While they were able to isolate CBG from some samples of hashish, the full importance of CBG in cannabis chemistry wouldn’t be understood for another decade. Before he passed, Dr. Mechoulam created multiple derivatives of CBG which showed anti-inflammatory, pain relieving, and obesity preventing properties in rodents. In 1975, Yukihiro Shoyama led a team of researchers who were the first to show the biosynthesis of cannabinoid acids, including how cannabigerolic acid (CBGa) is formed and how it converts into other cannabinoids, like CBG.

  For many years it was believed that CBG was exclusively produced by cannabis, but recent research definitively confirmed it is also produced by the wooly umbrella plant, which produces the largest number of cannabinoids found anywhere other than cannabis. This discovery gives cannabis companies interested in CBG an additional source they can extract from. While much is still unknown about cannabis biochemistry and we are constantly learning more, we do have a clearer picture of how CBG and other cannabinoids get made than in 1975.

Though there are a few earlier steps in the conversion process (as shown in Figure 4), most sources online focus on olivetolic acid as the starting chemical. When olivetolic acid combines with geranyl diphosphate, CBGa is formed, which then combines with various synthases to create CBG, THCa, CBDa, and CBCa (which further convert into THC, CBD, and CBC). This is why many researchers have referred to CBGa, and in some cases, CBG, as the “mother of all cannabinoids” or the “stem cell” cannabinoid.

There is some mixed opinion on if CBG itself can convert into THC, CBD, and CBC, or if just CBGa. Some of the most current research on CBG, contains a flowchart showing the biochemical pathways that can be taken, and on that chart (Figure 4 above), CBG is clearly a dead-end. That seems to indicate that once CBGa becomes CBG it will remain in a somewhat stable form (as stable as THC or CBD at least, which are both known to break down into other cannabinoids).  A few years ago I interviewed Seth Crawford, one of the founders of Oregon CBD, who told me about their CBG breeding efforts.

“We developed the first pure CBG Type IV line,” said Crawford, noting “I know GW developed those years back, but they are held proprietorially. We are a seed farm and sell seeds to farmers.” For anyone not sure what he meant by a “Type IV,” that is a way to describe cannabis cultivars by their chemotype rather than indica or sativa. The first Type IV chemotypes were identified in 1987, but it still has not seen widespread use, likely because so few plants exist. “Our ratio is 100-1 CBG to THC, Crawford boasted, adding “Some individual varieties can go over 300-1.

” Since I spoke to Crawford, many other breeders have begun to breed for CBG, and there are several CBG-rich cultivars available.  Since CBGa becomes more than just CBG, leaving only trace amounts of CBG in most plants, you might be wondering how people were ever able to breed CBG-rich plants. In 2005, Etienne de Meijer followed up on his previous research on cannabis genetics, aiming to “clarify the genetic mechanism that is responsible for the accumulation of cannabigerol (CBG) in certain phenotypes of Cannabis.

” They found a genetic mutation in certain cultivars of European hemp that caused dramatically increased CBG production, from about 10% of the “cannabinoid fraction” to up to 90%. Now, thanks to years of breeding those CBG-rich lines, we have stabilized CBG cultivars and are seeing more and more CBG products every week. In 2008, GW Pharmaceuticals applied for, and eventually received US and EU patents on CBG in the manufacture of medications to treat “diseases and conditions benefiting from concurrent agonism of the CBi [sic] and the CB2 cannabinoid receptors.

” The now withdrawn or abandoned patents listed examples of those diseases, including: “pain, neurodegenerative disease, ischemic disease, brain injury or damage, acquired brain injury, age related inflammatory or autoimmune disease, cachexia, nausea and vomiting, glaucoma, movement disorders, rheumatoid arthritis, asthma, allergy, psoriasis, Crohn’s disease, systemic lupus erythematosus, diabetes, cancer, osteoporosis, renal ischemia and nephritis.” Aside from GW’s research, several studies over the past decade or so have substantiated CBG’s benefits for a range of medical conditions in cats and rodents.

We’ve known since 1984 that CBG has benefits to animals suffering from glaucoma (specifically cats), lowering intraocular pressure like THC without the feeling of being high. A 2009 study followed up on that research and showed CBG and THC had notable benefits to both cats and rats, finding “cannabigerol and related cannabinoids may have therapeutic potential for the treatment of glaucoma.” Aside from glaucoma, CBG has also shown multiple mechanisms to treat the inflammation that leads to inflammatory bowel disease.

Those anti-inflammatory effects are not limited to the bowels and a 2012 study noted “CBD and CBG also have analgesic and antiinflammatory effects.” Perhaps one of the most unique properties of CBG is that it has been shown to aid “neuronal regeneration” in recovery after spinal cord injuries. One potential downside could be nausea, where it has been suggested that “Interactions between moderate doses of CBG and CBD may oppose one another at the 5-HT(1A) receptor in the regulation of nausea and vomiting.

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