Digital methylation assessments of alcohol and cigarette consumption account for common variance in accelerated epigenetic ageing.
Level 4 - case-series / case-control
Cross-sectional observational analysis within a cohort wave
PubMed 35866695 · doi:10.1080/15592294.2022.2100684
What was done
Researchers evaluated whether objective biological measures of substance use correlate better with epigenetic aging than self-report. Using methylation-sensitive digital PCR (MSdPCR) assays for smoking and heavy alcohol consumption (HAC), they analyzed cross-sectional data from 437 African American participants in Wave 7 of the Family and Community Health Study Offspring Cohort. They compared self-reported vs. MSdPCR-assessed substance use against seven distinct epigenetic aging indices.
What was found
MSdPCR assessments of smoking and HAC were strongly associated with accelerated epigenetic aging, whereas self-reported alcohol consumption was not. Objective MSdPCR assessments accounted for 57% of GrimAge acceleration and accounted for the shared variance between GrimAge and DunedinPOAM accelerated aging. Specific numerical values for the remaining five epigenetic aging indices were not reported in the abstract.
Why it matters
Self-reported smoking and drinking often underestimate exposure, potentially explaining why earlier epigenetic aging studies showed weak associations. Objective digital methylation assays substantially clarify the contribution of substance use to biological aging clocks.
Limits
The abstract reports on a single cohort wave of 437 African American individuals, limiting immediate generalizability across other racial and demographic groups. The design is cross-sectional, precluding causal determination, and quantitative effect sizes are omitted for five of the seven epigenetic aging indices evaluated.
Cited by
- supports Smoking has a positive correlation of 0.4 to 0.45 with GrimAge epigenetic age acceleration.