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.
Smokes two or three cigars a day. Also drinks Manhattans | Those interventions entail sacrifices that most people probably aren’t willing to make. But further research may yield more palatable strategies. In August researchers announced that a compound called resveratrol, found in red wine, mimics calorie deprivation and prolongs the life span of yeast cells by 70 percent. Some scientists doing that work said they had taken to drinking a glass of red wine each day. In the last decade, animal studies also turned up dozens of genes that can extend life span. For example, a single mutation in a roundworm can extend its life 600 percent. The genes involved code for proteins that control basic physiological processes such as energy consumption, growth rate, and cell division. Some of the genes protect critical proteins from damage due to stress. Scientists speculate that mild, chronic stress—like a low-calorie diet or a cold room—may spark these genes into action. |
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.
