Stability Constants (log K1) of Various Metal Chelates

from
Chapter 6 - Sequestrants in Foods, by Thomas E. Furia, in CRC Handbook of Food
Additives,
2nd ed. 1972 as revised by cited authors (where data shows a letter corresponding to
citation at bottom of table)

latest revision October 26, 2006

NOTE: THIS FILE IS UPDATED UPON FINDING USEFUL FOOD CHEMISTRY DATA

webmaster - George Eby

What are " Stability Constants"

The A. E. Martell's NIST Critically Selected Stability Constants of Metal Complexes is the Bible
for stability data for metal and ligand reactions. However, it is an expensive and vast document.
Stability constants for very strong chelators is found on the Stanford MAXCHELATOR page. A
general search for A.E. Martell's critical stability constants is here. Unfortunately, Dr. Martell
died in 2003.

Metal (to right) Co(I Fe(I Fe(II

Al(II Ba Ca Cu Hg Mg Mn Ni Sr Zn
Ligand (below) I) I) I)
I)
Acetic acid 0.39 0.53 2.24 3.7d 0.51 0.74 0.43 1.03
Adenine
Adipic acid 1.92 2.19 3.35
ADP 2.36 2.82 3.68 5.90 3.11 3.54 4.50 2.50 4.28
Alanine 0.80 1.24 4.82 8.18 3.24 5.96 0.73 5.16
β-Alanine 7.13 4.63 4
Albumin 2.20
Arginine 3.20 2.0
Ascorbic acid 0.19 0.35
Asparagine 0 0.43
5.84
Aspartic acid 1.14 1.16 5.90 8.57 2.43 3.74 7.12 1.48 2.90
a
ATP 9.8 3.29 3.60 4.62 6.13 4.0 3.98 5.02 3.03 4.25

Benzoic acid 1.6 0.9 0.9

n-Butyric acid 0.31 0.51 2.14 0.53 0.36 1.00
Casein 2.23
Citraconic acid 1.3 1.3
10.9
Citric acid 11.7e 2.3 3.5 4.4 6.1 3.2 11.85 2.8 3.2 4.8 2.8 4.5
d
14.4
Cysteine 9.3 19.2 6.2 < 4 4.1 10.4 9.8
d

Dehydracetic acid 5.6 4.1

Desferri-
29.9
ferrichrysin
Desferri-
29.0
ferrichrome
Desferri-
11.8 13.7 32.5 12.2 12.0
ferrioxamin E
3,4-
12.7
Dihydroxybenzoic 3.71 7.96 5.67 7.22 8.27 8.91
9
acid
11.9
Dimethylglyoxime 14.6 7.7
4
O,O-
Dimethylpurpuroga 4.5 6.6 9.2 4.9 6.7 6.8
llin
DNA <5.6e

Metal (to right) Co(I Fe(I Fe(II

Al(II Ba Ca Cu Hg Mg Mn Ni Sr Zn
Ligand (below) I) I) I)
I)
10.7 21.5 13.5 18.5
EDTA 16.13 7.78 16.21 18.8 14.3 25.7 8.69 8.63 16.5
0 d 6 6

Formic acid 0.60 0.80 1.98 3.1 0.66 0.60

Fumaric acid 1.59 2.00 2.51 0.99 0.54

Globulin 2.32
18.2
Gluconic acid 0.95 1.21 0.70 1.00 1.70
9
Glutamic acid 1.28 1.43 5.06 7.85 4.6 1.9 3.3 5.9 1.37 5.45
Glutaric acid 2.04 1.06 2.4 1.08 0.6 1.60
0.80 1.18 0.86 0.89 1.80
Glyceric acid
b b b b b
Glycine 0.77 1.43 5.23 8.22 4.3 10.0 10.3 3.45 3.2 6.1 0.91 5.16
 d
0.92 0.80 1.92
Glycolic acid 0.66 1.11 1.60 2.81 4.7
b b b
Glycylglycine 1.24 3.00 6.7 2.62 9.1 1.34 2.19 4.18 3.91
Glycylsarcosine 3.91 6.50 2.29 4.44
Guanosine 3.2 6 4.3 3.0 3.8 4.6

