Why would you want to lower LDL in general when it is oxidised LDL that is partly responsible for arterial endothelial damage?Surely decreasing the underlying mechanism for ‘damaging’ LDL is a more effective strategy ie reducing mitochondrial dysfunction by decreasing insulin resistance ie adopting a LCHF or ketogenic diet.
And is the intimal damage not secondary to factors that damage the endothelial glycocalyx ie diet and shear factors within arteries resulting in damage/repair cycles hence the layered appearance of atheromatous plaques?Surely if it was a ‘cholesterol’ problem veins too would have atheromatous plaques?
My ApoB is in good shape based on substracting HDL-C from total LDL, but not my Lp(a), which my doc tested for recently. Does Lp(a) significantly increase risk independent of ApoB? The European Atherosclerosis Society identified Lp(a) it as a significant risk factor and I've been seeing lots of info about clinical studies for drugs seeking to reduce Lp(a).
Why would you want to lower LDL in general when it is oxidised LDL that is partly responsible for arterial endothelial damage?Surely decreasing the underlying mechanism for ‘damaging’ LDL is a more effective strategy ie reducing mitochondrial dysfunction by decreasing insulin resistance ie adopting a LCHF or ketogenic diet.
And is the intimal damage not secondary to factors that damage the endothelial glycocalyx ie diet and shear factors within arteries resulting in damage/repair cycles hence the layered appearance of atheromatous plaques?Surely if it was a ‘cholesterol’ problem veins too would have atheromatous plaques?
My ApoB is in good shape based on substracting HDL-C from total LDL, but not my Lp(a), which my doc tested for recently. Does Lp(a) significantly increase risk independent of ApoB? The European Atherosclerosis Society identified Lp(a) it as a significant risk factor and I've been seeing lots of info about clinical studies for drugs seeking to reduce Lp(a).