Eat less, live longer: It works for animals, but most people would like to have the second part without doing the first.

It may someday be possible, says an MIT aging researcher who has discovered that a gene previously found to control longevity in yeast does the same thing in an animal - a common roundworm - and maybe in many other animals including humans.

The gene normally extends life only when the animal is deprived of food. But MIT biology professor Leonard Guarente believes it might be possible to switch on the gene with a drug, adding years to life while eating a normal diet.

``You might be able to harvest the benefits of (a longer) life span without having to go through that rigorous regimen,'' said Leonard Guarente, whose report, co-authored with Heidi A. Tissenbaum of the MIT biology department, appears in the current journal Nature.

Researchers have long known that some animals actually live longer when their food supply is drastically reduced, a genetic coping mechanism that helps them survive hard times. The strategy hasn't been proven yet in humans - though some pioneers are trying it on themselves.

The MIT biologists found that the roundworms lived 50 percent longer than their usual two-week life span when the researchers added extra copies of a gene called sir2. Best of all, Guarente and Tissenbaum extended the worms' lives without a starvation diet.

However, the added genes increased the likelihood that infant roundworms would go into a dormant stage called a dauer, in which the worms can survive for months without food.

The gene is similar to one previously found to regulate longevity in baker's yeast. The publication is the first to show that the sir2 mechanism regulates longevity in the animal kingdom.

``What's true in yeast and worms is probably generally true in all organisms, because these organisms are so divergent,'' said Guarente, who recently founded a Cambridge, Mass., company, Elixir Pharmaceuticals, to search for anti-aging drugs.

Aging ``is one of the few parts of biology that's still a mystery,'' said Cynthia Kenyon, a biochemist and aging researcher at the University of California in San Francisco, calling the MIT findings ``very intriguing and thought-provoking,''

She said that the sir2 gene mechanism is another example of the way evolution has resulted in important genes being shared among many species. Kenyon discovered another gene in roundworms which, when mutated, doubled their life span. But the sir2 gene mechanism is probably more universal, she said.

She also agreed that drugs might one day be found to increase longevity without requiring semi-starvation diets.

The creation of the long-lived worms is striking because it seemed unlikely that the same gene would control aging in yeast, which are single-celled fungi, as well as complex animals.

``After more than a decade of guessing that studies'' of the yeast ``might teach us about general mechanisms of aging, the gamble has paid off,'' wrote David Gems, a biologist at University College in London, in a commentary in Nature.

In the earlier yeast studies, Guarente showed that the sir2 gene was a key regulator of aging.

``We could remove the gene and it shortened the life span of cells, or we could increase the life span by adding the gene,'' he said.

The sir2 gene, however, needed input from a molecule called NAD in order to lengthen or shorten the life span. NAD can ``sense'' when nutrition is abundant or scarce, said the MIT scientist.

``Our concept is that when nutrition is scarce, then it is advantageous to slow down the aging process and hunker down until things get better,'' he said. ``Sir2 is perfectly positioned to do this.''

• More news on Seniors' Health (General)

Related MEDLINEplus Pages:

• Seniors' Health (General)