OSA risk was significantly correlated with biological age acceleration measured by PhenoAge and pace of biological aging (DunedinPACE), and mediation analysis detected indirect effects of OSA risk on chronic pain outcomes through the pace of biological aging.
Key Findings
Results
Individuals with low OSA risk reported increased DunedinPACE (pace of biological aging) compared to those with intermediate or high OSA risk.
The difference in DunedinPACE between low OSA risk and intermediate/high OSA risk groups was statistically significant (p < 0.001).
This finding was counterintuitive, as lower OSA risk was associated with faster pace of biological aging by this measure.
DunedinPACE is the Dunedin Pace of Aging Computed from the Epigenome.
The sample included 104 individuals with low OSA risk and 95 with intermediate or high OSA risk.
Results
There was a significant correlation between OSA risk and biological age acceleration measured by PhenoAge.
The correlation between OSA risk and PhenoAge-based biological age acceleration was statistically significant (p < 0.05).
Five epigenetic clocks were used: DunedinPACE, Horvath's, Hannum's, PhenoAge, and GrimAge.
The analysis was conducted in 199 adults aged 18–82 years who completed both STOPBANG and pain questionnaires.
Results
There was a significant correlation between OSA risk and pace of biological aging.
The correlation between OSA risk and pace of biological aging was statistically significant (p < 0.05).
OSA risk was assessed using the STOPBANG questionnaire.
Participants were classified as low OSA risk (n = 104) or intermediate/high OSA risk (n = 95).
Results
Mediation analysis detected indirect effects of OSA risk on chronic pain outcomes through the pace of biological aging.
The mediation analysis identified the pace of biological aging as a mediator in the relationship between OSA risk and chronic low back pain outcomes.
The study focused on nonspecific chronic low back pain (CLBP) as the chronic pain outcome.
This suggests a mechanistic pathway linking sleep-disordered breathing risk to chronic pain via accelerated biological aging.
Methods
The study sample consisted of 199 adults with nonspecific chronic low back pain who completed both STOPBANG and pain questionnaires.
Participants ranged in age from 18 to 82 years.
This was a secondary data analysis and cross-sectional study design.
104 participants had low OSA risk and 95 had intermediate or high OSA risk based on STOPBANG scoring.
Five biological aging measures were assessed: DunedinPACE, Horvath's clock, Hannum's clock, PhenoAge, and GrimAge.