Thanks to North for mentioning that article - link to the full PDF is in the upper left corner of the URL you posted - I just finished reading it, and it's pretty clear MO is not inert as AMRN claimed - even at such a low dose it did something bad - but finding out why would be very expensive and may not reveal a direct cause/affect relationship - metabolic processes are beyond complicated. (see links below).
From your article - shocking that no anti-inflammatory effects were found in the EPA group - almost all of us on V have reported greatly reduced inflammation, like DES being cured with V - for me it relieved a lifetime of chronic lower back pain plus DES - JL claimed DES was an inflammatory disease. EPA must reduce inflammation via a pathway that didn't have it's biomarkers measured in R-IT.
The data presented by Ridker and colleagues raises the difficult question, not of whether or not icosapent ethyl improves clinical outcomes in high-risk cardiovascular patients but of the magnitude of that benefit and whether that benefit is sufficiently robust for recommendations to guide clinical practice. Icosapent ethyl was superior to mineral oil in a large, well-designed RCT in reducing important clinical events. But the mechanistic work presented here by the investigators also shows that mineral oil was not inert with a number of pro-inflammatory markers increased over timeand no measured anti-inflammatory effects associated with icosapent ethyl, only a decline, as expected, in TG.
Here's a couple links to chew on as far as how complicated metabolic processes are - 8 diagrams at this site, just for methylation, which includes the Kreb's cycle, how your body produces ATP:
The most complicated one from that site is here - see text on left side that explains some of the steps involved and how genetics and toxins like heavy metals, (something I've been treated for via chelation therapy) can interfere with these cycles: