Recent studies using the MAOA genotype to detect G × E in CD among females have not addressed the effect of X-inactivation as a result of inconsistency in determining whether this locus is subject to X-inactivation and whether inactivation of this locus was non-random (Benjamin et al. 2000; Carrel & Willard, 2005; Fraga et al. 2005; Nordquist & Oreland, 2006; Pinsonneault et al. 2006). Consequently, our understanding of the effect of this X-linked marker on CD risk in females and any gender differences that may arise from G × E is limited. Additionally, prior studies in females have not controlled for the effects of rGE, restricting the ability to address the role of G × E in the etiology of CD in this population. Therefore, to understand the role of an X-linked marker on risk for CD and any influence it may have on gender differences in CD, females with homozygous and heterozygous MAOA genotypes were used to test for the main effects of MAOA and childhood adversity as well as any effects associated with G × E in the presence of passive rGE, defined by parental ASP, as risk factors for CD.
