Background: The Behavioral Susceptibility Theory proposes that inherited variation in appetitive traits shapes vulnerability to obesity in environments with abundant high-energy foods, yet the mechanisms linking genetic variation to early-life eating behavior remain insufficiently understood. Using data from ~31,000 children in the Norwegian Mother, Father and Child Cohort Study (MoBa), we characterized appetitive phenotypes at age 8 using domain- and item-level scores from the Child Eating Behaviour Questionnaire (CEBQ). In what is currently the largest attempt to date, we first quantified associations between appetitive traits and longitudinal BMI from infancy to age 8 followed by genome-wide association analyses for all appetite domains and items. We identified ten risk loci with distinct profiles for Food Responsiveness (e.g. near FTO, TMEM18, MC4R, ADCY3, SEC16B, TFAP2B, KDM4C), Satiety Responsiveness (near ADCY3, SEC16B) and Food Fussiness (near SIX3 and the common large 17q21.31 inversion). We then applied LD-score regression to estimate genetic correlations with anthropometric, metabolic, dietary, hormonal, and psychological traits across development. To assess how established obesity loci influence appetite, we further examined 25 known childhood BMI-associated loci from the largest independent study and evaluated their association patterns across the CEBQ domains. Further mediation analyses showed that FTO predominantly affects Food Responsiveness (FR), with up to 38.7% of its effect on BMI mediated through FR. This approach, combining behavioral phenotyping, longitudinal growth data, genome-wide analyses, and targeted evaluation of BMI loci, provides a framework for distinguishing shared versus trait-specific biological pathways underlying childhood eating behavior and its contribution to early-life obesity risk.