The high genetic correlation and lack of difference in polygenic burden between male and female ADHD cases support combining GWAS data from both sexes in ADHD meta-analyses and further suggest that current clinical practices of diagnosing ADHD are capturing a clinical phenotype that is similar at the level of common genetic risk variants in both sexes. Thus, our results indicate that genome-wide autosomal common variants largely do not explain the observed sex bias in ADHD prevalence. On the other hand, the epidemiological results also suggest some degree of clinical heterogeneity, with ADHD showing a stronger phenotypic association with comorbid ASD, congenital malformations, and mild ID in female individuals. We also found evidence for a modest increase in familial risk for ADHD in female individuals based on sibling analysis. Further work simultaneously examining variants across the spectrum of frequencies is needed to comprehensively determine the role of genetic risk in the sex bias in ADHD prevalence.
