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By Michelle Roberts Health editor, BBC News online People prescribed anti-depressants should be aware they could be at increased risk of type 2 diabetes, say UK researchers. The University of Southampton team looked at available medical studies and found evidence the two were linked. But there was no proof that one necessarily caused the other. It may be that people taking anti-depressants put on weight which, in turn, increases their diabetes risk, the team told Diabetes Care journal. Or the drugs themselves may interfere with blood sugar control. Their analysis of 22 studies involving thousands of patients on anti-depressants could not single out any class of drug or type of person as high risk. Prof Richard Holt and colleagues say more research is needed to investigate what factors lie behind the findings. And they say doctors should keep a closer check for early warning signs of diabetes in patients who have been prescribed these drugs. With 46 million anti-depressant prescriptions a year in the UK, this potential increased risk is worrying, they say. Prof Holt said: "Some of this may be coincidence but there's a signal that people who are being treated with anti-depressants then have an increased risk of going on to develop diabetes. BBC © 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 18697 - Posted: 09.25.2013

By Sarah Amandolare Decades of research and billions of dollars go into developing and marketing drugs. Here's the life span of a typical brain drug—Cymbalta, a popular antidepressant Tuberculosis researchers discover that a drug that treats infections, called iproniazid, also boosts patients' mood. They learn that iproniazid slows the breakdown of three chemicals in the brain— serotonin, norepinephrine and dopamine. These molecules take center stage in the next two decades, as scientists search for antidepressants. 1974 Eli Lilly researchers develop fluoxetine (Prozac), the first selective serotonin reuptake inhibitor. Fluoxetine thwarts the absorption, or “reuptake,” of serotonin. This boosts levels of the chemical in the pockets of space between neurons. Prozac does not hit drugstore shelves until 1988. 1980s Scientists start tinkering with the reuptake of norepinephrine and dopamine, which, in addition to elevating mood, can relieve muscle and joint pain. They dub this new class of antidepressants serotonin-norepinephrine reuptake inhibitors (SNRIs). At Eli Lilly, scientists begin developing an SNRI with a special focus on norepinephrine. One of their molecules becomes known as duloxetine, later branded Cymbalta. 1986 © 2013 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: 18660 - Posted: 09.18.2013

By Gary Stix New types of drugs for schizophrenia, depression and other psychiatric disorders are few and far between—and a number of companies have scaled back or dropped development of this class of pharmaceuticals. One exception stands out. Ketamine, the anesthetic and illegal club drug, is now being repurposed as the first rapid-acting antidepressant drug and has been lauded as possibly the biggest advance in the treatment of depression in 50 years. A few trials by large pharma outfits are now underway on a new, purportedly improved and, of course, more profitable variant of ketamine, which in its current generic drug form does not make pharmaceutical marketing departments salivate. Some physicians have decided they simply can’t wait for the lengthy protocols of the drug approval process to be sorted out. They have read about experimental trials in which a low-dose, slow-infusion of ketamine seems to produce what no Prozac-like pill can achieve, lifting the black cloud in hours, not weeks. With nothing to offer desperate, sometimes suicidal patients, physicians have decided against waiting for an expensive, ketamine lookalike to arrive and have started writing scripts for the plain, vanilla generic version that has been used for decades as an anesthetic. Ketamine, it seems, has captivated a bunch of white coats with the same grassroots energy that has propelled the medical marijuana movement. © 2013 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: 18640 - Posted: 09.12.2013

Linda Carroll TODAY contributor Whether it’s “One Flew Over the Cuckoo’s Nest,” “Girl Interrupted,” or “Homeland,” Hollywood’s portrayals of electroconvulsive therapy have never been pretty. And the images from those movies and TV shows have only added to a stigma that keeps many desperate patients from opting for a therapy that might turn their lives around, experts say. “We can’t get past the stigma of all the visuals we’ve seen from movies and the fact that it seems so antiquated when you consider modern medicine,” NBC chief medical editor Dr. Nancy Snyderman told TODAY’s Matt Lauer. “But time and time and time again if you look at patients who have severe depression who don’t respond to medications, they will tell you that ECT works.” That’s certainly true in Denise Stewart’s case. Stewart, a mother of two, suffers from schizoaffective disorder. Her hallucinations were pushing her closer and closer to suicide each day. “There would be voices in my head that would sit there and say, ‘Denise, see the knife in the kitchen? Cut your wrists. Denise, see those pills over there? Take all those pills,’” she told TODAY. After antidepressants made Stewart’s condition worse, her doctors suggested ECT. And the change was dramatic. “If it hadn’t been for the electroconvulsive therapy, I wouldn’t be alive right now,” Stewart said. These days an estimated 100,000 Americans undergo ECT each year – and the process is a lot different from what you see in the media, experts say.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 17: Learning and Memory
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18541 - Posted: 08.21.2013

