Evolutionary and comparative animal studies indicate that mammalian aging is a result of “passive” rather than “active” biochemical mechanisms. That is, aging is not a “genetic program” evolutionarily selected to limit health duration or life span but, rather, is a side-product of essential processes of differentiation and development which are found in all mammalian species. Thus, the physiological and biochemical nature of mammalian aging is qualitatively similar in different species because of common mechanisms of causation. It then follows that mechanisms determining extent of health maintenance or life span are “active” in nature and operate by reducing the time-dependent accumulation of these “passive” aging effects. These “active” mechanisms are called “longevity determinant processes” (LDPs) and act to preserve and maintain the biological functional integrity of an animal. Thus, longevity and not aging has evolved in mammalian species, where LDPs have evolved through positive evolutionary selection and exist as a genetic program of global health maintenance processes. Many LDPs may exist, but much evidence suggest that they are remarkably similar in different mammalian species and are governed in their temporal and extent of expression by relatively few regulatory genes, or “longevity determinant genes”. LDPs may also be primarily responsible for stabilizing the proper differentiated state of cells, where aging is viewed as being a result of genetic instability leading to dysdifferentiation. Oxidative stress represents an ideal candidate as a “passive” aging process, and the repair and defense mechanisms acting to determine the oxidative stress state would represent a class of LDPs. Much experimental data now supports this LDP hypothesis, which carries with it the far-reaching prediction that, in spite of the vast complexity of mammalian aging, relatively simple means may now prove possible to further increase the maintenance of biological functions — and thus the healthy and productive years of human life span.
Source: https://link.springer.com/chapter/10.1007/978-3-0348-7337-6_2
