By controlling environmental factors for genetic confounding (and vice versa) and longitudinal effects for baseline variations, our study design also allows certain etiologic inferences. Cross-sectional correlation between BPD 4 and AUD was partly driven by shared environmental factors, but when controlling for baseline value, BPD 4 predicted future AUD only through shared genetic factors. In contrast, childhood conduct disorder implied both current and future risk due to both shared environmental and shared genetic factors. This suggests that while shared environmental factors may link acute AUD with other self-harming impulsive behaviors in short term, their long-term (~10-year) association appears to derive from shared genetic liabilities. In contrast to self-harming impulsive behaviors, environmental factors influencing childhood conduct disorder may predispose to a life course where accumulating life events (environment) keep increasing or sustaining the future risk of AUD.
