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A drug that works through the same brain mechanism as the fast-acting antidepressant ketamine briefly improved treatment-resistant patients' depression symptoms in minutes, with minimal untoward side effects, in a clinical trial conducted by the National Institutes of Health. The experimental agent, called AZD6765, acts through the brain's glutamate chemical messenger system. Existing antidepressants available through prescription, which work through the brain’s serotonin system, take a few weeks to work, imperiling severely depressed patients, who can be at high risk for suicide. Ketamine also works in hours, but its usefulness is limited by its potential for dissociative side-effects, including hallucinations. It is being studied mostly for clues to how it works. "Our findings serve as a proof of concept that we can tap into an important component of the glutamate pathway to develop a new generation of safe, rapid-acting practical treatments for depression," said Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health, which conducted the research. Zarate, and colleagues, reported on their results online Dec. 1, 2012 in the journal Biological Psychiatry. AZD6765, like ketamine, works by blocking glutamate binding to a protein on the surface of neurons, called the NMDA receptor. It is a less powerful blocker of the NMDA receptor, which may be a reason why it is better tolerated than ketamine.

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17594 - Posted: 12.11.2012

By BENEDICT CAREY They plotted a revolution, fell to debating among themselves, and in the end overturned very little except their own expectations. But the effort itself was a valuable guide for anyone who has received a psychiatric diagnosis, or anyone who might get one. This month, the American Psychiatric Association announced that its board of trustees had approved the fifth edition of the association’s influential diagnostic manual — the so-called bible of mental disorders — ending more than five years of sometimes acrimonious, and often very public, controversy. The committee of doctors appointed by the psychiatric association had attempted to execute a paradigm shift, changing how mental disorders are conceived and posting its proposals online for the public to comment. And comment it did: Patient advocacy groups sounded off, objecting to proposed changes in the definitions of depression and Asperger syndrome, among other diagnoses. Outside academic researchers did, too. A few committee members quit in protest. The final text, which won’t be fully available until publication this spring, has already gotten predictably mixed reviews. “Given the challenges in a field where objective lines are hard to draw, they did a solid job,” said Dr. Michael First, a psychiatrist at Columbia who edited a previous version of the manual and was a consultant on this one. Others disagreed. “This is the saddest moment in my 45-year career of practicing, studying and teaching psychiatry,” wrote Dr. Allen Frances, the chairman of a previous committee who has been one of the most vocal critics, in a blog post about the new manual, the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders, or DSM5. © 2012 The New York Times Company

Related chapters from BP6e: 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: 17593 - Posted: 12.11.2012

Cognitive behavioural therapy (CBT) can reduce symptoms of depression in people who fail to respond to drug treatment, says a study in the Lancet. CBT, a type of psychotherapy, was found to benefit nearly half of the 234 patients who received it combined with normal care from their GP. Up to two-thirds of people with depression do not respond to anti-depressants. Patients should have access to a range of treatments, the charity Mind said. CBT is a form of talking psychotherapy to help people with depression change the way they think to improve how they feel and alter their behaviour. The study followed 469 patients with treatment-resistant depression picked from GP practices in Bristol, Exeter and Glasgow over 12 months. One group of patients continued with their usual care from their GP, which could include anti-depressant medication, while the second group was also treated with CBT. After six months, researchers found 46% of those who had received CBT reported at least a 50% reduction in their symptoms. This compared with 22% experiencing the same reduction in the other group. The study concluded CBT was effective in reducing symptoms and improving patients' quality of life. The improvements had been maintained for a period of 12 months, it added. BBC © 2012

