of symptom clustering, indicating that clustering contributed almost no additional genetic information (Grant et al. 2009). That study also found a genetic correlation of 0.96 for AD symptom count and alcohol abuse, suggesting that abuse and dependence symptoms tapped the same underlying genetic liability. In the current study, therefore, the use of AUD symptom count without clustering is supported by evidence showing that abuse and dependence are genetically correlated and that symptom clustering adds little genetic information to the phenotype. The AUD phenotype is also consistent with evidence from other twin samples that the magnitude of genetic influences on risk are similar for narrowly defined alcohol dependence and for broadly defined problem drinking (Prescott & Kendler, 1999; Prescott et al. 1999).
