Modnote: This post was moved out of the Firefly thread.
I've had some CannaQuin (Cannatonic x Harlequin) and Sour D back to back and mixed, was a very interesting experience. The CannaQuin didn't give me any real high but was excellent for pain, and the SD was the perfect sativa addition to it. Really nice uplifting high with analgesia but no grogginess from a strong indica
Yah, we on our way here. It happens that SD, while being recognized as a clear head energy boost, works 10x better for my lumbar pain & sciatica, below the belt, than ANY other strain I've tried so far. It's so specific to the lower spinal cord that I don't think it would work as well on (mid-level) thoracic nerves.
What I noticed, though, and is REALLY interesting, is that if I 1) lay down some Sour Diesel as base, for reduced pain and boosted energy, and 2) I add another strain that's not so analgesic but is a great energy boost, say Red Congolese, the pain pops right up again, like there's a competitive relationship knocking out the analgesia.
Same with Harlequin (high CBD strain). I thought it could be used in a blend to block excess confusion due to high THC levels, but it reverses Sour Diesel's analgesia as well. And the vaping at different temps seems to suggest that SD's analgesia arrives with the very first fraction that has that dieselly taste, not in the compounds that cross over later, at higher temp.
This all also suggests that some of the effects that, these days, are often credited to CBD or terpenes, including analgesia, may be (in part at least) caused/mediated/boosted by Delta9 THC itself or other low temp fraction elements. The reversal suggests that these elements probably interact in classical "competitive agonist-antagonist" pharmacology, and intertwine with the Endocannabinoid system we are born with.
This is well-known with our natural Endorphins and other morphine derivatives. For instance at a high enough level Codeine, a weaker mu receptor activator (agonist), can still competitively displace Morphine from the receptors, but being a weaker activator, it blocks/reverses some of the analgesic action instead of lightly supplementing it.
Also this is how naloxone reverses respiratory depression in an OD, because it's strongly bound to the mu receptors, thus competing with Morphine and pushing it out, but it's in itself such a weak agonist that it leaves practically no effect. Result: total reversal.
The point is that we see signs of similar complex actions between the Cannabinoids, though it may take a very long time to sort out how they all interact.
