SLEEP

Espie, Colin A.; Kyle, Simon D.

doi: 10.1093/sleep/31.5.591pmid: 18517027

Young, Terry

doi: 10.1093/sleep/31.5.593pmid: 18517028

Horne, James

doi: 10.1093/sleep/31.5.595pmid: 18517029

Edinger, Jack D.; Means, Melanie K.; Carney, Colleen E.; Krystal, Andrew D.

doi: 10.1093/sleep/31.5.599pmid: 18517030

AbstractObjective:To examine psychomotor (reaction time) performance defcits and their relation to subjective and objective sleep measures among individuals with primary insomnia (PI).Design and Setting:This study was conducted at affliated VA and academic medical centers using a matched-groups, cross-sectional research design.Participants:Seventy-nine (43 women) individuals with PI (MAge = 50.0 ± 17.1 y) and 84 (41 women) well-screened normal sleepers (MAge = 48.6 ± 16.8 y).Methods and Measures:Participants underwent 3 nights of polysomnography (PSG) followed by daytime testing with a 4–trial multiple sleep latency test (MSLT). Before each MSLT nap, they rated their sleepiness and completed a performance battery that included simple reaction time (SRT), continuous performance (CPT), and 4 switching attention (SAT) tests. Performance measures included the mean response latency and the standard deviation of each subject's within-test response latencies.Results:PI sufferers reported greater (P = 0.001) daytime sleepiness, but were significantly (P = 0.02), more alert than normal sleepers on the MSLT. Multivariate analyses showed the PI group had significantly longer response latencies and greater response variability across many of the subtests than did the controls. Regression analyses showed that both PSG- and diary-based sleep measures contributed to the prediction of daytime performance indices, although objective wake time after sleep onset appeared the best single predictor of the daytime measures.Conclusions:Results confirm that PI sufferers do show relative psychomotor performance deficits when responding to challenging reaction time tasks, and these deficits appear related to both objective and subjective sleep deficits. Findings support PI patients' diurnal complaints and suggest the usefulness of complex reaction time tasks for assessing them.

Archer, Simon N.; Viola, Antoine U.; Kyriakopoulou, Vanessa; von Schantz, Malcolm; Dijk, Derk-Jan

doi: 10.1093/sleep/31.5.608pmid: 18517031

AbstractStudy Objectives:Individual sleep timing differs and is governed partly by circadian oscillators, which may be assessed by hormonal markers, or by clock gene expression. Clock gene expression oscillates in peripheral tissues, including leukocytes. The study objective was to determine whether the endogenous phase of these rhythms, assessed in the absence of the sleep-wake and light-dark cycle, correlates with habitual sleep-wake timing.Design:Observational, cross-sectional.Setting:Home environment and Clinical Research Center.Participants:24 healthy subjects aged 25.0 ± 3.5 (SD) years.Measurements:Actigraphy and sleep diaries were used to characterize sleep timing. Circadian rhythm phase and amplitude of plasma melatonin, cortisol, and BMAL1, PER2, and PER3 expression were assessed during a constant routine.Results:Circadian oscillations were more robust for PER3 than for BMAL1 or PER2. Average peak timings were 6:05 for PER3, 8:06 for PER2, 15:06 for BMAL1, 4:20 for melatonin, and 10:49 for cortisol. Individual sleep-wake timing correlated with the phases of melatonin and cortisol. Individual PER3 rhythms correlated significantly with sleep-wake timing and the timing of melatonin and cortisol, but those of PER2 and BMAL1 did not reach signifcance. The correlation between sleep timing and PER3 expression was stronger in individuals homozygous for the variant of the PER3 polymorphism that is associated with morningness.Conclusions:Individual phase differences in PER3 expression during a constant routine correlate with sleep timing during entrainment. PER3 expression in leukocytes represents a useful molecular marker of the circadian processes governing sleep-wake timing.

Cappuccio, Francesco P.; Taggart, Frances M.; Kandala, Ngianga-Bakwin; Currie, Andrew; Peile, Ed; Stranges, Saverio; Miller, Michelle A.

doi: 10.1093/sleep/31.5.619pmid: 18517032

AbstractBackground:Recent epidemiological studies suggest that short sleep duration may be associated with the development of obesity from childhood to adulthood.Objectives:To assess whether the evidence supports the presence of a relationship between short sleep duration and obesity at different ages, and to obtain an estimate of the risk.Methods:We performed a systematic search of publications using MEDLINE (1996–2007 wk 40), EMBASE (from 1988), AMED (from 1985), CINHAL (from 1982) and PsycINFO (from 1985) and manual searches without language restrictions. When necessary, authors were contacted. Criteria for inclusion were: report of duration of sleep as exposure, BMI as continuous outcome and prevalence of obesity as categorical outcome, number of participants, age, and gender. Results were pooled using a random effect model. Sensitivity analysis was performed, heterogeneity and publication bias were also checked. Results are expressed as pooled odds ratios (OR [95% confidence intervals, CIs]) and as pooled regression coefficients (β 95% CIs).Results:Of 696 studies identified, 45 met the inclusion criteria (19 in children and 26 in adults) and 30 (12 and 18, respectively) were pooled in the meta-analysis for a total of 36 population samples. They included 634,511 participants (30,002 children and 604,509 adults) from around the world. Age ranged from 2 to 102 years and included boys, girls, men and women. In children the pooled OR for short duration of sleep and obesity was 1.89 (1.46 to 2.43; P < 0.0001). In adults the pooled OR was 1.55 (1.43 to 1.68; P < 0.0001). There was no evidence of publication bias. In adults, the pooled β for short sleep duration was −0.35 (−0.57 to −0.12) unit change in BMI per hour of sleep change.Conclusions:Cross-sectional studies from around the world show a consistent increased risk of obesity amongst short sleepers in children and adults. Causal inference is difficult due to lack of control for important confounders and inconsistent evidence of temporal sequence in prospective studies.

