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By JAN HOFFMAN From the shock of the cancer diagnosis onward, depression can take its well-documented toll on patients. Even patients who appear to pack away their fears during the grinding treatment journey to becoming cancer-free concede that when the regimen ends, they unspool emotionally. There has been less attention paid to the disease’s emotional impact on spouses. They, too, can become depressed. But with the roles of caregiver and cheerleader thrust upon them, they may feel constrained about expressing their darker feelings. Now a new analysis finds that within two years of a cancer diagnosis, the pervasiveness of depression in patients and their spouses tends to drop back to roughly the same levels as in the general population, only to be replaced by another mind-demon: anxiety, which can even intensify as time passes. 48 Were you a caretaker for someone with cancer? How did you take care of yourself while your partner was going through treatment? Join in the discussion below. The analysis, which looked at 43 studies involving 51,381 patients with a range of cancers, found that over all, nearly 18 percent of patients experienced serious anxiety two to 10 years after their diagnosis, compared with about 14 percent of the general population. But in a cluster of studies that looked at couples, anxiety levels in that time frame grew to as high as 28 percent in patients and 40 percent in their spouses. Copyright 2013 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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18372 - Posted: 07.13.2013

By NICHOLAS BAKALAR Using functional magnetic resonance imaging, researchers have found brain changes in preschool-age children with depression that are not apparent in their nondepressed peers. The study, in the July issue of The Journal of the American Academy of Child & Adolescent Psychiatry, examined 23 children 4 to 6 years old who had been diagnosed with depression and 31 of their healthy peers. Researchers used well-validated tests to diagnose depression, and eliminated from the study children with neurological disorders, autism or developmental disorders, or who had been born prematurely. None of the subjects was taking antidepressants. The children underwent M.R.I. brain scans while viewing pictures of happy, sad, fearful or neutral faces. The researchers found that right amygdala and right thalamus activity was significantly greater in the depressed children than in the others, a finding that has also been observed in depressed adolescents and adults. “We found something in the brain that is aligned with the idea of neurobiological models of depression — which parts of the brain are involved and how they interact,” said the lead author, Michael S. Gaffrey, an assistant professor in the department of psychiatry at Washington University in St. Louis. “We can begin to use this information in conjunction with other information — symptoms, other biological markers — to identify and eventually prevent and treat this disorder.” Copyright 2013 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: Biological Basis of Behavioral Disorders; Chapter 13: Memory, Learning, and Development
Link ID: 18371 - Posted: 07.13.2013

By Bruce Bower A surprisingly simple decision-making tool shows promise as a way for physicians to identify people with depression. An answer to the first of four questions was all that researchers usually needed to identify women who weren’t depressed, say psychologist Mirjam Jenny of the Max Planck Institute for Human Development in Berlin and her colleagues. Using all four questions, this tool spotted depressed women about as well as two more-complex methods, Jenny’s team reports June 24 in the Journal of Applied Research in Memory and Cognition. If the findings hold up in other studies, physicians and other professionals with no mental-health training could use this brief technique to tag individuals who need thorough depression evaluations. “This decision tree can be used to screen for depression, but not to reach a final diagnosis,” Jenny says. Her team drew on data from 1,382 German women who completed a 21-item screening questionnaire for depression on two occasions, separated by 18 months. Based on this measure, depression initially affected 3.6 percent of the sample, or 50 individuals, and later appeared in 1.9 percent of the sample, or 26 individuals. Women’s initial responses to a handful of items that best predicted whether they would rank as depressed 18 months later were used to create a four-question decision tree. The first question in the tree — “Have you cried more than usual in the last week?” — led the pack in identifying cases of depression. A “no” response to this or any of the other three questions — which inquired about feelings in the last week of disappointment or self-hate, discouragement about the future and personal failure — exempted women from being categorized as depressed. Those who responded “yes” to all four questions were classified as depressed. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18370 - Posted: 07.13.2013

