Panu on Statins

This is in fact precisely the story of torcetrapib. This drug cost Pfizer over 800 million dollars to develop. Torcetrapib is an inhibitor of CETP - cholesterol ester transfer protein. CETP facilitates the transfer of cholesterol from HLD to VLDL or LDL. Now, if you believe version 3.0 of the lipid hypothesis, there are these things called "good" and "bad" cholesterol. This is cardiologist shorthand for lipoprotein-cholesterol complexes that cause or prevent heart disease. HDL is the good one and we want it to be high, so it can hoover up the cholesterol from arterial plaque (a ridiculous idea that as Malcolm Kendrick pointed out defies physical chemistry - Ornish's "garbage trucks") and shrink them. LDL is the bad one and we want it to be low, as it is constantly fighting to transport cholesterol to the arterial plaque.
Cardiologists and Pfizer actually believe that LDL is trying to kill you and HDL is trying to save you at the same time. They figured, why not throw our pharmacological weight into the fight? If we inhibit CETP, the level of HDL will rise, and the level of LDL will fall. They actually combined torcetrapib with an extant statin (atorvastatin or Lipitor) to really, really get the LDL down as well as the HDL up.
So how did it work? Well, it worked spectacularly. HDL levels soared and LDL levels went down. I mean, we are talking HDL to LDL ratios that epidemiologists and cardiologists would say should reduce the risk of heart attack to zero. There was a glitch, though. Although the HDL and LDL went exactly the way they wanted, the risk of death in the group that got the torcetrapib was 60% higher. The trial was halted early.

I suggest:
1) Avoidance of excess PUFA in the diet that leads to oxidized LDL and possible endothelial damage
2) Avoidance of all the causes of leaky gut that may lead to the suite of inflammatory processes known as the metabolic syndrome - avoid excess PUFA (esp. linoleic acid), wheat, and fructose
3) Plenty of saturated fat intake
4) If your glucoregulation is impaired, reduce carbohydrate consumption to whatever is necessary to minimize glycation and endothelial damage. Minimize glycated hemoglobin (Hemoglobin A1c) to the degree possible
5) Replacement of essential micronutrients that may be deficient on the SAD. Magnesium, sunshine, pastured butter for Vit K2.
Those are my general recommendations for everyone.

http://www.paleonu.com/panu-weblog/2010/7/21/statins-and-the-cholesterol-hypothesis-part-i.html