Third, estimates of latent genetic factors in the Classical Twin Design (CTD) formally assume additive genetic effects. The meager proportions of variance that are accounted for by individual genetic variants have led some to conclude that gene–environment interactions or non-additive genetic factors (such as epistasis or dominance) may play pivotal roles in the etiology of AUD. With the CTD it is generally not possible to disentangle the effects of non-additive genetic factors from additive genetic factors (Martin et al. 1978; Neale et al. 1994) due to the lack of power to disentangle these highly collinear genetic factors. Furthermore, when the DZ correlation is greater than half the MZ correlation, most researchers do not even test for dominance as the correlations are more consistent with the shared environment playing a role in the development of the phenotype. More recent evidence, however, suggests that non-additive genetic variation is absorbed into the additive genetic factor (Keller et al. 2010), suggesting that the genetic variance component should be interpreted as a broad genetic factor. This interpretation is consistent with our interpretation of the current results.
