Chapter 16. Psychopathology: Biological Basis of Behavior Disorders
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Ian Sample Science editor The risks of heavy cannabis for mental health are serious enough to warrant global public health campaigns, according to international drugs experts who said young people were particularly vulnerable. The warning from scientists in the UK, US, Europe and Australia reflects a growing consensus that frequent use of the drug can increase the risk of psychosis in vulnerable people, and comes as the UN prepares to convene a special session on the global drugs problem for the first time since 1998. The meeting in New York next week aims to unify countries in their efforts to tackle issues around illicit drug use. While the vast majority of people who smoke cannabis will not develop psychotic disorders, those who do can have their lives ruined. Psychosis is defined by hallucinations, delusions and irrational behaviour, and while most patients recover from the episodes, some go on to develop schizophrenia. The risk is higher among patients who continue with heavy cannabis use. Public health warnings over cannabis have been extremely limited because the drug is illegal in most countries, and there are uncertainties over whether it really contributes to mental illness. But many researchers now believe the evidence for harm is strong enough to issue clear warnings. “It’s not sensible to wait for absolute proof that cannabis is a component cause of psychosis,” said Sir Robin Murray, professor of psychiatric research at King’s College London. © 2016 Guardian News and Media Limited
By Amy Ellis Nutt I saw it all: The beginning of Time and the end of Time. Creation and annihilation. Somehow I’d slipped through a seam in the space-time continuum, and from my privileged mental perch I'd peered into the center of the universe. I was exhilarated and drew diagrams of my visions, trying to figure out what it all meant. But when I shared those visions with friends, they were confused and concerned. I was manic, they said, and making no sense. We were at an impasse. Was I sick – or simply in search of myself? Those questions from my own past hovered in the background while I watched two very different documentaries recently. Both explore bipolar illness -- a diagnosis I received more than 25 years ago and one that 5.5 million Americans share. But the films come from very different perspectives. The first, "Ride the Tiger: A Guide Through the Bipolar Brain," was produced by Detroit Public TV and airs on PBS Wednesday. It chronicles the latest in cutting-edge research into bipolar disorder and in doing so firmly plants its flag in the biological camp: The disorder is about misfiring brain circuits, genetic mutations, neurochemical disruptions and other neurological processes not yet delineated. The result is dramatic swings in mood and behavior that affect a person's ability to think clearly. "Ride the Tiger" features appearances by former congressman Patrick Kennedy and the late actress Patty Duke, both of whom talk about their own experiences. The second documentary, "Bipolarized: Re-Thinking Mental Illness," questions the very reality of the disorder -- at least for one former psychiatric patient.
Link ID: 22104 - Posted: 04.14.2016
Scott O. Lilienfeld1*, Katheryn C. Sauvigné2, Steven Jay Lynn3, Robin L. Cautin4, Robert D. Latzman2 and Irwin D. Waldman1 The goal of this article is to promote clear thinking and clear writing among students and teachers of psychological science by curbing terminological misinformation and confusion. To this end, we present a provisional list of 50 commonly used terms in psychology, psychiatry, and allied fields that should be avoided, or at most used sparingly and with explicit caveats. We provide corrective information for students, instructors, and researchers regarding these terms, which we organize for expository purposes into five categories: inaccurate or misleading terms, frequently misused terms, ambiguous terms, oxymorons, and pleonasms. For each term, we (a) explain why it is problematic, (b) delineate one or more examples of its misuse, and (c) when pertinent, offer recommendations for preferable terms. By being more judicious in their use of terminology, psychologists and psychiatrists can foster clearer thinking in their students and the field at large regarding mental phenomena. Scientific thinking necessitates clarity, including clarity in writing (Pinker, 2014). In turn, clarity hinges on accuracy in the use of specialized terminology. Clarity is especially critical in such disciplines as psychology and psychiatry, where most phenomena, such as emotions, personality traits, and mental disorders, are “open concepts.” Open concepts are characterized by fuzzy boundaries, an indefinitely extendable indicator list, and an unclear inner essence (Pap, 1958; Meehl, 1986). © 2007 - 2015 Frontiers Media S.A
