Although our estimates surpass results from GWASs, estimates are still lower than heritability estimates reported in twin and family studies. The discrepancy can be attributed to several factors. First, heritability estimates from twin and family studies include the effects of all causal variants, whereas heritability estimated using the methods employed in this study include only the effects of variants that are in (sufficient) LD with the genotyped SNPs included in the analyses. LD is especially low if the causal variant has a different MAF than the genotyped marker. Consequently, contribution of rare variants (MAF <0.5%) and variants with low MAF (0.5% < MAF <1%) is included in the heritability estimates from twin and family studies but is generally not included in the variance explained by common SNPs. As causal variants are unknown, we cannot estimate LD between genotyped SNPs and causal variants directly. However, assuming that LD between the causal variants and genotyped SNPs is as strong as between the genotyped SNPs (that is, adjustment for prediction error of causal variants that have the same allelic frequency spectrum as genotyped
