Study raises questions about how we age

Los Angeles Times

Countering the prevailing theory that aging is the accumulation of wear and tear in cells, scientists studying worms have found that aging might be hard-wired, a sort of unintentional sabotage by genes gone wild.

The study, published Thursday in the journal Cell, found that metabolic processes important during development might shift later in life in ways that unintentionally sabotage the worms, causing them to age and die.

The scientists studied a tiny worm called Caenorhabditis elegans, which is popular in aging studies because it lives only two weeks.

Of the worms’ approximately 20,000 genes, 1,256 were regulated differently in young worms versus old worms.

In particular, the aged worms had different levels of transcription factors, key genes that influence development by turning other genes on and off.

Chemically squelching certain overactive genes later in life made the worms live a few days longer, said Stanford University developmental biologist Stuart Kim, who led the research.

The researchers also found that the age-related molecular switches weren’t affected by stresses such as radiation, heat, infection and oxidation, which are thought to cause aging through gradual accumulation of damage, a process akin to rusting away molecule by molecule.

Kim acknowledged that rusting played a role but doubted it was the sole force that made living things wither and die of old age.

“I don’t think there are any theories that account for the vast differences in life spans between animals. Nobody knows why we age in 80 years and chimpanzees age in 40,” he said.

Kim said he thinks the worm results one day might answer questions such as why the human kidney ages faster than the liver or why some clams live for 400 years and whales can live for 200 years.

“Why can’t I live as long as a whale? How hard would it be?” he asked.