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 - 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
PY - 2019/6
Y1 - 2019/6
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.
U2 - 10.1098/rsos.190420
DO - 10.1098/rsos.190420
M3 - Article
C2 - 31312500
SN - 2054-5703
VL - 6
JO - Royal Society Open Science
JF - Royal Society Open Science
IS - 6
M1 - 190420
ER -