detect odds ratios of this magnitude, given the observed minor allele frequencies for current ADHD-risk alleles. Genome-wide association studies (GWAS), in which “a dense set of SNPs [single nucleotide polymorphisms] across the genome is genotyped to survey the most common genetic variation for a role in disease or to identify the heritable quantitative traits that are risk factors for disease,”12 offer promise due to their increased power to detect such small effect sizes. However, currently no genomewide significance levels have been reached for ADHD traits (see Franke et al.13 for a review). Thus, to date, molecular genetic studies have accounted for less than 5% of the estimated heritability in ADHD symptoms,14,15 and although this is common to many neuropsychiatric and other phenotypes, it has lead some researchers to conclude that there is a disparity between molecular and quantitative approaches to understanding the genetic etiology of ADHD.
