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Objectives: We hypothesize that prostaglandins and oxytocin administered during the perinatal period to initiate or enhance labor alter fetal neurobehavioral development.
Methods: The CHARGE (Childhood Autism Risk from Genetics and the Environment) Study is an ongoing case-control study of the environmental etiology of autism. The study population consists of 232 children with autism and 129 population-based controls for which we have medical records documenting their mother’s labor. Demographic data, use of drugs to induce or augment labor, and covariates related to the labor and delivery process were abstracted in a systematic fashion. Logistic regression was used to examine the relationships between use of such drugs and autism status.
Results: After adjustment for mother’s education, preeclampsia, cesarean delivery, and date of delivery, use of oxytocin was less common among mothers whose children developed autism compared with those whose babies developed typically (30% vs 40%, AOR 0.46, 95% CI 0.27, 0.80). After controlling for oxytocin administration, use of vaginal prostaglandins was more common among mothers of children with autism compared with controls, although this association failed to achieve statistical significance (13% vs 9%, AOR 2.10, 95% CI 0.93, 5.00).
Conclusions: Oxytocin is released in the hypothalamus and amygdala in response to stimuli including stress, and modulates pro-social, anxiolytic and antistress actions. Fetal exposure to exogenous oxytocin during the perinatal period may enhance or protect neurodevelopment. Prostaglandins regulate many immunological processes, including cytokines IL-1, IL-4, IL-6 and TNFa & ß, which critically influence brain development and function. It is plausible that perinatal exposure to exogenous prostaglandins may result in abnormal brain development, possibly via disruption of normal immune function.