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Sci Rep. 2019 Feb 4;9(1):1193. doi: 10.1038/s41598-018-38009-0.

A distinctive DNA methylation pattern in insufficient sleep.

Author information

1
Department of Public Health Solutions, Genomics and Biomarkers Unit, National Institute for Health and Welfare, PO Box 30, FI-00271, Helsinki, Finland. alexandra.lahtinen@helsinki.fi.
2
Department of Psychiatry, University of Helsinki and Helsinki University Central Hospital, PO Box 590, FIN-00029, HUS, Helsinki, Finland. alexandra.lahtinen@helsinki.fi.
3
Work Ability and Working Career, Finnish Institute of Occupational Health, PO Box 40, FI-00032, Työterveyslaitos, Helsinki, Finland.
4
Finnair Health Services, HEL-IF/67, FI-01053, Finnair, Finland.
5
Department of Public Health Solutions, Genomics and Biomarkers Unit, National Institute for Health and Welfare, PO Box 30, FI-00271, Helsinki, Finland.
6
Department of Psychiatry, University of Helsinki and Helsinki University Central Hospital, PO Box 590, FIN-00029, HUS, Helsinki, Finland.
7
Estonian Genome Center, Institute of Genomics, University of Tartu, Tartu, 51010, Estonia.
8
Diabetes and Obesity Research Program, University of Helsinki, PO Box 63, FI-00014, Helsinki, Finland.
9
Department of Public Health Solutions, Genomics and Biomarkers Unit, National Institute for Health and Welfare, PO Box 30, FI-00271, Helsinki, Finland. tiina.paunio@helsinki.fi.
10
Department of Psychiatry, University of Helsinki and Helsinki University Central Hospital, PO Box 590, FIN-00029, HUS, Helsinki, Finland. tiina.paunio@helsinki.fi.

Abstract

Short sleep duration or insomnia may lead to an increased risk of various psychiatric and cardio-metabolic conditions. Since DNA methylation plays a critical role in the regulation of gene expression, studies of differentially methylated positions (DMPs) might be valuable for understanding the mechanisms underlying insomnia. We performed a cross-sectional genome-wide analysis of DNA methylation in relation to self-reported insufficient sleep in individuals from a community-based sample (79 men, aged 39.3 ± 7.3), and in relation to shift work disorder in an occupational cohort (26 men, aged 44.9 ± 9.0). The analysis of DNA methylation data revealed that genes corresponding to selected DMPs form a distinctive pathway: "Nervous System Development" (FDR P value < 0.05). We found that 78% of the DMPs were hypomethylated in cases in both cohorts, suggesting that insufficient sleep may be associated with loss of DNA methylation. A karyoplot revealed clusters of DMPs at various chromosomal regions, including 12 DMPs on chromosome 17, previously associated with Smith-Magenis syndrome, a rare condition comprising disturbed sleep and inverse circadian rhythm. Our findings give novel insights into the DNA methylation patterns associated with sleep loss, possibly modifying processes related to neuroplasticity and neurodegeneration. Future prospective studies are needed to confirm the observed associations.

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