Aging isn’t cumulative process of progressive chemical damage — it can stop

In 1939, British statisticians Major Greenwood and J.O. Irwin published a little-noticed article in the journal Human Biology that contained a profoundly unexpected discovery. Greenwood and Irwin were studying mortality figures for women 93 and older. They expected to see the death rate rising with age, as it does throughout adult life. But they did not. Instead, between age 93 and 100, the acceleration in death rates came to a screeching stop. Little old ladies who were 99 were no more likely to die than those who were 93.

The authors were dismayed. “At first sight this must seem a preposterous speculation,” they wrote. After all, like every other respectable biologist of the time, they assumed that “decay must surely continue.”

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But what if it doesn’t? What if aging stops? And if it stops very late in our lives, is there any way we can make it stop earlier, when we are in better health?

Dropping like flies

The fact of aging has been well known to biology and medicine from their earliest days. Aristotle wroteon the topic more than 2,300 years ago. Like pretty much every biologist since then, he thought of aging as a remorseless process of falling apart, until death finally puts us out of our misery.

Present molecular and cell theories of aging assume that aging is a physiological process involving some type of cumulative damage, disrepair or disharmony. The theories differ only over which kind of cumulative breakdown happens. Evolutionary biologists such as myself who work on aging likewise used to think that we were studying how natural selection might allow the cumulative damage to happen.

All that started to change in 1992, when the labs of Jim Carey at the University of California at Davis and Jim Curtsinger at the University of Minnesota independently published landmark articles in the journal Science.

Carey and Curtsinger studied not humans but those stalwarts of the lab, flies — hundreds of thousands of them. They kept groups of thousands of flies of the same age in carefully controlled conditions and meticulously recorded the death of every fly until the whole group was dead.

Amazingly, they found the same thing as Greenwood and Irwin. At first, the mortality rate increased exponentially. But after a few weeks, death rates stopped rising. Some of Carey’s results were breathtaking: Once death rates leveled off, there were months of stable or even declining death rates. It looked as if a relatively brief period of aging was followed by a long plateau when aging stopped. This time, everybody noticed.

Soon, other biologists were looking for signs of life after aging. To our collective astonishment, they were found in every laboratory experiment of sufficient size, whether flies, nematode worms or beetles. Admittedly, there aren’t many studies that have used large-enough cohorts to see the effect, and nobody has studied it in mice or other mammals. But that merely showed why we hadn’t noticed it before: Almost no one had thought to keep large enough cohorts to measure death rates at later ages accurately. Once we started doing experiments on the right scale, it was obvious that what Greenwood and Irwin found in their old ladies was generally true: Look late enough in the aging process and it seems to stop.