Mineralization by ionic calcium of plaque, forming around localized lesions, seems to have attracted a great deal of medical attention. Not only do these contain various forms of calcium, such as carbonate apatite - Ca10(PO4)CO3, but also concretions containing barium, strontium or lead. However, we should not underestimate the progressive damage resulting from generalized arterial calcification with its slowly progressive loss of elasticity and circulatory capacity.

Both forms of arterial degeneration involve ionic calcium to some extent and both are amenable to chelation therapy's ability to start the process by which calcium and other metals are removed from such concretions, initiating (relative) normalization.

It was never the intention of this chapter to explore fully all possible causes of atherosclerosis (other more comprehensive texts exist which do this perfectly adequately - see Further Reading), but rather to point to the need in many such conditions to deal with both ongoing contributory causes of calcium imbalance/cardiovascular dysfunction (acid/alkaline imbalance, calcium/phosphorus imbalance, calcium/magnesium imbalance, high fat intake, low vegetable/complex carbohydrate intake, etc.), as well as having a strong image of the need that may exist for a method simultaneously (together with the correction of the imbalances mentioned) to remove deposits of metastatic calcification.

Dr Elmer Cranton (Cranton and Frackelton 1982) explains a fundamental and somewhat revolutionary concept of atherosclerosis development when he reminds us of another slant to chelation therapy using not EDTA but deferoxamine: 'This has been shown to improve cardiac function in patients with increased iron stores . . . as well as reducing inflammatory responses in animal experiments'. EDTA also has a strong affinity for iron and Cranton suggests that the individual's iron status is a critical element in the background to atherosclerosis development.

Women of menstrual age are four times less likely to develop such arterial changes as men of the same age. Also, men accumulate iron in the blood (serum ferritin) at precisely four times the rate of pre-menopausal women and it is no coincidence that these two factors have the same degree of measurable numerical similarity (four times the iron and four times the arterial damage), since iron is a potent catalyst of lipid peroxidation with all its potentially devastating circulatory repercussions.

It could be argued that this protection from atherosclerosis is all down to hormonal influences present in young women and not men. But this is not so, says Cranton, as he provides us with the clinching link between iron and the damage discussed above.

When women are studied following hysterectomy, it is observed that there is an immediate rise in their iron levels to equal that of men of the same age and their susceptibility to atherosclerotic changes also rises to that of men (Cranton and Brecher 'Bypassing Bypass'). These changes after removal of the womb (thereby stopping menstruation) are seen whether the ovaries (which produce oestrogen) are retained or not. Clearly, the monthly blood loss is protective and Cranton suggests that a good way for men and post-menopausal women to reduce the risk of atherosclerosis would be to become regular blood donors.

Chelation therapy of course offers another way of reducing excessive iron levels. We have seen above that calcium in its ionic form is reasonably easily chelated by EDTA. However, calcium is not high on the list of substances to which EDTA is most attracted. In descending order, the stability of a chelation link between EDTA and various metals (at normal levels of acidity of the blood) is as follows:

Chromium2
Iron3
Mercury2
Copper2
Lead2
Zinc2
Cadmium2
Cobalt2
Aluminium3
Iron2
Manganese2
Calcium2
Magnesium2

How toxic metals such as lead interfere with protection
Elmer Cranton and James Frackelton (1982) explain the ways in which lead toxicity can prevent the body from doing its natural protective work against free radical activity: 'Lead reacts vigorously with sulfur-containing glutathione peroxidase (a major antioxidant enzyme used by the body against free radicals) and prevents it reacting with free radicals' They also explain how reduced glutathione further harms the body by preventing the recycling of antioxidant (protective) vitamins such as E and C and other enzymes: 'Lead therefore cripples the free radical protective activity of that entire array of antioxidants'

And EDTA was developed precisely to remove lead from the system.

These insights into how circulatory damage occurs and the ways in which EDTA helps prevent or repair such happenings, as explained by experts in the field of chelation, should help us understand the irrelevance of trying to state precisely how and why EDTA therapy works so well in any given case. What is important is its proven value and relative safety.