Axiom 1: Because of the mechanics of copying DNA, telomeres always grow shorter with cell divisions.
Axiom 2: Stem cells and Cancer cells (possible mutant stem cells) are capable of self-immortalizing by lengthening their telomeres with telomerase.
Corollary 2.1: telomere length in stem cells is dynamic and lengthens or shortens as a function of telomerase activation, replicative burden, and environmental effects.
Axiom 3: Differentiated, or non-stem cells cannot be younger (telomere length) or healthier (genetic integrity) than their most recent stem cell progenitor.
Corollary 3.1: Since T-cells of the cellular immune system are all stem-like in nature, a senescence of T-cells results in worsening immune function reflected in higher rates of infection and cancer
Axiom 4: For non-stem cells, which don’t produce an active form of telomerase, the Hayflick Limit is the cause of apoptosis (“programmed” cell death) and teleologically serves to protect us from rogue cell lines that have acquired dangerous changes from DNA transcription errors, erroneous splicing, and oxidative or ionizing stresses.
HYPOTHESIS: Aging is caused by the shortening of telomeres in stem cells. If the stem cells’ telomeres can be protected by telomerase activation, then the effects of aging may be slowed and possibly reversed