Links for Keyword: Depression

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Heart risk link to SSRI antidepressants confirmed

Some but not all antidepressant drugs known as SSRIs pose a very small but serious heart risk, say researchers. Citalopram and escitalopram, which fall into this drug group, can trigger a heart rhythm disturbance, a new study in the British Medical Journal shows. UK and US regulators have already warned doctors to be extra careful about which patients they prescribe these medicines to. And they have lowered the maximum recommended dose. The UK's Medicines and Healthcare products Regulatory Agency (MHRA) says people with pre-existing heart conditions should have a heart trace before going on these drugs, to check for a rhythm disturbance known as long QT interval. Experts reassure that complications are very rare and that in most cases the benefits for the patient taking the drug will outweigh the risks. Long QT QT interval is measured with an electrocardiogram (ECG) and varies with the heart rate - it gets longer when the heart beats slower and is shorter when the heart beats faster. Some variation is normal, but if it gets too long it can upset the timing of heartbeat with potentially dire consequences - dizziness, faints and, rarely, sudden death. To assess how common a problem long QT linked to SSRI use might be, US researchers decided to look at the medical records of more than 38,00 patients from New England. BBC © 2013

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: 17736 - Posted: 01.30.2013

Published clinical trials shown to be misleading

By Rachel Ehrenberg A rare peek into drug company documents reveals troubling differences between publicly available information and materials the company holds close to its chest. In comparing public and private descriptions of drug trials conducted by pharmaceutical giant Pfizer, researchers discovered discrepancies including changes in the number of study participants and inconsistent definitions of protocols and analyses. The researchers, led by Kay Dickersin, director of the Center for Clinical Trials at the Johns Hopkins Bloomberg School of Public Health, gained access to internal Pfizer reports after a lawsuit made them available. Dickersin and her colleagues compared the internal documents with 10 publications in peer-reviewed journals about randomized trials of Pfizer’s anti-epilepsy drug gabapentin (brand name Neurontin) that tested its effectiveness for treating other disorders. The results, the researchers say, suggest that the published trials were biased and misleading, even though they read as if standard protocols were followed. That lack of transparency could mean that clinicians prescribe drugs based on incomplete or incorrect information. We could see all of the biases right in front of us all at once,” says Dickersin, who was an expert witness in the suit, which was brought by a health insurer against Pfizer. Pfizer lost the case in 2010, and a judge ruled it should pay $142 million in damages for violating federal racketeering laws in promoting Neurontin for treating migraines and bipolar disorder. Pfizer had in 2004 settled a case and paid $430 million in civil fines and criminal penalties for promoting Neurontin for unapproved use. © Society for Science & the Public 2000 - 2013

Depression gene search disappoints

By Laura Sanders A massive effort to uncover genes involved in depression has largely failed. By combing through the DNA of 34,549 volunteers, an international team of 86 scientists hoped to uncover genetic influences that affect a person’s vulnerability to depression. But the analysis turned up nothing. The results are the latest in a string of large studies that have failed to pinpoint genetic culprits of depression. “I’m disappointed,” says study coauthor Henning Tiemeier of Erasmus Medical Center in Rotterdam, Netherlands. The negative finding, published online January 3 in Biological Psychiatry, “tells us that we have to be very modest,” he says. “Yet we think it’s doable to find some of the genes involved.” Depression seems to run in families, leading scientists to think that certain genes are partially behind the disorder. But so far, studies on people diagnosed with depression have failed to reveal these genes. Unlike earlier studies, the new study ignored depression diagnoses and instead focused solely on symptoms. Researchers combined the results of 17 studies that asked volunteers the same set of 20 questions about their emotional health at the time of the questionnaire. A person with many signs of depression scored high on the index (called CES-D), while a person with few signs scored low. The researchers hoped that capturing the continuum of symptoms — instead of a black-and-white depression diagnosis — would be a better way to ferret out the genes involved in depression. © Society for Science & the Public 2000 - 2013

