replicated or supported by evidence from multiple samples, which is the case for the associations that we reported. Also, although our sample size is reasonable, experience has shown that many true associations are detected only in samples or meta-analyses that are much larger. The relatively small size of the sample used in Phase 3 for the primary trait analyses and as replication for the OD subtype findings is in our view the most likely cause of few replication observations in that sample. Specifically, there were proportionally fewer AAs available for Phase 3 (n= 805, ~24% as large as the discovery sample), which is the part of the sample in which most positive results were initially observed. Ideally, the replication sample would be larger than the discovery sample. It is also noteworthy that there was little evidence of association in EAs for any of our top findings in AAs, however, all but one of the SNPs reported in Table 1 were monomorphic in EAs. Finally, our findings are not adjusted for testing association in two populations and with two trait models (case-control and ordinal). Bonferroni correction is too conservative given the high correlation between the traits and distinct hypotheses for EAs
