With this said, we did not examine intermediate variables, or individual-specific consequences of EAU, that may explain the causal link between EAU and SA. For example, it’s possible that EAU may exert risk for SA via the development of more problematic alcohol use, such as an alcohol use disorder, which is elevated among those reporting early onset drinking (Grant and Dawson 1997;Sartor et al. 2007). Furthermore, the median age of onset of SA in the current study is identical to the median age of onset for both alcohol abuse and dependence in the Australian population (i.e., 20 years; Teesson et al. 2010), which indicates that alcohol use disorders may be an important phenotype to consider in this pathway. It is also possible that EAU contributes to alterations in brain regions that influence response inhibition, which in turn increases risk for later SA. Wetherill and colleagues (2013) found differences in activation of brain regions associated with inhibitory control (e.g., frontal regions) both before and after the onset of heavy drinking among adolescents relative to non-drinking controls. Alterations in frontal brain regions