Link ID: 22096 - Posted: 04.12.2016
By Nicholas Bakalar Hormone therapy for prostate cancer may increase the risk for depression, a new analysis has found. Hormone therapy, or androgen deprivation therapy, a widely used prostate cancer treatment, aims to reduce levels of testosterone and other male hormones, which helps limit the spread of prostate cancer cells. From 1992 to 2006, researchers studied 78,552 prostate cancer patients older than 65, of whom 33,382 had hormone therapy. Compared with those treated with other therapies, men who received androgen deprivation therapy were 23 percent more likely to receive a diagnosis of depression, and they had a 29 percent increased risk of having inpatient psychiatric treatment. Longer hormone treatment increased the risk: Researchers found a 12 percent increased relative risk with six or fewer months of treatment, a 26 percent increased risk with seven to 11 months, and a 37 percent increased risk with a year or more. The study, in The Journal of Clinical Oncology, is observational, and does not prove causation. The senior author, Dr. Paul L. Nguyen, of Brigham and Women’s Hospital, said that research is finding “almost an avalanche of side effects” with hormone therapy. Still, for some patients, especially those with severe disease, it can be a life saver. “You have to know what the potential upside is. For some guys it will still be worth it, but for some not.” © 2016 The New York Times Company
By Jordana Cepelewicz The brain relies on a system of chemical messengers, known as neurotransmitters, to carry missives from cell to cell. When all is well, these communications enable the brain to coordinate various functions, from complex thought to quick, knee-jerk reactions—but when the system is out of whack, serious disease or disorder can ensue. A team of researchers at the Technical University of Denmark (D.T.U.) and University of Oxford have for the first time identified the molecular structure of dopamine beta-hydroxylase (DBH), the enzyme that controls the conversion between dopamine and norepinephrine, two major neurotransmitters. Understanding the crystal structure of the enzyme could provide an ideal target for drug development. Dopamine and norepinephrine play key roles in many brain functions such as learning, memory, movement and the fight-or-flight response. Imbalances in the levels of these neurotransmitters—and the role DBH plays in regulating them—have been implicated in a wide range of disorders, including hypertension, congestive heart failure, anxiety, depression, post-traumatic stress disorder, Alzheimer’s, schizophrenia, Parkinson’s and even cocaine addiction. DBH has long intrigued biochemists but it has been challenging to perform the analyses needed to determine the protein’s structure. “This enzyme has been particularly difficult,” says Hans Christensen, a chemist at D.T.U. and the study’s lead researcher. “We tried many different expression systems before we finally succeeded. Now that we have the structure it is clear why—[it] is very intricate, with different parts of the enzyme interacting very tightly.” © 2016 Scientific American,
Sara Reardon Prozac (fluoxetine) and similar antidepressants are among the most prescribed drugs in the United States, but scientists still don’t know exactly how they work. Now one piece of that puzzle — the structure of a protein targeted by several widely used antidepressants — has been solved. The finding, reported on 6 April in Nature1, could enable the development of better, more-targeted depression drugs. But it may come too late for drug companies, many of which have abandoned the search for depression treatments. Prozac and its kin — drugs called selective serotonin reuptake inhibitors (SSRIs) — were first discovered2 in 1972. They address one hallmark of depression: low levels of the molecule serotonin, which neurons use to signal one another. By preventing a protein called serotonin transporter (SERT) form absorbing the serotonin back into neurons that release it, the drugs boost serotonin levels in the junctions between cells. But the details of this mechanism have long eluded researchers, who