Sun, Qian, Oltra, Elisa, Dijck-Brouwer, D A Janneke et al. · Redox biology · 2023 · DOI
Some people with ME/CFS have antibodies that attack a protein called selenoprotein P, which normally helps transport selenium (a mineral needed for thyroid function) throughout the body. This study found that ME/CFS patients with these antibodies have lower selenium levels and struggle to convert thyroid hormone into its active form, which could explain why they feel tired and have other thyroid-like symptoms even when standard thyroid tests appear normal.
This research identifies a potential biomarker (SELENOP-aAb) and biological mechanism that could explain thyroid-like symptoms in a subset of ME/CFS patients whose standard thyroid tests appear normal—a long-standing clinical puzzle. If confirmed, this could lead to new diagnostic tests and targeted treatments specifically for SELENOP-aAb-positive patients, potentially offering relief to patients currently dismissed as having normal thyroid function.
This study does not prove that SELENOP-aAb directly causes ME/CFS or that correcting selenium deficiency will reverse the illness—correlation does not equal causation. The cross-sectional design cannot establish whether autoantibodies are a cause or consequence of the disease. Additionally, the findings in this specific subgroup may not apply to all ME/CFS patients, and clinical benefit from selenium or other interventions remains unproven.
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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