Iron metabolism panels should be a first

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Iron metabolism panels should be a first

Postby Merlyn » Sun Mar 07, 2010 2:10 pm

Can anybody give me a logical reason why these doctors are not running iron metabolism panels on people that are clearly clogged up with iron. Varcies (twisted veins in the neck) are a well recognized complication of hemochromatosis, which is the most common genetic disorder ever recognized. I am frankly disgusted that they are not first and foremost running a simple blood test to see whether people are developing these twisted veins due to overloading iron. There is no excuse for not doing this, it is a simple blood test. Most of us that are running these things are showing nonstandard results. Please please please do this for the sake of science.
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Postby LR1234 » Sun Mar 07, 2010 2:23 pm

I agree Merlyn. I had a long chat with my neuro back in June about HH and have just forwarded your letter to him as well, he knows there is an iron metabolism prob in MS but he does not agree with the HH idea (I think he is wrong though!). i am trying to encourage him to do the iron panels on his progressive patients. What does he have to lose?? Also Jimmy Legs is right about Zinc balancing iron. Maybe in HH there is a problem with Zinc metabolism or something. Maybe Zinc could be used as a treatment along with phlebotemies. Zinc is low in a lot of MS patients. Did you get yours checked?
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Postby cheerleader » Sun Mar 07, 2010 4:48 pm

Merlyn-The stenosis being found are congenital truncular venous malformations or created by impingement. You are referring to varices, which are created by the damaged organ (like the liver) being unable to process blood, which creates enlarged veins above the organ. Varices are literally stretched out veins, the opposite of stenosied veins. These are two different medical conditions. One does not need to have hemochromatosis in order to have CCSVI.
The iron deposition in brain tissue is created by reflux and microbleeds breaking thru the BBB....not excess iron. My Jeff had all the iron panels run, and he was perfectly normal. His jugular veins were not.
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Postby Merlyn » Sun Mar 07, 2010 6:12 pm

Cheerleader-what puzzles me is that we find iron in the brains of people with Parkinson's, Alzheimer's, Huntington's. And Zamboni says he only finds these twisted veins in people with multiple sclerosis. And yet all of these conditions feature neurodegeneration... they know that in Parkinson's, Alzheimer's, Huntington's there is loss of iron homeostasis, very often due to the genetic mutation for hemochromatosis. And very often in MS. We have not even identified all of the mutations, so the genetic testing is not definitive.

I still see no rationale for not first doing an iron metabolism panel given the cost of the blood test. I know I have had an amazing reaction to two phlebotomies and I am concluding that what I have been told about primary progressive MS is not at all true. What if we could be helping people with primary progressive MS because even Zamboni says there are too many veins too close to the brain blocked with iron? What if we are treatable through phlebotomy? Since phlebotomy has never been done with MS, we cannot deny that it might be totally effective.

It turns out that abnormal iron metabolism has been studied in MS for a long time. Even Zamboni was studying iron deposits in the legs, which he attributes to venous insufficiency. But he also says that having the genetic mutation for hemochromatosis makes them more likely to result in ulcers. Anyway, I see the ultimate reason for people to test their iron metabolism, is that we seem to be finding have rather high rate of people showing abnormal iron panels. We need all the data we can get to rule out the possibility it is not the iron itself that is causing stress on the vascular system because of thick blood. I know I am amazed at the result of two phlebotomies that is in no way explicable by the standard present understanding of what causes MS symptoms.
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Postby Merlyn » Mon Mar 08, 2010 12:18 pm

Cheerleader-I forgot to ask you in the last post who tested the iron? Was that your own initiative, or did they do this before the procedure, because it seems like most people are not having a simple blood test before the CCSVI. Also, my Dr. thought my iron metabolism panel was normal, when it was clearly not. Same with Erika, her iron was considered normal until she questioned further. Can you post the numbers of the full iron panel just to reassure all of us readers that it is indeed perfectly normal, because most people's are not. I just found another person who was told that iron was normal when he is clearly iron poisoned.

I think they are finding these veins in normal people also, how is that being explained?

