chas123...
Excellent post I agree with almost everything you say except two points...
The first is I believe the effects of EPA to repair the damage to the cardio-vascular elements caused by CVD are accomplished over short periods of time..Some like the effect on platelet aggregation are almost instantaneous , even the re arrangement of unstable plaques into stable plaques takes weeks and not years..EPA can not correct all forms of damage including dysfunctional valves, or dysfunctional left ventricles..EPA probably can and does decrease the extent of ischemic damage in the heart or in the brain. EPA can also probably head off events..by moderating inflammation (same as aspirin) but these effects are present shortly after taking the medication.
The second is the statin issue. The first case being JELIS where the LDL-Cs were relatively high, (>150mg/dl) and the statin doses were low..The JELIS skeptics point to this observation and say.."You could have similar risk reductions if you increased the statin doses". Well that is one way to look at it, but that is ignoring the fact these Japanese patients with their higher EPA blood levels had lower pre-trial CVD risk and lower risk in the P arm on these low doses of statins and higher LDL-C levels, than westerners matched for age and gender, who were fully statinized and had lower LDL-C levels than the Japs. The lower CVD risk was clearly due to the higher EPA levels and were low despite higher LDL-C levels..In R-I we see high CVD risk in patients taking high doses of statins despite the LDL-Cs which are under 100 mg?dl..The problem is they do not have the high EPA levels of the Japanese..
So I ask all of you If you can have low risk of CVD with high LDL-C and low statin doses, if your EPA levels are high...And you could have can be at high risk with low LDL-C and high statin doses if your EPA are low..If you could only chose one which would rather have high EPA levels...or Low LDL-C/high statin levels
":>) JL
AI
Market Data 
Markets 
