Two Natural Protocols Shown to Reverse Heart Disease.

Join the growing number of people that are tracking the reversal of their heart disease on the Track Your Plaque Message BoardsThere you can read about many cases of regression of atherosclerotic disease with protocols based on Natural Protocol #1. (There is a modest membership fee for TYP) 

Natural Protocol #1: These are the natural products (existing in the body), primarily based on the research from Dr Linus Pauling and his colleagues, that Dr. Owen Fonorrow (don’t be dissuaded by the negative posts regarding a business he used for marketing) used as he demonstrated a reversal of heart disease in his patients. In 1996, a CAT scan coronary calcium score study validated the protocol showing a 15% reversal of calcification indicating reversal of coronary artery disease. Complementary Medicine doctors such as Dr. Dach are seeing similar results using this protocol.

  1. Take Vitamin C as ascorbic acid (3 to 18 g per day in divided doses, 3-4 times a day)

High doses can cause loose stools, so you may find your own body’s limit.

  1. Take Lysine. 2 to 3 g daily for prevention and from 3 to 6 g daily for the greatest therapeutic benefit.

  2. Take Proline from 250 mg to 2000 mg daily. Recently, this amino acid was found to be an even more effective Lp(a) binding inhibitor than lysine in vitro

  3. Supplement Coenzyme Q10 (100-300 mg/day) CoQ10 is a vital substance for energy and proper heart function. Beware that Statins and Red Yeast Rice block the enzyme for your body’s production of CoQ10 in addition to cholestereol.

These supplements can be obtained at any the health food store as tablets or capsules for 40 to 50 dollars a month.  A convenient powder form can be obtained at Tower Laboratories.  They have a product called Heart-Tech  which provides the Linus Pauling Protocol in powder form.  There is also the Vitamin C FoundationCardio-C which provides 2500 mg vitamin C and 2500 mg lysine per serving plus 500 mg proline.

Of further interest, Steve Hickey and Hilary Roberts come right out on page 167 of their book, and make the statement, “Vitamin C and Tocotrienols can reverse coronary artery disease”.  They would add the Tocotrienol form of Vitamin E to the Linus Pauling Protocol.  Regarding heart disease, and atherosclerotic vascular disease, the authors state that “on the available evidence, the combination of Vitamin C and Tocotrienols could be curative with no known harmful effects.”

See Linus Pauling Background Research Below

Natural Protocol #2: Dr. Dean Ornish has documented the reversal of Heart Disease using a multi-disciplinary approach:

Linus Pauling Background Research

See  for more details, examples and ordering supplements.

In 1989, after the discoveries of the Lp(a) cholesterol molecule (circa 1964) and its lysine binding sites (circa 1987), Linus Pauling and his associate Matthias Rath formulated a unified theory of heart disease and invented a treatment. Vitamin C and lysine (and proline) in large amounts become Lp(a) binding inhibitors that restore vascular health and are patented to destroy atherosclerotic plaques

Humans have a genetic mutation (GULO genetic defect in primate DNA) that make them one of the few species that fail to synthesize ascorbic acid (vitamin C). The theory that Cardiovascular Disease (CVD) is related to a deficiency of vitamin C was first proposed by the Canadian physician G. C. Willis in 1953. He found that atherosclerotic plaques form over vitamin-C-starved vascular tissues in both guinea pigs and human beings.

Willis devised a method of photographing plaques with X-rays and observed that atherosclerotic plaques were not uniformly distributed throughout the vascular system; rather these “blockages” are concentrated near the heart, where arteries are constantly bent or squeezed. Imagine stepping on your garden hose a thousand times a day.  You will soon notice cracks in the wall of the garden hose. This is the same process that happens in the artery

Another Canadian, Paterson, had found that the tissues of heart patients were generally depleted of vitamin C, and it was well known that vitamin C is required for strong and healthy arteries. Willis reasoned that only the mechanical stress caused by the pulse could explain the typical pattern of atherosclerosis. To Willis, the body was laying down plaque precisely where it was needed in order to “patch over” the tiny cracks from the bending of the arteries.  