CCSVI does not seem to explain some of the other characteristics of MS. Do these veins just open up during pregnancy? Why do women go into remission during pregnancy if these congenital veins are problematic every day? Do these veins open and close accounting for relapsing remitting symptomatology? How does CCSVI account for the hypercortisalism always found in MS, or the low uric acid? How does that explain the growing gender discrepancies? It used to be that the ratio was one man to one woman with MS, it is now like three women to one male. It also seems to totally ignore that there is a genetic factor in MS, that the North American aboriginal and the Inuit have very low incidence of MS, whereas hemochromatosis would account for that.

I just don't see people asking enough questions. And there can be no absolutely no argument against running iron metabolism tests.

I am not picking on you, but if you could post those iron numbers I would be grateful. And also why you ran them in the first place... is Jeff on an iron chelator now?
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Postby cheerleader » Mon Mar 08, 2010 12:31 pm

The origin of increased leg iron stores is extravasation of red blood cells (erythrocytes) in conditions of significant venous stasis. Erythrocytes are degraded by the interstitial macrophages, with the released iron incorporated into ferritin. Over time, with increasing overload of iron, the structure of ferritin changes to haemosiderin.4-9 In 1988, Ackermann found a twenty-fold higher average concentration of iron in lower limbs affected by venous ulcers as compared to the upper arm of the same subjects.8 The phenomenon of leg haemosiderin deposits seems to be significant for the entire body, since this protein has been demonstrated in the urine of patients affected by CVD.9


Merlyn, not to pick on you....but you misunderstood Zamboni's research. What causes the increase of iron stores is venous stasis....not anything regarding iron levels in the blood. Please read his paper again:
link to The Big Idea Paper


What Zamboni has found is that when the blood flow is slowed, this degrades the erythrocytes to the extent that iron is released, and ferritin changes to haemosiderin. It is not because of hemochromatosis. (Jeff's iron panels were done by our GP, at my request and were found to be normal. I'm not going to dig them up right now and post, but you'll need to trust me, she did all the panels at our request and it cost us. He didn't have iron issues, he had jugular occlusion. This is why people with varying iron levels have CCSVI, and blood-letting will not change venous stasis- the cause of iron deposition.)

Jeff takes EGCG, a natural chelator which permeates the BBB, to remove iron deposited there by venous stasis.
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Postby Merlyn » Mon Mar 08, 2010 1:56 pm

Cheerleader-there is still nothing that you have said that would justify not running iron metabolism panels on every one. Just because Jeff does not show hemochromatosis, does not mean that it would exclude everyone from that condition. Five out of five of us are showing it, another person is waiting for their results. There is also iron loading anemia etc. They used to think hemochromatosis affected maybe one in 100,000 people, they now say one in 200. But that is the full-blown variety. The homozygous people. They have not really studied what happens to the heterozygote population, this is the genetic mutation that is most commonly associated with loss of iron homeostasis. Nor do you answer how iron gets into the brains of people with Parkinson's and Alzheimer's and Huntington's. I just watched the video by Zamboni once again, and he never ever mentions that iron is found in other conditions in the brain. He makes it sound like it is only MS, and that is not true! Most people on here were surprised to find out that iron accumulates in the brain in other conditions, conditions that do not feature CCSVI. You have any explanation for this, does Zamboni???

We have no idea what phlebotomy will do for MS. None. It's never been done! Nor do I hear any reasonable explanations for why MS goes into remission during pregnancy, nor does CCSVI make any sense genetically.
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Postby cheerleader » Mon Mar 08, 2010 2:57 pm

Merlyn: Why no iron panels?...because it is not necessary to diagnose CCSVI.

1. Because iron does not cause stenosis. Truncular venous malformations and external impingement cause stenosis. Not iron.

2. Zamboni does actually discuss other neurological diseases, which he tested for CCSVI. Please read his original CCSVI paper, he discusses this.
45 patients affected by other neurological diseases (OND) (table 2); this group was composed of patients affected by neurodegenerative disorders (Parkinson disease and amyotrophic lateral sclerosis-ALS), other neuroimmunological disorders including myasthenia gravis and multifocal motor neuropathy (MMN), and cerebrovascular disease (ischaemic stroke, transient ischaemic attack (TIA)).

none had CCSVI. Their brains may have iron deposition, but it is not related to venous stasis. Zamboni never said this group didn't have iron in their brains. He said they didn't have CCSVI.

Iron is essential for brain health, and myelination. Oligodendrocytes need iron to remyelinate the white matter. It is a very complex relationship....

