Chapter 16. Psychopathology: Biological Basis of Behavior Disorders

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 1 - 20 of 2888

By Diana Kwon MDMA, or ecstasy, once had the reputation of exclusively being an illicit party drug popular at raves and dance clubs. That view has changed in recent years. The substance, known for its ability to produce feelings of euphoria and affection for others, has developed a new identity as a promising therapeutic tool. Researchers are currently investigating MDMA-assisted therapy as a potential treatment for post-traumatic stress disorder in late-stage clinical trials. The drug’s capacity to enhance sociability has also led to studies investigating its benefits for other conditions, such as social anxiety in individuals with autism spectrum disorder. Despite the promise of its therapeutic benefits, concern persists among some scientists that MDMA could be abused because its pleasurable effects can make it addictive. “By no means [does the drug] have the addictive liability of methamphetamine or certain opioids,” says Robert Malenka, a professor of psychiatry and behavioral sciences at Stanford University. “But it does have abuse potential.” A new study by Malenka and his team suggests it may be possible to circumvent this risk. The findings, published today in Science Translational Medicine, reveal that MDMA’s sociability-enhancing abilities and its pleasurable properties are controlled by distinct pathways in the brain—at least in mice. That insight opens the possibility of developing a safer version of the drug. Previous research by Malenka’s group and others had revealed that MDMA stimulated the release of both serotonin and dopamine in the brain. The existing evidence suggested the drug’s effects on sociability were linked to serotonin and its addictive potential to dopamine, but the extent to which these pathways were distinct was unknown. “Separating out the prosocial from the addictive effects has tremendous implications for drug development,” says Boris Heifets, an anesthesiologist at Stanford and lead author of the latest study. A key question is, “Can we make something with the same kind of prosocial effect that maybe isn’t as prone to abuse?” © 2019 Scientific American

Keyword: Drug Abuse; Depression
Link ID: 26891 - Posted: 12.12.2019

By Andrea Petersen Anne Firmender, 74, was working with her psychologist to come up with a list of her positive attributes. “I cook for others,” said Ms. Firmender. “It’s giving,” encouraged the psychologist, Dimitris Kiosses. “Good kids,” continued Ms. Firmender, who has four grown children and four grandchildren. “And great mother,” added Dr. Kiosses. Ms. Firmender smiled. Dr. Kiosses typed up the list and handed a printout to Ms. Firmender to take home. “When you’re feeling down and hard on yourself, you can remind yourself of your strengths,” he told her. Ms. Firmender, who has a history of mental health problems, was in therapy for depression. But she also has mild cognitive impairment and can have trouble remembering what day it is. So Dr. Kiosses was treating her with a novel approach called Problem Adaptation Therapy, or PATH. The therapy, developed at Weill Cornell Medicine in New York City and White Plains, N.Y., focuses on solving tangible problems that fuel feelings of sadness and hopelessness. It incorporates tools, like checklists, calendars, signs and videos, to make it accessible for people with memory issues. A caregiver is often involved. The approach is one of several new psychotherapies to treat anxiety and depression in people with cognitive impairments, including early to moderate dementia. Another, the Peaceful Mind program, developed by researchers at Baylor College of Medicine and elsewhere for patients with anxiety and dementia, simplifies traditional cognitive behavioral therapy and focuses on scheduling pleasurable activities and skills, like deep breathing. Therapy sessions are short and take place in patients’ homes. A program designed by researchers at University College London gives cards to patients to take home to remind them of key strategies. One that says “Stop and Think” prompts them to pause when they have panicky and unhelpful thoughts to help keep those thoughts from spiraling and creating more anxiety. © 2019 The New York Times Company

