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Is extending lifespan the next stage of evolution?


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Is extending lifespan the next stage of evolution?

by Valentina Lencautan Published on 25th Jun 2015

by Valentina Lencautan Published on 25th June 2015

A new study: “Programmed death is favoured by natural selection in spatial systems” asks the question why do lifespans of different organisms vary so much? The aim being to determine whether humans can and perhaps even should be reprogrammed to live longer.

Initiated by head of NECSI Yaneer-Bar-Yam and Donald Ingber, director of Harvard Wyss Institute, the study applied a spatial evolutionary algorithm to show that short lifespans can be of greater advantage to the lineage of the species, in direct contradiction to the old theory that a species' short lifespan is beneficial. The aim of the study is to prove that life expectancy is determined by the evolutionary processes we are all subjected to.

According to standard evolutionary theory, “intrinsic mortality” is the result of either mutation accumulation or genes that predispose species to reproductive success in the initial stages of life, which comes with late detrimental effects. These factors account for species' senescence, also known as ageing and ultimate death. But findings show that there are registered cases of genetic modification which lead to changes in lifespan expectations, unusual longevity and senescence patterns and phenomena of programmed death, making traditional aging theories and medicine appear inexact.

To demonstrate the mechanism for adaptive limitations of lifespan, researchers also aim to turnover the old interpretations of the ageing process. They argue that if evolution truly is responsible for our lifespan, we have the power to execute modifications in the mechanisms employed in regulating our lifespan. Evidence that ageing is genetic and that previous theories may be false is shown by including local context into the theory. Local context creates a bond between organism and environment, with the environment being directly affected by the organism.

What is interesting is that these new assumptions are not a novelty in the field of research: “The idea that shorter lifespans can be and are selected for directly goes back to at least 1870. It was later rejected based on theoretical arguments that evolution of such a trait opposed to individual self-interest, like other altruistic behaviors, must require group selection, whose applicability should be accepted only as a last resort.”

Regarding humans, the model shows that we can significantly extend our lifespan as ageing is not inherent, but rather genetic. In fact, researchers feel that we should not only consider the idea, but expect scientific discoveries to lead to an increase in average life expectancy. As stated in the conclusion of the study, “If aging is programmed, rather than a collection of secondary break-downs or genetic tradeoffs, then effective health and life extensions through dietary, pharmacological, or genetic interventions are likely to be possible, with potential for significant impact.” 

Although still a relatively formative concept, and one which largely stems from long-held assumptions, if the results of the ongoing tests prove to be accurate, it could lead to a new understanding of aging - legitimising the notion that we are not programmed to lead short lives. In turn, this may translate to greater advocacy for life extension, and accelerate the rate of research and development of treatments designed to prolong lifespan.