Sleep duration and fragmentation in relation to leukocyte DNA methylation in adolescents

Jansen, Erica C.; Dolinoy, Dana C.; O’Brien, Louise M.; Peterson, Karen E.; Chervin, Ronald D.; Banker, Margaret; Téllez-Rojo, Martha M.; Cantoral, Alejandra; Mercado‐García, Adriana; Sánchez, Brisa N.; Goodrich, Jaclyn M.

doi:10.1093/sleep/zsz121

Cited by 11 publications

(12 citation statements)

References 49 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…UK Biobank 23andMe Jansen, Dolinoy, et al, 2019, Jansen, Watanabe, et al, 2019 Multi‐ancestry Genome‐Wide Association Study of Stroke (MEGASTROKE) dataset was based on a meta‐analysis of 29 European‐ancestry GWAS…”

Section: Resultsmentioning

confidence: 99%

Potential genetic and epigenetic mechanisms in insomnia: A systematic review

Palagini

Geoffroy

Gehrman

et al. 2023

Journal of Sleep Research

View full text Add to dashboard Cite

SummaryInsomnia is a stress‐related sleep disorder conceptualised within a diathesis‐stress framework, which it is thought to result from predisposing factors interacting with precipitating stressful events that trigger the development of insomnia. Among predisposing factors genetics and epigenetics may play a role. A systematic review of the current evidence for the genetic and epigenetic basis of insomnia was conducted according to Preferred Reporting Items for Systematic Reviews and Meta‐Analyses (PRISMA) system. A total of 24 studies were collected for twins and family heritability, 55 for genome‐wide association studies, 26 about candidate genes for insomnia, and eight for epigenetics. Data showed that insomnia is a complex polygenic stress‐related disorder, and it is likely to be caused by a synergy of genetic and environmental factors, with stress‐related sleep reactivity being the important trait. Even if few studies have been conducted to date on insomnia, epigenetics may be the framework to understand long‐lasting consequences of the interaction between genetic and environmental factors and effects of stress on the brain in insomnia. Interestingly, polygenic risk for insomnia has been causally linked to different mental and medical disorders. Probably, by treating insomnia it would be possible to intervene on the effect of stress on the brain and prevent some medical and mental conditions.

show abstract

Section: Resultsmentioning

confidence: 99%

Potential genetic and epigenetic mechanisms in insomnia: A systematic review

Palagini

Geoffroy

Gehrman

et al. 2023

Journal of Sleep Research

View full text Add to dashboard Cite

show abstract

“…During remethylation, under the action of MTHFR and cofactor vitamin B12, Hcy receives a methyl group produced from OCM and is remethylated back to methionine, and methionine could be converted into Hcy with the donation of a methyl group for cellular methylation. Both OCM and DNA methylation may be affected by long sleep durations [ 37 , 38 ]. People with a long sleep duration usually had lower levels of vitamin B12 [ 37 ], which could lead to Hcy accumulation and reduced cellular methylation.…”

Section: Discussionmentioning

confidence: 99%

Sleep Duration, Midday Napping, and Serum Homocysteine Levels: A Gene–Environment Interaction Study

Wang

Gao

et al. 2023

Nutrients

View full text Add to dashboard Cite

The associations of sleep duration and midday napping with homocysteine (Hcy) levels, and whether these sleep behaviors modify the association between genetic predisposition and Hcy levels, has yet to be investigated. We included 19,426 participants without severe health conditions at baseline from the Dongfeng–Tongji cohort. In a subgroup of 15,126 participants with genetic data, a genetic risk score (GRS) based on 18 Hcy-related loci was constructed to test the gene–sleep interactions in Hcy. Hcy levels were higher in subjects with a long sleep duration (≥9 h) and midday napping (>90 min), as compared to those who reported a moderate sleep duration (7 to <8 h) and midday napping (1–30 min) (all p values < 0.05). A long sleep duration and midday napping showed a joint effect in increasing Hcy (p for trend < 0.001). Significant interactions regarding Hcy levels were observed for a long sleep duration with GRS and MTHFR rs1801133, and long midday napping with DPEP1 rs12921383 (all p values for interaction < 0.05). Overall findings indicated that a long sleep duration and midday napping were associated with elevated serum Hcy levels, independently and jointly, and amplified the genetic susceptibility to higher Hcy.

show abstract

“…For example, even one-night acute sleep loss in adults resulted in 148 significant lipid metabolism-related differentially methylated regions in the subcutaneous adipose tissue [ 61 ]. Additionally, both objectively measured shorter sleep duration and higher sleep fragmentation in adolescents were associated with the DNA methylation of metabolism-related genes in the blood [ 62 ]. As specific to the intrauterine impact of maternal sleep, only animal studies were conducted and showed that the sleep fragmentation during the late gestation induced the offspring’s AdipoQ methylation modification along with the higher weight and other metabolic syndrome-like phenotypes [ 16 , 63 ].…”

Section: Discussionmentioning

confidence: 99%

The mediating effect of DNA methylation in the association between maternal sleep during pregnancy and offspring adiposity status: a prospective cohort study

et al. 2022

View full text Add to dashboard Cite

Background Childhood overweight/obesity is a global public health concern. It is important to identify its early-life risk factors. Maternal poor sleep is common in late pregnancy, and previous studies indicated that poor sleep may influence the offspring’s adiposity status. However, very few studies in humans investigated the effect of the different sleep parameters (sleep quantity, quality, and timing) on the offspring’s adiposity indicators, and long-term studies are even more scarce. In addition, the underlying mechanism remains unclear. The present study therefore aimed to examine the association between the three maternal sleep dimensions in the late pregnancy and the offspring adiposity indicators and to explore the potential mediating effect of the cord blood DNA methylation in the above association. Methods Included participants in the current study were 2211 healthy pregnant women with singleton gestation from the Shanghai Birth Cohort (SBC) and Shanghai Sleep Birth Cohort (SSBC). Maternal nighttime sleep duration, quality, and midpoint (an indicator of circadian rhythm) were assessed by the same instrument in both cohorts during late pregnancy, and the offspring’s body mass index (BMI) and subcutaneous fat (SF) were measured at 2 years old. Additionally, in 231 SSBC samples, the genome-wide DNA methylation levels were measured using the Illumina Infinium Methylation EPIC BeadChip. The multivariate linear regression was used to determine the associations between the maternal sleep parameters and the offspring adiposity indicators. The epigenome-wide association study was conducted to identify the maternal sleep-related CpG sites. The mediation analysis was performed to evaluate the potential intermediate role of DNA methylation in the association between maternal sleep and offspring adiposity indicators. Results The mean maternal nighttime sleep duration and the sleep midpoint for combined cohorts were 9.24 ± 1.13 h and 3.02 ± 0.82, respectively, and 24.5% of pregnant women experienced poor sleep quality in late pregnancy. After adjusting for the covariates, the maternal later sleep midpoint was associated with the increased SF in offspring (Coef. = 0.62, 95% CI 0.37–0.87, p < 0.001) at 2 years old. However, no significant associations of the nighttime sleep duration or sleep quality with the offspring adiposity indicators were found. In the SSBC sample, 45 differential methylated probes (DMPs) were associated with the maternal sleep midpoint, and then, we observed 10 and 3 DMPs that were also associated with the offspring’s SF and BMI at 2 years, of which cg04351668 (MARCH9) and cg12232388 significantly mediated the relationship of sleep midpoint and SF and cg12232388 and cg12225226 mediated the sleep midpoint–BMI association, respectively. Conclusions Maternal later sleep timing in late pregnancy was associated with higher childhood adiposity in the offspring. Cord blood DNA methylation may play a mediation role in that relationship.

show abstract

Sleep duration and fragmentation in relation to leukocyte DNA methylation in adolescents

Cited by 11 publications

References 49 publications

Potential genetic and epigenetic mechanisms in insomnia: A systematic review

Potential genetic and epigenetic mechanisms in insomnia: A systematic review

Sleep Duration, Midday Napping, and Serum Homocysteine Levels: A Gene–Environment Interaction Study

The mediating effect of DNA methylation in the association between maternal sleep during pregnancy and offspring adiposity status: a prospective cohort study

Contact Info

Product

Resources

About