Skip to content

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

Research output: Contribution to journalArticle

  • Melissa Bateson
  • Abraham Aviv
  • Laila Bendix
  • Athanase Benetos
  • Yoav Ben-Shlomohttp://orcid.org/0000-0001-6648-3007
  • Stig E. Bojesen
  • Cyrus Cooper
  • Rachel Cooper
  • Ian J. Deary
  • Sara Hägg
  • Sarah E. Harris
  • Jeremy D. Kark
  • Florian Kronenberg
  • Diana Kuh
  • Carlos Labat
  • Carmen M. Martin-Ruiz
  • Craig Meyer
  • Børge G. Nordestgaard
  • Brenda W.J.H. Penninx
  • Gillian V. Pepper
  • Dóra Révész
  • M. Abdullah Said
  • John M. Starr
  • Holly Syddall
  • William Murray Thomson
  • Pim Van Der Harst
  • Mary Whooley
  • Thomas Von Zglinicki
  • Peter Willeit
  • Yiqiang Zhan
  • Daniel Nettle
Original languageEnglish
Article number190420
Number of pages16
JournalRoyal Society Open Science
Volume6
Issue number6
DOIs
DateAccepted/In press - 3 May 2019
DatePublished (current) - 5 Jun 2019

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.

    Research areas

  • Biological age, Longitudinal, Smoking, Telomere attrition, Telomere length

Download statistics

No data available

Documents

Documents

  • Full-text PDF (final published version)

    Rights statement: This is the final published version of the article (version of record). It first appeared online via the Royal Society at https://royalsocietypublishing.org/doi/10.1098/rsos.190420 . Please refer to any applicable terms of use of the publisher.

    Final published version, 951 KB, PDF document

    Licence: CC BY

DOI

View research connections

Related faculties, schools or groups