Fiona B. A. T. Agbor

Nonspecific chronic low back pain (NSCLBP) is associated with central sensitization, and both diet quality and epigenetic aging are proposed modifiable, mechanistic contributors to this process. We examined how dietary profiles and epigenetic aging affect central sensitization in NSCLBP. Participants completed dietary, epigenetic aging (DunedinPACE, GrimAge), and central sensitization indicators, including conditioned pain modulation (CPM), heat and mechanical temporal summation (TS), and pain sensitivity questionnaire (PSQ). Dietary profiles were derived from latent profile analysis of dietary inflammatory index components. Nested regression models examined how dietary profiles and epigenetic aging predict central sensitization, adjusting for age, sex, BMI, and race, followed by Benjamini-Hochberg’s false discovery rate correction. We included 200 adults with NSCLBP: mean age 44 years; 62% African American; 55% female; mean BMI 31.33 kg/m². Five tests remained significant after Benjamini-Hochberg correction. DunedinPACE acceleration increased PSQ (β = 2.936, raw p = .034, FDR p = .034), GrimAge acceleration decreased mechanical TS (β = -0.270, raw p = .008, FDR p = .016). Increased low pro-inflammatory diet increased CPM only after accounting for DunedinPACE (β = 49.788, SE = 15.433, raw p = .002, FDR p = .013) and GrimAge (β = 52.685, SE = 15.281, raw p = .001, FDR p = .013). Increased low pro-inflammatory diet decreased heat TS facilitation in the GrimAge-adjusted model (β = -22.028, SE = 8.270, raw p = .009, FDR p = .049). Diet and epigenetic aging jointly, rather than independently, shape central pain processing in NSCLBP, suggesting protective effects of healthier diets.

This secondary data analysis aimed to determine the nature of the relationship between obstructive sleep apnea (OSA) risk, biological age acceleration, and nonspecific chronic low back pain (CLBP). In total, 199 adults aged 18–82 years who filled both STOPBANG and pain questionnaires subsetted for secondary analysis. Based on the STOPBANG questionnaire, 104 had a low OSA risk and 95 had an intermediate or high OSA risk. Dunedin Pace of Aging Computed from the Epigenome (DunedinPACE), Horvath’s, Hannum’s, PhenoAge, and GrimAge clocks were used to determine biological age and pace of biological aging. Individuals with low OSA risk reported increased DunedinPACE compared to those with intermediate/high OSA risk ( p < 0.001). There was a significant correlation between the risk for OSA and biological age acceleration measured by PhenoAge as well as pace of biological aging ( p < 0.05). Mediation analysis detected indirect effects of OSA risk on chronic pain outcomes through the pace of biological aging. Targeted interventions addressing OSA risk offers a promising therapeutic strategy. This could be particularly valuable for aging populations where both accelerated biological aging and chronic pain conditions are prevalent, offering a more holistic approach to improving nonspecific chronic pain outcomes through quality of sleep and restfulness.

In this study, we aimed to investigate if the pace of biological aging serves as a critical mediator in the relationship between chronic pain resilience and chronic low back pain intensity and disability. Two hundred seven community-dwelling non-Hispanic Black (NHB) and non-Hispanic White (NHW) adults completed the Pain Resilience Scale (PRS) and Graded Chronic Pain Scale (GCPS). Blood genomic DNA was sequenced using Illumina’s MethylationEPIC, and the pace of biological aging estimated using the DunedinPACE (the Dunedin Pace of Aging Calculated from the Epigenome) algorithm. In bivariate correlations, DunedinPACE significantly correlated with pain intensity (r = 0.40), and disability (r = 0.39), at p < .05. Pain resilience negatively correlated with pain intensity (rs = −0.22), pain disability (rs = −0.30), and DunedinPACE (r = −0.11). After controlling for chronological age, sex, race, and BMI, mediation analyses revealed a significant indirect association of pain resilience on pain intensity through the pace of biological aging (β = −0.66 (SE); Boot 95% CI [−1.06, −0.25]). Similarly, DunedinPACE partially mediated the relationship between resilience and pain disability (β = −0.82; 95% CI, [−1.20 to −0.44]). We found that higher levels of resilience correlate with a slower pace of biological aging, which in turn correlates with better pain outcomes. The pace of biological aging emerged as an important potential target for future interventions studies for pain management.