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Smoking does not accelerate leukocyte telomere attrition: a meta-analysis of 18 longitudinal cohorts

Research output: Contribution to journalArticle

Original languageEnglish
JournalRoyal Society Open Science
DateAccepted/In press - 3 May 2019

Abstract

Smoking is associated with shorter leukocyte telomere length (LTL), a biomarker of increased morbidity and reduced longevity. This association is widely interpreted as evidence that smoking accelerates LTL attrition. However, an alternative hypothesis is that individuals with shorter telomeres are more likely to start smoking. Both hypotheses predict a cross-sectional difference in LTL between smokers and non-smokers, but the acceleration hypothesis additionally predicts an association between smoking and LTL attrition. 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 78.83 bp shorter in smokers (95% CI: 21.09 to 136.58). However, LTL attrition was a negligible 0.44 bp/year faster in smokers than in non-smokers (95% CI: -1.83 to 0.95), a difference that equates to only 1.23% of the estimated age-related loss of 35.71 bp/year. Assuming a linear effect of smoking, at least 177 years of smoking would be required to generate the observed cross-sectional difference in LTL. It is therefore unlikely that smoking causes the difference in LTL between smokers and non-smokers.

    Research areas

  • biological age, telomere length, telomere attrition, smoking, longitudinal

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