years vs. 15.9 years, p < 0.003), and had comorbid Axis I disorders (75% cannabis use disorder, 72% lifetime major depressive episode, 69% attention deficit/hyperactivity disorder, and 63% conduct disorder) whereas such diagnoses were exclusionary for controls. These comorbid disorders have previously been linked to white matter abnormalities (Matochik et al., 2005; McAlonan et al., 2007; Medina et al., 2007a; Steingard et al., 2002). Thus, there is much difficulty extricating potential interactive effects of these conditions. However, both the present study and De Bellis and colleagues (2008) offer interesting contributions to understanding the relationships between adolescent alcohol involvement and white matter integrity. The present study examined sub-clinical drinking to better isolate alcohol effects on typically developing teenagers. Binge drinking teens are of particular interest, as it is estimated that more than 30% of minors who begin drinking before age 16 will develop alcohol dependence (Grant and Dawson, 1997). Indeed, studying nondisordered adolescent drinkers is of substantial import due to the increased risk for binge drinking teens to transition into an AUD by adulthood (Hawkins et al., 1992; Viner and Taylor, 2007). The sample in the De Bellis paper is representative of adolescents with an AUD, especially due to high rates
