Cross-sectional findings from the Whitehall II cohort showed that shorter duration of sleep was significantly associated, in a linear fashion, with greater body weigh and risk of obesity, which is consistent with previous cross-sectional reports (14
). Specifically, the regression coefficient of −0.36 (−0.49 to −0.24) for the cross-sectional association between the number of hours of sleep and BMI is consistent with the magnitude of the association observed in a recently published cross-sectional analysis from a population-based sample in the US (21
). Moreover, unlike previous investigations, which did not include measures of body fat distribution and central adiposity, in the cross-sectional analyses we also found a significant, inverse association between hours of sleep and waist circumference. Finally, individuals sleeping 5 hours or less had a 65% increased risk of obesity compared to those sleeping 7 hours, in fully adjusted models, which is consistent with pooled estimates reported in a meta-analysis of cross-sectional studies (34
The prospective analyses, however, did not show a significant association between sleep duration and future changes in body weight or waist circumference, therefore not supporting a temporal relationship between short sleep duration and obesity, an essential criterion to infer causality. Indeed, most of the evidence so far comes from cross-sectional analyses (14
), which preclude the possibility of sorting out the bidirectional relationship between sleep duration and body weight. On the other hand, change models offer the possibility of controlling for all time-stable confounders. Obesity is often co-morbid with several medical conditions that in turn may impair the quality and duration of sleep (29
). Findings from a few longitudinal investigations have been inconsistent (23
). First, Hasler et al
found that short sleep time was associated with subsequent obesity in subjects younger than 35 years but the association diminished in older participants (23
). However, this study was based on a small sample (n
= 496) with over-representation of cases with psychiatric disorders and, thus, with a limited generalizability. In addition, in this study the potential for reverse causality could not be excluded because the authors also found an association between earlier obesity and future short sleep duration. Second, Gangwisch et al
reported inconsistent findings from cross-sectional and longitudinal analyses on the large US sample of the NHANES-I (24
). Similar to our study, the authors found significant cross-sectional associations between short sleep duration and high body weight and obesity, whereas sleep duration at baseline was not associated with significant future changes in BMI over a mean follow-up of 8–10 years (β = −0.053, p
=0.27), consistent with our findings. It should be noted, however, that this analysis was based on self-reported weights to compute BMI during the follow-up and did not include measures of body fat distribution. Third, a recently published report from the large sample of the Nurses’ Health Study (n
= 68,183) has shown that a habitual sleep time of less than 7 hours predicted a modest increase in weight over a mean follow-up of 16 years (26
). In addition, the relative risks for incident obesity were 1.15 (1.04, 1.26) and 1.06 (1.01, 1.11) for women sleeping 5 and 6 hours, respectively, compared to those sleeping 7 hours, which resemble our point risk estimates. However, this analysis was based on self-reported measures of body weight, did not include measures of body fat distribution, and was limited to a large cohort of middle-aged women from the nursing profession, thus with a limited generalizability. Conversely, there were no significant associations between sleep duration at baseline and weight gain (and incident type 2 diabetes) in a population-based study of 1,462 Swedish women followed for 32 years (25
). It should be noted that in this study the authors did find significant, inverse associations between sleep duration and BMI and waist-to-hip ratio in cross-sectional analyses at baseline, which is consistent with our findings. In summary, our results are consistent in showing inverse cross-sectional relationships between short sleep and obesity but no prospective associations.
The biological mechanisms underlying the observed associations between short sleep duration and increased body weight are unclear, although the evidence from physiological studies suggests some possible explanations. For example, sleep deprivation has been found to influence hormones that control appetite. In a small study on 12 young, healthy men, an induced short-term sleep restriction was associated with a reduction in the levels of the anorexigenic hormone leptin on one hand and an increase in the levels of the orexigenic hormone ghrelin, and thus increased hunger (35
). Similar associations were found in cross-sectional analyses from the Wisconsin Sleep Cohort Study, suggesting that these effects may persist with long-term sleep restriction (19
). Glucose homeostasis is also affected by sleep deprivation since glucose uptake varies through different phases of sleep, and adverse effects of sleep deprivation have been reported on cortisol levels, glucose tolerance, and growth hormone secretion (36
). Moreover, sleep deprivation has been associated with changes in levels of circulating catecholamines and alterations of neurovegetative responses (39
). Recent findings also suggest that sleep may have powerful effects on the immune function and that inflammatory responses to sleep deprivation may represent one mechanism linking short sleep duration to obesity and other metabolic disorders (40
). Finally, we cannot exclude that sleep deprivation may represent a risk marker for poorer health outcomes and impaired quality of life rather than a casual factor for obesity and other related diseases (11
). Indeed, our descriptive analyses showing a poorer health status and lifestyle profile associated with shorter duration of sleep strongly suggest that other factors and co-morbidities could confound the associations between duration and quality of sleep and health outcomes.
There are some limitations in our study. First, the population is an occupational cohort of white-collar workers and limited to whites, which may reduce the generalizability of our findings to other populations. However, this would not affect the internal validity of our results with respect to the longitudinal analyses. Second, information about sleep duration was self-reported by the participants. Nevertheless, self-report assessments of sleep have been shown to be valid measures compared to quantitative sleep assessments with actigraphy (44
). Moreover, because outcomes were assessed prospectively, any misclassification of sleep duration would be non-differential with respect to weight gain, thus resulting in underestimation of the true effects. A further limitation of this study is the relatively short time of follow-up (5 years), which may have precluded us from detecting larger and significant effects of sleep deprivation on future changes in body weight and fat distribution. However, other longitudinal analyses (23
), but one (26
), based on longer follow-ups, still failed to detect significant and consistent associations. The strengths of this study include the simultaneous inclusion of a number of covariates known to be related to both sleep habits and obesity. A further strength is that anthropometric measures of relative weight and body fat distribution were directly measured at both examinations and were not based on questionnaire like in previous longitudinal investigations, thus minimizing the potential of recall bias and misclassification that occurs when using self report alone.
In summary, consistent with previous investigations, this study demonstrates significant associations between short duration of sleep and greater body weight, central adiposity and risk of obesity, in cross-sectional analyses. However, prospective analyses do not support a temporal relationship between short duration of sleep and gains in body weight or central adiposity, which is consistent with all (23
) but one (26
) previous longitudinal studies. While sustained sleep curtailment and ensuing excessive daytime sleepiness are undoubtedly cause for concern, our study suggests that short duration of sleep might represent a risk marker rather than a causative risk factor for obesity. Further prospective studies with objective assessment of long-term exposure (e.g., repeated actigraphy), more specific outcomes (including direct measures of adiposity) and better control for confounders are needed before causality can be determined.