The comorbidity problem is by no means unique to psychiatry. Similar sets of results with respect to familial clustering, cross-disorder treatment effects, and high levels of pleiotropy are observed across autoimmune disorders including Crohn’s disease, rheumatoid arthritis, and type 1 diabetes (for review see Cotsapas & Hafler, 2013). This has resulted in analogous conversations surrounding revision of autoimmune nosology and highlights an important point: Type 1 diabetes and arthritis certainly appear quite different, but despite our observation the biology points towards a conglomeration of both cross-cutting and distinct pathways. Within psychiatry, many disorders also seem dissimilar, but their general co-occurrence at levels far higher than chance necessitate understanding the underlying causes of this overlap. Cross-disorder genomics is converging on the ability to fill in major gaps in our understanding of comorbidity via emerging evidence across genome-wide, mechanistic, and individual variant levels of analysis. As genomic research continues to progress, it will likely play an increasingly important role in the process of “epistemic iteration,” whereby our diagnostic categories are iteratively updated to reflect an evidence base that gradually approximates the latent structure of psychopathology (Kendler, 2009).
