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.
we know that there's evidence of atherosclerosis in familial partial lipid dystrophy called dunigan type without elevated ldl gsd1a glycogen storage disease 1a have hyperlipidemia with no atherosclerosis there's an atherosclerosis escape phenomenon you must have insulin resistance to develop atherosclerosis
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there's a monogenic form of insulin resistance known as dunigan familial lipodystrophy where people do not have elevated levels of LDL but they are insulin resistant and they develop massive atherosclerosis
I don't think clinically meaningful atherosclerosis, except for maybe a few genetic conditions, we can talk about those, you know, familial, you know, like like dislip you know, like um what am I thinking of? FH, familial hyperlipidemia. FH or Dunnigan lipodystrophy, you know, um but that but those people are insulin resistant at I, you know, by default anyway. So, I don't think a lot of cardiovascular disease I don't think there's a significant amount of cardiovascular disease that's clinically meaningful for humans that happens independent of insulin resistance.
envelope of a cell that changes and causes insulin resistance profound insulin resistance these people have light dystrophy they have abs but they have visceral fat because they have insulin resistance due to their monogenic condition they do not have elevated LDL and they have massive aggressive atherosclerosis