These n-3 PUFAs frequently substitute n-6 PUFAs like ARA, resulting in decreased availability of ARA for eicosanoid synthesis. EPA also inhibits ARA metabolism as a competitive substrate for COX-2, decreasing prostaglandin E2 (PGE2) production. In rats, dietary supplementation with ALA inhibits PG biosynthesis from ARA, while equivalent quantities of ALA and LA decreased up to 40% n-6 PUFAs incorporation in phospholipids (Calder, 2017). Furthermore, Rees et al. observed that a daily EPA intake of 2.7 g or 4.05 g for 3 months decreases the PGE2 production by lipopolysaccharide-stimulated mononuclear cells, while a lower dose of 1.35 g did not. EPA was integrated in a linear dose-dependent manner into mononuclear cell phospholipids and plasma. This study suggested a daily threshold in the range of 1.35–2.7 g EPA for the anti-inflammatory action (Rees et al., 2006).