Chapter 12. Psychopathology: The Biology of Behavioral Disorders

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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.

Keyword: Depression
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.

Keyword: Depression
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,

Keyword: Depression; Drug Abuse
Link ID: 27361 - Posted: 07.14.2020

Research shows that adolescents who live in areas that have high levels of artificial light at night tend to get less sleep and are more likely to have a mood disorder relative to teens who live in areas with low levels of night-time light. The research was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health, and is published in JAMA Psychiatry. “These findings illustrate the importance of joint consideration of both broader environmental-level and individual-level exposures in mental health and sleep research,” says study author Diana Paksarian, Ph.D., a postdoctoral research fellow at NIMH. Daily rhythms, including the circadian rhythms that drive our sleep-wake cycles, are thought to be important factors that contribute to physical and mental health. The presence of artificial light at night can disrupt these rhythms, altering the light-dark cycle that influences hormonal, cellular, and other biological processes. Researchers have investigated associations among indoor artificial light, daily rhythms, and mental health, but the impact of outdoor artificial light has received relatively little attention, especially in teens. In this study, Paksarian, Kathleen Merikangas, Ph.D., senior investigator and chief of the Genetic Epidemiology Research Branch at NIMH, and coauthors examined data from a nationally representative sample of adolescents in the United States, which was collected from 2001 to 2004 as part of the National Comorbidity Survey Adolescent Supplement (NCS-A). The dataset included information about individual-level and neighborhood-level characteristics, mental health outcomes, and sleep patterns for a total of 10,123 teens, ages 13 to 18 years old.

Keyword: Biological Rhythms; Depression
Link ID: 27348 - Posted: 07.08.2020

By Pam Belluck Kim Victory was paralyzed on a bed and being burned alive. Just in time, someone rescued her, but suddenly, she was turned into an ice sculpture on a fancy cruise ship buffet. Next, she was a subject of an experiment in a lab in Japan. Then she was being attacked by cats. Nightmarish visions like these plagued Ms. Victory during her hospitalization this spring for severe respiratory failure caused by the coronavirus. They made her so agitated that one night, she pulled out her ventilator breathing tube; another time, she fell off a chair and landed on the floor of the intensive care unit. “It was so real, and I was so scared,” said Ms. Victory, 31, now back home in Franklin, Tenn. To a startling degree, many coronavirus patients are reporting similar experiences. Called hospital delirium, the phenomenon has previously been seen mostly in a subset of older patients, some of whom already had dementia, and in recent years, hospitals adopted measures to reduce it. “All of that has been erased by Covid,” said Dr. E. Wesley Ely, co-director of the Critical Illness, Brain Dysfunction and Survivorship Center at Vanderbilt University and the Nashville Veteran’s Administration Hospital, whose team developed guidelines for hospitals to minimize delirium. Now, the condition is bedeviling coronavirus patients of all ages with no previous cognitive impairment. Reports from hospitals and researchers suggest that about two-thirds to three-quarters of coronavirus patients in I.C.U.’s have experienced it in various ways. Some have “hyperactive delirium,” paranoid hallucinations and agitation; some have “hypoactive delirium,” internalized visions and confusion that cause patients to become withdrawn and incommunicative; and some have both. © 2020 The New York Times Company

