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The Journal of Clinical Endocrinology & Metabolism Vol. 86, No. 2 517-520
Copyright © 2001 by The Endocrine Society


From the Clinical Research Centers

Polycystic Ovary Syndrome Is Associated with Obstructive Sleep Apnea and Daytime Sleepiness: Role of Insulin Resistance1

Alexandros N. Vgontzas, Richard S. Legro, Edward O. Bixler, Allison Grayev, Anthony Kales and George P. Chrousos

Sleep Research and Treatment Center (A.N.V., E.O.B., A.K.), Department of Psychiatry, and Department of Obstetrics and Gynecology (R.S.L., A.G.), Penn State University College of Medicine, Hershey, Pennsylvania 17033; and Pediatric and Reproductive Endocrinology Branch (G.P.C.), National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland 28092

Address correspondence and requests for reprints to: Alexandros N. Vgontzas, M.D., Sleep Research and Treatment Center, Department of Psychiatry, The Pennsylvania State University, College of Medicine, 500 University Drive, Hershey, Pennsylvania 17033. E-mail: axv3{at}psu.edu

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder of premenopausal women, characterized by chronic hyperandrogenism, oligoanovulation, and insulin resistance. Obstructive sleep apnea (OSA) and excessive daytime sleepiness (EDS) are strongly associated with insulin resistance and hypercytokinemia, independently of obesity. We hypothesized that women with PCOS are at risk for OSA and EDS. Fifty-three women with PCOS (age range, 16–45 yr) and 452 control premenopausal women (age range, 20–42), from a general randomized sample for the assessment of prevalence of OSA, were evaluated in the sleep laboratory for 1 night. In addition, women with PCOS were tested for plasma free and weakly bound testosterone, total testosterone, and fasting blood glucose and insulin concentrations. In this study, PCOS patients were 30 times more likely to suffer from sleep disordered breathing (SDB) than the controls [odds ratio = 30.6, 95% confidence interval (7.2–139.4)]. Nine of the PCOS patients (17.0%) were recommended treatment for SDB, in contrast with only 3 (0.6%) of the control group (P < 0.001). In addition, PCOS patients reported more frequent daytime sleepiness than the controls (80.4% vs. 27.0%, respectively; P < 0.001). PCOS patients who were recommended treatment for SDB, compared with those who were not, had significantly higher fasting plasma insulin levels (306.48 ± 52.39 vs. 176.71 ± 18.13 pmol/L, P < 0.01) and a lower glucose-to-insulin ratio (0.02 ± 0.00 vs. 0.04 ± 0.00, P < 0.05). Plasma free and total testosterone and fasting blood glucose concentrations were not different between the two groups of PCOS women. Our data indicate that SDB and EDS are markedly and significantly more frequent in PCOS women than in premenopausal controls. Also, insulin resistance is a stronger risk factor than is body mass index or testosterone for SDB in PCOS women. These data support our proposal that, independently of gender, sleep apnea might be a manifestation of an endocrine/metabolic abnormality in which insulin resistance plays a principal role.




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