Cannabis seed, commercially known as hemp seed, is a protein-rich food available in several forms. Anyone can order hemp seed, hemp protein powder, or hemp seed oil from online retailers or most grocery stores. In addition to protein, hemp seed contains Omega-6 and Omega-3 fatty acids, fiber, and a wide variety of minerals, making it a particularly healthy food. While hemp seed has generally been consumed for overall health or muscle building, a 2021 study in the journal Food Science & Nutrition by researchers in China now points to the potential of peptides (small proteins) from hemp seed to act as anticancer agents.

The researchers first prepared hemp peptides (HP) by using enzymes to break down large hemp proteins, then used a filtration system to capture the compounds, which were freeze-dried in preparation for use. The HP treatment was applied to both human liver cancer cells and normal human liver cancer cells. The normal cells were unaffected in any way, but the liver cancer cells showed reduced viability, proliferation, and migration. Apoptosis (programmed cell death) was also only observed in the cancer cells, indicating selective cytotoxicity. The relationship between cell viability of cancer cells (Hep3B), healthy cells (L02), and concentration of HP is shown below.

Interestingly, the mechanisms by which HP caused the above effects overlap with the primary phytocannabinoids tetrahydrocannabinol (THC), cannabidiol (CBD), and cannabigerol (CBG). For example, HP treatment stimulated an increase in reactive oxygen species (ROS), highly reactive molecules that damage structures within cancer cells. Numerous other studies have linked increased ROS generation by phytocannabinoids, mainly CBD, with cancer cell death. These include studies on CBD and breast cancer, CBG and colon cancer, CBD and leukemia, CBD and multiple myeloma, and THC and breast cancer.

Another effect of HP treatment was upregulation of a protein called Bad, which helps initiate apoptosis. Activation of this protein has also been connected with THC inducing apoptosis in leukemia cells.

It would be interesting for further studies to examine whether unprocessed hemp protein exerts anticancer effects in animals following natural digestion. Research into the impact of whole hemp seed on cancer development, with its rich array of essential fatty acids, fibers, and minerals, is also warranted. In the future, comprehensive cannabis therapy may include high doses of phytocannabinoids/terpenoids/flavonoids along with some forms of hemp protein, peptides, or seed meal. Only further research will determine what approaches are most efficacious.

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Before examining combinations of different phytocannabinoids, each isolated compound was tested on established GB cell lines and GB cells derived from surgical biopsies. CBG and THC possessed similar potencies in reducing the viability of these cells, while CBD was about 20% more potent. The results were different when examining glioblastoma stem cells (GSCs), which are undifferentiated cells that contribute to resistance of GB tumors to conventional therapy. In this case, CBD and THC were similar in their viability-reducing potency, while CBG was substantially weaker. CBD was still slightly stronger than THC though, indicating it was the most effective phytocannabinoid at reducing viability in both GB cells and GSCs. Further experiments revealed the viability-lowering effect was likely due to induction of programmed cell death (apoptosis). Interestingly, GSCs were more sensitive to apoptosis induced by all the phytocannabinoids than the differentiated GB cells. In the chart below, U87 and NIB138 are GB cells, and NCH644 and K26 are GSCs.

Caspase-3, a key enzyme involved in apoptosis, was not increased substantially in GB cell lines in response to CBD or CBG, as reflected by the low apoptotic rates shown above. However, combining CBD and CBG massively increased caspase-3 activation. Temozolomide (TMZ), a standard chemotherapeutic agent for GB, also barely increased caspase-3 on its own, but when combined with CBD and CBG, levels of the enzyme were raised tremendously. However, CBG and CBD were more effective on their own than with TMZ in two of the three tested cell lines (U373 and T98), whereas the U87 cell line showed the highest caspase-3 expression when all three compounds were mixed. Therefore, CBG and CBD sometimes worked better on their own, but TMZ was always more effective when combined with phytocannabinoids than on its own.

Researchers also tested different combination ratios of CBD and CBG together to examine potential synergy against GB cells and GSCs. Interestingly, the optimal ratios were essentially reversed depending on the cell type. For GB cells, the optimal ratio reported was 1:4 CBD:CBG, while for GSCs it was 3:1 CBD:CBG. The addition of THC at low concentrations did not significantly enhance the effects of the CBD:CBG combinations, although at higher concentrations appeared to contribute some benefit. Ultimately, researchers stated, “We have demonstrated that THC has little added value in combined-cannabinoid glioblastoma treatment, suggesting that this psychotropic cannabinoid should be replaced with CBG in future clinical studies of glioblastoma therapy.”

Despite these observations, this study only used isolated phytocannabinoids, and the effects in humans using whole-plant cannabis extracts can be quite different. Extrapolating dosing from cell studies to humans is also difficult, but such studies do provide indications for what may work in further animal or human studies. It is too soon to say whether THC could be replaced by CBG for GB treatment, but this possibility is worth exploring, especially in patients who cannot tolerate the intoxicating nature of THC. The promise of using nonintoxicating phytocannabinoids to treat cancer is exciting, as more patients would be able to comply with high doses and more medical professionals would be open to using them.

The post 2021 Study Shows the Potential of CBG to Treat Glioblastoma appeared first on The Cannabis for Cancer Declaration.

A new January 2021 study published in the journal BMC Complementary Medicine and Therapies tested the Echinacea purpurea species along with a whole-plant cannabis extract on lung cancer cells. The roots of Echinacea were extracted with dichloromethane while cannabis flowers were extracted with methanol. The cannabinoid composition of the cannabis product was not clear but appeared to be CBD-rich. Both Echinacea and cannabis were shown to induce programmed cell death (apoptosis) in A549 lung cancer cells through CB2 receptor activation. Furthermore, the downstream effects were also similar, with both extracts leading to accumulation of reactive oxygen species and activation of the caspase-3 enzyme, which is involved in breaking down proteins as part of the apoptosis process.

Both plants also induced cell death in a time- and dose-dependent manner. As concentrations of the extracts were increased and allowed to interact with the lung cancer cells for a longer time, more of those cells died. The following chart demonstrates the reduction in viable cells following cannabis exposure for various timeframes (A = 24 hours, B = 36 hours, C = 48 hours). The next chart shows results for Echinacea.
Reduction of Lung Cancer Cell Viability in Response to Cannabis Extract

Reduction of Lung Cancer Cell Viability in Response to Echinacea Extract

More research is needed to clarify how these effects could translate to humans. For patients who do not respond to cannabis or cannot tolerate it for some reason, using other natural means of stimulating the endocannabinoid system may be appropriate.

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