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Claudia M. Gold At the recent gubernatorial candidates forum on mental health, Martha Coakley repeated the oft-heard phrase that depression is like diabetes. Her motivation was good, the idea being to reduce the stigma of mental illness, and to offer "parity" or equal insurance coverage, for mental and physical illness. However, I am concerned that this phrase, and its companion, "ADHD is like diabetes," will, in fact, have the exact opposite effect. A recent New York Times op ed, The Trouble with Brain Science, helped me to put my finger on what is troubling about these statements. Psychologist Gary Marcus identifies the need for a bridge between neuroscience and psychology that does not currently exist. Diabetes is a disorder of insulin metabolism. Insulin is produced in the pancreas. The above analogies disregard the intimate intertwining of brain and mind. For the pancreas, there is no corresponding "mind" that exists in the realm of feelings and relationships. While there is some emerging evidence of the brain structures involved in the collection of symptoms named by the DSM (Diagnostic and Statistical Manual of Mental Disorders,) there are no known biological processes corresponding to depression, ADHD or any other diagnosis in the DSM. There is, however, a wealth of new evidence showing how brain structure and function changes in relationships. ©2014 Boston Globe Media Partners, LLC

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: 19836 - Posted: 07.16.2014

By Sharon Oosthoek, CBC News Mounting evidence that gut bacteria affect mood and behaviour has researchers investigating just how much power these tiny microbes wield over our mental health. "Many people with chronic intestinal conditions also have psychological disturbances and we never understood why," says McMaster University gastroenterologist Dr. Stephen Collins. Now, scientists such as Dr. Collins are starting to come up with answers. Our lower gastrointestinal tract is home to almost 100 trillion microorganisms, most of which are bacteria. They are, by and large, "good" bacteria that help us digest food and release the energy and nutrients we need. They also crowd out bacteria that can trigger disease. But when things go awry in our guts, they can also go awry in our brains. Up to 80 per cent of people with irritable bowel syndrome experience increased anxiety and depression. And those with autism — a syndrome associated with problems interacting with others — are more likely to have abnormal levels of gut bacteria. Dr. Collins and fellow McMaster gastroenterologist Premysl Bercik have done some of the seminal research into the bacteria-brain-behaviour connection. In a study published last year, they changed the behaviour of mice by giving them fecal transplants of intestinal bacteria. It involved giving adventurous mice bacteria from timid ones, thereby inducing timid behaviour. Before the transplant, adventurous mice placed in a dark, protected enclosure spent much of their time exploring an attached bright, wide-open area. After the transplant, they rarely ventured beyond their enclosure. © CBC 2014

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 19827 - Posted: 07.14.2014

|By Roni Jacobson Prozac, Paxil, Celexa, Zoloft, Lexapro. These so-called selective serotonin reuptake inhibitors (SSRIs) are among the most widely prescribed drugs in the U.S. Although they are typically used to treat depression and anxiety disorders, they are also prescribed off-label for conditions such as chronic pain, premature ejaculation, bulimia, irritable bowel syndrome, premenstrual syndrome and hot flashes. Even if you have never taken an SSRI, chances are you know someone who has. About one in every 10 American adults is being prescribed one now. For women aged 40 to 59 years old, the proportion increases to one in four. SSRIs block the body from reabsorbing serotonin, a neurotransmitter mostly found in the brain, spinal cord and digestive tract whose roles include regulation of mood, appetite, sexual function and sleep. Specifically, SSRIs bind to the protein that carries serotonin between nerve cells—called SERT, for serotonin transporter—intercepting it before it can escort the released neurotransmitter back into the cell. This action leaves more active serotonin in the body, a chemical effect that is supposed to spur feelings of happiness and well-being. But there are hints that SSRIs are doing something other than simply boosting serotonin levels. First, people vary in their response to SSRIs: Studies have shown that the drugs are not very effective for mild to moderate depression, but work well when the disorder is severe. If low serotonin were the only culprit in depression, SSRIs would be more uniformly helpful in alleviating symptoms. Second, it takes weeks after starting an SSRI for depression and anxiety to lift even though changes in serotonin ought to happen pretty much right away. © 2014 Scientific American

