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By Benedict Carey At a recent visit to the Veterans Affairs clinic in the Bronx, Barry, a decorated Vietnam veteran, learned that he belonged to a very exclusive club. According to a new A.I.-assisted algorithm, he was one of several hundred V.A. patients nationwide, of six million total, deemed at imminent risk of suicide. The news did not take him entirely off guard. Barry, 69, who was badly wounded in the 1968 Tet offensive, had already made two previous attempts on his life. “I don’t like this idea of a list, to tell you the truth — a computer telling me something like this,” Barry, a retired postal worker, said in a phone interview. He asked that his surname be omitted for privacy. “But I thought about it,” Barry said. “I decided, you know, OK — if it’s going to get me more support that I need, then I’m OK with it.” For more than a decade, health officials have watched in vain as suicide rates climbed steadily — by 30 percent nationally since 2000 — and rates in the V.A. system have been higher than in the general population. The trends have defied easy explanation and driven investment in blind analysis: machine learning, or A.I.-assisted algorithms that search medical and other records for patterns historically associated with suicides or attempts in large clinical populations. Doctors have traditionally gauged patients’ risks by looking at past mental health diagnoses and incidents of substance abuse, and by drawing on experience and medical instinct. But these evaluations fall well short of predictive, and the artificially intelligent programs explore many more factors, like employment and marital status, physical ailments, prescription history and hospital visits. These algorithms are black boxes: They flag a person as at high risk of suicide, without providing any rationale. But human intelligence isn’t necessarily better at the task. “The fact is, we can’t rely on trained medical experts to identify people who are truly at high risk,” said Dr. Marianne S. Goodman, a psychiatrist at the Veterans Integrated Service Network in the Bronx, and a clinical professor of medicine at the Icahn School of Medicine at Mount Sinai. “We’re no good at it.” © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27600 - Posted: 11.30.2020

By Jelena Kecmanovic Across the spectrum, mental health problems seem to be on the rise. One-quarter of Americans reported moderate to severe depression this summer and another quarter said they suffered from mild depression, a recent study reported. These findings are similar to surveys done by the Census Bureau and the Centers for Disease Control and Prevention. A third of Americans now show signs of clinical anxiety or depression, Census Bureau finds. Former first lady Michelle Obama highlighted the problem for many when she said in August that she has been dealing with “low-grade depression.” As a psychologist, I hear almost daily how the combination of coronavirus, racial unrest, economic uncertainty and political crisis are leading many people to feel a lot worse than usual. “It is not at all surprising that we are seeing the significant increase in distress. It’s a normal reaction to an abnormal situation,” said Judy Beck, president of the Beck Institute for Cognitive Behavior Therapy in Philadelphia and author of the widely used mental health textbook “Cognitive Behavior Therapy: Basics and Beyond.” But an important difference exists between having depressive symptoms — such as sadness, fatigue and loss of motivation — and a full-blown major depressive episode that can affect your ability to function at work and home for weeks or months. The amount and duration of the symptoms, as well as the degree to which they impair one’s life all play a role in diagnosing clinical depression. Extensive research suggests that certain ways of thinking and behaving can hasten the plunge into clinical depression, while others can prevent it. As we head into winter, which can stress the coping skills of many people, here are some strategies that can help you resist the depressive downward spiral. 1. Reduce overthinking. When we feel down, we tend to think about the bad things repeatedly, often trying to figure out why they’ve happened. Research shows that some people are especially prone to this kind of “depressive rumination.” They overanalyze everything, hoping to think their way out of feeling bad, and fret about consequences of their sadness.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27599 - Posted: 11.30.2020

By Linda Searing The “baby blues” that women can experience after giving birth usually go away within a week or two, but it now appears that more severe depressive symptoms, known as postpartum depression, may affect some new mothers for at least three years. Research from the National Institutes of Health, which tracked 4,866 women for three years after childbirth, found that about 25 percent of the women reported moderate to high levels of depressive symptoms at some point and that the remaining 75 percent experienced low-level depressive symptoms throughout the study. The “baby blues” typically include such symptoms as mood swings, anxiety and trouble sleeping, whereas postpartum depression symptoms — generally more intense and longer lasting — may include excessive crying, overwhelming fatigue, loss of appetite, difficulty bonding with the baby, feelings of inadequacy, hopelessness and more. The NIH research, published in the journal Pediatrics, encourages pediatricians to screen their tiny patients’ mothers for depressive symptoms during the children’s regular checkups, noting that “mothers’ mental health is critical to children’s well-being and development.” The researchers note that maternal depression increases a child’s risk for cognitive, emotional and behavioral problems. Getting treatment, however, should not only ease a mother’s symptoms but also improve her child’s odds for a favorable developmental outcome.