Histamine 5.16 9.55 9.60 3.72 6.88 5.96

10.6
Histidine 7.30 5.89 4.00 3.58 8.69 6.63
0
0.43 0.60 0.60 0.47 1.06
β-Hydroxybutyric
b b b b b
13.2
3-Hydroxyflavone 9.91 9.70
0

Inosine 2.6 5 3 3.3

Inosine
3.76 4.74 4.04 4.57
triphosphate
Iron-free
24.6
ferrichrome
Isovaleric acid 0.20 2.08
Itaconic acid 1.20 2.8 1.8 0.96 1.9

Kojic acid 7.7 2.5 7.11 6.6 9.2 3.0 7.4 4.9

Lactic acid 0.55 1.07 1.89 3.02 6.4 0.93 1.19 2.21 0.70 1.86
Leucine 4.49 7.0 3.42 9.9 2.15 5.58 4.92
Lysine 4.5 2.18

Maleic acid 2.26 2.43 3.90 1.68 2.0 1.1 2.0

Malic acid 1.30 1.80 3.4 1.55 2.24 1.45 2.80
Methionine 3.24 9.1 5.77 4.38
Methylsalicylate 5.90 9.77

12.6 11.2 10.4

NTA >10 4.82 6.41 10.6 8.84 15.87 5.41 7.44 4.98
8 6 5

Metal (to right) Ba Ca Co(I Cu Fe(I Fe(II Hg Mg Mn Ni Sr Zn

Ligand (below) Al(II I) I) I)
I)
6.82 6.42
Orotic acid 6.39c
c c
Ornithine 4.02 6.90 3.09 8.7 <2 4.85 4.10
Oxalic acid 7.26 2.31 3.0 4.7 6.3 >4.7 9.4 2.55 3.9 5.16 2.54 4.9

β-Phenylalanine 7.74 3.26 8.9

Pimelic acid 1.08
Pivalic acid 0.55 2.19
Polyphosphate 3.0 3.5 3.0 3.2 5.5 3.0 2.5
Proline 4.07 10.0 3.34
Propionic acid 0.34 0.50 2.2 3.45 0.54 0.43 1.01
Purine 6.90 4.88
Pyrophosphate 5.0 6.7 22.2 5.7 5.8 8.7
Pyruvic acid 0.8 2.2

Riboflavin 3.9 <6 3.4 4.1 <4

Salicylaldehyde 4.67 7.40 4.22 8.70 3.69 3.73 5.22 4.50

14.11 10.6
Salicylic acid 6.72 6.55 16.35 4.7 2.7 6.95 6.85
e 0
Sarcosine 4.34 7.83 3.52 9.7 5.41
Serine 1.43 3.43 9.2 5.44
Succinic acid 1.57 1.20 2.08 3.3 7.49 1.2 2.11 2.36 0.9 1.78

( + )-Tartaric acid 1.95 1.80 3.2 7.49 1.36 3.78 1.94 2.68
Tetrametaphosphat
4.9 5.2 3.18 5.17 4.95 2.8
e
Threonine 3.30 8.6
Transferrin 12.3e
Trimetaphosphate 2.50 1.55 1.11 3.57 3.22 1.95
Triphosphate 6.3 6.5 9.8 5.8 3.80 9.7
Tryptophan 9.0

