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By Sara Chodosh Although scientists have learned a lot about the brain in the last few decades, approaches to treating mental illnesses have not kept up. As neuroscientists learn more about brain circuits, Stanford psychiatrist Amit Etkin foresees a time when diagnoses will be based on brain scans rather than symptoms. Etkin, who will be speaking at the World Economic Forum’s Annual Meeting of the New Champions in Tianjin, China, from June 26 to 28, spoke with Scientific American about his research on the neurological basis of emotional disorders and the future of mental health treatment. The high cost of treating mental illness doesn’t get talked about very much. Why is that? It’s a really interesting issue. The costs associated with mental illness are not just the care of people who have an illness, which often starts early in life and continues as a lifelong process, but also the cost to employers in decreased productivity and the cost to society in general. A report that came out recently in Health Affairs showed that spending within our health system in the U.S. is greater for mental illness than for any other area of medicine, and yet our understanding of these illnesses is incredibly backwards. Treatments are no different than they were 40 years ago, so that feels like a problem that is only getting bigger without an obvious solution. Why hasn’t there been much progress? It was really not until about 10 years ago that [mental health professionals] started realizing how little difference we have made. There are a few fundamental issues and mistakes we’ve made. One is that in the absence of knowing what the causes of the illnesses that we treat are, we focus on the symptoms, and that has already led us down the wrong path. If you go to another country and you ask somebody to tell you their symptoms, as a clinician you might have the sense that they have anxiety or depression. In Asian countries they express that in a somatic way: “I can’t sleep” or “I feel weak.” The biology cannot be that different, but the symptoms are different because they’re culturally bound. If you look at different parts of the U.S. you’ll see people expressing symptoms in different ways depending on their local culture. If that’s the case, then a symptom-based definition is problematic. The long and short of it is that people have named syndromes or disorders that they don’t actually know represent a valid entity that is distinct from another entity. © 2016 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22364 - Posted: 06.27.2016

Most available antidepressants do not help children and teenagers with serious mental health problems and some may be unsafe, experts have warned. A review of clinical trial evidence found that of 14 antidepressant drugs, only one, fluoxetine – marketed as Prozac – was better than a placebo at relieving the symptoms of young people with major depression. Another drug, venlafaxine, was associated with an increased risk of suicidal thoughts and suicide attempts. Blood test could identify people who will respond to antidepressants Read more But the authors stressed that the true effectiveness and safety of antidepressants taken by children and teenagers remained unclear because of the poor design and selective reporting of trials, which were mostly funded by drug companies. They recommended close monitoring of young people on antidepressants, regardless of what drugs they were prescribed, especially at the start of treatment. Professor Peng Xie, a member of the team from Chongqing Medical University in China, said: “The balance of risks and benefits of antidepressants for the treatment of major depression does not seem to offer a clear advantage in children and teenagers, with probably only the exception of fluoxetine.” Major depressive disorder affects around 3% of children aged six to 12 and 6% of teenagers aged 13 to 18. In 2004 the US Food and Drug Administration (FDA) issued a warning against the use of antidepressants in young people up to the age of 24 because of concerns about suicide risk. Yet the number of young people taking the drugs increased between 2005 and 2012, both in the US and UK, said the study authors writing in the Lancet medical journal. In the UK the proportion of children and teenagers aged 19 and under taking antidepressants rose from 0.7% to 1.1%. © 2016 Guardian News and Media Limited

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22303 - Posted: 06.09.2016

By Perri Klass, M.D. When girls come in for their physical exams, one of the questions I routinely ask is “Do you get your period?” I try to ask before I expect the answer to be yes, so that if a girl doesn’t seem to know about the changes of puberty that lie ahead, I can encourage her to talk about them with her mother, and offer to help answer questions. And I often point out that even those who have not yet embarked on puberty themselves are likely to have classmates who are going through these changes, so, again, it’s important to let kids know that their questions are welcome, and will be answered accurately. But like everybody else who deals with girls, I’m aware that this means bringing up the topic when girls are pretty young. Puberty is now coming earlier for many girls, with bodies changing in the third and fourth grade, and there is a complicated discussion about the reasons, from obesity and family stress to chemicals in the environment that may disrupt the normal effects of hormones. I’m not going to try to delineate that discussion here — though it’s an important one — because I want to concentrate on the effect, rather than the cause, of reaching puberty early. A large study published in May in the journal Pediatrics looked at a group of 8,327 children born in Hong Kong in April and May of 1997, for whom a great deal of health data has been collected. The researchers had access to the children’s health records, showing how their doctors had documented their physical maturity, according to what are known as the Tanner stages, for the standardized pediatric index of sexual maturation. Before children enter puberty, we call it Tanner I; for girls, Tanner II is the beginning of breast development, while for boys, it’s the enlargement of the scrotum and testes and the reddening and changing of the scrotum skin. Boys and girls then progress through the intermediate changes to stage V, full physical maturity. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 22288 - Posted: 06.06.2016

