In a series of classic studies, Webb and colleagues [49, 50] found that short sleep in the laboratory was associated with less stage 2 and rapid eye movement (REM) sleep but equivalent amount of slow wave sleep (SWS) as compared to normal and long sleep. These findings were later replicated by Benoit and colleagues [51–53], who found that short sleepers do not exhibit different amounts of SWS (whole night) nor do they exhibit cycle by cycle differences in SWS as compared to normal duration sleepers.

Perhaps the most proximal consequence of sleep loss is a resultant increase in “sleepiness” (sleep propensity). Assessment of sleepiness usually involves measurement of sleep in situations in which sleep is not appropriate or desired [54]. Individuals who experience partial or total sleep deprivation demonstrate increased sleepiness [39, 55]. This finding has been replicated across three methods of objective assessment of sleepiness: the multiple sleep latency test, maintenance of wakefulness test, and measurements of oculomotor activity [39, 56–58].

Assessments of neurobehavioral consequences of sleep loss are among the most common outcomes assessed in sleep deprivation studies. This is usually operationalized as sustained attention [38]. The most well-validated measure of sustained attention in this context is the psychomotor vigilance task (PVT) [38, 59]. The PVT has been consistently used to show that sustained attention decreases with sleep restriction in a dose–response manner as sleep opportunity is reduced from 7 to 3 h [38, 39]. Additionally, deficits accumulate across several days [38, 39]. Other work has demonstrated that sleep deprivation is also associated with deficits in executive function [60], learning [61], and memory [62].

There has been significant discussion of the role of impaired functioning due to sleep loss in auto accidents [63–68]. There is a strong evidence that sleepiness is a major factor contributing to automobile accidents [69–71]. Several papers have shown that accidents are related to sleepiness caused by sleep apnea [69, 72, 73] and prolonged wakefulness [71, 74, 75]. Some evidence also suggests that short sleepers may exhibit more sleepiness than average [76, 77], but currently there are very limited data to support the claim that short sleepers are more likely to experience auto accidents [78], though some evidence exists [79].

In his classic series of studies subjecting rats to extreme sleep deprivation, Rechschaffen and colleagues found that sleep-deprived rats became hyperphagic, even though they demonstrated a depletion of energy reserves [80]. At the time, this was not generally considered in a context of linking sleep with metabolism. However, in a landmark study published in 1991, Van Cauter and colleagues studied metabolic effects of sleep deprivation in eight healthy subjects [81]. This study found that sleep deprivation had a negative impact on glucose tolerance and insulin resistance, but problems resolved with recovery sleep. Since then, several studies have replicated and extended those findings.

Spiegel and colleagues studied 11 young men in the laboratory following a condition of 12 or 4 h in bed [82]. Insulin and glucose measures were obtained during intravenous glucose tolerance test (IVGTT) and after meals 5 and 10 h later. No differences were seen following the meals. However, during the fasting IVGTT, glucose and insulin were both lower, reflected in a lower homeostatic model assessment of insulin resistance value (HOMA-IR—a product of insulin and glucose readings that denote insulin resistance). In a follow-up study, Spiegel and colleagues [83] studied subjects who spent two nights of 10 h in bed (2200–0800), versus two nights of 4 h in bed (0100–0500) in a crossover design. After the second night of each bedtime condition, caloric intake was replaced by an intravenous glucose infusion at a constant rate to avoid fluctuations of hunger and appetite related to meal ingestion. Even though sleep duration was manipulated for only two nights, the glucose and insulin profiles obtained during continuous glucose infusion were consistent with the results obtained using IVGTT in a previous study of six nights. In the early part of the day, after 2 days of short bedtimes, glucose levels were higher and insulin levels were lower than after 2 days of longer bedtimes. These findings have since been replicated in other studies that have shown that sleep deprivation can lead to insulin dysregulation [84–86] .

