title: [The phylogenic theory of disease formation, theory of pathology, pathogenesis of "metabolic pandemics" and the role of clinical biochemistry].
abstract: The R. Virchow concept of cellular pathology contains indirect evidences that in vivo there are structural and functional units between cell and organ and the mechanisms of formation health and disease conditions are common. The phylogenetic theory is proposed to understand the unity of pathogenesis of atheroslerosis, diabetes mellitus, metabolic syndrome and obesity. This theory includes three positions. 1. The consideration of physiology and pathology processes in vivo from a position of biologic functions and biologic reaction. 2. In phylogenesis, the formation of metabolism regulation on three levels: cell (autocrine level), paracrine cells cenosis i.e. structural and functional units of every organ (paracrine level) and whole organism (organism level). The biologic functions are: the trophology function, homeostasis, endoecology function (intercellular medium "purity"), adaptation, locomotion function (motion), species continuation function and cognitive function. 3. The consideration of formation in phylogenesis the biologic functions and pathology process reactions on three stages sequentially. The methodic modes in phylogenesis are: the continuity of formation of biologic functions and reactions and biologic subordination. In the last case, the humoral mediators formed in phylogenesis later cannot reverse the action of phylogenetically earlier mediators. The discordance of humoral regulation on phylogenesis different degrees, on autocrine, paracrine and organism levels is the foundation and unity of pathogenesis of all metabolic pandemics, the essential arterial hypertension and insulin resistance syndrome included.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
mesh_terms: D000222:Adaptation, Physiological; D019898:Autocrine Communication; D003324:Coronary Artery Disease / Q000209:etiology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D007333:Insulin Resistance; D050356:Lipid Metabolism; D008928:Mitochondria / Q000378:metabolism / Q000473:pathology; D008962:Models, Theoretical; D019899:Paracrine Communication