Using these endophenotypes collectively, then, has the potential to overcome the problem of heterogeneous subject samples by increasing the ability to identify those in the population with the endophenotypes who are at especially high risk for EXT disorders (and, thus, more likely to be true gene carriers; e.g. Iacono et al., 2000). The small to moderate effect sizes we found when comparing EXT between those scoring high and low on the endophenotypes provides initial evidence supporting this hypothesis. A multivariate endophenotype could also be advantageous given the polygenic influences on the general vulnerability to EXT. Endophenotypes are putatively less genetically complex correlates of the disorder that, because they tap the neurobiological basis of gene effects, are closer to gene action. The extent to which the genetic influences overlap between the endophenotypes and EXT, then, may provide increased power to detect "hits" for genetic linkage and association studies that may account for exceedingly small proportions of variance in the EXT phenotype (Gottesman & Gould, 2003). These are necessary avenues of future research in evaluating the utility of this multivariate approach to defining endophenotypes for EXT.