Susan Nolen-Hoeksema, Psychologist Who Studied Depression in Women, Dies at 53

By BENEDICT CAREY Susan Nolen-Hoeksema, a psychologist and writer whose work helped explain why women are twice as prone to depression as men and why such low moods can be so hard to shake, died on Jan. 2 in New Haven. She was 53. Her death followed heart surgery to correct a congenitally weak valve, said her husband, Richard Nolen-Hoeksema. Dr. Nolen-Hoeksema, a professor at Yale University, began studying depression in the 1980s, a time of great excitement in psychiatry and psychology. New drugs like Prozac were entering the market; novel talking therapies were proving effective, too, particularly cognitive behavior therapy, in which people learn to defuse upsetting thoughts by questioning their basis. Her studies, first in children and later in adults, exposed one of the most deceptively upsetting of these patterns: rumination, the natural instinct to dwell on the sources of problems rather than their possible solutions. Women were more prone to ruminate than men, the studies found, and in a landmark 1987 paper she argued that this difference accounted for the two-to-one ratio of depressed women to depressed men. She later linked rumination to a variety of mood and behavior problems, including anxiety, eating disorders and substance abuse. “The way I think she’d put it is that, when bad things happen, women brood — they’re cerebral, which can feed into the depression,” said Martin Seligman, a professor of psychology at the University of Pennsylvania, who oversaw her doctoral work. “Men are more inclined to act, to do something, plan, beat someone up, play basketball.” © 2013 The New York Times Company

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: 17679 - Posted: 01.14.2013

Little Mind Benders: Parasites that sneak into the brain may alter your behavior and health

By Susan Milius Imagining tiny creatures infiltrating human brains is creepy enough. But Marion Vittecoq knows she has been invaded. Her inner companions may be just hanging out — or they may be subtly changing her personality, manipulating her behavior or altering her risk of disease. Yet she doesn’t sound particularly upset. Not once in the course of a phone conversation and many e-mails did Vittecoq recommend wearing tinfoil hats or mention mind control by the CIA, the United Nations or little green men beaming rays from the moons of Uranus. She studies the ecology of parasites, especially the one-celled Toxoplasma gondii, which coincidentally is the creature that has invaded her brain. She doesn’t see it as an extra-ordinary intrusion. The parasite has wormed its way into an estimated one-third of people on the planet. In France, where Vittecoq works at both a CNRS national research lab in Montpellier and the Tour du Valat research center in Arles, nearly one-third to about one-half of adults carry hitchhiking T. gondii. CNRS research colleague Frédéric Thomas is also infected, and also doesn’t fret about it. In the United States, almost one in four residents over the age of 12 has the infection. In other parts of the world, rates are as high as 95 percent. An unlucky minority of these infected people become quite ill. Most, however, don’t even know that their muscles and brains carry the parasite. © Society for Science & the Public 2000 - 2013

Related chapters from BP6e: Chapter 16: Psychopathology: Biological Basis of Behavior Disorders; Chapter 6: Evolution of the Brain and Behavior
Related chapters from MM:Chapter 12: Psychopathology: Biological Basis of Behavioral Disorders
Link ID: 17677 - Posted: 01.12.2013

Diet drinks' 'link to depression' questioned

Experts are questioning whether diet drinks could raise depression risk, after a large study has found a link. The US research in more than 250,000 people found depression was more common among frequent consumers of artificially sweetened beverages. The work, which will be presented at the American Academy of Neurology's annual meeting, did not look at the cause for this link. Drinking coffee was linked with a lower risk of depression. People who drank four cups a day were 10% less likely to be diagnosed with depression during the 10-year study period than those who drank no coffee. But those who drank four cans or glasses of diet fizzy drinks or artificially sweetened juice a day increased their risk of depression by about a third. Lead researcher Dr Honglei Chen, of the National Institutes of Health in North Carolina, said: "Our research suggests that cutting out or down on sweetened diet drinks or replacing them with unsweetened coffee may naturally help lower your depression risk." But he said more studies were needed to explore this. BBC © 2013

