MOJ ISSN: 2381-179X MOJCR

Clinical & Medical Case Reports
Editorial
Volume 2 Issue 3 - 2015
Sleep and Sleep Medicine. From Exotic Research to a Public Health Problem
Richard Staats
Department of Pneumology, University Hospital de Santa Maria, Portugal
Received: April 29, 2015 | Published: May 08, 2015
*Corresponding author: Richard Staats, Department of Pneumology, University Hospital de Santa Maria, Centro Hospitalar Lisboa Norte, Hospital da Luz, Portugal, Tel: 00351913646987; Email: @
Citation: Staats R (2015) Sleep and Sleep Medicine. From Exotic Research to a Public Health Problem. MOJ Clin Med Case Rep 2(3): 00021. DOI: 10.15406/mojcr.2015.02.00021

Abbrevations

EEG: Electroencephalography; REM: Rapid Eye Movement; NREM: Non-Rapid Eye Movement ; OSAS: Obstructive Sleep Apnea Syndrome

Editorial

For many years sleep research and sleep medicine have been restricted to a small number of scientists mainly active in the field of Neurology, Neurophysiology, and Psychiatry. Following the description of the electroencephalography (EEG) by Berger [1], the knowledge of sleep and sleep disturbances increased exponentially in the last six decades. The beginning of modern sleep medicine was developing the discovery of the typical EEG sleep pattern of both normal sleep or non REM sleep (NREM) and paradoxical sleep or REM sleep [2-5]. Sleep disorders appear early in human written history. Insomnia, for example, was described in the oldest human story “Gilgamesh” the king of Uruk [6]. There are a huge amount of nowadays celebrities who have declared problems of insomnia including George Clooney or Michael Jackson. Although insomnia clearly reduces the quality of life it has taken a long time until both health professional and the general population accepted insomnia as a disease. Sleeplessness is a frequent disorder with about 10 % of the population refering chronic insomnia.

A short-term or intermitted insomnia reaches values up to 35% of the population [7]. It is now considered a fact, that insomnia and also sleep deprivation or sleep restriction may lead to a reduction in the physical capability and is an important risk factor for car accidents [8,9]. Besides insomnia sleep related breathing disorders have been intensively investigated in the last decades. The most frequent one is the obstructive sleep apnea syndrome (OSAS). Also, here celebrities are not excluded with famous examples including Quincy Jones or Shaquille O´Neal. The most frequently cited prevalence of OSAS is 4 % in men and 2 % in women [10]. However, due to the increased obesity in the industrialized countries the actual prevalence is possibly much higher. Recent studies indicate higher numbers with 15 % of the US population and 30% of a São Paulo cohort fulfilling the criterias of sleep apnea [11,12].

Considering these numbers, it is highly probable that physicians not directly related to sleep medicine will encounter patients with relevant sleep disorders. Patients are frequently not aware that common health problems are influenced or even have their origin in the presence of sleep disorders. The relationship between OSA and cardiovascular diseases has been established for a long time with first descriptions in the 1980th just after the invention of positive pressure therapy [13,14]. In several epidemiological studies, OSA was found to increase the risk of hypertension, especially nocturnal hypertension and coronary heart disease [15-17]. Patients benefit of an adequate therapy of OSAS by a decrease of the cardiovascular diseases and the mortality. There exists a sufficient body of evidence that intermittent hypoxia is the key mechanism for the higher prevalence of cardiovascular diseases in OSAS [18-20]. Nevertheless, other non-hypoxic sleep diseases like insomnia and restless legs syndrome are also found to be related to hypertension and non-dipping blood pressure [21-25].

The interaction of sleep disorders with metabolic alterations is less clear but there is now ample evidence that sleep disturbances are associated with the metabolic syndrome [26-30]. Recent cross sectional and longitudinal studies have found more and more confirmation that Type 2 diabetes is associated with the presence of OSAS [31-33]. Positive pressure therapy abbreviates some of the altered parametres. OSAS is therefore in the interesting position that it helps to understand the pathogenesis leading to Type 2 diabetes but also, from the clinical point of view, that it is relevant for disease control [34-38]. Similary to the above stated association between OSAS and cardiovascular diseases, the intermittent hypoxia is considered one of the major risk factors to develop metabolic alterations [39-41]. Both insulin resistance and lipid metabolism are connected to the liver function. In fact, the repitetive hypoxemia in OSAS patients has been recently linked to the development of non-alcoholic steatohepatitis and OSAS has been found associated with the prevalence of non-alcoholic fatty liver disease [42-44]. This closes the circle of interacting metabolic diseases including obesity, OSAS, hypoxemia, liver dysfunction and altered glucose and insulin metabolism [45].

