( hG2) for height, BMI, vWF and QTi in each cohort and the combined data where applicable (Online Methods, Table 1 and Supplementary Table 1). The traits vWF and QTi were available from the ARIC sample only. We show that 44.8% (s.e = 2.9%) of phenotypic variance for height can be explained by all the autosomal SNPs, in line with an estimate of 44.5% (s.e. = 8.3%) in a similar analysis of an Australian cohort (3,925 unrelated individuals genotyped by 294,831 SNPs on Illumina arrays, in contrast to the Affymetrix arrays in the present study)4. We show for the first time that 16.5% (s.e. = 2.9%), 25.2% (s.e. = 5.1%) and 20.9% (s.e. = 5.0%) of variances for BMI, vWF and QTi can be explained by all the autosomal SNPs, approximately 10-fold, 2-fold and 3-fold larger than the variance explained by all known validated loci found by GWAS for BMI12–15, vWF16 and QTi17, respectively. We note that the ABO blood group locus on chromosome 9 is known to explain approximately 10% of phenotypic variation for vWF16, through modification of the amount of H antigen expression on the circulating vWF glycoprotein18,19. The estimate of hG2 for weight is 18.6% (s.e. =