Keyword: Alzheimers; Depression
Link ID: 26884 - Posted: 12.09.2019

By Laura Sanders “Does the pill cause depression?” the news headline asked. Prompted by a recent study that described a link between taking birth control pills as a teenager and depression in adulthood, the news got some doctors hopping mad. Early research hints that there are reasons to look more closely at hormonal birth control’s side effects. But so far, the link is less than certain. “This is a premature connection,” says pediatrician Cora Breuner of Seattle Children’s Hospital. Putting too much stock in preliminary evidence may lead to fewer teenagers getting birth control and, in turn, more unwanted pregnancies among teens — a situation that can upend young lives, Breuner says. Headlines that frighten teens, their families and doctors are “yet another barrier in place for accessing a completely effective way to prevent unplanned pregnancies.” Ob-gyn and contraception researcher Katharine O’Connell White agrees. “Birth control gets all of the worry and concern,” says White, of Boston University School of Medicine. “But we know that other things are much more dangerous.” Teen pregnancy, for instance. Access to effective birth control is vital for sexually active teenagers, the doctors say. “I don’t think the evidence is there right now to say that this is a threat,” adds epidemiologist and public health researcher Sarah McKetta of Columbia University, who has studied birth control use in teens. Still, she sees value in more research on the issue. “Women deserve good medication … that’s not giving them problems.” If there are risks that come with the pill, then scientists ought to get a handle on them. © Society for Science & the Public 2000–2019

Keyword: Depression; Hormones & Behavior
Link ID: 26864 - Posted: 12.02.2019

By Nick Chrastil In May of 2016, not long after his release from a psychiatric hospital, Colby Crawford, a 23-year old black man, was booked into the Orleans Justice Center (OJC) — a new $150-million-dollar jail opened a year earlier to replace the crumbling and now shuttered Orleans Parish Prison complex, and touted as a symbol of a more progressive approach to incarceration in New Orleans. Ten months later, he was dead. Colby Crawford was diagnosed with schizophrenia, bipolar disorder, and substance use disorder. A lawsuit argues that his death at Orleans Parish jail was in part due to a profound lack of treatment for his mental illness. Visual: Courtesy of the Crawford family. Prior to Crawford’s incarceration, he had been diagnosed with schizophrenia, bipolar disorder, and substance use disorder. A psychiatrist at OJC noted that he was prone to “seeing spirits and ghosts, insomnia, anxiety, paranoia, and bad dreams,” and prescribed an antipsychotic and anticonvulsant. A month after Crawford’s arrest on allegations that he hit his mother and sister, he was transferred about an hour outside of New Orleans to a state prison called the Elayn Hunt Correctional Center — the one place he received adequate mental health care while incarcerated, according to a wrongful death suit filed by his mother. But two months later, Crawford was transferred back to OJC and placed in “disciplinary segregation” for 20 days. Upon release back into the general population, he deteriorated. He stopped taking his medications consistently and started hearing voices and seeing spirits. He couldn’t sleep and got in fights. Jail records cited in the complaint show that medical staff was aware of Crawford’s declining condition. He requested to be moved to a psychiatric tier. He never was.

Keyword: Schizophrenia
Link ID: 26839 - Posted: 11.21.2019

Robin McKie Major psychological disorders such as schizophrenia will continue to affect humans because men and women are continually generating genetic mutations that disrupt brain development. This will be the key conclusion of Professor Sir Michael Owen, director of Cardiff University’s centre for neuropsychiatric genetics and genomics, when he gives the annual Darwin Lecture at the Royal Society of Medicine this week. Understanding such conditions at an evolutionary level will be crucial to developing treatments, Owen believes. Thirty years ago, the new technology of DNA analysis raised hopes that schizophrenia – a condition that can track through families – would soon reveal links to one or two specific genes, said Owen. Treatments might then be relatively easy to develop, it was thought. Instead scientists found that hundreds of genes, each having a tiny effect, dictate whether or not a person will be susceptible to the condition. Characterised by profound behavioural changes, hallucinations, and delusions, these transformations in behaviour can have profound consequences, he added. For example, men with schizophrenia have – on average – only a quarter as many children as males in the general population while women with the condition have about half as many as unaffected females. That low reproduction rate should have had one clear result, Owen told the Observer last week. “Schizophrenia cases should have declined and disappeared long ago as those affected were out bred by those unaffected. This has not happened. A steady level of 1% people continue to be affected.” © 2019 Guardian News & Media Limited

