Programmed Theories of Aging

The process of aging is a subject matter of intense interest to the public, to health professionals, and to scientists in the fields of gerontology and life-span human development. Over the past century, more than 300 different theories of aging have been proposed. To advance the understanding of any biological process, scientists seek to construct useful conceptual frameworks that enable future observations to be tested for compatibility, so that confidence in predictions can be gained. Two such conceptual frameworks used to portray the process of aging are (a) the programmed theory of aging and (b) the nonprogrammed theory of aging. Both frameworks see organismal aging as a biological process characterized by the progressive accumulation of damage leading to physiological decline, which in turn culminates in an increased likelihood of mortality. It is these time-dependent deteriorative changes—termed organismal senescence by biogerontologists—that constitute the aging process. Nonprogrammed theories of aging envision this deterioration to be the result of the organism’s inability to defend itself from the intrinsic threat of damage accumulation over the life span. In contrast, programmed theories propose that each organism possesses a gene or set of genes that activate a pathway whose exclusive function is to trigger this functional decline. For more than 50 years, the popularity of nonprogrammed theories of aging has prevailed among most biogerontologists. But recent findings, including single gene mutations that extend life span in fruit flies (Drosophila) and worms (Caenorhabditis elegans), have stimulated a more spirited reexamination of whether nonprogrammed theories are telling the entire story. This entry, with its goal of better understanding programmed theories of aging, provides a below-the-surface look at some of the observations and inferences that are currently shaping contemporary thinking about programmed versus nonprogrammed theories.