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Increasing absorption of amines in the stomach

aced126

aced126

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May 18, 2015
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Does taking antacids like tums really improve the absorption of amines from the stomach?

The pH of the stomach is 1-2 meaning that essentially a negligible amount of amine compound (pka ~7-8) will be in the unprotonated form which can easily diffuse through the stomach membrane. Raising the pH by one or two units is not going to do anything to the amount of unprotonated amine, which will still be negligible at pH 3-4.

So I'm assuming the bulk of the compound (obviosuly assuming it isn't transported via other means like endocytosis, facilitated diffusion etc) will be absorbed in the small intestines where the pH is much higher (~7.4). Is this where the antacids have their effect of increased absorption? I would've thought all the carbonate ions would've reacted in the stomach and none would reach as far as the intestine.
 
Acid-base reactions are extremely fast, so if you take a carbonate, it will have reacted long before reaching the intestines. Is there empirical data suggesting that taking an antacid improves the absorption of amines?
 
A lot of people say taking a few tums before dropping an e pill potentiates it 1.5 times or even more.
 
Potentiates the rush or the whole experience (I've never taken MDMA)? Because if it only increased the speed of absorption, the "area under the curve" would still stay the same, so the experience would be stronger but shorter, am I right? Perhaps the low pH of the stomach is able to hydrolyze some of the MDMA before it is absorbed, so when you increase it by a bit, that effect is significantly decreased? Honestly though I have no idea, maybe someone else does.
 
I think AUC increases because the actual bioavailability is claimed to be raised by prior antacid administration. It seems to prolong effects as well. Even so, it seems irrelevant; if the antacids are long gone when the amines reach the small intestines, how is this supposed increase in either absorption speed or AUC mediated?
 
According to Adder, the 1,3-benzodioxole system of MDMA is way more stable than normal acetals and is resistant to hydrolysis. Seems to make sense considering that the system is (nearly) planar rather than bent.
 
Yeah under normal conditions it is quite stable, but it may not be so at pH of 1, but that was just a suggestion.
 
Ok, there are also many anecdotal reports that plain amphetamine sulphate is made to have a much longer and more intense duration of action with prior antacid consumption. Here the argument of acetal hydrolysis cannot be used and the only factor involved is supposed deprotonation of the primary amine salt.
 
Well, then there's something else at play here. I'm not much of a biologist unfortunately, so I can't speculate farther than the basic stuff. Anyway, as you said, even at pH of like 4 there's negligible amount of deprotonated amines, and besides intestines have higher pH and way more surface area than the stomach. Perhaps there's some kind of transporter/mechanism that works better for amines at higher pH? Sorry if that sounds stupid.
 
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