[Clinical biochemistry methods in objectiva evalution of overeating foood of carnivores (meat)by a phylogenetically herbivorous homo sapiens (a patient).]

The abuse of food of carnivores (meat) by phylogeneticallyI herbivorous Homo sapiens (a patient) initiates atherosclerosis. Addressing biogenetic law of E. Haeckel that ontogeny recapitulates phylogeny (a universal anamnesis), we suggest a diagnostic technique that allows evaluation of the meat diet abuse by a herbivorous Homo sapiens. This technique is based on application of phylogenetic theory of general pathology to clinical practice. The degrees of objective evaluation of nonphysiological overeating of meat are: the first, an increase in the fast plasma content of oleic triglycerides palmitoyl-oleyl-palmitate (POP). The second, hyperglyceridemia + an increase in low density lipoprotein cholesterol (LDL-CL) content. The third, increased plasma content of apoС-III. The fourth, an increase in the concentration of apoВ-48. If electrophoregrams are analyzed and hyperlipoproteinemia (HLP) type is determined according to WHO classification, the first degree of meat overeating is not informative, the second, corresponds to type IV HLP; the third, to type IIb HLP, and the forth, to type V HLP, i.e, the patient diet consists practically of the food of carnivores. Hyperlipoproteinemia coincides with insulin resistance syndrome, hyperglycemia and hyperinsulinemia, which is based on blood increase of fatty acids in the form of polar unesterified fatty acids (UFA). According to phylogenetic theory of general pathology, in vivo cells do not internalize glucose if there is a possibility to internalize UFA. Preventive examination allows evaluation of disorders in the biological function of trophology (food consumption). Thus, the use of different methods in the analysis of this function offers evaluation of the effectiveness of diet therapy from the level of disorders when treatment was started.

[Clinical biochemistry methods in objectiva evalution of overeating foood of carnivores (meat) by a phylogenetically herbivorous homo sapiens (a patient).]

The abuse of food of carnivores (meat) by phylogeneticallyI herbivorous Homo sapiens (a patient) initiates atherosclerosis. Addressing biogenetic law of E. Haeckel that ontogeny recapitulates phylogeny (a universal anamnesis), we suggest a diagnostic technique that allows evaluation of the meat diet abuse by a herbivorous Homo sapiens. This technique is based on application of phylogenetic theory of general pathology to clinical practice. The degrees of objective evaluation of nonphysiological overeating of meat are: the first, an increase in the fast plasma content of oleic triglycerides palmitoyl-oleyl-palmitate (POP). The second, hyperglyceridemia + an increase in low density lipoprotein cholesterol (LDL-CL) content. The third, increased plasma content of apoС-III. The fourth, an increase in the concentration of apoВ-48. If electrophoregrams are analyzed and hyperlipoproteinemia (HLP) type is determined according to WHO classification, the first degree of meat overeating is not informative, the second, corresponds to type IV HLP; the third, to type IIb HLP, and the forth, to type V HLP, i.e, the patient diet consists practically of the food of carnivores. Hyperlipoproteinemia coincides with insulin resistance yndrome, hyperglycemia and hyperinsulinemia, which is based on blood increase of fatty acids in the form of polar unesterified fatty acids (UFA). According to phylogenetic theory of general pathology, in vivo cells do not internalize glucose if there is a possibility to internalize UFA. Preventive examination allows evaluation of disorders in the biological function of trophology (food consumption). Thus, the use of different methods in the analysis of this function offers evaluation of the effectiveness of diet therapy from the level of disorders when treatment was started.

[The individual fatty acids of blood plasma: biological role of substrates, parameters of quantity and quality, diagnostic of atherosclerosis and atheromotosis.]

The atherosclerosis and atheromotosis are supposed to be, according to phylogenetic theory of general pathology, two etiologically different aphysiological processes, unified by community of pathogenesis. The atherosclerosis is a derangement of biological function of trophology (feeding), biological reaction of exotrophy (external feeding) and biological function of adaptation, biological reaction of compensation in response to deficiency of ῳ-3 and ῳ-6 polyenoic fatty acids. In case of deficiency of polyenoic fatty acids in cells and during synthesis of eicosanoids of group I from unsaturated endogenous ῳ-6 С20: 3 digomo-γ-linoleic unsaturated fatty acid, atherosclerosis is developed, a complex metabolism disorder in vivo. The atheromotosis is a derangement of biological function of endoecology, biological reactions of inflammation and inherent immunity. This incomplete utilization in intima of arteries of non-ligand palmitic lipoproteins of very low → low density under effect not of polyfunctional resident macrophage but monocytes of hematogenic origin without expression of acid hydrolase of polyenoic ethers of cholesterol. In intima, in area of cumulation of endogenous phlogogens (initiator of inflammation) from the pool of intra-vascular medium, polyenoic unsaturated fatty acids are cumulated that were not absorbed by cells in structure of ligand low density palmitic lipoproteins using apoB-100- endocytosis. The pathogenic factor of atherosclerosis - derangement of biological function of trophology. biological function of exotrophy under alimentary deficiency of in vivo of ῳ-3 and ῳ-6 polyenoic fatty acids with physiological parameters of feeding. The pathogenic factor of atheromotosis - phylogenetically herbivorous (carnivorous) human misusing of animal (meat) food, palmitic unsaturated fatty acids, development by hepatocytes of a large number of palmitic triglycerides and lipoproteins of very low density of the same name. The late in phylogenesis insulin-dependent lipoproteins of very low density transfer palmitic lipoproteins of very low density to cells slowly. The cells absorb them also slowly. The cumulation of non-ligand palmitic lipoproteins of very low density → low density in blood competitively blocks physiological absorption of polyenoic unsaturated fatty acids by cells in structure of physiological palmitic lipoproteins of low density. The atherosclerosis occurs blood flow and atheromotosis in intima of arteries of elastic type.

[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.

Inhibitor of beta-hydroxy-beta-methylglutaryl coenzyme A reductase decreases energy supply to the myocardium in rats.

Hypocholesterolemic preparations, inhibitors of the key enzyme of cholesterol biosynthesis beta-hydroxy-beta-methylglutaryl coenzyme A reductase (statins), block the synthesis of ubiquinone Q10, intermediate electron carrier in the mitochondrial respiratory chain. This should decrease energy supply to tissues. Daily peroral administration of beta-hydroxy-beta-methylglutaryl coenzyme A reductase inhibitor simvastatin (24 mg/kg perorally) for 30 days had no effect on the contents of macroergic phosphates (ATP and creatine phosphate) in the liver, but decreased these parameters in the myocardium.