To chelate or not to chelate...?

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To chelate or not to chelate...?

Postby gainsbourg » Sat Jan 17, 2009 6:12 am

Oh well, nobody else seems to want to start this thread so here goes! I should point out that I know little about this subject apart from what I’ve learned from this forum and Google..

For anyone who is new to the term ‘chelation’ it means (in non technical terms) the removal of unwanted substances, such as heavy metals, from the body. An iron chelator is a substance which binds with iron and removes it from the body.

Things have been changing a lot recently…. Its beginning to look like MS is yet another neurodegenerative illness. In other words the initial cause may not be the immune system. So, could that pathogen be iron? I don’t personally think it’s quite that simple. In my view, something else is causing the initial disruption within nerve cells, which then results in the iron accumulations (which in turn creates more damage). In any case, you do not have to believe that iron is the primary cause of MS to consider going ahead with chelation, you simply have to be aware of how much damage these iron deposits can do!

Iron is a potent cause of oxidative stress. It brings disruption and death to nerve cells and could even explain the changes in the vasculature.

Scientists have discovered that heavy metal deposition plays a key role in neurodegenerative illnesses like Parkinson’s Disease and Alzheimer’s. A very large and recent study showed that people who consumed the most vegetable source of iron were 30% more likely to develop Parkinson’s Disease…I find that scary - it is a disease my mother died from - maybe this accounts for my big interest in all this.

Also, in Friedreich’s Ataxia, (a disease with many MS-like symptoms which is often mistaken for MS) a gene which causes faulty iron metabolism is now known to be the sole cause. The sole cause!


And now...evidence has been increasing that iron may also play a big role in MS

1. New imaging studies (e.g. Bashi November 2008) have shown that iron deposits are more common than previously thought near the sites of MS damage and also in grey matter axons. Bashi found that the worse the symptoms the more the iron. Whether it is there by cause or effect - iron is now there.
2. The remarkable discovery, also in 2008 that iron metabolism is faulty in MS (could this account for the deposits?).
3. Mice with the MS like disease EAE show significant improvement following iron chelation.


Iron has been overlooked as a major culprit in MS for several possible reasons:

1. Some with MS suffer from anaemia.
2. Iron is essential for healthy nerve function and myelin repair.
3. It gives us energy and is essential for metabolism.
4. For decades MS has been thought to be primarily an autoimmune illness, i.e. an inflammatory illness where the damage has been thought to have been primarily caused by the body attacking itself.


So...to chelate or not to chelate? That is the question!

Assuming the research is to be believed, if you have MS (or just about any neurological illness) there are definitely toxic iron accumulations in your brain and spine sitting there right now! Deposits are rare in healthy people but in MS it is common for deposits to be easily visible (even in those with anaemia). They are mostly located - as are plaques - around the blood vessels in the white matter. They are also found in the grey matter axons beneath the main cortex, where, incidentally, MS brains are known to be gradually shrinking!

The natural iron chelator IP6 (rice bran) sounds promising but there are things that concern me

1. Is it possible to maintain healthy levels of iron whilst chelating excess iron from deposits in the brain and spine? (low iron can also cause oxidative stress)
2. How well does IP6 do the job?
3. How long should chelation last?
4. What is the best way to maintain levels of other minerals that are removed along with the iron?
5. Is it safe for those with low levels of iron to attempt removing iron deposits?
6. Many antioxidants are also iron chelators but some say excessive antioxidants do even more damage.

Sorry for such a long post but I just hope someone out there can shine some light on some of this.


…if only iron wasn’t so complicated!



