beta-endorphin and Premature-Birth

Postpartum depression (PPD) is one of the most frequent complications of childbirth affecting ~500,000 women annually (prevalence 10% to 15%). Despite the documented adverse outcomes for mother and child, there remains a great need to develop prospective approaches to identify women at risk. This review examines some of the best-characterized molecular and clinical risk factors for PPD. We illustrate that this is a growing literature but there remains a lack of reliable molecular predictors for PPD. Current best predictors are clinical assessments for psychiatric history and adverse life events, highlighting the need for increased depression screening across the perinatal period.

Topics: beta-Endorphin; Biomarkers; C-Reactive Protein; Corticotropin-Releasing Hormone; Depression, Postpartum; Epigenesis, Genetic; Female; Genetic Predisposition to Disease; Humans; Hydrocortisone; Interleukin-6; Life Change Events; Maternal Age; Mental Disorders; Oxytocin; Pregnancy; Pregnanolone; Premature Birth; Race Factors; Risk Factors; Social Class; Thyroid Function Tests

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 (F3,603 = 5.73, p < .001). Simple effects indicated that CRH levels only at 31 weeks predicted preterm birth (F1,201 = 5.53, p = .02). Levels of cortisol were higher in women who delivered preterm at 15 weeks gestation (F1,201 = 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, Fchange = 61.78, p < .0001). Every unit of change in cortisol (microg/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.

Topics: Adrenocorticotropic Hormone; Adult; beta-Endorphin; Corticotropin-Releasing Hormone; Female; Humans; Hydrocortisone; Mothers; Placenta; Pregnancy; Pregnancy Trimester, Third; Premature Birth; Regression Analysis; Risk