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.
The Birth of an Atherosclerotic Lesion
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.
The free radical and the arterial wall
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 fat connection
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.
Where does calcium come into the picture?
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.