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Chunk #21 — Discussion

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The etiology of DSM-5 alcohol use disorder: Evidence of shared and non-shared additive genetic effects.
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The incorporation of previous DSM-IV abuse symptoms and craving for alcohol enhanced the definition of problematic alcohol use. Estimated effects of genetic variation on the newly added alcohol symptoms ranged from 0.10–0.37. Notably, the SNP-heritability of DSM-5 AUD factor was similar to what was previously reported for DSM-IV alcohol dependence as a factor score (Palmer et al., 2015b, Brick et al., 2017). Moreover, our examinations of the genetic influences on the 11 symptoms supports the underlying assumptions of (1) a single underlying dimension of risk that is captured by the symptoms, and (2) common genetic pathways that contribute to ‘craving’, ‘using longer than intended’, ‘withdrawal’, and the other symptoms. These findings align with previous examinations of alcohol symptoms in genetically informed samples, which suggested a single underlying latent trait that is polygenic in nature. It was for this reason that we opted to use Genomic Restricted maximum likelihood (GREML) to understand the relationship among the 11 AUD symptoms because our sample sizes precluded the use of genomewide association analysis which would have resulted in biased SNP-estimates that reflect only a