A Biopsychosocial Framework to Examine Risk for Type 2 Diabetes in Asian Pacific Islander Immigrants.

There is large disparity in the incidence of Type 2 diabetes (T2D) for Asian Pacific Islanders (APIs), one of the fastest growing minority populations in the United States. It is critical to examine biopsychosocial pathways and vulnerability factors that intensify risk for T2D in API. Increasing evidence links chronic stress to poor health outcomes and accelerated development and progression of diseases of aging, such as diabetes. Immigrant populations face unique life stressors, including the challenges associated with the process of adapting to a new environment, new language, and cultural differences. In addition, immigrants experience high levels of psychological distress related to changes of identity and values, loss of support, discrimination, and disempowerment. The purpose of this article is to propose a biopsychosocial framework to explicate potential mechanistic pathways that link cumulative life stress to risk for T2D in the API immigrant population. Unique to the proposed framework is the emphasis on inflammatory processes and accelerated cellular aging (telomere biology). A deeper understanding of biopsychosocial pathways can lead to tailored and targeted interventions to reduce the incidence of T2D in the API immigrant population.

Epigenetics and social context: implications for disparity in cardiovascular disease.

BACKGROUND: Although it is well established that African Americans (AA) experience greater social stressors than non-Hispanic Whites (NHW), the extent to which early life adversity and cumulative social stressors such as perceived discrimination, neighborhood violence, subjective social status, and socioeconomic status contribute to disparity in coronary heart disease (CHD) and stroke between AA and NHW are not well understood. PURPOSE: The purpose of this paper is to propose a conceptual model based upon McEwen's Allostatic Load Model suggesting how the relationships among social context, early life adversity, psychological stress, inflammation, adaptation, and epigenetic signature may contribute to the development of CHD and ischemic stroke. We hypothesize that social context and prior life adversity are associated with genome-wide as well as gene-specific epigenetic modifications that confer a proinflammatory epigenetic signature that mediates an enhanced proinflammatory state. Exposure to early life adversity, coupled with an increased allostatic load places individuals at greater risk for inflammatory based diseases, such as CHD and ischemic stroke. RESULTS: Based on a review of the literature, we propose a novel model in which social context and psychological stress, particularly during early life, engenders a proinflammatory epigenetic signature, which drives a heightened inflammatory state that increases risk for CHD and stroke. In the proposed model, a proinflammatory epigenetic signature and adaptation serve as mediator variables. CONCLUSIONS: Understanding the extent to which epigenetic signature bridges the psycho-social environment with inflammation and risk for CHD may yield novel biomarkers that can be used to assess risk, development, and progression of CHD/stroke. Epigenetic biomarkers may be used to inform preventive and treatment strategies that can be targeted to those most vulnerable, or to those with early signs of CHD, such as endothelial dysfunction. Furthermore, epigenetic approaches, including lifestyle modification and stress reduction programs, such as mindfulness-based stress reduction, offer promise to reduce health inequity linked to social disadvantage, as emerging evidence demonstrates that adverse epigenetic marks can be reversed.