Important considerations for the current study were our inability to model dominance and epistatic effects from genomewide loci, which is a growing area of interest in the field of psychiatric genetics, but is an approach that was not feasible with our current sample size. As such, readers should interpret these effects as the cumulative/additive effect of genomewide SNPs, which is akin to the additive genetic variance component (A) typically examined in the twin literature and that largely contributes to the correlation among relatives. Likewise, an examination of gender was prohibited due to sample size, but twin studies that have explored gender differences (i.e., qualitative and quantitative) have been mixed (Verhulst et al., 2015). Another important consideration to arise from this study is, the varied h2SNP effect sizes across symptoms suggest that larger samples are needed to study individual symptoms with limited (<0.30) genetic effects, particularly if the variance across the set of SNPs influencing each symptom is not constant. We have cautiously interpreted our study findings because of the limited power to detect modest SNP-heritability estimates and genetic correlations, especially
