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By Melissa Healy The nature of psychological resilience has, in recent years, been a subject of enormous interest to researchers, who have wondered how some people endure and even thrive under a certain amount of stress, and others crumble and fall prey to depression. The resulting research has underscored the importance of feeling socially connected and the value of psychotherapy to identify and exercise patterns of thought that protect against hopelessness and defeat. But what does psychological resilience look like inside our brains, at the cellular level? Such knowledge might help bolster peoples' immunity to depression and even treat people under chronic stress. And a new study published Thursday in Science magazine has made some progress in the effort to see the brain struggling with -- and ultimately triumphing over -- stress. A group of neuroscientists at Mount Sinai's Icahn School of Medicine in New York focused on the dopaminergic cells in the brain's ventral tegmentum, a key node in the brain's reward circuitry and therefore an important place to look at how social triumph and defeat play out in the brain. In mice under stress because they were either chronically isolated or rebuffed or attacked by fellow littermates, the group had observed that this group of neurons become overactive. It would logically follow, then, that if you don't want stressed mice (or people) to become depressed, you would want to avoid hyperactivity in that key group of neurons, right? Actually, wrong, the researchers found. In a series of experiments, they saw that the mice who were least prone to behave in socially defeated ways when under stress were actually the ones whose dopaminergic cells in the ventral tegmental area displayed the greatest levels of hyperactivity in response to stress. And that hyperactivity was most pronounced in the neurons that extended from the tegmentum into the nearby nucleus accumbens, also a key node in the brain's reward system.

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19511 - Posted: 04.21.2014

Scientists have traced vulnerability to depression-like behaviors in mice to out-of-balance electrical activity inside neurons of the brain’s reward circuit and experimentally reversed it – but there’s a twist. Instead of suppressing it, researchers funded by the National Institutes of Health boosted runaway neuronal activity even further, eventually triggering a compensatory self-stabilizing response. Once electrical balance was restored, previously susceptible animals were no longer prone to becoming withdrawn, anxious, and listless following socially stressful experiences. “To our surprise, neurons in this circuit harbor their own self-tuning, homeostatic mechanism of natural resilience,” explained Ming-Hu Han, Ph.D External Web Site Policy., of the Icahn School of Medicine at Mount Sinai, New York City, a grantee of the NIH’s National Institute of Mental Health (NIMH) and leader of the research team. Han and colleagues report on their discovery April 18, 2014 in the journal Science. Prior to the new study, the researchers had turned resilience to social stress on and off by using pulses of light to manipulate reward circuit neuronal firing rates in genetically engineered mice – optogenetics. But they didn’t know how resilience worked at the cellular level. To find out, they focused on electrical events in reward circuit neurons of mice exposed to a social stressor. Some mice that experience repeated encounters with a dominant animal emerge behaviorally unscathed, while others develop depression-like behaviors.

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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19510 - Posted: 04.19.2014

By DORIS IAROVICI, M.D. “I think our experiment failed,” the young graduate student told me, referring to our attempt to take her off the antidepressant she’d been on for seven years. She was back in my campus office after a difficult summer break, and as she talked about feeling unsettled and upset, I wondered about the broader experiment playing out on college campuses across the country. Antidepressants are an excellent treatment for depression and anxiety. I’ve seen them improve — and sometimes save — many young lives. But a growing number of young adults are taking psychiatric medicines for longer and longer periods, at the very age when they are also consolidating their identities, making plans for the future and navigating adult relationships. Are we using good scientific evidence to make decisions about keeping these young people on antidepressants? Or are we inadvertently teaching future generations to view themselves as too fragile to cope with the adversity that life invariably brings? My patient had started medication as a college freshman, after she’d become depressed and spent much of her time in bed. She was forced to take a medical leave but improved quickly, returned to school and graduated. She married soon after and worked for a few years, feeling well all the while. Professional guidelines recommend six to nine months of medicine for first episodes of depression. But my patient had never been advised to stop taking it. She reluctantly agreed to my recommendation to taper off her antidepressant. © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19502 - Posted: 04.17.2014

