# Telomere Shortening Theory of Aging

Telomere dysfunction causes defined cellular and tissue disease; telomere attrition as a primary cause of ordinary human aging remains unestablished.

Registered primary-subclaim aggregation returns Γ from SC3, despite Ε for SC1 and SC2. Severe telomere dysfunction is a causal pathology in defined contexts. The positive model and syndrome results cannot establish that gradual attrition is a primary rate-limiting cause of ordinary human aging. Human genetic disease trade-offs and bounded negative functional/lifespan findings constrain scope; they do not show all telomere biology is causally irrelevant.

Contexts were mapped positively: critical deficiency, initial reserve, stem-cell dependence and checkpoint status predict tissue effects. Species, rare disease and mean-LTL population studies differ. This mapped restricted causality warrants Ε for narrow subclaims; it does not make broad SC3 causal.