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 19822 - Posted: 07.14.2014

By Adam Carter, CBC News Women who take antidepressants when they’re pregnant could unknowingly predispose their kids to type 2 diabetes and obesity later on in life, new research out of McMaster University suggests. The study, conducted by associate professor of obstetrics and gynecology Alison Holloway and PhD student Nicole De Long, found a link between the antidepressant fluoxetine and increased risk of obesity and diabetes in children. Holloway cautions that this is not a warning for all pregnant women to stop taking antidepressants, but rather to start a conversation about prenatal care and what works best on an individual basis. “There are a lot of women who really need antidepressants to treat depression. This is what they need,” Holloway told CBC. “We’re not saying you should necessarily take patients off antidepressants because of this — but women should have this discussion with their caregiver.” “Obesity and Type 2 diabetes in children is on the rise and there is the argument that it is related to lifestyle and availability of high calorie foods and reduced physical activity, but our study has found that maternal antidepressant use may also be a contributing factor to the obesity and diabetes epidemic.” According to a study out of Memorial University in St. John's, obesity rates in Canada have tripled between 1985 and 2011. Canada also ranks poorly when it comes to its overall number of cases of diabetes, according to international report from the Organization for Economic Co-operation and Development, released last year. © CBC 2014

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: 19760 - Posted: 06.23.2014

By Brady Dennis Government warnings a decade ago about the risks associated with children and adolescents taking antidepressants appear to have backfired, causing an increase in suicide attempts and discouraging many depressed young people from seeking treatment, according to a study published Wednesday in the academic journal BMJ. Researchers said their findings underscore how even well-intentioned public health warnings can produce unintended conseque­n­c­­es, particularly when they involve widespread media attention and sensitive topics such as depression and suicide. In 2003 and 2004, the Food and Drug Administration issued a series of warnings based on data that pointed to an increase in suicidal thinking among some children and adolescents prescribed a class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs. They included such drugs as Paxil and Zoloft. In late 2004, the agency directed manufacturers to include a “black box” warning on their labels notifying consumers and doctors about the increased risk of suicidal thoughts and behaviors in youths being treated with these medications. The FDA warnings received a flood of media coverage that researchers said focused more on the tiny percentage of patients who had experienced suicidal thinking due to the drugs than on the far greater number who benefited from them. “There was a huge amount of publicity,” said Stephen Soumerai, professor of population medicine at Harvard Medical School and a co-author of Wednesday’s study. “The media concentrated more on the relatively small risk than on the significant upside.”

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: 19747 - Posted: 06.19.2014

By PAM BELLUCK Cindy Wachenheim was someone people didn’t think they had to worry about. She was a levelheaded lawyer working for the State Supreme Court, a favorite aunt who got down on the floor to play with her nieces and nephews, and, finally, in her 40s, the mother she had long dreamed of becoming. But when her baby was a few months old, she became obsessed with the idea that she had caused him irrevocable brain damage. Nothing could shake her from that certainty, not even repeated assurances from doctors that he was normal. “I love him so much, but it’s obviously a terrible kind of love,” she agonized in a 13-page handwritten note. “It’s a love where I can’t bear knowing he is going to suffer physically and mentally/emotionally for much of his life.” Ms. Wachenheim’s story provides a wrenching case study of one woman’s experience with maternal mental illness in its most extreme and rare form. It also illuminates some of the surprising research findings that are redefining the scientific understanding of such disorders: that they often develop later than expected and include symptoms not just of depression, but of psychiatric illnesses. Now these mood disorders, long hidden in shame and fear, are coming out of the shadows. Many women have been afraid to admit to terrifying visions or deadened emotions, believing they should be flush with maternal joy or fearing their babies would be taken from them. But now, advocacy groups on maternal mental illness are springing up, and some mothers are blogging about their experiences with remarkable candor. A dozen states have passed laws encouraging screening, education and treatment. And celebrities, including Brooke Shields, Gwyneth Paltrow and Courteney Cox, have disclosed their postpartum depression. © 2014 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: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 19743 - Posted: 06.17.2014