In addition to insulin and glucose, the hormones leptin and ghrelin have also been studied relative to sleep deprivation. Leptin is a hormone that plays a key role in regulating energy intake and energy expenditure. It is secreted by adipose tissue and inhibits appetite at the level of the hypothalamus by counteracting neuropeptide Y (an appetite stimulant) and promoting aMSH (an appetite suppressant). Leptin is generally viewed as an adiposity signal. It decreases with fasting, increases with stress, and decreases with physical activity. Elevated leptin is associated with decreased food consumption, though obese individuals become resistant to its effects. Ghrelin, on the other hand, is a hormone that is frequently considered as the counterpart to leptin. It increases prior to meals and is associated with hunger. It stimulates food intake and activates reward pathways that play a role in the “reward” function of foods. Ghrelin is decreased in obesity, and the normal nocturnal rise in ghrelin is blunted by obesity. Several studies have shown that sleep deprivation is associated with decreased leptin and increased ghrelin [83, 87–89]. If this is the case, a decrease in leptin and an increase in ghrelin (especially in an individual who is obese) would likely lead to an orexigenic eating pattern that could result in weight gain and diabetes over time.

Cardiovascular end points are usually difficult to measure in short-term human laboratory studies, since only indirect markers of cardiovascular health are possible and these tend to change very slowly. However, there are several laboratory studies that suggest a causal role of sleep deprivation in cardiovascular disease (CVD) risk. Lusardi and colleagues [90] studied ambulatory blood pressure in 18 healthy subjects across a typical night of sleep, and sleep restricted to the second half of the night only, 1 week later. They observed that the sleep restriction condition was associated with elevated systolic and diastolic blood pressure, especially in the early parts of the night (no normal nighttime dipping when the subject was awake). These blood pressure changes may translate into daytime effects as well. Tochikubo and colleagues found that daytime mean systolic and diastolic blood pressure increased after a night of restricted sleep (mean 3.6 h) [91]. The mechanism for this is not clear. One study found that restriction to five nights of < 5 h of sleep caused a significant increase in cardiac and peripheral sympathetic modulation, associated with a decrease in endothelial-dependent venodilation, suggesting that acute sleep loss affects endothelial function, potentially through the acetylcholine system [92]. Also, in a study of 27 individuals whose sleep opportunity was less than half of usual, the sleep deprivation condition was associated with a reduction in left atrial early diastolic strain rate in the absence of geometric alterations, suggesting that sleep deprivation may be associated with functional impairments in the left atrium [93].

Sleep deprivation may also interact with cardiovascular responses to stress. For example, sleep deprivation amplified the increased systolic blood pressure associated with psychological stress [94]. Also, 24-h total sleep deprivation was found to amplify heart rate increases in response to mental stress and a cold pressor test, even after recovery [95].

Inflammation is well established as a key mechanism in the development of CVD [96]. Recently, the following pro-inflammatory biomarkers have demonstrated (or suggested) associations with sleep deprivation in the laboratory: tumor necrosis factor α (TNFα); interleukins 1 (IL-1), 6 (IL-6), and 17 (IL-17); and C-reactive protein (CRP).

Regarding TNFα, in a study that evaluated the effects of 12 nights of sleep restriction to 6 h, 24-h TNFα secretion was elevated in men, but not in women [97]. Several laboratory studies have also assessed interleukins. In a study of five nights of sleep restriction to 4 h, 13 healthy young men demonstrated elevated IL-1β at the messenger RNA (mRNA) level but not the protein level [98]. Regarding IL-6, in a study by Haack and colleagues, IL-6 was elevated after 12 days of 4 h of sleep, relative to 8 h. These elevations were associated with increased pain ratings [99]. In another study, after 12 nights of 6 h of sleep, 24-h IL-6 secretion was elevated, relative to 8 h [97]. In a more recent study, after five nights of sleep restriction to 4 h, 13 healthy young men demonstrated elevated IL-6 at the mRNA level but not the protein level [98]. To date, one study has examined sleep restriction in the context of IL-17. After five nights of sleep restricted to 4 h, 13 healthy young men demonstrated elevated IL-17 at the mRNA level and at the protein level [98].

