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Abstract
The purposes of this study were to determine the intervals when placental corticotrophic-releasing hormone (CRH) was most responsive to maternal cortisol. A sample of 203 women each were evaluated at 15, 19, 25 and 31 weeks gestation and followed to term. Placental CRH and maternal adrenocorticotropin hormone (ACTH), B-endorphin and cortisol were determined from plasma. CRH levels increased faster and were higher in women who delivered preterm compared with women who delivered at term ( F 3,603 = 5.73, p < .001). Simple effects indicated that CRH levels only at 31 weeks predicted preterm birth ( F 1,201 = 5.53, p = .02). Levels of cortisol were higher in women who delivered preterm at 15 weeks gestation ( F 1,201 = 4.45, p = .03) with a similar trend at 19 weeks gestation. Hierarchical regression suggested that the influence on birth outcome of maternal cortisol early in pregnancy was mediated by its influence on placental CRH at 31 weeks. Elevated cortisol at 15 weeks predicted the surge in placental CRH at 31 weeks ( R = .49, d.f. = 1,199, F change = 61.78, p < .0001). Every unit of change in cortisol (μg/dl) at 15 weeks was associated with a 34 unit change of CRH (pg/ml) at 31 weeks. These findings suggested that early detection of stress signals by the placenta stimulated the subsequent release of CRH and resulted in increased risk for preterm delivery.
Highlights
Remarkable surveillance and response systems have evolved and are conserved so that many species from the desert dwelling Western Spadefoot tadpole to the human fetus can detect threats to survival and adjust their developmental trajectory [3,40]
Consistent with previous studies [29,45,46], placental corticotrophicreleasing hormone (CRH) levels in women destined to deliver preterm had faster rates of increase (F3,603 = 5.73, p < .001 [group  weeks gestation]) and significantly higher levels of CRH confined to the beginning of the early third trimester (F1,201 = 5.53, p = .02 [post hoc comparison at 31 weeks]) than women who subsequently delivered at term (Fig. 2)
New findings from this study indicate that a plausible stress-related endocrine signal, elevated cortisol [22,37] from the mother very early in pregnancy predicts the precocious rise in CRH leading to an abbreviated gestational period
Summary
Remarkable surveillance and response systems have evolved and are conserved so that many species from the desert dwelling Western Spadefoot tadpole to the human fetus can detect threats to survival and adjust their developmental trajectory [3,40]. The human placenta is both a sensory and effector organ that incorporates and transduces information peptides 27 (2006) 1457–1463 from its maternal host environment into the fetal developmental program It has receptors and expresses the genes for major stress systems, including the endocrine system and CRH [10,11,20,23,28,34,35,48]. To the inhibitory influence on the promoter region of the CRH gene in the hypothalamus, maternal stress signals (glucocorticoids) from the adrenal glands activate the promoter region in the placenta and stimulate its synthesis [21,41] This positive feedback system contains both a signal to the fetus (elevated glucocorticoids) that the host environment (the mother) is threatened [44], potentially compromising fetal survival, and a response from the fetus (increased placental CRH production) that shortens gestation. The purposes of our study are to determine the critical intervals during which CRH influences the length of human gestation and the critical periods during gestation when the placenta is most vulnerable to the biological signals of threat
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