Incidence of psychiatric diagnoses in offspring prenatally exposed to SSRIs

A recent article in the Journal of the American Academy of Child and Adolescent Psychiatry presents a study looking at prenatal exposure to selective serotonin reuptake inhibitors (SSRIs) and associated increased rates of depression diagnoses in early adolescence. The report stresses that these findings are preliminary and should not be construed to change clinical practice.

The study is the first to investigate the incidence of psychiatric diagnoses in offspring prenatally exposed to SSRIs as far out as adolescence, noting however the vital importance of treating maternal depression, which can have significant adverse effects on offspring. Untreated maternal depression has been shown to increase risks of several perinatal outcomes including preterm birth, delivery by C-section, and bleeding during delivery.

Researchers used Finnish national birth registry data to determine the cumulative incidence of depression, anxiety disorders, autism spectrum disorder, and attention-deficit/hyperactivity disorder in the offspring of four groups of mother-offspring dyads: mothers exposed to SSRIs during pregnancy, mothers exposed to psychiatric disorder but not to antidepressants, mothers who used SSRIs only before pregnancy), and children of mothers unexposed to either antidepressants or psychiatric disorders.

They found the cumulative incidence of depression among offspring exposed prenatally to SSRIs was 8.2% by age 14.9 years, compared with 1.9% in the psychiatric disorder/no medication group and 2.8% in the SSRI-discontinued group. In contrast, SSRI prenatal exposure was not associated with an increased risk of autism spectrum disorder, ADHD, or anxiety.

When Happiness and Depression Meet

About a year ago I wrote about happiness and what it is that makes us happy. It turns out that what makes us happy, what motivates us, follows the philosophy of Autonomy, Mastery and Purpose. We do things for ourselves that help grow us and are important to us, we do things that we have to struggle with to improve ourselves, and we do things that make us part of a bigger world, and all of these three things have the capacity to make us happy or happier. Follow link below.

http://appliedpsychologyresearch.blogspot.com.au/2012/03/happiness-is-synthetic-so-why-not.html

I wanted today to check, basically, how users of Google search for information associated with happiness and depression. This is essentially search volume index over time. As you can see above there is a fascinating convergence between these two search volumes. As the search volume for Depression decreases over time, the search volume for Happiness has increased to almost the same volume matching Depression. Even when you ask Google to extrapolate these trends (in dotted lines) the trend continues.

Clinical depression and smoking

Jack Dikian

October 2011

Not long ago I was using the Google trends tool to look at various search volume correlations for clinical depression and other factors including smoking. I noticed Australians are in the top three countries using Google to search “depression”. The first was Ireland followed by South Africa. Another interesting thing, albeit, without a real hard look seems like there is about half the volume of searches for depression now compared to 5 or 6 years ago.

As I mentioned, my real objective was to see if there was anything to glean from data reflecting people’s propensity to use a search engine for perceived tag combinations such as “depression” and “smoking”.

Indeed, a study by the Toronto-based Centre for Addiction and Mental Health reports that the same enzyme, Monoamine oxidase (MAO), is found in elevated levels in both people suffering from clinical depression as well as heavy smokers in the early stages of abstaining from smoking. This could be why people struggle to quit the habit.

Smokers in the study also reported increased feelings of sadness in questionnaires done as part of the study. The researchers said such findings could explain why smokers are at a higher risk of suffering from depression — almost twice that of the general population, according to Jeffrey Meyer, a senior scientist with the Centre for Addiction who led the study.

Mouse Model That Replicates Human OCD Can Point To More Effective Treatments

Jack Dikian

September 2011

Researchers at the University of Chicago are using a new model of obsessive-compulsive disorder (OCD) that mirrors both symptoms of the disease and the timing of its treatment in humans. In the paper published in Biological Psychiatry the researchers report that they have been able to use the model to isolated a single neurotransmitter receptor in a specific brain region responsible for their model's OCD-like symptoms, offering new insight into the cause of the disorder.

Having a model that seems to mimic the disorder so well, especially in terms of the time course of treatments that work in humans, is potentially very useful for researching novel therapeutics. It’s possible that with further research the model may point the way to new treatments for both OCD and autism.

With a model that replicates aspects of OCD, researchers can dig deeper into the specific neurotransmitters and systems involved in the disorder. A drug that is used to treat migraines, but also known to have the unintended effect of increasing anxiety and compulsions in people with OCD was shown to bring about highly repetitive patterns of locomotion in mice.

The drug-treated mice also exhibited deficits in prepulse inhibition, a form of startle plasticity thought to measure the brain's ability to filter out intrusive thoughts, which plague OCD patients. To determine whether these drug-induced behaviors reflected the neurobiology of OCD, the researchers tested the same drugs used to treat the disorder in humans. After four weeks of pre-treatment with SRIs - the same duration required to see therapeutic effects in humans - drug-induced OCD behaviors were reduced in the mice.

The researchers then looked for a specific brain region where activation of 1b serotonin receptors creates OCD-like symptoms. In humans, scientists have identified a region called the orbitofrontal cortex that is more active in OCD subjects. Again matching the human data, selectively activating 1b receptors in the orbitofrontal cortex with the drug was sufficient to produce the OCD-like symptoms in the mice.

The results offer promising ideas about developing new treatments for OCD. A drug that blocks the serotonin 1b receptors may be effective in reducing OCD symptoms; however, no such chemical is currently available according to the researchers.

Researchers

Stephanie Dulawa, PhD, assistant professor in the Department of Psychiatry and Behavioral Neuroscience at the University of Chicago Medical Center and senior author of the study

Nancy Shanahan, PhD, lead author of the paper in Biological Psychiatry

Tuberculosis antibiotic treating phobias

Jack Dikian

September 2011

A phobia is defined as the unrelenting fear of a situation, activity, or thing that causes one to want to avoid it. Lifetime prevalence of specific phobias appears to be approximately 5%. However, rates vary widely in different countries, from less than 1% in Northern Ireland to approximately 9% in the United States.

Specific phobias have effectively been treated with behavior therapy1 where classical conditioning thinking is that the response of phobic fear is a reflex acquired to non-dangerous stimuli. Therapy sometimes involves setting up phobic treatment involving exposure to the phobic stimulus in a safe and controlled setting. Flooding, physical and imaginative until the fear fades away can also be used.

Pharmacology, including SSRIs, MAOIs, RIMAs, TeCA, Benzodiazepines have been used as treatment options but more recently It has been shown that a combination of acute dosing of d-cycloserine, an old antibiotic medication used for treating tuberculosis, with exposure therapy facilitates the effects of exposure therapy of social phobia.

1. Marks, I. M. (1987). Fears, phobias, and rituals: Panic, anxiety, and their disorders. New York: Oxford University Press.