This very interesting short article regards the evolving problems with the simple HDL/LDL conception of coronary disease:
"Lilly’s evacetrapib did just you would want a CETP inhibitor, or any lipid-targeting cardiovascular drug, to do. It raised HDL by 130% compared to placebo, and lowered LDL by 35%. But the cardiovascular outcomes (MI, angina, stroke, and so on) were absolutely identical between the treatment group and the placebo group. At one point, if you’d asked cardiologists to predict the effects of a compound that affected cholesterol levels in this way, you’d have gotten some pretty enthusiastic guesses. But not now."
I found this comment to be much better, and more interesting, than the original article:
>The other side of the third possibility is that LDL and HDL levels are indicators of some underlying process, and not causative at all. So CETP inhibitors might just be changing the indicator while doing nothing to the actual cause of the heart disease, while statins are doing something to the underlying cause, which in turn changes cholesterol levels. IE the old “correlation is not causation” coming to bite us yet again.
"Lilly’s evacetrapib did just you would want a CETP inhibitor, or any lipid-targeting cardiovascular drug, to do. It raised HDL by 130% compared to placebo, and lowered LDL by 35%. But the cardiovascular outcomes (MI, angina, stroke, and so on) were absolutely identical between the treatment group and the placebo group. At one point, if you’d asked cardiologists to predict the effects of a compound that affected cholesterol levels in this way, you’d have gotten some pretty enthusiastic guesses. But not now."