As noted earlier, individuals at risk for AUD tend to exhibit anomalies in their response to aversive stimuli as indicated by elevations in heart rate and blunted cortisol levels. In the presence of alcohol, the HPA system seems to be differentially affected by stress in high risk youth compared to control subjects. The HPA system regulates multiple components of the body's autonomic response to stress and prepares mechanisms in the brain for responsive action and survival (de Kloet et al. 1999). The HPA system is an important regulatory system that acts through hormone cascades to support both behavioral and physiological responses to threat (de Kloet et al. 1998). Alteration in HPA functioning associated with alcoholism risk may negatively impact an individual's ability to respond to internal and external challenges (i.e. cope with stress). In addition, cognitive deficits are associated with HPA system dysfunction (e.g. Cushings disease), so it is equally plausible that altered neurohormone levels in the offspring of alcoholics can disrupt cognitive processes (Starkman et al. 2001).
