The UK Health Education Council tells us that almost 40 per cent of all deaths of people between the ages of 35 and 74 arise as the result of stroke or heart attack. The majority of these crises result from circulatory restrictions or obstructions which are both preventable and treatable by chelation therapy.
Those problems arising from atherosclerosis are far and away the greatest health problem in industrialized societies. And as most people now know, cardiovascular and circulatory degenerative changes are to a very great extent preventable, since it is now well established that life-style practices and dietary habits contribute significantly towards their causation. So not only are most diseases which stem from circulatory degeneration largely preventable, in many instances they are at least partly reversible if causative factors are stopped and positive action taken.
However, the range of contributory factors is very wide indeed and no single method of prevention can possibly cover all of them, ranging as they do from the unavoidable – inherited tendencies, age and sex – to the (usually) controllable – smoking, dietary habits, stress coping abilities and exercise patterns. It has been demonstrated, in the Pritikin programme for example (Pritikin 1980), that much can be achieved through the application of self-applied dietary strategies, avoidance of known irritants (smoke, high-fat diet, etc.), combined with the application of aerobic exercise methods. Just how such methods can help, either on their own, or as part of a wider; therapeutic approach – whether this involves drugs, surgery or chelation therapy – will become clearer once the known causes of circulatory obstruction are examined.
The value of chelation as an intervention strategy will also be seen to have marked advantages over many ‘high-tech’ approaches, in such conditions, once we comprehend that the entire arterial network is frequently damaged, requiring a method of treatment which addresses all 40,000 miles of it, rather than just local, isolated points of major blockage receiving attention.
There is no absolute consensus as to the causes of atherosclerosis, which probably means that all, or a number, of the theories are at least partially correct. It is therefore necessary to examine the most popular of these hypotheses.
In good health an artery (or arteriole) is far more than a simple plumbing conduit. As with so many parts of the body it also acts as a mini-factory, producing a large number of vital biochemical agents such as enzymes which act to protect it from damage which could arise via the action of a number of agencies (see below), such as excess fat in the bloodstream or other potential sources of free radical activity (see Chapter 2). The ability of such enzymes to perform their defensive and other functions depends on the abundant presence of co-factors vitamins such as A, C, E, D) and an army of minerals and adequate protein sources for the amino and nucleic acids needed for regeneration and repair functions.
Nutritional excellence is therefore the essential background to all other potential causes of arterial damage. If the nutritional status of the region is sound, the resulting abundant supply of defending substances will provide a powerful protective shield. Conversely, if nutrition is poor, vulnerability is greater and far fewer and lesser stress factors will be required before serious damage is caused.
We therefore need to keep in mind the underlying degree of (or lack of) nutritional soundness along with the list of constant influential factors (age, sex, inherited tendencies) in order to establish a base of vulnerability, susceptibility towards cardio-vascular disease.
In other words, we are not all starting from the same place, and noxious influences, whether these are toxic, dietary or life-style in origin, will affect one person quite differently from another because of this base-line susceptibility.
The shield will be weaker, the damage greater, the chances of recovery slighter, if nutrition is not dealt with as a primary and ongoing priority, whatever else is done in therapeutic terms. Basic guidance to the ‘ideal’ dietary pattern has been given by a variety of governmental and medical agencies over the past few years and this is discussed more fully in Chapter 8.
In Chapter 2 we discussed the way in which the hooligan-like behaviour of a free oxidizing radical might begin. Here we have, as the end-result of oxidation, highly reactive, electrically charged, molecular fragments with unpaired electrons in their outer shell, capable of grabbing on to other molecules in order to achieve the paired status to which all electrons aim. In capturing this new electron, forming a new chemical bond, the molecules from which the electrons have been taken become damaged and new free radicals are formed. Chain reactions can continue in this way until antioxidant substances (vitamins A, C, E, or enzymes such as catalase, or minerals such as selenium, or amino acids such as cysteine) quench the reaction. A single free radical can produce reactions involving thousands of damaged molecules, along with new free radicals, before the process burns itself out or is deactivated.
Why should such activity occur in the arteries?
Firstly, there is a plentiful supply of oxygen which fuels the free radical explosion. Secondly, there may be a relative lack of antioxidant substances (which is one reason why cardio-vascular disease is so much more evident where selenium or vitamins A or C are in poor nutritional supply). Thirdly, there may be present substances which easily generate free radical activity, such as fats and unbound (ionic) forms of metals such as iron and copper.
The walls of the cells of our bodies are made up to a large extent of lipids, which are extremely prone to peroxidation (rancidity), a process which involves massive free radical activity.