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26831 - Posted: 11.19.2019

By Jane E. Brody There‌ are‌ ‌some‌ ‌crimes‌ ‌that‌ ‌are‌ almost‌ ‌impossible‌ ‌to‌ ‌forget. ‌ ‌ For‌ me, ‌they‌ ‌include‌ ‌the‌ ‌death‌ ‌in‌ ‌1999‌ ‌of‌ ‌Kendra‌ ‌Webdale, ‌an‌ ‌aspiring‌ ‌young‌ ‌journalist‌ ‌who‌ ‌was‌ ‌pushed‌ ‌in‌ ‌front‌ ‌of‌ ‌a‌ ‌New‌ ‌York‌ ‌subway‌ ‌train‌ ‌by‌ ‌a‌ ‌29-year-old‌ ‌man‌ ‌with‌ ‌schizophrenia‌ ‌who‌ ‌had‌ ‌stopped‌ ‌taking‌ ‌his‌ ‌medication. ‌That‌ ‌same‌ ‌year, ‌two‌ ‌mentally‌ ‌ill‌ ‌teenage‌‌‌ ‌boys‌ ‌massacred‌ ‌12‌ ‌students‌ ‌and‌ ‌one‌ ‌teacher‌ ‌at‌ ‌Columbine‌ ‌High‌ ‌School‌ ‌in‌ ‌Colorado. ‌ ‌ Thirteen‌ ‌years‌ ‌later, ‌a‌ ‌seriously‌ ‌emotionally‌ ‌disturbed‌ ‌20-year-old‌ ‌man‌ ‌murdered‌ ‌20‌ ‌young‌ ‌children‌ ‌and‌ ‌six‌ ‌adults‌ ‌at‌ ‌Sandy‌ ‌Hook‌ ‌Elementary‌ ‌School‌ ‌in‌ ‌Connecticut. ‌This‌ ‌year, ‌a‌ ‌homeless‌ ‌24-year-old‌ ‌man‌ ‌bludgeoned‌ ‌four‌ ‌men‌ ‌to‌ ‌death‌ ‌while‌ ‌they‌ ‌slept‌ ‌on‌ ‌the‌ ‌streets‌ ‌of‌ ‌my‌ ‌city. ‌ ‌ Although‌ ‌New York is now far‌ ‌safer‌ ‌than‌ ‌when‌ ‌I‌ ‌was‌ ‌a‌ ‌child‌ ‌in‌ ‌the‌ ‌1940s‌ ‌and‌ ‌’50s‌ ‌who‌ ‌walked‌ ‌to‌ ‌and‌ ‌from‌ ‌school‌ ‌unescorted, ‌like‌ ‌most‌ ‌big‌ ‌cities, ‌it still‌ ‌harbors‌ ‌untold‌ ‌numbers‌ ‌of‌ ‌men‌ ‌and‌ ‌women‌ ‌with‌ ‌known‌ ‌or‌ ‌undiagnosed‌ ‌severe‌ ‌mental‌ ‌illness‌ ‌that‌ ‌can‌ ‌and‌ ‌should‌ ‌be‌ ‌treated‌ ‌before‌ ‌yet‌ ‌another‌ ‌personal‌ ‌or‌ ‌societal‌ ‌tragedy‌ ‌occurs. ‌ ‌ What, ‌I‌ ‌wondered, ‌is‌ ‌or‌ ‌can‌ ‌be‌ ‌done‌ ‌to‌ ‌help‌ ‌them‌ ‌and‌ ‌avert‌ ‌further‌ ‌disasters? ‌ ‌ Contrary‌ ‌to‌ ‌politically‌ ‌motivated‌ ‌claims, ‌I‌ ‌learned‌ ‌that‌ ‌people‌ ‌with‌ ‌serious‌ ‌mental‌ ‌ills‌ ‌are‌ ‌not‌ ‌necessarily‌ ‌prone‌ ‌to‌ ‌commit‌ ‌violent‌ acts‌ ‌ — ‌they‌ ‌are‌ ‌far‌ ‌more‌ ‌likely‌ ‌to‌ ‌become‌ ‌‌victims‌‌ ‌of‌ ‌crime. ‌Rather, ‌the‌ ‌issue‌ ‌is‌ ‌that‌ ‌treatments‌ ‌known‌ ‌to‌ ‌be‌ ‌effective‌ ‌are‌ ‌underfunded‌ ‌or‌ ‌wrongly‌ ‌dismissed‌ ‌as‌ ‌ineffective‌ ‌or‌ ‌too‌ ‌dangerous; ‌basic‌ ‌research‌ ‌in‌ ‌university‌ ‌and‌ ‌government‌ ‌laboratories‌ ‌into‌ ‌new‌ ‌and‌ ‌better‌ ‌drugs‌ ‌is‌ ‌limited‌ ‌and‌ ‌also‌ ‌underfunded; ‌and‌ ‌pharmaceutical‌ ‌companies‌ ‌have‌ ‌shown‌ ‌little‌ ‌interest‌ ‌in‌ ‌developing‌ ‌and‌ ‌testing‌ ‌treatments‌ ‌for‌ ‌severe‌ ‌mental‌ ‌illness. ‌ ‌ Also‌ ‌at‌ ‌issue‌ ‌is‌ ‌that, ‌as‌ ‌was‌ true‌ for‌ ‌cancer‌ ‌until‌ ‌recently, ‌acknowledgment‌ ‌of‌ ‌mental‌ ‌illness‌ ‌carries‌ ‌a‌ ‌stigma‌ ‌that‌ ‌impedes‌ ‌its‌ ‌early‌ ‌recognition, ‌when‌ ‌it‌ ‌can‌ ‌be‌ ‌most‌ ‌effectively‌ ‌treated‌ ‌or‌ ‌reversed. ‌ ‌ © 2019 The New York Times Company

