A major motivation for the genetic analysis is to get information about the causal mechanisms behind an observed association between an exposure of interest and its presumed outcome. When designing interventions, it is important to understand whether an association is due to shared genetic factors or due to some sequences of developmental events. Covariation between an exposure and an outcome captured in the “E” component of an ACE model is closely related to results from “co-twin control” analysis, because the additive genetic effects and the family environment have been controlled for [45–47]. The logic of co-twin control is that if an exposure difference between genetically identical MZ twins is associated with a difference in an outcome, then the observed association is likely to be environmentally mediated because there is no genetic variance to explain it. Thus, ACE modeling results carry implications about environmental causation or lack of it. While the ACE model is effective in using both MZ and DZ twins, it is blind for non-additive genetic effects. That is why we also provide the within- and between-MZ-twin pair logistic
