Results from linear regression analyses are displayed in Table 3. Model 1, which included the standard covariates, PC1 by sex and age by AD interactions but no genetic component, accounted for 8.3% of the variance in BMI. Model 2, which added the SNP-GRSS and the 21-kb deletion on 16p12.3 to the base model, fit significantly better [F(3 2335) = 25.3, p = 3.34x−54] and accounted for an additional 3.2% of phenotypic variance (3.1% due to SNP-GRSS, 0.1% due to deletion on 16p12.3) in BMI for a total of 11.5%. Interactions between the covariates and the SNP-GRSS were not significant except for sex, which suggested that the SNP-GRSS was statistically similar in EA and AA and across age but tended to account for more of the variation in females. No significant interactions between the covariates and the 21-kb deletion on 16p12.3 were found, which indicated that the CNV was comparably associated with BMI in males and females, EA and AA and across the age range observed in SAGE. Additional file 5: Table S5 gives full model statistics by ancestry. We have
