Its a FACT, LDL cholesterol particles sticks to the walls of the arteries causing blockages. That cannot be disputed. This is most certain in those with a high LDL particle number. Throw high tryglycerides into the mix and you are asking for serious trouble if not addressed.
Having some sort of gene mutation is very rare and not part of the normal cholesterol risk calculus. Some of us naturally and genetically produce too much LDL cholesterol and thats where statins can be very beneficial. Some people can barely diet and have stellar lipid numbers while some can diet like a competitive bodybuilder one month before the Olympia and still have high LDL numbers.
'familial hypercholesterolemia' is THE genetic mutation which creates a higher level of LDL concentration. People with fH have very high levels of LDL-c. Yet, many with fH suffer no CVD at all,..none, nada. Hence the reality that LDL-c levels have nothing to do with CVD.
LDL-p becomes a different issue , and has a small relevance to CVD, and only when severe oxidation is taking place, (which can be negated through high dose vit e )but still, however, this is almost negligible when put next to TG, systemic inflammation and clotting abnormalities.
LDL is found to be deposited in the thrombus in the lining of the intima in arterial plaque, yet, the percentage by which the LDL is deposited has no bearing on the level of LDL-c or -p circulating. ( The LDL in the plaque deposits dont correlate to high LDL-c or -P)
Hence why heart attacks through infarction is seen with patients with low, medium and high LDL-c and -P numbers
The other problem is that the majority of stain medicines have little or no effect on LDL-p (which is only mildly correlated to cvd), and no effect at all on Lp(a) which is a better risk factor in the relms of lipid issues than LDL-p is.
The actual reason why statins do have a positive effect on CVD is nothing to do with the ldl-c lowering properties (which are pointless), but everything to do with the mechanism by which they promote anti inflammation in the endothelial lining of the coronary artery wall.
Its actually just damn good luck they they (statins) exhibit these properties. Otherwise, theyd be beyond pointless.
The same results for FMD and correction of endothelial dysfunction can be created by using ACE inhibitors and folate.
If youd like any info on this CVD, feel free to pm me, im up to 328 clinical trials read now in the last 13 years involving CVD, plus can put u in touch with the cardiologists who arent 'statin whisperers'