Study Questions Effectiveness of Therapy for Suicidal Teenagers

By BENEDICT CAREY Most adolescents who plan or attempt suicide have already received at least some mental health treatment, raising questions about the effectiveness of current approaches to helping troubled youths, according to the largest in-depth analysis to date of suicidal behaviors in American teenagers. Matt Nock, a professor of psychology at Harvard and the lead author of a study on the mental health treatment of troubled young people, said his research showed that “we’ve got a long way to go to do this right.” The study found that 55 percent of adolescents who plan or attempt suicide have already received some therapy. The study, in the journal JAMA Psychiatry, found that 55 percent of suicidal teenagers had received some therapy before they thought about suicide, planned it or tried to kill themselves, contradicting the widely held belief that suicide is due in part to a lack of access to treatment. The findings, based on interviews with a nationwide sample of more than 6,000 teenagers and at least one parent of each, linked suicidal behavior to complex combinations of mood disorders like depression and behavior problems like attention-deficit and eating disorders, as well as alcohol and drug abuse. The study found that about one in eight teenagers had persistent suicidal thoughts at some point, and that about a third of those who had suicidal thoughts had made an attempt, usually within a year of having the idea. © 2013 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: 17665 - Posted: 01.10.2013

Walking the Tightrope on Mental Health Coverage

By RON LIEBER Insurance covers more mental health care than many people may realize, and more people will soon have the kind of health insurance that does so. But coverage goes only so far when there aren’t enough practitioners who accept it — or there aren’t any nearby, or they aren’t taking any new patients. In the days after the Newtown, Conn., school shooting, parents and politicians took to the airwaves to make broad-based proclamations about the sorry state of mental health care in America. But a closer look reveals a more nuanced view, with a great deal of recent legislative progress as well as plenty of infuriating coverage gaps. The stakes in any census of mental health insurance coverage are high given how many people are suffering. Twenty-six percent of adults experience a diagnosable mental disorder in any given year, and 6 percent of all adults experience a seriously debilitating mental illness, according to the National Institute of Mental Health. Twenty-one percent of teenagers experience a severe emotional disturbance between the ages of 13 and 18. According to this year’s Society for Human Resource Management survey of 550 employers of all sizes, including nonprofits and government entities, 85 percent offer at least some mental health insurance coverage. A 2009 Mercer survey found that 84 percent of employers with more than 500 employees covered both in-network and out-of-network mental health and substance abuse treatments. © 2012 The New York Times Company

Regular marijuana use by teens continues to be a concern

Continued high use of marijuana by the nation's eighth, 10th and 12th graders combined with a drop in perceptions of its potential harms in this year's Monitoring the Future survey, an annual survey of eighth, 10th, and 12th-graders conducted by researchers at the University of Michigan. The survey was carried out in classrooms around the country earlier this year, under a grant from the National Institute on Drug Abuse (NIDA), part of the National Institutes of Health. The 2012 survey shows that 6.5 percent of high school seniors smoke marijuana daily, up from 5.1 percent five years ago. Nearly 23 percent say they smoked it in the month prior to the survey, and just over 36 percent say they smoked within the previous year. For 10th graders, 3.5 percent said they use marijuana daily, with 17 percent reporting past month use and 28 percent reporting use in the past year. The use escalates after eighth grade, when only 1.1 percent reported daily use, and 6.5 percent reported past month use. More than 11 percent of eighth graders said they used marijuana in the past year. The Monitoring the Future survey also showed that teens' perception of marijuana’s harmfulness is down, which can signal future increases in use. Only 41.7 percent of eighth graders see occasional use of marijuana as harmful; 66.9 percent see regular use as harmful. Both rates are at the lowest since the survey began tracking risk perception for this age group in 1991. As teens get older, their perception of risk diminishes. Only 20.6 percent of 12th graders see occasional use as harmful (the lowest since 1983), and 44.1 percent see regular use as harmful, the lowest since 1979.

