Direct and Mediating Pathways Linking Personal Networks with Cardiovascular Disease

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PROJECT SUMMARY/ABSTRACT Personal networks are important for cardiovascular functioning; they not only serve as sources of support and burden, but may also pattern psychosocial stress generated by major and negative life events and the environment. While much research has examined these relationships broadly, few studies have assessed data that combine extensive and rich personal network measurement with clinical indicators of cardiovascular disease (CVD) phenotype, including hypertension (HTN) and atrial fibrillation (AFib), to illuminate potential associations. The primary aim of this award is to provide necessary training and research experience to facilitate my transition to an independent researcher in the field of social networks and cardiovascular health. As a highly- trained public health scientist with specialization in social networks, I am seeking additional training in psychosocial stress theory and cardiovascular pathophysiology. I will pursue rigorous training and research during this award that will add essential skills and knowledge regarding theory of psychosocial stressors and measurement of CVD to my existing toolkit with the aim of lowering rates of CVD across broad populations. The objective of this award is to extend existing knowledge of how personal networks influence CVD by elucidating psychosocial and biological pathways in which personal networks pattern stressors that affect HTN, often the first clinical symptom of CVD. Understanding how network characteristics translate to HTN, however, requires further clarification of physiological and psychosocial processes. The proposed research examines links among personal network composition, including sources of burden and support, significant life events, and environmental stressors in association with HTN with the objective of gaining new knowledge about the specific mechanisms through which personal networks influence CVD risk. This proposal is highly significant because it will advance scientific understanding of complex relationships between personal networks and HTN and AFib. I will achieve these objectives by leveraging two existing longitudinal studies currently being conducted at Berkeley and UCSF, world-class research institutions with a long history of collaboration. I will draw on a broad range of resources, training opportunities, and mentors at both institutions to obtain the necessary skills to pursue a research career that integrates my prior background with new clinical knowledge of stress and cardiovascular pathophysiology. These new proficiencies, combined with unique cohort data highlighting specific associations linking personal networks with HTN and AFib will prepare me to write an R01 to examine how personal networks can be leveraged to lower rates of HTN and CVD.