Effects of Chelation With Edta and Vitamin B Therapy on Nitric Oxide‐related Endothelial Vasodilator Function

Abstract

1. 'Chelation therapy' with EDTA is being frequently used in patients with cardiovascular disease, despite limited objective evidence of effectiveness. Depressed nitric oxide (.NO)-related endothelial function accompanies atherosclerosis, and even the vascular risk factors alone, and is improved by numerous interventions that also improve prognosis in vascular disease. 2. The aim of the present study was to determine the influence of chelation therapy with EDTA alone and EDTA in combination with B vitamins on endothelial function. 3. After a control series of saline infusions, we examined the effects of a series of EDTA infusions (1.5 g, 10 times over 6 weeks) in eight subjects with coronary artery disease. In addition, because EDTA is commonly supplemented by other components, particularly B group vitamins, we subsequently examined the effect of a similar series of vitamin-supplemented EDTA infusions. 4. Forearm blood flow (FBF) was assessed by plethysmography and graded intrabrachial infusions of the endothelium-dependent vasodilator acetylcholine (ACh) and the endothelium-independent dilator sodium nitroprusside (SNP). 5. There was no difference in vasodilation to either drug after EDTA alone compared with the control periods, but the response to ACh was augmented after combined therapy (P < 0.03, ANOVA). The latter was accompanied by a small but consistent mean (+/- SEM) fall in plasma homocysteine of 1.6 +/- 0.5 mumol/L (P < 0.05). 6. The selective increase in the vasodilator response to ACh after therapy with EDTA and several B group vitamins indicates that NO-related endothelial function was improved. 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. These results, along with the current interest in the possible cardioprotective effects of vitamins and the increasing administration of 'chelation therapy', call for more definitive studies on these aspects of 'alternative medicine'.

EDTA chelation therapy for cardiovascular disease: a systematic review

“…Proposed mechanisms of action for the reversal of cardiovascular disease by EDTA include: calcium chelation resulting in dissolution of atheromatous plaques, free radical scavenging action, reduction of total body iron stores, cell membrane stabilization, arterial dilatation due to calcium channel blocking action, improvement of arterial wall elasticity and increased production of nitric oxide [ 4 , 21 ]. Critics have taken issue with some of these mechanisms, however, claiming the use of outdated concepts on the pathophysiology of atherosclerosis and for instance, the inability of EDTA, a water soluble compound, to effectively complex with plaque calcium [ 3 ].…”

Endothelial dysfunction in spontaneously hypertensive rats: focus on methodological aspects

“…Along with other authors, we have also used it to prevent oxidation of unstable substances, for example catecholamines [30,51]. Although EDTA is not a classic antioxidant, it chelates free metals, which can catalyse the non-enzymatic generation of hydroxyl radical [2], and there is clinical evidence from forearm blood flow plethysmography studies that this compound improves acetylcholine relaxations when used together with vitamins [54]. Although the direct antioxidant effect of EDTA in endothelium-dependent relaxations in vitro has not been thoroughly addressed, Table 1 provides information that EDTA itself does not affect vascular function significantly, but EDTA might have an influence on vasodilator responses if ascorbic acid is present [25,26,32,55].…”

Inhibition of CEM calcification by the sequential pretreatment with ethanol and EDTA

“…29 The proposed mechanism behind the chelation therapy was that EDTA chelates calcium from atheromatous plaques and thus favorably alters the plaque and the arterial wall, for example, by altering endothelial function. 30 Other postulated mechanisms of EDTA action included (a) inhibition of platelet aggregation, 31 (b) stimulation of parathormone (PTH) release that in turn mobilizes calcium from plaques and reduces pro- *Statistically significant differences between values with the same superscript letter (a-h); p < 0.05; n = 6 each.…”