Hypothyroidism, an underactive thyroid gland, is a significant and well-documented contributing factor that can initiate or worsen sleep apnea. Clinical research confirms this association, though it may not be the sole cause of every case. Medical guidelines often recommend screening for one condition when the other is diagnosed.
Understanding Hypothyroidism and Sleep Apnea
Hypothyroidism is an endocrine disorder where the thyroid gland fails to produce sufficient amounts of thyroid hormones (T4 and T3). Since these hormones regulate nearly every metabolic process, a deficiency causes a systemic slowdown, affecting functions from heart rate to energy use. This reduction in metabolic activity leads to symptoms like fatigue, weight gain, and an inability to tolerate cold.
The form of sleep apnea most closely linked to thyroid dysfunction is Obstructive Sleep Apnea (OSA). OSA is characterized by the recurrent collapse of the upper airway during sleep, causing a significant decrease or cessation of airflow. These episodes lead to drops in blood oxygen levels and brief awakenings, resulting in fragmented sleep and excessive daytime sleepiness. The physical blockage of the throat, often due to soft tissue enlargement, is the defining feature of OSA.
The Established Connection
Medical observations show a high statistical overlap between these two conditions; patients diagnosed with one are significantly more likely to have the other. Studies indicate the prevalence of OSA in hypothyroid patients is high, often ranging from 10% to 25%, with some cohorts reporting rates as high as 74%.
Individuals with hypothyroidism are approximately twice as likely to be diagnosed with sleep apnea compared to those with normal thyroid function. When sleep apnea is present alongside hypothyroidism, the severity is greater. Patients with both conditions show a significantly higher apnea-hypopnea index (AHI)—the measure of apnea events per hour—than those with OSA alone. This suggests low thyroid function actively contributes to the severity of sleep-disordered breathing.
Biological Mechanisms Linking the Two Conditions
The connection between low thyroid hormone and breathing issues lies in three distinct physiological changes that occur when the body is in a hypometabolic state.
One direct mechanism is myxedematous infiltration, the accumulation of mucopolysaccharides in the soft tissues. This fluid retention causes the tongue (macroglossia) and the tissues lining the upper airway to swell and thicken. This physical enlargement narrows the passage, making it susceptible to collapse during sleep.
The second mechanism involves the impact of thyroid hormone deficiency on the muscles that maintain airway patency. Hypothyroidism leads to myopathy, or muscle weakness, affecting the dilator muscles responsible for keeping the upper airway open. Their reduced tone makes them less effective, creating an environment highly conducive to recurrent obstruction.
A third contributing factor is a reduction in the central respiratory drive, the brain’s signal to breathe. Low thyroid hormone levels decrease the brainstem’s sensitivity to changes in carbon dioxide and oxygen concentrations. This blunted response means the brain is slower to recognize a lack of airflow and initiate a corrective breath, which can prolong apnea periods and worsen oxygen desaturation.
Treatment Considerations
Treating the underlying thyroid deficiency is a primary step in management, typically using levothyroxine replacement therapy. This treatment can improve or significantly reduce the frequency of apneic episodes and daytime sleepiness in some patients. Improvement is often attributed to the reduction of myxedematous swelling and the restoration of muscle function.
However, thyroid treatment alone does not guarantee a complete resolution of sleep apnea. Many patients with moderate to severe OSA continue to require traditional interventions like Continuous Positive Airway Pressure (CPAP) therapy. Experts advise against delaying CPAP while waiting for thyroid levels to normalize, as concurrent management of both conditions is the safest and most effective strategy.