DMPS Chelation Push

Full ingredient list

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

Supporting studies

• 1

  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 ↗

• 2

  Intravenous DMPS is absorbed instantly, cleared by the kidneys, and its metal-carrying capacity tracks directly with how much mercury comes out in the urine.

  Five healthy volunteers received 3.0 mg/kg of DMPS intravenously with detailed pharmacokinetic sampling. DMPS is rapidly converted to disulfide forms and eliminated primarily by the kidneys — by 96 hours, 10% of the dose was recovered as parent drug and 74% as disulfide metabolites. Parent drug half-life was 1.8 hours; total DMPS half-life was 20 hours. Critically, mercury excretion correlated almost perfectly with urinary output of both the parent drug (r-squared = .94) and its disulfide metabolites (r-squared = .96). Intravenous DMPS bypasses the roughly 39% oral bioavailability of the drug, delivering the full dose.

  Clinical pharmacokinetic study (intravenous) Hurlbut KM, Maiorino RM, Mayersohn M, Dart RC, Bruce DC, Aposhian HV Determination and metabolism of dithiol chelating agents. XVI: Pharmacokinetics of 2,3-dimercapto-1-propanesulfonate after intravenous administration to human volunteers. Journal of Pharmacology and Experimental Therapeutics. 1994. PMID 8113976 ↗

• 3

  DMPS dramatically mobilizes stored mercury — up to 88-fold increases in urinary mercury excretion in exposed workers — and also shifts arsenic toward more readily excreted forms.

  This landmark human review and study series from the University of Arizona documented DMPS challenge testing across multiple populations. Dental technicians excreted 88 times more mercury after DMPS, dentists 49 times more, and non-dental personnel 35 times more. Roughly two-thirds of the mercury excreted by college volunteers was traceable to dental amalgam fillings, and post-challenge urinary mercury correlated with amalgam surface area. In people exposed to arsenic-contaminated water, DMPS tripled the proportion of monomethylarsonic acid in urine, demonstrating active mobilization of arsenic as well.

  Human challenge-test studies and review Aposhian HV, et al. Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS). Environmental Health Perspectives. 1998. PMID 9703487 ↗

• 4

  A course of DMPS lowered mercury body burden in occupationally exposed workers and returned their urinary mercury to normal levels.

  Workers occupationally exposed to mercurous chloride during calomel lotion manufacturing were treated with DMPS in three sequential cycles. During DMPS treatment, urinary mercury output surged to 1,754, 314, and 173 micrograms per 24 hours across the three cycles, against baseline periods of 106, 48, and 53 micrograms per 24 hours — the steadily falling peaks showing the mercury reservoir being emptied. The investigators concluded that DMPS treatment was effective in lowering the body burden of mercury and in decreasing urinary mercury concentration to normal levels. Route in this study: oral; the same agent is given intravenously for faster, complete delivery.

  Clinical trial Gonzalez-Ramirez D, Aposhian HV, et al. DMPS (2,3-dimercaptopropane-1-sulfonate, dimaval) decreases the body burden of mercury in humans exposed to mercurous chloride. Journal of Pharmacology and Experimental Therapeutics. 1998. PMID 9765315 ↗

• 5

  In mercury-intoxicated residents of a gold-mining region, DMPS treatment produced measurable improvement in tremor, coordination, memory and sleep.

  Ninety-five mercury-intoxicated inhabitants of Mt. Diwata in the Philippines were treated with DMPS as part of a UNIDO mercury-abatement project, with neurological and neuropsychological testing before and after. Most participants reported marked symptom improvement including reduced tremor, better memory, and improved sleep. Objective examination findings improved significantly, including facial expression (hypo-mimia), the Romberg balance test, and tremor/ataxia testing, as did neuropsychological pencil-tapping and Frostig test scores. Urinary mercury excretion rose substantially during therapy. The investigators described DMPS as highly effective, with adverse effects rare. Route in this study: oral.

  Prospective clinical treatment study Böse-O'Reilly S, Drasch G, et al. The Mt. Diwata study on the Philippines 2000-treatment of mercury intoxicated inhabitants of a gold mining area with DMPS (2,3-dimercapto-1-propane-sulfonic acid, Dimaval). Science of the Total Environment. 2003. PMID 12711426 ↗

• 6

  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 ↗

• 7

  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 ↗

• 8

  Glutathione is the molecule liver enzymes attach to toxins during Phase II detoxification so they can be excreted.

  This Annual Review of Pharmacology and Toxicology review covers the three mammalian glutathione transferase (GST) families - cytosolic, mitochondrial, and microsomal. These Phase II enzymes conjugate glutathione onto electrophilic xenobiotics such as carcinogens and environmental pollutants, and also onto endogenous compounds including aldehydes, quinones, and lipid hydroperoxides generated during oxidative stress. The review also describes glutathione transferases' roles in leukotriene, prostaglandin, and steroid hormone biosynthesis, and in modulating gene expression through nuclear receptor pathways. Glutathione is the required cofactor for this entire conjugation system.

  Mechanistic review Hayes JD, Flanagan JU, Jowsey IR Glutathione transferases. Annual Review of Pharmacology and Toxicology. 2005. PMID 15822171 ↗

References

• 1Sears ME. Chelation: harnessing and enhancing heavy metal detoxification--a review. The Scientific World Journal. 2013. PMID 23690738 ↗
• 2Hurlbut KM, Maiorino RM, Mayersohn M, Dart RC, Bruce DC, Aposhian HV. Determination and metabolism of dithiol chelating agents. XVI: Pharmacokinetics of 2,3-dimercapto-1-propanesulfonate after intravenous administration to human volunteers. Journal of Pharmacology and Experimental Therapeutics. 1994. PMID 8113976 ↗
• 3Aposhian HV, et al. Mobilization of mercury and arsenic in humans by sodium 2,3-dimercapto-1-propane sulfonate (DMPS). Environmental Health Perspectives. 1998. PMID 9703487 ↗
• 4Gonzalez-Ramirez D, Aposhian HV, et al. DMPS (2,3-dimercaptopropane-1-sulfonate, dimaval) decreases the body burden of mercury in humans exposed to mercurous chloride. Journal of Pharmacology and Experimental Therapeutics. 1998. PMID 9765315 ↗
• 5Böse-O'Reilly S, Drasch G, et al. The Mt. Diwata study on the Philippines 2000-treatment of mercury intoxicated inhabitants of a gold mining area with DMPS (2,3-dimercapto-1-propane-sulfonic acid, Dimaval). Science of the Total Environment. 2003. PMID 12711426 ↗
• 6Flora SJS, Mittal M, Mehta A. Heavy metal induced oxidative stress & its possible reversal by chelation therapy. Indian Journal of Medical Research. 2008. PMID 19106443 ↗
• 7Forman HJ, Zhang H, Rinna A. Glutathione: overview of its protective roles, measurement, and biosynthesis. Molecular Aspects of Medicine. 2009. PMID 18796312 ↗
• 8Hayes JD, Flanagan JU, Jowsey IR. Glutathione transferases. Annual Review of Pharmacology and Toxicology. 2005. PMID 15822171 ↗