Chelation involves an intravenous drip of molecules into the bloodstream called ‘chelators’, which can remove toxic metals such as lead, mercury and aluminium from the body. The chelating agent most often used is ethylenediaminetetraacetic acid (EDTA), which can supposedly mop up the metals that, if left alone, can trigger the production of free radicals. They are also supposed to clean up the calcium deposited in the arteries, although it’s recognised that calcium is an effect, not a cause, of arterial plaque.

Although chelation practitioners pointed to the thousands of patients they said they helped, doctors nevertheless maintained that there was no scientific evidence for these claims. Things came to a head in 2003 with the release of the results of the PATCH study, which had monitored the progress of 47 heart patients, half of whom had been given EDTA chelation, and the remainder, a placebo. After six months, the chelation group’s arterial flow was no better than that in the placebo group. Chelation practitioners have since argued that the study was too small – and flawed.

The study appears to have only hardened the positions of both camps, leaving patients as puzzled as ever (J Am Coll Cardiol, 2003; 41: 420-5).

What is EDTA?

EDTA is a substance which removes undesirable metals from the body. Some metals, such as lead, mercury and cadmium are poisons. Lead and cadmium levels correlate with high blood pressure. All metals, even essential nutritional elements, are toxic in excess or when abnormally situated. EDTA normalizes the distribution of most metallic elements in the body. EDTA improves calcium and cholesterol metabolism by eliminating metallic elements in the body. EDTA improves calcium and cholesterol metabolism by eliminating metallic catalysts which cause damage to cell membranes by producing “oxygen free radicals.” Free radical pathology is now believed by many scientists to be an important contributing cause of atherosclerosis, cancer, diabetes and other diseases of aging. EDTA helps to prevent the production of harmful free radicals.

What is it used for?

Chelation therapy is used to reverse symptoms of hardening of the arteries, also known as atherosclerosis or arteriosclerosis. Atherosclerosis is caused by multiple complex factors, including abnormal accumulations of metallic elements. The end result is plaque formation within arteries which blocks the flow of blood. Plaques are composed of fibrous tissue, cholesterol and calcium. Atherosclerosis leads to heart attack, stroke, senility and may lead to amputation of extremities. Every single study of the use of chelation therapy for atherosclerosis which has ever been published, without exception, has described an improvement in blood flow and symptoms. Adverse editorial comment to the contrary lacks evidence and stems primarily from physicians with a vested interest in catheterization and surgery.

How Does Artery Disease Affect Health?

Blockage of blood vessels by plaque (atheroma) reduces the flow of blood, starving vital organs for oxygen and other nutrients. Cell walls then become leaky, allowing excessive calcium, sodium and other elements to enter. When calcium accumulates to a critical point, deposits form, like concrete. These calcifications can often be seen on xray. Disordered calcium metabolism can also cause coronaries and other arteries to go into spasm, further reducing blood to vital organs.

How Does Chelation Therapy Affect Health?

Chelation therapy promotes health by correcting the major underlying cause of arterial blockage. Damaging oxygen free radicals are increased by the presence of metallic elements and act as a chronic irritant to blood vessel walls and cell membranes. EDTA removes those metallic irritants, allowing leaky and damaged cell walls to heal. Plaques smooth over and shrink, allowing more blood to pass. Arterial walls become softer and more pliable, allowing easier expansion. Scientific studies have proven that blood flow increases after chelation therapy. A complete program of chelation therapy involves a broad-based health care program of regular exercise, proper nutrition, vitamin and mineral supplementation and avoidance of tobacco and other damaging habits.

What are the interactions between Chelation Therapy and other treatments for Artery Disease?

Chelation therapy can be utilized in conjunction with most other therapies for cardio-vascular disease. EDTA is compatible with blood thinners, blood vessel dilators, medicines for blood pressure and heart arrhythmias, calcium blockers and beta blockers. The need for drugs is often reduced or eliminated after a course of chelation therapy.

What is the cost comparison?

Bypass surgery is the mechanical repair of only a small portion of the arterial tree. Total costs average about $45,000 and can be as high as $60,000 or even more. Chelation therapy is an office treatment which improves blood flow throughout the entire vascular system at a fraction of the cost of bypass surgery. For example, if 20 to 40 four-hour chelation treatments in a physician’s office were required for a given patient, it would cost an estimated $2000-$4000.

What about safety and side effects?

Chelation therapy is among the safest of medical procedures. More than 400,000 patients have received over four million treatments during the past 30 years. Not one death has been directly caused by chelation therapy, when properly administered by a physician who was fully trained and competent in the use of this therapy. Side effects are possible, as with any drug therapy. Vein irritation, mild pain, headache and fatigue may occur. Occasionally a mild and transient fever occurs. These and other minor side effects, if they occur, are easily controlled by adjusting the duration and frequency of treatment, or with the use of other simple measures. Side effects tend to diminish after the first few treatments. Most patients experience few or no side effects.

How do I know if I need or can benefit from Chelation Therapy?

If you have chest pain or leg pain on walking; shortness of breath; painful, discolored feet; transient loss of vision; paralysis; or rapidly failing memory, see a physician! Any unexplained or persistent symptoms which affect your heart, head or limbs should be explored for circulatory blockage.

How will I be able to tell it Chelation Therapy has helped me?

Patients routinely report reduction or elimination of their symptoms with an increasing sense of well being after chelation therapy. Family and friends are often the first to notice and report improvement in appearance, behavior and performance. Comparison of pre- and post-therapy diagnostic tests can provide objective evidence of effectiveness.

Can my personal physician give this treatment?

Any licensed physician can legally administer this treatment. Courses to train physicians in the safe use of chelation therapy are offered twice yearly by the American College for Advancement in Medicine. Interested physicians should contact ACAM for information about training and certification in this important type of medical therapy.

Can Chelation Therapy be used after Bypass Surgery?

Yes! Although chelation therapy is best utilized to avoid bypass surgery, many patients who have previously undergone one or more bypass procedures, often with little or no benefit, have subsequently benefitted greatly from chelation therapy. Treatment for each patient must be individualized. If all else fails, including chelation therapy, bypass remains available as a last resort.

Is Chelation Therapy legal treatment?

Yes! Chelation therapy is completely legal. A licensed physician is free to utilize any therapy of acceptable risk which, in his or her professional judgement, is of potential benefit — even if advertising claims for treatment are not yet approved by the FDA. The FDA does not regulate the practice of medicine but only limits marketing and advertising claims for drugs. The FDA has approved marketing claims for the use of EDTA to treat lead poisoning and several other conditions. Treatment of atherosclerosis is not yet an allowable claim for inclusion in the marketing literature of EDTA.

Do medical insurance companies pay for Chelation Therapy?

Most medical insurance companies, including Medicare, have been financially depleted by paying for so many expensive surgeries. Segments of the health care industry which profit greatly from surgical procedures are politically powerful. Physicians who review claims for medical insurance companies often favor the extremely expensive and risky procedures, such as bypass surgery, while refusing payment for equally beneficial, far less expensive and immeasurably safer chelation therapy. While insurance policies do not specifically exclude chelation therapy in their policies, patients have often had to resort to the courts in order to collect their insurance benefits.

How do I find a physician who is trained and competent in Chelation Therapy?

The American College for Advancement in Medicine provides a free national listing of its member doctors, most of whom include chelation therapy in their practice. To receive this list, send a self-addressed, business-size (#10) envelope with .55 cents postage to:

The reader is advised that varying and even conflicting views are held by other segments of the medical profession. The information presented here is educational in nature and is not intended as a basis for diagnosis or treatment.

This information represents the current opinion of independent physician consultants to ACAM at the time of publication.

ACAM publishes and distributes this information as a courtesy to the public.

The reason you have “high cholesterol” is probably because you hae eaten too much saturated fat (from animals) over
the years. Some people, however, have an inherited type of high cholesterol. For more information on familial
hypercholesterolemia please see the conventional diagnosis section.

Clinical high cholesterol is usually found in the blood values on a annual check-up. No signs or symptoms may
be present even with life threatening atherosclerotic disease. This diagnosis may be a result of a life of poor eating
habits, sedentary lifestyle, smoking, excessive drinking, etc. You may be experiencing angina, hypertension, or kidney
disease as well as the elevated blood lipids. Even though it’s quite likely you can control your high cholesterol with
some basic dietary changes, there are some other disease problems which can cause this syndrome. Make sure your
doctor has discussed the “rule-outs” with you; in other words make sure your high cholesterol is NOT
because of:

• von Gierke’s disease
  
• “sluggish” liver syndrome
  
• hypothyroidism
  
• pregnancy
  
• pancreatic dysfunction
  
• nephrosis

In industrial countries, people who are apparently symptom-free may suddenly have a massive MI (myocardial
infarction, or heart attack). It may be the first indicator of disease. Therefore yearly cholesterol screens are highly
recommended. Hypercholesterolemia in Western countries seems well-linked to significant morbidity (hypertension,
angina) and mortality (MI, CVA or cerebral vascular accident, which usually refers to stroke). It is estimated that half
the population in the U.S. will die from Congestive Heart Disease (CHD) and the results of atherosclerosis. Coronary
bypass surgery is one of the most common operations now performed, even though it carries inherent risks and research
has shown that its effect is generally transient, with patients often experiencing repeat symptoms only 2-3 years
post-surgery. Chelation therapy offers some hope, but it remains controversial and only a few physicians have
adequate training to perform this technique. New research suggests that prevention and natural treatment offer
the healthiest, most lasting and least costly route to recovery.

Cholesterol levels have become the source of much national fear, even though cholesterol is one of the most
valuable substances in the human body. Cholesterol is needed for strong cell walls, as a precursor for hormone
production, and as a coating around nerves, to name just a few of its very important functions. Cholesterol is made
in the liver in amounts up to 2000 mg/day. Cholesterol associated with high density lipoprotein, HDL (and
Apolipoprotein A-1), is generally considered to be beneficial to the body, as it works to remove cholesterol from
blood vessel walls and the the blood itself, bringing it to the liver for processing and excretion. Cholesterol associated
with the low density lipoprotein, LDL (and Apolipoprotein B), is generally thought to be harmful to the body as it carries
cholesterol into the bloodstream and can therefore place it into the intima of the arterial walls, promoting
atherosclerotic processes. Very low density lipoproteins, VLDLs, become LDLs in the liver and are therefore also
generally thought to be harmful.

