Several other factors related to our sample composition constrain our interpretations. We were not able to examine sex differences, as our sampling strategy was designed to minimize differences by matching the alcohol dependent and healthy control groups for this and other demographic characteristics. We did not measure cognitive ability (e.g., IQ) or match groups on it, but this characteristic could have contributed to function in the circuits of interest in the current study. In addition, we did not collect detailed information about family history of alcohol dependence beyond its presence or absence of a first- or second-degree relative. As a result, we were not able to investigate the effects of family history density (e.g., as applied in work by Stoltenberg et al. [60] and Zucker et al. [61]) or of alcohol dependence in particular family members (e.g., mothers) on neural response or functional connectivity. Finally, we did not collect data on alcohol use from participants in our healthy control group, and this would have allowed us to draw stronger conclusions about the mechanisms of group differences in frontostriatal function.
