While there are numerous strengths to the presented systematic review, including that reviewed studies represent an important first step towards synthesizing the empirical data around human adolescent AU and brain function and structure, the findings should be interpreted in light of the following limitations.1Presence of potential confounds. Due to the established role of co-occurring psychiatric factors (e.g., Dalwani et al., 2014), co-occurring substance use (e.g., Baker, Yücel, Fornito, Allen, & Lubman, 2013), and family history of AU (e.g., Spadoni et al., 2013) in AU youths' brain structure and function, we intentionally omitted studies that explicitly targeted these factors (e.g., evaluations of co-occurring psychopathology, those in which the primary focus was not on alcohol, evaluations of family history) in the absence of examining actively drinking youth. However, we recognize that this approach may still have limitations, and have therefore detailed potential 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
