Strong evidence has accrued indicating that inflammation (INF) predicts the onset of chronic, age-related diseases. Although psychosocial stress is a major determinant of INF, we know little about the role of stress contagion from romantic partners, a prominent social context in early adulthood, or the role of childhood stressors in amplifying INF response to adult stress. Evidence has accumulated indicating that early stress experiences may shift propensity to respond with INF due to early calibration of Inflammation Related Transcriptional Response (IRTR). However, we have little information regarding the extent to which IRTR predicts amplified INF response to adult stressors or the extent which it accounts for the impact of early stressors on INF. In addition, we do not know the extent to which persistent, supportive relationships in young adulthood have the potential to ameliorate the impact of earlier stressors by modifying IRTR and so reducing INF in response to adult stressors. Finally, prior research has largely focused on White samples, thereby limiting our understanding of the causes of INF among African Americans, a group at elevated risk for age- related chronic illness. This application seeks funding to add assessment of romantic partners and to directly assess IRTR for both targets and partners who are participating in a recently funded application. In the parent application we assess INF and collect telephone interview data from targets regarding stress and health behaviors in a sample of roughly 700 African Americans (now 28 years of age). In the current application we add parallel interview assessments and assessment of INF for N = 320 romantic partners. In addition we add assessment of IRTR for both targets and romantic partners. This additional data collection will allow us to address the following specific aims: 1) Identify the effect of stress contagion on young adult INF among African Americans, controlling for own stressors and history of early exposure to stressors; 2) Test hypothesized amplification of effect on INF of own stress, stress contagion, and dyad-level effects due to exposure to early stressors, and examine the hypothesis that calibration of Inflammation Related Transcriptional Response (IRTR) is the mechanism by which early stress influences INF; and 3) Test the hypothesized role of persistent supportive romantic relationships (PSR) in recalibrating stress biology, i.e., examine the hypothesis that among those in persistent supportive relationships in young adulthood we will see reduced impact of early stress exposure on IRTR. The Institute of Medicine prescribes development of prevention based on longitudinal, epidemiological research with target populations. Currently, no prospective investigations identify the protective factors that interrup the impact of stress on INF for African Americans. The results of the proposed research will identify protective processes and serve as the basis for empirically- based, health disparities prevention programs as well as provide a basis for ongoing policy discussions, e.g. the Healthy Marriage Initiative.
Improving quality of longer lives requires information about sources of the inflammation linked to age- related, chronic diseases; causes that include social relationships and may lie at earlier stages of development. Building on prior research documenting the role of childhood stress in amplifying inflammatory responses to adult stress, the present study examines the interaction of child stress with stress contagion from adult romantic partners as well as ameliorative effects due to persistent, supportive romantic relationships, and so provides a foundation for development of preventative interventions to protect against amplified inflammation and a framework for ongoing policy discussions such as the healthy marriage initiative.