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Postby lionheart » Sat Jan 17, 2009 7:19 am

How about any doctor's view? Or articles on this issue?
It sounds interesting and complicated :(, but some doctor somewhere must have tackled the problem?
Have you referred it to your neuro?
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Question for gainsbourg

Postby lyndacarol » Sat Jan 17, 2009 8:21 am

gainsbourg--Is iron removed from the bloodstream in plasmapheresis? (I know it removes calcium.) This procedure improves symptoms for some on a temporary basis. Why? Could it be because iron is removed? My personal belief (as the "insulin girl,") has been that insulin is removed (until the pancreas can replace it), but could it be iron?
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Postby DIM » Sat Jan 17, 2009 9:09 am

Great thread Gainsburg, as I say in the "iron" thread wife has had high normal levels of iron and TIBC, waiting this week results from ferritin and transferrin but I am sure she has some type of iron dysregulation!
She has had brown spots in her face before MS diagnosis most of them fade away with BBDiet, supplementation and LDN but who knows what her iron levels were before!
She takes plenty of supplements that cause iron chelation, EGCG, pycnogenol, quercetin, curcumin etc they are also antioxidants but as you say if iron is high they may work the opposite way.
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Postby gainsbourg » Sun Jan 18, 2009 3:16 pm

lyndacarol - I'm afraid I do not know if iron is removed in plasmapheresis, but I believe those who benefit genuinely do so because apparent autoimmune damage is reduced when inflammatory antibodies are temporarily removed from the blood.

I have to say I am very open minded about the role of insulin in MS because of a growing suspicion that faulty metabolism plays a part in the disease. As you know, iron and insulin are key players in metabolism - but I get lost in this area because it is so highly technical and complicated.

In case anyone still hasn't read how iron metabolism is faulty in MS its here:

http://www.ncbi.nlm.nih.gov/pubmed/18408021

But right now I'm more concerned about getting rid of the iron deposits with chelation before searching for ways to fix the faulty metabolsm of iron (Idebenone is a possibility).

With regard to asking how doctors are takling the iron/MS link, you must be kidding! My neurologist at Charring Cross just finds the idea amusing. I gave her a list of supplements I am currently taking. She looked at it and said:

"I see you're taking a chelator"

"....for a while crocodile!"

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Postby RedSonja » Tue Jan 20, 2009 5:11 am

Is chelation back in fashion? haven't seen it for years:

http://www.healthwatcher.net/Quackerywa ... index.html
Bibo ergo sum
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Postby DIM » Tue Jan 20, 2009 6:11 am

RedSonja wrote:Is chelation back in fashion? haven't seen it for years:

http://www.healthwatcher.net/Quackerywa ... index.html

They mention cardiovascular diseases and chelation with known medicines not with "nutraceuticals" as EGCG, quercetin, IP6 etc
The above substances are useful to MSers even as antioxidants so why to be harmfull?
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Postby gainsbourg » Tue Jan 20, 2009 2:27 pm

If removing toxic iron deposits from the brain becomes fashionable - so be it! Caution is always wise but from what I have read the natural chelator IP6 (rice bran) is safe.

In 2001 Food and Drug Administration researchers reported that 8 out of 12 chelating agents tested caused gene mutations....but among the four completely non-toxic chelators was IP6

Anyone who only trusts prescription drugs should read this...
http://www.newsweek.com/id/92265

DIM, I came across an interesting article about iron which includes a protocol for using IP6 as an iron chelator here:

http://www.chiro.org/nutrition/FULL/Iro ... hing.shtml



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Postby chrishasms » Tue Jan 20, 2009 7:16 pm

I still think MS must be some form of auto immune just because treatments like Revimmune or Cytoxan couldn't work if it wasn't. I'm definitely interested in this concept of the Iron being an issue. It would explain why I feel like crud if I eat too much red meat.

Tomorrow I see my doctor to have a slough of blood tests done to check me for everything. "The Ultra Mind Solution by Dr. Mark Hyman" is a book my wife read and it's similar to Dr. Eric Braverman "The Edge Effect" but more detailed, it's where we got all the tests from. I am also going to talk to him about the tests for the blockages. Here in Denver we have the machines and they may be interested in trying it.
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Postby gainsbourg » Wed Jan 21, 2009 10:41 am

chrishasms said:
I still think MS must be some form of auto immune just because treatments like Revimmune or Cytoxan couldn't work if it wasn't.

Good point Chris. The question is, is MS primarily autoimmune? Drugs may help with inflammation but they can't actually heal MS if some other process is triggering the immune response in first instance (this could be a vascular problem; BBB; iron; virus; stress; insulin etc....take your pick!)

