Association between telomere length in blood and mortality in people aged 60 years or older
Abstract
During normal ageing, the gradual loss of telomeric DNA in dividing somatic cells can contribute to replicative senescence, apoptosis, or neoplastic transformation. In the genetic disorder dyskeratosis congenita, telomere shortening is accelerated, and patients have premature onset of many age-related diseases and early death. We aimed to assess an association between telomere length and mortality in 143 normal unrelated individuals over the age of 60 years. Those with shorter telomeres in blood DNA had poorer survival, attributable in part to a 3.18-fold higher mortality rate from heart disease (95% CI 1(.)36-7.45, p=0.0079), and an 8.54-fold higher mortality rate from infectious disease (1.52-47.9, p=0.015). These results lend support to the hypothesis that telomere shortening in human beings contributes to mortality in many age-related diseases.
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Telomere length has been shown to predict the replicative capacity of human cells and the appearance of certain age-associated pathologies in humans.
“telomere length has been shown to predict the replicative capacity of human cells and the appearance of certain age-associated pathologies in humans 54, 55”
From The common biology of cancer and ageing (2007) · cites this paper as [55]
In several studies, baseline LTL predicted the subsequent development of cancers, cardiovascular disease, diabetes or mortality.
“In several studies, not only did baseline LTL correlate with medical illnesses cross-sectionally but predicted the subsequent development of cancers, CVD, diabetes or mortality (Cawthon et al., 2003; Willeit et al 2010; Zhao et al., 2014).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Cawthon et al., 2003
Shorter LTL is linked with premature mortality and a reduction in years of healthy living.
“There are some studies linking shorter LTL with premature mortality (Cawthon et al., 2003; Fitzpatrick et al., 2011; Weischer et al., 2012) and a reduction in years of healthy living (Njajou et al., 2009).”
From Psychiatric disorders and leukocyte telomere length: Underlying mechanisms linking mental illness with cellular aging (2015) · cites this paper as Cawthon et al., 2003
Short telomeres have been linked to numerous diseases of aging and, in many but not all cases, to all-cause and disease-specific mortality.
“Short telomeres have been linked to numerous diseases of aging and in many but not all cases, to all-cause and disease-specific mortality (12–17).”
From Determinants of telomere attrition over 1 year in healthy older women: stress and health behaviors matter (2015) · cites this paper as [17]
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Does oxidative stress shorten telomeres in vivo ? A review
Reichert, S., & Stier, A. (2017) · Biology Letters · doi:10.1098/rsbl.2017.0463 · Cited by 324 · see citing works
T Cell Replicative Senescence in Human Aging
P. Chou, J., & B. Effros, R. (2013) · Current Pharmaceutical Design · doi:10.2174/138161213805219711 · Cited by 323 · see citing works
Shortened Telomeres in Circulating Leukocytes of Patients with Chronic Obstructive Pulmonary Disease
Savale, L., Chaouat, A., Bastuji‐Garin, S., Marcos, É., Boyer, L., Maître, B., Sarni, M., HOUSSET, B., Weitzenblum, E., Matrat, M., et al. (2009) · American Journal of Respiratory and Critical Care Medicine · doi:10.1164/rccm.200809-1398oc · Cited by 322 · see citing works
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Molecular and biological hallmarks of ageing
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Telomere Length and All-Cause Mortality: A Meta-analysis
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Self-citationShort Telomeres Are Associated With Increased Carotid Atherosclerosis in Hypertensive Subjects
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Short Telomeres, even in the Presence of Telomerase, Limit Tissue Renewal Capacity
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- Authors
- Cawthon, R. M., Smith, K. R., O'Brien, E., Sivatchenko, A., & Kerber, R. A.
- Affiliations
- University of Utah (US)
- Corresponding author
- Cawthon, Richard M
- Venue
- The Lancet
- Publisher
- Elsevier BV
- Published
- 2003-02
- Volume
- 361
- Issue
- 9355
- Pages
- 393-395
- ISSN
- 0099-5355 (ISSN-L)
- 0140-6736
- OpenAlex
- W2145859123
- Cited by
- 1,761
- References
- 5
- Citations by year
- 2026: 14 · 2025: 32 · 2024: 52 · 2023: 57 · 2022: 64 · 2021: 68 · 2020: 90 · 2019: 75 · 2018: 101 · 2017: 102 · 2016: 100 · 2015: 91 · 2014: 122 · 2013: 79 · 2012: 87
- FWCI
- 36.88
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- The Lancet (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ag013478-04, 5k01ag000767-05)
- National Institute on Aging (AG13478, K01 AG00767)
- National Cancer Institute (R29CA069421, R29 CA69421)
- NIH Clinical Center
- Topics
- Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- telomere length, mortality, aging, replicative senescence, dyskeratosis congenita, heart disease mortality, infectious disease mortality, age-related diseases, blood DNA, older adults
- MeSH terms
- Aged, Aged, 80 and over, Aging, Blood Donors, Cause of Death, Communicable Diseases, Female, Heart Diseases, Humans, Male, Middle Aged, Mortality, Population Surveillance, Utah, Proportional Hazards Models, Survival Analysis, Telomere, Apoptosis, Age Distribution, Dyskeratosis Congenita
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