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I am confused about the iron anc Vitamin C debate......have been taking 500mg. daily....would it be wise not to take it?

Vitamin C aids the absorption of iron, so if you want to keep taking Vit.C. then do not take it at the same time of the day as you eat foods high in iron, ie: meat, iron fortified cereals etc.
Hope that helps.

So how long after having vitamin c does it take to wear off and not cause the iron to be absorbed? Does it cause it to be absorbed more all day? or just a few hours? Thanks!

I'm not sure, I've just read not to take them together. People with iron overload are advised not to take Vit.C. supplements, but OK to eat foods with Vit.C., maybe just don't eat together with meat. Meat is heme iron so readily absorbed, but things like spinach are non-heme and although high are not as readily absorbed in the gut.

Maybe oranges in the morning and meat at night

I just will wait a few hours after drinking orange juice to eat from now on i guess Hopefully thats okay. Why do they have to make MS so complicated LOL!

How do you know if you have iron overload?

i was liberated in December 2010 (balloon angio - IJVs
+ Azy) and have been taking 1000mg vit C with my lunch for the last 3 years,

should i stop the vitamin C?

I'm not a doctor or health professional, but I'm not convinced that vitamin C is a problem as far as iron overload. The theory is that with CCSVI, iron eventually leaks across the blood brain barrier due to poor blood drainage.
I don't think it has anything to do with iron overload. Needless to say, everyone has iron in their blood, and if you have CCSVI some of it may wind up where it's not supposed to be, even if you are anemic. Vitamin C is crucial to cell repair and is a valuable antioxidant.
Please correct me if you know otherwise.

Interestingly I took at least 1000mg vit C daily for 25 years prior to my diagnosis.

Mixing Vit.C with iron enhances iron absorption. If you are anemic I suppose it would help boost up your iron levels taking them together.

If you actually have an iron overload, you are advised not to take them together. It's as simple as that.

I have never taken Vit.C. supplements and still got an iron overload, as in my case it's a genetic problem.

Have a look at this please

http://en.wikipedia.org/wiki/File:Multi ... HO2002.svg

and this.

http://www.who.int/vmnis/anaemia/preval ... naemia.pdf

It is the iron in our diets combined with CCSVI that causes MS.

Of note is this country, it sticks out like a sore thumb.... and is a paradox

http://geography.about.com/library/cia/ ... guiana.htm

Why do they have such a prevalence of MS when the others surrounding countries do not ???

The Geology of this nation tells the story, High in water soluble iron it looks like, and it gets into all the foods, plants etc, ( still researching). Friends of mine are from the area have have extremely high levels of iron in their blood that has alarmed their Canadian Doctors.

If you draw a venn diagram and assign Stenosis to one circle, Time to the other and Diet / iron to the third the intersection of these produces MS

The larger any one of the circles is the greater the chance of having MS. If you do not have CCSVI then you will not get Clinically defined MS. If you have a diet with no iron, you will not get MS. (this is impossible though as Iron is in everything). Time is time and you cannot eliminate that.

I have reduced iron in my diet. I have reduced Vitamin C in all forms completely becuase

http://www.ncbi.nlm.nih.gov/pubmed/3304065

Ann N Y Acad Sci. 1987;498:324-32.

Is there a physiological role of vitamin C in iron absorption?
Hallberg L, Brune M, Rossander-Hulthén L.

Nonheme iron usually constitutes more than 90% of the dietary iron. Its absorbability is a resultant of the balance between factors enhancing and inhibiting the absorption. Ascorbic acid is the most potent enhancer, and is the same for native and synthetic AA. The enhancing effect is strongly dose related (log dose/effect), and is different for different meals probably mainly due to varying content of inhibitors in the meals. AA also increases the iron absorption from simple meals with no known inhibitor, probably because AA impairs the formation of unavailable iron complexes with ligands normally present in the gastrointestinal lumen. The effect of AA is so unequivocal and marked that it must be considered as a physiological factor essential for the absorption of dietary iron.

Iron is essential, we need it, but I think the important thing here is the balance of iron and where the body stores it. You can be anemic and have organs overloaded with iron at the same time, so there is no clear cut answer at this stage to the iron question.

Usually the body is very good at maintaining the balance, once you have enough in storage hepcidin increases, which in turn reduces absorption.
People with hemochromatosis genes have low hepcidin, hence their body has trouble cutting off the intake.

I believe myself that we have plenty of iron in our diets, it's forced on us through iron enriched food products, and the marketing complex that pushes that iron is good. Both too little and too much cause problems.

There is no answer to the first question. You need to find out your iron status and work from there.

I got very sick when my iron levels were high. The symptoms are similar to MS, I even got a brain lesion! My sister has MS DX for 20 years, she also had high iron levels. I reduced my iron levels and became well again. But my case was clear cut.

Maybe my sister doesn't have MS, maybe she has a mild iron overload.
Don't know, they won't reduce her iron levels
My brain went quite queer when my iron levels were high (the brain lesion formed and also epilepsy showed up on an EEG) and also when I was de-ironing by phlebotomy I had an episode of involuntary arm and leg movements, just for one day. The more iron I got out the better I felt, and now I'm de-ironed I'm a box of birds, no more brain events, no fatigue.

I don't know the connection, but there is one, of that I'm sure.
just wish my sister could try it too!

When I was first diagnosed I was intrigued to hear of some people who had a type of MS that was involved with iron. At the time I was doing all kinds of dietary experimenting and one thing I decided was that iron in vitamins did not agree with me. At around the same time vitamin C seemed to make a difference, and I took it every day for many years. When I found out about CCSVI I sought and found a daily vitamin with no iron in it, which I have taken since.

