The global population is undergoing significant transformation. We are living longer than ever before, and older individuals make up an increasingly large segment of the world’s inhabitants. Yet, these extra years are not necessarily spent in good health.
How, then, do these demographic shifts interact with our understanding of genetics and evolution? How might aging—a relatively recent concept in the history of Homo sapiens—reshape our species?
And is the connection between aging and declining health unavoidable?
To explore these questions, evolutionary geneticists Handan Melike Dönertaş and Linda Partridge analyzed several massive, modern genetic datasets to test an idea that has persisted since the mid-20th century: the “shadow of selection effect.” The findings of their study have been published in the journal Nature Reviews Genetics.
“Advances in comparative genomics, large-scale human genetics studies, and multi-omic biomarkers of aging now enable rigorous testing of evolutionary predictions,” the researchers write in their published paper.
The concept of the “shadow of selection” is rooted in the notion that natural selection, driven by evolutionary pressures—the classic principle of “survival of the fittest”—is fueled by the need for a species to reproduce.
However, once the next generation arrives, our evolutionary fitness becomes much less consequential.
This impacts health in later life in several ways. First, harmful genetic mutations that manifest in old age are not weeded out by evolution—by that time, we have already had our children.
Second, genes that are beneficial in youth but detrimental in old age also persist, as evolution largely favors advantages that appear early in life.
For example, if a gene or gene variant increases the risk of developing cancer in later years but simultaneously helps you have children in your 20s and 30s, from an evolutionary standpoint, this is a favorable trade-off.
That is the theory, and with the vast increase in genetic data now available for analysis, Dönertaş and Partridge were able to compare it against existing evidence.
“An evolutionary perspective on aging is not just a historical curiosity,” says Dönertaş from the Fritz Lipmann Institute in Germany. “It points to conserved, ancient mechanisms whose continued activity in later life contributes to age-related diseases, and it is precisely here that interventions are most likely to be effective.”
The researchers cited several studies encompassing hundreds of thousands of individuals that indicate a weakening of natural selection in later life, essentially confirming the reality of the “shadow of selection.”
Dönertaş and Partridge also examined how aging differs across species, such as the long-lived naked mole rat. The biological tricks these species employ to bypass the “shadow of selection” effect could aid research into healthy aging in humans as well.
In other words, gaining a deeper understanding of aging from an evolutionary perspective provides clues on how the aging process might be modified.
“It also reframes the goal: not simply to extend lifespan, but to partially reduce the late-life costs associated with biological features that natural selection optimized for early life—so that a greater portion of life is spent in good health,” says Partridge from University College London.
Of course, human lifespan also varies greatly, a point the researchers themselves noted.
Essentially, we age and ultimately die because our cells wear out.
Yet, there is a tantalizing possibility that ways might be found to somewhat alter the priorities of this biological clock, and this review offers a fresh perspective on how that could be achieved.
“Ecological selection, which allowed the aging process to evolve, now offers a framework for reversing its effects,” the researchers write. “Aligning evolutionary theory with mechanistic studies and human genomics will enable science to move beyond merely cataloging age-related changes to rationally targeting their root causes, thereby reducing disease burden and extending healthy lifespan in humans.”
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