<p>Could epigenetics help explain racial disparities in chronic pain?</p>

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.

Identification of DNA methylation associated enrichment pathways in adults with non-specific chronic low back pain

“…Thus, a mechanism such as epigenetics that links stressful environmental factors to alterations in genetic expression may play a significant role in cLBP. 21…”

Placebo hypoalgesia: racial differences

“…Future research with neurobiological approaches can further explore other potential race-based mechanistic differences (i.e. epigenetic differences [3], DNA hypermethylation [5; 90]).…”

Differential DNA methylation in Black and White individuals with chronic low back pain enrich different genomic pathways

“…This may be related to the fact that race is a socially constructed categorization of people, different from biological traits such as ancestry, and not an inherent disease risk. ( Aroke et al, 2019 )…”

“…( Kanherkar et al, 2014 , Syed and Nemeroff, 2017 ) DNA methylation (DNAm) is a stable, heritable, and well-studied epigenetic modification. ( Aroke et al, 2019 , Dupont et al, 2009 ) Generally, DNAm is tissue-specific, however, in rat models with chronic pain, Massart and colleagues found a strong correlation between DNAm in the prefrontal cortex and peripheral blood T-cells; peripheral T-cell methylation predicted chronic pain with 80% accuracy. ( Massart et al, 2016 ) Other researchers have also utilized peripheral blood methylation as a less-invasive sample to study methylation patterns in chronic pain conditions, including fibromyalgia, persistent post-mastectomy pain, generalized musculoskeletal pain, and cLBP.…”

“…We previously suggested that a lifetime of adversity, chronic stress, poor coping, and racial discrimination may induce epigenetic modifications, affecting adaptation and resulting in racial differences in adulthood disorders such as chronic pain. ( Aroke et al, 2019 ) Emerging evidence suggests that DNAm changes that occur throughout the lifetime may play an essential role in the pathology of cLBP. ( Gerra et al, 2017 ) Tajerian and colleagues have previously reported cLBP correlated with DNAm levels in secreted protein acidic and cysteine-rich (SPARC) gene.…”