By RICHARD A. FRIEDMAN, M.D. Fully 1 in 5 Americans take at least one psychiatric medication. Yet when it comes to mental health, we are facing a crisis in drug innovation. Sure, we have many antidepressants, antipsychotics, hypnotic medications and the like. But their popularity masks two serious problems. First, each of these drug classes is filled with “me too” drugs, which are essentially just copies of one another; we have six S.S.R.I. antidepressants that essentially do the same thing, and likewise for the 10 new atypical antipsychotic drugs. Second, the available drugs leave a lot to be desired: patients with illnesses like schizophrenia, major depression and bipolar disorder often fail to respond adequately to these medications or cannot tolerate their side effects. Yet even though 25 percent of Americans suffer from a diagnosable mental illness in any year, there are few signs of innovation from the major drug makers. After a series of failed clinical trials in which novel antidepressants and antipsychotics did little or no better than placebos, the companies seem to have concluded that developing new psychiatric drugs is too risky and too expensive. This trend was obvious at the 2011 meeting of the American Society for Clinical Pharmacology and Therapeutics, where only 13 of 300 abstracts related to psychopharmacology and none related to novel drugs. Instead, they are spending most of their research dollars on illnesses like cancer, heart disease and diabetes, which have well-defined biological markers and are easier to study than mental disorders. © 2013 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: 18531 - Posted: 08.20.2013

What if a psychiatrist could tell whether someone was about to commit suicide simply by taking a sample of their blood? That’s the promise of new research, which finds increased amounts of a particular protein in the bloodstream of those contemplating killing themselves. The test was conducted on only a few people, however, and given that such “biomarkers” often prove unreliable in the long run, it’s far from ready for clinical use. Suicide isn’t like a heart attack. People typically don’t reveal early symptoms to their doctor—morbid thoughts, for example, instead of chest pain—and there’s no equivalent of a cholesterol or high blood pressure test to identify those at most risk of killing themselves. "We are dealing with something more complex and less accessible," says Alexander Niculescu III, a psychiatrist at the Indiana University School of Medicine in Indianapolis. So some researchers are eager to find physical signs, called biomarkers, that can be measured in the bloodstream to signal when a person is at a high likelihood of committing suicide. Over the past decade, Niculescu and his colleagues have been refining a method for identifying biomarkers that can distinguish psychological states. The technique depends on blood samples taken from individuals in different mental states over time—for example, from people with bipolar disorder as they swing between the disorder’s characteristic high and low moods. The researchers test those samples for differences in the activity, or expression, of genes for of different proteins. After screening the blood samples, the scientists “score” a list of candidate biomarker genes by searching for related results in a large database of studies by other groups using a program that Niculescu compares to the Google page-ranking algorithm. In previous published studies, Niculescu and other groups have used the technique to probe for biomarkers in disorders such as bipolar disorder, psychosis, and alcoholism. © 2012 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: Biological Basis of Behavioral Disorders
Link ID: 18530 - Posted: 08.20.2013

By RONI CARYN RABIN Over the past two decades, the use of antidepressants has skyrocketed. One in 10 Americans now takes an antidepressant medication; among women in their 40s and 50s, the figure is one in four. Experts have offered numerous reasons. Depression is common, and economic struggles have added to our stress and anxiety. Television ads promote antidepressants, and insurance plans usually cover them, even while limiting talk therapy. But a recent study suggests another explanation: that the condition is being overdiagnosed on a remarkable scale. The study, published in April in the journal Psychotherapy and Psychosomatics, found that nearly two-thirds of a sample of more than 5,000 patients who had been given a diagnosis of depression within the previous 12 months did not meet the criteria for major depressive episode as described by the psychiatrists’ bible, the Diagnostic and Statistical Manual of Mental Disorders (or D.S.M.). The study is not the first to find that patients frequently get “false positive” diagnoses for depression. Several earlier review studies have reported that diagnostic accuracy is low in general practice offices, in large part because serious depression is so rare in that setting. Elderly patients were most likely to be misdiagnosed, the latest study found. Six out of seven patients age 65 and older who had been given a diagnosis of depression did not fit the criteria. More educated patients and those in poor health were less likely to receive an inaccurate diagnosis. 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: 18499 - Posted: 08.13.2013