Keyword: Schizophrenia; Aggression
Link ID: 26829 - Posted: 11.18.2019

National Institutes of Health researchers found that a single, low-dose ketamine infusion was relatively free of side effects for patients with treatment-resistant depression. Elia Acevedo-Diaz, M.D., Carlos Zarate, M.D., and colleagues at the NIH’s National Institute of Mental Health (NIMH) report their findings in the Journal of Affective Disorders. Studies have shown that a single, subanesthetic-dose (a lower dose than would cause anesthesia) ketamine infusion can often rapidly relieve depressive symptoms within hours in people who have not responded to conventional antidepressants, which typically take weeks or months to work. However, widespread off-label use of intravenous subanesthetic-dose ketamine for treatment-resistant depression has raised concerns about side effects, especially given its history as a drug of abuse. “The most common short-term side effect was feeling strange or loopy,” said Acevedo-Diaz, of the Section on the Neurobiology and Treatment of Mood Disorders, part of the NIMH Intramural Research Program (IRP) in Bethesda, Maryland. “Most side effects peaked within an hour of ketamine administration and were gone within two hours. We did not see any serious, drug-related adverse events or increased ketamine cravings with a single-administration.” The researchers compiled data on side effects from 163 patients with major depressive disorder or bipolar disorder and 25 healthy controls who participated in one of five placebo-controlled clinical trials conducted at the NIH Clinical Center over 13 years. While past studies have been based mostly on passive monitoring, the NIMH IRP assessment involved active and structured surveillance of emerging side effects in an inpatient setting and used both a standard rating scale and clinician interviews. In addition to dissociative (disconnected, unreal) symptoms, the NIMH IRP assessment examined other potential side effects — including headaches, dizziness, and sleepiness. The study did not address the side effects associated with repeated infusions or long-term use.

Keyword: Depression
Link ID: 26822 - Posted: 11.16.2019

By Kristopher Nielsen Have you ever heard of a condition known as “general paresis of the insane”? Probably not. In the 19th century general paresis was one of the most commonly diagnosed mental disorders. Its symptoms included odd social behaviors, impaired judgment, depressed mood and difficulty concentrating. Around the turn of the 20th century, though, we figured what it really was—a form of late-stage syphilis infecting the brain and disrupting its function. A few decades later we discovered a highly effective treatment: penicillin. Although general paresis is now very rare, its example is still instructive. Any honest researcher will tell you we don’t currently have good explanations for most mental disorders. Depression, obsessive-compulsive disorder, schizophrenia—we don’t really know how these patterns of disrupted thought, behavior and emotion develop or why they stick around. Yet the hope remains that, much like with general paresis, we may soon discover the root causes of these illnesses, and this knowledge may tell us how to treat them. An example of this hope can be seen in the popular notion that a “chemical imbalance” causes depression. This might turn out to be true, but the truth is we don’t know. Some researchers are starting to think that for many mental disorders, such hope might be based on incorrect assumptions. Instead of having one root cause, as general paresis did, mental disorders might be caused by many mechanisms acting together. These mechanisms might be situated in the brain, but they could also be located in the body and even in the external environment, interacting with one another in a network to create the patterns of distress and dysfunction we currently recognize and label as varieties of mental illness. In this more complex view, patterns such as depression and generalized anxiety arise as tendencies in the human brain-body-environment system. Once the patterns are established, they are hard to change because the network continues to maintain them. © 2019 Scientific American

