Aging Is a Disease. Is There a Cure?


CAMBRIDGE (Jun 12, 2015) -- Nobody lives forever, but a new approach to understanding human evolution suggests we are living shorter life spans than we could, and that aging should be thought of as a treatable disease, rather than a byproduct of time. A new paper, published this week in Physical Review Letters, argues the mathematics underpinning our understanding of evolution is fundamentally flawed.

Rather than naturally selecting for the longest possible lives, as the prevailing theory holds, evolution frequently opts for shorter life spans in environments where resources are scarce and the pressures to reproduce are especially intense. As a result, humans have been genetically conditioned to live shorter lives than we otherwise could, just as we retain a number of traits chosen for life on the prehistoric savannah rather than 21st century cities.

The paper’s authors — a team from the New England Complex Systems Institute (NECSI) in collaboration with the Harvard Wyss Institute for Biologically Inspired Engineering — show that because traditional theories describe only average environments and not the local variations that are present in nature, they miss the need to regulate lifespans to leave sufficient resources for their descendants.

These findings have a number of implications, the most important of which concern aging. If life spans are not necessarily finite, then genetic therapies could both extend life and delay the effects of aging. Evidence for this theory exists in other species. For example, a female octopus typically dies shortly after giving birth. If her optic gland is removed, however, she lives longer and may reproduce again. Other researchers have found genetic mutations in the nematode worm that may extend its life fivefold.

This study is the first contribution made toward understanding aging theory from a complex systems perspective. The authors have not identified the specific mechanism needed to achieve longer lifespans. “It has to be more complicated than a single mutation,” says NECSI president Yaneer Bar-Yam, “but it can’t be so complicated that evolution wouldn’t be able to make changes to extend or shorten the lifespan depending on environmental conditions.” He suggests that a detailed study of what sets off or stops aging can lead to treatments for aging and ultimately change the genetic program.

 

 

Phone: 617-547-4100 | Fax: 617-661-7711 | Email: office at necsi.edu

277 Broadway Cambridge, MA USA