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By Jessica Hamzelou JACK NICHOLSON has a lot to answer for. One of the knock-on effects of hit 1975 movie One Flew Over the Cuckoo’s Nest was a public backlash against electroconvulsive therapy (ECT). The treatment, used since the 1930s for a wide range of mental health conditions, delivers a jolt of electricity to the brain big enough to trigger a seizure. The film’s brutal depiction of ECT and lobbying helped it fall out of favour in the 1980s and 1990s. But ECT may now be undergoing a revival, led by psychiatrists who champion it because of its success rate. “It’s the most effective treatment we have in psychiatry,” says George Kirov at Cardiff University, UK, who oversees ECT treatments in the area. A report from the UK Royal College of Psychiatrists last September showed that three-quarters of people with mental health problems felt improvement after having ECT. And psychiatrists say that a similar percentage of people who have schizophrenia that doesn’t respond to drug treatment find ECT effective. “I’ve never seen an ECT treatment that doesn’t work,” says Helen Farrell, a psychiatrist at the Beth Israel Deaconess Medical Center in Boston. “People have such a skewed view of electroconvulsive therapy. It is seen as primitive and horrific“ Mounting evidence has convinced the US Food and Drug Administration (FDA) to consider reclassifying ECT devices to make the technology more accessible for people with depression or bipolar disorder. The public will still take some convincing, however. In a 2005 survey in Switzerland, for example, 56 per cent were against ECT, while just 1 per cent said they were in favour. © Copyright Reed Business Information Ltd.

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: 22571 - Posted: 08.18.2016

Laura Sanders A busy protein known for its role in aging may also have a hand in depression, a study on mice hints. Under certain circumstances, the aging-related SIRT1 protein seems to make mice despondent, scientists report August 10 in the Journal of Neuroscience. The results are preliminary, but they might ultimately help find new depression treatments. Today’s treatments aren’t always effective, and new approaches are sorely needed. “This is one potential new avenue,” says study coauthor Deveroux Ferguson of the University of Arizona College of Medicine in Phoenix. Ferguson and colleagues subjected mice to 10 days of stressful encounters with other mice. After their demoralizing ordeal, the mice showed signs of depression, such as eschewing sugar water and giving up attempts to swim. Along with these signs of rodent despair, the mice had more SIRT1 gene activity in the nucleus accumbens, a brain area that has been linked to motivation and depression. Resveratrol, a compound found in red grapes, supercharges the SIRT1 protein, making it more efficient at its job. When Ferguson and colleagues delivered resveratrol directly to the nucleus accumbens, mice displayed more signs of depression and anxiety. When the researchers used a different compound to hinder SIRT1 activity, the mice showed the opposite effect, appearing bolder in some tests than mice that didn’t receive the compound. |© Society for Science & the Public 2000 - 2016.

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: 22537 - Posted: 08.10.2016

Nicola Davis Scientists have discovered 17 separate genetic variations that increase the risk of a person developing depression. The findings, which came from analysing DNA data collected from more than 300,000 people, are the first genetics links to the disease found in people of European ancestry. The scientists say the research will contribute to a better understanding of the disease and could eventually lead to new treatments. They also hope it will reduce the stigma that can accompany depression. According to Nice, up to 10% of people seen by practitioners in primary care have clinical depression, with symptoms including a continuously low mood, low self-esteem, difficulties making decisions and lack of energy. Both environmental and genetic factors are thought to be behind depression, with the interaction between the two also thought to be important. But with a large number of genetic variants each thought to make a tiny contribution to the risk of developing the condition, unravelling their identity has proved challenging. While previous studies have turned up a couple of regions in the genome of Chinese women that might increase the risk of depression, the variants didn’t appear to play a role in depression for people of European ancestry. © 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: 22504 - Posted: 08.02.2016

