July 24 (HealthDay News) -- Aging may be part of your genetic plan, not the result of wear-and-tear on your body, a new study of worms suggests.

The finding contradicts a commonly held theory and gives hope that science eventually may find a way to stop or reverse the aging process.

Comparing young and old C. elegans nematode worms, researchers at the Stanford University School of Medicine found that shifts in levels of three transcription factors -- the molecular switches that turn genes on and off -- appeared to trigger genetic pathways that age the worms.

This finding would back the less-popular theory that genetic programming, rather than a lifelong accumulation of toxins and damage, make organisms grow old.

"Our data just didn't fit the current model of damage accumulation, and so we had to consider the alternative model of developmental drift," senior author Stuart Kim, a professor of developmental biology and of genetics, said in a Stanford news release.

The researchers, whose report was published in the July 24 issue of Cell, found hundreds of age-regulated genes operated by elt-3, a transcription factor that becomes more abundant with age. Two other transcription factors that regulate elt-3 also changed with age.

The same process may not happen in humans, Kim said, but the finding should start scientists on a mission to find whether this aging mechanism is also in people.

"Everyone has assumed we age by rust. But then how do you explain animals that don't age?" said Kim, who cited tortoises that lay eggs at 100 and whales that live to 200.

"A free radical doesn't care if it's in a human cell or a worm cell," he said.

SOURCE: Stanford University School of Medicine, news release, July 24, 2008