Smoking does not accelerate leucocyte telomere attrition: a meta-analysis of 18 longitudinal cohorts. Issue 6 (5th June 2019)

• Record Type: Journal Article
• Authors: Bateson, Melissa; Aviv, Abraham; Bendix, Laila; Benetos, Athanase; Ben-Shlomo, Yoav; Bojesen, Stig E.; Cooper, Cyrus; Cooper, Rachel; Deary, Ian J.; Hägg, Sara; Harris, Sarah E.; Kark, Jeremy D.; Kronenberg, Florian; Kuh, Diana; Labat, Carlos; Martin-Ruiz, Carmen M.; Meyer, Craig; Nordestgaard, Børge G.; Penninx, Brenda W. J. H.; Pepper, Gillian V.; Révész, Dóra; Said, M. Abdullah; Starr, John M.; Syddall, Holly; Thomson, William Murray; van der Harst, Pim; Whooley, Mary; von Zglinicki, Thomas; Willeit, Peter; Zhan, Yiqiang; Nettle, Daniel;
• Is Part Of: Royal Society open science. Volume 6:Issue 6(2019)
• Publication Date: 2019-06-05
• Subjects: biological age -- telomere length -- telomere attrition -- smoking -- longitudinal; Science -- Periodicals; 500
• DOI: 10.1098/rsos.190420
• Languages: English
• ISSNs: 2054-5703

Abstract

Abstract : Smoking is associated with shorter leucocyte telomere length (LTL), a biomarker of increased morbidity and reduced longevity. This association is widely interpreted as evidence that smoking causes accelerated LTL attrition in adulthood, but the evidence for this is inconsistent. We analysed the association between smoking and LTL dynamics in 18 longitudinal cohorts. The dataset included data from 12 579 adults (4678 current smokers and 7901 non-smokers) over a mean follow-up interval of 8.6 years. Meta-analysis confirmed a cross-sectional difference in LTL between smokers and non-smokers, with mean LTL 84.61 bp shorter in smokers (95% CI: 22.62 to 146.61). However, LTL attrition was only 0.51 bp yr −1 faster in smokers than in non-smokers (95% CI: −2.09 to 1.08), a difference that equates to only 1.32% of the estimated age-related loss of 38.33 bp yr −1 . Assuming a linear effect of smoking, 167 years of smoking would be required to generate the observed cross-sectional difference in LTL. Therefore, the difference in LTL between smokers and non-smokers is extremely unlikely to be explained by a linear, causal effect of smoking. Selective adoption, whereby individuals with short telomeres are more likely to start smoking, needs to be considered as a more plausible explanation for the observed pattern of telomere dynamics.