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: Specific information concerning the solution chemistry of zinc compositions used in common cold treatments is found at http://george-eby-research.com/html/solution-chemistry.html .

webmaster - George Eby
http://george-eby-research.com/gif/webmail.bmp

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)
Ligand (below)

   Al(III)

Ba

Ca

Co(II)

Cu

Fe(II)

Fe(III)

Hg

Mg

Mn

Ni

Sr

Zn

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

b-Alanine

 

 

 

 

7.13

 

 

 

 

 

4.63

 

4

Albumin

 

 

2.20

 

 

 

 

 

 

 

 

 

 

Arginine

 

 

 

 

 

3.20

 

 

 

2.0

 

 

 

Ascorbic acid

 

 

0.19

 

 

 

 

 

 

 

 

0.35

 

Asparagine

 

 

0

 

 

 

 

 

 

 

 

0.43

 

Aspartic acid

 

1.14

1.16

5.90

8.57

 

 

 

2.43

3.74

7.12

1.48

5.84 2.90a

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

 

Citric acid

 11.7e

2.3

3.5

4.4

6.1

3.2

11.85

10.9d

2.8

3.2

4.8

2.8

4.5

Cysteine

 

 

 

9.3

19.2

6.2

 

14.4d

< 4

4.1

10.4

 

9.8

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Dehydracetic acid

 

 

 

 

5.6

 

 

 

 

 

4.1

 

 

Desferri-ferrichrysin

 

 

 

 

 

 

29.9

 

 

 

 

 

 

Desferri-ferrichrome

 

 

 

 

 

 

29.0

 

 

 

 

 

 

Desferri-ferrioxamin E

 

 

 

11.8

13.7

 

32.5

 

 

 

12.2

 

12.0

3,4-Dihydroxybenzoic acid

 

 

3.71

7.96

12.79

 

 

 

5.67

7.22

8.27

 

8.91

Dimethylglyoxime

 

 

 

 

11.94

 

 

 

 

 

14.6

 

7.7

O,O-Dimethylpurpurogallin

 

 

4.5

6.6

9.2

 

 

 

4.9

 

6.7

 

6.8

 DNA

 <5.6e

 

 

 

 

 

 

 

 

 

 

 

 

Metal (to right)
Ligand (below)

   Al(III)

Ba

Ca

Co(II)

Cu

Fe(II)

Fe(III)

Hg

Mg

Mn

Ni

Sr

Zn

EDTA

16.13

7.78

10.70

16.21

18.8

14.3

25.7

21.5d

8.69

13.56

18.56

8.63

16.5

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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

 

 

 

 

 

 

 

 

 

 

Gluconic acid

 

0.95

1.21

 

18.29

 

 

 

0.70

 

 

1.00

1.70

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

Glyceric acid

 

0.80b

1.18b

 

 

 

 

 

0.86b

 

 

0.89b

1.80b

Glycine

 

0.77

1.43

5.23

8.22

4.3

10.0

10.3d

3.45

3.2

6.1

0.91

5.16

Glycolic acid

 

0.66

1.11

1.60

2.81

 

4.7

 

0.92b

 

 

0.80b

1.92b

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

Histidine

 

 

 

7.30

10.60

5.89

4.00

 

 

3.58

8.69

 

6.63

b-Hydroxybutyric

 

0.43b

0.60b

 

 

 

 

 

0.60b

 

 

0.47b

1.06b

3-Hydroxyflavone

 

 

 

9.91

13.20

 

 

 

 

 

 

 

9.70

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Inosine

 

 

 

2.6

5

3

 

 

 

 

3.3

 

 

Inosine triphosphate

 

 

3.76

4.74

 

 

 

 

4.04

4.57

 

 

 

Iron-free ferrichrome

 

 

 

 

 

 

24.6

 

 

 

 

 

 

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

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

NTA

>10

4.82

6.41

10.6

12.68

8.84

15.87

 

5.41

7.44

11.26

4.98

10.45

 

 

 

 

 

 

 

 

 

 

 

 

 

 

Metal (to right)
Ligand (below)

   Al(III)

Ba

Ca

Co(II)

Cu

Fe(II)

Fe(III)

Hg

Mg

Mn

Ni

Sr

Zn

Orotic acid

 

 

 

6.39c

 

 

 

 

 

 

6.82c

 

6.42c

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

 

 

 

 

 

 

 

 

 

 

 

 

 

 

b-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

Salicylic acid

14.11e

 

 

6.72

10.60

6.55

16.35

 

4.7

2.7

6.95

 

6.85

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

Tetrametaphosphate

 

4.9

5.2

 

3.18

 

 

 

5.17

 

4.95

2.8

 

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 diphosphate

 

 

 

 

 

 

 

 

3.17

 

 

 

 

Uridine triphosphate

 

 

3.71

4.55

 

 

 

 

4.02

4.78

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

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)
Ligand (above)

Al(III)

Ba

Ca

Co(II)

Cu

Fe(II)

Fe(III)

Hg

Mg

Mn

Ni

Sr

Zn

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 Parkinsonís 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.

Quack QuackChelation 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