But once again, although well designed studies brought evidence that intermittent hypoxemia leads to metabolic alteration, it is yet in the discussion if sleep fragmentation, restriction, and insomnia are also important risk factors. Both quality and quantity of sleep predict the risk of type 2 diabetes [46]. Female shift workers with a rapid forward shift rotation are more prone to reach criteria of the metabolic syndrome when compared to colleagues working on a regular basis during the day [35]. In an animal model, alteration of the circadian rhythm may cause hyperlipidaemia via clock gene regulations [47]. The effect of sleepiness, fatigue and non-restoring sleep on cardiovascular and metabolic disorders is still unclear. At present it remains in the discussion if sleep apneas without sleepiness are in fact at an increased risk of cardiovascular diseases or metabolic disorders [48-53].

Conclusion

We know that sleep effects various functions of the homeostasis. To address correctly the health problems of their patients any physician should be aware of this relationship. Although the impact of OSAS on cardiovascular and metabolic disorders is well established, there is still some uncertainty if sleep quality, sleep duration, and sleep fragmentation are not of relevance as well. To elucidate this complicated relationship between sleep, mental and physical health the publication of case reports will be of considerable importance.

References

  1. Berger H ( 1929) Über das Elektroenzephalogramm des Menschen. Arch f Psychiat 87: 527-570.
  2. Davis H, Davis PA, Loomis AL, Harvey EN, Hobart G (1937) Changes in Human Brain Potentials during the Onset of Sleep. Science 86(2237): 448-450.
  3. Aserinsky E, Kleitman N (1953) Regularly occurring periods of eye motility, and concomitant phenomena, during sleep. Science 118(3062): 273-274.
  4. Aserinsky E, Kleitman N (1955) Two types of ocular motility occurring in sleep. J Appl Physiol 8(1): 1-10.
  5. Kleitman N, Engelmann G (1955) The development of the diurnal (24-hour) sleep-wakefulness rhythm in the infant. Acta med Scand Suppl 307: 106.
  6. Summers-Bremner E (2008) Insomnia : a cultural history. Reaktion Books, London, UK.
  7. Medicine AAoS (2014) International classification of sleep disorders. (3rd edn), In: Sateia M (Ed.), American Academy of Sleep Medicine, USA, pp. 389.
  8. Williamson AM, Feyer AM (2000) Moderate sleep deprivation produces impairments in cognitive and motor performance equivalent to legally prescribed levels of alcohol intoxication. Occup Environ Med 57(10): 649-655.
  9. Léger D, Bayon V, Ohayon MM, Philip P, Ement P, et al. (2014) Insomnia and accidents: cross-sectional study (EQUINOX) on sleep-related home, work and car accidents in 5293 subjects with insomnia from 10 countries. J Sleep Res 23(2): 143-152.
  10. Young T, Palta M, Dempsey J, Skatrud J, Weber S, et al. (1993) The occurrence of sleep-disordered breathing among middle-aged adults. N Engl J Med 328(17): 1230-1235.
  11. Young T, Palta M, Dempsey J, Peppard PE, Nieto FJ, et al. (2009) Burden of sleep apnea: rationale, design, and major findings of the Wisconsin Sleep Cohort study. WMJ 108(5): 246-249.
  12. Tufik S, Santos-Silva R, Taddei JA, Bittencourt LR (2010) Obstructive sleep apnea syndrome in the Sao Paulo Epidemiologic Sleep Study. Sleep Med 11(5): 441-446.
  13. Sullivan CE, Issa FG, Berthon-Jones M, Eves L (1981) Reversal of obstructive sleep apnoea by continuous positive airway pressure applied through the nares. Lancet 1(8225): 862-865.
  14. Kales A, Bixler EO, Cadieux RJ, Schneck DW, Shaw LC, et al. (1984) Sleep apnoea in a hypertensive population. Lancet 2(8410): 1005-1008.
