Lp(a) and cardiovascular diseases

Many large-scale studies have explored the relationship between Lp(a) and cardiovascular diseases, consistently finding an association between high Lp(a) levels and atherosclerosis, heart attacks, or stroke; Lp(a) has been validated as a significant, independent risk factor for heart disease.

Lp(a) promotes the recruitment of immune cells called monocytes to the intima, the innermost layer of blood vessels and arteries facing the blood stream. Once monocytes have migrated to the intima, they can become engorged with oxidized LDL—becoming “foam”cells—and initiate atherosclerotic lesion formation.

Lp(a) contributes to thrombosis (blood clot formation) that could result in a heart attack or stroke. Clot formation in the arterial wall, called “mural thrombosis,” contributes to the growth of atherosclerotic lesions; “occlusive thrombosis,” on the other hand, blocks an artery and triggers a heart attack or stroke. Lp(a) may also enhance coagulation, which could further contribute to thrombotic events.

Lp(a) is found in few species, mainly those that do not synthesize vitamin C. Since the absence of detectable Lp(a) in most species—almost all of which synthesize vitamin C—does not seem to be biologically disadvantageous, it was also proposed that vitamin C serves as a surrogate for Lp(a).

As a surrogate for vitamin C and owing to its pro-clotting functions, Pauling and his colleague suggested that Lp(a) might help repair lesions in the arterial wall caused by mechanical stress, free radicals, and/or sub-optimum collagen synthesis when vitamin C concentrations are insufficient. However, atherosclerosis results from the chronic, pathological deposition of Lp(a). A corollary is that adequate vitamin C status in humans, such as that achieved by sufficient intake, may help prevent arterial damage and reduce the need for the deposition of Lp(a) and/or lower its levels, thus preventing the development of atherosclerotic plaque.

Depletion of vitamin C increases the permeability of the vascular wall, thereby contributing to the infiltration of Lp(a) and leading to plaque formation and mural thrombosis. In chronic vitamin C insufficiency, the prolonged action and accumulation of Lp(a) may result in the development of plaque (mural thrombosis)

 

Lysine—by binding to Lp(a)—may quickly remove Lp(a) from plaque and also prevent its deposition in developing plaque.

Unfortunately, no controlled clinical trials have yet been published to validate or refute this.

Lysine is found in the diet, and it can be used in the body as a precursor to synthesize carnitine, an amino acid critical for mitochondrial energy production in cells. In his first case report on the amelioration of angina with vitamin C and lysine, Pauling noted that vitamin C is important in the hydroxylation reactions that synthesize carnitine from lysine. A number of studies have found that carnitine supplementation, as an adjunct to conventional therapy, is useful in treating heart disease, including heart attacks, heart failure, angina, and peripheral arterial disease.

 

Source:

Linus Pauling Institute | Oregon State University

Stephen Lawson
LPI Administrative Officer

VITAMIN C, LYSINE, AND LIPOPROTEIN(a) IN ATHEROSCLEROSIS AND ANGINA PECTORIS