Research Project
10403771
PROJECT SUMMARY As society seeks to understand the etiology of human emotional and behavioral disorders, increasing attention must focus on the earliest determinants of vulnerability to these disorders, including those existing during prenatal life. Maternal stress during pregnancy contributes to this vulnerability by derailing many aspects of fetal development, including those underlying the infant?s later physiological and behavioral responses to stress. Dysregulation of these stress-coping systems is known to put infants at tremendous risk for later emotional and behavioral problems. What remains virtually unknown, however, is how the differential timing of prenatal stress affects the degree of impairment in infants? biobehavioral regulation to stress. In the first longitudinal prospective study of its kind, we propose to use unprecedented high-frequency sampling to measure the occurrence of a common major stressor in a cohort of 335 women starting as early as week 15 of pregnancy, and then determine precisely when during pregnancy (early, mid, late) the stress exposure had the greatest impact on their 6-month-old infants? physiological responses to stress (i.e., hypothalamic-pituitary axis and sympathetic nervous system reactivity) and their behavioral responses to stress. The prenatal stressor we will use as a model is intimate partner violence (IPV). IPV is ideal to study for this purpose because, unlike many stressors studied in previous research on prenatal stress, IPV is an extremely common stressor experienced by pregnant women and its timing during pregnancy can be very precisely assessed. Furthermore, women can experience IPV during pregnancy, postpartum, or both. Therefore, in addition to determining the critical periods during fetal life when exposure to this major stressor is particularly detrimental to later infant stress responsivity, we can determine how those effects compare with postnatal exposure to the same stressor. Based on knowledge about the developmental milestones for the neural substrates involved in the physiological and behavioral responses to stress, we hypothesize in Aim 1 that early gestation stress will have the greatest effects on infant SNS stress responsivity, but that mid-gestation stress will have the greatest effects on infant HPA-axis responsivity and their behavioral responses to stress. In Aim 2 we will examine the maternal HPA axis and SNS functioning during her pregnancy as a mediator of the effects of prenatal IPV on later infant stress responsivity. Knowledge about the sensitive periods to stress that exist within prenatal life will have profound implications for pinpointing the cellular and molecular mechanisms that are derailed in the fetus and responsible for the negative outcomes seen after birth. This knowledge will also greatly inform strategies for prevention and intervention that will help avoid the negative effects of stress during this exquisitely sensitive period for human psychological and behavioral development and, thus, improve the lives of millions of women and their infants.
