N&PD Moderators: Skorpio | thegreenhand
It has since been disproven by mephedrone, which simultaneously releases tons of DA and 5-HT but yet does not cause "MDMA type neurotoxicity."
But Neurotic I could be remembering wrong but I was under the impression it was catecholamines being metabolized by MAO-B that might've damaged the serotonin axons to an extent https://www.erowid.org/references/refs_view.php?ID=974 The damage was attenuated by MAO-B inhibitors and increased by more dopamine, while lack of dopamine through different methods meant less to no serotonin damage. Although I should mention a great portion of the increase in neurotoxicity with more dopamine is probably from increased temperature. But I do wonder what the consequence is of having dopamine inside a serotonin axon if that is indeed a thing. One study said even dopamine itself is toxic to serotonin neurons, hydrogen peroxide aside.
That's because it's just plain ibuprofen as the free acid, it's not a salt.
I can't give an answer, but you definitely have the enzymes right. The mechanism you describe would be the same as the one causing Tramadol to be potentiated through grapefruit juice. 3A4 metabolizes to N-Desmethyltramadol, 2D6 to O-Desmethyltramadol, resulting in higher plasma levels of the latter which is a much stronger mu opioid receptor agonist.After a fairly short search, I didn't find any suggestions that grapefruit inhibits CYP2D6, only 3A4. So according to my understanding, 3A4 is responsible for N-dealkylation of codeine producing the inactive norcodeine while 2D6 is responsible for 3-dealkylation producing morphine. This should mean that if 3A4 is inhibited, more codeine will follow the 3-dealkylation path resulting in more morphine, thus increased opioid effect. My question is, why do people suggest against using grapefruit to potentiate codeine and why do some people say that in their experience grapefruit actually decreases the effects of codeine?