Sustained wakefulness and visual attention: moderation by chronotype

Introduction - Attentional networks are sensitive to sleep deprivation and increased time awake. However, existing evidence is inconsistent and may be accounted for by differences in chronotype or time-of-day. We examined the effects of sustained wakefulness over a normal “socially constrained” day (following 18 h of sustained wakefulness), following a night of normal sleep, on visual attention as a function of chronotype. Methods - Twenty-six good sleepers (mean age 25.58; SD 4.26; 54 % male) completed the Attention Network Test (ANT) at two time points (baseline at 8 am; following 18-h sustained wakefulness at 2 am). The ANT provided mean reaction times (RTs), error rates, and the efficiency of three attentional networks—alerting, orienting, and executive control/conflict. The Morningness–Eveningness Questionnaire measured chronotype. Results - Mean RTs were longer at time 2 compared to time 1 for those with increasing eveningness; the opposite was true for morningness. However, those with increasing morningness exhibited longer RT and made more errors, on incongruent trials at time 2 relative to those with increasing eveningness. There were no significant main effects of time or chronotype (or interactions) on attentional network scores. Conclusion - Sustained wakefulness produced differential effects on visual attention as a function of chronotype. Whilst overall our results point to an asynchrony effect, this effect was moderated by flanker type. Participants with increasing eveningness outperformed those with increasing morningness on incongruent trials at time 2. The preservation of executive control in evening-types following sustained wakefulness is likely driven by differences in circadian phase between chronotypes across the day

The Association between Daytime Napping and Cognitive Functioning in Chronic Fatigue Syndrome

OBJECTIVES The precise relationship between sleep and physical and mental functioning in chronic fatigue syndrome (CFS) has not been examined directly, nor has the impact of daytime napping. This study aimed to examine self-reported sleep in patients with CFS and explore whether sleep quality and daytime napping, specific patient characteristics (gender, illness length) and levels of anxiety and depression, predicted daytime fatigue severity, levels of daytime sleepiness and cognitive functioning, all key dimensions of the illness experience. METHODS 118 adults meeting the 1994 CDC case criteria for CFS completed a standardised sleep diary over 14 days. Momentary functional assessments of fatigue, sleepiness, cognition and mood were completed by patients as part of usual care. Levels of daytime functioning and disability were quantified using symptom assessment tools, measuring fatigue (Chalder Fatigue Scale), sleepiness (Epworth Sleepiness Scale), cognitive functioning (Trail Making Test, Cognitive Failures Questionnaire), and mood (Hospital Anxiety and Depression Scale). RESULTS Hierarchical Regressions demonstrated that a shorter time since diagnosis, higher depression and longer wake time after sleep onset predicted 23.4% of the variance in fatigue severity (p <.001). Being male, higher depression and more afternoon naps predicted 25.6% of the variance in objective cognitive dysfunction (p <.001). Higher anxiety and depression and morning napping predicted 32.2% of the variance in subjective cognitive dysfunction (p <.001). When patients were classified into groups of mild and moderate sleepiness, those with longer daytime naps, those who mainly napped in the afternoon, and those with higher levels of anxiety, were more likely to be in the moderately sleepy group. CONCLUSIONS Napping, particularly in the afternoon is associated with poorer cognitive functioning and more daytime sleepiness in CFS. These findings have clinical implications for symptom management strategies

Genetic and Environmental Influences on Sleep Quality: Quantitative and Molecular Genetic Approaches to an Understanding of Individual Differences