Related chapters from BN: 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 and Learning
Link ID: 27573 - Posted: 11.10.2020

By Nicholas Bakalar A mother’s psychological distress during pregnancy may increase the risk for asthma in her child, a new study suggests. Researchers had the parents of 4,231 children fill out well-validated questionnaires on psychological stress in the second trimester of pregnancy, and again three years later. The mothers also completed questionnaires at two and six months after giving birth. The study, in the journal Thorax, found that 362 of the mothers and 167 of the fathers had clinically significant psychological distress during the mothers’ pregnancies. When the children were 10 years old, parents reported whether their child had ever been diagnosed with asthma. As an extra measure, the researchers tested the children using forced expiratory volume, or FEV, a standard clinical test of lung function. After controlling for age, smoking during pregnancy, body mass index, a history of asthma and other factors, they found that maternal depression and anxiety during pregnancy was significantly associated with both diagnoses of asthma and poorer lung function in their children. There was no association between childhood asthma and parents’ psychological distress in the years after pregnancy, and no association with paternal psychological stress at any time. “Of course, this could be only one of many causes of asthma,” said the lead author, Dr. Evelien R. van Meel of Erasmus University in Rotterdam, “but we corrected for many confounders, and we saw the effect only in mothers. This seems to suggest that there’s something going on in the uterus. But this is an observational study, and we can’t say that it’s a causal effect.” © 2020 The New York Times Company

Related chapters from BN: 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 and Learning
Link ID: 27534 - Posted: 10.21.2020

By John Horgan One of the most impressive, disturbing works of science journalism I’ve encountered is Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs, and the Astonishing Rise of Mental Illness in America, published in 2010. In the book, which I review here, award-winning journalist Robert Whitaker presents evidence that medications for mental illness, over time and in the aggregate, cause net harm. In 2012, I brought Whitaker to my school to give a talk, in part to check him out. He struck me as a smart, sensible, meticulous reporter whose in-depth research had led him to startling conclusions. Since then, far from encountering persuasive rebuttals of Whitaker’s thesis, I keep finding corroborations of it. If Whitaker is right, modern psychiatry, together with the pharmaceutical industry, has inflicted iatrogenic harm on millions of people. Reports of surging mental distress during the pandemic have me thinking once again about Whitaker’s views and wondering how they have evolved. Below he answers some questions. —John Horgan
 Horgan: When and why did you start reporting on mental health? Whitaker: It came about in a very roundabout way. In 1994, I had co-founded a publishing company called CenterWatch that covered the business aspects of the “clinical trials industry,” and I soon became interested in writing about how financial interests were corrupting drug trials. Risperdal and Zyprexa had just come to market, and after I used a Freedom of Information request to obtain the FDA’s review of those two drugs, I could see that psychiatric drug trials were a prime example of that corruption. In addition, I had learned of NIMH-funded research that seemed abusive of schizophrenia patients, and in 1998, I co-wrote a series for the Boston Globe on abuses of patients in psychiatric research. My interest was in that broader question of corruption and abuse in research settings, and not specific to psychiatry. © 2020 Scientific American

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: Development of the Brain
Link ID: 27531 - Posted: 10.19.2020

By Lisa Grossman Clues from a chemical — Science News, October 3, 1970 An experimental drug’s effects on the sexual behavior of certain animals is arousing interest among investigators.… The drug, para-chlorophenylalanine … reduces the level of a naturally occurring neurochemical, serotonin, in the brain of rats, mice and dogs.… Little is known about how serotonin acts in the brain, and investigators quickly recognized that PCPA could be used to study this brain chemical. Update PCPA helped e­stablish serotonin’s role in regulating sexual desire, as well as sleep, appetite and mood. The chemical messenger has become key to one common class of antidepressant drugs called selective serotonin r­euptake inhibitors. Identified in 1974, SSRIs work by increasing the brain’s serotonin levels. But such drugs can hinder sexual desire. One SSRI that failed to relieve depression in humans found a second life as a treatment for sexual dysfunction. Approved by the U.S. Food and Drug Administration in 2015, this “little pink pill,” sold as Addyi, may boost sex drive in women by lowering serotonin in the brain’s reward centers. H.A. Croft. Understanding the role of serotonin in female hypoactive sexual desire disorder and treatment options. Journal of Sexual Medicine. Vol. 14, December 2017, p. 1575. Doi: 10.1016/j.jsxm.2017.10.068. © Society for Science & the Public 2000–2020.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 27497 - Posted: 09.30.2020

