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The etiology of autism spectrum disorder (ASD) is multifactorial, complex, and likely involves interactions among genetic, epigenetic, and environmental factors. With respect to environmental influences, a growing literature implicates intrauterine experiences in the origin of this pervasive developmental disorder. In this prospective longitudinal study, we examined the hypothesis that fetal exposure to maternal cortisol may confer ASD risk. In addition, because ASD is four times more prevalent in males than in females, and because sexually dimorphic responses to intrauterine experiences are commonly observed, we examined whether or not any associations differ by fetal sex. Maternal plasma cortisol was measured at 15, 19, 25, 31, and 37 weeks’ gestation in a sample of 84 pregnant women. ASD symptoms were assessed in their 5-year-old children with the Social Communication Questionnaire (SCQ). Fetal exposure to lower levels of maternal cortisol was associated with higher levels of ASD symptoms only among boys. The observed hypocortisolemic profile exhibited by these mothers may indicate a risk factor that precedes the stress of caregiving for a child with ASD and may not be solely a consequence of the stress of caregiving, as previously thought. These findings confirm the value of examining prenatal hormone exposures as predictors of ASD risk and support the premise that altered prenatal steroid exposures may play a role in the etiology of ASD.


This is a pre-copy-editing, author-produced PDF of an article accepted for publication in Clinical Psychological Science, volume 7, issue 2, in 2019 following peer review. The definitive publisher-authenticated version is available online at


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