Uridine
3.17
diphosphate
Uridine
3.71 4.55 4.02 4.78
triphosphate

n-Valeric acid 0.20 0.30 2.12

Valine 7.92 3.39 9.6 2.84 5.37 5.0

Xanthosine 2.8 3.4 <2 3.0 2.4

Metal (to right) Al(III Co(I Fe(I Fe(II
Ba Ca Cu Hg Mg Mn Ni Sr Zn
Ligand (above) ) I) I) I)
a. Berthon G et al., Agents and Actions, 1982;12:619-629. (considering protonated ammonium
group)
b. Cannan, RK et al., Journal of American Chemical Society, 1938;60:2314-2320.
c. Tucci, ER et al., Journal of Inorganic Neuclear Chemistry, 1967;29:1657-1667.
d. Martell et al., Critical Stability Constants, 1998.
e. R. Bruce Martin, Accounts of Chemical Research, volume 27, number 7, 1994, pages 204-210
In the distribution of the zinc and gluconic acid system, pK values are used as shown after these
reactions: Zn2+ + L_ <=> ZnL+ (1.62) and ZnL+ + OH_ <=> ZnL(OH)0 (8.14). The pK values
are courtesy of Gerritt Bekendam, Akzo Chemicals BV Research Centre, Deventer, The
Netherlands, 1989. The Zn2+ fraction over pH 6 is strongly affected by the second pK value.
Precipitates of hydroxides of zinc result in supersaturated solutions. Page 1185, vol. 2, Handbook
of metal-Ligand Interactions in Biologic Fluids - Bioinorganic Medicine, ed. Berthon , Marcel
Dekker, NY, 1995.

k1=2.3 for zinc sulfate

What are Stability Constants and Why Are They Important?

Stability constants are well known tools for solution chemists, biochemists and chemist in
general to help determine the properties of metal-ligand reactions in water and biological
systems. Metals, like aluminum, are well known by name, and ligands are what the metals are
attached to, such as "acetate" (acetic acid), or "aluminum acetate". In general terms, the stability
constant of a metal complex can be calculated as follows: K = [ML] / [M][L], where K is the
stability constant (expressed as a logarithm); M is the amount of metal ion such as Zn2+ ion, and
L is the amount of a ligand such as gluconate or acetate. The total concentration of metal CM can
be computed with specialized computation programs. The basic equation CM = [M] + [ML] with
[ML] = K [M] [L] becomes CM = [M] (1 + K [L]); hence [M] = CM / (1 + K [L]) shows that the
concentration of M depends on the stability constant of the complex and free concentration of the
ligand which is dependent upon corresponding pK and pH values.

What does all of this mean to non professionals? Life, good health, bad health or death!

Very low stability constant numeric values (between negative values and 1) mean that the metal-
ligand is not only soluble in water but readily dissociates into the metal ionic form shown and the
ligand, yielding essentially all metal in ionic form at pH as low as stomach acid (about pH 2 to 3)
to as high as physiologic pH 7.4 (the pH of the main extracellular body fluids such as serum and
lymph). Consequently these metallic ions are available for absorption from the digestive tract
and allow life to be sustained in the case of metals that are nutrients, and harm life or terminate
life if the metal is a toxin like Cd (Cadmium) or promote tissue (brain and bone) injury in the
case of biologically absorbable complexes of Al (Aluminum).

Generally, metal-ligands with stability constants of 3 and lower are soluble and substantially
(~over 5%) ionized at physiologic pH 7.4. Between 3 and perhaps as high as 6, metal-ligands are
likely to disassociate in stomach acid, but not greatly at physiologic pH 7.4. For stability
constants above 6, there is less and less metal released regardless of how low the pH may be, and
such compounds are essentially useless in biological systems which use (stomach) acids to
dissociate metal from ligand. In the case of mercury, cysteine, citric acid and glycine tightly
complex mercury, making it less toxic. These too are capable of sustaining life, harming life or
terminating life dependent on whether the metal is a nutrient or toxin. Consequently, mineral
dietary supplements must remain biologically available, and metals for human and animal use
must not be associated with ligands where the stability constant is much greater than 5.8. The
stability constants of amino acid complexes of many biologically important metals are in the 4 to
5 range and are highly absorbed even though they are not necessarily broken down by acids.

Generally, ionized metals in water consist of the metallic ion attached to a few H2O molecules
and carry the positive electric charge of the metal ion. Stability constants numbers are expressed
as the logarithm of the real stability value (number). For instance, the stability constant in real
numbers for zinc acetate is a bit over 10 (101), while the stability constant for copper gluconate is
over 100,000,000,00,000,000 (1018). Consequently, the logarithm of the actual stability of the
compound offers an easy way to write and understand how stable a metal-ligand is. Obviously
copper gluconate is not biologically available. Some substances, like EDTA are so strong in their
chelating, sequestering, binding power that they are used to bind metals, particularly zinc, from
DNA, resulting an a soup of simple amino acids, having no genetic utility.

