Autoantibodies to selenoprotein P in chronic fatigue syndrome suggest selenium transport impairment and acquired resistance to thyroid hormone. — ME/CFS Atlas
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Autoantibodies to selenoprotein P in chronic fatigue syndrome suggest selenium transport impairment and acquired resistance to thyroid hormone.
Sun, Qian, Oltra, Elisa, Dijck-Brouwer, D A Janneke et al. · Redox biology · 2023 · DOI
Quick Summary
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.
Why It Matters
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.
Observed Findings
SELENOP-aAb prevalence was 9.6–15.6% in CFS patients versus 0.9–2.0% in healthy controls.
In SELENOP-aAb-positive patients, the expected correlation between selenium and glutathione peroxidase activity was absent, suggesting impaired selenium delivery to tissues.
SELENOP-aAb-positive CFS patients had significantly lower deiodinase activity, free T3 levels, and T3/T4 ratios compared to negative patients.
24-hour urinary iodine was significantly lower in SELENOP-aAb-positive patients (median 43.2 μg/L) versus negative patients (58.9 μg/L) and controls (89.0 μg/L).
Selenium, glutathione peroxidase, and SELENOP levels showed linear correlations without saturation across samples, indicating selenium deficiency.
Inferred Conclusions
SELENOP-aAb impairs selenium transport and selenoprotein expression in target tissues, reducing the activity of thyroid hormone-converting enzymes (deiodinases).
In SELENOP-aAb-positive CFS patients, thyroid hormone activation is reduced as an acquired condition that may not be reflected by standard blood TSH and T4 measurements.
A subset of CFS patients have an autoimmune mechanism targeting selenoprotein P that could account for thyroid-like symptoms despite normal conventional thyroid tests.
Remaining Questions
Does correcting selenium deficiency or blocking SELENOP-aAb improve ME/CFS symptoms in affected patients—i.e., is this association causal?
What This Study Does Not Prove
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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