By ANNA FELS ONE of the most painful experiences of being a psychiatrist is having a patient for whom none of the available therapies or medications work. A while back, I was asked to do a consultation on just such a patient. This person had been a heroin addict in her early 20s. She had quit the opioid five years earlier, but her life was plagued with anxiety, apathy and self-doubt that prior treatments had not helped. At the end of the session, almost as an afterthought, she noted with irony that the only time in her adult life when she had been able to socialize easily and function at work was when she had been hooked on heroin. We are in the midst of a devastating and often lethal opioid epidemic, one of whose victims, we learned last week, was the pop star Prince. At such a time, it is hard to remember that there are multiple opioids naturally produced in our brains and required for our well-being. The neural circuitry utilizing these substances controls some of our most fundamental feelings of pain, stress and hopelessness, as well as pleasure and even euphoria. There is obviously a need for extreme caution, but research suggests that certain opioids may actually be useful in treating psychiatric diseases that have proved frustratingly unresponsive to current medications. It is the potentially addictive subset of opioids, whose natural ancestors were originally derived from poppies, that we associate with the word. These substances have been with us for most, if not all, of human civilization. Poppy seeds have been found at archaeological sites of Neolithic man. The Sumerians wrote about “the joy plant”; an Egyptian papyrus from the second millennium B.C. described the use of a product of poppies to stop the crying of children. Hippocrates suggested its use for female ailments, and a ninth-century Persian physician advocated the use of opium for melancholia. Millenniums later, during the American Civil War, the Union Army used 10 million opium pills to treat wounded soldiers. And then there were the two Opium Wars fought between China and Britain. Unquestionably, no other psychoactive substance has played such a central role in human affairs. © 2016 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 8: General Principles of Sensory Processing, Touch, and Pain
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 22287 - Posted: 06.06.2016

Amanda Aronczyk At first Giselle wasn't sure what to put on her medical school application. She wanted to be a doctor, but she also wanted people to know about her own health: years of depression, anxiety and a suicide attempt. (We're using only her first name in this story, out of concern for her future career.) "A lot of people were like, you don't say that at all," she said. "Do not mention that you have any kind of weakness." Giselle remembers having her first intense suicidal thoughts when she was 10 years old. Her parents had split up and she had moved from the coast of Colombia to Chicago. She started having extreme mood swings and fighting with her mom. And then, when she was 16 years old, she tried to kill herself. "Yeah, lots of pills." After her suicide attempt she began therapy and eventually started taking antidepressants. That worked extremely well. After finishing high school, she took an unconventional route. She went to Brazil to work with a women's community health group, worked as a research assistant for a doctor, and trained as a doula to assist women in labor. It was while working as a doula and witnessing what she saw as insensitive behavior from a doctor that she resolved her own career indecision: She would become a different kind of doctor. When she applied to medical school, she told them this whole story in her application. In the fall of 2014, she started at the University of Wisconsin School of Medicine and Public Health. © 2016 npr

