Links for Keyword: Depression

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By BENEDICT CAREY Curing insomnia in people with depression could double their chance of a full recovery, scientists are reporting. The findings, based on an insomnia treatment that uses talk therapy rather than drugs, are the first to emerge from a series of closely watched studies of sleep and depression to be released in the coming year. A student demonstrating equipment at Colleen Carney’s sleep lab at Ryerson University. Dr. Carney is the lead author of a new report about the effects of insomnia treatment on depression. The new report affirms the results of a smaller pilot study, giving scientists confidence that the effects of the insomnia treatment are real. If the figures continue to hold up, the advance will be the most significant in the treatment of depression since the introduction of Prozac in 1987. Depression is the most common mental disorder, affecting some 18 million Americans in any given year, according to government figures, and more than half of them also have insomnia. Experts familiar with the new report said that the results were plausible and that if supported by other studies, they should lead to major changes in treatment. “It would be an absolute boon to the field,” said Dr. Nada L. Stotland, professor of psychiatry at Rush Medical College in Chicago, who was not connected with the latest research. “It makes good common sense clinically,” she continued. “If you have a depression, you’re often awake all night, it’s extremely lonely, it’s dark, you’re aware every moment that the world around you is sleeping, every concern you have is magnified.” The study is the first of four on sleep and depression nearing completion, all financed by the National Institute of Mental Health. They are evaluating a type of talk therapy for insomnia that is cheap, relatively brief and usually effective, but not currently a part of standard treatment. © 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: 18945 - Posted: 11.19.2013

By Julianne Chiaet Kate wanted to die. She remembers the moment the psychiatrist said “the antidepressant isn’t going to work right away. Can you promise to be here next week and not kill yourself?” “I told her no,” Kate says. “I couldn’t promise my doctor I’d make it a week. That’s how bad my life had to be before I got help. When you’re struggling to stay alive every single day, and then your doctor tells you it’s going to take two to six weeks before the medications they give you are going to work, it’s devastating.” To make matters worse, after those weeks, the drug didn’t work. Kate went through five different anti-depressants over the course of six months before confirming that none of them worked. The debilitating disorder kept her out of school for extended periods of time. The National Center for Health Statistics estimates more than 1 in 10 Americans over the age of 12 took antidepressants between 2005 and 2008, the last time period for which the data are available. The rate of antidepressant use increased 400 percent from 1998 to 2008. Traditional antidepressants go after serotonin neurotransmitters, which sit in the membrane of the brain. Some antidepressants also target norepinephrine and dopamine. The drug keeps the transmitters from performing their normal function of transporting serotonin from the outside to the inside of the brain cells. People with depression have a normal amount of serotonin inside of their brain cells, however they have an insufficient amount on the outside of their cells. Thus by inhibiting the transmitter, the drug blocks the transportation of serotonin being taken into the cell, thus building up the serotonin outside of the 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: 18919 - Posted: 11.13.2013

By Michelle Roberts Health editor, BBC News online Depression can make us physically older by speeding up the ageing process in our cells, according to a study. Lab tests showed cells looked biologically older in people who were severely depressed or who had been in the past. These visible differences in a measure of cell ageing called telomere length couldn't be explained by other factors, such as whether a person smoked. The findings, in more than 2,000 people, appear in Molecular Psychiatry. Experts already know that people with major depression are at increased risk of age-related diseases such as cancer, diabetes, obesity and heart disease. This might be partly down to unhealthy lifestyle behaviours such as alcohol use and physical inactivity. But scientists suspect depression takes its own toll on our cells. To investigate, Josine Verhoeven from the VU University Medical Centre in the Netherlands, along with colleagues from the US, recruited 2,407 people to take part in the study. More than one third of the volunteers were currently depressed, a third had experienced major depression in the past and the rest had never been depressed. The volunteers were asked to give a blood sample for the researchers to analyse in the lab for signs of cellular ageing. The researchers were looking for changes in structures deep inside cells called telomeres. BBC © 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: 18913 - Posted: 11.12.2013

