Abstract
The metabolic syndrome, an emerging public health problem, represents a constellation of cardiovascular risk factors. It has been suggested that the presence of obstructive sleep apnea (OSA) may increase the risk of developing some of the features of the metabolic syndrome, including hypertension, insulin resistance, and type 2 diabetes. In this article, we discuss the parallels between the metabolic syndrome and obstructive sleep apnea and describe possible OSA-related factors that may contribute to the metabolic syndrome, specifically the roles of obesity, hypertension, dyslipidemia, sex hormones, inflammation, vascular dysfunction, leptin, insulin resistance, and sleep deprivation.
Similar content being viewed by others
References and Recommended Reading
Carlson JT, Hedner JA, Ejnell H, et al.: High prevalence of hypertension in sleep apnea patients independent of obesity. Am J Respir Crit Care Med 1994, 150:72–77.
Stoohs RA, Facchini F, Guilleminault C: Insulin resistance and sleep-disordered breathing in healthy humans. Am J Respir Crit Care Med 1996, 154:170–174.
Elmasry A, Janson C, Lindberg E, et al.: The role of habitual snoring and obesity in the development of diabetes: a 10-year follow-up study in a male population. J Intern Med 2000, 248:13–20.
Must A, Spadano J, Coakley EH, et al.: The disease burden associated with overweight and obesity. JAMA 1999, 282:1523–1529.
Overweight, obesity, and health risk. National Task Force on the Prevention and Treatment of Obesity [no authors listed]. Arch Intern Med 2000, 160:898–904.
Young T, Palta M, Dempsey J, et al.: The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 1993, 328:1230–1235.
Shamsuzzaman AS, Gersh BJ, Somers VK: Obstructive sleep apnea: implications for cardiac and vascular disease. JAMA 2003, 290:1906–1914. Obstructive sleep apnea may be characterized by sleep fragmentation, increased sympathetic activity, endothelial dysfunction, inflammation, increased oxidative stress, platelet aggregability, and metabolic dysregulation. Through these mechanisms, OSA may worsen cardiac and vascular disease.
Wilcox I, McNamara SG, Collins FL, et al.: "Syndrome Z": the interaction of sleep apnoea, vascular risk factors and heart disease. Thorax 1998, 53(suppl_3):S25-S28.
Coughlin SR, Mawdsley L, Mugarza JA, et al.: Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J 2004, 25:735–741.
Anstead M, Phillips B: The spectrum of sleep-disordered breathing. Respir Care Clin N Am 1999, 5:363–377.
Malhotra A, White DP: Obstructive sleep apnoea. Lancet 2002, 360:237–245.
Young T, Shahar E, Nieto FJ, et al.: Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med 2002, 162:893–900.
Vgontzas AN, Tan TL, Bixler EO, et al.: Sleep apnea and sleep disruption in obese patients. Arch Intern Med 1994, 154:1705–1711.
van Boxem TJ, de Groot GH: Prevalence and severity of sleep disordered breathing in a group of morbidly obese patients. Neth J Med 1999, 54:202–206.
Peppard PE, Young T, Palta M, et al.: Longitudinal study of moderate weight change and sleep-disordered breathing. JAMA 2000, 284:3015–3021.
Smith PL, Gold AR, Meyers DA, et al.: Weight loss in mildly to moderately obese patients with obstructive sleep apnea. Ann Intern Med 1985, 103:850–855.
Schwartz AR, Gold AR, Schubert N, et al.: Effect of weight loss on upper airway collapsibility in obstructive sleep apnea. Am Rev Respir Dis 1991, 144:494–498.
Vgontzas AN, Bixler EO, Chrousos GP: Metabolic disturbances in obesity versus sleep apnoea: the importance of visceral obesity and insulin resistance. J Intern Med 2003, 254:32–44.
Phillips BG, Kato M, Narkiewicz K, et al.: Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea. Am J Physiol Heart Circ Physiol 2000, 279:H234-H237.
Phillips BG, Hisel TM, Kato M, et al.: Recent weight gain in patients with newly diagnosed obstructive sleep apnea. J Hypertens 1999, 17:1297–1300.
Chin K, Shimizu K, Nakamura T, et al.: Changes in intra-abdominal visceral fat and serum leptin levels in patients with obstructive sleep apnea syndrome following nasal continuous positive airway pressure therapy. Circulation 1999, 100:706–712.
Nieto FJ, Young TB, Lind BK, et al.: Association of sleep-disordered breathing, sleep apnea, and hypertension in a large community-based study. Sleep Heart Health Study. JAMA 2000, 283:1829–1836.
Peppard PE, Young T, Palta M, et al.: Prospective study of the association between sleep disordered breathing and hypertension. N Engl J Med 2000, 342:1378–1384.
Peker Y, Hedner J, Norum J, et al.: Increased incidence of cardiovascular disease in middle-aged men with obstructive sleep apnea: a 7-year follow-up. Am J Respir Crit Care Med 2002, 166:159–165.
Weiss JW, Launois SH, Anand A, et al.: Cardiovascular morbidity in obstructive sleep apnea. Prog Cardiovasc Dis 1999, 41:367–376.
Stradling JR: Sleep apnoea and systemic hypertension. Thorax 1989, 44:984–989.
Young T, Peppard P, Palta M, et al.: Population-based study of sleep-disordered breathing as a risk factor for hypertension. Arch Intern Med 1997, 157:1746–1752.
