LAUSR

Substance use disorders are complex psychiatric conditions that impose a significant burden on affected individuals, their families, and communities broadly. They are highly prevalent worldwide, influenced by a tangled constellation of interrelated environmental and biological factors. Notably, individuals struggling with substance use problems often use more than one substance, complicating efforts to understand, prevent, and treat these conditions. Advances in psychiatric genetics suggest that high rates of comorbidity among substance use disorders may be partly explained by a shared genetic etiology. That is, while some genetic influences may be fairly specific to a particular substance (e.g., ADH1B and alcohol), research suggests a considerable proportion of genetic risk operates via more general pathways to addiction. Such pleiotropic effects may be more the norm than the exception in psychopathology, as studies routinely find that genetic influences on psychiatric disorders cross diagnostic boundaries [1]. In this issue of Neuropsychopharmacology, Hatoum et al. [2] report an ambitious study that interrogates the genetic influences that cut across substance use disorders. To do so, they use Genomic Structural Equation Modeling (Genomic SEM), a statistical framework and software for applying structural equation modeling techniques to genome-wide association study (GWAS) summary statistics, to model the joint genetic architecture of several substances use disorder phenotypes. This approach enabled the authors to conduct a series of analyses that addressed the following questions: