Autopsy studies of heart attack victims have shown that many have clean vessels and normal cholesterol levels. It is obvious that there are other causes for heart disease. Indeed, researchers with the Framingham Heart Study (the decades-long study that brought us the term "risk factor") identified a relative of LDL-cholesterol called lipoprotein (a) [Lp(a)], which is now recognized as a major independent risk factor for heart disease. While LDL cholesterol maybe known as the "bad" cholesterol, Lp(a) is even worse. Lp(a) is a plasma lipoprotein that structurally resembles LDL, but with additional adhesive properties. Some of the natural cholesterol produced by the liver in response to free radical damage is converted into LDL cholesterol and its relative Lp(a). Lp(a) fosters cholesterol deposition by enhancing oxidation of LDL-cholesterol. It is the oxidized form of cholesterol that penetrates the endothelium, leading to both the buildup of plaque and vascular disease. It should be noted that artery blockage (plaque) is composed mainly of Lp(a) and not of ordinary cholesterol.

Oxidized cholesterol is a free radical generator. Research has shown that rabbits that consumed a small amount of oxidized cholesterol for merely 12 weeks had atherosclerosis plaques that were two times as big as the control population. Studies reveal that heart attack risk falls 2% for every 1% drop in LDL cholesterol level.

Studies have also shown that Lp(a) holds fast to damaged blood vessels, attracting other Lp(a) molecules, and finally constituting the atherosclerotic plaques. In fact, a high Lp (a) level (more than 30 mg/dl) has been revealed to carry a 10 times greater risks for heart disease than LDL cholesterol level.

Linus Pauling, two-time Nobel Laureate, postulated that Lp(a) may be the surrogate for ascorbate in humans. Low dietary intake of ascorbate leads to weaken blood vessels because ascorbate is required for the synthesis of collagen and elastin, which strengthen the blood vessel wall. In the absence of ascorbate, Lp(a) is mobilized to repair these structural defects in arterial walls by being deposited to strengthen the tissue. However, if the plasma concentration of Lp(a) is too high, the process goes too far. Too much Lp(a) gets deposited in the arterial wall, and plaque formation is initiated.

Chronic depletion of these essential nutrients such as vitamin C, lysine, and proline in the endothelial and vascular smooth muscle cells impairs their ability to function properly. Guinea pigs fed a diet low in ascorbate rapidly developed atherosclerotic plaques, similar to those found in humans. When large amounts of supplementary ascorbate were given to these guinea pigs, there was a regression in plaque formation.

Because humans, other primates, and guinea pigs do not produce ascorbate endogenously, they have to be supplemented from external sources. Dr. Pauling concluded that the optimum intake of Vitamin C is perhaps 100 times more than the RDA (85 mg). During the last 25 years of his life (he died at age 93 from cancer), Dr Pauling increased his own intake of Vitamin C many times, taking 3,000 mg to 18,000 mg per day. This amount is consistent with the amount of ascorbate in animals that are capable of producing their own on a daily basis. Dr. Pauling believed that cardiovascular disease is the general result of ascorbate deficiency.

Lp(a) is a simple blood laboratory test to perform. The optimum laboratory level should be under 20 mg/dl and preferably under 14 mg/dl. Currently, there is no medicine or drugs that effectively lowers Lp(a) to this level.

A high Lp(a) is genetically linked. The most effective and natural way to normalize it is a nutritional cocktail consisting of high dose Vitamin C ( 4-6 grams), L-lysine (2-4 grams), and L-proline ( 1-2 grams). Other synergistic amino acids such as glutamine, ornithine, and pine bark extract should also be included. Because high dose vitamin C can lead to diarrhea, it is very important to incorporate the fat-soluble form called ascobyl palmitate. Being fat soluble, this form of vitamin C stays in the body much longer than regular vitamin C and extends the efficacy of vitamin C in the body. At the same time it reduces the amount of vitamin C needed.

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

· Strengthening and healing damaged blood vessels
· Lowering LP(a) blood levels
· Inhibiting the binding of LP(a) molecules on the walls of blood vessels

This concept of endothelial repair advanced by Dr Pauling to lower Lp(a) is simple and logical. Once the endothelium is healed, the body will not send a signal to the liver to produce cholesterol and its related products such as LDL and Lp(a). The key is to focus on the endothelium and not focus on the liver.

Many conventionally trained physicians uses niacin or statin drugs to reduce Lp(a). This works to a limited extent. Statin drugs have some Lp(a) lowering effects by suppressing its production in the liver, but this is a band-aid approach and comes with side effects. Niacin also reduces the production of Lp(a) in the liver and helps to reduce its blood level . However, this approach has its limitations because until the endothelial wall is optimized and cleared, the Lp(a) level will not be reduced significantly. The effects of niacin or statin drug therapy usually hit a plateau after 9-12 months of therapy. The Lp(a) level seldom goes below 30mg/dl because until the endothelium is healed, the body will always instruct the liver to make cholesterol.

On the other hand, with the proper nutritional cocktail focusing on endothelial repair, drastic improvements on Lp(a) level can usually be seen within the same time frame for the majority of people. The higher the starting value, the more significant the reduction.