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17582 - Posted: 12.08.2012

Scicurious Guest Writer, Nicole Baganz! 4:02 PM. It took every ounce of energy I had to drag myself to the bathroom. Arriving in the room that is located 2 feet from my bed felt like a victory. I rifled through the medicine cabinet, stuck the thermometer in my mouth and collapsed on the bathroom floor. 103.2° F. Yep, I’m sick. Sleepiness. Fatigue. Loss of appetite and motivation. Lethargy. Leave me alone. We all know what it feels like to be sick. Clinicians collectively describe this group of symptoms as “sickness behavior”. Evolutionarily speaking, the idea that the immune system would produce these symptoms makes sense. An organism infected with a pathogenic bug should retreat from its social group to protect others from the spread of infection. The organism essentially shuts down in order to send every ounce of energy to the immune system to battle the bug that has invaded the body’s cells. This sickness state would facilitate recovery of the organism and also protect the community from the spread of the infection by limiting the interaction of the infected party from its entire social group. All of the symptoms of sickness behavior are displayed not only by people who have an infection, but also by those who have been diagnosed with Major Depressive Disorder (MDD). Could sickness behavior and MDD be linked? What happens in the brain to produce sickness behaviors, and how might these relate to depression? Mice are good models for scientists to use to study the effect of immune system activation on brain function and behavior (research studies that subject people to infectious agents before probing their brains in the name of science draw few willing volunteers). Laboratory mice also display sickness behavior when their immune systems are turned on. Sick rodents sleep more, eat less, and lose interest in drinking sugary water (usually a scrumptious treat for mice). They also stop interacting socially – mice are, by nature, very social creatures that like to sniff, groom, lick and cuddle up to their roommates. © 2012 Scientific American

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17551 - Posted: 11.29.2012

Richard A. Lovett Scientists have known for years that human medications, from anti-inflammatories to the hormones in birth-control pills, are ending up in waterways and affecting fish and other aquatic organisms. But researchers are only beginning to compile the many effects that those drugs seem to be having. And it isn't good news for the fish. One such drug, fluoxetine, is the active ingredient in the antidepressant Prozac. Like some other pharmaceuticals, fluoxetine is excreted in the urine of people taking it, and reaches lakes and waterways through sewage-treatment plants that are unequipped to remove it. To investigate the effects of fluoxetine, researchers have turned to a common US freshwater fish species called the fathead minnow (Pimephales promelas). Normally, fathead minnows show a complex mating behaviour, with males building the nests that females visit to lay their eggs. Once the eggs are laid and fertilized, the males tend to them by cleaning away any fungus or dead eggs. But when fluoxetine is added to the water, all of this changes, said Rebecca Klaper, an ecologist at the University of Wisconsin-Milwaukee's Great Lakes Water Institute. Klaper presented her results this week at the 2012 meeting of the North American division of the Society of Environmental Toxicology and Chemistry in Long Beach, California. © 2012 Nature Publishing Group,

Related chapters from BP6e: 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: 17506 - Posted: 11.19.2012

Danish researchers Krogh and colleagues randomly 115 assigned depressed people to one of two exercise programs. One was a strenuous aerobic workout - cycling for 30 minutes, 3 times per week, for 3 months. The other was various stretching exercises. The idea was that stretching was a kind of placebo control group on the grounds that, while it is an intervention, it's not the kind of exercise that gets you fit. It doesn't burn many calories, it doesn't improve your cardiovascular system, etc. Aerobic exercise is the kind that's most commonly been proposed as having an antidepressant effect. So what happened? Not much. Both groups got less depressed but there was zero difference between the two conditions. The cyclists did get physically fitter than the stretchers, losing more weight and improving on other measures. But they didn't feel any better. If this is true, it might mean that the antidepressant effects of aerobic exercise are psychological rather than physical - it's about the idea of 'exercising', not the process of becoming fitter. While many trials have found modest beneficial effects of exercise vs a "control condition", the control condition was often just doing nothing much - such as being put on a waiting-list. So the placebo effect or the motivational benefits of 'doing something', rather than the effects of exercise per se, could be behind it. In the current study though the stretching avoided that problem.

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 11: Motor Control and Plasticity
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 5: The Sensorimotor System
Link ID: 17463 - Posted: 11.07.2012

By Stephanie Pappas, An over-excited immune system may explain why some people are susceptible to depression, according to new research on mice. Mice whose immune systems responded to stress by overproducing an inflammatory compound called Interleukin-6 were more likely to become the mousy versions of depressed than mice with non-overactive immune systems, the research found. This same compound is elevated in depressed humans, said study researcher Georgia Hodes, suggesting hope for new depression treatments. "There's probably a subset of people with depression who have this over-sensitive inflammatory response to stress and that this is leading to the symptoms of depression," Hodes, a postdoctoral researcher at the Mount Sinai Medical Center in New York, told LiveScience. Hodes added that stress could be thought of as an allergen, like pet dander, with the over-reactive immune system making you depressed rather than giving you runny nose. "In some ways, it is an analogy to an allergy," Hodes said. "You have something that is not really dangerous, but your body thinks it is, so you have this massive immune response. In this case, the stressor is what they're having this massive immune response to." Some of the symptoms of depression — lack of energy, loss of appetite — mirror the body's response to physical illness, Hodes noted. © 2012 Yahoo! Inc.

