Several studies suggest that high risk individuals display a blunted neuroendocrine response to stress (Dai et al. 2002; Dawes et al. 1999; Sorocco et al. 2006), similar to those observed in children with ADHD (Hastings et al. 2009; King et al. 1998; Shin and Lee 2007), conduct disorder (Fairchild et al. 2008; McBurnett et al. 2005) and ASPD (O'Leary et al. 2007). It has been reported that 10- to 12-year-old offspring of alcoholics show reduced reactivity of the hypothalamic-pituitary-adrenocortical (HPA) system to a potentially anxiety-provoking situation and an attenuated return to baseline cortisol levels (Moss et al. 1995, 1999). In contrast, other studies have shown that cortisol response to psychosocial stress is significantly increased in offspring with a family history of AUD compared to those with no family history of AUD (Uhart et al. 2006; Zimmermann et al. 2004). These contradictory findings may be due to varying psychological comorbidity, previous drug and alcohol use, gender distribution, and personality traits all of which that have been shown to influence HPA functioning. Interestingly, conduct disorder symptoms in children may contribute to the
