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We set out to examine how chronotype (diurnal preference) is connected to ability to function in natural conditions where individuals cannot choose their sleep schedule. We conducted a cross-sectional study in military conscript service to test the hypothesis that sleep deprivation mediates the adverse effects of chronotype on cognitive functioning. We also examined the effects of time of day.One hundred forty participants (ages 18–24 years) completed an online survey, including the Morningness-Eveningness Questionnaire and a Cambridge Neuropsychological Test Automated Battery. Most (n = 106) underwent an actigraphy recording. After bivariate analyses, we created a mediation model (self-reported sleepiness and sleep deprivation mediating effect of chronotype on cognition) and a moderation model (synchrony between most alert time and testing time).Reaction times in inhibition task correlated negatively with sleep efficiency and positively with sleep latency in actigraphy. There was no relation to ability to inhibit responses. More significantly, spatial working memory performance (especially strategicness of performance) correlated positively with morning preference and negatively with sleep deprivation before service. Synchrony with most alert time of the day did not moderate these connections. No other cognitive task correlated with morningness or sleep variables.In line with previous research, inhibitory control is maintained after insufficient sleep but with a tradeoff of slower performance. The connection between morning preference and working memory strategy is a novel finding. We suggest that diurnal preference could be seen as an adaptive strategy, as morningness has consistently been associated with better academic and health outcomes. ; publishedVersion ; Peer reviewed

To access publisher full text version of this article. Please click on the hyperlink in Additional Links field. ; Common sequence variants have recently joined rare structural polymorphisms as genetic factors with strong evidence for association with schizophrenia. Here we extend our previous genome-wide association study and meta-analysis (totalling 7 946 cases and 19 036 controls) by examining an expanded set of variants using an enlarged follow-up sample (up to 10 260 cases and 23 500 controls). In addition to previously reported alleles in the major histocompatibility complex region, near neurogranin (NRGN) and in an intron of transcription factor 4 (TCF4), we find two novel variants showing genome-wide significant association: rs2312147[C], upstream of vaccinia-related kinase 2 (VRK2) [odds ratio (OR) = 1.09, P = 1.9 × 10(-9)] and rs4309482[A], between coiled-coiled domain containing 68 (CCDC68) and TCF4, about 400 kb from the previously described risk allele, but not accounted for by its association (OR = 1.09, P = 7.8 × 10(-9)). ; European Union LSHM-CT-2006-037761 PIAP-GA-2008-218251 HEALTH-F2-2009-223423 National Genome Research Network of the German Federal Ministry of Education and Research (BMBF) 01GS08144 01GS08147 National Institute of Mental Health R01 MH078075 N01 MH900001 MH074027 Centre of Excellence for Complex Disease Genetics of the Academy of Finland 213506 129680 Biocentrum Helsinki Foundation Faculty of Medicine, University of Helsinki Stanley Medical Research Institute Danish Council for Strategic Research 2101-07-0059 H. Lundbeck A/S Research Council of Norway 163070/V50 South-East Norway Health Authority 2004-123 Medical Research Council Ministerio de Sanidad y Consumo, Spain PI081522 Xunta de Galicia 08CSA005208PR Swedish Research Council Wellcome Trust 083948/Z/07/Z Max Planck Society Eli Lilly and Company ; info:eu-repo/grantAgreement/EC/FP7/218251