‘There is no individual thing in nature, than which there is not another more powerful and strong. Whatsoever thing be given, there is something stronger whereby it can be destroyed.’ –Spinoza
Is Aging a Disease?
One argument against treating aging is that it is not a disease. To an extent, this view stems from the fact that the word aging refers to different things. One is the experience of the passage of time. Another is the acquisition of experience and wisdom that can come from living long. To avoid confusion with these benign aspects, biologists use the term “senescence” for the increasing frailty and risk of disease and death that come with aging. Put more precisely, then, the question at hand is this: Is human senescence a disease?
One approach to defining illness has been to compare a given condition to good health. Is someone’s condition typical of a person of a given gender or age? For instance, the possession of ovaries is healthy for a woman, but not a man. Likewise, one might consider muscle wasting to indicate serious disease in a 20-year-old, but not a 90-year-old. Given that everyone who lives long enough will eventually experience senescence, I can appreciate the view that it is a normal condition and therefore not pathological. Still, from my perspective as someone working on the biological basis of aging, it is hard not to see it as a disease.
Senescence is a process involving dysfunction and deterioration at the molecular, cellular and physiological levels. This endemic malfunction causes diseases of aging. Even if one ages well, escaping the ravages of cancer or type II diabetes, one still dies in the end, and one dies of something. Moreover, in evolutionary terms, aging appears to serve no real purpose, meaning it does not contribute to evolutionary fitness. Why, then, has aging evolved?
The main theory dates back to the 1930s and was developed by J. B. S. Haldane and, later, Peter Medawar—both of University College London—and by the American biologist George C. Williams of the State University of New York, Stony Brook. It argues that aging reflects the decline in the force of natural selection against mutations that exert harmful effects late in life. An inherited mutation causing severe pathology in childhood will reduce the chances of reproduction and so disappear from the population. By contrast, another mutation with similar effects—but which surfaces after a person’s reproductive years—is more likely to persist. Natural selection can even favor mutations that enhance fitness early in life but reduce late-life health. This is because the early-life effects of genes have much stronger effects on fitness. Consequently, populations accumulate mutations that exert harmful effects in late life, and the sum of these effects is aging. Here evolutionary biology delivers a grim message about the human condition: Aging is essentially a multifactor genetic disease. It differs from other genetic diseases only in that we all inherit it. This universality does not mean that aging is not a disease. Instead, it is a special sort of disease.
photo { Noritoshi Hirakawa }