Keyword: Schizophrenia; Depression
Link ID: 26815 - Posted: 11.12.2019

Maheen Mausoof Adamson, Ph.D. The 1982 science fiction film classic Blade Runner is a gritty detective story set in the dystopian future that raises questions about what it means to be human. In the film, Harrison Ford plays Rick Deckard, a police officer turned bounty hunter searching the streets of Los Angeles for a replicant (human-like androids) rebellion leader Roy Batty. Batty is presented as a technologically perfected being fitted with a human-template brain completely rewired to create an enemy to be deathly feared. Fear of the perfect altered brain is prominent in science fiction—and may be particularly prevalent today, amid growing concerns about genetic editing and artificial intelligence. The prospect of a fully artificial human brain remains very distant. However, we are in the midst of a neuromodulation revolution that will increase our ability to treat disease and optimize human performance. We must, however, carefully consider the benefits and risks of these techniques in fully evaluating their potential for society as well as the individual. A large number of patients suffering from neurological or psychiatric disorders—depression, pain, and post-traumatic stress disorder among them—are resistant to or can develop resistance to standard medication and psychotherapy, suggesting the need for new approaches. Neuromodulation may possibly be such an approach. The term (aka neurostimulation) refers to direct stimulation and modification of the nervous system through the use of electrical, chemical, or mechanical signals. Neuromodulation therapy is already used to treat many brain disorders, most commonly movement disorders, chronic pain, and depression. © 2019 The Dana Foundation.

Keyword: Parkinsons; Depression
Link ID: 26797 - Posted: 11.07.2019

By Emily Eakin Ten years ago, Susannah Cahalan was hospitalized with mysterious and terrifying symptoms. She believed an army of bedbugs had invaded her apartment. She believed her father had tried to abduct her and kill his wife, her stepmother. She believed she could age people using just her mind. She couldn’t eat or sleep. She spoke in gibberish and slipped into a catatonic state. Had it not been for an ingenious doctor brought in to consult on her case, Cahalan might well have ended up in a psychiatric ward. Instead, as she recounted in “Brain on Fire,” her best-selling 2012 memoir about her ordeal, she was eventually found to have a rare — or at least newly discovered — neurological disease: anti-NMDA-receptor autoimmune encephalitis. In plain English, Cahalan’s body was attacking her brain. She was only the 217th person in the world to be diagnosed with the disorder and among the first to receive the concoction of steroids, immunoglobulin infusions and plasmapheresis she credits for her recovery. Cahalan’s condition is what in medicine is called a “great pretender”: a disorder that mimics the symptoms of various disorders, confounding doctors and leading them astray. “The Great Pretender” also happens to be the title of Cahalan’s new book, which comes out on Tuesday. It, too, is a medical detective story, only this time at the heart of the mystery is not a patient or a disease but a member of the profession: David Rosenhan, a Stanford psychologist and the author of “On Being Sane in Insane Places,” a landmark 1973 study that, by questioning psychiatrists’ ability to diagnose mental illness, plunged the field into a crisis from which it has still not fully recovered. Cahalan, 34, learned about Rosenhan six years ago, while on tour for the paperback edition of “Brain on Fire.” She was inundated with letters, hundreds a week, from desperate patients and their families, convinced that they too might have a neurological condition masquerading as mental illness. She was haunted by the idea that sheer luck had allowed her to escape a similar fate. © 2019 The New York Times Company

Keyword: Schizophrenia
Link ID: 26784 - Posted: 11.02.2019

Ricardo F. Muñoz I have been convinced of the importance of prevention in addressing mental-health problems since the early 1970s, when I began my doctorate in clinical psychology. But only now is there sufficient evidence from clinical trials of the effectiveness of preventive interventions, using approaches derived from interpersonal and cognitive behavioural therapy, to justify deploying them. And only now are the tools available to make such interventions available to people worldwide. Two recent reports underline this conclusion. In February, the US Preventive Services Task Force, an independent panel of experts in evidence-based medicine, urged clinicians to “provide or refer pregnant and postpartum persons who are at increased risk of perinatal depression to counseling interventions”1. And last month, the US National Academies of Sciences, Engineering, and Medicine (NASEM) released a report2 calling on various stakeholders, from educators to policymakers, to prevent mental-health disorders and to promote healthy mental, emotional and behavioural development in the under 25s. (I was a member of the committees that prepared this document and two previous NASEM reports in 1994 and 2009 on preventive interventions3,4.) The latest NASEM call to action2 is so all-encompassing, it is hard to know where to begin. I propose that initial efforts focus on preventing depression in pregnant women or in women who have recently given birth (perinatal depression). There is substantial evidence for the effectiveness of providing such women with basic skills in mood management5. These interventions could have an impact across generations, because better maternal mental health is linked to babies’ healthier development2. And if researchers and health-care systems were to monitor and compare the epidemiology of depression in thousands of mothers and their children in areas that have or have not deployed preventive interventions, stakeholders could measure their effect on entire communities. © 2019 Springer Nature Limited

