disorders, Martin and colleagues (2017) describe the multiple, not mutually exclusive, interpretations of a given genetic correlation, which may signify: 1) the same risk variants are directly, causally impacting different phenotypes; 2) the same risk variants could be impacting a third, unmeasured phenotype that underlies both conditions; 3) there are in fact different risk variants between the two disorders but these variants are highly correlated and acting through different mechanisms to result in the conditions; 4) one phenotype mediates the association between genetic risk and the other phenotype. At present, it is difficult to distinguish among these explanations. Therefore, the next step in research in this area is to conduct longitudinal prospective studies and/or Mendelian Randomization methods (e.g., Polimanti et al., 2018) that can disentangle causality, and for this, better-powered GWAS of these two phenotypes would be helpful. Current study results do support the common, third-variable approach and support new avenues for research, setting the stage for identification of common mechanisms that are genetically informed.
