Anandamide prevents cancer by starving food cells

A previously unknown driver of a cancer-friendly environment was discovered by the Sloan Kettering Institute and published in early 2021. Immune cells have been reinvented. We now better understand how cannabinoids interact with cancer, including recent research that may explain how anandamide prevents this.

A century for cancer research

dr Otto Warburg discovered the process cancer uses to use up glucose a century ago. Essentially, cancer sucks at energy production. Glucose is consumed by cancer in a low-oxygen environment aptly named the Warburg effect. A century later, in 2021, a known mechanism was identified as a key factor in anaerobic glucose metabolism in cancer cells.

The metabolism in cancer cells is unorthodox and is called anaerobic glycolysis. Don’t be discouraged as the discovery in 2021 means drugs can attack and block the process of treating and preventing cancer.

The endocannabinoid system and phytocannabinoids are well suited for this role. The unique cannabinoids that our bodies and cannabis plants produce both regulate the mechanism and prevent cancer cells from feeding and producing waste. However, preventing glucose from doing other things it’s not supposed to do can also starve cancer.

For example, under certain conditions, anandamide (AEA) can prevent skin cancer by regulating glucose radicals in the body. According to a study published in 2022, anandamide increases efficient glucose metabolism in skin cancer cells by 40%. Increased metabolic efficiency prevents free radicals from binding elsewhere in the body, which inhibits cancer development.

Speaking of radicals, anandamide affects the production of reactive oxygen species (ROS). This effect provides further anti-cancer properties.

Endocannabinoids for regeneration, phytos for killing

While low doses of anandamide failed to prevent skin cancer under certain conditions. The right concentrations of AEA can kill cancer cells that don’t have protection. However, the researchers could not elucidate the exact mechanisms that anandamide uses to tame glucose radicals and prevent cancer. However, a function involved in energy regulation has been pinned as the prime suspect.

Finding an answer in the immuno-oncology haystack

Any research identifying the role of the ECS in cancer therapy is easily misunderstood. Our dynamic immune system interacts with cancer cells through multiple targets. In addition, there are different immune cells known as “don’t eat me” signals. Four troublesome immune agents that protect cancer from attack have been identified.

A subtype of the T cell is a “don’t eat me” signal. Although the mechanisms driving a cancerous environment (P1K3/AKT and MAPk) also result in T cell activation. If anandamide or THC are truly regulating glucose metabolism, then they may prevent cancer-protective “don’t eat me” signals. This would allow the body to kill cancer more easily once its food supply is cut off.

Harvard Med School previously worked with Sloan Kettering on P1K3 regulators in 2018. mRNA vaccines currently being developed by the Havard Med School focus on indirectly regulating this process to treat cancer. The mechanism also lowers the programmed cell death factor 1 (PD1/PD-L1) axis — one of the four signals that don’t eat me.

Increased glucose in the cell. Decreases the production of Purvyat. Changes in glycosylation profile, MAPk are important as well as other metabolic mechanisms. Further research is needed to better understand the mechanism behind glycosylation regulation.

Sources

1. Xu K, Yin N, Peng M, Stamatiades EG, Shyu A, Li P, Zhang X, Do, MH, Wang Z, Capistrano KJ, Chou C ., Levine, AG, Rudensky, AY, & Li, MO (2021). Glycolysis drives phosphoinositide 3-kinase signaling to boost T cell immunity. Science (New York, NY), 371 (6527), 405-410.
2. Sobiepanek A, Milner-Krawczyk M, Musolf P, Starecki T, & Kobiela T (2022). Anandamide-modulated changes in metabolism, glycosylation profile, and migration of metastatic melanoma cells. Cancer, 14(6), 1419. https://doi.org/10.3390/cancers14061419