By BENEDICT CAREY The relationship had become intolerably abusive, and after a stinging phone call one night, it seemed there was only one way to end the pain. Enough wine and pills should do the job — and would have, except that paramedics barged through the door, alerted by her lover. “I very rarely tell the story in detail publicly, it’s so triggering and sensational,” said Dese’Rae L. Stage, 30, a photographer and writer living in Brooklyn who tried to kill herself in 2006. “I talk about what led up to it, how helpless I felt — and what came after.” The nation’s oldest suicide prevention organization, the American Association of Suicidology, decided in a vote by its board last week to recognize a vast but historically invisible portion of its membership: people, like Ms. Stage, who tried to kill themselves but survived. About a million American adults a year make a failed attempt at suicide, surveys suggest, far outnumbering the 38,000 who succeed, and in the past few years, scores of them have come together on social media and in other forums to demand a bigger voice in prevention efforts. Plans for speakers bureaus of survivors willing to tell their stories are well underway, as is research to measure the effect of such testimony on audiences. For decades, mental health organizations have featured speakers with schizophrenia, bipolar disorder and depression. But until now, suicide has been virtually taboo, because of not only shame and stigma, but also fears that talking about the act could give others ideas about how to do it. “This is a real shift you’re seeing,” said Heidi Bryan, 56, of Neenah, Wis., who has been speaking for years about suicide attempts she made in the 1990s. “For people working in suicide prevention, they always told us not to talk about our own experience, like they were afraid to tip us over the edge or something. Honestly, we’re the ones who know what works and what doesn’t.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19481 - Posted: 04.14.2014

|By Scott O. Lilienfeld and Hal Arkowitz A rabble-rousing patient on a psychiatric ward is brought into a room and strapped to a gurney. He is being punished for his defiance of the head nurse's sadistic authority. As he lies fully awake, the psychiatrist and other staff members place electrodes on both sides of his head and pass a quick jolt of electricity between them. Several orderlies hold the patient down while he grimaces in pain, thrashes uncontrollably and lapses into a stupor. This scene from the 1975 Academy Award–winning film One Flew Over the Cuckoo's Nest, starring Jack Nicholson as the rebellious patient, has probably shaped the general public's perceptions of electroconvulsive therapy (ECT) far more than any scientific description. As a result, many laypeople regard ECT as a hazardous, even barbaric, procedure. Yet most data suggest that when properly administered, ECT is a relatively safe and often beneficial last-resort treatment for severe depression, among other forms of mental illness. One Flew Over the Cuckoo's Nest is far from the only negative portrayal of ECT in popular culture. In a 2001 survey of 24 films featuring the technique, psychiatrists Andrew McDonald of the University of Sydney and Garry Walter of Northern Sydney Central Coast Health of New South Wales reported that the depictions of ECT are usually pejorative and inaccurate. In most cases, ECT is delivered without patients' consent and often as retribution for disobedience. The treatment is typically applied to fully conscious and terrified patients. Following the shocks, patients generally lapse into incoherence or a zombielike state. In six films, patients become markedly worse or die. Probably as a result of such portrayals, the general public holds negative attitudes toward ECT. © 2014 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19475 - Posted: 04.12.2014

By NICHOLAS BAKALAR A new study adds to the evidence that the use of antidepressants during pregnancy is associated with a higher risk of premature birth, though many factors most likely play a role and the relationship is complex. Researchers reviewed data from 41 studies, some of which controlled for factors like smoking, alcohol or coffee drinking, weight gain during pregnancy, and other behavioral and health issues. They found no increase in the risk of early birth with the use of antidepressants during the first trimester, a 53 percent higher risk over all and a 96 percent higher risk with antidepressant use late in pregnancy. Depression itself is a risk factor for premature births, and a few studies tried to account for this by using, as a control, a group of women with a diagnosis of depression who did not take antidepressants during their pregnancy. Generally, researchers still found a higher, though diminished, risk from taking antidepressants. The review was published in March in PLOS One. Does this mean that all pregnant women should avoid these drugs? No, said the senior author, Dr. Adam C. Urato, an assistant professor of maternal-fetal medicine at Tufts University. Risks and benefits have to be balanced, he said. “It’s very complex, and depends on the severity of the disease,” Dr. Urato added. “The point is that we have to get the right information out so that we can let pregnant women make an informed decision.” © 2014 The New York Times Company

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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 19454 - Posted: 04.08.2014

By James Gallagher Health and science reporter, BBC News The illegal party drug ketamine is an "exciting" and "dramatic" new treatment for depression, say doctors who have conducted the first trial in the UK. Some patients who have faced incurable depression for decades have had symptoms disappear within hours of taking low doses of the drug. The small trial on 28 people, reported in the Journal of Psychopharmacology, shows the benefits can last months. Experts said the findings opened up a whole new avenue of research. Depression is common and affects one-in-10 people at some point in their lives. Antidepressants, such as prozac, and behavioural therapies help some patients, but a significant proportion remain resistant to any form of treatment. A team at Oxford Health NHS Foundation Trust gave patients doses of ketamine over 40 minutes on up to six occasions. Eight showed improvements in reported levels of depression, with four of them improving so much they were no longer classed as depressed. Some responded within six hours of the first infusion of ketamine. Lead researcher Dr Rupert McShane said: "It really is dramatic for some people, it's the sort of thing really that makes it worth doing psychiatry, it's a really wonderful thing to see. He added: "[The patients] say 'ah this is how I used to think' and the relatives say 'we've got x back'." Dr McShane said this included patients who had lived with depression for 20 years. Stressed man The testing of ketamine has indentified some serious side-effects The duration of the effect is still a problem. Some relapse within days, while others have found they benefit for around three months and have since had additional doses of ketamine. There are also some serious side-effects including one case of the supply of blood to the brain being interrupted. Doctors say people should not try to self-medicate because of the serious risk to health outside of a hospital setting. BBC © 2014

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: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19444 - Posted: 04.03.2014

|By Hal Arkowitz and Scott O. Lilienfeld A commercial sponsored by Pfizer, the drug company that manufactures the antidepressant Zoloft, asserts, “While the cause [of depression] is unknown, depression may be related to an imbalance of natural chemicals between nerve cells in the brain. Prescription Zoloft works to correct this imbalance.” Using advertisements such as this one, pharmaceutical companies have widely promoted the idea that depression results from a chemical imbalance in the brain. The general idea is that a deficiency of certain neurotransmitters (chemical messengers) at synapses, or tiny gaps, between neurons interferes with the transmission of nerve impulses, causing or contributing to depression. One of these neurotransmitters, serotonin, has attracted the most attention, but many others, including norepinephrine and dopamine, have also been granted supporting roles in the story. Much of the general public seems to have accepted the chemical imbalance hypothesis uncritically. For example, in a 2007 survey of 262 undergraduates, psychologist Christopher M. France of Cleveland State University and his colleagues found that 84.7 percent of participants found it “likely” that chemical imbalances cause depression. In reality, however, depression cannot be boiled down to an excess or deficit of any particular chemical or even a suite of chemicals. “Chemical imbalance is sort of last-century thinking. It's much more complicated than that,” neuroscientist Joseph Coyle of Harvard Medical School was quoted as saying in a blog by National Public Radio's Alix Spiegel. © 2014 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: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19432 - Posted: 04.01.2014

By Lenny Bernstein After 60 years of refusing, the people who run the Golden Gate Bridge are moving toward installing a suicide barrier, the New York Times reports. As soon as May, the Golden Gate Bridge, Highway and Transportation District is expected to approve construction of a steel mesh net 20 feet below the California landmark’s sidewalk. A record 46 people jumped to their deaths from the span in 2013, and another 118 were stopped before they could. According to the Times, they have tended to be younger than in the past. Experts have long known, and good research shows, that barriers are highly effective at halting suicides, the 10th-leading cause of death in the United States at 38,364 fatalities in 2010. This is true not just of bridges or other high places: locking up firearms and individually bubble-wrapping pills both limit suicides by those methods, said Jill Harkavy-Friedman, vice president of research for the American Foundation for Suicide Prevention. The key is the characteristics of a person on the verge of committing suicide, even someone who has been contemplating it for a while. Suicides are impulsive acts, and the people who commit them are not thinking clearly, have trouble solving problems, have difficulty shifting gears and weigh risks differently. If thwarted in that first, impulsive attempt, they often do not adjust and seek another way to take their lives, Harkavy-Friedman said. “In a suicidal crisis, it’s all about time,” she said. “They’re going to grab whatever is available. They don’t change gears if that is thwarted, because they have rigid thinking in that moment. They’re not thinking about dying. They’re thinking about ending the pain. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19423 - Posted: 03.29.2014

