Somatic mutations impose an entropic upper bound on human lifespan

Evgeniy Efimov, Vlad Fedotov, Leonid Malaev, Ekaterina E. Khrameeva, Dmitrii Kriukov

1. 01

   Incremental survival-dynamics modeling framework layering aging contributors one at a time

2. 02

   In post-mitotic cells (neurons, cardiomyocytes) somatic mutation alone reduces median lifespan from a theoretical non-aging baseline of 1,759 years to 156 years

3. 03

   Proliferating tissues such as liver maintain function for thousands of years through cellular replacement, effectively neutralising mutation-driven decline

4. 04

   Multi-organ integration predicts median lifespan of 146-194 years — roughly twice current human longevity

5. 05

   The reduction is substantial but incomplete, implying other hallmarks contribute comparably to observed mortality

6. 06

   Bounds radical life-extension and longevity escape velocity claims while also indicating mutation-focused programmes alone are insufficient

Study Design

Review

Sample Size

Not reported

Study Duration

Not applicable (in silico)

Methodology

Computational incremental modeling framework integrating organ-specific somatic mutation accumulation into population survival dynamics; sequential inclusion of aging factors to isolate the contribution of somatic mutation.

Limitations

A model, not an observation. Outputs are only as reliable as its organ-failure and mutation-accumulation assumptions, and it cannot account for hallmarks or failure modes not represented in the framework. It should be used to calibrate expectations, not to make any claim about an individual patient's achievable lifespan.