- Email: [email protected]
S23.A OSA and lipids
Parallel Symposia / Sleep Medicine 8 Suppl. 1 (2007) S11–S47 • 1st speaker: Mary IP, M.D., Ph.D., Prof., Department of Medicine, The University of Hong Kong, China • 2nd speaker: Joachim Ficker, M.D., Ph.D., Prof., Department of Respiratory Medicine, Allergology, Sleep Medicine, Klinikum Nuernberg, Teaching Hospital of Friedrich-Alexander-University ErlangenNuernberg, Germany • 3rd speaker: Olli Polo • 4th speaker/discussant: Tarja Saaresranta Sleep loss, sleeping difficulties and sleep-disordered breathing are hot topics, which interest many research groups around the world. The proposal "Sleeping problems and metabolism" will cover sleep loss, menopausal sleeping problems, sleep-disordered breathing and their impact on metabolism. Sleep loss is becoming more and more common in our 24/7 societies in east and west, and concern of its harmful metabolic effects is growing. Menopausal sleeping problems deserve our attention, since the mean age is increasing and third or even more of woman’s life span is postmenopausal in western societies. Menopause impacts on metabolism as well. Besides a clinical problem, menopause is an important model of sleep disturbance, where subjective reports and objectively measured sleep often disagree. In this respect, menopause remains a methodological challenge for sleep researchers. Sleep-disordered breathing is a combination of sleep and breathing disorders. The effects of sleep-disordered breathing on metabolism differ to some extent from those of “pure” sleep loss. Sleep-disordered breathing becomes more common after menopause. The role of menopausal hormonal changes in pathophysiology of sleep-disordered breathing and the role of menopausal hormone therapy will be discussed. The topic would be fresh and update. It would give a comprehensive review of the sleep difficulties across menopause and sleep-disordered breathing on metabolism.
S23.A OSA and lipids M. Ip. Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China Abstract not available at time of printing.
S23.B Adipokines and sleep-disordered breathing J. Ficker. Department of Respiratory Medicine, Allergology, Sleep Medicine, Klinikum Nuernberg, Teaching Hospital of Friedrich-AlexanderUniversity Erlangen-Nuernberg, Nuernberg, Germany SDB is associated with an increased prevalence of cardiovascular disease (CVD). The risk factors for SDB and CVD are highly interrelated. For example, obesity is a major risk factor for SDB, hypertension, and CVD. Obesity and SDB may interact to produce CVD, possibly through the secretion of adipokines. The aim of this presentation is to present and discuss the current data on the effects of sleep-disordered breathing on adipokines in this context. Body fat content is tightly controlled by a homeostatic mechanism linking adipocyte mass with central nervous system control of appetite and metabolic rate. The adipocyte-derived hormone leptin acts as the afferent signaling limb of this negative feedback loop to decrease appetite and increase energy expenditure. Paradoxically, human obesity is associated with hyperleptinemia, suggesting resistance to leptin’s actions. Patients with SDB may be at increased risk for weight gain. Resistance to appetitesuppressant effects of leptin may be involved because SDB patients have higher leptin levels than similarly obese controls. Furthermore, increased leptin levels associated with SDB decline after treatment with CPAP. Many adipokines such as leptin, adiponectin, tumor necrosis factoralpha and IL-6 have known roles in the development of hypertension and atherosclerosis. Moreover, differential expression of these adipokines between subcutaneous and visceral fat may account for specific cardiovascular risks between those with and without SDB. It has been shown that serum adiponectin levels inversely correlate with obesity and insulin resistance. Evidence for the role of adiponectin in metabolic consequences of sleep apnea remains controversial up to now.
