Links for Keyword: Schizophrenia

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By Sharon Begley, STAT Lab mice whose brains were injected with cells from schizophrenia patients became afraid of strangers, slept fitfully, felt intense anxiety, struggled to remember new things, and showed other signs of the mental disorder, scientists reported on Thursday. The latest advance in “chimeras,” animals created by transplanting cells from one species into another, demonstrated the value of the technique, scientists not involved in the study said, but is likely to draw renewed attention to a controversial field that opponents see as deeply immoral and undermining the natural order. Under a 2015 moratorium, the National Institutes of Health does not fund research that transplants human stem cells into early embryos of other animals. When the NIH asked for public comment on lifting the moratorium, it received nearly 20,000 responses, almost all objecting to “grossly unethical research”; many mentioned Frankenstein. But the new study, in Cell Stem Cell, injected human cells into newborn mice, not embryos. It received funding from the NIH as well as private foundations, to unravel how brain development goes off the rails to cause schizophrenia. Although the prevailing idea has been that the devastating disease, which strikes some 1 percent of U.S. adults, is primarily caused by something going wrong with neurons, the scientists suspected the brain’s support cells, called glia. © 2017 Scientific American,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 23863 - Posted: 07.22.2017

By Aaron Reuben, Jonathan Schaefer Most of us know at least one person who has struggled with a bout of debilitating mental illness. Despite their familiarity, however, these kinds of episodes are typically considered unusual, and even shameful. New research, from our lab and from others around the world, however, suggests mental illnesses are so common that almost everyone will develop at least one diagnosable mental disorder at some point in their lives. Most of these people will never receive treatment, and their relationships, job performance and life satisfaction will likely suffer. Meanwhile the few individuals who never seem to develop a disorder may offer psychology a new avenue of study, allowing researchers to ask what it takes to be abnormally, enduringly, mentally well. Epidemiologists have long known that, at any given point in time, roughly 20 to 25 percent of the population suffers from a mental illness, which means they experience psychological distress severe enough to impair functioning at work, school or in their relationships. Extensive national surveys, conducted from the mid-1990s through the early 2000s, suggested that a much higher percentage, close to half the population, would experience a mental illness at some point in their lives. These surveys were large, involving thousands of participants representative of the U.S. in age, sex, social class and ethnicity. They were also, however, retrospective, which means they relied on survey respondents’ accurate recollection of feelings and behaviors months, years and even decades in the past. Human memory is fallible, and modern science has demonstrated that people are notoriously inconsistent reporters about their own mental health history, leaving the final accuracy of these studies up for debate. Of further concern, up to a third of the people contacted by the national surveys failed to enroll in the studies. Follow-up tests suggested that these “nonresponders” tended to have worse mental health. © 2017 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23837 - Posted: 07.14.2017

By Sharon Begley, STAT Living in a city makes people develop schizophrenia. Tell me more: The claim is not quite that stark, but it’s close. For a study published last week, researchers interviewed 2,063 British twins (some identical, some not) at age 18 about “psychotic experiences” they’d had since age 12—such as feeling paranoid, hearing voices, worrying their food might be poisoned, and having “unusual or frightening” thoughts. Among those who lived in the most densely populated large cities, 34 percent reported such experiences; 24 percent of adolescents in rural areas did. The twins are part of a long-running study that has followed them from birth in 1994-95, so the researchers— led by Helen Fisher of King’s College London and Candice Odgers of Duke University—also knew the teens’ family income, parents’ education, where they lived, and more. Conclusion: 18-year-olds raised in big cities were 67 percent more likely to have had psychotic experiences, the researchers reported in Schizophrenia Bulletin. They then used standard statistics tools to account for possible psychosis-related factors other than cities per se. Cities have more people who are poor and uneducated, which are risk factors for schizophrenia and other forms of psychosis, so they controlled for socioeconomic status. Family psychiatric history raises the risk of an individual’s developing psychosis, and since there is some evidence that people with mental illness move to cities, which have more treatment facilities, the researchers controlled for this, too. They also controlled for drug use, some forms of which are more common in urban than rural areas. These calculations brought the extra risk of psychosis among urban teens down to 43 percent. © 2017 Scientific American,

