Nowadays, several alternative aging theories partly contradict and complement each other. Modern biology pays much attention to the issue of aging, and every year unique facts emerge that allow a deeper understanding of the mechanisms of this process. One of the most exciting and rational theories is the free radical view. Almost simultaneously put forward by D. Harman (1956) and N.M. Emanuel (1958), the free radical theory explains the mechanism of aging and a wide range of related pathological processes (Pomatto & Davies, 2018). According to this theory, cell malfunction is caused by free radicals, which are necessary for numerous biochemical processes like reactive oxygen species synthesized mainly in mitochondria, the energy factories of cells. If a very aggressive, chemically active free radical accidentally leaves the place where it is needed, it can damage DNA, RNA, proteins, and lipids.
Nature has provided a mechanism to protect against excess free radicals: in addition to superoxide dismutase, many substances from food, including vitamins A, C, and E, have antioxidant properties. Regular consumption of fruits and vegetables and even a few cups of tea or coffee daily will provide one with enough polyphenols, which are good antioxidants (Pomatto & Davies, 2018). Unfortunately, excessive antioxidants such as in an overdose of supplements are not only not helpful but can even increase cell oxidative processes. Biological systems are imperfect, and this imperfection makes obvious sense: nature does not need immortal organisms for apparent reasons. Therefore, biosystems at all levels of the organization have limited reliability. All humans are victims of a genetically programmed deficiency in the reliability of molecular and cellular machines (Pomatto & Davies, 2018). Except for free radicals, there are other failures; however, free oxygen radicals are, after all, universal means of implementing one of the essential ideas of being.
Aging processes are inevitable, but scientists have been trying to understand them for decades. Nowadays, there are numerous theories about the mechanisms of age-related changes, and another such hypothesis is the theory of somatic mutations or mutation theory. Its meaning is that genes with harmful mutations that manifest themselves in old age do not meet significant resistance to natural selection, so changes in such genes accumulate and cause aging. According to the theory of mutation accumulation, genes useful in early human life are maintained by natural selection, in contrast to genes useful in old age (Al et al., 2020). Thus, it is the younger generation that makes the main contribution to the creation of new generations. On this basis, Peter Medawar concluded that older individuals are too few and cannot influence the population’s gene pool either in favor of or against aging (Al et al., 2020). Mutation accumulation theory advocates the absence of specific genes that cause programmed aging.
That is, the changes an organism undergoes after reproductive age have no meaning for evolution. At the same time, harmful mutations manifested in youth meet stiff resistance to natural selection because of the negative effect on reproductive fitness. Similar mutations appearing in old age are relatively neutral since their carriers have already passed their genes to their offspring. According to this theory, people with a deleterious mutation are less likely to reproduce if its negative effect occurs earlier (Al et al., 2020). For example, progeria patients live only about twelve years, so they cannot pass on their mutant genes to the next generation. In such conditions, progeria comes only from new mutations, not parental genes. In contrast, people who show the mutation at an older age can reproduce before the disease occurs, like inherited Alzheimer’s disease (Al et al., 2020). As a result, progeria is less common than diseases such as Alzheimer’s because the mutant genes responsible for the disease are not removed from the gene pool as quickly as progeria genes.
References
Al, O., Rimental, P., Basic, M., & Ien, S. (2020). Effects of DNA Methylation on Cancer and Aging. Journal of Experimental and Basic Medical Sciences, 1(3), 126-130. doi: 10.5606/jebms.2020.75627
Pomatto, L. C., & Davies, K. J. (2018). Adaptive homeostasis and the free radical theory of ageing. Free Radical Biology and Medicine, 124, 420-430. doi:10.1016/j.freeradbiomed.2018.06.016