Like many other complex traits, alcoholism appears to be clinically and etiologicaly hetrogenous[13]. This implies that there might be several steps and intermediate conditions in the development of AUD. Information about the underlying genetic factors that influence risk to AUD can be derived from multiple levels of AUD including amounts of drinks (Alcohol consumption), severity and symptoms of alcohol abuse and dependence. Commonly, genome wide association studies (GWAS) of alcoholism have focused on phenotypes based on the Diagnostic & Statistical Manual of Mental Disorders (DSM)[14]. In the 4th edition of the DSM (DSM-IV), alcohol dependence (AD) and abuse were considered as mutually exclusive diagnoses that together made up AUDs. DSM-V[14, 15] on the other hand consolidated AD and abuse as a single disorder as AUD[15],[16]. By considering AD and abuse under single umbrella increased the number of diagnosed subjects, but this number was still not large enough to design powerful GWAS studies. Therefore, many genetic studies of alcoholism also concentrated on nonclinical phenotypes, such as alcohol consumption and Alcohol Use Disorders Identification Test (AUDIT)[17–19], from large population based cohorts. The
