Abstract
This study aimed to dissect the direct effect of smoking and its indirect effect through body mass index (BMI) on leukocyte telomere length (LTL) and to distinguish the mediation and suppression effects of BMI. The study cohort included 1,037 adults (729 Whites and 308 African Americans; 42.1% males; mean age: 40.3 years) with LTL measurements by Southern blotting. General third variable models were used to distinguish the mediation and suppression effects of BMI on the smoking-LTL association. After adjusting for age, race, sex and alcohol drinking, the total effect of smoking on LTL was significant (standardized regression coefficient, β= -0.061, p=0.034) without BMI included in the model. With additional adjustment for BMI, the indirect effect of smoking on LTL through BMI was estimated at β= 0.011 (p=0.023), and the direct effect of smoking on LTL was strengthened to β= -0.072 (p=0.012). The results were similar when pack-years of smoking was used. The effect parameters did not differ significantly between race and sex groups. These results suggest that BMI has a suppression effect, not a mediation effect, on the smoking-LTL association, which potentially contributes to previous inconsistencies in the effect of smoking on LTL.
Highlights
Telomeres, the TTAGGG tandem repeats at the ends of chromosomes that protect the end of chromosomes, become progressively shortened with each cell division [1]
The present study aims to dissect the direct effect of smoking on leukocyte telomere length (LTL) and its indirect effect through body mass index (BMI) and to distinguish the mediation and suppression effects of body weight in a study cohort of African American (AA) and white adults from the Bogalusa Heart Study
Our findings suggest that BMI modifies the association between cigarette smoking and LTL by suppressing the effect of smoking, which potentially contributes to the mixed findings reported on the smoking-LTL association in previous studies [13]
Summary
The TTAGGG tandem repeats at the ends of chromosomes that protect the end of chromosomes, become progressively shortened with each cell division [1]. Telomere length has been considered as a marker of biological aging, cardiovascular aging [2, 3]. Extensive evidence has shown that agedependent leukocyte telomere length (LTL) attrition is associated with cardiovascular risk factors such as race, sex, obesity, and unhealthy lifestyles, including excessive alcohol consumption, lack of physical activity and cigarette smoking [3,4,5,6,7]. Effects of cigarette smoking on inflammation and oxidative stress in humans, animals, and in vitro models are well documented [8, 9]. Exposure to harmful chemicals in cigarettes induces irreparable damage to the telomeric DNA through the mechanisms of increased inflammation and oxidative stress [10,11,12]. The role of a third variable is a potential explanation for these inconsistencies
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