title: The pathogenesis and prevention of atherosclerosis.
abstract: Most measures taken to prevent atherosclerosis still aim at lowering the cholesterol content of the plasma lipoproteins by dietary and pharmacological means. This approach has only proved successful to a limited extent. Diseases secondary to atherosclerosis are still the commonest cause of death in western industrialized countries. As all metabolic processes are regulated by opposing processes of equilibrium, i.e. by processes directed towards performance and recovery, we asked ourselves whether the fatty degeneration and sclerosis of the arteries could be causally related to a continuous dysregulation of these processes. We consider this to be the case, with a continuous deficiency of glycosaminoglycans (heparin, heparinoids) on the endothelial surface of the vessels. Numerous studies indicate that in the case of thinning of the anionic glycosaminoglycan film on the endothelial surface, the lipoprotein-lipase and antithrombin III activity induced by heparin is reduced, as result of which hyperlipoproteinaemia and increased tendency to thrombosis can only by compensated for to an inadequate extent. The formation of glycosaminoglycans is a characteristic of all mesenchymal cells, whereby the exogenous introduction of glycosaminoglycans into the extracellular space is of decisive importance for adequate glycosaminoglycan synthesis. Since Engelberg reported outstanding results obtained with heparin injections in the prevention and treatment of atherosclerotic disorders of the cardiac circulation, we considered it appropriate to use the well-proven dietary supplement of glycosaminoglycans in rheumatology, in the treatment of arthrosis, as well as in the prevention and treatment of atherosclerosis.
authors.affiliation: Study Group Nutrition and Immunity, Bern, Switzerland.
authors.forename: A
authors.initials: A
authors.lastname: Hässig
authors.forename: L
authors.initials: L
authors.lastname: Wen-Xi
authors.forename: K
authors.initials: K
authors.lastname: Stampfli
mesh_terms: D000818:Animals; D000990:Antithrombin III / Q000378:metabolism; D001158:Arteries / Q000502:physiology / Q000503:physiopathology*; D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology* / Q000517:prevention & control*; D004730:Endothelium, Vascular / Q000502:physiology / Q000503:physiopathology; D006025:Glycosaminoglycans / Q000502:physiology; D006493:Heparin / Q000502:physiology; D006801:Humans; D008071:Lipoprotein Lipase / Q000378:metabolism; D008955:Models, Cardiovascular; D011480:Protease Inhibitors / Q000378:metabolism; D012697:Serine Endopeptidases / Q000378:metabolism
chemical_list: D006025:Glycosaminoglycans; D011480:Protease Inhibitors; D000990:Antithrombin III; D006493:Heparin; D008071:Lipoprotein Lipase; D012697:Serine Endopeptidases