For newer folks into the cannabis sector the sheer volume of cannabinoids can be overwhelming, and unless you are going to become a scientist there are only really 6 or 7 you need to be familiar with, learning all 114 would be quite a task. One of those 6 or 7 is CBG (Cannabigerol).
CBG Solves Problems
CBG is one of the least abundant and highest sought after cannabinoids, making its stock extremely valuable.CBG is also non-psychoactive, which can assist the more well known CBD in solving common problems. It’s also receiving growing interest for its pharmacological properties. Like THC and CBD, it is found as cannabigerolic acid (CBGA) within the plant and is decarboxylated to CBG with heat, light and time.
In the study CBG attenuated murine colitis, reduced nitric oxide production in macrophages (effect being modulated by the CB2 receptor) and reduced ROS formation in intestinal epithelial cells. CBG reduced colon weight/colon length ratio, myeloperoxidase activity, and iNOS expression, increased SOD activity and normalized interleukin-1β, interleukin-10 and interferon-γ changes associated to DNBS administration.
The conclusion of the study was that CBG could be considered for clinical experimentation in IBD/IBS patients.
Huntington’s disease (HD) is a fatal genetic disorder that causes the progressive breakdown of nerve cells in the brain. It deteriorates a person’s physical and mental abilities during their prime working years and has no cure.
According to The Mayo Clinic, Huntington’s disease is an inherited disease that causes the progressive breakdown (degeneration) of nerve cells in the brain. Huntington’s disease has a broad impact on a person’s functional abilities and usually results in movement, thinking (cognitive) and psychiatric disorders. Most people with Huntington’s disease develop signs and symptoms in their 30s or 40s. But the disease may emerge earlier or later in life.
According to the study CBG was extremely active as a neuroprotectant in mice intoxicated with 3-nitropropionate (3NP), improving motor deficits and preserving striatal neurons against 3NP toxicity.
The study found significant reduction in the aggregation of mutant huntingtin in the striatal parenchyma in CBG-treated animals. In conclusion, our results open new research avenues for the use of CBG, alone or in combination with other phytocannabinoids or therapies, for the treatment of neurodegenerative diseases such as Huntington’s disease.
A number of cell-based studies have shown that CBG is anti-tumoral. This has been demonstrated by the ability of CBG to inhibit cancer cell growth and induce programmed cell death in human colon cancer cells, and in breast, prostate and stomach cancer cells. In colon cancer, this may be because of anti-inflammatory effects of CBG.
A reduction in cell infiltrates, mainly CD4+ T cells, was observed, and Th1 and Th17 responses were inhibited in the spinal cord of VCE-003-treated mice, accompanied by weaker microglial activation, structural preservation of myelin sheets and reduced axonal damage.
The conclusion of the study was that CBG exhibited the highest growth-inhibitory activity against the cancer cell lines.
Several cannabinoids were tested on mouse bladder contractility in vitro. CBG, THCV, CBD and CBDV.
CBG ranked as the most effective followed by THCV>CBD>CBDV. In depth studies on CBG showed that the effect of this phytocannabinoid on acetylcholine-induced contractions was not affected by CB1 or CB2 receptor antagonists. Additionally, CBG also reduced acetylcholine-induced contractions in the human bladder.
Jokes about cannabis munchies go back decades, but, studies have shown that non-psychoactive cannabinoids like CBG can greatly stimulate appetite, without the psychoactive effect of THC. This can strip away the image of someone passing out on a couch out of their tree with a bowl of cheetos.
The objective of this study was to assess the effects of CBG on food intake and feeding patterns. The appetite-stimulating properties of cannabis are well documented and have been predominantly attributed to the hyperphagic activity of the psychoactive phytocannabinoid.
CBG produced no adverse effects on any parameter in the neuromotor tolerability test battery. In the feeding assay, 120-240 mg/kg CBG more than doubled total food intake and increased the number of meals consumed, and at 240 mg/kg reduced latency to feed. However, the sizes or durations of individual meals were not significantly increased.
There are a lot of people walking around saying cannabis prevents can cure cancer, but those are bold claims. Originally when medical cannabis was given to cancer patients was for things like peace of mind, sleep and appetite stimulation. However, studies do show that in cases like colon cancer CBG is effective in halting progression of the disease.
According to a 2014 study, CBG potently blocks transient receptor potential (TRP) M8 (TRPM8), activates TRPA1, TRPV1 and TRPV2 channels, blocks 5-hydroxytryptamine receptor 1A (5-HT1A) receptors and inhibits the reuptake of endocannabinoids.
CBG inhibited the growth of xenograft tumours as well as chemically induced colon carcinogenesis. CBG hampers colon cancer progression in vivo and selectively inhibits the growth of CRC cells, an effect shared by other TRPM8 antagonists.
THCA, THCV, CBG and CBC have anti-inflammatory properties in various models, with curative applications against a broad array of inflammatory diseases. CBDA, CBG and CBC have potential anti-tumoral properties. THCV and CBG might also be protective in various neurological disorders. Much further research is required to translate a few of the promising findings to clinical trials to prove effectiveness of the substances either as single chemicals or as combinations of phytocannabinoids, in people.