EDTA Chelation and the Removal of Toxic Metals
The concept of EDTA 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 EDTA chelation therapy exerts its cardiovascular effect primarily at the endothelium level and not simply a “router-rooter” type concept we were once led to believe.
Let us take a closer look.
EDTA and Endothelium
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:
- Vasodilatation to increase blood flow to the area.
- Increase vascular permeability to allow diffusible components to enter the site.
- Cellular infiltration by chemotaxis, or the directed movement of inflammatory cells through the walls of blood vessels to the site of injury.
- Changes in biosynthetic, metabolic, and catabolic profiles of many organs.
- 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.
EDTA Chelation and Cancer
Modern humans have 1,000 times more lead in their bones than their ancestors just 400 years ago. Lead from automobile exhausts, petrochemicals from wear of automobile tires, cadmium, and other carcinogens are omnipresent. Ongoing exposure to thousands of US workers and recent research indicates that asymptomatic and sub-clinical lead exposure can result in chronic toxicity manifestations, such as hypertension, kidney impairment, and symptoms of dementia. Other toxic metals include mercury, a potent neurotoxin even at minute doses, as seen in dentists’ offices. Arsenic is clearly carcinogenic, and cadmium is now being recognized as a contributor to osteoporosis.
These substances cause cancer and potentate other carcinogens. EDTA is a highly effective way to bind excessive lead and lower the lead level from tissues and organs (but not from bones where the majority of lead is stored and released slowly with time).
In addition to lead, EDTA also removes unwanted nutritional elements such as excessive free iron, which promotes cancer by catalyzing free radical pathology. Most cancer cells have a strong affinity for iron. Removal of excessive iron is an important factor of many anti-cancer therapies.
In a study conducted by Walter Blumer, M.D. published in Journal of Advancement in Medicine ( Volume 2, Numbers 1/2, Spring/Summer 1989), it was found that mortality from cancer was reduced 90% during an 18-year follow-up of 59 patients treated with an IV push of calcium EDTA. It is important to note that treated patients had no evidence of cancer at the time of entry into this study. Observations relate only to long-term prevention of death from malignant disease, if chelation therapy is begun before clinical evidence of cancer occurs. The use of chelation as a cancer prevention tool should be on the minds of all those at high risk for cancer.
In this study, control and treated patients were selected from the same neighborhood in a small town in Europe. Both groups lived next to a heavily traveled highway. Both groups were exposed to the same amount of lead from automobile exhaust, industrial pollution and other carcinogens. The level of exposure was measured and was found to be no greater than those existing in most other metropolitan areas throughout the world. Specifically, the traffic flow past the residences of the study subjects, was 4000 vehicles per day in 1956 and increased to 8000 vehicles per day in 1968. Of those, 7000 were passenger cars and 400 were diesel trucks.
The results of this longitudinal study are quite remarkable. Over a period of 18 years, only one of 59 treated patients (1.7%) died of cancer while 30 of 172 non treated control subjects (17.6%) died of cancer. Statistical analysis showed EDTA chelation therapy to be the only significant difference between controls and treated patients and serves to explain the marked reduction in cancer mortality.
IV EDTA Chelation
EDTA is a chemical that is widely used as a food preservative (and therefore generally recognized as safe). We are in fact exposed to about 20- 50 mg of this everyday simply from the food that we eat. It is approved by the FDA in treatment of lead toxicity. Usually a solution mixed with magnesium bound EDTA is the agent of choice in IV chelation therapy practiced during the past 50 years by American doctors. Because EDTA has a higher affinity towards calcium in comparison to magnesium; magnesium is released while calcium is picked up. Too fast of a removal of calcium from the blood stream, however, is not productive and it can lead to a dangerous condition known as hypocalcaemia and serious medical side effects. For this reason, the IV drip must be administered slowly. One session of IV chelation takes about 2-3 hours, infusing 1.8 to 3 grams of sodium-EDTA intravenously. A course of treatment usually entails 30 sessions, with one to three treatments per week. The patient sits in a comfortable chair, and the EDTA is painlessly dripped into the veins via an intravenous solution ( or “soup” ) mixed with minerals and vitamins. In addition to the traditional form, a quicker IV push format, advanced by Dr. Walter Blumer of Switzerland, also proved to be very beneficial as well. In this process, the calcium bound EDTA is used. There is no worry about calcium depletion because the calcium is delivered together with the EDTA. The calcium is given up, as the EDTA binds metals it has a higher affinity for, such as lead. The best news is that this can be administered painlessly over a matter of minutes instead of hours.
According to Dr Robert Rowen, a noted alternative medicine doctor and editor-in-chief of Second Opinion, Dr Blumer’s research showed remarkable cardiovascular benefits of IV push calcium EDTA. There is an astonishing 90% reduction in heart attacks in Dr Blumer’s patients receiving only calcium EDTA by the quick-push method, over decades of clinical use. In his study, 343 patients were studied with an average age of 44 and were administered 2-3 grams of calcium EDTA twice a week for 5 -10 weeks. He noted complete resolution of cardiac symptoms.
