Could epigenetics help explain racial disparities in chronic pain?
- PMID: 30863142
- PMCID: PMC6388771
- DOI: 10.2147/JPR.S191848
Could epigenetics help explain racial disparities in chronic pain?
Abstract
African Americans disproportionately suffer more severe and debilitating morbidity from chronic pain than do non-Hispanic Whites. These differences may arise from differential exposure to psychosocial and environmental factors such as adverse childhood experiences, racial discrimination, low socioeconomic status, and depression, all of which have been associated with chronic stress and chronic pain. Race, as a social construct, makes it such that African Americans are more likely to experience different early life conditions, which may induce epigenetic changes that sustain racial differences in chronic pain. Epigenetics is one mechanism by which environmental factors such as childhood stress, racial discrimination, economic hardship, and depression can affect gene expression without altering the underlying genetic sequence. This article provides a narrative review of the literature on epigenetics as a mechanism by which differential environmental exposure could explain racial differences in chronic pain. Most studies of epigenetic changes in chronic pain examine DNA methylation. DNA methylation is altered in the glucocorticoid (stress response) receptor gene, NR3C1, which has been associated with depression, childhood stress, low socioeconomic status, and chronic pain. Similarly, DNA methylation patterns of immune cytokine genes have been associated with chronic stress states. Thus, DNA methylation changes may play an essential role in the epigenetic modulation of chronic pain in different races with a higher incidence of epigenetic alterations contributing to more severe and disabling chronic pain in African Americans.
Keywords: DNA methylation; chronic pain; epigenetics; epigenomics; racial health disparities; stress.
Conflict of interest statement
Disclosure The content expressed herein and the interpretation and reporting of these data are the responsibility of the authors and should not be seen as an official recommendation or interpretation of the National Institutes of Health or the University of Alabama Birmingham. The authors report no conflicts of interest in this work.
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