Guan, Zhiwei; Vgontzas, Alexandros N.; Bixler, Edward O.; Fang, Jidong

doi: 10.1093/sleep/31.5.627pmid: 18517033

AbstractObjective:To determine whether weight loss could reverse excessive sleep in high-fat diet-induced obesity.Design:Three groups of mice participated in the study. A weight gain/ loss group was fed with high-fat food for 6 weeks (weight gain), and regular food again for 4 weeks (weight loss). A control group and a weight gain only group were fed with regular food and high-fat food, respectively, for 10 weeks after the baseline.Participants:Adult male C57BL/6 mice.Measurements:The amounts of wake, rapid eye movement sleep (REMS) and non-REM sleep (NREMS) were determined at week 0 (baseline), week 6, and week 10.Results:The weight gain/loss group displayed a significant decrease in wakefulness and increases in NREMS and episodes of NREMS during 6 weeks of weight gain, which were reversed during subsequent 4 weeks of weight loss. The weight gain only group displayed significant decrease in wakefulness and increase of NREMS and REMS at both week 6 and week 10. The control group did not show significant sleep alterations during the experiment.Conclusion:These observations indicate that sleep alterations induced by weight gain are reversed by weight loss in obese animals. These data may shed light on the mechanisms underlying the well-established association between obesity and sleepiness in humans and may lead to new therapeutic strategies for these 2 increasingly prevalent problems in the modern societies.

Hall, Martica H.; Muldoon, Matthew F.; Jennings, J. Richard; Buysse, Daniel J.; Flory, Janine D.; Manuck, Stephen B.

doi: 10.1093/sleep/31.5.635pmid: 18517034

AbstractStudy objective:Short and long sleep duration have been linked to various risk factors for cardiovascular disease. In the present study, we evaluated the relationship between sleep duration and presence of the metabolic syndrome, which is a cluster of physiologically interrelated risk factors for cardiometabolic disease.Design/Setting:Cross-sectional community-based cohort study.Participants:One thousand two hundred fourteen participants from the Adult Health and Behavior Project registry (aged 30 to 54 years).Measurements:Participants were divided into 4 groups based upon their reported sleep duration. The metabolic syndrome was defined according to the American Heart Association/National Heart Lung and Blood Institute's criteria. Logistic regression was used to test the hypothesis that sleep duration is a significant correlate of the metabolic syndrome and its components.Results:The observed metabolic syndrome rate (22%) was similar to that of published health statistics for American adults. After covariate adjustment, the odds for having the metabolic syndrome increased by more than 45% in both short and long sleepers, compared with those sleeping 7 to 8 hours per night. Sleep duration was also associated individually with abdominal obesity, elevated fasting glucose, and hy-pertriglyceridemia. After further adjustment for use of antihypertensive medication, prevalence of the metabolic syndrome and its components remained elevated in short sleepers only.Conclusion:These data suggest that sleep duration is a significant correlate of the metabolic syndrome. Additional studies are needed to evaluate temporal relationships among these measures, the behavioral and physiologic mechanisms that link the two, and their impact on subsequent cardiometabolic disease.

Kaneita, Yoshitaka; Uchiyama, Makoto; Yoshiike, Nobuo; Ohida, Takashi

doi: 10.1093/sleep/31.5.645pmid: 18517035

AbstractStudy Objectives:We examined the individual association between sleep duration and a high serum triglyceride, low HDL cholesterol, or high LDL cholesterol level.Design and Setting:The present study analyzed data from the National Health and Nutrition Survey that was conducted in November 2003 by the Japanese Ministry of Health, Labour and Welfare. This survey was conducted on residents in the districts selected randomly from all over Japan.Participants:The subjects included in the statistical analysis were 1,666 men and 2,329 women aged 20 years or older.Intervention:N/AMeasurements and results:Among women, both short and long sleep durations are associated with a high serum triglyceride level or a low HDL cholesterol level. Compared with women sleeping 6 to 7 h, the relative risk of a high triglyceride level among women sleeping <5 h was 1.51 (95% CI, 0.96–2.35), and among women sleeping ≥8 h was 1.45 (95% CI, 1.00–2.11); the relative risk of a low HDL cholesterol level among women sleeping <5 h was 5.85 (95% CI, 2.29–14.94), and among women sleeping ≥8 h was 4.27 (95% CI, 1.88–9.72). On the other hand, it was observed that the risk of a high LDL cholesterol level was lower among men sleeping ≥8 h. These analyses were adjusted for the following items: age, blood pressure, body mass index, plasma glucose level, smoking habit, alcohol consumption, dietary habits, psychological stress, and taking cholesterol-lowering medications.Conclusions:Usual sleep duration is closely associated with serum lipid and lipoprotein levels.

Walsh, James K.; Snyder, Ellen; Hall, Janine; Randazzo, Angela C.; Griffin, Kara; Groeger, John; Eisenstein, Rhody; Feren, Stephen D.; Dickey, Pam; Schweitzer, Paula K.

doi: 10.1093/sleep/31.5.659pmid: 18517036