Keyword: Schizophrenia
Link ID: 27336 - Posted: 06.29.2020

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

Keyword: Depression; 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

Keyword: Depression; 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

Keyword: Depression
Link ID: 27258 - Posted: 05.20.2020

Alejandra Manjarrez The brain is a master of forming patterns, even when it involves events occurring at different times. Take the phenomenon of trace fear conditioning—scientists can get an animal to notice the relationship between a neutral stimulus and an aversive stimulus separated by a temporal chasm (the trace) of a few or even tens of seconds. While it’s a well-established protocol in neuroscience and psychology labs, the mechanism for how the brain bridges the time gap between two related stimuli in order to associate them is “one of the most enigmatic and highly investigated” questions, says Columbia University neuroscientist Attila Losonczy. If the first stimulus is finished, the information about its presence and identity “should be somehow maintained through some neuronal mechanism,” he explains, so it can be associated with the second stimulus coming later. Losonczy and his colleagues have recently investigated how this might occur in a study published May 8 in Neuron. They measured the neural activity in the hippocampal CA1 region of the brain—known to be crucial for the formation of memories—of mice exposed to trace fear conditioning. The team found that associating the two events separated by time involved the activation of a subset of neurons that fired sparsely every time mice received the first stimulus and during the time gap that followed. The pattern emerged only after mice had learned to associate both stimuli. The study highlights “the important question of how we link memories across time,” says Denise Cai, a neuroscientist at the Icahn School of Medicine at Mount Sinai who was not involved in the work. Studying the basic mechanisms of temporal association is critical for understanding how it goes wrong in disorders such as post-traumatic stress disorder (PTSD) or Alzheimer’s disease, she says. © 1986–2020 The Scientist

Keyword: Learning & Memory; Stress
Link ID: 27254 - Posted: 05.18.2020

Michael Marshall In 2018, psychiatrist Oleguer Plana-Ripoll was wrestling with a puzzling fact about mental disorders. He knew that many individuals have multiple conditions — anxiety and depression, say, or schizophrenia and bipolar disorder. He wanted to know how common it was to have more than one diagnosis, so he got his hands on a database containing the medical details of around 5.9 million Danish citizens. He was taken aback by what he found. Every single mental disorder predisposed the patient to every other mental disorder — no matter how distinct the symptoms1. “We knew that comorbidity was important, but we didn’t expect to find associations for all pairs,” says Plana-Ripoll, who is based at Aarhus University in Denmark. The study tackles a fundamental question that has bothered researchers for more than a century. What are the roots of mental illness? In the hope of finding an answer, scientists have piled up an enormous amount of data over the past decade, through studies of genes, brain activity and neuroanatomy. They have found evidence that many of the same genes underlie seemingly distinct disorders, such as schizophrenia and autism, and that changes in the brain’s decision-making systems could be involved in many conditions. Researchers are also drastically rethinking theories of how our brains go wrong. The idea that mental illness can be classified into distinct, discrete categories such as ‘anxiety’ or ‘psychosis’ has been disproved to a large extent. Instead, disorders shade into each other, and there are no hard dividing lines — as Plana-Ripoll’s study so clearly demonstrated. © 2020 Springer Nature Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27235 - Posted: 05.06.2020

by Peter Hess The mood-stabilizing drug lithium eases repetitive behaviors seen in mice missing SHANK3, an autism gene, according to a new study1. The findings suggest lithium merits further study as a treatment for some people with autism, even though the drug has troublesome side effects, including tremors and impaired memory. “Lithium is, of course, a rather difficult, non-ideal treatment,” says lead investigator Gina Turrigiano, professor of vision science at Brandeis University in Waltham, Massachusetts. “It’s really hard to get people on a lithium regimen that they can tolerate well.” But understanding why lithium works may set the stage for better treatments, she says. About 1 percent of people with autism have mutations in SHANK3. Deletion or mutation of the gene can also lead to Phelan-McDermid syndrome, which is characterized by intellectual disability, delayed speech and, often, autism. Case studies of people with Phelan-McDermid syndrome also suggest that lithium eases behavior problems associated with the condition2. Previous work has shown that SHANK3 helps stabilize neuronal circuits by adjusting excitatory and inhibitory signaling like a thermostat. This process, called homeostatic plasticity, allows neurons to respond to changes in sensory input. © 2020 Simons Foundation