For many years, this theory placed the effect of high cholesterol as the major etiologic agent in the epidemic
of heart attacks and cardiovascular disease experienced in Western nations. However, recent evidence suggests
other important factors, such as atherosclerosis.

The best approach to prevention of high cholesterol is regular aerobic exercise and a low animal-fat diet.
There are also specific nutritional approaches which include eating a low sugar diet (because where there’s sugar,
there’s often fat too), with a high fiber content and, of course, low or no extra cholesterol and a low Sodium or
Sodium-restricted diet . To get to the point of prevention, in other words to bring down you high cholesterol at the
beginning of your therapy, try 2 or 3 weeks of a vegetarian cleansing diet or a series of short juice-only fasts .
Do not attempt a fast unsupervised. Work with a doctor or an experienced friend.

Foods that have specific ability to dissolve blood fats and therefore can hlep reduce high cholesterol
include:

• garlic, wheat germ, liquid chlorophyll, alfalfa sprouts, buckwheat, watercress, rice polishings, apple, celery,
  cherries

  
  

• foods high in water-soluble fiber: flax seed, pectin, guar gum, oat bran

  
  

• onions, beans, legumes, soy, ginger, alf
  

Our entire universe is made up of combinations of elements the smallest unit of which is the atom. Each atom consists of a central nucleus, made up of protons, which is positively charged electrically. The number of protons in an atom determines what the element is. In the case of hydrogen, for example, there is just one proton, whereas carbon has 6 protons, sodium 11, calcium 20 and uranium 92.

Spinning around the central core of protons – in orbit, so to speak – are precisely the same number of negatively charged electrons, or, in the case of hydrogen, one electron. Electrons are much smaller than protons; by weight it actually takes 1835 electrons to equal one proton. Despite this imbalance in weight, the negative electrical charge of one electron is just as powerful as the positive electrical charge of one proton. Thus in a stable, electrically neutral atom, the electrical charge of the proton(s) is precisely in balance with that of the electron(s).

Electrons (much like people) have a natural tendency to find partners so that they can become paired. When this does not happen, as during radiation or certain chemical processes, a ‘free radical’ or a molecule (combination of atoms) with an unpaired electron may evolve (see below for more on these miniscule troublemakers).

The electrons which spin in orbit around the protons are arranged in such a way as to form layers, or ‘shells’ each such shell being placed just a little further out than the previous one from the nucleus. The arrangement of electrons in each ‘shell’, or layer (in most atoms) is always the same, with two electrons in the inner shell and eight electrons in the next. In some instances atoms, instead of having their own complement of negatively charged electrons (which provide electrical balance and harmony to the positive electrical charge of the protons) actually share electrons with other atoms.

This is the way molecules (combinations of atoms) are formed, allowing, for example, the two gases hydrogen and oxygen to combine together to form water. Some atoms find that they can gain or lose anything from one to three electrons when necessary, thus turning themselves into ions. An ion is simply an atom or group of atoms which has lost or gained one or more of these orbiting electrons, for one of a number of reasons, and which has therefore in the process become capable of conducting electricity.

Technically, a cation is an ion with a positive electrical charge (this happens to an ion which has lost one or more electrons) and an anion is an ion which is negatively charged (this happens to an ion which has gained one or more electrons).

If we look at what happens when this process occurs between sodium and chlorine it should become clearer.

The process of crystallization of salt


The sodium atom (Na) has 11 protons at its core and therefore (since the number of protons equals the number of electrons) requires 11 electrons to balance it electrically.

As in other atoms the first ‘shell’ contains two electrons, and the second ‘shell’, eight. Simple arithmetic tells us that there is one more electron needing a home in the case of sodium, and this is found in orbit, on its own, in the third ‘shell’ This so-called ‘valency’, electron is therefore available to attach itself easily to any passing atom which might be in need of an extra electron to complete its own electrical balance.

Chlorine (Cl) has 17 protons and 17 electrons. Again the ‘shell’ system demands two electrons in the inner layer, eight in the next and in chlorine an unbalanced seven electrons (remember eight is the ideal) are found in the outer ‘shell’. When sodium and chlorine are brought together, the ‘odd’ electron in sodium latches on to the seven in the chlorine to create a perfect ‘shell’ of eight electrons.

This process of combination creates a salt in which sodium and chlorine are bound together (in this case as table salt, NaCI) in a crystalline form. The sodium which has lost its free spinning electron (see above) is therefore now a positive ion, and this is expressed as Na+, while the chlorine which has gained an electron has become a negative ion, expressed Cl-. Chelation (pronounced key-lay-shin) is a natural interaction between an organic compound which has two or more ‘available attachment points’ (scientifically termed ‘reactive sites’) in its outer shell, with which it can link (co-ordinate) with a metal which happens to have two free electrons in its outer shell. It is axiomatic that a true chelation reaction has two or more such bonds or links. Together the organic compound (chelating agent) and the metal form a stable ring-like structure when they combine.

You (or indeed any living thing) could not survive without the constant benefits of chelation taking place, all the time, throughout your body. Digestion and assimilation of foods involves, for example, the ongoing process of chelation in which your body uses protein substances (amino acids) to chelate with minerals for transportation to their destinations, or in which blood cells latch on to, and thus acquire, iron. Indeed, haemoglobin is a chelate of iron (as is the enzyme catalase, which your body uses to ‘switch off’ the free radical activity of hydrogen peroxide). When you eat meat or green vegetables which contain iron, after the digestive process has released the iron from the food in which it is bound it has to be combined (chelated) with amino acids (protein fractions) so that it can be carried through the intestinal mucous membranes into the bloodstream.

However, if you drink tea at the same meal, the tannin in the tea will chelate with the iron (forming insoluble iron tannate) before it gets a chance to be absorbed, thus depriving your body of the iron. Should you, though, take some ascorbic acid (vitamin C) or eat vitamin C-rich food at the same meal as an iron-rich food, this will chelate with the iron and actually enhance and speed its absorption. The iron, once in the bloodstream, is released from the proteins with which it was chelated for transportation, so that it can recombine, in another chelating process, with blood chemicals to form transferrin which is then stored for later use.

Literally tens of thousands of body processes, involving the formation and function of enzymes, hormones and vitamins constantly utilize similar chelation mechanisms. Similarly, countless examples of natural chelation are found in relation to plant life; for example, chlorophyll is a chelate of magnesium which has been processed during photosynthesis.

The word itself is derived from the Greek word (chela) which describes the prehensile claw of a scorpion or crab. This graphically evokes a picture of one substance grabbing or clutching and embracing another, as the chelation process takes place. Chelation therapy is the extension of this natural process to enable the removal from the body of undesirable ionic material by the infusion, or taking orally, of an organic compound which has suitable chelating properties.

One of the major substances being influenced during chelation therapy is calcium, as this process causes it to be removed from metastatic deposits while at the same time encouraging recalcification of bone (see description of atherosclerosis in Chapter 4). If calcium happens to be inappropriately present in certain body tissues (in a layer of plaque in the lining of an artery, or in excessive amounts on the surface of a joint in arthritis), it is of benefit, in health terms, to remove this, and chelation therapy safely allows exactly this to be done.

The number of electrons in a calcium atom is 20. This has an inner ‘shell’, of 2 electrons, two complete shells of 8 electrons each, and an outer shell of 2 ‘spare’, electrons, which are therefore free to attach to a suitable molecule or atom which may be in need of 2 electrons often called a ‘complexing agent’). The symbol for the calcium cation, because of its two free electrons, is Ca++.

In chelation therapy the ‘suitable molecule’, or ‘complexing agent’, with which this can link is a compound called EDTA (ethylene-diamine-tetra-acetic acid). Together EDTA and a metallic cation form a stable complex which can then be excreted from the system. The stability of this bond is vital to success in chelation therapy, for if there is a weak linkage other reactions breaking the bond could take place should the compound come into contact with suitable chemicals.

A chelating reaction which produces equilibrium, a strong and stable ring structure between the metal ion (calcium is a weakish link, iron, lead and copper are far stronger) and the chelating agent (such as EDTA), is effective in achieving the safe removal of the ion from the body.

When you use a water softener you are chelating calcium (and other minerals) out of the water. When you use a detergent in washing clothes or dishes, this chelates with minerals in the ‘dirt’ allowing the now soluble compounds to be washed away by water.

The brief survey of the early history of EDTA (see Chapter 3) will help to explain its tortuous route towards medical respectability as a means of removing unwanted mineral/metal substances. Before we look at the fascinating background to chelation therapy, one more facet of the imbalance which can result from unpaired electrons is worth examination.

Radiation is often described as ionizing radiation. This is because, by definition, it is able to dislodge individual electrons out of atoms and molecules, leaving unpaired electrons behind. This is one way in which free radicals are created. Some such molecules, with unpaired electrons, are extremely dangerous and can have very damaging effects on body tissues. Bleach (hydrogen peroxide), for example, does its damage to tissue (just think what it does to hair) through free radical action, as a deluge of these reactive entities chaotically bounce around, creating local havoc by grabbing on to any accessible electrons with which they come in contact (in this case from the hair itself).

Radiation is an example of how free radicals may be produced in the body when such an outside force acts on its cells. Perhaps more surprisingly there is almost continuous production of free radicals by some of the defending cells of the body. These are used as a means of destroying invading micro-organisms or cancer cells.

Since this is a natural process which is going on all the time in the body, there must exist control mechanisms to prevent undesirable effects from free radicals on healthy body cells, and this is the case when we are in good health.

Just as iron rusts, and an exposed apple or potato will turn brown when its surface meets the air, so do our bodies endure oxidation (ageing), for all of these are examples involving free radical activity. In the same way that the placing of lemon juice on an apple will stop it from turning brown by ‘mopping up’ the unpaired electrons, thanks to the antioxidant vitamin C in the juice, your body contains numerous antioxidant and free radical deactivating substances (specific enzymes, amino acids, vitamins, minerals, uric acid, etc.). The body can protect itself with these substances by quenching those free radicals which it produces itself, or which are created by radiation or from other sources. At least, it has these defensive substances to hand when it is well nourished. As we will see in Chapter 4, the processes which produce atherosclerosis have much to do with both free radical activity and with the accumulation of obstructive deposits, in which calcium acts as a cement or binding agent.

