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dibenzylamine (DBA) and L-BHB (levo-beta-hydroxybutyrate)

(zonk)

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according to some studies L-BHB is a prodrug to DBA which are considered both analgesic and antiepileptic however this is because bhb is a prodrug to dba which is an nmda antagonist and both . My question is if someone could fill me in on just how much of an antagonist in relation to it's potential toxicity. At what level if any would dba exert any significant effect or even possible dissociation or relaxation etc... I was thinking it may make a good supplement, agmatine was a huge dissappointment.
 
The studies I'm looking at suggest that dibenzylamine is an impurity present and not a metabolite.[ref][ref2]

I can't see how betahydroxybutyrate would metabolise to dibenzylamine. It's also weird that the anticonvulant activity is only seen in the commerical L-BHB and pure DBA, and not racemic BHB (which should be 50% L-BHB!)... suggesting that it's contaminated with DBA and it's not a natural metabolite.
 
I'm positive it is both a metabolite and an impurity, i have no idea on the metabolic pathway but that is what the study indicated as they tested L-BHB, D-BHB, BHB and DBA and found that DBA had a higher effect because obviously it's a instant pure concentration vs L-BHB which was slightly slower and lower. They stated L-BHB has no direct action and it was due to the conversion to DBA. Also the D-BHB blocked the effects altogether so this is why BHB had little effect vs L-BHB. Perhaps I misread though?
 
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Can you post a reference to that paper?

I just don't see how you go from this:
200px-Beta-Hydroxybutyric_acid-2D-skeletal.svg.png

to this:
05203959.png

metabolically.
 
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