Is Aging an Inevitable Characteristic of Organic Life or an Evolutionary Adaptation?

Abstract

Aging is an evolutionary paradox. Several hypotheses have been proposed to explain it, but none fully explains all the biochemical and ecologic data accumulated over decades of research. We suggest that senescence is a primitive immune strategy which acts to protect an individual’s kin from chronic infections. Older organisms are exposed to pathogens for a longer period of time and have a higher likelihood of acquiring infectious diseases. Accordingly, the parasitic load in aged individuals is higher than in younger ones. Given that the probability of pathogen transmission is higher within the kin, the inclusive fitness cost of infection might exceed the benefit of living longer. In this case, programmed lifespan termination might be an evolutionarily stable strategy. Here, we discuss the classical evolutionary hypotheses of aging and compare them with the pathogen control hypothesis, discuss the consistency of these hypotheses with existing empirical data, and present a revised conceptual framework to understand the evolution of aging. Electronic supplementary material The online version contains supplementary material available at 10.1134/S0006297922120021.

Aging clocks based on accumulating stochastic variation

“…Mutations that abruptly limit post-reproductive life are observed in semelparous species, whereas iteroparous species typically show a gradual functional decline because of insufficient maintenance and repair mechanisms, leading to stochastic damage accumulation with aging 7 . Progress on aging clocks has revived the idea of a potential aging program 8 , questioning whether aging is primarily a stochastic entropy-driven event, whether aging clocks could show a causal relationship 9 , 10 and whether it involves programmatic aspects 11 – 16 . Intrinsic flaws in a software code of life 17 , an adaptive pathogen control program 11 , 18 or developmental processes 13 , 15 were suggested to cause aging.…”

“…Progress on aging clocks has revived the idea of a potential aging program 8 , questioning whether aging is primarily a stochastic entropy-driven event, whether aging clocks could show a causal relationship 9 , 10 and whether it involves programmatic aspects 11 – 16 . Intrinsic flaws in a software code of life 17 , an adaptive pathogen control program 11 , 18 or developmental processes 13 , 15 were suggested to cause aging. Age-dependent selective mortality may depend not only on remaining fertility, but also on intergenerational resource transfer, explaining a quantity–quality tradeoff, and potentially allowing a programmed process to affect aging 19 .…”

El transhumanismo y la mejora de la calidad de vida de las personas mayores: ¿Cómo podría configurar el futuro del dolor y el sufrimiento en las personas mayores?

“…Sin embargo, basta decir que el envejecimiento es una parte inexorable de la vida humana y que, en última instancia, conduce a la muerte, con el colapso de todas las funciones fisiológicas y biológicas que mantienen la vida de la persona humana junto con su dignidad (8).…”

Accurate aging clocks based on accumulating stochastic variation

“…Recent progress on aging clocks, however, has revived the idea of a potential program involved in aging 8,9 . Currently, it is controversially discussed whether aging is purely a stochastic entropy-driven event in line with the evolutionary theory of aging, whether the existence of aging clocks could show a causal relationship to aging 10,11 , and whether other programmatic aspects of aging could exist [12][13][14][15][16] . Rather than a consequence of inevitable molecular damage, intrinsic flaws in a software code of life 17 , an adaptive pathogen control program 12,18 , or developmental processes 14,16 were suggested to cause aging.…”