Chapter 12. Psychopathology: The Biology of Behavioral Disorders
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Symptoms of depression that steadily increase over time in older age could indicate early signs of dementia, scientists have said. Other patterns of symptoms, such as chronic depression, appear not to be linked, a study found. Dutch researchers looked at different ways depression in older adults progressed over time and how this related to any risk. They concluded worsening depression may signal the condition is taking hold. The research, published in The Lancet Psychiatry, followed more than 3,000 adults aged 55 and over living in the Netherlands. All had depression but no symptoms of dementia at the start of the study. Dr M Arfan Ikram of the Erasmus University Medical Center in Rotterdam said depressive symptoms that gradually increase over time appear to be a better predictor of dementia later in life than other paths of depression. "There are a number of potential explanations, including that depression and dementia may both be symptoms of a common underlying cause, or that increasing depressive symptoms are on the starting end of a dementia continuum in older adults," he said. Only the group whose symptoms of depression increased over time were found to be at increased risk of dementia - about one in five of people (55 out of 255) in this group developed dementia. Others who had symptoms that waxed and waned or stayed the same were not at increased risk. For example, in those who experienced low but stable levels of depression, around 10% went on to develop dementia. The exact nature of depression on dementia risk remains unknown. © 2016 BBC
People who've recovered from depression stave off relapses with mindfulness therapy as well as with antidepressants, a new review finds. Mindfulness-based cognitive therapy (MBCT) is an eight-week group program that helps people become better observers of their own thoughts and emotions and to learn to distance themselves before ruminations spiral downwards. An international team of psychiatry researchers combined data from nine randomized trials of 1,258 patients total with recurrent depression to compare the mindfulness therapy to placebo, treatment as usual and other active treatments including antidepressants. People suffering from depression who received the mindfulness therapy were 31 per cent less likely to suffer a relapse during the next 60 weeks compared with those who did not receive it, Willem Kuyken of the University of Oxford, in England and his co-authors reported in a meta-analysis review in Wednesday's issue of the journal JAMA Psychiatry. "If you compare MBCT against antidepressant medication it basically holds its own, which means it provides protection on par with what people would get from continuing to take to take medications for one, two or three years after they've recovered from depression," said co-author Dr. Zindel Segal, a professor of psychology at the University of Toronto Scarborough. No one reported side-effects associated with participating in the therapy. ©2016 CBC/Radio-Canada.
By ERICA GOODE PORTLAND, Ore. — The 911 caller had reported a man with a samurai sword, lunging at people on the waterfront. It was evening, and when the police arrived, they saw the man pacing the beach and called to him. He responded by throwing a rock at the embankment where they stood. They shouted to him from a sheriff’s boat; he threw another rock. They told him to drop the sword; he said he would kill them. He started to leave the beach, and after warning him, they shot him in the leg with a beanbag gun. He turned back, still carrying the four-foot blade. In another city — or in Portland itself not that long ago — the next step would almost certainly have been a direct confrontation and, had the man not put down the weapon, the use of lethal force. But the Portland Police Bureau, prodded in part by the 2012 findings of a Justice Department investigation, has spent years putting in place an intensive training program and protocols for how officers deal with people with mental illness. At a time when police behavior is under intense scrutiny — a series of fatal shootings by police officers have focused national attention on issues of race and mental illness — Portland’s approach has served as a model for other law enforcement agencies around the country. And on that Sunday last summer, the police here chose a different course. At 2:30 a.m., after spending hours trying to engage the man, the officers decided to “disengage,” and they withdrew, leaving the man on the beach. A search at daylight found no signs of him. People with mental illnesses are overrepresented among civilians involved in police shootings: Twenty-five percent or more of people fatally shot by the police have had a mental disorder, according to various analyses. © 2016 The New York Times Company
Link ID: 22150 - Posted: 04.27.2016
