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programmed. Proponents of this view point out that animals of similar species and exposure to wear and tear have markedly different life spans. The Canada goose has a longevity of 23.5 years; the emperor goose only 6.3 years. Perhaps animals are like plants, with lives that are, to a large extent, internally governed. Certain species of bamboo, for instance, form a dense stand that grows and flourishes for a hundred years, flowers all at once, and then dies.
    The idea that living things shut down instead of wearing down has received substantial support in recent years. Researchers working with the now famous worm
C. elegans
(twice in one decade, Nobel Prizes went to scientists doing work on the little nematode) were able, by altering a single gene, to produce worms that live more than twice as long and age more slowly. Scientists have since come up with single-gene alterations that increase the life spans of fruit flies, mice, and yeast.
    These findings notwithstanding, the preponderance of the evidence is against the idea that our life spans are programmed into us. Remember that for most of our hundred-thousand-year existence—all but the past couple of hundred years—theaverage life span of human beings has been thirty years or less. (Research suggests that subjects of the Roman Empire had an average life expectancy of twenty-eight years.) The natural course was to die before old age. Indeed, for most of history, death was a risk at every age of life and had no obvious connection with aging, at all.As Montaigne wrote, observing late-sixteenth-century life, “To die of age is a rare, singular, and extraordinary death, and so much less natural than others: it is the last and extremest kind of dying.” So today, with our average life span in much of the world climbing past eighty years, we are alreadyoddities living well beyond our appointed time. When we study aging what we are trying to understand is not so much a natural process as an unnatural one.
    It turns out thatinheritance has surprisingly little influence on longevity. James Vaupel, of the Max Planck Institute for Demographic Research, in Rostock, Germany, notes that only 3 percent of how long you’ll live, compared with the average, is explained by your parents’ longevity; by contrast, up to 90 percent of how tall you are is explained by your parents’ height. Even genetically identical twins vary widely in life span: the typical gap is more than fifteen years.
    If our genes explain less than we imagined, the classical wear-and-tear model may explain more than we knew. Leonid Gavrilov, a researcher at the University of Chicago, argues that human beings fail the way all complex systems fail: randomly and gradually. As engineers have long recognized, simple devices typically do not age. They function reliably until a critical component fails, and the whole thing dies in an instant. A windup toy, for example, works smoothly until a gear rusts or a spring breaks, and then it doesn’t work at all. But complex systems—power plants, say—have to survive and function despite having thousands of critical, potentially fragile components. Engineers therefore design these machines with multiple layers of redundancy: with backup systems, and backup systems for the backup systems. The backups may not be as efficient as the first-line components, but they allow the machine to keep going even as damage accumulates. Gavrilov argues that, within the parameters established by our genes, that’s exactly how human beings appear to work. We have an extra kidney, an extra lung, an extra gonad, extra teeth. The DNA in our cells is frequently damaged under routine conditions, but our cells have a number of DNArepair systems. If a key gene is permanently damaged, there are usually extra copies of the gene nearby. And, if the entire cell dies, other cells can fill in.
    Nonetheless, as the defects in a complex system increase, the time comes when just one more defect is enough to