Such is the case of the α-linolenic acid dietary intake, which interacted with FADS1 genetic variability to affect serum non-HDL-cholesterol concentrations in European adolescents [122], or another study where the genetic liability to obesity, assessed by a obesity polygenic risk score (PRS), was attenuated by a higher fiber intake [123]. This evidence concerns the gene FADS1 and obesity due to melanocortin 4 receptor deficiency.