Posted 17 July 2007 - 04:13 AM
I thought the article seemed oddly biased. Nevertheless by all appearances DMAE is NOT an aCH precursor, even though that's what it is usually described as. Whatever DMAE does seems to have something to do with the fact that it causes the production of phosphatidyl-DMAE in lieu of phosphatidylcholine, on top of raising choline levels. On the other hand, DMAE actually *reduces* choline uptake, which gives me some pause. Frankly I'm beginning to have less of a clue of what DMAE even *does* the more I read. But Dave's article didn't help that uncertainty at all. I had to hit the journal articles myself, and I still haven't found good answers.