The Weight of Lost Sleep: An Epidemiological Perspective

Fay
12 minutes ago
5 min read

Epidemiology of sleep

Sleep is a periodic, reversible state of rest that is not easily interrupted by the outside world and is widespread in all multicellular animals, suggesting that it serves an important biological function. If sleep were not beneficial, natural selection would have eliminated it long ago. Its necessity is also reflected in the “homeostatic drive for sleep”: similar to hunger or thirst, the longer the absence of sleep, the stronger the urge to fall asleep. Animal studies have further demonstrated this - complete sleep deprivation can lead to death within a few weeks.

In human studies, the most commonly used indicator of sleep is sleep duration. A large body of evidence shows that chronic sleep deprivation increases health risks. For this reason, the U.S. government included sleep as a public health goal for the first time in its “Healthy People 2020” program, suggesting that children, adolescents, and adults should all achieve the appropriate minimum amount of sleep (8-16 hours for children and adolescents and at least 7 hours for adults). However, epidemiologic surveys have found that the reality is far from ideal. For example, U.S. Youth Risk Behavior Surveillance data show that up to 95 percent of high school students do not get the recommended amount of sleep, and that the average amount of sleep for children and adolescents has decreased by more than an hour over the past century.

Adults also face sleep deprivation. While experts recommend getting at least seven hours of sleep a night, surveys show that about one-third of U.S. adults fall short. From 1985 to 2012, the average number of minutes of self-reported sleep decreased by 10-15 minutes, and the percentage of people sleeping less than six hours a night rose from 22.3 percent to nearly 30 percent. The reasons for this decrease in sleep are complex and include increased lighting at night, the proliferation of electronic devices, and longer work hours.

Sleep and obesity

Over the past few decades, shorter sleep duration has occurred almost in tandem with rising obesity rates. Epidemiologic data from 2011-2014 show that obesity rates in the United States have reached 37.7% among adults and 17.0% among children and adolescents. This trend, coupled with pathophysiologic evidence, suggests a possible link between sleep deprivation and obesity.

There is a considerable body of research on the relationship, including several systematic reviews and meta-analyses. Early studies relied primarily on cross-sectional studies, making it difficult to determine the direction of causality; also, most of the data came from self-reports, a subjective measure that tends to be overestimated by approximately 1 hour compared with objective tools (eg, activity loggers), which also increases interstudy variability. In addition, the definition of “short sleep” is not uniform, further complicating comparisons.

Results for children and adolescents were relatively consistent: sleep deprivation significantly increased the risk of obesity. In adults, the association was not as clear as expected, with some studies showing positive associations, some showing U-shaped curves, and some finding no significant associations. For example, in the Nurses' Health Study, the risk of obesity was about 15% higher among people who slept less than 5 hours per night than among those who slept 7 hours per night; however, short sleep was not associated with weight gain in the longitudinal cohorts of CARDIA and SWAN. Evidence from randomized controlled trials is similarly limited and mixed, suggesting that the relationship between sleep and obesity may be influenced by age, measurement method, or study design.

The relationship between prolonged sleep and obesity has also received attention, but the biological mechanisms are unclear. Some studies have found positive associations, which may reflect reporting errors (e.g., bedtime as sleep time) or be influenced by confounding factors such as depression and socioeconomic level.

From a mechanistic perspective, sleep-deprived individuals have more opportunities to eat because they are awake longer; meanwhile, fatigue may promote obesity by reducing physical activity and increasing sedentary behavior. However, experimental studies have found that the effects of short sleep on energy expenditure and basal metabolism are not significant, suggesting that mechanisms beyond energy balance still need to be further explored.

Obesity comorbidities associated with sleep

While a large number of studies have explored whether sleep deprivation contributes to obesity, the inverse relationship is equally noteworthy: obesity itself can significantly affect sleep. The classic example is obstructive sleep apnea (OSA), one of the most common complications of obesity, which is characterized by recurrent collapse of the upper airway. Numerous studies have shown a dose-response relationship between BMI and the severity of OSA, with higher body weight being associated with more severe OSA. Longitudinal studies have further shown that both high baseline weight and weight gain are associated with the progression of OSA, whereas weight loss interventions improve the symptoms and severity of OSA. This evidence supports a causal role for obesity in OSA. Specific mechanisms may include airway compression due to fat deposition in the neck, abdominal obesity that reduces lung volume and thus tracheal traction, and impaired dilatation due to fat deposition within the tongue muscles.

In addition to OSA, obesity is strongly associated with a variety of comorbidities that may disrupt sleep:

Depression: Obesity and depression are bi-directionally linked in both adults and adolescents. Obesity may increase the risk of depression through insulin resistance, chronic inflammation, or psychological burdens (e.g., lowered self-esteem, somatic dissatisfaction). In turn, depression is often accompanied by sleep disorders (insomnia, abnormal sleep duration, etc.) and can further exacerbate obesity through poor lifestyle behaviors.
Gastroesophageal reflux disease (GERD): Obese individuals are more likely to develop GERD and its complications, such as erosive esophagitis and esophageal adenocarcinoma. Mechanisms may involve elevated abdominal pressure, hiatal hernia formation, and lower esophageal sphincter relaxation.GERD is often exacerbated at night or while lying down, which can result in sleep fragmentation. A few studies have suggested a possible bidirectional association between sleep deprivation and GERD, but the results have been inconsistent.
Osteoarthritis: Obesity increases joint burden, is an important risk factor for osteoarthritis, and is associated with disease progression and symptom exacerbation. Joint pain not only interferes with daytime activities but also often leads to sleep disturbances. Weight loss can significantly improve joint loading and sleep quality.
Asthma: Obesity is associated with both risk and severity of asthma. Obese asthmatics tend to be more symptomatic and less responsive to treatment, and nocturnal asthma exacerbations often disrupt sleep.

In addition, even in the absence of significant comorbidities, obese individuals are more likely to experience daytime sleepiness and decreased sleep quality. It has been suggested that this may be related to chronic inflammation or hypothalamic-pituitary-adrenal axis dysfunction. Patients following bariatric surgery commonly report improved sleep, further suggesting that obesity may directly affect sleep through independent pathways.

Conclusion

Available epidemiologic evidence suggests a complex bidirectional relationship between sleep deprivation and obesity. Reduced sleep duration may increase energy intake and decrease physical activity, thereby promoting weight gain; at the same time, obesity, especially when accompanied by comorbidities such as obstructive sleep apnea, depression, and gastroesophageal reflux, can further disrupt sleep. Long-term and longitudinal studies emphasize the importance of healthy sleep for weight management despite differences in the associations observed across age groups and study designs. Future studies need to incorporate objective sleep measures and intervention trials to clarify causal mechanisms and explore the potential for preventing or mitigating obesity and related comorbidities through improved sleep. This direction is not only critical for individual health but also has far-reaching implications for the development of public health strategies.