The evidence is convergent. Multiple independent sources reach the same conclusion, the underlying mechanism is well-characterized, and even the field's most cautious voices treat it as worth doing.
I think that the research around the byproducts of linolic acid specifically linolic acid leading to 2 Ag and a nide I'm gonna talk about studies with that which are endogenous cannabinoids binding to CB1 so cannaboid one and canono 2 receptors in the brain leading to overeating
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when you eat linoleic acid whether it's a human or a mouse and this has been shown in both mouse and human models a molecule is produced called 2ag which is a cannabinoid and that cannabinoid activates that cb1 receptor
in their studies in mice their studies in c elegans c elegans is a worm you can make worms fat by giving them linoleic acid because of these probably this mechanism of satiety in the human brain
this study dietary linoleic acid elevating endogenous 2h in an animide inducing obesity
And we know that eating more seed oils, at least in mice, tickles that receptor more because endogenous cannabinoids, or I should say, because cannabinoids, 2-AG and anandamide, appear to be overproduced.