OSA epidemiology and risk factors
The prevalence of OSA varies considerably between studies, mainly due to differences in the population studied, study designs, and the method and criteria used to diagnose OSA. A prevalence of 4% in men and 2% in women  has traditionally been quoted in many populations. The prevalence from three well-conducted studies with similar design from Wisconsin, Pennsylvania, and Spain showed an OSA prevalence of 17–26% in men and 9–28% in women and a prevalence of 9–14% and 2–7% for men and women with moderate to severe OSA . These studies used a two-stage sampling design which allows some degree of estimate of the “self-selection” bias which is usually a significant problem in OSA studies.
OSA prevalence is affected by many risk factors such as obesity, age, ethnicity, and gender. The large majority of epidemiologic OSA studies took place in Western societies (particularly in the USA) and included mainly white Caucasians; hence data about the prevalence in other ethnicities is rather limited. In African Americans, the available results are conflicting. While some studies showed a higher adjusted OSA prevalence in Afro-Caribbeans (increased twofold) , others did not show such a difference . Chinese have a high OSA prevalence (8.8% in men and 3.7% in women) despite being less obese than white Europeans [12,13]. This highlights the importance of factors other than obesity (such as the anatomy of upper airways) in the development ofOSA. Chinese were shown to have more crowded upper airways with higher Mallampati score and shorter thyromental distance . Data regarding the prevalence of OSA in South Asians are also limited. In a semi-urban population in Delhi, the OSA prevalence was 3.7% , this rose to 9.3% in middle-aged urban Indians , and 19.5% in middle-aged urban men .
The impact of gender on OSA status has been well recognized; men have two to three times increased risk of OSA compared to women . The exact mechanisms behind the gender differences in OSA prevalence are not clear but several possible factors have been proposed. Sex hormones have been implicated, since men receiving testosterone replacement are at higher risk of OSA and the prevalence of OSA in postmenopausal women is higher than in premenopausal women. Hormone-replacement therapy also reduces the risk of OSA in postmenopausal women . In addition, hyperandrogenemia was associated with higher risk of OSA and oral contraceptives were associated with lower OSA risk in women with polycystic ovarian syndrome . Differences in upper airway size and ventilator control between men and women have also been implicated but the results are conflicting .
Several studies have shown that the prevalence of OSA increases with age . In men, OSA (AHI ≥10 events per hour) was present in 3.2%, 11.3%, and 18.1% of the 20–44, 45–64, and 61–100-year-old age groups, respectively . In another study from Spain, the prevalence of any OSA was three times higher and the prevalence of moderate to severe OSA was four times higher in older patients (>70 years old) compared to middle-aged participants . On the other hand, in the Sleep Heart Health Study, OSA prevalence increased with age but reached a plateau at the age of 65 years, which may be related to survival effect . The relationship with age seems to be due to changes in pharyngeal anatomy and upper airway collapsibility .
Excess body weight is an essential risk factor for OSA, although not all OSA patients are obese or overweight. In the Wisconsin Sleep Cohort Study, each increase in BMI by one standard deviation, resulted in a fourfold increase in OSA prevalence . Several other studies have shown the strong link between OSA and excess body weight . Prospective studies showed that weight gain is associated with the development of or worsening pre-existing OSA [23,24]. This was further supported by a randomized controlled trial which showed that weight loss (vital lifestyle modifications or surgical intervention) improve/cure OSA [25,26]. The mechanisms that link obesity to OSA are not entirely clear but several mechanisms have been proposed; weight gain can alter normal upper airway mechanics during sleep by increased parapharyngeal fat deposition resulting in a smaller upper airway, altering the neural compensatory mechanisms that maintain airway patency, reducing the functional residual capacity with a resultant decrease in the stabilizing caudal traction on the upper airway and affecting the chemosensitivity to O2 and CO2 which reduces ventilator drive .
There are several other predisposing risk factors to OSA such as current smoking, excess alcohol intake, and genetic factors [10,18].