at 4.1%, 2/4 at 12.8%, 4/7 at 27.4%, and 4/4 at 39.3%. Regenotyping ~10% of the samples revealed an error rate of 7.5% (4/53). For the present study, DRD4 variability was coded on the basis of the presence (7+) versus absence (7−) of at least one copy of the DRD4 7-repeat allele. For clarity, based on this coding scheme, adolescents without a 7-repeat but with at least one longer allele (i.e. 8, 9, or 10) were included in the 7− category. When the alleles are collapsed to 7+ and 7− the error rate falls to 5.7% (3/53) due to one of the four errors not changing their status as being 7+. This rate is not surprising given the difficulty of amplifying the 7-copy allele in the presence of the 4-copy allele. In addition, the genotypes were in Hardy–Weinberg equilibrium, χ2(1) = 0.03, ns, increasing confidence that the number of individuals who were 7+ heterozygotes (the difficult genotype to assess) was accurately reported. It is important to note that if error were nonrandom, bias might be introduced into our results. To explore this possibility, we examined correlations between variables that are included in the path model and DRD4 (see Table 1).
