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Tuesday, 03/31/2020 8:07:33 PM

Tuesday, March 31, 2020 8:07:33 PM

Post# of 426441
I'm trying to just forget about this, but the more I try to ignore it the more ridiculous I think it is. In addition to all the other faults of the Mori study (small sample, no females, low TGs, etc.), wasn't it also just 1.8g of EPA? In that instance, if EPA increased LDL, but was statistically insignificant, couldn't you reasonably conclude that raising the dose to 4g would actually produce a significant increase in LDL?

Or to look at this another way...let's pretend raising LDL was a good thing and Amarin had a patent for EPA to raise LDL. In this instance, the generics would be arguing that Mori proved it was obvious that EPA would also raise LDL just like DHA did, even though it wasn't statistically significant (especially
at a higher dose). This seems like the more convincing argument. Using Du's reasoning then, Mori could pretty much be clear and convincing either way. In the real (non-Du) world, we call this inconclusive, or hypothesis generating at best.

I have to stop now before I lose my mind.
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