By NICHOLAS BAKALAR A large study has linked several common anti-anxiety drugs and sleeping pills to an increased risk of death, although it’s not certain the drugs were the cause. For more than seven years, researchers followed 34,727 people who filled prescriptions for anti-anxiety medications like Valium and Xanax, or sleep aids like Ambien, Sonata and Lunesta, comparing them with 69,418 controls who did not. After adjusting for a wide variety of factors, the researchers found that people who took the drugs had more than double the risk of death. The study appears online in BMJ. The researchers tried to account for the use of other prescribed drugs, age, smoking, alcohol use, socioeconomic status, and other health and behavioral characteristics. Most important, the investigators also controlled for sleep disorders, anxiety disorders and other psychiatric illnesses, all of which are risk factors for mortality. The lead author, Dr. Scott Weich, a professor of psychiatry at the University of Warwick, said that while he and his colleagues were careful to account for as many potential risks as possible, they were not able to control for the severity of the illnesses suffered by the study participants. Still, he said, the research “adds to an accumulating body of evidence that these drugs are dangerous.” He added: “I prescribe these drugs, and they are difficult to come off. The less time you spend on them the better.” © 2014 The New York Times Company

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19419 - Posted: 03.29.2014

By Gisela Telis, Jodi Corbitt had been battling depression for decades and by 2010 had resigned herself to taking antidepressant medication for the rest of her life. Then she decided to start a dietary experiment. To lose weight, the 47-year-old Catonsville, Md., mother stopped eating gluten, a protein found in wheat and related grains. Within a month she had shed several pounds — and her lifelong depression. “It was like a veil lifted and I could see life more clearly,” she recalled. “It changed everything.” Corbitt had stumbled into an area that scientists have recently begun to investigate: whether food can have as powerful an impact on the mind as it does on the body. Research exploring the link between diet and mental health “is a very new field; the first papers only came out a few years ago,” said Michael Berk, a professor of psychiatry at the Deakin University School of Medicine in Australia. “But the results are unusually consistent, and they show a link between diet quality and mental health.” “Diet quality” refers to the kinds of foods that people eat, how often they eat them and how much of them they eat. In several studies, including a 2011 analysis of more than 5,000 Norwegians, Berk and his collaborators have found lower rates of depression, anxiety and bipolar disorder among those who consumed a traditional diet of meat and vegetables than among people who followed a modern Western diet heavy with processed and fast foods or even a health-food diet of tofu and salads. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19403 - Posted: 03.25.2014

By BENEDICT CAREY He heard about the drug trial from a friend in Switzerland and decided it was worth volunteering, even if it meant long, painful train journeys from his native Austria and the real possibility of a mental meltdown. He didn’t have much time, after all, and traditional medicine had done nothing to relieve his degenerative spine condition. “I’d never taken the drug before, so I was feeling — well, I think the proper word for it, in English, is dread,” said Peter, 50, an Austrian social worker, in a telephone interview; he asked that his last name be omitted to protect his identity. “There was this fear that it could all go wrong, that it could turn into a bad trip.” On Tuesday, The Journal of Nervous and Mental Disease is posting online results from the first controlled trial of LSD in more than 40 years. The study, conducted in the office of a Swiss psychiatrist near Bern, tested the effects of the drug as a complement to talk therapy for 12 people nearing the end of life, including Peter. Most of the subjects had terminal cancer, and several died within a year after the trial — but not before having a mental adventure that appeared to have eased the existential gloom of their last days. “Their anxiety went down and stayed down,” said Dr. Peter Gasser, who conducted the therapy and followed up with his patients a year after the trial concluded. The new publication marks the latest in a series of baby steps by a loose coalition of researchers and fund-raisers who are working to bring hallucinogens back into the fold of mainstream psychiatry. Before research was banned in 1966 in the United States, doctors tested LSD’s effect for a variety of conditions, including end-of-life anxiety. But in the past few years, psychiatrists in the United States and abroad — working with state regulators as well as ethics boards — have tested Ecstasy-assisted therapy for post-traumatic stress; and other trials with hallucinogens are in the works. © 2014 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: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 19322 - Posted: 03.04.2014

