## 4 Discussion  
The scientific literature supports that childhood eating behaviors may be modulated by genetic factors [25]. The behavioral susceptibility theory hypothesizes that genetics influences the obesity phenotype by regulating appetite, expressed in eating behavior. The review by [PERSON] et al. [10] is illuminating, as it highlights the value of studies associating the genetic risk scores and the psychometric measures of eating behaviors. The same authors highlight the need for further research, particularly longitudinal studies in children. In the present study, an association was found between GRS and obesity and the food responsiveness (FR) subscale, in addition to the subscales related to emotional eating, both by excess (EOE) and deficiency (EUE). The results using other subscales are generally in line with the expectations that the average scores increase with higher genetic risk scores in the pro-intake scales and decrease in the anti-intake scales, following the trend of previous studies, which highlight the more significant evidence concerning the ability to satiate and the demand to food [10]. Some studies have observed that schoolchildren genetically predisposed to obesity show a more significant response to or enjoyment of food, greater appetite, and less responsiveness [24; 26]. In the present study, despite not finding such an association with the total risk score, the trend of the averages is along the same lines. In turn, in the literature, a more significant response to food, understood as a greater desire to consume food, is associated with a greater risk of being overweight. The literature concludes that children who enjoy or express a greater desire for food consume more daily energy on average [27]. These schoolchildren also eat more processed products of low nutritional quality, which are high in calories, refined and saturated fats, and free or added sugars, a dietary pattern associated with an increased risk of obesity [28]. Genetic predisposition to emotional eating is controversial. Further evidence is still required in school populations, and previous studies reached contradictory results. Some authors suggest that the genetic component predisposes a greater or lesser tendency to emotional eating [29], an observation in line with the findings of the present study. However, other studies find that the heritability of the emotional eating behavior is low and, in any case, is less deterministic than learned behavior [30; 31]. Certain studies report associations between a lower genetic risk for obesity and slower eating, leading to earlier satiety and lower food intake, possibly because of less responsiveness to internal satiety cues and greater appetite [32]. Our study finds both trends, although without significant association with GRS. Children who are pickier and who reject new foods might have a less varied and obesogenic diet [10]. However, the present study found no relationship between food pickiness and genetic predisposition to obesity, as previous studies have described [33]. On the other hand, 14 of 32 SNPs analyzed could be independently associated with eating behaviors. Thus, five SNPs from different loci were associated with the anti-eating subscale of emotional undereating (EUE) and two other SNPs with the pro-intake subscale of increased risk of emotional overeating (EOE). In particular, the SNPs of the FTO gene, rs1421085 (significant in the present study) and rs9939609, have been associated in the literature with uncontrolled eating (loss of control eating), which is usually accompanied by a preference for more palatable foods, usually higher in calories and rich in fat or sugar [34]. In the anti-intake subscale of slowness in eating (SE), lower scores have also been found in children with the risk genotype in three SNPs, implying a possible higher eating speed. Scientific evidence shows that eating slowly reduces food intake, a protective factor against weight gain. Eating slowly promotes earlier satiety, while eating fast means higher total intake [6].