Jim Hammond is an elite athlete. He works out two hours a day with a trainer, pushing himself through sprints, runs, and strength-building exercises. His resting heart rate is below 50. He’s won three gold medals and one silver in amateur competitions this year alone, running races from 100 to 800 meters. In his division, he’s broken four national racing records. But perhaps the most elite thing about Hammond is his age.
He is 93. And really, there’s nothing much wrong with him, aside from the fact that he doesn’t see very well. He takes no drugs and has no complaints, although his hair long ago turned white and his skin is no longer taut.
His secret? He doesn’t have one. Hammond never took exceptional measures during his long life to preserve his health. He did not exercise regularly until his fifties and didn’t get serious about it until his eighties, when he began training for the Georgia Golden Olympics. “I love nothing better than winning,” he says. “It’s been a wonderful thing for me.” Hammond is aging, certainly, but somehow he isn’t getting old—at least, not in the way we usually think about it.
They say aging is one of the only certain things in life. But it turns out they were wrong. In recent years, gerontologists have overturned much of the conventional wisdom about getting old. Aging is not the simple result of the passage of time. According to a provocative new view, it is actually something our own bodies create, a side effect of the essential inflammatory system that protects us against infectious disease. As we fight off invaders, we inflict massive collateral damage on ourselves, poisoning our own organs and breaking down our own tissues. We are our own worst enemy.
This paradox is transforming the way we understand aging. It is also changing our understanding of what diseases are and where they come from. Inflammation seems to underlie not just senescence but all the chronic illnesses that often come along with it: diabetes, atherosclerosis, Alzheimer’s, heart attack. “Inflammatory factors predict virtually all bad outcomes in humans,” says Russell Tracy, a professor of pathology and biochemistry at the University of Vermont College of Medicine, whose pioneering research helped demonstrate the role of inflammation in heart disease. “It predicts having heart attacks, having heart failure, becoming diabetic; predicts becoming fragile in old age; predicts cognitive function decline, even cancer to a certain extent.”
The idea that chronic diseases might be caused by persistent inflammation has been kicking around since the 19th century. Only in the past few years, though, have modern biochemistry and the emerging field of systems biology made it possible to grasp the convoluted chemical interactions involved in bodywide responses like inflammation. Over a lifetime, this essential set of defensive mechanisms runs out of bounds and gradually damages organs throughout the body.
When you start to think about aging as a consequence of inflammation, as Tracy and many prominent gerontologists now do, you start to see old age in a different, much more hopeful light. If decrepitude is driven by an overactive immune system, then it is treatable. And if many chronic diseases share this underlying cause, they might all be remedied in a similar way. The right anti-inflammatory drug could be a panacea, treating diabetes, dementia, heart disease, and even cancer. Such a wonder drug might allow us to live longer, but more to the point, it would almost surely allow us to live better, increasing the odds that we could all spend our old age feeling like Jim Hammond: healthy, vibrant, and vital. And unlike science fiction visions of an immortality pill, a successful anti-inflammatory treatment could actually happen within our lifetime.
For the last century and a half, the average life span in wealthy countries has increased steadily, climbing from about 45 to more than 80 years. There is no good reason to think this increase will suddenly stop. But longer life today often simply means taking longer to die—slowly, expensively, and with more disease and disability. “If you talk to many old people, what they are really desperate about is not the fact that they’re going to die but that they are going to be sick, dependent, have to rely on others,” says Luigi Ferrucci, chief of the longitudinal studies section at the National Institute on Aging and director of the Baltimore Longitudinal Study of Aging, the nation’s longest-running study of old age.
Biologists have known for a while that inflammation increases with age, but until recently, given everything else that slumps, spikes, or goes off the rails as we get old, it didn’t seem especially important. Some researchers on aging still think that way.
But a big clue linking inflammation with aging came in the late 1990s, when Tracy and his colleagues showed that C-reactive protein (CRP), an inflammatory protein, is an amazingly accurate predictor of a future heart attack—as good as or better than high blood pressure or high cholesterol. At least in heart disease, inflammation isn’t just a bystander. What’s more, we could do something to decrease it. Aspirin, which was already known to help people with heart disease, seems to work primarily by reducing inflammation.
So why should our own immune system rely on such an apparently dangerous mechanism? The answer lies in the fact that infectious disease has historically been the number one killer of human beings, and responding to this threat has profoundly shaped our biology. Possessing a fierce and ferocious immune response primed to keep us alive long enough to reproduce was an evolutionary no-brainer.
