**14. The origin of MetS**

The results of genetics studies on the potential hereditary predisposition to MetS were analyzed by Stančakova and Laakso [132]. They concluded that there is only a limited evidence for common genetic background explaining the clustering of the metabolic trait. Instead, the existing evidence suggests the importance of epigenetic mechanisms [132]. This conclusion supports our earlier suggestion [55, 66, 67] that the external appearances and metabolic features of MetS reflect the genetic properties of our distant ancestors. So far, however, aging and MetS have been commonly regarded as the result of accumulation of different kinds of damages caused by oxidative stress and/or improper life style [8–11, 133–135].

As we have stressed earlier, all human beings after birth undergo changes during postembryonic ontogenesis. One of the theories of aging suggests that with the advanced age, the loss of heterochromatin results in altered gene expression [1, 2]. The epigenetic alterations resulting from global heterochromatin loss may be at the root of the various molecular events associated with aging and may tie together the various models of aging [2]. However, the process of ontogenesis in humans suggests that each transition to a new stage switches conversion of a new

#### *Metabolic Syndrome as the First Stage of Eldership; the Beginning of Real Aging DOI: http://dx.doi.org/10.5772/intechopen.95464*

portion of heterochromatin into euchromatin, and new genes begin to work, and then during transition to a the next stage, the "previous" portion of euchromatin does not turn back into heterochromatin, but becomes lost. Therefore, the so called "general loss" of the heterochromatin with advancing age simply reflects the advancement of individual ontogeny. Evidently, when men and women enter the post-reproductive stage of ontogenesis, they have lost much of the heterochromatin that was present in a newborn baby. The genes that govern the postreproductive stage were not the subject for natural selection, and therefore they are the same, or almost the same, genes that our distant ancestors had. This can be proved by many qualities in our bodies that appear after the age of 55: bulky body structure, dark spots of myelin in the skin, hair distribution, etc. Evidently, after transition to the post-reproductive stage many metabolic features also become distinct from the previous stages. There is a lot of evidence that elderly people of the northern Europe and Siberia acquire external and metabolic features common to the people living in the Northern Polar Regions. Inhabitants of the North, for example Eskimos, Dolgans, Innuits, do not consume a lot of plant foods rich in carbohydrates. Their diet is based on meat, animal fat and fish.

Again, the clue to understanding the nature of MetS, we can find in the sex associated differences in the energy metabolism and the transition of men and women from reproductive to the post-reproductive stage of ontogenesis, which is commonly regarded as the stage of aging [92]. This usually occurs between the ages of 50 and 55, when women go through menopause. The sharp changes in appearance and metabolism are particularly evident in women during and after the menopause, which increases the risk of MetS by 60% [136]. It is important, that the occurrence of MetS in the post-menopause period does not depend on the body mass index (BMD) and physical activity [137], but may depend in women on the dynamics of estrogen decline with age [138]. Interestingly, studies on sex hormone replacement in animals have shown that males receiving testosterone showed MetS deterioration, while females with estrogen replacement showed improvement in their MetS symptoms such as decreased hypertension [139]. This agrees with the suggestion that the genetically predetermined transition to the post-reproductive stage during normal ontogenesis, which is accompanied by changes in the hormone status, is the major natural cause of MetS. Thus some features of MetS, namely insensitivity to insulin and gain of fat, particularly visceral obesity, simply reflect a new type of metabolism. From this point of view, T2D may result from the excessive consumption of unnecessary carbohydrates at the post-reproductive stage.
