Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

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By Neuroskeptic If you delve into the wildest depths of the scientific literature, you will find a trilogy of papers so weird, that they have become legendary. In these articles, spanning a 12 year period, author Jarl Flensmark says that heeled shoes cause mental illness, while flat footwear promotes brain health: Is there an association between the use of heeled footwear and schizophrenia? (2004) Physical activity, eccentric contractions of plantar flexors, and neurogenesis: therapeutic potential of flat shoes in psychiatric and neurological disorders (2009) Flat shoes increase neurogenesis (2016) The abstract of the first paper gives a good sense of Flensmark’s ideas: A selective literature review and synthesis is used to present a hypothesis that finds support in all facts and is contradicted by none. Heeled footwear began to be used more than a 1000 years ago, and led to the occurrence of the first cases of schizophrenia. Industrialization of shoe production increased schizophrenia prevalence. The neurobiological mechanism for this shoe-induced psychosis is said to be that: During walking synchronised stimuli from mechanoreceptors in the lower extremities increase activity in cerebello-thalamo-cortico-cerebellar loops through their action on NMDA-receptors. Using heeled shoes leads to weaker stimulation of the loops. Reduced cortical activity changes dopaminergic function which involves the basal ganglia-thalamo-cortical-nigro-basal ganglia loops. And so it goes on.

Keyword: Schizophrenia
Link ID: 26305 - Posted: 06.06.2019

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.

Keyword: Depression; Schizophrenia
Link ID: 26270 - Posted: 05.28.2019

By Anna Groves | Bipolar patients are seven times more likely to develop Parkinson’s disease, according to a new study. Though the news may be disheartening to those suffering from the already-trying condition, the link might also lead to clues about the causes behind the two conditions. Parkinson’s is a complex disease associated with a gradual decline in dopamine levels produced by neurons, or brain cells. It eventually leads to impaired movements and other bodily functions. The causes are unknown, and there is no cure. Bipolar disorder, also known as manic-depressive illness, is characterized by episodic fluctuations in mood, concentration or energy levels. Its causes are also unknown, though some bipolar-associated genes have been identified. Researchers are still figuring out how brain structure and function changes under the disease. Previous research has linked Parkinson’s with depression. So when the authors of the new study, most of whom are practicing physicians, noticed some of their bipolar patients developing Parkinson’s, they wondered if there was a connection. The study, out today in Neurology, was led by Huang Mao-Hsuan, who practices in the department of psychiatry at Taipei Veterans General Hospital. The researchers compared data from two groups of adults in the Taiwan National Health Insurance Research Database. Members of one group — over 56,000 individuals — were diagnosed with bipolar disorder between 2001 and 2009. The other — 225,000 individuals — had never been diagnosed with the disorder. No one in either cohort had received a Parkinson’s diagnosis and all the patients were over 20. And researchers ensured the two groups had similar ages, socioeconomic status, and other traits that might influence health.

Keyword: Parkinsons; Schizophrenia
Link ID: 26264 - Posted: 05.23.2019

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.

Keyword: Depression; Genes & Behavior
Link ID: 26261 - Posted: 05.22.2019

By Emily Willingham As anyone who’s dealt with substance addiction can tell you, breaking the physical intimacy with the drug isn’t always the most challenging part of treatment. People trying to avoid resurrecting their addiction also must grapple with reminders of it: the sights, sounds and people who were part of their addictive behaviors. These cues can trigger a craving for the drug, creating anxiety that steers them straight back into addiction for relief. The opioid epidemic in the United States has taken more than 300,000 lives, and support for people working to keep these drugs out of their orbit has become crucial. Methadone and buprenorphine, the current medical treatment options, help break the physical craving for opioids by targeting the same pathways that opioids use. Although these drugs can ease physical need, they don’t quiet the anxiety that environmental cues can trigger, leaving open a door to addiction reentry. The cannabis compound cannabidiol (CBD), a nonpsychoactive component of cannabis, might be the key to keeping that door locked. Researchers report that among people with opioid addiction, CBD dampens cue-triggered cravings and anxiety, along with reducing stress hormone levels and heart rate. The results were published May 21 in the American Journal of Psychiatry. “These findings provide support for an effect of cannabidiol on this process,” says Kathryn McHugh, assistant professor in the department of psychiatry at Harvard Medical School’s Division of Alcohol and Drug Abuse, who was not involved in the study. However, she cautions, the results are preliminary, and behavioral therapies are also quite effective at dimming the signal from cues. © 2019 Scientific American