Related chapters from BP7e: 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: 23683 - Posted: 05.31.2017

Nicola Davis People from ethnic minorities have up to a five times greater risk of psychotic disorders than the white British population, researchers say. A new study reveals that the trend holds in both urban and rural settings, with first-generation migrants who arrive in the UK in childhood among those at increased risk. The team behind the study say a number of factors could be at play, including stresses related to the migration process, discrimination and issues related to isolation and integration. James Kirkbride, a psychiatric epidemiologist from University College London and co-author of the research, described the figures as shocking. It’s time to tackle mental health inequality among black people “If this was any other disorder we would be horrified and up in arms and we would be campaigning from a public health perspective on how we could reduce this level of suffering,” he said. “There is a massive health inequality and it hasn’t got much attention.” While psychosis is rare – rates in England stand at about 30 cases per 100,000 people per year – Kirkbride says more should be done to offer services to those in need and to unpick drivers behind raised risks. “In the present climate when issues about migration are at the forefront of the public’s mind, people from ethnic minority backgrounds may face additional stresses that could potentially contribute to mental health problems,” he added. Writing in the journal Schizophrenia Bulletin, Kirkbride and colleagues from the University of Cambridge and a collection of NHS foundation trusts describe how they looked at trends among 687 people in the east of England.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23678 - Posted: 05.30.2017

By Daniel Barron Earlier this month, JAMA Psychiatry published a land-breaking editorial. A group of psychiatrists led by David Ross described how and why post-traumatic stress disorder (PTSD) should be clinically evaluated from a neuroscience framework. The fact that this editorial was published in one of psychiatry’s leading journals is no small feat. Psychiatry houses a large and powerful contingency that argues neuroscience has little clinical relevance. The relevance of neuroscience to psychiatry was the subject of a recent Op-Ed debate in the New York Times: “There’s Such a Thing as Too Much Neuroscience” was rebutted with “More Neuroscience, Not Less.” This specific debate—and the dense politics as a whole—exists because competing frameworks are vying for competing funding, a conflict that pre-dates Freud’s departure from neurology. That the relevance of neuroscience to psychiatry is still questioned is blatantly outlandish: what organ do psychiatrists treat if not the brain? And what framework could possibly be more relevant than neuroscience to understanding brain dysfunction? In his editorial, Ross tactfully presented his case for neuroscience, describing the obvious choice for a clinical framework as one “perspective,” making a delicate intellectual curtsey while supporting his case with data. Ross discussed five “key neuroscience themes” (read: lines of evidence from burgeoning sub-fields) relevant to understanding and treating PTSD: fear conditioning, dysregulated circuits, memory reconsolidation, and epigenetic and genetic considerations. Each theme accounts for the diverse biological, psychological and social factors involved in PTSD—which is to say, these factors all have some affect on the brain mechanisms. Most importantly, Ross describes how a mechanistic approach allows clinicians to trace the specific causes of PTSD to specific treatments that can target those causes. © 2017 Scientific American,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 23536 - Posted: 04.26.2017

