There are mechanisms by which omega 6 fatty acids might be inflammatory, and an association with the modern diet of omega 6 fatty acids also came with increases in inflammation... when it comes down to it, it's just as easy to make linoleic acid look like a dietary villain as it is to make saturated fat look bad. And maybe just as warranted.
There are some studies showing that extreme avoidance of omega fatty acids can be anti-inflammatory, but this is at a level of avoidance that it's very hard to achieve, especially on a high fat diet, we're talking taking barely enough to avoid essential fatty acid deficiencies. Inflammation happens for a reason, and it's not simply that the body had enough materials to drive the inflammatory process.
One study I was looking at the other day gave rats endotoxin to initiate inflammation. This illustrates what I'm talking about, they fed hydrogenated coconut oil as the fat source to deny the animals enough omega 6 to have a normal reaction, and endotoxin resulted in less inflammation. Those endotoxins signal the body that there are pathogenic bacteria present, this is what the immune response/inflammation are intended to protect against.
On the other hand, I think whatever contributes to donuts, pizza, and potato chips also contributes to modern diseases. Walnuts might be a wonderful food, but if they make me more likely to eat high-sugar ice cream, that can be a problem.
Arachidonic acid and docosahexaenoic acid supplemented to an essential fatty acid-deficient diet alters the response to endotoxin in rats.
Ling PR1, Malkan A, Le HD, Puder M, Bistrian BR.
This study examined fatty acid profiles, triene-tetraene ratios (20:3n9/20:4n6), and nutritional and inflammatory markers in rats fed an essential fatty acid-deficient (EFAD) diet provided as 2% hydrogenated coconut oil (HCO) alone for 2 weeks or with 1.3 mg of arachidonic acid (AA) and 3.3 mg of docosahexaenoic acid (DHA) (AA + DHA) added to achieve 2% fat. Healthy controls were fed an AIN 93M diet (AIN) with 2% soybean oil. The HCO and AA + DHA diets led to significant reductions of linoleic acid, α-linolenic acid, and AA (20:4n6) and increases in Mead acid (20:3n9) in plasma and liver compared with the AIN diet; but the triene-tetraene levels remained well within normal. However, levels of 20:3n9 and 20:4n6 were lower in liver phospholipids in the AA + DHA than in HCO group, suggesting reduced elongation and desaturation in ω-9 and -6 pathways. The AA + DHA group also had significantly lower levels of 18:1n9 and 16:1n7 as well as 18:1n9/18:0 and 16:1n7/16:0 than the HCO group, suggesting inhibition of stearyl-Co A desaturase-1 activity. In response to lipopolysaccharide, the levels of tumor necrosis factor and interleukin-6 were significantly lower with HCO, reflecting reduced inflammation. The AA + DHA group had higher levels of IL-6 and C-reactive protein than the HCO group but significantly lower than the AIN group. However, in response to endotoxin, interleukin-6 was higher with AA + DHA than with AIN. Feeding an EFAD diet reduces baseline inflammation and inflammatory response to endotoxin long before the development of EFAD, and added AA + DHA modifies this response.
Controls ate 2 percent soybean oil, if you manage to get your omega 6 intake that low while eating a high fat diet, you are working very hard to do so.
I think intervention studies might be a problem for this stuff. I've seen studies from the sixties where body fat was maybe 4 percent linoleic acid. And more recent studies where human body fat was more like 25 percent linoleic acid. You could see that really interfering with finding out whether getting linoleic acid levels right down there would benefit people with inflammatory disease, the figure I've seen put out for body fat half life for people at a stable body weight is around 600 days.