Are Limited Lifespans An Evolutionary Adaptation?

Since the time of Darwin, evolutionary biologists have wondered why the lifespans of different species vary so significantly. A new model now suggests that the life expectancy of any given species is a function of evolutionary pressures — a conclusion that hints at the potential for powerful anti-aging interventions in humans.

The new paper, which now appears in Physical Review Letters, challenges popular conceptions about the nature of aging and why it manifests at different rates in different organisms, including species that are closely related.


By running variations of their model hundreds of thousands of times, a research team led by Yaneer Bar-Yam from the New England Complex Systems Institute (NECSI), in collaboration with the Harvard Wyss Institute for Biologically Inspired Engineering, observed that evolution favors shorter lifespans in environments where resources are scarce and when pressures to procreate are particularly intense. The simulations appeared to show that lifespans of animals — humans included — are genetically conditioned, and not the result of gradual wear-and-tear. It’s a surprising result, one that gives added credence to the burgeoning paradigm known as “programmed aging.” At the same time, the study shows that current efforts to develop anti-aging interventions may be based on incorrect assumptions.

Why We Age

As it stands, there are two prevailing theories that explain “intrinsic mortality,” i.e. death that occurs when an animal dies of “old age” rather than from external causes, such as predation or starvation.

First, there’s the “mutation accumulation” theory posited by Oxford University biologist and Nobel Laureate Peter Medawar. He argued that certain adaptations, or mutations, can produce detrimental effects late in life that are not strongly selected against in evolution. Collectively, these “detrimental” effects manifest as the symptoms of aging and eventually death.

The second theory, called “antagonistic pleiotropy” — or the “pay later theory” — is the idea that a single gene, or characteristic, is beneficial early in life, but then turns detrimental at a later stage. A good example is cellular senescence, which acts beneficially early life by suppressing cancer, but then turns against us later on by causing frailty and, paradoxically, cancer. Antagonistic pleiotropy was conceived by Michigan State University biologist George Williams back in 1957.


There are some problems with these theories, however.

First, they both place an undue emphasis on math — a product of the neo-Darwinian approach to evolution popularized by the likes of Williams and British statistician and mathematician Sir Ronald A. Fisher. The neo-Darwinian synthesis, with its declaration of the gene as the basic unit of evolution, inspired mathematical analyses of phenomena such as kin selection, altruism, and speciation. At the same time, however, the approach has resulted in a subsequent dearth of empirical evidence.


Second, so-called “selfish genes” should work to favor extreme longevity among animals, yet that’s something we don’t observe. As explained to me by Josh Mitteldorf, co-author of the upcoming book, DNA of Death, and an expert on the genetic underpinnings of aging, a primary disadvantage of aging is that an animal eventually dies and leaves less offspring.

Because of these shortcomings, and owing to a growing body of phenomenological data that has been emerging since the 1990s, there’s a third explanation, a theory known as “programmed aging” that was first proposed by biologist August Weismann back in the 1880s. That aging is a deliberate function of our genetics remains a controversial idea, but it’s an idea that’s steadily acquiring adherents.


Programmed Death

One of these adherents is NECSI president Yaneer Bar-Yam, who in the new paper contends that popular approaches to the aging problem fail to address a very important constraint, namely the ways lifespans are genetically controlled according to the resource limitations of a given environment. Without genetically programmed aging, he argues, animals wouldn’t be able to leave sufficient resources for their offspring. And this holds true for all animals, whether they be rabbits, dolphins, or humans.


Mule deer grazing in Zion Canyon. If these creatures had longer lifespans, would there be enough food to go around? (Credit: Itsmine/cc)

Bar-Yam and his team reached this conclusion by developing a simple model that analyzed how the lifespans of simulated organisms would change and evolve over time under spatially constrained conditions.


Instead of looking at the average conditions of environments over time, this model took local variations into account in environments where organisms evolve. In their simulations, the researchers used cellular automata to observe the evolution of lifespan limits and the onset of intrinsic mortality. Though the simulation took place within a tight spatial system, some variables were adjusted, including the presence of self-renewing resources (which in a real life scenario would be akin to the re-growth of grass for grazing animals, available fish stock for dolphins, and so on).

