Dear Editor,
With great interest, I read the Review Paper recently created by Zhao et al.1 The authors conducted a study to explore the correlations among metabolic syndrome (MetS), obstructive sleep apnea (OSA), and hypertension.
To date, the prevalence of obesity is increasing rapidly worldwide and is especially common among patients with hypertension, OSA, and MetS, which suggested probable important mechanistic links between these conditions. Due to the prevalence of obesity, MetS is an emerging public challenge that represents a constellation of cardiovascular risk factors. The rising prevalence of sleep apnea, paralleled by a trend of reducing sleep duration (SD), is increasing because of the ongoing epidemic of obesity. Short SD has been suggested to play a key role in the development of MetS.2 Short SD is associated with adverse cardiometabolic manifestations including hypertension, MetS, and cardiovascular consequences.3, 4
OSA is a sleep respiratory disorder characterized by recurrent episodes of complete or partial airway obstruction, resulting in arousal, sleep fragmentation, short SD, and intermittent hypoxia. Biological markers of cardiovascular risk, including oxidative stress, sympathetic activation, systemic inflammation, and endothelial dysfunction, are significantly increased in obese patients with OSA versus those without OSA, suggesting that OSA is not simply an epiphenomenon of obesity. The evidence supports the concept that sleep disorder exacerbates the cardiometabolic risk and MetS through numerous biological pathway.5 It seems like a chicken‐and‐egg problem in some way. However, it is still not completely clear whether this association is unique or is mediated by coexisting disorders frequently seen in patients with OSA. Which is the axis of vicious circle in the complex relationships? It may be not only just one factor in different pathophysiological stages.
Studies suggest that circadian rhythm is a key factor regulation of metabolic systems. Disruption of the circadian rhythm is a contributory factor to clinical and pathophysiological conditions, including cardiovascular disease, MetS, and inflammation.6 We always ignore the universality and importance of circadian rhythms. Circadian rhythms were generated by a transcriptional autoregulatory feedback loop involving core clock genes. Lemmer7 suggested that circadian rhythm disruption is a risk factor for metabolic and cardiovascular disorders, while clinical disease feedback on clock function is limited. Recent studies suggested lose weight by dieting and regular exercise may result in change in circadian clock gene expression.8 Given the complexity of circadian clock gene regulation, the final answer to this question could not be evaluated in an all‐or‐none point of view; otherwise, we will make a mistake. New insight into circadian biology is vital for a new approach to treatment of OSA and MetS.
We should pay more attention to pregnant women with OSA. The prevalence of OSA during pregnancy is greater than that observed in the general population. Immoderate increasing levels of weight and pregnancy‐related weight gain are certainly independent risk factors for OSA during pregnancy. Experimental and prospective studies in humans have demonstrated that OSA is associated with adverse maternal and fetal outcomes.9 There is no doubt that obesity and MetS increased the risk. Because of an overlap in symptoms of OSA and normal pregnancy findings, the diagnosis of OSA in pregnancy is delayed. Current OSA screening tools may not perform well in high‐risk pregnant women.10 Systematic evaluation and grading criteria including accurate recognition and management of prenatal sleep disorders may be solved in time.
According to recent surveys, the percentage of some certain type of shift work is much higher in developing countries than in developed countries, approximately from 15% to 30%. Shift work sleep disorder is a common and overlooked problem in the worldwide, condition with potentially serious medical, social, and economic consequences.11 Nonetheless, shift work will remain a vital component of the modern society and civilization. Shift work sleep disorder is associated with an increased occurrence of cognitive impairment and comorbidities, such as obesity, insulin resistance, diabetes, dyslipidemia, and MetS. Further research is needed to evaluate different treatment approaches for shift work sleep disorder. A new grading system should be established to assess health costs and economics.
CONFLICT OF INTEREST
None.
REFERENCES
- 1. Zhao X, Xu H, Zou J, et al. Joint interaction effect of metabolic syndrome and obstructive sleep apnea on hypertension. J Clin Hypertension. 2018; 20:1551-1552. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Min H, Um YJ, Jang BS, et al. Association between sleep duration and measurable cardiometabolic risk factors in healthy korean women: The Fourth and Fifth Korean National Health and Nutrition Examination Surveys (KNHANES IV and V). Int J Endocrinol. 2016;2016:3784210. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Lucas‐de la Cruz L, Martin‐Espinosa N, Cavero‐Redondo I, et al. Sleep patterns and cardiometabolic risk in schoolchildren from Cuenca, Spain. PloS one. 2018;13(1):e0191637. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Itani O, Kaneita Y, Tokiya M, et al. Short sleep duration, shift work, and actual days taken off work are predictive life‐style risk factors for new‐onset metabolic syndrome: a seven‐year cohort study of 40,000 male workers. Sleep Med. 2017;39:87‐94. [DOI] [PubMed] [Google Scholar]
- 5. Kuwabara M, Tomitani N, Shiga T, Kario K. Polysomnography‐derived sleep parameters as a determinant of nocturnal blood pressure profile in patients with obstructive sleep apnea. J Clin Hypertension. 2018;20(6):1039‐1048. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6. Arble DM, Bass J, Behn CD, et al. Impact of sleep and circadian disruption on energy balance and diabetes: a summary of workshop discussions. Sleep. 2015;38(12):1849‐1860. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7. Lemmer B, Oster H. The role of circadian rhythms in the hypertension of diabetes mellitus and the metabolic syndrome. Curr Hypertens Rep. 2018;20(5):43. [DOI] [PubMed] [Google Scholar]
- 8. Pivovarova O, Gogebakan O, Sucher S, et al. Regulation of the clock gene expression in human adipose tissue by weight loss. Int J Obesity. 2016;40(6):899‐906. [DOI] [PubMed] [Google Scholar]
- 9. Li L, Zhao K, Hua J, Li S. Association between sleep‐disordered breathing during pregnancy and maternal and fetal outcomes: an updated systematic review and meta‐analysis. Front Neurol. 2018;9:91. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 10. Tantrakul V, Numthavaj P, Guilleminault C, et al. Performance of screening questionnaires for obstructive sleep apnea during pregnancy: A systematic review and meta‐analysis. Sleep Med Rev. 2017;36:96‐106. [DOI] [PubMed] [Google Scholar]
- 11. Wickwire EM, Geiger‐Brown J, Scharf SM, Drake CL. Shift work and shift work sleep disorder: clinical and organizational perspectives. Chest. 2017;151(5):1156‐1172. [DOI] [PMC free article] [PubMed] [Google Scholar]