By RONI CARYN RABIN Martha Rhodes experienced her first bout of depression at 13. By her late 50s, she had taken just about every antidepressant there is, including Zoloft, Lexapro and Paxil — which did the trick for many years, but had side effects — then Effexor, Lamictal, Seroquel and Abilify. After a suicide attempt in 2009, she tried something radically different: transcranial magnetic stimulation, or TMS, a treatment in which magnetic pulses are used to stimulate parts of the brain believed to be involved in mood regulation. Unlike electroconvulsive or shock therapy, which is also used to treat stubborn depression, TMS does not generally produce seizures. Every day, she spent just over half an hour in a chair with a powerful magnet affixed to the front left side of her head. After four weeks, “I woke up and something was different,” said Mrs. Rhodes, who wrote a book, “3,000 Pulses Later” describing the treatment. “I felt lighter. I didn’t wake up in the morning and wish I were dead.” For Mrs. Rhodes, 63, a former advertising executive in Danbury, Conn., TMS treatment was transformative, and she no longer needs antidepressants. But there are still many questions about just how many severely depressed patients respond to TMS, which requires daily office visits for several weeks, costs thousands of dollars and is often not covered by insurance. For the therapy, patients sit in a doctor’s office with a large magnet pressed to the left side of their heads. The idea is that a pulsed magnetic field, similar to that used in M.R.I.’s, creates an electrical current in the surface of the brain that “resets” the patient’s mood regulatory system. Copyright 2013 The New York Times Company

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18337 - Posted: 07.02.2013

By DAVID DOBBS On average, about 700 Americans kill themselves each week — but in the fine-weather weeks of May and June, the toll rises closer to 800, sometimes higher. Every year, suicide peaks with the tulips and lilacs — increasing roughly 15 percent over the annual average to create one of psychiatry’s most consistent epidemiological patterns. It may seem perverse that the period of spring and early summer, as the psychologist Kay Redfield Jamison puts it in her splendid book “Night Falls Fast,” should contain “a capacity for self-murder that winter less often has.” Yet it does. This grim spring growth confounds conventional belief that suicides peak in winter. It also confounds researchers — and fascinates them. As they discover more angles into the biology of mood and behavior, they are finding new clues about why suicides rise with the sun’s arc. They hope solving this puzzle will help us better understand why people commit suicide at all — and perhaps reduce the numbers year-round. This effort takes an extra urgency from what Dr. Adam Kaplin, a psychiatrist at Johns Hopkins University, calls a “suicide epidemic” — a sharp increase in both absolute and per-capita rates since the recession that began in 2007, particularly among the middle-aged. More than 38,000 people committed suicide in the United States in 2010 — a 16.5 percent jump from the 32,600 suicides five years before, and a new high. The stakes involved in figuring out the dynamics of self-murder seem only to rise with time. The spring surge in suicides is actually the largest of a few oscillations throughout the year. After dropping to an annual low in February (October in the southern hemisphere), rates climb sharply through spring; fall slowly in summer; show a slight rise, according to some studies, in fall; and then begin a steep winter drop. The spring peak generally runs 10 to 25 percent above the yearly average and 20 to 50 percent above the February low. Copyright 2013 The New York Times Company

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: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 18308 - Posted: 06.25.2013

