Atherosclerosis and atheromatosis are consequtive metabolic disordes. Pathology of the biological functions of trophology and endoecology is the basis for ischemic heart disease prevention.

Abstract

Atherosclerosis and atheromatosis are different nonphysiological processes with different etiology and pathogenesis. They manifest alterations in different biological functions. According to our original phylogenetic theory of general pathology, atherosclerosis is associated with altered biological function of trophology, eating, biological reaction of exotrophy. Atherosclerosis is induced by eating of nonoptimal for phylogenetically herbivorous Homo sapiens meat diet with high content of palmitic saturated fatty acid (SFA), which leads to in vivo formation of phylogenetically early low-efficient palmitic pathway of FA metabolism instead of highly-efficient oleic pathway operating in herbivores. Accumulation of nonligand palmitic very low density lipoproteins (VLDL) and low density lipoproteins (LDL) in the bloodstream results from nonphysiological reaction of compensation upon transport of palmitic SFA to cells. An increase in blood content of palmitic triglycerides (TG) and nonligand palmitic VLDLЛ→LDL coincides with the development of hypercholesterolemia: type IV→ type IIb → type V. Atheromatosis compensates changes in lipoproteins by activation of the biological function of endoecology (purity of the extracellular medium) in vivo, thus fulfilling the biological reaction of inflammation. This is physiological denaturation of apoВ-100 in nonligand VLDL→LDL by neutrophils via peroxidation, opsonization by the complement components, transcytosis across the endothelial monolayer and removal to the intima of elastic arteries that serves as a collection and utilization pool for phogogens from local intravascular pool of the intercellular medium. Endogenous phlogogens are utilized by phylogenetically early polyfunctional resident macrophages which are small in number and do not proliferate. Blood-borne monocytes-macrophages are also involved in this process, however, they do not express acid hydrolase of polyenic cholesteryl esters. Atheromatous masses are partially catabolized polyenic FA esterified by the alcohol cholesterol which were not internalized by cells. Atheromatosis is a process of pathological compensation in the realization of the function of endoecology. Prevention of atherosclerosis and atheromatosis should be based on elimination of the effects produced by a nonphysiological meat diet.