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Chunk #2 — Introduction

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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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As part of the debate on the utility and suitability of the dichotomous measure of alcohol dependence (AD), as opposed to a continuous measure of alcohol problem severity in genetic research, we recently examined the assumption of genetic homogeneity across all DSM-IV dependence symptoms using genomewide SNP data (Palmer et al., 2015b). Validation of the assumption across the seven symptoms affirmed the utility of a factor score across the indices as much of the observed genetic variance was shared across the comorbid items, suggesting common genetic factors underlie the addiction state (Koob et al., 2014), which is reflected in behavioral symptoms included in DSM-5 AUD (American Psychiatric Association, 2013). The results also indicated that effects observed upon a latent continuum of AD risk (as indicated by DSM-IV dependence symptoms) may not be truly reflective of the entire liability continuum, as there also exists symptom-specific genetic variance that may be imparted by the study of multiple factors (as previously suggested using a multivariate twin study approach (Kendler et al., 2012)). This latter point was recently reflected in a report by Hart