By Bruce Bower To a cacophony of boos, so-whats and even a few cheers, the American Psychiatric Association released the fifth edition of its Diagnostic and Statistical Manual of Mental Disorders, DSM-5, on May 18 at its annual meeting in San Francisco. Controversy always flares when psychiatrists redefine which forms of human suffering will count as real and reimbursable by medical insurance. This time, though, the stakes are raised by competing efforts to classify mental disorders. The World Health Organization plans to release a new version of its own system for identifying mental ailments in 2015 as part of the 11th edition of the International Classification of Diseases. It’s not clear how much the ICD will mirror DSM-5. Some differences have already emerged. Clinicians working on the international classification report in the May 11 Lancet that they plan to pare down the number and types of symptoms needed to diagnose post-traumatic stress disorder, or PTSD, and add a severe form of the condition triggered by long-lasting or frequent harrowing events. These departures from DSM-5 would make it easier for mental health workers to help victims of conflict and natural disasters in poor, non-Western countries, say psychologist Andreas Maercker of the University of Zurich and his colleagues. Meanwhile, the National Institute of Mental Health in Rockville, Md., has launched the Research Domain Criteria, or RDoC, a 10-year effort to define mental disorders based on behavioral and brain measures. DSM’s approach, by contrast, relies on rulings by groups of psychiatrists about which symptoms characterize particular disorders. The approach has yielded imprecise diagnostic labels that advance neither treatment nor research, argued psychiatrist and NIMH director Thomas Insel in an April 29 blog post. © Society for Science & the Public 2000 - 2013

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18276 - Posted: 06.15.2013

by Jennifer Couzin-Frankel Publish your data, or else we will—that's the stark warning to drug companies in a new proposal released today. Peter Doshi (shown right), a postdoctoral fellow at Johns Hopkins University in Baltimore, Maryland, and his colleagues are fed up that only about half of all clinical trials are published. They want to change that, by convincing researchers and journals to print data that have been publicly released through other means, such as litigation and Freedom of Information Act requests, but, practically speaking, are sitting dormant in the filing cabinets or computers of individual scientists. The unusual proposal is called RIAT, for Restoring Invisible and Abandoned Trials. It was published today in BMJ and also endorsed by PLOS Medicine. Doshi, who studies comparative effectiveness research, came up with the idea when his colleague, Swaroop Vedula, was analyzing reporting biases involving the drug gabapentin. Gabapentin's maker Pfizer had been sued for the way in which they marketed the drug for unapproved indications. During litigation, Pfizer had released thousands of pages involving gabapentin trials, and Vedula was poring through them. (One of the authors of the RIAT paper, Kay Dickersin, served as an expert witness against Pfizer in gabapentin litigation.) Pfizer had published only 12 of its 20 trials in gabapentin. But Doshi's center at Hopkins had the clinical study reports detailing the results of the other eight. At the time, "it just hits me," Doshi says. "Why are we still referring to these as unpublished trials? Why aren't we publishing them ourselves?" © 2010 American Association for the Advancement of Science

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: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18275 - Posted: 06.15.2013

Alison Abbott A simple brain scan may offer a way to predict which people being treated for depression will respond to drugs, and which will respond to cognitive behavioural therapy. Neurologist Helen Mayberg from Emory University in Atlanta, Georgia, and her colleagues have run the first systematic, well-controlled study to identify the first potential biomarker that distinguishes between treatment responses. The work is published in JAMA Psychiatry1. Psychiatrists are desperate for such biomarkers, because fewer than 40% of people with depression go into remission after initial treatment. “It could be fabulous,” says Steven Zalcman, chief of clinical neuroscience research at the US National Institute of Mental Health (NIMH) in Bethesda, Maryland. But he cautions that the brain-scan biomarker still has to be validated in further trials — a process that could take a couple of years. Mayberg and her colleagues selected 82 people with untreated depression, and measured glucose metabolism in their brains using positron emission tomography (PET) scans. They then randomly assigned the subjects to treatment groups. One group received the common antidepressant drug escitalopram oxalate (a selective serotonin reuptake inhibitor, or SSRI) for 12 weeks. The other group received 16 sessions of cognitive behavioural therapy over the same period. © 2013 Nature Publishing Group

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: Biological Basis of Behavioral Disorders; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 18269 - Posted: 06.13.2013