have sought to crystallize and visualize the SERT protein since the early 1990s. “It’s tough to make, and once you make it, it tends to fall apart in your hands,” says Eric Gouaux, a crystallographer at Oregon Health & Science University in Portland. Gouaux and his colleagues finally succeeded by creating small mutations in the SERT gene to make the protein more stable. For the first time, they were able to see the pocket in which two SSRIs — Paxil (paroxetine) and Lexapro (escitalopram) — bind. They also identified a second pocket, called an allosteric site. When escitalopram binds to both sites, the transporter protein and the drug bond more tightly, which increases the medicine's effect. © 2016 Nature Publishing Group
Link ID: 22083 - Posted: 04.07.2016
Emily Anthes Type 'depression' into the Apple App Store and a list of at least a hundred programs will pop up on the screen. There are apps that diagnose depression (Depression Test), track moods (Optimism) and help people to “think more positive” (Affirmations!). There's Depression Cure Hypnosis (“The #1 Depression Cure Hypnosis App in the App Store”), Gratitude Journal (“the easiest and most effective way to rewire your brain in just five minutes a day”), and dozens more. And that's just for depression. There are apps pitched at people struggling with anxiety, schizophrenia, post-traumatic stress disorder (PTSD), eating disorders and addiction. This burgeoning industry may meet an important need. Estimates suggest that about 29% of people will experience a mental disorder in their lifetime1. Data from the World Health Organization (WHO) show that many of those people — up to 55% in developed countries and 85% in developing ones — are not getting the treatment they need. Mobile health apps could help to fill the gap (see 'Mobilizing mental health'). Given the ubiquity of smartphones, apps might serve as a digital lifeline — particularly in rural and low-income regions — putting a portable therapist in every pocket. “We can now reach people that up until recently were completely unreachable to us,” says Dror Ben-Zeev, who directs the mHealth for Mental Health Program at the Dartmouth Psychiatric Research Center in Lebanon, New Hampshire. Public-health organizations have been buying into the concept. In its Mental Health Action Plan 2013–2020, the WHO recommended “the promotion of self-care, for instance, through the use of electronic and mobile health technologies.” And the UK National Health Service (NHS) website NHS Choices carries a short list of online mental-health resources, including a few apps, that it has formally endorsed. © 2016 Nature Publishing Grou
By Rachel Zelniker, A long dark winter can be mentally and physically exhausting, but a recent study published in the journal of Clinical Psychological Science challenges the idea that it's making people depressed. Seasonal affective disorder (SAD) is commonly believed to affect a significant portion of the population in the Northern Hemisphere during the darker winter months. As many as 35 per cent of Canadians complain of having the "winter blues," according to the Centre for Addiction and Mental Health. Another 10 to 15 per cent have a mild form of seasonal depression, while about two to five per cent of Canadians will have a severe, clinical form of SAD. The disorder is based on the theory that some depressions occur seasonally in response to reduced sunlight — but recent research says that theory may be unsubstantiated. "We conducted a study using data that looked at the relationship between depression in a fairly large sample of people distributed over several degrees latitude in the United States," said Steven G. LoBello, a psychology professor at Auburn University in Montgomery, Ala., and one of the study's authors. "We looked across the four seasons to see if there was an association with sunlight, and we simply didn't find a direct relationship with sunlight, the seasons, or latitude." LoBello's study does not look at populations north of the 49th parallel, but he is confident his findings hold. "We cite in our paper a paper by [Vidje Hansen] that looked at this problem in Norway, which is north of the Arctic Circle, and they experience the polar night." According to LeBello, that research "did not find any relationship between an increase in depression and the duration of the polar night." A "seasonal pattern" modifier for depression diagnoses was officially added to the Diagnostic and Statistical Manual of Mental Disorders (DSM) in 1987. ©2016 CBC/Radio-Canada.