By James Gallagher Health and science reporter, BBC News A tool for predicting the risk of clinical depression in teenage boys has been developed by researchers. Looking for high levels of the stress hormone cortisol and reports of feeling miserable, lonely or unloved could find those at greatest risk. Researchers at the University of Cambridge want to develop a way of screening for depression in the same way as heart problems can be predicted. However, their method was far less useful in girls. Teenage years and early adulthood are a critical time for mental health - 75% of disorders develop before the age of 24. But there is no way to accurately say who will or will not develop depression. Risky combination Now researchers say they have taken the "first step" towards a screening tool. Tests on 1,858 teenagers, reported in Proceedings of the National Academy of Sciences, combined hormone levels and mood questionnaires to assess risk. They showed that having both high cortisol levels and depressive mood symptoms posed a higher risk of depression than either factor alone and presented a risk of clinical depression 14 times that of those with low cortisol and no depressive symptoms. Around one in six boys was in the high-risk category and half of them were diagnosed with clinical depression during the three years of study. One of the researchers, Prof Ian Goodyer, said: "Depression is a terrible illness that will affect as many as 10 million people in the UK at some point in their lives. "Through our research, we now have a very real way of identifying those teenage boys most likely to develop clinical depression. BBC © 2014

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 19261 - Posted: 02.18.2014

|By Simon Makin For decades two very different treatments of depression have existed side by side. Medications act on molecules, cells and synapses in the brain. Psychological therapies focus on cognition and behavior, trying to alter negatively biased thinking. Now a new theory suggests that these interventions may work in more similar ways than anyone realized, providing an opportunity to better integrate the two approaches. More important, it may help provide patients faster, more reliable relief from this crippling condition. Antidepressant drugs increase the levels of certain chemical messengers in the brain, such as serotonin and norepinephrine. Yet exactly how these neurotransmitters affect mood is unknown. “There was a missing link between the cellular, molecular and synaptic bases of these drugs, on the one hand, and what they affect in humans, which is their experiences, perceptions, memories and feelings,” says Catherine Harmer, a neuroscientist at the University of Oxford. The psychological explanation, meanwhile, describes depression in terms of distorted information processing. Depressed people are thought to process perceptions, experiences and memories with a negative bias. Many studies confirm that depressed individuals show increased sensitivity to sad faces, greater memory for negative material and reduced responsiveness to rewards as compared with healthy people. Successful therapies teach patients how to correct for this clouded vision. Harmer now believes that antidepressants may also work by altering this negative emotional processing. About a decade ago she and her colleagues tested the effects of commonly prescribed antidepressants on healthy volunteers and found that many of the drugs skewed emotional processing to the positive. Previous research had shown that antidepressants also change these measures in depressed people, but studies included only patients who had been on medication for six to eight weeks because the drugs were assumed to take that long to kick in. © 2014 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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19231 - Posted: 02.10.2014