Free radical activity, now generally accepted to play a large part in the development of atherosclerosis as well as many other forms of damage to the body, including soft tissues, bone surfaces and nerve structures, is often associated with the presence in the body of heavy metals. Chelation can remove these metals before they do their damage. EDTA can also create the situation (low serum calcium, leading to parathyroid hormone production, leading to metastatic calcium removal, etc) which starts the process of dissolution of atheromatous deposits which may be obstructing an artery in an area where free radical damage has already taken place. If such an approach is combined with nutritional patterns which encourage the intake of antioxidant substances (vitamins A, C, E, minerals such as selenium and zinc, etc.) an even better end result should be anticipated.

Dr Elmer Cranton’s view


A leading American physician, Elmer Cranton, MD, states his expert view of the importance of using EDTA to counteract the free radical scourge (Cranton and Frackelton 1982):

EDTA can reduce the production of free radicals by a million-fold, for it is not possible for free radical pathology to be catalytically accelerated by metallic ions in the presence of EDTA. Traces of unbound metallic ions are necessary for uncontrolled proliferation of free radicals in living tissue and EDTA binds these ionic metal catalysts making them chemically inert and removing them from the body.

He continues:

Two essential nutritional elements, iron and copper, are the most potent catalysts of lipid peroxidation [the degradation of fats by free radicals]. Catalytic iron and copper accumulate near phospholipid cell membranes, in joint fluid, and in cerebrospinal fluid with age and are released into tissue fluids following trauma or ischaemia [lack of oxygen supply due to circulatory inefficiency]. These unbound extracellular iron and copper ions have been shown to potentiate free radical tissue damage.

We will learn more about free radical activity, the damage caused by toxic heavy metals (and some apparently useful ones such as iron when in excess of requirements) and of the many protective functions of EDTA chelation therapy in relation to both free radical activity and heavy metal toxicity in later chapters, especially Chapter 5.

Acetic acid is a mild chelator, far weaker than EDTA. Nevertheless, you can demonstrate for yourself the chelation process in action using the organic acid in vinegar (acetic acid).

Take an eggshell and place this in a bowl with some vinegar. Over a period of several days the eggshell will become increasingly thin, as the acetic acid progressively chelates the calcium out of the shell. Add more vinegar and the shell will eventually have all of its calcium removed, leaving it in solution, bound (chelated) to the acetic acid.

It is just this process, much more efficiently performed, that EDTA achieves in the body when it acts on unwanted calcium deposits which are obstructing normal function.

Remember that EDTA only does this with ionic, unbound, calcium and thus will not leach calcium out of the normal bound sites such as the bones and teeth. By removing ionic, free calcium from the bloodstream, EDTA triggers parathyroid hormone to be released, which in turn compels the body to unbind metastatic calcium which may be cementing atheromatous plaque deposits in the blood vessels. In this way circulatory normality is encouraged.

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.

Vulnerability/susceptibility


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.

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:

• The bulk of stored stable calcium in the body is approximately 1 kilo in the bones and teeth.
  

  
  

• Between 2 and 4 grams of the calcium in the bones is in the ionic form which is ‘exchangeable’ with the amount of calcium ‘transported’ daily, into and out of bone, commonly around 3 grams.
  

  
  

• This interchange is between bone and the calcium held extracellularly (around 1-1.5 grams) and intracellularly (4-10 grams), in the plasma (less than .5 gram) and in interstitial fluids (under 1 gram).
  

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.

Age


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:

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.

Supporters of chelation therapy claim just these benefits and yet, despite the many published papers supporting these claims (see References), many doctors find such claims for the usefulness of chelation therapy to be controversial, and tend to dismiss out of hand the chance that they might just possibly be
accurate.

Prevention and treatment of degenerative diseases




Although chelation therapy for prevention and treatment of degenerative circulatory diseases is practiced by hundreds of medical doctors in the USA and Europe, it remains controversial, inasmuch as it is misunderstood, its use being grossly underinvestigated by mainstream medicine except in treating a narrow range of conditions such as lead and other heavy metal toxicity or acute hypercalcaemia (increased calcium levels in the blood). Ironically, as will be explained in later chapters, it was the medical use of chelation therapy in removing toxic metals which first led to the discovery of its hugely beneficial ‘side-effects’ of dramatically enhanced circulatory function.

Those doctors who have examined chelation therapy in action and who have seen its outstanding results in preventing and reversing so many degenerative diseases, usually change rapidly from critics to supporters of this essentially safe system.

Imagine someone (a loved one, friend, a patient if you are a physician, or even yourself) being in great pain, or being virtually disabled, as a result of chronic circulatory dysfunction. It might be that there is so much narrowing of the blood vessels to the heart muscle itself that any exertion would be enough to produce the agony of angina, a fist-like gripping in the chest, accompanied by severe pain, a vice-like pressure, gasping for breath and almost total helplessness. Or it might be that the circulation to the legs is so impeded that taking just a few steps across the room brings on cramp-like gripping of the muscles of the lower leg, or severe aching of the upper leg, or both. These symptoms can be so severe that only a few steps can
be taken before stopping is imperative while the circulation trickles through and the cramp eases (often taking several minutes), followed by a few more staggering steps as the cycle of intermittent claudication repeats itself. Or it might be that the abilities to function at all, perhaps to speak or to use one or other limb, or even to be able to think rationally, have been largely lost due to impeded circulation to the brain.

Imagine any one of these catastrophes and consider what options remain open to the person facing this hell.

What choices are there?


Chelation is one. In several hundreds of thousands of cases such as those briefly listed above, chelation therapy has helped to restore normal function.

It does not always do so, damage may be too severe and irreversible. But it offers a chance for a very safe form of intervention which can often take the person involved to the stage where surgery and increased medication become unnecessary and where effective long-term preventive methods, including exercise and dietary strategies, can be introduced.

Is chelation natural?


Given the nature of the damage which has already taken place in such conditions, of the dangers which apply and of the emergency status existing in many such cases, it is as natural an option as is likely to be found, and is certainly the safest.

What does medicine have to offer?


Many of the problems listed above relate specifically to obstruction, to the impeding of the flow of blood, often caused directly by the presence of concretions in the lining of major arteries.

Drugs can certainly help, but frequently at the cost of severe side-effects, and none address the causes of the problem, thus leaving the likelihood of the development of further disasters. Certainly there are now a host of drugs of varying degrees of effectiveness, all of which have major side-effects and some of which, while reducing the risks of the patient dying from the particular circulatory problem, actually increase the risks of their dying from other causes (see EDTA: how it works and what it does).

Surgery?


Bypass and other interventions may be possible. These methods (see EDTA: how it works and what it does) help some but not all, and most are risky in themselves or have major drawbacks and few can do anything for brain function if this is the area of the body most affected.

Without question modern surgeons have evolved amazingly skilful techniques, including the following:

• Balloons are carefully threaded into an appropriate artery before being inflated in order to compress the concretions, thus making more space through which the blood can flow.

• Alternatively, instead of a balloon, a minute laser might be threaded along the artery to the place where there are concretions so that these can be ‘blasted and burned’ away.

• By means of the similar insertion of a minute, high-power drill or cutting instruments, the obstruction is partially chiselled or cut away.

• There is perhaps the choice of the grafting of veins from other regions of the body, or use of those donated by animals or manufactured from special plastics, by which means the circulatory obstruction may be bypassed.
  

It is against the considerable known risks and variable and often very short-lived benefits – and of the limited success rate – which most of these methods offer, that we should measure the ‘naturalness’ or otherwise of a series of gentle infusions into the bloodstream of a synthetic amino acid, EDTA (ethylene-diamine-tetra-acetic acid).

This was initially thought to ‘lock on’ to the calcium cementing material which binds these concretions together and, by removing it from the scene, to allow the absorption of the rest of the material in the concretion (cholesterol, etc.). This somewhat simplistic picture of what happens has since been replaced by more recent research (described in Chapters 2, 3, 4 and 5), which explains a scientifically more acceptable concept of just how the improvements seen in chelation therapy actually do take place. It was originally thought that as well as leaching out calcium from atheromatous deposits, chelation therapy removed ionic calcium from cells in which it should not be present, thus reducing the chances of local arterial muscle spasms, increasing the free flow of tissue-enhancing, nutritive-rich blood. These benefits are certainly often apparent after chelation therapy, even if the precise mechanisms are not as simple as those which pioneer chelation therapists imagined.

What is known is that once atheromatous concretions lose the calcium which bind them, after a series of chelation infusions, the innate natural defence mechanisms of the body aided by dietary and exercise methods where appropriate, safely take over the removal of the remaining debris which is impeding the blood flow.

Diet and exercise


For many, these can certainly offer help in the long term and should be included whatever else is done (drugs, surgery or chelation), but may not offer the speedy result needed. The exercise element may also be virtually impossible for anyone with intermittent claudication and out of the question, or at best extremely difficult, for someone with cerebral ischaemia or who has had a stroke.

Chelation therapy (combined where possible with dietary and exercise strategies, and by means of mechanisms which will be discussed in later chapters) encourages the circulatory obstructions to be dissolved by the body’s own efforts after the concrete binding the blocking material has been dissolved and removed.

Without doubt it would be better to use totally natural methods such as exercise and preventive nutritional approaches. But even if the person so affected were able to comply with the strenuous demands for compliance in such a programme there might not be time to do this before time ran out. Compromise as to what is totally ‘natural’ would seem to be a small price to pay if the method chosen is safe and is used as part of a comprehensive approach which not only attempts to restore normality to the circulation, but to ensure prevention of any recurrence.

A full medical case history
and examination is the first prerequisite, including a comprehensive
personal and family history detailing all aspects of previous
health problems and current status. Questions relating to diet,
habits, emotional status, exercise, stress levels and a detailed
listing of symptoms is part of this. A full physical examination
is also required, most notably of all aspects of the circulatory
and respiratory systems.

