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Aging and Disease    2014, Vol. 5 Issue (5) : 346-355     DOI: 10.14336/AD.2014.0500346
Epigenetics and Social Context: Implications for Disparity in Cardiovascular Disease
Karen L. Saban1, 2, Herbert L. Mathews3, Holli A. DeVon4, Linda W. Janusek1
1Marcella Niehoff School of Nursing, Loyola University Chicago, Maywood, IL, USA
2Center of Innovation for Complex Chronic Healthcare, Edward Hines Jr. VA Hospital, Hines, IL, USA
3Stritch School of Medicine, Loyola University Chicago, Maywood, IL, USA
4College of Nursing, University of Illinois at Chicago, Chicago, IL, USA
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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.


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.


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.


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.

Keywords Stroke      Cardiovascular Disease      Epigenetics      Epigenomics      Health Status Disparities      Cytokines     
Corresponding Authors: Karen L. Saban   
Issue Date: 12 November 2014
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Karen L. Saban
Herbert L. Mathews
Holli A. DeVon
Linda W. Janusek
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Karen L. Saban,Herbert L. Mathews,Holli A. DeVon, et al. Epigenetics and Social Context: Implications for Disparity in Cardiovascular Disease[J]. Aging and Disease, 2014, 5(5): 346-355.
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Figure 1:  Epigenetics over the lifespan. Source: Figure is used with permission and is from “Prospects for Epigenetic Epidemiology” by D.L. Foley, J.M. Craig, R. Morely, C.A. Olsson, T. Dwyer, K. Smith et al. 2009, American Journal of Epidemiology, 169, pp. 389–400. Copyright 2009 by Oxford University Press [95].
Figure 2  The Figure depicts the proposed conceptual model. The model is based on allostatic load theory, which posits that cumulative life stress results in an altered calibration of the physiological response to acute stress, which predisposes individuals to inflammatory diseases, such as CHD and ischemic stroke [61,96,97]. Behavioral (i.e. symptoms such as fatigue), psychological (i.e. depression and anxiety), and inflammatory (i.e. elevated proinflammatory cytokines) responses are driven by cumulative life stressors. 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. Furthermore, the degree of predisposition to disease subsequent to psychological stress and inflammatory response are modulated by an individual’s adaptive capacity [11].
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