EDTA enhances the cardiovascular system by enhancing endothelial function through the removal of toxic metals that are detrimental to endothelial health. It chelates heavy metal from the vascular wall, kidney and brain. EDTA binds to toxic metals such as lead, free iron, cadmium, arsenic, and to a lesser extent, mercury When the level of toxic metal is reduced, the endothelium will function better. Increased levels of nitrous oxide will be released, and the peripheral vascular flow will increase while blood pressure is normalized. Calcium from the endothelium wall is not removed by EDTA.
Oral EDTA Chelation
While most IV EDTA chelation doctors are trained to believe that IV EDTA chelation is the only way that works, advanced researches have now shown that oral EDTA chelation therapy can also have beneficial effects, although less potent than the IV form.
There are various forms of EDTA available in oral form. The most common of which is calcium-bound EDTA. Calcium, however, is not the best mineral for the aging body. Contrary to popular belief from research over 30 years old, the newer longitudinal studies are showing that calcium, in excess of 300 mg a day, does not contribute to bone strength. Excess calcium can lead to increased cardiac irritability and arrhythmia. In fact, calcium-channel blockers are routinely used by doctors world-wide to treat hypertension. Excessive calcium also leads to calcium deposits in soft tissues. What our body needs is more magnesium, an increasing 80% of Americans are deficient in even getting the RDA suggested dose of 350 mg of Magnesium per day. EDTA has a higher affinity for calcium than magnesium. Oral EDTA chelation goes to work not only by binding the unwanted toxic metals, but also leads to the release of magnesium from the EDTA molecule while binding excessive calcium from our body. Because the oral form works slowly, there is no worry about dropping the amount of calcium in our body too quickly, as in the case of IV chelation.
The best form of oral EDTA chelation product should contain magnesium bound EDTA. As the EDTA is delivered, magnesium is released. Magnesium is needed in over 300 enzymatic reactions in the body. It helps to relax smooth muscles of the heart and lowers blood pressure. It is nature’s calcium-channel blocker. It also helps relax the mind and act as a natural sleeping pill and tranquilizer.
Taking 1,800 mg a day of oral magnesium bound EDTA chelation for 20 days (300 mg x6 tablets daily) at a 5% intestinal absorption rate, will deliver the same amount of EDTA to the blood stream as one IV session of 1,800 mg.
90% of the oral EDTA pass through the gut. In this process, it binds to ingested toxic metals, such as mercury found in fish. A complete chelation program should therefore consist of an intravenous component as well as an oral component. The oral component works on the gut to remove ingested toxic metal. It also serves as a long term maintenance program to remove the slow leakage of lead from its reserve in our bones (where it is kept). Without an ongoing oral maintenance, to remove the lead released from our bones, IV EDTA chelation will not be able to keep the lead level in check once IV therapy is stopped. Separately, the IV form works on the endothelial cells. Therefore, both the oral and IV form work on very different pathways and, in fact, complement each other.
Before embarking on oral or IV EDTA chelation treatment, accurate determination of the degree of minerals and toxic element presence should be carried out. Since serum levels are not accurate, it is best to perform a pack red blood cell intracellular element analysis. Hair mineral analysis is another method of measuring the amount of mineral present in the body. Though the result reflects historical data, a standardized reference standard is not readily available, and interpretation can vary from laboratory to laboratory.
Alternatively, a 24 hour, 6 hour, or spot urine (pre and post-provocation study using oral chelation agents such as EDTA-Mg K2 or DMPS) is a good way to yield a qualitative and quantitative analysis of the amount of mineral and toxic metal load in the body prior to starting of chelation treatment to remove toxic metal. Such tests can be repeated 3 months after treatment in order to determine the degree of toxic metal removal.
It is important to note that anyone on EDTA chelation treatment must be supplemented with a high potency, anti-oxidant and mineral, formula which adequately protects against chromium deficiency. Up to 400 mcg of chromium polynicotinate is needed for the healthy, and up to 800 mcg for those with diabetes because chromium is easily bounded to EDTA and excreted out of the body.
In addition to EDTA, garlic and selenium are good chelators of mercury; and malic acid is a good chelator of iron.
Dr. Guy Abraham is a recognized authority on oral chelation. Here is what he has to say about it.
Dr. Abraham’s Abstract on Oral EDTA Chelation:
By Guy E. Abraham, M.D. FACN
It is estimated that over 400,000 individuals have undergone intravenous (IV) EDTA chelation therapy since its inception some 50 years ago (1). The usual dosage per session is 3 grams of the disodium salt. Magnesium is added to the IV fluid for its known biological effects. Since only a few milligrams of lead and other toxic metals are excreted in the urine in response to IV EDTA, the use of 3 grams of EDTA seems excessive.