An electrocardiogram and chest
X­ray might be required as well as a number of blood tests.
Exercise tolerance tests may be used to see just how the functioning
of the heart, lungs and circulation responds to activity. A commonly
used procedure, before chelation therapy is started, and of major
importance in establishing a ‘before’ picture of circulatory efficiency,
is the use of what is known as bi­directional Doppler (sound
wave) examination.

This is a painless, non­invasive
use of sound waves (ultrasonic) which is used to investigate six
major arterial sites which relate to circulation to the brain,
as well as eight sites which relate to circulation to the legs.
The Doppler equipment gives readings which tell the doctor running
the tests three important pieces of information at each site:

1. It shows whether there is any turbulence which could relate to breakaway deposits of plaque,
etc., which could be involved in production of a stroke.



2. It checks for any signs of capillary hardening in the brain, often associated with memory
loss and age­related brain changes.



3. The major arteries are assessed for obstructions to normal flow of blood which could relate to over­burdened heart function or deficient circulation to the legs.

This sound­wave testing
takes about an hour and all findings are recorded on charts so
that later tests can be compared. This is also an excellent way
for the patient to appreciate visually the degree of current circulatory
difficulty.

Use of thermographically (heat)
sensitive film allows areas of the body which are not receiving
their full circulatory servicing to be photographed as a record
which can be compared with the same region after treatment.

Among other tests, an initial
one is performed (not for people with diabetes) after overnight
fasting (14 hours without food). This test is usually done around
mid­morning, the last food (or coffee or sugar) having been
consumed around 9 pm the previous night. The fasting blood test
gives an accurate idea of cholesterol levels as well as other
key markers. Periodic monitoring of blood levels of cholesterol
and other elements (giving evidence of levels of blood fats, carbohydrates,
whether or not there is anaemia, infection, immune system problems,
liver or kidney dysfunction, etc.) is made during the chelation
treatment which can last for some months, with two or three infusions
per week.

Depending upon the condition
of the patient a blood sample may be required before each treatment,
or periodically.

A 24­hour sample is required
for assessment of normal urinary output of creatinine, a key guide
as to kidney status. A periodic assessment is made of the creatinine
levels of the urine as the series of chelation treatments progress,
but this does not require collection of 24­hour samples.
As with blood testing, the frequency of urine testing during a
series of chelation infusions will vary, depending on the nature
of the problem being treated and the health of the patient.

If there is any evidence that
the kidneys could not be expected to deal efficiently with the
elimination of EDTA during infusion, then the treatment series
would be delayed or stopped until this factor had been dealt with
appropriately. As we will see in a description of important research
by Doctors McDonagh, Rudolph and Cheraskin later in this chapter,
kidney dysfunction is often capable of being normalized by EDTA
chelation therapy

A computerized dietary analysis
(based on the filling in of lengthy questionnaires) of what the
patient eats is often required so that comprehensive dietary and
supplementation advice can be given to the person being chelated,
to complement the treatment.

In addition, saliva, sweat
and faeces may need to be tested for a variety of reasons, including
assessment of what the patient’s current metabolic and nutrient
status is, how well foods are being digested and absorbed, etc.
Whether such tests are needed will depend upon the individual
problems being dealt with.

This non­invasive and
inexpensive method is also sometimes used to provide an accurate
indication of heavy metal toxicity as well as to give some idea
of the current mineral status of the body. The findings from this
and the other tests allow the doctor in charge to decide just
what balance of minerals should be added to the basic EDTA infusion
solution in order to obtain the best results.

Once it has been established
that there is a problem which could benefit from EDTA infusion,
a series of treatments are scheduled, either two or three times
per week. Most chelation centres treat patients in a group setting.

A large room with appropriate
seating (usually comfortable recliners) is all that is needed
(not unlike a hairdressing or beauty salon). There are several
advantages to this approach:

1. The mutual support of people
having the same procedure is reassuring and encouraging. There
will almost always be someone present who has had a number of
infusions and who can give a personal account of what to expect.



2. The costs can be reduced,
since fewer supervisory staff are required if patients are grouped
together in this way.



3. During the 3 1/2 hours of
the infusion the patient can read, doze, chat, watch TV, listen
to a pep talk on diet or exercise from a clinician (this is a
truly ‘captive audience’).

The infusion itself involves
the insertion into a vein (usually in the hand or forearm, but
sometimes the lower leg) of a needle which is attached to the
container (hung on an adjustable stand), from which is drip­fed
around half a litre of fluid over the 3 1/2 hours’ duration of
each treatment. This liquid usually contains 2 to 3 grams of EDTA
and whatever additional minerals the doctor has decided will best
help achieve a balanced blood content.

EDTA mixture

Among the other substances
often placed in solution with the EDTA are a complex of B vitamins,
vitamin C, magnesium (extremely useful for cardiovascular health)
and heparin (an anti­coagulant, enough of which is sometimes
used just to prevent any clotting at the injection site). Cranton
suggests (Cranton and Frackelton, 1982) that since magnesium is
a natural calcium antagonist and also the ion least likely to
be removed by EDTA (see Chapter 4), and that it is relatively
deficient in many people with cardiovascular and circulatory problems,
it should be supplied with the chelation process. He suggests
that the best way to do this is to use magnesium­EDTA, which
would provide an efficient delivery system and thereby increase
magnesium stores in the body.

When the infusion is being
performed, the arm is kept stable as a rule by being taped to
a padded board which rests on a cushion for comfort. It is usually
quite possible (although it is not encouraged) for the patient
to move around freely during treatment (to visit the toilet, for
example) as long as the mobile infusion is wheeled alongside.

The rate at which the EDTA
solution is dripped into the bloodstream can be varied but usually
it is at a rate of one drop per second.

As a general rule, two, but
sometimes three, treatments are given each week, and a total of
anything from 20 (for relatively mild problems) to 30 infusions
in all comprise one complete series.

On a number of occasions (sometimes
at each visit) blood and urine testing (as well as other tests)
may be carried out to ensure that kidney and other functions are
operating sufficiently well to cope with the EDTA detoxification.
This is obviously more important in elderly patients or anyone
with compromised kidney function. In some instances where a great
deal of circulatory pathology exists, follow­up series of
chelation infusions might be encouraged, with many people showing
benefits after up to 100 infusions.

The EDTA is eliminated from
the body, 95 per cent via the kidneys and 5 per cent via the bile,
along with the toxic metals and free ionic calcium which it has
locked on to in its transit through the circulatory system.

In hospital settings, EDTA
infusions have in the past been given daily for up to five days,
followed by a two­day rest period for the kidneys. This protocol
is now discouraged by the American medical group with the most
experience of chelation, the American Academy of Medical Preventics.

General toxicity

Walker and Gordon (1982) inform
us that EDTA is far safer than aspirin, digoxin, tetracyclin,
ethyl alcohol or the nicotine from two cigarettes, in equivalent
therapeutic doses. EDTA is used in thousands of food products
(it is in most canned foods) and its toxicity is known to be extremely
low.

In assessing the relative
toxicity of a substance a therapeutic index is established. Firstly,
the amount of the substance which would prove lethal to half the
animals in an experimental setting is discovered by the gruesome
process of increasing their intake until half of them die. This
is the LD­50 measurement (LD for lethal dose). When this
amount is divided by the amount required for a therapeutic effect
we end with a number which is the therapeutic index.

The LD­50 of EDTA is
2000 milligrams per kilo of body weight, whether taken orally
or intravenously. In comparison aspirin has a toxicity equal to
558 milligrams per kilo of body weight. So in general there is
no need for concern as to general toxicity with
EDTA usage, whether by mouth (see Chapter 9) or directly into the blood.

Kidney toxicity

In the early 1950s several
deaths occurred from nephrotoxicity after EDTA treatment. At that
time the dosage used was around 10 grams per infusion, whereas
the recommended dose now adays is 3 grams.

Halstead (1979) states:

The problem in EDTA nephrotoxicity
is based upon two fundamental principles of toxicology: dosage and route of administration. Dosage is concerned with both the amount administered and the rate
of administration, or the time period in which the EDTA is given.

It appears that toxicity for
the kidneys may relate directly to too large a dose infused at
too fast a rate. In general, if no more than 3 grams is infused
in any 24­hour period (diluted with 500 ml sterile Lactated
Ringer’s solution or-except in the case of diabetes-5 per cent
dextrose solution), with a 24­hour rest period between chelation
infusions (2­3 per week) and if the infusion of these 3 grams (less than 50 milligrams per kilo of body weight) is timed to take around three hours, little if any danger exists of producing toxicity for the kidneys.

Indeed, research has shown
that in general chelation therapy improves kidney function, particularly
if any impairment to these vital organs relates to circulatory
problems.

Improved kidney function
after EDTA

McDonagh, Rudolph and Cheraskin
(1982d) have investigated the alleged toxicity of EDTA in relation
to kidney function and their results are worth some consideration.

They examined the results
of treating 383 people with a variety of chronic degenerative
disorders (primarily occlusive arterial disease) with EDTA chelation
therapy (plus supportive multivitamin/mineral supplementation)
for 50 days.

The measurement of the levels
of creatinine in the blood is commonly used in medicine as a guide
to kidney efficiency.

Creatinine is the end breakdown
product of muscle activity which is cleared from the body by filtration
through the normal kidney. The levels found in the bloodstream
are known to correlate well with the rate and efficiency of clearance,
giving a simple way of judging kidney function. The researchers
made specific measurements of the levels of creatinine in the
blood of these patients at the first visit (fasting levels) and
then gave 10 infusions of 3 grams of EDTA in a solution of 1000
cc normal saline with an interval of five days between each infusion
(supplementation was also given). After this the serum creatinine
was again assessed.

They found that a very interesting
balancing effect could be seen when the overall picture was revealed,
very similar to that noted when cholesterol ratios were examined
(see Chapter 4). Those people who initially had low levels of
serum creatinine showed a very slight increase; those in the mid­range
(normal?) showed no change and those above the mid­range
of normal and actually with a creatinine excess (therefore indicating
poor clearance by the kidneys) showed a drop towards normal.

