Palmitoylethanolamide (PEA) is a breakthrough in medicine. It is a so called Amide of a long-chain fatty acid: Amides of long-chain fatty acids have numerous actual and potential uses was a topic presented already in 1949 by the chemist EDWARD T. ROE during his presentation at the Meeting of the Philadelphia Section of the American Chemical Society (Jan. 20, 1949).
Now, more than half a century after his lecture we know the numerous and potential uses of PEA; more than 400 scientific articles have been written were PEA has been mentioned and/or explored.
Nobel laureate Professor Rita Levi-Montalcini already demonstrated in 1993 that PEA could inhibit overactive (substance P-stimulated) mast cells. In the paper “Endocannabinoids inhibit release of nerve growth factor by inflammation-activated mast cells” of 2011 more insight is gained on the molecular mechanism behind the peace bringing effects of PEA on inflammatory cells such as the mast cell.
In a series of elegant experiments Cantarella and colleagues (2011) showed that overactive mast cells can be inhibited in their overactivity via PEA, and that this effect can be understood via PEA’s interaction with a Cannabinoid-like receptor, the GPR55 receptor.
PEA however thus has great biological relevant effects, as they clearly found out and we quote:
In synthesis, these data are suggestive for a substantial contribution of NGF to the inflammatory activity of mast cells in the human cell line HMC-1 and that, in particular, it also exerts a potent proliferative effect upon human endothelial cells, the first phase of angiogenesis.
…PEA, effectively inhibit NGF release from mast cells and consequent endothelial cell proliferation, an effect mediated by the orphan receptor GPR55.
In conclusion, we hypothesize that inhibition of the GPR55 receptor might be envisioned as a novel candidate mode for treatment of human inflammatory disorders of various origins, by restraining the angiogenic component.
Source: G. Cantarella et al. Endocannabinoids inhibit release of nerve growth factor by inflammation-activated mast cells. Biochemical Pharmacology 82 (2011) 380–388