My lawn is kept under control very well without pesticides using a product which is mainly iron. But I don't spray it on, myself.

Iron is such a basic part of us that I don't see how it can be tightly controlled. In Canada you cannot give blood if you have 'MS'.

I have seen some of Dr. Haacke's work but I don't think it has been proven that the iron deposits in brains correlate with anything. Anyone have answers on this?

some deposition is normal:

Normal deposition of brain iron in childhood and adolescence: MR imaging at 1.5 T
Abstract
Magnetic resonance (MR) images of the brain in 285 patients between the ages of 2 and 25 years were retrospectively studied to determine the appearance of brain iron accumulation. ... The temporal sequence of normal iron deposition as detected with MR imaging is helpful not only in the diagnosis of known iron-deposition diseases but also in the detection of iron-related pathologic changes.

certain inherited conditions such as hemochromatosis which lead to iron overload are associated with deposition:

http://www.ncbi.nlm.nih.gov/pubmed/20293593
Deposition of Iron in Paraventricular Areas of the Human Brain in Hemochromatosis

sometimes ms patients have iron dysregulation:

http://www.ncbi.nlm.nih.gov/pubmed/15957506
Serum ferritin, transferrin and soluble transferrin receptor levels in multiple sclerosis patients.
Over the last few years, increased evidence has supported the role of iron dysregulation in the pathogenesis of multiple sclerosis (MS), as iron is essential for myelin formation and oxidative phosphorylation. We studied indices of iron metabolism, such as serum iron, ferritin, transferrin and soluble transferrin receptor (sTFR) levels in 27 MS patients. Seven patients had chronic progressive active disease (CP-A), six had chronic progressive stable (CP-S), ten had relapsing—remitting active (RR-A) and four had relapsing—remitting stable (RR-S) disease. sTFR levels were found to be significantly higher in CP-A (P=0.021) and RR-A (P= 0.004) patients than in controls. sTFR levels were also elevated in CP-S patients but did not reach significance (P=0.064). sTFR values in RR-S patients were comparable to those found in controls (P=0.31). Ferritin levels were significantly elevated only in CP-A patients (P= 0.002). Patients of the CP group had significantly higher ferritin values than the RR patients (P= 0.004). Haemoglobin values as well as iron and transferrin levels were within normal limits in all patients. In conclusion, the increased serum sTFR and ferritin levels in nonanaemic MS patients with active disease reflect the increased iron turnover. The mild elevation of sTFR levels in CP-S patients may indicate active inflammation with ongoing oxidative damage that is not detectable by history or examination.

and bringin it home:

http://www.ncbi.nlm.nih.gov/pubmed/18073202
J Biol Chem. 2008 Feb 22;283(8):5168-77.
Zinc deficiency-induced iron accumulation, a consequence of alterations in iron regulatory protein-binding activity, iron transporters, and iron storage proteins.
Abstract
One consequence of zinc deficiency is an elevation in cell and tissue iron concentrations. To examine the mechanism(s) underlying this phenomenon, Swiss 3T3 cells were cultured in zinc-deficient (D, 0.5 microM zinc), zinc-supplemented (S, 50 microM zinc), or control (C, 4 microM zinc) media. After 24 h of culture, cells in the D group were characterized by a 50% decrease in intracellular zinc and a 35% increase in intracellular iron relative to cells in the S and C groups. The increase in cellular iron was associated with increased transferrin receptor 1 protein and mRNA levels and increased ferritin light chain expression. The divalent metal transporter 1(+)iron-responsive element isoform mRNA was decreased during zinc deficiency-induced iron accumulation. Examination of zinc-deficient cells revealed increased binding of iron regulatory protein 2 (IRP2) and decreased binding of IRP1 to a consensus iron-responsive element. The increased IRP2-binding activity in zinc-deficient cells coincided with an increased level of IRP2 protein. The accumulation of IRP2 protein was independent of zinc deficiency-induced intracellular nitric oxide production but was attenuated by the addition of the antioxidant N-acetylcysteine or ascorbate to the D medium. These data support the concept that zinc deficiency can result in alterations in iron transporter, storage, and regulatory proteins, which facilitate iron accumulation.

and of course ms patients tend to be low in zinc.

That first study is from 1947! Sometimes you have to go back to go forwards
I wonder if anyone has looked at hepcidin levels in MS?
Does zinc have any effect on hepcidin levels?

Wow, zinc does have an effect on hepcidin levels.
And very noteworthy also, hepcidin is repressed by hypoxia.
Meaning you will load more iron with low hepcidin caused by hypoxia (like someone with hemochromatosis, but from a different path)

.

FEBS Lett. 2010 Feb 19;584(4):719-25. Epub 2009 Dec 22.

Divalent metal-dependent regulation of hepcidin expression by MTF-1.
Balesaria S, Ramesh B, McArdle H, Bayele HK, Srai SK.

Department of Structural and Molecular Biology, Division of Biosciences, University College London, London, United Kingdom. sara@biochem.ucl.ac.uk

Abstract
Hepcidin is a small acute phase peptide that regulates iron absorption. It is induced by inflammation and infection, but is repressed by anaemia and hypoxia. Here we further reveal that hepcidin transcription also involves interactions between functional metal response elements (MREs) in its promoter, and the MRE-binding transcription factor-1. Analysis of hepcidin mRNA and protein levels in hepatoma cells suggests that its expression may be regulated by divalent metal ions, with zinc inducing maximal effects on hepcidin levels. These data suggest that this peptide may be a pleiotropic sensor of divalent metals, some of which are xenobiotic environmental toxins.

Copyright 2009 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

http://www.ncbi.nlm.nih.gov/pubmed/20026331