Overall, the published literature supports the presence of an association between sleep duration and weight. However, substantial differences in study designs including whether sleep duration was modeled as a cause or consequence of obesity preclude direct comparisons across studies or quantitative synthesis through meta-analysis. Differences in definitions of normal and short sleep durations also varied substantially across studies. Among children, short sleep duration was defined anywhere from less than 8 hours to less than 11 hours per night while definitions of normal sleep duration ranged from at least 8 hours to more than 12 hours.10, 13
A 6 year old with 9 hours of sleep could be classified as having short, intermediate, or long sleep duration depending on the study.7, 9, 13
Even in studies of adults where greater consensus regarding sleep needs exists, the definitions of normal sleep duration ranged greatly across studies from at least 6 hours to at least 9 hours.34, 35
Despite this variability in defining exposure, across the 13 pediatric studies, results were fairly uniform: short sleep duration was positively associated with increased weight. The findings among adult studies were more mixed. This may in part reflect a more complex relationship between sleep duration and weight in this age group with many studies reporting a U-shaped cross-sectional association. Some of the negative results may therefore be due to the fact that in these studies, long sleepers were not specifically separated from normal sleepers. Interestingly, both the NHANES and Nurses Health Study found a positive association between long sleep durations and obesity assessed simultaneously but no association with future obesity, suggesting the cross-sectional relationship might be due to reverse causation or residual confounding.3, 6
Potential mechanisms for an association between long sleep duration and obesity, whether causal or not, include depression, low socioeconomic status, and societal isolation.39
The robust pediatric data as well as the negative findings in the two studies focusing on geriatric cohorts suggest the relationship between sleep duration and weight may weaken with age. Data from prospective studies support this hypothesis.6, 38
In the Zurich Cohort Study, the cross-sectional relationship between sleep duration and weight weakened as participants aged. In the NHANES population, the association between short sleep duration and weight was most apparent in the youngest tertile. Thus, overall, the literature suggests short sleep duration may represent an independent risk factor for weight gain and obesity particularly in children and younger adults.
A number of causal pathways linking short sleep duration with obesity have been suggested based on experimental studies of sleep deprivation (). One mechanism by which sleep deprivation might predispose to weight gain is by increasing caloric intake. Total sleep deprivation experiments in animals have consistently found sleep deprivation produces hyperphagia.40
Partial sleep deprivation experiments in humans suggest a similar effect. Comparing 4 hours of sleep opportunity per night to 10 hours over a period of 2 days, both hunger and appetite scores on a visual analog scale were elevated by sleep deprivation.4
Furthermore, these increases were particularly notable for high fat and high carbohydrate foods. These changes corresponded with elevations in serum ghrelin and reductions in serum leptin suggesting sleep deprivation may impact peripheral regulators of hunger. A study restricting sleep for six consecutive days found a similar reduction in leptin that persisted throughout the 24 hour day.41
Alternatively, some have argued that in an environment where food is readily available, curtailed sleep may simply represent an increased opportunity to eat especially if most of wake-time is spent in sedentary activities such as watching television where snacking is common.42
In the epidemiologic literature, those studies that attempted to quantify caloric intake found no relationship between sleep duration and dietary consumption.3, 9, 36, 37
However, two epidemiologic studies have demonstrated that short sleepers have reduced levels of leptin and elevated levels of ghrelin study supporting an effect of short sleep durations on appetite regulation.27, 29
Potential mechanisms by which sleep deprivation may predispose to obesity.
