TL correlates with age.
The authors of this article studied the telomere structures that are part of one’s chromosomes. Individuals are born with telomeres of certain length, and in many cells, telomeres shorten as the cells divide and age. TL is therefore considered a marker of biological aging [7–10, 43, 44]. Advocates of human life extension promote the idea of lengthening the telomeres in certain cells through temporary activation of telomerase (by drugs) or possibly permanently by gene therapy. They reason that this would extend human life. It has been hypothesized that there is a tradeoff between cancerous tumor suppression and tissue repair capacity, in that lengthening telomeres might slow aging and in exchange increase vulnerability to cancer . That concept, coupled with recent findings in oncology and gerontology, provides the foundation for an integrative theory of vertebrate senescence that reconciles aspects of the “accumulated damage”, “metabolic rate”, and “oxidative stress” models. Changing TL is usually associated with changing speed of senescence. This telomere shortening, however, might be a consequence of, and not a reason for, aging.