Comedian and writer Ruby Wax, a regular on British television, has clinical depression. In her book published last week, Sane New World (Hodder & Stoughton, 2013), she describes her struggles with different therapies and her fear of being ‘found out’. She is not alone. A 2010 survey in Europe revealed that 38% of people had a diagnosed mental disorder — including 7% with major depression. The proportion is likely to be similar in all populations, even in Africa, where psychiatric disease barely features on the health agenda. The stigma attached to such disorders means that many people do not admit to their illness. The same stigma discourages investment, so that research funding is not proportional to the distress these disorders cause. Why lobby for better treatments for depression or schizophrenia when there are ‘real’ diseases out there, such as cancer? Wax has been through the catalogue of available therapies and says that she has settled on an approach known as ‘mindfulness’, which helps to keep her depression under control. It may seem that the various therapies are inadequate, given that initial treatment of depression fails in 60% or more of cases. It is true that more treatment options are badly needed. Yet evidence-based cognitive behavioural therapies and drugs already developed by the pharmaceutical industry can work splendidly for long periods — if they are given to the right patients. How do you recognize the right patients? Treatment decisions tend to be based on the preferences of physicians or their patients, often with a missionary zeal that gives no credence to the idea that a personalized approach would be more appropriate. © 2013 Nature Publishing Group

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18268 - Posted: 06.13.2013

By Scicurious Most people have heard of ECT: Electroconvulsive Therapy. A lot of people will immediately think of the scene during One Flew Over the Cuckoo’s Nest, which doesn’t give you a very good picture. People think of ECT and think of horrible seizures, something terribly dangerous. But it’s not like that anymore. Now, ECT is usually done during a light anesthesia as well as a muscle relaxant. The huge seizures don’t happen anymore, though it’s still uncomfortable to watch (that’s a warning for the video below). So while ECT is no longer horrifying, it’s not something to be taken lightly. Aside from the fact that you’re getting an induced seizure, there are side effects, often people have deficits in working memory for a while afterward. But for people with severe depression who are truly desperate, it’s sometimes their best hope. But while we know that, in many patients, ECT does work, we still don’t know HOW. There are lots of antidepressants on the market today. All of them currently act on neurotransmitters, chemical messengers in the brain, and most of them act, at least in part, on serotonin. But the problem is, antidepressants don’t work for everyone. In fact, about 60% of patients being treated for depression won’t respond to the first drug they are given, and require trials of several different different drugs. And, sadly, 20% of patients don’t respond to all of the drugs tried. That’s a lot of people. And those people, who have often exhausted all of the drug options, sometimes turn to ECT. © 2013 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18229 - Posted: 06.04.2013

By Scicurious My eye was caught last week by a piece in Scientific American proper asking “is ketamine the next big depression drug?” It’s a good piece, and I appreciate the balance in the article, but I was also kind of surprised that…it took so long. There have been previous media rumblings (and blog) about ketamine through the years, so I’m rather curious as to why the article came out now (maybe there’s another new paper out? I didn’t see any referenced and couldn’t find anything). To be honest, while yes, ketamine has a lot of interesting potential, it’s not really quite as “new” as you might think. The first major clinical reports of ketamine as an effective antidepressant actually date back to 2000. Since then, scientists have been spending a lot of time trying to figure out WHY a drug usually used to knock out horses, or abused for its perception-changing qualities, acts as an antidepressant. And not just any antidepressant, but an almost miracle drug (maybe), helping people who respond to no other treatment, and with effects of a single dose occurring within hours (currently antidepressants take weeks), and lasting for weeks. And for all that…they don’t know how it works. So I saw the article, and I wanted to write a bit of follow-up. Because yes, while we don’t know QUITE how ketamine works…we have some ideas. And here is one of them. Ketamine isn’t like the current drugs used as antidepressants. Current drugs, like Prozac affect chemical neurotransmitters like serotonin. © 2013 Scientific American