Overall the total measurement
showed an average decline in serum levels (indicating improved
kidney function), but far more significant, according to the judgement
of the researchers, is the homoeostatic effect in which ­
whether high or low to start with ­ a tendency towards the
mid­range (between 0.5 and 1.7 milligrams/decilitre) is observed.

It seems that EDTA therapy
may actually improve kidney function if it is applied slowly
with normal dosages.

One exception


These researchers make note
of one exceptional case amongst nearly 400 patients tested in
this way, and the progression of events is worth noting as an
example which highlights both the initial concerns which some
patients might produce and the long­term benefits of chelation
therapy.

This was an 86­year­old
female in whom the initial measurement of creatinine was 1.9 mg/dl,
which is regarded as abnormally high and therefore indicative
of poor kidney function. After starting chelation every five days,
a rise was seen in the creatinine levels by day 25 (fifth infusion)
to a very unhealthy 3.5 mg/dl. As treatment progressed, it dropped
to 2.8 mg/dl by day 60 and had dropped to 1.8 mg/dl by day 100,
some time after the course of chelation therapy had finished.

As the researchers point out:
‘this emphasizes the need to follow renal function during EDTA
therapy, and, one might add, for a while after, as the benefits
frequently are not fully manifest before about three months after
treatment is over.

Special considerations:
age, heavy metals or parathyroid deficiency

If the patient is very elderly,
or has low parathyroid activity or is suffering from heavy metal
toxicity which is damaging kidney tubules, treatment should be
modified to use less EDTA less frequently (once weekly perhaps).
Heavy metals damage the kidneys and too rapid infusion can overload
them. Heavy metals most likely to produce kidney damage during
infusion therapy (if this is done too rapidly, that is) are lead,
aluminium, cadmium, mercury, nickel, copper and arsenic.

Renal function tests should
always be performed before chelation therapy is started in which
serum nitrogen (BUN) and serum creatinine is examined. In any
case of significant renal impairment, lower dosage EDTA infusions
should be used with extreme caution with suitable periods of rest
between.

Too much calcium removed

If, through inexperience or
error, there is too rapid an infusion (or too much EDTA used),
levels of calcium in the blood can drop rapidly, resulting in
cramps, tetany, convulsions, etc. An injection of calcium gluconate
will swiftly control such abnormal reactions. This hypocalcaemia
reaction is almost unheard of where the guidelines given above
are followed as to dosage, speed of infusion and spread of treatments.

Inflammation of a vein

If an infusion into a vein
is performed too rapidly, inflammation may occur (thrombophlebitis).
This is unlikely in the extreme if guidelines as described above
are followed concerning dilution of EDTA with Ringers solution
or dextrose solution and slow infusion.

Should the needle carrying
the infusion slip, a local soft tissue irritation may develop.
This may best be treated with use of alternate hot and cold packs.
Supplementation with antioxidant nutrients such as vitamins C
and E (make sure of a good source) and the mineral selenium should
protect against such an incident.

Care regarding insulin
shock and hypoglycaemia

During EDTA infusion it is
possible for blood glucose to drop, leading to insulin shock.
This is more likely amongst diabetics in whom no dextrose solution
should be used. Patients having EDTA infusions are advised to
have a snack before or during the three hours plus treatment period.
Walker and Gordon (1982) recommend the following strategy:

You should eat something before
the three to four hour infusions, but not high­calcium­containing
foods such as dairy products. Rather, eat adequate unrefined complex
carbohydrates and avoid most sugars, including overripe bananas.

During an infusion they recommend
eating fruit.

In diabetic individuals, using
zinc­bound insulin involves a risk of too rapid a release
of insulin, leading to hypoglycaemia and shock. A rapid introduction
of sugar is needed in such an instance and a change in the form
of insulin used before further EDTA infusions are tried. Most
people with known diabetes find that with chelation therapy their
requirement for insulin declines.

Congestive heart failure

If the heart is already unable
to cope adequately with movement of fluids, and there is evidence
of congestive heart failure (extreme shortness of breath, swollen
ankles) and/or if digitalis­like medication is being taken,
extreme care is needed over chelation infusions, since EDTA prevents
digitalis working adequately. Sodium EDTA would appear to be undesirable
in such people as it could increase the fluid retention tendency.
However, Halstead is adamant that:

Na2 EDTA does not appear to
have any significant deleterious effects in congestive heart patients
since the sodium (Na2) is apparently excreted intact with the
metal chelate. However, the use of 5 per cent dextrose and water
is recommended in such cases.

Short­term side­effects

A number of variable side­effects
have been observed with use of intravenous EDTA infusion, including
the following:

• Headaches ­
  which often relate
  to the same phenomenon discussed above, of low blood sugar. Eating
  before treatment, or during it, will usually prevent this possibility.
  It is reported that a common recommendation which prevents ‘EDTA­headaches’
  is that a banana, not overripe, be eaten during the first hour
  of infusion.
  
• Diarrhoca ­ this
  unusual side­effect should be treated with rest and a bland
  diet with plenty of liquids for a day or so. Urinary frequency is common
  as kidney efficiency improves and a weight loss (from fluid excretion)
  of 3­5 pounds (1.3­2.2 kg) is common after an infusion
  if fluid retention was previously evident.
  
• Local skin irritation
  may result and
  is usually associated with a reduction in zinc and vitamin B6
  (pyridoxine). For this reason supplementation of these nutrients
  is usually suggested during chelation therapy.
  
• Nausea or stomach upset
  may also be related
  to vitamin B6 deficiency in the less than one patient in 100 receiving
  chelation therapy who feels this side­effect. It is best
  treated by B6 supplementation, although short­term relief
  (up to eight hours) from nausea can be achieved by applying thumb
  pressure to a point two thumb­widths above the wrist crease
  on either forearm (acupuncture point P6) for a minute or so whenever
  the symptom is felt.
  
• Feeling faint may
  relate to a drop in blood pressure. It is common for those who
  start treatment with high blood pressure to see a return to more
  normal levels. If it were normal to start with, it could drop
  slightly as well as leading to feelings of faintness on standing
  after sitting or lying. Treatment is to rest for an hour or so
  when this happens, ideally with the feet slightly higher than
  the head. The amino acid tyrosine can safely be supplemented to
  help restore normal pressure levels if this symptom persists.
  
  
• Fever may
  develop in a very few people during the day after chelation therapy
  sessions (approximately one in 5000). Whoever is in charge of
  the treatment should be told, although the condition normally
  resolves on its own.
  
• Extreme fatigue may be felt in some people and this is usually the result of a general
  nutrient deficiency in minerals such as magnesium, zinc or potassium.
  Taking a potassium­rich supplement and/or the regular eating
  of potassium­rich foods is suggested before and during chelation
  (grapes, bananas, peaches, potato skins), as this mineral may
  be removed by the process itself.
  
• Pains in the joints
  are more likely
  where infusions are frequent (three weekly). An immediate reduction
  to once weekly is suggested, and also possibly a reduction in
  dosage of EDTA being used, if strong flu­like aches develop.
  The symptoms should pass fairly soon if these strategies are adopted.
  
  
• Cramps in
  the legs are not uncommon (one patient in 20), usually at night.
  The supplementation of magnesium (either by mouth or in the El)TA
  infusions)
  will usually prevent this happening. If it is added to the infusion
  this could be in the form of magnesium chloride or magnesium sulphate.
  Such additions also reduce the chance of local skin irritation
  at the site of the infusion.
  

Other minor side­effects
have been reported in the many millions of chelation infusions
already given, but all seem to vanish when the therapy is reduced
or stopped. As Bruce Halstead states: ‘The number of significant
untoward reactions is probably less than in any other major therapeutic
modality’

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.

A further well­established
effect of EDTA infusion involves the improvement of cell membrane
integrity and consequent protection of mitochondria activity.
If this is happening in the heart muscle itself, such improvement
in cell function (enhanced energy production via enhanced mitochondria
activity) often allows a strong chance of salvaging and regenerating
previously damaged muscle function, with benefits to the heart
and therefore the body as a whole.

Research by Dr C Gallagher
as long ago as 1960 (Gallagher, 1960) showed that the natural
ageing of the mitochondria could be counteracted by use of EDTA.

Not only does EDTA remove
circulating ionic calcium from the blood, but it also acts directly
on improving the function of blood platelets. These (which contain
granules, lysosomes, mitochondria and glucose), along with red
and white blood cells (erythrocytes and leucocytes), make up much
of the ‘solid’ material suspended in the blood plasma which itself
is made up of a complex of protein­based substances including
fibrinogen, albumin and globulin, as well as carrying in solution
salts, hormones and a variety of metabolic products and wastes.

Platelets have as a major
function the role of initiating repair of any damaged internal
lining in blood vessels. This they accomplish, under the direction
of prostaglandin hormones called prostacyclin (which discourages
clotting and reduces muscle spasm) and thromboxane (which encourages
muscle spasm and the stickiness of blood), firstly by adhering
to the damaged surface, gradually covering the region of injury,
while at the same time reducing the danger of hemorrhage by encouraging
a degree of coagulation of the blood. As all this happens, the
shape of the platelets alters from a disc shape to a more irregular
form, with radiating filaments known as pseudopodia extending
from them as well as developing inside them. These protective
functions of platelets are therefore life­enhancing. But,
should the process of organization of clots (coagulation) take
place in a cerebral artery the consequences could well be life­threatening
and would certainly pose a hazard until it resolved.

Just how EDTA reduces these
dangers is not clear, but it does. The reduction, after use of
EDTA, in the tendency to overcoagulation is thought by some to
relate to the way EDTA removes ionic calcium from the membrane
of the platelet. Or it may be that a more healthy, balanced production
of the prostaglandins which control platelet function and activity
are influenced by the way EDTA inhibits lipid peroxidation, since
prostoglandins are the product of lipids which can be severely
damaged by free radical activity.

Normalizing abnormal cholesterol
and high density lipoprotein (HDL) levels

As we age there is an increasing
tendency for our bloodcholesterol levels to rise. High blood cholesterol
was for many years used alone as a marker of increased risk of
cardiovascular disease. The fashion for blaming all cholesterol
has only partly been reduced in the public mind through education,
but medical practitioners now know that it is only some forms
of cholesterol which pose a real threat ­ the low density
forms (LDL). Indeed the ratio between total cholesterol and HDL
(high density lipoprotein beneficial form) is now used as a clear
indication of relative safety or danger, in terms of being a predictor
of cardiovascular disease.

