those with abundant, high amplitude alpha activity showed a blunted EEG response to alcohol. Based on the evidence that “desynchronized”, low-alpha EEG is indicative of higher level of tonic arousal and is prevalent among alcoholics, the authors proposed a model of alcoholism risk, according to which individuals with higher level of tonic central nervous system excitation may be predisposed to alcoholism because they experience greater relaxation after alcohol intake and therefore may be more sensitive to the rewarding and reinforcing effects of alcohol. Finally, MZ similarity on EEG measures tended to increase, while DZ similarity tended to decrease after alcohol intake, suggesting that genetic influences on brain oscillations are increased in the state of alcohol intoxication. These results have been corroborated in a later study (Sorbel et al., 1996) that, using a larger twin sample, showed increased heritability of EEG spectral band power in all frequency bands after alcohol intake, which was mainly due to decrease in within-pair differences of MZ twins. Taken together, these studies suggest that EEG under alcohol may be influenced by an additional set of genes specific to this condition, perhaps with non-additive affects, and these genetically determined differences in brain function may be important for
