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.
More of that LDL more of that APO B is retained in the proteoglycans in the sub-intominal space that LDL is enriched in linoleic acid I know we're going to get to that therefore it's more likely to be oxidized and taken up by the macrophages and made into foam cells made into these fatty streaks
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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if you have some degree of insulin resistance you are at a higher risk of atherosclerosis not because of your elevated apob because of the way those LDL particles those apob particles are retained in the arterial wall
in people who have some degree of insulin resistance they're not doing wound healing well... in people who have some degree of insulin resistance that atherosclerotic plaque begins to develop because that wound healing at the level of the endothelium is not proceeding properly
if you have some degree of insulin resistance you are at a higher risk of atherosclerosis not because of your elevated apob because of the way those LDL particles those apob particles are retained in the arterial wall
More of that LDL more of that APO B is retained in the proteoglycans in the sub-intominal space that LDL is enriched in linoleic acid I know we're going to get to that therefore it's more likely to be oxidized and taken up by the macrophages and made into foam cells made into these fatty streaks