by Clare Wilson People who begin antidepressant treatment must face a gruelling wait of several weeks before they find out whether or not the drug will work for them. A new take on the causes of depression could lead to a blood test predicting who will be helped by medication – taking the guess work out of prescribing. "A test would be a major advance as at the moment millions of people are treated with antidepressants that won't have any effect," says Gustavo Turecki of McGill University in Montreal, Canada, who led the study. The research centres on miRNAs, small molecules that have an important role in turning genes on and off in different parts of the body. MiRNAs have already been implicated in several brain disorders. In the latest study, Turecki and his colleagues measured the levels of about 1000 miRNAs in the brains of people who had committed suicide. These were compared to levels in brains of people who had died from other causes. A molecule called miRNA-1202 was the most altered, being present at significantly lower levels in the brains of people who died from suicide. Crucially, this molecule seems to damp down the activity of a gene involved in glutamate signalling in the brain. That's significant because recent research has highlighted the importance of glutamate signalling in depression. © 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: 19731 - Posted: 06.14.2014

The financial crisis has been linked to a 4.5 per cent increase in Canada’s suicide rate, according to a study that estimates at least 10,000 extra suicides could be connected to economic hardship in EU countries and North America. Researchers compared suicide data from the World Health Organization before and after the onset of the recession in 2007. "A crucial question for policy and psychiatric practice is whether these suicide rises are inevitable," Aaron Reeves of Oxford University’s sociology department and his co-authors said in Wednesday’s issue of the British Journal of Psychiatry. Given that the rise in suicides exceeded what would be expected and the large variations in suicide rates across countries, the researchers suspect some of the suicides were "potentially avoidable." In Canada, the suicides rose by 4.5 per cent or about 240 suicides more than expected between 2007 and 2010. In the U.S.A, the rate increased by 4.8 per cent over the same period. Before 2007 in Europe, suicide rates had been falling, but the trend reversed, rising by 6.5 per cent by 2009 and staying elevated through 2011. Two countries, Sweden and Finland, bucked the trend in the early 1990s. Job loss, home repossession and debt are the main risk factors leading to suicide during economic downturns, previous studies suggest. © CBC 2014

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: 19722 - Posted: 06.12.2014

By Chris Wodskou, CBC News For the past 25 years, people suffering from depression have been treated with antidepressant drugs like Zoloft, Prozac and Paxil — three of the world’s best-selling selective serotonin reuptake inhibitors, or SSRIs. But people are questioning whether these drugs are the appropriate treatment for depression, and if they could even be causing harm. The drugs are designed to address a chemical imbalance in the brain and thereby relieve the symptoms of depression. In this case, it’s a shortage of serotonin that antidepressants work to correct. In fact, there are pharmaceutical treatments targeting chemical imbalances for just about every form of mental illness, from schizophrenia to ADHD, and a raft of anxiety disorders. Hundreds of millions of prescriptions are written for antipsychotic, antidepressant and anti-anxiety medications every year in the United States alone, producing billions of dollars in revenue for pharmaceutical companies. But what if the very premise behind these drugs is flawed? What if mental illnesses like depression aren’t really caused by chemical imbalances, and that millions of the people who are prescribed those drugs derive no benefit from them? And what if those drugs could actually make their mental illness worse and more intractable over the long term? Investigative journalist Robert Whitaker argued that psychiatric drugs are a largely ineffective way of treating mental illness in his 2010 book called Anatomy of an Epidemic: Magic Bullets, Psychiatric Drugs and the Astonishing Rise of Mental Illness in America. Whitaker maintains that the foundation of modern psychiatry, the chemical imbalance model, is scientifically unproven. © CBC 2014

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: 19712 - Posted: 06.09.2014

