Placental corticotropin-releasing hormone (CRH), spontaneous preterm birth, and fetal growth restriction: A prospective investigation

Wadhwa, Pathik D.; Garite, Thomas J.; Porto, Manuel; Glynn, Laura M.; Chicz-DeMet, Aleksandra; Dunkel-Schetter, Christine; Sandman, Curt A.

doi:10.1016/j.ajog.2004.06.070

Cited by 344 publications

(277 citation statements)

References 36 publications

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“…The second possibility is that under stressful conditions, the fetus must compete with its host (the mother) for resources required for coping and survival (Stearns, 2005). This possibility is consistent with findings indicating that fetal exposure to stress hormones and synthetic corticosteroid administration are associated with fetal growth restriction (Bloom et al, 2001;French et al, 1999;Reinisch et al, 1978;Wadhwa et al, 2004). The purposes of the present study were to (1) test these competing hypotheses by evaluating the consequences of exposure to stress hormones during pregnancy for physical and neuromuscular development in infants and (2) determine the specific periods during pregnancy during which stress hormones influence newborn physical and neuromuscular maturation.…”

Section: Introductionsupporting

confidence: 75%

“…Despite the necessity of cortisol for fetal maturation, it has been repeatedly demonstrated that women receiving synthetic corticosteroids (administration commencing typically around the 24th week gestation) were more likely to deliver infants with fetal growth restriction and low birth weight, even when controlling for length of gestation, suggesting that high levels of glucocorticoids may be detrimental to fetal growth (Bloom, Sheffield, McIntire, & Leveno, 2001;French, Hagan, Evans, Godfrey, & Newnham, 1999;Reinisch, Simon, Karow, & Gandelman, 1978). Similarly, exposure to CRH at 33 weeks' gestation has been associated with fetal growth restriction (Wadhwa et al, 2004). Nevertheless, no study has examined whether the timing of prenatal exposure to stress hormones affects fetal growth and maturation.…”

Section: Introductionmentioning

confidence: 99%

“…One of the major placental stress signals in pregnant primates is the peptide corticotropin-releasing hormone (CRH). This peptide plays a key role in the maturation of the fetal hypothalamic-pituitary-adrenal-axis (HPA-axis) and other systems, and coordinates events that underlie both fetal growth and maturation and the time of onset of parturition (Hobel, Dunkel-Schetter, Roesch, Castro, & Arora, 1999;Sandman et al, 2006;Sandman et al, 2003;Sandman et al, 1999b;Wadhwa et al, 2004;Wadhwa, Porto, Garite, Chicz-DeMet, & Sandman, 1998).…”

Section: Introductionmentioning

confidence: 99%

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Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Ellman

Schetter

Hobel

et al. 2008

Developmental Psychobiology

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153

146

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The purpose of the study was to determine the specific periods during pregnancy in which human fetal exposure to stress hormones affects newborn physical and neuromuscular maturation. Blood was collected from 158 women at 15, 19, 25, and 31 weeks' gestation. Levels of placental corticotropin-releasing hormone (CRH) and maternal cortisol were determined from plasma. Newborns were evaluated with the New Ballard Maturation Score. Results indicated that increases in maternal cortisol at 15, 19, and 25 weeks and increases in placental CRH at 31 weeks were significantly associated with decreases in infant maturation among males (even after controlling for length of gestation). Results also suggested that increases in maternal cortisol at 31 weeks were associated with increases in infant maturation among females, although these results were not significant after controlling for length of gestation. Findings suggest that stress hormones have effects on human fetal neurodevelopment that are independent of birth outcome.

