A lack of consensus persists in aging research about how to define, measure, and explain aging, with mechanistic (molecular) and evolutionary models often remaining disconnected.

To bridge this gap, 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.

Core Insights of the Model

• Explaining Interventions: The framework accounts for why heterochronic parabiosis benefits older individuals while harming younger ones, and why regeneration produces global tissue rejuvenation in aging planarians.
• Classical Theories Re-framed: Traditional evolutionary theories like antagonistic pleiotropy and mutation accumulation are positioned as secondary mechanisms layered atop fundamental information-theoretic processes.
• A Testable Prediction: The unified perspective yields a specific 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.

Key Conceptual Sections

1. Types of Damage to Somatic Tissue

Somatic damage is categorized into external insults (which drive the evolution of targeted repair and regenerative pathways) and internal, continuous metabolic insults (combated by constitutive molecular quality-control networks). Aging, however, represents a third, distinct class: a system-wide, cumulative breakdown where repair mechanisms themselves gradually lose efficacy rather than simple wear-and-tear.

2. Loss of Information is Irrecoverable

While physical components continually turn over in tissues (such as the mammalian intestine or constituent cellular proteins), the progressive degradation of fundamental information stores—specifically genomic DNA and the epigenetic landscape—leads to the erosion of cellular identity and function. Epigenetic drift and loss of heterochromatin contribute significantly to transcriptional noise and cellular senescence.

3. Reversal and Epigenetic Maintenance

Because somatic cells lose precise regulatory coordinates over time, true rejuvenation requires the re-execution of developmental programs or their functional equivalents (as observed in somatic cloning or extreme regeneration models like planarians). Differentiated cells slow this epigenomic degradation through sustained resource investment and binary maintenance strategies.