Our fifth conclusion addresses what these data mean in terms of clinical prevention and intervention implications. Ultimately, these collective data suggest that there is a different pattern of brain structure and function for AU versus non-AU youth. Concretely, these brain-based differences are relevant because they have been found to place youth at greater risk for future binge drinking and sustained AUDs long into adulthood (e.g., King, de Wit, McNamara, & Cao, 2011; Spear, 2014). While there are concerns about how this trajectory would progress unchecked, there is also room for optimism. The broader human adolescent addiction literature suggests that observed differences return to typical patterns when AU is discontinued (Lisdahl et al., 2013a; Monnig et al., 2013; Welch et al., 2013). Thus, the human adolescent brain may be able to get back on track once youth are able to reduce or abstain from AU. One promising clinical avenue may be to bolster and strengthen prefrontal/executive control skills, to help AU youth improve their decision-making in favour of reducing AU. Similarly, approaches that re-orient AU youth to the relationship between incentive
