What is CBG?
CBG in cannabis was first detected and synthesized by Gaoni and Mechoulam at the Hebrew University of Jerusalem in 1964. Five years later, its psychopharmacological effects were tested at the same university. It was evaluated as non-psychoactive. CBG is formed by the decarboxylation of CBGA.
CBG – Cannabigerol
CBG in cannabis was first detected and synthesized by Gaoni and Mechoulam at the Hebrew University of Jerusalem in 1964 [Mechoulam, 1970]. Five years later, its psychopharmacological effects were tested at the same university. It was evaluated as non-psychoactive [Grunfeld, 1969]. CBG is formed through the decarboxylation of CBGA. This process also produces other yet unidentified by-products, likely belonging to the group of minor cannabinoids [Wang, 2016]. As CBGA is usually mostly converted into other cannabinoid acids (THCA, CBDA, CBCA) before it undergoes decarboxylation, the content of CBG (i.e., CBG + CBGA) in dried cannabis typically does not exceed 1%. However, there are strains with genetic mutations that prevent CBGA from being processed, resulting in higher amounts of this compound and lower levels of THC and CBD [Morales, 2017]. CBG and its derivatives are also found in the South African perennial plant of the family Asteraceae (daisy family), Helichrysum umbraculigerum. The CBGA content in the dried herb of this plant is typically around 0.2% by weight [Izzo, 2009].
Therapeutic Use
CBG shows potential in the treatment of glaucoma [Colosanti, 2009], psoriasis [Wilkinson, 2007], and chronic pain [Petrocellis, 2008]. In cell culture tests, it also exhibited anticancer effects [Ligresti, 2006], for example, on colorectal cancer cells [Borrelli, 2014]. Experimental evidence shows that this compound is a mild deactivator of the serotonin 5-HT1A receptor and a highly effective activator of the norepinephrine α2 receptor [Gascio, 2010] and that CBG deactivates the CB1 receptor at higher concentrations [Navarro 2018]. CBG, like other cannabinoids, can also act on temperature receptors (e.g., TRPA1), which likely plays a role in its analgesic and anti-inflammatory effects [Petrocellis, 2008]. CBG acts as an antioxidant [Izzo, 2009] and also suppresses the production of prostaglandin E2 (a major pro-inflammatory signaling molecule in the body) [Granja, 2012]. In a mouse model of colitis, CBG alleviated symptoms of chronic inflammation [Borrelli, 2013]. CBG was also shown to be highly effective as a neuroprotectant in mouse tests [Valdeolivas, 2014]. In tests on human keratinocyte cultures (skin cells), CBG showed a strong ability to suppress their excessive proliferation [Wilkinson, 2007]. It is also possible that CBG blocks the reuptake of norepinephrine, causing its accumulation at α2 receptors and thereby suppressing natural norepinephrine secretion. This corresponds to the antidepressant activity observed in rat tests [Musty, 2006; p.32.].
Like other cannabinoids, CBG has strong antibacterial effects, including against the feared resistant form of Staphylococcus aureus (MRSA) [Appendino, 2008].
Side Effects
CBG has been observed to significantly reduce the antiemetic (anti-nausea) effects of CBD when administered simultaneously. This may be related to the opposing effects of these cannabinoids on the serotonin 5-HT1A receptor. [Gauson, 2010]. It cannot be ruled out that CBG may similarly affect the efficacy of other drugs acting on serotonin receptors (e.g., SSRI antidepressants), although there is currently no evidence of such interaction.
Interested in cannabinoids and their effects? Read more on our blog about CBD and CBN.