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      Leukocyte Telomere Length and All-Cause, Cardiovascular Disease, and Cancer Mortality: Results From Individual-Participant-Data Meta-Analysis of 2 Large Prospective Cohort Studies

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          Abstract

          We studied the associations of leukocyte telomere length (LTL) with all-cause, cardiovascular disease, and cancer mortality in 12,199 adults participating in 2 population-based prospective cohort studies from Europe (ESTHER) and the United States (Nurses' Health Study). Blood samples were collected in 1989-1990 (Nurses' Health Study) and 2000-2002 (ESTHER). LTL was measured by quantitative polymerase chain reaction. We calculated z scores for LTL to standardize LTL measurements across the cohorts. Cox proportional hazards regression models were used to calculate relative mortality according to continuous levels and quintiles of LTL z scores. The hazard ratios obtained from each cohort were subsequently pooled by meta-analysis. Overall, 2,882 deaths were recorded during follow-up (Nurses' Health Study, 1989-2010; ESTHER, 2000-2015). LTL was inversely associated with age in both cohorts. After adjustment for age, a significant inverse trend of LTL with all-cause mortality was observed in both cohorts. In random-effects meta-analysis, age-adjusted hazard ratios for the shortest LTL quintile compared with the longest were 1.23 (95% confidence interval (CI): 1.04, 1.46) for all-cause mortality, 1.29 (95% CI: 0.83, 2.00) for cardiovascular mortality, and 1.10 (95% CI: 0.88, 1.37) for cancer mortality. In this study population with an age range of 43-75 years, we corroborated previous evidence suggesting that LTL predicts all-cause mortality beyond its association with age.

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          Most cited references 25

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          Meta-analysis formulating evaluating combining and reporting

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            White cell telomere length and risk of premature myocardial infarction.

            Biological age may be distinct from chronological age and contribute to the pathogenesis of age-related diseases. Mean telomeres lengths provide an assessment of biological age with shorter telomeres, indicating increased biological age. We investigated whether subjects with premature myocardial infarction (MI) had shorter leukocyte telomeres. Mean terminal restriction fragment (TRF) length, a measure of average telomere size, was compared in leukocyte DNA of 203 cases with a premature MI (<50 years) and 180 controls. Age- and sex-adjusted mean TRF length of cases was significantly shorter than that of controls (difference 299.7+/-69.3 base pairs, P<0.0001) and on average equivalent to controls 11.3 years older. The difference in mean TRF length between cases and controls was not accounted for by other coronary risk factors. Compared with subjects in the highest quartile for telomere length, the risk of myocardial infarction was increased between 2.8- and 3.2-fold (P<0.0001) in subjects with shorter than average telomeres. The findings support the concept that biological age may play a role in the etiology of coronary heart disease and have potentially important implications for our understanding of its genetic etiology, pathogenesis, and variable age of onset.
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              Is telomere length a biomarker of aging? A review.

               K Mather,  A Jorm,  R. PARSLOW (2011)
              Telomeres, the DNA-protein structures located at the ends of chromosomes, have been proposed to act as a biomarker of aging. In this review, the human evidence that telomere length is a biomarker of aging is evaluated. Although telomere length is implicated in cellular aging, the evidence suggesting telomere length is a biomarker of aging in humans is equivocal. More studies examining the relationships between telomere length and mortality and with measures that decline with "normal" aging in community samples are required. These studies would benefit from longitudinal measures of both telomere length and aging-related parameters.
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                Author and article information

                Journal
                American Journal of Epidemiology
                Oxford University Press (OUP)
                0002-9262
                1476-6256
                June 15 2017
                June 15 2017
                April 28 2017
                June 15 2017
                June 15 2017
                April 28 2017
                : 185
                : 12
                : 1317-1326
                Affiliations
                [1 ]Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany
                [2 ]Network Aging Research, University of Heidelberg, Heidelberg, Germany
                [3 ]German Cancer Consortium, Heidelberg, Germany
                [4 ]Genomics and Proteomics Core Facility, German Cancer Research Center, Heidelberg, Germany
                [5 ]Department of Epidemiology and Public Health, Faculty of Population Health Sciences, University College London, London, United Kingdom
                [6 ]Channing Laboratory, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
                [7 ]Program in Genetic Epidemiology and Statistical Genetics, Harvard School of Public Health, Boston, Massachusetts
                [8 ]Hellenic Health Foundation, Athens, Greece
                [9 ]Department of Hygiene, Epidemiology and Medical Statistics, Medical School, University of Athens, Athens, Greece
                [10 ]Institute for Translational Epidemiology and Tisch Cancer Institute, Icahn School of Medicine at Mount Sinai, New York, New York
                Article
                10.1093/aje/kww210
                5860628
                28459963
                © 2017

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