In addition to AUD, BCHE (and/or surrounding region, 3q26) has previously been associated with behavioral conditions relevant to fast beta EEG, including ADHD and cocaine use/problems. In four independent studies, variations within or surrounding BCHE have also been associated with ADHD.49–52 Jacob et al.50 report that, when meta-analyzing the results of their study with three additional GWAS for copy number variations, they found that individuals with ADHD were more likely to have a deletion in the BCHE promoter region. Given several lines of evidence suggesting the involvement of BCHE in the etiology of ADHD,50 post hoc we re-examined the association between 3q26 variants and fast beta EEG, adjusting for ADHD. When the GWAS of fast beta EEG included ADHD as a covariate in the model, results (Supplementary Figure S3C) show that the 3q26 association is significantly reduced, with the top SNP no longer meeting genome-wide significance criteria. This suggests an important connection between ADHD, 3q26 and fast beta EEG that future studies with longitudinal designs should disentangle (for example, does fast beta EEG mediate the association between 3q26 and ADHD?).
