Arguing for Aging to Influence Natural Selection through Loss of Parental Contributions to Early Life Evolutionary Fitness
It seems that ever more people these days argue for aging to influence natural selection through effects on the group, or at least on offspring. The core argument made here, as I understand it, is that a sort of inverse Grandmother effect can allow a rapid pace of aging to reduce fitness in early life by reducing parental or grandparental contributions to survival. If the case, then this means that age-related diseases are not just side-effects of a relentless evolutionary focus on early life at the expense of later life, but are actively involved in selection in some way, perhaps as a buffer against more subtly harmful mutations. Like most of the more abstruse discussion of evolution, proof is hard to come by - most arguments at this level are a matter of model versus model and assumption versus assumption. The line between hypothesis and opinion is more blurred than it might be elsewhere in the life sciences.
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 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. 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 gives a benefit to the species through the selection against germ line genes that disrupt homeostasis.