Keyword: Depression
Link ID: 26778 - Posted: 11.01.2019

Terry Gross Ever since childhood, author Kevin Wilson has lived with disturbing images that flash through his mind without warning. "I've always had this kind of agitation and looping thoughts and small tics," he says. "Falling off of tall buildings, getting stabbed, catching on fire — they were these just quick, kind of violent bursts in my head." Not that Wilson would ever harm anyone else — the harm in these quick, intrusive thoughts was strictly internal. The images fed off of his own anxiety, and left him feeling terrified. It wasn't until Wilson was diagnosed with Tourette's syndrome as an adult that he began to understand what he was seeing. At first, he was skeptical of the diagnosis; Tourette's is a neurological disorder often characterized by involuntary vocal or motor tics, and Wilson's version wasn't what he'd seen portrayed on TV or in books. "Mine is so much more internal," he says. "Those images and looping tics are in my head. And so a lot of the work that I'm doing is just keeping it in there." One way that Wilson helps control the images is to include them through his writing. His new novel, Nothing to See Here, is about a woman who takes over the care of twin children who burst into flames when they're afraid or angry. "Writing is, I think, the thing that saved me — being able to transfer what was in my head onto the page," he says. "There's this freedom that once it ... goes out into the world and you publish it, you're kind of free of it for a little while — at least it's somebody else's problem." © 2019 npr

Keyword: Tourettes
Link ID: 26774 - Posted: 10.31.2019

By Nicholas Bakalar A healthy diet may help relieve the symptoms of depression. There is good evidence from observational studies that diet can affect mood, and now a randomized controlled trial suggests that healthy eating can modestly improve clinical levels of depression. The study, in PLOS One, randomized 76 college students with poor diet and depression symptoms to two groups. One group was put on a Mediterranean-style diet high in fruits, vegetables, fish, olive oil, nuts and seeds, and low in refined carbohydrates, sugar and saturated fat. The other continued their usual eating habits. At the beginning and end of the three-week trial, all participants were assessed with well-validated scales measuring depression, anxiety, current mood, memory and self-efficacy (confidence in one’s ability to exert control over behavior). Symptoms of depression improved, on average, in the diet group, shifting from the moderate severity range to the normal range. Depressive symptoms among the controls, meanwhile, remained stable, staying within the moderate severity range. On tests of anxiety and stress, the diet group had significantly lower scores than the controls, after controlling for levels of anxiety and stress at the start of the study. There were no differences between the two groups in memory or self-efficacy scores. The study controlled for smoking, physical activity, B.M.I. and other factors. © 2019 The New York Times Company

Keyword: Depression; Obesity
Link ID: 26772 - Posted: 10.31.2019

Sarah Boseley Health editor The use of cannabis medicines to treat people with depression, anxiety, psychosis or other mental health issues cannot be justified because there is little evidence that they work or are safe, according to a major new study. A review of evidence from trials conducted over nearly 40 years, published in the journal Lancet Psychiatry, concludes that the risks outweigh the benefits. And yet, say the authors, they are being given to people with mental health problems in Australia, the US and Canada, and demand is likely to grow. Prof Louisa Degenhardt of the National Drug and Alcohol Research Centre at UNSW Sydney, Australia, lead author of the study, said the findings had important implications in countries where medical use was allowed. “There is a notable absence of high-quality evidence to properly assess the effectiveness and safety of medicinal cannabinoids compared with placebo, and until evidence from randomised controlled trials is available, clinical guidelines cannot be drawn up around their use in mental health disorders,” she said. “In countries where medicinal cannabinoids are already legal, doctors and patients must be aware of the limitations of existing evidence and the risks of cannabinoids. These must be weighed when considering use to treat symptoms of common mental health disorders. Those who decide to proceed should be carefully monitored for positive and negative mental health effects of using medicinal cannabinoids.” © 2019 Guardian News & Media Limited

