I have had great success using Cannabigerol (CBG) for pain. Two years ago I broke six ribs and as usual declined pain pills, using only high doses of CBD and CBG, etc. Then nine years ago I was contemplating surgery due to pain for months in my upper back and arm, but one 100 mg dose of full-spec CBD and an hour later the pain was gone, never to return. Same supplier for both, which is crucial for successful treatment.
It appears CBD is great for pain caused by inflammation. Even brain issues due to inflammation, such as temporary dementia and psychosis. But CBG acts on pain differently, and when they say it is better for pain than THC, it appears true; to me THC seems to act more as a “pain distractor” than a pain killer, whereas CBG was the one that actually made the noninflammatory pain less.
CBG activates the TRPV1 receptor to desensitize it and block the transmission of pain signals, and the pain relief from CBG is from endorphin release. It actually increases endorphins, which are part of the brain’s “reward centers.” They can improve your sense or feeling of wellbeing. That’s one reason CBG is important as happiness is no laughing matter.
Your body releases endorphins in response to pain or stress or during pleasurable activities like exercise, sex, laughing, or falling in love. You can also boost your endorphins by eating dark chocolate or spicy foods, the subject of many a breathless magazine story. Endorphins help by reducing stress, anxiety, and depression, boosting self-esteem, improving cognitive function, and regulating appetite.
They are profoundly important in life, and highlight the importance of including CBG in a daily wellness regimen for psychological and physical support.
There was a study recently on Cannabigerol (CBG), the “mother” cannabinoid in the plant, for pain. “The antinociceptive activity and mechanism of action of cannabigerol” was published by Chinese researchers in “Biomedicine & Pharmacotherapy,” in February 2023. Here is my summary:
CBG has been shown to have stronger antinociceptive activity [pain relief] than CBC and CBD, and CBG has been reported to have a stronger antinociceptive effect than THC.
Accordingly, we finally selected the compound CBG for follow-up experimental studies combined with our preliminary screening results. Using the same model, we explored the onset time of action, effective dose, and comparison of CBG antinociceptive with multiple antinociceptive agents.
CBG begins to work at 60 min and gradually weakens over time, and its antinociceptive effect were not dose-dependent, which works best at 2 mg/kg [150 mg for a 165-pound person], and there is no significant difference in antinociceptive effects compared with antinociceptive effects such as indometacin [arthritis NSAID], aspirin and ibuprofen.
For neuropathic pain, CBG can exert antinociceptive effect; for arthritis pain CBG has no effect but CBG may be more effective in local administration and can be developed as an external preparation.
TRPV1 is a temperature receptor and key nociceptor [pain receptor]. The literature reports that cannabinoids can activate the TRPV1 channel. Our results indicated that CBG can bind and interact with the TRPV1 protein, and we demonstrated that CBG may be antinociceptive by activating the TRPV1 channel and desensitizing it. [Could this have implications in treating CHS, thought to be a disorder of TRPV1?]
Cannabinoid receptors include CB1R and CB2R, and CB2R agonists have been reported to promote the release of β-endorphin, which then act on the ends of nociceptors and analgesia.
Based on experiments on the efficacy of CBG, the results showed that CBG local administration is more effective than injection. As a result, we speculated that CBG may exert antinociceptive effects by activating CB2R on HaCaT cells to promote the secretion of β-endorphin.
It was shown that activating CB2R increased the release of β-endorphin, which is consistent with previously reported results. Correspondingly, we demonstrated that CBG promoted the release of β-endorphin, and PCR experiments also showed that CBG upregulated the mRNA levels of POMC, which is the precursor of β-endorphin.
Therefore, all of the above results show that CBG may exert antinociceptive effects by activating TRPV1 to desensitize it and activating CB2R to promote β-endorphin release (Fig. 8):
Conclusions
In this study, we demonstrated the antinociceptive activity of CBG in different pain models and elucidated the mechanism by which CBG targets two receptors, TRPV1 and CB2R, to produce antinociceptive effects. CBG may activate the TRPV1 receptor to desensitize it and block the transmission of pain signals; antinociception of CBG may be mediated by stimulation of β-endorphin release from HaCaT cells. In addition, CBG is safe and nontoxic and is promising for development as a topical formulation for pain management.
Read the study at: https://www.sciencedirect.com/science/article/pii/S0753332222015529?via%3Dihub
[Edited for brevity and clarity but not content by RR, other than bracketed comments]