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: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18197 - Posted: 05.28.2013

by Sara Reardon As suicide rates climb steeply in the US a growing number of psychiatrists are arguing that suicidal behaviour should be considered as a disease in its own right, rather than as a behaviour resulting from a mood disorder. They base their argument on mounting evidence showing that the brains of people who have committed suicide have striking similarities, quite distinct from what is seen in the brains of people who have similar mood disorders but who died of natural causes. Suicide also tends to be more common in some families, suggesting there may be genetic and other biological factors in play. What's more, most people with mood disorders never attempt to kill themselves, and about 10 per cent of suicides have no history of mental disease. The idea of classifying suicidal tendencies as a disease is being taken seriously. The team behind the fifth edition of the Diagnostic Standards Manual (DSM-5) – the newest version of psychiatry's "bible", released at the American Psychiatric Association's meeting in San Francisco this week – considered a proposal to have "suicide behaviour disorder" listed as a distinct diagnosis. It was ultimately put on probation: put into a list of topics deemed to require further research for possible inclusion in future DSM revisions. Another argument for linking suicidal people together under a single diagnosis is that it could spur research into the neurological and genetic factors they have in common. This could allow psychiatrists to better predict someone's suicide risk, and even lead to treatments that stop suicidal feelings. © Copyright Reed Business Information Ltd.

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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18165 - Posted: 05.18.2013

20:00 13 May 2013 by Douglas Heaven Genes in cells throughout the body switch on and off throughout the day in a coordinated way. Or at least they should. In people with clinical depression, genes in their brain tissues appear to be significantly out of sync – a finding that could lead to new treatments for the condition. We know from previous studies that genes in cells elsewhere, such as the skin, follow a 24-hour cycle of activity. But identifying patterns of genetic activity in a living brain isn't easy to do. "We always assumed we would have a clock [in our brain]," says Huda Akil at the University of Michigan in Ann Arbor. "But it had never been shown before." Akil and her colleagues examined the brains of 55 people with a known time of death, looking at around 12,000 genes in tissues from six brain regions. By matching the time of death with molecular signs of genetic activity – whether each gene was actively expressing itself or not – the team identified hundreds of genes that follow a daily cycle. Sudden death Akil says it was important to look at the brains of individuals who had died suddenly – through a heart attack or car accident, for example. Slower deaths can cause dramatic changes in the brain that would have obscured what they were looking for, but sudden death freezes the genetic activity. "We can capture an instant," she says. © Copyright Reed Business Information Ltd.

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: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 18158 - Posted: 05.14.2013

By Samyukta Mullangi A recent article in NYTimes [1] declared that the rising rate of suicides among our baby boomer generation now made suicides, by raw numbers alone, a bigger killer than motor vehicle accidents! Researchers quoted within the article pointed to complex reasons like the economic downturn over the past decade, the widespread availability of opioid drugs like oxycodone, and changes in marriage, social isolation and family roles. Then I scrolled down, as I always do, to peruse some of the readers’ comments, and that’s when I paused. I suppose in hindsight that I had expected readers to exclaim at the shocking statistics (suicide rates now stand at 27.3 per 100,000 for middle aged men, 8.1 per 100,000 for women), or lament over personal stories of relatives or friends who took their own lives. While I certainly saw a few such comments, I was amazed to discover the number of readers who were sympathetic to the idea of suicide. “Molly” wrote “Why is suicide usually looked upon as a desperate and forbidden act? Can’t we accept that in addition to poverty, loneliness, alienation, ill health, life in world [sic] that is sometimes personally pointless means that death is a relief? I believe the right to die, in a time and place (and wishfully peacefully without violence) is a basic human right.” This post was ‘recommended’ by 351 other readers at the time of this essay being written. © 2013 Scientific American

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: Biological Basis of Behavioral Disorders; Chapter 10: Biological Rhythms and Sleep
Link ID: 18157 - Posted: 05.14.2013

