Polli, Andrea, Hendrix, Jolien, Ickmans, Kelly et al. · Journal of translational medicine · 2022 · DOI
This study looked at how genes and chemical changes in DNA affect a protein called COMT, which plays a role in pain and inflammation in ME/CFS and fibromyalgia. Researchers compared 28 patients with these conditions to 26 healthy people and measured pain sensitivity, genetic variants, and immune markers. They found that certain genetic patterns and DNA changes were linked to symptoms and immune responses, suggesting that how our genes are "switched on or off" may contribute to these conditions.
This research provides mechanistic evidence that epigenetic modifications—reversible DNA changes that don't alter genes themselves—may contribute to ME/CFS and fibromyalgia pathophysiology, particularly through altered pain processing and immune regulation. Understanding these molecular mechanisms could eventually lead to better diagnostic biomarkers and personalized treatment strategies for these poorly understood conditions.
This study does not establish causation—increased methylation may be a consequence rather than a cause of disease. The findings are not specific to ME/CFS or fibromyalgia alone, so they do not explain what makes these conditions distinct. Results from a small sample cannot be generalized to all ME/CFS patients without larger replication studies.
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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