We are thus led to the frustrating conclusion that anything we say about G × E in psychiatric genetics is critically dependent on the interface between biology and psychometrics to the point that analysis symptom counts and dichotomous outcomes is likely to be seriously mis-leading since estimates are biased and/or the type I error rates are higher than assumed. Patterns of main effect and interaction change as a function of the items chosen for measurement and the underlying truth about the genetic architecture of liability.
