The first stage of pathogenesis, with a similar beginning of aging, can be designated as "metabolic chaos", which eventually leads to the second stage – a "black box", about which, in principle, we do not know anything. And unexpectedly, at the later stages of pathogenesis, the interaction of these two sets – pathogenic factors and targets, leads to a quite definite set of one and a half dozen proliferative-degenerative senile pathologies with quite predictable general unified events of pathogenesis.
Trying to explain this paradoxical phenomenon, I came to the conclusion that the listed pathogenic factors on their own can hardly be the cause of physiological aging.
As for pathological aging, which can be influenced by a huge number of pathogenic factors of a very different nature, even in this case, I doubt that each pathogenic factor that provokes or aggravates pathological aging has its own unique mechanism of action on this disease. I assumed that a huge variety of pathogenic factors of the most diverse nature affects pathological aging through a unified mechanism.
The path to the main and unique pathogenic factor, the same for physiological and pathological aging, which not only initiates, but also prolongs this disease at different stages of pathogenesis, turned out to be quite long and with numerous dead ends.
Analyzing the research results of V. M. Dilman [4] regarding age-related coarsening of the sensitivity of the hypothalamus functions to peripheral regulatory signals of negative feedback (peripheral hormones and key metabolites), accompanied by an increase in the basal level of one of the stress hormones, cortisol, I suggested that in addition to hormonal and metabolic signals that determine this phenomenon, there is a more powerful and significant regulator of the activity of the hypothalamus – the peripheral part of the autonomic nervous system (ANS) – evolutionary metabolic regulation system No. 1, which ensures the rapid adaptation of the body to changing conditions as the environment and the internal environment of the body. I was convinced of this by the results of experiments W. B. Cannon [5] by removing in animals the sympathetic ganglia of the ANS, which provide the neural connection of the brain stem structures with the periphery.