By Bret Stetka The multibillion-dollar supplement industry spews many dubious claims, but a new study suggests that some nutritional supplements, including omega-3 fatty acids and vitamin D, may boost the effectiveness of antidepressants. If so, the supplements might help relieve symptoms for the millions of people who don’t immediately respond to these drugs. The meta-analysis—published Tuesday in the American Journal of Psychiatry—reviewed the results of 40 clinical trials that evaluated the effects of taking nutritional supplements in conjunction with several major classes of antidepressants, including selective serotonin reuptake inhibitors (SSRIs), serotonin-norepinephrine reuptake inhibitors (SNRIs) and tricyclic antidepressants. It revealed that four supplements in particular upped the potency of the medications, compared with a placebo. The researchers, based at Harvard University and the University of Melbourne, found the strongest evidence for an omega-3 fish oil called eicosapentaenoic acid, or EPA. In general, people with depression who took an antidepressant drug and an omega-3 sourced from fish oil experienced a significant reduction in their symptoms as assessed by a the Hamilton Depression Rating Scale, a common measure used by most of the studies in the review. The same was true, although to a lesser extent, for S-adenosylmethionine, methylfolate (a form of the B vitamin folic acid) and Vitamin D. A few isolated studies found some benefit from augmenting treatment with creatine, while adding zinc, vitamin C, the amino acid tryptophan and folic acid produced mixed results. The authors deemed all of these supplements relatively safe. © 2016 Scientific American,
Link ID: 22149 - Posted: 04.27.2016
By Nicholas Bakalar Treating pregnant women for depression may benefit not just themselves but their babies as well. A study, in the May issue of Obstetrics & Gynecology, included 7,267 pregnant women, of whom 831 had symptoms of depression. After controlling for maternal age, race, income, body mass index and other health and behavioral characteristics, the researchers found that depressive symptoms were associated with a 27 percent increased relative risk of preterm birth (less than 37 weeks of gestation), an 82 percent increased risk of very preterm birth (less than 32 weeks of gestation), and a 28 percent increased risk of having a baby small for gestational age. They also found that among those who were treated with antidepressants for depression — about a fifth of those with the diagnosis — there was no association with increased risk for any of these problems. But they acknowledge that this group was quite small, which limits the power to draw conclusions. Still, the lead author, Dr. Kartik K. Venkatesh, a clinical fellow in obstetrics and gynecology at Harvard, said that it was important to screen mothers for depression, not only for their health but for that of their babies. “By screening early in pregnancy, you could identify those at higher risk and counsel them about the importance of treatment,” he said. “Treating these women for depression may have real benefits.” © 2016 The New York Times Company
Anna Nowogrodzki Prions, the misfolded proteins that are known for causing degenerative illnesses in animals and humans, may have been spotted for the first time in plants. Researchers led by Susan Lindquist, a biologist at the Whitehead Institute for Biomedical Research in Cambridge, Massachusetts, report that they have found a section of protein in thale cress (Arabidopsis) that behaves like a prion when it is inserted into yeast. In plants, the protein is called Luminidependens (LD), and it is normally involved in responding to daylight and controlling flowering time. When a part of the LD gene is inserted into yeast, it produces a protein that does not fold up normally, and which spreads this misfolded state to proteins around it in a domino effect that causes aggregates or clumps. Later generations of yeast cells inherit the effect: their versions of the protein also misfold. This does not mean that plants definitely have prion-like proteins, adds Lindquist — but she thinks that it is likely. “I’d be surprised if they weren’t there,” she says. To prove it, researchers would need to grind up a plant and see whether they could find a protein such as LD in several different folded states, as well as show that any potential prion caused a misfolding cascade when added to a test-tube of protein. Lindquist adds that because she's not a plant scientist — her focus is on using yeast to investigate prions — she hasn't tried these experiments. The study is reported on 25 April in the Proceedings of the National Academy of Sciences1. © 2016 Nature Publishing Group
