As hypothesized, we found main effects of condition (corticotropin: F2,135 = 3.12; P < .05; cortisol: F2,136=10.04; P<.001; cortisol to corticotropin ratio: F2,135=5.35; P<.005) and group × condition (corticotropin: F2,135 = 5.64; P = .004; cortisol: F2,136 = 3.25; P=.04; cortisol to corticotropin ratio: P<.53), time (corticotropin: F6,420 = 4.35; P < .001; cortisol: F6,420=20.85; P<.001; cortisol to corticotropin ratio: F6,420 =12.6; P<.001), and group × time interaction (corticotropin: P<.57; cortisol: F6,420=4.29; P<.001; cortisol to corticotropin ratio: P<.34) for each measure. Condition main effects indicated greater responses in the stress (corticotropin: P<.02; cortisol: P<.003; cortisol to corticotropin ratio: P<.003) and alcohol cue (corticotropin: P<.61; cortisol: P<.001; cortisol to corticotropin ratio: P<.007) conditions relative to the neutral condition. Significant interactions were a result of higher corticotropin response in the neutral, relaxing condition in the alcohol-dependent patients relative to controls (P < .01), with no stress- and cue-induced corticotropin and cortisol responses to stress and to cues relative to the neutral condition in the patients relative to controls (Figure 4 highlights group × condition interactions showing baseline-adjusted mean responses of corticotropin and cortisol levels in the neutral, stress, and alcohol cue conditions for each group).