Related chapters from BP6e: 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: 17462 - Posted: 11.07.2012

By WILLIAM C. RHODEN We’ve seen it hundreds of times. An athlete is injured and within seconds is surrounded by an armada of medical personnel: trainers, assistant trainers, team doctors. The athlete is helped off the field, given a diagnosis, treated and sent to physical therapy, often to return miraculously in a week or two. But when that same athlete has a mental disorder, there is no armada of trainers, no team doctors. That athlete is often abandoned. For all of the current focus on traumatic brain injury as a result of concussions, mental illness, often overlooked, exists at every level of sports. Sports too often is a masking agent that hides deeply rooted mental health issues. The better the athlete, the more desperate to reach the next level, the less likely he or she will reach out for help. The gladiator mentality remains a primary barrier. “Mental health has a stigma that is tied into weakness and is absolutely the antithesis of what athletes want to portray,” said Dr. Thelma Dye Holmes, the executive director of the Northside Center for Child Development, one of New York’s oldest mental health agencies, serving more than 1,500 children and their families. “Mental health is not something that you can easily know,” Holmes said. “You feel a pain in your side, you have discomfort. Mental illness is vague and makes us uneasy. Especially when it comes to athletes, there tends to be a stigma around coming forward.” © 2012 The New York Times Company

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17436 - Posted: 10.30.2012

By ARTHUR A. STONE DESPITE the beating that Mondays have taken in pop songs — Fats Domino crooned “Blue Monday, how I hate blue Monday” — the day does not deserve its gloomy reputation. Two colleagues and I recently published an analysis of a remarkable yearlong survey by the Gallup Organization, which conducted 1,000 live interviews a day, asking people across the United States to recall their mood in the prior day. We scoured the data for evidence that Monday was bluer than Tuesday or Wednesday. We couldn’t find any. Mood was evaluated with several adjectives measuring positive or negative feelings. Spanish-only speakers were queried in Spanish. Interviewers spoke to people in every state on cellphones and land lines. The data unequivocally showed that Mondays are as pleasant to Americans as the three days that follow, and only a trifle less joyful than Fridays. Perhaps no surprise, people generally felt good on the weekend — though for retirees, the distinction between weekend and weekdays was only modest. Likewise, day-of-the-week mood was gender-blind. Over all, women assessed their daily moods more negatively than men did, but relative changes from day to day were similar for both sexes. And yet still, the belief in blue Mondays persists. Several years ago, in another study, I examined expectations about mood and day of the week: two-thirds of the sample nominated Monday as the “worst” day of the week. Other research has confirmed that this sentiment is widespread, despite the fact that, well, we don’t really feel any gloomier on that day. © 2012 The New York Times Company

Related chapters from BP6e: 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: 17366 - Posted: 10.13.2012

By RICHARD A. FRIEDMAN, M.D. Speed, instant gratification, accessibility — these are a few of the appealing hallmarks of digital technology. It’s no coincidence that we love our smart wireless devices: Humans are a notoriously impatient species, born with a preference for immediate rewards. But the virtues of the digital age are not always aligned with those of psychotherapy. It takes time to change behavior and alleviate emotional pain, and for many patients constant access is more harmful than helpful. These days, as never before, therapists are struggling to recalibrate their approach to patients living in a wired world. For some, the new technology is clearly a boon. Let’s say you have the common anxiety disorder social phobia. You avoid speaking up in class or at work, fearful you’ll embarrass yourself, and the prospect of going to a party inspires dread. You will do anything to avoid social interactions. You see a therapist who sensibly recommends cognitive-behavioral therapy, which will challenge your dysfunctional thoughts about how people see you and as a result lower your social anxiety. You find that this treatment involves a fair amount of homework: You typically have to keep a written log of your thoughts and feelings to examine them. And since you see your therapist weekly, most of the work is done solo. As it turns out, there is a smartphone app that will prompt you at various times during the day to record these social interactions and your emotional response to them. You can take the record to your therapist, and you are off and running. © 2012 The New York Times Company

