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Research Paper|Volume 8, Issue 7|pp 1398—1415

Longitudinal decline of leukocyte telomere length in old age and the association with sex and genetic risk

Kari Berglund1, Chandra A. Reynolds2, Alexander Ploner1, Lotte Gerritsen1,3, Iiris Hovatta4,5, Nancy L. Pedersen1, Sara Hägg1
  • 1Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, 171 77 Stockholm, Sweden
  • 2Department of Psychology, University of California-Riverside, Riverside, CA 92521, USA
  • 3Department of Clinical Psychology, Faculty of Social Sciences, Utrecht University, Utrecht, the Netherlands
  • 4Department of Biosciences, Viikki Biocenter, University of Helsinki, Helsinki, Finland
  • 5Department of Health, National Institute for Health and Welfare, Helsinki, Finland
Received: April 19, 2016Accepted: June 20, 2016Published: July 7, 2016
https://doi.org/10.18632/aging.100995

Copyright: © 2016 Berglund et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Telomeres are DNA-protein structures at the ends of chromosomes. Leukocyte telomere length (LTL) shortening has been associated with advanced age. However, most studies use cross-sectional data, hence, the aim of our study was to model longitudinal trajectories of LTL attrition across 20 years at old age. Assessments of LTL were done by qPCR in SATSA (Swedish Adoption/Twin Study of Aging; N=636 individuals). Cross-sectional and longitudinal associations with age were estimated, the latter using latent growth curve analysis. A genetic risk score (GRS) for LTL was further assessed and included in the models. We confirmed an inverse cross-sectional association of LTL with age (B=−0.0022 T/S-ratio; 95% CI: −0.0035, −0.0009, p-value=0.0008). Longitudinal LTL analyses adjusted for sex (1598 samples; ≤5 measurements) suggested modest average decline until 69 years of age but accelerating decline after 69 years, with significant inter-individual variation. Women had on average ∼6% T/S-ratio units longer LTL at baseline, and inclusion of the GRS improved the model where four risk alleles was equivalent to the effect size difference between the sexes. In this cohort of old individuals, baseline LTL varied with age, sex and genetic background. The rate of change of LTL accelerated with age and varied considerably between individuals.