Leukocyte Telomere Dynamics: Longitudinal Findings Among Young Adults in the Bogalusa Heart Study

Abstract

Leukocyte telomere length (LTL) is ostensibly a biomarker of human aging. Cross-sectional analyses have found that LTL is relatively short in a host of aging-related diseases. These studies have also provided indirect estimates of age-dependent LTL shortening. In this paper, the authors report findings of the first comprehensive longitudinal study of 450 whites and 185 African Americans in Louisiana (aged 31.4 and 37.4 years at baseline (1995–1996) and follow-up (2001–2006) examinations, respectively) participating in the Bogalusa Heart Study. Rate of change in LTL was highly variable among individuals, with some displaying a paradoxical gain in LTL during the follow-up period. The most striking observation was that age-dependent LTL shortening was proportional to LTL at baseline examination. At both baseline and follow-up examinations, African Americans had longer LTLs than whites, and smokers had shorter LTLs than nonsmokers. The longer LTL in African Americans than in whites explained in part the faster rate of LTL shortening observed among African Americans. These findings underscore the complexity of leukocyte telomere dynamics in vivo and suggest that determinants in addition to the “end-replication problem” contribute to telomere shortening in vivo.

Short telomere length is associated with NOTCH1/SF3B1/TP53 aberrations and poor outcome in newly diagnosed chronic lymphocytic leukemia patients

“…In line with this reasoning, CLL cases with the longest telomeres at diagnosis showed the most pronounced yearly telomere loss. It is noteworthy that similar data showing base line dependent TL alterations by time have been shown in normal blood cells indicating similar mechanisms for telomere maintenance in leukemic and normal cells [16][17][18].…”

“…In line with this reasoning, CLL cases with the longest telomeres at diagnosis showed the most pronounced yearly telomere loss. It is noteworthy that similar data showing base line dependent TL alterations by time have been shown in normal blood cells indicating similar mechanisms for telomere maintenance in leukemic and normal cells [16][17][18].Finally, we assessed TL and clonal evolution defined by the acquisition of new copy number aberrations (CNAs) in 47 cases of which 11 were previously found to display clonal evolution [19]. These cases were mainly IGHV unmutated (64% vs. 31% for cases without clonal evolution) and had distinctly shorter TL at diagnosis (average 1,791 U vs. 2,770 U, P 5 0.052).…”

Telomere length and adiposity in a racially diverse sample

“…Some studies have shown that minorities have longer telomere length, although they suggest quicker shortening in minorities. 14,15 Another study demonstrated that blacks and Hispanics had shorter telomeres than whites. 16 One possible reason for these differences could be a differential impact of adiposity on telomere length by race, similar to the differential impact of adiposity on mortality that has been previously demonstrated between Whites and Blacks.…”

Telomeres and Lifestyle Choices

“…While cross-sectional studies are abundant, there have been very few longitudinal studies of telomere length [Aviv et al, 2009;Ehrlenbach et al, 2009;Epel et al, 2009;Nordfjall et al, 2009;Farzaneh-Far et al, 2010]. One consistent finding from the published longitudinal data is that the rate of telomere length change over time is inversely related to the baseline telomere length [Aviv et al, 2009;Farzaneh-Far et al, 2010].…”