Several studies have investigated whether partial sleep deprivation results in increased CRP levels. Meier-Ewert and colleagues [100] found that during partial sleep deprivation, CRP levels increased significantly. A more recent study by van Leeuwen and colleagues [98] also found that following sleep restriction, CRP was increased compared to baseline (145 % of baseline, p< 0.05), and continued to increase during recovery (231 % of baseline, p< 0.05).

Self-reported short sleepers likely include many individuals who also suffer from sleep disorders or, at least, report significant levels of sleep symptoms. This is important to consider, since sleep duration is often discussed as either a separate construct from sleep disturbance or synonymous with sleep disturbance. These data suggest a more complicated picture, where short sleep findings not only partly reflect effects of duration per se but also partly reflect issues of sleep quality. For example, a study by Grandner and Kripke [101] found that habitual short sleepers are more likely to report difficulty falling asleep, difficulty maintaining sleep, nonrestorative sleep, and daytime sleepiness, compared to 7–8-h sleepers. Although several studies of sleep duration have accounted for some of these issues, it is important to note that many do not.

Over 40 years of evidence indicates a strong association between nightly sleep duration and mortality risk [102, 103]. Overall, sleep duration is associated with mortality in a U-shaped fashion, with the highest risk found for short and long sleepers and the lowest risk in individuals who report average sleep durations of 7–8 h. Gallicchio and Kalesan [104] conducted a meta-analysis of 23 studies investigating the association between sleep duration and mortality conducted from 1979 to 2007. Using random-effects meta-analysis, the authors report that the pooled relative risk (RR) for all-cause mortality for short sleep was 1.10 (95 % CI = (1.06, 1.15)), with cardiovascular-related RR at 1.06 (95 % CI = (0.94, 1.30)) and cancer-related RR at 0.99 (95 % CI = (0.88, 1.13)). For long sleep, RR for all-cause mortality was 1.23 (95 % CI = (1.16, 1.30)), with cardiovascular RR at 1.38 (95 % CI = (1.13, 1.69)) and cancer RR at 1.21 (95 % CI = (1.11, 1.32)). In a more recent meta-analysis, including 16 published studies from 1993 to 2009, Cappuccio and colleagues examined whether evidence supports the presence of a relationship between duration of sleep and all-cause mortality and to obtain an estimate of the risk [105]. This meta-analysis demonstrated larger effects, including an RR = 1.12 (95 % CI = (1.06, 1.18)) for short sleep and RR = 1.30 (95 % CI = (1.22, 1.38)) for long sleep. In general, habitual sleep duration is associated with mortality. Specifically, both short and long sleep durations are associated with elevated risk, albeit through potentially different mechanisms [15, 21, 106, 107]. The exact pathways by which this risk is conferred are not well known. One possibility is that both short and long sleep durations are associated with elevated risk of cardiometabolic disease, which could contribute to mortality.

Several dozen studies, in various settings, using various approaches, have documented that short sleep duration (variously defined) is associated with obesity and/or adiposity and/or weight gain [106, 108–120]. As an example of one such study, sleep duration from the 2009 Behavioral Risk Factor Surveillance System (BRFSS) was assessed relative to obesity. In unadjusted analyses, sleep duration of less than 5 h was associated with an additional 2.7 body mass index (BMI) points, and sleep duration of 5–6 h was associated with an additional 0.8 BMI points (relative to 7 h) [121]. In a separate analysis, each day of the week, the participants reported insufficient sleep were associated with 0.2 more BMI points. After adjusting for numerous covariates, relationships for < 5 h of sleep and insufficient sleep remained. When insufficient sleep and sleep duration were entered into the same statistical model, along with covariates, the effect for < 5 h of sleep remained. This suggests that there is a robust association between very short sleep duration and BMI, which is not accounted for by perceived insufficient sleep.

