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—the average 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 already
oddities 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 that inheritance 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 DNA repair 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
impair the whole, resulting in the condition known as
frailty. It happens to power plants, cars, and large
organizations. And it happens to us: eventually, one too
many joints are damaged, one too many arteries calcify.
There are no more backups. We wear down until we can’t
wear down anymore.
It happens in a bewildering array of ways. Hair grows
gray, for instance, simply because we run out of the
pigment cells that give hair its color. The natural life
cycle of the scalp’s pigment cells is just a few years. We
rely on stem cells under the surface to migrate in and
replace them. Gradually, however, the stem-cell reservoir
is used up. By the age of fifty, as a result, half of the
average person’s hairs have gone gray.
Inside skin cells, the mechanisms that clear out waste
products slowly break down and the residue coalesces
into a clot of gooey yellow-brown pigment known as
lipofuscin. These are the age spots we see in skin. When
lipofuscin accumulates in sweat glands, the sweat glands
cannot function, which helps explain why we become so
susceptible to heat stroke and heat exhaustion in old age.
The eyes go for different reasons. The lens is made of
crystallin proteins that are tremendously durable, but they
change chemically in ways that diminish their elasticity
over time—hence the farsightedness that most people
develop beginning in their fourth decade. The process
also gradually yellows the lens. Even without cataracts
(the whitish clouding of the lens that occurs with age,
excessive ultraviolet exposure, high cholesterol, diabetes,
and cigarette smoking), the amount of light reaching the
retina of a healthy sixty-year-old is one-third that of a
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