By JACKIE CALMES and ROBERT PEAR WASHINGTON — The Obama administration on Friday will complete a generation-long effort to require insurers to cover care for mental health and addiction just like physical illnesses when it issues long-awaited regulations defining parity in benefits and treatment. The rules, which will apply to almost all forms of insurance, will have far-reaching consequences for many Americans. In the White House, the regulations are also seen as critical to President Obama’s program for curbing gun violence by addressing an issue on which there is bipartisan agreement: Making treatment more available to those with mental illness could reduce killings, including mass murders. In issuing the regulations, senior officials said, the administration will have acted on all 23 executive actions that the president and Vice President Joseph R. Biden Jr. announced early this year to reduce gun crimes after the Newtown, Conn., school massacre. In planning those actions, the administration anticipated that gun control legislation would fail in Congress as pressure from the gun lobby proved longer-lasting than the national trauma over the killings of first graders and their caretakers last Dec. 14. “We feel actually like we’ve made a lot of progress on mental health as a result in this year, and this is kind of the big one,” said a senior administration official, one of several who described the outlines of the regulations that Kathleen Sebelius, the secretary of health and human services, will announce at a mental health conference on Friday in Atlanta with the former first lady Rosalynn Carter. While laws and regulations dating to 1996 took initial steps in requiring insurance parity for medical and mental health, “here we’re doing full parity, and we’ve also taken steps to extend it to the people covered in the Affordable Care Act,” the senior official said. “This is kind of the final word on parity.” © 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: 18901 - Posted: 11.09.2013

By Helen Briggs BBC News Depression is the second most common cause of disability worldwide after back pain, according to a review of research. The disease must be treated as a global public health priority, experts report in the journal PLOS Medicine. The study compared clinical depression with more than 200 other diseases and injuries as a cause of disability. Globally, only a small proportion of patients have access to treatment, the World Health Organization says. Depression was ranked at number two as a global cause of disability, but its impact varied in different countries and regions. For example, rates of major depression were highest in Afghanistan and lowest in Japan. In the UK, depression was ranked at number three in terms of years lived with a disability. Dr Alize Ferrari from the University of Queensland's School of Population Health led the study. "Depression is a big problem and we definitely need to pay more attention to it than we are now," she told BBC News. "There's still more work to be done in terms of awareness of the disease and also in coming up with successful ways of treating it. "The burden is different between countries, so it tends to be higher in low and middle income countries and lower in high income countries." Policy-makers had made an effort to bring depression to the forefront, but there was a lot more work to be done, she added. BBC © 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: 18883 - Posted: 11.07.2013

By DAN HURLEY This couldn’t possibly be a good idea. On Friday the 13th of September, in an old brick building on 13th Street in Boston’s Charlestown neighborhood, a pair of electrodes was attached to my forehead, one over my brain’s left prefrontal cortex, the other just above my right eye socket. I was about to undergo transcranial direct-current stimulation, or tDCS, an experimental technique for delivering extremely low dose electrical stimulation to the brain. Using less than 1 percent of the electrical energy necessary for electroconvulsive therapy, powered by an ordinary nine-volt battery, tDCS has been shown in hundreds of studies to enhance an astonishing, seemingly implausible variety of intellectual, emotional and movement-related brain functions. And its side effects appear limited to a mild tingling at the site of the electrode, sometimes a slight reddening of the skin, very rarely a headache and certainly no seizures or memory loss. Still, I felt more than a bit apprehensive as I prepared to find out if a little bit of juice could amp up my cognitive reserves and make me, in a word, smarter. With the electrodes in place, J. León Morales-Quezada, senior research associate at Harvard’s Laboratory of Neuromodulation, pressed a button on his computer and I felt . . . absolutely nothing. No pain. No tingling. Not even a little muscle twitching. “Is it on?” I asked. Morales-Quezada assured me it was. For proof, he pointed to a flat-screen on the wall, displaying signals from six electroencephalogram (EEG) monitors also attached to my head. After 10 minutes of charging my brain, he turned on a computerized exercise I was supposed to practice while the current continued flowing. Called an attention-switching task, it’s used by psychologists as a measure of “executive function” or “cognitive control”: the ability to overrule your urges, to ignore distractions and to quickly shift your focus. Young adults generally do better than older people; people with greater overall cognitive abilities generally perform better than those with less. © 2013 The New York Times Company

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: 18870 - Posted: 11.04.2013

by Bethany Brookshire In pharmacology research, it seems like one test is never enough. If you want to test a new antidepressant, reviewers (and good logic) often demand that you use more than one test. A locomotor assay to see whether the new drug depresses or increases how much a mouse moves. A forced swim test or tail suspension test to see how it stacks up against other, known antidepressants. Does it increase swimming? Or climbing? Does it decrease immobility more or less than known antidepressants? You may want to use a chronic mild stress test, which exposes mice over a long period of time to things like mild cold, noise or light to induce stress. Does chronic exposure to your new antidepressant relieve the stress like other antidepressants do? What about responses to things like chronic bullying by other mice? Does it work then? You don’t necessarily need to run all of these tests, but you usually do need to run more than one. After all, what if the drug decreases immobility in a forced swim test, like other antidepressants, but it also makes them race around the room … because it’s cocaine? These are the kind of questions that pharmacologists end up asking. Often, to find new, potential antidepressants, for example, we end up matching them against other, known antidepressants in a series of these tests. If the drug performs well in all of them, doesn’t decrease locomotor activity but keeps the mice swimming and stops them from looking stressed after bullying, we might have something new. © Society for Science & the Public 2000 - 2013.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18859 - Posted: 10.31.2013