In addition to cross-sectional studies, several prospective studies have linked short sleep duration with incident weight gain. Data from the Nurse’s Health Study found that sleep duration of less than 6 h increased likelihood of gaining > 15 kg over 16 years [122]. In a study of Japanese men, a similar pattern was found, with incident obesity over 1 year significantly higher among 5-h sleepers (odds ratio (OR) = 1.5) and < 5-h sleepers (OR = 1.9), relative to 7-h sleepers [123].

Several studies have demonstrated population-level associations between short sleep duration and diabetes. There are a number of reviews that summarize many of these studies [108, 109 115, 116, 124, 125]. Since the publication of these reviews, there have been a number of studies that further extend our understanding of this association. Buxton and Marcelli [126] found that sleep duration of < 7 h, as assessed using the 2004–2005 National Health Interview Survey (NHIS), was associated with elevated diabetes risk in the American population. Using the 2008 BRFSS, Shankar and colleagues found that self-reported insufficient sleep was positively associated with prevalence of diabetes [127]. However, Vishnu and colleagues note that, in this same sample, the relationship depended on race/ethnicity—it was significant in all groups except non-Hispanic Blacks [128]. In an analysis of the 2005 NHIS, Zizi and colleagues, however, found that both Black and White respondents who were short sleepers (6 h or less) were at increased risk of also reporting diabetes, and that this relationship was significantly stronger in the Black respondents [129]. Complaints of sleep disturbance may also play a role. Using the 2006 BRFSS, Grandner and colleagues showed that sleep disturbances (broadly defined as difficulty initiating or maintaining sleep or sleeping too much) were associated with diabetes prevalence [130, 131]. The extent to which the relationship depends on sleep duration itself or the perceived unmet sleep need is unclear. To address this question, Altman and colleagues used the 2009 BRFSS, which assessed sleep duration and insufficient sleep. This study found that any association is likely driven more by short sleep duration, rather than perceived unmet sleep need [121].

In a study of Japanese men, sleep duration of < 5 h was associated with approximately 63 % elevated risk for diabetes [132]. Another study of Japanese men found that sleep of 5 h or less was associated with greater likelihood of untreated diabetes [133]. Similarly, a study from Iran found that 5 h or less of sleep was associated with impaired fasting glucose [134].

Short sleep duration may also be associated with development of diabetes. In the Western New York Study, Rafaelson and colleagues found that sleep duration < 6 h was associated with development of impaired fasting glucose [135]. This relationship appeared to be partially mediated by insulin resistance. In a study of nondiabetic Japanese government workers, short sleep duration of 5 h or less was associated with a greater than fourfold increased likelihood of developing diabetes [136]. Data from the National Cheng Kung University Hospital in Taiwan showed that short sleepers (< 6 h) were approximately 55 % more likely to present with newly diagnosed diabetes, but not prediabetes. However, a study from New Zealand did find an association between short sleep duration and prediabetes [137]. This study also documented an association between sleep duration at age 32 and HbA_1C levels.

Hoevenaar-Blom and colleagues [138] conducted a 12-year prospective study of 20,432 men and women in the Netherlands with no history of CVD to investigate the association between short and long sleep duration and total CVD and coronary heart disease (CHD) incidence, independent of other modifiable lifestyle factors . Compared to people who slept 7–8 h, short sleepers (defined as those individuals who slept ≤ 6 h) had a 15 % higher risk of total CVD incidence (hazard ratio (HR): 1.15; 95 % CI: 1.00–1.32) and a 23 % higher risk of CHD incidence (HR: 1.23; 95 % CI: 1.04–1.45). It also appears that the quality of sleep for those people sleeping ≤ 6 h adds additional risk for CVD. When compared to individuals with normal sleep duration and good sleep quality, short sleepers with poor subjective sleep had a 63 % higher risk of CVD (HR: 1.63; 95 % CI: 1.21–2.19) and 79 % higher risk of CHD incidence (HR: 1.79; 95 % CI: 1.24–2.58) .