Metallic ions can pass between cells as simply as marbles falling through a room full of
basketballs. They are under control of the biologically closed electric circuit (BCEC), gravity,
moving body fluids, the electric charge of cell membranes, and many other biophysical and
biochemical means. Metallic ions may interact with cell membranes and/or be taken up by cells.
By example, the zinc ion is tightly controlled at the cell membrane and does not pass into the
cell, where it would be a cytotoxin. This does not mean that zinc is not used in the cell, rather its
concentration in the cell is much lower than in serum. On the other hand, magnesium ions are
present in much greater concentration inside cells than in the serum, being actively brought into
the cell as the cell needs them - with devastating health results if such nutrient is not available for
cellular uptake.

All metal-ligand compositions release increasingly more metal ion as pH is lowered towards
increased acidity, and more metal hydroxides are released as pH is raised into the basic end of
the pH scale.

The complexity of these systems can range from the very simple to the very complex. Here is a
simple example of the computed amount of zinc ion from zinc acetate across the lower half of
the pH scale (stability constant of 1.03). Another example, although more complex, is the
computed amount of zinc ion and other zinc species in zinc gluconate (stability constant of 1.7).
Here is an example of an equal molar ratio of zinc, gluconic acid and glycine, showing the
increased complexity of the zinc and mixed ligand system across the pH scale, with positive,
neutral and negatively charged zinc species. Even more complex relationships can exist where
there is more ligand than needed for complete complexation, yielding metal-ligand water soluble
complexes that carry, positive, and more neutral and negative electrical charges such as this
1:1:10 mole ratio of zinc, gluconic acid and glycine (respectively) system. In all metal-ligand
systems, there may be more than one metal-ligand combination at each pH. For example, in the
zinc gluconate system, there may be Zn2+ ions, zinc gluconate1+ positively charged species, zinc
gluconate neutrally charged and zinc hydroxide species having no charge or negative charges
dependent upon pH. Add a second ligand and one gets even more species. To determine the
amount of all positively charged metal species, the individual species are summed for each pH.
Summed positively charged species at each pH for zinc gluconate, zinc gluconate and glycine,
zinc acetate, and zinc gluconate with citric acid are shown in this graphic, along with links to the
original graphical computations by Berthon.

Even though metal-ligand systems can be quite complex, the stability constant of equal molar
metal-ligand complexes tells a large part of the story concerning the availability of the ionic
metal in aqueous solution, particularly in the acidic to neutral pH range applicable to biological
species.

Other ways of accessing bioavailability

There are other ways of assessing biological availability, and the simplest is direct measurement
of serum changes upon administration of the metal-ligand. Generally, metal oxides, hydroxides,
oleates and stearates are either very poorly utilized or not biologically available. They are too
tightly bound together for the stomach acid to dissociate into ionic form and they will not benefit
humans or animals. Unfortunately, many human and animal foods rely upon magnesium oxide as
the dietary source of magnesium, which likely produces dietary deficiencies of magnesium and
most likely, much poor health and early death. Concerning magnesium oxide, this article abstract
reported that "taking magnesium citrate was best absorbed, and that magnesium oxide was no
better than taking placebo." This medical journal article reported that "Results indicated
relatively poor bioavailability of magnesium oxide (fractional absorption 4 per cent) but
significantly higher and equivalent bioavailability of magnesium chloride, magnesium lactate
and magnesium aspartate." Another article reported "The increment in urinary magnesium
following magnesium citrate load (25 mMol) was significantly higher than that obtained from
magnesium oxide load (during 4 hours post-load, 0.22 vs 0.006 mg/mg creatinine, p less than
0.05; during second 2 hours post-load, 0.035 vs 0.008 mg/mg creatinine, p less than 0.05). Thus,
magnesium citrate was more soluble and bioavailable than magnesium oxide."

