The Best Way to Utilize Cannabigerol (CBG)

A new era has arrived, folks. We have entered the era of minor cannabinoids. And one of the most promising, making up just 1% of cannabis and hemp plants, is CBG or cannabigerol. 

Much like CBD, CBG is a non-psychoactive cannabinoid that can have profound effects on inflammation and neuroprotection. However, there are some key differences between the two as well.

Read on to learn about CBG, its many mechanisms of action, and why it’s poised to get its own star on the cannabinoid walk of fame. 

CBG's History

Cannabinoids were first isolated from the cannabis plant in the early 1940s by American scientist Robert S. Cahn. His research brought about a wave of research into the many different cannabinoids. 

CBG was first isolated in 1964 in Israel by Raphael Mechoulam and Yehlel Gaoni. They isolated CBG, THC, and CBD using gas chromatography mass spectrometry. CBG was nicknamed the “mother of all cannabinoids” because most of it was converted into other cannabinoids as the plant matured [1]. This is why CBG is found in such little quantities in the mature plant and its optimum extraction window is early in the cannabis or hemp plant’s life cycle. 

How CBG Works

Like many other cannabinoids, CBG acts on the cannabinoid receptors CB1 and CB2 in a complex way that’s not completely understood [2]. For a quick refresher, CB1 and CB2 receptors are a part of the body’s endocannabinoid system. The system is composed of the endogenous cannabinoids, enzymes which act on them, and receptors. 

The CB1 receptors are found in high numbers in the brain, while CB2 receptors are found in immune cells and in a few neurons [3]. Typically, when a cannabinoid binds to these receptors they can activate a number of different cellular responses which can include increased appetite, decreased inflammation, mood changes, and memory changes. More research on CBG is needed to fully elucidate its effect on these downstream functions.

In addition to the endocannabinoid system, CBG is a PPAR-gamma agonist. This particular PPAR transcription factor causes insulin sensitization and enhances glucose metabolism. The PPAR family of transcription factors plays a major regulatory role in energy homeostasis and metabolic function [7]. 

CBG is also a potent agonist of the alpha-2-adrenoreceptor, which may mean that it has utility as an anti-hypertensive, sedative, and pain reliever. So far, all studies have been done in non-human animals but those are coming soon [7]!

CBG’s interaction with TRP receptors, a class of receptor that regulates temperature, may explain how CBG can potentially help with chronic pain, inflammation, and skin health [7].

Finally, CBG is a potent antagonist (blocker) of the 5HT1A serotonin receptor, but the exact effect on serotonin has not been studied in detail as of yet [7]. 

CBG's Potential Benefits

• Neuroprotection [4] 
• Decreased inflammation [4]
• Pain relief 
• Relaxation
• Anticancer [6]
• Antibacterial [4]
• Glaucoma treatment [5]

CBG Dosing

Much like other cannabinoids found on the market, CBG can be consumed in a variety of ways, including oils, gummies, creams, suppositories, and now in troche form too! Just like other cannabinoid dosing, it's best to start low and go slow when trying CBG.

Dosing also depends on a variety of factors including, but not limited, to:

• Body weight
• Body composition
• Liver metabolism
• Reason for using CBG
• Product potency 
• Product delivery method 

Always make sure that your CBG is purity and potency tested before using it!

CBG Safety

CBG has been found to be a well-tolerated molecule. However, taking heroic doses may result in:

• Nausea
• Vomiting
• Diarrhea 

CBG in our Products

CBG works in synergy with CBD, kava, and N-nicotinoyl-GABA in Tro Calm, one of the most novel and most powerful anti-anxiety products on the market. All ingredients are precision dosed and pharmaceutical grade, and Tro Calm was extensively tested before launching in November of 2021.

Let the troche dissolve between your upper cheek and gums. In 15 to 30 minutes, you’ll feel the chill and the calm... so you can carry on!

References

1. Aizpurua-Olaizola, Oier & Soydaner, Umut & Öztürk, Ekin & Schibano, Daniele & Simsir, Yilmaz & Navarro, Patricia & Etxebarria, Nestor & Usobiaga, Aresatz. (2016). Evolution of the Cannabinoid and Terpene Content during the Growth of Cannabis sativa Plants from Different Chemotypes. Journal of Natural Products. 79. 10.1021/acs.jnatprod.5b00949. 
2. Navarro, G., Varani, K., Reyes-Resina, I., Sánchez de Medina, V., Rivas-Santisteban, R., Sánchez-Carnerero Callado, C., Vincenzi, F., Casano, S., Ferreiro-Vera, C., Canela, E. I., Borea, P. A., Nadal, X., & Franco, R. (2018). Cannabigerol Action at Cannabinoid CB1 and CB2 Receptors and at CB1-CB2 Heteroreceptor Complexes. Frontiers in pharmacology, 9, 632. https://doi.org/10.3389/fphar.2018.00632
3. Mackie K. Cannabinoid receptors: where they are and what they do. J Neuroendocrinol. 2008 May;20 Suppl 1:10-4. doi: 10.1111/j.1365-2826.2008.01671.x. PMID: 18426493.
4. Nachnani R, Raup-Konsavage WM, Vrana KE. The Pharmacological Case for Cannabigerol. J Pharmacol Exp Ther. 2021 Feb;376(2):204-212. doi: 10.1124/jpet.120.000340. Epub 2020 Nov 9. PMID: 33168643. 
5. Tomida, I., Pertwee, R. G., & Azuara-Blanco, A. (2004). Cannabinoids and glaucoma. The British journal of ophthalmology, 88(5), 708–713. https://doi.org/10.1136/bjo.2003.032250 
6. Dariš, B., Tancer Verboten, M., Knez, Ž., & Ferk, P. (2019). Cannabinoids in cancer treatment: Therapeutic potential and legislation. Bosnian journal of basic medical sciences, 19(1), 14–23. https://doi.org/10.17305/bjbms.2018.3532 
7. https://cannigma.com/plant/what-is-cbg/