Third, beyond the point estimates of effect size reported above, there was often substantial heterogeneity across studies. Although some of this variability could be explained by differences in gender composition, assessment of stimulation or sedation, and limbs of the BAC curve, other unmeasured differences between studies may have also contributed to effect heterogeneity. For example, studies differed on definitions of risk status, alcohol dosage, and other design components. Although we found little evidence that dosage moderated risk-group differences, the limited descriptions of other study factors—including participant ethnicities, dose pacing, time of day, and other contextual variables—presented in many studies precluded quantitative evaluations. Given that social context can increase subjective stimulant response to alcohol (Ray et al., 2010) and that some East Asians report greater subjective response as a function of genetic differences in alcohol metabolism (Hendershot et al., 2009), further study of these potentially important factors is warranted. As recommended by Morean and Corbin (2010), the use of standardized alcohol-administration procedures and risk-group categorization methods (e.g., binge drinking; Wechsler and Isaac, 1992)—along with validated measures of subjective stimulation and sedation
