GWAS summary statistics for all the diseases and quantitative traits are publicly available (Supplementary Data 1). We removed ambiguous (A/T and C/G) SNPs and mapped the genetic markers to the Genome Reference Consortium human genome build 37. SNP heritability for each disease and trait was estimated using GWAS summary statistics and LD score regression23. Heritability estimates for diseases on the observed scale were transformed to the liability scale as described in Lee et al.58 using the assumed population and sample prevalences shown in Supplementary Table 13. For unadjusted PRS and P+T, we used all the genetic markers that are present in the summary statistics, LD reference panel and the Partners Biobank genetic data. For LDpred(-inf) and PRS-CS(-auto), we further restricted the genetic markers to the HapMap3 panel to reduce memory and computational cost. Table 1 shows the total number of markers included in the analysis for each disease and quantitative phenotype. We note that the GWAS samples and the Partners Biobank sample may have overlap. However, by carefully examining the sample composition of each GWAS study, we believe that sample overlap is minimal (if any) and does not impact the comparison among polygenic prediction methods.
