Genetic determinants of daytime napping and effects on cardiometabolic health

Dashti, Hassan S.; Daghlas, Iyas; Lane, Jacqueline M.; Huang, Yaoguo; Udler, Miriam S.; Wang, Heming; Ollila, Hanna; Jones, Samuel E.; Kim, Jaegil; Wood, Andrew R.; Weedon, Michael N.; Aslibekyan, Stella; Garaulet, Marta; Saxena, Richa

doi:10.1101/2020.06.12.20129858

Cited by 10 publications

(20 citation statements)

References 98 publications

(163 reference statements)

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“…Genetic associations for sleep traits were obtained from published 9,10,12,21 and unpublished GWAS summary statistics in UK Biobank (UKB) participants of European ancestry (methodologic details given in Data S1; GWAS characteristics listed in Table S1). We considered GWAS for all sleep traits ascertained in UKB: sleep duration, 12 morning diurnal preference (also referred to as "chronotype"), 10 daytime napping frequency, 22 snoring, insomnia symptoms, 9 difficulty awakening, and daytime sleepiness 23 (phenotype definitions and GWAS procedures are provided in Data S1 and Table S2). We selected all available sleep traits so as to provide an unbiased survey of the relationship between sleep health and migraine.…”

Section: Sleep Traits In Uk Biobankmentioning

confidence: 99%

Habitual sleep disturbances and migraine: a Mendelian randomization study

Daghlas

Vgontzas

Guo

et al. 2020

Ann Clin Transl Neurol

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Objective: Sleep disturbances are associated with increased risk of migraine, however the extent of shared underlying biology and the direction of causal relationships between these traits is unclear. Delineating causality between sleep patterns and migraine may offer new pathophysiologic insights and inform subsequent intervention studies. Here, we used genetic approaches to test for shared genetic influences between sleep patterns and migraine, and to test whether habitual sleep patterns may be causal risk factors for migraine and vice versa. Methods: To quantify genetic overlap, we performed genome-wide genetic correlation analyses using genome-wide association studies of nine sleep traits in the UK Biobank (n ≥ 237,627), and migraine from the International Headache Genetics Consortium (59,674 cases and 316,078 controls). We then tested for potential causal effects between sleep traits and migraine using bidirectional, two-sample Mendelian randomization. Results: Seven sleep traits demonstrated genetic overlap with migraine, including insomnia symptoms (rg = 0.29, P < 10 À31) and difficulty awakening (rg = 0.11, P < 10 À4). Mendelian randomization analyses provided evidence for potential causal effects of difficulty awakening on risk of migraine (OR [95% CI] = 1.37 [1.12-1.68], P = 0.002), and nominal evidence that liability to insomnia symptoms increased the risk of migraine (1.09 [1.02-1.16], P = 0.02). In contrast, there was minimal evidence for an effect of migraine liability on sleep patterns or disturbances. Interpretation: These data support a shared genetic basis between several sleep traits and migraine, and support potential causal effects of difficulty awakening and insomnia symptoms on migraine risk. Treatment of sleep disturbances may therefore be a promising clinical intervention in the management of migraine.

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Section: Sleep Traits In Uk Biobankmentioning

confidence: 99%

Habitual sleep disturbances and migraine: a Mendelian randomization study

Daghlas

Vgontzas

Guo

et al. 2020

Ann Clin Transl Neurol

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“…We would expect this to bias results towards the null. To address this, we identified subsets of genome-wide significance SNPs of some sleep traits (i.e., 108 for insomnia, 14 19 for daytime sleepiness, 18 17 napping, 19 and 72 for chronotype 20 ) in other independent GWAS that did not include UKB. Details of these subsets were provided in Supplementary Methods .…”

Section: Methodsmentioning

confidence: 99%

“…Our primary aim was to explore effects of sleep traits (i.e., insomnia, 14 sleep duration, 17 daytime sleepiness, 18 daytime napping, 19 and chronotype 20 ) on average glycaemic levels assessed by HbA1c in general population. Our secondary aim was to assess the effects of these sleep traits on non-fasting glucose levels.…”

Section: Introductionmentioning

confidence: 99%

Assessing the causal role of sleep traits on glycated haemoglobin: a Mendelian randomization study

