ArticleFrontiers in aging2025
Accelerated biological aging as potential mediator in the relationship between central obesity and lung cancer risk.
Article in Frontiers in aging, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed.
- Accelerated biological aging and underlying epigenetic modification mediated the association between obesity and asthma.Clinical epigenetics · 2026Article
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9 authors.
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Abstract
Background: The increased prevalence of obesity and incidence of lung cancer have raised significant concerns worldwide. However, the relationship between obesity and lung cancer risk, and the potential mediating effect of biological aging remains poorly understood. Methods: Using UK Biobank database, this population-based cohort study employed multivariable Cox regression to estimate HRs (Hazard Ratios) for obesity indices (waist circumference [WC], waist-hip ratio [WHR], body shape index [ABSI], conicity index [C-Index]) and lung cancer risk. Biological aging was evaluated via PhenoAge and Klemera-Doubal method age (KDMAge), with acceleration calculated by regressing biological on chronological age. Longitudinal mediation analysis explored their mediating effects. Results: Among the 301,398 participants in the study, 2,466 incident cases of lung cancer were identified. All central - obesity - related indices were significantly associated with elevated risk of lung cancer, with (WC: HR = 1.10, 95% CI 1.02-1.19; WHR: 1.10, 1.03-1.18; ABSI: 1.73, 1.54-1.94; C-Index: 1.51, 1.35-1.69). Notably, PhenoAge/KDMAge acceleration mediated the associations between WHR, ABSI, C -Index and the lung cancer risk, with mediated proportions from 1.85% to 32.67%. Conclusion: This study highlights central obesity was significantly associated with incident risk of lung cancer, emphasizing biological aging's mediating role.
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