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By Chris Wodskou, CBC News For the past 25 years, people suffering from depression have been treated with antidepressant drugs like Zoloft, Prozac and Paxil — three of the world’s best-selling selective serotonin reuptake inhibitors, or SSRIs. But people are questioning whether these drugs are the appropriate treatment for depression, and if they could even be causing harm. The drugs are designed to address a chemical imbalance in the brain and thereby relieve the symptoms of depression. In this case, it’s a shortage of serotonin that antidepressants work to correct. In fact, there are pharmaceutical treatments targeting chemical imbalances for just about every form of mental illness, from schizophrenia to ADHD, and a raft of anxiety disorders. Hundreds of millions of prescriptions are written for antipsychotic, antidepressant and anti-anxiety medications every year in the United States alone, producing billions of dollars in revenue for pharmaceutical companies. But what if the very premise behind these drugs is flawed? What if mental illnesses like depression aren’t really caused by chemical imbalances, and that millions of the people who are prescribed those drugs derive no benefit from them? And what if those drugs could actually make their mental illness worse and more intractable over the long term? Investigative journalist Robert Whitaker argued that psychiatric drugs are a largely ineffective way of treating mental illness in his 2010 book called Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs and the Astonishing Rise of Mental Illness in America. Whitaker maintains that the foundation of modern psychiatry, the chemical imbalance model, is scientifically unproven. © CBC 2014

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: 19712 - Posted: 06.09.2014

By Meeri Kim, Many of us find ourselves swimming along in the tranquil sea of life when suddenly a crisis hits — a death in the family, the loss of a job, a bad breakup. Some power through and find calm waters again, while others drown in depression. Scientists continue to search for the underlying genes and neurobiology that dictate our reactions to stress. Now, a study using mice has found a switch-like mechanism between resilience and defeat in an area of the brain that plays an important role in regulating emotions and has been linked with mood and anxiety disorders. (Bo Li/Cold Spring Harbor Laboratory) - Researchers at Cold Spring Harbor Laboratory identify the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (top, green image) become hyperactive in depressed mice. The bottom panel is close-up of above image - yellow indicates activation. The team showed that this enhanced activity causes depression. After artificially enhancing the activity of neurons in that part of the brain — the medial prefrontal cortex — mice that previously fought to avoid electric shocks started to act helpless. Rather than leaping for an open escape route, they sat in a corner taking the pain — presumably out of a belief that nothing they could do would change their circumstances. “This helpless behavior is quite similar to what clinicians see in depressed individuals — an inability to take action to avoid or correct a difficult situation,” said study author and neuroscientist Bo Li of the Cold Spring Harbor Laboratory in New York. The results were published online May 27 in the Journal of Neuroscience. © 1996-2014 The Washington Post

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: Biological Basis of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 19704 - Posted: 06.06.2014

Joy Jernigan TODAY contributor Depression is a serious medical condition that affects millions of Americans — and nearly twice as many women as men. Symptoms can include persistent feelings of sadness or hopelessness and loss of interest in activities that were once pleasurable, according to the National Institute of Mental Health. Other symptoms include feelings of guilt or worthlessness, irritability, changes in appetite, increased fatigue, difficulty concentrating — even recurrent thoughts of suicide. About 12 million American women suffer from depression each year, women like Debi Lee. Although depression is treatable, most commonly with medications or counseling, many never seek help, often because they are too embarrassed or ashamed. "Depression is really a physical illness," said Dr. Andrew Leuchter, a psychiatrist at the Semel Institute for Neuroscience and Human Behavior at University of California, Los Angeles. It's a disorder that even can be seen in brain scans, with images clearly showing the difference between a normal functioning brain and the brain of someone suffering from depression. "When you show this image to a person who's struggling with depression and you show them that their brain looks different than the quote so-called healthy person, what's their reaction?" Shriver asked. "It's commonly one of relief," Leuchter said. Now, Dr. Leuchter says there's an innovative new treatment called synchronized transcranial magnetic stimulation, or sTMS, that may have the potential to provide relief. Dr. Leuchter, a consultant and stockholder in the company behind sTMS, says it syncs to each patient's brain, then stimulates it with low levels of magnetic energy, 30 minutes a day for several weeks.

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: 19689 - Posted: 06.04.2014

Jyoti Madhusoodanan Most people handle stress well, but some find it difficult to cope and as a result develop depression and other mood disorders. Researchers have previously been able to identify the part of the brain that controls this response, but not exactly how it does so. Now, a study in mice identifies a small group of neurons that could be responsible. The research might also help elucidate the mechanism of deep brain stimulation, a therapy that uses electrical impulses to treat depression and other neurological disorders. How an animal deals with stress is controlled by a part of the brain known as the prefrontal cortex, and the neurons in this part of the brain are known to change in structure and function in response to stressful situations1. To look at the cellular basis of the responses, neuroscientist Bo Li of Cold Spring Harbor Laboratory in New York and his colleagues subjected mice to small electric shocks at random intervals to produce stress. Most of the mice tried to avoid the shocks, but just over one-fifth did not. They also started to avoid other animals or failed to choose tasty foods over plain ones — typical signs of depressive behaviour. The researchers then looked at the animals' brains and found that a specific set of neurons in the prefrontal cortex were easily excitable in depressed mice, but much harder to excite in those resilient to the stress. Furthermore, artificially increasing the activity of these neurons caused mice that were once resilient to become susceptible to depressive behaviours. “We were surprised that we were able to see a difference between depressed and resilient animals at the level of synaptic transmission,” says Li. © 2014 Nature Publishing Group,

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: 19674 - Posted: 05.31.2014

