Healthy Sleep Education—A Salve for Obesity?

There is increasing recognition that there is an epidemic of obesity in this country. As noted in a report from the Robert Wood Johnson Foundation and the Trust for America's Health, obesity rates range from 18.9% (Colorado) to 32.5% (Mississippi). Furthermore, in 30 states, the percent of obese or overweight children exceed 30%.1 The public health implications of obesity are enormous. For sleep clinicians the link between obesity and obstructive sleep apnea is well known. However, obesity is a risk factor for many of the most common chronic illnesses afflicting Americans today including coronary heart disease, hypertension, asthma, diabetes mellitus, degenerative joint disease, and some cancers. The medical conditions caused or worsened by obesity translate into reduced quality of life and an enormous economic burden. A 1995 estimate of the total cost of overweight and obesity in the United States was $99.2 billion, including approximately $51.6 billion in direct medical costs and $47.6 billion in indirect costs related to absenteeism, presenteeism, and reduced productivity.2 As a result of the prevalence and economic data as well as empiric observations of the populace, state and federal health care agencies, as well as private foundations have increased research funding and have started public awareness campaigns designed to prevent and ultimately reverse the rising tide of obesity. Studies in twins have been used to better understand the effect of diverse genetic, environmental, and social variables on health and disease.3–4 In this issue of the Journal, Watson et al. utilized data from the University of Washington Twin Registry to assess genetic and non-genetic determinants of BMI and sleep duration within this cohort.5 They found that BMI was higher among those with short sleep durations. In addition, although there was strong heritability of BMI and borderline heritability of sleep duration, there was no apparent evidence of common genetic or environmental factors between sleep duration and BMI. Several issues potentially confound the association between sleep duration and BMI. Is shorter sleep driven by external constraints or behavioral traits, both of which can simultaneously contribute to decreased physical activity and unhealthy diet as well? While environmental differences have been reported even in younger twins living in same household, a more apparent divergence of environments can be expected in many twins in third and fourth decades of life. What is also not clear is why the differences were not significant in the dizygotic twins. A smaller sample size could be one explanation. It is also possible that genetics modify the influence of sleep duration on body weight. This may have attenuated the sleep-duration related differences in BMI in dizygotic twins, who share only 50% of their genetics. Indeed, studies have suggested genetic factors influence the effect of overfeeding in twins.4 Finally, can a higher BMI indirectly result in shorter sleep duration? People with higher BMI are at increased risk of diverse medical disorders such as diabetes, hypertension, and other cardiovascular disorders. These disorders have been associated with poor sleep efficiency and shorter self-reported sleep. However, the presence of such chronic disorders is less likely in this cohort with a relatively young mean age. Regardless of these limitations, this is an important study. It employs a substantial sample size and utilizes different models to control for additional genetic and environmental influences to assess the relationship between BMI and sleep duration. Thus, the data provide further evidence that there are unique environmental factors responsible for the inverse association between BMI and sleep duration. The most likely unique factor is voluntary or externally imposed sleep restriction. As discussed in this paper, there are a number of possible mechanisms responsible for the relationship between short sleep duration and higher BMI. However, irrespective of the underlying mechanism, in most cases, the remedial solution is conceptually simple: more sleep. Despite the evidence implicating inadequate sleep as an important factor in mediating obesity, public health interventions generally fail to incorporate healthy sleep education as part of their overall strategy. For example, the American Heart Association and the Clinton Foundation recently formed the Alliance for a Healthier Generation to combat childhood obesity. However, their strategies focus on better diet and increased physical activity for children. There is no mention of improving sleep hygiene.6 Recent data suggest that decreased sleep time in children may be associated with increased screen time (e.g., computer gaming, television watching) and use of caffeinated beverages.7 These behaviors are potentially correctable but rarely mentioned in obesity prevention programs. Why has not sleep hygiene education become more visible in the war against obesity? Two possible explanations come to mind. First, most studies have been cross-sectional observations. There are few longitudinal studies and no large scale intervention studies which have proven the value of sleep hygiene in decreasing the development of obesity. Second, the sleep medicine community has not assumed a sufficient advocacy role in informing their obesity prevention counterparts about the importance of adequate sleep. Watson and colleagues are to be congratulated in highlighting the significant relationship between short sleep duration and increased BMI. Continued exploration of such data will help better confirm the association and elucidate the mechanistic paradigm between sleep duration and obesity. Meanwhile, we as a sleep medicine community need to help translate such findings by designing intervention trials to demonstrate the usefulness of sleep interventions in reducing obesity, and to advocate to the medical and public health community at large about the importance of sufficient sleep.