Chapter 12. Psychopathology: Biological Basis of Behavioral Disorders
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By Scicurious People who suffer from obsessive compulsive disorder (OCD) can’t help some of their actions. They suffer from severely intrusive thoughts and anxiety, which they know are not right. And they feel a compulsion to do rituals to get rid of them. Maybe it’s repetitive hand washing. Maybe it’s checking that the stove is off exactly 7 times each night. Whatever it is, the symptoms can cause severely interfere with their daily lives. What causes these compulsive, repetitive behaviors? We’re not sure, but today’s paper suggests a role of the circuit between the striatum and the orbitofrontal cortex, areas associated with impulsivity and repetitive behaviors. And it could be that increasing activity within certain parts of this circuit might help shut down some repetitive behaviors, giving us important insight into how repetitive behaviors work. I should begin by noting that Ed also covered this paper over at Not Exactly Rocket Science, along with another paper about making compulsive behaviors. It’s a really cool look at the two papers and you should definitely check it out! Me, I’m interested in the circuit involved here, and why stimulating one part may end up inhibiting behavior. The authors of this study started with a model of obsessive behavior, the SAPAP3 knockout mouse, which I actually wrote a bit about recently. This mouse has a knockout of a special protein associated with synapses. Without it, mice display obsessive (well, repetitive, we can’t really ask the mouse if they are obsessing) grooming behavior, grooming their faces so much that they will cause lesions to form. The authors wanted to look at what caused this behavior, and what could potentially stop it. © 2013 Scientific American
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18285 - Posted: 06.18.2013
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
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
Published by scicurious What do the overconsumption of food and Obsessive-Compulsive Disorder (OCD) have in common? At first, this sounds like a trick question. But deep in the brain, the molecules underlying our behavior may come together for these two conditions. The first is MC4R, a receptor for melanocortin. It binds hormones and affects feeding behavior, mutations in MC4R are associated with severe overcomsumption of high fat, high calorie foods and with obesity. A mouse without an MC4R gene will become severely obese compared to its wildtype counterparts. SAPAP3 is a protein that is associated with synapses, the spaces between neurons. It can regulate things like receptor levels that determine how well a neuron responds to excitatory input. But a knockout of SAPAP3 in mice produces something very different: severe overgrooming, a model of OCD. All rodents groom themselves, it's necessary to keep clean. But SAPAP3 knockouts groom themselves far, far too much, to the point of creating terrible lesions on their skin. This has been proposed as a model of OCD, as many people with OCD become obsessed with cleanliness, and will do things like, say, washing their hands, to the point of severely damaging their skin. So a knockout of MC4R creates obese mice. A knockout of SAPAP3 creates overgrooming mice. You might think that if you combined the two knockouts, you would get severely obese mice that also overgroomed. But you don't. Instead, you get mice that, to all appearances, seem completely normal. No obesity. No overgrooming. Neurotic Physiology Copyright © 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
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
Link ID: 18268 - Posted: 06.13.2013
Kerri Smith Researchers have both created and relieved symptoms of obsessive-compulsive disorder (OCD) in genetically modified mice using a technique that turns brain cells on and off with light, known as optogenetics. The work, by two separate teams, confirms the neural circuits that contribute to the condition and points to treatment targets. It also provides insight into how quickly compulsive behaviours can develop — and how quickly they might be soothed. The results of the studies are published in Science1, 2. Brain scanning in humans with OCD has pointed to two areas — the orbitofrontal cortex, just behind the eyes, and the striatum, a hub in the middle of the brain — as being involved in the condition's characteristic repetitive and compulsive behaviours. But “in people we have no way of testing cause and effect”, says Susanne Ahmari, a psychiatrist and neuroscientist at Columbia University in New York who led one of the studies. It is not clear, for example, whether abnormal brain activity causes the compulsions, or whether the behaviour simply results from the brain trying to hold symptoms at bay by compensating. “There’s been a big debate in the field,” says Satinder Kaur Singh of Yale University in New Haven, Connecticut, who studies molecules involved in OCD-like disorders but was not involved in the new studies. “What the Ahmari paper shows is that it is causative.” © 2013 Nature Publishing Group
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18248 - Posted: 06.08.2013
by Jennifer Viegas Dogs with obsessive compulsive disorder show nearly the same brain abnormalities of humans who have OCD, a new study finds. The discovery, published in Progress in Neuro-Psychopharmacology & Biological Psychiatry, adds another notch to the dog-human connection and holds promise for better treatments for OCD. “While the study sample was small and further research is needed, the results further validate that dogs with CCD (Canine Compulsive Disorder) can provide insight and understanding into anxiety disorders that affect people,” Nicholas Dodman, a professor of clinical sciences at the Cummings School of Veterinary Medicine at Tufts University who worked on the study, said in a press release. Dodman said that, in addition to having the same structural brain abnormalities as people with OCD, dogs also show similar behaviors, respond to the same medications and seem to have similar genetic roots to the disorder. Dogs with CCD engage in repetitious and destructive behaviors, such as flank and blanket-sucking, tail chasing and chewing. The main thing — and this is true for humans as well — is that the activity or thought is repetitive and persistent, such that it’s time consuming and interferes with normal daily routines. For dogs, Dobermans appear to be a breed that is most at risk, likely due to their genetics. © 2013 Discovery Communications, LLC
