ing that causes OSA (Robinson et al., 2004a). Menopause also increases the risk of OSA (Bixler et al., 2001; Young et al., 2003), possibly through lower levels of progestational hormones that influence the respiratory system through changes in body fat distribution (Vgontzas and Kales, 1999). However, recent studies suggest that there may be a referral bias that results in a lower apparent rate of sleep apnea in females than in males (Kapsimalis and Kryger, 2002; Shepertycky et al., 2005). Epidemiological evidence suggests that hormone replacement therapy lessens the risk of OSA (Shahar et al., 2003). In children, the main risk factor for OSA is tonsillar hypertrophy, although OSA may also occur in children with congenital and neuromuscular disorders and in children who were born prematurely (Rosen et al., 2003). Asthma, a common childhood respiratory illness, is also associated with OSA in children (Sulit et al., 2005).
In adolescents, risk factors may be more similar to those seen in adults and include obesity (Redline et al., 1999). Being a minority is a risk factor for both increased prevalence and severity of sleep-disordered breathing in both children and adults (Rosen et al., 1992; Ancoli-Israel et al., 1995; Rosen et al., 2003). The prevalence of sleep-disordered breathing in the United States is approximately three times higher in middle-aged members of minority groups compared to non-Hispanic whites (Kripke et al., 1997). African American children are at increased risk, even after adjusting for obesity or respiratory problems (Redline et al., 1999; Rosen et al., 2003). Familial and probably genetic factors strongly contribute to OSA (Buxbaum et al., 2002; Palmer LJ et al., 2003; Palmer et al., 2004).
Patients with cardiovascular disease and diabetes are also at higher risk for developing both OSA and central sleep apnea (Sin et al., 1999).
Patients with impaired baroreflexes (e.g., patients with hypertension or heart failure and premature infants) may be especially susceptible to excessive autonomic responses to chemoreflex stimulation during periods of apnea. In these patient groups, bradyarrhythmias, hypoxia, hypoperfusion, and sympathetic activation during apnea may predispose to sudden death (Somers et al., 1988; 1992).
Limited evidence suggests that sleep-disordered breathing may affect an individual’s mortality (Young et al., 2002a,b; Lavie et al., 2005). Studies of patients at sleep clinics tend to show an association between sleep apnea and mortality (He et al., 1988), but several well-designed, population-based studies failed to find an association (Ancoli-Israel et al., 1996; Lindberg et al., 1998; Kripke et al., 2002), except in one subgroup of patients below age 60 with both snoring and excessive daytime sleepiness. The subgroup experienced twice the risk of mortality (Lindberg et al., 1998). A recent observa-