For example, according to the “free radical” hypothesis of aging, we get older because of constant cellular damage caused by reactive oxygen compounds that are a natural product of metabolism. Inflammation can partly explain how this might work. Macrophages, as part of the inflammatory response, produce reactive oxygen species in order to attack bacteria. Oxidative stress and inflammation clearly egg each other on, and calming one can inhibit the other.
To take another prominent example, a low-calorie diet is known to increase the life spans of creatures ranging from flatworms to rats, but no one knows why, or whether it will help humans live longer. Inflammation provides a clue: Dietary restriction sharply inhibits the inflammatory response, and that may be part of why it promotes longevity at the same time that it reduces insulin resistance and slows dementia. Yet another widely discussed theory of why we age blames the shortening of telomeres, chromosomal structures that, in most cells, dwindle with each division and may ultimately limit the number of times any cell can divide. It is possible that inflammation could play a role here, too, because it prompts the faster turnover of cells in the immune system and other tissues.
Still, nobody thinks that there is a single root cause of aging—different species may age in different ways, and multiple mechanisms are probably at work. “I think it would be a mistake to suggest that inflammation is the cause of aging, or that all theories of aging must be tied to it,” Cohen says. Then again it may not ultimately matter whether inflammation is the most significant cause of our decay. More important is that inflammation offers an unparalleled opportunity to do something about it.
Some ways to reduce inflammation are elementary. It is impossible to know exactly what is going on in Jim Hammond’s body, but all the aspects of his regimen—healthy food, exercise, and a good attitude—reduce systemic inflammation. Those of us without his tenacity can turn to drug companies, which are exploring new anti-inflammatory drugs like flavonoids. Researchers are also looking at new uses for old drugs—trying to prevent Alzheimer’s using ibuprofen, for example. “The research is really to prevent the chronic debilitating diseases of aging,” says Nir Barzilai, a molecular geneticist and director of the Institute for Aging Research at the Albert Einstein College of Medicine in New York. “But if I develop a drug, it will have a side effect, which is that you will live longer.”
Some of this research stretches the boundaries of what we know. Rudi Westendorp, head of the department of gerontology and geriatrics at the Leiden University Medical Center, is trying to treat old-age depression with drugs that are currently used for autoimmune conditions like rheumatoid arthritis. Harvard University researchers are considering a vaccine against atherosclerosis, which may provoke a reaction that suppresses inflammation.
The caveat with these experiments is that by modifying inflammation, we are playing with fire. After all, fighting off infection is an absolutely essential bodily function. “The danger of monkeying around in a system like that is that you may do more harm than good,” Cohen says. But humans appear willing to renegotiate the ancient evolutionary bargain that traded robust reproductive health for frail old age.
Think of Jim Hammond if you have any doubts. In his blog, he describes running the 800-meter race in the 2007 National Senior Olympics games. “I won in a photo finish, and I broke the national record,” he wrote. The crowd went nuts. At the age of 93, Hammond had the most exhilarating experience of his entire life.
