Theory and modeling dominates the study of the evolution of aging, as is the case in any field in which one is presented with a snapshot of a very complex environment and no ability to conduct directly relevant experiments on that environment. Beyond the state of the natural world here on earth, astrophysics is another good example: a zoo of diverse phenomenon out there in the universe and a great deal of highly mathematical back and forth here on Earth over exactly why the night sky looks the way it does.
Given the nature of the field, any discussion of the fine details of the evolution of aging should be taken as speculative. Evolution as a whole is well supported by the evidence, and a demonstrably useful concept that has informed and accelerated progress in the life sciences. But many of the specific hypotheses and mathematical models that foam and compete under the surface of the bigger picture are likely incorrect in some or all of their details.
The commentary on the evolution of aging in today's open access paper might be taken as the polar opposite of programmed aging hypotheses. Here, aging is envisaged as an inevitable byproduct of the way that natural selection operates, stronger in its effects on early life. Early reproduction is an effective strategy across near all niches, since the occupants of near all niches are affected by predation, disease, and other forms of mortality. Thus mechanisms and systems that aid in early life success at the cost of late life health are selected, despite reducing the hypothetical overall number of offspring that could be produced over a lifetime absent predation, disease, and other extrinsic causes of mortality. Evolution as a process produces imperfect machines, good enough at the outset, but which fall apart thereafter.
Evolutionary theory allows for various types of byproduct effects that can affect late life, both negatively and positively. If pleiotropy is viewed mechanistically, molecule-based and network-based pleiotropy make late life effects likely. Research on model systems has already shown that there are a large number of mechanisms by which single mutations can affect late life, supporting the possibility that populations accumulate diverse positive and negative late life effects. It is likely that late life is subject to little selection due to rapidly decreasing population size and lack of late life reproduction in most species, making it unlikely that aging is under simple regulatory control. Instead, it could potentially be an emergent property of the many byproduct effects that affect late life (both selection-based and neutrality-based) and the accumulation of mutations primarily affecting late life. Each species will have its own constellation of byproduct effects and late acting mutations.
This will translate into a large and complex mixture of genetic variation that will distribute across the individuals in populations. Some of the mutations affecting aging may be shared between species, due to conservation of molecules or networks, while others will be species specific. Characteristic lifespans for different species would be another emergent property. Superimposed upon this pattern of aging would be physiological responses to environmental insults common to aging animals, such as stress and infection. Such responses could contribute to the aging pattern. These responses would also consist of both conserved and species-specific components. While it is unclear how age-related tissue dysfunction connects to organism mortality, tissue specific changes with age would be expected to contribute to the species-specific pattern.
One of the most prominent theories accounting for aging and age-dependent mortality rates postulates cumulative damage leading to stochastic failure of tissues and the organism. Specific mechanisms included in this theory are oxidative damage or somatic mutation. The disposability model states that repair capacities are limited by evolutionary constraints, leading to this cumulative damage. At the present time these theories cannot account for the full range of aging patterns in all species. Perhaps aging can be viewed as the net result of hundreds of byproduct effects combined with the accumulation of late-acting mutations, encompassing both positive and negative effects upon mortality and vigor.
Aging is correlated with a large number of species, tissue, and cell type specific changes at the molecular level. It is possible that aging is an emergent property of hundreds of effects, some conserved, some fixed at the species level, and some that are variable at the population level. According to this view, it would only be a modest exaggeration to say aging is all trees and no forest.