Links for Keyword: Depression

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By Zheala Qayyum A nurse showed me the newspaper just as I was walking in. I saw the smiling face of the young man I had taken care of since he was a teenager. Several times after hurting himself or threatening suicide he had been admitted to the Connecticut hospital where I work as a child and adolescent psychiatrist. I wished I had seen that smile during our interactions. It looked genuine. But this was an obituary. I was devastated. I didn’t know what to do with how I felt, and too ashamed to let people know. Suicide assessments were a fundamental part of my psychiatric training, but what to do when suicide occurs was not. This is true for many psychiatry training programs across the country. The emphasis lies on suicide prevention but there is not enough focus on preparing psychiatry trainees for the loss of a patient due to suicide or how to deal with the aftermath. This young man’s death was particularly painful because he was not a complete stranger. His last hospitalization, a couple of months before his death had been the first time I didn’t care for him. Just before that hospitalization, the lovely lady who altered my clothes mentioned that her grandson had been hospitalized several times. She knew I was a psychiatrist and started telling me about the arduous journey her family had faced because of her grandson’s mental health struggles. Then she mentioned his name. © 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: 26468 - Posted: 07.31.2019

By Kent Babb MINNEAPOLIS — On the day he’d bury his daughter, Mark Catlin stepped out of a chapel and into the fresh air. “Nice day for a walk,” he said, looking up, and on this morning in late March, the weather was flawless: cloudless, crisp, a bright blue sky. He took a breath and set off, heading down the cemetery’s path and falling behind the procession of cars ahead, talking as gravel crunched beneath his shoes. He asked if the memorial service, laboriously planned near the lakefront cycling trails Kelly Catlin had explored before becoming a silver medalist in the 2016 Olympics, had been good enough. He apologized if it had been too sad. The afternoon reception, he assured friends and visitors, should be more lively. A few paces up the winding path, a longtime friend shook his head. Mark, the friend whispered, would do anything to distract himself — he always had — in this case to avoid facing “the darkness”: Kelly’s suicide two weeks earlier, her thoughts during those final days and weeks, the way she’d planned her death in the same meticulous, results-oriented way she’d lived her life. Back on the walkway, Mark wore a blank expression as he accepted condolences and told people about his plans for the coming weeks. Eventually he reached a gravesite surrounded by mourners, and he stopped at the rear of the group as if happening upon a stranger’s funeral. Gradually the faces turned, and after a moment Mark noticed his wife and two other children waiting near a charcoal-colored casket. “I guess we’ll go lay her to rest now,” he said, stepping forward.

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: 26462 - Posted: 07.30.2019

By Kelli María Korducki The antidepressant Prozac came on the market in 1986; coincidentally, it was the year I was born. By the time I saw my first psychiatrist, as an early-2000s teenager, another half-dozen antidepressants belonging to the same class of drugs, selective serotonin reuptake inhibitors, or S.S.R.I.s, had joined it on the market — and in the public consciousness. The despondent cartoon blob from a memorable series of TV ads for the S.S.R.I. drug Zoloft became a near-instant piece of pop culture iconography after its May 2001 debut. It was commonplace through much of my childhood to find ads for other S.S.R.I.s tucked into the pages of the women’s magazines I’d leaf through at the salon where my mother had her hair cut, outlining criteria for determining whether Paxil “may be right for you.” In my depressed, anxious, eating disordered adolescence, I knew by name the pills that promised to help me. The mainstreaming of S.S.R.I.s and other psychopharmaceuticals didn’t eradicate stigmas against mental illness, but it certainly normalized a sense of their prevalence. (A 2003 study concluded that child and adolescent psychotropic prescription rates alone had nearly tripled since the late 1980s.) It also shaped the tone of conversation. No longer were mental illnesses necessarily discussed as a shameful aberration, but rather as chemically preordained sicknesses: functions of what became known as a “chemical imbalance.” As a teenager entering the psychiatric care system, I found this logic tremendously reassuring. I came from an extended family of medical providers and had been raised to trust in the hard, scientific grounding of modern medicine. © 2019 The New York Times Company