Keyword: Autism
Link ID: 27215 - Posted: 04.27.2020

by Lauren Schenkman Mice with mutations in a gene called DLG2 are anxious and asocial; they also sleep poorly and overgroom themselves, according to a new study1. These characteristics resemble those seen in some people with autism. The results offer the first evidence that mutations in DLG2 may account for some of the condition’s behavioral traits. “This study is a baby step indicating DLG2’s implication in [autism’s] core behavioral symptoms,” says lead investigator Soo Young Kim, assistant professor of pharmacy at Yeungnam University in Gyeongsan, South Korea. A 2013 study reported that mice and people with DLG2 mutations have differences in learning, attention and other cognitive processes2. Last year, a study of nearly 500 families with two or more autistic children identified DLG2 as a candidate gene for autism3. The new work offers “a more full picture” of DLG2’s effect on behavior, says Seth Grant, professor of molecular neuroscience at the University of Edinburgh in Scotland. Grant led the 2013 work but was not involved in the new study. “It’s a useful contribution.” Kim and her colleagues bred male mice that have two mutant copies of DLG2. The animals lack the corresponding protein, which forms part of a neuron’s scaffolding. DLG4, another gene implicated in autism, has a similar role. © 2020 Simons Foundation

Keyword: Autism; Schizophrenia
Link ID: 27212 - Posted: 04.24.2020

By Kelly Servick For the first time in decades, researchers may have a new way to tweak brain signals to treat psychosis and other symptoms of schizophrenia. Results from a 245-person clinical trial hint that a compound called SEP-363856, which seems to act on neural receptors involved in dopamine signaling, might address a broader range of schizophrenia symptoms than currently available drugs do—and with fewer side effects. “If these results are confirmed, this will be big, big news,” says Jeffrey Lieberman, a psychiatrist at Columbia University. The drug’s developer, Sunovion Pharmaceuticals Inc., identified it through an unusual screening process not guided by the brain circuits and receptors already implicated in the disease, Lieberman says. “It was a big gamble on their part. This study suggests that it may pay off.” The biological basis of schizophrenia remains a puzzle, but researchers have linked patients’ hallucinations and delusions to an excess of the chemical messenger dopamine. To inhibit dopamine signaling, existing antipsychotic drugs bind to a type of dopamine receptor on neurons called D2. These drugs help control abnormal perceptions and thoughts—the “positive” symptoms of schizophrenia. But they don’t do much to address either cognitive impairments or the “negative” symptoms, including lack of motivation, dulled emotion, and social withdrawal. “Those negative symptoms are often the most devastating,” says Diana Perkins, a psychiatrist at the University of North Carolina, Chapel Hill. “A person can become, at the most extreme, robotlike.” © 2020 American Association for the Advancement of Science.

Keyword: Schizophrenia
Link ID: 27200 - Posted: 04.16.2020

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.

Keyword: Depression; 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

Keyword: Depression; Stress
Link ID: 27183 - Posted: 04.13.2020

By Katherine Rosman The coronavirus outbreak has turned many of us into nervous germophobes, seeking to protect ourselves from infection by washing our hands methodically and frequently, avoiding unnecessary contact with so called high-touch surfaces and methodically sanitizing packages, our homes and our bodies. For people diagnosed with obsessive-compulsive disorder, or O.C.D., the worry created by the threat of coronavirus has the potential for more intense and longer-lasting implications. According to the International OCD Foundation, there are about three million Americans who have been diagnosed with O.C.D. It’s a condition characterized by unwanted thoughts or urges that generate high levels of anxiety and repetitive acts meant to neutralize the obsessional thought. The cleaning and sanitizing practices that help prevent coronavirus infection are bringing people with O.C.D. into closer orbit to behaviors that are a gateway to detrimental patterns that could interfere with their ability to engage meaningfully with the world outside their homes for years to come. Courtenay Patlin, a 28-year-old in Los Angeles, is trying to find balance between appropriate caution and overreaction. Several weeks ago, before the California shelter-in-place order, Ms. Patlin decided to mostly stay indoors. She had read enough about how quickly coronavirus had spread in China, Italy and then Seattle, and how very sick it was making so many. She felt she could rely on only herself and her Clorox to stay healthy. “I keep a very clean apartment, and I feel safe at home,” she said. Ms. Patlin, a graduate student studying clinical psychology, was diagnosed with O.C.D. about five years ago, she said, after years of being afraid of public toilets, refusing to eat off dishes that she hadn’t scrubbed herself or witnessed being sufficiently cleaned by others and being fearful of being hugged by basically anyone. ImageMs. Patlin’s hands. She used to clean her hands and apartment with pure bleach and cleaning solutions until the skin on her fingers started to peel off, which she would take as a sign that she was cleaning the proper amount. © 2020 The New York Times Company

Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 27167 - Posted: 04.03.2020

By Jennifer Szalai Donald Galvin was a sophomore at Colorado State when he first checked into the campus health clinic to get treated for a cat bite, offering no further explanation of what had occurred. Two years and several visits later, he arrived at the clinic with another cat bite — only this time he told a doctor what happened to the cat. “He killed a cat slowly and painfully,” the doctor recorded in his notes. “Doesn’t know why he killed the cat nor why he tormented. Got emotionally upset as he discussed the behavior.” The oldest of 12 siblings, Donald was the first to be told he was schizophrenic. Five of his brothers would eventually get the same diagnosis. Even the healthy children in the Galvin family were beset in a sense, forced to live with an affliction that inevitably shaped their relationships to their parents and to one another. As the journalist Robert Kolker writes in “Hidden Valley Road,” having just one schizophrenic family member is bound to reorient the experiences of everyone else; having six made the Galvins extraordinary, not least to the medical researchers who eventually studied them. Kolker’s previous book, “Lost Girls,” traced the lives of five murdered women on Long Island and told a story of sex work and law enforcement during a time of technological change. His new book is a comparable feat of empathy and narrative journalism, as he coaxes out the struggles of the Galvin family, showing how they embodied the roiling debates over the science of schizophrenia — not just its causes, “but what it actually is.” The Galvin children were all born between 1945 and 1965, during the two decades of the baby boom. It was a time when the psychoanalytic approach to mental illness, with its theory of the cold and domineering “schizophrenogenic mother,” reigned supreme. What began as a more holistic rejoinder to the crude biological reductionism of the early 20th century soon hardened into its own orthodoxy. According to its proponents, mental illness was a disease of nurture, not nature; as one psychiatrist put it, the schizophrenic patient “is always one who is reared by a woman who suffers from a perversion of the maternal instinct.” © 2020 The New York Times Company

Keyword: Schizophrenia; Genes & Behavior
Link ID: 27161 - Posted: 04.02.2020

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.

Keyword: Depression
Link ID: 27152 - Posted: 03.31.2020

Jonathan Kanter and Adam Kuczynski To fight the spread of coronavirus, government officials have asked Americans to swallow a hard pill: Stay away from each other. In times of societal stress, such a demand runs counter to what evolution has hard-wired people to do: Seek out and support each other as families, friends and communities. We yearn to huddle together. The warmth of our breath and bodies, of holding hands and hugging, of talking and listening, is a primary source of soothing. These connections are pivotal for responding to and maximizing our survival in times of stress. Priority number one is to follow the recommended social distancing guidelines to control the virus. The cure is definitely not worse than the disease – experts’ projections of disease spread and mortality without strong intervention make this clear. But as with any pill, there are side effects. As psychological scientists at the University of Washington’s Center for the Science of Social Connection, our lab studies social connectedness, why it is important and how to maximize its benefits. Our clinical and research experiences help us understand the side effects of social distancing and suggest strategies for addressing them. In times of stress and illness, being deprived of social connection can create more stress and illness. People who are lonely have higher levels of the hormone cortisol, an indicator of stress; show weaker immune responses to pathogens; and are at increased risk for premature death. Isolation can lead to depression, suicidal thoughts and other clinical conditions. © 2010–2020, The Conversation US, Inc.

Keyword: Stress
Link ID: 27127 - Posted: 03.17.2020

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

Keyword: Depression
Link ID: 27112 - Posted: 03.12.2020