Lipoprotein(a): A Cardiovascular Nightmare

A lipoprotein is a biochemical assembly that contains both proteins and lipids bound together. Lipoprotein(a), also known as Lp(a), is a combination of two types of lipoproteins: low density lipoprotein (LDL) and apolipoprotein(a) also known as apo(a).

Lipoprotein(a) was not discovered until 1963. This is a fairly recent discovery compared to cholesterol which was first identified in 1769.[6] Lp(a) levels are hereditary and not affected by diet or exercise. That means even vegan raw food eaters can have elevated levels. I know this from personal experience as well as listening to what the experts have found.

Elevated levels of LDL have been associated with heart disease. But when LDL and apo(a) combine to form Lp(a), and the Lp(a) becomes elevated, they create an even greater risk factor. When elevated, Lp(a) predicts the risk of early atherosclerosis independently of other cardiac risk factors, including elevated LDL. Numerous epidemiologic studies concluded that Lp(a) is a risk factor for atherosclerotic diseases such as coronary heart disease and stroke.[1][2][3][4][5] In addition, Lp(a) is a proinflammatory molecule containing oxidized phospholipids that have been shown to contribute directly to vascular disease progression.

Lp(a) concentrations vary over one thousandfold between individuals, from < 0.2 to > 200 mg/dL. This range of concentrations has been observed in all populations studied. Currently, a level of over 30 mg/dL is said to be elevated.

A recent study followed 3467 African Americans and 9851 Caucasians for 20 years. The researchers found that an elevated Lp(a) conferred the same risk in each group. However, African Americans had roughly three times the level of Lp(a), and Lp(a) also predicted an increased risk of stroke.[7]

Lp(a) remains in the bloodstream for about 3 to 7 days.[8] The kidneys have been identified as playing a role in Lp(a) clearance from the bloodstream.[9] This means that people with kidney failure may develop elevated levels of Lp(a).

The commonly prescribed lipid-reducing pharmaceutical drugs have little or no effect on Lp(a) concentrations. Furthermore, diet, exercise, and other environmental factors have little to no effect on Lp(a) concentrations.

Fortunately for us, Niacin (nicotinic acid)—but not the no-flush type—may possibly reduce elevated levels of Lp(a) 20 by 30% (according to Sotirios Tsimikas MD) when taken in medicinal doses. And there are some new pharmaceutical drugs waiting for approval that show promise in lowering Lp(a). But if approved, one should also consider the possible side effects of such a drug.

The European Atherosclerosis Society recommends that all people with a moderate or high risk of cardiovascular disease have their lipoprotein(a) levels measured. According to the society, any person with one of the following risk factors should be tested;

• Family history of hypercholesterolaemia (a genetic disorder characterized by high cholesterol levels).
• Premature cardiovascular disease or a family history of premature cardiovascular disease.
• Family history of elevated lipoprotein(a).
• Recurrent cardiovascular disease despite statin treatment.

Lowering Lp(a) can be difficult to achieve. If you find out that your Lp(a) is elevated, there are other things that you can do to reduce your risk. Eliminating other risk factors for heart disease, adopting a healthy lifestyle, and taking high quality omega 3 supplements may indeed help.

In conclusion, knowing your personal risk factors and taking steps toward eliminating then and incorporating a healthier lifestyle could really pay off in the long run.

1. Nordestgaard BG, Chapman MJ, Ray K, Borén J, Andreotti F, Watts GF, Ginsberg H, Amarenco P, Catapano A, Descamps OS, Fisher E, Kovanen PT, Kuivenhoven JA, Lesnik P, Masana L, Reiner Z, Taskinen MR, Tokgözoglu L, Tybjærg-Hansen A (December 2010)."Lipoprotein(a) as a cardiovascular risk factor: current status". Eur. Heart J. 31 (23): 2844–53.doi:10.1093/eurheartj/ehq386.PMC3295201.PMID20965889.
2. Kamstrup PR, Tybjærg-Hansen A, Nordestgaard BG (April 2011). "Lipoprotein(a) and risk of myocardial infarction--genetic epidemiologic evidence of causality". Scand. J. Clin. Lab. Invest. 71 (2): 87–93.doi:10.3109/00365513.2010.550311. PMID21231777.
3. Danesh J, Collins R, Peto R (2000). "Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies".Circulation 102 (10): 1082–5.doi:10.1161/01.CIR.102.10.1082. PMID10973834.
4. Smolders B, Lemmens R, Thijs V (2007). "Lipoprotein (a) and stroke: a meta-analysis of observational studies". Stroke 38(6): 1959–66.doi:10.1161/STROKEAHA.106.480657. PMID17478739.
5. Schreiner PJ, Morrisett JD, Sharrett AR, Patsch W, Tyroler HA, Wu K, Heiss G (1993)."Lipoprotein(a) as a risk factor for preclinical atherosclerosis".Arterioscler. Thromb. 13 (6): 826–33.doi:10.1161/01.ATV.13.6.826.PMID8499402.
6. Albers JJ, Koschinsky ML, Marcovina SM (2007). "Evidence mounts for a role of the kidney in lipoprotein(a) catabolism".Kidney Int.71(10): 961–2.doi:10.1038/sj.ki.5002240.PMID17495935.

1. Chevreul (1816) "Recherches chimiques sur les corps gras, et particulièrement sur leurs combinaisons avec les alcalis. Sixième mémoire. Examen des graisses d'homme, de mouton, de boeuf, de jaguar et d'oie" (Chemical researches on fatty substances, and particularly on their combinations o filippos ine kapios with alkalis. Sixth memoir. Study of human, sheep, beef, jaguar and goose fat), Annales de Chimie et de Physique, 2 : 339-372. From page 346 : "Je nommerai cholesterine, de χολη, bile, et στερεος, solide, la substance cristallisée des calculs biliares humains, ... " (I will name cholesterine — from χολη (bile) and στερεος (solid) — the crystalized substance from human gallstones ... )
2. Virani SS, Brautbar A, Davis BC, Nambi V, Hoogeveen RC, Sharrett AR, Coresh J, Mosley TH, Morrisett JD, Catellier DJ, Folsom AR, Boerwinkle E, Ballantyne CM (January 2012). "Associations Between Lipoprotein(a) Levels and Cardiovascular Outcomes in Black and White Subjects: The Atherosclerosis Risk in Communities (ARIC) Study".Circulation 125 (2): 241–9.doi:10.1161/CIRCULATIONAHA.111.045120. PMID22128224.
3. Rader DJ, Cain W, Zech LA, Usher D, Brewer HB (February 1993)."Variation in lipoprotein(a) concentrations among individuals with the same apolipoprotein (a) isoform is determined by the rate of lipoprotein(a) production".J. Clin. Invest.91(2): 443–7.doi:10.1172/JCI116221.PMC287951.PMID8432853.