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: 26459 - Posted: 07.29.2019

Mariam Alexander It might come as quite a surprise to learn that, as a psychiatrist, if I ever had the misfortune to develop severe depression, my treatment of choice would be electroconvulsive therapy (ECT). Why? Well, to put it simply, ECT is the most rapid treatment for severe depression that we currently have to offer – with a recent study in the BMJ highlighting its effectiveness. For the uninitiated, ECT is a medical procedure in which an anaesthetised patient has a small electrical current applied to their scalp in order to induce a seizure for the purposes of treating severe mental illnesses and occasionally neurological disorders too. Each treatment takes just a few minutes and is usually administered two or three times a week. ECT course length varies depending on the needs of the patient, but on average eight to 12 treatments are given. It’s almost impossible to discuss ECT without the word “barbaric” being used. For anyone who is familiar with the psychiatric era of One Flew Over the Cuckoo’s Nest, this is understandable. But things have moved on a great deal since then. Indeed, if you’re looking for a “b” word to describe the process of contemporary ECT, top of my list would be “boring” – the use of a general anaesthetic and muscle relaxant means there’s probably more drama involved in having a filling than ECT. That’s not to say ECT isn’t a significant intervention, but treatments should always be considered in relation to the condition that needs to be managed. Most people would be totally opposed to the idea of a surgeon amputating their leg. However, if there was an infection rapidly rising from their foot and an amputation was the best option to save their life, I suspect most people would then see it as a necessity. Context is key. © 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: 26438 - Posted: 07.23.2019

Sara Reardon Nearly every scientist who has used mice or rats to study depression is familiar with the forced-swim test. The animal is dropped into a tank of water while researchers watch to see how long it tries to stay afloat. In theory, a depressed rodent will give up more quickly than a happy one — an assumption that has guided decades of research on antidepressants and genetic modifications intended to induce depression in lab mice. But mental-health researchers have become increasingly sceptical in recent years about whether the forced-swim test is a good model for depression in people. It is not clear whether mice stop swimming because they are despondent or because they have learnt that a lab technician will scoop them out of the tank when they stop moving. Factors such as water temperature also seem to affect the results. “We don’t know what depression looks like in a mouse,” says Eric Nestler, a neuroscientist at the Icahn School of Medicine at Mount Sinai in New York City. Now, the animal-rights group People for the Ethical Treatment of Animals (PETA) is jumping into the fray. The group wants the US National Institute of Mental Health (NIMH) in Bethesda, Maryland, to stop supporting the use of the forced-swim test and similar behavioural assessments by its employees and grant recipients. The tests “create intense fear, anxiety, terror, and depression in small animals” without providing useful data, PETA said in a letter to the agency on 12 July. © 2019 Springer Nature Publishing AG

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: 26431 - Posted: 07.19.2019

By Courtenay Harris Bond Before I started ketamine infusions this spring, I was milling around my house, unhinged, ducking into my bedroom to weep behind the closed door whenever my three young children were occupied. I felt like an actor playing a wife and mother. I had been having trouble concentrating on anything for several months, including my work as a journalist. Unable to read a book or watch a crime thriller — diversions I usually love and use to unwind — and in a torturous limbo with no plan, I felt hopeless, full of self-loathing, even suicidal. The only thing keeping me from hurting myself was the thought of what that would do to my family. Globally, nearly 800,000 people die by suicide each year, according to the World Health Organization, which also reports that more than 300 million people worldwide suffer from depression. Approximately 10 to 30 percent of those with major depressive disorder have treatment-resistant depression, typically defined as a failure to respond to at least two different treatments. I have treatment-resistant depression, as well as generalized anxiety disorder. Throughout my life, I have been on a quest to conquer these formidable demons. I am 48 and have been in therapy off and on — mostly on — since the fourth grade. I have tried approximately 14 different antidepressants, but they either haven’t worked, or they’ve caused insufferable side effects. I have done a full course of transcranial magnetic stimulation, during which magnetic fields were applied to my scalp at specific points that affect depression and anxiety. And I recently tried Nardil, a first-generation antidepressant that requires a special diet. I was dizzy at times with blurred vision and felt overwhelming fatigue to the point where I feared I might fall asleep while driving. Copyright 2019 Undark

