1 Eating Disorders Continuum, Douglas Institute, Montreal, Canada.
2 Department of Psychiatry, McGill University, Montreal, Canada.
3 Research Centre, Douglas Institute, Montreal, Canada.
4 Department of Psychology, Concordia University, Montreal, Canada.
5 Sainte-Justine Hospital Research Centre, University of Montreal, Montreal, Canada.
6 Department of Pharmacology and Therapeutics, McGill University, Montreal, Canada.

Objectives: Recent studies have reported altered methylation levels at disorder-relevant DNA sites in people who are ill with Anorexia Nervosa (AN) compared to findings in people with no eating disorder (ED) or in whom AN has remitted. The preceding implies state-related influences upon gene expression in people with AN. The present study further examined this notion. Methods: We measured genome-wide DNA methylation in 145 women with active AN, 49 showing stable one-year remission of AN, and 64 with no ED. Results: Comparisons revealed 205 differentially methylated sites between active and no ED groups, and 162 differentially methylated sites between active and remitted groups (Q < 0.01). Probes tended to map onto genes relevant to psychiatric, metabolic and immune functions. Notably, several of the genes identified here as being differentially methylated in people with AN (e.g., SYNJ2, PRKAG2, STAT3, CSGALNACT1, NEGR1, NR1H3) have figured in previous studies on AN. Effects also associated illness chronicity and lower BMI with more pronounced DNA methylation alterations, and remission of AN with normalization of DNA methylation. Conclusions: Findings corroborate earlier results suggesting reversible DNA methylation alterations in AN, and point to particular genes at which epigenetic mechanisms may act to shape AN phenomenology.