EDTA Chelation IV

Full ingredient list

Exact amounts delivered in each size. Formulas are compounded per patient and can be adjusted by your provider.

Supporting studies

• 1

  In the largest randomized trial of IV chelation ever conducted, EDTA infusions reduced major cardiovascular events by 18% in heart attack survivors.

  The NIH-funded Trial to Assess Chelation Therapy (TACT) randomized 1,708 patients aged 50 and older with a prior myocardial infarction to 40 intravenous EDTA-based infusions or placebo. The primary composite endpoint — death, recurrent heart attack, stroke, coronary revascularization, or hospitalization for angina — occurred in 26% of the chelation group versus 30% on placebo (hazard ratio 0.82; 95% CI 0.69-0.99; P = .035). This was a double-blind, placebo-controlled trial using the intravenous route.

  Randomized controlled trial Lamas GA, et al. Effect of disodium EDTA chelation regimen on cardiovascular events in patients with previous myocardial infarction: the TACT randomized trial. JAMA. 2013. PMID 23532240 ↗

• 2

  Among TACT participants with diabetes, IV EDTA chelation cut cardiovascular events by 41% and all-cause death by 43% over five years.

  A prespecified subgroup analysis of the 633 TACT participants who had diabetes found that EDTA infusions reduced the primary endpoint from 38% to 25% (hazard ratio 0.59; 95% CI 0.44-0.79; P < 0.001, still significant after Bonferroni adjustment at P = 0.002). All-cause mortality fell from 16% to 10% (HR 0.57; 95% CI 0.36-0.88; P = 0.011) and cardiovascular death, reinfarction, or stroke fell from 17% to 11% (HR 0.60; 95% CI 0.39-0.91; P = 0.017). The number needed to treat was 6.5 patients over five years, and the treatment-by-diabetes interaction was significant at P = 0.004. Route: intravenous.

  Prespecified subgroup analysis of a randomized controlled trial Escolar E, Lamas GA, et al. The effect of an EDTA-based chelation regimen on patients with diabetes mellitus and prior myocardial infarction in the Trial to Assess Chelation Therapy (TACT). Circulation: Cardiovascular Quality and Outcomes. 2014. PMID 24254885 ↗

• 3

  Patients with both diabetes and peripheral artery disease — among the highest-risk vascular patients — saw a 48% reduction in cardiovascular events with IV EDTA.

  This analysis looked at the 162 TACT participants who had diabetes, a prior heart attack, and peripheral artery disease. Active intravenous EDTA infusions reduced the primary composite endpoint compared with placebo (hazard ratio 0.52; 95% CI 0.30-0.92; P = 0.0069), with mortality falling from 24% to 11%. Only 3.3 patients needed to be treated to prevent one event over five years. The authors concluded that having advanced atherosclerosis across multiple vascular beds did not diminish the benefit observed.

  Post-hoc subgroup analysis of a randomized controlled trial Ujueta F, Lamas GA, et al. The effect of EDTA-based chelation on patients with diabetes and peripheral artery disease in the Trial to Assess Chelation Therapy (TACT). Journal of Diabetes and Its Complications. 2019. PMID 31101487 ↗

• 4

  A systematic review published by the American Heart Association found that most studies of EDTA chelation in cardiovascular patients reported improvement, including measurable gains in leg circulation.

  Researchers at Columbia University systematically reviewed 24 studies of EDTA chelation in patients with pre-existing cardiovascular disease, including 4 randomized controlled trials and 15 prospective before-after studies. Seventeen of the 24 studies reported improved outcomes after treatment. A meta-analysis of ankle-brachial index — an objective measure of blood flow to the legs — showed an improvement of 0.08 from baseline (95% CI 0.06-0.09). The largest benefits were consistently seen in patients with diabetes and severe peripheral arterial disease.

  Systematic review with meta-analysis Ravalli F, Navas-Acien A, et al. Chelation Therapy in Patients With Cardiovascular Disease: A Systematic Review. Journal of the American Heart Association. 2022. PMID 35229619 ↗

• 5

  Calcium disodium EDTA is an established, well-tolerated treatment for lead poisoning and is the most effective agent for pulling lead out of tissue stores.

  In a comparative clinical study of 37 adults with elevated blood lead, patients received either oral DMSA or intravenous calcium disodium EDTA (CaNa2EDTA) over two five-day courses. Both antidotes substantially reduced symptom prevalence, blood lead concentrations, and mobilizable lead stores, and both were well tolerated. CaNa2EDTA was significantly better at mobilizing lead out of tissue stores (P = .04), and on an equivalent molar-dose basis showed superior overall efficacy (P < .001). Route: intravenous CaNa2EDTA — the same form used in our infusions.

