Date:   5/24/2013 1:18:53 PM ( 11 y ago)
Hits:   1,035
URL:   https://www.curezone.org/forums/fm.asp?i=2068481

the odd thing is that MSM had no effect on me some years back. For me it seems like other things had to be fixed before the sulfur could work. A chain of events.

Edit; a good article IMO about the co-relation of minerals; also possibly a missing link, rubidium.

"Iron absorption and regulation, according to the literature, is poorly understood. It is known to occur at the membrane of the ileum, and our experience suggests that there is a screening device, which we refer to affectionately as the "iron gate." This consists of a membrane regulator that calls for the exchange of the position of rubidium and selenium within the transfer pores.

So far, we have deduced that iron is regulated in this way: when the iron sensor perceives a shortage of iron in the blood, rubidium stays behind the gate, (at the surface of the lining that is exposed to the capillary bed) and selenium swings to the front of the gate, (toward the surface of the lining of the ileum that is exposed to the nutrient fluid.) This position of selenium invites the iron molecule to separate out of the nutrient broth in the ileum, migrate across the entry pore, and slip into the receptor sites of the capillaries at the back of the pore, and then into the bloodstream. If the sensor perceives that there is already enough iron in the blood, then selenium slides behind the gate, and rubidium comes up to the nutrient surface, and it closes off access to iron. The presence of rubidium at the nutrient surface of the ileum lining prevents further uptake of iron.

If this is true, then we might deduce that in a shortage of rubidium, the absorption of excessive iron could be due to the inability to screen it out, because the iron gate is stuck in the "open" position. In that case selenium would be too abundant at the nutrient surface, and not enough rubidium would be available to trade places and serve as a screen. Iron has an open invitation to continue to enter the bloodstream. In time this would be likely to lead to hemosiderosis.

On the other hand, if there were a shortage of selenium, iron might not be able to gain access to the capillary structure. The transfer pores would be guarded by rubidium, and would remain closed. In that case, iron uptake would be less than optimal, resulting in a form of anemia that would not yield to iron supplements, and would not be related to B-12/folic deficiency. Oddly enough, if there is no rubidium available at all, and only selenium is present, the iron will also be refused entry. Possibly rubidium, stationed at the rear position of the regulatory pore, serves as a sort of magnetic-like draw that pulls the iron in. Both Se and Rb have to be present for the "iron gate" to work.
http://www.balancingcenter.com/articles/rubidium.html




 

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