Keyword: OCD - Obsessive Compulsive Disorder
Link ID: 18241 - Posted: 06.06.2013
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
Link ID: 18229 - Posted: 06.04.2013
by Douglas Heaven Putting a digital face to the abusive voices in their head could help people with schizophrenia. Results of a preliminary trial, announced today at the Wellcome Trust in London, demonstrated how people with schizophrenia could overcome their auditory hallucinations by conversing with an avatar representation of the voice in their head. At the start of the trial, 16 people with schizophrenia created an on-screen avatar that best matched what they imagined the voice in their head to look like – much like a police photo-fit. They then chose a male or female voice closely resembling the one they hear. By conversing with a therapist via the avatar, the volunteers reported reduced levels of distress and higher self-esteem. Three people stopped hearing the hallucinatory voice altogether – including one who had lived with it for 16 years. Hearing voices is a common symptom of schizophrenia, which affects about 1 per cent of the population worldwide. The hallucinations can stop people from thinking clearly and prevent them from working and sustaining social relationships. The voices are also typically abusive, telling the person to harm themselves or others. "It's hard to imagine what it's like to hear a disembodied voice," says Julian Leff at University College London, who led the trial. People often say that the helplessness is the worst thing, he says. They cannot control the voices and they feel dominated. © Copyright Reed Business Information Ltd.
Link ID: 18203 - Posted: 05.30.2013
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
Link ID: 18197 - Posted: 05.28.2013
Scientists have reversed behavioral and brain abnormalities in adult mice that resemble some features of schizophrenia by restoring normal expression to a suspect gene that is over-expressed in humans with the illness. Targeting expression of the gene Neuregulin1, which makes a protein important for brain development, may hold promise for treating at least some patients with the brain disorder, say researchers funded by the National Institutes of Health. Like patients with schizophrenia, adult mice biogenetically-engineered to have higher Neuregulin 1 levels showed reduced activity of the brain messenger chemicals glutamate and GABA. The mice also showed behaviors related to aspects of the human illness. For example, they interacted less with other animals and faltered on thinking tasks. “The deficits reversed when we normalized Neuregulin 1 expression in animals that had been symptomatic, suggesting that damage which occurred during development is recoverable in adulthood,” explained Lin Mei, M.D., Ph.D.External Web Site Policy , of the Medical College of Georgia at Georgia Regents University, a grantee of NIH’s National Institute of Mental Health (NIMH). “While mouse models can’t really do full justice to a complex brain disorder that impairs our most uniquely human characteristics, this study demonstrates the potential of dissecting the workings of intermediate components of disorders in animals to discover underlying mechanisms and new treatment targets,” said NIMH Director Thomas R. Insel, M.D. “Hopeful news about how an illness process that originates early in development might be reversible in adulthood illustrates the promise of such translational research.” Schizophrenia is thought to stem from early damage to the developing fetal brain, traceable to a complex mix of genetic and environmental causes. Although genes identified to date account for only a small fraction of cases, evidence has implicated variation in the Neuregulin 1 gene. For example, postmortem studies have found that it is overexpressed in the brain's thinking hub, or prefrontal cortex, of some people who had schizophrenia. It codes for a chemical messenger that plays a pivotal role in communication between brain cells, as well as in brain development.
By Jeffrey A. Lieberman Like many psychiatrists, I have been amazed by the debates surrounding the DSM-5, the first major revision of the American Psychiatric Association’s Diagnostic and Statistical Manual of Mental Disorders in nearly twenty years, which was just released. Never before has a thick medical text of diagnostic nomenclature been the subject of so much attention. Although I was heartened to see more and more people discussing the real-world issues and challenges—for patients, families, clinicians and caregivers–within mental health care, for which the book offers an up-to-the-minute diagnostic GPS, I was also alarmed at the harsh criticism of the field of psychiatry and the APA. Consequently, I believe that as you read and watch this increased coverage, it’s important to understand the difference between thoughtful, legitimate debate, and the inevitable outcry from a small group of critics –made louder by social media and support from dubious sources —who have relentlessly sought to undermine the credibility of psychiatric medicine and question the validity of mental illness.. DSM-5 has ignited a broad dialogue on mental illness and opened up a conversation about the state of psychiatry and mental healthcare in this country. Critiques have ranged in focus from the inclusion of specific disorders in DSM-5, to the concern over a lack of biological measures which define them. Some have even questioned the entire diagnostic system, urging us to look with an eye focused on the impact to patients. These are the kinds of debate that I hope will continue long after DSM-5’s shiny cover becomes warn and wrinkled. Such meaningful discourse only fuels our ability to produce a manual that best serves those touched by mental illness. But there’s another type of critique that does not contribute to this goal. These are the groups who are actually proud to identify themselves as “anti-psychiatry.” © 2013 Scientific American
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.