By Melissa Healy Adolescents treated with the antidepressant fluoxetine -- better known by its commercial name, Prozac -- appear to undergo changes in brain signaling that result in changed behavior well into adulthood, says a new study. Adult mice and rats who were administered Prozac for a stretch of mid-adolescence responded to daunting social and physical challenges with less despair than animals who passed their teen years unmedicated, a team of researchers found. But, even as adults long separated from their antidepressant days, the Prozac veterans reacted to stressful situations with greater anxiety than did the adult Prozac virgins. The latest research, published Wednesday in the Journal of Neuroscience, offers evidence that treatment with a selective serotonin reuptake inhibitor -- an SSRI antidepressant -- has long-lived effects on the developing brain. It also zeroes in on how and where fluoxetine effects those lasting changes: by modifying the cascade of chemical signals issued by the brain's ventral tegmentum -- a region active in mood regulation -- in stressful situations. Yet, the new research raises more questions than it answers, since the changes in adults who were treated with Prozac as adolescents seem contradictory. Sensitivity to stress appears to predispose one to developing depression. So how does a medication that treats depression in children and teens -- and that continues to protect them from depression as adults -- also heighten their sensitivity to stress?

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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 19146 - Posted: 01.18.2014

By Megan Wiegand and Slate, Tips for beating the seasonal blues are as numerous as the winter night is long. Light boxes, touted to “uplift people’s spirits” and “improve mood and energy,” offer a New-Agey-seeming solution to propel us into the cold as if it’s the first beautiful day of spring. But can sitting in front of a light for a few minutes a day actually counteract the dreariest months? Yes, in many cases. Light-box therapy has been shown to alleviate symptoms in people who suffer from seasonal affective disorder, or SAD. Symptoms of this form of depression — they can include lost interest in beloved activities, overeating, loss of energy, disrupted sleep cycles and feelings of hopelessness or guilt — typically appear in late fall or early winter and dissipate in spring. Women are twice as likely as men to seek treatment for SAD, and those farther away from the equator are more likely to be diagnosed: About 11 percent of Mainers have a clinical SAD diagnosis, but only 2 percent of Floridians report the illness, according to Kathryn Roecklein, an assistant professor of psychology at the University of Pittsburgh. One tool doctors use to treat SAD is light-box therapy. Light boxes use bright white fluorescent bulbs (or sometimes blue light) that reproduce some wavelengths of the sun’s light. They contain filters to block harmful UV rays and come in various shapes, sizes, light types and price points. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 19125 - Posted: 01.14.2014

By Sandra G. Boodman, Bebe Bahnsen remembers the night, alone in her small cottage on the Alabama coast, that she felt a strong urge to drink a can of drain cleaner. For years, antidepressants combined with talk therapy had enabled Bahnsen, whose first name is Beatrice, to function well, establishing a thriving public relations business in Washington followed by a career as a newspaper reporter. But those days had been supplanted by a prolonged suicidal depression that had proved impervious to electroshock treatments, periodic hospitalizations and a raft of psychiatric drugs. The phone call in which Bahnsen confided her desire to drink poison seemed to confirm the worst fears of one of her closest friends. “I figured, well, she was one of those people who just was not ever going to get better,” said Paddy Bowman, a folklore specialist who lives in Alexandria. Bahnsen, now 73, traces the beginning of her psychological slide to the mid-1990s, when she decided that, after two decades, she’d had enough of Washington. She moved back to her home state of Georgia and her life slowly began to unravel. She felt estranged from her large and devoted circle of friends, began having problems at work, and grew restless and increasingly depressed. “I felt as though I was on a large island and everyone was slowly moving away and I was there by myself,” Bahnsen recalled. For the first time in her life, she said, she was intermittently psychotic. Periodic suicide attempts, some involving overdoses of prescribed sleeping pills, landed her in a series of mental hospitals. In November 2006 she was hospitalized in Las Vegas, where she was then living with one of her sons. Doctors, baffled by her longstanding failure to improve, decided to take a closer look at her case. What they found resulted in an entirely different treatment, one that had a rapid and dramatic effect on her mental state. © 1996-2013 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 15: Language and Our Divided Brain
Link ID: 19069 - Posted: 12.24.2013

