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Aging, inflammation & the body electric.

Publication: Daedalus
Publication Date: 01-JAN-06
Format: Online
Delivery: Immediate Online Access

Article Excerpt
In a famous photograph of Walt Whitman taken in the 1860s (see inside back cover), the great American bard looks wizened--his hair white, his face weathered. He looks, in short, like an old man. In fact, he was only in his forties.

During the Civil War, Whitman spent hours each day in to...

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...hospital wards attending desperately sick soldiers, which exposed him to dysenteries and horribly infected wounds. As a result, a bad infection in one hand climbed up into his shoulder, and he became beset by chronic headaches and fevers.

One hundred and fifty years after Whitman sang "the body electric," we can find in Whitman's fate some clues to the nature of aging. For much of his adult life, he complained of chronic headaches, fevers, and weakness. At the age of 55, he suffered a stroke that paralyzed his left side. Other strokes followed, though without noticeably impairing his memory. Whitman eventually lived to the age of 72, exceeding his generation's life expectancy by about thirty years. Yet shortly before his death, one of his doctors noted, "His apparent age was greater than his real years."

A postmortem by experts in gross morbid anatomy showed that Whitman had long suffered from both meningitis and tuberculosis. Tuberculous meningitis may have contributed to his strokes and would have been consistent with his other reported ailments. Both infections inflame arteries at the base of the brain, which, in turn, increases the risk of infarcts and strokes that selectively damage deep brain centers in a 'TB zone,' but usually spare higher cognitive functions. Although tuberculous meningitis is a rare disease, the 'Whitman case' points us to more general principles in aging.

Inflammation is increasingly recognized as fundamental to aging. As modern medicine has brought infectious diseases like tuberculosis and meningitis under control, successive generations have had to carry less of the inflammatory burden of such diseases--which may help account for recent improvements in human longevity. Changes of the inflammatory burden may also anticipate limits ahead. Aging, of course, is an immensely complex process governed by multiple gene-environment interactions. No single factor governs aging--biogerontology is a graveyard of single-cause hypotheses.

In the past century and a half, human life spans have increased remarkably, with one year added to the life span for every three to four years of calendar time. Before the Industrial Revolution, the average life span was about thirty-five to forty years. Even if one survived the hazards of childhood to reach maturity, the remaining life span was still shorter than today's. Currently, life expectancy in most developed countries has doubled to about eighty years and continues to climb. The result is a major shift in population age structure, from broad-based pyramids with younger groups in the majority, to skyscraper-shaped structures, which are arising everywhere because of the steadily growing rates of survival at younger ages and survival to increasingly older ages. In fact, centenarians are the fastest expanding age group. Sitting on the topmast is Jean Calment (1875-1997) who tested cognitively normal at 119. Her 122-year longevity may yet be superseded.

The decline in childhood mortality rates is yet another remarkable change that has occurred in recent generations. Not so long ago, infant and childhood mortality rates were very high almost everywhere; rates of 30 percent were very common in Europe and North America until the Industrial Revolution, when early-age mortality began to decrease. This is significant because childhood mortality trends are the strongest predictors of later mortality. In following birth cohorts over their life spans, Eileen Crimmins and I discovered that the survivors in birth cohorts with high early-age mortality rates showed much higher mortality rates at all later ages than survivors in birth cohorts with lower early-age mortality rates. (1) Evidence from Sweden, which has kept remarkably complete records of mortality since 1750, makes a very strong case for this.

We hypothesized that this outcome was the result of chronic infections and inflammations accelerating aging processes. For example, rheumatic fever, the result of streptococcus infections, killed many children in the 'bad old days' before antibiotics. But the disease continued to affect even its survivors, who rarely lived beyond middle age, because the bacterial colonization of the...

NOTE: All illustrations and photos have been removed from this article.



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