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.

中文翻译：

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DHEA：一种被忽视的生物信号，可能影响胎儿和儿童发育

背景通过最终产物皮质醇的压力敏感的母亲下丘脑-垂体-肾上腺（HPA）轴代表了母亲经历塑造胎儿发育并对儿童神经发育产生长期影响的主要途径。然而，在人类妊娠研究中，还有另一种 HPA 轴终产物被广泛忽视。脱氢表雄酮 (DHEA) 的合成和释放与皮质醇相似，因此它是一种可能影响胎儿神经发育的看似合理但被忽视的生物信号。DHEA 还可能与皮质醇相互作用来决定发育结果。令人惊讶的是，对于人类胎儿在产前接触母体 DHEA 和后代神经发育的情况几乎一无所知。本研究首次探讨了胎儿在产前接触母体 DHEA 和皮质醇对婴儿情绪反应的联合影响。方法参与者为 124 名母婴组合。在 15 周（妊娠早期）和 35 周（妊娠晚期）时从母亲的头发中测量 DHEA 和皮质醇。当婴儿 6 个月大时，在实验室获得了积极和消极情绪反应的观察评估。Pearson 相关性用于检查产前母亲皮质醇、产前母亲 DHEA 与婴儿积极和消极情绪反应之间的关联。进行调节分析以调查 DHEA 是否可能改变皮质醇和情绪反应之间的关联。结果妊娠早期和晚期母亲 DHEA 水平较高与婴儿的积极情绪反应程度较高有关。妊娠晚期母亲皮质醇升高与更大的负面情绪反应相关。最后，只有当 DHEA 较低时，才能观察到胎儿皮质醇暴露与婴儿情绪反应之间的关联。结论这些新观察结果表明，DHEA 是参与产前编程的潜在母体生物信号。它似乎可以独立地或与皮质醇共同作用来确定孩子的情绪反应。它作为 HPA 轴的主要最终产物的作用，加上这里显示的新记录的与产前发育的关联，强烈呼吁将 DHEA 纳入未来的胎儿编程研究中。