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

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: 26784 - Posted: 11.02.2019

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

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 4: Development of the Brain
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.

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: 26750 - Posted: 10.25.2019

By Liz Eavey My brother Roland’s Facebook post set off a flurry of concern throughout his social network. He’d been assaulted, he wrote, by “old-world mentality Agent Smiths who are threatening our ability to bring natural plant-based Medicine and intelligent health care to the world.” In caps, he told his followers to ALERT THE PRESS AND BRING SIGNS OF PROTEST. The yogis sent positive vibes; the rebels cried fight the man; the good Samaritans offered to jump in their cars and rescue him. Except that Roland hadn’t exactly been assaulted. He’d been placed under an involuntary psychiatric hold and forcibly subdued in an emergency room at the same institution where he was training to become a psychiatrist. And, with that, four years ago, Facebook snitched our big family secret: Roland, the literary prodigy, the tenderhearted musician, the Ivy League grad, was bipolar. Roland — who read and approved this essay — is the effortlessly brilliant middle child who takes up a disproportionate amount of space in a room, with a booming voice and the charisma of a megachurch pastor. After college, he moved to Hollywood and landed, with zero experience or connections, a coveted job with an A-list director. Then, he decided to become a doctor, enrolling in a top-tier M.D./M.B.A. program. Everything about my brother is superlative, including his demons: crippling insomnia, legendary alcoholism and a chemical imbalance that has repeatedly imploded his life. I, the firstborn, am diplomatic and obedient, less concerned with standing out than blending in. Just 17 months apart, Roland and I constantly butted heads trying to assert our individuality growing up. In seventh grade, I wrote “An Older Sister’s Guide to Having Younger Brothers,” which began: “A smart idea, which would prevent use of this guide, would be to just not have younger brothers.” Yet, when we weren’t vying for sibling dominance, we were always looking out for each other. © 2019 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: 26652 - Posted: 09.27.2019

Researchers have discovered that gene expression regulators work together to raise an individual’s risk of developing schizophrenia. Schizophrenia-like gene expression changes modeled in human neurons matched changes found in patients’ brains. The researchers, led by Kristen Brennand, of the Icahn School of Medicine at Mount Sinai, New York City, report on their findings in Nature Genetics. The work was funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Genome-wide association studies have revealed at least 143 chromosomal sites associated with risk for schizophrenia. However, individually, each of these sites can explain only a small fraction of the risk. Even when the effects of disease-linked rare genetic variants are factored in, most of schizophrenia’s known high inheritance remains unexplained. One possible clue: more than 40% of the suspect chromosomal sites contain regulators, called expression quantitative trait loci, or eQTLs, that govern the expression of multiple genes. “Individually, these gene regulators have a modest effect on the brain. Working in concert, they exert different and more significant effects on the brain — effects that boost schizophrenia risk,” explained David Panchision, chief of the Developmental Neurobiology Program at NIMH. “Learning more about the downstream cellular and molecular effects of such synergy holds hope for advances in precision psychiatry and more personalized medicine.” To explore the role of these regulators, Brennand and colleagues studied them in induced neurons using a molecular modeling technology. This induced pluripotent stem cell method makes it possible to grow a person’s unique neurons in a petri dish using stem cells derived from their skin cells.

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 4: Development of the Brain
Link ID: 26643 - Posted: 09.24.2019

By Jane E. Brody Tiffany Martinez was a 17-year-old college freshman when she began hearing voices, seeing shadowy figures and experiencing troubling, intrusive thoughts. Her friends at the University of Southern Maine, where she was majoring in psychology, noticed that she was acting strangely and urged her to get help. They most likely saved her from a crippling mental health crisis, prevented the derailment of her education and ultimately enabled her to become a psychiatric nurse practitioner who can help other young people avert a psychiatric crisis. Tiffany’s friends convinced her to go to the university’s health center, where she met with a nurse who had just attended an educational seminar about identifying the early signs of mental illness in young adults. The nurse suspected that Tiffany was at risk of developing a psychotic episode and referred her to the Portland Identification and Early Referral, or PIER, program at the Maine Health Center. The program was developed in 2001 by Dr. William R. McFarlane, a psychiatrist who suspected that if early intervention could reverse the course of diseases like cancer and heart disease, it should do likewise for psychosis. Despite conventional wisdom suggesting otherwise, he persevered in the belief that an impending psychotic break could be identified and prevented if it was recognized early and appropriate steps taken to head it off. Tiffany, who said her father had schizophrenia, was an early beneficiary of his vision and has become a poster child for what can be done to prevent a devastating, costly illness that afflicts up to 3 percent of the population. After the PIER program was extended to 25 school districts in and around Portland, there was a 35 percent decline in new hospital admissions for psychotic symptoms, Dr. McFarlane said. © 2019 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: 26562 - Posted: 09.02.2019

