Dhea

A neglected biological signal that may affect fetal and child development

Bibliographic Data

ID21345008
AuthorsNatasha A Bailey (Department of Psychology University of Virginia Charlottesville VA USA), Natasha Bailey (0000-0002-8144-6762, Department of Psychology University of Virginia Charlottesville VA USA), E P Davis (0000-0001-6345-9271, Department of Psychology University of Denver Denver CO USA), Curt A Sandman (0000-0003-3876-8528, Department of Psychiatry and Human Behavior University of California Irvine CA USA), Laura M Glynn (0000-0001-5903-8685, Department of Psychology Chapman University Orange CA USA, corresponding author)
Year2024
Volume65
Issue9
Pages1145-1155
Publication date2024-09-01
Peer ReviewedYes
Open AccessYes
TypeARTICLE
VenueJournal of Child Psychology and Psychiatry (JOURNAL)
Journal identifiersISSN: 0021-9630 • E-ISSN: 1469-7610
PublisherWiley (PUBLISHER • GB)
DOI10.1111/jcpp.13952
PMID38426566
OpenAlexW4392355781
LanguageEN
Citations received1
References cited77

BACKGROUND: The 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. METHODS: Participants 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. RESULTS: Higher 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. CONCLUSIONS: These 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

Affect (linguistics) · Developmental psychology · Fetus · Pregnancy · Communication · Genetics · Hormonal Regulation and Hypertension · Maternal Mental Health During Pregnancy and Postpartum · Neuroscience · Psychology · Stress Responses and Cortisol

Tools

Open DOIOpen Access