When food supplements of an oily nature (oil of evening primrose, for example) are marketed, they are usually combined with antioxidant substances such as vitamin E or wheatgerm oil (which is rich in vitamin E) in order to damp down any free radical activity, allowing the product to remain stable for longer. A similar protective effect is constantly at work in the body itself if adequate antioxidant nutrients are present. In fact the most potent enzyme used by the body to protect its cells against lipid peroxidation is glutathione peroxidase, which is dependent on the antioxidant mineral selenium. If antioxidants such as these are lacking, or if other free radical generating factors are at work (alcohol, heavy metals or cigarette smoke, for example), a chain reaction of free radical activity can take place in the lipids of cell walls, severely damaging these.
It is now known that as we age, and certainly by middle age (45-55 approximately), a great many of the protective enzymes in the blood vessels and their walls are in rapid decline or are totally absent. Also apparent as we age is a build-up in the bloodstream of forms of cholesterol which increase the risks of cardiovascular disease, the low density lipoproteins (LDL). As we will discover in the next chapter, EDTA therapy has a remarkable normalizing effect on this dangerous build-up.
The seeds of later degeneration of arterial wall cells (and high levels of LDL-cholesterol) are often present in schoolchildren and certainly in most people in industrialized countries far earlier than middle age. According to major research in the USA and Europe, the first signs of degeneration of the arteries start early in childhood, often before schooling begins. Whether because of enzyme lack, metal toxicity or cholesterol (LDL) excess, free radical activity increases under such circumstances. The damage which takes place in cells during a free radical chain reaction goes beyond just the cell wall, often involving alterations to the genetic material of the cell, the DNA and RNA. If this happens, the way the cell reproduces itself will be altered, frequently leading, it is thought by many experts, to the beginning of atheromatous development (or of cancer, see Chapter 5).
A researcher in the USA, Earl Benditt, MD, first published in February 1977 (Scientific American) the theory of monoclonal proliferation. This suggested that damage to cells in the smooth muscles which lie below the inner lining of the artery are the initial site where damage occurs. It is here that we see the gradual evolution of atheromatous plaque which eventually erupts through the inner lining of the blood vessel. Whether the trigger for the original vessel-wall injury derives from free radical activity, excess cholesterol levels or from specific chemical or metal toxicity, or even from mechanical insult due perhaps to increased blood pressure, is not at issue (perhaps all or some of these, as well as other factors, interrelate in any given case and EDTA is able to normalize most of these).
Among EDTA chelation therapy’s most important contributions to cardiovascular health are the ways in which it deactivates free radical activity and normalizes cholesterol excess. Indeed, some experts believe these to be even more important than its effects on calcium status. Elmer Cranton, MD, states (Cranton and Brecher 1984):
If, as the newest research indicates, the free radical theory of degenerative disease is correct, then reversing free radical pathology would be the key to the treatment and prevention of such major age-related ailments as atherosclerosis. Specifically, EDTA reduces the rate of pathological free radical chemical reactions by a million-fold, below the level at which the body’s defences can take over, and so provides time for free radical damage to be repaired by natural healing.
McDonagh and his colleagues (McDonagh, Rudolph and Cheraskin 1982b) report: ‘Notwithstanding the general traditional consensus that serum cholesterol is physiologically different at different ages, our research shows that following EDTA plus supportive multivitamin/mineral supplementation the serum cholesterol approaches about 200mg% (normal) in all age groups.’
Some researchers see the development (after free radical activity) of atheromatous plaque as a defensive, protective reaction, whereas others do not agree with this concept. Whichever is correct, a sequence is commonly observed in which the inner lining (the intima which lies below the surface lining) of an artery becomes damaged, followed by the development of what seems to be an accumulation of debris at the site, consisting of a combination of connective tissue, elastin, collagen, cholesterol, polysaccharides and various protein fractions. If calcium also links up with such atheromatous deposits, a concrete-like state develops. Calcium, in its ionic form, is attracted to link and bind with the developing atheroma due to its electrical attraction to the substances in it.
It surely matters that largely preventable factors contribute to arterial damage, but it is to the processes which follow on from these developments, which ensure that the artery will become severely obstructed, that we need to turn.
To summarize, therefore, we see that a combination of low levels of antioxidant substances together with increased levels of free radical activity (for whatever reason and there are many possible, including excess presence of forms of cholesterol (LDL) and heavy metal imbalances), results in damage to cells deep within the arterial walls. This is usually followed or accompanied by the evolution of thickening of the arterial walls and the development of atheromatous changes.
We need to look briefly at the enormous subject of calcium and its functions, its balance and imbalance in the blood vessels and bloodstream, along with calcium’s link with diet, exercise, the ageing process, free radical damage and subsequent atherosclerosis.
Calcium is one of the most important elements in the body and, together with magnesium, is vital for cardiovascular health. In the main calcium is used by the body extracellularly (along with sodium), as opposed to potassium, magnesium and zinc which are largely found intracellularly.
Ninety-nine per cent of all calcium in the body is found bound to phosphorus in bones and teeth. However, more important to us is the ionic form of calcium which is found in the body. Around 60 per cent of all the calcium in the bloodstream is in the ionic form (Ca++) where its degree of concentration ranges from 9 to 11 milligrams per 100 millilitres of serum. This ionic calcium is very important in the body economy, being instantly available for use chemically, especially in relation to coagulation of blood, as well as heart, muscle and nerve function and the permeability of cell membranes.
The distribution of calcium in the body in good health and disease varies greatly. Under ideal conditions, largely controlled by the activity of the parathyroid hormone, calcium levels are as follows:
Under certain circumstances, as in osteoporosis, deposition of calcium takes place around joints (soft tissues) and in arteries. Such abnormal calcium deposits are known as metastatic or dystrophic deposits, some of which contain ionic calcium.
Parathyroid hormone (which is markedly influenced by the degree of acidity of the blood, and production of which is stimulated by EDTA infusion – see below), as well as calcitonin and vitamin D3, control and regulate calcium flux between extracellular and intracellular calcium, so vital in cellular function as well as in those enzyme systems which influence muscle contractility, nerve transmission and some hormone activities.
The transfer of substances including water across cell membranes involves the activity of ionic forms of many minerals including sodium, potassium, magnesium and calcium. It is in the mitochondria of cells that intracellular calcium is found, most usually bound as a phosphate rather than in ionic (free) form.
In an adult, 20 per cent of the total bone calcium is re-absorbed and replaced each year, in normal health, but when replacement is inadequate, serious problems arise. Thus, apart from its role in providing structural integrity to the skeleton and teeth, calcium is also of vital importance in the processes of growth and development, and the maintenance of health, and yet it presents us with an apparent paradox.
It is now known that, if overall nutrient imbalances exist, a high-protein diet is capable of speeding up the removal of calcium from bones and of contributing to osteoporosis. This has occurred in many millions of women in Europe, America and other industrialized nations of the world. Post-menopausa women in particular are thus vulnerable to easily fractured bones, after even slight injury. Many factors contribute towards this, but one of the major elements appears to be an imbalance in the ratio of calcium-to-phosphorus in the diet. Phosphorus is found in very large quantities in meat and in most other proteins as well as in carbonated drinks.
Stone-age man ate abundant meat (in excess of 700 grams daily), as do current hunter gatherers, and yet their bone structures remained, and remain, sound into old age.
This is a paradox.
The complex process which occurs when a high-protein diet is consumed may be linked to a high degree of acidity in the body. Increased acidity increases parathyroid hormone production and a consequence of this is additional resorption of calcium from bone into the bloodstream. If additional vitamin D is also present in the body this progression may be limited (and the body of course makes vitamin D when sufficient sunlight is available to it).
Another factor which appears to prevent decalcification is exercise. It is possible that these two protective factors, sunshine and exercise, which were abundantly available to stone-age man, may account for the difference noted in the effect of a high-protein diet in those people, as opposed to such a diet in a sedentary individual, where decalcification is more common.
We are obliged to ask therefore why, if an EDTA infusion stimulates parathormone production and subsequent calcium withdrawal from bone (as well as from pathological deposits in atheromatous plaque, etc.), this does not lead to osteoporosis?
Bruce Halstead (1979) answers this as follows:
Physicians having extensive clinical experience with EDTA in the treatment of atherosclerosis have generally observed that the bone structure improves with the administration of EDTA. The explanation of the apparent paradox is to be found in the role parathormone plays in relationship to osteoblastic function. When EDTA is administered intravenously into the body there is a rapid complexing of ionic serum calcium and excretion of calcium EDTA through the renal tubules. This causes a drop in circulating calcium and a stimulation of parathormone production . . . which results in withdrawal of ionic calcium from metastatic deposits and also increases the conversion of preosteoblasts to osteoblasts . . . leading to an increase in total collagen synthesis or new bone formation . . . This basic biochemical mechanism of bone metabolism has been well documented experimentally and provides a reasonable explanation as to why EDTA generally improves bone structure rather than producing osteoporosis clinically.
Increased sugar in the blood causes a decrease in the circulation of vitamin D, which if present helps to neutralize the sequence of events described:
High protein = high acidity levels in the blood = high parathyroid hormone = low levels of calcium in the blood = decalcification.
(Recall that if EDTA infusion is the cause of this sequence the final result is not decalcification of bone, only of metastatic deposits.)
Interestingly there is a family of plants which contain a material which acts very much like vitamin D in protecting against bone decalcification where blood acidity stimulates decalcification. This is the solanaceous family of plants, which includes tomatoes, potatoes, green peppers and aubergine.
One of the most critical elements in the whole equation of balances and imbalances involved in this highly complex scenario relates to the ratio between calcium and phosphorus in the diet. It has been found that the demineralization of bones ceases, and actually reverses (bone begins to remineralize) when the ratio of calcium to phosphorus is 1 (that is, one part of calcium for every one part of phosphorus in the diet: 1 / 1 = 1). Commonly the diet in Western society achieves a ratio of less than 0.5 parts of calcium to each part of phosphorus (1/2 / 1 = 1).
Stated simply this means that whilst experimentally it can be shown that a high-protein diet increases calcium excretion and bone loss, this does not appear to be nearly so likely when the overall diet is balanced, even though there is a high protein intake.
Some experiments which appeared to implicate a high-protein diet as the major cause of calcium loss have been shown to be seriously flawed, as the type of protein used was a concentrated, often liquid, protein, bearing little resemblance to the forms of protein normally eaten. Such concentrated purified proteins are the types often used in crash slimming programmes as well as in some emergency refeeding programmes, where malnutrition exists.
Phosphorus itself is now seen to be useful and necessary in achieving a balance against the acid side-effects of a high-protein diet. So phosphorus and calcium, in balance, produce the situation in which a sound bone structure can be achieved even where there is a high meat intake. A high vegetable content in the diet ensures lowered acidity as well as calcium replenishment.
Calcium from vegetables
Some of the best sources of calcium are from green leafy vegetables such as dandelion greens, mustard greens, turnip and beet tops, watercress, broccoli and kale.
Other protective factors
The other important elements in maintaining healthy nerve and bone structures include exercise and daylight. Exercise taken in an environment in which light is available is therefore important. Direct sunlight is not important as even indirect daylight has beneficial effects in the production of vitamin D.
Thus there is no real paradox: a high-protein diet is not going to result in decalcification unless there is an imbalance between calcium and phosphorus and unless acidity clearly outweighs alkalinity. Neither of these is likely if sound eating patterns are followed, and even less likely if exercise and light are obtained in liberal quantities.
We have seen a variety of often interacting influences on calcium status in the body. If for any reason calcium levels in the blood are too low, the action of parathyroid hormone withdraws ionic calcium from other (often metastatic) sources to meet this imbalance. If EDTA is the cause of the reduction in ionic calcium levels in the blood, then (as explained by Bruce Halstead above) osteoblasts are stimulated to start the process of bone calcification. However, if calcium levels increase in the bloodstream (as they would if withdrawn from bone as in osteoporosis), calcitonin produced by the thyroid lowers it, often causing it to be deposited in metastatic forms. In good health, around one gram of calcium should be absorbed from the intestines daily, but if far more calcium is ingested, or the intake of magnesium is low, excess calcium will either be excreted via the kidneys or added to the dystrophic depositions in soft tissues (arteries, etc.). If this occurs in arteries it may be in one of two forms. There might be localized, discrete deposits which show up well as radiopaque shadows on X-ray; or there may be a more generalized, diffuse deposition in which calcium is secreted in the previously elastic fibres of the arteries. Generalized calcification of arteries is not radiopaque until it is well advanced.
With passing time multifaceted influences (diet, life-style, toxic exposure, stress, lack of exercise, etc.), interacting with the normal ageing process may lead to one or other of these forms of arterial degeneration. As the general calcification described above proceeds, there is a gradual lessening of the ability for oxygen and nutrients to be transported and absorbed, with consequent deterioration of the status of the tissues being fed. This is arteriosclerosis and it may impair circulation to any body part, including the brain, leading in such a case to impaired ability to concentrate, remember or think, or to transient dizziness; hearing and sight might be impaired; tinnitus might develop; the extremities, especially the legs, might feel colder or be subject to cramp; the heart muscle itself might become starved of oxygen and nutrients, developing the symptoms of angina; the ageing process may be seen to be advanced steadily, and as it progresses, in time muscular spasm may completely shut down one or other of the arterial channels of circulation.
In atherosclerosis, where more localized deposits of atheromatous material form on the artery wall, there is an inevitable turbulence and increased pressure of the flow of blood at that point. The atheromatous deposit could continue to increase in size until it obstructed the artery or there is always the chance of a fragment of such a plaque deposit breaking away and being carried to a point too narrow for its passage, completely or partially blocking this. A cerebral accident or coronary infarct would then have occurred.
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:
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.