The cellular automaton interpretation of aging and cancer

Scientific Essay from the year 2018 in the subject Biology – Diseases, Health, Nutrition, language: English, abstract: Cells of multicellular organisms communicate with each other through gap junctions composed of connexin proteins. The totality of gap junction communication among a group of cells is a Gap Junction Bioelectric Network (GJBN). Even though the rule governing a GJBN may be simple, its computations can be complex. The Principle of Computational Equivalence (PCE) holds that Wolfram cellular automaton #110 is sufficiently complex to model the computations of a complex GJBN. The Principle of Computational Irreducibility (PCI) maintains that a complex GJBN cannot be modeled accurately and comprehensively by ‘shortcut’ equations. Instead, the system must be ‘run’ to observe its outcome. It is proposed that aging and cancer are the result of chronic entropic dysregulation of the complex asymmetric GJBN modeled by cellular automaton #110 into a symmetric random network modeled by cellular automaton #30. Consequently, asymmetric morphogen gradients necessary for the geometric stability of the organism (morphostasis) are gradually lost, and the organism ‘grows’ old and develops cancer. The Hayflick limit, shortening of telomeres, and telomerase activity are not the proximate causes of aging and cancer. Successful cancer prevention/treatment, and anti-aging or rejuvenation strategies will require a systems approach that maintains or restores the complex GJBN modeled by Wolfram cellular automaton #110.