Fight Aging!

Two more or less opposing ways to think about the evolution of aging are as follows (a) aging is actively selected for because it provides some benefit to species survival, such as increased adaptability to environmental change, or (b) aging occurs in a post-reproductive part of life that is not under selection pressure, and is thus a side-effect of mechanisms that are selected for because they provide benefits during the earlier period of reproductive life span, but which systematically fail over time. To a certain extent the former viewpoint is associated with the minority position that aging is a genetic program of deterioration while the latter viewpoint is associated with the majority position that aging is caused by an accumulation of cellular and molecular damage.

That sweeping generalization obscures a lot of important subtlety, however. The evolution of aging is a fairly dynamic field of theory, and probably won't settle down until the progression of aging from young to old in individuals is cataloged and understood to a far greater level of detail than is presently the case. That will probably post-date the first rejuvenation treatments, however, as that full understanding isn't necessary in order to construct treatments that repair age-related damage. Or at least it is not necessary provided that aging is caused by damage, as I think to be the case, rather than being a very complicated program of genetic changes that cause damage. If aging is a genetic program, then we are in for a very long and expensive road to any meaningful extension of healthy life.

I ran across an open access paper today that presents a novel view of the evolution of aging, one with a focus on our microbial fellow travelers. It is clear that gut bacteria have a modest degree of influence on aging, but is this large enough for microbial populations to be significant in the evolution of aging? This paper takes more of a programmed aging position in arguing that microbial species that help to wear down and kill the host in later life - that promote faster aging through mechanisms such as chronic inflammation, in other words - are selected for because of this outcome, and not just due to an ability to provide benefits in early life.

Does any of this theorizing matter in a practical sense? Yes in the long term: evolution has proven to be a powerful tool in many fields of medicine. Yes for researchers working on understanding the detailed progression of aging. No if we are focused on repair of the cellular and molecular damage that causes aging, as this repair approach enables us to sidestep a full understanding of how aging progresses. The research community has a robust list of the differences between old and young tissues, so we should be working now to fix them all regardless of how they come about or what exactly their role might be or why they evolved in the first place. Still, this is an interesting enough paper and point of view for me to point it out, and you can probably see why the title caught my eye:

Host Demise as a Beneficial Function of Indigenous Microbiota in Human Hosts

The age structure of human populations is exceptional among animal species. Unlike with most species, human juvenility is extremely extended, and death is not coincident with the end of the reproductive period. We examine the age structure of early humans with models that reveal an extraordinary balance of human fertility and mortality. We hypothesize that the age structure of early humans was maintained by mechanisms incorporating the programmed death of senescent individuals, including by means of interactions with their indigenous microorganisms.

First, before and during reproductive life, there was selection for microbes that preserve host function through regulation of energy homeostasis, promotion of fecundity, and defense against competing high-grade pathogens. Second, we hypothesize that after reproductive life, there was selection for organisms that contribute to host demise. While deleterious to the individual, the presence of such interplay may be salutary for the overall host population in terms of resource utilization, resistance to periodic diminutions in the food supply, and epidemics due to high-grade pathogens.

We provide deterministic mathematical models based on age-structured populations that illustrate the dynamics of such relationships and explore the relevant parameter values within which population viability is maintained. We argue that the age structure of early humans was robust in its balance of the juvenile, reproductive-age, and senescent classes. We hypothesize that the human microbiome evolved mechanisms specific to the mortality of senescent individuals among early humans because their mortality contributed to the stability of the general population. The hypothesis that we present provides new bases for modern medical problems, such as inflammation-induced neoplasia and degenerative diseases of the elderly. We postulate that these mechanisms evolved because they contributed to the stability of early human populations, but their legacy is now a burden on human longevity in the changed modern world.