Shared genetic risk between anorexia nervosa and cardiovascular disease events: Evidence from genome‐wide association studies

• Published in: Brain and behavior 2024-02, Vol.14 (2), p.e3294-n/a
• Main Authors: Qi, Baiyu, Graff, Mariaelisa, Eating Disorders Working Group of the Psychiatric Genomics Consortium, Bulik, Cynthia M, North, Kari E, Munn‐Chernoff, Melissa A
• Format: Article
• Language: English
• Subjects: Anorexia; Binge eating; Biobanks; Brief Report; Brief Reports; Cardiac arrhythmia; Cardiomyopathy; Cardiovascular disease; Consortia; Coronary vessels; Diabetes; Eating disorders; genetics; Genomes; Genomics; Genotype & phenotype; Health risk assessment; Heart attacks; heart disease; Heart failure; Insulin resistance; medical complications; Medicin och hälsovetenskap; Mortality; Risk factors; Self report; Stroke; Vein & artery diseases; Working groups
• ISSN: 2162-3279; 2162-3279
• DOI: 10.1002/brb3.3294

Objective Cardiovascular complications occur in up to 80% of patients with anorexia nervosa (AN), yet the underlying mechanisms warrant further investigation. We assessed the genetic correlation (rg) between AN and cardiovascular disease (CVD) events to inform whether elevated cardiovascular risk among individuals with AN is due to shared genetic effects. Method We used genome‐wide association study summary statistics for AN (N = 72,517), AN with binge eating (N = 12,630), AN without binge eating (N = 12,516), and six CVD events (N = 390,142 to 977,323). We calculated the rgs via linkage disequilibrium score regression and corrected for multiple testing using false discovery rate. Results Significant rgs emerged between AN with heart failure (rg = –0.11, SE = 0.05, q = .04) and myocardial infarction (rg = –0.10, SE = 0.03, q = .01). AN with binge eating had a significant rg with myocardial infarction (rg = –0.15, SE = 0.06, q = .02). No significant rg emerged between AN without binge eating and any CVD event. Discussion Some loci affect the liability to AN and CVD in opposite directions and the shared genetic effects may not be consistent across all CVD events. Our results provide further evidence suggesting that the elevated cardiovascular risk in AN may not be due to shared genetic underpinnings, but more likely a downstream consequence of the disease. We calculated the genetic correlation between three anorexia nervosa (AN) phenotypes and six cardiovascular disease (CVD) events. We observed significant (q