Research Project
10204749
Chronic pain is a major public health challenge, affecting 100 million adults in the United States and resulting in over $600 billion annually in treatment costs and lost productivity. African-American (AA) adults are disproportionately affected by daily and chronic pain and report higher pain severity and greater pain-related disability across a variety of conditions. Compared to non-minorities with similar pain conditions, AA adults have poorer physical functioning, greater impairment at work and home, and lower quality of life. Daily bodily pain is common and often a precursor to chronic pain. Understanding the mechanisms that contribute to daily pain in AA adults is critical for prevention efforts targeting vulnerable adults before they develop debilitating and difficult to treat chronic pain conditions. Daily pain is more likely to become chronic in adults who have experienced adversity. Compared to non-minorities, AA adults report greater exposure to childhood trauma, family adversity, interpersonal violence, and racial discrimination. Thus, AA adults are impacted by disparities in risk factors for pain (adversity) and by chronic pain itself. Although the mechanisms linking adversity to daily pain in AA adults have not been clearly delineated, two promising pathways involve alterations of stress response systems (i.e., hypothalamic-pituitary-adrenal [HPA] axis) and pain sensitivity. The HPA axis plays an important role in stress-induced analgesia and may account, in part, for the relation between adversity and pain. Chronic and traumatic stressors are associated with diminished cortisol secretion. In turn, lower cortisol levels predict higher subsequent pain severity. Preliminary data suggest that prolonged HPA hypo-activity, indexed by hair cortisol concentration (HCC), is associated with greater pain intensity and pain-related disability. Despite theoretical models implicating HPA hypo-activity as a consequence of adversity and a risk factor for chronic pain, no studies have investigated HPA function as a mechanism linking adversity to daily pain in AA adults. Experimental pain responses correlate with pain intensity and predict risk for developing pain. Adversity is associated with altered evoked pain sensitivity. In turn, experimental pain responses predict daily and chronic pain. Although racial differences in experimental pain responses are well-established, no studies have tested altered pain sensitivity as a mechanism linking adversity to pain in AA adults. We will recruit 160 participants (~50% female), 18-45 years of age, without chronic pain, who self-identify as AA. Assessments at baseline, 6- and 12 months will determine exposure to adversity (self-report, geocoded crime report data), daily pain (intensity/disability), HCC (hair samples), and experimental pain facilitation and inhibition. Anticipated findings will highlight two novel mechanistic pathways linking cumulative adversity, which is more common in AA adults, to subsequent daily pain and disability. This proposal will also set the stage for secondary prevention efforts aimed at eliminating racial disparities in chronic pain by identifying HPA hypo- activity and evoked pain sensitivity as early risk markers for screening and potential targets for intervention.