By TANYA FRANK It begins in the laundry room in the early hours of the morning. I find him alone, tracing the wires of the telephone circuit board. “This is how they are monitoring us,” my son whispers. “We have to cut some stuff out, change the receiver, I can do it.” “Who?” I ask. “Who is monitoring us? And why?” He puts a finger to his lips to quiet me, and begins rifling through the tool kit. He doesn’t seem quite sure what he is looking for. He has never rerouted wires in his life, and besides, it is 2009 and we have suspended our landline. These wires that my 19-year-old is obsessing over are part of a defunct apparatus from a bygone age. I shiver in this damp afterthought of a room, but not from the concrete floor under my bare feet. I’m a Londoner with a tolerance for winter. It’s nerves that have me shaking. I am scared of my own child. My partner is in San Francisco, and we are in Los Angeles. There is no national health system here. We are unmoored, just my boy and me above a twinkling metropolis of strangers. “We can’t trust anybody,” he writes. “Our computers and phones are bugged. Listen, hear that?” I shake my head, unable to detect anything. “It’s a helicopter spying on us.” When it sinks in that this is not a delirium that can be eased with Advil and a good night’s sleep, and when I stop denying that my son is armed, I take him to the closest psychiatric hospital, where he is involuntarily held for 72 hours, considered a danger to himself or others. His symptomology is examined and classified as if he is some rare and delicate butterfly, and he emerges with a label: schizoaffective disorder. It is a complex condition with traits of both schizophrenia (a thought disorder) and bipolar (a mood disorder). Basically, my son had a psychotic break. That’s what they call it when someone disintegrates from his psyche. © 2017 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23518 - Posted: 04.21.2017

By CLYDE HABERMAN In America’s most storied political family, Rosemary Kennedy was the first in her generation to die of natural causes. Before then, a brother had been killed in war, a sister in a plane crash and two other brothers in assassinations. Not much of Ms. Kennedy’s life qualified as natural, though. Intellectually challenged from birth, she became increasingly erratic after entering womanhood. Her tempestuous mood swings troubled the family patriarch so much that he approved controversial surgery, which he was led to believe would calm her. In 1941, at age 23, Ms. Kennedy underwent a prefrontal lobotomy. It went badly. For her remaining 63 years, she led an institutionalized existence, out of public view, unable to speak clearly or walk without a limp. Retro Report, a series of video documentaries exploring major news stories of the past, harks back to that botched lobotomy and the neurologist who effectively sealed the young woman’s fate, Dr. Walter J. Freeman. The purpose is to show how the past informs the present. Psychosurgery endures, as with a procedure called a cingulotomy, which is used to treat depression and obsessive-compulsive disorder and involves severing fibers deep in the frontal lobe. But attention these days is keenly focused on stimulating discrete areas of the brain with electrical charges in the hope of easing torments like Parkinson’s disease, O.C.D. and depression. “What Walter Freeman was doing was crude and barbaric and harmful in many cases,” said Jack El-Hai, who wrote a 2005 biography of him, “The Lobotomist: A Maverick Medical Genius and His Tragic Quest to Rid the World of Mental Illness.” Referring to cingulotomies, Mr. El-Hai told Retro Report, “But what does remain is the idea that the brain can be physically manipulated, surgically manipulated, to help treat psychiatric illnesses.” The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23505 - Posted: 04.18.2017

Emily Corwin Michael Treadwell sat at the back of a courtroom in New Hampshire. He wore a windbreaker and khaki pants and leaned over his work boots with his elbows on his knees. At first it looked like he was chewing gum — a bold choice in a courtroom. But when he spoke it was clear: He wasn't chewing gum, he was chewing his own gums. Michael doesn't have any teeth. Taxpayers in Hillsborough County, N.H., have spent $63,000 over the last six years keeping Treadwell in jail for little more than trespassing. Law Investigation Into Private Prisons Reveals Crowding, Under-Staffing And Inmate Deaths For years now, his life has looked like this: Trespass in an apartment building, spend 30 days in jail; bother restaurant customers, spend 42 days in jail; panhandle aggressively, spend 30 days in jail. "When you live in a town like Nashua, there's not a lot of homelessness there, and it kinda like focuses, puts you in the spotlight," Treadwell says. "Especially if you drink alcohol and stuff." His charges all come from some combination of being homeless and getting drunk. Still, he says, jail is no worse than the streets. "People kill homeless people, violence and everything else," Treadwell says. "It can be a very dangerous life to live in. I don't suggest jail as an alternative. Ain't no kinda life." © 2017 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23497 - Posted: 04.17.2017

