Existing molecular biology indicates a path to biological immortality

This preprint argues that complementary single strand lesions (CSSLs) are the primary irreversible form of nuclear DNA damage driving aging. A simple Bayesian model using average literature values for daily new damage (~70,000 lesions/cell) and steady damage (~38,000 lesions/cell) quantitatively reproduces the observed human lifespan (~76 years) and the ~3,000 somatic mutations/cell limit observed in mammals. The model also predicts extremely long lifespans for elevated DNA repair or chromatid redundancy. It then introduces the Artificial Biological Immortality System (ABIS): a novel synthetic system that maintains permanently “sisterized” chromatid redundancy throughout the entire cell cycle via alternating orthogonal sets of MEIKIN, cohesin and separase, enabling continuous high fidelity DNA repair by sister chromatid exchange. ABIS is assembled entirely from existing biological components and is designed to be testable in mammalian cells. A compatible, simpler “little ABIS” path based on enhanced SSB repair and high affinity nuclear antioxidants is also outlined. Because DNA damage is not the sole driver of functional decay over time, complementary solutions are proposed for polymerase fidelity, nucleotide repeat instability, mitotic segregation errors, cancer, senescence, bioaccumulation, tissue overgrowth and regeneration.