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To investigate the causal relationship between sleep duration and heart failure (HF) in a European population. We focused on the continuous sleep duration of 460,099 European individuals as our primary exposure. Genome-wide significant single nucleotide polymorphisms (SNPs, n = 9851,867) linked to continuous sleep duration were adopted as instrumental variables. The outcome of interest was based on HF events in a European cohort (n = 977,323; with 930,014 controls and 47,309 cases). We employed a two-sample Mendelian randomization (MR) approach to infer causality between sleep duration and the incidence of HF. For validation purposes, an additional cohort of 336,965 European individuals diagnosed with insomnia was selected as a secondary exposure group. Using its SNPs, a subsequent two-sample MR analysis was conducted with the HF cohort to further corroborate our initial findings. Employing the MR methodology, we selected 57 SNPs that are associated with sleep duration, and 24 SNPs that are associated with insomnia as instrumental variables. We discerned a substantial association between genetically inferred sleep duration and HF risk (odds ratio: 0.61; 95% confidence interval: 0.47-0.78, P < .0001). Our subsequent analysis highlighted a pronounced increased HF risk associated with insomnia (odds ratio: 1.54; 95% confidence interval: 1.08-2.17, P < .02). These conclusions were further bolstered by consistent results from sensitivity analyses. Our study suggests a causal linkage between sleep duration and the onset risk of HF in the European population. Notably, shorter sleep durations were associated with a heightened risk of HF., Competing Interests: The authors declare no conflict of interest, financial or otherwise. We declare that we have no financial and personal relationships with other people or organizations that can inappropriately influence our work. There is no professional or other personal interest in any product, service, and/or company that could be construed as influencing the position presented in the manuscript entitled., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Study Objectives: To analyze the association between sleep-related symptoms and sleep length in parents and their children in relation to other risk factors in both generations., Method: The participants were parents (n = 5,855, age 54.3 ± 6.5 years, 45.2% men) who participated in the community-based Respiratory Health in Northern Europe (RHINE) study and one random member of their adult offspring (n = 5,855, age 30.2 ± 7.7 years, 41.5% men) who participated in the Respiratory Health in Northern Europe, Spain and Australia (RHINESSA) study. Both generations responded to identical questionnaires on sleep symptoms, including difficulty initiating sleep (DIS), difficulty maintaining sleep (DMS), early morning awakening (EMA), snoring, nocturnal sweating, nocturnal gastroesophageal reflux (nGER), sleep time and excessive daytime sleepiness (EDS). Insomnia was defined as either, or both, DIS and DMS in combination with EDS., Results: All sleep variables except nocturnal sweating were more common in offspring whose parents had reported the same symptom. After adjusting for age, gender, BMI, smoking, physical activity, education, center and parents' total number of children, there were independent associations between sleep symptoms in parents and offspring for DIS (adj. OR, 95% CI: 1.52, 1.20-1.93), DMS (1.34, 1.15-1.56), snoring (1.45, 1.15,1.83), nGER (1.65, 1.15-2.37), insomnia (1.39, 1.13-1.73), short sleep time (<6 h/night) (2.51, 1.72-3.68) and EDS (1.48, 1.26,1.72). There were no independent relationships between symptoms in parents and offspring for EMA, nocturnal sweating or long sleep time (>9 h/night)., Conclusion: The familiar aggregation of many sleep disturbances was not explained by investigated lifestyle and environmental factors. This supports a heritable factor in sleep problems., (Copyright © 2020 Elsevier B.V. All rights reserved.)

For nearly half a century, jobs have become increasingly characterized by employment insecurity. We examined the implications for sleep disturbance with cross-sectional data from the European Working Conditions Survey (2010). A group of 24,553 workers between the ages of 25 and 65 years in 31 European countries were asked to indicate whether they suffered from "insomnia or general sleep difficulties" in the past 12 months. We employed logistic regression to model the association between employment insecurity and sleep disturbance for all countries combined and each individual country. For all countries combined, employment insecurity increased the odds of reporting insomnia or general sleep difficulties in the past 12 months. Each unit increase in employment insecurity elevated the odds of sleep disturbance by approximately 47%. This finding was remarkably consistent across 27 of 31 European countries, including Albania, Austria, Belgium, Bulgaria, Croatia, Cyprus, Czech Republic, Denmark, Estonia, Finland, France, Germany, Greece, Hungary, Ireland, Italy, Latvia, Lithuania, Luxembourg, the Netherlands, Norway, Slovakia, Slovenia, Spain, Sweden, Turkey and UK. These results persisted with adjustments for age, gender, immigrant status, household size, partnership status, number of children, child care, elder care, education, earner status, precarious employment status, workplace sector, workplace tenure and workplace size. Employment insecurity was unrelated to sleep disturbance in four European countries: Malta, Poland, Portugal and Romania. Our research continues recent efforts to reveal the human costs associated with working in neoliberal postindustrial labour markets. Our analyses contribute to the external validity of previous research by exploring the impact of employment insecurity across European countries., (© 2018 European Sleep Research Society.)

Biological circadian clocks oscillate with an approximately 24-hour period, are ubiquitous, and presumably confer a selective advantage by anticipating the transitions between day and night. The circadian rhythms of sleep, melatonin secretion and body core temperature are thought to be generated by the suprachiasmatic nucleus of the hypothalamus, the anatomic locus of the mammalian circadian clock. Autosomal semi-dominant mutations in rodents with fast or slow biological clocks (that is, short or long endogenous period lengths; tau) are associated with phase-advanced or delayed sleep-wake rhythms, respectively. These models predict the existence of familial human circadian rhythm variants but none of the human circadian rhythm disorders are known to have a familial tendency. Although a slight 'morning lark' tendency is common, individuals with a large and disabling sleep phase-advance are rare. This disorder, advanced sleep-phase syndrome, is characterized by very early sleep onset and offset; only two cases are reported in young adults. Here we describe three kindreds with a profound phase advance of the sleep-wake, melatonin and temperature rhythms associated with a very short tau. The trait segregates as an autosomal dominant with high penetrance. These kindreds represent a well-characterized familial circadian rhythm variant in humans and provide a unique opportunity for genetic analysis of human circadian physiology.