Genetic architecture of eating disorder risk and specific symptoms in the general adult population
Abstract
Abstract Eating disorders (EDs) affect 2%–5% of the population, while subclinical symptoms are more prevalent. Previous diagnosis-based genome-wide association studies (GWASs) identified risk variants, but the genetic architecture of ED symptoms in the general population remains unclear. Using the five-item SCOFF screening tool, we conducted six GWASs in the Estonian Biobank (EstBB; N = 212,000): one for higher ED risk and one for each SCOFF item. We estimated genetic correlations with 59 external phenotypes, evaluated polygenic risk scores (PRSs) for uncontrolled eating in an independent subsample, and performed phenome-wide association studies (PheWAS) linking genetic risk to medical diagnoses. We found 14 independent genome-wide significant SNPs associated with increased ED risk and cognitive-behavioral symptoms like loss of control and food dominates , with SNP heritability ranging from 2% to 8%. Notably, variants in FTO and MC4R were linked to both higher ED risk and cognitive-behavioral symptoms , while ROBO2 and TMEM18 correlated with higher ED risk and loss of control , highlighting appetite regulation pathways. Cognitive-behavioral symptoms exhibited moderate-to-strong genetic correlations with anthropometric, psychiatric, lifestyle, personality, and somatic traits. PheWASs identified associations between PRSs of ED symptoms and medical conditions (28, 27, and 24 significant associations for higher ED risk , loss of control , and food dominates , respectively),…
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