Do we need to age? Extending the arc of life

by Matthew Hardcastle and Yaneer Bar-Yam


Despite efforts by alchemists and mystics to forestall the effects of aging and the inevitability of death, traditional science has firmly supported the necessity of mortality. When it comes to survival of the fittest, having an expiration date seems like a clear disadvantage, so aging must be an unavoidable necessity of biology. According to this line of thought, if lifespans could be any longer evolution would have already made them so. However, new research [1] conducted at the New England Complex Systems Institute (NECSI) now provides an evolutionarily-sound basis for pre-programmed death, and, in turn, hope for extending the arc of life.

Figure 1. Our results show that research focused on the mechanism of aging can extend youthfulness and lifespan many times, until the actual limit from intrinsic biological mortality is reached.


The mathematical basis of traditional evolutionary theory is rooted in several assumptions and simplifications. For example, the success of individuals in a population is only considered as an average: The circumstances of any member of a population are considered to be equivalent. NECSI expands these standard models by including a spatial component, where resource availability varies by region and the effects of resource exploitation extend over time. Eliminating the longstanding assumption reveals a net evolutionary benefit from mortality: Death at a given age leaves resources for descendants that inherit the local environment. NECSI’s simulations are remarkably robust, showing a direct evolutionary benefit for a limited lifespan in a variety of contexts.

From NECSI’s simulations, we can expect to see programmed death throughout nature. And indeed there is extensive evidence [2] for this result, from the widespread variability of lifespans across the animal kingdom, to the high degree of lifespan plasticity achieved in laboratory settings. For example, the lifespan of a nematode can be increased fivefold through two mutations. If lifespans as we experience them are not determined by an inherent biological limit, then they must be predetermined by a genetic mechanism. In humans and many other animals, that mechanism is explicitly apparent as senescence, or the process of aging. A understanding of the mechanism that causes aging could lead to a means of opposing it.

Figure 2. The traditional theory that evolution selects for the longest possible life leads biologists to think that lifespans are inherently limited to the ones we have today. In this view, aging cannot be stopped and lives can be extended only to about 120 years. The new understanding that evolution selects for shorter lifespans implies that aging is a mechanism for limiting lifespans which can be changed. Aging as we experience it is unnecessary, and can be postponed until the actual intrinsic lifespan limit is reached.


NECSI’s simulations provide a theoretical basis for extending the state of youthfulness and postponing the changes we associate with old age (see Figures 1 and 2). More than life extension, the trajectory of the human condition could be redrawn. Both youthfulness and life could be extended manyfold. Already, some researchers are looking to understand the mechanism of aging. For example, the shortening of the telomeres at the end of our chromosomes has been linked to aging. While today the actual mechanisms of aging remain unknown, a redirection of research priorities could provide a scientific approach to discovering the fountain of youth.

References

  1. J. Werfel, D.E. Ingber, Y. Bar-Yam, Programmed death is favored by natural selection in spatial systems. Physical Review Letters (June 12, 2015).
  2. J. Werfel, D.E. Ingber, Y. Bar-Yam, Theory and associated phenomenology for intrinsic mortality arising from natural selection. arXiv (June 12, 2015).


 

 

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