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Rethinking aging and life span

A new evolutionary model linked to aging raises the question: can life span be tuned?

(BOSTON) — Why do organisms grow old and die? Standard evolutionary theory has had an answer for this ancient question for decades: senescence_aging-related degradation_is due to genetic flaws that selection is powerless to eliminate and gene effects that give early-life benefits but late-life problems. And yet lifespans between closely related species can differ by a factor of ten and more. For instance, the rougheye rockfish lives for about 200 years, while its close relative, the blue rockfish has a lifespan of only 26. Animals like salmon live until they reproduce a single time and then die and, on the other hand, in a non-parasitic roundworm, C. elegans, just a single or few-gene mutations have been shown to extend lifespan significantly. Could all this suggest an active lifespan control mechanism within every organism and what role does it play?

Older ideas, first proposed in the 19th century, suggesting that shortened lifespans can be beneficial to a species, have been discarded. Now a new computer model of evolution, published in the Physical Review Journal, shows that limited lifespan can be detrimental to an individual in the short term but beneficial to its far descendants, conferring an advantage to the whole species in the long run.

A team of scientists at the Wyss Institute of Biologically Inspired Engineering and the New England Complex Systems Institute have demonstrated in a new more complete computer model that genetically programmed life span limitations, although shortening the individual organism’s life, confer long-term benefits for the species many generations later. The findings are reported in the June 12 issue of Physical Review Letters. Credit: majivecka/Shutterstock.com

“It seems very clear intuitively that shorter lifespan should be selected against a gene that contributes to the death of its owner logically ought to be eliminated,” said Justin Werfel who is a Senior Research Scientist at Harvard’s Wyss Institute for Biologically Inspired Engineering. “But what our model shows is that, while living longer can give a reproductive advantage for many generations, much further down the line the longer-lived ones get outcompeted by shorter-lived variants.”

Spearheaded by Werfel, a study performed at the Cambridge-based New England Complex Systems Institute (NECSI) and the Wyss Institute has now identified a new evolutionary effect that shows how an active mechanism of life span control can improve success of a lineage over long time scales-helping to account for apparent exceptions to the traditional theoretical understanding of aging, and raising important possible implications for human medicine.

The co-authors on this study include Wyss Institute Founding Director Donald Ingber, M.D., Ph.D. who is also the Judah Folkman Professor of Vascular Biology at Harvard Medical School and Boston Children’s Hospital and Professor of Bioengineering at Harvard John A. Paulson School of Engineering and Applied Sciences (SEAS) and Yaneer Bar-Yam, Ph.D., the President of NECSI where the work was begun. Bar-Yam is also an affiliate of the Massachusetts Institute of Technology (MIT) Media Lab.

Standard mathematical models of life span in an evolutionary context assume a homogeneous environment where individuals all have the same amount of resources (food) at their disposal. These models predict that longer lifespan and increased reproduction are always favored, in accordance with existing evolutionary dogma. The Wyss Institute and NESCI researchers took a radically different modeling approach. They modeled a more real-life scenario in which organisms change the local levels of resources available to them over time: resources in this ‘spatial’ model are progressively depleted locally by the organism, and replenished when left untouched. The organism thus shapes its own environment: heavy resource use may let an individual reproduce more, but over time results in a depleted environment for its descendants.

Giving organisms in the model the ability to limit their own lifespan, as a heritable trait, revealed a surprising result: an optimum lifespan appeared. The exact length of the lifespan that was most beneficial varied with the environmental conditions, but some degree of lifespan self-limitation was always favored over no lifespan limitation in the spatial model with limited resources. Longer-lived variants had a competitive advantage for many generations, but in the longer term, they were eliminated compared to the more age-limited strains. “We show that mechanisms for active lifespan limitation can actually have a long-term benefit to one’s descendants, even if they’re obviously not in one’s own best self-interest. The result gives a new way to interpret observations in nature, and helps to explain the ones that have posed problems for the standard understanding,” said Werfel.

“Previous models about aging and evolution were implemented only under specific conditions, which is why they did not have a more general impact and why standard evolutionary theory maintained its dominance. Our approach is fundamentally generic, resulting in the most general model that can be made. We therefore expect it to have a much larger impact,” said Bar-Yam. “The model also implies that there are intrinsic genetic mechanisms that limit life span. Intervening in them could extend our healthy lifespans dramatically.”

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