A multiyear clinical trial comparing medication and mental health counseling in the treatment of post-traumatic stress disorder shows that patients who chose their form of treatment — whether drugs or therapy — improved more than those who were simply prescribed one or the other regardless of the patient’s preference.
The study, led by the University of Washington and Case Western Reserve University, was conducted at outpatient clinics in Seattle and Cleveland. It found that both a medication — Sertraline, marketed as Zoloft — and a specific form a therapy known as prolonged exposure were effective in reducing PTSD symptoms during the course of treatment, with improvements maintained at least two years later. But patients who received their choice between the two possible treatments showed greater reduction in symptoms, were more apt to stick to their treatment program and even lost their PTSD diagnosis over time.
The study, published Oct. 19 in the American Journal of Psychiatry, is the first large-scale trial of hundreds of PTSD patients, including veterans and survivors of sexual assault, to measure whether patient preference in the course of treatment impacts the effectiveness of a type of cognitive behavioral therapy and use of selective serotonin reuptake inhibitors, a type of antidepressant often prescribed for PTSD.
Researchers funded by the National Institutes of Health have shown that a therapy-based treatment for disruptive behavioral disorders can be adapted and used as an effective treatment option for early childhood depression. Children as young as 3-years-old can be diagnosed with clinical depression, and although preschool-aged children are sometimes prescribed antidepressants, a psychotherapeutic intervention is greatly needed. The study, funded by the National Institute of Mental Health (NIMH), part of NIH, appears online June 20 in the American Journal of Psychiatry.
The researchers adapted Parent-Child Interaction Therapy (PCIT), which has been shown to be an effective way to treat disruptive behavioral disorders in young children. In standard PCIT treatment, parents are taught techniques for successfully interacting with their children. They then practice these techniques in controlled situations while being coached by a clinician.
Postpartum affective disorder (AD), including postpartum depression (PPD), affects more than one in two hundred women with no history of prior psychiatric episodes, and raises the risk of later affective disorder for those women, according to a new study published in PLOS Medicine by Marie-Louise Rasmussen from Statens Serum Institut, Denmark, and colleagues.
PPD is estimated to affect more than 5 percent of all women following childbirth, making it the most common postnatal complication of childbearing. In the new study, researchers analyzed data from the Danish national registries on 457,317 women who had a first child (and subsequent births) between 1996 and 2013 and had no prior psychiatric hospital contacts or use of antidepressants. Postpartum AD was defined as an antidepressant prescription fill or hospital contact for depression within six months after birth.
The use of antidepressants has been on the rise for many years. Between 2 and 8% of pregnant women are on antidepressants. Now researchers from the National Centre for Register-based Research at Aarhus BSS show that there is an increased risk involved in using antidepressants during pregnancy.
The researchers, headed by Xiaoqin Liu, have applied register-based research to the study of 905,383 children born between 1998 and 2012 with the aim of exploring the possible adverse effects of the mother’s use of antidepressants during her pregnancy.
They found that out of the 905,383 children in total, 32,400 developed a psychiatric disorder later in life. Some of these children were born to mothers who were on antidepressants during their pregnancy, while other children had not been exposed to medication.
Antidepressants treat symptoms of depression by increasing levels of brain signaling molecules (neurotransmitters) such as serotonin, as with the most widely used type of antidepressant, selective serotonin reuptake inhibitors (SSRIs). However, many of the 350 million people worldwide thought to be affected with depression do not respond to SSRI treatment.
Now, researchers in the Department of Neuroscience and Cell Biology at Osaka University have found that an activator of the serotonin type 3 receptor (5HT3R) produces antidepressant effects in mice and increases nerve cell growth in the part of the brain responsible for memory and spatial navigation (the hippocampus). They also showed that it functions using a different mechanism than the commonly used SSRI fluoxetine, and therefore may be suitable for patients with depression who do not respond favorably to current medication.
When they work, antidepressant medications may take weeks or months to alleviate symptoms of depression. Progress in developing new and more effective antidepressant treatments has been limited, though a new study published in Biological Psychiatry offers new insights into how antidepressants work.
Using a mouse model of depression, researchers found that a therapeutic response to antidepressant medication may stem from changes in gene expression that induce resilience and reverse vulnerability to exhibiting depression-like responses to stress. The study, led by Dr. Eric Nestler of the Icahn School of Medicine at Mount Sinai in New York, teases apart the mechanisms of two different antidepressant drugs- the conventional tricyclic antidepressant imipramine and fast-acting ketamine.
Despite the fact that more than four percent of the world’s population suffer from depression, and even though approximately 1,500 individuals commit suicide each year in Sweden, the understanding of the pathophysiology of depression remains unclear and only a few new discoveries of mechanisms behind it have been made in recent years. New approved pharmacological interventions are mainly absent, despite intensive research on the subject.
Researchers at Karolinska Institutet have characterized the role of the enzyme CYP2C19 in depression and functional and morphological changes in the brain. The enzyme is responsible for the metabolism of many neuroactive compounds, including antidepressants, and is located in the fetal brain and adult liver.
SSRI antidepressants (Selective Serotonin Reuptake Inhibitors, the best known being Prozactm) are amongst the most commonly taken medicines. However, there seems to be no way of knowing in advance whether or not SSRIs will work effectively. Now a group of European researchers has developed a new theory of SSRI action, and tested it in stressed mice. The results, which are presented at the ECNP conference in Vienna, show why the circumstances we find ourselves in may influence whether an antidepressant works or not.
According to researcher, Silvia Poggini (Istituto Superiore di Sanità, Rome), “There is no doubt that antidepressants work for many people, but for between 30 and 50% of depressed people, antidepressants don’t work. No-one knows why. This work may explain part of the reason.”
Psychiatrists nearly always responded with prescriptions for antidepressants when clients complained of bad marriages, according to a new study spanning 20 years at a Midwestern medical center.
The assumption that people struggling with their marriages or other domestic issues are suffering from depression is not supported by the way depression is defined medically, said Jonathan M. Metzl, Frederick B. Rentschler II Professor of Sociology and Medicine, Health and Society at Vanderbilt and the study’s lead author. The study, conducted using a Midwestern medical center’s records from 1980 to 2000, appears in the current issue of the Yale Journal of Biology and Medicine
Notably, Metzl said, the time period of analysis followed a 1974 decision that removed the term “homosexuality” from the Diagnostic and Statistical Manual of Mental Disorders (DSM), the standard reference book of psychiatric illnesses.
In a study appearing in the June 28 issue of JAMA, Christiane E. Angermann, M.D., of University Hospital Wurzburg, Germany, and colleagues examined whether 24 months of treatment with the antidepressant escitalopram would improve mortality, illness, and mood in patients with chronic heart failure and depression.
Previous meta-analysis indicates that depression prevalence in patients with heart failure is 10 percent to 40 percent, depending on disease severity. Depression has been shown to be an independent predictor of mortality and rehospitalization in patients with heart failure, with incidence rates increasing in parallel with depression severity. Long-term efficacy and safety of selective serotonin reuptake inhibitors (SSRIs), which are widely used to treat depression, is unknown for patients with heart failure and depression.