Chris Woolston Signs of depression among graduate students in the United States have apparently doubled during the COVID-19 pandemic, according to a survey that drew responses from more than 15,000 graduate and 30,000 undergraduate students at 9 US research universities. The survey, conducted by the Student Experience in the Research University (SERU) Consortium — a collaboration between the University of California, Berkeley (UC Berkeley), and the University of Minnesota Twin Cities in Minneapolis — found that indications of anxiety among graduate students rose by 50% this year compared with last year. “It’s very alarming that so many students are suffering from mental-health issues,” says Igor Chirikov, director of SERU and a senior researcher in higher education with the Center for Studies in Higher Education at UC Berkeley. “The pandemic has obviously had a big impact.” The survey, which ran from 18 May to 20 July, used simple two-item questionnaires — the Generalized Anxiety Disorder-2 and Patient Health Questionnaire-2 — to screen for symptoms of anxiety disorders and major depression. Thirty-nine per cent of graduate students (a group that includes law- and medical-school students) screened positive for anxiety, and 32% screened positive for depression. When the same screening questions were asked in March to July 2019, 26% of graduate students had signs of anxiety and 15% showed depression symptoms. © 2020 Springer Nature Limited

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27427 - Posted: 08.20.2020

Jon Hamilton The Food and Drug Administration has approved a variant of the anesthetic and party drug ketamine for suicidal patients with major depression. The drug is a nasal spray called Spravato and it contains esketamine, a chemical cousin of ketamine. In 2019, the FDA approved Spravato for patients with major depressive disorder who hadn't responded to other treatments. Now, the agency is adding patients who are having suicidal thoughts or have recently attempted to harm themselves or take their own lives. "Spravato is the first approved antidepressant medication that's been able to demonstrate a reduction in symptoms of major depressive disorder within 24 hours after the first dose," says Dr. Michelle Kramer, a psychiatrist and vice president of U.S. neuroscience, medical affairs at Janssen Pharmaceuticals, which makes the drug. Janssen is part of Johnson & Johnson. The drug's quick action is potentially important for suicidal patients because "existing drugs typically can take weeks or longer before you really get noticeable clinical benefit," says Dr. Gerard Sanacora, a professor of psychiatry at Yale University and director of Yale's depression research program. He was involved in the studies leading to the FDA approval and has consulted for Janssen. So a dose of esketamine "could potentially get a person out of a difficult, horrible situation when they're feeling so overwhelmed," says Dr. Charles Conway, a professor of psychiatry at Washington University School of Medicine in St. Louis who wasn't involved in the study. "This could be a significant improvement in how we can help people who have intense suicidal thinking." © 2020 npr

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27416 - Posted: 08.12.2020

By Hannah Sparks For communities with a low rate of depression and suicide, there may be something in the water, according to a new study. A comprehensive analysis of findings from previous studies has revealed that regions where the public drinking water contains a high level of naturally occurring lithium — a mineral used most often for the treatment of depression and bipolar disorder — also boast a lower rate of suicide than other areas. The review included all prior research on the effects of lithium, as well as regional water samples and suicide data from 1,286 locales in Austria, Greece, Italy, Lithuania, the UK, Japan and the United States. “Naturally occurring lithium in drinking water may have the potential to reduce the risk of suicide and may possibly help in mood stabilization, particularly in populations with relatively high suicide rates and geographical areas with a greater range of lithium concentration in the drinking water,” the authors concluded in their report. Denoted as “Li” on the periodic table, the element is found in varying concentrations in crops, rocks, soil and ground water — thus how it seeps into our water supply. In a statement on the King’s College London website, lead study author and chairman of epidemiology and public health at Brighton and Sussex Medical School Anjum Memon said, “It is promising that higher levels of trace lithium in drinking water may exert an anti-suicidal effect and have the potential to improve community mental health.” The results, published in the British Journal of Psychiatry, “are also consistent with the finding in clinical trials that lithium reduces suicide and related behaviors in people with a mood disorder,” said Allan Young, a professor at King’s College’s Institute of Psychiatry, Psychology & Neuroscience.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27408 - Posted: 08.08.2020

