The conclusion to today's open access paper opens with the following declaration: “There is still no agreement among gerontologists as to the main aging-related issue: whether it is an accidental accumulation of damage in the organism or a result of the operation of a specially evolved program.”
This is true in the sense that a minority of scientists (one in ten, perhaps – it is hard to count heads on this topic) consider aging to be programmed, a phenomenon that is under evolutionary selection, rather than an unselected side-effect of other selected traits.
A new study by UConn researchers and others increases the number of genetic variants linked to lifespan to 25. These markers offer potentially modifiable targets to reduce the risk of an early death and improve health. Image credit: sylviebliss via Good Free Photos, Public Domain
The consensus views on the evolution of aging is that it is an outcome of antagonistic pleiotropy. Selection operates most strongly on factors leading to early life reproductive success, regardless of later consequences. Evolution thus produces outcomes such as (a) an adaptive immune system that cannot operate indefinitely because it must store information about every pathogen encountered, or (b) mammalian biochemistries that cannot effectively break down certain rare metabolic byproducts, and so this metabolic waste accumulates over a lifetime to cause late-life pathologies. In other words, systems and organs that function well at the outset, but accumulate damage and dysfunction and fall apart over time.
Programmed aging theories, on the other hand, are somewhat more varied. There are some, like the hyperfunction theory, focused on processes of development that do not stop and run wild with age, are hard to distinguish from antagonistic pleiotropy. Others, such as the concept that aging is a group selection outcome that exists because other options lead to ecosystem collapse due to excessive reproduction, are quite alien in comparison to the consensus. But the core idea is that aging is a selected process, not just an unfortunate side-effect of selection and the fact that early reproduction is always favored.
The authors of this paper are on the programmed aging side of the house, seeing aging as experienced by humans as simply a slower form of phenoptosis, the abrupt decline and death following mating that is observed in species such as salmon. They are also interested in oxidative stress in aging, being one of the groups that worked on mitochondrially targeted antioxidants capable of improving mitochondrial function and modestly slowing aging in short-lived laboratory species.
Armed with that understanding, it is worth reading the paper for their take on on exceptional human longevity and why it evolved. Humans have much longer lives than other primates, and in some ways this appears to be an extension of childhood features into later life, a process called neoteny – though by no means clearly so. This increased life span may have been driven by our intelligence, and then our technology (in the broadest sense), as described by the Grandmother hypothesis. It is a selection effect that promotes longer survival of grandparents once they can assist in increasing the fitness of their descendants. But that isn't the only possible explanation.
Link: Perspectives of Homo sapiens lifespan extension: focus on external or internal resources?
Source: Fight Aging!