Here is a special note about aluminum toxicity. Tea grown in China has been reported to be high
in non-biologically available aluminum. However, acid rain is increasing its bioavailability.
Addition of milk to tea does not change its availability, but adding lemon juice, due to its citric
acid content, converts the tea to aluminum citrate which is highly soluble and highly bioavailable
reports R. Bruce Martin (Acc. Chem. Res., Vol 27, No.7, 1994, pp. 204-210). In fact, ingesting
any form of aluminum when taken with citrate will make the aluminum highly bioavailable, and
such may be the main source of aluminum in plaques of Alzheimer's Disease and it may be the
cause of Parkinson’s and amyotrophic lateral sclerosis in parts of the world where magnesium
content of foods is low. All biological processes involving magnesium are subject to attack
(replacement) by aluminum, causing much illness. Magnesium deficiency affects about 70
percent of Americans and much of the West and causes much mental illness as shown in this
report.

Chelation therapy

People repeatedly ask me about "chelation therapy" with EDTA and calcium or
sodium EDTA and cardiovascular health, mainly to remove extra calcium or
heavy metals. I generally tell them that EDTA will bind various metals from the
blood, specifically lead, zinc, cadmium, aluminum and calcium, perhaps with
benefit to health (with the exception of removal of vital zinc, which is easily replaced). EDTA
chelation does not appear to affect cobalt, chromium, or copper, and it seems to help retain
magnesium according to a 2001 article by Waters et al.. On the other hand, significant increases
were found in urinary excretion of manganese, chromium, lead, zinc, and copper after the start of
CaEDTA injection according to Sata et al., suggesting that there is some disagreement as to
which metals, specifically chromium and copper, are removed. Progressive renal insufficiency
may be improved for at least 1 year after lead chelating therapy with EDTA according to Lin et
al.. Detoxification of cadmium by EDTA on kidney function failed, even though EDTA
treatment continued many years after cessation of cadmium exposure according to Wu et al..
However, according to the Center for disease Control, EDTA (not CaEDTA) has caused death by
inducing a lethal state of hypocalcemia as shown in this report, apparently by overdose.

The actual effect on coronary calcification is not as clear as one might expect. For example, in
2002 Villarruz et al., having reviewed the literature, concluded: "At present, there is insufficient
evidence to decide on the effectiveness or ineffectiveness of chelation therapy in improving
clinical outcomes of patients with atherosclerotic cardiovascular disease. This decision must be
preceded by conducting randomized controlled trials that would include endpoints that show the
effects of chelation therapy on longevity and quality of life among patients with atherosclerotic
cardiovascular disease."

One major problem is the confusion between chelation therapy with "calcium EDTA", "sodium
EDTA", and plain "EDTA". Each of these produces different results since EDTA is either bound
with either calcium or sodium, or it is unbound and is free, highly reactive EDTA. For example
calcium EDTA could hardly be expected to bind calcium from the blood to benefit
cardiovascular calcification since it (calcium EDTA) is already bound to calcium! Clearly a
bogus and useless treatment! However, it does not produce the side effects that result from use of
either sodium EDTA or EDTA.

