The concept of sleep health provides a positive holistic framing of multiple sleep characteristics, including sleep duration, continuity, timing, alertness, and satisfaction. Sleep health promotion is an underrecognized public health opportunity with implications for a wide range of critical health outcomes, including cardiovascular disease, obesity, mental health, and neurodegenerative disease. Using a socioecological framework, we describe interacting domains of individual, social, and contextual influences on sleep health. To the extent that these determinants of sleep health are modifiable, sleep and public health researchers may benefit from taking a multilevel approach for addressing disparities in sleep health. For example, in addition to providing individual-level sleep behavioral recommendations, health promotion interventions need to occur at multiple contextual levels (e.g., family, schools, workplaces, media, and policy). Because sleep health, a key indicator of overall health, is unevenly distributed across the population, we consider improving sleep health a necessary step toward achieving health equity.
Poor sleep health is an underrecognized public health challenge strongly associated with morbidity and mortality (30). For example, more than 80% of older adults who report sleep disturbances describe at least one major mental or physical disorder, particularly depression, heart disease, pain, and memory problems (41). This strong overlap between sleep problems and other mental and physical health morbidities has led to a common misconception that sleep problems are merely an epiphenomenon of other conditions. However, over the past three decades, converging evidence demonstrates that sleep problems not only commonly co-occur with other morbidities, but also can play a causal role in the development of these conditions. This paradigmatic shift in viewing poor sleep health as a critical indicator and risk factor for health problems, rather than simply being secondary to those conditions, has important etiological and clinical implications for public health.
In this review, we describe current conceptualizations of sleep health and highlight findings linking sleep with cardiovascular disease (CVD), obesity, mental health, and neurodegenerative disease. Our review focuses on adults because most data address the health problems of midlife and older adults; understanding sleep health implications in childhood remains a pressing research priority. We also discuss the socioecological model of sleep health and the potentially mediating role of sleep in understanding health disparities. We conclude with recommendations and opportunities for interventions, future research areas, and the importance of promoting sleep health for achieving health equity. This review should not be considered exhaustive, but rather a summary of key, contemporary findings that, in our opinion, represent the state of the science on the role of sleep in public health and promising future directions.
SLEEP HEALTH: IT IS MORE THAN THE SUM OF ITS PARTS
In prior decades of sleep research, scholars tended to focus on a narrow range of sleep problems, which were disease oriented rather than positively framed as health oriented (17). The most common sleep characteristics studied were short and long sleep duration; the most common symptoms studied were insomnia symptoms (e.g., trouble falling asleep, staying asleep, and waking up too early), and the most common disorder studied was sleep apnea.
Epidemiologic data on each of these sleep indicators present an alarming picture. For example, current consensus panel recommendations indicate that adults should sleep a minimum of 7 h per night (15, 36), yet the Centers for Disease Control and Prevention (CDC) reports that about 35% do not meet that recommendation (20). Insomnia symptoms refer to patient-reported difficulty falling asleep or staying asleep or awakening too early. Insomnia disorder refers to insomnia symptoms that persist for some duration (typically 1–3 months) and that cause significant distress or impaired waking function. Worldwide between 30% and 35% of adults suffer from insomnia symptoms, and about 10% of the population meet diagnostic criteria for insomnia disorder (93). Obstructive sleep apnea (OSA), another prevalent sleep disorder with public health implications, is defined by recurrent episodes of not breathing (apnea) or reduced airflow (hypopnea) during sleep, despite continued respiratory effort. OSA leads to intermittent hypoxemia and repeated arousals, which can compromise cardiovascular function. Prevalence estimates for OSA vary widely, between 3% and 10% of the general population; however, OSA is likely severely underdiagnosed, particularly among African Americans, overweight individuals, and older adults (42, 69). These statistics highlight the multidimensional nature of sleep and suggest that poor sleep characteristics, sleep symptoms, and sleep disorders are common and costly to public health.
The emerging concept of “sleep health” presents a more holistic view of sleep, including multiple domains of sleep characteristics, including regularity, alertness, timing, efficiency, and satisfaction, rather than individual symptoms and disorders (17). Unlike sleep symptoms and disorders, multidimensional sleep health can be measured as a continuous variable to characterize every individual in the population. The concept of sleep health provides a useful heuristic for integrating existing research, identifying gaps in the literature, and recognizing promising future directions for research and clinical intervention. Furthermore, this broader conceptualization of sleep as a multidimensional entity of health coheres with the World Health Organization's view, which describes “health” in general, as a “state of complete physical, mental and social well-being and not merely the absence of disease or infirmity” (140). Multidimensional sleep health recognizes that sleep occurs at the individual level and also in a larger socioecological context. This perspective is consistent with two key developments in sleep science over the past two decades: the recognition of substantial inequities in sleep that parallel other racial/ethnic and socioeconomic disparities in other health outcomes (53, 54, 67, 102), and the recognition that determinants of sleep health go beyond the individual, encompassing socioenvironmental influences as well (55, 66). Thus, sleep health not only serves as a key indicator of overall health and equity, but also provides an opportunity for multiple levels of intervention (66). Although sleep health and its components are associated with a broad range of morbidities, we next highlight examples from the recent literature on the association between sleep and key health outcomes, including CVD, obesity, mental health, and neurogenerative diseases.