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22276 - Posted: 06.02.2016

By Gary Stix Scientists will never find a single gene for depression—nor two, nor 20. But among the 20,000 human genes and the hundreds of thousands of proteins and molecules that switch on those genes or regulate their activity in some way, there are clues that point to the roots of depression. Tools to identify biological pathways that are instrumental in either inducing depression or protecting against it have recently debuted—and hold the promise of providing leads for new drug therapies for psychiatric and neurological diseases. A recent paper in the journal Neuron illustrates both the dazzling complexity of this approach and the ability of these techniques to pinpoint key genes that may play a role in governing depression. Scientific American talked with the senior author on the paper—neuroscientist Eric Nestler from the Icahn School of Medicine at Mt. Sinai in New York. Nestler spoke about the potential of this research to break the logjam in pharmaceutical research that has impeded development of drugs to treat brain disorders. Scientific American: The first years in the war on cancer met with a tremendous amount of frustration. Things look like they're improving somewhat now for cancer. Do you anticipate a similar trajectory may occur in neuroscience for psychiatric disorders? Eric Nestler: I do. I just think it will take longer. I was in medical school 35 years ago when the idea that identifying a person's specific pathophysiology was put forward as a means of directing treatment of cancer. We're now three decades later finally seeing the day when that’s happening. I definitely think the same will occur for major brain disorders. The brain is just more complicated and the disorders are more complicated so it will take longer. © 2016 Scientific American

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22267 - Posted: 05.31.2016

Sara Reardon Children from impoverished families are more prone to mental illness, and alterations in DNA structure could be to blame, according to a study published on 24 May in Molecular Psychiatry1. Poverty brings with it a number of different stressors, such as poor nutrition, increased prevalence of smoking and the general struggle of trying to get by. All of these can affect a child’s development, particularly in the brain, where the structure of areas involved in response to stress and decision-making have been linked to low socioeconomic status. Poor children are more prone to mental illnesses such as depression than their peers from wealthier families, but they are also more likely to have cognitive problems. Some of these differences are clearly visible in the brain structure and seem to appear at birth, which suggests that prenatal exposure to these stressors can be involved2. But neurodevelopment does not stop at birth. Neuroscientist Ahmad Hariri of Duke University in Durham, North Carolina, suspected that continual exposure to stressors might affect older children as well. He decided to test this idea by studying chemical tags known as methyl groups, which alter DNA structure to regulate how genes are expressed. There is some evidence that methylation patterns can be passed down through generations, but they are also altered by environmental factors, such as smoking. © 2016 Nature Publishing Group,

Related chapters from BP7e: Chapter 7: Life-Span Development of the Brain and Behavior; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 13: Memory, Learning, and Development; Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22248 - Posted: 05.25.2016

By Diana Kwon More than one in 10 Americans older than 12 takes antidepressants, according to a 2011 report by the National Center for Health Statistics. A significant but unknown number of children younger than 12 take them, too. Although most such drugs are not approved for young children, doctors have prescribed them off-label for years because they have been thought to have relatively mild side effects. Yet recent reports have revealed that important data about the safety of these drugs—especially their risks for children and adolescents—have been withheld from the medical community and the public. In the latest and most comprehensive analysis, published in January in the BMJ, researchers at the Nordic Cochrane Center in Copenhagen showed that pharmaceutical companies have not been revealing the full extent of serious harm in clinical study reports, which are detailed documents sent to regulatory authorities such as the U.S. Food and Drug Administration and the European Medicines Agency (EMA) when applying for approval of a new drug. The researchers examined reports from 70 double-blind, placebo-controlled trials of two common categories of antidepressants—selective serotonin reuptake inhibitors (SSRIs) and serotonin and norepinephrine reuptake inhibitors (SNRIs)—and found that the occurrence of suicidal thoughts and aggressive behavior doubled in children and adolescents who used these drugs. The investigators discovered that some of the most revealing information was buried in appendices where individual patient outcomes are listed. For example, they found clear instances of suicidal thinking that had been passed off as “emotional lability” or “worsening depression” in the report itself. This information, however, was available for only 32 out of the 70 trials. “We found that a lot of the appendices were often only available on request to the authorities, and the authorities had never requested them,” says Tarang Sharma, a Ph.D. student at Cochrane and lead author of the study. “I'm actually kind of scared about how bad the actual situation would be if we had the complete data.” © 2016 Scientific American