Oligodendrocytes are the predominant iron-containing cells in the brain. Iron-containing oligodendrocytes are found near neuronal cell bodies, along blood vessels, and are particularly abundant within white matter tracts. Iron-positive cells in white matter are present from birth and eventually reside in defined patches of cells in the adult. These patches of iron-containing cells typically have a blood vessel in their center. Ferritin, the iron storage protein, is also expressed early in development in oligodendrocytes in a regional and cellular pattern similar to that seen for iron. Recently, the functionally distinct subunits of ferritin have been analyzed; only heavy (H)-chain ferritin is found in oligodendrocytes early in development. H-ferritin is associated with high iron utilization and low iron storage. Consistent with the expression of H-ferritin is the expression of transferrin receptors (for iron acquisition) on immature oligodendrocytes. Transferrin protein accumulation and mRNA expression in the brain are both dependent on a viable population of oligodendrocytes and may have an autocrine function to assist oligodendrocytes in iron acquisition. Although apparently the majority of oligodendrocytes in white matter tracts contain ferritin, transferrin, and iron, not all of them do, indicating that there is a subset of oligodendrocytes in white matter tracts. The only known function of oligodendrocytes is myelin production, and both a direct and indirect relationship exists between iron acquisition and myelin production. Iron is directly involved in myelin production as a required co-factor for cholesterol and lipid biosynthesis and indirectly because of its requirement for oxidative metabolism (which occurs in oligodendrocytes at a higher rate than other brain cells). Factors (such as cytokines) and conditions such as iron deficiency may reduce iron acquisition by oligodendrocytes and the susceptibility of oligodendrocytes to oxidative injury may be a result of their iron-rich cytoplasm. Thus, the many known phenomena that decrease oligodendrocyte survival and/or myelin production may mediate their effect through a final common pathway that involves disruptions in iron availability or intracellular management of iron.

http://www3.interscience.wiley.com/jour ... 1&SRETRY=0


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Last edited by cheerleader on Tue Mar 09, 2010 10:41 am, edited 1 time in total.
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Postby Bethr » Mon Mar 08, 2010 4:58 pm

I think there is a connection between high iron levels and MS symptoms. I'm living proof of it. I have the C282Y gene, so does my sister with MS.
We both have highish iron levels. I developed my lesion when my transferrin saturation was at it's highest levels (note not "serum iron"), Serum Iron was never above high/normal levels. Transferrin saturation is not normally tested for (it was, once upon a time).

One good phlebotomy put me right back on my feet. It lasted six weeks, I'm going downhill again now. What happened to me, wonderful that it is, may be unique to me as I have high T-Lymphoctes because I am asplenic, much higher than most people I would guess. So the process was amplified in me, and the cure was also amplified.

The connections lies here, but please put me right Cheer if you will

Hypothetical molecular mechanisms by which local
iron overload facilitates the development of
venous leg ulcers and multiple sclerosis lesions
M. Simka a,*, Z. Rybak b
a Department of Angiology, Wodzislawska 78, 43-200 Pszczyna, Poland
b Department of Vascular, General and Transplantation Surgery, Medical University, Wroclaw, Poland
Received 4 December 2007; accepted 23 February 2008
Summary 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 INFcR2
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.


and added to this:

J Vasc Surg. 2005 Aug;42(2):309-14.

Hemochromatosis C282Y gene mutation increases the risk of venous leg ulceration.
Zamboni P, Tognazzo S, Izzo M, Pancaldi F, Scapoli GL, Liboni A, Gemmati D.

Inter-Departmental Vascular Disease Center, University of Ferrara, Italy. zmp@unife.it

