Double bond location to the side, I'm more concerned about polyunsaturated oil's increased susceptibility to oxidative (ROS) damage. Traveling today so no links, but I buy into the "your body incorporates what you eat". So, eat polyunsaturated FAs, most of it is esterified into trigs and stored - but a good bit also goes into structures like cell membranes (a lipid bilayer) - and if you're unhealthy enough to be building up a fatty liver, oxidative damage seems to be what triggers that into steatosis. I'd somewhat agree on saturated FAs, but there's a lot of genetic variability as to how well we handle them. I've seen a couple of studies in PubMed indicating that stearic FA (primarily in meat) does positive things for serum lipids, some others indicating palmitic FA (coconut) is good, so WTH knows? I would point out that we make our own fats from carbs - and we can only make stearic - but we're omnivores - so there's always been at least some fats in our diets.

Back to bond location. I've read that APOE4, which is associated with a higher risk of AD, blocks serum omega-3 (double bond 3 in from the tail) FAs at the BBB (probably tighter 'tight' inter-epithelial bonds in the capillaries, but also maybe in the choroid plexus which filters blood into CS fluid). Again, WTH knows - both where this is happening or whether it's contributing to that increased risk.

TL;DR: yeah, fraught subject