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rafunrafun

02/08/16 1:06 PM

#71619 RE: Whalatane #71618

So are you refusing to answer how 15 trials that lowered LDL-C did lower CVD?

marzan

02/08/16 1:12 PM

#71621 RE: Whalatane #71618

I guess 'how low is low enough' still a question anyone couldn't answer. When it comes to LDL and linearly extrapolating like kiwi wants is non sense. And when you extrapolate it to zero, it would definitely make no sense even to kiwi because he knows the body needs some amount of LDL. Kiwi wants to poke holes, the wind will change direction, and hopefully he stops some point and start covering.

zumantu

02/08/16 1:54 PM

#71624 RE: Whalatane #71618

Kiwi, you said;

"Amarin has warned against extrapolating to much from JELIS .... but those who are supposed to be smart enough to know better ...do it anyway."

We both know it is Amarin's responsibility to safeguard / qualify their communication to investors to project against making speculative and or potentially misleading statements.

But contrary to your point, Amarin also makes it clear they designed reduce it using the chort getting a 53% RRR reduction as a model / criteria. Conclusion: So on the BS meter, you get "mostly BS"

If Kiwi conducted duplicate experiments, does Kiwi expect different results between the two experiments?

An illogical conclusion suggesting different results is often used as an example of insanity




HDGabor

02/08/16 1:57 PM

#71625 RE: Whalatane #71618

K-

JL and others here , are being selective regarding Amarin's presenting of truthful and non misleading information.
They choose to accept that which confirms their existing pt of view and ignore that which doesn't.

It's funny from you ... e.g.

1.) 967th event and interim readout (The Co said that the date of the DMC's rec. depends on the process duration only, but you ignore it)
2.) Despite lower LDL level, stronger statin and higher dose of EPA (resulted in same EPA level) you think R-IT's active arm will not have a rate per year similar / near to JELIS's p arm, meanwhile R-IT's p arm will have a lower rate than the required minimum (5.2%).
3.) Acc. to you lower LDL level and stronger statin affect the RRR, meanwhile these are exist in both arms (fyi: 20 vs 10 and 10 vs 5 has the SAME RRR ...)

Amarin has warned against extrapolating to much from JELIS .... but those who are supposed to be smart enough to know better ...do it anyway

Using data from JELIS with caution and do not use are two different things. I (and I think JL also) am using JELIS as indicative source and not as a 'confirmation'.

Best,
G

oneragman

02/08/16 8:54 PM

#71656 RE: Whalatane #71618

Kiwi,
"The cohort that JL likes to cite in JELIS were not on optimal statin therapy. Therefore their LDL and levels of inflammation were not lowered as much as we will see in R-It."
Are you trying to say if JELIS had been on optimal statin therapy, it would have lowered events because the statins would have lowered events more than what happened causing the 1.8g of EPA to be less effective? What about the fact that in JELIS, the population as a whole, because of diet, had approximately 2g of EPA in their blood. You have acknowledged here many times EPA lowers inflammation but keep discounting that when comparing the 2 studies and only focusing on LDL. So basically you are saying max dose statin is more effective than EPA in lowering inflammation. To take a page out of your book, could you post that study so I can check it out. I feel you focus on LDL while basically ignoring the effects of EPA, especially when comparing the 2 trials. I was under the impression that when you add V to a statin, it's like 2+2=5 while you seem to feel its like 2+2=3.