Paul Saladino· MD
there's also things like polyunsaturated fatty acids which can also bring down your LDL through a myriad of different mechanisms but they are also preferentially quarantined in the pathway of ketogenesis
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there's also things like polyunsaturated fatty acids which can also bring down your LDL through a myriad of different mechanisms but they are also preferentially quarantined in the pathway of ketogenesis
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how much does having high levels of polyunsaturated fatty acids actually reduce reduce the amount of ldl particles because quite literally they're just getting removed more by scavenger receptors because they're getting modified faster
for one for example there is a uh higher ketogenesis inducing effect of pufas so there's more that gets shuttled towards the ketogenesis pathway if and and if so that would be in opposition of the triglyceride assembly and therefore vldl secreting pathway and therefore succeeding LDL if that's if that is one path there's also a greater um Siobhan found this paper and we ended up looking it up in a couple other places but that basically a greater degree of uh we'll call it manufactur bias there's a there's a higher problematic creation of lipoproteins in that they can sometimes get shuttled and this happens in the ER if I'm not mistaken but I'd have to look that up but basically there's more manufactured bias that happens in that case where there's less that's going to get secreted for that reason but the one that I'm especially interested in is how much of those that do get secreted when the monolayer has more um polyunsaturated fat is more susceptible to oxidation in other words the lipoprotein entirely is more likely to get oxidized in circulation now I'm not saying that's necessarily good or bad but I will say with a lot of confidence it does mean it's going to get removed sooner by scavenger receptors that's literally what the scavenger receptors are waiting around for is if they um if they connect with more oxidized LDL particles they're going to get removed from circulation sooner than the typical two to four day um uh persistence that you typically would see with an LDL particle right and then there's the hatle model which I'm not sure if that was the one you were talking about earlier but the hatle model I think came out last year or this year but they were describing why it is that perhaps for the membrane fluid fluidity maintenancing that there's more uptake of lipoproteins in order to compens for this uh abundance of Pua and actually of the models that sounds the most concerning their model sounds the worst in other words your your body's uh creating a compensatory effect of having to take up more lipoproteins in order to fix an issue of there being too much of an abundance of a particular fatty acid right um so they those are just the ones I could think oh and I'm sorry let me throw in one more which is that there is a higher expression of ldo receptors with a greater degree of Pua that one I I'd want to see a little bit more that would convince me of it but that one um at the time that I was researching it wasn't as strong I'd have to take another look at it again the point is there's a big spectrum of different things for which Pua can have an impact on your LDL