Trial results have been mixed regarding the association of Lp(a) with CHD, with most showing a higher incidence in patients with elevated levels (greater than 30 mg/dL) and some not.5 Yet, excessive amounts have been identified in 19% of families with a member in whom CHD has been diagnosed before age 60. In particular, Lp(a) seems to potentiate the consequences wrought by increased LDL-cholesterol levels, as often seen in familial hypercholesterolemia.

Treatment with cholesterol-lowering agents offers little benefit. A possible exception in some patients is nicotinic acid, in dosages of 1 to 4 g/d, which may lower Lp(a) as much as 15% to 20%, but this response is highly variable. Estrogen replacement therapy (ERT) may be of limited value for postmenopausal women with elevated Lp(a) levels, though other investigators add that estrogen also drives CRP levels up. One treatment regime that has been totally ignored by conventional medical circles had been proposed by the two-time Nobel Prize winning Linus Pauling. The Pauling Therapy consists of orthomolecular substances that inhibit the binding of lipoprotein(a) Linus Pauling explained:

"Many investigators contributed to demonstrating that it is lipoprotein(a) that is deposited in plaques, not merely LDL, but Lp(a). If you have more than 20 mg/dl in the blood it begins to deposit plaques and cause atherosclerosis. The question then is: What causes Lp (a) to stick to the wall of the artery and form these plaques? "Well countless biochemists and chemists discovered what in the wall of the artery causes Lp(a) to adhere and form atherosclerotic plaques and ultimately lead to heart disease, strokes, and peripheral arterial disease. The answer is that there is a particular amino acid in a protein in the wall of the artery - lysine - which is one of the twenty amino acids that binds the Lp(a) and causes atherosclerotic plaques to develop. I THINK IT IS A VERY IMPORTANT DISCOVERY" [Linus Pauling, JON, 1994]

Furthermore he stated “ Knowing that lysyl residues are what causes lipoprotein(a) to get stuck to the wall of the artery and form atherosclerotic plaques, any physical chemist would say at once that the thing to do is prevent that by putting the amino acid lysine in the blood to a greater extent than it is normally. You need lysine to be alive, it is essential: You have to get about 1 gram a day to keep in protein balance, but you can take lysine, pure lysine, a perfectly non toxic substance in food, as pills, which puts extra lysine molecules in the blood. They enter into competition with the lysyl residues on the wall of arteries and accordingly count to prevent Lp(a) from being deposited, or even will work to pull it loose and destroy atherosclerotic plaques." [Linus Pauling, JON, Aug 1994]

Treatment of elevated Lp(a) has be proposed by Pauling in U. S. Patent # 5,278,189 for the prevention and treatment of occlusive cardiovascular disease with vitamin C and substances that inhibit the binding of lipoprotein-(a). The patent provides a method for the prevention and treatment of cardiovascular disease, such as atherosclerosis, by administering therapeutically effective dosages of a formula composed of vitamin C, lipoprotein- (a) binding inhibitors (e.g., lysine and proline or their analogs) and antioxidants.

Now since conventional medicine offers use no treatment regime for elevated Lp (a) other then the use of niacin I believe that Linus Pauling prevention and treatment plans offers us a viable and safe option.