Reducing the Risk for Cardiovascular Disease with Nutritional Supplements

Reducing the risk for cardiovascular disease (CVD) is a primary goal of any health care system in the industrialized world. The success of this world-wide effort will largely depend on the proper understanding of the mechanisms responsible for development of this disease. This paper marshals the scientific evidence for the predominant pathome-chanisms of CVD and presents new therapeutic approaches. Human atherosclerotic lesions are primarily composed of lipoprotein-a. The extracellular deposition of this lipoprotein directly parallels the extent of the atherosclerotic lesion. The frequency of this pathomechanism today is directly related to its efficacy as a defense mechanism during the evolution of man, particularly in stabilizing the vascular wall during ascorbate deficiency. The deposition of lipoprotein-a in form of largely intact particles implies the reversibility of this mechanism. On the basis of an improved understanding about the pathogenesis of CVD new therapeutic approaches are defined. Certain vitamins and amino acids are of particular importance for these approaches. Ascorbate is essential for preserving and restoring the integrity and stability of the vascular wall. Niacin and ascorbate were reported to lower lipoprotein-a plasma levels. It is proposed that this effect is mediated by NADPH. The amino acids L-lysine and L-proline competitively interfere with the binding of lipoprotein-a to constituents of the vascular wall and atherosclerotic lesions. The therapeutic use of these amino acids could prevent further buildup of lipoprotein-a accumulation in the vascular wall. More importantly, optimum concentrations of L-lysine and L-proline could release deposited lipoprotein-a but also other atherogenic lipoproteins from the vascular wall. This paper defines a new therapeutic goal: The pharmaceutical, non-invasive reversal of existing CVD with nutritional supplements. 1. 880 Bear Gulch Road, Woodside, CA 94062. Introduction Cardiovascular Disease (CVD) is the most frequent cause of death in the industrialized world. In a series of recent papers I have contributed to an improved understanding about the pathogenesis of human CVD. It was shown that ascorbate deficiency is an important underlying factor and that all mechanisms known today leading to CVD can be triggered by ascorbate deficiency. This remarkable fact reflects the strong pressure during the evolution of man after loss of endogenous ascorbate synthesis. This pressure favored genetic and metabolic features contributing to avoidance of the fatal consequences of ascorbate deficiency and scurvy. The different mechanisms of human CVD known today therefore all compensate for impaired integrity and stability of the vascular wall caused by chronically low dietary ascorbate intake. If these mechanisms overshoot, heart attack, stroke and other forms of CVD develop. In the first part of this paper I will marshal the evidence for the most frequent of these pathomechanisms. I will focus here on mechanisms related to lipid and lipoprotein deposition in the vascular wall and re-evaluate existing hypotheses. This re-evaluation is particularly necessary since cholesterol lowering concepts have become dominant factors in the public health debate. I will show that the most important among these overshooting defense mechanism is the extracellular deposition of lipoprotein-a in the vascular wall. On the basis of an improved understanding of these pathomechanisms I will present new therapeutic approaches including the reversibility of existing atherosclerotic deposits. Finally I will marshal the evidence for the particular value of nutritional supplements to achieve this therapeutic aim. Lipoprotein-a, not LDL, is the Primary Risk Factor for CVD in Plasma Present theories of human CVD are based on the concept that low-density lipoprotein (LDL) or LDL-cholesterol is the primary risk