Elsevier

Experimental Gerontology

Volume 33, Issues 1–2, January–March 1998, Pages 95-112
Experimental Gerontology

Original Articles
Extending Functional Life Span

https://doi.org/10.1016/S0531-5565(97)00059-4Get rights and content

Abstract

Average life expectancy at birth is a rough measure of the span of healthy, productive life—the functional life span. In the developed countries average life expectancies at birth now range from 76–79 years, six to nine years less than the limit of about 85 years imposed by aging. Aging is the accumulation of changes that increase the risk of death. Aging changes can be attributed to development, genetic defects, the environment, disease, and the inborn aging process. The latter is the major risk factor for disease and death after age 28 in the developed countries. The free radical theory of aging arose in 1954; it postulated that aging changes were caused by free radical reactions. There is now a growing consensus, largely based on the results of measures to minimize more-or-less random endogenous free radical reactions, that such reactions are a major cause of aging, possibly the only one. Some of these studies are presented following a brief discussion of free radical reactions.

Section snippets

In Appreciation

I am privileged to have an opportunity to contribute a chapter to this book in honor of Alex Comfort. I first met Alex during a symposium on experimental gerontology organized by Professor F. Bourliere, April 2–4, 1962, in Paris. Summaries of the lectures have been published (Bourliere 1962); Alex reported on the effect of restricted feeding on growth and longevity on fish.

Alex is a man of many interests—a true renaissance man. His contributions to biomedical gerontology have added

Free Radical Theory of Aging

Many theories have been advanced to account for aging (Rockstein et al 1974; Warner et al 1987; Medvedev 1990). No one theory is generally accepted (Schneider 1987; Viig 1990). The free radical theory of aging arose in 1954 (Harman 1986, Harman 1992, Harman 1993) from a consideration of aging phenomena from the premise that a single common process, modifiable by genetic and environmental factors, was responsible for the aging and death of all living things, in 1972 the theory was expanded (

Free Radical Reactions

Free radical reactions can be divided into three stages (Pryor 1966; Nonhebel 1974): 1) initiation, 2) propagation, and 3) termination—as illustrated by the reaction of O2 with organic compounds (Fig. 2). The amount converted to products per unit time of a compound involved in a free radical reaction depends on the: 1) rate of initiation and 2) the number of times the propagation phase (see Fig. 2) is repeated before termination, i.e., the chain length. The propagation phase can be shortened

Minimizing Free Radical Reaction Damage

Many studies now attest to the beneficial effects on life span and disease of measures designed to minimize endogenous free radical reactions in the body (Harman 1986, Harman 1993, Harman 1994). Three experiments illustrating the effects of decreased initiation rates are presented below followed by a discussion of the use of antioxidants such as vitamin E to limit free radical damage.

Comment

The participation of free radical reactions in normal metabolism and in the pathogenesis of many diseases is now generally accepted. Whether or not these reactions are responsible for aging is still being debated (Mehlhorn 1985; Rothstein 1986; Schneider 1987; Weindruch et al 1993; Sohal 1993).

Criticism of a theory is helpful, and as a consequence, it is either destroyed, modified, or confirmed; in either case it contributes to the solution of the problem for which the theory was formulated—in

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