Now, since we know that inflammation stems primarily from PUFA metabolites, it would be sensible to propose that may be PUFA is involved in the pathogenesis of depression. Also, given their effects on the entire body, depression would be a systemic disease. This is exactly what a recent study I posted found.
Much of what you say makes sense to me, but I doubt this reasoning a bit. This is one of the only topics I've really tried to study (back in 2012, but nevertheless), and I think this kind of reasoning is only partly true. I was just rereading some log I wrote in 2012. And I was saying something along these lines:
Without inflammatory stimuli much AA stays in the membrane phospholipids. In response to inflammatory stimuli, AA is released from membrane phospholipids by phospholipase A2. So therefore, much AA in the membrane, is not really causing inflammation, but causing excess inflammation when there are already inflammatory stimuli.
Besides that, PGE2 seems to be down regulated in asthma and hair loss for example (maybe also depression). While PGD2 is upregulated. So it is not only about PUFA, but also about what is done with the PUFA, if is it converted to PGD2 or PGE2, seems to make a difference.
So I have this note, in my log, "Which factor cause an increase of intracellular calcium???" I can remember that, the more I read about this stuff (and I have read a LOT of studies back then, because I was desperate to cure my hair loss), the more it all seem to do with an increase of intracellular calcium. Both the release of AA from the membrane (which then can be further metabolized), PGD2 formation (instead of PGE2) and mast cell degranulation.
So here my log stops, because I could just not find out what causes intracellular calcium to increase, and I kind of decided I probably need to do a biology study to understand concepts like this. But now I find that taurine seems to be very effective in preventing intracellular calcium to increase, and this is also proven to help with hair loss
In short my point is, yes PUFA is bad, also because it just get rancid like crazy, but I think for many people it is (almost) impossible to eat so little PUFA so that you can't produce things like PGD2 anymore (and just produce mead acid metabolites). I think limiting PUFA means to I don't know 5 gram a day or something will mostly cause less inflammation where there are inflammatory stimuli, not curing inflammation. To make sure the inflammation stops, I think it is more important, is to make sure that AA is not released from the membrane, and is not converted in PGD2 and other bad guys. This seems to do with preventing intracellular calcium to increase, where taurine seems to help, and probably just things that make sure your cells stay in their healthy restfull state (with potassium and magnesium high, and natrium and calcium low).