Faccenda JF, Mackay TW, Boon NA, et al.: Randomized placebo-controlled trial of continuous positive airway pressure on blood pressure in the sleep apnea-hypopnea syndrome. Am J Respir Crit Care Med 2001, 163:344–348.
Pepperell JC, Ramdassingh-Dow S, Crosthwaite N, et al.: Ambulatory blood pressure after therapeutic and subtherapeutic nasal continuous positive airway pressure for obstructive sleep apnoea: a randomised parallel trial. Lancet 2002, 359:204–210. A randomized trial comparing changes in blood pressure in 118 men with OSA who were assigned to either therapeutic or subtherapeutic nasal continuous positive airway pressure (nCPAP) for 1 month. Therapeutic nCPAP reduced mean arterial ambulatory blood pressure by 2.5 mm Hg (during both sleep and wakefulness), whereas subtherapeutic nCPAP increased blood pressure by 0.8 mm Hg.
Becker HF, Jerrentrup A, Ploch T, et al.: Effect of nasal continuous positive airway pressure treatment on blood pressure in patients with obstructive sleep apnea. Circulation 2003, 107:68–73. The effect of nCPAP on arterial hypertension was studied in 60 patients with OSA randomly assigned to either effective or subtherapeutic nCPAP for 9 weeks. Mean arterial pressure decreased by 9.9 mm Hg with effective nCPAP. Mean, diastolic, and systolic blood pressure decreased significantly by approximately 10 mm Hg during the night and the day, a change predicted to reduce the risk of coronary heart disease by 37% and risk of stroke by 56%.
Somers VK, Dyken ME, Clary MP, et al.: Sympathetic neural mechanisms in obstructive sleep apnea. J Clin Invest 1995, 96:1897–1904.
Kiely JL, McNicholas WT: Cardiovascular risk factors in patients with obstructive sleep apnoea syndrome. Eur Respir J 2000, 16:128–133.
Ip MS, Lam KS, Ho C, et al.: Serum leptin and vascular risk factors in obstructive sleep apnea. Chest 2000, 118:580–586.
Tishler PV, Larkin EK, Schluchter MD, et al.: Incidence of sleep-disordered breathing in an urban adult population: the relative importance of risk factors in the development of sleep-disordered breathing. JAMA 2003, 289:2230–2237.
Matsumoto AM, Sandblom RE, Schoene RB, et al.: Testosterone replacement in hypogonadal men: effects on obstructive sleep apnoea, respiratory drives, and sleep. Clin Endocrinol (Oxf) 1985, 22:713–721.
Dexter DD, Dovre EJ: Obstructive sleep apnea due to endogenous testosterone production in a woman. Mayo Clin Proc 1998, 73:246–248.
Cistulli PA, Grunstein RR, Sullivan CE: Effect of testosterone administration on upper airway collapsibility during sleep. Am J Respir Crit Care Med 1994, 149:530–532.
Schneider BK, Pickett CK, Zwillich CW, et al.: Influence of testosterone on breathing during sleep. J Appl Physiol 1986, 61:618–623.
Punjabi NM, Sorkin JD, Katzel LI, et al.: Sleep-disordered breathing and insulin resistance in middle-aged and overweight men. Am J Respir Crit Care Med 2002, 165:677–682. A study of 150 men without diabetes and cardiopulmonary disease showed that impairment of glucose tolerance is related to the severity of oxygen desaturation. After adjusting for percent body fat, BMI, and AHI, a 4% decrease in oxygen saturation was associated with the 1.99 odds ratio for worsening glucose tolerance. Increase in AHI was associated with worsening insulin resistance independent of obesity.
Abate N: Obesity and cardiovascular disease. Pathogenetic role of the metabolic syndrome and therapeutic implications. J Diabetes Complications 2000, 14:154–174.
VanHelder T, Symons JD, Radomski MW: Effects of sleep deprivation and exercise on glucose tolerance. Aviat Space Environ Med 1993, 64:487–492.
Spiegel K, Leproult R, Van Cauter E: Impact of sleep debt on metabolic and endocrine function. Lancet 1999, 354:1435–1439.
Vgontzas AN, Zoumakis M, Bixler EO, et al.: Impaired nighttime sleep in healthy old versus young adults is associated with elevated plasma interleukin-6 and cortisol levels: physiologic and therapeutic implications. J Clin Endocrinol Metab 2003, 88:2087–2095.
Redwine L, Hauger RL, Gillin JC, et al.: Effects of sleep and sleep deprivation on interleukin-6, growth hormone, cortisol, and melatonin levels in humans. J Clin Endocrinol Metab 2000, 85:3597–3603.
Kato M, Phillips BG, Sigurdsson G, et al.: Effects of sleep deprivation on neural circulatory control. Hypertension 2000, 35:1173–1175.
Mullington JM, Chan JL, Van Dongen HP, et al.: Sleep loss reduces diurnal rhythm amplitude of leptin in healthy men. J Neuroendocrinol 2003, 15:851–854. Sleep may influence the nocturnal leptin profile. In a study of 10 healthy men, diurnal amplitude of leptin was reduced during days of sleep deprivation (88 hours), and recovered during recovery sleep.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Svatikova, A., Wolk, R., Gami, A.S. et al. Interactions between obstructive sleep apnea and the metabolic syndrome. Curr Diab Rep 5, 53–58 (2005). https://doi.org/10.1007/s11892-005-0068-2
Issue Date:
DOI: https://doi.org/10.1007/s11892-005-0068-2