These results should be evaluated in the light of the following limitations. First, we were unable to estimate risk for CD among females with low MAOA activity also experiencing three or more exposures to childhood adversity because of a lack of observations (Fig. 2). Consequently, G × E may have been initially overestimated and after transformation was lost. The variable strength of G × E highlights the issue of scale in our measurement and treatment of environmental exposure towards the detection of G × E and genetic effects in humans, reinforcing the need for better measures of environmental risk for psychiatric disorders. Second, this study is a cross-sectional analysis of longitudinal data from four waves of data. Age was not included as a covariate and these results therefore reflect the risk for CD associated with childhood adversity, maternal ASP and MAOA throughout adolescence. Third, these analyses treated CD as a categorical outcome and ignored the additional information that might be reflected by using indices of severity such as symptom counts or by differentiating subtypes such as aggressive and non-aggressive behaviors.