Richard A. Friedman DRUG companies are eager to tell you about their newest medicines. Turn on your TV or go online and there’s a new drug — with a hefty price tag — for whatever ails you, from antidepressants to painkillers to remedies for erectile dysfunction. The pharmaceutical industry spends lavishly to get your attention: In 2014, drug makers poured $4.5 billion into so-called direct-to-consumer advertising, a 30 percent increase over two years. Drug makers claim they are educating the public with their ads, providing information that will help you make better choices about your medical care. So in the spirit of education, let’s consider a recent online ad for Latuda, a new antipsychotic medication. A young woman rides a bike off into the sun as we are told that Latuda has been shown to be effective for many people with bipolar depression, followed by that staccato recitation of potential side effects that most viewers tune out. Here’s what a helpful prescription drug label could look like, with facts that are now out of reach. These are question marks because, although many clinical trial results are published, they are difficult to find and compare. Rules should mandate that all studies are accessible. Note the same high cost for a four-fold range of Latuda doses. Often the lowest dose is just as effective; some low-dose consumers realize they can save money by ordering the higher-dose units and splitting them into pieces. The ideal label would have statistics on how many people have serious side effects. Data are not included for these drugs because they may take years to emerge, if ever. Other drugs have well-known side effects. Fair enough. But the ad omits something that most consumers would like to know: There are many older and cheaper treatments that are just as effective. In fact, Latuda is one of 10 “second generation” antipsychotic medications, many available in generic forms, that essentially work the same way. Of course, the goal of drug companies is not to educate, but to sell products. We could ban the ads, as almost every other country does, and which I’d strongly support. But such a campaign in the United States would face fierce legislative and legal challenges. Instead, let’s help the drug companies make their ads truly educational. © 2016 The New York Times Company
It was December 2012 when the country learned about the massacre at Sandy Hook Elementary School, that left 20 children dead at the hands of 20-year-old shooter Adam Lanza. After the shock and the initial grief came questions about how it could have happened and why. Reports that Adam Lanza may have had some form of undiagnosed mental illness surfaced. The tragedy drove Liza Long to write a blog post on that same day, titled "I Am Adam Lanza's Mother." She wasn't Lanza's mom, but she was raising a child with a mental disorder. Her 13-year-old son had violent rages on a regular basis. He was in and out of juvenile detention. He had threatened to kill her. She detailed all this in her essay that took off online. Now, four years later, her son is speaking out too. This week on For The Record: a mother, a son and life on the edge of bipolar disorder. Eric Walton, Liza Long's son, is now a 16-year-old high school sophomore in Boise, Idaho. After a series of misdiagnoses, he's been diagnosed with bipolar disorder. But four years ago, he didn't know much about his condition. "I knew that there were times when I would have rages, didn't like them. I knew that I wanted them to stop," Walton says. Except he felt a loss of control in those moments. He describes the onset of these rages as a "blackout" of sorts. "I would start getting angry," he says. "Then it's like being trapped inside a box inside your own head. It was like a television on the wall that shows you what you're seeing. You can feel everything, but you no longer have the video game controller to control your own body." Walton's mom says when Eric would get into those states, "he would express a lot of suicidal thoughts, and hearing him just say, 'I want to die, I just want to end it.'" Then, two days before the Newtown shooting, Eric Walton had another episode. © 2016 npr
By SABRINA TAVERNISE WASHINGTON — Suicide in the United States has surged to the highest levels in nearly 30 years, a federal data analysis has found, with increases in every age group except older adults. The rise was particularly steep for women. It was also substantial among middle-aged Americans, sending a signal of deep anguish from a group whose suicide rates had been stable or falling since the 1950s. The suicide rate for middle-aged women, ages 45 to 64, jumped by 63 percent over the period of the study, while it rose by 43 percent for men in that age range, the sharpest increase for males of any age. The overall suicide rate rose by 24 percent from 1999 to 2014, according to the National Center for Health Statistics, which released the study on Friday. The increases were so widespread that they lifted the nation’s suicide rate to 13 per 100,000 people, the highest since 1986. The rate rose by 2 percent a year starting in 2006, double the annual rise in the earlier period of the study. In all, 42,773 people died from suicide in 2014, compared with 29,199 in 1999. From 1999 to 2014, suicide rates in the United States rose among most age groups. Men and women from 45 to 64 had a sharp increase. Rates fell among those age 75 and older. “It’s really stunning to see such a large increase in suicide rates affecting virtually every age group,” said Katherine Hempstead, senior adviser for health care at the Robert Wood Johnson Foundation, who has identified a link between suicides in middle age and rising rates of distress about jobs and personal finances. Researchers also found an alarming increase among girls 10 to 14, whose suicide rate, while still very low, had tripled. The number of girls who killed themselves rose to 150 in 2014 from 50 in 1999. “This one certainly jumped out,” said Sally Curtin, a statistician at the center and an author of the report. © 2016 The New York Times Company