By Matthew Sitman As I read George Scialabba’s new book How To Be Depressed, I recalled that I’d been introduced to his writing almost a decade ago by a schizophrenic, manic-depressive homeless man. R. might have protested that term—technically, he lived in a small garage that a fellow parishioner at the church we all attended let him use. It was shocking to visit him there for the first time; nearly every square inch of the place was filled with musty stacks of the New York Review of Books, assorted newspapers, and books, leaving only a narrow path that led to a mattress. Before adding something to one of these piles, he’d open his latest acquisition and run his finger down its pages, searching for matches or “sparks” that might cause a destructive fire—a phobia caused by a traumatic incident in R.’s childhood. My friends and I tried to look after R., taking him to dinner or paying his phone bill or letting him do laundry in our homes. I was drawn to R. partly because I couldn’t help but see some of myself in him, and had a gnawing fear that his plight would one day be my own. He was, in his way, an intellectual, who actually read at least a few of the periodicals he collected and enjoyed arguing about politics. I’d often see him in the local used bookstore I frequented, and that must have been where he pressed Scialabba’s What Are Intellectuals Good For? into my hands. “This is the good shit,” he solemnly professed, and he was right. R. had been an alcoholic, and I’d gleaned that when he finally kicked booze the withdrawal caused a breakdown from which he’d never quite recovered. I knew I sometimes drank too much, too, and for the wrong reasons—enough to watch myself. We shared both hypochondria and a dread of visiting the doctor. I wasn’t a manic depressive, but for much of the time I knew R. I was in the throes of the worst severe depression of my life. © 2020 Commonweal Magazine.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27365 - Posted: 07.15.2020

Amy Fleming Taking a stroll with Shane O’Mara is a risky endeavour. The neuroscientist is so passionate about walking, and our collective right to go for walks, that he is determined not to let the slightest unfortunate aspect of urban design break his stride. So much so, that he has a habit of darting across busy roads as the lights change. “One of life’s great horrors as you’re walking is waiting for permission to cross the street,” he tells me, when we are forced to stop for traffic – a rude interruption when, as he says, “the experience of synchrony when walking together is one of life’s great pleasures”. He knows this not only through personal experience, but from cold, hard data – walking makes us healthier, happier and brainier. We are wandering the streets of Dublin discussing O’Mara’s book, In Praise of Walking, a backstage tour of what happens in our brains while we perambulate. Our jaunt begins at the grand old gates of his workplace, Trinity College, and takes in the Irish famine memorial at St Stephen’s Green, the Georgian mile, the birthplace of Francis Bacon, the site of Facebook’s new European mega-HQ and the salubrious seaside dwellings of Sandymount. O’Mara, 53, is in his element striding through urban landscapes – from epic hikes across London’s sprawl to more sedate ambles in Oxford, where he received his DPhil – and waxing lyrical about science, nature, architecture and literature. He favours what he calls a “motor-centric” view of the brain – that it evolved to support movement and, therefore, if we stop moving about, it won’t work as well. © 2020 Read It Later, Inc.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 27364 - Posted: 07.15.2020

By Erica Rex In 2012, I had my first psychedelic experiences, as a subject in a clinical trial at Johns Hopkins University School of Medicine’s Behavioral Pharmacology Research Unit. I was given two doses of psilocybin spaced a month apart to treat my cancer-related depression. During one session, deep within the world the drug evoked, I found myself inside a steel industrial space. Women were bent over long tables, working. I became aware of my animosity towards my two living siblings. A woman seated at the end of a table wearing a net cap and white clothes, turned and handed me a tall Dixie cup. “You can put that in here,” she said. The cup filled itself with my bilious, sibling-directed feelings. “We’ll put it over there.” She turned and placed the cup matter-of-factly on a table at the back of the room. Then she went back to her tasks. Whenever I speak with her, Mary Cosimano, the director of guide/facilitator services at Johns Hopkins Center for Psychedelic and Consciousness Research, mentions the women in the chamber and the cup. My experience struck a chord. For me, the women in the chamber have become a transcendent metaphor for emotional healing. “I’ve thought about having a necklace made, with the cup, as a momento,” she said the last time I saw her at a conference. “Have you thought about it?” Prior to their 1971 prohibition, psilocybin and LSD were administered to approximately 40,000 patients, among them people with terminal cancer, alcoholics and those suffering from depression and obsessive-compulsive disorder. The results of the early clinical studies were promising, and more recent research has been as well. The treatment certainly helped me. Eight years after my sessions, researchers continue to prove the same point again and again in an ongoing effort to turn psychedelic drug therapy into FDA-sanctioned medical treatment. This can’t happen soon enough. © 2020 Scientific American,

