Читать книгу Aging - Harry R. Moody - Страница 72
Wear-and-Tear Theory
ОглавлениеThe wear-and-tear theory of aging sees aging as the result of chance. The human body, like all multicellular organisms, is constantly wearing out and being repaired. Each day, thousands of cells die and are replaced, and damaged cell parts are repaired. Like components of an aging car, parts of the body wear out from repeated use, so the wear-and-tear theory seems plausible.
The wear-and-tear theory is a good explanation for some aspects of aging—for example, the fact that joints in our hips, fingers, and knees tend to become damaged over the course of time. A case in point is the disease of osteoarthritis, in which cartilage in joints disintegrates. Another is cataracts, in which degeneration causes vision loss. Our hearts beat several billion times over a lifetime, so with advancing age, the elasticity of blood vessels gradually weakens, causing normal blood pressure to rise and athletic performance to decline.
The wear-and-tear theory of aging goes back to Aristotle but in its current form was expanded by one of the founding fathers of modern biogerontology, August Weismann (1834–1914). He distinguished between the two types of cells in the body: germ plasm cells, such as the sperm and egg, which are capable of reproducing and are in some sense “immortal,” and somatic cells comprising the rest of the body, which die. Weismann (1889), in his famous address “On the Duration of Life,” argued that aging takes place because somatic cells cannot renew themselves, so living things succumb to the wear and tear of existence.
What we see as aging, then, is the cumulative, statistical result of wear and tear. Consider the case of glassware in a restaurant, which follows a curve similar to that for human populations. Over time, fewer and fewer glasses are left unbroken, until finally all are gone. The life expectancy or survival curve of the glassware follows a linear path over time, but the result for each individual glass comes about because of chance. Nothing decrees in advance that a specific glass will break at a fixed time. Glasses are just inherently breakable, so normal wear and tear in a restaurant will have its inevitable result. Like everyone born in a certain year (e.g., 1880), the “glasses” disappear one by one until none are left.
Some modern biological theories of aging are more sophisticated versions of this original wear-and-tear theory. For example, the somatic mutation theory of aging notes that cells can be damaged by radiation and, as a result, mutate or experience genetic changes (Szilard, 1959). The somatic mutation hypothesis would seem to predict higher cancer rates with age, yet survivors of the atomic bomb at Hiroshima showed higher rates of cancer but no acceleration of the aging process.
Even without actual mutation, over time, cells might lose their ability to function as a consequence of dynamic changes in DNA. According to the so-called error accumulation theory of aging, or error catastrophe theory, decremental changes of senescence are essentially the result of chance or random changes that degrade the genetic code (Medvedev, 1972). The process is similar to what would happen if we were to use a photocopy to make another copy. Over time, small errors accumulate. The errors eventually make the copies unreadable. Similarly, the error catastrophe theory suggests that damaged proteins eventually bring on what we know as aging through dysfunction in enzyme production.
The accumulative waste theory of aging points to the buildup in the cells of waste products and other harmful substances. The accumulation of waste products eventually interferes with cell metabolism and leads to death. Although waste products do accumulate, there is little evidence of harm to the organism. The key to longevity may be the extent to which cells retain the capacity to repair damage done to DNA. In fact, DNA repair capacity is correlated with the metabolic rate and life span of different species. Some studies suggest that DNA damage in excess of repair capacity may be linked to age-related diseases such as cancer.