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In summary, the anti-inflammatory effect of EFA deficiency was more marked that that of dietary (n-3) fatty acid supplementation in acute inflammation.
Thanks haidut!!So, @Makrosky and @ReSTART, check this out from another thread (courtesy of @paymanz). It is official information on IV nutrition, which says that PUFA (linoleic acid) is what causes NAFLD in up to 50% of patients on TPN, and of those up to 50% die.
More Evidence That Omega-3 Supplements Don't Work
"...Fatty liver is usually a more long term complication of TPN, though over a long enough course it is fairly common. The pathogenesis is due to using linoleic acid (an omega-6 fatty acid component of soybean oil) as a major source of calories.[10][11] TPN-associated liver disease strikes up to 50% of patients within 5–7 years, correlated with a mortality rate of 2–50%. Onset of this liver disease is the major complication that leads TPN patients to requiring an intestinal transplant.[12]
Oxidized metabolites of linoleic acid as biomarkers of liver injury in nonalcoholic steatohepatitisIn fact, because LA cannot be synthesized de novo in humans, dietary LA is the sole source of LA for the human body, therefore also being the sole source for OXLAM synthesis. Lowering LA in the diet might help to reduce OXLAMs in the blood and other tissues such as the liver, leading to an improvement of liver histology.