Eating disorders (ED) such as anorexia nervosa (AN), bulimia nervosa (BN), and binge-eating disorder (BED) are debilitating and costly with few effective treatments. Comorbidity between ED and anxiety (ANX) and obsessive-compulsive disorder (OCD) is typical, with about two-thirds of individuals with ED also reporting lifetime ANX (including OCD). Comorbidity adversely impacts prognosis and time to recovery. Most ED and ANX phenotypes onset during adolescence, and evidence points to shared risk at the genetic level. ED and ANX phenotypes are moderately heritable. Genetic risk scores (GRS), which combine weighted risk from common variant single-nucleotide polymorphisms (SNPs) across the genome, are effective in defining psychiatric risk, although the focus has typically been on diagnoses. Integrating genetic risk information across multiple ED- and ANX- phenotypes could enhance predictive power of GRS while also specifying whether this genetic risk is best understood through a single factor vs. multiple factors. For instance, multiple metabolic, anthropometric, and psychiatric traits share genetic risk with AN. ANX also shows significant genetic overlap with psychiatric traits but less so with anthropometric and metabolic traits, suggesting shared risk between ED and ANX with psychiatric traits, but differential risk with metabolic and anthropometric traits. We will investigate this empirically using genomic structural equation modeling (GSEM) to identify genomic factors associated with ED and ANX phenotypes.
Additionally, we propose a fine-grained investigation of the association between ED and ANX by examining ED and ANX symptom trajectories across adolescence and into adulthood; to hone in on the biology that underlies ED and ANX change over time. At present, little is known about how ED and ANX symptoms affect each other across development, and how genetic risk influences their onset and course, though it is likely that genetic risk affects onset and course differently in adolescence vs. adulthood. Studying how ED and ANX are associated, both genetically and phenotypically, across development will advance early identification and targeted prevention and treatment of these conditions before threshold diagnoses crystallize.