Original ArticleThe relationship between weight change and daytime sleepiness: the Sleep Heart Health Study
Introduction
The association between obesity and excessive daytime sleepiness (EDS) has long been accepted; however, to our knowledge, its causality has not been formally assessed. Whether weight change has a causal effect on daytime sleepiness, and what the pathways are remain largely unexplored. EDS, the irresistible urge to fall asleep despite one's intention to remain awake [1], is highly prevalent in the general population (up to 30%) [2] and is known to affect work performance [3], [4], mental health [5], [6], quality of life [5] and motor-vehicle-related deaths [7], [8].
A recent longitudinal study by Fernandez-Mendoza et al. [9] found that weight gain over 7.5 years was associated with incident and persistent EDS over the same duration; whilst weight loss was associated with its remission. Similarly, in another study by Palm et al. [10], increase in body mass index (BMI) over 10–13 years was associated with incident EDS over the same duration. However, these studies used one-/two-item non-validated questionnaires to assess EDS, and they did not assess potential mediating pathways between weight change and daytime sleepiness, which may provide useful information for interventions targeting EDS remission.
Using the Sleep Heart Health Study (SHHS) dataset, a large population-based multicentre cohort study for assessing the cardiovascular outcomes of sleep apnoea, and a causal framework, we aimed to study the relationship between weight change and daytime sleepiness, measured through the Epworth Sleepiness Scale, a validated [11], and widely used eight-item questionnaire to measure daytime sleepiness. We also performed mediation analyses to assess the likely pathways through which weight change may affect daytime sleepiness. Potential mediators considered include obstructive sleep apnoea, mental health, physical health, and sleep duration, as suggested by a previous review [12].
Section snippets
Data source
We used the SHHS dataset; a large population-based multicentre cohort study in the US, which aimed to assess the cardiovascular outcomes of sleep apnoea in community-dwelling adults. A total of 6441 individuals were recruited from six ongoing, population-based, parent cohorts: Atherosclerosis Risk in Communities Study, Cardiovascular Health Study, Framingham Heart Study, New York Cohorts, Strong Heart Study and Tucson Cohorts. To be recruited into the SHHS, individuals were required to be 40
Baseline characteristics, and levels of exposure and outcome
The study participants were on average 55 years old, 46% were female, the mean baseline BMI was 28 kg/m2, and 25% had EDS. Compared to men, women were more likely to have lower education, weight, BMI, ESS scores, OAHI, AHI, and SF-36 physical and mental component score at baseline. They were also more likely to have longer objective sleep duration, worse sleep disturbance score, insomnia, used benzodiazepines and antidepressants, and less likely to be a current or former smoker at baseline (
Discussion
In this study, through a causal framework, we have consistently found evidence supporting an association between weight gain and worse daytime sleepiness that may be partly mediated by severity of obstructive sleep apnoea. The relationship seemed to be more pronounced in women and those with poorer mental health.
A recent study by Fernandez-Mendoza et al. [9] similarly found higher risk of incident EDS with weight gain, and remitted EDS with weight loss. Another recent longitudinal study by
Conclusion
Our study showed, for the first time, that weight gain is associated with daytime sleepiness as assessed through the ESS, and that approximately one-fifth of this relationship occurs through obstructive sleep apnoea, and approximately one-sixth through poor overall physical health. We explicitly described the extent to which the assumptions of ‘no unmeasured confounding’ and ‘well-defined intervention’, may affect causal inference from our study findings. This provides further understanding of
Acknowledgements
WLN is supported by a Monash Graduate Scholarship, a Monash International Post-graduate Research Scholarship and a Baker Bright Sparks Top-Up Scholarship. JES is funded by an NHMRC Senior Research Fellowship. AP is supported by an NHMRC Development Fellowship and is a researcher within a National Health and Medical Research Council, Centre for Research Excellence in Obesity Policy and Food Systems grant (APP1041020).
This study was supported in part by the Victorian Government's Operational
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