Very good thoughts...I wonder if those that experience headaches with DAA would notice little to no headaches if they used agmatine in conjunction with DAA....?
'...Agmatine is also believed to be able to prevent the highly unlikely event of D-Aspartic Acid induced neuro-toxicity. In short, Agmatine is believed to do so by preventing over-excitation of NMDA receptors and reversing the levels of activation.
The important thing to distinguish here is that exogenous application of Agmatine and D-Aspartic acid work on different mechanisms for the NMDA receptor, so regardless of one being an antagonist and the other an agonist, they do not overlap. Exogenous D-aspartic acid application utilizes the R-type VGCCs and none of the others, while exogenous Agmatine is said to use the L-type VGCCs and shows no signs of inhibition of the R-type VGCCs. Exogenous application of Agmatine will enhance its regulatory role in the body so that in higher levels of NMDA receptor activation, it will inhibit the receptor from higher glutamate release (so over-excitation leading to potential neuro-toxicity) by inhibiting the receptor.'