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22242 - Posted: 05.24.2016

Zoe Cormier A hallucinogenic drug derived from magic mushrooms could be useful in treating depression, the first safety study of this approach has concluded. Researchers from Imperial College London gave 12 people psilocybin, the active component in magic mushrooms. All had been clinically depressed for a significant amount of time — on average 17.8 years. None of the patients had responded to standard medications, such as selective serotonin re-uptake inhibitors (SSRIs), or had electroconvulsive therapy. One week after receiving an oral dose of psilocybin, all patients experienced a marked improvement in their symptoms. Three months on, five patients were in complete remission. “That is pretty remarkable in the context of currently available treatments,” says Robin Carhart-Harris, a neuropsychopharmacologist at Imperial College London and first author of the latest study, which is published in The Lancet Psychiatry1. The equivalent remission rate for SSRIs is around 20%. The study's authors are not suggesting that psilocybin should be a treatment of last resort for depressed patients. “Our conclusion is more sober than that — we are simply saying that this is doable,” says Carhart-Harris. “We can give psilocybin to depressed patients, they can tolerate it, and it is safe. This gives us an initial impression of the effectiveness of the treatment.” © 2016 Nature Publishing Group

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22224 - Posted: 05.17.2016

By CLYDE HABERMAN At respected research centers in the United States and other countries, scientists have spent much of their professional lives in drug rehabilitation. It is not because they themselves struggle with addiction. What they are trying to rehabilitate are the drugs. Their focus is on mind-altering compounds that fell far from grace nearly half a century ago, LSD prominent among them. Along with other psychedelics, it was outlawed by the federal government, damned as bearing a high potential for abuse and offering no accepted medical benefit. But in recent years, researchers have sought to rescue hallucinogens from exile by examining their efficacy in treating certain disorders of the mind, and perhaps even in understanding the nature of consciousness and spirituality. The work of these scientists now draws the attention of Retro Report, a series of video documentaries that examine major news stories of the past and their enduring significance. Psychoactive substances, often derived from mushrooms, have been part of human cultures from Central and South America to the Sahara for thousands of years. But there is no need to look that far back; 1938 will do. That was when Albert Hofmann, a Swiss chemist searching for a drug to combat circulatory ailments, happened to synthesize lysergic acid diethylamide: LSD or, more familiarly, acid. Five years later, Dr. Hofmann, who died in 2008 at age 102, accidentally ingested a small dose of his creation and discovered its mind-blowing potential as he embarked on the first known acid trip. Many more such journeys would follow, for him and for countless others. © 2016 The New York Times Company

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: The Biology of Behavioral Disorders
Link ID: 22219 - Posted: 05.16.2016

Laura Sanders Ketamine, a drug that has shown promise in quickly easing depression, doesn’t actually do the job itself. Instead, depression relief comes from one of the drug’s breakdown products, a new study in mice suggests. The results, published May 4 in Nature, identify a potential depression-fighting drug that works quickly but without ketamine’s serious side effects or potential for abuse. The discovery “could be a major turning point,” says neuroscientist Roberto Malinow of the University of California, San Diego. “I’m sure that drug companies will look at this very closely.” Depression is a pernicious problem with few good treatments. Traditional antidepressants don’t work for everyone, and when the drugs do work, they can take weeks to kick in. Ketamine, developed in the 1960s as a sedative for people and now used commonly by veterinarians to knock out animals, can ease depression in minutes, not weeks, small studies show. But the new study suggests that a metabolite of ketamine — not the drug itself — fights depression. Inside the body, ketamine gets converted into a slew of related molecules. One of these breakdown molecules, a chemical called (2R,6R)-hydroxynorketamine, is behind the benefits, neuropharmacologist Todd Gould of the University of Maryland School of Medicine in Baltimore and colleagues found. On its own, a single dose of (2R,6R)-HNK reduced signs of depression in mice, restoring their drive to search for a hidden platform in water, to try to escape a shock and to choose sweet water over plain. A type of ketamine that couldn’t be broken down easily into HNKs didn’t ease signs of depression in mice. Finding that a breakdown product, and not ketamine itself, was behind the results was a big surprise, Gould says. © Society for Science & the Public 2000 - 2016

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 22184 - Posted: 05.05.2016

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

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22165 - Posted: 05.02.2016

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.

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: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22154 - Posted: 04.28.2016

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,

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
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

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: The Biology of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 22148 - Posted: 04.27.2016

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

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: The Biology of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 22132 - Posted: 04.23.2016

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 22126 - Posted: 04.21.2016

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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 12: Sex: Evolutionary, Hormonal, and Neural Bases
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 22092 - Posted: 04.12.2016

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

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: The Biology of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
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

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders
Link ID: 22075 - Posted: 04.06.2016