By D. D. GUTTENPLAN LONDON — With its battered desks, fluorescent lights and interactive whiteboard showing an odd creature that, depending on how you look at it, could be either a duck or a rabbit, this could be a class in any university philosophy department. But this is a class with a difference. It is the Maudsley Philosophy Group, a seminar that meets regularly on the grounds of the Maudsley Hospital, Britain’s largest mental health teaching hospital, which is affiliated with the Institute of Psychiatry at King’s College London. Participants at the last session included psychiatrists, psychologists, philosophers and an actor who had just finished working as a chaplain in a locked men’s ward at the hospital and who was about to organize a storytelling group there. “We started out as a reading group for trainee psychiatrists,” said Gareth S. Owen, a researcher at the Institute of Psychiatry who co-founded the group in 2002. “Then, gradually, we developed and started inviting philosophers — at first it was quite low key. We would talk about our clinical experiences and then they would relate those experiences to their way of thinking.” Robert Harland, another co-founder of the group, said he had known Dr. Owen since they “cut up a corpse together at medical school.” “The analytic philosophers brought a real clarity to our discussions,” Dr. Harland said. “We were looking at various models to help us understand what we were doing as psychiatrists. “There is lots of applied science now in psychiatry: neuroimaging, genetics, epidemiology. But they don’t have much to say about sitting with a patient and trying to understand that person’s experiences.” © 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 1: Biological Psychology: Scope and Outlook
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 1: An Introduction to Brain and Behavior
Link ID: 18489 - Posted: 08.12.2013

Women living in urban centres in Canada with more than 500,000 inhabitants are at higher risk of postpartum depression than women in other areas, suggests a new study in the Canadian Medical Association Journal. Looking at the experiences of over 6,000 women who lived in rural, semi-rural, semi-urban or urban areas from the 2006 Canadian Maternity Experiences Survey, the study suggests that women in urban areas were at higher risk, with almost 10 per cent reporting postpartum depression compared with six per cent of women in rural areas, almost seven per cent of women in semirural areas and about five per cent in semiurban areas. Urban areas were found to have higher numbers of immigrant populations, and more women in these areas reported lower levels of social support during and after pregnancy. "We found that Canadian women who lived in large urban areas … were at higher risk of postpartum depression than women living in other areas," said Dr. Simone Vigod, psychiatrist at Women's College Hospital and scientist at Women's College Research Institute in Toronto. "The risk factors for postpartum depression [including history of depression, social support and immigration status] that were unequally distributed across geographic regions accounted for most of the variance in the rates of postpartum depression." The reason why immigrant woman appear to be at higher risk is not really known, she said. "Some theories are that it's related to social support or being away from their family." They could also have cultural barriers or needs that are not being met, she added. © 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: 18467 - Posted: 08.07.2013

By Scicurious Most current treatments for depression target the serotonin system, a chemical messenger that plays a role in mood (though it also plays a role in many, many other things). Most of the antidepressant drugs on the market (such as Prozac, Celexa, and Zoloft) that target serotonin do it by blocking the recycling of serotonin, keeping it in the spaces between neurons and allowing it to be active for far longer than it might otherwise. The problem is, these drugs take a long time to work. Often many weeks. In that time, patients may grow frustrated as side effects happen and the needed effects don’t. Patients may be in very desperate straights when they first go on medication, and any extra time before the drugs work becomes that much more dangerous. The drugs may not work at all, causing doctors and patients to have to go through the entire, weeks long process over and over again. Scientists are looking for new antidepressant mechanisms, and trying to create more effective drugs. But there are various ways to go about it. You can go looking for an entirely new way of working, but you can also look at ways to make the current drugs work faster. One target that might help antidepressant drugs work faster is one of the many receptors for serotonin, the 5-HT1A receptor. Receptors are proteins that sit on cell surfaces, and bind chemicals. When they bind a chemical, they cause change, maybe by opening a channel, or starting a signal to make a neuron fire more, or less. What a receptor does depends on its type, but also where in the brain it is located and on what type of cell. © 2013 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: 18463 - Posted: 08.06.2013

