Author: Glei DA1, Goldman N2, Weinstein M3, Risques RA4.
Affiliation:
1Center for Population and Health, Georgetown University, Washington, District of Columbia. dag77@georgetown.edu. 2Office of Population Research, Princeton University, Princeton, New Jersey. 3Center for Population and Health, Georgetown University, Washington, District of Columbia. 4Department of Pathology, University of Washington, Seattle, Washington.
Conference/Journal: J Gerontol A Biol Sci Med Sci.
Date published: 2014 Oct 17
Other:
Pages: glu191 , Word Count: 234
Recent studies have found mixed results regarding the association between leukocyte telomere length (LTL)-thought to be a marker of cellular aging-and all-cause mortality. Some studies have reported a significant inverse relationship, but others have not, perhaps in part owing to insufficient power. We examine the relationship using data from a nationally representative sample of older Taiwanese (54+ in 2000), which is larger (n = 942) than most previous studies, and which includes comprehensive information on potential confounders including white blood cell distribution and inflammatory markers. Results from a Cox hazards model demonstrate a small, but significant, association between LTL and mortality that is independent of age, sex, and lifestyle factors. White blood cell distribution, especially the proportion of neutrophils, is an important predictor of LTL; however, the association between LTL and mortality changes little controlling for white blood cell distribution. In contrast, the association between LTL and mortality weakens considerably (by 48%) after adjustment for inflammatory markers and homocysteine. Our results suggest that the relationship between short telomeres and mortality is tied to inflammation and homocysteine. Longitudinal studies are needed to explore bidirectional influences resulting from the fact that inflammation leads to shorter leukocyte telomeres, which in turn results in senescence, which exacerbates inflammation.
© The Author 2014. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.
KEYWORDS:
Biological aging; Inflammation.; Mortality; Taiwan; Telomeres
PMID: 25326284