Our findings suggest that a sample of ∼10 000 individuals (with 25% cases) is not sufficient—in EAs or in AAs—to identify robust risk loci. A larger sample size and greater genotyping coverage (particularly in AA individuals) will afford greater power in future single variant association analyses. As well, it is possible that highly standardized phenotyping and/or ascertainment of more specific populations may increase power by decreasing phenotypic heterogeneity, as is arguably the explanation for success of the CONVERGE consortium.55 Future work needs to more carefully consider trauma exposure, a necessary though not sufficient condition for the development of PTSD. Although the majority of controls (87.7%) in the current analysis were trauma exposed, the inclusion of nontrauma-exposed controls may have reduced power to detect PTSD loci. Moreover, sex differences in both type and quantity of trauma exposure are well documented56 and will be important to consider in future research examining sex differences in heritability. In the interim, the successful polygenic analyses discussed above (that is, significant heritability estimates and genetic correlations) mean that the summary statistics made available with this report will be informative for PTSD studies when used with appropriate polygenic methods (for example, PRS and LDSC).