“We simply designed an understanding of what happens when we don’t make the assumption of the same environment,” Bar-Yam told io9. “The only thing it relies upon is spatial locality, which, along with resource limitation, is generally the case in nature.”


Fascinatingly, group selection — the idea that natural selection acts at the group level — was never a consideration in the model. Yet the simulations consistently showed that a built-in life expectancy emerged among the simulated organisms to preserve the integrity of their species over time. This is surprising because a pro-group result was produced via an individualized selectional process.

“Beyond a certain point of living longer, you over-exploit local resources and leave reduced resources for your offspring that inhabit the same area,” Bar-Yam said. “And because of that, it turns out that it’s better to have a specific lifespan than a lifespan of arbitrary length. So, when it comes to the evolution of lifespans, the longest possible lifespans are not selected for.”


Bar-Yam’s work suggests that aging is a mechanism — if not the mechanism — that works to define and limit the lifespans of animals. And if the biological and medical communities can figure out how our genes control these developmental processes, he says we may be able to develop powerful anti-aging interventions. Simply put, the researchers see aging as a genetic disease that can and should be treated.

Tradeoffs and Scaling for Time

These are clearly remarkable claims, so I contacted gerontologist and anti-aging expert Aubrey de Grey to get his take on the paper.


“My initial take is that it’s in line with what is already well known about kin selection and ‘population viscosity,’” he says. “Basically, if one’s nearest relatives are also one’s physically closest neighbours, it’s to be expected that there will be a non-individual benefit from suicide when resources are limited.”

As for the study’s claim that “Intrinsic mortality is not favored for long-range spatial mixing,” de Grey says one can’t extrapolate to any situation in which there’s lots of long-range spatial mixing, “which is of course the case for animals.” On this point de Grey and Bar-Yam disagree, the latter of whom claims that long-range spatial mixing — when two species or populations exist in the same geographic area and regularly encounter and/or compete for resources with one another — is “limited” in the “typical real-world systems.”


de Grey doesn’t buy the programmed aging hypothesis. He recently published a paper at Current Aging Science on this exact topic, concluding that:

...however much we might wish that aging were programmed and thus that the ill-health of old age could be greatly postponed just by disabling some aspect of our genetic makeup, the unfortunate truth is that no such program exists, and thus that our only option for substantial extension of healthspan is a divide-and-conquer panel of interventions to repair the damage that the body inflicts upon itself throughout life as side-effects of its normal operation. I explicitly avoid arguments that rely on unnecessarily abstruse evolutionary theory, in order to render my line of reasoning accessible to the broadest possible audience.


I also contacted S. Jay Olshansky to get his opinion. He’s a professor in the School of Public Health at the University of Illinois at Chicago and Research Associate at the Center on Aging at the University of Chicago.

Here’s what Olshansky said to me in an email:

I would take issue with their final and most important point. If senescence is programmed, manipulating genes to favor greater longevity is likely to have tradeoffs for other attributes of the life history — which the authors never even mention. Since most tradeoffs are negative or undesirable, it is unlikely that such an intervention would actually work. To the contrary, we’re better off without programmed aging — this way, interventions that modulate the rate of senescence (either indirectly or directly) are not battling against a genetic program. Interventions that do not battle against our own genes are more likely to have a substantive impact.

Finally, the authors made the fundamental error of comparing the longevity of species without scaling time. Since species live life on different time scales, failing to scale for time leads some to believe that because the longevity of flies or worms can be increased several fold, therefore the same can be accomplished for humans. My colleague and I wrote an e-book to explain scaled time; unfortunately, it appears to have not been read by these authors. The title is “A Measured Breath of Life”.


I offered Bar-Yam an opportunity to respond to Olshansky’s criticisms.

“That there has to be a tradeoff is exactly what our theory disproves,” he told io9. “The fact that these lifespans are specifically being selected for shows there aren’t such tradeoffs.”


Bar-Yam says it’s true that there might be tradeoffs for particular adaptations, but the mechanism as a whole is precisely and exclusively one of lifespan control.