As the father of two sons with schizophrenia, author Ron Powers is familiar with the pain and frustration of dealing with a chronic, incurable disease of the brain. Powers' younger son, Kevin, was a talented musician whose struggles with schizophrenia began at age 17. Just before his 21st birthday, in 2005, Kevin took his own life. A few years later, Powers' older son, Dean, started experiencing symptoms of schizophrenia and had a psychotic break. "There is no greater ... feeling of helplessness than to watch two beloved sons deteriorate before [your] eyes, not knowing what to do to bring them back," Powers tells Fresh Air's Terry Gross. Powers' new book, No One Cares About Crazy People, is both a memoir about his sons and a history of how the mentally ill have been treated medically, legally and socially. Although Dean is now medicated and doing well, Powers notes that many people with schizophrenia don't receive the treatment they need — in part because they often don't believe they are ill. "This unwillingness to believe that one is afflicted has led to tremendous problems," Powers says. "To force that person into being helped is a violation of his or her civil rights ... and the law may penalize the care workers who give [people with schizophrenia] medications or admit them to a hospital against their will. ... That is the great reigning Catch-22 of the way our society deals — or fails to deal — with schizophrenia." © 2017 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23383 - Posted: 03.21.2017

By Taylor Beck LSD, “magic” mushrooms and mescaline have been banned in the U.S. and many other countries since the 1970s, but psychedelic medicine is making a comeback as new therapies for depression, nicotine addiction and anxiety. The drugs have another scientific use, too: so-called psychotomimetics, or mimics of psychosis, may be useful tools for studying schizophrenia. By creating a brief bout of psychosis in a healthy brain, as indigenous healers have for millennia, scientists are seeking new ways to study—and perhaps treat—mental illness. “We think that schizophrenia is a group of psychoses, which may have different causes,” says Franz Vollenweider, a psychiatrist and neuroscientist at the University of Zurich. “The new approach is to try to understand specific symptoms: hearing voices, cognitive problems, or apathy and social disengagement. If you can identify the neural bases of these, you can tailor the pharmacology.” Vollenweider and his colleagues have found an existing drug for anxiety that blocks specific effects of psilocybin, the psychoactive ingredient in magic mushrooms. When healthy people were given the drug before tripping, they did not report visual hallucinations and other common effects, according to a study published in April 2016 in European Neuropsychopharmacology. The effort is part of a burgeoning movement in pharmacology that seeks to induce psychosis to learn how to treat it. And schizophrenia desperately needs new treatments. Seventy-five percent of afflicted patients have cognitive problems. And most commonly used drugs do not treat the disorder's “negative” symptoms—apathy, social withdrawal, negative thinking—nor the cognitive impairments, which best predict how well a patient will fare in the long term. © 2017 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 23375 - Posted: 03.19.2017

By James Gallagher Health and science reporter, Maps have revealed "hotspots" of schizophrenia and other psychotic illnesses in England, based on the amount of medication prescribed by GPs. The analysis by the University of East London showed North Kesteven, in Lincolnshire, had the highest rates. The lowest rate of schizophrenia prescriptions was in East Dorset. However, explaining the pattern across England is complicated and the research team says the maps pose a lot of questions. They were developed using anonymous prescription records that are collected from doctors' surgeries in England. They record only prescriptions given out by GPs - not the number of patients treated - so hospital treatment is missed in the analysis. Data between October 2015 and September 2016 showed the average number of schizophrenia prescriptions across England was 19 for every 1,000 people. Prof Allan Brimicombe, one of the researchers from UEL, said: "The pattern is not uniformly spread across the country." He suggests this could be due to "environmental effects" such as different rates of drink or drug abuse. Prof Brimicombe told the BBC: "The top one is in the Lincolnshire countryside and there are others in the countryside." © 2017 BBC