By the late 1980s, medical researchers confirmed that heart disease begins with a lesion or crack in the arterial wall. Then a variant of the so-called “bad” LDL cholesterol called lipoprotein(a), or Lp(a), was studied and found to be really bad.  Lp(a) is sticky because of receptors on the surface of the molecule called lysine binding sites. Work that led to the 1987 Nobel prize in medicine discovered that lysine (and proline) binding sites cause the formation of atherosclerotic plaques. Then, Beisiegel et. al. in Germany examined plaques post mortem and found only Lp(a), not ordinary LDL cholesterol.

Lp(a) was the genetic difference between beings that suffer cardiovascular disease and those that do not. Lp(a) had evolved only in species that do not make their own vitamin C – e.g. humans and guinea pigs.

Pauling and Rath researched Lp(a). They discovered that it becomes elevated in guinea pigs deprived of vitamin C, but not in the controls. They realized that in most species, sufficient ascorbic acid will prevent cracks in the vessel wall, but in those species that suffer chronic low Vitamin C levels, Lp(a) had evolved to patch cracked blood vessels.

As this process progresses, the liver produces more Lp(a) molecules. As the number of Lp(a) molecules increases, they tend to deposit on top of existing plaque formations. When the healing process overshoots, the arteries narrow and the flow of blood is reduced.

This problem has a solution. The Lp(a) molecule has a finite number of lysine binding sites – points of attachment to lysine. Pauling’s invention – his treatment for heart disease – is to increase the serum concentration of the amino acid lysine, and as more lysine enters the blood stream, the probability increases that floating Lp(a) molecules will bind with it (rather than with the patches of plaques growing on the arterial walls.)

After all the Lp(a) molecule’s binding receptors are filled with the free lysine floating in the blood, the Lp(a) molecule becomes as harmless as ordinary LDL cholesterol.

Pauling and Rath called the substances that destroy existing plaques Lp(a) binding inhibitors. Vitamin C, to increase collagen production and to improve the health and strength of arteries, and lysine, to prevent and to dissolve Lp(a) plaques, are the primary binding inhibitors. These substances taken together are clinically effective.

Linus Pauling believed that chronic scurvy can be prevented with a daily intake of between 3,000 to 10,000 mg or more vitamin C. This amount approximates what the animals synthesize, and matching animal production is the reason Pauling ingested 18,000 mg daily.

Pauling and Rath’s invention for destroying existing atherosclerotic plaques is the large amount of another essential nutrient, the amino acid lysine. Pauling filmed a video lecture in which he recommended that heart patients take between 2,000 and 6,000 mg of lysine daily with their vitamin C (more if serum Lp(a) is elevated). Neither vitamin C nor lysine have any known lethal dose.

The Lp(a) binding inhibitors become the Pauling Therapy for heart disease only at high dosages, between 3 to 18 g ascorbic acid and 3 to 6 g lysine. In his video, Pauling recounts the first cases where his high vitamin C and lysine therapy quickly resolved advanced cardiovascular disease in humans. The effect is so pronounced, and the inhibitors are so nontoxic, that Pauling doubted a clinical study was even necessary.

Recently, the amino acid proline was found to be an even more effective Lp(a) binding inhibitor than lysine in vitro. Adding between .5 and 2 g proline may be of significant additional benefit.

When serum Lp(a) is elevated, Lp(a) binding inhibitors can profoundly interfere with the disease process. Binding inhibitor formulas that include proline have been documented to lower Lp(a) in six to 14 months. In cases where Lp(a) is not reduced, binding inhibitors become even more important to neutralize Lp(a) regardless of their effect on serum Lp(a).

Recently a reevaluation of the Framingham Heart study that Lp(a) and not ordinary LDL is highly predictive of CVD and Oxford found that elevated Lp(a) increases the risk of heart attack and stroke by 70%.



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