By RICHARD A. FRIEDMAN, M.D. When will we ever get depression under control? Of all the major illnesses, mental or physical, depression has been one of the toughest to subdue. Despite the ubiquity of antidepressant drugs — there are now 26 to choose from — only a third of patients with major depression will experience a full remission after the first round of treatment, and successive treatments with different drugs will give some relief to just 20 to 25 percent more. About 30 percent of people with depression have some degree of treatment resistance. And the greater the degree of resistance, the more likely a future relapse, even if the patient continues taking the drug. Although we have learned much about depression — for example, the recent research showing that the successful treatment of insomnia in depressed patients essentially doubles their response to a drug like Prozac — we still don’t understand its fundamental cause. The old idea that the disease results from a deficiency of a single neurotransmitter like serotonin or dopamine is clearly simplistic and wrong. Maybe psychiatrists and neuroscientists have something to learn from the successful hunt for the Higgs boson. Of course a debilitating disease has nothing in common with a subatomic particle, except that both are mysterious and elusive. But it was those very qualities that inspired international teams of physicists to work together for years until they finally identified the boson last year. Among biomedical scientists, who compete for the same research dollars and want to be first across the finish line with an important finding, such cooperation is hardly the norm. But there are signs that this is changing. Not long ago, I sat in at a meeting of the Hope for Depression Research Foundation. Audrey Gruss, the knowledgeable and energetic philanthropist who started the foundation, has corralled a group of senior basic and clinical neuroscientists to look for solutions. (It is not the first to try a collaborative approach; others are being sponsored by the MacArthur Foundation and the Pritzker Consortium.) Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19068 - Posted: 12.24.2013

By John Chipman, CBC News Andrew Solomon is not your typical depressive, if such a thing exists. Most people struggling with clinical depression do not like to talk about it. Depression is usually suffered in silence, because of the stigma that still clings to it. Many people still see depression as a sign of weakness, or believe that if you just cheered up or had a better attitude you'd feel so much better. Solomon has heard the wrong-headed chatter most of his life. But rather than shy away, the journalist and best-selling author wrote a book about it, detailing his own struggles with depression. It’s called The Noonday Demon: An Atlas of Depression. And he has become a vocal advocate, calling for more progressive attitudes about the disease so that people suffering from it can step out of the shadows and feel comfortable getting the help they need to survive, and to thrive. So it was with some shock and dismay that Solomon learned about Ellen Richardson, a Canadian woman turned back at the U.S. border last month because she was hospitalized last year for her depression. Richardson was told she could only enter the U.S. if a doctor — not her own, but one from a shortlist of others whom she had never met — signed a document vouching for her. She would also have to pay a fee of $500. U.S. border guards are allowed to bar anyone they deem a threat to themselves, to other Americans, or their property. They have access to police records — including even uneventful encounters with officers — but medical records are supposed to be held in the strictest confidence. © CBC 2013

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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 19038 - Posted: 12.16.2013

By ROBERT PEAR WASHINGTON — Psychiatrists are significantly less likely than doctors in other specialties to accept insurance, researchers say in a new study, complicating the push to increase access to mental health care. The study, published Wednesday in the journal JAMA Psychiatry, found that 55 percent of psychiatrists accepted private insurance, compared with 89 percent of other doctors. Likewise, the study said, 55 percent of psychiatrists accept patients covered by Medicare, against 86 percent of other doctors. And 43 percent of psychiatrists accept Medicaid, which provides coverage for low-income people, while 73 percent of other doctors do. The lead author of the study, Dr. Tara F. Bishop of Weill Cornell Medical College in New York, said: “In the wake of the school killings in Newtown, Conn., and other recent mass shootings, the need for increased mental health services is now recognized. But unless patients have deep pockets, they may have a hard time finding a psychiatrist who will treat them.” Mental health care is one of 10 types of “essential health benefits” that must be provided by insurers under the new health care law. A federal rule issued last month requires insurers to cover care for mental health and addiction on the same terms as treatments for physical illnesses, without charging higher co-payments or deductibles or imposing stricter limits on services. Starting next year, Medicare will end a discriminatory policy that for decades has required people to pay a larger share of the bill for mental health care than for other outpatient services. However, the study suggests that expanding coverage may not by itself guarantee access to psychiatrists. “Even if you have good insurance that covers mental health care, you may still have a problem if there’s no doctor who accepts your insurance,” Dr. Bishop said. © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 19031 - Posted: 12.12.2013