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Exploring the Relationship Between Thyroid Hormones and Obstructive Sleep Apnea Severity in Euthyroid Patients
Marsida Teliti1,2, Laura Croce1,2, Caterina Pronzato3
1Department of Internal Medicine and Therapeutics, University of Pavia, Pavia, Italy.
Journal of Sleep Research
|August 2, 2026
Summary
Higher free triiodothyronine levels in obstructive sleep apnea patients correlate with respiratory event severity, not just low oxygen. This suggests free triiodothyronine may indicate the body's response to intermittent hypoxia.
Area of Science:
- Endocrinology
- Sleep Medicine
- Respiratory Medicine
Background:
- Obstructive sleep apnea (OSA) involves intermittent hypoxia and sleep fragmentation, potentially affecting thyroid hormone regulation.
- Existing research on thyroid function in OSA, especially free triiodothyronine (fT3), is inconsistent.
Purpose of the Study:
- To investigate the association between thyroid hormone levels (fT3, free thyroxine (fT4), thyroid-stimulating hormone (TSH)) and OSA severity.
- To determine if fT3 is a sensitive marker for intermittent hypoxia in OSA patients.
Main Methods:
- Cross-sectional study of 168 adults with polysomnography-confirmed OSA, excluding thyroid disease and relevant medications.
- Collected demographic data, BMI, polysomnography indices, and serum thyroid hormone levels.
- Assessed OSA severity using apnea-hypopnea index (AHI), oxygen desaturation index (ODI), mean nocturnal oxygen saturation, and % sleep time with SpO2 < 90%.
Main Results:
- Patients with higher AHI (above cohort median) had significantly higher fT3 levels (p=0.014).
- fT3 independently predicted AHI (p=0.004) and ODI (p=0.001) in multivariable analyses.
- No significant associations were found for fT4 or TSH with respiratory indices, nor for fT3 with measures of hypoxemia severity (mean SpO2, % time SpO2 < 90%).
Conclusions:
- Elevated fT3 concentrations in OSA are linked to the burden of respiratory events (AHI) rather than the severity of hypoxemia.
- fT3 may serve as a sensitive indicator of the physiological response to intermittent hypoxia in obstructive sleep apnea.
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