Keyword: Drug Abuse; Schizophrenia
Link ID: 26769 - Posted: 10.30.2019

By Jocelyn Kaiser HOUSTON, TEXAS—Schizophrenia tends to run in families, which suggests it’s largely inherited. But a long-running search for genes underlying this severe psychiatric condition has yielded only indirect clues. Now, by scouring the DNA of tens of thousands of people, gene hunters have for the first time nabbed a handful of rare genes that, when mutated, appear to be direct contributors to the disease—and may shed light on what goes awry in a schizophrenia patient’s brain. “These are concrete genes with mutations with a clear molecular mechanism,” says Mark Daly of the Broad Institute in Cambridge, Massachusetts, and the University of Helsinki, who is principal investigator for a consortium that presented the work last week at the annual meeting of the American Society of Human Genetics (ASHG) here. “It was a fabulous talk,” says Jennifer Mulle of Emory University in Atlanta, who studies the genetics of psychiatric disorders. “We don’t understand anything about the biological pathways [in schizophrenia]. Now, these genes give us an avenue.” People with schizophrenia, which afflicts about 0.7% of the U.S. population, have a distorted sense of reality and confused thinking; they may have hallucinations and delusions. Some patients share similar genetic abnormalities, such as missing specific chunks of DNA, but how those gaps may contribute to disease isn’t known. © 2019 American Association for the Advancement of Science

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26756 - Posted: 10.26.2019

Researchers have discovered in mice how one of the few genes definitively linked to schizophrenia, called SETD1A, likely confers risk for the illness. Mice genetically engineered to lack a functioning version of the enzyme-coding gene showed abnormalities in working memory, mimicking those commonly seen in schizophrenia patients. Restoring the gene’s function corrected the working memory deficit. Counteracting the gene’s deficiencies also repaired neuronal circuit deficits in adult mice – suggesting clues for potential treatment strategies. A team of scientists led by Joseph Gogos, M.D., Ph.D., of Columbia University, New York City, reported on their research – supported by the National Institutes of Health – in Neuron. “You could call SETD1A a master regulator,” explained David Panchision Ph.D., of the NIH’s National Institute of Mental Health (NIMH), which co-funded the study. “This schizophrenia risk gene codes for an enzyme that influences the expression of many other genes. In mice, a hobbled version of SETD1A disrupted gene expression in a network harboring other genomic suspects in schizophrenia. Remarkably, the resulting abnormalities were reversible.” Researchers have identified both common and rare genetic variations that contribute to risk for schizophrenia. Mutant SETD1A is one of just a few rare genes known to unequivocally confer risk for schizophrenia. While common genetic variations linked to schizophrenia individually exert only tiny effects on risk, having just one mutant copy of SETD1A is sufficient to confer a large increase in disease risk. SETD1A plays a key role in epigenomic regulation – the switching on-and-off of genes in response to experience – a molecular process widespread in the brain. Mutations in SETD1A have primarily been found in people with schizophrenia, suggesting that this rare gene variation might hold important clues to the underlying disease process.

Keyword: Schizophrenia; Genes & Behavior
Link ID: 26750 - Posted: 10.25.2019

By Jonathan Lambert Prozac, a commonly prescribed medication for kids and teens with autism, is no more effective than a placebo at treating obsessive-compulsive behaviors, a small study finds. The results of the randomized clinical trial, published October 22 in JAMA, cast further doubt on the widespread practice of prescribing a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs, to treat children with autism who have these behaviors, says pediatric neurologist Ann Neumeyer. “We really don’t have any good medications that have yet been studied in children with autism for these behaviors,” says Neumeyer, the medical director of the Massachusetts General Hospital Lurie Center for Autism in Lexington, who wasn’t involved in the study. “That’s a problem.” Autism spectrum disorders encompass a diversity of symptoms, but common among them are obsessive-compulsive behaviors (SN: 10/16/18). Individuals with autism can become hyperfocused on specific ideas or objects and can engage in ritualistic “tics,” such as rocking or hand-waving. For many individuals, these symptoms interfere with everyday functioning. SSRI antidepressants account for a quarter to a third of all prescriptions to children and teens with autism, according to pediatrician Dinah Reddihough at the Murdoch Children’s Research Institute in Melbourne, Australia. “Despite their widespread use, there is no evidence of effectiveness of SSRIs for autism spectrum disorders in children,” she says. © Society for Science & the Public 2000–2019.

