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Free Radical Theory of Aging: An Update
Increasing the Functional Life Span
DENHAM HARMAN
Department of Medicine, University of Nebraska College of Medicine, 984635 Nebraska Medical Center, Omaha, Nebraska, 68198-4635, USA
Key Words: aging • mitochondria • mutations • free radicals • longevity • origin of life • evolution
Address for correspondence: Denham Harman, M.D., Ph.D., Department of Medicine, University of Nebraska College of Medicine, 984635 Nebraska Medical Center, Omaha, Nebraska, 68198-4635, USA. Voice: 402-559-4416; fax: 402-559-7330. e-mail: vcerino{at}unmc.edu
Aging is the progressive accumulation of diverse, deleterious changes with time that increase the chance of disease and death. The basic chemical process underlying aging was first advanced by the free radical theory of aging (FRTA) in 1954: the reaction of active free radicals, normally produced in the organisms, with cellular constituents initiates the changes associated with aging. The involvement of free radicals in aging is related to their key role in the origin and evolution of life. Aging changes are commonly attributed to development, genetic defects, the environment, disease, and an inborn aging process (IAP). The latter produces aging changes at an exponentially increasing rate with age, becoming the major risk factor for disease and death for humans after the age of 28 years in the developed countries. In them the IAP limits human average life expectancy at birth (ALE-B)—a rough measure of the healthy life span—to about 85 years; few reach 100 years and only one is known to have lived to 122 years. In these countries, improvements in living conditions (ILC) have gradually raised ALE-Bs to 76–79 years, 6–9 years less than the limit imposed by aging, with no change in the maximum life span (MLS). The extensive studies based on the FRTA hold promise that ALE-B and the MLS can be extended, the ALE-B possibly by a few years, and the MLS somewhat less.
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