I was actually thinking that the other day.
Dutch pills with coating will indeed take longer.
But I've crushed them up to try see if there was any difference. None what so ever. Same effect except come up was dramatically faster.
So it sends me right back to the glycidate if racemic etc isn't the cause.
I don't touch MDxx in either form these days but my position has remained the same since the first time this was brought up: the drug is not magic, it is not unique, it is governed by chemistry in production, psychopharmacology in recreation, and biology in absorption in just the same way as every other drug.
If there is an actual difference then consideration of such factors will be far more productive than the blind guesses and ridiculous myths this debate seems to attract.
A combination of the coating and excipients of the pill make a massive difference.
The exact ratio of enantiomers in a drug that only works fully if used as an equal mix of D- and L- is even bigger. Quite a few of the posters in this thread were oh so ready to jump on my suggesting it as a possibility because, and there's a few key words, the
standard synthetic routes produce the racemic compound. Funnily enough the time frame of the change is right around the time many labs stopped using the
standard synthetic routes because the main reactant was changed to one that will not form a true (50:50) racemic mixture but instead selectively generate a higher proportion of the isomer that corresponds with its own.
A new reagent of a majorly different structure at the atomic level will not react at the same rate when undergoing the same catalytic process if the duration of exposure is a constant. Black market superlabs have
a lot to lose if their production rate falls by the tiniest fraction.
Funny how a combination of those three factors goes a long way to explaining the debate, isn't it?
8)
