Sleep apnea (SA) is a disorder characterized by repeated pauses in breathing or periods of shallow breathing during sleep, leading to fragmented rest and reduced oxygen levels. SA is not a primary disease but is secondary to underlying anatomical, physiological, or neurological factors. The two main forms are Obstructive Sleep Apnea (OSA), where the airway collapses despite breathing effort, and Central Sleep Apnea (CSA), where the brain fails to send the signal to breathe. Effective management requires addressing the primary condition responsible for the respiratory disruption.
Physical Characteristics and Airway Structure
The most frequent cause of Obstructive Sleep Apnea is related to physical and anatomical features that mechanically narrow the upper airway. Excess body weight, particularly fat deposits around the neck and throat, creates external pressure that predisposes the pharynx to collapse during sleep. A large neck circumference is a common physical marker indicating increased soft tissue volume, which reduces the space available for air passage.
Obesity is a major driver because fat infiltration occurs within the tongue and lateral pharyngeal walls, making the airway more pliable and prone to collapse. During sleep, the muscle tone that normally keeps the airway open decreases, allowing the additional soft tissue volume to fall inward. Furthermore, the reduced lung volume experienced in the supine position decreases the downward pull on the trachea, further destabilizing the upper airway.
Structural characteristics of the head and neck, independent of body weight, can also be major contributing factors. A small or recessed lower jaw (micrognathia or retrognathia) limits the skeletal space for the tongue and soft palate, pushing them backward. Similarly, naturally enlarged tonsils or adenoids, especially in children, or a large tongue size can physically encroach upon the limited airway space. Nasal obstructions, such as a severely deviated septum or nasal polyps, increase the negative pressure needed to draw air past the blockage, which can then cause the soft tissues of the pharynx to collapse more easily.
Another physical mechanism involves fluid redistribution within the body, often linked to conditions like heart failure or chronic kidney disease. When an individual lies down to sleep, fluid that has accumulated in the legs during the day shifts toward the upper body, increasing the fluid volume and swelling in the neck and pharyngeal tissues. This nocturnal swelling further narrows the already compromised upper airway, directly contributing to the severity of the obstruction.
Systemic Metabolic and Endocrine Disorders
Systemic diseases and hormonal imbalances can contribute to sleep apnea by altering tissue structure, muscle function, or metabolic control. Hypothyroidism, a condition of low thyroid hormone levels, can lead to the accumulation of mucopolysaccharides in soft tissues, causing swelling of the tongue and throat. This tissue enlargement physically narrows the airway, increasing the likelihood of obstruction.
Acromegaly, a disorder caused by excess growth hormone, similarly promotes the overgrowth of soft tissues, including the tongue and laryngeal structures. This results in an anatomically narrow pharynx that is highly susceptible to collapse, even in individuals who are not significantly overweight. Type 2 diabetes and the associated metabolic syndrome are frequently observed alongside OSA, often due to shared mechanisms involving systemic inflammation and insulin resistance.
The hormonal milieu can also influence sleep apnea risk, particularly in women. Polycystic Ovary Syndrome (PCOS) is associated with hormonal changes, including increased androgen levels, which may affect fat distribution and upper airway anatomy. Menopause brings a reduction in protective hormones like progesterone and estrogen, which normally help maintain muscle tone in the upper airway, potentially leading to increased collapsibility. Insulin resistance and altered fat distribution may also influence the function of the pharyngeal dilator muscles, impairing the neuromuscular responsiveness needed to keep the airway open.
Medications and Central Nervous System Interference
Central Sleep Apnea (CSA) occurs when the brain’s respiratory control centers fail to generate the necessary signal for the diaphragm and chest muscles to breathe. This neurological signal failure is often secondary to underlying medical conditions or the use of certain substances. Heart failure is a primary cause of CSA, specifically leading to a pattern known as Cheyne-Stokes respiration. In Cheyne-Stokes breathing, the body’s control over carbon dioxide and oxygen levels becomes unstable, causing a cyclical pattern of breathing that waxes and wanes, interspersed with central apneas.
Neurological injuries, such as a stroke or trauma involving the brainstem, can directly damage the respiratory control centers, impairing the brain’s ability to initiate a breath. These conditions disrupt the precise feedback loop that regulates ventilation.
Certain medications strongly suppress the central respiratory drive, which is a common mechanism for medication-induced CSA. Opioids are the most recognized agents, as they act on mu-opioid receptors in the brainstem, which are involved in controlling the breathing rhythm. High doses of opioids can dramatically dull the body’s sensitivity to rising carbon dioxide levels, leading to long pauses in breathing.
Other central nervous system depressants, including sedatives like benzodiazepines, as well as some non-opioid pain or seizure medications such as baclofen and valproic acid, can also induce CSA. These drugs often work by increasing the effect of GABA, a calming neurotransmitter, which inadvertently slows the brain’s signal to breathe.