Currently, there are no medications or drugs that can effectively lower your Lp(a). A high Lp(a) is genetically linked.
Fortunately, Mother Nature has provided us a much better
non-toxic alternative. It consist of large
doses of vitamin C, L-lysine, and L-proline. Vitamin C, L-Lysine and
L-proline are the basic building blocks of collagen. When these vitamins enter
our bodies, they form collagen in large amounts. This is necessary, as collagen
must be replenished in blood vessels to remain healthy and plaque free over
periods of time. The reason is simple - Lp(a) is manufacturered in the liver in
response to aging vascular system and "micro-fissures" in the endothelial
vascular wall. The body, in its attempt to patch up these fissures, produce
cholesterol and its relative Lp(a).
Unfortunately, Both cholesterol and Lp(a) are sticky , making them perfect for the job.
Lp(a) is many times more
potent than cholesterol in its patching ability and has a tendency to attract
other Lp(a) particles. The aggregation of Lp(a) forms a plaque that leads
to vascular occlusion.
This mega vitamin cocktail therapy will increase blood concentrations of important substances and focuses on:
- Strengthen and heal blood vessels
- Lower LP(a) blood levels
- Inhibit the binding of LP(a) molecules in the walls of blood vessels
Only a few animals do not produce their own vitamin C, and humans are one of them. Vitamin C must therefore be taken from external source.
The amount varies between individuals and depends on
the individual's health condition. Heart patients with serious conditions
require more than normal individuals with high Lp(a). Vitamin C is water-soluble. A large amount is needed in order to reach adequate blood and tissue concentration. The amount
of ascorbic acid can be reduced if ascobyl palmitate,
In addition to the above triple cocktail (vitamin C, L-lysine, and L-proline), other foundational nutrients are important to enhance vascular wall function. These include vitamin E and L-carnitine, a natural compound stimulating fatty acid oxidation in the mitochondria. To further enhance the effectiveness of the cocktail, it is important to use bioflavonoids and ascobyl palmitate . Many conventionally trained physician uses niacin to reduce Lp(a). This does work to a limited extend. Niacin reduces the production of lipoprotein A in the liver, and helps to bring down the lipoprotein A in the blood. This is what most conventional doctors use. However, this approach has its limitations because until the endothelial wall is optimized and cleared, the lipoprotein A level will not be able to reduce significantly. The effects of niacin usually hit a plateau after 6-9 months of therapy. If you are on niacin, make sure the liver enzyme levels are taken periodically to make sure the liver is able to handle the high dose of the niacin.
Vitamin C is water-soluble. A large amount is needed in order to reach adequate blood and tissue concentration. The amount of ascorbic acid can be reduced if ascobyl palmitate,the fat-soluble form of ascorbic acid, is used at the same time. This combination is also more effective, as it allows vitamin C can stay in the body much longer.
For those who are unfamiliar with Lp(a), here are some articles on this subject:
RESEARCH ARTICLES ON LP(A)
Angles-Cano ; Structural basis for the pathophysiology of lipoprotein(a) in the athero-thrombotic process. Braz J Med Biol Res 1997 Nov;30(11):1271-80.
Lipoprotein Lp(a) is a major and independent genetic risk factor for atherosclerosis and cardiovascular disease. It is relative of LDL or bad cholesterol The difference between Lp(a) and low density lipoproteins (LDL) is apolipoprotein apo(a), a glycoprotein structurally similar to plasminogen, the precursor of plasmin, the fibrinolytic enzyme.
Lp(a) has the capacity to bind, fibrin and membrane proteins of endothelial cells and monocytes. It also stops plasminogen binding and plasmin generation. The inhibition of plasmin generation and the accumulation of Lp(a) on the surface of fibrin and cell membranes favor fibrin and cholesterol deposition at sites of vascular injury.
Price KD; Price CS; Reynolds RD; Hyperglycemia-induced latent scurvy and atherosclerosis: the scorbutic-metaplasia hypothesis. Med Hypotheses 1996 Feb;46(2):119-29.
Latent scurvy is characterized by a reversible atherosclerosis that closely resembles the clinical form of the disease.
Acute scurvy is characterized by microvascular complications such as widespread capillary hemorrhaging. Vitamin C (ascorbate) is required for the synthesis of collagen, the protein that is most critical in the maintenance of vascular integrity.
In latent scurvy, it has been suggested that large blood vessels use modified LDL, in particular lipoprotein(a) and collagen to maintain macrovascular integrity. This is because collagen will be spared for the maintenance of capillaries, the sites of gas and nutrient exchange.
The foam-cell phenotype of atherosclerosis is identified as a mesenchymal genetic program, regulated by the availability of ascorbate. When vitamin C is limited, foam cells develop and induce oxidative modification of LDL. This stabilizing large blood vessels via the deposition of LDL. The structural similarity between vitamin C and glucose suggests that hyperglycemia will inhibit cellular uptake of ascorbate, inducing local vitamin C deficiency.
Chong PH; Bachenheimer BS Current, new and future treatments in dyslipidaemia and atherosclerosis. Drugs 2000 Jul;60(1):55-93.
Nicotinic acid has been made tolerable with sustained-release formulations, and is still considered an excellent choice in elevating HDL cholesterol. It is also potentially effective in reducing lipoprotein(a) [Lp(a)] levels.
Although LDL cholesterol is still the major target for therapy, it is likely that in future, other lipid/lipoprotein and nonlipid parameters will also become targets for specific therapeutic interventions. Other significant lipid/lipoprotein parameters that have been associated with CHD include elevated triglyceride, oxidized LDL cholesterol and Lp(a) levels, elevated C Reactive Protein, elevated homocysteine, and low HDL levels.