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23281 - Posted: 02.25.2017

By BENEDICT CAREY She was all there, all the time: exuberant in describing her mania, savage and tender when recalling her despair. And for decades, she gracefully wore the legacy of her legendary role as Princess Leia, worshiped by a generation of teenage girls as the lone female warrior amid the galactic male cast of the “Star Wars” trilogy. In her long, openhearted life, the actress and author Carrie Fisher brought the subject of bipolar disorder into the popular culture with such humor and hard-boiled detail that her death on Tuesday triggered a wave of affection on social media and elsewhere, from both fans and fellow bipolar travelers, whose emotional language she knew and enriched. She channeled the spirit of people like Patty Duke, who wrote about her own bipolar illness, and Kitty Dukakis, who wrote about depression and alcoholism, and turned it into performance art. Ms. Fisher’s career coincided with the growing interest in bipolar disorder itself, a mood disorder characterized by alternating highs and lows, paralyzing depressions punctuated by flights of exuberant energy. Her success fed a longstanding debate on the relationship between mental turmoil and creativity. And her writing and speaking helped usher in a confessional era in which mental disorders have entered the pop culture with a life of their own: Bipolar is now a prominent trait of another famous Carrie, Claire Danes’s character Carrie Mathison in the Showtime television series “Homeland.” “She was so important to the public because she was telling the truth about bipolar disorder, not putting on airs or pontificating, just sharing who she is in an honest-to-the-bone way,” said Judith Schlesinger, a psychologist and author of “The Insanity Hoax: Exposing the Myth of the Mad Genius.” © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 23035 - Posted: 12.29.2016

By Arlene Karidis As a young teenager, Inshirah Aleem was sure she’d be heading to Harvard Law School in a few years. But the straight-A student went down another road. Within months of her 14th birthday, the quiet girl was telling outrageous lies, running away from home and stealing. She eventually landed in front of a judge and later was sent to foster care, where she lived in a basement, her belongings stuffed into a trash bag. It would be a year before Aleem, now a 38-year-old schoolteacher living in Greenbelt, was diagnosed with bipolar disorder. The brain condition is characterized by high (manic) moods and low (depressed) moods as well as by fluctuating energy levels. These unstable states are coupled with impaired judgment. The diagnosis explained her racing, disjointed thoughts and almost completely sleepless nights. And it explained her terrifying hallucinations, which were followed by a catatonic state where Aleem couldn’t move or talk. About 2.6 percent of adults and about 11.2 percent of 13- to-18-year-olds have bipolar disorder, according to the Substance Abuse and Mental Health Services Administration. The disorder can be hard to recognize and harder to treat. Combining medications often brings substantial improvement, but some patients experience side effects and show minimal improvement. Researchers, who have found that bipolar disorder is inherited more than 70 percent of the time, hope to identify drugs to target the 20 genetic variations known to be associated with the disorder. © 1996-2016 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22864 - Posted: 11.14.2016

Mo Costandi Stem cells obtained from patients with schizophrenia carry a genetic mutation that alters the ratio of the different type of nerve cells they produce, according to a new study by researchers in Japan. The findings, published today in the journal Translational Psychiatry, suggest that abnormal neural differentiation may contribute to the disease, such that fewer neurons and more non-neuronal cells are generated during the earliest stages of brain development. Schizophrenia is a debilitating mental illness that affects about 1 in 100 people. It is known to be highly heritable, but is genetically complex: so far, researchers have identified over 100 rare genetic variations and dozens of mutations associated with increased risk of developing the disease. One of the best characterised mutations associated with the disease is a microdeletion on chromosome 22, within a region containing dozens of genes known to be involved in the development, maturation, and function of brain circuits. This deletion is found in 1 in every 2,000 – 4,000 live births; all patients carrying it exhibit various psychiatric symptoms and conditions, with just under a third of them developing schizophrenia in adolescence or early adulthood. Manabu Toyoshima of the RIKEN Brain Science Institute and his colleagues obtained skin cells from two female schizophrenic patients diagnosed with the chromosome 22 deletion and two healthy individuals, then reprogrammed them to generate induced pluripotent stem cells (iPSCs), unspecialised cells which, like embryonic stem cells, retain the ability to differentiate into all the different cell types in the body. They then compared the properties of iPSCs obtained from the schizophrenic patients with those from the healthy controls. © 2016 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22822 - Posted: 11.02.2016