Trevor Stokes Reuters Talk therapy may be a helpful supplemental treatment for people with depression who have not responded to medication, a new study from the United Kingdom suggests. Researchers found that people with depression who had not improved despite taking antidepressants were three times more likely to experience a reduction in their depression symptoms if talk therapy was added to their treatment regimen compared with those who continued to take only antidepressants. The study is one of the first large trials to test the effectiveness of talk therapy given in tandem with antidepressants, the researchers said. Up to two-thirds of people with depression don’t respond fully to antidepressant treatment, and the findings suggest a way to help this group, the researchers said. “Until now, there was little evidence to help clinicians choose the best next step treatment for those patients whose symptoms do not respond to standard drug treatments," study researcher Nicola Wiles of the University of Bristol's Centre for Mental Health, Addiction and Suicide Research said in a statement. The study followed patients for one year. Future studies should examine the effectiveness of this treatment combination over the long term, as patients with depression can relapse after treatment, the researchers said.

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: 18375 - Posted: 07.15.2013

By JAN HOFFMAN From the shock of the cancer diagnosis onward, depression can take its well-documented toll on patients. Even patients who appear to pack away their fears during the grinding treatment journey to becoming cancer-free concede that when the regimen ends, they unspool emotionally. There has been less attention paid to the disease’s emotional impact on spouses. They, too, can become depressed. But with the roles of caregiver and cheerleader thrust upon them, they may feel constrained about expressing their darker feelings. Now a new analysis finds that within two years of a cancer diagnosis, the pervasiveness of depression in patients and their spouses tends to drop back to roughly the same levels as in the general population, only to be replaced by another mind-demon: anxiety, which can even intensify as time passes. 48 Were you a caretaker for someone with cancer? How did you take care of yourself while your partner was going through treatment? Join in the discussion below. The analysis, which looked at 43 studies involving 51,381 patients with a range of cancers, found that over all, nearly 18 percent of patients experienced serious anxiety two to 10 years after their diagnosis, compared with about 14 percent of the general population. But in a cluster of studies that looked at couples, anxiety levels in that time frame grew to as high as 28 percent in patients and 40 percent in their spouses. Copyright 2013 The New York Times Company

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: 18372 - Posted: 07.13.2013

By NICHOLAS BAKALAR Using functional magnetic resonance imaging, researchers have found brain changes in preschool-age children with depression that are not apparent in their nondepressed peers. The study, in the July issue of The Journal of the American Academy of Child & Adolescent Psychiatry, examined 23 children 4 to 6 years old who had been diagnosed with depression and 31 of their healthy peers. Researchers used well-validated tests to diagnose depression, and eliminated from the study children with neurological disorders, autism or developmental disorders, or who had been born prematurely. None of the subjects was taking antidepressants. The children underwent M.R.I. brain scans while viewing pictures of happy, sad, fearful or neutral faces. The researchers found that right amygdala and right thalamus activity was significantly greater in the depressed children than in the others, a finding that has also been observed in depressed adolescents and adults. “We found something in the brain that is aligned with the idea of neurobiological models of depression — which parts of the brain are involved and how they interact,” said the lead author, Michael S. Gaffrey, an assistant professor in the department of psychiatry at Washington University in St. Louis. “We can begin to use this information in conjunction with other information — symptoms, other biological markers — to identify and eventually prevent and treat this disorder.” Copyright 2013 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: 18371 - Posted: 07.13.2013

By Bruce Bower A surprisingly simple decision-making tool shows promise as a way for physicians to identify people with depression. An answer to the first of four questions was all that researchers usually needed to identify women who weren’t depressed, say psychologist Mirjam Jenny of the Max Planck Institute for Human Development in Berlin and her colleagues. Using all four questions, this tool spotted depressed women about as well as two more-complex methods, Jenny’s team reports June 24 in the Journal of Applied Research in Memory and Cognition. If the findings hold up in other studies, physicians and other professionals with no mental-health training could use this brief technique to tag individuals who need thorough depression evaluations. “This decision tree can be used to screen for depression, but not to reach a final diagnosis,” Jenny says. Her team drew on data from 1,382 German women who completed a 21-item screening questionnaire for depression on two occasions, separated by 18 months. Based on this measure, depression initially affected 3.6 percent of the sample, or 50 individuals, and later appeared in 1.9 percent of the sample, or 26 individuals. Women’s initial responses to a handful of items that best predicted whether they would rank as depressed 18 months later were used to create a four-question decision tree. The first question in the tree — “Have you cried more than usual in the last week?” — led the pack in identifying cases of depression. A “no” response to this or any of the other three questions — which inquired about feelings in the last week of disappointment or self-hate, discouragement about the future and personal failure — exempted women from being categorized as depressed. Those who responded “yes” to all four questions were classified as depressed. © Society for Science & the Public 2000 - 2013