OBJECTIVE: Chronic venous disease (CVD) is the most common vascular disorder, progressing in approximately 10% of cases toward chronic venous leg ulceration, whereas the hemochromatosis gene (HFE) C282Y mutation is the most common recognized genetic defect in iron metabolism. Because CVD leads to local iron overload in the affected legs, we investigated whether two common HFE mutations could increase the risk of chronic venous leg ulceration. METHODS: This was a case-control study at the Vascular Diseases Center, University of Ferrara, Italy. From a cohort of 980 consecutive patients affected by severe CVD (CEAP clinical classes C4 to C6) we selected 238 cases with the exclusion of any other comorbidity factor potentially involved in wound etiology (group A). They were subdivided into group B, including 137 patients with ulcer (classes C5 and C6: 98 primary and 39 postthrombotic cases), and group C, including 101 cases with no skin lesions (class C4). They were completely matched for sex, age, and geographic origin with 280 healthy controls (group D). A total of 518 subjects were polymerase chain reaction genotyped for HFE mutations (C282Y and H63D). We assessed the risk of ulceration by comparing the prevalence of ulcer in homogenous cases with and without the HFE variants. Other main outcome measures were the sensitivity, specificity, and predictive values of the genetic test in CVD cases. RESULTS: C282Y mutation significantly increases the risk of ulcer in primary CVD by almost seven times (odds ratio, 6.69; 95% confidence interval, 1.45-30.8; P = .01). Application of the HFE test in primary CVD demonstrated increased specificity and positive predictive values (98% and 86%, respectively), with negligible sensitivity and negative predictive values. CONCLUSIONS: The overlap of primary CVD and the C282Y mutation consistently increases the risk of developing venous leg ulceration. These data, which have been confirmed in other clinical settings, suggest new strategies for preventing and treating primary CVD. CLINICAL RELEVANCE: The number of patients affected by primary CVD is so great that the vast majority of ulcers are also related to this common problem. On the other hand, there is not a reliable way for identifying in advance, from the broad base of primary CVD patients (20-40% of the general population), the high risk minority (10% of primary CVD cases) who will develop a venous ulcer. In such cases, a simple C282Y blood genetic test demonstrated an elevated specificity in predicting ulcer development (98%, CI 95%, 92.8-99.7). The genetic test could be applied starting from the C2 class, varicose veins, the most common situation observed in clinical practice. In perspective, the presence of the C282Y mutation would strengthen the indications and priorities for surgical correction of superficial venous insufficiency.

PMID: 16102632 [PubMed - indexed for MEDLINE]


Publication Types, MeSH Terms


Surely there must be a tie in somewhere.

JMHO

Cheers.........
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Postby Merlyn » Mon Mar 08, 2010 5:20 pm

How in the world can you tell if somebody has a problem with iron unless they test for it? No, maybe you do not need to test this to diagnose CCSVI but on the other hand doctors do not run this iron metabolism panel routinely, so it seems to me that it would be money well spent, and would add to our knowledge base of MS and the iron factor. Iron seems to be implicated in the autoimmunity cascade in MS, so I assume keeping it low would help control that... I assume that is why they are putting people on iron chelators after this procedure. I also wonder if the reduction in relapses are not due to keeping the iron down. It strikes me as kind of bad science to credit CCSVI with a reduction in relapses if one is also automatically taking iron chelators. How do you know what is doing what? How do you know if not simply keeping the iron down doesn't help MS progression? People who take iron supplements are 2.1 more likely to develop Parkinson's.

Your quote about the various groups of people that were tested for CCSVI all have neurological problems, the Parkinson's, ALS etc., and when you study these conditions you will find that the degeneration is attributed to the accumulation of iron. Iron causes cell death through oxidative stress. Lipid peroxidation, free radicals etc. etc. etc., the same as any heavy metal.

Why do people that have the stenosis, 29% of normal people I understand, not have iron in their brains? I'm just asking questions, because I don't think enough questions have been asked. I understand what you are saying, but maybe there is more than one way to skin a cat so to speak. As I have said many times, it is important that we identify those people with high iron levels, and this is pretty economically done. Because of the extra volume of blood during pregnancy, women are very often low in iron during pregnancy.

http://pregnancy.about.com/cs/anemia/a/enoughironhtm
Anemia in pregnancy is common and it is most often caused by an iron deficiency. Iron is a mineral that everyone needs. Pregnant women need more iron for a variety of reasons. The biggest reason is that iron helps your body make new blood to carry the oxygen and nutrients to the baby during pregnancy. By the end of pregnancy you will have twice as much blood in your body than when you began the pregnancy. Your need for iron will increase 100% over your requirements pre-pregnancy.
[/quote]

Maybe it is not all that important how iron gets into the brain, just that it is there. I come at this from a different perspective, the question of heavy metals and how they impact health. We do not know at this point whether just keeping the iron down results in positive outcome for those of us with higher iron, of which there seems to be quite a number. I know in my case, this is true, just a couple of phlebotomies has resulted in better neurological functioning, major reduction in spasticity! If there is an easier way to treat MS, through iron reduction, it would be an incredible savings economically. We cannot make the assumption at this point that CCSVI the only way to treat the iron problem. It seems to me that there might be a number of ways. And this of course is not even addressing the rather cavalier dismissal of a whole group of us with primary progressive MS. What we need is a clinical trial, CCSVI versus phlebotomy to see who has the better outcome.

