confounding factors in Table 2, Table 3 to aid reader interpretation of the presented synthesis.2Causation versus correlation. The majority of studies included in this systematic review were cross-sectional. Subsequently, it is not possible to disentangle whether brain-based differences represent an antecedent risk factor that predated youth alcohol consumption (potentially placing youth at greater risk for AU), whether they reflect a consequence of adolescent drinking, and/or whether they indicate some unmeasured (and potentially unexpected) third factor that contributes to both.3Lack of longitudinal research that follows AU youth into adulthood. Human and animal neuro-developmental research suggests that even slight and subtle changes in brain structure and function during adolescence can have long standing effects upon neurodevelopmental and socio-emotional growth, including the potential to develop psychopathology and engage in future substance use (Jacobus & Tapert, 2013; Spear, 2014). However, the limited body of longitudinal studies that follow AU youth into adulthood makes definitive conclusions about the sustained behavioural or neural sequelae of adolescent AU impossible at this time.4Interpretation of adolescent MRI/fMRI research. As with all neuroimaging studies that compare groups, there is no clear way to interpret differences in brain structure and function between the two groups. For example, we are still far