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Section: Introductionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Ellman

Schetter

Hobel

et al. 2008

Developmental Psychobiology

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153

146

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“…42 Other studies have found associations between stress hormones (i.e., cortisol and adrenocorticotrophin-releasing hormone) and PTB, though IPV as a stressor was not specifically measured. [43][44][45] These findings highlight the need for further research on the neuroendocrine changes evident in pregnant women experiencing IPV. An enhanced understanding of the links between violence, HPA activation, utero-placental perfusion, and adverse neonatal outcomes may provide an important pathway to reducing disparities in neonatal outcomes.…”

Section: Severity Of Violence and Adverse Neonatal Outcomesmentioning

confidence: 99%

Intimate Partner Violence During Pregnancy and Adverse Neonatal Outcomes in Low-Income Women

Alhusen

Bullock

Sharps

et al. 2014

Journal of Women's Health

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Background: Intimate partner violence (IPV) affects an estimated 1.5 million U.S. women annually. IPV impacts maternal and neonatal health with higher rates of depression and low birth weight (LBW). Less studied is experiencing IPV and delivering a small for gestational age (SGA) baby. SGA neonates are at increased risk of developmental and behavioral problems. The negative sequelae persist into adulthood with increased rates of diabetes mellitus and coronary heart disease. Methods: In a sample of 239 pregnant women experiencing IPV, in urban and rural settings, we examined cross-sectional associations of severity of IPV and neonatal outcomes (i.e., birth weight and gestational age). Severity of IPV was measured by the Conflict Tactics Scale 2 and neonatal outcomes were collected at the time of delivery. Results: Outcomes were collected on 194 neonates; 14.9% (n = 29) were classified as LBW, 19.1% (n = 37) classified as SGA, and 9.8% (n = 19) as LBW and SGA. Women reporting higher severity of IPV during pregnancy had a greater likelihood of delivering an SGA neonate (odds ratio [OR] 4.81; 95% confidence interval [95% CI] 1.86-12.47), and LBW neonate (OR 4.20;. Conclusions: In a sample of pregnant women experiencing perinatal IPV, women experiencing greater severities of IPV were more likely to deliver a neonate with an adverse outcome. Early recognition and intervention of IPV is essential to reduce disparities in birth outcomes and long-term health outcomes for these neonates.

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“…Obstetric risk was defined as the presence of medical complications in the index pregnancy. Risk conditions were ascertained by extensive medical chart review and coded as a binary variable as previously described (82). The study population was predominantly (72%) at low risk with respect to adverse birth outcomes.…”

Section: Methodsmentioning

confidence: 99%

Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems

Buß

Davis²,

Shahbaba³

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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537

496

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Stress-related variation in the intrauterine milieu may impact brain development and emergent function, with long-term implications in terms of susceptibility for affective disorders. Studies in animals suggest limbic regions in the developing brain are particularly sensitive to exposure to the stress hormone cortisol. However, the nature, magnitude, and time course of these effects have not yet been adequately characterized in humans. A prospective, longitudinal study was conducted in 65 normal, healthy mother-child dyads to examine the association of maternal cortisol in early, mid-, and late gestation with subsequent measures at approximately 7 y age of child amygdala and hippocampus volume and affective problems. After accounting for the effects of potential confounding pre-and postnatal factors, higher maternal cortisol levels in earlier but not later gestation was associated with a larger right amygdala volume in girls (a 1 SD increase in cortisol was associated with a 6.4% increase in right amygdala volume), but not in boys. Moreover, higher maternal cortisol levels in early gestation was associated with more affective problems in girls, and this association was mediated, in part, by amygdala volume. No association between maternal cortisol in pregnancy and child hippocampus volume was observed in either sex. The current findings represent, to the best of our knowledge, the first report linking maternal stress hormone levels in human pregnancy with subsequent child amygdala volume and affect. The results underscore the importance of the intrauterine environment and suggest the origins of neuropsychiatric disorders may have their foundations early in life.developmental programming | fetal origins | hypothalamus-pituitaryadrenal axis | depression | emotion regulation

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Placental corticotropin-releasing hormone (CRH), spontaneous preterm birth, and fetal growth restriction: A prospective investigation

Cited by 344 publications

References 36 publications

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Timing of fetal exposure to stress hormones: Effects on newborn physical and neuromuscular maturation

Intimate Partner Violence During Pregnancy and Adverse Neonatal Outcomes in Low-Income Women

Maternal cortisol over the course of pregnancy and subsequent child amygdala and hippocampus volumes and affective problems

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