Wyns, Arne, Hendrix, Jolien, Van Campenhout, Jente et al. · International journal of molecular sciences · 2026 · DOI
This study examined whether changes in how a gene called OPRM1 (which controls opioid receptors in the body) are chemically marked in people with ME/CFS and fibromyalgia. Researchers found that people with these conditions had higher levels of these chemical marks on the OPRM1 gene compared to healthy people, even after accounting for how severe their symptoms were. This suggests that problems with the body's natural pain-relief system may be a fundamental part of these illnesses.
This is the first study to identify epigenetic modifications of the opioid receptor gene in ME/CFS and fibromyalgia, providing potential biological evidence for abnormalities in natural pain-modulation systems that could explain why these patients experience disproportionate pain and fatigue. Understanding this mechanism may eventually lead to new diagnostic tools and targeted treatments for these poorly understood conditions.
This study does not prove that increased OPRM1 methylation causes ME/CFS or fibromyalgia, only that an association exists. It also does not demonstrate that this methylation actually reduces opioid receptor function or activity—only that the chemical modification is present. Finally, because methylation patterns were measured at single timepoints, the study cannot determine whether these changes are stable, develop before symptom onset, or represent a consequence of disease.
About the PEM badge: “PEM required” means post-exertional malaise was an explicit required diagnostic criterion for participant inclusion in this study — not that PEM was studied, observed, or discussed. Studies using criteria that do not require PEM (e.g. Fukuda, Oxford) are tagged “PEM not required”. How the atlas works →
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