Blood DNA methylation patterns in anorexia nervosa: a longitudinal study on the role of illness duration and symptom remission

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Previous studies have shown state-related alterations of peripheral DNA methylation levels in people with Anorexia Nervosa (AN). The aim of the present study was to investigate the extent to which illness duration in AN impacts DNA methylation changes and to examine any effects of illness duration upon the stability of methylation changes following symptom remission. We assessed leukocyte genome-wide DNA methylation in 198 women with active AN, 62 showing one-year weight restoration after a full-threshold episode of AN (AN-remitted) and 92 who never had an eating disorder (NED). Follow-up data (after 15.3 weeks of treatment, on average) were available for 108 AN-active participants. Compared to NED and AN-remitted participants, women with active AN had altered DNA methylation in genes involved in mental status, metabolism and immune function. Subsequent analyses highlighted differentially-methylated regions at LRRC8D , PRKAG2 , CCDC6 , and STAT3 genes. Additionally, in AN-active participants, longer illness duration was associated with lower methylation levels (7 CpG sites) in the serotonin receptor 2A gene ( HTR2A ) promoter region. Irrespective of illness duration, increases in body mass index were associated with methylation changes in genes involved in lipid and glucose metabolism, cellular functions, and immune processes. Results suggest chronicity-linked, reversible alterations of DNA methylation in AN, and support a pathophysiological model of AN involving psychiatric, metabolic, and immune components. In particular, our findings point to an epigenetically-regulated effect by which a long-standing eating disorder may adversely affect the serotonin system--which is thought to mediate various features that are prominent in individuals with AN.

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