Replies to post #350855 on Amarin Corp Plc (AMRN)

[lettruthringout]

I did notice the mention of increased inflammation

You are buying into language that Nissen undoubtedly wanted in the article. What it really says is "In conclusion, we show that chronic oral administration of mineral oil in a mouse model with human-like lipoprotein metabolism caused an increase in intestinal permeability, potentially leading to pro-inflammatory effects"

"Potentially leading to" does not mean there was increased inflammation. On the other hand there were statistically significant reductions in triglyceride levels and cholesterol concentrations with mineral oil. Not potential reductions but statistically significant reductions. Maybe REDUCE-IT results would have been even more significant with a corn oil placebo.

Cholesterol concentrations were significantly lower in the 30 µL mineral oil group than in the 30 µL corn oil group at the four post-baseline time points (mean [SD], mmol/L – 4 weeks: 14.0 [3.4] versus 16.6 [2.4], p = 0.02; 8 weeks: 12.3 [2.9] versus 15.3 [3.5], p = 0.02; 12 weeks: 11.6 [2.8] versus 15.1 [3.7], p < 0.01; 16 weeks: 10.6 [2.5] versus 14.1 [3.4], p < 0.01) (Figure 3A).

Mean triglyceride concentrations were statistically significantly lower in the 30 µL mineral oil group than in the 30 µL corn oil group at 8, 12, and 16 weeks (mean [SD], mmol/L – 8 weeks: 3.5 [1.2] versus 4.7 [1.6], p = 0.03; 12 weeks: 3.1 [1.0] versus 4.8 [1.8], p < 0.01; 16 weeks: 3.2 [1.1] versus 4.6 [2.0], p = 0.02), and were significantly lower in the 15 µL mineral oil group than in the 15 µL corn oil group at 8 and 12 weeks (mean [SD], mmol/L – 8 weeks: 4.6 [1.0] versus 6.1 [1.6], p < 0.01; 12 weeks: 3.3 [1.1] versus 5.2 [1.5], p < 0.01) (Figure 3B). The AUC for triglycerides was significantly lower in the mineral oil group than in the corn oil group, both for the 30 µL dose (p < 0.01) and for the 15 µL dose (p = 0.01).

[sts66]

EVAPORATE is under attack as well - right before the ESC conf. too - this was published in the ESC's "European Heart Journal", equivalent to our AHA journal:

https://academic.oup.com/eurheartj/article/42/31/3023/6273098?login=true

Underlying mechanisms involved in the icosapent ethyl reduction of cardiovascular events still cannot be attributed to an anti-atherosclerotic effect

Read all of it - they accuse Budhoff for manipulating the randomization process, impugn his scientific integrity, and claim he didn't run the trial correctly. Again I ask who is behind these constant attacks on V research and what do they have to gain by discrediting AMRN and V?