In eukaryotes, the C20:4 polyunsaturated fatty acid arachidonic acid (AA) plays important roles as a phospholipid component, signaling molecule and precursor of the endocannabinoid-prostanoid axis. Accordingly, the absence of AA causes detrimental effects. Here, compensatory mechanisms involved in AA deficiency in <i>Caenorhabditis elegans</i> were investigated. We show that the -3 C20:4 polyunsaturated fatty acid juniperonic acid (JuA) is generated in the <i>C. elegans</i><i>
fat-3(
wa22)</i> mutant, which lacks 6 desaturase activity and cannot generate AA and -3 AA. JuA partially rescued the loss of function of AA in growth and development. Additionally, we observed that supplementation of AA and -3 AA modulates lifespan of <i>
fat-3(
wa22)</i> mutants. We described a feasible biosynthetic pathway that leads to the generation of JuA from <i></i>-linoleic acid (ALA) via elongases ELO-1/2 and 5 desaturase which is rate-limiting. Employing liquid chromatography mass spectrometry (LC-MS/MS), we identified endocannabinoid-like ethanolamine and glycerol derivatives of JuA and -3 AA. Like classical endocannabinoids, these lipids exhibited binding interactions with NPR-32, a G protein coupled receptor (GPCR) shown to act as endocannabinoid receptor in <i>C. elegans</i>. Our study suggests that the eicosatetraenoic acids AA, -3 AA and JuA share similar biological functions. This biosynthetic plasticity of eicosatetraenoic acids observed in <i>C. elegans</i> uncovers a possible biological role of JuA and associated -3 endocannabinoids in 6 desaturase deficiencies, highlighting the importance of ALA.