“And it has to be that way according to the theory — that’s the whole point,” he says. “The theory is telling us that evolution is selecting for that trait in the same way it selects for height, weight, color, and other things. The fact that evolution is selecting for a particular trait implies that there isn’t a necessary tradeoff with other traits.”


To which he added: “The gut reaction from people engaging in this field who feel there have to be tradeoffs are driven by a 40 year old theory that says the only way you can have longer lifespans is by virtue of the fact that there are these tradeoffs.”

As for Olshansky’s point about failing to scale for time, Bar-Yam points to how crocodiles barely seem to age at all, and how some species of birds live for only several years, while others, like the albatross, live for nearly five decades. There are also rockfishes to consider; check out this chart showing the incredible variations in lifespan among its member species:


“There’s no particular lifespan,” he says. “And there’s no reason to believe that particular lifespans have a scale that’s inherent. Lifespans of organisms vary in related species by huge variations.”

Bar-Yam also brought up nematode worms. Researchers have shown that a single gene deletion can extend the lives of these worms by a five-fold increase. Olshansky says it’s not fair or accurate to compare anti-aging interventions between nematodes and humans because of time-scaling. But Bar-Yam argues that time scales are not an important factor.


“If there was a really well defined lifespan, we would be seeing it in a systematic process that would be related to biological size or something else like that, but we don’t really observe that,” he says. “The idea that short lifespans can be extended, but long lifespans cannot, is an idea without a lot of phenomenological support.”

At the same time, there are some biological data points that appear to strengthen the programmed aging hypothesis.


As Josh Mittledorf told me, cellular senescence is a “classic example” of this process at work — a mechanism of programmed death that’s been around ever since the first eukaryotes emerged billions of years ago. There’s also the octopus to consider, an organism that simply stops eating after it’s done reproducing.

“There are many species where death is clearly programmed and there’s no reason for this animal to die,” says Mittledorf.


Implications to Life Extension

The Bar-Yam study was a mathematical, simulation-based investigation of evolution, not a biological one. Consequently, any inferences made by the researchers beyond that — namely those that pertain to potential life extension interventions in humans — need to be taken with a fistful of salt. Biological studies will be required to show if these researchers are on the right track. That said, anti-aging scientists need to take notice.


For example, gerontologists like de Grey are working to repair the damage done by aging. Bar-Yam admits that degradation happens over time, but he says biological systems show a remarkable capacity for self-repair.


“The question is, why do self-repairing organisms age?,” he asks. “So in the context of where self-repair is an effective process, why does it not work well enough to keep us alive for 150 to 200 years?”

He says the answer from the traditional theory is not based upon any understanding of biology that tells us aging is necessary, “but it’s only and solely based upon solutions that are based on mathematical approximations.”


Mittledorf says that rather than trying to repair the processes of aging, scientists should try to trick the body into thinking it’s younger. That way, the body will work to repair itself. Experiments in mice, where the blood of the old is replaced with the blood the young, has been shown to reduce the effects of cognitive decline, among other age-related disorders.

“Experiments like these suggest that aging is controlled by factors in the blood, such as hormones and small RNA and gene promoters,” Mittledorf told io9. “Little molecules that stick onto the DNA and program it epigenetically, and then turn on or turn off that gene. We have hundreds, possibly thousands of them in our blood — and they have tremendous influence on the health and destiny of a cell.”


Bar-Yam says there’s both popular hope and fatalism about the nature of aging and death. He claims that many scientists today have placed themselves in direct opposition to the hope, while favoring the fatalism — and they’re doing so by honoring theories based on incorrect assumptions.


“When we remove those assumptions we find that the opposite conclusion is reached,” he says. “So if we have the opposite conclusion, we suddenly have a very different scientific framework that impacts dramatically on the nature of public understanding. It should shift the dialogue dramatically. And that’s really my hope. By shifting the dialogue, I’m hoping we can shift the priorities of analysis of research in a direction that, because of what the theory says, is likely to be a fruitful direction of inquiry.”

Read the entire study at Physical Review Letters: “Programmed death is favored by natural selection in spatial systems”.


Contact the author at and @dvorsky. Top image by Tara Jacoby

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