An American born a century ago would have been expected to live, on average, just 54 years. Many children died young, and giving birth was one of the most dangerous things a woman would do. But thanks to vaccinations, antibiotics, sanitation and better maternal care, we are now much more likely to die in old age than in our youth. An infant born today should live to see a 78th birthday.
The easy gains against the grim reaper have been won. Now as people live to ever older ages, they confront two broad sets of forces that conspire to impose the ultimate human limit. First, each extra year we live means another year of accumulated damage to the body's cells and organs—damage that slower cellular-repair systems cannot quite fix. In addition, age is the biggest risk factor for common deadly ailments that researchers have been relatively powerless against, such as cancer, heart disease and Alzheimer's.
Researchers looking to push the limits of human life span are thus asking: Which of these two forces should we bet our research money on? Is it a more effective strategy to attempt to slow the aging process or to fight individual diseases? In other words, do most of us die because we get old—or because we get sick?
On supporting science journalism
If you're enjoying this article, consider supporting our award-winning journalism by subscribing. By purchasing a subscription you are helping to ensure the future of impactful stories about the discoveries and ideas shaping our world today.
Scientists who support the antidisease route argue that a piecemeal approach stands the best chance of pushing life span out past a century. “If we can focus on the major causes of death—cancer, cardiovascular disease—if we can really conquer those diseases and replace parts of the body if they wear out, that is the best possible outcome,” says Sarah Harper, a gerontologist at the Oxford Institute of Population Aging in England. She expects that if we can continue to beat back cancer and heart disease and improve stem cell technologies, such as personalized, laboratory-grown tissues, we could reasonably expect to live relatively healthy lives to 100—perhaps even 120—in the not too distant future.
Extending the active life span by this model requires that we figure out how to fix the body's naturally aging pieces. Scientists have already used stem cells to grow whole tracheae and jawbones. If research continues apace, as Harper and others in the field expect it will, tissues, organs and bones to replace those that fail will soon no longer be science fiction. “The small advances we are making in technology—in genetics, in stem cell research—are the kind of advances that are pushing back life span,” she says.
Other investigators argue that we need to fight the aging process itself. Even if we are able to cure cancer, says S. Jay Olshansky, a researcher at the University of Illinois at Chicago School of Public Health, we will still experience heart problems or Alzheimer's—or at least macular degeneration. Similarly, regenerative medicine would solve problems only one organ at a time. “A new esophagus would be a nice thing to have,” he says, “but that hasn't influenced anything else.”
That state of affairs will not be so if we can retard the aging process at the molecular level, Olshansky says. His approach would not target just one organ or system but the brain and body as a whole. He and his colleagues are launching what he calls “a Manhattan-style Project to slow aging.” They are aiming for an across-the-board healthy life extension of seven years, which, he says, might easily be achieved in the next decade or two. And because the risk of disease doubles every seven years or so, by slowing aging by seven years, Olshansky reasons, we can cut disease risk roughly in half.
He has long held the human body's natural, biological expiration date to be about 85. By that time, our cells have typically suffered an insurmountable amount of oxidative stress—damage stemming from the production of oxygen free radicals that harm DNA, proteins and other important cellular components. Olshansky and his colleagues are studying those rare superlong-lived individuals who make it past 100 or 110 in good physical and mental health. These people, he notes, might already be going through cellular aging at a slower pace, perhaps because their cells can better resist oxidative stress. Locating a genetic link for this slowdown might lead to the development of systemic antiaging therapies.
A “treatment” for aging, beyond the usual healthy diet and exercise advice, might eventually come in the form of a pill. Yet developing something so complex as a compound that might help retard the body's aging process requires serious scientific effort. And that often means starting back at the molecular and mouse levels. The Mprize, which is sponsored by the Methuselah Foundation, awards teams of researchers who break the record for the longest-lived mice. One current candidate compound is rapamycin, which works along the same cellular pathway that calorie restriction does. Both rapamycin and calorie restriction have been shown to extend life span in mice. Like many other proposed panaceas, however, rapamycin is not without drawbacks. The drug suppresses the immune system, making it not terribly desirable for a large-scale rollout anytime soon. And cautionary tales do abound: resveratrol, the “red wine” drug that had previously been the big antiaging hope, has faltered in recent studies. Not everyone in the longevity field is expecting rapamycin to work as well in humans as it appears to work in rodents.
Indeed, life-extension research has long been a pseudoscience backwater, swamped with snake oil and short-lived hopes. Both Olshansky and Harper are wary of claims that we will soon be able to live to 150 and beyond. Ultimately the most successful way to increase life span for the majority of people will likely be an all-of-the-above strategy. We are going to need better disease therapies, advances at the molecular level, regenerative medicine and good old-fashioned healthy living.
Even without any exceptional scientific breakthroughs in longevity and disease research, our plodding scientific progress—not to mention advances in health care and sanitation—continues to extend our life span. Average life expectancy worldwide increases by three months every year. That is not a bad return. Even developed regions such as Europe continue to gain about two years every decade. With luck—and more hard work—those living a century from now will consider our life expectancy pitifully short.