No genetic instructions are required to age animals, just as no instructions on how to age inanimate machines are included in their blueprints.79,80 Molecular disorder occurs and accumulates within cells and their products because the energy required for maintenance and repair processes to maintain functional integrity for an indefinite time is unnecessary after reproductive success. Survival beyond the reproductive years and, in some cases, raising progeny to independence, is not favored by evolution because limited resources are better spent on strategies that enhance reproductive success to sexual maturity rather than longevity.81 Although genes certainly influence longevity determination, the processes of aging are not genetically programmed. Overengineered systems and redundant physiological capacities are essential for surviving long enough to reproduce in environments that are invariably hostile to life. Because humans have learned how to reduce environmental threats to life, the presence of redundant physiological capacity permits them and the domesticated animals we protect to survive beyond the reproductive ages. Studies in lower animals that have led to the view that genes are involved in aging have demonstrated that significant declines in mortality rates and large increases in average and maximum life span can be achieved experimentally.82,83,84,85 Without exception, however, these genes have never produced a reversal or arrest of the inexorable increase in mortality rate that is one important hallmark of aging. The apparent effects of such genes on aging therefore appear to be inadvertent consequences of changes in other stages of life, such as growth and development, rather than a modification of underlying aging processes. Indeed, the evolutionary arguments presented above suggest that a unitary programmed aging process is unlikely to even exist and that such studies are more accurately interpreted to have an effect on longevity determination, not the various biological processes that contribute to aging. From this perspective, longevity determination is under genetic control only indirectly.86,87 Thus, aging is a product of evolutionary neglect, not evolutionary intent.88,89,90,91
79Hayflick L. The Future of aging. Nature. 2000;408:267-269.
80Miller RA. Kleemeier award lecture: are there genes for aging? J Gerontol A Biol Sci Med Sci. 1999;54(7):B297-307.
81Kirkwood TBL. Evolution of aging. Nature. 1977;270:301-304.
82Johnson TE. Aging can be genetically dissected into component processes using long-lived lines of Caenorhabditis elegans. Proc Natl Acad Sci. USA. 1987;84:3777-3781.
83Johnson TE. Increased life span of age-1 mutants in Caenorhabditis elegans and lower Gompertz rate of aging. Science. 1990;249:908-912.
84Vaupel JW, Carey JR, Christensen K, et al. Biodemographic trajectories of longevity. Science. 1998;280:855-859.
85Johnson TE, Wu D, Tedesco P, Dames S, Vaupel JW. Age-specific demographic profiles of longevity mutants in Caenorhabditis elegans show segmental effects. J Gerontol Bio Sci. 2001;56:B331-339.
86Hayflick L. How and Why We Age. 1994. Ballantine Books: New York.
87Demetrius L. Mortality plateaus and directionality theory. Proc R Soc Lond B; 2001,268:1-9.
88Olshansky SJ, Carnes BA, Butler RA. If humans were built to last. Sci Am; 2001.
89Carnes BA, Olshansky SJ, Gavrilov L, Gavrilova N, Grahn D. Human longevity: nature vs. nurture -- fact or fiction. Perspect Biol Med. 1999;42(3):422-441.
90Robert L. Cellular and molecular mechanisms of aging and age related diseases. Pathol Oncol Res. 2000;6:3-9.
91Robert L. Aging of the vascular wall and atherosclerosis. Exp Gerontol. 1999;34:491-501.
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