We might finally be figuring out how an increasingly popular therapy that uses electricity to boost the brain’s functioning has its effects – by pushing up levels of calcium in cells. Transcranial direct current stimulation (tDCS) involves using electrodes to send a weak current across the brain. Stimulating brain tissue like this has been linked to effects ranging from accelerating learning to improving the symptoms of depression and faster recovery from strokes. The broad consensus is that tDCS does this by lowering the threshold at which neurons fire, making it easier for them to pass on electrical signals. This leads to changes in the connectivity between neurons and alters information processing. But the cellular mechanisms that lead to such broad neurological changes are not clear and some researchers suggest that tDCS may not have any effect on the brain. Despite the doubts, devices are being developed for sale to people keen to influence their own brains. Now Hajime Hirase at the RIKEN Brain Science Institute in Tokyo, Japan, and his colleagues may have found an answer. They have identified large, sudden surges in calcium flow in the brains of mice seconds after they receive low doses of tDCS. These surges seem to start in cells called astrocytes – star-shaped cells that don’t fire themselves, but help to strengthen the connections between neurons and regulate the electrical signals that pass between them. © Copyright Reed Business Information Ltd.
By Simon Makin Brain science draws legions of eager students to the field and countless millions in dollars, euros and renminbi to fund research. These endeavors, however, have not yielded major improvements in treating patients who suffer from psychiatric disorders for decades. The languid pace of translating research into therapies stems from the inherent difficulties in understanding mental illness. “Psychiatry deals with brains interacting with the world and with other brains, so we're not just considering a brain's function but its function in complex situations,” says Quentin Huys of the Swiss Federal Institute of Technology (E.T.H. Zurich) and the University of Zurich, lead author of a review of the emerging field of computational psychiatry, published this month in Nature Neuroscience. Computational psychiatry sets forth the ambitious goal of using sophisticated numerical tools to understand and treat mental illness. Psychiatry currently defines disorders using lists of symptoms. Researchers have been devoting enormous energies to find biological markers that make diagnosis more objective with only halting success. Part of the problem is there is usually no one-to-one correspondence between biological causes and disorders defined by their symptoms, such as those in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). A specific disorder, like depression or schizophrenia, may result from a range of different underlying causes (biological or otherwise). On the other hand, the same cause might ultimately lead to different disorders in different people, depending on anything from their genetics to their life experiences. One of the goals of computational psychiatry is to draw connections between symptoms and causes, regardless of diagnoses. © 2016 Scientific American
Alison Abbott In the 25 years that John Collinge has studied neurology, he has seen hundreds of human brains. But the ones he was looking at under the microscope in January 2015 were like nothing he had seen before. He and his team of pathologists were examining the autopsied brains of four people who had once received injections of growth hormone derived from human cadavers. It turned out that some of the preparations were contaminated with a misfolded protein — a prion — that causes a rare and deadly condition called Creutzfeldt–Jakob disease (CJD), and all four had died in their 40s or 50s as a result. But for Collinge, the reason that these brains looked extraordinary was not the damage wrought by prion disease; it was that they were scarred in another way. “It was very clear that something was there beyond what you'd expect,” he says. The brains were spotted with the whitish plaques typical of people with Alzheimer's disease. They looked, in other words, like young people with an old person's disease. For Collinge, this led to a worrying conclusion: that the plaques might have been transmitted, alongside the prions, in the injections of growth hormone — the first evidence that Alzheimer's could be transmitted from one person to another. If true, that could have far-reaching implications: the possibility that 'seeds' of the amyloid-β protein involved in Alzheimer's could be transferred during other procedures in which fluid or tissues from one person are introduced into another, such as blood transfusions, organ transplants and other common medical procedures. © 2016 Nature Publishing Group,