SLEEP HEALTH AS A KEY HEALTH INDICATOR
CVD is the leading cause of death globally (141). While sleep disturbances are common among individuals with CVD (85), a burgeoning evidence base demonstrates the role of sleep characteristics and disorders in contributing to CVD morbidity and mortality (57).
Most of the existing epidemiologic evidence on sleep and CVD risk has focused on isolated sleep characteristics, primarily sleep duration, or specific sleep disorders, primarily OSA. For example, a 2011 meta-analysis of 15 studies, involving more than 400,000 individuals, showed that short sleep duration (<7 h) is associated with incident coronary heart disease (CHD) and stroke, as well as increased risk of CHD mortality (20). Long sleep duration (>9 h) is associated with increased risk of incident CHD, stroke, and total CVD events (20). While much of this research comes from studies of single-item, self-reported assessments of habitual sleep duration (20), these findings are supported by studies that objectively measured (i.e., via actigraphy or polysomnography) sleep characteristics (7, 62, 133). Other sleep characteristics including sleep quality, regularity, and timing of sleep have been associated with CVD risk factors (62, 80). For example, Huang & Redline (62) found that greater objectively measured variability in sleep timing and duration was associated with higher prevalence and incidence of metabolic dysregulation, independent of sleep duration and other lifestyle risk factors.
Beyond these isolated sleep characteristics, research has also examined links between clinical sleep disorders (e.g., OSA and insomnia) and CVD risk and events. A meta-analysis of prospective cohort studies indicates that moderate-to-severe OSA predicts increased CVD risk, particularly stroke risk (36). Insomnia has been examined in relation to CVD both as a symptom and as a discrete disorder. Although insomnia is the most common sleep disorder and insomnia symptoms are highly prevalent in the general population, relatively less research has focused on insomnia as a risk factor for the development of CVD risk, compared with OSA. The available evidence is somewhat equivocal, perhaps owing to heterogeneity in the correlates and consequences of insomnia symptoms versus disorder and because certain subtypes or combinations of symptoms may be more strongly linked with CVD risk than others (68). For example, Troxel and colleagues (125) found that specific symptoms of insomnia, including difficulty falling asleep and poor-quality sleep, but not a syndromal definition of insomnia, were significant predictors of the development of metabolic syndrome in a cohort of black and white men and women. Furthermore, in a series of landmark studies, Vgontzas and colleagues (40, 131, 132, 134) demonstrated that insomnia coupled with short polysomnographic sleep duration strongly and significantly predict hypertension, metabolic dysfunction, depression, and mortality relative to insomnia with normal sleep duration. Thus, the insomnia short sleep phenotype may specifically convey higher risk for cardiovascular outcomes.
Collectively, these findings demonstrate the importance of considering multiple indicators of sleep health simultaneously as they relate to CVD and the underlying mechanisms that may explain why some sleep symptoms or disorders are more strongly linked with CVD outcomes. For example, laboratory-based studies provide convincing evidence that short sleep duration may contribute to CVD risk, in part through disruptions in metabolic dysregulation, autonomic functioning, and inflammatory processes (125). Similarly, insomnia is conceptualized as a disorder of physiologic and emotional hyperarousal, which may be associated with heightened sympathetic nervous system activation, hypercortisolemia, and activation of nuclear factor (NF)-κB [which serves a critical role in cellular inflammatory signaling (65)], all of which are implicated in the pathogenesis of CVD.
Building on the robust evidence linking sleep symptoms and disorders with CVD risk, intervention studies would provide the strongest demonstration of sleep as a causal risk factor. Such intervention-focused research (51, 114), however, has lagged far behind the observational studies of sleep and CVD risk, and the limited data to date are inconclusive. For example, a large, randomized clinical trial found that CPAP (continuous positive airway pressure) treatment did not prevent CVD events among patients with prevalent CVD (92). However, these findings have several limitations, including the fact that patients in this trial generally presented with OSA without daytime sleepiness and that CPAP compliance was low (3.3 h per night, on average). Future research should explore the hypothesis that specific OSA phenotypes, particularly those who present with more severe OSA and those with daytime sleepiness, may derive the greatest cardiovascular benefits from CPAP treatment (44). Furthermore, behavioral strategies to support the uptake of and compliance with treatments for OSA require further investigation (32). Finally, short-term studies focused on interventions to extend sleep duration and/or improve sleep quality suggest that improving sleep health holds promise as a strategy to reduce cardiovascular risk (51).