Emily Sohn After a mother killed her four young children and then herself last month in rural China, onlookers quickly pointed to life circumstances. The family lived in extreme poverty, and bloggers speculated that her inability to escape adversity pushed her over the edge. Can poverty really cause mental illness? It's a complex question that is fairly new to science. Despite high rates of both poverty and mental disorders around the world, researchers only started probing the possible links about 25 years ago. Since then, evidence has piled up to make the case that, at the very least, there is a connection. People who live in poverty appear to be at higher risk for mental illnesses. They also report lower levels of happiness. That seems to be true all over the globe. In a 2010 review of 115 studies that spanned 33 countries across the developed and developing worlds, nearly 80 percent of the studies showed that poverty comes with higher rates of mental illness. Among people living in poverty, those studies also found, mental illnesses were more severe, lasted longer and had worse outcomes. And there's growing evidence that levels of depression are higher in poorer countries than in wealthier ones. Those kinds of findings challenge a long-held myth of the "poor but happy African sitting under a palm tree," says Johannes Haushofer, an economist and neurobiologist who studies interactions between poverty and mental health at Princeton University. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22811 - Posted: 10.31.2016

By Tori Rodriguez Uric acid is almost always mentioned in the context of gout, an inflammatory type of arthritis that results from excessive uric acid in the blood. It may be surprising, then, that it has also been linked with a vastly different type of disease: bipolar disorder. Elevated uric acid has been observed in patients with acute mania, and reducing uric acid improves symptoms. New evidence supports its potential as a treatment target. Uric acid is a by-product of the breakdown of compounds called purines, found in many foods and manufactured by the body. High levels of uric acid can indicate that these compounds, such as the neurotransmitter adenosine, are being broken down too readily in the body. “Adenosine might play a key role in neurotransmission and neuromodulation, having sedative, anticonvulsant and antiaggressive effects,” says physician Francesco Bartoli, a researcher at the University of Milano-Bicocca in Italy. Bartoli's new study, published in May in the Journal of Psychosomatic Research, examined uric acid levels in 176 patients with bipolar disorder or another severe mental illness and 89 healthy controls. The results show that bipolar disorder was the only diagnosis significantly linked with levels of uric acid. Excess uric acid was found to be linked to male gender, metabolic syndrome, waist size and triglyceride levels. Beyond the too rapid breakdown of adenosine, other potential explanations for increased uric acid include the metabolic abnormalities often present in people with bipolar disorder and frequent consumption of purine-rich foods and drinks, such as liver, legumes, anchovies and alcohol. Fructose consumption can also be a problem because the sugar inhibits uric acid excretion. Dietary interventions may reduce levels, but medication is typically required if dietary changes are insufficient. © 2016 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22790 - Posted: 10.26.2016

Bret Stetka Every day in the United States, millions of expectant mothers take a prenatal vitamin on the advice of their doctor. The counsel typically comes with physical health in mind: folic acid to help avoid fetal spinal cord problems; iodine to spur healthy brain development; calcium to be bound like molecular Legos into diminutive baby bones. But what about a child's future mental health? Questions about whether ADHD might arise a few years down the road or whether schizophrenia could crop up in young adulthood tend to be overshadowed by more immediate parental anxieties. As a friend with a newborn daughter recently fretted over lunch, "I'm just trying not to drop her!" Yet much as pediatricians administer childhood vaccines to guard against future infections, some psychiatrists now are thinking about how to shift their treatment-centric discipline toward one that also deals in early prevention. In 2013, University of Colorado psychiatrist Robert Freedman and colleagues recruited 100 healthy, pregnant women from greater Denver to study whether giving the B vitamin choline during pregnancy would enhance brain growth in the developing fetus. The moms-to-be were randomly given either a placebo or a form of choline called phosphatidylcholine. Choline itself is broken down by bacteria in the gut; by giving it in this related form the supplement can more effectively be absorbed into the bloodstream. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22777 - Posted: 10.22.2016