By Gretchen Reynolds Meditating before running could change the brain in ways that are more beneficial for mental health than practicing either of those activities alone, according to an interesting study of a new treatment program for people with depression. As many people know from experience, depression is characterized in part by an inability to stop dwelling on gloomy thoughts and unhappy memories from the past. Researchers suspect that this thinking pattern, known as rumination, may involve two areas of the brain in particular: the prefrontal cortex, a part of the brain that helps to control attention and focus, and the hippocampus, which is critical for learning and memory. In some studies, people with severe depression have been found to have a smaller hippocampus than people who are not depressed. Interestingly, meditation and exercise affect those same portions of the brain, although in varying ways. In brain-scan studies, people who are long-term meditators, for instance, generally display different patterns of brain-cell communication in their prefrontal cortex during cognitive tests than people who don’t meditate. Those differences are believed to indicate that the meditators possess a more honed ability to focus and concentrate. Meanwhile, according to animal studies, aerobic exercise substantially increases the production of new brain cells in the hippocampus. Both meditation and exercise also have proven beneficial in the treatment of anxiety, depression and other mood disorders. These various findings about exercise and meditation intrigued researchers at Rutgers University in New Brunswick, N.J., who began to wonder whether, since meditation and exercise on their own improve moods, combining the two might intensify the impacts of each. So, for the new study, which was published last month in Translational Psychiatry, the scientists recruited 52 men and women, 22 of whom had been given diagnoses of depression. The researchers confirmed that diagnosis with their own tests and then asked all of the volunteers to complete a computerized test of their ability to focus while sensors measured electrical signals in their brains. © 2016 The New York Times Company
Link ID: 21998 - Posted: 03.17.2016
By Victoria Sayo Turner Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Credit: ©iStock Around March, some of us take a kick at the snow mounded on the curb and wonder if spring is finally going to drop by. The sun sets before we go home, and the cold coops us up except for runs to the grocery store. All of this amounts to something known informally as the winter blues, because those wintry days and dead trees can put us in a glum mood. But in the 1980s, research at the National Institutes of Mental Health led to recognition of a form of depression known as seasonal affective disorder (shortened, of course, to SAD). Seasonal affective disorder was categorized under major depression to signify depression with a yearly recurrence, a condition far more debilitating than your average “winter blues.” Mention of SAD in research and books peaked in the 1990s, and today SAD is considered a diagnosable (and insurable) disorder. Treatment ranges from psychotherapy to antidepressants to light therapy — large boxes filled with lightbulbs that look like tanning beds for your face. However, a recent study questions the existence of seasonal depression entirely. Each year, the Centers for Disease Control conducts a large cross-sectional study of the US population. A group of researchers realized they could use the CDC results independently to investigate how much depression changes by season. The 2006 version of the CDC study included a set of questions typically used to screen for depression. By analyzing the answers gathered from 34,000 adults over the course of the year, the researchers might detect flareups of seasonal affective disorder. They might see wintertime surges in depression. “To be honest, we initially did not question the [SAD] diagnosis,” writes investigator Dr. Steven LoBello, the goal being “to determine the actual extent to which depression changes with the seasons.” © 2016 Scientific American
Deborah Orr The psychologist Oliver James has for many years been a part of the cultural landscape, writing best-selling books, making television programmes, contributing articles to newspapers and generally offering his views. As a practicing psychotherapist of many years’ standing, he has good reason to believe that he has important insights to offer. James is particularly exercised by the damage caused by casual emotional abuse – the explosive parent who shouts and swears at their kids, displays resentment against them or tries to coerce them into doing things instead of employing reason. No sensible person disagrees with him on this, and only a harsh critic would deny that James has played a strong and positive part in popularising these simple, important wisdoms. That’s why it’s so very odd that James has chosen now to perpetrate casual emotional abuse on a grand scale. His latest book, Not in Your Genes: The Real Reason Parents Are Like Their Children, expands on an argument he’s been making for years: that there is no scientific basis for belief in the idea that there is any genetic element to any psychological trait. Even illnesses such as schizophrenia and bipolar disorder are completely down to the environment in which you grew up, not the complex interplay between nature and nurture that mainstream science espouses. Even if James had conclusive evidence to back up his absolutist claim – which he does not – I would suggest that such news should be broken gently. © 2016 Guardian News and Media Limited
