Anandamide prevents cancer by starving cells of food



A previously unknown driver of a cancer-friendly environment was discovered by Sloan Kettering Institute and published in early 2021. Immune cells were reimagined. Now, we better understand how cannabinoids interact with cancer, including recent research that might explain how anandamide prevents it.

A century for cancer research

Dr. Otto Warburg discovered the process that cancer uses to consume glucose a century ago. Essentially, cancer sucks at energy production. Glucose is used up by cancer in an oxygen-starved environment aptly named the Warburg Effect. A century later, in 2021, a well-known mechanism was identified as a key driver of anaerobic glucose metabolism in cancerous cells.

Metabolism in cancer cells is unorthodox and known as anaerobic glycolysis. Not to be discouraged since the discovery in 2021 means that drugs can target and block the process to treat and prevent cancer.

The endocannabinoid system and phytocannabinoids are well fitted for this role. The unique cannabinoids our bodies and cannabis plants produce both regulate the mechanism, stopping cancerous cells from consuming food and producing waste. Although, blocking glucose from doing other things it’s not supposed to do can also starve cancer.

For example, anandamide (AEA) can, under special conditions, prevent skin cancer by regulating glucose radicals in the body. According to research published in 2022, anandamide boosts efficient glucose metabolism by 40% inside cancerous skin cells. Increased metabolic efficiency prevents radicals from binding to other sites in the body, which inhibits cancer formation.

Speaking of radicals, anandamide affects the production reactive oxygen species (ROS). This effect delivers further anticancer properties.

Endocannabinoids for regeneration, phytos for the kill

While low doses of anandamide under specific conditions failed to prevent skin cancer. The right concentrations of AEA can kill cancer cells that have no protection. Researchers, however, failed to elucidate the exact mechanisms that anandamide uses to tame glucose radicals and prevent cancer. Although, a function involved in energy regulation was pinned as a prime suspect.

Finding an answer in a haystack of immuno-oncology

Any investigation identifying the ECS’s role in cancer therapy becomes easily misconstrued. Our dynamic immune systems interact with cancerous cells through multiple targets. Adding to this, different immune cells exist known as don’t eat me signals. Four troublesome immune agents have been identified that protect cancer from attack.

A subtype of T cell is one don’t eat me signal. Although the mechanisms that drive a cancerous environment, (P1K3/AKT and MAPk), also lead to T cell activation. If anandamide or THC truly regulates glucose metabolism, then they can prevent cancer-protecting don’t eat me signals. This would allow the body to more easily kill off cancer as soon as its food supply is shut off.

Havard Med School previously worked with Sloan Kettering on P1K3 regulators in 2018. mRNA vaccines now in development by Havard Med School focus on regulating that process indirectly to treat cancer. The mechanism also lowers the Programmed Cell Death Factor-1 (PD1/PD-L1) axis — one of the four don’t eat me signals.

Increased glucose in the cell. Decreases purvyate production. Changes in glycosylation profile, MAPk are important as are other metabolic mechanisms. More research is needed to better under the mechanism behind glycosylation regulation.

Sources

  1. Xu, K., Yin, N., Peng, M., Stamatiades, E. G., Shyu, A., Li, P., Zhang, X., Do, M. H., Wang, Z., Capistrano, K. J., Chou, C., Levine, A. G., Rudensky, A. Y., & Li, M. O. (2021). Glycolysis fuels phosphoinositide 3-kinase signaling to bolster T cell immunity. Science (New York, N.Y.)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. Cancers14(6), 1419. https://doi.org/10.3390/cancers14061419





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