Douwe Draaisma Some 70 years ago, John Cade, an Australian psychiatrist, discovered a medication for bipolar disorder that helped many patients to regain stability swiftly. Lithium is now the standard treatment for the condition, and one of the most consistently effective medicines in psychiatry. But its rise was riddled with obstacles. The intertwined story of Cade and his momentous finding is told in Lithium, a compelling book by US psychiatrist Walter Brown. Bipolar disorder, labelled manic-depressive illness until 1980, affects around 1 in 100 people globally. Without treatment, it can become a relentless cycle of emotional highs and lows. Suicide rates for untreated people are 10–20 times those in the general population. Fortunately, lithium carbonate — derived from the light, silvery metal lithium — can reduce that figure tenfold. Brown’s telling of Cade’s eventful life covers much of the same ground as Finding Sanity (2016), a rather hagiographic biography by Greg de Moore and Ann Westmore. What Brown does superbly well is to show that Cade made his discovery without access to advances in technology or to modern facilities — and almost despite them. His finding was the happy result of being forced to work with the simplest of means. During the Second World War, Cade was interred for more than three years in the notorious Japanese prisoner-of-war camp at Changi in Singapore. He was put in charge of the psychiatric section, where he began to note the decisive link between certain food deficiencies and diseases in his fellow prisoners. A lack of B vitamins, for instance, caused beriberi and pellagra.

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: 26544 - Posted: 08.27.2019

Natalie Parletta Poor air quality has been associated with higher rates of bipolar disorder and major depression in observational research involving more than 150 million people in the US and Denmark. The link was found to be more pronounced in Denmark, with research also suggesting that pollution exposure during childhood more than doubled the risk of schizophrenia and personality disorders. Genetic studies now reveal that genes only explain a small fraction of psychiatric illness onset. Therefore, researchers are exploring environmental factors in the search to comprehend the global increase in these complex disorders of brain function. “We were hoping to understand what aspects of human environments are driving psychiatric and neurological disease prevalence,” says senior author Andrey Rzhetsky from the University of Chicago, US. The findings are published in the journal PLOS ONE. The search thus far has focussed largely on family environments and childhood trauma, including prenatal influences. Other possible avenues include social circumstances, stressful life events, substance abuse, and emerging evidence for poor diet. Far less attention has been given to physical environments. Yet as the numerous adverse health impacts of air pollution have come to light, inspection of its potential role in neurological disorders has lagged.

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: 26525 - Posted: 08.21.2019

Etelka Lehoczky Like any good story about a scientific discovery, Walter A. Brown's account of the history of lithium features plenty of improvisation, conjecture and straight-up kismet. Unlike many such stories, though, it also features a fair share of personal bias, senseless puttering and random speculation — on part of these scientific researchers. Brown, a practicing psychiatrist and university professor of more than 40 years, seems to have been drawn to write Lithium: A Doctor, A Drug and a Breakthrough as much because of lithium's fluky history and overlooked importance (for many years, he argues, it was "the Cinderella of psychiatric drugs") as by the profound impact it's had on countless sufferers of bipolar disorder and depression. Lithium is a homage, not just to a drug, but to the renegade side of science. Its heroes are researchers scattered around the globe, short on funding and frequently unaware of each other's work, without whom a commonly available substance would never have been recognized as a treatment for one of the most baffling psychiatric illnesses. By celebrating these men, Brown hopes to do a lot more than simply raise awareness about an underappreciated substance. He aims to demolish what remains of the myth that scientific progress is driven by rigorous dispassion. The story of lithium's use in medicine is certainly colorful, as is the history of the illness it's become known for. Brown doesn't stint on either tale. He goes all the way back to the first century to find a would-be description of manic depression by the Greek doctor Aretaeus of Cappadocia. These patients, Aretaeus wrote, "'laugh, play, dance night and day, and sometimes go openly to the market crowned, as if victors in some contest of skill,'" only to become "'torpid, dull and sorrowful.'" © 2019 npr

