Alcohol is a physiological stressor, which in turn, influences alcohol consumption. The mechanisms underlying this complex interaction, however, remain unknown. Acute alcohol consumption can activate the HPA axis and release glucocorticoids in a dose-dependent manner (Boyd, Kumar et al. 2010). Acute alcohol intake in social drinkers increases cortisol levels, though with the transition from social drinking to alcohol dependence, the HPA axis response is attenuated and the cortisol response is decreased (King, Munisamy et al. 2006). Similarly, acute ethanol voluntary self-administration in rats stimulated release of corticosterone and ACTH, but chronic exposure sufficient to produce dependence decreased the neuroendocrine response (Richardson, Lee et al. 2008). The impact of alcohol on HPA activation/function depends on several factors such as: 1) the timing of alcohol administration relative to stimulus, 2) duration of stressful stimulus (chronic vs. acute), and 3) whether individuals usually experience stimulant-like or sedative-like effects of alcohol under normal conditions. In healthy males given the Trier Social Stress Test, production of salivary cortisol was inhibited when ethanol was administered intravenously after a stressor to achieve a breath alcohol concentration of