Based on studies performed with radioactive EDTA in young adult male subjects, oral EDTA is poorly absorbed by the intestinal tract, with an estimated bioavailability of less than 5 percent (2). However, one must keep in mind the fact that detoxification of heavy metals by EDTA occurs also in the gastrointestinal tract by blocking reabsorption of these metals after secretion by the liver in the bile, which is then excreted in the intestinal tract. The intestinal route of detoxification of toxic metals by EDTA is as important as their renal excretion. The binding affinity of EDTA for heavy metals is high enough to prevent their intestinal reabsorption, after EDTA chelation of these metals in the intestinal tract.
The first study on oral EDTA in human subjects was published in 1953, some 50 years ago (3). Seven patients with increased levels of blood and urine lead levels were treated with Ca EDTA both orally and intravenously. The urinary excretion of lead was 10 to 40 times above baseline following IV EDTA, whereas it was 5 to 10 times higher with oral EDTA. The blood lead levels and red blood cell abnormalities improved in patients receiving IV and oral EDTA. Considering the fact that IV EDTA is at least 20 times more bioavailable than the oral route, enteral EDTA compares favorably to the IV route.
The second study of oral Ca EDTA disodium was published in 1954, using a daily dose of 2 grams for 7 days (4). In the symptomatic patients with lead intoxication, the symptoms improved remarkably following oral EDTA and the blood profile returned to normal. No disturbance of serum electrolytes was observed.
In 1956, a third publication reported the results of a study using a daily oral dose of 4 grams of Ca EDTA disodium in 14 patients with industrial lead poisoning (5). There was a marked increase in urine lead excretion, from 5 to 35 times baseline levels. There was a marked increase in fecal lead excretion also, above the estimated oral intake of lead. By the second and third day, most patients experienced very considerable improvements in their subjective symptoms, a feeling of general well being replacing the fatigue, weakness and loss of appetite. Based on their calculations, the authors concluded that this approach increases both urine and fecal lead levels, and most likely resulted in the removal of lead from bones. Several other studies (6-8), confirmed the effectiveness of oral EDTA.
The question then is: Why are we using relatively large doses of EDTA intravenously for detoxification of toxic metals, when the oral route worked very well, is non invasive and does not require constant visits to medical clinics which disrupt daily routine? At four hours per session and three sessions per week, this represents a loss of 12 hours per week. The ideal form of oral EDTA would be the di-potassium salt of the magnesium chelate, since these two very important intracellular minerals would be dissociated in the intestinal tract and available for absorption.
The affinity of EDTA for magnesium is very low, resulting in exchange of magnesium for toxic metals in the intestinal tract. This is the approach of choice and preliminary data so far suggest that with the exception of chromium, red cell levels of trace elements do not decrease following 3 months of oral Mg EDTA K2 at a daily dosage of 1.8 gm In some subjects, there is a slight drop in red cell chromium, which is correctable with chromium supplementation. The red cell levels of mercury, lead and cadmium decreased Significantly following 3 months on oral EDTA. There is so far no side effects except urinary urgency in some subjects during the first hour after ingestion.
Oral route for EDTA chelation therapy using the di-potassium salt of EDTA magnesium chelate, based on the above rationale should be considered.
This approach is practical, noninvasive, and based on preliminary data, effective. More studies are needed however in order to fully validate this approach.
1. Elmer Cranton, M.D., Bypassing Bypass The New Technique of Chelation Therapy. 2nd Edition, Hampton Roads Publishing Co. 1997. Pg 35.
2. Foreman, EI., and Trujillo, T. T.: The Metabolism of C14 Labedled Ethylenediaminetetraacetic Acid in Human Beings, J. Lab. & Clin. Med. 43:566-571 (April) 1954.
3. Sidbury, J. B., Jr.: Bynum, J. C.; and Fetz, L. L.: Effect of Chelating Agent on Urinary Lead Excretion: Comparison of Oral and Intravenous Administration, Proc. Soc. Exper. Biol. & Med. 82:226, 1953.
4. Cotter, L. H.: Treatment of Lead Poisoning by Chelation, J.A.M.A.155:906-908 (July 3) 1954.
5. Shiels, D. O.; Thomas, D. L. G.; and Kearley, E.: Treatment of Lead Poisoning by Edathamil Calcium Disodium, A.M.A. Arch. Indust. Health 13:489-498 (May) 1956.
6. Pagnotto, L.D.; Elkins, H. B.: and Bayka, I.: Oral Administration of Edathamil Calcium Disodium (Calcium Disodium Versenate), A.M.A. Arch. Indust. Health 17:29-33 (Jan.) 1958.
7. Bell, R. F.; Gilliland, J. C.: Boland, J. R.; and Sullivan, B. R.: Effect of Oral Edathamil Calcium Disodium on Urinary and Fecal Lead Excretion, A.M.A. Arch. Indust. Health 13:366-371. (April) 1956.
8. Manville, I. A., and Moser, R.: Recent Developments in the Care of Workers Exposed to Lead, A.M.A. Arch. Indust. Health 12:528-538 (Nov.) 1955.
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