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.
the um saturated F and some people too also turn on the enzymes that induce cholesterol synthesis so now if the liver starts overproducing cholesterol then the lipid pool is out of whack the same nuclear transcription factors go in and say stop making your retiv we don't want to pull in more cholesterol into this liver that's over synthesizing cholesterol
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Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
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so in many many people exposure to saturated fat the nuclear transcription factors realize oh my God the fatty liver uh fatty acid toxicity is going to occur to this liver we have to uh take our defensive mechanisms on that so what they first thing they do is say my God we don't want more lipids being pulled into the liver by these LDL receptors so the nuclear transcription factors go into your DNA and say stop making these LDL receptors stop sending out the signal that will be translated into an LDL receptor so of course if you eat saturated fat and your liver stops expressing LDL receptors your apob is going to go through the roof
the um saturated F and some people too also turn on the enzymes that induce cholesterol synthesis so now if the liver starts over producing cholesterol then the lipid pool is out of whack
I was aware of the importance for, you know, of of fat, particularly like, you know, a certain amount of saturated fat, which is known to increase endogenous cholesterol production.