Animal studies show that prenatal maternal stress (PNMS) results in maternal glucocorticoids passing the placental barrier and disrupting fetal brain development, particularly the hypothalamic-pituitary-adrenal axis. This in turn influences pregnancy outcomes and offspring development. To date, however, there have been no prospective studies of pregnant women exposed to a sudden-onset natural disaster that have been able to elucidate the biopsychosocial mechanisms responsible for the wide variety of consequences of prenatal stress seen in human and animal offspring. As such, the goal of this project is to increase our understanding of the mechanisms responsible for the effects of maternal exposure to varying levels of hardship, and the pregnant women's subjective reactions to these hardships, imposed by a severe, independent stressor: the U.S. Midwest floods of June 2008. We will determine the extent to which the effects of various components of disaster on the mother, the pregnancy and infant may be moderated by biological, psychological, and social factors on a sample of approximately 420 women who had either given birth shortly before the flooding, or who were pregnant during the flooding, or who became pregnant within 3 months after the flooding.
An important element of this study is that pre-flood data are available on the psychological functioning, coping, and social support in 135 pregnant and postpartum women. Here, we propose to augment this on-going study with a new protocol involving two timelines. One data collection timeline will be linked to the flooding, and will assess symptoms of post-traumatic stress disorder (PTSD) and coping, and collect diurnal salivary cortisol, at recruitment, 6- and 12-months post-flood. A second timeline is linked to the pregnancy and involves data collection at recruitment, at 30-32 weeks gestation, delivery, and 6-months postpartum; these will assess maternal mood, biomarkers from maternal blood, and infant behavior over time. We predict that higher levels of PNMS will be associated with poorer maternal health outcomes (PTSD, postpartum depression). We also predict that higher levels of PNMS and higher pregnancy cortisol levels will be associated with more obstetric and newborn complications, poorer infant health, poorer neuromotor maturity at birth, blunted reactive cortisol levels, as well as more difficult temperament. We believe that placental functioning will be a central mechanism for these effects: prenatal stress will be associated with altered placental functioning which will be associated with poorer perinatal and infant outcomes. This RAPID grant will enable us to collect (and to a limited extent analyze) the most comprehensive data set ever obtained for studying the effects of an independent stressor on PTSD, postpartum depression, pregnancy outcomes and infant development. By obtaining a multitude of maternal and infant biomarkers and by evaluating the functioning of the placenta, we will be in a position to test a comprehensive biopsychosocial model of prenatal maternal stress. The results of this collaboration should point us towards interventions that will effectively limit the damage to mother and fetus when disasters occur.