As consumers dig through various Hemp products,  CBG is something relatively newer on the shelves to ponder. "I'm not sure what it does, can you explain this one to me?" a patient recently asked when sending in a bottle of a brand that had 500mg per oz. One thing the GCRC can do is explain that research is still unfolding on the mechanisms, actions, and promises of both CBGa and CBG. What we do know is that is causes endocannabinoid and cannabinoid receptor activity unlike what's been seen with other plant constituents - but in line with the 'major activity' the minor cannabinoids create. 

In this research we examine this study that tells us exactly that. When some cannabinoids are used (THC/CBN for example) they mimic natural endorphins (endocannabinoids like Anandamide) and they utilize the receptor system made for them. This causes two things 1.) A reduced production of the endocannabinoid as the availability of receptor sites diminishes and it's need does as well due to the mimicking action of the plant constituents. 2.) A reduction in receptor site growth as they are created by the body for new endorphins, not so much for what mimics them. 

But, when other cannabinoids are used such as CBG, it spurs action that actually creates endocannabinoids. These newly created endorphins will immediately antagonize the receptors that THC and CBN do. In status quo with all other receptor systems this  builds more receptors for the endogenous ligand THC to bind to (THC) due to the new availability of increased amounts of the minor cannabinoids. CBD has shown the same response but not as intense as CBG.  What does this do for the average patient? They gain a greater efficacy. 

But what about the THC user - does this competition cause them to have less of 'medicated feeling'? No, actually it reduces the THC tolerance as now the ECS is functioning in balance and doesn't over engage the plant constituent trying to replace an endocannabinoid. With the continued use of the minor cannabinoids the efficacy of all constituents increases. "I'm using less THC now" is a common statement of patients that have been introduced the right ratios of constituents that act in this manner. 

For the more scientific crowd: 

Cannabinoid compounds bind and activate cannabinoid CB1 (CB1R) and CB2 (CB2R) receptors, which belong to the superfamily of G-protein-coupled receptors. There are many ways to classify them, but the most used distinguishes between endogenous molecules (endocannabinoids), phytocannabinoids and synthetic cannabinoids. Endocannabinoids and one of the most studied phytocannabinoids, Δ9-tetrahydrocannabinol (Δ9-THC), are agonists with more or less CB1R/CB2R selectivity. Furthermore, synthetic cannabinoids mainly act (as agonists or antagonists) by binding to the orthosteric site of receptors (Mechoulam, 2016). Indeed, there is a limited number of molecules, either synthetic or phytocannabinoids, that behave as allosteric modulators of cannabinoid receptor function.

Anandamide and 2-arachidonoyl glycerol (2-AG) are the two main endocannabinoids, being synthesized from membrane lipids and having an alkyl-amide chemical structure. They are retrograde effectors being produced in the post-synaptic neuron to act in the pre-synaptic neuron where they regulate the release of neurotransmitters (Diana and Marty, 2004).

Phytocannabinoids are phenolic terpenes biosynthesized in nature nearly exclusively in the Cannabis sativa L. plant. In the Cannabis plant, all cannabinoids are biosynthesized in the acid form, mainly Δ9-THCA, CBDA, etc. CBGA is the first molecule formed in the biosynthetic pathway and the substrate of Δ9-tetrahydrocannabinol-synthase and CBD-synthase (Fellermeier and Zenk, 1998). The pharmacologic effects of Cannabis components, traditionally consumed through inhalation, are attributed to the decarboxylated neutral products of above mentioned acids: Δ9-THC, CBD, and CBG.

Synthetic cannabinoids are very different in chemical structure. For instance, they may be indoles like WIN-55,212-2, AM-1241 or JWH-018, or phenolic, phenols lacking the pyrene ring, like CP-55,940 or HU-308. All these compounds have been used in cannabinoid research and have helped to unveil pharmacological aspects of the endocannabinoid system. It should be noted that some of these compounds have recently arrived at the streets sold as legal highs, thus raising Public Health concerns (Adams et al., 2017; Weinstein et al., 2017).

The endocannabinoid system is constituted by the endogenous cannabinoids, the enzymes that produce and degrade them, and by the receptors that mediate their actions. Whereas endocannabinoids consist of molecules with aliphatic structure, AEA and 2-AG, the structure of natural cannabinoids, derived from C. sativa L., is fairly different [see (Lu and Mackie, 2016) and references therein]. Although it is well established that one of the main active components of the plant and one of the few that are psychoactive, namely Δ9-THC, acts via cannabinoid receptors, there is controversy on whether these receptors mediate the action of phytocannabinoids such as CBN, CBD or CBG. As happened the last years for CBD, a new research and revision of the cannabinoid receptor pharmacology must be done with the rest of phytocannabinoids as CBG. A further phenomenon that may be considered to understand the action of molecules from C. sativa L. and its extracts is the fact that cannabinoid receptors may form heteromers, namely CB1–CB2 heteroreceptors, which display particular functional properties (Callén et al., 2012).

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Everyday cannabis science takes another leap and bound - in jumping back two years we find information that many are digging for toady in asking "What does CBG do". 

The answer?  A lot more than most think - and much more than any of us know. 

Please go to the NCBI Publication to read the entire research study - due to copyright law the GCRC will only publish the ABSTRACT: 

 Gemma Navarro, and co.  Front Pharmacol. 2018; 9: 632.
Published online 2018 Jun 21. doi: 10.3389/fphar.2018.00632

Abstract

Cannabigerol (CBG) is one of the major phytocannabinoids present in Cannabis sativa L. that is attracting pharmacological interest because it is non-psychotropic and is abundant in some industrial hemp varieties. The aim of this work was to investigate in parallel the binding properties of CBG to cannabinoid CB1 (CB1R) and CB2 (CB2R) receptors and the effects of the compound on agonist activation of those receptors and of CB1–CB2 heteroreceptor complexes. Using [3H]-CP-55940, CBG competed with low micromolar Ki values the binding to CB1R and CB2R. Homogeneous binding in living cells, which is only technically possible for the CB2R, provided a 152 nM Ki value. Also interesting, CBG competed the binding of [3H]-WIN-55,212-2 to CB2R but not to CB1R (Ki: 2.7 versus >30 μM). The phytocannabinoid modulated signaling mediated by receptors and receptor heteromers even at low concentrations of 0.1–1 μM. cAMP, pERK, β-arrestin recruitment and label-free assays in HEK-293T cells expressing the receptors and treated with endocannabinoids or selective agonists proved that CBG is a partial agonist of CB2R. The action on cells expressing heteromers was similar to that obtained in cells expressing the CB2R. The effect of CBG on CB1R was measurable but the underlying molecular mechanisms remain uncertain. The results indicate that CBG is indeed effective as regulator of endocannabinoid signaling.

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