There may be longer-lasting consequences of repeated exposure to alcohol during adolescence as well. Substantial research has shown that the younger individuals are when they begin to drink, the more likely they are to develop risky drinking patterns, display later stress-induced drinking, and become dependent on alcohol (e.g., Grant & Dawson, 1997; Ehlers et al., 2006; Young et al., 2006). Alterations in regional brain volumes, white-matter integrity, and brain activation patterns during cognitive tasks also have been reported in youth after one to two years of binge drinking (Squeglia et al., 2009). Some of the neural differences seen among individuals with a history of high levels of adolescent alcohol use may be associated with toxicity due to the early alcohol exposure itself (e.g., reductions in the size of the limbic region known as the hippocampus), whereas other changes (e.g., decreases in PFC volume) may reflect premorbid characteristics that serve to increase risk for early alcohol use (e.g., De Bellis et al., 2005). Thus, early use of alcohol may not necessarily be causal in producing these neural alterations or the elevated
