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Mind over matter. New research explains how abstract benefits of exercise—from reversing depression to fighting cognitive decline—might arise from a group of key molecules. While our muscles pump iron, our cells pump out something else: molecules that help maintain a healthy brain. But scientists have struggled to account for the well-known mental benefits of exercise, from counteracting depression and aging to fighting Alzheimer’s and Parkinson’s disease. Now, a research team may have finally found a molecular link between a workout and a healthy brain. Much exercise research focuses on the parts of our body that do the heavy lifting. Muscle cells ramp up production of a protein called FNDC5 during a workout. A fragment of this protein, known as irisin, gets lopped off and released into the bloodstream, where it drives the formation of brown fat cells, thought to protect against diseases such as diabetes and obesity. (White fat cells are traditionally the villains.) While studying the effects of FNDC5 in muscles, cellular biologist Bruce Spiegelman of Harvard Medical School in Boston happened upon some startling results: Mice that did not produce a so-called co-activator of FNDC5 production, known as PGC-1α, were hyperactive and had tiny holes in certain parts of their brains. Other studies showed that FNDC5 and PGC-1α are present in the brain, not just the muscles, and that both might play a role in the development of neurons. © 2013 American Association for the Advancement of Science.

Related chapters from BP7e: Chapter 11: Motor Control and Plasticity; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 5: The Sensorimotor System; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18781 - Posted: 10.12.2013

Children whose mothers are depressed during pregnancy have a small increased risk of depression in adulthood, according to a UK study. Medical treatment during pregnancy could lower the risk of future mental health problems in the child, say researchers at Bristol University. The study followed the offspring of more than 8,000 mothers who had postnatal or antenatal depression. The risk is around 1.3 times higher than normal at age 18, it found. The study is published in JAMA Psychiatry. Lead researcher Dr Rebecca Pearson told the BBC: "Depression in pregnancy should be taken seriously and treated in pregnancy. It looks like there is a long-term risk to the child, although it is small." She said it was an association, not a causal link, and needed further investigation. Prof Carmine Pariante of King's College London's Institute of Psychiatry said the development of an individual's mental health did not start at birth but in the uterus. "The message is clear - helping women who are depressed in pregnancy will not only alleviate their suffering but also the suffering of the next generation." Prof Celso Arango of Gregorio Maranon General University Hospital, Madrid, said stress hormones may affect the child's development in the womb. "Women with depression would ideally be treated before getting pregnant, but if they are already pregnant when diagnosed with depression it is even more important that they are treated as it will impact on the mother and child." The researchers think different factors may be involved in antenatal and postnatal depression, with environmental factors such as social support having a bigger impact in postnatal depression. BBC © 2013

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: 18777 - Posted: 10.12.2013

by Linda Geddes There's little doubt that smoking during pregnancy is bad for the baby. But besides stunting growth and boosting the risk of premature birth, it seems that tobacco smoke leaves a lasting legacy on the brain. Children whose mothers smoked during pregnancy have altered brain growth, which may put them at greater risk of anxiety and depression. Hanan El Marroun at Erasmus Medical Center in Rotterdam, the Netherlands, and her colleagues had previously seen impaired brain growth in babies born to women who smoked throughout their pregnancy, although no differences were seen if women stopped smoking soon after learning that they were pregnant. The question was whether these changes were permanent, or would correct themselves as the child developed. So El Marroun's team used MRI to look at the brains of 113 children aged between 6 and 8 years old whose mothers smoked during pregnancy, and another 113 children whose mums did not. The children's behavioural and emotional functioning was also tested. Depression link Those whose mothers smoked throughout pregnancy had smaller total brain volumes and reduced amounts of grey and white matter in the superior frontal cortex, an area involved in regulating moods. What's more, these structural differences correlated with symptoms of depression and anxiety in the children. Not every child whose mother smoked showed these symptoms, and the study could not definitively prove cause and effect. However, because we already know that smoking is bad for babies, pregnant women should continue to be advised not to smoke, El Marroun says. © Copyright Reed Business Information Ltd.

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: 18760 - Posted: 10.08.2013

By Gary Stix Psychological depression is more than an emotional state. Good evidence for that comes from emerging new uses for a technology already widely prescribed for Parkinson’s patients. The more neurologists and surgeons learn about the aptly named deep brain stimulation, the more they are convinced that the currents from the technology’s implanted electrodes can literally reboot brain circuits involved with the mood disorder. Thomas Schlaepfer, a psychiatrist from the University of Bonn Hospital and a leading expert in researching deep brain stimulation, describes in the interview that follows the workings of the technique and why it may help the severely depressed. Can you explain what deep brain stimulation is and what it is currently used for? Deep brain stimulation refers to the implantation of very small electrodes in both hemispheres of the brain, which are connected to a neurostimulator, usually placed under the skin on the right chest. This device is in size and function very similar to a heart pacemaker. It allows stimulations of different pulse width and frequency. Depending on the chosen stimulation parameters the electrodes in the brain are able to “neuromodulate” – to reversibly alter the function – of the surrounding brain tissue. Deep brain stimulation has gained widespread acceptance as a successful treatment for tremor associated with Parkinson’s disease. More than 80,000 patients worldwide have been treated with this method. Some see deep brain stimulation as a much less invasive and fully reversibly alternative to historical neurosurgical interventions, which require tiny amounts of brain tissue to be destroyed in order to have clinical effects. © 2013 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: 18747 - Posted: 10.05.2013

