Heroic intervention, high­technology diagnostic and monitoring methods, skilled nursing, intensive and complex medication and, where appropriate, surgery of sometimes mind­boggling complexity, all add up to a magnificent refinement of those many skills required for the saving of life after a sudden infarct, thrombosis or embolism, as well as other major causes of emergency circulatory mayhem.

But . . .

There is a darker side to the brilliant progress exemplified by such medical techniques, relating to an apparent lack of awareness of, or interest in, safer alternative treatment methods for dealing with pre­crisis conditions. Among these relatively inexpensive and safe preventive measures must be numbered chelation therapy. (It is also useful in treatment of coronary thrombosis ­ see below.)

Many of the drugs used by conventional medicine for prevention and treatment of such conditions do not address causes but rather tamper with symptoms (for example, drugs which lower blood pressure, while ignoring the causes of its elevation, or which interfere with calcium uptake without dealing with the long­term effect of residual calcification, or drugs which attempt to reduce heightened cholesterol levels, proving themselves successful at this task but leading to a higher mortality rate from other causes than were nothing done at all). Most such drugs create at least as many problems as they solve (compare this with the results of EDTA treatment on cholesterol as described below).

There is also strong evidence of the overuse of surgical methods, such as bypass surgery; indeed, a recent US survey indicated that almost half of bypass operations were not essential, even though this survey took orthodox criteria as to what was 'essential' as the yardstick.

And what­about transplants? The concentration of surgical experts and their back­up teams with high­tech, spectacular, surgical methods (such as are employed in transplant surgery) benefit very few (albeit often amazingly so), while depriving or delaying care for many more through such allocation of scarce resources.

In the USA, where chelation now has a 30­year track record it might be expected that insurance companies would be supportive of chelation therapy as a cheaper alternative to bypass surgery. And yet this not yet so. A recent legal action, brought by a patient against his insurance company (for refusing to pay his expenses for highly successful chelation treatment) led to some pertinent comments from the judge trying the case. The case was heard in Lorain County, Ohio where the judge, George Ferguson, ordered Aetna Insurance to pay the chelation expenses, stating in his judgement:

It is interesting to note that the Defendant (insurance company) would presumably pay for very expensive bypass surgery where there have been 4000 deaths in 300,000 cases, but is refusing to pay for chelation therapy where there have been approximately 20 deaths in 300,000 cases. Insurance companies are repeatedly urging second opinions where surgery is recommended. The Plaintiff was advised to have surgery on June 2 1987, at Elyria Memorial Hospital. Plaintiff obtained a second opinion from a duly licensed physician, followed the second physicians advice (chelation therapy), is alive today and saved the insurance company the expensive coronary bypass surgical operation. (Day vs. Aetna Life Insurance Company, 87CV12710, Elyria Municipal Court, Lorain County, Ohio, 1988)

The complexities of prejudice, ignorance of alternatives, and in some cases outright vested commercial interest, are all sometimes involved in the antagonism of many medical practitioners to chelation therapy. Nevertheless, hundreds of physicians support its simpler and safer approaches to degenerative cardiovascular conditions, and its safety record is evident to all who wish to investigate it.

Just what does EDTA do when it is infused? In order to appreciate its activities we need to return to cellular metabolism for a short while.

Body cells contain miniature factories in which complex biochemical processes are continuously underway with raw materials being turned into energy and protein compounds. Within the cell there exist internal transportation mechanisms and also the means for the transfer of raw materials into the cell, as well as of processed products and wastes out of it. These precise and dynamic functions, however, many of which depend upon complex enzyme activity, are vulnerable should the materials which surround the cell become damaged.

The intracellular membrane which surrounds the cell is far from being a mere envelope, but is involved in important organizational functions, including the control of what passes through it. The active cell membrane is itself made up of lipids (and cholesterol), proteins and water. Should free radical activity take place in its vicinity, destructive effects occur, producing lipid peroxidation (this is what happens when fats become rancid). When this occurs the functioning of cell 'factories' would be either severely disorganized or put out of action, the organizational enzymes could be lost, the distribution of raw material and finished manufactured products and energy disorganized, and a process started of local tissue degeneration.

This is the picture of what happens when atherosclerosis begins in an artery wall. Much lipid peroxidation activity involves the presence of metal ions such as iron, copper or calcium and it is these which EDTA so effectively locks onto, preventing their destructive influence from operating.

