Acute ethanol (EtOH) administration impairs circadian clock phase-resetting, suggesting a mode for the disruptive effect of alcohol abuse on human circadian rhythms. Here, we extend this research by characterizing the chronobiological effects of chronic alcohol consumption. First, daily profiles of EtOH were measured in the suprachiasmatic nucleus (SCN) and subcutaneously using microdialysis in hamsters drinking EtOH. In both cases, EtOH peaked near lights-off and declined throughout the dark-phase to low day-time levels. Drinking bouts preceded EtOH peaks by ~20 min. Second, hamsters chronically drinking EtOH received a light pulse during the late dark-phase (Zeitgeber time [ZT] 18.5) to induce photic phase-advances. Water controls had shifts of 1.2±0.2 h, while those drinking 10% and 20% EtOH had much reduced shifts (0.5±0.1 h and 0.3±0.1 h, respectively; p<0.001 vs. controls). Third, incremental decreases in light intensity (270 lux to 0.5 lux) were used to explore chronic EtOH effects on photic entrainment and rhythm stability. Activity onset was unaffected by 20% EtOH at all light intensities. Conversely, the 24 h pattern of activity bouts was disrupted by EtOH under all light intensities. Finally, replacement of chronic EtOH with water was used to examine withdrawal effects. Water controls had photic phase-advances of 1.1±0.3 h, while hamsters deprived of EtOH for 2-3 days showed enhanced shifts (2.1±0.3 h; p<0.05 vs. controls). Thus, in chronically-drinking hamsters, brain EtOH levels are sufficient to inhibit photic phase-resetting and disrupt circadian activity. Chronic EtOH did not impair photic entrainment, however its replacement with water potentiated photic phase-resetting.