By Meredith Wadman The second century C.E. Greek physician and philosopher Galen advised patients suffering from disorders of the spirit to bathe in and drink hot spring water. Modern day brain scientists have posited that Galen’s prescription delivered more than a placebo effect. Lithium has for decades been recognized as an effective mood stabilizer in bipolar disease, and lithium salts may have been present in the springs Galen knew. Yet exactly how lithium soothes the mind has been less than clear. Now, a team led by Ben Cheyette, a neuroscientist at the University of California in San Francisco (UCSF), has linked its success to influence over dendritic spines, tiny projections where excitatory neurons form connections, or synapses, with other nerve cells. Lithium treatment restored healthy numbers of dendritic spines in mice engineered to carry a genetic mutation that is more common in people with autism, schizophrenia, and bipolar disorder than in unaffected people, they report today in Molecular Psychiatry. The lithium also reversed symptoms in these mutant mice—lack of interest in social interactions, decreased motivation, and increased anxiety—that mimic those in the human diseases. “They showed there’s a correlation between the ability of lithium to reverse not only the behavioral abnormalities in the mice, but also the [dendritic] spine abnormalities,” says Scott Soderling, a neuroscientist at Duke University in Durham, North Carolina, who studies how dysfunctions in signaling at brain synapses and lead to psychiatric disorders. Soderling adds that the work also sheds light on the roots of these diseases. “It gives further credence to this idea that these spine abnormalities are functionally linked to the behavioral disorders.” © 2016 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22764 - Posted: 10.18.2016

By MICHAEL HEDRICK My father said on numerous occasions when I was growing up that he would see other families that had problems like divorce and drug use, and he would thank God that his family was so perfect. Things would change, though. They always do. And that perfect family would face just as much struggle as any other. Growing up in the mountains above Boulder, Colo., our life was good. My parents had left their life in Chicago behind for an ideal they saw in a piece of art they found at a flea market, a haphazardly painted picture of a cabin next to a river with the mountains towering in the background. Born in the early ‘80s, my brothers and I shared a bond as best friends in our small neighborhood, isolated from town, where we spent time outside sledding, building forts and making dams in the ditch that ran by our house. The biggest problems we seemed to face were bloody knees and the occasional broken bone from snowboarding and bike accidents. My dad, a subscriber to “Mother Earth News,” relished our family’s home in the mountains. There were backpacking trips to the national park 30 miles away, where he taught us how to build a fire and to hang our food from tree limbs to keep it out of reach of bears. Other times he would take us on long father-son road trips, where we would drive the long highways with nothing to look at but the passing fields and nothing to pay attention to but the books on tape from Focus on the Family that my father put on the car stereo. Those tapes provided a Christian look at what it meant to be a man, covering issues like lust, sex and puberty, and he’d answer our questions about girls and all manner of things relating to our growing into healthy young men. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22686 - Posted: 09.23.2016

By Helen Thomson High levels of inflammation as a child may predict a higher risk of manic behaviour in later life, a finding that could lead to new ways of treating conditions like bipolar disorder. Hypomania involves spells of hyperactivity and is often a symptom of mood disorders, including bipolar disorder, seasonal affective disorder and some kinds of psychosis. People experiencing hypomania may take more risks, feel more confident and become impatient with others. After spells like this, they may “crash”, needing to sleep for long periods and sometimes remembering little about the previous few days. Earlier studies suggested a link between inflammation and mood disorders, prompting Joseph Hayes at University College London and his team to see if inflammation as a child might lead to mental health problems later. Analysing data from more than 1700 people, his team identified a significant link between high levels of a chemical involved in inflammation at age 9, and experiencing aspects of hypomania at age 22. The chemical, called IL-6, is normally secreted by white blood cells to stimulate an inflammatory immune response to infection or trauma. Hayes’s team says it is unclear how inflammation in childhood could induce symptoms of hypomania but IL-6 is known to affect the brain. A study that used injections to increase IL-6 in the blood of healthy volunteers found that this caused symptoms of anxiety, and reduced performance in memory tests. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22636 - Posted: 09.07.2016