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17345 - Posted: 10.09.2012

By Tori Rodriguez A common complaint about wrinkle-masking Botox is that recipients have difficulty displaying emotions on their faces. That side effect might be a good thing, however, for people with treatment-resistant depression. In the first randomized, controlled study on the effect of botulinum toxin—known commercially as Botox—on depression, researchers investigated whether it might aid patients with major depressive disorder who had not responded to antidepressant medications. Participants in the treatment group were given a single dose (consisting of five injections) of botulinum toxin in the area of the face between and just above the eyebrows, whereas the control group was given placebo injections. Depressive symptoms in the treatment group decreased 47 percent after six weeks, an improvement that remained through the 16-week study period. The placebo group had a 9 percent reduction in symptoms. The findings appeared in May in the Journal of Psychiatric Research. Study author M. Axel Wollmer, a psychiatrist at the University of Basel in Switzerland, believes the treatment “interrupts feedback from the facial musculature to the brain, which may be involved in the development and maintenance of negative emotions.” Past studies have shown that Botox impairs people's ability to identify others' feelings, and the new finding adds more evidence: the muscles of the face are instrumental for identifying and experiencing emotions, not just communicating them. © 2012 Scientific American

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 1: An Introduction to Brain and Behavior
Link ID: 17315 - Posted: 10.02.2012

Moms suffering the blues in the months after giving birth may be more likely to end up with kids who are shorter than their peers, a new study shows. Researchers who followed more than 6,000 mothers and babies found that when moms reported moderate to severe symptoms of depression in the nine months following delivery, their children were more likely to be shorter than others as kindergarteners, according to the report published in the journal Pediatrics. In fact, 5-year-olds with moms who’d suffered symptoms of postpartum depression were almost 50 percent more likely than their peers to be in the shortest 10 percent of kids that age. The new research doesn’t explain how kids with depressed moms end up shorter. That’s something the researchers are looking into right now, said the study’s lead author Pamela J. Surkan, an assistant professor at the Johns Hopkins Bloomberg School of Public Health. Surkan suspects, however, that depression might get in the way of nurturing. “We think that mothers who are depressed or blue might have a hard time following through with caregiving tasks,” Surkan said. “We know that children of depressed mothers often suffer from poor attachment and the depression seems to have effects on other developmental outcomes. It makes sense that mothers who have depressive symptoms might have reduced ability to take care of infants, that they might not always pick up cues from their kids.” © 2012 NBCNews.com

Related chapters from BP6e: 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: 17244 - Posted: 09.11.2012

By Carrie Arnold Like an overwhelmed traffic cop, the depressed brain may transmit signals among regions in a dysfunctional way. Recent brain-imaging studies suggest that areas of the brain involved in mood, concentration and conscious thought are hyperconnected, which scientists believe could lead to the problems with focus, anxiety and memory frequently seen in depression. Using functional MRI and electroencephalography (EEG), psychiatrist Andrew Leuchter of the University of California, Los Angeles, and his colleagues measured the activity of depressed patients' brains at rest. They found that the limbic and cortical areas, which together produce and process our emotions, sent a barrage of neural messages back and forth to one another—much more than in the brains of healthy patients. These signals, Leuchter says, can amplify depressed people's negative thoughts and act like white noise, drowning out the other neural messages telling them to move on. A separate study by psychiatrist Shuqiao Yao of Central South University in Hunan, China, produced a more nuanced view of these two areas' hyperconnectivity. In work published in Biological Psychiatry in April, Yao and his colleagues reported that stronger links among certain corticolimbic circuits are seen in patients more prone to rumination, the act of continuously replaying negative thoughts. Less connectivity in other corticolimbic circuits corresponded to autobiographical memory impairments, which is another common feature that appears in depression. © 2012 Scientific American

Related chapters from BP6e: 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: 17197 - Posted: 08.25.2012

