Sun, Nov 20, 2005 - Page 19 News List

Long live the thin, new findings show

Cells genetically tricked into slow-aging mode by starving seem to live up to six times longer


A genetic experiment to unlock the secrets of the aging process has created organisms that live six times their usual lifespan, raising hopes that it might be possible to slow aging in humans.

The geneticists behind the study say the increase in lifespan is so striking, they believe they have found one of the most fundamental mechanisms that controls the rate at which living creatures age.

The tests were carried out in single-celled organisms, forcing them into what the researchers refer to as an "extreme survival mode."

Instead of growing quickly and showing signs of aging, the organisms became resilient to damage and were better able to repair the genetic defects that build up with age, often leading to cancer in later life.

"When you do this genetic manipulation, you can get some of the longest lifespans ever described," said Valter Longo, a biomedical gerontologist at the University of Southern California. "We have good reason to believe this genetic effect is conserved in other organisms. We're working with mice and human cells now and are already starting to see the same response."

A large body of research has already shown that severely restricting diet can boost the lifespan of flies, worms and mice by around 40 percent. Scientists believe that drastically cutting calories triggers a switch in an organism's behavior, from growing and being able to reproduce, to a state of stasis in which growth and aging are put on hold at the expense of reproductive capability, until more food is available.

Scientists are now trying to mimic the effect by tinkering with genes in the hope of developing anti-aging treatments that work without having to cut food intake.

"We're not too far from being able to exploit this understan-ding to at least start thinking about drugs that can put humans in an anti-aging mode. That doesn't mean we'll necessarily live six times longer, but it means we could slow down the DNA damage we accumulate as we age, and that could protect us from cancer," he said.

In the experiment, Dr Longo's team took yeast cells and knocked out two key genes, named Sir2 and SCH9. The latter governs the cells' ability to convert nutrients into energy.

They found that instead of dying after a week, the cells lived for up to six weeks. Dr Longo said parallel experiments on human liver cells appeared to replicate the effect, but refused to elaborate until the results have been published.

The researchers believe that the Sir2 gene normally plays a role in restricting an organism's lifespan, and allows energy from the food it eats to be directed into growth and reproduction. By blocking the gene, the cells were essentially tricked into believing food was scarce and switched them into a survival mode.

"When you start increasing lifespan by five or six times, it means you're really playing with the life and death programs of organisms. We're telling the organisms to go into a completely different mode of slow aging, said Dr Longo.

"What they're doing is saying `I cannot afford to age. I still have to generate offspring, but I don't have enough food to do it now.'"

Research has now begun to test whether the effect works in mice. According to Dr Longo, lab mice bred with the equivalent gene knocked out appear to live longer, but are smaller, infertile and often suffer muscular defects, suggesting the gene is necessary for normal foetal development.

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