  15. Peppard PE, Young T, Palta M, Skatrud J (2000) Prospective study of the association between sleep-disordered breathing and hypertension. N Engl J Med 342(19): 1378-1384.
  16. Seif F, Patel SR, Walia HK, Rueschman M, Bhatt DL, et al. (2014) Obstructive sleep apnea and diurnal nondipping hemodynamic indices in patients at increased cardiovascular risk. J Hypertens 32(2): 267-275.
  17. Hla KM, Young T, Hagen EW, Stein JH, Finn LA, et al. (2014) Coronary Heart Disease Incidence in Sleep Disordered Breathing: The Wisconsin Sleep Cohort Study. Sleep 00357-14.
  18. Lavie L, Lavie P (2009) Molecular mechanisms of cardiovascular disease in OSAHS: the oxidative stress link. Eur Respir J 33(6): 1467-1484.
  19. Garvey JF, Taylor CT, McNicholas WT (2009) Cardiovascular disease in obstructive sleep apnoea syndrome: the role of intermittent hypoxia and inflammation. Eur Respir J 33(5): 1195-1205.
  20. Bradley TD, Floras JS (2009) Obstructive sleep apnoea and its cardiovascular consequences. Lancet 373(9657): 82-93.
  21. Walters AS, Rye DB (2009) Review of the relationship of restless legs syndrome and periodic limb movements in sleep to hypertension, heart disease, and stroke. Sleep 32(5): 589-597.
  22. Vgontzas AN, Liao D, Bixler EO, Chrousos GP, Vela-Bueno A (2009) Insomnia with objective short sleep duration is associated with a high risk for hypertension. Sleep 32(4): 491-497.
  23. Bruno RM, Palagini L, Gemignani A, Virdis A, Di Giulio A, et al. (2013) Poor sleep quality and resistant hypertension. Sleep Med 14(11): 1157-1163.
  24. Faraut B, Boudjeltia KZ, Vanhamme L, Kerkhofs M (2012) Immune, inflammatory and cardiovascular consequences of sleep restriction and recovery. Sleep Med Rev 16(2): 137-149.
  25. Palagini L, Bruno RM, Gemignani A, Baglioni C, Ghiadoni L, et al. (2013) Sleep loss and hypertension: a systematic review. Curr pharma Des 19(13): 2409-2419.
  26. Spiegel K, Leproult R, Van Cauter E (1999) Impact of sleep debt on metabolic and endocrine function. Lancet 354(9188): 1435-1439.
  27. Grandi AM, Laurita E, Marchesi C, Maresca AM, Solbiati F, et al. (2012) OSA, metabolic syndrome and CPAP: effect on cardiac remodeling in subjects with abdominal obesity. Respir Med 106(1): 145-152.
  28. Hall MH, Okun ML, Sowers M, Matthews KA, Kravitz HM, et al. (2012) Sleep is associated with the metabolic syndrome in a multi-ethnic cohort of midlife women: the SWAN Sleep Study. Sleep 35(6): 783-790.
  29. Hung HC, Yang YC, Ou HY, Wu JS, Lu FH, et al. (2013) The association between self-reported sleep quality and metabolic syndrome. PLoS One 8(1): 54304.
  30. Drager LF, Lopes HF, Maki-Nunes C, et al. (2010) The impact of obstructive sleep apnea on metabolic and inflammatory markers in consecutive patients with metabolic syndrome. PLoS One 5(8): 12065.
  31. Reichmuth KJ, Austin D, Skatrud JB, Young T (2005) Association of sleep apnea and type II diabetes: a population-based study. Am J Respir Crit Care Med 172(12): 1590-1595.
  32. Lindberg E, Theorell-Haglow J, Svensson M, Gislason T, Berne C, et al. (2012) Sleep apnea and glucose metabolism: a long-term follow-up in a community-based sample. Chest 142(4): 935-942.
  33. Kent BD, Grote L, Bonsignore MR, Saaresranta T, Verbraecken J, et al. (2014) Sleep apnoea severity independently predicts glycaemic health in nondiabetic subjects: the ESADA study. Eur Respir J 44(1): 130-139.
  34. Coughlin SR, Mawdsley L, Mugarza JA, Calverley PM, Wilding JP (2004) Obstructive sleep apnoea is independently associated with an increased prevalence of metabolic syndrome. Eur Heart J 25(9): 735-741.
  35. Sharma SK, Agrawal S, Damodaran D, Sreenivas V, Kadhiravan T, et al. (2011) CPAP for the metabolic syndrome in patients with obstructive sleep apnea. N Engl J Med 365(24): 2277-2286.
