Together, the 32 confirmed BMI loci explained 1.45% of the inter-individual variation in BMI of the stage 2 samples, with the FTO SNP accounting for the largest proportion of the variance (0.34%) (Table 1). To estimate the cumulative effect of the 32 variants on BMI, we constructed a genetic-susceptibility score that sums the number of BMI-increasing alleles weighted by the overall stage 2 effect sizes in the ARIC study (N = 8,120), one of our largest population-based studies (Online Methods). For each unit increase in the genetic-susceptibility score, approximately equivalent to one additional risk allele, BMI increased by 0.17 kg/m2, equivalent to a 435–551 g gain in body weight in adults of 160–180 cm in height. The difference in average BMI between individuals with a high genetic-susceptibility score (≥38 BMI-increasing alleles, 1.5% (n=124) of the ARIC sample) and those with a low genetic-susceptibility score (≤21 BMI-increasing alleles, 2.2% (n=175) of the ARIC sample) was 2.73 kg/m2, equivalent to a 6.99 to 8.85 kg body weight difference in adults 160–180 cm in height (Fig. 2a). Still, we note that the predictive
