Study offers "radical change" in cellular aging concept

March 30, 2000
Web posted at: 5:25 p.m. EST (2225 GMT)

By Laura Lane

(WebMD) -- Scientists have long blamed saggy wrinkles and creaky arthritic joints on aging cells that stop dividing often enough to maintain our bodies in their fresh and youthful form.

But a new study could turn that theory on its head. Aging cells do continue to divide, according to a study published in this week's issue of Science. The problem is that the older cells have accumulated genetic damage; thus, they turn out flawed cells that eventually contribute to the diseases of aging.

"This represents a radical change in the way people have thought about aging," says Richard Lerner, M.D., co-author of the study, which involved researchers from The Scripps Institute of Research and the Genomics Institute of the Novartis Research Foundation, both of San Diego, California.

"While scientists have believed that aging is a disease in which cells stop dividing, this study suggests that aging is really a disease of quality control," says Lerner, president of Scripps. "In this case, the manufactured product is a new cell. As we get older, altered gene expression results in cells with diminished function."

Damaged genes turn out flawed cells

The scientists analyzed the genes of cells taken from people who were young, middle-aged and elderly, and those of children suffering from progeria, a devastating disease that causes premature aging. The researchers looked at genes of cells known as fibroblasts -- commonly found in the skin, bones and cartilage -- and found 61 genes that changed significantly with age.

The researchers say that they believe the genes may contribute to diseases such as Alzheimer's, cataracts, arthritis, breast cancer and other conditions of the kidneys, heart and ovaries.

Why do genes go awry as we get older? One theory is that free radicals -- unpaired electrons that roam the body stealing matching electrons from our molecules -- damage the genes, says lead author Danith Ly, Ph.D. The damaged genes regulate cell division, among other processes.

Researchers say it's far too early to know if this shift in understanding of the biology of aging will someday help prevent age-related diseases. But there's no question that this information is an important piece of the larger puzzle, says Lerner. As scientists piece together a more comprehensive picture of how age-related diseases develop, better drugs to treat or prevent such ailments could follow.

A diet for youth

While we wait for scientists to hammer out the details, there is one sure way to slow aging, says longtime aging researcher Roy Walford, M.D., professor of pathology at the University of California, Los Angeles, School of Medicine: Eat less.

"The only thing that retards aging is calorie restriction," Walford says. "As genetic studies go forward, we'll find out why."

Among his many studies in mice, Walford has found that when mice ate 30 percent less than usual, their 39-month lifespan increased to 56 months. Translated into human years, that's an increase of 52 years. He's also found that a low-calorie diet can help prevent the immune system from weakening.

His theory? The less food you eat, the fewer the free radicals you'll have wreaking havoc on your genes. While the USDA recommends that a sedentary woman eat only 1,600 calories a day, the average American eats well over 2,000 calories.

Of course, no one knows if this theory would prove true in humans. To benefit from Walford's youth-preserving formula, you'd have to subsist on a 1,400-calorie daily diet, packed with fruits, vegetables and fish that have antioxidants to fight free radicals.

So far, scientists haven't been able to find enough volunteers willing to live on such a diet to know if it would prolong the human lifespan.

© 2000 Healtheon/WebMD. All rights reserved.

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