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Biophile Magazine -- » Your healthy heart

"We are constantly taking ideas from the spiritual world and forming them into our own conception of the things we desire. Sometimes the finished product does not satisfy or please us. That is because we have taken the idea away from its true parents, wisdom and love." Daily Guru

Your healthy heart

by Dr Elizna Hanekom

FILED IN: Health and Food · Issue 17


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Blaming cholesterol for atherosclerosis (hardening and thickening of arteries) makes as much sense as blaming paramedics for the carnage they face after arriving at a road accident scene. It is therefore time for the unifying perspective of coronary heart disease (CHD), found in the nutrition oriented theory as explained by Thomas E. Levy, a board certified American cardiologist and world expert on vitamin C.

Simply stated, atherosclerosis is a disease that appears to be initiated by a deficiency of vitamin C in the innermost lining of the arteries (blood vessels).. This innermost lining of the arteries once damaged by a lack of vitamin C, initiates and stimulates a host of different plaque-building processes.

Vitamin C:
Vitamin C helps to make the mortar of the structural cement (connective tissue) between cells. This connective tissue is the elastin and collagen fibre and water-filled mesh ’cartilage’ that regulates nutrient access and supports and position artery muscle and lining cells.

Long term or periodically low vitamin C weakens this connective tissue. (Fisher E, et al 1991. Diabetes: 40;3), which then allows blood to enter the artery walls, thickening and hardening them with repair and clotting materials, with calcium and with cholesterol crystals. Muscle cells then multiply inside the connective tissue to strengthen the wall, increasing the risk for heart disease and stroke. (NEJM Jan. 1999)

Vitamin C is essential for producing and maintaining the “intercellular glue” that keeps arteries strong and intact. (Pauling 1983 Aggresology: 24;7) Vitamin C deficiency has been shown to break down the “intercellular glue” into components that “leak” into the bloodstream. When the intercellular glue in the arteries becomes watery due to lack of vitamin C, the first step of atherosclerosis has taken place.
If no compensatory mechanism existed, the blood vessel would relentlessly continue its degeneration, until it became so weak that it eventually failed, with progressive enlarging of the vessel’s diameter, leaking of blood, and/or frank rupture. Photos taken of the retina (cardioretinometry) confirm that vitamin C can reverse artery disease.

Cholesterol
Cholesterol only adds to the development of atherosclerosis after the process has been initiated by degenerative arterial changes taking place because of vitamin C deficiency.
Vitamin C interacts with, and affects cholesterol metabolism in various ways. Turley et al (Atherosclerosis : 24;1-2. 1976) reviewed the literature and concluded that chronic, but latent Vitamin C deficiency leads to increased blood cholesterol.

Ginter (International J for Vitamin. and Nutrition Research :48;4.1977) showed that 1,000mg of vitamin C daily for a full year, significantly lowered serum cholesterol.
Elevated cholesterol is the body’s natural method for coping with the “lack” of vitamin. C. Artificially lowering this marker (cholesterol elevation) with drugs, has no effect on the underlying problem.

Toxin-fighting capabilities of cholesterol
Vitamin C also relates to cholesterol levels in the body in another extremely important, though indirect fashion. The scientific literature reveals an abundance of evidence, in both animal and human studies, indicating that cholesterol serves as a primary neutraliser, or inactivator of a wide array of toxic substances.. (Figueiredo et al. Medical Microbiology and Immunology: 38;1.2003). Alouf (International J. of Medical Microbiology: 290;4. 2000) reported the ability of cholesterol to neutralise a large number of different bacterial toxins capable of causing direct cellular damage.

Chi et al (1981) published data that indicated elevated serum cholesterol seemed to be a marker, if not a direct response, to a variety of toxic exposures. Finally, Huggins and Levy(Uninformed consent: The hidden dangers in Dental Care. 1999) have repeatedly observed significant drops in serum cholesterol levels in patients who have had mercury amalgams, root canals and other sources of heavy metal and infective toxicity removed from their mouths.