Other recent studies have also demonstrated an association between short sleep duration and CVD. For example, using the Coronary Artery Risk Development in Young Adults (CARDIA) data, Knutson and colleagues found that shorter sleep durations were associated with elevated systolic and diastolic blood pressure , as well as adverse changes in blood pressure over 5 years [139]. Also, Buxton and Marcelli [126] found that short sleep duration is associated with increased prevalence of hypertension and CVD, using the 2004–2005 NHIS data. In a recent analysis of data from the BRFSS, Altman and colleagues [121] found that short sleep duration was associated with elevated prevalence of hypertension, hyperlipidemia, and history of heart attack and stroke. This study also found that the risk was particularly elevated in those reporting < 5 h of sleep (though there was some elevated risk associated with 5–6 h). Also, when self-reported insufficient sleep was assessed, irrespective of sleep duration, days per week of insufficient sleep was also associated with these outcomes. When sleep duration and insufficient sleep were evaluated simultaneously (looking for unique effects of one or the other), insufficient sleep was uniquely predictive of hypertension and hyperlipidemia, whereas sleep duration was uniquely predictive of hypertension, heart attack, and stroke history .

The role of short sleep in predicting cardiovascular mortality has also been assessed via meta-analysis. In a review of 15 studies including 474,684 male and female participants, Cappuccio and colleagues [140] found that short sleep (defined as ≤ 5–6 h) was associated with an RR of 1.48 (95 % CI: 1.22–1.80) and long sleep (defined as > 8–9 h) was associated with an RR of 1.38 (95 % CI: 1.15–1.66) of dying or developing CHD. Similarly, the RR of developing CHD or dying from stroke was 1.15 (95 % CI: 1.00–1.31) for short sleep and 1.65 (95 % CI: 1.45–1.87) for long sleep .

Several studies have assessed inflammatory markers in population samples that assessed self-reported sleep duration. In a study of mothers, sleep duration of < 5 h at 1 year post partum was associated with elevated IL-6 at 3 years post partum [141]. Large epidemiologic cohorts have been leveraged to examine associations between sleep duration and CRP levels in general population samples. Miller and colleagues reported a null association between short and long sleep durations and CRP among men in that cohort after adjusting for covariates. Among women, though, long sleep (≥ 9 h) was associated with a 35 % increase in CRP levels after adjusting for age, marital status, BMI, smoking, systolic blood pressure, and triglyceride levels [142]. Evidence of a significant association between short sleep and CRP among women was also reported in fully adjusted models. A significant relationship between short sleep duration (assessed using polysomnography) and CRP was also found for women enrolled in the Study of Women’s Health across the Nation (SWAN) Study [143]. Further analysis showed a significant interaction with race/ethnicity, and post hoc analyses clarified that this relationship only existed among African American women. However, not all studies have documented significant relationships. In the Wisconsin Sleep Cohort ( N = 907), no association was seen between CRP and short or long sleep duration in adjusted models [144]. In this case, investigators examined self-reported as well as polysomnography-assessed sleep duration, and also evaluated quadratic terms in their analysis. This study also did not demonstrate sex-stratified or race-stratified results; however, these findings are based on a sample of predominantly Caucasian participants. Additionally, Suarez and colleagues [145] did not report a significant association between sleep duration and CRP among men, but the small sample size ( N = 210) and younger age group (mean age 28) may account for this.

