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Back in 1957, when an evolutionary biologist named George C. Williams introduced his “antagonistic pleiotropy” theory of aging, I was slogging through first grade at Red Oak Elementary School and blissfully unaware of the particular genetic advantages Williams had identified in the young. I recall being more preoccupied at the time wondering how the “duck-and-cover” drills we practiced in our classroom would save us when the Russians dropped the A-bomb. Growing old seemed like a distant, slightly tenuous possibility.

Williams posited that our genes affect more than one human trait (pleiotropy) and do so in both positive and negative ways (antagonistic) at various points in our lifespan. More importantly to my fellow aging boomers today, he argued that natural selection is always “biased in favor of youth over age whenever a conflict of interest arises.”

This may seem obvious — evolutionary progress depends on the young procreating, after all — but the notion that our genes engage in some sort of capricious behavior has flummoxed researchers for the past 60 years. Why, for instance, should genetic mutations that cause overproduction of sex hormones in young adults also cause prostate and ovarian cancers in geezers? It’s as if our genes are practicing mutually assured destruction.

I recall Williams and my youthful Cold War angst in light of last week’s news that Chinese researchers are challenging his theory with a study suggesting, however vaguely, that natural selection may not be as unkind to the elderly as we’ve been led to believe.

Working with the popular laboratory nematode Caenorhabditis elegans, CAI Shiqing, PhD, and his colleagues at the Chinese Academy of Sciences set out to examine the genetic reasons why some nematodes (and by extension, humans) age at different rates than others. Their findings, published in the journal Nature, focus on genetic variations in certain coding (rgba-1) and receptor (npr-28) genes that trigger serotonergic and dopaminergic neurons in the brain. This interaction apparently disrupts the “unfolded” protein in the mitochondria and modulates the aging process. These genes, they argue, “might have been subjected to a recent selective sweep” that made them more likely to extend longevity.

“This study suggests that the evolutionary selection of genes that offer benefits in early life could also result in a concomitant extension of lifespan or extension of health span, or both,” Shiqing explains in a statement released by the academy. “This research indicates that aging rates may have been affected by the emergence of new genes, natural selection, and interaction between different genetic loci, thus providing new insights into the evolutionary theory of aging.”

Nematodes are not humans, of course, and Shiqing’s findings offer about as much assurance as my grade school civil-defense drills. Still, it’s nice to know my genes may be open to change as I totter through my golden years. I’d hate to think evolution has it in for us.

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