EDTA ­ How it Works and What it Does

Current medical crisis care
in dealing with many acute manifestations of cardiovascular and
circulatory disease, such as coronary thrombosis and cerebrovascular
accidents, is superbly efficient and often surprisingly successful
at saving life (surprising considering the state of the patients,
that is).

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.