Aging takes place in a cell, an organ, or the total organism with the passage of time. It is a process that goes on over the entire adult life span of any living thing. Gerontology, the study of the aging process, is devoted to the understanding and control of all factors contributing to the finitude of individual life. It is not concerned exclusively with debility, which looms so large in human experience, but deals with a much wider range of phenomena. Every species has a life history in which the individual life span has an appropriate relationship to the reproductive life span and to the mechanism of reproduction and the course of development. How these relationships evolved is as germane to gerontology as it is to evolutionary biology. It is also important to distinguish between the purely physicochemical processes of aging and the accidental organismic processes of disease and injury that lead to death.
Gerontology, therefore, can be defined as the science of the finitude of life as expressed in the three aspects of longevity, aging, and death, examined in both evolutionary and individual (ontogenetic) perspective. Longevity is the span of life of an organism. Aging is the sequential or progressive change in an organism that leads to an increased risk of debility, disease, and death; senescence consists of these manifestations of the aging process.
Genetic theories
One theory of aging assumes that the life span of a cell or organism is genetically determined—that the genes of an animal contain a “program” that determines its life span just as eye colour is determined genetically. Although long life is recognized often as a familial characteristic, and short-lived strains of fruit flies, rats, and mice can be produced by selective breeding, other factors clearly can significantly alter the basic genetic program of aging.
Non-genetic theories
Other theories of aging focus attention on factors that can influence the expression of a genetically determined “program.” One of these is the “wear-and-tear” theory, which assumes that animals and cells, like machines, simply wear out. Animals, however, unlike machines, have some ability to repair themselves, so that this theory does not fit the facts of a biological system. A corollary to the wear-and-tear theory is the presumption that waste products accumulate within cells and interfere with function. The accumulation of highly insoluble particles, known as “age pigments,” has been observed in muscle cells in the heart and nerve cells of both human beings and other animals.
With increasing age, tendons, skin, and even blood vessels lose elasticity. This is due to the formation of cross-links between or within the molecules of collagen (a fibrous protein) that give elasticity to these tissues. The “cross-linking” theory of aging assumes that similar cross-links form in other biologically important molecules, such as enzymes. These cross-links could alter the structure and shape of the enzyme molecules so that they are unable to carry out their functions in the cell.
Another theory of aging assumes that immune reactions, normally directed against disease-producing organisms as well as foreign proteins or tissue, begin to attack cells of the individual's own body. In other words, the system that produces antibodies loses its ability to distinguish between “self” and foreign proteins. This “autoimmune” theory of aging is based on clinical rather than on experimental evidence.
These theories all attempt to explain aging in terms of cellular and molecular changes. Actually, age changes are much more marked in the overall performance of an individual than in cellular processes that can be measured. The age decrement in the ability to perform muscular work is much greater than any changes that can be detected in the enzyme activities of the muscles that perform the work. It is possible that aging in an individual is actually due to a breakdown in the control mechanisms that are required in a complex performance.
Reproduction is an all-important function of an organism's life history, and all other vital processes, including senescence and death, are shaped to serve it. The distinction between semelparous and iteroparous modes of reproduction is important for an understanding of biological aging. Semelparous organisms reproduce by a single reproductive act. Annual and biennial plants are semelparous, as are many insects and a few vertebrates, notably salmon and eels. Iteroparous organisms, on the other hand, reproduce recurrently over a reproductive span that usually covers a major part of the total life span.
In semelparous forms, reproduction takes place near the end of the life span, after which there ensues a rapid senescence that quickly leads to the death of the organism. In plants the senescent phase is usually an integral part of the reproductive process and essential for its completion. The dispersal of seeds, for example, is accomplished by processes—including ripening and fall (abscission) of fruits and drying of seed pods—that are inseparable from the overall senescence process. Moreover, the onset of plant senescence is invariably initiated by the changing levels of hormones, which are under systemic or environmental control. If, for example, the hormone auxin is prevented, by experimental means, from influencing the plant, the plant lives longer than normal and undergoes an atypical prolonged pattern of senescent change.
Useful inferences can be drawn from the study of the aging processes of insects that display two distinct kinds of adaptive coloration: the procryptic, in which the patterns and colours afford the insect concealment in its native habitat; and the aposematic, in which the vivid markings serve as a warning that the insect is poisonous or bad tasting. The two adaptation patterns have different optimal species survival strategies: the procryptics die out as quickly as possible after completing reproduction, thus reducing the opportunity for predators to learn how to detect them; the aposematics have longer post-reproductive survival, thus increasing their opportunity to condition predators. Both adaptations are found in the family of saturniid moths, and it has been shown that the duration of their post-reproductive survival is governed by an enzyme system that controls the fraction of time spent in flight: procryptics fly more, exhaust themselves, and die quickly; aposematics fly less, conserve their energies, and live longer.
These examples indicate that in semelparous forms, in which full vigour and function are required until virtually the end of life, senescence has an onset closely coupled with the completion of the reproductive process and is governed by relatively simple enzymatic mechanisms that can be modified by natural selection. Such specific, genetically controlled senescence processes are instances of programmed life termination.
The iteroparous forms include most vertebrates, most of the longer-lived insects, crustaceans and spiders, cephalopod and gastropod mollusks, and perennial plants. In contrast to semelparous forms, iteroparous organisms need not survive to the end of their reproductive phase in order to reproduce successfully, and the average fraction of the reproductive span survived varies widely between groups: small rodents and birds in the wild survive on the average only 10 percent to 20 percent of their potential reproductive lifetimes; whales, elephants, apes, and other large mammals in the wild, on the other hand, live through 50 percent or more of their reproductive spans, and a few survive beyond reproductive age. In iteroparous forms the onset of senescence is gradual, with no evidence of specific systemic or environmental initiating mechanisms; senescence manifests itself early as a decline in reproductive performance. In species that grow to a fixed body size, decline of reproductive capacity begins quite early and accelerates with increasing age. In large egg-laying reptiles, which attain sexual maturity while relatively small in size and continue to grow during a long reproductive span, the number of eggs laid per year increases with age and body size but eventually levels off and declines. The reproductive span in such cases is shorter than the life span.
These comparisons illustrate the influence exerted by factors of population dynamics on the evolution of reproductive and bodily (somatic) senescence. The proportional contribution of an individual to the rate of increase of the iteroparous population obviously diminishes as the number of his living progeny increases. In addition, his reproductive capacity diminishes with age. These facts imply that there is an optimum number of litters per lifetime. Whether or not these influences of population dynamics lead to the evolution of adaptive senescence patterns has long been debated by gerontologists but has not yet been investigated definitively.
