Scientific research can tell us why and how we age, but does this insight help us stay younger, longer? Until very recently, most experts would have said no. Many held that the aging of cells, and of multicellular organisms like humans, was inevitable—and therefore, there was a limit to how long each species could live. One theory held that the biological life span of any species is roughly six times the stretch between birth and maturity. Using this formula, the maximum lifespan for humans is 120 years. In fact, one well-documented contender for the title of longest-lived person is a French woman believed to be 122 years old when she died in 1997.

Today, some researchers are having second thoughts about a maximum life span, and indeed about the inevitability of aging. While nothing may seem more unavoidable than aging and death—not even taxes—some animals do not seem to age. Many cold-water ocean fish, some amphibians, and the American lobster never reach a fixed size. They continue to grow bigger, reproduce, and live until something—an accident, a predator, or a disease—kills them.

Clearly, though, this is not the case for humans. So why do some scientists think we might be able to overcome the biological cap on aging? Recent research indicates that while our genes may indeed “program” us for a particular life span by affecting how rapidly our cells age, we may be learning enough about how the “program” works to change it.

Calorie restriction and aging

The first suggestion that the process of aging might not be inevitable—or at least that it could be slowed—emerged about 70 years ago. Scientists discovered that when animals are forced to live on 30% to 40% fewer calories than they would normally consume, something unusual happens: they become resistant to most age-related diseases—cancer, heart disease, diabetes, Alzheimer’s disease—and live 30% to 50% longer.

Scientists set out to understand what genes are turned on by calorie restriction because if they could figure that out, they might be able to develop medications that turn those genes on just like calorie restriction does (but without people having to drastically reduce food intake). Over the past 15 years, scientists at MIT and Harvard Medical School identified a family of genes called sirtuins that are responsible for the health benefits of calorie restriction. Then they developed compounds called sirtuin-activating compounds (STACs) that turn on the sirtuin genes. The first STAC is called resveratrol, which is found in red wine. Resveratrol can extend the life span of simple organism like yeast, fruit flies, worms, and fish. In late 2006, resveratrol was shown to extend the life span of mice fed a high-calorie, high-fat diet. Not only did it extend life span in all these animals, but the animals were protected against several diseases of aging and remained physically active and vital until very late in their extended lives.

It’s easy to see why this research is potentially relevant to humans. Like the mice in these studies, many of us are middle-aged mammals who eat a high-calorie, high-fat diet. While research results in mice do not always prove true in humans, they often do. Still, we are a long way from knowing whether human life span can be extended, and the added years made vital and active, by such knowledge of the biology of aging.

Antioxidants

If oxidants damage cells and contribute to cellular aging, it seems logical that increasing levels of antioxidants might help. Several vitamins are antioxidants—particularly vitamins E, C, and beta carotene (a form of vitamin A). Foods rich in those vitamins seemed to be associated with improved health. That led to the attractive theory that supplements of vitamins E and C and beta carotene might as well.  But the evidence so far has been disappointing. At the same time, there are other clues that finding other ways of harnessing the body’s antioxidant systems might prove valuable. For example, there is a genetic mutation in worms that triggers an overabundance of the antioxidant enzymes superoxide dismutase (SOD) and catalase—the result being a doubled lifespan for the worms. These enzymes work in concert to neutralize oxidants and help prevent oxidative damage.

Other researchers found the gene that churned out SOD was more active in a group of longer-lived fruit flies than in flies of average life span. Likewise, fruit flies given extra copies of the SOD gene lived longer.

The Daf genes

A series of genes dubbed Daf—decay accelerating factor—in worms has a counterpart in humans that helps manage insulin levels and a growth factor called IGF-1. When researchers deliberately immobilize certain Daf genes in worms, they can live up to five times longer and continue to be active and capable of reproducing until late in their greatly lengthened lives.

The Indy gene

When researchers introduced any one of five mutations into a single gene dubbed Indy—an acronym inspired by a Monty Python line, “I’m not dead yet”—the flies’ life span nearly doubled. Moreover, the long-lived flies stayed frisky and reproduced far longer. When the mutation was reversed, fly life span returned to normal. This research not only identified another gene of possible importance in aging, it demonstrated that even when engaged in the serious business of discovering and naming new genes, scientists can have a sense of humor.