Statistics might well be misleading when it comes to predicting trends in aging, so another kind of analysis seems in order. What’s needed is a model that describes how and why age kills us—a model that explains what it means to die of “natural causes.” So far, that model doesn’t exist. Biomedical research has produced vast stores of knowledge about the diseases of old age, but scientists still don’t understand why our bodies begin to deteriorate when we reach our thirties. It’s not even clear that aging, as a process, can be separated from its pathologies.

“Opinions go from nothing ever dies from old age to everything dies from old age,” says Austad. “We don’t really know very well why people age to death.”

Most researchers agree that the biggest boost in human life expectancy will not come from curing diseases. Instead, the rate of aging itself has to be slowed down. Richard Miller, a biogerontologist at the University of Michigan, says Olshansky’s research shows that the average 50-year-old woman would live to be 95 if cancer, heart disease, stroke, and diabetes were curable. But studies with rodents, Miller says, indicate that if her aging could be retarded, she’d live to be 115. Most important, those extra years would be lived in good health.

There is tantalizing evidence from laboratory studies that aging can be slowed. Experiments with mice, fruit flies, yeast cells, and tiny worms called nematodes, or roundworms, have pointed to environmental modifications that can extend life span dramatically. Mice fed an austere low-calorie diet, for example, will live up to 40 percent longer. Fruit flies kept in refrigerators can live six times as long as unrefrigerated flies. Cats, dogs, and even humans live years longer than average when they are castrated. And the bonus years seem to be truly golden: Methuselan mice are strong, healthy, and alert.

Nonetheless, not a single life-extending gene has been found in the human genome yet. “We know a lot about genes that make humans live shorter lives,” says Austad. “But we don’t know any genes that make humans live to extreme old age.”

Given Olshansky’s confidence that humans won’t live to be 150, it may be surprising to learn that he thinks there’s no predetermined biological limit to the human life span. He agrees with Austad and other researchers that there aren’t any physiological determinants of mortality: no molecular switch that gets thrown, no ticking chromosomal clock that says your time is up, no somatic schedule for checkout. There are no death genes that terminate life the way that countless other genes orchestrate growth, metabolism, and reproduction.

And nature supplies ample evidence that the rate of aging is flexible rather than predetermined. The evidence comes from comparisons between species. A fruit fly lives three weeks, a mouse three years, a quahog clam 200 years, and a bristlecone pine 4,000 years. In each of these species, the same cellular processes are at work.

“To me,” says Austad, “the interesting thing has always been, why does [life span] differ so much in different species?” A number of theories have addressed that question. One notion, the influential rate-of-living theory first advanced about 100 years ago, is that the speed of an animal’s metabolism limits its life span. Hence, cold-blooded animals like turtles live longer than warm-blooded ones like hares, and fast-living creatures die young. Body size also seems to have something to do with it. Larger animals have slower metabolisms and tend to have longer lives than small animals.

The rate-of-living model gives rise to some seductively simple ideas. It suggests, for example, that all species of mammal have the same number of heartbeats in a lifetime. And it was buttressed by evidence that the normal metabolic consumption of energy generates reactive molecules called free radicals that damage DNA, enzymes, and cell membranes. The damage accumulates over time and results in an organism’s increased susceptibility to cancer, or its inability to repair clogged arteries, or a slide into senility. The free-radical model is now a leading theory of aging, and it fits neatly with the rate-of-living theory of life span: The faster the metabolism, the faster free radicals do their damage.

But the rate-of-living theory succumbed to the weight of exceptions. Birds, for example, have metabolisms twice as fast as those of mammals, yet they can live much longer. Parrots can outlive elephants; hummingbirds have been known to survive to 14—the equivalent, in terms of energy consumption per pound, of a human living to 500. A species of North American bat half as big as a mouse can live 30 years in the wild. Opossums, on the other hand, rarely last more than two years, even in captivity. Yet they are the size of house cats and cannot by any measure be accused of living fast.

There is one more glaring exception: Humans live four times longer than they should based on their size and metabolic rate.

A new perspective on mortality came in the 1950s from distinguished British immunologist Sir Peter Medawar. Inspired by evolutionary theory, Medawar pointed out that death and disease are staved off by natural selection, which impels all living things to survive long enough to reproduce. Natural selection favors any trait, genetic or otherwise, that helps an organism live to reproductive age: mechanisms for DNA repair, robust immune systems, good eyesight, strong bones, quick thinking. The downside, of course, is that natural selection doesn’t promote an individual’s survival past reproductive age. In people there’s no evolutionary advantage to fending off cancer, heart disease, stroke, arthritis, cataracts, Alzheimer’s, and other banes of the aged, because these conditions usually show up long after genes have been passed on to the next generation.

Experiments with fruit flies published in the 1980s proved there was a causal connection between the timing of reproduction and the evolution of life span. By culling and fertilizing eggs from only older females for many generations, Michael Rose of the University of California at Irvine managed to double his flies’ life span. If an environment allows or requires fecundity late in life, then life gets longer. Austad speculates that a similar experiment performed on humans would produce a measurable increase in life expectancy in 10 generations, or about 250 years.

