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This provided some initial evidence for an additive relationship, with each additional T allele associated with greater basal cortisol output. FIGURE 1 Effects of CRHR1 genotype on basal cortisol levels. Alcohol Consumption and Perceived Stress Differences in the CAR We tested to see if some of the variability in CAR could be accounted for by perceived stress over the past month and standard drinks consumed over the past 90 days. Perceived stress had a significant inverse relationship with CAR [��21 = �C0.007, t(68) = �C2.33, p = 0.023]. More specifically, rural African American emerging adults had a blunted CAR when experiencing higher levels of perceived stress. Furthermore, alcohol consumption also had a significant independent inverse relationship with CAR [��22 = �C0.003, t(68) = �C2.13, p = 0.037] such that the CAR was blunted in individuals who consumed higher amounts of alcoholic beverages. Moreover, the CAR was essentially non-existent in #find more randurls[1|1|,|CHEM1|]# participants who reported higher levels of stress and alcohol consumption (Figure ?(Figure2).2). The interaction between reported stress and alcohol consumption was not a predictor of CAR suggesting additive effects of perceived stress and alcohol consumption. Additionally, there wasn��t a gender effect in predicting CAR. FIGURE 2 The effects of alcohol consumption and perceived stress on the cortisol awaking response. Discussion The CAR has been identified as a reliable indicator of HPA-axis functioning (Chida and Steptoe, 2009; Gonzalez et al., 2009; Thorn et al., 2009). In this study, rural African American emerging adults exhibited a blunted CAR when reporting higher levels of stress or alcohol consumption. Moreover, these effects were additive, such that the CAR was obliterated for participants who reported both the experience of higher stress and increased alcohol consumption. While stress was only measured quantitatively over the past month, this outcome is consistent with previous studies that found a hypoactive CAR to be linked to chronic stress, fatigue, burnout, and hopelessness (Chida and Steptoe, 2009; Fries et al., 2009). This is further substantiated by the types of chronic stressors that were identified by the stress card sort. Furthermore, previous research linked alcohol abuse with hyperactive HPA activity (Adinoff et al., 2003). It is our hypothesis, that alcohol is being consumed as a negative coping strategy for addressing unmitigated stressors that this community endures on a daily basis. The long-term effect of heavy alcohol use will primarily mirror that of the stress model where acute alcohol consumption aimed at coping with daily life stress will initially lead to a hyperactive HPA-axis. However, the body��s chronic exposure to increased levels of alcohol will consequentially cause wear-and-tear on this regulatory system and ultimately result in a hypoactive HPA-axis due to allostatic load (Lovallo et al.