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: 18370 - Posted: 07.13.2013

By RONI CARYN RABIN Martha Rhodes experienced her first bout of depression at 13. By her late 50s, she had taken just about every antidepressant there is, including Zoloft, Lexapro and Paxil — which did the trick for many years, but had side effects — then Effexor, Lamictal, Seroquel and Abilify. After a suicide attempt in 2009, she tried something radically different: transcranial magnetic stimulation, or TMS, a treatment in which magnetic pulses are used to stimulate parts of the brain believed to be involved in mood regulation. Unlike electroconvulsive or shock therapy, which is also used to treat stubborn depression, TMS does not generally produce seizures. Every day, she spent just over half an hour in a chair with a powerful magnet affixed to the front left side of her head. After four weeks, “I woke up and something was different,” said Mrs. Rhodes, who wrote a book, “3,000 Pulses Later” describing the treatment. “I felt lighter. I didn’t wake up in the morning and wish I were dead.” For Mrs. Rhodes, 63, a former advertising executive in Danbury, Conn., TMS treatment was transformative, and she no longer needs antidepressants. But there are still many questions about just how many severely depressed patients respond to TMS, which requires daily office visits for several weeks, costs thousands of dollars and is often not covered by insurance. For the therapy, patients sit in a doctor’s office with a large magnet pressed to the left side of their heads. The idea is that a pulsed magnetic field, similar to that used in M.R.I.’s, creates an electrical current in the surface of the brain that “resets” the patient’s mood regulatory system. 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: 18337 - Posted: 07.02.2013

By DAVID DOBBS On average, about 700 Americans kill themselves each week — but in the fine-weather weeks of May and June, the toll rises closer to 800, sometimes higher. Every year, suicide peaks with the tulips and lilacs — increasing roughly 15 percent over the annual average to create one of psychiatry’s most consistent epidemiological patterns. It may seem perverse that the period of spring and early summer, as the psychologist Kay Redfield Jamison puts it in her splendid book “Night Falls Fast,” should contain “a capacity for self-murder that winter less often has.” Yet it does. This grim spring growth confounds conventional belief that suicides peak in winter. It also confounds researchers — and fascinates them. As they discover more angles into the biology of mood and behavior, they are finding new clues about why suicides rise with the sun’s arc. They hope solving this puzzle will help us better understand why people commit suicide at all — and perhaps reduce the numbers year-round. This effort takes an extra urgency from what Dr. Adam Kaplin, a psychiatrist at Johns Hopkins University, calls a “suicide epidemic” — a sharp increase in both absolute and per-capita rates since the recession that began in 2007, particularly among the middle-aged. More than 38,000 people committed suicide in the United States in 2010 — a 16.5 percent jump from the 32,600 suicides five years before, and a new high. The stakes involved in figuring out the dynamics of self-murder seem only to rise with time. The spring surge in suicides is actually the largest of a few oscillations throughout the year. After dropping to an annual low in February (October in the southern hemisphere), rates climb sharply through spring; fall slowly in summer; show a slight rise, according to some studies, in fall; and then begin a steep winter drop. The spring peak generally runs 10 to 25 percent above the yearly average and 20 to 50 percent above the February low. Copyright 2013 The New York Times Company

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: 18308 - Posted: 06.25.2013

By Bruce Bower To a cacophony of boos, so-whats and even a few cheers, the American Psychiatric Association released the fifth edition of its Diagnostic and Statistical Manual of Mental Disorders, DSM-5, on May 18 at its annual meeting in San Francisco. Controversy always flares when psychiatrists redefine which forms of human suffering will count as real and reimbursable by medical insurance. This time, though, the stakes are raised by competing efforts to classify mental disorders. The World Health Organization plans to release a new version of its own system for identifying mental ailments in 2015 as part of the 11th edition of the International Classification of Diseases. It’s not clear how much the ICD will mirror DSM-5. Some differences have already emerged. Clinicians working on the international classification report in the May 11 Lancet that they plan to pare down the number and types of symptoms needed to diagnose post-traumatic stress disorder, or PTSD, and add a severe form of the condition triggered by long-lasting or frequent harrowing events. These departures from DSM-5 would make it easier for mental health workers to help victims of conflict and natural disasters in poor, non-Western countries, say psychologist Andreas Maercker of the University of Zurich and his colleagues. Meanwhile, the National Institute of Mental Health in Rockville, Md., has launched the Research Domain Criteria, or RDoC, a 10-year effort to define mental disorders based on behavioral and brain measures. DSM’s approach, by contrast, relies on rulings by groups of psychiatrists about which symptoms characterize particular disorders. The approach has yielded imprecise diagnostic labels that advance neither treatment nor research, argued psychiatrist and NIMH director Thomas Insel in an April 29 blog post. © Society for Science & the Public 2000 - 2013