There are vast inter-individual differences in sleep quality in the general population – whilst some individuals sleep well with little or no sleep disturbance, others experience frequent sleep disturbances, problems which often manifest into chronic sleep disorders such as insomnia. The aim of this thesis is to explore factors accounting for these observed differences in sleep quality between individuals. Using data from a large-scale twin study this thesis uses behavioural genetic techniques to investigate genetic and environmental influences on sleep quality in a sample of 1,556 twins and siblings aged 18-27 years. The first four studies use quantitative genetic techniques to investigate 1) associations between components of sleep quality and the overlap in the genetic and environmental influences accounting for them; 2) specific non-shared environmental influences on global sleep quality; 3) the presence of gene-environment interplay between sleep quality and dependent negative life events; and 4) the association between sleep quality and diurnal preference, and the overlap in their aetiological influences. Most importantly, there was substantial genetic overlap between individual components of sleep quality (rA mostly ≥.50); sleep quality and diurnal preference (rD = .52[95% CI=.37-.70]); and sleep quality and dependent negative life events (rD = .63[.45-.83]) – the latter finding providing evidence of gene-environment correlation. In general, non-shared environmental overlap was small (rE mostly ≤.40). The final study used a candidate gene approach to investigate associations between sleep quality and diurnal preference with 5HTTLPR, PER3, and CLOCK 3111 – polymorphisms hypothesized to be implicated in sleep and/or the circadian system. An association was found between the ‘long’ allele of 5HTTLPR and poor sleep quality (β = -.34, p<.01). This thesis utilises the twin method in novel ways in the context of sleep research and advances knowledge of the genetic and environmental underpinnings of the variation in sleep quality in healthy young adults

Revising the Intolerance of Uncertainty Model of Generalized Anxiety Disorder: Evidence from UK and Italian Undergraduate Samples

The Intolerance of Uncertainty Model (IUM) of Generalized Anxiety Disorder (GAD) attributes a key role to Intolerance of Uncertainty (IU), and additional roles to Positive Beliefs about Worry (PBW), Negative Problem Orientation (NPO), and Cognitive Avoidance (CA), in the development and maintenance of worry, the core feature of GAD. Despite the role of the IUM components in worry and GAD has been considerably demonstrated, to date no studies have explicitly assessed whether and how PBW, NPO, and CA might turn IU into worry and somatic anxiety. The current studies sought to re-examine the IUM by assessing the relationships between the model’s components on two different non-clinical samples made up of UK and Italian undergraduate students. One-hundred and seventy UK undergraduates and 488 Italian undergraduates completed measures assessing IU, worry, somatic anxiety, depression, and refined measures of PBW, NPO, and CA. In each sample, two mediation models were conducted in order to test whether PBW, NPO, and CA differentially mediate the path from IU to worry and the path from IU to somatic anxiety. Secondly, it was tested whether IU also moderates the mediations. Main findings showed that, in the UK sample, only NPO mediated the path from IU to worry; as far as concern the path to anxiety, none of the putative mediators was significant. Differently, in the Italian sample PBW and NPO were mediators in the path from IU to worry, whereas only CA played a mediational role in the path from IU to somatic anxiety. Lastly, IU was observed to moderate only the association between NPO and worry, and only in the Italian sample. Some important cross-cultural, conceptual, and methodological issues raised from main results are discussed

Genetic and environmental influences on sleep quality : quantitative and molecular genetic approaches to an understanding of individual differences

There are vast inter-individual differences in sleep quality in the general population – whilst some individuals sleep well with little or no sleep disturbance, others experience frequent sleep disturbances, problems which often manifest into chronic sleep disorders such as insomnia. The aim of this thesis is to explore factors accounting for these observed differences in sleep quality between individuals. Using data from a large-scale twin study this thesis uses behavioural genetic techniques to investigate genetic and environmental influences on sleep quality in a sample of 1,556 twins and siblings aged 18-27 years. The first four studies use quantitative genetic techniques to investigate 1) associations between components of sleep quality and the overlap in the genetic and environmental influences accounting for them; 2) specific non-shared environmental influences on global sleep quality; 3) the presence of gene-environment interplay between sleep quality and dependent negative life events; and 4) the association between sleep quality and diurnal preference, and the overlap in their aetiological influences. Most importantly, there was substantial genetic overlap between individual components of sleep quality (rA mostly ≥.50); sleep quality and diurnal preference (rD = .52[95% CI=.37-.70]); and sleep quality and dependent negative life events (rD = .63[.45-.83]) – the latter finding providing evidence of gene-environment correlation. In general, non-shared environmental overlap was small (rE mostly ≤.40). The final study used a candidate gene approach to investigate associations between sleep quality and diurnal preference with 5HTTLPR, PER3, and CLOCK 3111 – polymorphisms hypothesized to be implicated in sleep and/or the circadian system. An association was found between the ‘long’ allele of 5HTTLPR and poor sleep quality (β = -.34, p<.01). This thesis utilises the twin method in novel ways in the context of sleep research and advances knowledge of the genetic and environmental underpinnings of the variation in sleep quality in healthy young adults.EThOS - Electronic Theses Online ServiceGBUnited Kingdo

