Hazrati, Ebrahim, Eftekhar, Seyed Parsa, Mosaed, Reza et al. · Molecular pain · 2024 · DOI
This review examined how a specific pathway in the body that breaks down the amino acid tryptophan might contribute to chronic pain, including in ME/CFS patients. The review looked at research across various pain conditions and depression, finding that certain chemicals produced along this pathway can either protect or damage nerve cells. The authors suggest that targeting this pathway could lead to new, non-opioid treatments for chronic pain.
ME/CFS is explicitly included in this review's scope, making it directly relevant to understanding potential biological mechanisms underlying post-exertional malaise, pain, and fatigue. The identification of the kynurenine pathway as a druggable target could inform future research into non-opioid, mechanism-based treatments for ME/CFS patients who often experience multi-system pain and depression.
This narrative review does not establish causal relationships between kynurenine pathway dysregulation and ME/CFS symptoms—it synthesizes existing literature rather than providing new mechanistic evidence. The review does not prove that KP-targeting interventions will be effective in ME/CFS patients specifically, nor does it determine whether KP abnormalities are primary drivers or secondary consequences of chronic pain and fatigue.
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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