JL - Thanks for the kind words. Your post gave me some things to think about, as they often do.
You make some good points about the likely speed with which various V benefits influence event rate. Slow modes of action (more than a few months) would reduce at least slightly how much RI efficacy is implied by the JELIS results (at least for initial IA (interim analysis), not so much at final). I don't have the medical knowledge to judge, but CHERRY (a 6 month trial) seemed to me to indicates plaque stabilization is at least well under way within a few months. I'm encouraged to hear you say you think it may be as little as several weeks. I had also looked at arm separation on various event rate graphs. When you're looking for it, it is easy to see, or imagine you see, changes in the rate of arm separation, and the case can be made for those occurring as much as a year or more after inception of treatment. But, I consider those uncertain indications, within the margin of error due to random statistical effects, which can be substantial. There is no doubt there are multiple modes of action with varying speeds, but we don't have detailed info about their relative strengths and speeds.
I have tried to stay conservative in my assumptions. Even using assumptions I consider conservative, and seeking ways to challenge the bullish thesis, it's hard not to arrive at expectations of very strong RI performance.
It may or may not be that stronger statins for JELIS would have lowered CVD risk more, and if they did, you've convinced me that it may well have been more due to reduced inflammation than reduced LDL. And, if a dose of something was to be increased for JELIS, your posts have made me wonder if more EPA would have been the better choice, even on top of the high background levels. Certainly fewer side effects.
I suppose EPA studies are likely to continue for many years. Seems like one of them ought to evaluate combinations of more EPA and less statin (if any).
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