What are the risk factors for OSA?
Common risk factors or signs of OSA include:
- Increased daytime sleepiness
- Cognitive difficulties due to fatigue
- High blood pressure
- Narrowing of the nasopharynx (upper part of the throat behind the nose)
- Pulmonary hypertension (high blood pressure affecting arteries in the heart and lungs)
- Specific positions of the hyoid bone
- Tongue scalloping (tongues with rippled edges)
- Tongue fat
- Airway edema
Accumulation of fluid can increase the size of upper airway soft tissue is individuals with OSA and individuals that snore.
- Airway surface tension
Surface tension in the fluid lining the mucosa of the upper airway can also have an effect on its collapsibility. Individuals with OSA have been found to have higher surface tension in the upper airway walls. In turn, surfactant treatments have been shown to significantly reduce airway collapsibility and reduce AHI by up to 30% in individuals with OSA.
- Age (middle age)
As individuals age, they naturally experience more difficulties when sleeping. More than half of adults over the age of 65 years experience a chronic sleep-related issue. Sleep becomes more irregular impart due to OSA. Approximately 70% of men and 56% of women between 65 and 99 years of age have mild OSA. The development of OSA specifically has been shown to increase with age as well. However, it tends to level off after 60 years of age. It is believed that OSA increases with age because of increases in phat in the parapharyngeal area, lengthening of the soft palate and changes in body structure around the phaynx that occur with age.
- Sex (Male)
Men are more likely to experience OSA than women. One study found that 11.1% of men and 4.9% of women had moderate to severe OSA among a small community. Even when gaining weight, the risk for men increased twice as much as for women, when both gained a similar amount of weight. Other reasons that it may be more common in males could be related to the effects related to sex hormones on upper airway muscles and collapsibility and differences in pharyngeal anatomy and function between the sexes. The fact that prevalence increases in post-menopausal women compared to premenopausal women supports the hypothesis that hormones may play a role in gender differences.
- Excess body weight
Excess body weight is associated with approximately 60% of OSA causes. A 10% increase in weight has been shown to be associated with a 32% increase in their AHI, while the risk of developing moderate to severe OSA increases 6 times. Similarly, a 10% decrease in weight decreases AHI by 26%. Increasing body weight not only can increase the risk for OSA, but it can also accelerate the progression from a more moderate form to a severe form. There is evidence that weight loss, whether through, diet and exercise or surgical procedures, can reduce the risk for OSA. Mechanisms by which weight gain may increase the risk for OSA include:
o Increased parapharyngeal fat, resulting in a more restricted airway
o Alterations in neural pathways that maintain the airway opening
o Instability of respiratory control
o Reduced capacity and stability of the upper airway
- Large neck circumference (>17 inches in males and >16 inches in females)
The idea behind this risk factor is that the neck and similar central sections of the body, such as the waist, reflect the distribution of fat among the body in the center compared to the periphery. Some studies have found that a larger neck circumference is associated with moderate to severe OSA.
Studies comparing prevalence of OSA in different continents found that North America, Europe and Australia have a similar prevalence for OSA. This is surprising since white individuals tend to weigh more than those in Asia. Asians also have a greater disease severity compared to whites. This difference is thought to be related to the craniofacial feature differences between whites and Asians.
In general African-Americans have a similar rate of OSA to other racial groups. However, subsets of the African-American population, specifically those under the age of 25 years and those over the age of 65 years, have a higher prevalence of OSA than middle-aged African-Americans and individuals of other racial groups. These differences could be linked to increased morbidity often seen in minority populations such as obesity, and limited access to quality healthcare.
- Specific craniofacial morphology
Several facial bone and soft tissue features can contribute to sleep disorders including:
o Retrognathia (abnormal positioning of the upper or lower jaw)
o Tonsillar hypertrophy (enlarged tonsils)
o Enlarged tongue
o Enlarged soft palate
o Inferiorly positioned hyoid bone (U-shaped bone supporting the tongue)
o Maxillary retroposition (backward displacement of the upper jaw)
o Mandibular retroposition (backward displacement of the lower jaw)
o Decreased posterior airway space
The relationship of these craniofacial characteristics could account for differences in the causes of OSA in different racial groups.
- Familial and genetic predisposition
First degree relatives of an individual with OSA is more likely to develop the disease than those related to individuals without OSA. The risk of developing OSA also increases with the percentage of family members affected. Genetic factors are thought to account for up to 35% of disease severity experienced.
Smoking is associated with a higher prevalence of OSA. While OSA has not been linked to second-hand smoke, snoring, a sign of OSA has been linked to second-hand smoke inhalation. However, former smokers do not have the symptoms of OSA, suggesting it can be reversed. Smoking may promote OSA by inducing airway inflammation and increasing arousal from sleep due to nicotine withdrawals. OSA severity appears to increase with the number of cigarettes smoked a day.
- Alcohol Consumption
Drinking prior to sleep increases the collapsibility of the upper airway and the number of sleep apnea events that occur during sleep in both individuals with and without OSA. Alcohol consumption can also increase the length of the events and the severity of the resulting hypoxemia. Alcohol is thought to bring about these effects by reducing the activity of the oropharyngeal muscles. It is unclear if chronic alcohol use increases the risk of OSA.
- Polycystic ovary syndrome (PCOS)
PCOS is a collection of symptoms resulting from high level of androgen in females. Symptoms include no or heavy menstruation, excess body and facial hair, acne, difficulty getting pregnant and thick, dark skin. Notably, PCOS is associated with insulin resistance. There is evidence suggesting that insulin resistance in women with PCOS contributes to sleep disordered breathing.
- Visceral adiposity and high androgen levels
Similar to women with PCOS, men with insulin resistance and high levels of visceral adiposity have also been shown to experience OSA. This association may be caused by abnormal hormone levels resulting in altered upper airway passive mechanical properties.
Hypothyroidism is a condition in which the thyroid does not produce enough thyroid hormone. Associated conditions include weight gain, and thus it is unclear whether low thyroid levels or obesity may be driving OSA. Individuals with hypothyroidism experience and accumulation of hyaluronic acid in the skin leading to mucoproteins in the upper airway. The proteins cause the tongue, pharyngeal membrane and laryngeal membranes to become enlarged, increasing the collapsibility of the airway during sleep. Hypothyroidism may also reduce central respiratory control output as well. This combination of symptoms increase susceptibility to OSA.
Physical changes occurring during pregnancy can increase the risk for OSA. These changes include gestational weight gain, decreased pharyngeal luminal size, and changes in pulmonary physiology. OSA during pregnancy can put the baby at risk by reducing birth weights and physical condition of the newborn.
There is an increased prevalence of OSA in menoposaual and postmenopausal women compared to premenopausal women. This difference is thought to be due largely to hormonal differences among the two populations. This hypothesis is further supported by the fact that treatment with hormone replacement therapy reduces the prevalence of OSA, suggesting that progesterone and/or estrogen play a protective role against OSA by effecting the upper airway dilator muscle activity. Hormone replacement may not be the sole reason for reduced OSA. It is possible that women that chose to take hormone replacement therapy are healthier in general or are in earlier stages of menopause.