Another thread reminded me of one of my favourites, the endocannabinoid excess theory. Setting aside type I which is basically the munchies.
Type II is suppposed to be caused by an excess of omega 6 fatty acids in the diet. They fed mice a high fat diet with either 1 percent omega 6 linoleic acid or 8 percent. The 8 percent mice got fat, the 1 percent mice did not.
They got curious about how this related to other macronutrient ratios. They tried medium fat and very low fat at 8 and 1 percent linoleic acid--both of these were fattening at 8 percent but not at 1 percent. So that's interesting, because a diet with 8 percent linoleic acid as pretty much the only fat source is still a very low fat diet. (I believe the 1 percent linoleic was still an 8 percent fat diet, since otherwise the two wouldn't be properly comparable, I'll check after).
Endocannabinoids are lipid molecules, various fatty acids are used to synthesize various endocannabinoids, linoleic acid is one of these fatty acids.
There's an endocannabinoid drug that was trialed on obesity, they backed off because one of its effects is depression. And depression certainly does result, sometimes, in a decrease in appetite. Maybe this belongs in the "self-medication through food" basket, as well. But maybe the mice were perfectly happy at 1 percent linoleic acid, there's a difference between endocannabinoid blockade and greater sensitivity that might occur if your normal production of endocannabinoid is just a little lower.
Full study. I checked, and they replaced the excess linoleic acid with olive and coconut oils. The diets did contain sucrose.
One thing that bothers me with these studies is that they did nothing to look for a threshold. Saturation of this effect could occur at way below 8 percent linoleic acid. What happens at 4 percent? 2?
The actual endocannabinoids involved require desaturation of the linoleic acid to arachidonic acid. 1 percent fish oil (or was it dha?) anyways a fairly small amount protected against the effect of linoleic acid, desaturase enzymes that produce dha from alpha linolenic acid also produce arachidonic acid from linoleic acid, preformed dha downregulates the enzymes involved. That throws up the question of the effect of preformed arachidonic acid, but since the prediction there is that an all meat diet should be fattening and it doesn't seem to be, I don't see much point in going too far down that path--although I wouldn't be that shocked if in a mixed diet with sugar and starch etc. arachidonic acid from meat did play a role.