Obstructive Sleep Apnea (OSA) is a common sleep disorder where the airway repeatedly collapses during sleep, causing pauses in breathing, recurrent drops in blood oxygen levels, and fragmented sleep. Hypothyroidism is an endocrine disorder where the thyroid gland does not produce enough thyroid hormone. This underactive state slows down the body’s metabolism and affects nearly every system. While distinct, clinical evidence suggests a complex relationship exists between them. This article explores the physiological connections, focusing on whether OSA can influence thyroid function.
Hypothyroidism as a Contributor to Sleep Apnea
The association between these two conditions is most clearly understood by considering how an underactive thyroid can worsen or cause sleep apnea. Thyroid hormones are necessary for maintaining normal metabolic function and muscle tone. When these hormones are deficient, the physical structures of the upper airway are compromised, increasing the risk of collapse during sleep.
Thyroid deficiency causes the accumulation of mucoproteins and other hydrophilic substances in the soft tissues of the neck and tongue, a condition known as myxedema. This fluid retention causes the tissues to swell, resulting in an enlarged tongue (macroglossia) and a narrowing of the pharyngeal space. The bulk of these enlarged tissues directly predisposes the airway to obstruction and collapse, the defining characteristic of OSA.
Low thyroid hormone levels also reduce the neural output and muscle tone of the pharyngeal dilator muscles, which keep the airway open during sleep. This decrease in muscle activity makes the airway more susceptible to collapsing under the negative pressure generated by breathing. Patients with untreated hypothyroidism have a significantly higher prevalence of sleep-disordered breathing, with incidence estimates ranging from 25% to over 70%.
Sleep Apnea’s Effect on Thyroid Hormone Regulation
Mounting evidence suggests that sleep apnea can negatively impact thyroid hormone regulation, a process mediated by the body’s stress response. The hallmark of severe OSA is chronic intermittent hypoxia (CIH), the repeated cycle of oxygen deprivation followed by reoxygenation. CIH acts as a profound physiological stressor that triggers the activation of the sympathetic nervous system and promotes systemic inflammation.
This chronic stress and inflammation disrupt the hypothalamic-pituitary-thyroid (HPT) axis, the hormonal feedback loop controlling thyroid function. One consequence is the development of non-thyroidal illness syndrome (NTIS), or “euthyroid sick syndrome,” in a subset of patients with severe nocturnal hypoxemia. In NTIS, the body attempts to conserve energy by reducing the conversion of the inactive thyroid hormone, thyroxine (T4), into the biologically active form, triiodothyronine (T3).
This suppression of T3, often resulting in low serum T3 levels despite normal TSH, is an adaptive response to severe illness that CIH can mimic. Specific changes in deiodinase enzymes, which regulate this conversion, are observed, leading to increased reverse T3 (rT3). Some OSA patients may also develop subclinical hypothyroidism, characterized by an elevated TSH level but normal free T4. Proinflammatory cytokines, such as interleukin-1 beta (IL-1β), are elevated due to CIH and have been shown to directly inhibit thyroid cell function, providing a mechanism for this inflammatory link.
Shared Symptoms and Diagnostic Considerations
The clinical overlap between sleep apnea and hypothyroidism creates a significant diagnostic challenge. Both conditions commonly present with highly nonspecific symptoms that can easily be attributed to the other, or to general fatigue. These shared complaints include excessive daytime sleepiness, chronic fatigue, unexplained weight gain, and cognitive impairment often described as “brain fog.”
This symptom overlap underscores the necessity of comprehensive screening when one condition is diagnosed. A patient presenting with severe fatigue and weight gain could be suffering from primary hypothyroidism, severe OSA, or both. Failing to screen for a thyroid disorder in an OSA patient, or vice versa, risks incomplete diagnosis and ineffective treatment. Clinicians frequently recommend a thyroid-stimulating hormone (TSH) test as part of the initial workup for patients with suspected OSA.
Managing Both Conditions
When a patient is diagnosed with both obstructive sleep apnea and hypothyroidism, the treatment strategy must be coordinated. The primary treatment for hypothyroidism is thyroid hormone replacement therapy, usually with levothyroxine, which can sometimes improve or even resolve mild OSA. This medication helps reverse underlying physical mechanisms, such as fluid retention and reduced muscle tone in the upper airway.
However, the response to thyroid hormone replacement is variable, and many patients continue to have persistent sleep apnea even after achieving normal thyroid hormone levels. For these individuals, or those with moderate to severe OSA, continuous positive airway pressure (CPAP) therapy remains the standard of care. Initiating CPAP treatment for OSA has also been shown to improve abnormal thyroid hormone profiles, including recovery from NTIS and a decrease in TSH levels in those with subclinical hypothyroidism. The most effective management often involves a combined approach, utilizing thyroid hormone replacement and CPAP therapy simultaneously to address both the endocrine and respiratory components of the patient’s condition.