Keyword: Autism
Link ID: 26738 - Posted: 10.23.2019

By Marlene Cimons In 1991, Karestan Koenen was a recent college graduate and Peace Corps volunteer who arrived in a village in Niger eager to help local women start small businesses. When her sister came to visit during Christmas, the two decided to travel north to Agadez, a city in the Sahara. There, on the morning of Dec. 27, two male traders stopped by, trying to sell them jewelry. Koenen’s sister went to the market with one of men to have a look. While she was gone, the second man grabbed Koenen, held her down and raped her. Traumatized by the experience, Koenen was medically evacuated to the United States two days later and resigned from the Peace Corps. She returned to New Jersey to live with her parents, but the assault continued to haunt her. Increasingly, she became depressed. A psychologist diagnosed Koenen with post-traumatic stress disorder, or PTSD, a condition triggered by a traumatic, scary or dangerous event, and, for reasons still unclear, seems to disproportionately afflict women. These assaults can include combat, sexual assault, gun violence, accidents, natural disasters, even the death of a loved one. “I lay in bed, unable to sleep, thinking of ways to kill myself,” she recalls. “When I did sleep, I had nightmares. I lost interest in everything. I couldn’t read and was too jumpy to sit through a movie or watch TV. I was irritable with my family. I was always on guard — angry — and couldn’t stop thinking about what had happened. I felt like I was stuck in a dark tunnel, moving more and more quickly, but it only got darker.”

Keyword: Stress; Sexual Behavior
Link ID: 26726 - Posted: 10.21.2019

Dean Burnett It’s a damp, midweek afternoon. Even so, Cardiff’s walk-in stress management course has pulled in more than 50 people. There are teenagers, white-haired older people with walking aids, people from Caucasian, Asian and Middle Eastern backgrounds. There is at least one pair who look like a parent and child – I’m unsure who is there to support whom. The course instructor makes it clear that she is not going to ask people to speak out about their own stress levels in this first class: “We know speaking in public is stressful in itself.” She tells us a bit about previous attendees: a police officer whose inexplicable and constant worrying prevented him from functioning; a retired 71-year-old unable to shake the incomprehensible but constant fatigue and sadness that blighted his life; a single mother unable to attend her daughter’s school concert, despite the disappointment it would cause. What is the common theme that links these people – and the varied group sitting there this afternoon and listening? Stress may once just have been a kind of executive trophy – “I’m so stressed!” – but recent research suggests it is a key element in developing mental health problems such as depression and anxiety. The constant, stress-induced stimulation of key brain regions seems to be a major contributor to anxiety. And, in turn, vital brain regions becoming unresponsive and inflexible is believed to be a fundamental element of depressive disorders. Why do these regions become unresponsive? Possibly because they’re overworked, exhausted, by the effects of stress. This would explain why anxiety and depression regularly occur together. © 2019 Guardian News & Media Limited

Keyword: Depression; Stress
Link ID: 26701 - Posted: 10.15.2019

Allison Aubrey There's fresh evidence that eating a healthy diet, one that includes plenty of fruits and vegetables and limits highly processed foods, can help reduce symptoms of depression. A randomized controlled trial published in the journal PLOS ONE finds that symptoms of depression dropped significantly among a group of young adults after they followed a Mediterranean-style pattern of eating for three weeks. Participants saw their depression "score" fall from the "moderate" range down to the "normal" range, and they reported lower levels of anxiety and stress too. Alternatively, the depression scores among the control group of participants — who didn't change their diets — didn't budge. These participants continued to eat a diet higher in refined carbohydrates, processed foods and sugary foods and beverages. Their depression scores remained in the "moderate severity" range. "We were quite surprised by the findings," researcher Heather Francis, a lecturer in clinical neuropsychology at Macquarie University in Sydney, Australia, told NPR via email. "I think the next step is to demonstrate the physiological mechanism underlying how diet can improve depression symptoms," Francis said. In this study, participants in the "healthy eating" arm of the study ate about six more servings of fruits and vegetables per week, compared with the control group. Participants "who had a greater increase in fruit and vegetable intake showed the greatest improvement in depression symptoms," Francis said. © 2019 npr

Keyword: Depression; Obesity
Link ID: 26693 - Posted: 10.11.2019