Can the premises of the altered homeostatic theory permit improvement in the prevention of ischemic heart disease?
In this communication, the altered homeostatic theory will be discussed and updated, and evidence will be presented that the premises of the theory might permit improvement of the prevention of ischemic heart disease (IHD). This hypothesis, first described in 1999, argues that IHD is due basically to an inappropriate shift of homeostasis, and the theory includes the position that S-RV directly induces symptoms. In contrast, the standard approach to IHD is based fundamentally on two principles: that atherosclerosis is due fundamentally to lipid abnormalities, and that symptoms in IHD are due to obstructive complications of atherosclerosis in epicardial coronary arteries. Suggestions for prevention stem from the altered homeostatic theory's different basic conceptualization of this disorder, and it seems reasonable that accepted basic pathogenetic mechanisms help shape measures to prevent IHD. Many of the theory's positions for preventing IHD parallel standard views, but the theory's basic premises have resulted in significant differences between the standard and the theory's overall approach to the prevention of IHD. Positions for the prevention of IHD include: the possibility that any preventative factor can improve any risk factor, the use of substitute preventative factors to counter unmodifiable or difficult to correct risk factors, underestimation of the risk of IHD by the standard position in individuals with normal lipid levels but multiple other risk factors, the probable relative overemphasis of the risk factor of cholesterol, the value of a national program to reduce the incidence of multiple disorders with similar risk factors, an alternate approach to the use of statins, and the value of an evolutionary approach to preventing IHD and other disorders.
Hellstrom
H R
HR
College of Medicine, SUNY Upstate Medical University, Syracuse, New York 13210, USA. hellstrr@mail.upstate.edu
D001341:Autonomic Nervous System / Q000503:physiopathology; D001777:Blood Coagulation; D002784:Cholesterol / Q000097:blood; D006487:Hemostasis; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology; D007249:Inflammation / Q000503:physiopathology; D008077:Lipoproteins, LDL / Q000097:blood; D008955:Models, Cardiovascular; D017202:Myocardial Ischemia / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology / Q000517:prevention & control*; D012307:Risk Factors; D013564:Sympathetic Nervous System / Q000503:physiopathology
D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008077:Lipoproteins, LDL; D002784:Cholesterol