Overall then, it appears that one of cholesterol’s many functions in the body is that of a relatively non-specific toxin neutraliser and/or inactivator. The toxin-inactivating effects of cholesterol notwithstanding, vitamin C still appears to be the ultimate toxin neutraliser and inactivator. (virtually all toxins rapidly and significantly consume vitamin C). When higher levels of vitamin C are present to neutralise whatever toxins are present, cholesterol levels will not have to rise(and do not rise) in order to protect against those toxins.

Inflammation
Inflammation, by multiple mechanisms, appears to be a significant risk factor for atherosclerotic heart disease. Vitamin C deficiency appears to possibility help the inflammation process by the need to deliver more vitamin C to depleted areas. (Boos et al: 2006. Blood clotting, inflammation and thrombosis in cardiovascular events. Frontiers in Bioscience; 11. 2006) Also vitamin C deficiency definitely helps other inducers of inflammation to take hold in the body, such as bacterial and viral infections, as well as the toxins and autoimmune reactions they often produce.

Homocysteine
Homocysteine is an amino acid that is not found in the diet, but is formed exclusively as a breakdown product of another amino acid, methionine. New research from the prestigious Framingham Heart Study has confirmed that the first heart attacks are closely linked to high homocysteine levels—a link more evident in women Rasouli et al: (Atherosclerosis 181. 2005) showed that elevated homocysteine levels “strongly and independently” predict the progression of atherosclerosis.

When the levels of Vitamins B6, B12, and folate are too low, the conversion process of the amino acid methionine, into essential proteins gets stalled at the homocysteine level. (J. of American Medical Association 2003: 289)

Kanani also noted that oxidative stress appeared to play a role in the inability of the arteries to adequately relax in the presence of elevated homocysteine, and that vitamin C blocked this effect. (Circulation:100;11. 1999)

Lipoprotein (a)
Lp(a) is considered one of the best predictors of impending trouble with heart disease. (Von Eckardstein . J. of American College of Cardiology:37;2. 2001)

The story of Lp(a) goes back in our history some millions of years ago, when a mutation in our ancestors caused man and all primates to lose their ability to make vitamin C. Lp(a), a repair protein working like “radiator stop-leak”, uniquely developed in non vitamin C producing primates.
It is piggy-backed to LDL cholesterol, and has a sticky character, with a strong tendency to attach to sites of artery damage. This permits clumping, together with platelets, fibrin, calcium and cholesterol, at this location, decreasing the size of the artery.

Smoking
Smoking significantly lowers vitamin C content of blood.

Depression and psychosocial factors
Anxiety, stress, hostility, worry, irritability, dominance and anger all tied to the development of atherosclerosis and risk of heart attack. (Siegman et al. Psychosomatic Medicine: 62;2.2000a) All of these psychosocial factors, along with depression, appear to become most pronounced when toxin levels and cholesterol levels are high, and vitamin C levels low.

Some practical suggestions for stopping or reversing atherosclerosis:

Recommended Supplements
High vitamin C multivitamin compound
High potency vitamin B-complex
Copper and iron free multimineral
L-lysine: 3,000 to 6,000mg daily
L-proline: 500 to 1,500mg daily
Magnesium glycinate, (or other magnesium amino acid chelate): 200 to1,000 mg daily
Omega -3 fatty acids: 1,000 to 3000 mg daily with meals.
Rath and Niedzwiecki showed that a protocol involving supplementation could reliably lessen the natural progression rate of coronary artery calcification. (J. of Applied Nutrition:48:3 1996)

Minimisation of dietary toxicity
Avoid intake of high glycemic index foods, which cause a quick rush of glucose into the blood. It has been clearly established that glucose directly competes with vitamin C for the same transport mechanisms into the cells of the body. (Khatami et al. Investigative Ophthalmology ; 27:11.1986)
Emphasise fresh vegetable intake
Chew foods thoroughly
Minimise water and other liquids as drinks with meals
Minimise seafood intake (high mercury levels)

Total dental revision:
This includes proper removal of root-canal treated teeth, treatment of chronic periodontal disease, replacement of mercury amalgam and other toxic fillings and removal of dental implants.

Moderate non-competitive exercise:
Exercisers maintain significantly higher vitamin C levels than non-exercisers who consume identical amounts of dietary vitamin C.

Bibliography;
Stop America’s Nr 1 Killer. (Thomas E. Levy, MD, JD)
www.vitamincfoundation.org.

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