S27
One of the many open questions in this field, is whether CPAP can completely mitigate the effects of sleep apnea on glucose metabolism, adipokine effects and cardiovascular consequences in sleep apnea. S23.C Sleep across menopause O. Polo. Department of Respiratory Diseases, University of Tampere, Pikonlinna Hospital, Pikonlinna, Finland The prevalence of sleep problems in women increases in middle-aged women, and is usually attributed to menopause. However, the results from surveys, cross-sectional studies with objective measurements of sleep, and hormone-replacement trials with sleep studies, are inconsistent. Objective and subjective sleep quality seem to correlate poorly in middleaged women. Some studies have even shown that menopause is not associated with decreased objective sleep quality although those periand postmenopausal women were not satisfied with their subjective sleep quality. Do those women just complain for nothing? Can billions of postmenopausal women be wrong when they report sleeping problems? The discrepancy of subjective and objective sleep quality and possible contributing factors will be discussed. Reference(s) [1] Kalleinen N, Polo O, Himanen SL, Joutsen A, Urrila AS, Polo-Kantola P. Sleep deprivation and hormone therapy in postmenopausal women. Sleep Med. 2006; 7(5): 436−47. [2] Polo O. Sleep in postmenopausal women: better sleep for less satisfaction. Sleep 2003; 26(6): 652−3. [3] Young T, Rabago D, Zgierska A, Austin D, Laurel F. Objective and subjective sleep quality in premenopausal, perimenopausal, and postmenopausal women in the Wisconsin Sleep Cohort Study. Sleep. 2003; 26(6): 667−72. [4] Polo-Kantola P, Saaresranta T, Polo O. Aetiology and treatment of sleep disturbances during perimenopause and postmenopause. CNS Drugs 2001; 15(6): 445−52. [5] Polo-Kantola P, Rauhala E, Erkkola R, Irjala K, Polo O. Estrogen replacement therapy and nocturnal periodic limb movements: a randomized controlled trial. Obstet Gynecol 2001; 97(4): 548−54. [6] Polo-Kantola P, Erkkola R, Irjala K, Helenius H, Pullinen S, Polo O. Climacteric symptoms and sleep quality. Obstet Gynecol 1999; 94(2): 219−24. [7] Polo-Kantola P, Erkkola R, Irjala K, Pullinen S, Virtanen I, Polo O. Effect of short-term transdermal estrogen replacement therapy on sleep: a randomized, double-blind crossover trial in postmenopausal women. Fertil Steril 1999; 71(5): 873−80. Supported by Tampere University Hospital, Finnish Anti-Tuberculosis Association Foundation, Tampere Anti-Tuberculosis Foundation. S23.D Sex-hormones and sleep-disordered breathing T. Saaresranta. Department of Pulmonary Diseases and Sleep Research Unit, University of Turku, Turku, Finland Several hormones contribute to control of breathing [1,2]. Sleep-disordered breathing (SDB) has a male predominance suggesting a protective effect of female hormones and/or causative role of androgens in the pathogenesis of SDB. SDB is more prevalent also in polycystic ovary syndrome and after menopause. Sex steroid receptors are located in the central nervous system in the areas related to control of breathing. Sex steroids act directly or via neuromodulatory systems but also peripherally contributing to upper airway patency. High levels of estrogen and progesterone protect pregnant women from SDB. However, pre-existing SDB may deteriorate in obese pregnant women. Partial upper airway obstruction is common in pre-eclampsia and is associated with increased systemic blood pressure. Epidemiological studies show lower prevalencies of SDB in postmenopausal hormone therapy users than in non-users [3]. SDB with low AHI predominates in women, which does not mean fewer symptoms. This is likely due to high prevalence of partial upper airway obstruction in women resulting in low AHI.
S23.A OSA and lipids M. Ip. Department of Medicine, The University of Hong Kong, Queen Mary Hospital, Pokfulam, Hong Kong, China Abstract not available at time of printing.
S23.B Adipokines and sleep-disordered breathing J. Ficker. Department of Respiratory Medicine, Allergology, Sleep Medicine, Klinikum Nuernberg, Teaching Hospital of Friedrich-AlexanderUniversity Erlangen-Nuernberg, Nuernberg, Germany SDB is associated with an increased prevalence of cardiovascular disease (CVD). The risk factors for SDB and CVD are highly interrelated. For example, obesity is a major risk factor for SDB, hypertension, and CVD. Obesity and SDB may interact to produce CVD, possibly through the secretion of adipokines. The aim of this presentation is to present and discuss the current data on the effects of sleep-disordered breathing on adipokines in this context. Body fat content is tightly controlled by a homeostatic mechanism linking adipocyte mass with central nervous system control of appetite and metabolic rate. The adipocyte-derived hormone leptin acts as the afferent signaling limb of this negative feedback loop to decrease appetite and increase energy expenditure. Paradoxically, human obesity is associated with hyperleptinemia, suggesting resistance to leptin’s actions. Patients with SDB may be at increased risk for weight gain. Resistance to appetitesuppressant effects of leptin may be involved because SDB patients have higher leptin levels than similarly obese controls. Furthermore, increased leptin levels associated with SDB decline after treatment with CPAP. Many adipokines such as leptin, adiponectin, tumor necrosis factoralpha and IL-6 have known roles in the development of hypertension and atherosclerosis. Moreover, differential expression of these adipokines between subcutaneous and visceral fat may account for specific cardiovascular risks between those with and without SDB. It has been shown that serum adiponectin levels inversely correlate with obesity and insulin resistance. Evidence for the role of adiponectin in metabolic consequences of sleep apnea remains controversial up to now.
