Recently, medical literature has seen a significant rise in exploratory studies of cannabinoids other than THC and CBD. The cannabis plant contains many compounds that we still have limited knowledge about; it’s a wealth of healing.
Currently, one of the very hot topics is cannabgerol (CBG), a precursor to THC, CBD and CBC (cannabichromene). CBG has played in the background simply because it is present in very miniscule amounts, comprising about 1% of all cannabinoids in the plant, at its most abundant.
Short answer is: this has not been scientifically proven.
Long answer is that we can deduce this by comparing pharmacotherapeutic properties and pharmacodynamics of both CBG and CBD, side by side. When it comes to binding to cannabinoid receptors, neither CBG nor CBD activate CB receptors, but both do interfere with other cannabinoids binding. In this way, CBG and CBD both act as modulators of cannabinoids signaling.
This means that CBG (like CBD) can alter how our own endocannabinoids, such as anandamide, interact with receptors. An interesting, emerging point of study is looking at how cannabinoids relate to non-cannabinoid receptors, including those of serotonin and dopamine.
It has been shown that CBG acts as 5HT1A receptor (serotonin receptor) antagonist, while CBD is an agonist, therefore they could potentially exert different effects on molecular pathways affected by serotonin, such as sleep and breathing during sleep (i.e. sleep apnea). However, these are just speculations since studies exploring this topic are currently lacking.
Since CBG and CBD have similar effects on cannabinoid receptors, could we expect that CBG’s medicinal properties will be very similar to those of CBD?
Studies that are available are pointing to that direction. So far, pre-clinical studies have shown anti-inflammatory and neuroprotective properties of CBG in mouse models of autoimmune disease . Researchers have recently provided evidence that CBG induces a potent anti-inflammatory response in both a mouse model and in vitro, in cells grown in a Petri dish. This immunomodulatory response is characterized by the typical recruitment of anti-inflammatory cell types that reduce all the production of cytokines and chemokines that are collectively known as pro-inflammatory machinery.
Furthermore, the neuroprotective potential of CBG has been shown in the mouse model for Huntington’s disease. This study demonstrated that CBG has a great potential to improve motor deficits and to protect neurons from damage. As importantly, the researchers observed a significant reduction of huntingtin aggregates, which are clusters of a particular protein found in the brain of Huntington’s disease patients.
Additionally, recent evidence has emerged highlighting the anti-cancer potential for CBG. Treatment of colorectal cancer cells with CBG lead to cell death and further prevention of cell growth. For in vivo studies using mice, CBG inhibited growth of transplanted tumors and inhibited colon cancer progression.
With the above evidence presented, is CBG superior to CBD? The evidence is not sufficient to sway in either direction. Perhaps CBG and CBD have the potential to complement each other, working in synergy as potent anti-inflammatory, anti-cancer and neuroprotective phytocannabinoids. It doesn’t appear that they antagonize each other with respect to their interactions with cannabinoids receptors, which is crucial to support that possibility. The work seems to be cut out for the scientific community and it is just a matter of time before we can be more confident about pharmacotherapeutic properties of many different phytocannabinoids.