Smoking cessation associated with reversal of epigenetic aging in observational study of 1,911 US adults.
This observational study examined associations between smoking status and DNA methylation-based measures of biological aging in 1,911 US adults aged 50-84 years from NHANES 1999-2002. Former smokers with ≥20 years of cessation showed substantially reduced epigenetic age acceleration (GrimAge2: -12.66 years) approaching levels of never smokers (-13.88 years), with a dose-response pattern where longer cessation duration was associated with greater reversal of aging markers across multiple DNA methylation clocks.
What this changes
The finding has not established an approved change to our evidence assessment.
Source date: Sep 15, 2026 · Discovered: Sep 15, 2026 · Assessed: — · Research update
What it does not prove
- Limitations have not yet been verified. Read the primary source.
Extracted from supplied source material; model confidence is not a measured probability of correctness.
Study details
- Design
- Observational
- Sample size
- 1,911
- Duration
- —
- Population
- US adults aged 50-84 years from the National Health and Nutrition Examination Survey (NHANES) 1999-2002 cycles, n=1,911
- Primary outcome
- Epigenetic age acceleration (EAA) measured across six DNA methylation clocks: HorvathAge, HannumAge, SkinBloodAge, PhenoAge, GrimAge2, and DunedinPoAm
- Effect size
- Former smokers with ≥20 years of cessation: β = -12.66 years (95% CI: -14.56, -10.75) for GrimAge2; never smokers: β = -13.88 years (95% CI: -15.70, -12.05) for GrimAge2; current smokers exhibited highest EAA across all clocks; restricted cubic spline analysis revealed rapid initial declines in EAA during first decade post-cessation with continuous declines observed beyond 20 years for GrimAge2 and DunedinPoAm
- Significance
- Significant
- Journal
- GeroScience
- Published
- Sep 15, 2026
Sources
Primary source
- GeroScience ↗Peer reviewed
Assessment history
9/23/2026 · SUPERSEDED: Source updated; assessment withdrawn pending review.
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