[/quote]
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Postby MrSuccess » Mon Mar 08, 2010 5:41 pm

great discussion here . But I'm sensing an 'edge' that I can do without . The message seems to getting lost as a result. I like point -counterpoint as much as the next guy ...but ....

Is it possible you both are right ?





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Postby Merlyn » Mon Mar 08, 2010 5:41 pm

http://www.mssociety.org.uk/research/az ... ccsvi.html

More than 25 per cent of the 161 people scanned without MS (healthy control participants) also showed signs of CCSVI. This is surprising given that previous studies completed by Dr Zamboni suggested that CCSVI was a condition exclusively associated with MS.


Not Enough Information... do these people have iron in their brains, and if they do, why is it not causing problems, and if they don't, why don't they?
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Postby cheerleader » Mon Mar 08, 2010 5:48 pm

Beth-
those are great studies you posted. Let's break the information down into bite size chunks....we did this with the CCSVI papers last year, and it really helps to get a clearer picture. The first paper is from our beloved Dr. Simka. He really is an incredible doctor, and has a brilliant, inquisitive mind. This paper outlines a hypothetical situation- and he admits, it is still just a theory, but a good one.

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.

this is a great point to note- MS patients with the HFE mutation exhibit MS earlier and more frequently in some studies- and as Dr. Zamboni points out in the second study, the ulcers are worse with these mutations. But other recent studies say there is not a correlation between HFE and MS.

Here's a recent study on MS and HFE mutations:
Multiple sclerosis (MS) is a common inflammatory disease of the central nervous system unsurpassed for its variability in disease outcome. Given a possible role for dysregulation of iron metabolism in MS disease pathogenesis, we investigated whether or not mutations in the HFE gene influence the prognosis of the disease. A cohort of sporadic MS cases, taken from opposite extremes of the putative distribution of long-term outcome using the most stringent clinical criteria to date, was used to determine the role of HFE on MS disease severity. This approach increases the effective sample size by some 40-fold. Genotyping the two sets of MS patients (112 benign and 51 malignant) provided no evidence to suggest that mutations in HFE have any outcome modifying activity, although small effects cannot be ruled out. The frequency of HFE mutations was not different in MS compared to the general population.


http://linkinghub.elsevier.com/retrieve ... 2808002580

Back to Dr. Simka-

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.


This makes the most sense to me...Dr. Simka surmises that the activation of T-cells in this situation would lead to a more inflammatory response. Having an HFE mutation might make MS worse. Dr. Zamboni says this as well. But this does not mean it is causal.

Yes, there appears to be a tie in- it would be foolish to ignore the evidence....but it is not as black and white as saying people with HFE mutations get multiple sclerosis, and therefore blood letting or chelation will stop MS...there are many variables at play. The reason I am taking time out to write on these threads is to step in and say, wait....there is more going on.

I've researched endothelial disruption, nitric oxide and how this plays into oxidative stress, and have found more correlation to this process in MS than iron disregulation. But I would never say that stopping endothelial disruption will stop MS. There are many pieces to this puzzle, and by focusing on one to the exclusion of the others, we limit the big picture. That's all I'm trying to say.

Go ahead...if phlebotomy works for you, all the best!
Now I'm done :)
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Postby MrSuccess » Mon Mar 08, 2010 5:48 pm

Merlyn - I'll take a shot at this.

Can you assure me that the so-called healthy controls are not going to go on to develope iron deposits and then exhibit MS symptoms ?

Not wishing anything on anybody ....but it could happen.

As everyone knows ....healthy today ....but tomorrow ? Who knows.




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Postby Bethr » Mon Mar 08, 2010 8:01 pm

Thanks Cheer. Using genes is an incomplete science as yet. Many mutations are being discovered as we speak, for Hemochromatosis I think they are up to 38 this far. The studies only cover 2 genes. Many more types of genes that effect the iron metabolism and storage are being found that work in completely different ways than classic hemochromatosis.

I wish everyone the best for CCSVI and liberation.
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