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The Timing Of Prenatal Exposure To Maternal Cortisol And Psychosocial Stress Is Associated With Human Infant Cognitive Development

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The Timing of Prenatal Exposure to Maternal Cortisol and Psychosocial Stress Is Associated With Human Infant Cognitive Development

Elysia P. Davis and Curt A. Sandman University of California, Irvine

The consequences of prenatal maternal stress for development were examined in 125 full-term infants at 3, 6, and 12 months of age. Maternal cortisol and psychological state were evaluated 5 times during pregnancy. Exposure to elevated concentrations of cortisol early in gestation was associated with a slower rate of devel- opment over the 1st year and lower mental development scores at 12 months. Elevated levels of maternal cor- tisol late in gestation, however, were associated with accelerated cognitive development and higher scores at 12 months. Elevated levels of maternal pregnancy-specific anxiety early in pregnancy were independently associated with lower 12-month mental development scores. These data suggest that maternal cortisol and pregnancy-specific anxiety have programming influences on the developing fetus.

The prenatal period is a time of rapid change during which fetal organs and organ systems are forming and are vulnerable to both organizing and disorganizing influences. These influences on the fetus have been described as programming; the process by which a stimulus or insult during a vul- nerable developmental period has a long-lasting or permanent effect. The effects of programming are dependent on the timing of the exposure and on the developmental stage of organ systems. There is convincing support for fetal programming of adult health outcomes; however, the evidence comes pri- marily from retrospective studies that rely on birth phenotype (e.g., small size at birth or preterm delivery) as an index of fetal development (Barker, 1998, 2002). It is unlikely, however, that birth phe- notype alone is the cause of subsequent health out- comes. Birth phenotype, instead, reflects fetal adaptation to exposures that shape the structure and function of physiological systems that underlie health and disease risk (Gluckman & Hanson, 2004; Morley, Blair, Dwyer, & Owens, 2002). One emerg- ing risk factor for health outcomes resulting from fetal programming is prenatal exposure to maternal stress signals. The purpose of the present study was to investigate the programming influence of biological and psychosocial indicators of prenatal

maternal stress for fetal development and to evalu- ate the effects of timing of exposure to stress on infant development.

Fetal Programming: The Role of Glucocorticoids (GCs)

For a number of reasons, GCs have been pro- posed as a primary candidate for fetal program- ming. GCs cortisol in humans, are steroid hormones that play a critical role in normal devel- opment and are the end product of the hypotha- lamic–pituitary–adrenal (HPA) axis, one of the body’s major stress responsive systems. HPA axis activity is regulated by the release of hypothalamic corticotrophin-releasing hormone (CRH), which stimulates the biosynthesis and release of adreno- corticotropic hormone (ACTH). Release of ACTH from the pituitary into the blood stream triggers cortisol production and release from the adrenal cortex. Cortisol is released into the general circula- tion and has effects on nearly every organ and tissue in the body (Munck, Guyre, & Holbrook, 1984). In human pregnancy, regulation of the HPA axis changes dramatically with the production and release of CRH from the placenta. In contrast to the role of cortisol in the negative feedback regulation of the HPA axis, cortisol stimulates placental CRH production resulting in a positive feedback loop that allows for the simultaneous increase of CRH,This research was supported by a grant from the NIH (NS- 41298). The authors wish to thank the families who participated in this project. The assistance of Cheryl Crippen and Carol Holli- day is gratefully acknowledged. Correspondence concerning this article should be addressed to Elysia Davis, 333 City Boulevard West, Suite 1200, Orange, CA 92868. Electronic mail may be sent to

Child Development, January/February 2010, Volume 81, Number 1, Pages 131–148

 2010, Copyright the Author(s) JournalCompilation2010,SocietyforResearchinChildDevelopment,Inc. All rights reserved. 0009-3920/2010/8101-0009

ACTH, and cortisol in the maternal and fetal com- partments over the course of gestation (King, Nich- olson, & Smith, 2001; Petraglia, Florio, Nappi, & Genazzani, 1996). Maternal cortisol increases two- to fourfold over the course of normal gestation (Mastorakos & Ilias, 2003; Sandman et al., 2006). Fetal exposure to the increasing concentrations of maternal cortisol is regulated by a placental enzyme, 11b-hydroxyster- oid dehydrogenase type 2 (11b-HSD2), which oxi- dizes cortisol to its inactive form cortisone (Beitens, Bayard, Ances, Kowarski, & Migeon, 1973; Brown et al., 1996). Activity of placental 11b- HSD2 also increases as pregnancy advances, pro- viding partial protection for the fetus from mater- nal cortisol during critical stages of development. Toward the end of pregnancy, however, activity of the placental enzyme decreases, allowing a larger proportion of maternal cortisol to reach the fetus (Giannopoulos, Jackson, & Tulchinsky, 1982; Mur- phy, Smith, Giles, & Clifton, 2006). The normal increase in maternal cortisol during gestation and the decrease in placental 11b-HSD2 activity at the end of pregnancy ensure that the fetus is exposed to sufficient levels of cortisol during the third tri- mester, which are important for maturation of the fetal lungs and for preparation of the fetus for delivery (Austin & Leader, 2000; Hacking, Wat- kins, Fraser, Wolfe, & Nolan, 2001). Because pla- cental 11b-HSD2 is only a partial barrier, active maternal cortisol passes through the placenta, and fetal cortisol levels are significantly correlated with maternal levels throughout gestation (Gitau, Cam- eron, Fisk, & Glover, 1998; Gitau, Fisk, Teixerira, Cameron, & Glover, 2001). GC receptors are pres- ent throughout the central nervous system (Diorio, Viau, & Meaney, 1993; Jacobson & Sapolsky, 1991; Sanchez, Young, Plotsky, & Insel, 2000) and GCs easily pass through the blood–brain barrier (Zarrow, Philpott, & Denenberg, 1970). GCs play a critical role in normal brain development, which provides further evidence for GCs as a mechanism for programming the fetus (Matthews, 2000; Trejo, Cuchillo, Machin, & Rua, 2000; Welberg & Seckl, 2001). GCs shape the development of the neural sys- tems involved in the regulation of emotion and cognitive function. Furthermore, moderate increases in GCs have salutary effects on both brain


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