This study has several strengths and limitations. One limitation is that we used a relatively small number of participants to test a large number of putative predictors (genotypes). Despite the small sample, there is credible evidence that intermediate pharmacogenomic phenotypes might be more likely to have larger effect alleles [24]. Another potential limitation of this study was the use of participants that were not heavy drug abusers and thus might not have been at the highest genetic risk for developing drug abuse. Although our study was based on the idea that genetic variability in a population of healthy young adults is representative of the larger population, it is possible that our ascertainment procedures excluded relevant genetic variants. Similarly, we chose modest doses that were administered orally, whereas drug users typically ingest higher doses with faster routes of administration (intranasal, intravenous, or inhalation). Lastly, differences in drug metabolism may constitute an uncontrolled source of variability. Reducing the complex phenotype data to a small number of baseline and response factors is a strength of our study because baseline differences might otherwise confound
