A Phenoptosis Perspective on the Evolution of Exceptional Human Longevity
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.
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.
Perspectives of Homo sapiens lifespan extension: focus on external or internal resources?
The nature of the selection factors underlying the evolution of aging remains controversial. Many specialists in evolutionary gerontology support a set of ideas called the "evolutionary theory of aging". This theory is based on the idea that the selection efficiency decreases with age. It is also assumed that vitality and fertility are high in youth at the cost of reduced fitness at later ages. An alternative view is that programmed aging and death may be favored by some kind of selection.
A theoretical experiment called the "Fable about Fox and Hares" has been suggested. Two young hares differing "intellectually" have equal chances to escape from a fox since both hares are running faster than a fox. However, with age, the clever hare acquires some advantage, which becomes of crucial importance when the running speed of hares lowers to that of a fox. Now, the clever hare has a better chance to escape and, hence, to produce clever leverets than the stupid hare. Such an effect becomes possible due to age-dependent lowering of the running speed as a result of the operation of an aging program. This will facilitate the selection for cleverness.
The evolutionary changes in humans compared to other primates have the following distinguishing characteristics: large brain, exceptionally large life span, high paternal investment in offspring, and the role of older individuals as helpers in upbringing the children. The large brain is associated with a change in psychological characteristics: enhanced learning and cognition. Even human sleep is shorter, deeper, and has more rapid eye movement phases than that in other primates. Supposedly, the selection pressure in the direction of the reduction in sleep duration and its "quality" improvement were activated in the early stages of human evolution due to the change in the ecological niche and the development of overnight stays on the ground and not in the tree branches.
The evolution of these life history characteristics and extremely high intelligence was probably related to some degree to the dietary transition to high-quality, solid and hard-to-get food resources. In humans, technical progress leads to a sharp decrease in infant mortality and an increase in life expectancy, especially in comparison to wild chimpanzees. Despite the huge variation in the life span of various human populations, starting with preagricultural tribes and ending with the urban population in the developed countries, the differences between their survival curves are still smaller than those between the preagricultural human populations and the chimpanzees living in the wild. This relationship can be explained by the fact that neoteny prolongs life span and health span.
The change in survival curves of humans compared to chimpanzees occurs for two reasons: neoteny and very rapid technical progress. An analysis of time scales and survival curves allows us to separate these two causes. Thus, the evolution of neoteny requiring much more time may be responsible for the difference in the mortality curves of chimpanzees and hunter-gatherers, while technical progress is responsible for the great differences in the mortality curves of hunter-gatherers and Swedish individuals in the 20th century.
As someone with no biological background but a significant physical sciences background, I find a dichotomy (us vs them) discussion quite frustrating, as nothing is ever 'that simple'.
That being said, having a series of component (approach) solutions that serve to provide incremental fixes and perhaps contribute to reduced pathology always seems more compelling, even though it has been seemingly lumped under one side, but not the other.
Then: If ageing is an accidental accumulation of damage, is it unreasonable to say:
"An undamaged human is necessarily immortal." ?
Does damage then include the vastly different categories of (remember, no biological background) wear, injury, and 'used up' scenarios for each component and system.
Is an undamaged human identical in the first 10% of life, first 50% of life, and last 25% of life - assuming damage quantity is the only significant variable. Basic skeptics.
Some of the most convincing arguments for the survival of human women beyond menopause actually comes from sexual competition. In ancient societies, older men had a reproductive benefit when compared to younger men because they had more wealth. This selected for extremely long-lived men. However, women had no selective advantage for living longer and could even have a disadvantage because resources that could have gone into maturing faster or decreasing gestation times went into somatic maintenance instead. Since longevity is polygenic, it's not like one gene could be placed on the Y chromosome that increased longevity of solely men, so women got pulled along for the ride because the average selective advantage for male and female children was in favor of longer lives.
Bonduriansky, R., Maklakov, A., Zajitschek, F., & Brooks, R. (2008). Sexual selection, sexual conflict and the evolution of ageing and life span. Functional Ecology, 22(3), 443-453. https://doi.org/10.1111/j.1365-2435.2008.01417.x
Also, when programmed aging comes up, I like sharing this article from Kirkwood. He does some great simulations that I think plainly spell out how such selection cannot work.
Kowald, A., & Kirkwood, T. B. L. (2016). Can aging be programmed? A critical literature review. In Aging Cell (Vol. 15, Issue 6, pp. 986-998). Blackwell Publishing Ltd. https://doi.org/10.1111/acel.12510