Another dominant model to consider is the ‘disinhibitory/externalizing spectrum’ (DES) model (Gorenstein and Newman, 1980; Krueger et al., 2002; Iacono et al., 2003) which appears to have a similar cluster of disorders and similar etiological and neurocognitive explanations. Although, in many of our earlier studies, we have supported the DES model for alcoholism, especially to explain the neurocognitive disinhibition (Begleiter and Porjesz, 1999; Kamarajan et al., 2004, 2005a, 2005b, 2006; Porjesz et al., 2005a; Porjesz and Rangaswamy, 2007; Chen et al., 2007; Rangaswamy et al., 2007), the scope of the present study appears to fit well with the RDS model, as it specifically deals with reward processing deficiency in alcoholism which is not explicitly part of the DES model. Interestingly, a common underlying aspect to both models is the ability to identify and integrate the spectrum of disorders that share a common etiology, pathophysiology, biological markers and brain circuitry. In this regard, these models may be complementary to each other in explaining different dimensions of the spectrum rather than assumed being competitive. As a final note, it should be mentioned