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27361 - Posted: 07.14.2020

By Andrew McCormick The psychiatrist was bald, with kind eyes, a silver goatee and the air of exhaustion that follows a person who works hard in a difficult field. It was March 2019, and having let an old prescription expire months earlier, I had gone to the Veterans Affairs hospital in Manhattan — my first time at a V.A. — hoping to get antidepressants. In a small, sparsely decorated office, the doctor and I faced each other across a wide desk. He told me about various V.A. programs — counseling, group therapy, a veterans’ yoga class, each accompanied by a flier — and described at length the V.A.’s crisis hotline. I appreciated his care, but I wasn’t there to break any new emotional ground; I really just wanted a prescription and to be on my way. I answered briskly as he worked through the questions any mental health worker asks you on a first visit. Did I have a history of anxiety or depression? Yes. Had I had thoughts of hurting myself or of suicide? Not really. Did anyone in my family have a history of mental health issues? Suddenly, my brain went foggy and my thoughts failed to connect. My speech slowed, and I began struggling to form sentences. Weird, I thought. I hadn’t felt sick. I worried the doctor might think he’d hit a nerve, when in fact I had answered questions like these many times before, including in post-deployment health evaluations in the Navy. My vision blurred. Eyes aflutter, I motioned to the doctor to give me a minute. I think I laughed. With the calm dispassion of a man who’s seen it all, the doctor picked up a phone beside him: “I’m going to need some help,” he said. “He’s about to pass out. . . . Yeah, he looks like he might throw up.” I swallowed hard. I tried not to. “Yeah, he just threw up.” © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27319 - Posted: 06.24.2020

By Pooja Lakshmin After going through a harrowing bout of postpartum depression with her first child, my patient, Emily, had done everything possible to prepare for the postpartum period with her second. She stayed in treatment with me, her perinatal psychiatrist, and together we made the decision for her to continue Zoloft during her pregnancy. With the combination of medication, psychotherapy and a significant amount of planning, she was feeling confident about her delivery in April. And then, the coronavirus hit. Emily, whose name has been changed for privacy reasons, called me in late-March because she was having trouble sleeping. She was up half the night ruminating about whether she’d be able to have her husband with her for delivery and how to manage taking care of a toddler and a newborn without help. The cloud that we staved off for so long was returning, and Emily felt powerless to stop it. Postpartum depression and the larger group of maternal mental health conditions called perinatal mood and anxiety disorders are caused by neurobiological factors and environmental stressors. Pregnancy and the postpartum period are already vulnerable times for women due in part to the hormonal fluctuations accompanying pregnancy and delivery, as well as the sleep deprivation of the early postpartum period. Now, fears about the health of an unborn child or an infant and the consequences of preventive measures, like social distancing, have added more stress. As a psychiatrist who specializes in taking care of pregnant and postpartum women, I’ve seen an increase in intrusive worry, obsessions, compulsions, feelings of hopelessness and insomnia in my patients during the coronavirus pandemic. And I’m not alone in my observations: Worldwide, mental health professionals are concerned. A special editorial in a Scandinavian gynecological journal called attention to the psychological distress that pregnant women and new mothers will experience in a prolonged global pandemic. A report from Zhejiang University in China detailed the case of a woman who contracted Covid-19 late in her pregnancy and developed depressive symptoms. In the United States, maternal mental health experts have also described an increase in patients with clinical anxiety. © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27263 - Posted: 05.28.2020

