Why Patients Should be Wary of Chelation Therapy for Parkinson’s Disease

You can find out more about NPF's National Medical Director, Dr. Michael S. Okun, by also visiting the NPF Center of Excellence, University of Florida Center for Movement Disorders & Neurorestoration.

Over the last decade or more, several new therapies have emerged and subsequently been touted as restorative and/or curative for Parkinson’s disease.  In many cases, practitioners have offered a substantial fee for each treatment, and they have administered these treatments in an office or hospital setting – sometimes repeating the treatment 30 times or more.  Touted therapies, which have fallen into this “curative” category include fee for stem cell infusions, fee for glutathione infusions, and, most recently, fee for chelation.  Though there may be reasonable rationales for each of these therapies, scientific evidence is lacking, and chelation should only be administered under institutional review board-approved (IRB) protocols, and only for research purposes.  Parkinson’s disease patients should not be paying for chelators, and they should be warned of potential risks of therapy.  Past What’s Hot columns have focused on fee for stem cell and fee for glutathione therapies, and this month’s column will address chelation therapies.

Chelation is the process where a chemical forms a connection or complex with a heavy metal, and thereby functionally inactivates it.  The word chelate is derived from the Greek word meaning claw.  One way to remember what a chelator does is to remember that it simply claws or grabs a circulating metal ion.  Chelators can be used to detoxify heavy metals in the body, and are most commonly prescribed for lead, mercury or arsenic poisoning. 

Common uses for chelators include root canal treatments and agents used in contrast materials for MRI scanning (gadolinium).  Diseases such as hemochromatosis (iron overload) have been treated with the chelator defuroxamine.  This particular chelator can be very effective in addressing the iron overload which is known to result in the disease state – however, there may also be potential side effects associated with the drug such as cardiovascular, pulmonary, auditory and ocular issues.  Another common chelator that has been used is ethylenediamine tetra-acetic acid (EDTA).  EDTA was previously thought to possibly prevent atherosclerotic artery hardening.  The mechanism was theorized to act through removal of calcium deposits in blood vessel walls.  EDTA therapy has however, been disproven for atherosclerosis.  Similarly, EDTA has been turning up on websites and in doctor’s offices as the touted cure for other diseases including Alzheimer’s and Parkinson’s disease – despite a lack of scientific evidence or data from clinical trials. We do not recommend EDTA, or any other chelators for Parkinson’s disease. For those patients who are determined to try EDTA, please remember that using disodium EDTA instead of calcium EDTA has resulted in reported deaths.

The idea of using a chelator for Parkinson’s disease is not completely far-fetched.  It is known that iron accumulates in the Parkinsonian brain, and iron seems to accumulate in important brain areas known to be part of the neurodegenerative process – including the substantia nigra.  Additionally, there are a few animal experiments that have shown a protective effect of chelation against the development of Parkinson’s disease.  It has been hypothesized by many groups that oxidative stress may result in an iron imbalance, and this imbalance may in some way contribute to the brain degeneration seen in Parkinson’s disease patients.  However, it remains to be proven that removing iron from the brain of a Parkinson’s disease patient will have any clinically beneficial or disease-modifying effects.

Patients should be wary of any practitioner offering a fee for chelation therapy to treat or to cure Parkinson’s disease.  If a practitioner offers to send your blood, urine or hair to an expert (for a fee) in order to demonstrate a link to your Parkinson’s disease, we suggest that you consider declining this offer.  Many of the practitioners touting chelation will send the specimens to their own unregulated mail away laboratories, and results will often reveal positive or impossible scenarios – such as elevations in multiple heavy metals (for example, lead, mercury and arsenic are all elevated which is a very unlikely scenario).  If you are worried you have a heavy metal toxicity, you should see your neurologist for a comprehensive visit including an exposure history and examination.   A good neurologist should be able to detect common heavy metal clinical manifestations, such as neuropathy or unique lines on the finger nails (e.g. Mees lines).  Parkinsonian symptoms would represent an uncommon manifestation of heavy metal toxicity, except in the cases of Manganese exposure in miners and in welders.  In manganese exposure, the MRI is usually abnormal (as opposed to the relatively normal MRI in Parkinson’s disease, see previous What’s Hot column).  A neurologist can also send a urine sample to an approved and credible 24-hour laboratory to test for the presence of heavy metals. 

In conclusion, patients should be wary of any clinic performing chelation therapy for Parkinson’s disease.  These clinics should only be performing chelation under an IRB-approved research protocol, and patients and insurance companies should not be charged for what would be defined as an experimental therapy.  Further, patients should be informed that chelation therapy has many associated risks.  The storybook may not be completely closed on chelation therapy for Parkinson’s disease, however scientists and physicians must carry the burden of developing the direct link between iron deposition and neurodegeneration, and in proving that developing a drug that can cross the blood brain barrier and remove the iron will ultimately prove to be a viable and a meaningful treatment approach.

Selected References:

1. Budimir A. Metal ions, Alzheimer's disease and chelation therapy. Acta Pharm. 2011 Mar 1;61(1):1-14. PubMed PMID: 21406339.

2. Hider RC, Roy S, Ma YM, Le Kong X, Preston J. The potential application of iron chelators for the treatment of neurodegenerative diseases. Metallomics. 2011 Mar;3(3):239-49. Epub 2011 Feb 22. PubMed PMID: 21344071.

3. Bareggi SR, Cornelli U. Clioquinol: Review of its Mechanisms of Action and Clinical Uses in Neurodegenerative Disorders. CNS Neurosci Ther. 2010 Dec 27. doi: 10.1111/j.1755-5949.2010.00231.x. [Epub ahead of print] PubMed PMID: 21199452.

