Associations Between Alcohol Consumption and Leukocyte Telomere Length Modified by a Common Polymorphism of ALDH2.

Title
Associations Between Alcohol Consumption and Leukocyte Telomere Length Modified by a Common Polymorphism of ALDH2.
Publication type
Journal Article
Year of Publication
2016
Journal
Alcohol Clin Exp Res
Volume
40
Issue
4
Pagination
765-71
Date published
2016 Apr
ISSN
1530-0277
Abstract

BACKGROUND: Data on the association between alcohol consumption and telomere length, a marker of biological aging, are inconsistent. Moreover, the genetic modification of this association has been reported only rarely. To evaluate the association between alcohol consumption and leukocyte telomere length (LTL), and the effect modification of this association by a common polymorphism of the aldehyde dehydrogenase 2 (ALDH2) gene, we conducted a cross-sectional study in a general population including 1,771 middle-aged and elderly Koreans, aged 49 to 79 years.

METHODS: Study participants provided blood samples between 2011 and 2012 for the LTL assay, and between 2001 and 2002 for genomewide genotyping. Between 2011 and 2012, they also completed a questionnaire-based interview regarding their alcohol consumption. We examined effect modification by rs2074356, a surrogate marker of the ALDH2 polymorphism.

RESULTS: Heavy alcohol consumption (average daily alcohol consumption of >30 g) was inversely associated with LTL only among carriers of the mutant alleles (CT and TT) of rs2074356 (p < 0.01). Among these subjects, elderly drinkers in particular showed the strongest association (p < 0.001). Light-to-moderate alcohol consumption on an almost daily basis was positively associated with LTL (p < 0.001), and this association was significant among carriers of the wild-type allele (CC) of rs2074356 (p < 0.01) but not among those with the mutant alleles.

CONCLUSIONS: Our findings suggest that the potential benefit of light-to-moderate alcohol consumption and the detriment of heavy alcohol consumption on biological aging may depend on ALDH2 polymorphism.