By Julie Appleby, An increasing number of psychiatrists and hospitals — as well as entrepreneurs opening rTMS centers around the country — are betting that there are millions of people like Curtis, discouraged by depression treatments that have proved unsuccessful and willing to pony up thousands of dollars for the possibility of relief. The treatment, which has been approved by the Food and Drug Administration, is covered by Medicare in five states, but few private insurers pay for it routinely. While rTMS has ardent supporters, its effectiveness is still debated, and there is little evidence showing how long the results last. The technique has been shown to work better than a placebo, but the proportion of patients who show complete relief ranges widely, from as few as 10 percent to as many as 57 percent, according to various studies. The debate has huge implications, not just for many of the 14 million Americans who suffer from major depression every year but also for businesses eyeing a potentially lucrative market and insurers weighing whether to cover it. About half of those 14 million Americans seek relief through psychotherapy and prescription drug treatment, according to an evaluation by the federal Agency for Healthcare Research and Quality. But studies show that antidepressants provide complete cessation of symptoms only about a third of the time. Magnetic stimulation is aimed at patients with such “treatment-resistant depression.” Supporters say rTMS is worth the cost — between $6,000 and $12,000 for the four-to-six-week treatment — because it enables people such as Curtis to resume productive lives. Skeptics question the price tag in light of uncertain benefits. © 1996-2012 The Washington Post

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders; Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 17139 - Posted: 08.08.2012

Exercise and behavioural therapies are the most cost-effective and successful ways to treat Chronic fatigue syndrome, also known as ME, an analysis shows. A study of 640 patients showed these treatments had the potential to save the economy millions of pounds if they were widely adopted. The findings were published in the journal PLoS ONE. However, another treatment favoured by patients' groups was shown to offer little value. Nobody knows what causes the condition, yet a quarter of a million people in the UK are thought to have it. The symptoms include severe tiredness, poor concentration and memory as well as muscle and joint pain and disturbed sleep. An earlier version of this research, published last year, showed that cognitive behavioural therapy (changing how people think about their symptoms) and graded exercise therapy (gradually increasing the amount of exercise) were the most effective treatments. However, the study provoked anger from many patients' groups which argued that pacing therapies (learning to live within limits) were both better and safer for patients. Using data from the same set of patients, researchers compared improvements in levels of fatigue and activity with the cost to the NHS of providing the treatments. It concluded that only cognitive behavioural therapy and graded exercise therapy could be considered cost-effective. BBC © 2012

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17126 - Posted: 08.06.2012

Scientists have discovered a biological marker that may help to identify which depressed patients will respond to an experimental, rapid-acting antidepressant. The brain signal, detectable by noninvasive imaging, also holds clues to the agent’s underlying mechanism, which are vital for drug development, say National Institutes of Health researchers. The signal is among the latest of several such markers, including factors detectable in blood, genetic markers, and a sleep-specific brain wave, recently uncovered by the NIH team and grantee collaborators. They illuminate the workings of the agent, called ketamine, and may hold promise for more personalized treatment. "These clues help focus the search for the molecular targets of a future generation of medications that will lift depression within hours instead of weeks," explained Carlos Zarate, M.D., of the NIH’s National Institute of Mental Health (NIMH). "The more precisely we understand how this mechanism works, the more narrowly treatment can be targeted to achieve rapid antidepressant effects and avoid undesirable side effects." Previous research had shown that ketamine can lift symptoms of depression within hours in many patients. But side effects hamper its use as a first-line medication. So researchers are studying its mechanism of action in hopes of developing a safer agent that works similarly. Ketamine works through a different brain chemical system than conventional antidepressants. It initially blocks a protein on brain neurons, called the NMDA receptor, to which the chemical messenger glutamate binds.

Related chapters from BP6e: 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: 17124 - Posted: 08.04.2012

By Emily Selvadurai Health reporter, BBC News online People with mild mental illnesses such as anxiety or depression are more likely to die early, say researchers. They looked at the premature deaths from conditions such as heart disease and cancer of 68,000 people in England. The research suggested low level distress raised the risk by 16%, once lifestyle factors such as drinking and smoking were taken into account. More serious problems increased it by 67%, the University College London and Edinburgh University team said. The risk among those with severe mental health problems is already well documented. But researchers said the finding among those with milder cases - thought to be one in every four people - was concerning, as many would be undiagnosed. The Wellcome Trust-funded study, published in the British Medical Journal, looked at data over 10 years and matched it to information on death certificates. This is the largest study so far to show an association between psychological distress and death, according to scientists. Lead author Dr Tom Russ said: "The fact that an increased risk of mortality was evident, even at low levels of psychological distress, should prompt research into whether treatment of these very common, minor symptoms can modify this increased risk of death." BBC © 2012

