Not everything you put into your mouth makes it into the blood, let alone a target tissue.

I've had this same reservation about it. Theoretically, phosphatidate is digested via PLA2 at the 2nd carbon and then via lysophospholipase @ C1 to yield the FFAs for uptake into enterocytes w/ excretion of the glycerophosphorylcholine. That said, I tried to look up some data on it and they say the lysophospholipase can be absorbed directly itself, but I don't see how w/ the phosphate? And even if it was, you may get regeneration of the phosphatidate but again it's an issue of target specificity and utility. If it's not absorbed like that, it's random due to FFAs alone and there's no real net increase in phosphatidate per se. Some of the studies surmised that perhaps it was that the extracellular PA was distinct from the intracellular pool generated during contraction from PLD, or that metabolism to LPA (which will occur) induces distinct signaling modalities and activates ERK, which can also activate mTOR via TSC1/2 antagonism. That's the only plausible mechanism I could come up with, and it'd also be assuming there's somehow a net increase in plasma PA from its ingestion, which I still see as implausible tbh, but I may not know enough about SPECIFIC rxn mechanism to say with certainty.