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Aging is the process that converts young adults, most of them healthy and in no need of assistance from physicians, into older adults whose deteriorating physiological fitness leads to progressively increasing risks of illness and death. The effects of aging are so familiar to health professionals and aging adults that it is viewed by both parties as something immutable, taken for granted, an arena in which diseases and their treatments take place, but not itself subject to intervention or modulation. The major discovery in biogerontology, gradually emerging from decades of work in animal model systems, is that this old-fashioned viewpoint is wrong, and that the aging process can be delayed or decelerated in mammals, built very much like human beings, by simple manipulations of nutritional signals and genetic circuits similar to those already well-documented in people. It is now absolutely routine to extend lifespan, in rats and mice, by about 40%, i.e., about 10 times the increase in active life expectancy that would ensue from a complete elimination of all neoplastic illnesses, or all heart attacks, in a human population. It thus seems plausible that a more detailed understanding of the factors that determine aging and the processes by which aging increases the risk of such a wide range of lethal and nonlethal illnesses and disabilities could, in the foreseeable future, have a profound impact on preventive medicine.

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Aging is a mystery, in the same sense that infectious disease was once a mystery, and consciousness still is: an area of investigation in which well-informed researchers cannot really be confident that they have selected a line of investigation bound to be productive. Until recently, most published papers in biogerontology journals consisted of descriptions of the ways in which young mice, rats, or people differed from older ones, originally in terms of anatomy and physiology, as indicated by levels of enzymes or hormones, and more recently by exhaustive catalogs of protein and mRNA levels. This descriptive era is gradually being superseded by one focused on specific molecular hypotheses about the key factors that regulate aging. The foundation of this modern approach to the biology of aging was the development of genetic models and nutritional manipulations which could delay aging, and the exploitation of this leverage to test molecular ideas about the basis for the retardation of the aging process.

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This question—what is aging?—is posed not as an invitation to semantic quibbling, but to initiate reexamination of facts so familiar that they are seldom examined. A case history of an individual who has mild arthritis, some loss of hearing acuity, some evidence of incipient cataract, loss of muscle mass and strength, a progressive decline in capacity for aerobic exercise, troubles with learning and remembering, and an increased vulnerability to infectious illness would lead any physician to assume that the individual described is a man or woman of 60 or more years of age. But the list of signs and symptoms refers with equal accuracy ...

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