Across AUD symptoms, the pattern of inter-symptom SNP correlations was generally high (strong rG-SNP > 0.60), suggesting shared genetic variance across symptoms (see right side of Table 2). However it is important to recognize that several of these estimates were inflated in instances where the h2SNP of at least one of the symptoms was non-significant (i.e., only a small proportion of the phenotypic variance in the DSM-5 criterion is explained by genetic variation). Analysis of the 11×11 genetic variance/covariance matrix suggested a single genetic factor parsimoniously describes much of the shared genetic variance across the 11 criteria (see Supplementary Table S1 for the genetic variance/covariance matrix). Parallel analysis indicated that the first eigenvalue derived from this matrix exceeded the 95th percentile of the distribution of eigenvalues derived from random data (see Figure 1). Genetic factor loadings for AUD symptoms were high (>0.60) and the total genetic variance of each criteria attributable to the factor ranged from 38% for ‘craving’ to 89% for ‘failure to fulfill major roles’ (see Table 4 for a summary of factor loadings and percent variance explained