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: 26502 - Posted: 08.15.2019

By Simon Makin Can an Illusory World Help Treat Psychosis's Real-World Delusions? Scenes of everyday living within a virtual-reality simulation attempt to lessen social anxiety for people with psychosis. Credit: University of Oxford/Oxford VR Many people with psychosis suffer from persecutory delusions—beliefs that terrible things will happen to them in everyday situations, such as people trying to harm them. The disorder causes social anxiety, which can be exacerbated by other symptoms, such as hearing voices. All of this makes ordinary activities such as shopping or going to the doctor challenging. Often a person just withdraws entirely from social contact. In a vicious cycle, the ensuing isolation and rumination can exacerbate other symptoms, including those causing the withdrawal. The idea behind a virtual-reality system called gameChange is to help patients learn to feel safer, allaying social anxiety by putting them in simulations of situations they fear in which their worst dread does not materialize. Last month, clinical psychologist Daniel Freeman of the University of Oxford and his colleagues launched a clinical trial of gameChange, the biggest such trial to date of a VR treatment for schizophrenia. It will enroll 432 people with psychosis from five National Health Service (NHS) centers across the U.K. Researchers will assess participants’ avoidance and distress in real-world situations, using an established measure, before and after treatment and then do so again six months later. The hope is that the treatment will reduce participants’ anxiety, which will, in turn, improve other symptoms, particularly persecutory delusions. Freeman co-founded an Oxford spin-off company, Oxford VR, to develop and commercialize the technology. And if the trial is successful, gameChange could be rolled out by the NHS. © 2019 Scientific American

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: 26478 - Posted: 08.02.2019

By Emily Anthes In 2002, Marin Sardy and her younger brother Tom traveled to a small Costa Rican town for what they hoped would be a low-key beach vacation. The siblings, both in their 20s, planned to spend a few weeks relaxing, learning to surf, and just generally enjoying each other’s company. Sardy reveals what it means to love someone who is mentally ill and how hard it is to truly understand another person’s mind. And then, one day, Tom began to complain about his face. His bones, he said, had detached from each other, and his jaw had separated from his head. He couldn’t get his face back into alignment, he told Sardy. He began to talk — excitedly and cryptically — about “building matrices” and his plans to swim from Alaska to Japan. His facial expressions turned blank. Sardy observed these developments with growing alarm. She and Tom had grown up with a mother whose life had been derailed by schizophrenia, and she was well acquainted with its signs and symptoms. “Memories unfurl inside as I watch Tom,” Sardy writes in her intimate, multigenerational memoir, “The Edge of Every Day: Sketches of Schizophrenia.” “It is as if I already know that doctors and medications and hospitals and our efforts will all fail him.” “The Edge of Every Day” is Sardy’s attempt to come to terms with a fundamentally mysterious disease and how its effects ripple throughout her family. It’s a deeply compassionate book about what it means to love someone who is mentally ill — about how hard it is to truly understand another person’s mind and the importance of continuing to try. Copyright 2019 Undark

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: 26415 - Posted: 07.13.2019

By Bassey Ikpi This bipolar II. This many-sided creature. This life of mine. This brain constantly in conference with the racing heart, reminding me to slow down, stay calm. Remember the first time you were ever on a Ferris wheel? Remember when you got to the very top and just sat there, the entire world at your feet? You felt like you could reach up and grab the sky. Your entire body tingled with the intersection of joy and indestructibility and fearlessness and that good anxious recklessness. So damn excited to be alive at that moment. You could do anything. Now imagine feeling that every day for a week, or a month, or a few months. Twenty-four hours a day, seven days a week, without a break. So that everything you do feels like THE BIGGEST MOST AMAZING THING YOU HAVE EVER DONE IN YOUR LIFE! The first week or so, it’s great. Until it’s not. Because then the insomnia sets in. And you’re stacking days on top of one another, adding a new one before the last one ends. And you have to write the entire book tonight before you can sleep or eat or leave the house or do anything. But first you have to call your friends and your sister and the guy you just met and tell them all how much you love them. Tell each one that you’ve never felt this way about any other human being in the entire world and you’re so lucky and so glad and so grateful to have such an amazing, magical person in your life. And you believe it because it’s true. Until it isn’t. Until everything about them — the way their voices trail, the way their mouths move when they chew, the fact that he crosses his legs at the knee, the way she speaks about movies she’s never seen, the way they refer to celebrities by their first names — starts to make you feel like your blood is filled with snakes and you want to scream awful things at them about how the sounds of their voices feel like teeth on your skin and how much you hate their mother or their apartment or yourself. You want to bury your hatred in them, but you’re never quite sure who you hate the most. You, it’s always you. © 2019 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: 26395 - Posted: 07.08.2019

