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: 5.39). 08/2008; 32(7):1083-90. DOI: 10.1038/ijo.2008.57
Source: PubMed

ABSTRACT 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.


Available from: Henning Tiemeier, Mar 14, 2014
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The purpose of this study was to examine the association between objective measures of sleep quality and obesity in older community-dwelling people. This cross-sectional study included 189 community-dwelling adults aged ≥ 80 yr (83.4 ± 2.5 yr [age range, 80-95 yr]). Participants wore an accelerometer (ActiGraph GT3X+) on their non-dominant wrist 24 hr per day for 7 consecutive nights. Sleep parameters measured included total sleep time, sleep efficiency, and wake after sleep onset (WASO) during the night. Associations between sleep parameters and obesity were investigated by using multivariate logistic regression analysis. In multivariate models, those with sleep efficiency lower than 85% had a 2.85-fold increased odds of obesity, compared with those with sleep efficiency of 85% or higher. Similarly, those with WASO of ≥ 60 min (compared with < 60 min) had a 3.13-fold increased odds of obesity. However, there were no significant associations between total sleep time or self-reported napping duration and obesity. We found that poor sleep quality was an independent risk factor for obesity in community-dwelling Japanese adults aged ≥ 80 yr, even after controlling for potential confounding factors, including daily physical activity.
    Journal of Korean Medical Science 02/2015; 30(2):199-206. DOI:10.3346/jkms.2015.30.2.199 · 1.25 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Modern lifestyle has profoundly modified human sleep habits. Sleep duration has shortened over recent decades from 8 to 6.5 hours resulting in chronic sleep deprivation. Additionally, irregular sleep, shift work and travelling across time zones lead to disruption of circadian rhythms and asynchrony between the master hypothalamic clock and pacemakers in peripheral tissues. Furthermore, obstructive sleep apnea syndrome (OSA), which affects 4 - 15% of the population, is not only characterized by impaired sleep architecture but also by repetitive hemoglobin desaturations during sleep. Epidemiological studies have identified impaired sleep as an independent risk factor for all cause of-, as well as for cardiovascular, mortality/morbidity. More recently, sleep abnormalities were causally linked to impairments in glucose homeostasis, metabolic syndrome and Type 2 Diabetes Mellitus (T2DM). This review summarized current knowledge on the metabolic alterations associated with the most prevalent sleep disturbances, i.e. short sleep duration, shift work and OSA. We have focused on various endocrine and molecular mechanisms underlying the associations between inadequate sleep quality, quantity and timing with impaired glucose tolerance, insulin resistance and pancreatic β-cell dysfunction. Of these mechanisms, the role of the hypothalamic-pituitary-adrenal axis, circadian pacemakers in peripheral tissues, adipose tissue metabolism, sympathetic nervous system activation, oxidative stress and whole-body inflammation are discussed. Additionally, the impact of intermittent hypoxia and sleep fragmentation (key components of OSA) on intracellular signaling and metabolism in muscle, liver, fat and pancreas are also examined. In summary, this review provides endocrine and molecular explanations for the associations between common sleep disturbances and the pathogenesis of T2DM.
    Diabetology and Metabolic Syndrome 01/2015; 7:25. DOI:10.1186/s13098-015-0018-3 · 2.50 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: Obesity has long been recognised as the most important reversible risk factor for obstructive sleep apnoea (OSA). Analyses from the Wisconsin Sleep Cohort Study suggest that 41% of adult OSA cases, including 58% of moderate-to-severe cases, are attributable to overweight or obesity.1 As such, weight loss has long been recommended as an ancillary treatment for OSA. Longitudinal analyses from the Sleep Heart Health Study support the notion that weight loss is associated with improvements in OSA severity.2 However, the beneficial impact of weight loss was much less than the adverse effect of the same amount of weight gain in that study suggesting that the relationship between obesity and OSA is more complex than can be explained by an acute (and reversible) unidirectional causal model. Given evidence that short sleep durations and poor quality sleep predict an increased rate of weight gain,3 ,4 many have postulated that OSA may itself predispose to obesity. Retrospective data indicate that those with recently diagnosed OSA are more likely to have had recent weight gain.5 These findings have been used to support the contention that OSA causes weight gain but of course, this may simply reflect the impact of weight gain on OSA risk. An association between OSA and elevated leptin levels, which fall with CPAP therapy, suggests that an effect of OSA on weight gain may be mediated by leptin resistance whereby improvements in leptin resistance with OSA treatment would produce weight loss.6 Uncontrolled studies have reported that initiation of CPAP therapy is associated with induction of mild weight loss.7 However, given that most patients are educated on the association between obesity and OSA at … [Full text of this article]
    Thorax 12/2014; 70(3). DOI:10.1136/thoraxjnl-2014-206484 · 8.56 Impact Factor