Wagner A Silva1,2, Bianca Almeida-Pititto3,4, Ronaldo B Santos1,2, Aline N Aielo1,5, Soraya Giatti1,5, Barbara K Parise1,5, Silvana P Souza1,2, Sandra F Vivolo3, Paulo A Lotufo1, Isabela M Bensenor1, Luciano F Drager6,7,8. 1. Center of Clinical and Epidemiologic Research (CPCE), University of Sao Paulo, Av. Prof. Lineu Prestes, 2565-4 andar, Cidade Universitária, São Paulo, SP, 05508-000, Brazil. 2. Hypertension Unit, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil. 3. Department of Epidemiology, School of Public Health, University of Sao Paulo, Sao Paulo, Brazil. 4. Department of Preventive Medicine, Federal University of São Paulo (UNIFESP), São Paulo, Brazil. 5. Hypertension Unit, Renal Division, University of São Paulo, São Paulo, Brazil. 6. Center of Clinical and Epidemiologic Research (CPCE), University of Sao Paulo, Av. Prof. Lineu Prestes, 2565-4 andar, Cidade Universitária, São Paulo, SP, 05508-000, Brazil. luciano.drager@incor.usp.br. 7. Hypertension Unit, Heart Institute (InCor), University of Sao Paulo, Sao Paulo, Brazil. luciano.drager@incor.usp.br. 8. Hypertension Unit, Renal Division, University of São Paulo, São Paulo, Brazil. luciano.drager@incor.usp.br.
Abstract
PURPOSE: Obstructive sleep apnea (OSA) may contribute to metabolic and inflammatory deregulation but previous studies failed to consider sleep duration, sleep fragmentation, insomnia, and daytime sleepiness as potential confounders. METHODS: Consecutive non-diabetic middle-aged participants from the ELSA-Brasil cohort were invited to perform a clinical evaluation, home sleep study for 1 night, and wrist actigraphy for 7 days. OSA was defined by an apnea-hypopnea index ≥ 15 events/h. Participants were stratified according to the presence of OSA measuring the following markers: fasting glucose, glucose tolerance test, homeostatic model assessment of insulin resistance (HOMA-IR) index, fasting insulin, insulin after 2 h of glucose load, glycated hemoglobin, total cholesterol and their fractions, triglycerides, C-reactive protein, TNF-alpha, interleukin-6, interleukin-10, leptin, adiponectin, E-selectin, ADMA, MCP-1, TGF, apolipoprotein B, fibrinogen, and lipoprotein(a). Differences between groups were identified by chi-square test and ANOVA. RESULTS: We studied 708 participants (mean age: 46 ± 5 years, men: 44%, BMI 26.1 ± 4.1 kg/m2). Compared to no OSA, participants with OSA presented higher levels while fasting and after 2 h glucose load of insulin, HOMA-IR, cholesterol, triglycerides, and C-reactive protein (all p < 0.001). After linear regression analysis adjusting for traditional risk factors plus sleep duration, fragmentation, insomnia, and daytime sleepiness, OSA was negatively associated with adiponectin (β = - 0.271 CI 95% - 0.456 - 0.085) and positively associated with cholesterol (β = 9.707 CI 95% 2.737 16.678). Sex-stratification revealed that these associations were significant for men but not women. CONCLUSIONS: In non-diabetic middle-age adults, men with OSA presented with lower adiponectin and higher cholesterol levels independently of sleep duration, sleep fragmentation, insomnia, and daytime sleepiness.
PURPOSE: Obstructive sleep apnea (OSA) may contribute to metabolic and inflammatory deregulation but previous studies failed to consider sleep duration, sleep fragmentation, insomnia, and daytime sleepiness as potential confounders. METHODS: Consecutive non-diabetic middle-aged participants from the ELSA-Brasil cohort were invited to perform a clinical evaluation, home sleep study for 1 night, and wrist actigraphy for 7 days. OSA was defined by an apnea-hypopnea index ≥ 15 events/h. Participants were stratified according to the presence of OSA measuring the following markers: fasting glucose, glucose tolerance test, homeostatic model assessment of insulin resistance (HOMA-IR) index, fasting insulin, insulin after 2 h of glucose load, glycated hemoglobin, total cholesterol and their fractions, triglycerides, C-reactive protein, TNF-alpha, interleukin-6, interleukin-10, leptin, adiponectin, E-selectin, ADMA, MCP-1, TGF, apolipoprotein B, fibrinogen, and lipoprotein(a). Differences between groups were identified by chi-square test and ANOVA. RESULTS: We studied 708 participants (mean age: 46 ± 5 years, men: 44%, BMI 26.1 ± 4.1 kg/m2). Compared to no OSA, participants with OSA presented higher levels while fasting and after 2 h glucose load of insulin, HOMA-IR, cholesterol, triglycerides, and C-reactive protein (all p < 0.001). After linear regression analysis adjusting for traditional risk factors plus sleep duration, fragmentation, insomnia, and daytime sleepiness, OSA was negatively associated with adiponectin (β = - 0.271 CI 95% - 0.456 - 0.085) and positively associated with cholesterol (β = 9.707 CI 95% 2.737 16.678). Sex-stratification revealed that these associations were significant for men but not women. CONCLUSIONS: In non-diabetic middle-age adults, men with OSA presented with lower adiponectin and higher cholesterol levels independently of sleep duration, sleep fragmentation, insomnia, and daytime sleepiness.
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