Defeating Heart Disease
Therefore, heavy metal toxicity leads to decreased amounts of Nitric Oxide, which leads to unrelaxed blood vessels and associated decreased blood flow, AS WELL as vulnerability to infection of fresh cholesterol by low grade virus, such as Herpes, that can form and break a vesicle within an artery and cause an immediate Hypercoagulable state, with a subsequent blood clot formation and sudden death. Not only are scientists discovering that “normal” blood ranges of heavy metals are much too high for healthful longevity, but that unsuspected heavy metals are the cause of much cardiovascular disease, especially high blood pressure. It is especially imperative to correctly assay for lead if a patient has hypertension because it can not only destroy the kidneys but also brain function.
Chelation Therapy appears to restore the body’s ability to create the important substances, Nitric Oxide (N.O.), prostacyclin and heparin, by removing these metals from the endothelial lining. It’s been shown that EDTA blocks the slow calcium currents in the arterial wall, resulting in arterial vasodilation.
A formidable amount of data exists that clearly indicate the insidious toxicity of non-physiological metals such as mercury, lead, nickel, cadmium, arsenic and aluminum where specific mechanisms for the neurotoxic, nephrotoxic and immune-dysregulatory effects of these metals are identified.
High Blood Pressure
Today it is imperative for anyone with high blood pressure, heart disease, prostate issues, cardiovascular disease, chronic fatigue, or cancer, to rid the body of heavy metals. Heavy metal toxins such as lead, mercury, aluminum, cadmium and arsenic, have been clinically proven to damage and cause dysfunction in the lining of the arteries. Numerous established studies have confirmed that an impaired endothelial function (within the lining of the arteries) is linked to all major coronary heart diseases. Heart Disease is the end result of injury that started at the extremely thin layer of endothelial cells that line the inside surface of the heart and blood vessel walls.Endothelial cells play a vital role in the health and integrity of every tissue of the body.
Atherosclerosis is the main cause for heart attack and strokes. The endothelium is inner lining of blood vessels. This lining tissue generates the powerful arterial vessel dilator nitric oxide (N.O.). The endothelium also produces prostacyclin which slows the clotting of blood and also causes beneficial dilating of arteries. The third important endothelial product is heparin which prevents clots from forming without causing bleeding. Excessive deposition of heavy metals in the endothelium diminishes the endothelium’s ability to produce nitric oxide, prostacyclin, and heparin. *Iron and the sex differences in heart disease risk, Lancet, 1981 June 13; 1(8233):1293-1294. In addition, EDTA blocks the slow calcium currents in the arterial wall, resulting in arterial vasodilation.
One of these problem metals, mercury, is known to cause damage to enzymes so mercury removal should be beneficial. Removal of these metals appears to result in improved delivery of oxygen and nutrients to the tissues of the body. The theory of EDTA removing the solid sticky plaque with a unique mechanism, and dangerous solids being converted to a liquid, then transported away to be eliminated as a natural, normal phenomenon of body chemistry is still held by some. It does appear however that the discovery of N.O. production increasing with EDTA chelation is exactly what is happening, and that the excess plaque is removed through normal metabolic functions due to the body achieving a new level of homeostasis. This affords a possible explanation for the beneficial effects of chelation.
In 1999, Dr. Valentin Fuster, M.D. published a Book called The Vulnerable Atherosclerotic Plaque. Dr. Fuster was at the time the President of The American Heart Association, and also was and still is the Chairman of the Department of Cardiology at Mount Sinai School of Medicine in New York City. This book shows that heart attacks do not occur in areas of maximal plaque buildup where calcium has hardened large deposits of cholesterol, but in fact occur in fresh, “vulnerable” plaques that get INFECTED with germs, such as Epstein Barr Virus, Herpes Virus, Cytomegalovirus, and other low level germs that infect humans.
Toxic heavy metals are ever ready to attack the endothelium. The endothelium, in an attempt to heal itself, launches an inflammatory response to get rid of the unwanted guests. Researchers are now in the process of studying and proving that these germs are more prevalent and “infectious” when N.O. is not present in sufficient amounts. By removing the circulatory heavy metal toxins, EDTA enhances cardiovascular blood flow and function. N.O. is a potent vasodilator and a strong anti-oxidant. When the endothelium is damaged, N.O. production is reduced. This leads to the reduction of vasodilatation, or conversely, an increase in vascular constriction. Reduced N.O. production, as a result of toxic metal insult, leads to a reduction in vascular lumen size, restriction of blood flow, and ultimately an increase in blood pressure. This means, in layman’s terms, an increased risk of stroke and heart attack.
The proper amount of NO secretion is therefore of paramount importance, as imbalance of this contractility function will lead to hypertension, the silent killer. If the local vascular homeostasis is disturbed, it will result in platelet deposition, aggregation and a release of factors that promote smooth muscle proliferation. When this happens, you may get fibrosis, atherosclerosis and thrombus formation. As imbalances are first initiated at the endothelial level, where insults excite an inflammatory response, the endothelium is therefore the first link between inflammation and coagulation.
Meanwhile, a small amount of LDL (“Bad”) cholesterol that has built up in the artery wall becomes oxidized. Oxidized LDL is one of the triggers that set off a chain reaction. It causes the endothelium to express a special kind of molecule “glue” called ELAMS (endothelial-leukocyte adhesion molecules). These molecules, which happen to be floating by in the bloodstream causes certain kinds of white blood cells (monocytes and T lymphocytes) to stick to the endothelium. At this point in time, the inflammatory response is still well under control and normal, whether it is in the artery or in the tissue.
Beyond this point, the healing process goes off track. The white blood cells will start to move between and below the endothelium and cause damage in two major ways. Firstly, they will cause some of the muscles cells in the artery walls to grow and secondly, they incorporate particles into the artery wall, consuming the oxidized LDL particles. What results from here is a fatty streak that becomes a fibrous plaque.
This intricate process begins in the tissue under the endothelium. Due to inflammatory reactions, the endothelium’s structure becomes permeable to lipoproteins, particularly low- density lipoproteins (LDL) and macrophages. These particles will enter into the site of injury, accumulate cholesterol as cholesterylester and develop into foam cells. A raised LDL-cholesterol and related cholesterol carrier called lipoprotein (a) concentration is recognized by many as a major risk factor for heart disease as it appears to be the donor of cholesterol deposited in the atherosclerotic plaque. Being adhesive, the cells will attract other substances, resulting in a continuous deposition of unwanted conglomerate which we call fatty streak. The latter consists of lipids (fats), complex carbohydrates, blood, blood products, fibrous tissue, oxidized ascorbates and calcium deposits. As the fatty streak becomes increasingly larger, this resulting fibrosis forms an “endothelial tumor” or a plaque. The process of plaque formation is called atherosclerosis. Atherosclerosis blocks the blood’s pathway and narrows the arteries over time. This affords a possible explanation for the beneficial effects of chelation. In addition, EDTA blocks the slow calcium currents in the arterial wall, resulting in arterial vasodilation.
Probably the major underlying condition leading to cardiovascular disease is atherosclerosis, also known as hardening of the arteries. In time, this degenerative disease can narrow or block arteries in the heart, brain, and other parts of the body. It may begin early in life. The linings of the arteries become thickened and roughened by deposits of fat, cholesterol, fibrin (a clotting material), cellular debris, and calcium. As this buildup on the inner walls becomes hard and thick, arteries lose their ability to expand and contract. The blood moves with difficultly through the narrowed channels. This makes it easier for a clot to form that will block the channel (lumen) and deprive the heart, brain, and other organs of the necessary blood supply. In such a situation, how can dilator drugs possibly be effective?