By Meeri Kim, Many of us find ourselves swimming along in the tranquil sea of life when suddenly a crisis hits — a death in the family, the loss of a job, a bad breakup. Some power through and find calm waters again, while others drown in depression. Scientists continue to search for the underlying genes and neurobiology that dictate our reactions to stress. Now, a study using mice has found a switch-like mechanism between resilience and defeat in an area of the brain that plays an important role in regulating emotions and has been linked with mood and anxiety disorders. (Bo Li/Cold Spring Harbor Laboratory) - Researchers at Cold Spring Harbor Laboratory identify the neurons in the brain that determine if a mouse will learn to cope with stress or become depressed. These neurons, located in a region of the brain known as the medial prefrontal cortex (top, green image) become hyperactive in depressed mice. The bottom panel is close-up of above image - yellow indicates activation. The team showed that this enhanced activity causes depression. After artificially enhancing the activity of neurons in that part of the brain — the medial prefrontal cortex — mice that previously fought to avoid electric shocks started to act helpless. Rather than leaping for an open escape route, they sat in a corner taking the pain — presumably out of a belief that nothing they could do would change their circumstances. “This helpless behavior is quite similar to what clinicians see in depressed individuals — an inability to take action to avoid or correct a difficult situation,” said study author and neuroscientist Bo Li of the Cold Spring Harbor Laboratory in New York. The results were published online May 27 in the Journal of Neuroscience. © 1996-2014 The Washington Post

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 18: Attention and Higher Cognition
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 14: Attention and Consciousness
Link ID: 19704 - Posted: 06.06.2014

Joy Jernigan TODAY contributor Depression is a serious medical condition that affects millions of Americans — and nearly twice as many women as men. Symptoms can include persistent feelings of sadness or hopelessness and loss of interest in activities that were once pleasurable, according to the National Institute of Mental Health. Other symptoms include feelings of guilt or worthlessness, irritability, changes in appetite, increased fatigue, difficulty concentrating — even recurrent thoughts of suicide. About 12 million American women suffer from depression each year, women like Debi Lee. Although depression is treatable, most commonly with medications or counseling, many never seek help, often because they are too embarrassed or ashamed. "Depression is really a physical illness," said Dr. Andrew Leuchter, a psychiatrist at the Semel Institute for Neuroscience and Human Behavior at University of California, Los Angeles. It's a disorder that even can be seen in brain scans, with images clearly showing the difference between a normal functioning brain and the brain of someone suffering from depression. "When you show this image to a person who's struggling with depression and you show them that their brain looks different than the quote so-called healthy person, what's their reaction?" Shriver asked. "It's commonly one of relief," Leuchter said. Now, Dr. Leuchter says there's an innovative new treatment called synchronized transcranial magnetic stimulation, or sTMS, that may have the potential to provide relief. Dr. Leuchter, a consultant and stockholder in the company behind sTMS, says it syncs to each patient's brain, then stimulates it with low levels of magnetic energy, 30 minutes a day for several weeks.

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: 19689 - Posted: 06.04.2014

Jyoti Madhusoodanan Most people handle stress well, but some find it difficult to cope and as a result develop depression and other mood disorders. Researchers have previously been able to identify the part of the brain that controls this response, but not exactly how it does so. Now, a study in mice identifies a small group of neurons that could be responsible. The research might also help elucidate the mechanism of deep brain stimulation, a therapy that uses electrical impulses to treat depression and other neurological disorders. How an animal deals with stress is controlled by a part of the brain known as the prefrontal cortex, and the neurons in this part of the brain are known to change in structure and function in response to stressful situations1. To look at the cellular basis of the responses, neuroscientist Bo Li of Cold Spring Harbor Laboratory in New York and his colleagues subjected mice to small electric shocks at random intervals to produce stress. Most of the mice tried to avoid the shocks, but just over one-fifth did not. They also started to avoid other animals or failed to choose tasty foods over plain ones — typical signs of depressive behaviour. The researchers then looked at the animals' brains and found that a specific set of neurons in the prefrontal cortex were easily excitable in depressed mice, but much harder to excite in those resilient to the stress. Furthermore, artificially increasing the activity of these neurons caused mice that were once resilient to become susceptible to depressive behaviours. “We were surprised that we were able to see a difference between depressed and resilient animals at the level of synaptic transmission,” says Li. © 2014 Nature Publishing Group,

