Paul Saladino· MD
Without an understanding of the underlying metabolic health of an individual, markers like LDL, Lp(a), uric acid, and APOE genotype are essentially meaningless...
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.
Without an understanding of the underlying metabolic health of an individual, markers like LDL, Lp(a), uric acid, and APOE genotype are essentially meaningless...
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.
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it's the insulin resistance that is the atherogenic component rather than the LDL itself
in people who are insulin resistant if you have more LDO you may have more fuel for the fire but it's the insulin resistance that provide that is the total overarching context and I believe it's the insulin resistance that is the spark that burns the wood
the real targets are probably in my opinion insulin resistance first and foremost and then the subsequent increase in the susceptibility of LDL for oxidation and the connected increased cardiovascular risk with LP little a and those are very different targets than ldlc per se
I think that we should be focusing on LP little a which is a much better risk factor oxidized LDL in the RT material wall and most importantly insulin sensitivity
the real targets are probably in my opinion insulin resistance first and foremost and then the subsequent increase in the susceptibility of LDL for oxidation and the connected increased cardiovascular risk with LP level a and those are very different targets than ldlc per se