use disorder. This would have suggested frequency-specific alterations related to consumption of large quantities of the substance. To address this, we performed follow-up regression analyses that included number of use disorder symptoms, as well as measures of the frequency of alcohol and cannabis use to help decipher whether our findings were associated with addiction-related circuitry, or with amount of substance use. This is notable because, in the SCID interview, use disorder symptoms, and respective use disorder diagnosis, do not inquire about the amount or regularity of use. Ultimately, this showed that reduced alpha power was significantly associated with increased number of AUD symptoms, above and beyond the amount of alcohol and cannabis use, and the number of CUD symptoms. This statistically narrows our neural findings toward being specifically related to AUD symptom severity, further supporting that the alpha reductions we observed were addiction-related.