Research over the past 30 years has confirmed this benefit from EDTA (e.g. Barber and Bernheim). Of course, this protective influence would be much enhanced were there an appreciable presence of antioxidant nutrients such as vitamins C and E, selenium, and amino acid complexes such as glutathione peroxidase, which not only mop up free radical activity but also assist in building up cell membrane stability.

Within each cell there reside up to 2500 miniature energy producing factories, the mitochondria. One of the main functions of each mitochondria is to translate inorganic phosphate (ADP), sugar (glucose) and oxygen into adenosine triphosphate (ATP), the universal form of energy used by the body. This energy producing activity of the mitochondria involves a series of intricate, complex and vital biochemical processes dependent on vast numbers of enzymes (estimates vary from between 500 to 10,000 complete sets of oxidative enzymes in each mitochondria) which are themselves dependent upon dozens of nutrient factors and co­factors.

If calcium is abnormally deposited in arterial walls this inhibits some enzyme activity and negatively influences ATP (energy) production. If through free radical activity, or through any other disturbing influences on normal energy production or transfer by damaged mitochondria, cells can become energy starved, they tend then to become more acidic. This happens for a multitude of reasons: it may be to do with ageing or to calcium/magnesium ratios becoming unbalanced, due to free radical activity, local toxicity, oxygen deficit, nutritional imbalance, etc. Elmer Cranton, MD, reminds us that EDTA increases the efficiency of mitochondrial oxidative phosphorylation (energy production) quite independently of any effect on arterial blood supply' and let us not forget his statement that EDTA can reduce the production of free radicals by a million­fold.

Cells which have become energy starved and more acidic for whatever reason start to attract calcium ions, drawing them into the cell, further blocking energy production. An increase in calcium inside cells, accompanied by reduced oxygen and lower energy manufacture and availability, is a typical picture found in degenerative cardiovascular conditions. It is also a prescription for the muscles which surround the arteries to go into spasm. This is the reason for the use of calcium channel blocker drugs, which may be effective in blocking calcium uptake by muscle cells but do nothing about the underlying condition.

Morton Walker and Garry Gordon (1982) have discussed calcium channel­blocking drugs:

Calcium channel blockers are not as efficient in permanently restoring heart health as is EDTA chelation therapy, but even these calcium antagonists are clearly better, as a coronary medical programme, than open heart surgery. They inhibit the excessive accumulation of calcium in the heart cells and allow ATP production. Additionally, if you are the patient in heart spasm, you can help avoid death of the starved portion of your heart muscle. You will not show the elevated enzymes (CPK, LDH, SCOT and others)that your doctor measures in your blood test each day to see how many heart cells have really died and released their enzymes. An actual heart attack will be avoided . . . you will usually be able to go home from hospital the next day by having calcium channelblocking agents and/or chelation therapy.

Elmer Cranton and Arline Brecher (1984) describe some of the stages involved:

Impairment of the calcium/magnesium pump allows more ionized calcium to enter the cell, activating an enzyme that leads to the production of prostaglandin related leukotrienes, a chemical process which releases free radicals. When excessively stimulated by leukotrienes, white blood cells run amok and initiate free radical production, which causes increasing inflammatory damage to healthy tissues. Small blood vessels dilate, causing swelling, oedema, and leakage of red blood cells and platelets through blood vessel walls which result in microthrombi (microscopic clots). Some red blood cells then haemolyse releasing free copper and iron, which in turn catalyse an increase of free radical destruction to lipid membranes in the vicinity of a million­fold, triggering another vicious cycle.

This process is compounded by the presence of additional vitamin D and cholesterol because free radical activity helps to convert cholesterol into substances with vitamin D activity, resulting in plaque (in which cholesterol is usually bound) attracting calcium, thus cementing the material.

EDTA infusion, which has the ability to remove metal ions, stops or slows metals which are significant causes of free radical production. In removing metals, local toxicity is reduced and enzyme production and function improves. We should not underestimate the role of toxic metal ions in the body, whether these are of lead, mercury, cadmium, copper, iron or aluminum. Once these have been chelated by EDTA and removed from their deposition sites, free radical activity and consequent disruption of metabolic function is largely prevented. Once this has happened normal enzyme function resumes.