No explanation for why the MO group saw changes but the V group didn't , but they mentioned something might have been going on within other inflammatory pathways with biomarkers they didn't measure:
Despite our large sample size and randomized dou-ble-blind design, there are limitations to our analyses that merit consideration. First, care must be taken not to generalize these findings beyond what is presented here; for example, whereas we evaluated for effects in the canonical interleukin-1 to interleukin-6 to C-reactive protein pathway of innate immunity,4,5 we did not evaluate alternative pathways of inflammation that might also be involved in atheroprotection. Specialized pro-resolving and other anti-inflammatory mediators, for example, are powerful anti-inflammatory molecules produced from EPA, and EPA can reduce production of proinflammatory factors from arachidonic acid competitively. None of these, however, has been measured in REDUCE-IT; nor have alternative biomarkers such as ceramides and glycoprotein acetylation.