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: 19674 - Posted: 05.31.2014

André Aleman & Damiaan Denys According to the World Health Organization, almost 1 million people kill themselves every year. That is more than the number that die in homicides and war combined. A further 10 million to 20 million people attempt it. Suicide is one of the three leading causes of death in the economically most productive age group — those aged 15–44 years — and rates have risen since the economic crisis triggered by the banking crash in 2008 (see 'Suicide rates in Europe'). For example, the number of suicides per year in the Netherlands rose by 30% between 2008 and 2012, from 1,353 to 1,753. In the United States, the average suicide costs society US$1.06 million according to the US Centers for Disease Control and Prevention. Despite its enormous societal impact, little progress has been made in the scientific understanding or treatment of suicidal behaviour. We do know that up to 90% of suicides occur in people with a clinically diagnosable psychiatric disorder1. Large epidemiological studies have shown mental disorders, particularly depression and alcohol addiction, to be major risk factors2. And there is compelling evidence that adequate prevention and treatment of such disorders can reduce suicide rates2. But psychiatry has long neglected the topic. Other than as symptoms of borderline personality disorder and mood disorders, suicide, suicide attempts and suicidal thoughts were not listed in the fourth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-IV). The DSM-5 (published last year) does not code suicidal behaviour — the most prominent emergency in psychiatry in primary care. Suicidality is perceived as a medical complication rather than as a disorder in its own right. © 2014 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: 19642 - Posted: 05.21.2014

Eleven years on, I still remember the evening I decided to kill my baby daughter. It's not something you're supposed to feel as a new parent with a warm, tiny bundle in your arms. But this is how postnatal depression can twist your logic. At the time it made perfect sense. Catherine was screaming, in pain. She had colic, there was nothing I could do about it. If an animal were in this much pain you'd put it out of its misery, so why not a human? Postnatal depression can have this kind of effect even on the most reasonable woman, yet you won't find much about it in baby books. We're expected to love our kids the moment they pop out, even while the memory of the labour pains is still raw. I knew a baby would be hard work, of course, but I expected motherhood to be fulfilling. As it happened I had a wonderful pregnancy, followed by a quick and easy birth. But the problems started soon after. Catherine wouldn’t feed, her blood sugar levels tumbled and I ended up bottle-feeding her, in tears, in a hospital room filled with posters promoting the breast. I was a Bad Mother within 48 hours. Things were no better after the first month. This was meant to be a joyous time, but all I seemed to feel was rage and resentment. In pregnancy all the attention had been on me, and suddenly I was a sideshow to this wailing thing in a crib. I was tired, tetchy and resentful. My daughter had rapidly become a ball and chain. My freedom was over. I kept hoping this was just the “baby blues” and that it would soon pass, but things only got worse. When colic set in, for around five hours each evening Catherine would scream, her face a mix of red and purple rage. No amount of pacing, tummy-rubbing or soothing words could stop this tiny demanding creature. So one night, alone with her in her room, I decided it would be best to put her out of her misery. © 2014 Guardian News and Media Limited

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: Biological Basis of Behavioral Disorders; Chapter 8: Hormones and Sex
Link ID: 19626 - Posted: 05.16.2014

by Nathan Collins There's a new twist in mental health. People with depression seem three times as likely as those without it to have two brain lobes curled around each other. The brains of people with depression can be physically different from other brains – they are often smaller, for example – but exactly why that is so remains unclear. In humans, some studies point to changes in the size of the hippocampi, structures near the back of the brain thought to support memory formation. "There are so many studies that show a smaller hippocampus in almost every psychiatric disorder," says Jerome Maller, a neuroscientist at the Monash Alfred Psychiatry Research Centre in Melbourne, Australia, who led the latest work looking at brain lobes. "But very few can actually show or hypothesize why that is." Maller thinks he has stumbled on an explanation. He had been using a brain stimulation technique known as transcranial magnetic stimulation as a therapy for antidepressant-resistant depression. This involved using fMRI scans to create detailed maps of the brain to determine which parts to stimulate. While pouring over hundreds of those maps, Maller noticed that many of them showed signs of occipital bending. This is where occipital lobes – which are important for vision – at the back of the brain's left and right hemispheres twist around each other. So he and his colleagues scanned 51 people with and 48 without major depressive disorder. They found that about 35 per cent of those with depression and 12.5 per cent of the others showed signs of occipital bending. The difference was even greater in women: 46 per cent of women with depression had occipital bending compared with just 6 per cent of those without depression. © Copyright Reed Business Information Ltd.

Related chapters from BP7e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 19: Language and Hemispheric Asymmetry
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 15: Language and Our Divided Brain
Link ID: 19617 - Posted: 05.15.2014

by Michael Slezak Could preventing the brain shrinkage associated with depression be as simple as blocking a protein? Post-mortem analysis of brain tissue has shown that the dendrites that relay messages between neurons are more shrivelled in people with severe depression than in people without the condition. This atrophy could be behind some of the symptoms of depression, such as the inability to feel pleasure. As a result, drugs that help repair the neuronal connections, like ketamine, are under investigation. But how this shrinkage occurs has remained a mystery, limiting researchers' ability to find ways of stopping it. Ronald Duman at Yale University wondered whether a protein called REDD1, which was recently shown to reduce myelin, the fatty material that protects neurons, was the key. To find out, his team bred rats unable to produce REDD1 and exposed them to a prolonged period of unpredictable stress. In normal rats, this stress resulted in depressive-like behaviour and brain shrinkage, but Duman's rats were unaffected. In contrast, rats engineered to overproduce REDD1 became depressed and had brain shrinkage, even without being stressed. What's more, injecting normal rats with a stress hormone boosted levels of REDD1 in the brain. Giving them a drug that blocked the production of stress hormones stopped them producing the protein, even when they were externally stressed. Taken together, the experiments show that REDD1 is necessary to produce the brain shrinkage seen in stressed rats, and that stress hormones are involved in its production – offering a possible way to prevent the shrinkage. © 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: 19532 - Posted: 04.24.2014

By Melissa Healy The nature of psychological resilience has, in recent years, been a subject of enormous interest to researchers, who have wondered how some people endure and even thrive under a certain amount of stress, and others crumble and fall prey to depression. The resulting research has underscored the importance of feeling socially connected and the value of psychotherapy to identify and exercise patterns of thought that protect against hopelessness and defeat. But what does psychological resilience look like inside our brains, at the cellular level? Such knowledge might help bolster peoples' immunity to depression and even treat people under chronic stress. And a new study published Thursday in Science magazine has made some progress in the effort to see the brain struggling with -- and ultimately triumphing over -- stress. A group of neuroscientists at Mount Sinai's Icahn School of Medicine in New York focused on the dopaminergic cells in the brain's ventral tegmentum, a key node in the brain's reward circuitry and therefore an important place to look at how social triumph and defeat play out in the brain. In mice under stress because they were either chronically isolated or rebuffed or attacked by fellow littermates, the group had observed that this group of neurons become overactive. It would logically follow, then, that if you don't want stressed mice (or people) to become depressed, you would want to avoid hyperactivity in that key group of neurons, right? Actually, wrong, the researchers found. In a series of experiments, they saw that the mice who were least prone to behave in socially defeated ways when under stress were actually the ones whose dopaminergic cells in the ventral tegmental area displayed the greatest levels of hyperactivity in response to stress. And that hyperactivity was most pronounced in the neurons that extended from the tegmentum into the nearby nucleus accumbens, also a key node in the brain's reward system.

