Paul Saladino· MD
there's just a ton of evidence that this conversion of linolic acid to these oxy lipins is implicated in the development of all these uh diseases and the thing that controls that d6d activity is PPR Alpha
The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
there's just a ton of evidence that this conversion of linolic acid to these oxy lipins is implicated in the development of all these uh diseases and the thing that controls that d6d activity is PPR Alpha
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when something triggers this enzyme called PP alpha peroxone proliferator alpha it pushes linolic acid the 18 carbon polyant fat found in seed oils down a synthesis pathway that ends up in all of these Ox Lambs so what activates PPA are alpha we've talked about alic acid oxidized linolic acid alpha linolenic acid and other things do as well but those are those are big ones not regular linolic acid doesn't do it but alic acid does so if you end up with a seed oil like canola oil that has a lot of OIC acid plus linolic acid plus ala alpha linolenic acid an omega-3 plus an Omega 6 plus a monounsaturated fat you basically push a lot of things down this pathway linolic acid becomes arachadonic acid through GLA dlaa and then it becomes the Heats and Hodes and all of these Ox lams that I've talked about in the past people like Tucker good rich and these are strongly associated with many many bad diseases in humans heart disease diabetes obesity 5 and 11 heat associated with obesity in humans