Abstract:Nocturnal hypoxemia as determined by a polyvariable biomarker reliably predicted EDS in patients with severe OSA (AHI>50), indicating that oxygen fluctuation had a direct role in the development of EDS in patients with severe OSA.
“…Intermittent hypoxemia has been shown to result in disturbed sleep architecture or to damage neuronal structures that promote wakefulness in animal models ( 25 ). Indeed, higher degrees of hypoxemia predict both sleepiness and insulin resistance ( 1 , 26 ). According to these studies, we can expect that the effect of hypoxemia on glucose metabolism may be more evident in patients with OSA and EDS.…”
OBJECTIVEThe purpose of this study was to investigate whether the impact of obstructive sleep apnea (OSA) on glucose metabolism was different according to the presence or absence of obesity.RESEARCH DESIGN AND METHODSA total of 1,344 subjects >40 years old from the Korean Genome and Epidemiology Study were included. OSA was detected by home portable sleep monitoring. Plasma glucose, HbA1c, and insulin resistance were compared according to OSA and obesity status. The associations between OSA and impaired fasting glucose (IFG), impaired glucose tolerance (IGT), IFG + IGT, and diabetes were evaluated in subjects with and without obesity after adjusting for several confounding variables. The effect of visceral obesity on this association was evaluated in 820 subjects who underwent abdominal computed tomography scanning.RESULTSIn subjects without obesity, fasting glucose, 2-h glucose after 75-g glucose loading, and HbA1c were higher in those with OSA than in those without after controlling for age, sex, and BMI. In addition, the presence of OSA in nonobese subjects was associated with a higher prevalence of IFG + IGT and diabetes after adjusting for several confounding variables (odds ratio 3.15 [95% CI 1.44–6.90] and 2.24 [1.43–3.50] for IFG + IGT and diabetes, respectively). Further adjustment for visceral fat area did not modify this association. In contrast, in those with obesity, none of the abnormal glucose tolerance categories were associated with OSA.CONCLUSIONSThe presence of OSA in nonobese individuals is significantly associated with impaired glucose metabolism, which can be responsible for future risk for diabetes and cardiovascular disease.
“…Intermittent hypoxemia has been shown to result in disturbed sleep architecture or to damage neuronal structures that promote wakefulness in animal models ( 25 ). Indeed, higher degrees of hypoxemia predict both sleepiness and insulin resistance ( 1 , 26 ). According to these studies, we can expect that the effect of hypoxemia on glucose metabolism may be more evident in patients with OSA and EDS.…”
OBJECTIVEThe purpose of this study was to investigate whether the impact of obstructive sleep apnea (OSA) on glucose metabolism was different according to the presence or absence of obesity.RESEARCH DESIGN AND METHODSA total of 1,344 subjects >40 years old from the Korean Genome and Epidemiology Study were included. OSA was detected by home portable sleep monitoring. Plasma glucose, HbA1c, and insulin resistance were compared according to OSA and obesity status. The associations between OSA and impaired fasting glucose (IFG), impaired glucose tolerance (IGT), IFG + IGT, and diabetes were evaluated in subjects with and without obesity after adjusting for several confounding variables. The effect of visceral obesity on this association was evaluated in 820 subjects who underwent abdominal computed tomography scanning.RESULTSIn subjects without obesity, fasting glucose, 2-h glucose after 75-g glucose loading, and HbA1c were higher in those with OSA than in those without after controlling for age, sex, and BMI. In addition, the presence of OSA in nonobese subjects was associated with a higher prevalence of IFG + IGT and diabetes after adjusting for several confounding variables (odds ratio 3.15 [95% CI 1.44–6.90] and 2.24 [1.43–3.50] for IFG + IGT and diabetes, respectively). Further adjustment for visceral fat area did not modify this association. In contrast, in those with obesity, none of the abnormal glucose tolerance categories were associated with OSA.CONCLUSIONSThe presence of OSA in nonobese individuals is significantly associated with impaired glucose metabolism, which can be responsible for future risk for diabetes and cardiovascular disease.
“…The ESS is a self-administered questionnaire used to subjectively measure daytime sleepiness 10 . A score ≥ 10 is considered to represent excessive daytime sleepiness (EDS) 11 , 12 . The ODI is calculated as the number of times per hour that the blood’s oxygen desaturation is ≥ 3% or ≥ 4% from baseline during sleep 8 .…”
Gray matter (GM) anomalies may represent a critical pathology underlying obstructive sleep apnea (OSA). However, the evidence regarding their clinical relevance is inconsistent. We conducted a meta-analysis of voxel-based morphometry (VBM) studies of patients with OSA to identify their brain abnormalities. A systematic search was conducted based on PRISMA guidelines, and a meta-analysis was performed using the anisotropic effect-size-based algorithms (ASE-SDM) to quantitatively estimate regional GM changes in patients with OSA. Fifteen studies with 16 datasets comprising 353 untreated patients with OSA and 444 healthy controls were included. Our results revealed GM reductions in the bilateral anterior cingulate/paracingulate gyri (ACG/ApCG), left cerebellum (lobules IV/V and VIII), bilateral superior frontal gyrus (SFG, medial rostral part), right middle temporal gyrus (MTG), and right premotor cortex. Moreover, GM reductions in the bilateral ACG/ApCG were positively associated with body mass index (BMI) and age among patients with OSA, and GM reductions in the SFG (medial rostral part) were negatively associated with Epworth sleepiness scale (ESS) scores and sex (male). These abnormalities may represent structural brain underpinnings of neurocognitive abnormalities and respiratory-related abnormalities in OSA. In particular, this study adds to Psychoradiology, which is a promising subspecialty of clinical radiology mainly for psychiatric disorders.
“…In animal models, intermittent hypoxemia results in disturbed sleep architecture or damage to the neuronal structures that promote wakefulness [ 27 ]. Furthermore, a greater degree of hypoxemia predicts both sleepiness and insulin resistance [ 28 , 29 ]. Such findings suggest that the effects of hypoxemia on liver metabolism are likely to be more evident in individuals with comorbid OSA and EDS.…”
Background/Aims:Obstructive sleep apnea (OSA) is associated with an increased risk of obesity and non-alcoholic fatty liver disease (NAFLD), but it remains unclear whether the risk of NAFLD is independently related to OSA regardless of visceral obesity. Thus, the aim of the present study was to examine whether OSA alone or in combination with excessive daytime sleepiness (EDS) or short sleep duration was associated with NAFLD independent of visceral fat in Korean adults.Methods:A total of 621 participants were selected from the Korean Genome and Epidemiology Study (KoGES). The abdominal visceral fat area (VFA) and hepatic fat components of the participants were assessed using computed tomography scans and they were then categorized into four groups depending on the presence of OSA and EDS.Results:The proportions of NAFLD were 21.1%, 18.5%, 32.4%, and 46.7% in participants without OSA/EDS, with only EDS, with only OSA, and with both OSA and EDS, respectively. A combination of OSA and EDS increased the odds ratio (OR) for developing NAFLD (OR, 2.75; 95% confidence interval [CI], 1.21 to 6.28) compared to those without OSA/EDS, and this association remained significant (OR, 2.38; 95% CI, 1.01 to 5.59) even after adjusting for VFA. In short sleepers (< 5 hours) with OSA, the adjusted OR for NAFLD was 2.50 (95% CI, 1.08 to 5.75) compared to those sleeping longer than 5 hours without OSA.Conclusions:In the present study, OSA was closely associated with NAFLD in Korean adults. This association was particularly strong in those with EDS or short sleep duration regardless of VFA.
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