  36. Mota PC, Drummond M, Winck JC, Santos AC, Almeida J, et al. (2011) APAP impact on metabolic syndrome in obstructive sleep apnea patients. Sleep Breath 15(4): 665-672.
  37. West SD, Nicoll DJ, Wallace TM, Matthews DR, Stradling JR (2007) Effect of CPAP on insulin resistance and HbA1c in men with obstructive sleep apnoea and type 2 diabetes. Thorax 62(11): 969-974.
  38. Weinstock TG, Wang X, Rueschman M, Ismail-Beigi F, Aylor J, et al. (2012) A controlled trial of CPAP therapy on metabolic control in individuals with impaired glucose tolerance and sleep apnea. Sleep 35(5): 617-625.
  39. Olea E, Agapito MT, Gallego-Martin T, et al. (2014) Intermittent hypoxia and diet-induced obesity: effects on oxidative status, sympathetic tone, plasma glucose and insulin levels, and arterial pressure. J Appl Physiol 117(7): 706-719.
  40. Dewan NA, Nieto FJ, Somers VK (2015) Intermittent hypoxemia and OSA: implications for comorbidities. Chest 147(1): 266-274.
  41. Lévy P, Pépin JL, Arnaud C, Tamisier R, Borel JC, et al. (2008) Intermittent hypoxia and sleep-disordered breathing: current concepts and perspectives. Eur Respir J 32(4): 1082-1095.
  42. Corey KE, Misdraji J, Gelrud L, King LY, Zheng H, et al. (2015) Obstructive Sleep Apnea Is Associated with Nonalcoholic Steatohepatitis and Advanced Liver Histology. Dig Dis Sci .
  43. Minville C, Hilleret MN, Tamisier R, Aron-Wisnewsky J, Clement K, et al. (2014) Nonalcoholic fatty liver disease, nocturnal hypoxia, and endothelial function in patients with sleep apnea. Chest 145(3): 525-533.
  44. Sookoian S, Pirola CJ (2013) Obstructive sleep apnea is associated with fatty liver and abnormal liver enzymes: a meta-analysis. Obes Surg 23(11): 1815-1825.
  45. Paschetta E, Belci P, Alisi A, Liccardo D, Cutrera R, et al. (2015) OSAS-Related Inflammatory Mechanisms of Liver Injury in Nonalcoholic Fatty Liver Disease. Mediators inflamm 2015: 815721.
  46. Cappuccio FP, D'Elia L, Strazzullo P, Miller MA (2010) Quantity and quality of sleep and incidence of type 2 diabetes: a systematic review and meta-analysis. Diabetes Care 33(2): 414-420 .
  47. Pan X, Zhang Y, Wang L, Hussain MM. (2010) Diurnal regulation of MTP and plasma triglyceride by CLOCK is mediated by SHP. Cell Metab 12(2): 174-186.
  48. Barbé F, Durán-Cantolla J, Capote F, de la Peña M, Chiner E, et al. (2010) Long-term effect of continuous positive airway pressure in hypertensive patients with sleep apnea. Am J Respir Crit Care Med 181(7): 718-726.
  49. Barbé F, Mayoralas LR, Duran J, Masa JF, Maimó A, et al. (2001) Treatment with continuous positive airway pressure is not effective in patients with sleep apnea but no daytime sleepiness. a randomized, controlled trial. Ann Intern Med 134(11): 1015-1023.
  50. Robinson GV, Smith DM, Langford BA, Davies RJ, Stradling JR (2006) Continuous positive airway pressure does not reduce blood pressure in nonsleepy hypertensive OSA patients. Eur Respir J 27(6): 1229-1235.
  51. Huang JF, Chen LD, Lin QC, Chen GP, Yu YH, et al. (2015) The relationship between excessive daytime sleepiness and metabolic syndrome in severe obstructive sleep apnea syndrome. Clinical Respir J.
  52. Ronksley PE, Hemmelgarn BR, Heitman SJ, Hanly PJ, Faris PD, et al. (2009) Obstructive sleep apnoea is associated with diabetes in sleepy subjects. Thorax 64(10): 834-839.
  53. Pulixi EA, Tobaldini E, Battezzati PM, D'Ingianna P, Borroni V, et al. (2014) Risk of obstructive sleep apnea with daytime sleepiness is associated with liver damage in non-morbidly obese patients with nonalcoholic fatty liver disease. PLoS One 9(4): 96349.
© 2014-2016 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at http://medcraveonline.com
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy