Gene-x-environment analysis supports protective effects of eveningness chronotype on self-reported and actigraphy-derived sleep duration among those who always work night shifts in the UK Biobank.
Gene-x-environment analysis supports protective effects of eveningness chronotype on self-reported and actigraphy-derived sleep duration among those who always work night shifts in the UK Biobank.
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Previous research has linked having an eveningness chronotype with a higher tolerance for night shift work, suggesting the ability to work nights without health consequences may partially depend upon having a circadian clock optimized for these times. As chronotypes entrain over time to environmental cues, it remains unclear whether higher relative eveningness among healthy night workers reflects a moderating or mediating effect of chronotype on health. We address these concerns conducting a genome-wide association study and utilizing a polygenic score (PGS) for eveningness as a time-invariant measure of chronotype. On a sample of 53 211 workers in the UK Biobank (2006–2018), we focus on the effects of night shift work on sleep duration, a channel through which night shift work adversely affects health. We ask whether a higher predisposition toward eveningness promotes night shift work tolerance. Results indicate that regular night shift work is associated with a 13-minute (3.5%) reduction in self-reported sleep per night relative to those who never work these hours (95% confidence interval [CI] = −17:01, −8:36). We find that eveningness has a strong protective effect on night workers: a one-SD increase in the PGS is associated with a 4-minute (28%) reduction in the night shift work sleep penalty per night (CI = 0:10, 7:04). This protective effect is pronounced for those working the longest hours. Consistent patterns are observed with an actigraphy-derived measure of sleep duration. These findings indicate that solutions to health consequences of night shift work should take individual differences in chronotype into account.
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影响因子:
5.5
作者:
Gu F;Han J;Laden F;Pan A;Caporaso NE;Stampfer MJ;Kawachi I;Rexrode KM;Willett WC;Hankinson SE;Speizer FE;Schernhammer ES
通讯作者:
Schernhammer ES
影响因子:
3.7
作者:
Gamble KL;Motsinger-Reif AA;Hida A;Borsetti HM;Servick SV;Ciarleglio CM;Robbins S;Hicks J;Carver K;Hamilton N;Wells N;Summar ML;McMahon DG;Johnson CH
通讯作者:
Johnson CH
影响因子:
5
作者:
Fry A;Littlejohns TJ;Sudlow C;Doherty N;Adamska L;Sprosen T;Collins R;Allen NE
通讯作者:
Allen NE
影响因子:
30.8
作者:
Bulik-Sullivan, Brendan K.;Loh, Po-Ru;Finucane, Hilary K.;Ripke, Stephan;Yang, Jian;Patterson, Nick;Daly, Mark J.;Price, Alkes L.;Neale, Benjamin M.
通讯作者:
Neale, Benjamin M.
DOI:
10.1093/bioinformatics/btu848
发表时间:
2015-05-01
期刊:
Bioinformatics (Oxford, England)
影响因子:
--
作者:
Euesden J;Lewis CM;O'Reilly PF
通讯作者:
O'Reilly PF