By Janet Davison, CBC News Jason Novick has seen the darkness that mental health disorders can create. The 27-year-old Toronto man has also seen how advocacy — by himself and by others — has been vital in helping him cope with bipolar disorder, general anxiety disorder, mania and depression, particular during the stressful transition from his teenage years to leaving home for post-secondary school. "Mental health awareness … is still an issue that’s largely misunderstood," he said in a recent interview. "There’s a lot of [post-secondary] administrative workers and professors and program co-ordinators and what have you who won’t know the first thing about such issues, so your best ally is probably going to be yourself a lot of the time." Another ally can also be a caring friend or family member who steps up to help others understand the larger situation. Novick remembers going with his mother to "set the record straight" with a college professor. They wanted to explain to the instructor that it was his mental health that was his problem, not any lack of interest in the course. "It was my mental health that was causing me to be so withdrawn, that was causing me to be so unmotivated. I was passionate about the subject, but I was not passionate about life and living." Novick, who says he contemplated suicide at one point and has been in closed hospital wards three times because of his disorders, is much more passionate about life and living now, particularly after having completed an inpatient program at the Centre for Addiction and Mental Health in Toronto. © CBC 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: 18842 - Posted: 10.28.2013

By JAMES GORMAN Worldwide, 100,000 people have electrical implants in their brains to treat the involuntary movements associated with Parkinson’s disease, and scientists are experimenting with the technique for depression and other disorders. But today’s so-called deep brain stimulation only treats — it does not monitor its own effectiveness, partly because complex ailments like depression do not have defined biological signatures. The federal Defense Advanced Research Projects Agency, known as Darpa, announced Thursday that it intended to spend more than $70 million over five years to jump to the next level of brain implants, either by improving deep brain stimulation or by developing new technology. Justin Sanchez, Darpa program manager, said that for scientists now, “there is no technology that can acquire signals that can tell them precisely what is going on with the brain.” And so, he said, Darpa is “trying to change the game on how we approach these kinds of problems.” The new program, called Systems-Based Neurotechnology and Understanding for the Treatment of Neuropsychological Illnesses, is part of an Obama administration brain initiative, announced earlier this year, intended to promote innovative basic neuroscience. Participants in the initiative include Darpa, as well as the National Institutes of Health and the National Science Foundation. The announcement of Darpa’s goal is the first indication of how that research agency will participate in the initiative. The money is expected to be divided among different teams, and research proposals are now being sought. Darpa’s project is partly inspired by the needs of combat veterans who suffer from mental and physical conditions, and is the first to invest directly in researching human illness as part of the brain initiative. © 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: 18835 - Posted: 10.26.2013

by Simon Makin A drug similar to ketamine has been shown to work as an antidepressant, without the psychosis-like side effects associated with the party drug. In 2000, ketamine was seen to alleviate depression almost immediately in people for whom other treatments had failed. Larger clinical trials have since corroborated the findings. The drawback is that ketamine can cause hallucinations and other psychotic symptoms, making it unsuitable for use as a treatment. These effects also make it difficult to conduct randomised, placebo-controlled trials – the gold standard in clinical medicine – as it is obvious which participants have been given the drug. This meant that there was a possibility that the beneficial effects seen in previous trials were inflated. So a team led by Gerard Sanacora of Yale University and Mike Quirk of pharmaceutical firm AstraZeneca looked for an alternative compound. They decided to test lanicemine, a drug originally developed to treat epilepsy that targets the same brain receptors as ketamine. The team gave 152 people with moderate-to-severe depression and a history of poor response to antidepressants either lanicemine or a placebo three times a week, for three weeks. They were allowed to continue taking any medications they were already on. Before and after the trial the participants' level of depression was rated on a 60-point scale. After three weeks, those taking lanicemine were less depressed by an average of 13.5 points – 5.5 points better than those who took the placebo. The improvement was still statistically significant up to two weeks after the treatment ended. Dizziness was the only common side effect. © Copyright Reed Business Information Ltd.

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: 18793 - Posted: 10.16.2013

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