In fact, in the only formal study that I could find of EDTA chelation therapy for ischemic heart
disease, Knudtson et al. in 2002 found no evidence for efficacy. Here is what they found for
EDTA: "CONTEXT: Chelation therapy using EDTA is an unproven but widely used alternative
therapy for ischemic heart disease. OBJECTIVE: To determine if current EDTA protocols have a
favorable impact on exercise ischemia threshold and quality of life measures in patients with
stable ischemic heart disease. DESIGN: Double-blind, randomized, placebo-controlled trial
conducted between January 1996 and January 2000. SETTING: Participants were recruited from
a cohort of cardiac catheterization patients and the practices of cardiologists in Calgary, Alberta.
PARTICIPANTS: We screened 3140 patients, performed a qualifying treadmill test in 171, and
enrolled 84. Entry criteria included age at least 21 years with coronary artery disease proven by
angiography or a documented myocardial infarction and stable angina while receiving optimal
medical therapy. The required treadmill test used a gradual ramping protocol and patients had to
demonstrate at least 1-mm ST depression. INTERVENTIONS: Patients were randomly assigned
to receive infusion with either weight-adjusted (40 mg/kg) EDTA chelation therapy (n = 41) or
placebo (n = 43) for 3 hours per treatment, twice weekly for 15 weeks and once per month for an
additional 3 months. Patients in both groups took oral multivitamin therapy as well. MAIN
OUTCOME MEASURE: Change from baseline to 27-week follow-up in time to ischemia (1-
mm ST depression). RESULTS: Thirty-nine patients in each group completed the 27-week
protocol. One chelation patient had therapy discontinued for a transient rise in serum creatinine.
The mean (SD) baseline exercise time to ischemia was 572 (172) and 589 (176) seconds in the
placebo and chelation groups, respectively. The corresponding mean changes in time to ischemia
at 27 weeks were 54 seconds (95% confidence interval [CI], 23-84 seconds; P<.001) and 63
seconds (95% CI, 29-95 seconds; P><.001), for a difference of 9 seconds (95% CI, -36 to 53
seconds; P =.69). Exercise capacity and quality of life scores improved by similar degrees in
both groups. CONCLUSION: Based on exercise time to ischemia, exercise capacity, and quality
of life measurements, there is no evidence to support a beneficial effect of chelation therapy in
patients with ischemic heart disease, stable angina, and a positive treadmill test for ischemia."

Does chelation with these chemicals remove heavy metals in a manner that truly benefits health?
I could find much talk about this but precious little clinical evidence. In fact, I only found one
article about very aggressive treatment (three separate chelation therapies) to save the life of a
three-year old boy from massive lead poisoning. I assume there are other positive reports.

Still convinced EDTA is helpful? Here is a year 2000 review by complementary medicine
researchers of the literature that, again, reports no benefit. They write: BACKGROUND:
Chelation therapy is popular in the United States. The question of whether it does more good
than harm remains controversial. AIM: The aim of this systematic review was to summarize all
the clinical evidence for or against the effectiveness and efficacy of chelation therapy for
coronary heart disease. METHODS: A thorough search strategy was implemented to retrieve all
clinical investigations regardless of whether they were controlled or uncontrolled. RESULTS:
The most striking finding is the almost total lack of convincing evidence for efficacy. Numerous
case reports and case series were found, and the majority of these seem to indicate that chelation
therapy is effective. Only 2 controlled clinical trials were located, and they provided no evidence
that chelation therapy is efficacious beyond a powerful placebo effect. CONCLUSION: Given
the potential of chelation therapy to cause severe adverse effects, this treatment should now be
considered obsolete.

Still convinced EDTA is helpful? Here is a 2003 report showing no efficacy when combined
with vitamins and minerals. They write: OBJECTIVES: The purpose of this study was to
evaluate the effect of chelation therapy with ethylenediamine tetraacetic acid (EDTA) on
endothelium-dependent vasomotor responses in patients with documented coronary artery
disease (CAD). BACKGROUND: Oxidative stress plays an important role in the dysfunction of
endothelium and development of atherosclerosis. Modification of cardiac risk factors and
employment of antioxidants have been shown to improve endothelial function. Ethylenediamine
tetraacetic acid chelation therapy is considered to be a complementary therapy for patients with
CAD and is proposed to have antioxidant properties. METHODS: A total of 47 patients enrolled
in the Program to Assess Alternative Treatment Strategies to Achieve Cardiac Health (PATCH)
participated in this substudy and had complete data. High-resolution ultrasound was used to
assess endothelium-dependent brachial artery flow-mediated vasodilation (FMD) in patients with
CAD in a randomized, double-blind, and placebo-controlled fashion. Patients were randomized
to chelation therapy or placebo. The primary end point was the absolute difference in FMD after
the first and 33rd treatments (6 months) of study groups compared with their baselines.
RESULTS: At the baseline, the study population had mild impairment of FMD (7.2 +/- 3.4%).
The first chelation treatment did not change FMD as compared with placebo (chelation 6.5 +/-
3.5% vs. placebo 7.4 +/- 2.9%; p value = 0.371). The brachial artery studies at six months did not
demonstrate significant differences in FMD between study groups (placebo 7.3 +/- 3.4% vs.
chelation 7.3 +/- 3.2%; p value = 0.961). CONCLUSIONS: Our results suggest that EDTA
chelation therapy in combination with vitamins and minerals does not provide additional benefits
on abnormal vasomotor responses in patients with CAD optimally treated with proven therapies
for atherosclerotic risk factors.