By Clare Wilson People who develop schizophrenia may have been born with brains with a different structure. The finding adds further support to the idea that genetics can play a key role in schizophrenia, which involves delusions and hallucinations and is often a lifelong condition once it develops. Schizophrenia has been the subject of a fierce nature-versus-nurture debate: childhood abuse is linked with a raised risk of the condition, but 108 genes have been implicated, too. Probing the biology of schizophrenia is difficult because brain tissue sampled from people with the condition is rarely available to study. Kristen Brennand of the Icahn School of Medicine at Mount Sinai in New York and her colleagues got around this by taking skin cells from 14 people with schizophrenia, and reprogramming them into stem cells and then nerve cells. They found that on average these nerve cells had lower levels of a signalling molecule called miR-9 than similar cells developed from people who do not have schizophrenia. A small string of nucleic acids, miR-9 can change the activity of certain genes and is known to play a role in how neurons develop in the fetus. In further experiments, Brennand’s team showed that miR-9 might also affect how neurons migrate from where they form, next to the fetal brain’s central cavities, out to their final resting place in the brain’s outer layers. © Copyright Reed Business Information Ltd.
By Emily Underwood Earlier this month, György Buzsáki of New York University (NYU) in New York City showed a slide that sent a murmur through an audience in the Grand Ballroom of New York’s Midtown Hilton during the annual meeting of the Cognitive Neuroscience Society. It wasn’t just the grisly image of a human cadaver with more than 200 electrodes inserted into its brain that set people whispering; it was what those electrodes detected—or rather, what they failed to detect. When Buzsáki and his colleague, Antal Berényi, of the University of Szeged in Hungary, mimicked an increasingly popular form of brain stimulation by applying alternating electrical current to the outside of the cadaver’s skull, the electrodes inside registered little. Hardly any current entered the brain. On closer study, the pair discovered that up to 90% of the current had been redirected by the skin covering the skull, which acted as a “shunt,” Buzsáki said. For many meeting attendees, the unusual study heightened serious doubts about the mechanism and effectiveness of transcranial direct current stimulation (tDCS), an experimental, noninvasive treatment that uses electrodes to deliver weak current to a person’s forehead, and the related tACS, which uses alternating current. Little is known about how these techniques might influence the brain. Yet many scientific papers have claimed that the techniques can boost mood, alleviate chronic pain, and even make people better at math by directly affecting neuronal activity. This has spawned a cottage industry of do-it-yourself gadgets promising to make people smarter and happier. © 2016 American Association for the Advancement of Science
Link ID: 22126 - Posted: 04.21.2016
Rachel Becker A highly contagious and deadly animal brain disorder has been detected in Europe for the first time. Scientists are now warning that the single case found in a wild reindeer might represent an unrecognized, widespread infection. Chronic wasting disease (CWD) was thought to be restricted to deer, elk (Cervus canadensis) and moose (Alces alces) in North America and South Korea, but on 4 April researchers announced that the disease had been discovered in a free-ranging reindeer (Rangifer tarandus tarandus) in Norway. This is both the first time that CWD has been found in Europe and the first time that it has been found in this species in the wild anywhere in the world. “It’s worrying — of course, especially for animals. It’s a nasty disease,” says Sylvie Benestad, an animal-disease researcher at the Norwegian Veterinary Institute in Oslo who, along with colleague Turid Vikøren, diagnosed the diseased reindeer. A key question now is whether this is a rare — even unique — case, or if the disease is widespread but so far undetected in Europe. “If it’s similar to our prion disease in the United States and Canada, the disease is subtle and it would be easy to miss,” says Christina Sigurdson, a pathologist at the University of California, San Diego, who has shown that reindeer can contract CWD in a laboratory environment1. © 2016 Nature Publishing Group,
Link ID: 22117 - Posted: 04.19.2016
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.