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.
By Samyukta Mullangi A recent article in NYTimes  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
Pregnant mothers’ exposure to the flu was associated with a nearly fourfold increased risk that their child would develop bipolar disorder in adulthood, in a study funded by the National Institutes of Health. The findings add to mounting evidence of possible shared underlying causes and illness processes with schizophrenia, which some studies have also linked to prenatal exposure to influenza. “Prospective mothers should take common sense preventive measures, such as getting flu shots prior to and in the early stages of pregnancy and avoiding contact with people who are symptomatic,” said Alan Brown, M.D., M.P.H, of Columbia University and New York State Psychiatric Institute, a grantee of the NIH’s National Institute of Mental Health (NIMH). “In spite of public health recommendations, only a relatively small fraction of such women get immunized. The weight of evidence now suggests that benefits of the vaccine likely outweigh any possible risk to the mother or newborn.” Brown and colleagues reported their findings online May 8, 2013 in JAMA Psychiatry. Although there have been hints of a maternal influenza/bipolar disorder connection, the new study is the first to prospectively follow families in the same HMO, using physician-based diagnoses and structured standardized psychiatric measures. Access to unique Kaiser-Permanente, county and Child Health and Development Study External Web Site Policy databases made it possible to include more cases with detailed maternal flu exposure information than in previous studies.
Heidi Ledford Nassir Ghaemi, director of the Mood Disorders Program at Tufts Medical Center in Boston, Massachusetts, has felt shackled by the Diagnostic and Statistical Manual of Mental Disorders (DSM), often called the bible of psychiatry. Some of his depressed patients occasionally show manic behaviour but do not fulfil the DSM’s criteria for a diagnosis of bipolar disorder. Ghaemi is interested in whether such patients might respond better to drugs for bipolar disorder than for depression. But his colleagues warned him against straying from the DSM when he applied for funding at the US National Institute of Mental Health (NIMH), because peer reviewers tended to insist on research that hewed to DSM categories. Ghaemi held off from applying. If NIMH director Thomas Insel has his way, Ghaemi and other mental-health researchers will no longer feel the weight of the DSM. “NIMH will be re-orienting its research away from DSM categories,” Insel wrote in a blog entry on 29 April. The latest edition, the DSM-5, will be unveiled on 22 May at the annual meeting of the American Psychiatric Association in San Francisco, California. Like many psychiatrists, Insel questions whether the DSM’s categories accurately reflect the way the brain works. He is pushing a project that aims to create a new framework that classifies mental-health disorders according to their biological roots. “Going forward, we will be supporting research projects that look across current categories — or sub-divide current categories — to begin to develop a better system,” Insel wrote. The blog post made waves in the media and rattled some psychiatric clinicians and researchers. But Insel says that he has been talking about the issue since 2008. “The word was just still not out there,” he says. Insel says that he has increasingly received complaints from grant applicants who have tried to follow his guidance, only to be shot down by peer reviewers for eschewing DSM scripture. © 2013 Nature Publishing Group
by Claudia M Gold It seems that the National Institute of Mental Health (NIMH) may have dealt a death blow to the recently published Diagnostic and Statistical Manual of Mental Disorders (DSM 5) when the organization declared they would no longer fund research based on the DSM system of diagnosis. The views of NIMH director Thomas Insel were referenced in the recent New York Times article on the subject. His goal was to reshape the direction of psychiatric research to focus on biology, genetics and neuroscience so that scientists can define disorders by their causes, rather than their symptoms. I am no fan of the DSM system, which reduces complex experience to lists of symptoms; focusing on the "what" rather than the "why." However, the NIMH model has limits as well. There seems to be a wish to study mental illness in the same way we study cancer or diabetes. While I certainly have great respect for the complexity of the pancreas, or the process of malignant transformation of cells, trying to understand the brain/mind in an analogous way seems to be an unnecessary and even undesirable reduction of human experience. What is missing from both paradigms is recognition of the relational and historical context of being human. Fortunately there seems to be awareness that neither paradigm is complete. The Times article goes on to say: Dr. Insel is one of a growing number of scientists who think that the field needs an entirely new paradigm for understanding mental disorders, though neither he nor anyone else knows exactly what it will look like. © 2013 NY Times Co.
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