ArticleJournal of child psychology and psychiatry, and allied disciplines2024
DHEA: a neglected biological signal that may affect fetal and child development.
Article in Journal of child psychology and psychiatry, and allied disciplines, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it, 6 citations in OpenAlex.
- Adrenarche, social cognition, and the development and evolution of autism spectrum traits.Frontiers in psychiatry · 2025Pooled it
- Adrenarche as a regulator of sensitivity to early adversity.Journal of neuroendocrinology · 2026Review
- From womb to words: the sex-specific interplay of fetal sex hormones and maternal mood on infant language development.Frontiers in endocrinology · 2026Article
- The maternal-fetal communicatome: a scoping review and network physiology perspective on a unified, adaptive, and multiscale interaction network.Frontiers in network physiology · 2026Review
- Network analysis and trajectories of maternal emotional symptoms during labor.BMC psychology · 2025Article
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe stress-sensitive maternal hypothalamic-pituitary-adrenal (HPA) axis through the end-product cortisol, represents a primary pathway through which maternal experience shapes fetal development with long-term consequences for child neurodevelopment. However, there is another HPA axis end-product that has been widely ignored in the study of human pregnancy. The synthesis and release of dehydroepiandosterone (DHEA) is similar to cortisol, so it is a plausible, but neglected, biological signal that may influence fetal neurodevelopment. DHEA also may interact with cortisol to determine developmental outcomes. Surprisingly, there is virtually nothing known about human fetal exposure to prenatal maternal DHEA and offspring neurodevelopment. The current study examined, for the first time, the joint impact of fetal exposure to prenatal maternal DHEA and cortisol on infant emotional reactivity.
methodsParticipants were 124 mother-infant dyads. DHEA and cortisol were measured from maternal hair at 15 weeks (early gestation) and 35 weeks (late gestation). Observational assessments of positive and negative emotional reactivity were obtained in the laboratory when the infants were 6 months old. Pearson correlations were used to examine the associations between prenatal maternal cortisol, prenatal maternal DHEA, and infant positive and negative emotional reactivity. Moderation analyses were conducted to investigate whether DHEA might modify the association between cortisol and emotional reactivity.
resultsHigher levels of both early and late gestation maternal DHEA were linked to greater infant positive emotional reactivity. Elevated late gestation maternal cortisol was associated with greater negative emotional reactivity. Finally, the association between fetal cortisol exposure and infant emotional reactivity was only observed when DHEA was low.
conclusionsThese new observations indicate that DHEA is a potential maternal biological signal involved in prenatal programming. It appears to act both independently and jointly with cortisol to determine a child's emotional reactivity. Its role as a primary end-product of the HPA axis, coupled with the newly documented associations with prenatal development shown here, strongly calls for the inclusion of DHEA in future investigations of fetal programming.
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