Marian Simka, a phlebologist at the Department of Angiology, Wodzislawska, Poland (see Simka and Rybak article August 2008) believes iron may modulate and exagerate the immune process in MS. He goes on to suggest chelation:

http://www.ncbi.nlm.nih.gov/pubmed/18400414

This paper presents a hypothetical model of role for iron in the development of venous leg ulcers and multiple sclerosis. Elevated concentrations of iron were found in the skin affected by venous hypertension and also in the areas of brain with multiple sclerosis lesions. Individuals with hemochromatosis gene (HFE) mutations: C282Y and H63D, which result in a less efficient transport of iron by macrophages, are characterized by an increased risk for venous leg ulcer and multiple sclerosis. Multiple sclerosis is a T cell-mediated disease, and T cells probably participate in the development of venous ulcers. This deleterious role of ferric ions could be related to the regulation of T cell proliferation and apoptosis. Under normal conditions excessive accumulation of T cells cannot take place, because nitric oxide and interferon-gamma drive these cells toward apoptosis. However, in tissues with a high concentration of iron, T lymphocytes proliferate instead of undergoing apoptosis. This is possible due to the internalization of the INF-gammaR2 chain of the interferon-gamma receptor, the downregulation of inducible nitric oxide synthase expression in macrophages and the inactivation of the active site of caspases. Yet, it should be emphasized that this hypothesis does not claim for the increased concentration of iron as a direct causal factor for the development of venous ulcerations or multiple sclerosis, but rather, iron is a factor that modulates and exaggerates the autoimmune process. Iron chelators, administered systemically or locally, should potentially exhibit therapeutic and prophylactic activity against venous leg ulcers and multiple sclerosis.



Even man of the moment Zamboni describes the role of iron as 'pivotal' in MS in his (2006) article "The Big Idea: iron-dependent inflammation in venous disease and proposed parallels in multiple sclerosis"


Although investigations on the role of iron in MS are
still few, some evidence supports a pivotal role for iron in
MS inflammation
. The effect of manipulation of iron level
was investigated in EAE, a form of induced autoimmune
encephalomyelitis in mice used as an experimental model of
MS.31 The incidence of EAE was 60–70% in mice with a
normal iron level and in iron-overloaded mice, but 0% in
iron-deficient mice. The findings suggest that iron
deficiency provides protection from the development of
EAE31 and also challenge traditional views on what
constitutes a normal level of stored iron.14 The authors31
noted that, ‘The failure of iron-deficient mice to develop
EAE is impressive. Many of the pharmaceutical approaches
to inhibiting EAE are less effective than iron deficiency.’
Another group32 investigated the serum concentration
of soluble transferrin receptor (sTFR) in a group of MS
patients. The levels were found to be significantly higher in
patients with active MS, either in progressive or relapsingremitting
clinical form, than in controls. Serum ferritin
levels were also significantly elevated in patients affected by
the active and progressive form.32 Both findings support the
hypothesis above described, which proposes local iron
overload as the initial signal of the inflammatory chain in MS
.


http://www.societaitalianaflebologia.it ... amboni.pdf




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Last edited by gainsbourg on Mon Jan 04, 2010 12:04 pm, edited 1 time in total.
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Postby patientx » Wed Jan 21, 2009 11:19 am

Chris,

Where do things stand with your doctors at Hopkins? I think you were checking in with them because of a possible re-activation.
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Postby chrishasms » Wed Jan 21, 2009 4:48 pm

I have reactivated. I am not necessarily rapidly declining but I am getting worse again.

I had one little lesion. Little. Its not necessarily bad because one little lesion over 1.5 years is not bad for me. However, I am guessing I have more stuff than one going on now.

I go back at the beginning of March to re evaluate if I need to do it again. Until then I wait.
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Postby patientx » Wed Jan 21, 2009 6:53 pm

Yeah, I had read some of your posts where you mentioned that you had re-activated. Sorry to hear that. I was just wondering what the docs at JH were suggesting.
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Postby gainsbourg » Fri Jan 23, 2009 11:59 am

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."

http://www.medicalnewstoday.com/articles/128355.php


Image

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 so far:

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





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