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(2019) estimated that 23% of the variation in BMI is accounted for by common variants. To date, the largest meta-analysis of genome-wide association studies of BMI among adults has led to the discovery of 751 single nucleotide polymorphisms (SNPs) associated with BMI these SNPs collectively explain 6% of the phenotypic variance in BMI. With the advance of genomic research, there has been a shift from twin and family studies towards using measured genes in genome-wide association studies. Genetic factors explain between 40 to 60% of the proportion of the variability in body mass index (BMI) during childhood. Obesity is a heritable and highly polygenic chronic disease. Registry number: ISRCTN62310987 Retrospectively registered 17 September 2018. A better understanding of the genetic pathways that lead to childhood obesity can help to prevent weight gain. The findings suggest parental concern of overeating as a possible mediator in the genetic susceptibility to obesity and further highlight that other pathways are also involved. The findings suggest that the prospective associations between obesity indices and parental concern of overeating are likely bi-directional, but obesity indices have a stronger association with future parental concern of overeating than vice versa. To a lesser extent, baseline parental concern of overeating also mediated the association between the PRS-BMI and z-BMI at wave 3 ( β = 0.10, 95% CI: 0.07, 0.13) and z-WC at wave 3 ( β = 0.09, 95% CI: 0.07, 0.12). In mediation models, the association between the PRS-BMI and parental concern of overeating at wave 3 was mediated by baseline z-BMI ( β = 0.16, 95% CI: 0.10, 0.21) and baseline z-WC ( β = 0.17, 95% CI: 0.11, 0.23). In cross-lagged models, the prospective associations between z-score obesity indices and parental concern of overeating were bi-directional. Parental concern of overeating was derived from principal component analyses from an eating behavior questionnaire. Z-score BMI and z-score waist circumference (WC) were assessed and eating behaviors and relevant confounders were reported by parents via questionnaires. For 2656 children with genome-wide data we constructed a PRS based on 2.1 million single nucleotide polymorphisms. A total of 5112 children (49% girls) participated at waves 1, 2 and 3. The IDEFICS/I.Family study is a school-based multicenter pan-European cohort of children observed for 6 years (mean ± SD follow-up 5.8 ± 0.4).
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In this study we aim to examine the relationships between the polygenic risk score for body mass index (PRS-BMI), parental concern of overeating and obesity indices during childhood. A longitudinal approach is needed to assess the contribution of genetic risk during the development of obesity in childhood. Eating behaviors represent a plausible pathway, but because the relationships of eating behaviors and obesity may be bi-directional, it remains challenging to resolve the underlying pathways. Many genes and molecular pathways are associated with obesity, but the mechanisms from genes to obesity are less well known.