Actigraphic sleep duration and fragmentation are related to obesity in the elderly: The Rotterdam Study

Department of Epidemiology and Biostatistics, Erasmus Medical Center, Rotterdam, The Netherlands.
International journal of obesity (2005) (Impact Factor: 5). 08/2008; 32(7):1083-90. DOI: 10.1038/ijo.2008.57
Source: PubMed


The epidemiological evidence for the association between sleep duration and obesity in the elderly is inconsistent and has not been investigated with objective measures. Furthermore, the role of sleep fragmentation in this relationship is unknown. Our aim was to investigate the association of sleep measures with body mass index (BMI) and obesity in a normal elderly population.
Cross-sectional study.
A total of 983 community-dwelling elderly (mean age 68.4+/-6.9 years, range, 57-97).
Weight and height were measured, and sleep duration and fragmentation were assessed with on average six nights of actigraphy.
A quadratic model adequately described the association between continuous measures of sleep duration and BMI. Actigraphic sleep duration had a significant U-shaped relationship with BMI (beta of quadratic term=0.30, 95% confidence interval (CI): 0.08, 0.52). Both short sleepers (<5 h: OR, 2.76 (95% CI: 1.38, 5.49), 5 to <6 h: OR, 1.97 (95% CI: 1.26, 3.08)) and long sleepers (>or=8 h: OR, 2.93 (95% CI: 1.39, 6.16)) were more likely to be obese, compared to participants who slept 7 to <8 h. BMI increased with 0.59 kg m(-2) per standard deviation of sleep fragmentation (95% CI: 0.34, 0.84). After adjustment for sleep fragmentation, the association between short sleep and obesity was no longer significant. Exclusion of participants with probable sleep apnea only marginally changed these associations. Self-reported habitual sleep duration was not associated with BMI or obesity.
Sleep duration, as measured with actigraphy, had a U-shaped relationship with BMI and obesity in an elderly population. A highly fragmented sleep is associated with a higher BMI and a higher risk of obesity, and may explain why short sleep is related to obesity. To preclude bias that can be introduced by self-report measures of sleep duration, using multiple measures of sleep parameters is recommended in future research.

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Available from: Henning Tiemeier, Mar 14, 2014
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    • "More difficult to judge is whether environmental noise has also a long-term impact (tertiary effects). The question would have large relevance since recent general research into the long-term effects of poor sleep has established significant relationships with mortality [10], [11], cardiovascular disease[12], [13], diabetes and obesity [14] [15] [16] [17]. To establish such a relationship, longitudinal studies are needed over years. "
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    ABSTRACT: Background: The WHO-JCR has provided a general methodology to assess the health impact of environmental noise at larger scale. Switzerland used this methodology in a recent assessment. Other countries use their own assessment strategies. At smaller scales (regional, community) the application of this methodology is limited due to the use of standard exposure effect curves. In order to ensure to meet local needs (alpine valley) we adapted the methodology. Methods: We used actual GIS noise map information and merged it with GIS population information to get the number of noise exposed (30 to 70 dBA, L day , L evening and L night). On the effect side we used annoyance, sleep disturbance, hypertension and myocardial infarction. A mix of standard and regional exposure response information was applied. An upper and lower 95% confidence interval was derived for the prevalence estimates. With cost calculations we relied on the experience of the HEIMTSA-project. Results: The status quo yields high annoyance (3000-5000 persons) and high sleep disturbance (3000-4000 persons) as most important contributors. However, sleep disturbance shows the highest gain through a night curfew in truck traffic in health terms (number of affected, DALYs) and even more in health cost.
    INTER-NOISE and NOISE-CON Congress and Conference Proceedings; 09/2013
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    • "Indirect evidence of the relationship between insomnia and eating disorders emerged from studies indicating that poor sleep (or sleep of short duration) predicts obesity in children (Marshall, Glozierb, & Grunstein, 2008; Patel, 2009; Van Cauter & Knutson, 2008), in adults (Lauderdale et al., 2007; Patel et al., 2006) and in the elderly (Patel et al., 2008; Van der Berg et al., 2008). A second type of indirect evidence was also derived from laboratory studies demonstrating the sleep-disruptive effects of hunger. "
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    ABSTRACT: Background Insomnia is one of the most common sleep disorders, and it frequently co-occurs with several other psychiatric conditions. The relationship between insomnia and eating disorders is supported by clinical evidence indicating that patients with eating disorders experience poor sleep even if they rarely complain of it. Furthermore, indirect evidence comes from studies indicating that poor sleep predicts obesity and several studies also evidence that restrictive-type eating disorders are associated to objective reduction of sleep quality. Methods One thousand nineteen female university students volunteered for participating to the study. Valid and reliable questionnaires were used and the mediating role of depressive mood assessed. ResultsEvidence was found that increased severity of insomnia is associated with higher severity of disordered eating. Both insomnia and disordered eating symptoms were related to depression. The mediation analysis evidenced that both the direct path linking insomnia symptoms and eating disorder symptoms are significant and also the indirect paths related to the mediation of depression. Conclusions These findings support the existence of both a direct and an indirect relationship between insomnia symptoms and eating disorder symptoms.
    Clinical Psychologist 09/2013; 18(3). DOI:10.1111/cp.12023 · 0.93 Impact Factor
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    • "The results also show that increased food intake and body weight were accompanied by increased sleep fragmentation, which is similar to human studies showing a positive association between highly fragmented sleep and body mass index (1, 2, 6). Likewise, many rodent models show an association between sleep fragmentation and obesity, which includes obese leptin-deficient mice, leptin-resistant mice, obese Zucker rats and obesity resistant (OR) rats (13, 18, 37). "
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    ABSTRACT: Objective Sleep-restriction in humans increases risk for obesity, but previous rodent studies show weight loss following sleep deprivation, possibly due to stressful-methods used to prevent sleep. Obesity-resistant (OR) rats exhibit consolidated-sleep and resistance to weight-gain. We hypothesized that sleep disruption by a less-stressful method would increase body weight, and examined effect of partial sleep deprivation (PSD) on body weight in OR and Sprague-Dawley (SD) rats. Design and Methods OR and SD rats (n=12/group) were implanted with transmitters to record sleep/wake. After baseline recording, six SD and six OR rats underwent 8 h PSD during light-phase for 9 d. Sleep was reduced using recordings of random noise. Sleep/wake states were scored as wakefulness (W), slow-wave-sleep (SWS) and rapid-eye-movement-sleep (REMS). Total number of transitions between stages, SWS-delta-power, food intake and body weight were documented. Results Exposure to noise decreased SWS and REMS time, while increasing W time. Sleep-deprivation increased number of transitions between stages and SWS-delta-power. Further, PSD during the rest phase increased recovery-sleep during active phase. The PSD SD and OR rats had greater food intake and body weight compared to controls Conclusions PSD by less-stressful means increases body weight in rats. Also, PSD during rest phase increases active period sleep.
    Obesity 07/2013; 21(7). DOI:10.1002/oby.20182 · 3.73 Impact Factor
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