Recently, neuroimaging measures have been applied as an intermediate biological phenotype to investigate the effect of genes on human behavior. Genetic modulation of brain function is a plausible model for increased AUD risk (Hutchison, 2008). These brain based phenotypes are predominately determined from functional magnetic resonance imaging (fMRI) measurements and have been linked to predisposition from genetic variations of genes including DRD2, DRD4 OPRM1 and CNVs to AUD in several studies (Filbey et al., 2008; Heinz et al., 2004; Liu, Calhoun, Chen, Claus, & Hutchison, 2011). Several regions are implicated, including the ventral striatum, precuneus and prefrontal cortex. In addition to using fMRI to find genetic associations with AUD, magnetic resonance spectroscopy has also been used to find associations between metabolite concentrations in the brain and total CNV burden in an alcohol using population (Yeo, Gangestad, Gasparovic et al., 2011; Yeo, Gangestad, Liu et al., 2011). Similar to using intermediate functional and metabolic phenotypes, intermediate structural phenotypes have also been used to study predisposed risk to AUD from alcohol dependence families (Hill et al., 2007, 2011). While there has been
