Prenatal antidepressant exposure is associated with risk for attention-deficit hyperactivity disorder but not autism spectrum disorder in a large health system.

Previous studies suggested that risk for Autism Spectrum Disorder (ASD) may be increased in children exposed to antidepressants during the prenatal period. The disease specificity of this risk has not been addressed and the possibility of confounding has not been excluded. Children with ASD or attention-deficit hyperactivity disorder (ADHD) delivered in a large New England health-care system were identified from electronic health records (EHR), and each diagnostic group was matched 1:3 with children without ASD or ADHD. All children were linked with maternal health data using birth certificates and EHRs to determine prenatal medication exposures. Multiple logistic regression was used to examine association between prenatal antidepressant exposures and ASD or ADHD risk. A total of 1377 children diagnosed with ASD and 2243 with ADHD were matched with healthy controls. In models adjusted for sociodemographic features, antidepressant exposure prior to and during pregnancy was associated with ASD risk, but risk associated with exposure during pregnancy was no longer significant after controlling for maternal major depression (odds ratio (OR) 1.10 (0.70-1.70)). Conversely, antidepressant exposure during but not prior to pregnancy was associated with ADHD risk, even after adjustment for maternal depression (OR 1.81 (1.22-2.70)). These results suggest that the risk of autism observed with prenatal antidepressant exposure is likely confounded by severity of maternal illness, but further indicate that such exposure may still be associated with ADHD risk. This risk, modest in absolute terms, may still be a result of residual confounding and must be balanced against the substantial consequences of untreated maternal depression.

Discrimination between schizophrenic and control subjects by means of plasma dehydroepiandrosterone measurements.

In this study we were able to distinguish 10 schizophrenic subjects from 10 control subjects with 100% accuracy by measuring plasma dehydroepiandrosterone (DHEA) diurnal rhythms and analyzing the data using a linear function equation. Discrimination with this high level of accuracy is in contrast to most studies of altered biological functioning in schizophrenia which have yielded inconsistent results. These findings are regarded as preliminary; further study is necessary to elicit any consistent DHEA disturbance in schizophrenics and to discover the significance for the pathophysiology of the illness. Measurements of plasma cortisol, aldosterone, DHEA-SO4, and testosterone did not provide such a basis for discrimination.

Temporal variations in androgens and stress hormones in control and schizophrenic subjects.

Radioimmunoassay methods were employed to study the steroid hormones dehydroepiandrosterone (DHEA), cortisol, testosterone, and androstenedione in schizophrenic and control subjects. Observations were made at four different times during the day. Cortisol, testosterone, and androstenedione demonstrated no significant differences between the two subjects groups. DHEA was significantly below normal in the morning for the schizophrenic group, but within the range of the controls for subsequent determinations during the day. Control subjects show a similar circadian secretion pattern for both DHEA and cortisol. Schizophrenics show almost the same circadian secretion patterns for cortisol as do the controls.