Читать книгу The Power Of Youth. How To Tune Our Mind And Body For A Long And Healthy Life - Андрей Фоменко - Страница 7

While supporters of "programmed aging" theories view age-adverse changes as the result of an inevitable evolutionary program, followers of "damage theory" do not consider aging a "genetic doom." They believe that the body accumulates many "breakdowns" with age due to the influence of external factors, stress, etc. A gradual accumulation of such damages leads to the development of age-related diseases and, eventually, to death.

There are examples of damage accumulation theories.

● DNA damage theory. During cell division and copying of DNA molecules, there is always a risk of genetic errors (mutations) that accumulate with age and result in age-related diseases, primarily malignant tumors. In addition, adverse mutations, accumulating with age, can occur under the influence of factors external to the cell: ultraviolet radiation, virus entry, inserting their genome into hereditary material, etc.[9].

● Genetic instability theory. It is not about mutations associated with damage, but rather about various changes in the genome occurring in the chromosome division. For example, such things as aneuploidy, the presence of an abnormal number of chromosomes in a cell, are identified in the fetal brain at all stages of intrauterine development. After birth, the number of such neurons decreases significantly, but some of them remain and can cause brain cancer[10].

● Free radical theory. Supporters of this theory affirm that free radicals (particles, containing oxygen with one missing electron) are the cause of cellular malfunction. They are needed for many biochemical processes and are constantly formed in the body during breathing. By leaving the place where they needed, they sort of "take" an electron from the body, and this is called an oxidative reaction. Free radicals are a serious threat to cell activity because they damage proteins and lipids[11].

Among the numerous theories of aging today, the following concepts are also emphasized.

● Apoptosis theory. Body tissues are constantly updated: "worn-out" cells whose function is deteriorating, as well as cells damaged by infection, having genetic mutations, regularly commit "suicide." Programmed cellular self-destruction is called apoptosis. In Greek, ἀπόπτωσις means "leaf fall": old cells die, like autumn leaves, to make way for the younger generation. There is an apoptosis gene in the DNA of each cell that triggers cellular self-destruction in response to molecular signals. The problem is that over the years, the sensitivity of cells to signals, activating their "suicide," decreases, leading to an accumulation of damaged, low-functioning cells. The aging process is based on the decreased ability of tissues to remove aged cells[12].

● Elevational (ontogenetic) theory of aging. In the mid-twentieth century, the Soviet gerontologist V. M. Dilman related aging and ontogeny[13] (individual development) of the homeostatic systems of the organism. The scientist named an elevation in the hypothalamus sensitivity threshold – the "conductor" of an endocrine system – to homeostatic signals as the key mechanism of aging. In a series of experiments, it was proved that this mechanism is based on the adverse changes in the reproductive, hypothalamic-pituitary-adrenal axis, which provides the necessary number of glucocorticoids in the blood (the so-called stress hormones) and increases their secretion under stress, which eventually leads to hyperadaptosis, i.e., a condition of excessive body adaptation to stress. The same mechanism in the metabolic homeostasis system causes the accumulation of body fat, a decrease in tissue sensitivity to insulin, and the development of atherosclerosis. Dilman found that age-related transformations occurred because of homeostatic ontogenesis, creating conditions for the formation of malignancies. Thus, the scientist concluded that aging is not programmed, but is a byproduct of the genetic developmental program. This led to the belief that aging can be slowed down if homeostasis is stabilized at the level achieved by the end of the organism's development.

● Telomere theory of aging. The number of divisions of each cell in the body is limited. This is because the protective structures at the ends of chromosomes, called telomeres, shorten with each cell division[14]. Telomere shortening may be a molecular "clock" triggering aging. It was found that the enzyme telomerase, which protects telomeres from shortening, is actively produced in cancer cells, that can divide almost infinitely. Telomerase activity has been detected in more than 85 % of malignant tumors, whereas it is absent in cells of healthy tissues[15].

● Inflammatory theory of aging. This concept intersects with the immunologic theory of aging, but the priority here is given to the overblown immune response to various factors, including autoimmune responses – "aggression" directed at one's tissues – and not on the loss of the ability to fight off infections and recognize mutations. Under this theory, which is considered one of the most relevant today, aging is a general inflammatory process affecting all organs. It is inflammation that underlies the development of such age-related diseases as atherosclerosis, Alzheimer's disease, cardiovascular disease, diabetes mellitus type II[16].

We told only some theories of aging – there are many more. This large number of views on the causes and nature of age-related changes demonstrates the lack of a unified understanding of the process. It also suggests that aging is based not on a single mechanism, affecting which could indefinitely prolong youth, but on a complex set of causes operating at the genetic, molecular, and evolutionary levels. The multifactorial nature of aging helps us to understand that prevention of aging shall also be comprehensive and diversified.