By Benedict Carey The mental health toll of the coronavirus pandemic is only beginning to show itself, and it is too early to predict the scale of the impact. The coronavirus pandemic is an altogether different kind of cataclysm — an ongoing, wavelike, poorly understood threat that seems to be both everywhere and nowhere, a contagion nearly as psychological as it is physical. Death feels closer, even well away from the front lines of emergency rooms, and social isolation — which in pre-Covid times was often a sign of a mind turning in on itself — is the new normal for tens of millions of people around the world. The ultimate marker of the virus’s mental toll, some experts say, will show up in the nation’s suicide rate, in this and coming years. The immediate effect is not at all clear, despite President Trump’s recent claim that lockdown conditions were causing deaths. “Just look at what’s happening with drug addiction, look at what’s happening with suicides,” he said in a press briefing in the White House Rose Garden on Monday. In fact, doctors won’t know for many months if suicide is spiking in 2020; each death must be carefully investigated to determine its cause. The rolling impact of Covid-19 on these rates give scientists a sense of how extended uncertainty and repeating undercurrents of anxiety affect people’s will to live. “It’s a natural experiment, in a way,” said Matthew Nock, a psychology professor at Harvard. “There’s not only an increase in anxiety, but the more important piece is social isolation.” He added, “We’ve never had anything like this — and we know social isolation is related to suicide.” The earliest signs of whether the pandemic is driving up suicides will likely emerge among those who have had a history of managing persistent waves of self-destructive distress. Many of these people, who number in the millions worldwide, go through each day compulsively tuned to the world’s casual cruelties — its suspicious glances and rude remarks — and are prone to isolate themselves, at times contemplating a final exit plan. © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27258 - Posted: 05.20.2020

Carl Sherman The world of neuroscience and psychiatry sat up and took notice last March when the Food and Drug Administration (FDA) approved brexanolone (Zulresso) for postpartum depression. It was the first drug specifically approved for the condition, which afflicts some 15 percent of women just before or shortly after childbirth. The event was a pivotal chapter in a neuroscience story that began three-quarters of a century ago with the 1941 discovery by Hans Selye (best known for his pioneering research into the nature of stress) that hormones including progesterone could affect the brain to induce deep anesthesia. Fast-forward 40 years to the discovery that a number of hormones—termed “neurosteroids” by the neuroscientist/endocrinologist Étienne-Émile Baulieu, a key figure in this work—are synthesized within the nervous system itself. In their National Institutes of Mental Health (NIMH) lab, Steven Paul and colleagues showed that several of these compounds work by binding to receptors on brain cells that are activated by GABA, the most plentiful inhibitory neurotransmitter in the brain. The GABA-A receptor is the site of action of several sedating central nervous system (CNS) drugs, including benzodiazepines (Valium, Librium), barbiturates, and many anesthetics. Neurosteroids can also bind to receptors for glutamate, the brain’s principal excitatory neurotransmitter. Paul and Robert Purdy proposed that, with its effect on both GABAergic and glutaminergic systems, neuroactive steroids (a term they coined to include synthetic analogues as well as the naturally-occurring hormones themselves) help regulate excitation throughout the brain. Excitation is a major factor in conditions such as epilepsy. Although there are many neuroactive steroids, the lion’s share of research has focused on allopregnanolone, a progesterone derivative. © 2020 The Dana Foundation.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27197 - Posted: 04.16.2020

By Andrew Solomon For nearly 30 years — most of my adult life — I have struggled with depression and anxiety. While I’ve never felt alone in such commonplace afflictions — the family secret everyone shares — I now find I have more fellow sufferers than I could have ever imagined. Within weeks, the familiar symptoms of mental illness have become universal reality. A new poll from the Kaiser Family Foundation found nearly half of respondents said their mental health was being harmed by the coronavirus pandemic. Nearly everyone I know has been thrust in varying degrees into grief, panic, hopelessness and paralyzing fear. If you say, “I’m so terrified I can barely sleep,” people may reply, “What sensible person isn’t?” But that response can cause us to lose sight of the dangerous secondary crisis unfolding alongside the more obvious one: an escalation in both short-term and long-term clinical mental illness that may endure for decades after the pandemic recedes. When everyone else is experiencing depression and anxiety, real, clinical mental illness can get erased. While both the federal and local governments (some alarmingly slower than others) have responded to the spread of the coronavirus in critical ways, acknowledgment of the mental illness vulnerabilities has been cursory. Gov. Andrew Cuomo, who has so far enlisted more than 8,000 mental health providers to help New Yorkers in distress, is a fortunate exception. The Chinese government moved psychologists and psychiatrists to Wuhan during the first stage of self-quarantine. No comparable measures have been initiated by our federal government. The unequal treatment of the two kinds of health — physical over mental — is consonant with our society’s ongoing disregard for psychological stability. Insurance does not offer real parity of coverage, and treatment for mood disorders is generally deemed a luxury. But we are in a dual crisis of physical and mental health, and those facing psychiatric challenges deserve both acknowledgment and treatment. © 2020 The New York Times Company

