In addition, Obesity compromises placental function through multiple interconnected pathways: chronic inflammation and oxidative stress directly damage placental cells and impair nutrient exchange; epigenetic alterations (e.g., DNA methylation) disrupt gene expression patterns critical for placental development; and dysregulation of metabolic mediators (e.g., leptin, apelin) disrupts vascular tone and angiogenesis, while maternal vascular malperfusion is a well-established risk factor for indicated preterm birth (30). This evidence concerns the gene LEP and obesity due to melanocortin 4 receptor deficiency.