By Benedict Carey Last winter, several dozen people who were struggling with suicidal urges and bouts of intense emotion opened their lives to a company called Mindstrong, in what has become a closely watched experiment in Silicon Valley. Mindstrong, a venture co-founded by a former director of the National Institute of Mental Health, promised something that no drug or talk therapy can provide: an early-warning system that would flag the user when an emotional crisis seemed imminent — a personal, digital “fire alarm.” For the past year, California state and county mental health officials, along with patient representatives, have met regularly with Mindstrong and another company, 7 Cups, to test smartphone apps for people receiving care through the state’s public mental health system. Officials from 13 counties and two cities are involved, and the apps are already available to the public. The new users, most of whom have a diagnosis of borderline personality disorder, receive treatment through the Los Angeles County mental health network, and were among the first test subjects in this collaboration. They allowed Mindstrong to digitally install an alternate keyboard on their smartphones, embedded in the app, and to monitor their moment-to-moment screen activity. “People with borderline personality disorder have a very difficult time identifying when distress is very high,” said Lynn McFarr, director of the cognitive and dialectical behavior therapy clinic at Harbor U.C.L.A. Medical Center, which provides care for people in the Los Angeles County system. “If we can show them, in this biofeedback fashion, that the signals went off the rails yesterday, say, after they got into a fight with a co-worker, then they’d be able to anticipate that emotion and target it with the skills they’ve learned.” The potential for digital technology to transform mental health care is enormous, and some 10,000 apps now crowd the market, each promising to soothe one psychological symptom or another. Smartphones allow near continuous monitoring of people with diagnoses such as depression, anxiety and schizophrenia, disorders for which few new treatments are available. But there has been little research to demonstrate whether such digital supports are effective. © 2019 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: 26336 - Posted: 06.18.2019

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

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: 26305 - Posted: 06.06.2019

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

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: 26145 - Posted: 04.16.2019

By Nicholas Bakalar Urban air pollution is associated with an increased risk for psychotic experiences in teenagers, researchers report. A study published in JAMA Psychiatry included 2,063 British teenagers whose health had been followed from birth through age 18. Almost a third of them said they had at least one psychotic experience, ranging from a mild feeling of paranoia to a severe psychotic symptom, since age 12. Researchers linked air pollution data to locations where they spent most of their time — at home, school or work. Compared with teenagers who lived where pollution was lowest, those in the most polluted areas were 27 percent to 72 percent more likely to have psychotic experiences, depending on the type of pollutant; exposure to two pollutants, nitrogen dioxide and nitrogen oxides, accounted for 60 percent of the association. The study controlled for family psychiatric history, maternal psychosis, substance use, socioeconomic status, neighborhood social characteristics and other factors, but it is an observational study that does not prove causation. “From this one study, we can’t say that air pollution causes psychosis,” said the lead author, Helen L. Fisher, a research psychologist at King’s College London. “The study only says that these things commonly occur together.” © 2019 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 4: Development of the Brain
Link ID: 26085 - Posted: 03.28.2019

Text by David Gonzalez When the medical journal The Lancet asked Matthieu Zellweger to photograph any psychiatric condition that intrigued him, he thought of a close friend who has been living with bipolar disorder. He knew how his friend lamented that it was an “invisible handicap” that you couldn’t just snap out of, as some well-meaning but frustrated people would suggest. But Mr. Zellweger also recognized something in his friend that led him to propose a photo essay on bipolar disorder. “I’ve been around him quite a bit,” Mr. Zellweger said. “And the one thing that definitely surprised me is that — let’s face it — very intelligent people are overrepresented among bipolar people. A lot of them are very lucid about their disease. They have thought about how it impacts their lives. It was very stimulating to talk with them.” Mr. Zellweger spent 18 months in Switzerland, where he lives, and in Britain, photographing people with bipolar disorder, as well as their relatives or lovers who accompanied them, as they struggle with manic highs and depressive lows. He sought out subjects through patient advocacy groups and treatment centers who were open to sharing their experiences. “There are so many misconceptions about the disorder that a lot of the patients were happy to dispel that,” he said. “There is such a general stigma around mental disorders. One of the patients told me that when she told her friend about being bipolar, her friend said, ‘Oh, are you going to run after me with an ax?’ People think bipolar patients are uncontrollable or dangerous. But the only aggressive behavior I saw was people being aggressive against themselves.” © 2019 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: 26030 - Posted: 03.13.2019

