Reducing lipoprotein a

What is lipoprotein a ?

Lipoprotein A, commonly called Lp(a), is a major independent genetic risk factor for cardiovascular disease (CVD) and atherosclerosis. It is a 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. The optimum laboratory level should be under 20 mg/dl and preferrably under 14 mg/dl.

Frequently Asked Questions

  • 1How does lipoprotein a promote atherosclerosis?
  • 2When does one lower lipoprotein a?
  • 3In which patients should lipoprotein a be measured?
  • 4How do we reduce lipoprotein a at Health Renewal?
  • 5What other blood parameters have been associated with cardiovascular disease and atherosclerosis?
  • 6How does one treat Lipoprotein a?
  • 7How does Vitamin C, L-Lysine and L-proline work?
  • 8What other supplements does one need to help reduce lipo protein a?
  • 9What benefits does nicotinic acid / niacin have on atherosclerosis blood profile?
  • 10How long does it take to see an improvement in Lipoprotein a levels?
  • 11What are the additional benefits of nicotine acid supplementation?
  • 12Can Lipoprotein a be reduced with diet and lifestyle intervention ?
  • 13Can Prescription medication will help reduce Lipoprotein a?
  • 14What other medical options are there for compromised coronary artery disease and raised lipoprotein a?

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, produces cholesterol and its relative Lp(a). Unfortunately for patients with a raised lipoprotein a, both cholesterol and Lp(a) are sticky, and this ACCELERATES the "patching up" of the micro fissures and promotes atherosclerosis and plaque. 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.

There is also some experimental data suggesting that Lp(a) MAY PROMOTE CLOT FORMATION in arteries burdened by atherosclerotic plaque. This may be one of the mechanisms behind the involvement of Lp(a) in heart attack and stroke. 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 FAVOURS fibrin and cholesterol deposition at sites of vascular injury.

Consistent with treatment guidelines, reduction of elevated Lp(a) levels should be a secondary treatment priority, after maximal lowering of LDL-C.

The EAS Consensus panel recommends that Lp(a) should be measured in high risk individuals such as those with premature CVD, familial hypercholesterolemia, family history of premature CVD and/or elevated Lp(a), and individuals with recurrent CVD despite statin therapy.

At Health Renewal you will have a prolonged consultation with one of our experienced functional medicine doctors. After a thorough history taking and evaluation, specialized blood investigations will be requested to evaluate your cardiovascular risk factors. At your 2 week follow up the results will be discussed with you and lipoprotein a reducing supplements together with other vessel protective supplements.

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.

Currently, there are no prescription medications or drugs that can effectively lower your Lp(a).

A high Lp(a) is genetically linked. Fortunately, there is a non-toxic alternative to lower lipoprotein a which consists 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.

This mega vitamin cocktail therapy will increase blood concentrations of important substances and focuses on:

  • Strengthening and healing blood vessels
  • Lowering LP(a) blood levels
  • Inhibiting the binding of LP(a) molecules in the walls of blood vessels

In addition to the above triple cocktail (vitamin C, L-lysine, and L-proline), other foundational nutrients are important to enhance vascular wall function which include:

  • Vitamin E and L-carnitine, a natural compound.
  • To further enhance the effectiveness of the cocktail, it is important to use:
  • Bioflavonoids and ascorbyl palmitate stimulate fatty acid oxidation in the mitochondria.
  • 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 ascorbyl palmitate, the fat-soluble form of ascorbic acid, is used at the same time. This combination is also more effective, as it allows the vitamin C to stay longer in the body. The body does not produce its own vitamin C, and therefore must be taken from an external source.

Studies using niacin alone or in combination with, for example, statins have shown cardiovascular benefit:

Niacin reduces Lp(a) levels by up to 30–40% in a dose-dependent manner and in addition exerts other potential beneficial effects by reducing LDL cholesterol, total cholesterol, triglycerides, and remnant cholesterol and by raising HDL cholesterol. In a meta-analysis including 11 randomized controlled trials with 2682 patients in the active group and 3934 in the control group, niacin 1–3 g/day reduced major coronary events by 25%, stroke by 26% and any cardiovascular event by 27%.

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. 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. 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.

Improvements on Lp(a) level can usually be seen within weeks to months for the majority of the people. The higher the starting value, the more significant the reduction will be. Lp(a) can be completely normalized and bought to optimum level of under 14 mg/dl on nutritional therapies alone if treated properly. Unfortunately, not all people show positive signs of reduction. Some people are particularly resistant, and may take upwards of 1 year to effect minor change. In a small group or people, no change at all can be expected. All people with high Lp(a) should be started on a nutritional cocktail. Even if if repeat blood level do not show any improvement, vascular integrity is enhanced.

In addition to lowering Lp(a), niacin lowers:

  • LDL cholesterol,
  • total cholesterol,
  • triglycerides,
  • and remnant cholesterol,
  • and concomitantly increases HDL cholesterol levels.

Therefore, the favourable effects of niacin on CVD cannot be ascribed solely to Lp(a) reduction. Nevertheless, these studies clearly demonstrate that the use of niacin for reduction in Lp(a) to the suggested desirable levels is safe and in all likelihood beneficial.

Lp(a) is mainly genetically determined and therefore refractory to lifestyle intervention. Dietary changes, exercise and weight loss have not been shown to lower Lp (a). Compared with LDL, Lp(a) is relatively refractory to both lifestyle and drug intervention.

  • Fat consumption has NOT been shown to raise Lp(a). One study documented a lowering of plasma Lp(a) levels in individuals placed on diets RICH IN saturated fat (a palm oil enriched diet).
  • In keeping with this, other investigators have reported an INCREASE in Lp(a) levels in individuals after they reduced their saturated fat intake.
  • Monounsaturated fats also seem to reduce Lp(a) levels, as shown by a study that reported a significant decrease in Lp(a) levels in individuals whose diets were supplemented with almonds.

The data on the effects of statins (Zocor/ Crestor/ Lipitor) and fibrates on Lp(a) are limited and highly variable. Overall, statins have, however, been shown to consistently and modestly decrease elevated Lp(a) in patients with heterozygous familial hypercholesterolaemia.

What other prescription agents reported to decrease Lp(a) to a minor degree (<10%) ?

  • calcium antagonists,
  • angiotensin-converting enzyme inhibitors
  • thyroxine replacement in hypothyroid subjects
  • Aspirin is also known to modestly decrease lipoprotein a
  • Oestrogen replacement therapy in women has been shown to lower Lp(a), although by less than 10 percent
  • Androgens and anti-estrogens (e.g. tamoxifen) may lower lipoprotein a.

In young or middle-aged patients with evidence of progressive coronary disease and markedly elevated plasma Lp(a), serious consideration should be given to instituting LDL apheresis which removes Lp(a) efficaciously. This form of treatment is prohibitively expensive and impractical for most patients and most clinical centres.

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