To Chas and KIWI...
Chas, very good post. Nice to think someone gets it...It is possible in IMO
that later divergences are related to the fact that EPA not only prevents acute events, by actions like effecting platelet adhesiveness, but in repairing damaged areas, and slowing degeneration (aging) it cuts down the incidence of new events in one arm to levels seen in younger people.
KIWI..To accept your notions and whatever Ballantine might think, you would need the CVD risk in the R-I control arm to be much lower than it is. Since all are told the statin levels in R-I are optimal, and the LDL-Cs are under 100; then why is the annual CVD risk in this RI group two and one half times higher than The CVD risk in JELIS where the LDL-Cs are over 170..
There are limited numbers of ways to explain this discrepancy..Either LDL-C and statins are not really very important in reducing CVD..(that would explain why CVD risk is so high in R-I), or EPA levels are a much better indicator of CVD risk regardless of what your LDL-Cs are, or how much statin you are on...And increasing EPA levels are better at reducing CVD risk, than lowering LDL-C...Is irrefutable.
The idea statins would significantly lower ( the already low risk) in JELIS is nonsense.. In R-I the best the statins can do is to cut the CVD risk down to 5.7% or there abouts..The CVD rate in similar patients in JELIS was 2.3% due to higher EPA levels and little or no statins..Why would increasing statins cut the risk lower than 2.3% in JELIS if it could not get them lower than 5% in RI?
Please read my earlier post on the medical professors.
":>) JL
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