Keyword: Drug Abuse; Depression
Link ID: 26260 - Posted: 05.22.2019

Alison Abbott Pharmacologists gave mescaline a fair trial. In the early and mid-twentieth century, it seemed more than plausible that the fashionable hallucinogen could be tamed into a therapeutic agent. After all, it had profound effects on the human body, and had been used for centuries in parts of the Americas as a gateway to ceremonial spiritual experience. But this psychoactive alkaloid never found its clinical indication, as science writer Mike Jay explains in Mescaline, his anthropological and medical history. In the 1950s, the attention of biomedical researchers abruptly switched to a newly synthesized molecule with similar hallucinogenic properties but fewer physical side effects: lysergic acid diethylamide, or LSD. First synthesized by Swiss scientist Albert Hofmann in 1938, LSD went on to become a recreational drug of choice in the 1960s hippy era. And, like mescaline, it teased psychiatrists without delivering a cure. Jay traces the chronology of mescaline use. The alkaloid is found in the fast-growing San Pedro cactus (Echinopsis pachanoi) that towers above the mountainous desert scrub of the Andes, and the slow-growing, ground-hugging peyote cactus (Lophophora williamsii) native to Mexico and the southwestern United States. Archaeological evidence suggests that the use of these cacti in rites of long-vanished cultures goes back at least 5,000 years. © 2019 Springer Nature Publishing AG

Keyword: Drug Abuse; Depression
Link ID: 26255 - Posted: 05.21.2019

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.

Keyword: Depression; Development of the Brain
Link ID: 26248 - Posted: 05.20.2019

By LUKE DITTRICH On Valentine’s Day, 2018, five months after Hurricane Maria made landfall, Daniel Phillips stood at the edge of a denuded forest on the eastern half of a 38-acre island known as Cayo Santiago, a clipboard in his hand, his eyes on the monkeys. The island sits about a half-mile off the southeast coast of Puerto Rico, near a village called Punta Santiago. Phillips and his co-workers left the mainland shortly after dawn, and the monkeys had already begun to gather by the time they arrived, their screams and oddly birdlike chirps louder than the low rumble of the motorboat that ferried the humans. The monkeys were everywhere. Some were drinking from a large pool of stagnant rainwater; some were grooming each other, nit-picking; some were still gnawing on the plum-size pellets of chow that Phillips hurled into the crowd a half-hour before. Two sat on the naked branch of a tree, sporadically mating. They were all rhesus macaques, a species that grows to a maximum height of about two and a half feet and a weight of about 30 pounds. They have long, flexible tails; dark, expressive eyes; and fur ranging from blond to dark brown. Phillips’s notebook was full of empty tables. There were places for the monkeys’ ID numbers, which were tattooed on their chests and inner thighs, places for a description of their behavior, places for the time of day. There was a place for his own name, too, and he wrote it at the top of each page. Daniel Phillips is not a Puerto Rican name, whatever that means, but he was born here, in a big hospital in Fajardo. He arrived more than a month early and spent his first weeks in an incubator, but grew up to be a high school and college wrestler; as a biology major, he became interested in monkeys, and was invited by a primatologist from Duke University to take a job as a research assistant here on Cayo Santiago.

Keyword: Stress
Link ID: 26238 - Posted: 05.15.2019

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

Keyword: Depression; Schizophrenia
Link ID: 26220 - Posted: 05.09.2019

By Emilie Le Beau Lucchesi In 1945, Dorothy Still, a nurse in the United States Navy, met with a Navy psychiatrist to discuss disturbing symptoms she had been experiencing. Miss Still was one of 12 Navy nurses who had been held prisoner of war by the Japanese military in the occupied Philippines during World War II. For more than three years, Miss Still and the other nurses had provided care to diseased, starving and destitute civilian inmates in a makeshift infirmary at the P.O.W. camp. In the months after liberation, Miss Still found she often cried without provocation and had trouble stopping her tears. She most likely suffered from what today we could call post-traumatic stress disorder, but the Navy psychiatrist offered no support or solutions. Instead, he called her a “fake” and a “liar.” Nurses, he claimed could not suffer the kind of shell shock from war that sailors or soldiers could. Mental health experts now recognize that PTSD can indeed affect nurses, both military and civilian. As many as 28 percent of nurses experience PTSD at some point in their careers, said Meredith Mealer, an associate professor at the Anschutz Medical Campus at the University of Colorado, Denver, though health care providers still often struggle to treat it. “It’s probably improved from Dorothy’s experience, but we still have a ways to go,” Dr. Meal. PTSD, as defined by the DSM-5, the psychiatric professions’ official manual of mental health disorders, can arise after a person has been exposed to a traumatic event, typically involving or threatening death, injury or sexual violence. Someone might experience the trauma first-hand or witness it happening to someone else, learn it happened to a loved one or repeatedly hear details about a violent event. The result can be intrusive symptoms such as unwanted memories, nightmares, flashbacks and overwhelming feelings of stress when exposed to reminders of the event. © 2019 The New York Times Company

Keyword: Stress
Link ID: 26213 - Posted: 05.07.2019

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

Keyword: Depression; Drug Abuse
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

Keyword: Depression; Development of the Brain
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

Keyword: Depression; Schizophrenia
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

