How Long Can We Live? : We May Be Able to Push Our Life Spans Past Our 80s, but Would We Want to, Unless We Could Also Guarantee the Quality of Those Years? : Biologists Caleb Finch and Michael Rose are tackling the issue from different approaches, but both agree that aging can be postponed.

Life does not have to end at 85, or 100, or even 120. So says a small but elite group of researchers exploring the possibility of increasing our life span.

“Aging is no longer regarded as a monolith; an unmovable frontier,” says USC biologist Caleb E. Finch. Finch believes in using common good-health practices like eating right and exercising to control our environment and exploit the “plasticity” of life span.

“We probably, with existing technology, don’t have to invent anything new to get to the heart of biological aging,” he says. “I’m highly optimistic.”

Michael Rose of UC Irvine suggests the key to longer life lies in evolution and is studying a link between delayed reproduction and increased longevity in fruit flies.

“We have all the basic science to postpone human aging right now,” he says. “And I have a plan for doing it.”

The two researchers are old friends and colleagues who take very different approaches to the problem but reach the same conclusion:

Life expectancy is not capped by some unyielding force.

Their beliefs ignore the traditional consensus among researchers that life expectancy is controlled by an inevitable breakdown of body processes. In a recent article in Science magazine, scientists suggest that natural degeneration caps our life span at about 85 years.

In fact, no one knows how to dramatically increase how long we can live. But in recent years, scientists have moved away from believing that aging is the result of a single gene that goes awry late in life.

Instead, they believe theories that suggest aging is the result of many processes, linked to genes and the environment, working to wear down the body. These newer theories raise the possibility of intervening to stop the chain of events that cause aging.

“It’s now a question of whether people want to (pursue) this,” Rose says.

Finch and Rose have produced some of the most powerful evidence of the potential to extend the life span. And each has a new book that makes a strong case for going after the fountain of youth.

Rose, an evolutionary biologist, is the leading proponent of a theory of aging based on evolution.

With a youthful face and punk hair, Rose looks as if he would be more at home on MTV than on the seventh floor of the UCI Engineering Building. But he has turned many skeptics into supporters in recent years.

The purpose of his book, “Evolutionary Biology of Aging” (1991, Oxford University Press), “is to argue that aging can now be regarded as a problem that is well on its way toward a scientific solution.”

Scientists are more interested than ever in the longevity question because of recent success by Rose and others with experiments that have shown the life span can be extended in lab animals.

In experiments on fruit flies, worms and mice, it’s “very easy for us to . . . postpone aging so that life span can be doubled or the pattern of deterioration with aging can be vastly slower,” Rose says.

The experiments focus on finding which genes are important to the aging process in order to manipulate them.

Rose, for instance, is studying whether aging can be influenced by manipulating the process of natural selection--the force of nature that favors the young (who can reproduce) far more than the old.

Rose says his studies show that the age at which a species reaches maturity--and is able to reproduce--is linked to the onset of aging. That means that the way to keep natural selection working later in life is to postpone reproduction until a relatively advanced age.

Over the past 15 years, Rose has bred fruit flies at later and later ages--increasing their life span by 80%. He is selecting as parents only older flies that can pass on longevity genes.

Scientists have delayed reproduction and increased life span in other species, and are now trying to understand why the process works. They want to know which genes that affect life span are inherited or eliminated by postponing reproduction.

For the fruit fly, Rose has shown that at least 100 genes may be involved.

But the research will contribute little to the understanding of human aging, Rose says, unless the same experiments can be tried on mammals, such as mice. That is where his “plan” for expanding life span comes in.

“If we can use a mouse to postpone aging, than we will begin to find out how to do that in man,” he says. Ten years of work on mice, he suggests, could probably reveal the genes, processes and cell biology involved.

“Then we can try out direct interventions to postpone aging,” he says, first on mice, then on humans.

Finch also believes that plenty of evidence challenges the assumption that our life span has a limit. But he believes that study of common health practices--such as exercising and hormone treatments to reduce the risk of osteoporosis--will contribute significantly to the understanding of aging.

A professor of gerontology, Finch is a tall, thin Northeasterner who likes to joke about the way aging has left him balding. But beneath the congeniality is the kind of dedicated, no-nonsense scientist who would turn out a 842-page book called “Longevity, Senescence, and the Genome,” (1991, the University of Chicago Press). The title refers to the study of aging and the role of genes in that process.

Also an expert on Alzheimer’s disease, Finch says the potential to thwart disease and disability in old age is the force behind the research to extend our life span.

“The reason money is being put into research is in the belief . . . that we’ll be able to define, treat and prevent many disabilities of aging by medical practice,” Finch says.

“The number of people living beyond 80 is increasing and this has enormous implications for health programs and society in general. We can’t not do it.”

In his book, Finch has catalogued a lot of examples that show certain species have manipulated their environment to live longer. He calls this the “plasticity” of life span.

Finch said he sees no biological limits that predict a maximum life span in any species. However, he says, manipulating genes can affect how long we can live. “It’s a matter of programming genes in different sets of ways.”

For example, although queen bees and worker bees have the same genetic structure, queens live from five to 15 years while workers are lucky to live out a year. The difference, Finch says, is in their environment. Workers wear out from flying around while queens are pampered.

Some species apparently don’t age, Finch says. Scientists are studying a species of rock fish that are 100 years old and show no signs of aging, he says.

“Under some circumstances, aging may not occur in the natural world,” he says. “There are a lot of species of fish and other invertebrates that don’t seem to have an increased risk of disease or death.”

In the meantime, Finch suggests that people who are careful about their diet and exercise might live longer and healthier--and contribute to the advancement of science. After all, research showed that rats who receive special diets and hormone supplements live longer.

All of this means that such “interventions” can work in humans, Finch says. “Enough is now known to believe that (diseases of old age) are . . . not inevitable.”