow through neural circuits to govern these actions of the brain and body, and some scientists think that many neurological and psychiatric disorders may result from dysfunctional circuits. As this understanding has grown, some scientists have asked whether we could locate these faulty circuits, reach deep into the brain and nudge the flow to a more functional state, treating the underlying neurobiological cause of ailments like tremors or depression. The idea of changing the brain for the better with electricity is not new, but deep brain stimulation takes a more targeted approach than the electroconvulsive therapy introduced in the 1930s. DBS seeks to correct a specific dysfunction in the brain by introducing precisely timed electric pulses to specific regions. It works by the action of a very precise electrode that is surgically inserted deep in the brain and typically controlled by a device implanted under the collarbone. Once in place, doctors can externally tailor the pulses to a frequency that they hope will fix the faulty circuit. This week's Invisibilia podcast features the story of a woman with obsessive-compulsive disorder and depression who signed up for a deep brain stimulation trial. The story describes what it's like to be able to adjust her mood by adjusting the settings on her device. Listen to that story here. © 2019 npr

Related chapters from BN8e: 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: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26096 - Posted: 03.30.2019

Alix Spiegel We have the story of one woman who is taking part in an experiment on deep brain stimulation. RACHEL MARTIN, HOST: We are about to go deep - deep into your brain. STEVE INSKEEP, HOST: With a story about deep brain stimulation, or DBS, which sounds like a kind of massage, actually. But it means that patients get an implant that delivers small pulses of electricity to their brains. MARTIN: It's often used to treat Parkinson's disease. But for years, researchers have been trying to figure out how to use it to treat psychiatric disorders. INSKEEP: Results and experiments so far have been mixed. Many patients see no benefit. But some with obsessive-compulsive disorder have seen big changes. MARTIN: Like the next woman you're going to meet. For privacy, we are withholding her last name. Alix Spiegel from NPR's INVISIBILIA has her story. ALIX SPIEGEL, BYLINE: During the appointment, Megan didn't have to do that much, just sit in a chair while one of the doctors from the experiment used what looked like an oversized remote control to reprogram her electricity levels. Even after five years of having the implant, getting her electricity adjusted was unpredictable. Sometimes it went fine. But having electrodes in your brain is really complicated. And occasionally, the adjustments didn't go well. UNIDENTIFIED DOCTOR: While you were talking, I slowly ramped it up again. Anything different now? MEGAN: Slightly more aware. UNIDENTIFIED DOCTOR: OK. MEGAN: It's not like in the past, where it was like, oh, I feel good. But it's, like, a different feeling. SPIEGEL: After the doctor turned her up higher, Megan said she felt better. But then he decided to dial it back just a notch. He was worried that too much electricity might make her manic. UNIDENTIFIED DOCTOR: Now, if you notice me turning it down, then maybe I'll change my mind on that. MEGAN: (Crying) I'm sorry; don't do it. UNIDENTIFIED DOCTOR: Did you just feel it? MEGAN: (Crying) I don't feel very good at all right now. © 2019 npr

Related chapters from BN8e: 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: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 26095 - Posted: 03.30.2019

By Richard Schiffman The patient, a 48-year-old real estate professional in treatment for anxiety and mild depression, revealed that he had eaten three dozen oysters over the weekend. His psychiatrist, Dr. Drew Ramsey, an assistant clinical professor of psychiatry at Columbia University, was impressed: “You’re the only person I’ve prescribed them to who came back and said he ate 36!” Dr. Ramsey, the author of several books that address food and mental health, is a big fan of oysters. They are rich in vitamin B12, he said, which studies suggest may help to reduce brain shrinkage. They are also well stocked with long chain omega-3 fatty acids, deficiencies of which have been linked to higher risk for suicide and depression. But shellfish are not the only food he is enthusiastic about. Dr. Ramsey is a pioneer in the field of nutritional psychiatry, which attempts to apply what science is learning about the impact of nutrition on the brain and mental health. Dr. Ramsey argues that a poor diet is a major factor contributing to the epidemic of depression, which is the top driver of disability for Americans aged 15 to 44, according to a report by the World Health Organization. Together with Samantha Elkrief, a chef and food coach who sits in on many of his patient sessions, he often counsels patients on how better eating may lead to better mental health. The irony, he says, is that most Americans are overfed in calories yet starved of the vital array of micronutrients that our brains need, many of which are found in common plant foods. A survey published in 2017 by the Centers for Disease Control and Prevention reported that only one in 10 adults meets the minimal daily federal recommendations for fruit and vegetables — at least one-and-a-half to two cups per day of fruit and two to three cups per day of vegetables. © 2019 The New York Times Company

Related chapters from BN8e: 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: 26087 - Posted: 03.28.2019

By Laura Parker In the coming adventure video game Sea of Solitude, the main character — a young woman named Kay — navigates a partly submerged city as she faces a multitude of red-eyed scaly creatures. None are as terrifying as her own personal demons. As the game progresses, Kay realizes the creatures she is encountering are humans who turned into monsters when they became too lonely. To save herself, she fights to overcome her own loneliness. Kay was modeled after the game’s creative director, Cornelia Geppert of Jo-Mei Games, an independent game studio, who struggled after a 2013 breakup. “I felt like I was trapped in a cage,” Ms. Geppert, 37, said of her experience. Sea of Solitude, which Electronic Arts will publish this year, is among a growing number of video games that are tackling mental health issues. Last year, a game called Celeste explored depression and anxiety through a protagonist who had to avoid physical and emotional obstacles. In 2017’s fantasy action-adventure video game Hellblade: Senua’s Sacrifice, a young Celtic warrior deals with psychosis. Other games in recent years, including Night in the Woods and Pry, have delved into self-identity, anger issues and post-traumatic stress disorder. All followed the 2013 interactive fiction game Depression Quest, which asked players to step into the shoes of a character living with depression. These games are a far cry from the industry’s better-known story lines of battlefield heroics or the zombie apocalypse. But as a cultural conversation around mental health grows louder, makers of content are responding. According to the National Institute of Mental Health, one in five American adults lives with a mental illness. “Mental health is becoming a more central narrative in our culture, with greater efforts to normalize mental health challenges,” said Eve Crevoshay, executive director of Take This, a nonprofit that educates video game developers on best practices around portraying mental health. “With that trend comes response from creative industries, including games.” (Take This was founded in 2013 after the suicide of a video game journalist prompted a debate about the issue.) © 2019 The New York Times Company

Related chapters from BN8e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 26074 - Posted: 03.25.2019