My Alternative Hypothesis

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Hi ramakentesh, I am working on a similar model, but for calcium gated potassium channels. Note that sodium and potassium interfere with each other. My model also involves NFkB (and BH4, glutathione, NO, folic acid (synthetic folate), methylation cycle, COX-2 and perhaps COX-1) but not so much TNFa (though I have not explored immune hormones much yet). In particular there is upregulation of calcium gated potassium channels in the endothelium of blood vessels, especially the gut. This can trigger OI by increasing the amount of blood carried in the gut, together with secondary consequences of competitive inhibition from unmetabolized folic acid. This still needs a LOT of work for me to show its plausible and I am very busy on several other projects. Currently in this model the immune deficits are secondary consequences of toxicity from unmetabolized folic acid. Bye, Alex
 

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