Significance Aging is an evolutionary paradox. Traditionally, it is assumed as a maladaptive and nonprogrammed process of physical deterioration. Hypotheses of programmed aging are currently regarded as unfeasible since the evolutionary benefits of senescence are unclear. Here, we develop a model indicating that limiting lifespan is beneficial to control epidemics, providing a possible explanation for species lifespan setpoint selection and the absence of biologically immortal mutants. Our study suggests a unifying hypothesis in which lifespan is selected to prevent and limit outbreaks of chronic infectious diseases. Species-specific limits to lifespan (lifespan setpoint) determine the life expectancy of any given organism. Whether limiting lifespan provides an evolutionary benefit or is the result of an inevitable decline in fitness remains controversial. The identification of mutations extending lifespan suggests that aging is under genetic control, but the evolutionary driving forces limiting lifespan have not been defined. By examining the impact of lifespan on pathogen spread in a population, we propose that epidemics drive lifespan setpoints’ evolution. Shorter lifespan limits infection spread and accelerates pathogen clearance when compared to populations with longer-lived individuals. Limiting longevity is particularly beneficial in the context of zoonotic transmissions, where pathogens must undergo adaptation to a new host. Strikingly, in populations exposed to pathogens, shorter-living variants outcompete individuals with longer lifespans. We submit that infection outbreaks can contribute to control the evolution of species’ lifespan setpoints.
【저자키워드】 Evolution, aging, Epidemics, lifespan,