These results are consistent with a common liability model whereby overlapping genetic factors influence onset, SLE exposure, and alcohol consumption. Genetic overlap could arise because age at drinking onset, SLE, and past-year alcohol consumption are all influenced by another genetically influenced variable such as mood-related drinking motives. For example, if mood-related drinking motives are (i) genetically influenced, (ii) associated with early drinking onset, and (iii) increase risk for drinking in response to SLE, this would create shared genetic variation for early onset, SLE, and past-year drinking. Another explanation could be that genetic factors underlying early drinking onset influence risk for experiencing SLE. For instance, individuals who are genetically predisposed for sensation-seeking may both initiate drinking at an early age and place themselves at risk for experiencing various SLE (e.g., physical injury, legal problems). Thus, it is possible that increased rates of stress-related drinking observed among early drinkers are explained by their greater liability to engage in behaviors which potentially create life stress.
