A tentative molecular-biological hypothesis for arteriosclerosis

Abstract

In view of the fact that complications of arteriosclerosis are the most frequent causes of death in industrialized societies, its etiology is of enormous interest. The widely held lipid theory (detrimental effects of cholesterol) has been attacked because it cannot account for such facts as the homeostatic relationship of endogenous and exogenous cholesterol: for the "normal" cholesterol content of the early atheroma; for the distribution of the lesions, their spotty occurrence and their "programmed" appearance. Arteriosclerosis is part of the normal processes of aging which are related to molecular-biological changes. Autoimmune processes and the effects of extrachromosomal organisms of the genome (viruses, plasmids, viroids) are clinically of interest. Arteriosclerotic lesions are probably influenced by autoimmune processes; the variability and specificity of the non-chromosomal organisms may explain the location of the lesions; the end of the incubation period of the organisms may be responsible for the programmed appearance of clinical symptoms. The lipid changes are probably part of the adaptive mechanisms counteracting the rapid destruction of the vessels following the DNA alterations. Arteriosclerosis is part of normal evolution.