Shefali Luthra Depression prompts people to make about 8 million doctors' appointments a year, and more than half are with primary care physicians. A study suggests those doctors often fall short in treating depression because of insurance issues, time constraints and other factors. More often than not, primary care doctors fail to teach patients how to manage their care and don't follow up to see how they're doing, according to the study, which was published Monday in Health Affairs. Those are considered effective tactics for treating chronic illnesses. "The approach to depression should be like that of other chronic diseases," said Dr. Harold Pincus, vice chair of psychiatry at Columbia University's College of Physicians and Surgeons and one of the study's co-authors. But "by and large, primary care practices don't have the infrastructure or haven't chosen to implement those practices for depression." Most people with depression seek help from their primary care doctors, the study notes. That can be because patients often face shortages and limitations of access to specialty mental health care, including lack of insurance coverage, the authors write. Plus there's stigma: Patients sometimes feel nervous or ashamed to see a mental health specialist, according to the authors. Meanwhile, physicians and researchers have increasingly been calling for mental health conditions such as depression and anxiety to be treated like physical illnesses. Historically, those have been handled separately and not always with the same attention and care as things like high blood pressure and heart disease. © 2016 npr
Link ID: 21964 - Posted: 03.08.2016
Story by Amy Ellis Nutt She relaxed in the recliner, her eyes closed, her hands resting lightly in her lap. The psychiatrist’s assistant made small talk while pushing the woman’s hair this way and that, dabbing her head with spots of paste before attaching the 19 electrodes to her scalp. In the struggle over the future of psychiatry, researchers are looking deep within the brain to understand mental illness and find new therapeutic tools. As the test started, her anxiety ticked up. And that’s when it began: the sensation of being locked in a vise. First, she couldn’t move. Then she was shrinking, collapsing in on herself like some human black hole. It was a classic panic attack — captured in vivid color on the computer screen that psychiatrist Hasan Asif was watching. “It’s going to be okay,” he said, his voice quiet and soothing. “Just stay with it.” The images playing out in front of him were entirely unexpected; this clearly wasn’t a resting state for his patient. With each surge of anxiety, a splotch of red bloomed on the computer screen. Excessive activity of high-energy brain waves near the top of her head indicated hyper-arousal and stress. Decreased activity in the front of her brain, where emotions are managed, showed she couldn’t summon the resources to keep calm.
Tina Hesman Saey Sonia Vallabh knows what will probably kill her. In 2011, the Boston-area law school graduate learned she carries the same genetic mutation that caused her mother’s death from a rare brain-wasting prion disease. Prions are twisted forms of normal brain proteins that clump together and destroy nerves. About 10 to 15 percent of prion diseases are caused by a mutation in the PRNP gene, leading to such deadly diseases as Creutzfeldt-Jakob disease, Gerstmann-Sträussler-Scheinker syndrome and fatal familial insomnia, the disease that killed Vallabh’s mother. Grief, shared with family and friends, came first. Eventually, Vallabh realized, “We can’t get around this prognosis.… We’ve got to go through it.” So began her and husband Eric Minikel’s odyssey to learn about the disease that had turned their lives upside down. A scientist friend came by with a flash drive loaded with research papers about prion diseases. “We didn’t have the vocabulary” to understand the information, Vallabh says. So she took a sabbatical from her job to take biology and chemistry classes. Minikel kept writing transportation software, but attended night classes with his wife. Vallabh’s first foray into brain research was as a technician in a lab studying Huntington’s disease. During “science nights” at the couple’s home, scientist pals team-taught biology and biochemistry. The couple took the biggest step when Minikel left his consulting job and both enrolled in graduate school to study prion diseases. Prion proteins, some of which clump together or form fibrils, as in this E. coli bacteria, are often used to model how proteins misfold in some neurodegenerative disorders. © Society for Science & the Public 2000 - 2016
