What is CBG?
Cannabigerol (CBG) is a major cannabinoid, typically found in abundance in low THC high CBD varieties of cannabis, such as industrial hemp. It’s referred to as the parent cannabinoid, because other cannabinoids are derived from it.
CBG has been found to be non-psychoactive (1), even despite its ability to bind cannabinoid receptors 1 and 2 which may allow for direct modulation of the endocannabinoid system (2).
However, the activity at these receptors is relatively weak when compared to THC which may explain its lack of psychoactive effect.
Instead, CBG has been shown to be one of the most effective inhibitors of endocannabinoid reuptake (Anandamide), which may mean its effects on the endocannabinoid system are in fact indirect (3).
One such effect can be seen with relation to appetite stimulation.
A cannabinoid extract rich in CBG (with no THC) given at high doses (8400 and 16800mg equivalent for a 70g human) has been found to stimulate appetite in rats (4), possibly due to the indirect stimulation of cannabinoid receptors, which are involved in feeding behavior.
Lower doses (12 - 1232mg human equivalent) of pure CBG have been found to have no effect on appetite in rats (5), so dose is an important factor in seeing this effect.
CBG may therefore be useful for loss of appetite and cachexia in chronic illness, although doses used to demonstrate this effect in rats may be unrealistic for humans. Clinical studies are needed to clarify this.
CBG interacts with specific targets that are involved in carcinogenesis in colon cancer; the transient receptor potential channels (TRP).
CBG was shown to initiate cell death and reduce cell growth of colorectal cancer cells. In mice, CBG reduced the growth of tumours and colon carcinogenesis, demonstrating an inhibition of colon cancer progression (6).
CBG’s interaction with TRP channels may also implicate its utility in inflammation.
Inflammation is one of the driving forces of neurodegeneration in huntington's disease. CBG was shown to reduce proinflammatory markers, and immune cell activation in mice with huntingtons, preserving their neurons and motor activity (7). CBG may be a neuroprotectant in this case.
CBG has also been shown to reduce inflammation in mice with colitis, a form of inflammatory bowel disease. Other markers of colitis were inhibited by CBG, as well as colon measurements related to the disease (8). The inhibitory effect of CBG demonstrated here on colitis will be interesting to see clinically verified.
Interaction with TRP channels also implicates CBG in the management of pain (9). Although further studies are needed to clarify its magnitude of effect.
Unlike CBD, CBG is an antagonist of the 5HT1a serotonin receptor, which is involved in mood regulation as well as nausea and vomiting. Theoretically, the effects of CBG should be antagonistic to that of CBD with regards to nausea and vomiting.
In rats and shrews, CBG was shown to reverse the anti-vomiting effects of CBD, and also reversed anti-nausea effects (10). Therefore, the interaction between CBD and CBG may oppose one another with relation to nausea and vomiting.
Theoretically, the same could be true for the antidepressant effects of CBD, since these are largely a result of 5HT1a activation, whereas CBG antagonises this receptor. In line with this, CBG was found to exhibit no antidepressant effect in mice (11). However another study shows it did exhibit antidepressant activity (12). This difference may be due to the presence of other cannabinoids in the extract of the latter study.
Early studies of cannabinoids highlight CBG as a more potent GABA reuptake inhibitor than both CBD and THC (13), which may be efficacious for muscle relaxation, sleep and mood regulation.
CBG also displays activity as an antibacterial, and showed potent activity against methicillin (antibiotic) resistant Staphylococcus aureus (MRSA) strains of bacteria (14).