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Whalatane

02/08/16 2:31 PM

#71629 RE: HDGabor #71625

Gabor Re AMRN guidance .

Have they guided NOT to expect a stop at Interim.
OR
Have they guided to expect a stop or even hinted its "likely "

Please refresh my memory
thx
Kiwi

jessellivermore

02/08/16 3:35 PM

#71634 RE: HDGabor #71625

HDG..

I eventually had to put this poster on ignore, simply because he is unable to understand the the simple truth that the higher LDL-C >170) in JELIS resulted in a much lower CVD event rate than the lower level of LDL-C (<100) in REDUCE-IT..He steadfastly refuses to even consider the impact of that observation on the idea that the CVD event rate is directly related to LDL-C event risk..

As far as the preposterous information that large numbers (>150,000) patients gleaned from various "meta analysis" carry any true scientific information...All of these studies were Cherry picked using pre 2006-2007 studies run by and for the benefit of the statin companies who paid for them and bear sole responsibility for their accuracy...Call me a skeptic.

There has been one study since the 2006-2007 clinical trial reforms that has supported statin claims..The 15 cholesterol lowering drugs which actually increased CVD risk are hardly a testimonial to the idea lower LDL-C has any direct benefit regarding CVD..

This poster keeps introducing such suggestions that lowering the LDL-C in JELIS down to the 100 level would further lower the CVD risk (2.2% annual) down even farther, and this very well could be true. But it ignores the more important fact that unless the EPA/AA ratio is increased to the Japanese levels, a decrease in LDL-C to 100 results in an annual risk of over 5% if the EPA/AA ratio is as low as the R-I levels.

The point being EPA is a much more effective agent in reducing CVD event risk..Restating this: the pre trial levels in these two outcomes trials support the notion that high HDL-C levels with optimal EPA/AA ratios confer more protection than optimal LDL-C levels and low EPA/AA ratios...

":>) JL