By Emily Underwood Alert! “Cats Can Literally Make You Crazy.” Wait! “Cats Don't Cause Mental Illness.” The news headlines are as alarming as they are contradictory. All refer to Toxoplasma gondii, a brain parasite carried by our feline companions that infects roughly one in three people. Scientists have long hypothesized that T. gondii plays a role in mental illness, including schizophrenia. But though more than 100 studies have found a correlation, none has shown that the parasite actually causes mental illness. So what’s really going on? Here’s what you need to know: T. gondii is not a bacterium or a virus, but a single-celled microscopic organism distantly related to the parasite that causes malaria. Cats get T. gondii and the disease it causes, toxoplasmosis, by eating infected rodents, birds, and other animals. Estimates suggest about 40% of cats in the United States are infected; most don’t show any symptoms, but they can develop jaundice or blindness and experience personality changes if the parasite spreads to the liver or nervous system. In the first few weeks after infection, a cat can shed millions of hardy egg pods called oocysts into its litterbox each day. Although some people get toxoplasmosis from direct contact with domestic cats and cat feces, many more are infected when oocysts shed by cats make it into the soil and water, where they can survive for a year or longer. © 2019 American Association for the Advancement of Science.

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: 25968 - Posted: 02.15.2019

by Esmé Weijun Wang "Schizophrenia terrifies." Those are the first two words of The Collected Schizophrenias, Esmé Weijun Wang's new book — part memoir, part scientific chronicle of her journey towards a diagnosis of schizoaffective disorder. She first noticed that her brain worked differently than others, she says, when she was just five or six years old. And then, she says, "severe depression started when I was about 11, depression that was diagnosed by a doctor probably happened when I was 15 or 16. Bipolar disorder was diagnosed when I was about 17 or 18, and then the schizoaffective disorder, bipolar type, was diagnosed when I was in my late 20s." Interview Highlights On her experience of schizoaffective disorder I like to kind of jokingly say that it's like a marriage between schizophrenia and bipolar disorder. So my first hallucination that I ever had was actually when I was in the shower in college, and I heard a voice very clearly say to me, "I hate you." And it was so clear to me, and this is why I say that hallucinations really effectively kidnap the senses, because it's exactly like someone is standing next to you and saying this thing to you. And I started thinking, oh, is there something going on with the pipes, where I can hear maybe something on the floor below me, or maybe the floor above me, but it didn't really make sense to me physically, so I started thinking, maybe this is a hallucination, and it kind of went off from there ... and then later I started having delusions in which I was believing that my loved ones were replaced by doubles, or replaced by robots — so it's been an interesting journey. © 2019 npr

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: 25929 - Posted: 02.04.2019

Alison Abbott Neuroscientists have for the first time discovered differences between the ‘software’ of humans and monkey brains, using a technique that tracks single neurons. They found that human brains trade off ‘robustness’ — a measure of how synchronized neuron signals are — for greater efficiency in information processing. The researchers hypothesize that the results might help to explain humans’ unique intelligence, as well as their susceptibility to psychiatric disorders. The findings were published in Cell1 on 17 January. Scientists say that this type of unusual study could help them to better translate research in animal models of psychiatric diseases into the clinic. The research exploited a rare set of data on the activity of single neurons collected deep in the brains of people with epilepsy who were undergoing neurosurgery to identify the origin of their condition. The technique is so difficult that only a handful of clinics around the world can participate in this type of research. The study also used similar, existing data from three monkeys and collected neuron information from two more. Over the decades, neuroscientists have discovered many subtle and significant differences in the anatomy — the hardware — of the brains of humans and other primates. But the latest study looked instead at differences in brain signals. © 2019 Springer Nature Publishing AG

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 4: Development of the Brain
Link ID: 25889 - Posted: 01.21.2019