Is there any evidence to prove that THCp in use in Europe is the exact stereo isomer of material first identified, isolated and synthesized by Italian group i.e., “ The natural compound was isolated and fully characterized and its stereochemical configuration was assigned by match with the same compound obtained by a stereoselective synthesis. This new phytocannabinoid has been called (-)-trans -Δ9-tetrahydrocannabiphorol (Δ9-THCP)”
How do people who are experienced spice users of Huffman style full agonists say, the Euro-THCp that you refer to, compares to the Huffman full agonist e.g., JWH018 for instance? Granted that THCP may be well distributed In different strains at different concentrations…and that all marijuana users my be exposed to more or less of this on a regular basis.
What I am getting: is the CB1 bias- Radar plot for THCp agonism any different from JWH018? Since this is an important concept in the “drug action “ corner AND no scientific data is available…we need to ask users about the experiences. What makes THCp a marketable product?
What makes Hemp Bud sprayed with THCp a marketable product in Europe. Is this a top down product pushed on the Euro-market by business as a “money maker” or is this a product produced in such quantities as you suggest due to “local demand”. Who would want THCP on Hemp bud? Why not just vape the material as an oil…if you really want to get high.
If the Hemp bud is high in CBDA and CBD…you would be saturating the CB1 allosteric binding sight with CBD as well as agonizing the orthosteric site with THCP. Now this situation would attenuate the agonism and shift the whole experience more toward a THC like effect during the initial high. Perhaps vaping THCp and smoking THCp laced Hemp bud are two different experiences. Does CBD play a neuroprotective role?
It seems that tolerance does play an serious role in the amounts needed, as you suggest. Note that tolerance persists past 14 day window. So the euro-user. of SCB may well be a “different” animal so to speak.
From a review:
“More recently, the high-efficacy SCBs JWH-018 and JWH-073 were unable to induce hypothermia in mice previously made tolerant to hypothermic effects of low-efficacy Δ9-THC, suggesting that cross-tolerance developed to the hypothermic effects of the high-efficacy SCBs, despite the relatively large disparity in intrinsic activity [109]. In other words, unlike what is typically observed with other drugs (such as the opioids), tolerance to an effect induced by low-efficacy Δ9-THC was not surmounted by administration of higher-efficacy SCBs. Furthermore, cross-tolerance was still present 14 days after Δ9-THC cessation, suggesting that this cross-tolerance may be as persistent as the tolerance induced by repeated administration of the high-efficacy SCBs themselves [109]. Indeed, chronic treatment with high-efficacy SCBs results in rapid and persistent tolerance to some, but not all, in vivo effects, accompanied by region-specific downregulation and desensitization of central CB1 cannabinoid receptors 109–[111]”
Please advise. Thanks
Is see there is already judicious discussion of this subject by some notables please read.