In this book, as in most of the literature that deals with the biology of aging, the term aging is used more or less synonymously with the term senescing or senescence. These terms are meant to encapsulate the slow, insidious, and progressive declines in structure and function of an organism after it has attained sexual maturity and the adult phenotype. As such, it is distinct from what happens in development. Gene action in development, however, is clearly of great significance for what happens in the later half of the life span. Let us consider the metaphor of a protein-synthesizing factory to describe a living organism. The life span of that factory depends on how well it is constructed and how well it is maintained after construction has been completed. The latter involves a variety of quality control mechanisms to maintain macromolecular integrity and proliferative homeostasis.

Not all alterations that occur in old organisms are deleterious. Some are compensatory—adaptive responses to specific types of declines in structure and function. An example is the Starling phenomenon—the increased end-diastolic filling to maintain cardiac output in many old people (4). Such compensation has been referred to as sageing (5). But these compensations eventually fail, allowing the full emergence of senescent phenotypes.

Rates of aging are typically measured by the speed at which the probability of organismal death increases as a function of postmaturational age. These are exponential functions and often are referred to as Gompertz curves, named after the 19th century actuary who first described this relationship. Recent studies of the life tables of very large numbers of fruit flies, medflies, roundworms, and people, however, have shown that those rates appear to slow in extremely aged individuals (6). The underlying mechanisms are not yet understood.

Genetic loci that play major roles in the modulation of life span and senescent phenotypes have been referred to as gerontogenes (7). This term is becoming well entrenched in the gerontological literature, but it is perhaps an unfortunate choice, as its literal interpretation is that these are genes whose primary functions are to lead directly to senescence. As we shall see in Sec. V. Why Do We Age?, such an interpretation is not consistent with evolutionary biological explanations of the nature of aging. The term gerontogens has been coined to refer to putative environmental agents that have the potential to accelerate features of senescence (8). We have mutagens, carcinogens, and teratogens, so why not gerontogens? The best candidate for a "global gerontogen" (one that can essentially advance all features of senescence and thus shorten the life span) is gluttony! We shall learn more about the role of calories in modulating life span in Sec. VI. How Do We Age?

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