Aging and the Evolvability of Biological Immortality in Multicellular Organisms

Simon Scholz 

A lack of consensus persists in aging research about how to define, measure, and explain aging, and mechanistic (molecular) and evolutionary models remain disconnected.
A mechanistic–evolutionary model is proposed that integrates concepts from Kirkwood's disposable-soma theory and Sinclair’s information theory of aging, providing a concrete framework for the causes of aging and routes to its reversibility.
The model explains why heterochronic parabiosis benefits older individuals but harms younger ones and why regeneration produces global tissue rejuvenation in aging planarians.
Classical evolutionary theories such as antagonistic pleiotropy and mutation accumulation are framed as secondary mechanisms layered atop the central processes described here.
This unified perspective on mechanisms, evolution, and reversibility of aging yields a specific, testable prediction: a single differentiated somatic cell (or small graft), serially transplanted once per generation into a clonal youthful host at the previous host's old age, will retain youthful epigenetic and functional states and show a greatly extended lifespan, provided intercellular signals remain coherent and its genome is intact.