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Epigenetic factors in eating disorders: Clinical correlates and diagnostic specificity

AI Summary
  • Environmental exposures, including gestational, psychosocial, nutritional and metabolic factors, alter the epigenome and influence eating disorder development.
  • DNA methylation changes occur in genes regulating mental health, metabolism and immune function; some anorexia nervosa methylation patterns may reverse with remission.
  • Epigenetic findings mirror genome-wide association results and show overlap with psychiatric, metabolic and autoimmune disorders, informing integrated aetiologic models and clinical potential.
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Handb Clin Neurol. 2026;219:269-285. doi: 10.1016/B978-0-443-19043-8.00011-6.

ABSTRACT

In this chapter, we discuss epigenetic factors in eating disorders. Following a brief introduction to eating disorders, we review research on how different environmental factors – gestational, psychosocial, nutritional, and metabolic – could impact the epigenome and eating-disorder development. We review the literature providing evidence for DNA methylation alterations in eating disorders in genes regulating mental health, metabolism, and immune function. We also review researchthat has suggested that DNA methylation patterns in anorexia nervosa may be reversible upon remission. Although most epigenetic research in eating disorders focuses on anorexia nervosa, there is some evidence of epigenetic overlap between eating disorders, on the one hand, and other psychiatric metabolic and autoimmune disorders, on the other. Shared epigenetic alterations may contribute to comorbidity patterns. Overall, results of epigenetic genome-wide research in eating disorders mirror the findings from genome-wide association studies, and underscore the importance of incorporating metabolic, psychiatric, and immune components in etiologic models of eating disorders. We conclude our chapter with an integrated etiologic epigenetic model, provide avenues for future research, and discuss the clinical potentials, for eating disorders, of epigenetic markers.

PMID:42880840 | DOI:10.1016/B978-0-443-19043-8.00011-6

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