Still not sure about whether you’d like to get rid of iron deposits?
A four year research programme (Nov 2008) carried out by Dr. Rohit Bakshi, Associate Professor of Neurology and Radiology at the Brigham and Women's Hospital and Harvard Medical School has established that the amount of iron deposited in the grey matter is a more accurate indicator and predictor of MS progression and severity than the plaques in the white matter
Dr. Bakshi led a four year follow-up study, which found that patients with unnatural darkness of gray matter structures as seen on MRI pictures carried a higher risk for progression of physical disability. This abnormal darkness is referred to as T2 hypointensity, and is suggestive of excessive iron deposits. In addition, the researchers found that the new marker of gray matter damage showed closer correlations with patients' clinical status than other established MRI markers of disease severity, including lesions, also known as "plaques," and shrinkage of the brain, also know as "atrophy."
Iron in the brain of 43 yr old man with MS
(the one on the left)
Gray matter T2 hypointensity and brain atrophy in multiple sclerosis (MS). Fast spin-echo axial T2-weighted images are shown of a 43 year-old man with relapsing-remitting MS (disease duration of four years, mild-to-moderate physical disability - Expanded Disability Status Scale score 3.5, and an age-matched healthy subject. In the patient with MS, note the bilateral hypointensity of various gray matter areas compared to the healthy subject. The patient also has brain volume loss compared to the control (note prominence of ventricular and subarachnoid spaces). The T2 hypointensity most likely represents pathologic iron deposition.
Pirko I, Lucchinetti CF, Sriram S, Bakshi R. Neurology 2007;68:634–42.
Bakshi is the most prolific researcher in this area. He summarises chelation research
There is a relatively small body of literature regarding the effect of iron chelation therapy in MS. Trials of DES and dexrazoxane, a chelator similar to DES, have been completed in animals. Rats with EAE treated with DES before symptom development experienced total symptom suppression, while rats treated after symptom manifestation had a rapid marked attenuation of symptoms.117 A study with a myelin basic protein induced rat EAE model failed to show a treatment effect when DES was administered in the preclinical stage.118 Postulating that DES scavenges and prevents free radical formation and consequently will only be efficacious during active disease, Pedchenko et al.119 treated rats in the active stage of EAE and observed significantly reduced clinical signs when compared to vehicle-treated animals. Dexrazoxane, when injected alone into rats slightly attenuated the course of EAE, while rats given dexrazoxane concomitantly with mitoxantrone experienced improvement on clinical indices when compared with rats treated solely with mitoxantrone.120 This result is of special interest because mitoxantrone carries a significant risk of cardiotoxicity even though it is an effective FDA approved MS therapy while dexrazoxane is known to have cardioprotective effects.121 Only one human trial of iron-related therapy has been performed in human MS (DES in secondary progressive MS); after two years there was no significant improvement in disability score following up to eight courses of DES.25 This lack of treatment effect may potentially be attributed to the advanced disease in the patient population and the small number of the study participants (n=9).
It is evident from the studies presented above that iron deposition occurs in MS and that iron chelation is effective at ameliorating symptoms in animal models. It is unclear, however, the precise role that iron deposition plays in humans and whether chelation therapy or other therapies targeting iron related toxicity can benefit MS patients. Additional studies are warranted to further define the role of iron deposition in MS
If you want to read all of Bakshi’s meta-analysis on the precise role of iron in neurological illness - it’s technical but brilliant:
http://www.pubmedcentral.nih.gov/articl ... id=1963417