Keyword: Depression
Link ID: 26169 - Posted: 04.24.2019

By Dave Philipps Post-traumatic stress disorder has long been one of the hardest mental health problems to diagnose because some patients try to hide symptoms while others exaggerate them. But a new voice analysis technique may be able to take the guesswork out of identifying the disorder using the same technology now used to dial home hands-free or order pizza on a smart speaker. A team of researchers at New York University School of Medicine, working with SRI International, the nonprofit research institute that developed the smartphone assistant Siri, has created an algorithm that can analyze patient interviews, sort through tens of thousands of variables in their speech and identify minute auditory markers of PTSD that are otherwise imperceptible to the human ear, then make a diagnosis. The results, published online on Monday in the journal Depression and Anxiety, show the algorithm was able to narrow down the 40,500 speech characteristics of a group of patients — like the tension in the larynx and the timing in the flick in the tongue — to just 18 relevant indicators that together could be used to diagnose PTSD. Based on those 18 speech clues, the algorithm was able to correctly identify patients with PTSD 89 percent of the time. “They were not the speech features we thought,” said Dr. Charles Marmar, a psychiatry professor at N.Y.U. and one of the authors of the paper. “We thought the telling features would reflect agitated speech. In point of fact, when we saw the data, the features are flatter, more atonal speech. We were capturing the numbness that is so typical of PTSD patients.” As the process is refined, speech pattern analysis could become a widely used biomarker for objectively identifying the disorder, he said. © 2019 The New York Times Company

Keyword: Stress
Link ID: 26164 - Posted: 04.22.2019

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 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.

Keyword: Depression
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

Keyword: Depression; Drug Abuse
Link ID: 26148 - Posted: 04.17.2019

Alison Abbott In January 1973, Science published an article called ‘On being sane in insane places’. The author, psychologist David Rosenhan, described how he and seven other healthy people had reported themselves to a dozen psychiatric hospitals, claiming to hear voices uttering odd words such as ‘thud’ or ‘hollow’ — a symptom never reported in the clinical literature. Each person was diagnosed with either schizophrenia or manic-depressive psychosis, and admitted; once inside, they stopped the performance. They were released after an average of 19 days with diagnoses of ‘schizophrenia in remission’ (D. L. Rosenhan Science 179, 250–258; 1973). One research and teaching hospital, hearing about the study, declared that its own staff could never be so deceived. It challenged Rosenhan to send it pseudopatients. He agreed, but never did. Nonetheless, the hospital claimed to have identified 41 of them. Psychiatric hospitals, it seemed, could recognize neither healthy people nor those with mental illnesses. Rosenhan’s study exemplifies much of what went wrong in twentieth-century psychiatry, as biologists, psychoanalysts and sociologists struggled for supremacy. Science historian Anne Harrington takes us through the painful history of that struggle in the enthralling Mind Fixers, which focuses particularly on the United States. © 2019 Springer Nature Publishing AG

Keyword: Schizophrenia; Depression
Link ID: 26145 - Posted: 04.16.2019

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

Keyword: Depression; Drug Abuse
Link ID: 26141 - Posted: 04.15.2019

/ By Dan Falk It’s been 30 years since Bobby McFerrin urged us, “Don’t Worry, Be Happy.” But it’s not so easy, is it? In the modern world, there’s plenty that you could worry about — but what should you worry about? If you worry about everything, you end up paralyzed with fear; if, on the other hand, you never worry about anything, you’re likely to end up falling victim to circumstances that you could have prevented. We should only worry about things that are likely to happen, and which are likely to cause serious harm if they do happen — and which you can take reasonable measures to prevent from happening. Lise Johnson and Eric Chudler have written a new book to help you navigate the worrysphere. Johnson is a biomedical engineer and a science writer and Chudler is a neuroscientist, and together they lead us on a tour of 58 things that one might potentially worry about, and try to assess how much those things are actually worth worrying about. The authors shine a spotlight on everything from caffeine, fluoride, and the Ebola virus to bees, snakes, public restrooms, and cruise ships. If it were only a list, I suspect they’d have had trouble getting a book deal — but fortunately it’s more than that. The authors have found a nifty way of presenting the variables in graphic form (what they call a “worry index”), displaying each worry-item as a circle on a Cartesian graph: Likelihood is plotted on the x-axis, and preventability on the y-axis; meanwhile, the size of the circle reflects the consequences, or the severity, of the issue. For example, a flesh-eating infection gets a pretty big circle — the disease can be fatal if left untreated. Fortunately, your chances of getting it are very low, so the circle is placed on the far left-hand-side of the graph; and it’s also highly preventable (with good hygiene and prompt medical treatment), so the circle sits high up on the y-axis. In contrast, although “medical errors” get a similar-sized circle, it falls in the lower-right quadrant: Doctors and nurses make mistakes more often than we might imagine, and there’s not much you can do to prevent such errors from happening. Copyright 2019 Undark

Keyword: Stress; Emotions
Link ID: 26140 - Posted: 04.15.2019