The low level of response (LR) to alcohol is an endophenotype related to the future risk for heavy drinking, alcohol problems, and alcohol use disorders (AUDs) (Hu et al., 2005; Schuckit, 2002). The need to ingest more drinks to get the desired effects from early in life is hypothesized to increase the drinks consumed per occasion, which subsequently encourages selecting heavy-drinking peers and alters alcohol expectancies (Schuckit, 2002; Schuckit et al., in press, a). Following the guidelines for an endophenotype presented by Gottesman and Gould (2003), the less intense response to alcohol can be documented early in life (as young as age 12), predicts future alcohol-related problems, and has a heritability (or proportion of the variance explained by genes) of between 40% and 60% (Heath et al., 1999; Schuckit et al., 2006, 2007, in press, c). Several genes likely to contribute to the LR to alcohol in both animals and humans have been identified (Barr et al., 2003; Davies et al., 2003; Schuckit et al., 2005a), and structural equation as well as latent trajectory models have identified environmental components that