Although people would never tolerate Rose’s draconian methods, women in some developed countries are voluntarily delaying the age at which they start having children. “[Rose’s] experiment might be going on right now,” says gerontologist George M. Martin of the University of Washington in Seattle, “though we won’t see the results for hundreds of years.” The evolutionary theory of longevity “clearly predicts plasticity,” he says. “Given the right conditions, nature can evolve longer and longer life spans.”

Austad got a hint of what the right conditions might be 20 years ago. During a stay at a field station in Venezuela, he had his first exposure to the accelerated aging of the opossum. He trapped healthy 18-month-old opossums, then trapped them again just a few months later, and found them lame, half blind, balding, and full of parasites. Austad decided that opossums age and breed relatively quickly because they are easy targets for predators.

“Because they are slow moving and not terribly well armed with claws, teeth, brains, or agility, opossums will be killed by nearly every type of predator—owls, coyotes, wolves, feral dogs, cougars, bobcats. . . . ” Austad wrote in his 1997 book Why We Age. “If a predator is likely to kill you in the next few weeks or months, it makes little sense to waste resources on a long-lasting, effective immune system or an array of free-radical defenses. It is better evolutionarily to reproduce copiously, and the sooner the better.”

To test his theory, Austad located a group of opossums that had been isolated for thousands of years on an island off the coast of Georgia. The island had almost no natural opossum predators. He found that the animals’ reproductive systems aged more slowly than their mainland relations’ did: More than half enjoyed a second breeding season, a luxury for opossums. Brood sizes were smaller, too, in accordance with the quality versus quantity hypothesis. And sure enough, the average life expectancy was about 25 percent greater, while maximum life span—the longest any individual lived—was 50 percent longer.

And people? Austad ascribes our anomalous longevity to the low-risk environment we have created for ourselves. Human beings live twice as long as captive chimpanzees, he notes, despite the fact that the two species share 99 percent of their genes: “I think the key has been our social system—our mutual means of support and our ability to manipulate the environment.” Because one of the abiding aims of civilization is to make life safer for people, Austad says, the trend toward a longer life span will continue, and the luxury of long life, afforded by a civilized lifestyle, will eventually become encrypted in our DNA. Nurture becomes nature; culture dictates biological destiny.

“Evolution has definitely modified life span—it’s happening even as we speak,” says Judith Campisi, a molecular biologist at the Buck Institute for Age Research in Novato, California. “We’re already living 50 years beyond the natural life span determined by the environment in which we evolved.”

Therefore, Austad, unlike Olshansky, is unwilling to put a cap on the possible increase in life span that humans can achieve. “We can expect that within the next 20 to 30 generations, evolution will slow human aging considerably, by about 25 percent,” Austad says. That’s quick enough to demonstrate the flexibility of life span, but too slow to guarantee his heirs will beat out Olshansky’s. “I’m not counting on evolution to help out with the bet,” he admits.

So what is he counting on? Austad reasons that medical science can figure out ways to slow aging without waiting on generations of natural selection. The free-radical theory of aging offers helpful hints. Most of the nasty molecules produced by routine energy consumption in the body are oxidants. In 1998 Austad, his colleague Donna Holmes, an evolutionary gerontologist at the University of Idaho, and Martin demonstrated that bird cells suffer less oxidative damage than the cells of mice when exposed to free-radical stressors. Either birds have enzymes that combat oxidation better than mammalian enzymes do, or they produce fewer oxygen radicals. Until our physiology catches up, humans may be able to soften free-radical damage with antioxidants—compounds such as vitamin E that are found in foods and supplements.

Geriatrician Tom Perls of the Boston University School of Medicine runs the world’s largest ongoing study of people who are at least 100 years old, with more than 750 participants. His research has convinced him that, with proper care, the contemporary human’s genetic endowment will support a healthy life into the mid to late eighties. Centenarians, in contrast, seem to have congenital advantages. Perls calls them “genetic booster rockets.” He suspects that centenarians lack genes that predispose them to geriatric diseases and possess genes—as yet unidentified—that protect them from the ravages of time.

“We have a small number of people, particularly guys, who do everything short of throwing an atomic bomb at their bodies and still live to 100,” Perls says. Many members of his group ignore dietary guidelines and refuse to exercise; some have been smoking three packs a day for 50 years. “They have genes that allow them to get away with things that aren’t very good for them. We’d like to understand what’s going on.”

Perls says chance also plays a role in determining life span. Chance chooses the genes in which random mutations show up; chance takes the fatal step in front of the crosstown bus. And the longer you live, the more opportunity for misfortune. “It’s not just nature-nurture,” Martin agrees. “It’s nature, nurture, and luck. There is a lot of luck in being a centenarian.”

Thus Olshansky and other scientists like him say that while there may be no biological limits to the human life span, there are practical ones. In addition to luck, these include the amount of money society is willing to invest in antiaging research and the amount of time and effort that individuals are willing to spend on treatments that result from the research. Olshansky says that plenty of cheap, simple life-extending measures are already being ignored by a significant percentage of the general public. People still smoke, and most don’t exercise. In fact, Olshansky says, the threats posed by obesity and emerging infectious diseases such as AIDS are largely responsible for his pessimism about 150-year life spans.

“Technically, anything is possible,” he says. “But in the real world, we’re just getting fatter.”