S27
One of the many open questions in this field, is whether CPAP can completely mitigate the effects of sleep apnea on glucose metabolism, adipokine effects and cardiovascular consequences in sleep apnea. S23.C Sleep across menopause O. Polo. Department of Respiratory Diseases, University of Tampere, Pikonlinna Hospital, Pikonlinna, Finland The prevalence of sleep problems in women increases in middle-aged women, and is usually attributed to menopause. However, the results from surveys, cross-sectional studies with objective measurements of sleep, and hormone-replacement trials with sleep studies, are inconsistent. Objective and subjective sleep quality seem to correlate poorly in middleaged women. Some studies have even shown that menopause is not associated with decreased objective sleep quality although those periand postmenopausal women were not satisfied with their subjective sleep quality. Do those women just complain for nothing? Can billions of postmenopausal women be wrong when they report sleeping problems? The discrepancy of subjective and objective sleep quality and possible contributing factors will be discussed. Reference(s) [1] Kalleinen N, Polo O, Himanen SL, Joutsen A, Urrila AS, Polo-Kantola P. Sleep deprivation and hormone therapy in postmenopausal women. Sleep Med. 2006; 7(5): 436−47. [2] Polo O. Sleep in postmenopausal women: better sleep for less satisfaction. Sleep 2003; 26(6): 652−3. [3] Young T, Rabago D, Zgierska A, Austin D, Laurel F. Objective and subjective sleep quality in premenopausal, perimenopausal, and postmenopausal women in the Wisconsin Sleep Cohort Study. Sleep. 2003; 26(6): 667−72. [4] Polo-Kantola P, Saaresranta T, Polo O. Aetiology and treatment of sleep disturbances during perimenopause and postmenopause. CNS Drugs 2001; 15(6): 445−52. [5] Polo-Kantola P, Rauhala E, Erkkola R, Irjala K, Polo O. Estrogen replacement therapy and nocturnal periodic limb movements: a randomized controlled trial. Obstet Gynecol 2001; 97(4): 548−54. [6] Polo-Kantola P, Erkkola R, Irjala K, Helenius H, Pullinen S, Polo O. Climacteric symptoms and sleep quality. Obstet Gynecol 1999; 94(2): 219−24. [7] Polo-Kantola P, Erkkola R, Irjala K, Pullinen S, Virtanen I, Polo O. Effect of short-term transdermal estrogen replacement therapy on sleep: a randomized, double-blind crossover trial in postmenopausal women. Fertil Steril 1999; 71(5): 873−80. Supported by Tampere University Hospital, Finnish Anti-Tuberculosis Association Foundation, Tampere Anti-Tuberculosis Foundation. S23.D Sex-hormones and sleep-disordered breathing T. Saaresranta. Department of Pulmonary Diseases and Sleep Research Unit, University of Turku, Turku, Finland Several hormones contribute to control of breathing [1,2]. Sleep-disordered breathing (SDB) has a male predominance suggesting a protective effect of female hormones and/or causative role of androgens in the pathogenesis of SDB. SDB is more prevalent also in polycystic ovary syndrome and after menopause. Sex steroid receptors are located in the central nervous system in the areas related to control of breathing. Sex steroids act directly or via neuromodulatory systems but also peripherally contributing to upper airway patency. High levels of estrogen and progesterone protect pregnant women from SDB. However, pre-existing SDB may deteriorate in obese pregnant women. Partial upper airway obstruction is common in pre-eclampsia and is associated with increased systemic blood pressure. Epidemiological studies show lower prevalencies of SDB in postmenopausal hormone therapy users than in non-users [3]. SDB with low AHI predominates in women, which does not mean fewer symptoms. This is likely due to high prevalence of partial upper airway obstruction in women resulting in low AHI.