Still convinced EDTA is helpful? here is a 2005 report reporting no efficacy. They write:
BACKGROUND: Numerous practitioners of both conventional and complementary and
alternative medicine throughout North America and Europe claim that chelation therapy with
EDTA is an effective means to both control and treat cardiovascular disease. These claims are
controversial, and several randomized controlled trials have been completed dealing with this
topic. Objectives: To conduct a systematic review to evaluate the best available evidence for the
use of EDTA chelation therapy in the treatment of cardiovascular disease. METHODS: We
conducted a systematic review of 7 databases from inception to April 2005. Hand searches were
conducted in review articles and in any of the trials found. Experts in the field were contacted
and registries of clinical trials were searched for unpublished data. To be included in the final
systematic review, the studies had to be randomized controlled clinical trials. RESULTS: A total
of seven articles were found assessing EDTA chelation for the treatment of cardiovascular
disease. Two of these articles were subgroup analyses of one RCT that looked at different
clinical outcomes. Of the remaining five studies, two smaller studies found a beneficial effect
whereas the other three exhibited no benefit for cardiovascular disease from the use of EDTA
chelation therapy. CONCLUSIONS: The best available evidence does not support the
therapeutic use of EDTA chelation therapy in the treatment of cardiovascular disease. Although
not considered to be a highly invasive or harmful therapy, it is possible that the use of EDTA
chelation therapy in lieu of proven therapy may result in causing indirect harm to the patient.

Still convinced that EDTA chelation is beneficial? Click here for the world's literature (all 778
articles) on EDTA chelation.

Still convinced that EDTA chelation is beneficial? Check out the Quack Watch site.

Recently, I had a physician try to sell me on the idea that chelation would "increase nitric oxide"
production, thus benefiting the lining of the arteries. What did I find when I went to the medical
literature? Green et. al. found in 1999 that: "The selective increase in the vasodilator response to
acetylcholine after therapy with EDTA and several B group vitamins indicates that nitric oxide-
related endothelial function was improved. However, the absence of response to EDTA alone
suggests that the supplementary vitamins were necessary for this benefit, which may have been
related to the accompanying decrease in plasma homocysteine." See how they trick you? Benefit
resulted from additive B vitamins, and not EDTA. Remember that the B-vitamins are very often
added to the EDTA solutions, and you are paying a lot of money for something that you could
easily and cheaply obtain from a pharmacist or grocery store.

Want to be free of angina pectoris? Free of Reynaud's Disease? Better cardiovascular function?
Just use zinc as shown in this report and add magnesium as shown in this very long report on
magnesium in mental health and cardiology. Good cardiovasculat health is not quite that simple,
but supplemental zinc and magnesium are good starting points. Notice that EDTA removes zinc
and magnesium, thus potentially worsening cardiovascular health.

Still convinced that EDTA chelation is beneficial?

In conclusion

Hopefully, the reader will find this material of interest. Interested parties may submit properly
cited stabilty constant data for inclusion in this table. Data for aluminum is essentially missing,
but some is available and will be incorporated in the table as it is gathered. I thank Dr. thomas
Furia for starting this table in the "CRC Handbook of Food Additives", and hope to have many
contributors. I do not care how wide or long this table becomes. The data is important and needs
to be available. I will try to link citations above directly to Index Medicus links as they are
found.

The current author is not responsible for any of the data in the table, and has relied entirely on
the work of others. If I have made a mistake, please bring it to my attention and properly cited
work will be used to replace incorrect data.

Metal abreviations used in the above table are: Al (Aluminum), Ba (Barium), Co (Cobalt), Cu
(Copper), Hg (Mercury), Fe(II) Ferrous Iron, Fe(III) Ferric Iron, Mg (Magnesium), Mn
(Manganese), Ni (Nickel), Sr (Stronium), Zn (Zinc).
homepage - George Eby Research