56 4 GT

[56 4 GT @GTnate56]

@MohammedAlo Why LdL over ApoB?

[56 4 GT @GTnate56]

@NutritionMadeS3 @theproof @Marion436842126

[56 4 GT @GTnate56]

@Aku_700 They need to be rehabilitated with a bat, hot curling iron, scalpel, ants, and a rope.

[56 4 GT @GTnate56]

@markkaplan20 AI is wrong all the time. And one could say both those answers are correct. inflammation and metabolic syndrome are def contributing to ascvd. Kinda like gas on a fire. Maybe even the match that starts the fire depending on what you believe. Need apoB to have plaque though.

[56 4 GT @GTnate56]

@Marion436842126 This is THE question I cannot answer. I certainly think it’s possible. Would I have a clean cac if I didn’t have elevated glucose, I don’t know. I didn’t test my hs-crp back then so I don’t know what that was.

[56 4 GT @GTnate56]

@markkaplan20 I do take zetia

[56 4 GT @GTnate56]

@markkaplan20 My trigs 41 HDL 74. A1c 5.3 I’m not keto nor am I high carb nor am I plant based. I’m not carnivore or low fat either. I’ve been lifting weights for 34 years and eating clean for almost as long. I’m 50. I eat vegetables fruit meat grains legumes and even sweets sometimes

[56 4 GT @GTnate56]

@markkaplan20 @ironDPC

[56 4 GT @GTnate56]

@Marion436842126 A NAFLD metabolic trial doesn’t rebut IMPROVE-IT any more than a letter about apoB’s physiology rebuts Mendelian randomization.

[56 4 GT @GTnate56]

@nicknorwitz @bbenergy21st @Marion436842126 I’m on zetia. A1c is 5.3, HDL is 74, trigs are 41, apoB 61, ldl 74, hs-crp 0.6.

[56 4 GT @GTnate56]

@Marion436842126 @ElisaJ70 Untreated homozygous FH patients — with massively elevated apoB-carrying particles from birth due to LDLR loss-of-function — develop ascvd in childhood & die of MI in their teens or twenties without intervention. This is a natural human experiment. 0 confounders explain it.

[56 4 GT @GTnate56]

@Marion436842126 @ElisaJ70 Where’s the data in the last 12 years supporting this opinion “letter?”

[56 4 GT @GTnate56]

@Marion436842126 @ElisaJ70 A 2012 opinion letter sits far below:
•Mendelian randomization studies showing lifelong low apoB = proportionally lower ASCVD risk
•PCSK9 inhibitor RCTs (FOURIER, ODYSSEY OUTCOMES) where lowering apoB-carrying particles reduced events
•Familial hypercholesterolemia data

[56 4 GT @GTnate56]

@Marion436842126 @ElisaJ70 No serious lipidologist claims apoB is “bad” in a vacuum — the claim is that elevated apoB particle concentration drives atherogenesis through retention in the arterial intima. These aren’t in conflict.

[56 4 GT @GTnate56]

@Marion436842126 @ElisaJ70 Zetia only

[56 4 GT @GTnate56]

@Marion436842126 curious, since you point to insulin resistance and inflammation, what do you think of SGLT2 inhibitors like farxiga, jardiance, etc. they appear to have some cardiac longevity merits per the studies

[56 4 GT @GTnate56]

@Marion436842126 @ElisaJ70 Well my trigs are 41 and HDL was 74….

[56 4 GT @GTnate56]

@ElisaJ70 @Marion436842126 He’s talking about your trig/HDL ratio.

[56 4 GT @GTnate56]

@Marion436842126 My A1c is 5.3, my hs-crp is 0.6, fasting insulin was low normal. Please let me know when the A1c rise is coming.