We speculate that the genetic influences on alcohol problems in clinically ascertained populations may differ, in quantity or quality, from those within the general population. Symptom profiles or motives for alcohol use could, for example, define mechanisms by which different individuals develop the same AUD outcome, and these might differ systematically between populations. Clinical samples of substance dependent individuals are often not representative of the broader population (Blanco et al., 2008), and treatment-seeking individuals often have more severe illness and additional comorbidities (Kaufmann et al., 2014). Overall symptom endorsement rates are higher in clinical samples, but there could also be differences in endorsement profiles, since the syndromic criteria for AUD allows for many possible combinations of symptom subsets. Some evidence indicates unique genetic influences between symptom clusters (Kendler et al., 2012). There is also evidence that drinking for coping motives is more strongly tied to psychological dependence, while drinking for social or sensation-seeking motives are associated with heavy/frequent use (Kuntsche et al., 2005), but despite different underlying mechanisms both could lead to AUD symptoms/diagnoses. If any one of these pathways
