We selected 14,347 individuals from three population-based GWAS, i.e. the Health Professionals Follow-up Study (HPFS), the Nurses’ Health Study (NHS) and the Atherosclerosis Risk in Communities (ARIC) study6–8, and estimated the genetic relationship matrix (GRM) of all the individuals using 565,040 autosomal SNPs which passed quality control (Online Methods). We excluded one of each pair of individuals with an estimated genetic relationship > 0.025 (i.e. more related than third- to fourth-cousins) and retained a subset of 11,586 unrelated individuals. The reason for excluding related pairs is to avoid the possibility that the phenotypic resemblance between close relatives could be due to non-genetic effects (e.g. shared environment) and causal variants not tagged by SNPs but captured by pedigree10,11. We then fitted the GRM in a mixed linear model (MLM) to estimate the proportion of variance explained by all the autosomal SNPs ( 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