By DONALD G. McNEIL Jr. A baby with a shrunken, misshapen head is surely a heartbreaking sight. But reproductive health experts are warning that microcephaly may be only the most obvious consequence of the spread of the Zika virus. Even infants who appear normal at birth may be at higher risk for mental illnesses later in life if their mothers were infected during pregnancy, many researchers fear. The Zika virus, they say, closely resembles some infectious agents that have been linked to the development of autism, bipolar disorder and schizophrenia. Schizophrenia and other debilitating mental illnesses have no single cause, experts emphasized in interviews. The conditions are thought to arise from a combination of factors, including genetic predisposition and traumas later in life, such as sexual or physical abuse, abandonment or heavy drug use. But illnesses in utero, including viral infections, are thought to be a trigger. “The consequences of this go way beyond microcephaly,” said Dr. W. Ian Lipkin, who directs The Center for Infection and Immunity at Columbia University. Here is a look at the most prominent rumors and theories about Zika virus, along with responses from scientists. Among children in Latin America and the Caribbean, “I wouldn’t be surprised if we saw a big upswing in A.D.H.D., autism, epilepsy and schizophrenia,” he added. “We’re looking at a large group of individuals who may not be able to function in the world.” © 2016 The New York Times Company
By Nancy Szokan It’s well known that physical activity is a mood elevator. But writing in “The Athlete’s Way” blog on Psychology Today’s website, endurance athlete Christopher Bergland discusses a study indicating that combining movement with the attention-focusing benefits of meditation can be an extra-effective tool in fighting depression. The small study, conducted at Rutgers University in New Jersey, was based on a set of assumptions: Healthy brains are constantly producing neurons. Brains of people under stress or suffering depression produce fewer neurons. Physical activity increases neuron production, as do antidepressant medications. (Meanwhile, a certain number of newborn neurons die off.) Mental exercise — “effortful learning,” which requires focus — reduces those deaths. People with depression often have problems with focus. The researchers tested a novel intervention — it’s called MAP because it involves mental and physical training — aimed at both increasing neuron production and keeping those neurons alive. Fifty-two people completed the study — 22 with major depressive disorder, or MDD, and 30 who were not depressed. Twice a week, they performed 30 minutes of meditation during which they were directed to constantly focus on their breathing; they began each session seated, but for the last 10 minutes they meditated while walking slowly. Then they performed 30 minutes of moderate physical activity on a treadmill or stationary cycle. After eight weeks, the researchers found that the MDD patients’ depressive symptoms had been reduced by 40 percent. (The non-depressed participants also said they felt happier.)
Link ID: 21899 - Posted: 02.16.2016
By Dominic Howell BBC News A new therapy which involves a patient embodying themselves in a virtual reality avatar of a crying child could help with depression, research has suggested. Patients wear a headset that projects a life-sized image, firstly of an adult and then of a child. The new research tested the technology for the first time on patients with a mental health problem. The project is part of a continuing study at University College London. The university, which is working in collaboration with ICREA-University of Barcelona, has suspected for several years that virtual therapy could help with mental health conditions. This latest research - which has been published in the British Journal of Psychiatry Open and was funded by the Medical Research Council - lays the basis for a large-scale clinical trial to be carried out in the future. The study took 15 people who were all being treated by the NHS for depression and put them through the avatar experience. Firstly, the patients - 10 of whom were female and the rest male - put on a headset which projected an adult version of themselves into a virtual reality mirror. The patient was asked to mentally identify with the adult avatar, which exactly replicated the patient's body movements, in a process known as "embodiment". They then noticed a separate avatar of a small crying child, who was also in the mirror. They were told to say compassionate phrases to the child to try and comfort and console it. Patients asked the child to think of a time when it was happy, and to think of someone who loved them. At this stage of the experiment the roles were then reversed. © 2016 BBC
Link ID: 21897 - Posted: 02.15.2016