Telomere length behaves as biomarker of somatic redundancy rather than biological age.

5 Repeated evidence

How much this weighs: several studies in people, combined — the strongest kind of evidence there is.

Type of study: meta-analysis or systematic review
Studied in: people
Participants: not stated in the abstract
Published: 2013 in Aging cell
Cited: 93 times by other research
Who paid: Not declared. PubMed carries no conflict-of-interest statement for most articles; that is not the same as independent.
Source: PubMed 23346961 · doi 10.1111/acel.12050

The plain-language write-up of this study is still being written. Below is the abstract exactly as the researchers published it.

Abstract by the researchers — original text

Biomarkers of aging are essential to predict mortality and aging-related diseases. Paradoxically, age itself imposes a limitation on the use of known biomarkers of aging because their associations with mortality generally diminish with age. How this pattern arises is, however, not understood. With meta-analysis we show that human leucocyte telomere length (TL) predicts mortality, and that this mortality association diminishes with age, as found for other biomarkers of aging. Subsequently, we demonstrate with simulation models that this observation cannot be reconciled with the popular hypothesis that TL is proportional to biological age. Using the reliability theory of aging, we instead propose that TL is a biomarker of somatic redundancy, the body's capacity to absorb damage, which fits the observed pattern well. We discuss to what extent diminishing redundancy with age may also explain the observed diminishing mortality modulation with age of other biomarkers of aging. Considering diminishing somatic redundancy as the causal agent of aging may critically advance our understanding of the aging process, and improve predictions of life expectancy and vulnerability to aging-related diseases.