  Comparative clinical trial Sakthithasan K, Lévy P, Poupon J, Garnier R A comparative study of edetate calcium disodium and dimercaptosuccinic acid in the treatment of lead poisoning in adults. Clinical Toxicology (Philadelphia). 2018. PMID 29889577 ↗

• 6

  A course of 40 IV EDTA infusions lowered participants' blood lead levels by more than 60% in a large randomized trial.

  In TACT2, a second NIH-funded randomized double-blind trial of 959 patients with diabetes and a prior heart attack, intravenous edetate disodium infusions reduced median blood lead from 9.03 micrograms/L at baseline to 3.46 micrograms/L by the 40th infusion (P < .001). In the placebo group, blood lead was essentially unchanged over the same period (9.3 to 8.7 micrograms/L). This confirms in a rigorous randomized setting that a standard IV chelation course does what it is designed to do: measurably strip lead out of the body.

  Randomized controlled trial Lamas GA, et al. Edetate Disodium-Based Chelation for Patients With a Previous Myocardial Infarction and Diabetes: TACT2 Randomized Clinical Trial. JAMA. 2024. PMID 39141382 ↗

• 7

  A single IV EDTA infusion increased urinary lead excretion roughly 36-fold, and repeated infusions progressively drained the body's stored lead.

  Fourteen patients with coronary artery disease received a series of open-label intravenous edetate disodium infusions, with urine metals measured before and after and normalized to creatinine. After the first infusion, post-infusion urine lead rose 3,581% and cadmium rose 802% compared with pre-infusion values. Over the treatment course the body's reservoir of mobilizable lead visibly shrank: pre-infusion urine lead dropped 60% (P = 0.003), post-infusion lead dropped 36% (P = 0.0004) in 84% of patients, and pre-infusion lead became undetectable in nearly 40% of patients.

  Prospective clinical study (open-label, before-after) Alam ZH, Ujueta F, Lamas GA, et al. Urinary Metal Levels after Repeated Edetate Disodium Infusions: Preliminary Findings. International Journal of Environmental Research and Public Health. 2020. PMID 32610666 ↗

• 8

  Calcium EDTA chelation improved kidney filtration in patients with chronic kidney disease and elevated lead burden — while untreated patients continued to decline.

  Published in the New England Journal of Medicine, this randomized controlled trial studied patients with chronic renal insufficiency and mildly elevated body lead burden. Patients treated with intravenous calcium disodium EDTA gained kidney function, with a mean change in glomerular filtration rate of +2.1 mL/min/1.73 m2, while controls lost function at -6.0 mL/min/1.73 m2 (P < 0.001). The authors concluded that chelation with calcium disodium EDTA improved kidney function and slowed disease progression in this group. This trial used the same calcium-EDTA form given intravenously.

  Randomized controlled trial Lin JL, Lin-Tan DT, Hsu KH, Yu CC Environmental lead exposure and progression of chronic renal diseases in patients without diabetes. New England Journal of Medicine. 2003. PMID 12540640 ↗

• 9

  Even low-level lead burden — well below what was long considered safe — is strongly linked to cardiovascular death, making lead removal a meaningful health target.

  This population-based cohort study followed 14,289 US adults from NHANES III for a median of 19.3 years. Going from a blood lead of 1.0 to 6.7 micrograms/dL was associated with a 37% higher risk of all-cause mortality (HR 1.37; 95% CI 1.17-1.60), a 70% higher risk of cardiovascular death (HR 1.70; 95% CI 1.30-2.22), and more than double the risk of ischaemic heart disease death (HR 2.08; 95% CI 1.52-2.85). The authors estimated that 28.7% of cardiovascular mortality was attributable to lead exposure, establishing body lead burden as a large and modifiable contributor to heart disease.

  Prospective population-based cohort study Lanphear BP, Rauch S, Auinger P, Allen RW, Hornung RW Low-level lead exposure and mortality in US adults: a population-based cohort study. The Lancet Public Health. 2018. PMID 29544878 ↗

• 10

  Toxic metals cause damage largely by generating free radicals and draining the body's antioxidant reserves — and chelation therapy is a recognized way to reverse that oxidative burden.

  This comprehensive review examines how arsenic, lead, cadmium and mercury produce reactive oxygen species that injure cells, concluding that the toxic effects of these metals are caused primarily by an imbalance between pro-oxidant and antioxidant homeostasis — that is, oxidative stress. The authors evaluate the established chelating agents EDTA, DMPS, DMSA and BAL as the therapeutic answer to that metal-driven oxidative load, and note that pairing antioxidant support with chelation produces better outcomes than chelation alone — a rationale for combining chelation with antioxidant-containing IV protocols.

