Evidence Based Data


What is Chelation?


Chelation is an FDA-approved therapy for the safe elimination of toxic heavy metals from the body. During the chelation treatment, the patient is injected with a synthetic amino acid, EDTA (Ethylene Diamine Tetra Acetic Acid). This acid is remarkably capable of removing cholesterol, heavy metals, and plaque (which impedes blood flow,) from the body. Chelation is helpful for cancer patients as it binds with and eliminates excess free radicals, which contribute to the rapid progression of cancer.


How Does it Work?


Chelation therapy is a medical treatment that involves the use of chelating agents, which are chemical compounds that can bind to certain metals and minerals in the body and facilitate their elimination through urine. The goal of chelation therapy is to remove excess or toxic levels of metals or minerals from the body.


What are the Risks of Chelation?


While chelation therapy is generally considered safe when administered by a trained healthcare provider, it is not without risks. The most common side effects of chelation therapy include nausea, vomiting, and diarrhea. More serious side effects can occur in rare cases, including kidney damage, liver toxicity, and allergic reactions. 

In this video below, Dr. Steve Windley provides more detail on Chelation Therapy:

Local 10 News: Chelation therapy shows promise in the treatment of heart disease and diabetes.
Chelation Testimonial
Chelation Testimonial

Chelation- Relevant Research and News

The role of iron chelation in cancer therapy

This review focuses on advances and strategies in the use of iron chelators as anti-tumor therapies. Although the development of iron chelators for human disease has focused primarily on their use in the treatment of secondary iron overload, chelators may also be useful anti-tumor agents. They can deplete iron or cause oxidative stress in the tumor due to redox perturbations in its environment. Iron chelators have been tested for their anti-tumor activity in cell culture experiments, animal models and human clinical trials. Largely for pragmatic reasons, clinical studies of the anti-tumor activity of iron chelators have generally focused on desferrioxamine (DFO), a drug approved for the treatment of iron overload. These studies have shown that DFO can retard tumor growth in many different experimental contexts. However, the activity of DFO is modest, and advances in the use of chelators as anti-cancer agents will require the development of new chelators based on new paradigms. Examples of iron chelators that have shown promising anti-tumor activity (in various stages of development) include heterocyclic carboxaldehyde thiosemicarbazones, analogs of pyridoxal isonicotinoyl hydrazone, tachpyridine, O-trensox, desferrithiocin, and other natural and synthetic chelators. Apart from their use as single agents, chelators may also synergize with other anti-cancer therapies. The development of chelators as anticancer agents is largely an unexplored field, but one with extraordinary potential to impact human cancer.

Copper chelation selectively kills colon cancer cells through redox cycling and generation of reactive oxygen species

Background: Metals including iron, copper and zinc are essential for physiological processes yet can be toxic at high concentrations. However the role of these metals in the progression of cancer is not well defined. Here we study the anti-tumor activity of the metal chelator, TPEN, and define its mechanism of action.

Methods: Multiple approaches were employed, including cell viability, cell cycle analysis, multiple measurements of apoptosis, and mitochondrial function. In addition we measured cellular metal contents and employed EPR to record redox cycling of TPEN–metal complexes. Mouse xenografts were also performed to test the efficacy of TPEN in vivo.

Results: We show that metal chelation using TPEN (5μM) selectively induces cell death in HCT116 colon cancer cells without affecting the viability of non-cancerous colon or intestinal cells. Cell death was associated with increased levels of reactive oxygen species (ROS) and was inhibited by antioxidants and by prior chelation of copper. Interestingly, HCT116 cells accumulate copper to 7-folds higher levels than normal colon cells, and the TPEN-copper complex engages in redox cycling to generate hydroxyl radicals. Consistently, TPEN exhibits robust anti-tumor activity in vivo in colon cancer mouse xenografts.

Conclusion: Our data show that TPEN induces cell death by chelating copper to produce TPEN-copper complexes that engage in redox cycling to selectively eliminate colon cancer cells.

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