then we can perhaps hope to intervene to delay the process of aging (Finch, 1990).
Biological Theories of Aging
The facts about aging and maximum life span have led many biologists to believe that biophysical aging may have a single fundamental cause. In their efforts to find such a single primary process to explain those time-dependent changes that we recognize as biophysical aging, they have developed many different ideas. Biologist Zhores Medvedev (1972) enumerated more than 300 biological theories of aging. At present, no single theory of aging explains all the complex processes that occur in cells and body systems, but ongoing research is under way that is leading to new insights into why we grow old.
Broadly speaking, we can distinguish between two kinds of theories of aging (Finch & Kirkwood, 2000):
Chance. Some theories see aging as the result of external events, such as accumulated random negative factors that damage cells or body systems over time. For example, these factors might be mutation or damage to the organism from wear and tear.
Fate. Some theories see aging as the result of an internal necessity, such as a built-in genetic program that proceeds inevitably to senescence and death.
In either case, the question remains open: Is it possible to intervene to correct damage to the aging body or modify the genetic program? The most likely interventions are those that would make sense depending on which theory best explains the facts about aging (Ludwig, 1991).
Wear-and-Tear Theory
The 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.
Autoimmune Theory
The immune system is the body’s defense against foreign invaders such as bacteria. The immune system protects and preserves the body’s integrity, and it does this by developing antibodies to attack hostile invaders. We know that the immune system begins to decline after adolescence, and the weakening of immune function is linked to age-related vulnerability. According to the autoimmune theory of aging, the system may eventually become defective and no longer distinguish the body’s own tissues from foreign tissues. The body may then begin to attack itself, as suggested by the rising incidence of autoimmune diseases, such as rheumatoid arthritis, with advancing age (Kay & Makinodan, 1981).
Aging-Clock Theory
According to the aging-clock theory of aging, aging is programmed into our bodies like a clock ticking away from the moment of conception. One of the best examples of an aging clock in humans is the menstrual cycle, which begins in adolescence and ends with menopause. The aging-clock theory is part of programmed aging, in which aging is seen as a normal part of a sequence leading from conception through development to senescence and finally to death.
One version of the aging-clock theory emphasizes the roles of the nervous and endocrine systems. This version postulates that aging is timed by a gland, perhaps the hypothalamus, the thymus, or the pituitary gland. Such a gland acts like an orchestra conductor or a pacemaker to regulate the sequence of physiological changes that occur over time. Some support for this idea comes from observations that the hormone dehydroepiandrosterone (DHEA) is found in higher levels among younger people. Experimenters have also discovered that DHEA supplements help laboratory rats live longer.
The aging-clock theory has encouraged research on the role of hormones secreted by the thyroid, pituitary, and thymus glands (Lamberts, van den Beld, & van der Lely, 1997). These include human growth hormone, which can now be manufactured in quantity through genetic engineering. In experiments, volunteers injected with growth hormone lost flabby tissue and grew back muscle, essentially reversing some manifestations of the aging process for a time. Other investigators are interested in hormones produced by the pineal gland, which may help regulate the “biological clock” that keeps time for the body.
Hormones and the endocrine system clearly play a major role in the process of aging. Hormones
