Cannabinoid-induced inhibition of arachidonic acid acylation of membrane lipids leads to the buildup. THC also promotes increased concentrations of arachidonic acid metabolites, which leads to greater susceptibility to opportunistic bacterial pathogens such as Legionella in those already immune-compromised. Arachidonic acid, in addition to being a membrane component, is the biological precursor of the eicosanoids. Ethanolamine, a part of the phosphatidylethanolamine molecule, another cell-membrane component, is available for other cellular activity. And the endogenous ligand anandamide, mentioned previously, is the arachidonoyl amide of ethanolamine, a condensation product of arachidonic acid and ethanolamine.
Nature is indeed parsimonious.
Rather than create one more molecule from scratch, nature took two molecules already involved in the cell's economy and blended them into anandamide, to do whatever it is anandamide does-perhaps functioning indirectly in some manner to modulate brain dopaminergic activity, as several researchers have suggested. The fact that the cannabinoids fix themselves to receptor sites created for anandamide is incidental in the greater scheme of things, although not inconsequential. What has so facilely come to be called cannabinoid receptors should now be relabeled anandamide receptors. The cannabinoids are strictly chemical interlopers, hitching themselves to spaces reserved for the endogenous ligand anandamide. THC binds to anandamide receptors with only moderate affinity.