By NICHOLAS BAKALAR Depression may be an independent risk factor for Parkinson’s disease, a new study has found. In a retrospective analysis, researchers followed 4,634 patients with depression and 18,544 matched controls for 10 years. To rule out the possibility that depression is an early symptom of Parkinson’s disease, their analysis excluded patients who received a diagnosis of depression within five years of their Parkinson’s diagnosis. The average age of people with depression was 41, while it was 64 for those with both depression and Parkinson’s. The study, published online in Neurology, found that 66 patients with depression, or 1.42 percent, developed Parkinson’s disease, compared with 97, or 0.52 percent, among those who were not depressed. After controlling for age, sex, diabetes, hypertension and other factors, the researchers found clinical depression was associated with more than three times the risk for Parkinson’s disease. “Our paper does not convey the message that all depression leads to Parkinson’s disease,” said the senior author, Dr. Albert C. Yang, a professor of psychiatry at the National Yang-Ming University in Taiwan. “But particularly the depressed elderly and those with difficult-to-treat depression should be alert to the possibility of neurological disease and Parkinson’s.” Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 18735 - Posted: 10.03.2013

By Travis Riddle Humans like being around other humans. We are extraordinarily social animals. In fact, we are so social, that simply interacting with other people has been shown to be use similar brain areas as those involved with the processing of very basic rewards such as food, suggesting that interacting with people tends to make us feel good. However, it doesn’t take much reflection to notice that the way people interact with each other has radically changed in recent years. Much of our contact happens not face-to-face, but rather while staring at screen-based digital representations of each other, with Facebook being the most prominent example. This raises a very fundamental question – how does online interaction with other people differ from interacting with people in person? One possible way these two interaction styles might differ is through how rewarding we find them to be. Does interacting with Facebook make us feel good as does interacting with people in real life? A recent paper suggests that the answer is “probably not.” In fact, the data from this paper suggest that the more we interact with Facebook, the worse we tend to feel. Researchers recruited participants from around a college campus. The participants initially completed a set of questionnaires, including one measuring their overall satisfaction with life. Following this, participants were sent text messages 5 times a day for two weeks. For each text, participants were asked to respond to several questions, including how good they felt at that moment, as well as how much they had used Facebook, and how much they had experienced direct interaction with others, since the last text. At the end of the two weeks, participants completed a second round of questionnaires. Here, the researchers once again measured participants’ overall satisfaction with life. © 2013 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: 18734 - Posted: 10.02.2013

By BRANDON A. GAUDIANO PROVIDENCE, R.I. — PSYCHOTHERAPY is in decline. In the United States, from 1998 to 2007, the number of patients in outpatient mental health facilities receiving psychotherapy alone fell by 34 percent, while the number receiving medication alone increased by 23 percent. This is not necessarily for a lack of interest. A recent analysis of 33 studies found that patients expressed a three-times-greater preference for psychotherapy over medications. As well they should: for patients with the most common conditions, like depression and anxiety, empirically supported psychotherapies — that is, those shown to be safe and effective in randomized controlled trials — are indeed the best treatments of first choice. Medications, because of their potential side effects, should in most cases be considered only if therapy either doesn’t work well or if the patient isn’t willing to try counseling. So what explains the gap between what people might prefer and benefit from, and what they get? The answer is that psychotherapy has an image problem. Primary care physicians, insurers, policy makers, the public and even many therapists are largely unaware of the high level of research support that psychotherapy has. The situation is exacerbated by an assumption of greater scientific rigor in the biologically based practices of the pharmaceutical industries — industries that, not incidentally, also have the money to aggressively market and lobby for those practices. For the sake of patients and the health care system itself, psychotherapy needs to overhaul its image, more aggressively embracing, formalizing and promoting its empirically supported methods. My colleague Ivan W. Miller and I recently surveyed the empirical literature on psychotherapy in a series of papers we edited for the November edition of the journal Clinical Psychology Review. It is clear that a variety of therapies have strong evidentiary support, including cognitive-behavioral, mindfulness, interpersonal, family and even brief psychodynamic therapies (e.g., 20 sessions). © 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: 18722 - Posted: 09.30.2013

By REED ABELSON THE first time Melissa Morelli was taken to the hospital, she was suicidal and cutting herself, her mother says. She was just 13, and she had been transferred to a psychiatric hospital, where she stayed for more than a week. Her doctors told her mother, Cathy Morelli, that it was not safe for Melissa to go home. But the family’s health insurance carrier would not continue to pay for her to remain in the hospital. The second time, the same thing happened. And the third and the fourth. Over the course of five months, Ms. Morelli took Melissa to the hospital roughly a dozen times, and each time the insurance company, Anthem Blue Cross, refused to pay for hospital care. “It was just a revolving door,” Ms. Morelli said. “You had not been getting better in a significant way,” Anthem explained in one letter sent directly to Melissa, then 14, in July 2012. “It does not seem likely that doing the same thing will help you get better.” Desperate to get help for her daughter, Ms. Morelli sought the assistance of Connecticut state officials and an outside reviewer. She eventually won all her appeals, and Anthem was forced to pay for the care it initially denied. All told, Melissa spent nearly 10 months in a hospital; she is now at home. Anthem, which would not comment on Melissa’s case, says its coverage decisions are based on medical evidence. Melissa’s treatment did not come cheap: it ultimately cost hundreds of thousands of dollars, Ms. Morelli said. Patients often find themselves at odds with health insurers, but the battles are perhaps nowhere so heated as with the treatment of serious mental illness. © 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: 18710 - Posted: 09.28.2013

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