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17115 - Posted: 08.01.2012

By ANAHAD O'CONNOR Heart failure can take a heavy psychological toll, with many patients developing symptoms of depression. But a new study suggests that an exercise plan can ease the melancholy, creating improvements in mood that are comparable to the effects seen with medication. For roughly a year, researchers followed more than 2,000 people treated for congestive heart failure at 82 medical centers in the United States, France and Canada. Those who were assigned to a moderate aerobic exercise program — about 90 to 120 minutes a week — saw greater reductions in symptoms of depression than those who were not enrolled in such a program. “I think this shows that for patients who have heart failure, exercise is certainly an excellent treatment,” said Dr. James A. Blumenthal, a professor of medical psychology at Duke University Medical Center and the lead author of the study, which was published in The Journal of the American Medical Association. “It’s something that most patients can engage in. It results in improved cardiorespiratory fitness, they have more stamina, and now we see that not only do they derive these physical benefits, but they also derive psychological benefits as well.” An estimated five million Americans are living with heart failure, with more than half a million new cases diagnosed each year. Patients often experience a drastic decline in their physical abilities, and with it a blow to their mental health. Up to 75 percent of patients develop some symptoms of depression, with about 40 percent suffering from full-blown clinical depression, which can worsen their overall prognosis. Copyright 2012 The New York Times Company

Related chapters from BP6e: 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: 17111 - Posted: 08.01.2012

By PAULA SPAN Anna Hill’s mother-in-law had suffered from depression for years, it was clear in hindsight, and had denied it for years, too. Only 73, she’d lost interest in doing much of anything. In chronic pain after an earlier accident, she was taking high doses of methadone. Last November, she stunned her family by declining, at the eleventh hour, to come to Thanksgiving dinner. “I’d only seen her in a nightgown for a year straight,” said Ms. Hill, 42, an accountant in Atlanta. “She was just rotting away in bed, watching TV and taking methadone.” Depression in the elderly is a mixed picture these days. For years, mental health specialists lamented that depression was seriously underdiagnosed and undertreated in the elderly. Laypeople saw it not as a disease but as an inevitable part of aging. Doctors missed it because depression didn’t always look the way it did in younger patients — less sadness and weepiness, more physical symptoms and disengagement. Older people themselves often rejected help because mental illness carried a stigma. In primary care practices, Dr. Jürgen Unützer and colleagues found in a large study published in 2000, only 12 to 25 percent of older people with probable depression were getting a diagnosis and being treated. Not anymore. Over the past decade, “we’ve seen a really big increase in the recognition of depression and the initiation of treatment,” said Dr. Unützer, a geriatric psychiatrist now at the University of Washington. © 2012 The New York Times Company

Related chapters from BP6e: 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: 17090 - Posted: 07.26.2012

By Janet Raloff Psychiatrists sometimes prescribe light therapy to treat a form of depression in people who get too little morning sun. But too much light at other times may actually trigger such mood disorders. Chronic exposure to light at night unleashes depression, a new study finds — at least in animals. The new data confirm observations from studies of people who work night shifts, says Richard Stevens of the University of Connecticut Health Center in Farmington. Mood disorders join a growing list of problems — including cancer, obesity and diabetes — that can occur when light throws life out of balance by disrupting the biological clock and its timing of daily rhythms. In the new study, appearing online July 24 in Molecular Psychiatry, Tracy Bedrosian, Zachary Weil and Randy Nelson of Ohio State University exposed Siberian hamsters to normal light and dark cycles for four weeks. For the next four weeks, half of the animals remained on this schedule, and the rest received chronic dim light throughout their night. Compared with animals exposed to normal nighttime darkness, those getting dim light at night lost their intense preference for sweet drinks, “a sign they no longer get pleasure out of activities they once enjoyed,” Bedrosian says. In a second test, animals were clocked on how long they actively tried to escape a pool of water. Hamsters exposed to night lights stopped struggling and just floated in the water — a sign of “behavioral despair” — 10 times as long as animals that had experienced normal nighttime darkness, Bedrosian reports. © Society for Science & the Public 2000 - 2012

Related chapters from BP6e: 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: 17089 - Posted: 07.25.2012