Preterm delivery, an increasingly frequent occurrence in the United States, is associated with significant family burden and an estimated societal cost of at least $26 billion per year. In the U.S., the preterm birth rate is 12-13% as compared to 5-9% in other developed countries. Persistent racial disparities contribute to this discrepancy. Psychosocial stress and related physiological sequelae may contribute to preterm birth overall, as well as to racial disparities in preterm birth. The experience of chronic stress, such as that conferred by racial minority status, may sensitize physiological stress responses. Indeed, as compared to Caucasians, African-Americans exhibit greater cardiovascular reactivity to a variety of acute stressors. Importantly, blood pressure, glucocorticoid, and catecholamine responses to acute stress are attenuated during healthy pregnancy as compared to nonpregnancy. This adaptation may protect the mother and fetus from potentially detrimental effects of maternal physiological activation. Thus, women who exhibit greater and more extended physiological reactions to everyday stressors may be at increased risk for negative perinatal outcomes. Notably, no studies of acute stress during pregnancy have examined inflammatory immune responses or mechanisms underlying blood pressure change (i.e., cardiac output, total peripheral resistance). Moreover, limited information is available regarding effects of race on physiological adaptation to pregnancy. The current study will address important gaps in the literature by examining cardiovascular, endocrine, and immune reactivity to acute stress among 40 healthy pregnant women (20 Caucasian, 20 African-American) and 40 demographically matched nonpregnant control women. This research is designed to ultimately lead to the identification of women at greater risk for negative perinatal outcomes and elucidation of mechanisms underlying increased risk, providing a basis for individualized health care services.
Specific Aim #1 : To utilize more comprehensive and advanced methodology to assess physiological reactivity during pregnancy versus nonpregnancy, including measures of inflammation, impedance cardiography, and glucocorticoid receptor function. Hypothesis #1: Pregnant women will show attenuated physiological responses to acute stress as compared to nonpregnant women.
Specific Aim #2 : To examine racial differences in physiological reactivity during pregnancy versus nonpregnancy. Hypothesis #2: As compared to Caucasian women, African-American women will exhibit greater physiological reactivity to stress during pregnancy and nonpregnancy.
Specific Aim #3 : To examine psychosocial correlates of physiological reactivity during pregnancy and nonpregnancy. Hypothesis #3: Women reporting greater distress will exhibit greater physiological reactivity during pregnancy and nonpregnancy.
Specific Aim #4 : To examine associations between physiological reactivity and length of gestation. Hypothesis #4: Greater physiological reactivity to acute stress will predict shorter gestational length.
This study will fill important gaps in our knowledge regarding physiological adaption during pregnancy and effects of race on such adaptation. Information gained from this study will provide the groundwork for the following: 1) identification of women at greater risk of negative perinatal outcomes;2) describing physiological mechanisms underlying the link between stress and risk of preterm delivery;and 3) providing interventions designed to reduce the effects of stress and promote healthy pregnancy and fetal development.
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