It is not unusual for the Lp(a) level to be slightly elevated from its baseline level in the early months of therapy ( as it is cleared from the arterial wall into the lumen) before normalizing. This is normal and is not a cause for alarm. A follow up Lp(a) test should be done 9-12 months after starting the nutritional program. While a majority of people respond favorably, some are particularly resistant, and may take up to 1 year to see a minor change. In a very small group or people, no change at all can be expected after an extended period. The good news is that there are no negative side effects. All people with high Lp(a) should be started on a nutritional cocktail program. Even if repeated blood tests do not show any improvement, vascular integrity is enhanced. There is nothing to lose and everything to gain.

2. Homocysteine

Homocysteine is an amino acid by-product of food metabolism. It contributes to atherosclerosis, reduces the flexibility of blood vessels, and increases clotting by making platelets stickier and slowing blood flow. Studies show a direct positive correlation between high serum homocysteine levels and the risk of heart attack and stroke.

A high homocysteine level is also associated with Alzheimer's disease, as well as depression, multiple sclerosis, menopausal symptoms, and rheumatoid arthritis.

Homocysteine is formed naturally when protein is broken down. Too much of it causes oxidative damage to the endothelium. Oxidative damage is caused by free radicals (byproducts of the body's normal processes that can damage body tissues). In fact, the risk for heart disease triples when the homocysteine blood level exceeds 15.8 umol/L - a reading still considered by many to be within the "normal” range (The optimum target should be under 8 umol/L). Worse yet, the odds of heart disease are directly proportional to the homocysteine concentration. The higher the blood homocysteine level, the higher the risk of cardiac disease.

This direct correlation has been well researched, including a study conducted at the University of Bergen of 2127 men and 2639 women aged 65 to 67 years between 1992 and 1993. By February 1997, 162 men and 97 women had died; 121 from cardiovascular causes (including stroke), 103 from cancer, and 33 from other causes. Using a baseline homocysteine level of 9.0 umol/L the researchers found that for every 5.0 umol/L increment increase in homocysteine levels, all-cause mortality increased by 49%, cardiovascular mortality by 50%, cancer mortality by 26%, and deaths from other causes (respiratory, gastrointestinal and central nervous system diseases) by 104%.

Looking at it another way, dropping the homocysteine level by 5 points can reduce heart disease risk by 50%. These percentages refer to values obtained after adjusting for a variety of lifestyle factors including cholesterol level, blood pressure, smoking, body mass index, physical activity, and baseline cardiovascular disease risk, as well as a couple of non-changing factors such as age and gender. About 78% of this study group had homocysteine levels at or above 9.0 umol/L and 12% had levels exceeding 15 umol/L. It is interesting to note that smoking and drinking coffee were associated with higher homocysteine levels while taking vitamins and exercising were associated with lower levels. The result is clear – for optimum heart health, lower the homocysteine level.

In another study published in the Journal of the American College of Cardiology (June 1, 2001;37:1858-1863), researchers found that heart disease patients who took 5 milligrams (mg) of folic acid daily ( not microgram or mcg) for 12 weeks had slightly better functioning of their arterial inner lining, or endothelium, and a greater ability to widen their arteries appropriately, compared to those who took an inactive placebo.

It is sad to say, but only 11 percent of all Americans get enough folic acid from its main sources - liver, kidney, broccoli, beef, kale, turnip greens, and beats. Cooking destroys as much as 90 percent of a food's folic acid content. The average American over 50 years old only takes in 130 mcg of folic acid per day. The RDA (Recommended Daily Allowance) is 400 mcg a day. Its level is also depleted by chronic alcohol consumption and medications such as anticonvulsants. In fact, studies have shown that eating 400 mcg of folic acid from food alone does not raise the serum folic acid concentration anywhere close to that obtained by simple folic acid supplementation. You need more than what food can provide.

Drugs easily deplete folic acid as well. The NSAID anti-inflammatory drugs, including aspirin and ibuprofen, deplete folic acid. The popular class of anti-ulcer drugs known as the H-2 receptor antagonists [Zantac, Tagamet, Pepcid, etc.] also depletes folic acid.

Instead of encouraging simple folic acid supplementation, the US Food and Drug Administration implemented a policy of mandating that certain food be "enriched" with folic acid in 1998. Since that time, folic acid has been added to certain grain products including cereals, breads, pastas and flour. This has resulted in higher folic acid levels in adult Americans. Unfortunately, the amount of enrichment, while enough to protect a pregnant women and their fetus from neural tube defect, is hardly enough for optimum health. Only 636 mcg is present per pound of such "enriched food”. While some of these foods are good, the majorities fall in to the category of "junk food" because of its high grain and refined sugar content. Clearly, eating such “junk food” as a method to supplement folic acid is not the best way to optimize health.

There are no medications.

How much folic acid do you need?

RDA: 400 mcg a day
For heart heath: 400 mcg 800 mcg a day
To lower serum homocysteine level: 3-20 mg a day

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