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: 26391 - Posted: 07.05.2019

By Dana Najjar Four days after the birth of our daughter, my husband and I brought her home from the hospital. We were exhausted but giddy, ready to start our new lives. For nine months I had imagined what those first weeks at home would be like: sleepless nights, bleary-eyed arguments, a few late-night tears, all bundled up in the soft happy glow of new motherhood. In short, an adventure. But none of that materialized. What I came up against instead was a sheer wall of blinding panic. We had left the hospital with instructions to wake our newborn up every three hours to feed, but by the time we got home and settled in, five hours had elapsed, and nothing would rouse her long enough to nurse. She lay limp in my arms, drifting in and out of sleep, howling uncontrollably just long enough to tire herself out. We took our cues from the internet and tickled her feet with ice cubes, placed wet towels on her head and blew onto her face, but only managed to upset her more. And somewhere between trying to persuade her to latch for what felt like the hundredth time and willing my body to stay awake, it struck me that I had made a terrible mistake, one that I could never unmake. My stomach lurched, my hands and feet went numb and my heart began to pound. © 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: 26359 - Posted: 06.26.2019

New statistics suggest almost one-quarter of mothers experience either postpartum depression or an anxiety disorder in the months following birth, and that younger mothers are most at risk. The Statistics Canada survey analyzed the experiences of 7,085 respondents who gave birth in 2018 between January and the end of June. The women were surveyed online and by phone five to 13 months after delivery. The data found 23 per cent reported feelings consistent with either postpartum depression or an anxiety disorder — feelings that are more intense and longer-lasting than the so-called "baby blues" and may not resolve on their own. The rate ranged from 16 per cent in Saskatchewan to 31 per cent in Nova Scotia and was especially high among younger respondents. Among those under the age of 25 — numbering between 500 and 550 respondents — 30 per cent reported mental-health issues. That's compared to 23 per cent of mothers aged 25 and older. The survey also asked mothers about drug use and found 3 per cent used cannabis during pregnancy and 3 per cent used cannabis while breastfeeding. In addition, 1 per cent reported opioid use during pregnancy, including medical use and non-medical use. The survey was conducted in conjunction with the Public Health Agency of Canada and Health Canada and involved data collected from Nov. 29, 2018 to Feb. 5, 2019.

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: 26354 - Posted: 06.25.2019

By Benedict Carey and Jennifer Steinhauer Confronted by a rising rate of suicides in some groups of veterans., the Department of Veterans Affairs on Friday decided to approve the use of a new and costly depression drug, despite concerns among doctors and other experts about the drug’s effectiveness. The decision to endorse the drug — called Spravato, and manufactured by Janssen, a unit of Johnson & Johnson — came days after President Trump offered to negotiate a deal between the drug maker and the agency. Johnson & Johnson reportedly was working with associates at Trump’s Mar-a-Lago club, and the company has been supporting V.A. suicide-prevention efforts. A spokesman for the V.A. said that the decision to approve the drug, which would cover its use by doctors in its nearly 1,000 clinics nationwide, was a medical one. In a statement, the agency said, “V.A. will closely monitor the use of esketamine” — the generic name for Spravato — “in veterans to more fully understand its relative safety and effectiveness as compared to other available treatments. Based on this information, V.A. may revise its clinical guidance” and the availability of the drug. The V.A. stopped short of putting Spavato on its formulary, the list of drugs it requires to be carried in its 260 or so pharmacies. The approval enables V.A. doctors to offer the drug to patients they believe could benefit. Some Congressional Democrats expressed concern at the fast approval process. “I am incredibly alarmed by reporting today that suggests Spravato, a controversial new drug, is being rushed through critical reviews and may be prescribed to veterans before fully vetting the potential risks and benefits,” said Mark Takano, Democrat of California and chairman of the House Committee on Veteran’s Affairs, in a prepared statement released Wednesday. © 2019 The New York Times Company

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: 26351 - Posted: 06.24.2019

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.

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