Depression Surpasses Asthma as Top Disability Problem among U.S. and Canadian Teens

By Yevgeniy Grigoryev and Spoonful of Medicine The recent tragedy in Newtown, Connecticut, perpetrated by 20 year-old Adam Lanza, has intensified the discussion about how mental health is handled and documented in the US. Officials have not provided information about Lanza’s motivation and state of mind, and many are rightfully quick to point out that it is wrong to equate mental illness with the fatal sociopathic actions of a small group of individuals. The conversation about access to mental health care should, however, take into account new data showing an increasing contribution of mental and behavioral disorders to deterioration in the health-related quality of life among teenagers in the US and Canada over the last two decades, and increases elsewhere around the globe. The estimation of ‘years lived with disabilities’, or YLDs, is used as a collective metric to determine how much a particular disorder deprives the population of healthy years of life during a particular window of time. In 2010 just as in 1990, depression ranked as the number two contributor of YLDs, affecting 4% of the global population, eclipsed only by back pain that affected almost 10% of population worldwide. Among 10 to 14 year olds, the top contributor worldwide is iron deficiency. Asthma had been the largest contributor to YLDs for youths in that age range in the US and Canada in 1990, but the study published in The Lancet on Thursday led by researchers at the Institute of Health Metrics and Evaluation (IHME) at the University of Washington, Seattle showed that in this group depression surpassed asthma to claim the number one spot in 2010. In that group, the collective number of ‘years lost to disability’ grew from about 140,000 in 1990 to almost 180,000 in 2010, a 30% increase. Notably, global figures for the same age group show that the number of years lost to disability from depression grew from 4.9 million in 1990 to 5.5 million in 2010, a 13% increase as shown in the graphs below. © 2012 Scientific American

The dopamine side(s) of depression, part 2

By Scicurious Depression is a disease with a difficult set of symptoms. Not only are the symptoms difficult to describe (how do you really describe anhedonia, before you know the word for it?), symptoms of depression manifest in different ways for different people. One person will eat more, sleep all the time, move slowly. Another will eat almost nothing, never sleep, and be irritable and nervous. They are both depressed. The only universal symptom is the feeling of…depression, and the need for successful treatment. Treatments which often take several weeks to work, are often ineffective, and which come with a host of side effects. So I was particularly intrigued when Nature published two papers this week looking at the role of dopamine in depressive-like behavior. What I particularly like is that these two papers have somewhat opposite results, due to different behavioral methods, something which I think highlights some of the problems associated with studying depression. Ed Yong covered both of the studies together fabulously over at Not Exactly Rocket Science, but I’d like to look at them both separately, to take a deeper look at each one, see what they’ve achieved, and what other questions they raise. Today we are on the second of the two papers, one which has a similar angle to the first paper, but an entirely different result. Yesterday’s paper looked at how changes in dopamine cell firing from the ventral tegmental area (which projects to areas like the prefrontal cortex and the nucleus accumbens) can impact depressive-like behaviors in mice and rats. Today’s paper looks at the ventral tegmental area as well, but instead of cutting on or turning “off” cell firing, the authors of this study looked at different types of neuronal activity, and the effects in socially defeated mice. © 2012 Scientific American

