Early age at first drink has been linked to alcohol misuse in numerous studies over the last two decades. Whether interpreted as causal or as a marker of familial risk (King and Chassin, 2007; Prescott and Kendler, 1999) or moderator of genetic liability (Agrawal et al., 2009), early onset alcohol use is commonly viewed as a key factor to consider in prevention efforts to reduce alcohol-related problems. Although some of the evidence for elevated rates of heavy and problem drinking among early users comes from prospective studies (Grant et al., 2001; King and Chassin, 2007; Pedersen and Skrondal, 1998; Pitkanen et al., 2005; Warner and White, 2003), a large number of investigations of this pathway of risk are based on retrospective reports (Chou and Pickering, 1992; DeWit et al., 2000; Grant and Dawson, 1997; Grant et al., 2006; Hingson et al., 2006; McGue et al., 2001; Prescott and Kendler, 1999; Vieira et al., 2007). The cost, time, and logistical challenges of conducting prospective studies spanning the periods of risk for both initiation and the development of alcohol-related problems, particularly in
