Aging is an adaptation that selects in animals against disruption of homeostasis

During evolution, Muller's ratchet permanently generates deleterious germline mutations that eventually must be defused by selection. It seems widely held that cancer and aging-related diseases (ARDs) cannot contribute to this germline gene selection because they tail reproduction and thus occur too late, at the end of the life cycle. Here we posit however that by lessening the offspring's survival by proxy through diminishing parental care, they can still contribute to the selection. The hypothesis in detail: The widespread occurrence of aging in animals suggests that it is an adaptation. But to what benefit? Aging seems to have only drawbacks. In humans, ARDs cause today almost all mortality; they include heart disease, cerebrovascular disease, Alzheimer's disease, kidney disease and cancer. Compensation seems unthinkable. For cancer, the author proposed in a previous study a benefit to the species: purifying selection against deleterious germline genes that when expressed enhance intracellular energy dissipation. This multicausal energy dissipation, posited as the universal origin of cancer initiation, relates to cellular heat generation, disrupted metabolism, and inflammation. The organism reproduces during cancer's dormancy, and when approaching its end of life, the onset of cancer is accelerated in proportion to the cancer-initiating signal. Through cancer, the organism, now a parent, implements the self-actuated programmed death of Skulachev's phenoptosis. This "first death" enhances by proxy the offspring's chance of "second death" (or "double death") through diminished parental care. Repetition over generations realizes a purifying selection against genes causing energy dissipation. The removal of the deleterious germline gene mutations permanently generated by Muller's ratchet gives a benefit. We generalize, motivated by the parallels between cancer and aging, the purifying selection posited for cancer to aging. An ARD would be initiated in the organ by multicausal disruption of homeostasis, and be followed by dormancy and senescence until its onset near the end of the life cycle. Just as for cancer, the ARD eventually enhances double death, and the realized permanent selection gives a benefit to the species through the selection against germ line genes that disrupt homeostasis. Given their similarities, cancer and aging are combined in the posited Unified Cancer-Aging Adaptation (UCAA) model, which may be confirmed by next-generation sequencing data. Also because of the emerging important role of cellular senescence, the hypothesis may guide the development of therapies against both cancer and aging.