Paul Saladino· MD
they are carriers for fat soluble vitamins and antioxidants these are the functions of LDL vldl and other apolipoprotein B containing particles they seem like pretty important things to me
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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.
they are carriers for fat soluble vitamins and antioxidants these are the functions of LDL vldl and other apolipoprotein B containing particles they seem like pretty important things to me
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low density lipoprotein receptor deficient mice are protected against lethal endotoxemia and severe gram-negative infections this is of course a study in animal models but when the LDL receptor is deficient in mice they have more LDL in their bloodstream leading to higher levels of LDL and they are protected against lethal endotoxemia which is like a septic type reaction and inflammatory immune Cascade reaction in the mice when they have excess levels of endotoxin this is lipopolysaccharide in your bloodstream coming from the gut when they have gram-negative infections these are bacterial infections which are associated with LPS AKA endotoxin so LDL has an immune role in the human body and there is a strong argument to be made that perhaps in humans as well as animals having more LDL give given that you are insulin sensitive might actually be protective from things like infections
So there so there's two basic types of lipoprotein particles. There's those that contain this thing called apo B that's on uh LDL V bl and kyomicrons and the function of that type of uh B containing apol lipoprotein is to deliver uh lipids to sites that need it whether it's for uh growth or whether it's for repair and when the vascu is being uh I guess affected by chronic injury due to either high blood pressure or chronic inflammation, it needs uh these these building materials to be delivered from the liver or from the from the circulation. But when all the repair is done, then you can you can take that cholesterol that's been deposited in the vascule and you can remove it. And if the net effect is removal is better than deposit, then your arteries never have aththeroscerotic plaques. But if if uh you're depositing it faster than you're removing it, then you accumulate lipids in your blood vessel and that leads to aththeroscerosis.