By NICHOLAS BAKALAR Two studies have found that depression and the use of certain antidepressants are both associated with increased risk for Clostridium difficile infection, an increasingly common cause of diarrhea that in the worst cases can be fatal. Researchers studied 16,781 men and women, average age 68, using hospital records and interviews to record cases of the infection, often called C. diff, and diagnoses of depression. The interviews were conducted biennially from 1991 to 2007 to gather self-reports of feelings of sadness and other emotional problems. There were 404 cases of C. difficile infection. After adjusting for other variables, the researchers found that the risk of C. diff infection among people with a history of depression or depressive symptoms was 36 to 47 percent greater than among people without depression. A second study, involving 4,047 hospitalized patients, average age 58, found a similar association of infection with depression. In addition, it found an association of some antidepressants — Remeron, Prozac and trazodone — with C. diff infection. There was no association with other antidepressants. “We have known for a long time that depression is associated with changes in the gastrointestinal system,” said the lead author, Mary A.M. Rogers, a research assistant professor at the University of Michigan, “and this interaction between the brain and the gut deserves more study.” Both reports appeared in the journal BMC Medicine. Copyright 2013 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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18136 - Posted: 05.09.2013

By TARA PARKER-POPE Suicide rates among middle-aged Americans have risen sharply in the past decade, prompting concern that a generation of baby boomers who have faced years of economic worry and easy access to prescription painkillers may be particularly vulnerable to self-inflicted harm. More people now die of suicide than in car accidents, according to the Centers for Disease Control and Prevention, which published the findings in Friday’s issue of its Morbidity and Mortality Weekly Report. In 2010 there were 33,687 deaths from motor vehicle crashes and 38,364 suicides. Suicide has typically been viewed as a problem of teenagers and the elderly, and the surge in suicide rates among middle-aged Americans is surprising. From 1999 to 2010, the suicide rate among Americans ages 35 to 64 rose by nearly 30 percent, to 17.6 deaths per 100,000 people, up from 13.7. Although suicide rates are growing among both middle-aged men and women, far more men take their own lives. The suicide rate for middle-aged men was 27.3 deaths per 100,000, while for women it was 8.1 deaths per 100,000. The most pronounced increases were seen among men in their 50s, a group in which suicide rates jumped by nearly 50 percent, to about 30 per 100,000. For women, the largest increase was seen in those ages 60 to 64, among whom rates increased by nearly 60 percent, to 7.0 per 100,000. Suicide rates can be difficult to interpret because of variations in the way local officials report causes of death. But C.D.C. and academic researchers said they were confident that the data documented an actual increase in deaths by suicide and not a statistical anomaly. While reporting of suicides is not always consistent around the country, the current numbers are, if anything, too low. © 2013 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: Biological Basis of Behavioral Disorders; Chapter 11: Emotions, Aggression, and Stress
Link ID: 18118 - Posted: 05.04.2013

by Andy Coghlan and Sara Reardon The world's biggest mental health research institute is abandoning the new version of psychiatry's "bible" – the Diagnostic and Statistical Manual of Mental Disorders, questioning its validity and stating that "patients with mental disorders deserve better". This bombshell comes just weeks before the publication of the fifth revision of the manual, called DSM-5. On 29 April, Thomas Insel, director of the US National Institute of Mental Health (NIMH), advocated a major shift away from categorising diseases such as bipolar disorder and schizophrenia according to a person's symptoms. Instead, Insel wants mental disorders to be diagnosed more objectively using genetics, brain scans that show abnormal patterns of activity and cognitive testing. This would mean abandoning the manual published by the American Psychiatric Association that has been the mainstay of psychiatric research for 60 years. The DSM has been embroiled in controversy for a number of years. Critics have said that it has outlasted its usefulness, has turned complaints that are not truly illnesses into medical conditions, and has been unduly influenced by pharmaceutical companies looking for new markets for their drugs. There have also been complaints that widened definitions of several disorder have led to over-diagnosis of conditions such as bipolar disorder and attention deficit hyperactivity disorder. Now, Insel has said in a blog post published by the NIMH that he wants a complete shift to diagnoses based on science not symptoms. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18117 - Posted: 05.04.2013