André Aleman & Damiaan Denys According to the World Health Organization, almost 1 million people kill themselves every year. That is more than the number that die in homicides and war combined. A further 10 million to 20 million people attempt it. Suicide is one of the three leading causes of death in the economically most productive age group — those aged 15–44 years — and rates have risen since the economic crisis triggered by the banking crash in 2008 (see 'Suicide rates in Europe'). For example, the number of suicides per year in the Netherlands rose by 30% between 2008 and 2012, from 1,353 to 1,753. In the United States, the average suicide costs society US$1.06 million according to the US Centers for Disease Control and Prevention. Despite its enormous societal impact, little progress has been made in the scientific understanding or treatment of suicidal behaviour. We do know that up to 90% of suicides occur in people with a clinically diagnosable psychiatric disorder1. Large epidemiological studies have shown mental disorders, particularly depression and alcohol addiction, to be major risk factors2. And there is compelling evidence that adequate prevention and treatment of such disorders can reduce suicide rates2. But psychiatry has long neglected the topic. Other than as symptoms of borderline personality disorder and mood disorders, suicide, suicide attempts and suicidal thoughts were not listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The DSM-5 (published last year) does not code suicidal behaviour — the most prominent emergency in psychiatry in primary care. Suicidality is perceived as a medical complication rather than as a disorder in its own right. © 2014 Nature Publishing Group

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: 19642 - Posted: 05.21.2014

Eleven years on, I still remember the evening I decided to kill my baby daughter. It's not something you're supposed to feel as a new parent with a warm, tiny bundle in your arms. But this is how postnatal depression can twist your logic. At the time it made perfect sense. Catherine was screaming, in pain. She had colic, there was nothing I could do about it. If an animal were in this much pain you'd put it out of its misery, so why not a human? Postnatal depression can have this kind of effect even on the most reasonable woman, yet you won't find much about it in baby books. We're expected to love our kids the moment they pop out, even while the memory of the labour pains is still raw. I knew a baby would be hard work, of course, but I expected motherhood to be fulfilling. As it happened I had a wonderful pregnancy, followed by a quick and easy birth. But the problems started soon after. Catherine wouldn’t feed, her blood sugar levels tumbled and I ended up bottle-feeding her, in tears, in a hospital room filled with posters promoting the breast. I was a Bad Mother within 48 hours. Things were no better after the first month. This was meant to be a joyous time, but all I seemed to feel was rage and resentment. In pregnancy all the attention had been on me, and suddenly I was a sideshow to this wailing thing in a crib. I was tired, tetchy and resentful. My daughter had rapidly become a ball and chain. My freedom was over. I kept hoping this was just the “baby blues” and that it would soon pass, but things only got worse. When colic set in, for around five hours each evening Catherine would scream, her face a mix of red and purple rage. No amount of pacing, tummy-rubbing or soothing words could stop this tiny demanding creature. So one night, alone with her in her room, I decided it would be best to put her out of her misery. © 2014 Guardian News and Media Limited

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 19626 - Posted: 05.16.2014

by Nathan Collins There's a new twist in mental health. People with depression seem three times as likely as those without it to have two brain lobes curled around each other. The brains of people with depression can be physically different from other brains – they are often smaller, for example – but exactly why that is so remains unclear. In humans, some studies point to changes in the size of the hippocampi, structures near the back of the brain thought to support memory formation. "There are so many studies that show a smaller hippocampus in almost every psychiatric disorder," says Jerome Maller, a neuroscientist at the Monash Alfred Psychiatry Research Centre in Melbourne, Australia, who led the latest work looking at brain lobes. "But very few can actually show or hypothesize why that is." Maller thinks he has stumbled on an explanation. He had been using a brain stimulation technique known as transcranial magnetic stimulation as a therapy for antidepressant-resistant depression. This involved using fMRI scans to create detailed maps of the brain to determine which parts to stimulate. While pouring over hundreds of those maps, Maller noticed that many of them showed signs of occipital bending. This is where occipital lobes – which are important for vision – at the back of the brain's left and right hemispheres twist around each other. So he and his colleagues scanned 51 people with and 48 without major depressive disorder. They found that about 35 per cent of those with depression and 12.5 per cent of the others showed signs of occipital bending. The difference was even greater in women: 46 per cent of women with depression had occipital bending compared with just 6 per cent of those without depression. © Copyright Reed Business Information Ltd.

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: 19617 - Posted: 05.15.2014

by Michael Slezak Could preventing the brain shrinkage associated with depression be as simple as blocking a protein? Post-mortem analysis of brain tissue has shown that the dendrites that relay messages between neurons are more shrivelled in people with severe depression than in people without the condition. This atrophy could be behind some of the symptoms of depression, such as the inability to feel pleasure. As a result, drugs that help repair the neuronal connections, like ketamine, are under investigation. But how this shrinkage occurs has remained a mystery, limiting researchers' ability to find ways of stopping it. Ronald Duman at Yale University wondered whether a protein called REDD1, which was recently shown to reduce myelin, the fatty material that protects neurons, was the key. To find out, his team bred rats unable to produce REDD1 and exposed them to a prolonged period of unpredictable stress. In normal rats, this stress resulted in depressive-like behaviour and brain shrinkage, but Duman's rats were unaffected. In contrast, rats engineered to overproduce REDD1 became depressed and had brain shrinkage, even without being stressed. What's more, injecting normal rats with a stress hormone boosted levels of REDD1 in the brain. Giving them a drug that blocked the production of stress hormones stopped them producing the protein, even when they were externally stressed. Taken together, the experiments show that REDD1 is necessary to produce the brain shrinkage seen in stressed rats, and that stress hormones are involved in its production – offering a possible way to prevent the shrinkage. © Copyright Reed Business Information Ltd

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: 19532 - Posted: 04.24.2014

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