  Mechanistic review Flora SJS, Mittal M, Mehta A Heavy metal induced oxidative stress & its possible reversal by chelation therapy. Indian Journal of Medical Research. 2008. PMID 19106443 ↗

• 11

  The chemistry is well characterized: EDTA locks onto lead and cadmium through oxygen coordination bonds, while DMPS uses paired sulfur groups that preferentially capture mercury — making the two agents complementary.

  This peer-reviewed review of chelation chemistry and pharmacology explains that chelation — multiple coordination bonds between an organic molecule and a metal — is a normal biological process the body already uses through glutathione and metallothionein. Calcium disodium EDTA binds lead and cadmium strongly through oxygen-based coordination bonds and eliminates them in the urine, distributing mainly through extracellular fluid. DMPS, a dithiol, carries sulfur atoms for coordination, is rapidly converted to disulfide chelate forms, and is excreted largely in urine; it increases urinary excretion of arsenic, cadmium, lead, methylmercury and inorganic mercury. The differing binding chemistry is precisely why the two agents are used together.

  Review of chemistry and pharmacology Sears ME Chelation: harnessing and enhancing heavy metal detoxification--a review. The Scientific World Journal. 2013. PMID 23690738 ↗

• 12

  Glutathione is the body's most abundant intracellular antioxidant and its central redox regulator.

  This widely cited review in Molecular Aspects of Medicine describes glutathione as the most abundant low-molecular-weight thiol compound synthesized in human cells. The authors detail its role in protecting cells from oxidative damage and from the toxicity of reactive xenobiotic electrophiles, and in maintaining the cell's overall redox balance. The paper covers where oxidants and electrophiles come from, how glutathione eliminates them (by reduction and by conjugation), and how glutathione synthesis is regulated - including therapeutic strategies for raising cellular glutathione content.

  Mechanistic review Forman HJ, Zhang H, Rinna A Glutathione: overview of its protective roles, measurement, and biosynthesis. Molecular Aspects of Medicine. 2009. PMID 18796312 ↗

References

• 1Lamas GA, et al. Effect of disodium EDTA chelation regimen on cardiovascular events in patients with previous myocardial infarction: the TACT randomized trial. JAMA. 2013. PMID 23532240 ↗
• 2Escolar E, Lamas GA, et al. The effect of an EDTA-based chelation regimen on patients with diabetes mellitus and prior myocardial infarction in the Trial to Assess Chelation Therapy (TACT). Circulation: Cardiovascular Quality and Outcomes. 2014. PMID 24254885 ↗
• 3Ujueta F, Lamas GA, et al. The effect of EDTA-based chelation on patients with diabetes and peripheral artery disease in the Trial to Assess Chelation Therapy (TACT). Journal of Diabetes and Its Complications. 2019. PMID 31101487 ↗
• 4Ravalli F, Navas-Acien A, et al. Chelation Therapy in Patients With Cardiovascular Disease: A Systematic Review. Journal of the American Heart Association. 2022. PMID 35229619 ↗
• 5Sakthithasan K, Lévy P, Poupon J, Garnier R. A comparative study of edetate calcium disodium and dimercaptosuccinic acid in the treatment of lead poisoning in adults. Clinical Toxicology (Philadelphia). 2018. PMID 29889577 ↗
• 6Lamas GA, et al. Edetate Disodium-Based Chelation for Patients With a Previous Myocardial Infarction and Diabetes: TACT2 Randomized Clinical Trial. JAMA. 2024. PMID 39141382 ↗
• 7Alam ZH, Ujueta F, Lamas GA, et al. Urinary Metal Levels after Repeated Edetate Disodium Infusions: Preliminary Findings. International Journal of Environmental Research and Public Health. 2020. PMID 32610666 ↗
• 8Lin JL, Lin-Tan DT, Hsu KH, Yu CC. Environmental lead exposure and progression of chronic renal diseases in patients without diabetes. New England Journal of Medicine. 2003. PMID 12540640 ↗
• 9Lanphear BP, Rauch S, Auinger P, Allen RW, Hornung RW. Low-level lead exposure and mortality in US adults: a population-based cohort study. The Lancet Public Health. 2018. PMID 29544878 ↗
• 10Flora SJS, Mittal M, Mehta A. Heavy metal induced oxidative stress & its possible reversal by chelation therapy. Indian Journal of Medical Research. 2008. PMID 19106443 ↗
• 11Sears ME. Chelation: harnessing and enhancing heavy metal detoxification--a review. The Scientific World Journal. 2013. PMID 23690738 ↗
• 12Forman HJ, Zhang H, Rinna A. Glutathione: overview of its protective roles, measurement, and biosynthesis. Molecular Aspects of Medicine. 2009. PMID 18796312 ↗