Summary Obstructive sleep apnea (OSA) is an increasingly prevalent sleep disorder characterized by upper airway obstruction during sleep, resulting in breathing pauses, intermittent hypoxia, and fragmented sleep. In parallel, the constellation of adverse health outcomes associated with prolonged obesity, such as insulin resistance, elevated blood pressure, triglycerides, and reduced high-density lipoprotein cholesterol – termed metabolic syndrome –raises the risk of cardiovascular morbidity and mortality, type 2 diabetes, and all-cause mortality. Affecting 35–40% of U.S. adults, risk factors for metabolic syndrome, including obesity, middle age, sedentary behavior, and genetics, share considerable overlap with those for OSA. Thus, it has been difficult to disentangle cause, effect, and whether certain treatments, such as CPAP, can improve these outcomes. In this paper, we provide an update to our 2005 review which explored the association between OSA and metabolic syndrome, highlighting visceral obesity as the common etiological factor of both conditions. This update includes (a) recent data on physiological and biochemical mechanisms, (b) new data in nonobese men and women as well as children and adolescents, (c) insight from the latest treatment studies, (d) the role of aging in understanding clinically-meaningful phenotypes of the disorder, and (e) the potential diagnostic/prognostic utility of biomarkers in identifying OSA patients with the strongest cardiometabolic risk.
Because there is a lack of agreed upon diagnostic criteria, it is critical to understand the natural history of obstructive sleep apnoea (OSA) in children in order to establish treatment strategies based on objective data.The Penn State Child Cohort is a representative, general-population sample of 700 elementary school children at baseline, of whom 421 were reassessed 8 years later, during adolescence.The remission of childhood apnoea-hypopnoea index (AHI) ≥2 events per h in adolescence was 52.9%. Using the higher threshold of AHI ≥5 events per h, remission was 100.0%, with 50.0% partially remitting to AHI 2- <5 events per h and the other half remitting to AHI <2 events per h. The incidence of adolescent AHI ≥2 events per h in those with childhood AHI <2 events per h was 36.5%, while the incidence of AHI ≥5 events per h in those with childhood AHI <5 events per h was 10.6%. This longitudinal study confirms that prepubertal OSA tends to resolve naturally during the transition to adolescence, and that primary snoring and mild sleep disordered breathing (SDB) do not appear to be strongly associated with progression to more severe SDB.The key risk factors for SDB in adolescence are similar to those found in middle-aged adults (i.e. male sex, older age and obesity). Moreover, consistent with recent studies in adults, this study includes the novel cross-sectional finding that visceral fat is associated with SDB as early as adolescence.
Inflammation has been suggested as a potential pathway by which insomnia and short sleep can affect risk of morbidity in adults. However, few studies have examined the association of insomnia with inflammation in adolescents, despite accumulating evidence that pathophysiologic changes may already occur during this critical developmental period. The present study sought to examine the association of insomnia symptoms with systemic inflammation and the role of objective sleep duration in this association. Participants were 378 adolescents (16.9 ± 2.3y, 45.8% female) from the Penn State Child Cohort, a population-based sample who underwent 9-hour polysomnography (PSG) followed by a single fasting blood draw to assess plasma levels of C-reactive protein (CRP) and other inflammatory markers. Insomnia symptoms were defined by a self-report of difficulties falling and/or staying asleep, while objective sleep duration groups were defined as a PSG total sleep time ≥ 8, 8–7, and ≤ 7 hours. We assessed the association of insomnia symptoms, objective sleep duration, and their interaction with inflammatory markers, while adjusting for multiple potential confounders. Adolescents reporting insomnia symptoms had significantly higher levels of CRP compared to controls and a significant interaction (p < 0.01) showed that objective sleep duration modified this association. Elevated CRP was present in adolescents with insomnia symptoms and ≤ 7 hours of sleep (1.79 mg/L) as compared to controls or adolescents with insomnia symptoms and ≥ 8 hours of sleep (0.90 mg/L and 0.98 mg/L, respectively) or controls with ≤ 7 hours of sleep (0.74 mg/L; all p-values < 0.01). In sum, insomnia symptoms with objective short sleep duration are associated with systemic inflammation as early as adolescence. This study suggests that chronic low-grade inflammation may be a common final pathway towards morbidity in adulthood in this insomnia phenotype.
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