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: 18276 - Posted: 06.15.2013

by Jennifer Couzin-Frankel Publish your data, or else we will—that's the stark warning to drug companies in a new proposal released today. Peter Doshi (shown right), a postdoctoral fellow at Johns Hopkins University in Baltimore, Maryland, and his colleagues are fed up that only about half of all clinical trials are published. They want to change that, by convincing researchers and journals to print data that have been publicly released through other means, such as litigation and Freedom of Information Act requests, but, practically speaking, are sitting dormant in the filing cabinets or computers of individual scientists. The unusual proposal is called RIAT, for Restoring Invisible and Abandoned Trials. It was published today in BMJ and also endorsed by PLOS Medicine. Doshi, who studies comparative effectiveness research, came up with the idea when his colleague, Swaroop Vedula, was analyzing reporting biases involving the drug gabapentin. Gabapentin's maker Pfizer had been sued for the way in which they marketed the drug for unapproved indications. During litigation, Pfizer had released thousands of pages involving gabapentin trials, and Vedula was poring through them. (One of the authors of the RIAT paper, Kay Dickersin, served as an expert witness against Pfizer in gabapentin litigation.) Pfizer had published only 12 of its 20 trials in gabapentin. But Doshi's center at Hopkins had the clinical study reports detailing the results of the other eight. At the time, "it just hits me," Doshi says. "Why are we still referring to these as unpublished trials? Why aren't we publishing them ourselves?" © 2010 American Association for the Advancement of Science

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: 18275 - Posted: 06.15.2013

Alison Abbott A simple brain scan may offer a way to predict which people being treated for depression will respond to drugs, and which will respond to cognitive behavioural therapy. Neurologist Helen Mayberg from Emory University in Atlanta, Georgia, and her colleagues have run the first systematic, well-controlled study to identify the first potential biomarker that distinguishes between treatment responses. The work is published in JAMA Psychiatry1. Psychiatrists are desperate for such biomarkers, because fewer than 40% of people with depression go into remission after initial treatment. “It could be fabulous,” says Steven Zalcman, chief of clinical neuroscience research at the US National Institute of Mental Health (NIMH) in Bethesda, Maryland. But he cautions that the brain-scan biomarker still has to be validated in further trials — a process that could take a couple of years. Mayberg and her colleagues selected 82 people with untreated depression, and measured glucose metabolism in their brains using positron emission tomography (PET) scans. They then randomly assigned the subjects to treatment groups. One group received the common antidepressant drug escitalopram oxalate (a selective serotonin reuptake inhibitor, or SSRI) for 12 weeks. The other group received 16 sessions of cognitive behavioural therapy over the same period. © 2013 Nature Publishing Group

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: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 18269 - Posted: 06.13.2013

Comedian and writer Ruby Wax, a regular on British television, has clinical depression. In her book published last week, Sane New World (Hodder & Stoughton, 2013), she describes her struggles with different therapies and her fear of being ‘found out’. She is not alone. A 2010 survey in Europe revealed that 38% of people had a diagnosed mental disorder — including 7% with major depression. The proportion is likely to be similar in all populations, even in Africa, where psychiatric disease barely features on the health agenda. The stigma attached to such disorders means that many people do not admit to their illness. The same stigma discourages investment, so that research funding is not proportional to the distress these disorders cause. Why lobby for better treatments for depression or schizophrenia when there are ‘real’ diseases out there, such as cancer? Wax has been through the catalogue of available therapies and says that she has settled on an approach known as ‘mindfulness’, which helps to keep her depression under control. It may seem that the various therapies are inadequate, given that initial treatment of depression fails in 60% or more of cases. It is true that more treatment options are badly needed. Yet evidence-based cognitive behavioural therapies and drugs already developed by the pharmaceutical industry can work splendidly for long periods — if they are given to the right patients. How do you recognize the right patients? Treatment decisions tend to be based on the preferences of physicians or their patients, often with a missionary zeal that gives no credence to the idea that a personalized approach would be more appropriate. © 2013 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: 18268 - Posted: 06.13.2013