[The atherosclerosis and atheromatosis as two etiologically different aphysiological processes at single pathogenesis. Atheromatosis and pathogenetic role of insulin.].

It is supposed that at stages of phylogenesis seven biological functions was developed: 1) biological function of trophology; 2) homeostasis; 3) endoecology; 4) adaptation; 5) continuation of species; 6) locomotion; 7) cognitive function, including intellect. The function of trophology (feeding) is implemented by two biological reactions: exophilia - external feeding and endophilia - internal feeding. The function of endoecology prevents exceeding of upper limit of physiological interval by no substrate, catabolites and endogenous phlogogens. It is implemented by two biological functions: excretion and inflammation. The etiological factors of atherosclerosis are the following ones. The oleic mono-saturated fatty acid in chemical reactions is by far more active than palmitic fatty acid. In the ocean, all animals were carnivorous (piscivorous); species Homo Sapiens, in millions of years of life on dry land, forcedly became a herbivorousone. The main role in development of herbivorous animals belongs to insulin; the hormone regulating in the first-place metabolism of fatty acids, expresses transmutation of all endogenously synthesized from glucose palmitic saturated fatty acid in oleic monosaturated fatty acid. The late in phylogenesis insulin can't initiate transmutation of exogenous palmitic saturated fatty acid of food into oleic mono-saturated fatty acid. Under effect of insulin in vivo an active oleic type of metabolism of fatty acids is developed; and outside if effect of insulin palmitic type of metabolism of fatty acids is developed. In the ocean, synthesis of active eicosanoids occurs from ῳ-3 polyene fatty acids; there is no such fatty acids in dry land. The basis of pathogenesis of atherosclerosis is feeding of large amount of carnivorous (meat) food by phylogenetically herbivorous Homo Sapiens. This way a deficiency of palmitic saturated fatty acids in cells if developed blocking their bio-accessibility. The lipoproteins of low density are not developed in the initiated by insulin transfer of oleic triglycerides to cells in oleic apoE/B-100 lipoproteins of very low density and their absorption by cells. The transfer of triglycerides into lipoproteins of very low density is blocked under slow processes of transmutation of palmitic lipoproteins of very low density into lipoproteins of low density, retention cumulation of lipoproteins of low density in blood. Only because of partial utilization by monocytes of non-ligand palmitic lipoproteins of very low density →lipoproteins of low density that occurs in the intima of arteries of elastic type, atheromotosis is developed. The atheromotosis masses of intima are first of all interim catabolites of polyene fatty acids; the cells could not to absorb them by apoB-100-endocytosis in the content of lipoproteins of low density. The atherosclerosis, hyperlipoproteinemia, high content of lipoproteins of low density in blood and deficiency of polyene fatty acids in cells are a result of disorder of trophology function; the atheromotosis of arteries is only partial implementation of endoecology function.