in predicting relapse in abstinent individuals with AUD (Bauer, 2001; Saletu-Zyhlarz et al.). Since elevated beta EEG is present in the offspring of alcoholics prior to the onset of risky drinking (Begleiter and Porjesz, 1999; Deckel et al., 1996; Rangaswamy et al., 2002), it has been suggested that excess beta power precedes the development of AUDs and is likely related to an underlying genetic predisposition for developing AUD, rather than a consequence of heavy alcohol use. Begleiter and colleagues have suggested that this may be an electrophysiological index of an imbalance in the excitation–inhibition homeostasis in the cortex, which underlies a predisposition to develop AUD and related disorders (Begleiter and Porjesz, 1999; Porjesz et al., 2005). Further supporting this hypothesis is the association of beta EEG and other disorders characterized by behavioral disinhibition such as behavior problems and hyperactivity in children (Deckel et al., 1996), externalizing psychopathology (e.g., substance abuse symptoms) in a community sample of adolescents (Gilmore et al., 2010b), ADHD (Choi et al., 2013), and internet addiction with comorbid depression (Lee et al., 2014). Although the precise role of increased beta EEG in these behaviors and disorders remains unclear, this literature suggests that there is variation in fast