In a series of simple but
effective experiments, McDonagh, Rudolph, and Cheraskin (1982b)
have shown that EDTA infusion has a markedly beneficial effect
on this potentially serious problem.

The effects on over 200 patients
with varying levels of HDL cholesterol measurements were quite
dramatic. Those who initially showed low levels of HDL rose to
normal levels, those with normal levels remained unaltered, and
those with high levels of LDL (dangerous) dropped to normal ranges after EDTA­chelation therapy (supported with vitamin and mineral supplementation).

Thus we see a homoeostatic
(balancing, normalizing) effect after the use of EDTA, since it
supported a return towards normal HDL­cholesterol levels,
whether the initial abnormality was high or low.

How long before such change
starts to be significant?

This same team of researchers,
working in a private practice setting, found that: ‘ . . there
appears to be a significant reduction in serum cholesterol within
the first month or so (range of 12­36 days) of treatment
with EDTA . . . in private practice environment, irrespective
of the age or sex of the patient’ Excitingly, it was found that:
‘. . . those with the highest initial cholesterol scores decreased
about twice as much as those with the lower first score (approximately
17 per cent as against 9 per cent)’

With regard to the ratios
between total cholesterol and HDL, these homoeostatic effects
were measured as follows:

The ‘normal, balance between
total cholesterol and HDL is considered to be a ratio of 4.5:1. The McDonagh, Rudolph and Cheraskin team found that those with ‘relatively low ratios (under 4.0) tended to rise,
while those with relatively high ratios (over 5.0) tended to
decline, and those in the range 4.0­4.9 tended to remain
unchanged’

This important research is
deserving of far wider awareness and application since cardiovascular
disease is the number one killer and these risk factors are demonstrably
easy and safe to control or normalize (by EDTA, diet and life­style
changes).

In Chapter 4 we looked at
some of the ways in which cardiovascular disease developed. Once
a localized area of plaque has accumulated in an artery, following
some degree of local irritation and subsequent repair (which the
plaque represents to a large extent), there exists a strong case
for trying to remove any calcium in the plaque in order to prevent
its inevitable build up towards this becoming a complete obstruction. It is the loosely bound calcium in the plaque, held by an electrostatic charge, which prevents the
body from dissolving it. When EDTA is infused it mops up the
ionic (free) calcium in the blood serum, triggering release of parathormone.
This produces a demand for calcium in the blood and this is first mobilized from the calcium deposited in metastatic sites (plaque, soft tissue deposits, etc.), thus allowing the
process of resorption of the plaque material and restoration of
normal arterial status.

However, this does not happen
quickly. It is only by repetitive, very slow infusions of EDTA
that the process takes place safely

Does this not damage bone
and tooth structure?

On the contrary, the status
of bone is enhanced after a series of EDTA chelation infusions.
This is directly related to the influence of parathyroid hormone.
After EDTA infusion there is a rapid removal of ionic calcium
from the bloodstream (the EDTA/calcium complex is excreted via
the kidneys). The resulting drop in circulating calcium stimulates
parathyroid hormone production which results in the removal of
ionic calcium from metastatic deposits (such as occur in plaque).
At the same time a phenomenon occurs in response to parathormone,
described by Doctors Rasmussen and Bordier (1974), in which preosteoblasts
are converted into osteoblasts.

Since osteoblasts are the
cells which form bone, building the osseous matrix of the skeleton,
new bone formation is thus encouraged. This is often confirmed
by X­ray examination of bone before and after a series of
chelation infusions.

According to Cranton and Brecher
(1984):

Pulsed intermittent parathormone
stimulation, produced by each chelation (treatment) is known to
cause a lasting effect on osteoblasts of approximately three months’
duration. This is a proven effect of EDTA, and one that makes
perfect sense, for it provides a hypothetical explanation for
the three month waiting period for complete benefit following
a series of intravenous EDTA therapy infusions.

Walker and Gordon (1982) suggest
that:

Soft tissue pathological calcium
in plaques or arterial cells continues to diminish in order to
meet the need caused by the increased bone uptake of calcium.
The therapeutic cycle continues long after a series of chelation
treatment has been completed and patients continue to improve
all this time.

They describe the work of
Dr. Carlos Lamar who explained his findings on this topic at the
fourteenth annual meeting of the American College of Angiology
in 1968. Dr Lamar had demonstrated that as calcification of the
blood vessels decreased so did simultaneous recalcification take
place of previously osteoporotic vertebral and femoral bones.
Similarly, metastatic calcium deposits in arthritic joints was
often seen by Dr Lamar to decrease. In such cases deformity often
remained but symptoms of pain and immobility were reduced or absent
after chelation therapy. Walker and Gordon remind us, however,
that chelation itself is not the whole answer: ‘Hardened arteries
get softer and softened bones get harder following proper EDTA
chelation therapy ­where appropriate mineral
supplementation with zinc, magnesium and other minerals is being
given, dietary calcium/phosphorus ratio is balanced and active
exercise undertaken.’[original italics]

By now the concept of free
radical damage resulting in tissue damage and consequent deterioration
of circulatory function should be quite familiar. It is perhaps
less apparent that free radical damage is frequently the trigger
which leads to malignant changes in previously normal cells. Just
as the first benefits to circulation of EDTA chelation therapy
were discovered during treatment of heavy metal poisoning, so
was the way in which this same treatment could help prevent, and
indeed treat, cancer discovered.

Writing in a Swiss medical
journal in 1976, Dr W Blumen described the strange but potentially
very important discovery. In the late 1950s a group of residents
of Zurich who lived adjacent to a major traffic route were treated
for contamination by lead with EDTA chelation under the auspices
of the Zurich Board of Health. These people had all inhaled large
amounts of lead­laden fumes and were suffering from a range
of symptoms identified as being related to lead poisoning, including
stomach ache, fatigue, headache, digestive symptoms, etc. lead
deposits were found to be present in their gum tissues and specific
changes were found in their urine, linking their condition with
high lead levels.

Some years later, in the early
1970s, people living in the same area were being investigated
for the incidence of cancer, in an attempt to link the pollution
with a higher cancer rate than average. This link was easily established
as fully 11 per cent of the residents of the road had died of
cancer over the period 1959 to 1972, a rate some 900 per cent
above that expected when compared with people living in the same
community but not directly affected by lead pollution. The forms
of cancer most commonly related involved the lungs, colon, stomach,
breast and ovary.

But what of the people previously
treated with EDTA back in 1959?

Only one of the 47 people
in that group had developed cancer. The cancer rate in people
in the contaminated area who had not received EDTA was 600 per
cent above that of the group who had had chelation.

Far and away the best protection
from lead toxicity and its long­term effects is to avoid
it altogether. However, this is of course not always within the
control of the individual and a second best bet is to have the
lead removed via chelation as a protective measure against its
undoubted toxicity which can contribute towards the evolution
of cancer.

Australian research scientist
John Sterling, who has worked at the famous Issels clinic in Germany,
mentions in a personal communication that Issels had noted a marked
protective effect against cancer after use of EDTA chelation.

Animal studies (using mice)
have shown that intravenous EDTA plays a preventive role against
cancer, largely, it is thought, through removal of metallic ions
which seem to be essential for tumour growth.

Walker and Gordon believe
that the prevention offered to the citizens of Zurich was partly
as a result of removal of metal ions and of lead (which can chronically
depress immune function) and also due to the improvement in circulation
which chelation produced. Tumours flourish in areas of poor oxygenation
and the increase in the levels of this which chelation allows
would, they believe, be sufficient to retard cancer development.

Halstead (1979) points to
the significant increase in metal ions found as tissues age and
the increased likelihood of cancer developing. There is also a
proven link between high levels of certain metals in topsoil and
cancer in the same regions. Interestingly, he confirms that most
forms of chemotherapy involve drugs which have chelating effects
either directly or as a result of breakdown of their constituents.
He quotes experimental studies which show that in some forms of
cancer such as Ehrlich’s ascites tumour the use of EDTA was significantly
able to strip the tumour cells of their heavy protective coat,
allowing other mechanisms (such as protein digesting enzymes)
to destroy the tumours.

At the very least EDTA chelation
can be seen to offer a useful line of investigation in cancer
prevention, and possibly treatment, in some forms of this disease.

Dr Wayne Perry (1988) comments
on one of the beneficial ‘side effects’ of EDTA therapy when he
states: ‘Those who have used EDTA have been impressed by the dramatic
effects that can occur in some patients, and this action might
be explained by its powerful anti­depressant effect, shown
in a double blind trial over and above any placebo action’ (See
Kay et al 1984.) In discussing the objective evidence of general improvement amongst
patients having EDTA he includes ‘general alertness, concentration
and memory’ as common.

Clearly, if circulation to
the brain is enhanced the function of that organ should improve.
Equally important to mental function would be the removal of heavy
metals, the toxicity of which are common causes of a wide range
of problems affecting the brain and nervous system. It should
therefore not be surprising that EDTA often leads to improved
memory and reduced tendency to depression and other apparently
‘psychological’ symptoms.

The research team of McDonagh,
Rudolph and Cheraskin have looked at just this aspect of EDTA
chelation therapy’s effect ­ the psychotherapeutic benefits.
(McDonagh, Rudolph and Cheraskin, 1984, 1985a, 1985b) They used
a standard medical questionnaire (Cornell Medical Index ­
see Brodman et al 1949) at the first
consultation to allow 139 routine private­practice patients,
83 of whom were male, to answer questions from which ‘depression
‘tension’ and ‘anger’ tendencies could be discovered. These same
patients completed the same questionnaire at the end of a series
of EDTA infusions (plus multimineral/vitamin support supplementation)
over a two month period. There was a 40 per cent reduction in
depression indications amongst those patients who showed a tendency
towards depression in their first questionnaire. There was a 50
per cent reduction in ‘tension’ symptoms and a 46 per cent reduction
in ‘anger’ indications at the end of the treatment period.