A recent study utilizing the 2007–2008 National Health and Nutrition Examination Survey (NHANES) cohort aimed to discern relationships between sleep duration and CRP in the American population ( N = 5587), while addressing some of the sample size and generalizability limitations of previous studies. [146] To address issues of low variability of CRP in the population, a polynomial regression analysis examined whether there was a linear trend or a U-shape, even in the absence of any significant elevations among sleep duration groups, relative to 7 h. To address the issue of overly inclusive sleep duration categories (that may obscure effects at the extremes of sleep duration), sleep duration was assessed as < 5, 5, 6, 7, 8, 9, and 10 + h, with 7 h as the reference group. To address sex differences, analyses were conducted with men and women both combined and separate. To address race/ethnicity differences, interaction terms and stratified analyses looked at patterns in different groups. Linear and squared terms were significant in all models in the complete sample, with notable differences by sex and ethnoracial group. Overall, in models adjusted for sociodemographics and BMI, different patterns were observed for non-Hispanic White (elevated CRP for < 5 h and > 9 h), Black/African American (elevated CRP for < 5 and 8 h), Hispanic/Latino (elevated CRP for > 9 h), and Asian/other (higher in 9 and > 9 h and lower in 5 and 6 h) groups. Ethnoracial groups also demonstrated patterning by sex. For example, long sleep effects were more prominent among women.

When fibrin is degraded, one of the products is d-dimer, a biomarker of the formation of thrombotic disorders. Although d-dimer levels are usually very low, elevations have also been seen in other conditions such as liver disease, pregnancy , and post surgery. One previous study found that shorter sleep duration was associated with elevated d-dimer. In this same study, d-dimer was negatively associated with sleep quality measured with the Pittsburgh Sleep Quality Index [147]. Also, one previous study found that both short sleep duration (< 6 h) and long sleep duration (> 8 h) were associated with elevated intercellular adhesion molecule (ICAM) in a Taiwanese cohort. [148]

Several studies have examined associations between self-reported sleep and diet. In a study of adolescents , data from the Healthy Lifestyle in Europe by Nutrition in Adolescence (HELENA) study across several European countries found that short sleepers were less likely to be consuming the recommended levels of fruits, vegetables, fish, skim milk, breakfast cereals, and other foods. Also, shorter sleep duration was associated with increased consumption of pizza, burgers, and pasta [149]. In the Cleveland Children’s Sleep and Health Study, short sleep duration was associated with greater energy intake (~200 kcal), greater proportion of calories from fat, lower proportion of calories from carbohydrates, and more calorie consumption in early morning (5:00–7:00) [150].

In adults, data from a study of Japanese factory workers from 1992 to 1998 found that shorter seep duration was associated with more irregular meal timing and eating habits in general, more snacking between meals, more dining out, less consumption of vegetables, more preference for strongly flavored food, and no difference in preference for oily food [151]. Recent data from NHANES examined dietary data gathered from a comprehensive 24-h recall relative to sleep duration. Regarding sleep duration, food variety differentiated groups, with very short (< 5 h), short (5 h), and long (9 + h) sleepers, reporting fewer foods in their diet. Regarding macronutrients, after adjusting for overall diet, demographics, socioeconomics, and other health factors, a pattern was found where very short sleepers consumed less protein and carbohydrates than 7–8-h sleepers did. Analysis of micronutrients was done in two ways. First, nutrients were entered into linear regression analyses, adjusting for a number of covariates. From these analyses, very short sleep (< 5 h) was associated with less thiamin, folate, phosphorus, iron, zinc, and selenium. Short sleep (5–6 h) was associated with less water, and long sleep (9 + h) was associated with less phosphorus and more alcohol. In a stepwise regression analysis (which accounts for intercorrelations among nutrients), very short sleep (< 5 h) was associated with less water and lycopene; short sleep (5–6 h) was associated with less vitamin C, water, and selenium, and more lutein/zeaxanthin; and long sleep (9 + h) was associated with less theobromine and choline, and more alcohol [152].

