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Oral Chelation

Michael Lam, MD, MPH

The concept of chelation therapy as a way to remove heavy and toxic metal has been well established as a standard medical procedure for over 50 years. It is approved by the FDA for treatment of  lead toxicity.  The use of  IV chelation therapy for cardiovascular disease and atherosclerosis (made popular by a book called Bypassing Bypass) has met with extensive resistance from  mainstream medicine. There is little doubt that it works well when offered as a treatment of last resort, especially for those with end stage peripheral vascular disease needing amputation. While the precise mechanism is not well understood and  has been under intensive  debate over the years, modern research has shown that chelation therapy exerts its cardiovascular effect primarily at the endothelium level and not simply a "rooter-router" type concept we were once led to believe.

 Let us take a closer look.


We all know that atherosclerosis is the main cause for heart attack and strokes. It  is the end result of injury that started at the extremely thin layer of endothelial cells that line the inside surface (the lumina) of the heart and blood vessel walls. Circulatory toxins such as toxic metals ( lead, mercury, aluminum, cadmium, arsenic etc.), smoke, free radicals, sugar and infections cause these injuries. Numerous established studies have confirmed that an impaired endothelial function is linked to all major coronary heart diseases.

Although the endothelium is extremely thin, it is a highly complex structure in terms of function. It regulates the structural integrity of the vascular wall by secreting numerous factors that determine not only the contractility of the walls but also the homeostasis of the blood. One of the most important chemicals secreted by the endothelium is nitric oxide (NO). NO is a potent vasodilator and a strong anti-oxidant. When the endothelium is damaged, NO production is reduced. This leads to the reduction of vasodilatation, or conversely, an increase in vascular constriction. Reduced NO production, as a result of toxic metal, insult leads to  a reduction in vascular lumen size, restriction of blood flow, and ultimately increase in blood pressure. This means, in layman's terms, an increased risk of stroke and heart attack.  Fortunately, endogenous production of NO can be enhanced. The amino acid arginine is a direct precursor to the synthesis of NO. Those interested in helping the body produce more NO can consider taking a high dose of arginine ( 4 grams per day) together with 1 gram of vitamin C ( in the form of mineral and fat soluble ascorbates) and vitamin E ( 800 I.U.)

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, where insults excite an inflammatory response, the endothelium is therefore the first link between inflammation and coagulation. The endothelium also represents a surface where proteins are involved in coagulating. It is also here that the development of inflammation are expressed.

We will now look at the cascade of events a little closer. A high sugar diet  or heavy metal toxin, or  an environment full of cigarette smoke produces toxins, such as free radicals, that 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.

The characteristics of an inflammatory response are as follows: -

1. Vasodilatation to increase blood flow to the area.

2. Increase vascular permeability to allow diffusible components to enter the site.

3. Cellular infiltration by chemotaxis, or the directed movement of inflammatory cells through the walls of blood vessels to the site of injury.

4. Changes in biosynthetic, metabolic, and catabolic profiles of many organs.

5. Activation of cells of the immune system as well as of complex enzymatic systems of blood plasma.

During an inflammatory response, our blood flow is increased to transport more white blood cells to the injured area. The white blood cells first surround the damaged tissue, then together with the other cells in the damaged tissues neutralize, repair the damage and remove whatever is causing the injury. This reaction can be measured in the blood by the elevation of a substance called C reactive protein.

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.

By removing the circulatory heavy metal toxins, EDTA enhances cardiovascular blood flow and function.

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