By David Levine Almost seven percent of U.S. adults—about 15.7 million people—are diagnosed with major depression disorder, according to the National Institute of Mental Health (NIMH). The Centers for Disease Control and Prevention report that depression causes 200 million lost workdays each year at a cost to employers of between $17 billion and $44 billion. The statistics for anxiety disorders are not great either. The most common mental illnesses in the U.S., they affect 40 million adults age 18 and older, costing the economy more than $42 billion a year. In my twenties, I developed panic disorder. I failed to get better on most medications and therapy. As I reported in an article earlier this year, it took me years to find a medication that worked. Because it took me so long to be diagnosed and treated properly, I have always been interested in alternative treatments for depression and anxiety. Two years ago I attended two sessions at the World Science Festival on the use of electrical therapy to treat depression and anxiety. The first event was Spark of Genius? Awakening a Better Brain, a panel discussion moderated by ABC News Chief Health & Medical Editor Richard Besser. The panel discussed what is known about treating the brain and the ethical and legal complications of brain enhancement. (You can watch it online at the World Science Festival website.) The second panel, "Electric Medicine and the Brain" was moderated by John Rennie, former editor in chief of Scientific American His panel focused on the use of "electroceuticals," a term coined by researchers at GlaxoSmithKline to refer to all implantable devices being used to treat mental illnesses and being explored in the treatment of metabolic, cardiovascular and inflammatory disorders. © 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: 22462 - Posted: 07.20.2016

By Nicholas Bakalar A new study has identified a bacterial blueprint for chronic fatigue syndrome, offering further evidence that it is a physical disease with biological causes and not a psychological condition. Chronic fatigue syndrome is a condition that causes extreme and lasting fatigue, preventing people from taking part in even the most routine daily activities. There are no tests to confirm the diagnosis, which has prompted speculation that it is a psychological condition rather than a physical illness. In a study published in Microbiome, researchers recruited 48 people with C.F.S. and 39 healthy controls. Then they analyzed the quantity and variety of bacteria species in their stool. They also searched for markers of inflammation in their blood. The stool samples of those with C.F.S. had significantly lower diversity of species compared with the healthy people — a finding typical of inflammatory bowel disease as well. The scientists also discovered that people with C.F.S. had higher blood levels of lipopolysaccharides, inflammatory molecules that may indicate that bacteria have moved from the gut into the bloodstream, where they can produce various symptoms of disease. Using these criteria, the researchers were able to accurately identify more than 83 percent of C.F.S. cases based on the diversity of their gut bacteria and lipopolysaccharides in their blood. Finding a biomarker for C.F.S. has been an ongoing goal for researchers who hope to one day develop a diagnostic test for the condition. Still, the senior author of the study, Maureen R. Hanson, a professor of molecular biology at Cornell, said the bacteria blueprint in the new study is not yet a method of definitively diagnosing C.F.S. The importance of the finding, she said, is that it may offer new clues as to why people have these symptoms. © 2016 The New York Times Company

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: 22411 - Posted: 07.08.2016

Anthony Devlin/ Antidepressant use is at an all-time in high in England, where prescriptions filled for these drugs has doubled over the last decade. Figures from the Health and Social Care Information Centre show that in 2015, 61 million prescriptions were filled for antidepressant drugs, including citalopram and fluoxetine. This is up from 57.1 million in 2014, and 29.4 million back in 2005. “The reasons for this increase in antidepressant prescriptions could include a greater awareness of mental illness and more willingness to seek help,” says Gillian Connor of the charity Rethink Mental Illness. “However, with our overstretched and underfunded mental health services, too often antidepressants are the only treatment available.” UK guidelines suggest that people should be offered antidepressants as a first treatment option for moderate depression, but some critics argue that it would be better to steer people to talking therapies. In May, Andrew Green, a GP in East Riding and chairman of the British Medical Association’s Clinical and Prescribing Subcommittee, told a meeting of the UK’s All-Party Parliamentary Group for Prescribed Drug Dependence that one of the reasons doctors resort to prescribing antidepressants is because the waiting lists for talking therapies are so long. © Copyright Reed Business Information Ltd.

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: 22399 - Posted: 07.06.2016

By Tara Parker-Pope About one in eight women take an antidepressant at some time during pregnancy, reports Roni Rabin in today’s Science Times. But is it safe? Some new research shows that antidepressant use during pregnancy may be linked to certain problems in newborns. A new review of the medical literature concludes that treatment decisions for depression during pregnancy must be made on a case-by-case basis. “There’s not a one-size-fits-all answer,” said Dr. Kimberly Yonkers, a professor of psychiatry and obstetrics and gynecology at Yale School of Medicine who was the report’s lead author, and who acknowledged receiving research support from antidepressant manufacturers. “You can’t say, ‘Stop medication for all women because it’s harmful,’ and you can’t put all women on medication either.” To learn more, read the full story, “Depression Is a Dilemma for Women in Pregnancy,” and then please join the discussion below. Did you experience depression during pregnancy? Did you take medication to treat it? © 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: 22386 - Posted: 07.01.2016

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