ArticleClinical epigenetics2023
Epigenetic age acceleration mediates the association between smoking and diabetes-related outcomes.
Article in Clinical epigenetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Lung microbiome predictors of epigenetic aging and potential associations with smoking and electronic cigarette use.Clinical epigenetics · 2026Article
- Association of smoking behaviors with GOLD biological age acceleration and potential mediation: Evidence from NHANES 1999-2023.Tobacco induced diseases · 2026Article
- KoMethylNet: a novel epigenetic clock based on neural network analysis of DNA methylation data and epigenetic age acceleration in a Korean population.BMC medicine · 2025Article
- Three generations of epigenetic clocks in mediating the adverse effect of smoking on metabolic health.Epigenomics · 2025Article
- Cross-tissue comparison of epigenetic aging clocks in humans.Aging cell · 2025Article
- Environmental Health Is Overlooked in Longevity Research.Antioxidants (Basel, Switzerland) · 2025Review
- Causal Associations of Epigenetic Age Acceleration With Stroke and Its Functional Outcome: A Two-Sample, Two-Step Mendelian Randomization Study.Brain and behavior · 2025Article
- Association Between DNA Methylation ofJournal of diabetes research · 2025Article
- Causal relationship between type 2 diabetes and common respiratory system diseases: a two-sample Mendelian randomization analysis.Frontiers in medicine · 2024Article
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2 authors.
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Abstract
backgroundSmoking can lead to the deterioration of lung function and susceptibility to diabetes. Recently, smoking was found to induce DNA methylation (DNAm) changes in some cytosine-phosphate-guanine sites (CpGs). As linear combinations of DNAm levels of aging-related CpGs, five measures of epigenetic age acceleration (EAA) have received extensive attention: HannumEAA, IEAA, PhenoEAA, GrimEAA, and DunedinPACE. It is of interest to explore whether some measures of EAA can mediate the associations of smoking with diabetes-related outcomes and indices of ventilatory lung function. METHODS AND
resultsIn this study, we included self-reported smoking variables (smoking status, the number of pack-years, and years since smoking cessation), seven DNAm markers (HannumEAA, IEAA, PhenoEAA, GrimEAA, DNAm-based smoking pack-years, DNAm plasminogen activator inhibitor 1 [PAI-1] levels, and DunedinPACE), and four health outcomes (fasting glucose, hemoglobin A1C, forced expiratory volume in 1.0 s [FEV1], and forced vital capacity [FVC]) from 2474 Taiwan Biobank participants. Mediation analyses were conducted while adjusting for chronological age, sex, body mass index, drinking status, regular exercise status, educational attainment, and five cell-type proportions. We demonstrated that GrimEAA, DNAm-based smoking pack-years, DNAm PAI-1 levels, DunedinPACE, and PhenoEAA mediated smoking associations with diabetes-related outcomes. Moreover, current and former smoking both had an adverse indirect effect on FVC through DNAm PAI-1 levels. For former smokers, a long time since smoking cessation had a positive indirect impact on FVC through GrimEAA and on FEV1 through PhenoEAA.
conclusionsThis is one of the first studies to comprehensively investigate the role of five measures of EAA in mediating the associations of smoking with the health outcomes of an Asian population. The results showed that the second-generation epigenetic clocks (GrimEAA, DunedinPACE, and PhenoEAA) significantly mediated the associations between smoking and diabetes-related outcomes. In contrast, the first-generation epigenetic clocks (HannumEAA and IEAA) did not significantly mediate any associations of smoking variables with the four health outcomes. Cigarette smoking can, directly and indirectly, deteriorate human health through DNAm changes in aging-related CpG sites.
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