Peter Attia· MD
these are some of the papers that explain, IMO, the more likely mechanism for hyper apoB in high SFA intake subsets.
Loading…
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.
these are some of the papers that explain, IMO, the more likely mechanism for hyper apoB in high SFA intake subsets.
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
all right uh 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 the same nuclear transcription factors go in and say stop making re we don't want to pull in more cholesterol into this liver that's over synthesizing cholesterol so that's it it's another whole story as you know Peter why we don't necessarily tell people you have to restrict cholesterol in your diet that we're talking about saturated fat here and the absorption of steriles in your gut has nothing to do with the absorption of fatty acids in your gut totally different mechanisms that pull them in
For those with high triglycerides and small, dense LDL particles – a type of cholesterol profile associated with greater heart disease risk – reducing saturated fat intake can help lower ApoB.
Limit saturated fat consumption