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I have a question. I wrote to Ashton Embry (Best Bet Diet) asking whether his son had a Celtic background... and did not get a clear answer, but a notation that most people with MS did not carry the hemochromatosis gene according to PubMed. But we all know just how diligent science has been investigating this. The thing is, people of Irish descent have a one in six chance of carrying the carrier gene for hemochromatosis. It turns out that even if you are a carrier only, you have a slight increase in iron absorption. This iron gets deposited throughout the body including the pituitary etc., so it definitely gets into the brain. I am going to request this test to see whether I am a carrier which would predispose me to increase iron absorption. And if so, too much iron does all kinds of detrimental things including making the platelets sticky... sticky platelets/thick blood causes all kinds of circulation and other problems and I suspect it would cause stenosis etc. any thoughts on this? I think we are all victims of Celtic heritage.

http://www.ncbi.nlm.nih.gov/pubmed/568576
Hypovitaminemia A in idiopathic hemochromatosis and hepatic cirrhosis. Role of retinol-binding protein and zinc.
Brissot P, Le Treut A, Dien G, Cottencin M, Simon M, Bourel M.

Serum levels of vitamin A, its specific carrier protein retinol-binding protein (RBP), and zinc were determined in 34 cases of idiopathic hemochromatosis, 33 cases of alcoholic cirrhosis, 10 cases of non-alcoholic cirrhosis, and in 35 normal controls. In both alcoholic and non-alcoholic cirrhosis, vitamin A and RBP levels were very significantly reduced, whereas a significantly low zinc was observed only in the alcoholic cirrhosis group. In idiopathic hemochromatosis, vitamin A values were significantly lower compared to normals, whereas serum RBP levels were normal and serum zinc was very close to that of the controls. A significant correlation was found between vitamin A and RBP levels in the entire group of 112 patients. These results, (1) in alcoholic and non-alcoholic cirrhosis, confirm a dramatic vitamin A deficiency and the major role played by decreased RBP, but tend to deemphasize the possible role of zinc deficiency; (2) in idiopathic hemochromatosis, affirm a significant serum vitamin A deficiency supposedly by a different mechanism from that of alcoholic cirrhosis since in idiopathic hemochromatosis plasma RBP levels are normal. The role of this vitamin A disorder should be considered in the interpretation of clinical signs of idiopathic hemochromatosis such as ichthyosis and visual disorders.

without seeing the full text i can't see what 'very close' means in terms of zinc levels in patients and controls. however, if i do get a chance to go for the full text i am willing to bet it's not higher than controls, and also that the patient average is not 18.2 umol/L! it is known that the human body needs adequate zinc in order to handle vitamin A properly. AND, zinc repairs cirrhosis, which occurs both in alcoholism and iron overload.

Do pwMS who have a negative result for CCSVI still have Dawson’s fingers or venocentric lesions or damage occurring around veins? If so, then a blood flow problem is probably still associated with their MS. Would this show in venography? Maybe research should be looking for that to explain the results of SWI, rather than being preoccupied with percentages of CCSVI.