Lipoprotein(a) which is usually abbreviated to lp-a, is another type of cholesterol which occurs in animals that do not manufacture vitamin C. That includes humans, other primates and guinea pigs. Like total cholesterol and LDL, a high level of Lp-a is thought to be a risk factor for coronary heart disease and other diseases of the vascular system.
Nobel laureate Linus Pauling and Mathias Rath proposed that our bodies produce Lp-a to compensate for low levels of vitamin C. To demonstrate this, they caused atherosclerosis in guinea pigs by depleting their bodies of vitamin C. The Vitamin C depletion caused Lp-a to appear in the plaque.
But it may be a mistake to think of lp-a as a cause of atherosclerosis. Lp-a may just be an indicator; the cause may be vitamin C deficiency as supplementing with vitamin C reduces lp-a in the blood. Or it could be other factors, such as low levels of vitamin B3 (niacin), which also lowers lp-a.
It may also be significant that eating saturated fat lowers blood levels of Lp-a, whereas consumption of trans fatty acids causes levels of Lp-a to rise.[3,4]
1. Dahlen GH, et al. The importance of serum lipoprotein (a) as an independent risk factor for premature coronary artery disease in middle-aged black and white women from the United States. J Int Med 1998; 244: 417-24.
2. Rath M, Pauling L. Hypothesis: lipoprotein(a) is a surrogate for ascorbate. Proc Natl Acad Sci U S A. 1990; 87: 6204-7.
3. Khosla P, Hayes KC. Dietary trans-monounsaturated fatty acids negatively impact plasma lipids in humans: critical review of the evidence. J Am Coll Nutr 1996; 15: 325-339
4. Clevidence BA, Judd JT, Schaefer EJ, et al. Plasma lipoprotein (a) levels in men and women consuming diets enriched in saturated, cis-, or trans-monounsaturated fatty acids. Arterioscler Thromb Vasc Biol 1997; 17: 1657-1661