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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

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.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 14: Biological Rhythms, Sleep, and Dreaming
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 22063 - Posted: 04.04.2016

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.

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: 22049 - Posted: 03.30.2016

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

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: 21998 - Posted: 03.17.2016

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

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: 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.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 12: Psychopathology: The Biology of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 21932 - Posted: 02.25.2016

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.)

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: 21899 - Posted: 02.16.2016