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 27183 - Posted: 04.13.2020

A first-of-its-kind trial has demonstrated that a receptor involved in the brain’s reward system may be a viable target for treating anhedonia (or lack of pleasure), a key symptom of several mood and anxiety disorders. This innovative fast-fail trial was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, and the results of the trial are published in Nature Medicine. Mood and anxiety disorders are some of the most commonly diagnosed mental disorders, affecting millions of people each year. Despite this, available medications are not always effective in treating these disorders. The need for new treatments is clear, but developing psychiatric medications is often a resource-intensive process with a low success rate. To address this, NIMH established the Fast-Fail Trials program with the goal of enhancing the early phases of drug development. “The fast-fail approach aims to help researchers determine — quickly and efficiently — whether targeting a specific neurobiological mechanism has the hypothesized effect and is a potential candidate for further clinical trials,” explained Joshua A. Gordon, M.D., Ph.D., director of NIMH. “Positive results suggest that targeting a neurobiological mechanism affects brain function as expected, while negative results allow researchers to eliminate that target from further consideration. We hope this approach will pave the way towards the development of new and better treatments for individuals with mental illnesses.” In this study, researcher Andrew D. Krystal, M.D., who began the research while at the Duke University School of Medicine, Durham, North Carolina, and is now at the University of California, San Francisco, and colleagues report the first comprehensive application of this fast-fail approach. The researchers examined the kappa opioid receptor (KOR) as a possible neurobiological target for the treatment of anhedonia. Previous findings suggest that drugs that block the KOR, known as KOR antagonists, can affect reward-related brain circuits in ways that could improve reward processing and reverse anhedonia and associated symptoms.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27152 - Posted: 03.31.2020

By Alex Gatenby Victoria Derbyshire programme The mental health charity Mind says it is signposting people to street drug charities to help them withdraw from antidepressants because of the lack of alternatives available. Those affected can experience debilitating symptoms. "Within a couple of days of coming off, it was overwhelming - agitation, anxiety, akathisia [restlessness], just restlessness, can't sleep, suicidal ideations, all that stuff going on very quickly," Stuart Bryan tells the BBC's Victoria Derbyshire programme. The 48-year-old has been taking anti-depressants on and off for more than two decades. "The withdrawals are far worse than the original depression, for me and so many other people." Stuart has tried to stop more than 10 times, but has struggled with what he calls his withdrawal "hell" - and has now had to stop working. He says doctors have advised him to take anything between "a few weeks" to three months to slowly stop using the drugs. But he believes people coming off anti-depressants are being "abandoned by the system". Image caption Mind's Stephen Buckley says it is not fully understood how difficult a process coming off anti-depressants can be While antidepressants are not addictive, just over half of those who stop or reduce their dosage experience withdrawal symptoms, according to one review of 24 studies last year. The mental health charity Mind's head of information Stephen Buckley says it is having to signpost patients to street-drug charities, even though they have been prescribed the drugs on the NHS. Street-drug charities usually help those misusing alcohol and illegally-obtained drugs. © 2020 BBC

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 27112 - Posted: 03.12.2020

By Heather Jones I knew early on that my normal didn’t feel like everyone else’s. Even as early as kindergarten, I could tell that my brain worked differently than others, and that I seemed more listless than other children my age. Other kids felt sadness when they experienced a loss or something upsetting. I always felt sad. I didn’t question the cloudy lens through which I viewed the world, because I had never seen clearly. When I was 16, my family doctor asked me the questions that would change my worldview. Having treated me since childhood, she had noticed patterns. She asked me whether I was experiencing the list of symptoms associated with persistent depressive disorder. I had all of them — feeling down, feeling hopeless, sleep problems, avoidance of social activities, low self-esteem and the rest of the laundry list of warning signs. My doctor explained to me that persistent depressive disorder, also called dysthymia, was a type of “functional depression” that lasts for years and often for a lifetime. I had probably had it since early childhood. I burst into tears, finally knowing there was a reason I felt this way. Knowing what I had didn’t take away my depression — more than 20 years later, I am still living with this condition — but getting a proper diagnosis started me on a path to better management of my symptoms. I am not alone. According to the National Institute of Mental Health, 1.3 percent of American adults will experience persistent depressive disorder at some time in their lives.

Related chapters from BN: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 27104 - Posted: 03.09.2020