4. Li X, Jankovic J, Le W. Iron chelation and neuroprotection in neurodegenerative diseases. J Neural Transm. 2011 Mar;118(3):473-7. Epub 2010 Dec 16. PubMed PMID: 21161300.

5. Kakhlon O, Breuer W, Munnich A, Cabantchik ZI. Iron redistribution as a therapeutic strategy for treating diseases of localized iron accumulation. Can J Physiol Pharmacol. 2010 Mar;88(3):187-96. Review. PubMed PMID: 20393584.

6. Bolognin S, Messori L, Zatta P. Metal ion physiopathology in neurodegenerative disorders. Neuromolecular Med. 2009;11(4):223-38. Epub 2009 Nov 28. Review. PubMed PMID: 19946766.

7. Liu G, Men P, Perry G, Smith MA. Metal chelators coupled with nanoparticles as potential therapeutic agents for Alzheimer's disease. J Nanoneurosci. 2009 Jun 1;1(1):42-55. PubMed PMID: 19936278; PubMed Central PMCID: PMC2780350.

8. Aschner M, Erikson KM, Herrero Hernández E, Tjalkens R. Manganese and its role in Parkinson's disease: from transport to neuropathology. Neuromolecular Med. 2009;11(4):252-66. Epub . Review. Erratum in: Neuromolecular Med. 2009;11(4):267. Hernández, Elena Herrero [corrected to Herrero Hernández, Elena]. PubMed PMID:19657747.

Posted: 5/2/2011 12:23:48 PM by Cathy Whitlock


Browse current and archived What's Hot in PD? articles, the National Parkinson Foundation's monthly blog for people with Parkinson's written by our National Medical Director, Dr. Michael S. Okun. 

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May 2014
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April 2014
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March 2014
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February 2014
The Dream of a Pill Free Existence and the Continuous Dopaminergic Pump for the Treatment of Parkinson's Disease

January 2014
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December 2013
Could Fungus and Mold be an Important Contributor to Parkinson’s Disease?

November 2013
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October 2013
Halting of the Creatine Study

September 2013
The Importance of Identifying and Treating Caregiver Strain

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July 2013
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June 2013
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May 2013
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April 2013
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March 2013
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February 2013
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January 2013
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December 2012
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November 2012
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October 2012
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September 2012
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August 2012
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July 2012
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June 2012
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May 2012
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April 2012
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March 2012
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February 2012
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January 2012
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December 2011
Placing Stem Cells in Animal Models of Parkinson’s Disease: Another Important Step

November 2011
Important News for the Parkinson’s Disease Community: More Evidence that Sinemet and Madopar are Not Toxic and do Not Accelerate Disease Progression

October 2011
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September 2011
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August 2011
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July 2011
If you are Dizzy or Passing Out, it could be Your Parkinson’s Disease or Parkinson’s Disease Medications

June 2011
How Will Group Visits for Parkinson’s Disease Fit into the Future of Parkinson’s Disease Care?

May 2011
Why Patients Should be Wary of Chelation Therapy for Parkinson’s Disease

April 2011
Opening the Door to Gene Therapy in Parkinson’s Disease: The Need for Refinement of the Technology and Approach

March 2011
Does it Matter if I Can’t Get Brand Sinemet?

February 2011
Should I get a DaTscan or PET scan to confirm my diagnosis of Parkinson’s disease?

January 2011
A Critical Reappraisal of the Worst Drugs in Parkinson’s Disease

December 2010
Environmental Risks for PD: Manganese, Welding, Mining, and Parkinsonism

November 2010
Calling for the FDA to Revise the Eight Sinemet a Day Rule

October 2010
Dry Cleaning Solvents and Potential Environmental Risks for Developing Parkinson’s Disease

September 2010
Maintaining the Balance: Why Parkinson’s Disease Patients Need to Understand Drug Recalls, Withdrawals, and Safety Alerts

August 2010
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July 2010
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June 2010
Why Are Patches and Continuous Release Technology a Big Deal to Parkinson's?

May 2010
Is the PD SURG Trial Another Surge Forward for DBS Therapy?

April 2010
Cycling in PD in Those Who Can’t Walk: Is it Possible?

March 2010
New iPS Stem Cells for PD: What Does it Mean?

February 2010
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January 2010
Is Parkinson's Disease a Prion Disease?

December 2009
Parkinson's Disease Linked to Gaucher's Disease

November 2009
Brain Cells Keep Time Stamps: Implications for Parkinson's Disease Therapies

October 2009
Is it Safe to Have an MRI with a DBS in Place?

September 2009
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August 2009
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July 2009
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June 2009
Keeping an Eye on Trials Important to the Parkinson's Disease Patient

May 2009
Increased Risk of Melanoma in Parkinson's Disease

April 2009
Finally a DBS Expert Consensus Statement Aimed at Their True Customers: The Patients

March 2009
Pesticides and Environmental Exposure in Parkinson's disease: Should We Stay Away From the Stink Truck?

February 2009
Is Exercise Effective Treatment and Protection Against PD?

January 2009
Why are Transplant Trials Struggling to Succeed in the Treatment of PD?

December 2008
Are Monoamine Oxidase Inhibitors Disease Modifying or Neuroprotective in PD?

November 2008
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Each month, we will feature a new column by NPF's National Medical Director, Dr. Michael Okun, on the latest developments in Parkinson's disease research. Read the latest "What's Hot in PD?" below.

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