Chronic partial sleep deprivation also clearly leads to feelings of fatigue.2
This tiredness may lead to reductions in physical activity. In fact, cross-sectional studies in children have found short sleep durations to be associated with increased television viewing and reduced participation in organized sports.9, 10
In the Nurses’ Health Study and Nurses’ Health Study 2, short sleep durations were associated with reduced reported physical activity.3, 39
None of the epidemiologic studies that assessed physical activity found differences in activity could explain the sleep-weight association. Similarly, none of the studies that assessed television viewing found the sleep – obesity relationship could be explained by this factor.7, 9–11, 35–37
Finally, studies of acute sleep deprivation in humans have found a drop in core body temperature, suggesting sleep loss may impact energy expenditure through thermoregulation.43
No epidemiologic study of sleep duration to date has assessed thermoregulation. However, a recent study found no association between reported sleep duration and total energy expenditure measured using doubly labeled water.44
Despite the general consistency in the presence of a sleep – weight association, there are important limitations in the current literature that limit the ability to definitively conclude that short sleep duration causes accelerated weight gain. One concern is the rarity of objective measurements of sleep duration. Although polysomnography is infeasible in large cohorts and the recording instrumentation may itself interfere with sleep, other methods of objectively measuring sleep exist. Wrist actigraphy uses a monitor the size of a wristwatch to measure motion in the arm and has been validated against polysomnography.45, 46
Unfortunately, only two studies of sleep duration and obesity to date have utilized actigraphy and both used recording times that were too short to incorporate variability across the week.14, 32
Most studies have relied on questionnaires to assess sleep. However, the wording of these questions varies greatly across studies and few questions have been validated. The Nurses Health Study question is one of the few exceptions; in a subgroup of the cohort, this question showed good correlation (r=0.79) with one week of sleep diaries.47
However, the correlation between sleep diaries and actigraphy has been moderate at best (r=0.57 for nocturnal sleep and r=0.48 for daytime sleep).48
In addition, many studies asked only about nocturnal sleep which may substantially underestimate sleep duration in populations where napping or shift-work is common. The importance of this problem is demonstrated by the study by Ohayon et al where short nocturnal sleep durations were associated with obesity but no association was found with overall sleep duration because the obese were more likely to nap during the day.31
The large night to night variability in sleep duration may also lead to substantial measurement error. Of particular concern is the fact that sleep habits vary greatly between weekdays and weekends. Several studies have reported sleep duration is 0.6 hours longer on average on weekends.1, 32
These differences are even larger in those who have more severe sleep restriction during the week. It is unclear how accurately individuals are able to average their sleep habits over weekdays and weekends to answer a single question about usual sleep habits.
Given the lack of interventional trial data, another concern in inferring short sleep duration promotes obesity is the possibility of reverse causation. Obesity increases the risk of medical conditions such as osteoarthritis, gastroesophageal reflux, asthma, and heart failure that can disrupt sleep and lead to insomnia.49–52
Obesity is the strongest risk factor for obstructive sleep apnea which has as its hallmark disruption of sleep.53
Several studies have attempted to control for these co-morbidities by including the presence of these diseases as covariates in multivariate modeling.3, 23, 24, 28, 32, 33
Another argument against reverse causation comes from the positive findings in pediatric studies where the prevalence of co-morbid disorders related to obesity are rare. Whether obesity has an effect on sleep independent of its medical complications is unclear, but the data suggest any effect is in the opposite direction. Inflammation associated with obesity may lead to the release of soporific cytokines producing longer sleep durations.54
A mouse model of diet-induced obesity supports the notion that obesity increases sleep duration.55
The positive findings from all five longitudinal studies support the contention that short sleep duration causes weight gain rather than vice versa. However, only one study made repeated measurements of sleep to consider the opposite causal relationship.38
In that study, weight was a better predictor of future sleep duration than sleep duration was of future weight. This suggests the causal direction may be reversed, although the findings may also be explained by a waning effect of sleep duration on weight with aging.
The possibility of residual confounding is another concern. Conditions that have been associated with both short sleep durations and obesity and might therefore bias measures of the effect of sleep duration on weight include medical disorders such as chronic pain syndromes as well as psychiatric disorders such as depression. Such conditions may limit an individual’s ability to be physically active as well as interfere with sleep continuity. In addition, many medications can adversely affect both weight and sleep duration. Several studies have attempted to measure and control for co-morbid medical and psychiatric disorders as well as medication use through multivariate analysis.3, 6, 24, 28, 38
Because the Zurich Cohort Study was designed to investigate psychiatric outcomes, detailed assessments of depressive symptoms were performed and the sleep – weight association was found to be independent of depression.38
Again, findings from pediatric cohorts where co-morbidity and medication use are rare argue against the observed sleep – weight association being due to confounding from medical or psychiatric disease.
Socioeconomic status may also confound the sleep-weight relationship. People of lower socioeconomic status may have less favorable sleep environments, work longer hours, and work less desirable hours such as rotating or overnight shifts resulting in poor sleep. Low income has been associated with reduced sleep durations.32
However, many studies have adjusted for socioeconomic status in multivariate analyses and have found the sleep-weight association persisted.6, 9–11, 16, 26, 28, 35–38
The prevalence of chronic partial sleep deprivation has increased dramatically in the past half century, in parallel with the growing epidemics of overweight and obesity. Currently, 40% of American adults report obtaining less than 7 hours of sleep.1
In this systematic review, findings from many cross-sectional investigations as well as five prospective cohort studies suggest short sleep duration may be a novel and independent risk factor for weight gain and obesity, particularly in younger populations. Clearly, however, further research, particularly from large prospective cohort studies with objective measurement of sleep habits and repeated measures of both sleep duration and weight, is needed to more definitively establish a causal link and to better define the magnitude of any causal effect. In addition, further physiologic studies in both human and animal models are needed to better define the pathways by which sleep curtailment might impact weight regulation. In the end, controlled trials will be needed to assess the potential for sleep-promoting interventions to combat the obesity epidemic.