The dopamine side(s) of depression

By Scicurious Depression is a disease with a difficult set of symptoms. Not only are the symptoms difficult to describe (how do you really describe anhedonia, before you know the word for it?), symptoms of depression manifest in different ways for different people. One person will eat more, sleep all the time, move slowly. Another will eat almost nothing, never sleep, and be irritable and nervous. They are both depressed. The only universal symptom is the feeling of…depression, and the need for successful treatment. Treatments which often take several weeks to work, are often ineffective, and which come with a host of side effects. So I was particularly intrigued when Nature published two papers this week looking at the role of dopamine in depressive-like behavior. What I particularly like is that these two papers have somewhat opposite results, due to different behavioral methods, something which I think highlights some of the problems associated with studying depression. Ed Yong covered both of the studies together fabulously over at Not Exactly Rocket Science, but I’d like to look at them both separately, to take a deeper look at each one, see what they’ve achieved, and what other questions they raise. So I will start with one today, and post the other tomorrow, looking at both sides. While you often hear about serotonin in studies of depression (serotonin is, after all, a target of many current antidepressants), there are many other neurotransmitters and systems that are also under investigation, and many of them are bearing some fruitful results. Ketamine, for example. And of course there is the role of dopamine. © 2012 Scientific American

Brain stimulation alters depressive symptoms in mice

By Laura Sanders Signs of depression can be turned on and off in mice with the flip of a switch. Activating or silencing the behavior of certain brain cells with laser light causes the animals to change their depressive behavior, two new studies find. Although the experiments were done in rodents, the results have direct relevance to human depression, says neurologist Helen Mayberg of the Emory University School of Medicine in Atlanta. The new work may point out places in the human brain that doctors can similarly stimulate to treat depression. The results, published online December 13 in Nature, took advantage of a technique called optogenetics, which allows scientists to control nerve cell behavior with a tiny fiber-optic light. In the studies, mice were genetically engineered to harbor nerve cell proteins that respond to light. The researchers could make certain nerve cells fire off messages by shining blue light, and quiet them by shining yellow light. These cells, which produce the chemical messenger dopamine, nestle in a brain region called the ventral tegmental area, a spot known for handling rewards. This system may be skewed in people with depression, since the disorder often keeps people from responding normally to things that used to be enjoyable. One tiny fiber-optic flash had an instant and profound effect on the mice’s behavior, says psychiatrist and neuroscientist Karl Deisseroth of Stanford University, who coauthored both papers. “That was pretty amazing for us.” © Society for Science & the Public 2000 - 2012

The two faces of depression – two studies switch off symptoms in mice, but in opposite ways

By Ed Yong In a lab at Stanford University, a mouse is showing signs of depression. For around 10 weeks, it has experienced a series of irritations, from bouts without food or water, to erratic sleep patterns. Now, its motivation is low—when picked up by the tail, it makes few attempts to escape, and it doesn’t try to explore new spaces. It’s also less willing to sip from a sugary liquid– a sign that it gets less pleasure from normally pleasurable activities. It is never easy to assess the mental health of an animal, but this mouse is clearly showing some of the classic symptoms of depression. But not for long. Earlier, Kay Tye and Julie Mirzabekov altered the mouse so that a flash of light can activate a small part of its brain—the ventral tegmental area (VTA), near the bottom of the brain and close to the midline. A burst of light, and the mouse’s behaviour changes almost instantly. It struggles when held aloft, it explores open areas, and it regains its sweet tooth. A burst of light, and its symptoms disappear. But on the other side of the country, at the Mount Sinai School of Medicine, Dipesh Chaudhury and Jessica Walsh are doing the same thing to completely different effect. Their mice have been altered in a similar way, so that light can also switch on their VTA neurons. But these rodents have endured a shorter but more intense form of stress—10 days of being placed in cages with dominant, aggressive rivals. Because of the resulting attacks, some of them have developed depressive symptoms. Others are more resilient. But when Chaudhury and Walsh flashed the VTAs of these mice, resilient individuals transformed into susceptible ones.

Experimental agent briefly eases depression rapidly in test

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.

A Tense Compromise on Defining Disorders

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

Cognitive behavioural therapy 'can reduce depression'

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

Thoughts about depression from under the sheets

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

Human drugs make fish flounder

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,

Exercise And Depression Revisited

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

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