The researchers speculate
that the improvement was due to overall improvement in cellular
nutrition as a result of the enhanced circulation due to this
form of treatment. They note that the improvements in emotional
status, observed in this study, were superior in degree to any
physical improvements noted in their many previous studies.

Using the same approach these
researchers had over 100 patients complete the whole Cornell Medical
Index (CMI) questionnaire before and after a chelation series
which averaged 26 infusions over a two­month period. The
CMI questionnaire is designed to collect a great deal of information
in a short space of time. Anyone with more than 25 positive answers
out of the 195 questions is considered to be suffering from a
significant degree of current ill­health.

Before treatment, the average
number of positive answers amongst these patients was 31.7, indicating
an overall poor level of health. Some patients had as many as
95 ‘Yes’ answers, with the lowest score being 3; more than half
of the patients had over 25 positive answers. When the CMI questionnaire
was answered again after the therapy series there was a drop of
46 per cent in those with more than 25 positive answers and the
overall number of symptoms reported dropped by 15 per cent.

The CMI is divided into different
sections and when these were analysed for before­and­after
changes, the pattern that emerged was as follows:

Musculoskeletal symptoms declined
by 25 per cent; neurological symptoms by 19 per cent; cardiovascular
by 19 per cent; skin conditions by 18 per cent; respiratory by
17 per cent; genital by 13 per cent; gastro­intestinal by
11 per cent and urinary by 11 per cent.

Specific attention was paid
to fatigue in these patients, as this general symptom is amongst
the commonest and most worrying for many people in poor health.
Seven questions in the CMI relate specifically to the degree of
fatigue/tiredness felt. The percentage of those answering this
section who had no fatigue symptoms rose from 31 per cent to 56
per cent over the course of the treatment series, and of those
originally reporting fatigue as a symptom, fully 39 per cent showed
an appreciable improvement. Since most researchers and therapists
involved in chelation therapy report that the greatest beneficial
effect is not felt until up to 90 days after the cessation of
therapy, these results may well indicate only the beginning of
the benefits ultimately achieved.

Considering the fact that
over half those involved were by any definition in very poor health,
the improvements were remarkable, and the very general nature
of their spread supports the contention of these researchers that
they were due to generalized nutritional enhancement due to circulatory
improvements resulting from EDTA therapy.

We will discuss the controversial
oral EDTA approach after first looking at the nutritional approach.

The current vogue for oat­based
foods as a means of reducing cholesterol levels is but one form
of chelation which we take for granted. In fact the different
forms of fibre found in food, soluble pectin in apples and other
fruits, guar in beans as well as the forms found in grains, all
produce multiple chelating effects as they pass through the system.
These act largely in the bowel where they speed up transit time
and in this way prevent cholesterol reabsorption from bile as
well as clearing putrefactive material from the system more rapidly.
Fats in the bloodstream are reduced by soluble fibre in the diet,
reducing the potential for free radical activity.

The advice given in Chapter
8 regarding the ideal pattern of eating can easily produce just
these effects if followed reasonably closely. In addition many
basic nutrients such as vitamins C and E are natural chelators
and when in abundant supply act in the bloodstream to damp down
free radical activity as well as chelating toxic substances.

Several formulae have been
developed for oral chelation using variable combinations of substances.
Some are extremely complex and others simple enough to put together,
given a little patience and effort.

This is known as the Rinse
Formula, after Dr Jacobus Rinse of Vermont, who has popularized
this highly effective combination of substances, now advocated
by the Dutch National Health Board for the prevention of heart
disease

A daily intake of the following
is suggested:



4 grams of lecithin (try to
ensure a form which is high in phosphatidyl choline)



12 grams of coarsely chopped
sunflower seeds (for their linoleic acid, potassium and fibre
content)



5 grams debittered Brewer’s
yeast powder for its selenium, chromium and B vitamins (not suggested
for anyone with active Candida albicans overgrowth)



2 grams of bone­meal
as a source of calcium and magnesium, or a nutritional supplement
form of calcium and magnesium (in a ratio of 2:1)



5 grams unpasteurized or untreated
wheatgerm for its vitamin E and trace elements




500 milligrams of vitamin
C (as sodium ascorbate, in powder form if possible)



1001U vitamin E (make sure
this is D­Alpha tocopherol)



40 milligrams vitamin B6 (pyridoxine)



20­30 milligrams zinc
(picolinate or orotate)

Blend these ingredients
together in a food processor and keep refrigerated until use.

The amounts given are
for daily consumption (around 30 grams in total) and it is
probably wise to make up enough for a few weeks at a time and
to keep this well covered and chilled until it is consumed, as breakfast
or with any meal.

Research at the University
of Alabama by Drs C Butterworth and C Krumdieck (published
in 1974 in the American Journal of Clinical Nutrition) has
shown that the combination of linoleic acid and lecithin, as well
as the other nutrients such as vitamin C, act to form an enzyme Lecithin­Cholesterol­Acyl­Transferase (LCAT), which chelates cholesterol
deposits from arterial walls at normal body temperatures.
These foods are suggested by Dr Rinse as a means of ensuring
that the raw materials for formation of LCAT are readily
available.

Dr Kurt Donsbach, the dynamic
and controversial author of dozens of health booklets and pamphlets,
and director of an ‘holistic’ medical clinic in California, has
provided a chelation formula for oral use (Chelation pamphlet
1985, published by the author). He states:

Oral chelation is probably
a misnomer, since the formulation does not attach itself to, or
eliminate via the urine, the calcium in the bloodstream as does
the EDTA form of intravenous chelation. The term is used because
the end result is the same, with considerably less discomfort and
cost (approximately 1500 percent less).



The two chelation approaches,
intravenous infusion of EDTA and the oral nutrient approach, both
are lifesavers to countless individuals. Many physicians are now
opting for a combination of the two methods since they work in
different fashions and by doing so find that the intravenous infusions
can be cut down from a series of 30 to only 10 treatments. Furthermore,
by using a maintenance dose of the oral, the patient is protected
for the future so that he does not need to be rechelated with
EDTA.

John Stirling, an Australian
research scientist working in the UK compares oral and intravenous
chelation (although he is discussing oral use of EDTA, not oral
nutritional chelation) with intravenous EDTA (Stirling, 1989):

I would opt for intravenous
over oral EDTA in extreme life threatening situations. Intravenous
is more direct obviously, and results can be noticed sooner, and
the cost variance is considerable.

Vitamin A (fish liver oil
and beta carotene) 25,000IU



Vitamin D (fish liver oil)
400IU



Vitamin E
600IU



Vitamin C
3000mg



Vitamin Bl
200mg



Vitamin B2
50mg



Vitamin B6
150mg



Niacin (B3)
l00mg



Pantothenic acid (B5)
250mg



Vitamin B12
250mcg



Folic acid
400mcg



Biotin
100mcg



Choline
750mg



Inositol
100mg



PABA
150mg



Calcium carbonate
400mg



Magnesium oxide
500mg



Iodine (kelp)
225mcg



Copper gluconate
250mcg



Zinc gluconate
25mg



Potassium citrate and chloride 400mg



Manganese gluconate
10mg



Chromium
200mcg



Thymus extract
50mg



Spleen extract
50mg



Cod liver oil (EPA)
50mg



Hawthorn berry
25mg



Selenium
200mcg



Cysteine HCL
750mg



Methionine
200mg

Quite clearly, it is beyond
the means of most people to compile a collection of nutrients
which would meet these precise requirements. The particular formula
given above is available in the USA from health stores. Anyone
trying to put together an approximation of this suggested pattern
could ask for assistance from a health store assistant who would
doubtless with a little effort, be able to combine a number of
standard formulations and individual items towards this end.

It must be said that the combination
put together by Dr Donsbach seems heroic in its complexity and
although he explains precisely why each item is included, there
remains a faint suggestion of ‘shot­gun’ supplementation
in which the more things thrown together the greater the chance
that something might do some good. The author provides this formulation
as a matter of accuracy rather than as a strongly recommended
course. My preference would be for something along the lines of
Dr Rinse’s formulation or the using of individual nutrient supplementation
as outlined in Chapter 8.

Before we examine the use
of oral EDTA, a reminder is in order at this point of the value
of exercise as a chelation generating method. It is clear from
Nathan Pritikin’s work (Pritikin, 1980) that a combination of
diet and exercise can do as much as chelation therapy in normalizing
circulatory dysfunction; and remember that without attention to
these areas chelation therapy will produce results which will
not be sustained.

Dr Johan Bjorksten (1981)
states: ‘Lactic acid is not as effective as EDTA in speed, but
given enough time to act, it seems comparable in total removal
of chelatable metal’.

To achieve this effect, lactic
acid levels have to be raised regularly and for sustained periods
via endurance exercise patterns such as walking, swimming, cycling,
etc. This must not be confused with aerobic exercise in which
specific cardiovascular training is taking place only if a specific
degree of effort is sustained (see Chapter 8 on aerobic principles).
In order to achieve the lactic acid chelating effect it is more
important that duration (time spent exercising) is focused
on rather than degree of effort.

A combination of Dr Rinse’s
formula and regular exercise offers a means of self­chelation
of quite considerable sophistication.

However, when we speak of
oral chelation it is to oral EDTA that we should really be looking.

A leading British firm supplies
practitioners with their EDTA Complex supplement, which is based
on a formula originally used in the clinic of Dr Josef Issels
in West Germany and later used extensively in Australia by biologist
and naturopath John Stirling.

Stirling says:

EDTA is usually degraded in
the stomach and when given orally is of little value, with approximately
only 5 per cent being absorbed. However, when granulated and enteric
coated, then pressed into a tablet and coated again, the absorption
factor is almost 100 per cent.

Stirling recommends it as
a strong supportive agent along with diet and a correct organic
mineral replacement therapy:

The major advantage of using
low­dose EDTA orally is that it is non­invasive, does
not require electrolyte monitoring as the IV form does, and can
be used as a long­term method to slowly remove toxic metals
and arterial plaque from the system.

Stirling is also in favour
of the oral form because he prefers to avoid any possibility of
toxic overload on the kidneys and liver, the main organs of elimination
that are used in taking chelated material out of the body.

