IMHO, the CoQ10 "article" is nonsense.

There is reasonable evidence that higher doses of statins arrest plaque development and for plaque regression to occur somewhere after a 40-50% reduction in cholesterol. There are numerous studies out now that have measured this effect via intravascular ultrasonography (don't know about the US, but in Australia, this is still only a research tool). The hypothesis is that regression of atherosclerotic plaques would substantially reduce risk of cardiac events though this is not entirely clear. It has not been very long that there have been medications capable of reducing lipids to this degree. The following is a rather good commentary on the ASTEROID trial:

http://www.lipidsonline.org/commenta...entary_055.pdf

Certainly, there is plenty of evidence that the lower the LDL, the lower the cardiovascular risk with no real indication of there being a plateau limit (which is the reason why lipid targets keep dropping down).

There are no medications that are particularly good at raising HDL ("good" cholesterol). Statins can lead to very minor increases though atorvastatin is known to decrease both HDL and LDL. Gemfibrozil and nicotinic acid both increase HDL (and lower triglycerides) to a larger degree but both medications have problems with side-effects.

Aerobic exercise, cessation of smoking and mild alcohol consumption is associated with mild elevations of HDL. The following is a good guide on HDL (note: Australian/International units):

http://www.australianprescriber.com/...e/17/4/99/102/

Regards.