of genetic variance explained for height and BMI is approximately 0.07, so that the observed difference of 0.22 appears statistically significant. These results are consistent with the proportion of phenotypic variation for height and BMI explained by genome-wide significant SNPs, in that for height about 10% of phenotypic variance is explained yet for BMI less than 2%15,26, despite similar and large experimental sample sizes. These results imply that causal variants for BMI are in less LD with common SNPs than causal variants for height, possibly because, on average, causal variants for BMI have lower minor allele frequency than causal variants for height. Both observations from GWAS and our analyses are consistent with the allelic architecture for BMI being different from that for height. Different evolutionary pressures on obesity (or leanness) and height could account for such differences because natural selection will result in low frequencies of alleles that are correlated with fitness32. However, we do not provide direct evidence to support this hypothesis.
