\nFor this reason, the current AntiAging approach does not pretend in itself to “Anti-Aging”, what we intend is to age with quality of life, with health, maintaining a good physical and mental shape. <\/p>\n
In this article we will review in a simple way the best-known theories of prestigious researchers \u2013 some more accepted than others \u2013 and we will try to make a very brief review of caloric deprivation<\/strong> and sirtuins<\/strong>. <\/p>\n<\/p>\n As a first step, we must organize our knowledge in a methodical way in order to have a better understanding of the subject. (Orgel, 1963). (Denhan Harman, 1956). It means thinking that mitochondria accumulate oxidative damage<\/strong> through metabolites that they produce. (Bjorksten, 1968). (Alpatov and Pearl, 1929). (Walford, 1969). The basic idea of this genetic theory of aging is that a DNA mutation must alter the fidelity of protein synthesis<\/strong>, with consequent functional involution.<\/p>\n It postulates that each cell of the organism has in its genetic code the information to produce its own senescence in a programmed and orderly way, obeying<\/strong> internal signals and environmental effects. According to Hay Flick’s observations, human cells (in his study he used fibroblasts) maintained in vitro, lost the ability to divide when they reached a certain number of mitoses<\/strong>. In combination with the previous one and knowing that telomeres shorten with each mitotic division<\/strong>, this theory proposes that there is a limited number of mitoses, which is not true in cancer cells. It is a theory that points to its principle in the organization of the organism. It would result from certain genes that program maximum expression<\/strong>, especially for reproduction, but that after a while trigger the degeneration of the cells and organs they targeted. We know that there are numerous theories that we have not cited here. It is very difficult to bring them all together since, since man is a biopsychosocial being, we should also take into account evolutionary, environmental and even philosophical theories.<\/p>\n<\/p>\n To delve a little into the topic of how some theories have tried to explain the slowing of aging, we will now deal with caloric restriction.<\/p>\n A review published in Genes & Development<\/em> (Guarente 2000) hypothesized that calorie restriction (CR) slowed aging and the consequent decline in health by activating sirtuins.<\/p>\n A possible mechanism could be that less food slowed down the accumulation of oxidative damage.<\/p>\n This non-pharmacological scientific intervention<\/strong> proposes that, by reducing the number of calories ingested by an individual, not only could the aging process be slowed down but also the general state of health would improve.<\/p>\n Although most of the experiments have been developed in experimental models based on flies, yeasts and mice, it was shown that caloric deprivation would increase the expression of deacetylases that incorporate NAD+ for their functioning, sirtuins. The activation of these enzymes triggers nuclear transcriptional programs that improve metabolic efficiency and also upregulate mitochondrial oxidative metabolism and the resistance that accompanies it to oxidative stress.<\/p>\n Sirtuins promote this resistance by increasing antioxidant pathways (e.g., SOD2 and IDE2 in the mitochondria) and facilitating the repair of DNA damage through deacetylation or ADP-ribosylation of repair proteins. https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC4112140\/<\/a><\/p>\n<\/p>\n But eating less would not be the only way to achieve the beneficial effect of sirtuins. THEORIES OF AGING<\/h1>\n
\nThus, we will make a classification that will help us in the interpretation of the theories of aging. <\/p>\n Of the catastrophic error <\/h3>\n
\nThis hypothesis postulates that, as we advance in age, errors arise in the transcription mechanisms<\/strong>.
\nThese errors would cause the synthesis of defective proteins.
\nIn the event that these defective proteins were part of the transcription mechanisms, they would also generate defective products, which would prolong the damage successively, until reaching a catastrophe in cell homeostasis that would lead to cell death. <\/p>\n Free radical theory<\/h3>\n
\nIt is based on the assumption that there are mainly reactive oxygen species (ROS) that are generated as a result of cellular metabolism.
\nThese free radicals \u2013 among which the superoxide anion and hydroxyl stand out \u2013 are unstable elements that would cause cumulative damage to cellular structures such as DNA, proteins and lipids<\/strong>.
\nThere are also other sources of oxidants such as sunlight, tobacco, pesticides, heavy metals just to name a few.
\nAlthough cells have antioxidants capable of repairing damage, these would not be enough to recompose cellular homeostasis and would be reflected in a gradual loss of functional capacity. <\/p>\n Mitochondrial Damage Theory<\/h3>\n
\nOver time and progressively, they become less efficient and release more reactive oxygen molecules, which becomes a vicious circle and finally declines their activity.
\nThis theory would be related to the previous one. <\/p>\n Crosslinking theory <\/h3>\n
\nHere reference is made to the creation of harmful molecular bonds (such as glycosylation of connective tissue proteins, aldehydes, lipid oxidation products, alkylating agents, quinones, etc.) which produces tissue cross-linking<\/strong>.
\nCross-linking involves loss of elasticity, reduced bulking capacity, increased resistance to hydrolases, and thus an increase in molecular weight and a tendency to embrittlement of cellular structures. <\/p>\n Theory of wear and accumulation of internal cellular damage<\/h3>\n
\nThis theory is actually the sum of two theories that complement each other.
\nThey postulate that metabolites are generated throughout the cell cycle from the phagocytosis<\/strong> of organelles and other cellular detritus.
\nThis, added to the damage caused by aging, would accumulate to cause cellular senescence. <\/p>\n Immune System Theory<\/h3>\n
\nIn this theory \u2013 also called Human Immunosenscence \u2013 he tries to explain how the involutional changes of the immune system<\/strong> caused by aging cause alterations or decrease in the functions of the body.
\nEither due to susceptibility to certain diseases or due to increased production of T cells that ignore their own tissues (autoimmunity) or generate cytokine storms. <\/p>\n Genetic mutation theory<\/h3>\n
Apoptotic cell death theory<\/h3>\n
\nCancer cells would be the exception because they are not apoptotic and therefore immortal. <\/p>\n\n
Mitotic limit theory<\/h3>\n<\/li>\n<\/ul>\n
\nThis number was close to 50.
\nIn fact, part of his experiment was to freeze a group of cells that had reached 25 divisions and when he finally thawed them, they continued to divide until they completed the 50 and then perished. <\/p>\n Telomere theory<\/h3>\n
\nThese owe their eternity to telomerase, which replaces telomere sequences that are lost during mitosis.
\nThis enzyme is absent in the rest of the somatic cells. <\/p>\n\n
Disposable soma theory<\/h3>\n<\/li>\n<\/ul>\n
\nIt focuses on the fact that the priority of the entire cell complex would be the maintenance of the species<\/strong>, so survival would be in the background.
\nAccording to this theory, the body puts itself at the service of the reproductive cells until external agents finish off the rest of the other cells that served as support. <\/p>\n Williams’ theory of antagonistic pleitropy<\/h3>\n
\nThis case can be seen in the testicle and testosterone. \n\t <\/p>\n Other theories<\/h3>\n
\nAccording to Medvedev, who in 1990 took on the task of reviewing all those that had an applicable scientific basis, the number of theories amounted to more than 300<\/strong>. <\/p>\n SIRTUINS<\/h1>\n
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<\/a><\/p>\n
\nWithin the sirtuin group, SIRT1 and SIRT3 would be mostly related to the study objective. <\/p>\n
\nSince the 90s, a polyphenol that exerts antioxidant effects and has gained a lot of fame has been studied: resveratrol<\/strong><\/a>. <\/p>\n