Reader response: Insomnia symptoms and risk of cardiovascular diseases among 0.5 million adults: A 10-year cohort
HaoPeng, Neurologist, Department of Epidemiology, School of Public Health, Medical College of Soochow University
Submitted December 05, 2019
Sleep is of paramount importance for humans to synchronize behaviors with the 24-hour circadian rhythm. Poor sleep has been associated with disorders of metabolic and cardiovascular systems but with uncertain etiology. Dr. Zheng et al.1 found that insomnia symptoms accounted for about 10% higher risk of cardiovascular disease (CVD), leveraging a very large prospective cohort study. This finding increases the possibility that circadian disruption could be a risk factor for CVD. A better understanding of the mechanisms through which circadian disruption exerts cumulative toxic effects on cardiovascular system would undoubtedly improve the prevention and management of this debilitating epidemic for adults—and shift-workers in particular. The circadian clock is under tight control of an endogenous transcription-translation feedback loop, which is regulated by many circadian genes. As an interface between the fixed genome and dynamic environment, DNA methylation in the circadian genes may affect the genetic function and thereby regulate circadian rhythms.2 In fact, DNA methylation status changes dramatically in our lifetime in response to environment, and dysregulated DNA methylation was previously related to CVD and its risk factors.3–5 As a molecular modification, studying DNA methylation on circadian genes may uncover potential interventional targets for cardiovascular health.
Disclosure
The author reports no relevant disclosures. Contact journal@neurology.org for full disclosures.
References
Zheng B, Yu C, Lv J, et al. Insomnia symptoms and risk of cardiovascular diseases among 0.5 million adults: A 10-year cohort. Neurology 2019;93:e2110–2120.
Curradi M, Izzo A, Badaracco G and Landsberger N. Molecular mechanisms of gene silencing mediated by DNA methylation. Mol Cell Biol 2002;22:3157–3173.
Stoll S, Wang C, Qiu H. DNA Methylation and Histone Modification in Hypertension. Int J Mol Sci 2018;19: e1174.
Peng H, Zhu Y, Goldberg J, Vaccarino V, and Zhao J. DNA Methylation of Five Core Circadian Genes Jointly Contributes to Glucose Metabolism: A Gene-Set Analysis in Monozygotic Twins. Front Genet 2019;10:329.
Fernandez-Sanles A, Sayols-Baixeras S, Subirana I, Degano IR, and Elosua R. Association between DNA methylation and coronary heart disease or other atherosclerotic events: A systematic review. Atherosclerosis 2017;263:325–333.
Sleep is of paramount importance for humans to synchronize behaviors with the 24-hour circadian rhythm. Poor sleep has been associated with disorders of metabolic and cardiovascular systems but with uncertain etiology. Dr. Zheng et al.1 found that insomnia symptoms accounted for about 10% higher risk of cardiovascular disease (CVD), leveraging a very large prospective cohort study. This finding increases the possibility that circadian disruption could be a risk factor for CVD. A better understanding of the mechanisms through which circadian disruption exerts cumulative toxic effects on cardiovascular system would undoubtedly improve the prevention and management of this debilitating epidemic for adults—and shift-workers in particular. The circadian clock is under tight control of an endogenous transcription-translation feedback loop, which is regulated by many circadian genes. As an interface between the fixed genome and dynamic environment, DNA methylation in the circadian genes may affect the genetic function and thereby regulate circadian rhythms.2 In fact, DNA methylation status changes dramatically in our lifetime in response to environment, and dysregulated DNA methylation was previously related to CVD and its risk factors.3–5 As a molecular modification, studying DNA methylation on circadian genes may uncover potential interventional targets for cardiovascular health.
Disclosure
The author reports no relevant disclosures. Contact journal@neurology.org for full disclosures.
References