Anxiety mediates the relationship between perfectionism and insomnia symptoms: A longitudinal study

Objectives Individuals with insomnia often report aspects of perfectionism and symptoms of anxiety and depression. Investigation of these factors together has been limited. As such, the aim of the present study was to examine the extent to which the association between perfectionism and insomnia symptoms was mediated by anxiety and depression, concurrently and longitudinally. Methods Seventy-six members from the general-population participated at baseline. Data from 57 participants were subsequently analysed at twelve-month follow-up. Insomnia symptoms were assessed using The Insomnia Severity Index (ISI). Perfectionism was assessed using two Multidimensional Perfectionism Scales (F-MPS; HF-MPS). Symptoms of anxiety and depression were assessed using The Hospital Anxiety and Depression Scale (HADS). Correlational analysis examined longitudinal associations between perfectionism and insomnia symptoms. Hierarchical regression analysis examined whether significant associations remained after controlling for anxiety and depression. Results Baseline insomnia symptoms were associated with future doubts about action. Further, this relationship was mediated by preceding symptoms of anxiety and concurrent symptoms of insomnia. Similarly, baseline insomnia symptoms were also associated with future parental criticism. However this relationship was partially mediated by preceding symptoms of anxiety, and was not mediated by concurrent insomnia symptoms. Conclusions Symptoms of insomnia appear to be related to an increase in negative perfectionistic thinking in the form of doubts about action and parental criticism, however these relationships appear to be mediated by symptoms of anxiety. Therefore, treatments for insomnia should address anxiety symptoms with the prospect of preventing the accentuation of aspects of perfectionism due to poor sleep

Sleep duration, sleep variability, and impairments of visual attention

Attentional networks are sensitive to sleep deprivation. However, variation in attentional performance as a function of normal sleep parameters is under-studied. We examined whether attentional performance is influenced by 1) individual differences in sleep duration; 2) sleep duration variability; and/or 3) their interaction. Fifty-seven healthy participants (61.4% female; mean age=32.37 years; SD=8.68) completed questionnaires, wore wrist actigraphy for one week, and subsequently completed the Attention Network Test. Sleep duration and sleep duration variability did not predict orienting score, executive control score or error rates. Sleep duration variability appeared to moderate the association between sleep duration with overall reaction time (β = -.34, t= -2.13, p=.04) and alerting scores (β= .43, t=2.94, p=.01), though further inspection of the data suggested that these were spurious findings. Time of testing was a significant predictor of alerting score (β=.35, t=2.96, p=.01), chronotype of orienting (β=.31, t=2.28, p=.03) and age of overall reaction time (β=.35, t=2.70, p=.01). Our results highlight the importance of examining the associations between variations in sleep-wake patterns and attentional networks in samples with greater variation in sleep, as well as the importance of rigorously teasing apart mechanisms of the sleep homeostat from those related to the circadian rhythm in studies examining cognition

Polymorphisms in the circadian expressed genes PER3 and ARNTL2 are associated with diurnal preference and GNβ3 with sleep measures

Sleep and circadian rhythms are intrinsically linked, with several sleep traits, including sleep timing and duration, influenced by both sleep homeostasis and the circadian phase. Genetic variation in several circadian genes has been associated with diurnal preference (preference in timing of sleep), although there has been limited research on whether they are associated with other sleep measurements. We investigated whether these genetic variations were associated with diurnal preference (Morningness-Eveningness Questionnaire) and various sleep measures, including: the global Pittsburgh Sleep Quality index score; sleep duration; and sleep latency and sleep quality. We genotyped 10 polymorphisms in genes with circadian expression in participants from the G1219 sample (n = 966), a British longitudinal population sample of young adults. We conducted linear regressions using dominant, additive and recessive models of inheritance to test for associations between these polymorphisms and the sleep measures. We found a significant association between diurnal preference and a polymorphism in period homologue 3 (PER3) (P < 0.005, recessive model) and a novel nominally significant association between diurnal preference and a polymorphism in aryl hydrocarbon receptor nuclear translocator-like 2 (ARNTL2) (P < 0.05, additive model). We found that a polymorphism in guanine nucleotide binding protein beta 3 (GNβ3) was associated significantly with global sleep quality (P < 0.005, recessive model), and that a rare polymorphism in period homologue 2 (PER2) was associated significantly with both sleep duration and quality (P < 0.0005, recessive model). These findings suggest that genes with circadian expression may play a role in regulating both the circadian clock and sleep homeostasis, and highlight the importance of further studies aimed at dissecting the specific roles that circadian genes play in these two interrelated but unique behaviours

