What would Darwin say? It's the question I ask first when I'm looking for an answer about anything biological. Who am I to argue with Theodosius Grygorovych Dobzhansky who famously titled an essay, "Nothing in biology makes sense except in the light of evolution."
Yet aging presents an apparent paradox for evolutionary theory. The basic premise of evolution—natural selection—is that some randomly appearing traits are better fitted for survival than others. Individuals with those preferential traits will survive to pass them on to new generations. Among humans, mental acuity—the ability to plan the hunting and gathering—and physical prowess-the ability to execute the hunting and gathering are two of the human traits that with great success survived and evolved.
But with aging comes dementia and frailty. Where's the advantage in that?
Leonid A. Gavrilov and Natalia S. Gavrilova in "Evolutionary Theories of
Aging and Longevity," (The Scientific World Journal, 2002) ask how is it that evolution leads to "such bizarrely injurious features as senescence and late-life degenerative diseases instead of eternal youth and immortality. How does it happen that, after having accomplished the miraculous success that led us from a single cell at conception through birth and then to sexual maturity and productive adulthood...the developmental program formed by biological evolution fails even to maintain the accomplishments of its own work?"
The Gavrilovs point to another evolutionary quirk about aging. Quite obviously, aging occurs long after the necessary lifespan to continue our species—"beyond the reach of natural selection." For if natural selection is—in some simplistic way—the struggle to reproduce, that job is done decades before the ill effects of aging.
Years ago, I attended a lecture by the evolutionary biologist Richard Levins in which he noted that humans need to have a life expectancy of only twenty-five to ensure continuance of the species. We are well equipped to reproduce as teens, and a life expectancy of twenty-five left us with enough young-elders to pass on the full amount of culture needed to survive and evolve on the African plain to our current biological form. Not only old age, but middle-age appears to be totally irrelevant to survival.
The co-discover of natural selection, Alfred Rusell Wallace, hypothesized "programmed death" as an explanation for aging, "...when one or more individuals have provided a sufficient number of successors they themselves, as consumers of nourishment in a constantly increasing degree, are an injury to those successors. Natural selection therefore weeds them out."
This reminds me of the book, play, and movie, "On Borrowed Time," in which a man traps death in a tree. But he comes to see the consequences of nothing dying-individuals suffering from unalleviated pain, and scarce resources for all. Eventually he lets death out of the tree so that the cycle of life and death can go on.
Unfortunately, the programmed theory of death—that death has a competitive advantage for a species if not an individual—does not seem to have empirical support. Animals in captivity, and humans in our modern civilization, live much longer than in the wild, so it appears that natural lifespans are simply not long enough for the selection of programmed death in old age.
Aging presents what the Gavrilovs call a "timing problem," since, "Many manifestations of aging happen after the reproductive period of evolving organisms at ages which are beyond the reach of natural selection."
And they propose two—not mutually-exclusive—evolutionary theories to account for aging.
The mutation accumulation theory embodies the idea that although traits relating to aging—we reproduce years before we age—are not selected for survival, they are not selected against. A mutant gene that kills children will not be passed on to the next generation, but a negative gene—e.g., Alzheimer's disease—will be neutral to natural selection. Over time, these genes will not only be passed on to future generation, they will survive and accumulate in the human population.
Related to mutation accumulation is the antagonistic pleiotropy theory, which is the idea that some genes that have a survival value for reproduction carry within themselves negative effects as we age. Pleiotropic genes have more than one effect—in aging, antagonistic effects. Suppose there was a gene promoting the growth of calcium. This is good in youth. Strong bones promote the survival of hunter-gatherer evolving humans, but calcification promotes arthritis in old age. What's good for reproduction may not be good for longevity.
Behind all this is the idea that in the environment in which humans evolved, aging itself was not a normal part of the human life cycle. As late as the Middle Ages, the life expectancy of humans was only about Richard Levins' age necessary for survival of he species—about 25.
We apparently age because the genes for aging are either neutral for natural selection or the negative side effects of genes that earlier in life promote survival and reproduction.
For science, aging is actually a new phenomenon that is—so to speak—in its infancy.
In future postings, I will move beyond evolution and look at some of the mechanisms of aging-whatever their biological origins.