Abstract

The average lifespan of people in developed countries has tripled since ancient times while its maximum longevity (about 120 years) has remained invariable. The strategic goal of gerontology is to exceed this limit, i.e. to develop remedies which would allow the living of an indefinitely long life. However there have not been any significant advances in solving this problem so far. There is still no answer to even the fundamental question: what is the primary cause of degradation for all of an organism’s functions (otherwise known as aging)? Actually, there are too many answers to this question: over 300 aging theories have been developed, and each of them provides a different response (Medvedev, 1990), although the majority of these theories now have only historical importance. Theories of aging are traditionally divided into two alternative groups. First, stochastic theories claim that there are no specific aging genes and that an organism’s deterioration is the result of damaging factors. Second, and by way of contrast, programmed-aging theories assert that longevity is predetermined by a genetic program. Stochastic theories have dominated the discussion since gerontology became a branch of science, and the idea that aging is programmed has not yet received wide recognition, even though there is a lot of empirical evidence supporting it. There are several factors which impede the wide recognition of this idea. First, there is no evidence that longevity is under the control of natural selection; and second, there is no convincing mechanism the programmed of aging. Adherents of this view currently search for longevity genes in a practically blind or ad hoc fashion (Holzenberger et al., 2003; Kenyon, 2010). Many such genes have been found for various organisms, ranging from unicellular creatures to mammals, but it is still unclear what processes they control (Anisimov, 2003). There are several different theories which are currently under consideration and which are based on reliable, proven evidence: i) the free radical theory which claims that aging is caused by an increased damage rate in cell structures due to an increased generation-rate of reactive oxygen species (ROS) by their own mitochondria; ii) the protein error theory which states that the primary cause is the age-dependent retardation of the protein synthesis rate; iii) the replicative senescence theory which argues that an age-dependent organism’s senility is caused by the limitation of cell proliferation. There is also reliable evidence in support of other theories which are not as popular, for instance the immunological theory and several versions of neuroendocrinal theories.

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