TY - JOUR

T1 - Smoking does not accelerate leucocyte telomere attrition

T2 - A meta-analysis of 18 longitudinal cohorts

AU - Bateson, Melissa

AU - Aviv, Abraham

AU - Bendix, Laila

AU - Benetos, Athanase

AU - Ben-Shlomo, Yoav

AU - Bojesen, Stig E.

AU - Cooper, Cyrus

AU - Cooper, Rachel

AU - Deary, Ian J.

AU - Hägg, Sara

AU - Harris, Sarah E.

AU - Kark, Jeremy D.

AU - Kronenberg, Florian

AU - Kuh, Diana

AU - Labat, Carlos

AU - Martin-Ruiz, Carmen M.

AU - Meyer, Craig

AU - Nordestgaard, Børge G.

AU - Penninx, Brenda W.J.H.

AU - Pepper, Gillian V.

AU - Révész, Dóra

AU - Said, M. Abdullah

AU - Starr, John M.

AU - Syddall, Holly

AU - Thomson, William Murray

AU - Van Der Harst, Pim

AU - Whooley, Mary

AU - Von Zglinicki, Thomas

AU - Willeit, Peter

AU - Zhan, Yiqiang

AU - Nettle, Daniel

PY - 2019

Y1 - 2019

N2 - 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.

AB - 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.

KW - Biological age

KW - Longitudinal

KW - Smoking

KW - Telomere attrition

KW - Telomere length

U2 - 10.1098/rsos.190420

DO - 10.1098/rsos.190420

M3 - Journal article

C2 - 31312500

AN - SCOPUS:85068207350

VL - 6

JO - Royal Society Open Science

JF - Royal Society Open Science

SN - 2054-5703

IS - 6

M1 - 190420

ER -