Due to binge drinkers' relatively inchoate stages of alcohol use, results could alternatively highlight a premorbid white matter characteristic representing a vulnerability to risky drinking. However, the observed link between alcohol involvement (i.e., hangover) and reduced FA in this study lends support to a possible compromising influence of high-dose alcohol use on white matter quality. Several potential mechanisms could explain how FA might be reduced in heavy drinking teens. Years of alcoholism are linked to decreased N-acetylaspartate in white matter tissue, suggesting compounding axonal insult by chronic alcohol use (Meyerhoff et al., 2004; Schweinsburg et al., 2001). FA decrements could represent such a chemically induced axonal injury at a microstructural level. Animal models provide additional insights to rapid, alcohol-induced neural injury. Adult rats demonstrate neurodegeneration following once-daily ethanol exposure within as little as 5 days (Collins et al., 1998). Additionally, adolescent rats show differential sensitivity to brain damage compared to adults following 4 days of binge alcohol administration (Crews et al., 2000). Thus, human adolescents may be especially vulnerable to the deleterious effects of alcohol on neural tissues, including white
