Psychosocial Stress, Epigenetics, and Cardiovascular Disease: A Scoping Review of DNA Methylation’s Impact on Cardiovascular Disease in African Americans

Abstract

Introduction: African Americans experience a disproportionate burden of cardiovascular disease by up to 20% due to a combination of social and genetic factors. This paper will examine the potential contributions of DNA methylation to the burden of cardiovascular disease in African Americans in the context of psychosocial stress.

Methods: This scoping review examined peer-reviewed literature published between 1995 and 2025 using databases such as PubMed, Google Scholar, Scopus, and MedLine OVID. Inclusion criteria targeted studies on DNA methylation changes linked to stress and CVD, excluding studies focused on participants with diagnosed psychiatric stress disorders.

Results: Studies indicated that discrimination faced by the African American community correlated to DNA methylation in inflammatory genes such as tumor necrosis factor-α and other proteins implicated in cardiovascular disease pathology. There was a correlation with DNA methylation and altered protein expression potentially exposing an increased risk of cardiovascular disease for African Americans. Additionally, it was found that chronic maternal stress during and before pregnancy can reduce the expression of enzymes critical for oxidizing harmful maternal glucocorticoids. Consequently, the fetus becomes exposed to glucocorticoids such as cortisol and corticosterone that have been demonstrated to cause epigenetic modifications.

Discussion: Psychosocial stress contributes to cardiovascular disease in African American populations through both direct and intergenerational DNA methylation mechanisms. Chronic stress stemming from psychosocial stressors induce DNA methylation alterations in genetic pathways contributing to an increased prevalence of cardiovascular disease. Transgenerationally, chronic maternal stress can alter the expression of protective placental enzymes, potentially modifying the expression of IGF1 and IGF2 due to DNA methylation by maternal glucocorticoids. These findings underscore DNA methylation as a mechanism linking racial stress disparities to long-term cardiovascular outcomes.

Conclusion: Stress-induced DNA methylation affects vascular health both directly and transgenerationally, potentially contributing to the development of cardiovascular disease. This highlights a potential route by which African Americans are disproportionately burdened with rates of cardiovascular disease due to psychosocial stressors. The routes proposed here are based on correlational evidence and further directions should aim to highlight causal relationships between DNA methylation, psychosocial stress, and cardiovascular disease.