Thread by @holmanm

1/6 In the liver, INSULIN antagonises the ApoB secretion pathway at multiple sites:

- In DIABETES, ApoB secretion is INCREASED, and ApoB clearance is DECREASED

- Changes in ApoB metabolism drive cardiovascular disease in the Diabetic state

What does that tell you ?
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2/6 Isn’t it the case that modulating macrophage pro-inflammatory activity, and improving Insulin sensitivity is KEY in solving the CVD crisis ?

Lipoprotein particle levels and their constituents are extensively altered by insulin, acute inflammation and infection
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3/6 In fact, LOW Cholesterol has been consistently correlated with WORSE outcomes in critically ill patients. Measurements of various lipid parameters in patients with severe sepsis or septic shock indicate that apoB Lipoprotein levels can be very LOW ! Now why might that be?
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4/6 Apolipoprotein B : The association was found in nine studies (n = 1375). We found that COVID-19 patients with LOW ApoB values have a HIGHER risk of developing SEVERE disease (OR = 0.78; 95% CI 0.69 to 0.87; P < 0.001) with mild heterogeneity (I2 = 12%).
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5/6 Now stop being silly by merely trying to lower your cholesterol. Lipoproteins are our friends, provided we don’t oxidise them with sugars and seed oils ! Look after your Lipids and they in turn shall look after you !

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6/6 High time Cardiologists/Docs stopped substituting ApoB for LDL-C in CVD prevention. Lowering LDL-C didn’t lower mortality in CVD patients, and neither will lowering ApoB. This approach is unjustified IMO !