Chelation comes from the Greek word "claw," meaning "to grab," and that's exactly what chelating agents do. Chelating agents like EDTA travel through the bloodstream "grabbing" on to minerals and metals, such as calcium, lead, mercury, cadmium, copper, aluminum and iron, binding them, removing them from the bloodstream, and delivering them to the kidneys, which excrete them in the urine. Once bound by a chelating agent, the minerals are unable to react in undesirable ways.

The primary use of chelation therapy today is in the prevention and treatment of occlusive vascular disease, including atherosclerosis, coronary heart disease, and stroke. How does EDTA accomplish this remarkable feat? There appear to be several mechanisms involved.

  • Enhancing antioxidant activity. Free radicals produce lipid peroxidation in the bloodstream and in cell membranes. (Lipid peroxidation is the process that causes fats to become rancid.) Much lipid peroxidation involves the presence of metal ions such as iron, copper, and calcium. By effectively removing these metals and minerals, EDTA can reduce the production of free radicals and prevent their destructive influence. Thus, in concert with other antioxidant nutrients, such as vitamins C, E, selenium, glutathione peroxidase, and others, EDTA helps reduce atherosclerotic plaque.
  • Improving cellular energy production. Calcium that is abnormally deposited in arterial walls inhibits enzyme activity and negatively influences ATP (energy) production in mitochondria of the cells of arterial walls. Cells that become starved for energy become more acidic and start to attract more calcium ions, drawing these ions into the cell and further inhibiting cellular energy production. Degenerative cardiovascular conditions are typically marked by an increase in intracellular calcium accompanied by reduced oxygen and lower production and availability of energy. As a result of these imbalances, the muscles surrounding arteries may go into spasm. By removing metal ions, EDTA reduces local toxicity and thereby improves enzyme production and function.
  • Reducing blood "stickiness." EDTA also acts to directly improve blood platelet function, which is mainly to initiate repair of any damaged internal lining in blood vessels. When damage is detected, platelets adhere to the damaged surface, gradually covering the region. At the same time, they reduce the danger of hemorrhage by causing the blood to coagulate. While these protective effects are vital to life, if clot formation occurs inside a coronary or cerebral artery, it can cause a heart attack or stroke. EDTA appears to inhibit the tendency toward overcoagulation, probably by removing ionic calcium from the platelet membrane. EDTA may also help normalize the production of prostaglandins, which control platelet function and activity.
  • Normalizing blood cholesterol levels. EDTA treatment results in an increase in high-density lipoproteins (HDL), the "good" cholesterol, and a reduction in low-density lipoproteins (LDL), the "bad" cholesterol.
  • Removal of calcium from plaque. Calcium that is loosely held in plaque deposits by an electrostatic charge prevents the body from dissolving the plaque. EDTA binds with ionic (free) calcium in blood and thus triggers the release of parathormone. This increases the demand for calcium in blood, and the body responds by drawing from calcium deposits in plaque. With the calcium removed from the plaque, the plaque can be resorbed by the body, restoring the artery to its normal status.