[The basis principles of primary prevention of atherosclerosis]

Hypolipidemic drugs have a common algorithm of action despite differences in its mechanisms. They normalize interaction of cellular receptors with polyenic fatty acids (PFA), restore their functional, regulatory and structural action. Atherosclerosis is in vivo pathology of individual cells unable to incorporate PFA and a syndrome of ω-3 and ω-6 PFA deficiency. Compensatory synthesis of humoral mediators (eicosanoids). from endogenous unsaturated ω-9 C 20:3 dihomo-γ-linolenic (mead) FA imparts on them non-physiological properties and thereby affects in vivo activity of all functional processes and cellular functions, forms the multifaceted clinical picture of pathology and atheromatosis. Atherosclerosis and atheromatosis are related but different processes. Neither statins nor other hypolipidemic drugs exhibit pleiotropic action. They normalize active incorporation of PFA that possess intrinsic in vivo pleiotropic activity. Omega-3 eicosanoids act as peroxisome proliferators and oxidize excess palmitic acid The hypolipidemic action of insulin is mediated through transformation of all palmitic FA synthesized from glucose into oleinic FA. Hypolipidemic drugs are unsuitable for primary prophylaxis of HLP and atherosclerosis that should be based on (a) normalization ofbiological function of trophology and biological reaction ofexotrophy, (b) bringing (by substrate induction) qualitative and quantitative food composition in correspondence with real, rather limited functional capacity of Homo sapiens. Biological function of intellect plays an important role in primary prophylaxis of HLP and atherosclerosis.