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: 19511 - Posted: 04.21.2014

Scientists have traced vulnerability to depression-like behaviors in mice to out-of-balance electrical activity inside neurons of the brain’s reward circuit and experimentally reversed it – but there’s a twist. Instead of suppressing it, researchers funded by the National Institutes of Health boosted runaway neuronal activity even further, eventually triggering a compensatory self-stabilizing response. Once electrical balance was restored, previously susceptible animals were no longer prone to becoming withdrawn, anxious, and listless following socially stressful experiences. “To our surprise, neurons in this circuit harbor their own self-tuning, homeostatic mechanism of natural resilience,” explained Ming-Hu Han, Ph.D External Web Site Policy., of the Icahn School of Medicine at Mount Sinai, New York City, a grantee of the NIH’s National Institute of Mental Health (NIMH) and leader of the research team. Han and colleagues report on their discovery April 18, 2014 in the journal Science. Prior to the new study, the researchers had turned resilience to social stress on and off by using pulses of light to manipulate reward circuit neuronal firing rates in genetically engineered mice – optogenetics. But they didn’t know how resilience worked at the cellular level. To find out, they focused on electrical events in reward circuit neurons of mice exposed to a social stressor. Some mice that experience repeated encounters with a dominant animal emerge behaviorally unscathed, while others develop depression-like behaviors.

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: 19510 - Posted: 04.19.2014

By DORIS IAROVICI, M.D. “I think our experiment failed,” the young graduate student told me, referring to our attempt to take her off the antidepressant she’d been on for seven years. She was back in my campus office after a difficult summer break, and as she talked about feeling unsettled and upset, I wondered about the broader experiment playing out on college campuses across the country. Antidepressants are an excellent treatment for depression and anxiety. I’ve seen them improve — and sometimes save — many young lives. But a growing number of young adults are taking psychiatric medicines for longer and longer periods, at the very age when they are also consolidating their identities, making plans for the future and navigating adult relationships. Are we using good scientific evidence to make decisions about keeping these young people on antidepressants? Or are we inadvertently teaching future generations to view themselves as too fragile to cope with the adversity that life invariably brings? My patient had started medication as a college freshman, after she’d become depressed and spent much of her time in bed. She was forced to take a medical leave but improved quickly, returned to school and graduated. She married soon after and worked for a few years, feeling well all the while. Professional guidelines recommend six to nine months of medicine for first episodes of depression. But my patient had never been advised to stop taking it. She reluctantly agreed to my recommendation to taper off her antidepressant. © 2014 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: 19502 - Posted: 04.17.2014

By BENEDICT CAREY The relationship had become intolerably abusive, and after a stinging phone call one night, it seemed there was only one way to end the pain. Enough wine and pills should do the job — and would have, except that paramedics barged through the door, alerted by her lover. “I very rarely tell the story in detail publicly, it’s so triggering and sensational,” said Dese’Rae L. Stage, 30, a photographer and writer living in Brooklyn who tried to kill herself in 2006. “I talk about what led up to it, how helpless I felt — and what came after.” The nation’s oldest suicide prevention organization, the American Association of Suicidology, decided in a vote by its board last week to recognize a vast but historically invisible portion of its membership: people, like Ms. Stage, who tried to kill themselves but survived. About a million American adults a year make a failed attempt at suicide, surveys suggest, far outnumbering the 38,000 who succeed, and in the past few years, scores of them have come together on social media and in other forums to demand a bigger voice in prevention efforts. Plans for speakers bureaus of survivors willing to tell their stories are well underway, as is research to measure the effect of such testimony on audiences. For decades, mental health organizations have featured speakers with schizophrenia, bipolar disorder and depression. But until now, suicide has been virtually taboo, because of not only shame and stigma, but also fears that talking about the act could give others ideas about how to do it. “This is a real shift you’re seeing,” said Heidi Bryan, 56, of Neenah, Wis., who has been speaking for years about suicide attempts she made in the 1990s. “For people working in suicide prevention, they always told us not to talk about our own experience, like they were afraid to tip us over the edge or something. Honestly, we’re the ones who know what works and what doesn’t.” © 2014 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: 19481 - Posted: 04.14.2014