Could Cutting Calories Add Years to Your Life?

Reducing them turns on an anti-aging gene in yeast, studies find

WEDNESDAY, Dec. 31, 2003 (HealthDayNews) -- According to the results of two new studies done on yeast cells, reducing calories activates the silenced information regulator (Sir2) gene, which prolongs cell life.

It's still not quite clear, however, exactly how Sir2 is activated.

In one study, published in the Jan. 1 issue of Genes and Development, researchers found a coenzyme of nicotinamide adenine dinucleotide (NAD), called NADH, causes the activation of Sir2.

"We are interested in how diet influences health and longevity," says lead author Leonard Guarente, a professor of biology at the Massachusetts Institute of Technology. "Particularly in how lowering calories extends life and health."

The finding that limiting calories extends life and health is not a new finding, Guarente adds. But how this occurs remains a question.

In previous studies, Guarente's team had identified Sir2 as a key gene to extending cell life. In their current paper, the team studied what was happening in cells as calorie intake was reduced to activate this gene.

The researchers found levels of NADH, a molecule inside of cells, changed in response to a low-calorie diet. "When the levels of this molecule decrease, the activity of Sir2 goes up, making cells live longer," Guarente says.

The researchers found that by activating Sir2, cells extended their life span by 30 percent. "In human terms, that would be decades," Guarente says.

"Our hopes are to extend these studies beyond yeast to mammals," he adds.

This finding may lead to the creation of drugs that can offer the same benefit of a low-calorie diet without having to live on only 1,000 calories a day, Guarente says. "Right now, people can't expect to eat so little that this mechanism would be triggered. What they should do is eat a sensible diet."

In the second study, Dr. David Sinclair, an assistant professor of pathology at the Harvard Medical School, and his associates -- also working with yeast -- found it is not NADH that activates Sir2, but another gene called pyrazinamidase/nicotinamidase 1 (PNC1).

Their study appears in the Dec. 19 issue of Science.

"We both agree that Sir2 is key to understanding life span and the effect of calorie restriction on extending life," Sinclair says. "In reality, it may be a combination of NADH and PNC1."

"Our goal is to find drugs that use these molecules to fight the diseases of aging such as cancer, diabetes and heart disease, not to extend normal life," Sinclair says.

Dr. Ronen Marmorstein, a researcher from the Wistar Institute at the University of Pennsylvania, says both papers are very interesting. However, since the methods used in each study are different, it is hard to compare them, he adds.

Marmorstein agrees that both NADH and PNC1 may affect Sir2 function.

It is not clear what the ultimate clinical implication might be in humans, Marmorstein notes. "No one has showed that Sir2 functions to extend life in human cells. Whether or not any of the current experiments is relevant to human cells is an open question."

More information

To learn more about aging, visit the National Institute on Aging or the National Aging Association.

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