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Leveraging transdiagnostic genetic liability to psychiatric disorders to dissect clinical outcomes of anorexia nervosa

  • Zheng An Lu
  • , Alexander Ploner
  • , Andreas Birgegård
  • , Sarah L. Maguire
  • , Stephan Zipfel
  • , Eleftheria Zeggini
  • , D. Blake Woodside
  • , H. Erich Wichmann
  • , Thomas Werge
  • , Hunna J. Watson
  • , Tracey D. Wade
  • , Annemarie van Elburg
  • , Konstantinos Tziouvas
  • , Artemis Tsitsika
  • , Federica Tozzi
  • , Alfonso Tortorella
  • , Friederike I. Tam
  • , Beata Świątkowska
  • , Garret D. Stuber
  • , Michael Strober
  • Vidar W. Steen, Nicole Soranzo, Agnieszka Slopien, Marta Tyszkiewicz-Nwafor, Eric F. van Furth, Margarita C.T. Slof-Op’t, Lenka Slachtova, Alexandra Schosser, Nicholas J. Schork, Janet Treasure, Ulrike Schmidt, Stephen W. Scherer, André Scherag, Paolo Santonastaso, Filip Rybakowski, Alessandro Rotondo, Stephan Ripke, Samuli Ripatti, Valdo Ricca, Ted Reichborn-Kjennerud, Anu Raevuori, John F. Pearson, Jacques Pantel, Aarno Palotie, Julie O’Toole, Roel A. Ophoff, Martien J.H. Kas, Roger A.H. Adan, Jurjen Luykx, Bochao Danae Lin,

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Abstract

Anorexia nervosa (AN) has extensive genetic correlations with other psychiatric disorders, and genetic risk for different psychiatric disorders was associated with distinct clinical courses in AN. Uncovering associations between transdiagnostic psychiatric genetic liability and AN outcomes can facilitate its personalized treatment. In this study, we investigated the associations between transdiagnostic psychiatric genetic liability and outcomes of AN. Genomic structural equation models were fitted to genome-wide association data for AN and psychiatric disorders with high genetic correlations with AN (obsessive-compulsive symptoms [OCS], major depressive disorder [MDD], schizophrenia, and anxiety disorders) to extract one shared and five trait-specific genetic components. Next, we calculated the polygenic risk scores (PRS) for these components, including PRSshared, PRSAN-specific, PRSOCS-specific, PRSMDD-specific, PRSSCZ-specific and PRSANX-specific, which index the shared genetic liability to all five psychiatric traits, and genetic liability specific to AN, OCS, MDD, SCZ and ANX, respectively. We then tested associations between these PRSs and clinical outcomes reported between 1997 and 2018 among AN cases from the Anorexia Nervosa Genetics Initiative (ANGI), linked to Swedish National Registers. The clinical outcomes included cumulative disease burden (i.e., number of diagnoses, medication prescriptions, and inpatient days), risks of psychiatric comorbidities, and AN symptomatology. Among 4028 included AN cases, the mean (SD) birth year was 1985 (9), and 3947 (98.0%) were female. Within AN, +1 SD increase of PRSshared was associated with 9–39% excess risk of disease burden and psychiatric comorbidity, whereas the associations between PRSAN-specific and most clinical outcomes were statistically non-significant. +1 SD increase of PRSMDD-specific was associated with 3–29% increased risk of AN disease burden. Our findings show that shared psychiatric liability is associated with more adverse AN outcomes, whereas AN-specific liability is not a good indicator for its clinical course. This study provides a novel perspective on factors influencing heterogeneity in AN clinical course.

Original languageEnglish
Pages (from-to)1475-1484
Number of pages10
JournalMolecular Psychiatry
Volume31
Issue number3
Early online date2025
DOIs
Publication statusPublished - Mar 2026

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