Kidney function is not upset
by this approach any more than it is in intravenous applications,
and if there are concerns regarding kidney function this should
be monitored during any course of treatment. No electrolyte imbalances
have been observed with oral use of EDTA and diarrhoea is rarely
a side-effect.

EDTA was given orally to patients,
by the late Dr Issels at his cancer clinic in Germany, where it
proved ‘very useful’

It is now being used in the
UK by leading ‘holistic’ dentists such as Jack Levenson, who wish
to chelate mercury out of the system after it has entered via
the amalgam fillings of the patient. In such cases an antioxidant
formulation (vitamins A, C, E, etc.) as well as enzymes such as
Glutathione peroxidase are supplemented along with oral EDTA.
This form of EDTA should be seen as a form of maintenance rather
than having the potential for chelation held by intravenous infusion.
EDTA supplements for maintenance use are given morning and evening
with food ­ doses of 150 mg are usual.

First in Germany and then
in the USA, different methods were developed for the production
of chelating substances for specific industrial use, such as
the prevention of calcium in hard water from causing staining
or other problems in textile printing. Citric acid was commonly
used for this purpose until first a compound known as NTA, and
then EDTA (ethylenediamine­tetra­acetic acid), were
developed and patented to do the job more efficiently.

During the Second World War
research was carried out on sodium salts of EDTA in order to
establish whether these would be useful as an antidote to poison
gas. Earlier chelating compounds which had been used in this
role, such as BAL (British anti­Lewisite), had proved effective
when either externally applied or used systemically in neutralizing
the arsenic in poison gas, but had themselves been found to be
severely toxic in other ways.

A compound of sodium citrate
was used in 1941 to chelate lead from the bodies of people poisoned
by this heavy metal and later research established that EDTA
contained a highly effective antidote to heavy metal toxicity
(lead poisoning, for example), since it chelated just as well
with lead as it did with calcium when it was infused into the
bloodstream, and without any side effects.

It was at Georgetown University
that Dr. Martin Rubin (who had studied under Frederick Bersworth,
the major American pioneer researcher into EDTA)
conducted the first research into the biological effects of EDTA
on humans. These studies showed its effects on lowering calcium
levels, although this had not been the objective of the work,
which had focused on discovering its degree, or lack, of toxicity.

According to Dr Rubin, who
was the chief researcher into EDTA’s applications in treatment
of humans at that time, a Dr Geschikter was the first to use
an EDTA compound for treatment of a human. This work was also
done at Georgetown University, using the chelating ability of
EDTA to assist in the carrying into a patient of the heavy metal
nickel ­ with which it had been chemically bound ­
in a vain attempt to treat an advanced tumour. There were sadly
no benefits to the patient, but perhaps more importantly from
the viewpoint of the benefits later seen with EDTA usage, there
were no harmful effects either: all of the nickel­EDTA
complex which was put into the patient was found to be excreted
via the urine, unchanged.

It was in the early 1950s
that EDTA was first used in the treatment of lead poisoning,
with pleasantly surprising and often dramatically unexpected
results. Workers in battery factories frequently developed lead
poisoning, as did sailors in the US Navy who painted ships with
lead­based paint. Intravenous infusions of EDTA successfully
dealt with this problem, and indeed to this day the Food and
Drug Administration (FDA) in the USA suggests EDTA chelation
as the ideal method of treating not only lead poisoning but also
as the emergency treatment for hypercalcaemia. It was found that
there was often a marked improvement in the circulatory status
of patients with chronic lead poisoning, who also had atherosclerotic
(atheromatous deposits in the arteries) conditions and who were
being treated by EDTA infusion.

It is worth considering that
it is not just these naval personnel who are at risk from lead
toxicity. The degree of general human body contamination with
lead is now at five hundred times the level of people living
just two hundred years ago. Lead has many toxic effects on the
body, one of the more serious being its ability to prevent the
body’s natural control of free radical activity which itself
can result in circulatory incompetence as well as many other
problems.

Research studies by doctors
such as Belknap, Butler, Spencer, Foreman, Clarke, Dudley, Bechtel,
Jick, Surawicz, Boyle, Perry, Kitchell and many more (see References),
published in the early and middle 1950s, all relate to aspects of the treatment of arterial disease using EDTA.

Since those pioneering days,
techniques have evolved and have been improved for the successful
application of EDTA chelation treatment of the disastrous effects
not only of atherosclerosis, but also of circulatory obstructions
to the brain in people with some forms of senility. Similar benefits
have often been observed amongst those who have experienced cerebral
accidents (stroke) or who are suffering from early gangrenous
conditions. (The way in which EDTA is thought to work is discussed
in chapter 5.) Relief and marked symptomatic improvement has
been gained in countless instances of high blood pressure (essential
hypertension) and problems involving peripheral circulation (Reynaud’s
disease) as well as occlusion of blood flow to the extremities
(intermittent claudication).

A description of one of the
earliest uses of EDTA in treating chronic cardiovascular disease
was given in 1976 by Dr. Norman Clarke, Sr., to the California
Medical Association, in testimony before its Advisory Panel on
Internal Medicine. He described his introduction to the process
by research doctors (Drs. Albert Boyle and Gordon Myers) at Wayne University, Detroit in 1953.

They had had preliminary experience
in treating two patients at University Hospital, Detroit, who
had calcified mitral valves. The patients were almost completely
incapacitated . . . the doctors were very pleased with the results
[of chelation treatment] because they obtained very satisfactory
return of cardiac function.

Dr Clarke spent many years
investigating EDTA’s usefulness in treating cardiovascular disease,
and in his evidence stated: ‘In the last 28 years of my experience
with EDTA chelation I have given at least 100,000 to 120,000
infusions of EDTA and seen nobody harmed’.

He dramatically described
the successful treatment of gangrene using EDTA, perfused directly
into the site via a drip into the femoral artery, as well as
this method’s usefulness in cerebrovascular senility: ‘After
all these years, and with all that experience, I am just as certain
as can be that EDTA chelation therapy is the best treatment that
has ever been brought out for occlusive vascular disease’

Just as the use of EDTA in
treating lead poisoning revealed its ability to remove unwanted
calcium, so additional benefits were discovered when circulatory
conditions were being treated. Many patients with osteoarthritic
and similar problems reported relief of symptoms and an improved
range of movement in previously restricted joints. It seems that
obstructive calcium deposits in these areas were also being removed
during chelation treatment.

Other unexpected benefits
which chelation therapy has produced in many patients include
a reduction in the amount of insulin which diabetics require
to maintain a stable condition, as well as marked improvements
in many patients with kidney dysfunction (see also Chapter 6
on the potential danger to kidney function under certain conditions
of wrong use of EDTA). More surprisingly, perhaps, a great deal
of functional improvement in patients with Alzheimer’s disease
and Parkinson’s disease is sometimes seen. Just how chelation
could help in these states is not clear, apart from the unpredictable
benefits of circulatory enhancement, and it may be that patients
who appear to find relief from the symptoms of Alzheimer’s and
Parkinson’s diseases might have had a faulty diagnosis, despite
displaying all the classical signs associated with them.

New York studies on hyperactive
children, using EDTA, have shown remarkable benefits, thought
to relate to the removal of lead which may have accumulated in
greater quantities in some of these children, due to their relative
deficiency of major protective nutrients such as zinc and vitamin
C, not uncommonly observed in such children.

As described in Chapter 5,
there is also well­documented Swiss evidence of chelation
therapy offering marked protection against the development of
cancer as well as a suggestion that it could be useful in treating
some forms of this disease.

The safety aspect of the use
of EDTA in therapy has been phenomenal, with hardly any serious
reactions being recorded amongst the host of seriously ill people
to whom chelation therapy has been correctly applied. The commonest
short­term side­effects, as well as precautions associated
with EDTA usage, are discussed at length in Chapter 6.

By 1980 it was estimated by
Bruce Halstead, MD, (Halstead 1979) that
there had been over 2 million applications of EDTA therapy involving
some 100 million infusions, with not a single fatality, in the
USA alone. The most effective use of chelation therapy
has, over the 30 years of its successful application, been consistently
found to be related to those diseases in which heavy metal or
calcium deposits are major factors.

Have there been double blind
trials, the yardstick by which so much in medicine is judged?
Hardly any, because, as Halstead states: ‘It is impossible to
administer EDTA blindly (i.e., so that neither the doctor nor the patient knows whether
real EDTA or a substitute is being used), because it can be readily differentiated
from an innocuous placebo by even one unacquainted with the
compound’.

This is a major obstacle to
its acceptance by mainstream medicine, but should not prevent
those interested in its claims from examining the objective evidence.
It should not require double­blind control studies to impress
the observer with the possibility that people are actually getting
better when severely ill people, with advanced circulatory problems,
sometimes involving gangrene, show steady improvement in their
functions, better muscular co­ordination, the disappearance
of angina pain, increased ability to walk and work, restoration
or improvement of brain function, better skin tone and more powerful
arterial pulsations, along with the restoration of normal temperature
in the extremities. This is particularly true in many patients
who are slated to undergo bypass surgery, and this brings us
close to one reason for orthodox medicine’s rejection (in the
main) of chelation’s claims.

It might be that some of the
simplistic theories as to how EDTA achieved its results
may have prevented some scientists and physicians from taking
it seriously or of investigating its potential. The current theories
as to how calcium is encouraged to leave atheromatous deposits
in blocked arteries have been well investigated by the proponents
of chelation therapy and deserve to be seriously considered in
view of the vast amount of illness attached to this area of human
suffering and the remarkable results demonstrated by chelation
physicians.

Bypass surgery and drug treatment
of the conditions which chelation so often effectively deals with
are very big business indeed. In the USA
alone, $4 billion is
the current turnover per annum of the bypass industry. A
lesser, but nevertheless
enormous, sum is involved in medication for conditions which
the relatively cheap (and now out of patent) substance EDTA
can be shown to help. Such vested interests should
not be underestimated when it comes to the lengths to which they
will go to try to discredit methods which threaten their stranglehold
on the ‘market’ Chelation therapy continues to grow, however,
as public awareness and knowledge increases of this safe alternative
to surgery and drugs, many of which are of questionable safety
and value.