Aren't/isn't the active fraction of Nigella sativa (powdered fresh seed, its quite oily, and an electric spice grinder is the best way to do it, in a mortar, the pestle just crushes the buggers, turns them into greasy splats, and a very coarse, fragment-ey grind if one tries really hard) exerting the bioactivity of the plant through enkephalinase inhibition? because it certainly seems to strongly potentiate opioids if enough is taken. Will have to experiment again with doses, as its been
a long time since I tried it, and I had less tolerance at the time. But it certainly, definitely did not, subjectively, feel as though it was inactive.
Eur J Pharmacol. 2000 Jul 14;400(1):89-97.
Antinociceptive effects of Nigella sativa oil and its major component, thymoquinone, in mice.
https://www.ncbi.nlm.nih.gov/pubmed/10913589
31.184.194.81 Connect to this IP address for the full papers (its a website called sci-hub,they fight closed-access-enforcing, knowledge-thieving filth such as scientific publisher who use paywalls. One just puts in a PMID, DOI etc. and then usually at least it'll find the article. Sod paying those moneygrubbing swine publublising houses for a bloody lark!)
Interestingly, it seems that morphine, and other MOR agonists and possibly KOR, but not delta agonists are not crosstolerant when the tolerance is to the direct agonist, but that tolerance to thymoquinones effect induces a strong crosstolerance to conventional MOR agonists. Which strongly implies an indirect mechanism of action.
