I just saw these replies now. I tried to have a quick look in the book i mentioned and one thing he says in the chapter on amines is: "Hiistory of pseduoallergy should serve as a warning for the use of medications that inhibit AOC1. Similar warnings are appropriate for MAO and HNMt inhibiting medications. H2 blockers, although not strong inhibitors, are commonly used and available without a prescription". Ambifguous in this instance as to whether inhibits aoc1, mao, or hnmt. There were more extensive discussions elsewhere though, including those that singled out tagamet compared to the others- perhaps int he mast cell chapter- will look when I get a chance. When you both said that this claim was not in the book, were you referring to the table that suggests (arbuably) a different interpretation of this sentence?
Until i get a change too look in book, I was going to give the reference to another article, but looks like you have it- on mao-I like effects with cimedine. Note surew why you think it's just a drug-drug interaction (incidentally, i have not seen the drug drug paper one of the posters mention) and even if it is, raises the possiblity that cimetdine also interacts with endegenous MAO activity and not just exogeneous drugs that alter it.
There's also the work that finds that catecholamine levels in urine may be decreased with H2 blockers. I don't remember if they have a theory as to why, but decreased cat levels in urine can be due to decreased breakdown of the exisiting catecholamines, which would implicate with MAO, COMT, or the sulfer pathways. (or if it's jus tlowering the catecholamines, it still suggest h2 blockers are interacting with the whole catecholamine system).
thene there's the suspicious case study (haven't read it yet but its on the list) of someone who developed a pheochormocytoma after cessation of tagemet, suggesting again that its messing around with the whole catecholamine system
the book though was the one that was clearest on singling out tagamet vs other h2 blockers.
The poster who mentioned the antiviral effects of tagamet, I believe the theory of how this works would mean it should work for the other h2 blockers a s well. if memory serves (yes, by all means fact check), T supressor cells have receptors for H2. by blocking H2, the T supressor cells don't turn on so fast, and this allows viruses to be killed more effectively by immune system. the studies on the anti viral effect (not just EBV) were done with tagamet, but i think that's becasue they were done when that was the most popular (only?) drug in use. If all the h2 blockers have the antiviral activity, then won't hope the responder looking for what's special about tagamet. (though of course practice not same as theory; perhaps it works better in practice, and i've never had occasionto search for tagamet vs pepicd etc on anti-viral activity.
i'll look again - i'm coming from the perspective that i'm wildly sensitive with severe symptoms to even extremely small amounts of tyramines and in my case, i suspect at least some of the issue is poor supply of MAO-A (though not my only cause). So i might be biased when i see someone says stay away from tagamet (but the others ok) ifyou're senstivie to tyramines into thinking it further inhibits mao-a when wording is ambiguous.
What did you find is the difference between tagamet and the other h2 blockers when you looked into it to see why that one may have worked for you but not the others? What happens when you take a larger dose?
chemistry, especially biochem, is a good skill - will seek that poster out when questions arise
