The aches, pains and disease that come with age may be nature’s method of population control.
Aging is a genetic mechanism that prevents humans and other organisms from living as long as they could, scientists argue in a study published June 12 in Physical Review Letters. The scientists propose that age-related ailments provide the evolutionary benefit of shortening life span, which conserves resources for future generations. Scientists could greatly extend life expectancy by deactivating the machinery for aging embedded in our DNA, the researchers assert.
“I don’t think it’s unreasonable to think we could extend the human life span by multiples,” says study coauthor Yaneer Bar-Yam of the New England Complex Systems Institute in Cambridge, Mass.
Bar-Yam and his team’s conclusion that evolution shortens life spans is based on mathematical simulations showing that relatively short-lived organisms fared better over time than longer-lived and even immortal competitors.
It’s an impressive result, say scientists not involved with the research, but they are skeptical that the simulations reflect reality. “It’s certainly not your ordinary paper,” says Carl Bergstrom, an evolutionary biologist at the University of Washington in Seattle. “I’m intrigued but cautious.”
Many biologists have considered aging the result of an evolutionary trade-off: Mutations that promote reproductive success early in life can eventually become detrimental. Evolution does not select for truncated life spans, but an organism that avoids death from starvation, disease or other outside factors will ultimately succumb to those harmful mutations.
But past studies analyzing evolution’s impact on life span tended to oversimplify, says Justin Werfel at Harvard University’s Wyss Institute for Biologically Inspired Engineering. Some such studies assume “that every place is like every other place.” In reality, he says, organisms depend on the resources available where they live.
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Werfel, along with Bar-Yam and Harvard bioengineer Donald Ingber, devised simulations that tracked the evolution of organisms whose offspring inherit the resources left behind by previous generations. The resources came in the form of another species that served as prey. In one simulated scenario, an individual among a species of immortals, who die only from external factors such as starvation, obtains a genetic mutation for mortality. In many simulation runs, the mortality mutation spread through the population and overtook the immortals. In an opposing scenario, a mutation for immortality within a population of mortals never took hold.
Other simulations echoed the finding that having a truncated life span — in harsher terms, getting killed off prematurely — provides an evolutionary advantage. Werfel says that limited life spans enabled the predators to avoid depleting the prey many generations down the line, even if there was initially plenty of food for everyone.
Michael Rose, an evolutionary biologist at the University of California, Irvine, praises the researchers’ mathematical prowess in exploring whether longevity could pit organisms against their descendants in a battle for resources. But he says that humans and many other creatures can easily move and obtain new resources. He says the simulations may accurately describe a tree that drops seeds directly beneath it, forcing it to compete directly with its offspring. (Werfel says simulations that allowed the predators to move around produced the same results.) Rose also points out that many creatures, including humans before the era of modern medicine, usually get killed by predators, weather or disease long before they suffer from the effects of aging.
Bar-Yam says he is confident that shortened life spans are ubiquitous in nature, including in humans. If people are programmed to die, he says, then scientists should focus on discovering and deactivating the genetic mechanism. “Instead of treating age-related diseases, we can address them by intervening in the process of aging.”
Bergstrom isn’t as optimistic about significantly extending the human life span. Even if the new study is right about aging’s primary role, the trade-off mechanism for aging could also be at work. And Valter Longo, who studies aging at the University of Southern California in Los Angeles, says it’s not clear how long we would live even if evolution didn’t kill us off. A profit-hungry car company could design a vehicle to break down after a certain amount of time, he says. “But if it doesn’t do that, it doesn’t mean the car will last forever.”
Bar-Yam says he welcomes positive and negative feedback. “We expect this to be controversial,” he says. “I hope we end up shaking things up quite a bit.”