The short answer is no. But your question gets to the heart of an important problem that we have in this country: that all medications are approved by the Food and Drug Administration on the basis of relatively short-term studies, even though many are used long-term for medical and psychiatric disorders that are chronic, if not lifelong. The F.D.A. approves antidepressants like selective serotonin re-uptake inhibitors, or S.S.R.I.’s, if the drug beats a placebo in two randomized clinical trials that typically last 4 to 12 weeks and involve a few hundred patients. Longer-term maintenance studies, usually lasting one to two years, indicate that S.S.R.I.’s do not cause any serious harm, though they have plenty of side effects, like weight gain and sexual dysfunction. Once a drug hits the market, we have only a voluntary system of reporting adverse effects in the United States; there are no systematic long-term studies of any drug lasting 10 or more years. Still, S.S.R.I.’s have been used since the late 1980s and given to more than 40 million Americans, so it’s reasonable to say that if these drugs caused any significant toxic effects, we would have seen many such reports. Instead, we have some anecdotal reports claiming a wide range of S.S.R.I.-related toxicity, but one cannot know from these reports whether the symptoms are related to S.S.R.I. use or to medical illnesses that happen to develop over time in people taking these drugs. Copyright 2013 The New York Times Company

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: Biological Basis of Behavioral Disorders; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 18116 - Posted: 05.04.2013

By David Levine Sleep deprivation is a quick and efficient way to treat depression. It works 60 to 70 percent of the time—far better than existing drugs—but the mood boost usually lasts only until the patient falls asleep. As an ongoing treatment, sleep deprivation is impractical, but researchers have been studying the phenomenon in an effort to uncover the cellular mechanisms behind depression and remission. Now a team at Tufts University has pinpointed glia as the key players. The researchers previously found that astrocytes, a star-shaped type of glial cell, regulate the brain chemicals involved in sleepiness. During our waking hours, astrocytes continuously release the neurotransmitter adenosine, which builds up in the brain and causes “sleep pressure,” the feeling of sleepiness and its related memory and attention impairments. The neurotransmitter causes this pressure by binding to adenosine receptors on the outside of neurons like a key fitting into a lock. As more adenosine builds up, more receptors are triggered, and the urge to sleep gets stronger. In the new study, published online January 15 in the journal Translational Psychiatry, the scientists investigated whether this process is responsible for the antidepressant effects of sleep deprivation. Mice with depressivelike symptoms were administered three doses of a compound that triggers adenosine receptors, thus mimicking sleep deprivation. Although the mice continued to sleep normally, after 12 hours they showed a rapid improvement in mood and behavior, which lasted for 48 hours. © 2013 Scientific American

Related chapters from BP7e: Chapter 14: Biological Rhythms, Sleep, and Dreaming; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 10: Biological Rhythms and Sleep; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18083 - Posted: 04.27.2013

By Shaunacy Ferro When David Nichols earned a Ph.D in medicinal chemistry from the University of Iowa in 1973 by studying psychedelics, he thought he would continue studying hallucinogens indefinitely. "I thought I would work on it for the rest of my life," he says. His timing was less than fortuitous. In 1970, the year after Nichols started grad school, Richard Nixon signed into law the Controlled Substances Act, designed to clamp down on the manufacture and distribution of drugs in the U.S. The act classified hallucinogenic substances like LSD, DMT, psilocybin (the psychedelic alkaloid in mushrooms) and mescaline as Schedule I substances--the most restrictive use category, reserved for drugs with high potential for abuse and no accepted medical use. Marijuana was also placed in this category, and 15 years later when ecstasy came onto the scene, MDMA was emergency-classified as a Schedule I substance as well. By contrast, cocaine, opium and morphine are Schedule II substances, meaning they can be prescribed by a doctor. Despite some promising results from trials of psychedelics in treating alcoholism, psychiatric conditions and modeling mental illness, by the early '70s, the government had tightened control of Schedule I substances, even for research. It's only now that we're starting to return to the notion that these drugs could be medicine. © 2012 Popular Science

Related chapters from BP7e: Chapter 15: Emotions, Aggression, and Stress; Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 11: Emotions, Aggression, and Stress; Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 18056 - Posted: 04.22.2013