Liu

Richmond

Bowden

et al. 2020

Preprint

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ObjectiveTo examine the effects of sleep traits on glycated haemoglobin (HbA1c).DesignObservational multivariable regression (MVR), one-sample Mendelian randomization (1SMR), and two-sample summary data Mendelian randomization (2SMR).SettingUK Biobank (UKB) prospective cohort study and genome-wide association studies from the Meta-Analyses of Glucose and Insulin-related traits Consortium (MAGIC).ParticipantsIn MVR and 1SMR, participants were adults (mean (SD) age 57 (8) years; 54% female) from the UKB (n=336,999); in 2SMR, participants were adults (53 (11) years; 52% female) from MAGIC (n=46,368). All participants were adults of European ancestry.ExposuresSelf-reported insomnia frequency (usually vs sometimes or rarely/never); sleep duration: 24-hour sleep duration (hours/day); short sleep (≤6 hours vs 7-8 hours) and long sleep (≥9 hours vs 7-8 hours); daytime sleepiness and daytime napping (each consisting of 3 categories: never/rarely, sometimes, usually); chronotype (5 categories from definite morning to definite evening preference).Main outcome measureHbA1c in standard deviation (SD) units.ResultsAcross MV, 1SMR, 2SMR, and their sensitivity analyses we found a higher frequency of insomnia (usually vs sometimes or rarely/never) was associated with higher HbA1c (MVR: 0.053 SD units, 95% confidence interval (0.046 to 0.061), 1SMR: 0.52, (0.42 to 0.63), 2SMR: 0.22, (0.10 to 0.35)). Results remained significant but point estimates were somewhat attenuated after excluding people with diagnosed diabetes. For other sleep traits, there was less consistency with significant associations when using some, but not all methods.ConclusionsThis study suggests that insomnia increases HbA1c levels. These findings could have important implications for developing and evaluating strategies that improve sleep habits to reduce hyperglycaemia and prevent diabetes.SUMMARY BOXWhat is already known on this topicIn observational data, insomnia, short sleep duration, and evening preference are associated with higher risk for type 2 diabetes.Mendelian randomization (MR) studies have not found evidence of a causal effect of short sleep on type 2 diabetes or glycaemic traits but have indicated an effect of insomnia on type 2 diabetes. It is unclear whether insomnia influences HbA1c levels, a marker of long-term hyperglycaemia, in the general population.Recently identified genetic variants robustly associated with insomnia, sleep duration, daytime sleepiness, napping, and chronotype can be used in MR studies to explore causal effects of these sleep traits on HbA1c levels.What this study addsThis study suggests that a higher frequency of insomnia increases HbA1c levels in the general population and after excluding people with diabetes.We found no robust evidence for causal effects of other sleep traits on HbA1c levels.These findings improve our understanding of the impact of sleep traits on HbA1c levels and have important implications for developing and evaluating strategies that improve sleep habits to reduce hyperglycaemia and prevent diabetes.

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“…This shows that the interindividual variability in sleep traits is under substantial genetic control. Based on common genetic variations from genome-wide association studies (GWAS) in adults, a SNP-based heritability of 7.0% (Jansen et al, 2019) and 9.8% (Dashti et al, 2019) has been estimated for insomnia and sleep duration, respectively. These estimates are comparable with SNP-based heritability of other psychiatric traits [e.g.…”

Section: Introductionmentioning

confidence: 99%

“…Recent large genome-wide association studies (GWASs) in adults have identified 202 genetic loci associated with insomnia (Jansen et al, 2019) and 78 with self-reported habitual sleep duration (Dashti et al, 2019). Based on these studies, one can calculate quantitative polygenic risk scores (PRS), which represent individuals' genetic susceptibility for insomnia and sleep duration, as estimated by the additive effects of multiple alleles using summary statistics from GWAS.…”

Section: Introductionmentioning

confidence: 99%

Are some children genetically predisposed to poor sleep? A polygenic risk study in the general population

Kocevska,

Trajanoska,

Mulder

et al. 2023

Child Psychology Psychiatry

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BackgroundTwin studies show moderate heritability of sleep traits: 40% for insomnia symptoms and 46% for sleep duration. Genome‐wide association studies (GWAS) have identified genetic variants involved in insomnia and sleep duration in adults, but it is unknown whether these variants affect sleep during early development. We assessed whether polygenic risk scores for insomnia (PRS‐I) and sleep duration (PRS‐SD) affect sleep throughout early childhood to adolescence.MethodsWe included 2,458 children of European ancestry (51% girls). Insomnia‐related items of the Child Behavior Checklist were reported by mothers at child's age 1.5, 3, and 6 years. At 10–15 years, the Sleep Disturbance Scale for Children and actigraphy were assessed in a subsample (N = 975). Standardized PRS‐I and PRS‐SD (higher scores indicate genetic susceptibility for insomnia and longer sleep duration, respectively) were computed at multiple p‐value thresholds based on largest GWAS to date.ResultsChildren with higher PRS‐I had more insomnia‐related sleep problems between 1.5 and 15 years (BPRS‐I < 0.001 = .09, 95% CI: 0.05; 0.14). PRS‐SD was not associated with mother‐reported sleep problems. A higher PRS‐SD was in turn associated with longer actigraphically estimated sleep duration (BPRS‐SD < 5e08 = .05, 95% CI: 0.001; 0.09) and more wake after sleep onset (BPRS‐SD < 0.005 = .25, 95% CI: 0.04; 0.47) at 10–15 years, but these associations did not survive multiple testing correction.ConclusionsChildren who are genetically predisposed to insomnia have more insomnia‐like sleep problems, whereas those who are genetically predisposed to longer sleep have longer sleep duration, but are also more awake during the night in adolescence. This indicates that polygenic risk for sleep traits, based on GWAS in adults, affects sleep already in children.

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Genetic determinants of daytime napping and effects on cardiometabolic health

Cited by 10 publications

References 98 publications

Habitual sleep disturbances and migraine: a Mendelian randomization study

Habitual sleep disturbances and migraine: a Mendelian randomization study

Assessing the causal role of sleep traits on glycated haemoglobin: a Mendelian randomization study

Are some children genetically predisposed to poor sleep? A polygenic risk study in the general population

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