Few studies have assessed whether habitual short sleepers exhibit any neurobehavioral performance impairments. A recent study showed that among an epidemiologic sample in the USA, short sleepers were more likely to report nodding off or falling asleep at the wheel. Overall, 3.6 % of the population reported drowsy driving. Self-identified short sleepers reported drowsy driving more often, and long sleepers, less often. For example, compared to those reporting sleeping 7–8 h, those reporting 5 h or less per night were over 3.5 times as likely to report nodding off or falling asleep at the wheel and those reporting 6 h were nearly twice as likely. Participants in this study were also asked how often they experience insufficient sleep. Among those who reported insufficient sleep 7 nights/week, effects were greater. Compared to those reporting 7–8 h of sleep, those reporting less than 5 h were more than four times as likely and those reporting 6 h were more than three times as likely to report nodding off. Surprisingly, when analyses were restricted to only those who report 0 nights/week of insufficient sleep, significant differences remained. Compared to those reporting 7–8 h of sleep, those who reported less than 5 or 6 h were more than 2.5 times as likely to report nodding off at the wheel [79]. Although other research suggests that short sleepers may not be at higher risk for driving accidents [78], the above findings suggest that some cognitive impairments may exist due to inability to maintain vigilance.

Several studies have examined associations between sleep duration and race/ethnicity in cohort studies. Hale and Do found that, compared to White adults, Black, non-Mexican Hispanic, and other non-Hispanic minorities were more likely to be short sleepers, and Black adults were more likely to be long sleepers [166]. In a study by Nunes and colleagues that analyzed data from the NHIS, Black Americans were more likely than White Americans to sleep 5 or less, 6, and 9 h or more [167]. These data are supported by a meta-analysis, in which Ruiter and colleagues demonstrated that African Americans slept less than White Americans, whether sleep was assessed objectively or subjectively [168].

This relationship is complex in the consideration of differential experience of sleep difficulties. For example, Grandner and colleagues [169] assessed > 150,000 American respondents to the 2006 BRFSS and found that Black/African American, Hispanic/Latino, and Asian/other women were less likely than White women to report sleep disturbances, and Asian/other men were less likely than White men to report sleep disturbances. This finding may be partially due to response biases to the survey items. To illustrate this, in a more recent study, Grandner and colleagues [170] evaluated sleep symptoms asked as part of the 2007–2008 NHANES. Difficulty falling asleep was assessed via an elicited complaint (asking for how often respondents have difficulty) and by asking for a typical sleep latency (and dichotomizing around 30 min). When respondents were asked if they had difficulty falling asleep, those in minority groups generally reported fewer complaints than White respondents. However, when the question was asked in a nonjudgmental way (just asking for sleep latency, without any indication of what is a complaint of a problem), minority groups were more likely to report sleep latencies greater than 30 min. This suggests that assessing subjective sleep across racial/ethnic groups is complicated by how the question is asked.

In an analysis of NHIS data by Krueger and Friedman [171], sleep duration was associated with household income, such that the shortest and longest sleep durations were associated with the lowest household income. Similarly, Stamatakis and colleagues demonstrated that those in the lowest income quintile are 54 % more likely to report short sleep duration [172], and this likelihood declines in higher income categories in a dose–response manner. In a recent analysis of the 2009 BRFSS data, increased amounts of self-reported insufficient sleep were associated with decreased household income; however, these relationships were completely accounted for by other demographic, social, and health factors, suggesting that it is these factors that link income with insufficient sleep [173]. Other socioeconomic factors are also related to sleep difficulties. For example, Grandner and colleagues [170] showed that (in adjusted analyses) lower education is associated with long sleep latency, snorting/gasping during sleep, and snoring; lack of access to private health insurance is associated with long sleep latency; and food insecurity is associated with long sleep latency, difficulty falling asleep, difficulty maintaining sleep, early morning awakenings, nonrestorative sleep, sleepiness, snorting/gasping during sleep, and snoring. Although these relationships were adjusted for racial/ethnic variables, other studies have shown that the relationship between sleep quality and socioeconomics depends on race [174].

Several studies have shown that marital status and relationship quality are associated with sleep. For example, compared to married adults, those who are single, part of an unmarried couple, divorced, and separated are more likely to report sleep disturbance in general [169]. Being divorced is also associated with increased likelihood of early-morning awakenings, nonrestorative sleep, and daytime sleepiness [170]. A comprehensive review of research relating relationship quality to sleep is provided by Troxel and colleagues [175].