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Reducing Underage Drinking: A Collective Responsibility
hol use caused damage to the frontal regions of the brain (Crews et al., 2000).
New research using magnetic resonance imaging (MRI) technology to obtain a portrait of adolescent human brains support these animal studies, showing that the brain structure of youths with alcohol-use disorders is adversely affected. The hippocampus, which is responsible for forming new memories, was noticeably smaller in youth who abuse alcohol than in their nondrinking peers (De Bellis et al., 2000). Youth with alcohol-use disorders also performed worse on memory tests than nondrinkers, further suggesting that the structural difference in hippocampus size was affecting brain functioning. Neuropsychological studies also suggest that alcohol use during adolescence may have a direct effect on brain functioning: negative effects included decreased ability in planning and executive functioning, memory, spatial operations, and attention—all of which are important to academic performance and future functioning (Giancola and Mezzich, 2000; Brown et al., 2000; Tapert and Brown, 1999; Tapert et al., 2001).
THE CAUSATION QUESTION
Many consequences—both immediate and long-term—are correlated with youthful drinking. In the case of immediate consequences, drinking impairs one’s perceptual and motor skills, and this impairment clearly increases the risk of a car crash if one drives after drinking—a risk that is demonstrably higher for young drivers. Similarly, the disinhibiting effect of alcohol use impairs judgment and increases the risk of violence and unprotected sexual intercourse. In this sense, the causal link between alcohol use and the outcomes and problem behaviors just reviewed is not in doubt. The empirical evidence also shows a clear correlation between early drinking and problematic adult drinking and other related longer term problems: that is, the earlier that young people start drinking, the more likely they are to have problems in their adult lives.
However, these outcomes and behaviors may not be entirely attributable to alcohol. For example, some youths who have alcohol-related crashes or engage in alcohol-related violence or other risk-taking behavior may have been otherwise strongly predisposed to engage in problem behaviors of all sorts due to genetics, family circumstances, or other factors. Similarly, the higher rates of alcohol dependence, disease, and dysfunction among adults who began heavy drinking as youths may not be attributable to the early drinking per se. Some of these long-term outcomes are also consistent with the possibility that some individuals have a particular vulnerability to developing bad drinking habits and that one of the characteristics of these individuals is that they start drinking early. (For example, children of alco-