Experienced demand does not affect subsequent sleep and the cortisol awakening response

Purpose: Stress is associated with subjective and objective sleep disturbances; however, it is not known whether stress disrupts sleep and relevant physiological markers of stress immediately after it is experienced. The present study examined whether demand, in the form of cognitive tasks, disrupted sleep and the cortisol awakening response (CAR), depending on whether it was experienced or just anticipated. Participants and Methods: Subjective and objective sleep was measured in 22 healthy adults on three nights (Nights 0– 2) in a sleep laboratory using sleep diaries and polysomnography. Saliva samples were obtained at awakening, +15, +30, +45 and +60 minutes on each subsequent day (Day 1– 3) and CAR measurement indices were derived: awakening cortisol levels, the mean increase in cortisol levels (MnInc) and total cortisol secretion (AUCG). On Night 1, participants were informed that they were required to complete a series of demanding cognitive tasks within the sleep laboratory during the following day. Participants completed the tasks as expected or unexpectedly performed sedentary activities. Results: Compared to the no-demand group, the demand group displayed significantly higher levels of state anxiety immediately completing the first task. There were no subsequent differences between the demand and no-demand groups in Night 2 subjective sleep continuity, objective sleep continuity or architecture, or on any Day 3 CAR measure. Conclusion: These results indicate that sleep and the CAR are not differentially affected depending on whether or not an anticipated stressor is then experienced. This provides further evidence to indicate that the CAR is a marker of anticipation and not recovery. In order to disrupt sleep, a stressor may need to be personally relevant or of a prolonged duration or intensity

Longitudinal stability of genetic and environmental influences on the association between diurnal preference and sleep quality in young adult twins and siblings

Overlapping genetic influences have been implicated in diurnal preference and subjective sleep quality. Our overall aim was to examine overlapping concurrent and longitudinal genetic and environmental effects on diurnal preference and sleep quality over ~5 years. Behavioural genetic analyses were performed on data from the longitudinal British G1219 study of young adult twins and non-twin siblings. 1556 twins and siblings provided data on diurnal preference (Morningness-Eveningness Questionnaire) and sleep quality (Pittsburgh Sleep Quality Index) at time 1 (mean age=20.30 years, SD=1.76; 62% female); and 862 participated at time 2 (mean age=25.30 years, SD=1.81; 66% female). Preference for eveningness was associated with poorer sleep quality at both time-points (r=.25[95% confidence intervals, (CI)=.20-.30], and r=.21[CI=.15-.28]). There was substantial overlap in the genetic influences on diurnal preference and sleep quality individually, across time (genetic correlations [rA’s]: .64[95% CI = .59-.67] and .48[95% CI = .42-.53]). There were moderate genetic correlations between diurnal preference and sleep quality concurrently and longitudinally (rAs=.29-.60). Non-shared environmental overlap was substantially smaller for all cross-phenotype associations (non-shared environmental correlations [rE’s]=-.02-.08). All concurrent and longitudinal associations within and between phenotypes were largely accounted for by genetic factors (explaining between 60%-100% of the associations). All shared environmental effects were non-significant. Non-shared environmental influences played a smaller role on the associations between phenotypes (explaining between -.06%-40% of the associations). These results suggest that to some extent similar genes contribute to the stability of diurnal preference and sleep quality throughout young adulthood, but also that different genes play a part over this relatively short time-frame. While there was evidence of genetic overlap between phenotypes concurrently and longitudinally, the possible emergence of new genetic factors (or decline of previously associated factors) suggests that molecular genetic studies focussing on young adults should consider more tightly specified age-groups, given that genetic effects may be time-specific