Another possibility is that our measures of environmental risk would have the same moderating effects on the genetic and environmental risk for any form of psychopathology. However, in a separate analysis with the same sample13, we examined G-E interplay between INT disorders and the same measures of environmental risk, and found that the nonshared environment variance of INT increased at higher levels of each environmental risk factor while the genetic and shared environmental variance remained stable. That is, the same environmental adversity was associated with a different mechanism of G-E interplay in the emergence of INT compared to EXT psychopathology. Taken together, the pattern of results across the two studies provides impressive evidence of convergent and discriminant validity. The intriguing hypothesis of our work then is that the mechanism underlying environmental influence is relatively general, but will differ depending on the nature of the psychopathological condition.
