A SINGLE MECHANISM OF ACTION OF HYPOLIPIDEMIC DRUGS. BASIC PRINCIPLES OF PRIMARY PREVENTION OF ATHEROSCLEROSIS, ATHEROMATOSIS AND CORONARY SYNDROME

Abstract

Irrespective of differences in mechanism of action, hypolipidemic drugs develop their effects according to a single algorithm. They normalize receptor-mediated uptake of polyenic fatty acids (PFA) by cells, thus restoring their functional, regulatory and structural state. Atherosclerosis is an in vivo pathology of each individual cell that cannot actively internalize PFA. Atherosclerosis is a syndrome of intracellular deficiency of ω-3 and ω-6 PFA. Compensatory production of humoral mediators (eicosanoids) from endogenous ω-9 С20:3 digomo-ү-linolenic unsaturated fatty acids (FA) renders them aphysiological and capable of impairing all functional processes in vivo, which results in a multilevel clinical manifestations of atherosclerosis and development of atheromatosis. Although atherosclerosis and atheromatosis are related to each other, they are different processes. Neither statins, nor other hypolipidemic drugs have any pleiotropic activity. They normalize cellular uptake of PFA which produce their intrinsic pleiotropic effects. As peroxisomal prolilferators, ω-3 eicosanoids oxidize excessive exogenous palmitic acid. Hypolipidemic effect of insulin is realized in conversion of entire palmitic FA synthesized in vivo from glucose into oleic FA. Hypolipidemic drugs are not the means of primary prevention of hyperlipidemia and atherosclerosis. This prevention should be based on normalization of the biological function of trophology and biological reaction of exotrophy and correction of quality and quantity of food according to real, quite limited functional possibilities ofHomo sapiens. The biological function of intellect plays an important role in primary prevention of hyperlipidemias and atherosclerosis.

Keywords

• атеросклероз
• гиполипидемические препараты
• плейотропное действие
• ги-перлипопротеинемия
• никотиновая кислота