The obesity epidemic has multiple determinants ranging from genetics to eating behavior to environmental forces (33). Recent research on sleep health and circadian science highlights the role of sleep as an additional contributing factor to weight gain and obesity (6, 33, 86). Cross-sectional data indicate that short sleep duration is associated with increased odds of obesity among both children and adults. For example, a 2008 meta-analysis of data from 18 adult studies (n > 600,000) indicates that short sleep duration is associated with a 55% increase in odds for obesity (21). Although most of this research has relied on cross-sectional data, a meta-analysis of 11 studies (n ∼ 200,000) showed that the risk of incident obesity is 45% higher among those who report short sleep duration, with no longitudinal association between long sleep duration and incident obesity (144). Other dimensions of sleep health, including sleep variability, sleep timing, daytime napping, and low sleep efficiency, have all been associated with increased obesity, but they have been studied less frequently than sleep duration (96). There is less evidence of an association between insomnia disorder and obesity (25, 39). A meta-analysis of 67 studies showed no association between insomnia disorder and obesity and only a small positive association between insomnia symptoms and obesity (25).
Sleep health may influence obesity through multiple pathways, including the possibility that people who sleep less have more time available to eat per day (75, 115, 118). Experimental data show that sleep deprivation changes the hormones that regulate appetite, including increases in the hormone ghrelin, which causes hunger, and decreases in the hormone leptin, which regulates fullness (116, 122). In addition, sleep restriction causes behavioral changes such as larger portion size and food choices with higher caloric intake (19, 61). Finally, sleep loss also affects glucose metabolism (75, 115).
The circadian timing system may also serve as a critical link between sleep and metabolism. Circadian timing both influences and is influenced by the metabolic state of cells and organisms. Cellular energy metabolism at the molecular level is linked directly to the molecular circadian clock (88, 89). At the behavioral level, food can entrain the circadian timing system, and eating at an inappropriate circadian phase promotes weight gain and obesity in both animals and humans (6, 9, 88). Thus, restricting feeding/eating times within the appropriate circadian phase can both prevent obesity and result in weight loss (47, 59).
While there is strong and consistent evidence for the link between sleep health and obesity, it is essential to tease out the potential roles of reverse causality, bidirectionality, and third factors. Indeed, obesity (and related lifestyle factors such as diet and physical activity) may contribute to poor sleep health and sleep disorders, especially OSA (110). Despite these concerns, sleep and circadian-focused interventions, including sleep extension, regularizing sleep schedules, appropriate meal timing, and time-restricted eating, may serve as potential strategies for promoting weight loss, weight management, and improved glucose metabolism (28, 81, 123).
Depression and Mental Disorders
Sleep problems are a symptom of virtually every mental health condition, and sleep problems are even more prevalent in individuals with mental health problems as compared with the general population (78). For example, 65–90% of adults with major depressive disorder (MDD) report sleep problems, and 90% of children with depression report disturbed sleep (78). Sleep problems have traditionally been viewed as a consequence or symptom of a mental health condition rather than as a specific etiological agent that may play a causal role in the development of mental health issues. However, owing to robust, longitudinal, and prospective research, there is emerging consensus that sleep problems are a cause as well as a consequence of mental health problems. In fact, in 2005 the National Institutes of Health (NIH) issued a statement recommending that sleep problems no longer be routinely conceptualized as secondary to another disorder (95). This shift in recognizing the bidirectional associations between sleep and mental health has substantial implications for understanding the etiology of mental health.
The strongest evidence to date concerning a causal role of sleep in the development of mental health problems comes from prospective studies of sleep problems, particularly insomnia, and depression. For example, a meta-analysis of 34 cohort studies involving more than 170,000 participants with an average follow-up period of 60.4 months showed that insomnia symptoms significantly predicted the subsequent development of MDD (82). The pooled estimate across studies showed that those with insomnia at baseline had a more than twofold increased risk of developing MDD. Others have demonstrated prospective associations between insomnia and suicide (143) and anxiety (94, 103). More recent evidence has examined the role of insomnia in predicting the development of other mental health disorders including post-traumatic stress disorder (PTSD), bipolar disorder, and psychosis. For example, sleep problems and PTSD are highly prevalent in military populations and may be further heightened by prolonged and repeated deployments, as seen in the US military (124). Limited evidence suggests that insomnia predicts the development of PTSD in service members postdeployment (46, 138). Furthermore, sleep loss can precipitate mania symptoms in the context of bipolar disorder (58), and recent evidence indicates that sleep problems and disorders may increase the risk of psychosis and severity of psychotic episodes (84, 107).
The growing recognition that sleep problems not only co-occur with mental health problems but can also predict the onset of mental health problems has significant treatment implications and highlights important opportunities to identify transdiagnostic mechanisms that contribute to both poor sleep health and poor mental health. For example, untreated sleep problems predict poorer treatment prognosis (127) and greater likelihood of relapse (35), even for the most effective pharmacologic and/or behavioral treatments for depression. Moreover, recent findings from a large, randomized clinical trial demonstrated that treatment of insomnia, with cognitive behavioral therapy, led to reductions in psychotic experiences among university students (43). These promising findings provide strong evidence for a causal role of sleep disturbances in the development and exacerbation of mental health disorders and the potential for treating sleep problems as an important intervention target in the armament of strategies to support mental health.