Effects of Sleep Deprivation and Sleepiness on Society and Driving

Fig. 4.1

Social–ecological framework

The social–ecological model of sleep and health is based on this approach. The model, presented in Fig. 4.2, conceptualizes sleep in the context of both upstream and downstream factors. Downstream of sleep duration and quality lies adverse health outcomes of poor sleep. These may include weight gain/obesity, metabolic dysregulation, cardiovascular disease, inflammation, psychological disturbances, stress, and performance deficits. It is hypothesized that these, in aggregate, not only exacerbate each other but eventually contribute to overall morbidity and eventually mortality risk. Upstream of sleep lies the portion of the model that borrows heavily from the social–ecological framework. The model posits that sleep, as experienced by an individual, is best conceptualized in the context of three levels. First is the individual level. These are the individual’s own genetics, health, beliefs, choices, etc. These are the proximal causes of sleep experienced by that individual. Beyond the individual level, though, is the social level. This level, which borrows aspects of the microsystem, exosystem, and mesosystem, represents the immediate context of that individual. Factors at this level include neighborhood, culture, social networks, friends, and other systems that exist outside of the individual but to which the individual belongs. Two factors specifically stand out at this level and bridge most directly to the individual level. These include work/school and family/home. These two domains are hypothesized to exert the most influence (above individual-level factors) on sleep at the individual level. The third level is the societal level, within which the social level is situated. This borrows elements of the exosystem and macrosystem. Factors at this level represent structures that the elements at the social level are a part of, but exist outside of those factors. For example, factors at the societal level that influence sleep may include globalization, 24/7 society, public policy, and national geography.

Fig. 4.2

Social–ecological model of sleep and health. Adapted from Grandner, Hale, Moore, and Patel

Taken together, this model spells out the role of sleep on health, taking into account the individual and the social–environmental context. This way of thinking may be particularly useful about sleep. For example, when conceptualizing healthy sleep duration and quality, it is difficult to form a comprehensive understanding without taking into account work, family, and other contextual factors.

Health Effects of Sleep Deprivation

Sleep deprivation, whether in the laboratory or in “real-world” settings, is associated with a myriad of adverse outcomes. Any comprehensive summary would be beyond the scope of any single chapter. Of the outcomes that have been studied, effects can be generally conceptualized as neurocognitive (including stress, emotional processing, decision making, attention, and memory) and/or cardiometabolic (including obesity, cardiovascular disease, and diabetes).

Sleep-deprived persons report increased stress, and it is believed that both sleep loss and stress impact mood and emotion. Minkel et al. [7] compared stress handling in sleep-deprived participants with rested controls and reported greater subjective stress, anxiety, and anger in sleep-deprived participants than in rested controls following exposure to a low-stressor condition. High-stressor conditions did not produce varied response. Sleep deprivation may thus lower the psychological threshold for perception of stress from cognitive demands but does not selectively increase response magnitude to high stress performance demands [7]. In an earlier study, the same group had demonstrated that sleep-deprived healthy adults have less emotional expressiveness, especially in response to positive stimuli [8].

Van der Helm et al. investigated the impact of sleep deprivation on the ability to recognize the intensity of human facial emotions [9] in 37 healthy participants and randomly assigned them to total sleep-deprived (TSD) and sleep control (SC) group. This study found that sleep deprivation selectively impairs the accurate judgment of human facial emotions, especially threat relevant (anger) and reward relevant (happy) categories. This study suggests that sleep loss impairs discrete affective neural systems, disrupting the identification of salient affective social cues [9].

Many studies have examined the relationship between habitual short sleep duration and cardiometabolic disease [10, 11]. For example, a number of studies have found associations with obesity [10, 12–14], cardiovascular disease [10, 12, 15–18], stroke [12, 19], and diabetes [11, 12, 20–25]. Proposed mechanisms for these relationships include behavioral and physiological factors. Regarding behavioral factors, short sleep has been associated with overall unhealthy lifestyle choices [26–29] that could predispose to these conditions. Regarding physiological factors, four potential mechanistic pathways linking short sleep to cardiometabolic disease have been identified, representing metabolic, inflammatory, and sympathetic.

The metabolic pathway is represented by studies that have focused on food intake, insulin/glucose function, and secretion of hormones that play important roles in hunger and satiety [30]. Several studies have examined the role of sleep in food intake [31]. Overall, studies of laboratory samples have shown that acute sleep deprivation associated with an increase in energy intake of about 500 kcal per day [32–35]. In particular, the increase in energy intake seems largely confined to after dinner [34, 35]. Some studies have shown that acute sleep deprivation is associated with decreased leptin secretion and elevated ghrelin secretion. Leptin is a hormone secreted by adipose tissue and can be used as a marker of adiposity [36–38]. Some population-level studies have found that short sleepers secrete less leptin [39–44]. But this is complicated by the finding that short sleepers are more likely to be obese, thereby secreting more leptin due to more adipose tissue. This may explain why some studies have shown that short sleepers secrete more leptin overall [45, 46]. Ghrelin, a complement to leptin, is a hormone secreted by the stomach and tends to signal hunger [47–51]. Studies in the population have shown mixed results, perhaps due to a lack of sampling across the day and night [40, 41, 44, 52, 53]. The leptin/ghrelin system represents one aspect of the proposed metabolic pathway. The other main component is the insulin/glucose system. Studies in the laboratory show that acute sleep deprivation leads to temporary insulin resistance [54–60]. In addition, population-level studies have shown that habitual short sleepers are more likely to have diabetes, even using objective criteria including impaired fasting glucose [61].

The inflammatory pathway may also be relevant for the development of cardiometabolic disease. Inflammatory process contributes to all stages of cardiovascular disease, from the development of atherosclerostic plaques in the vascular wall to end-stage thrombotic complications [62]. Several studies have shown that acute sleep deprivation results in a pro-inflammatory state; in particular, studies have shown that sleep deprivation is associated with elevated levels of tumor necrosis factor alpha (TNF-α) [63, 64], interleukin-6 (IL-6) [63, 65, 66], and C-reactive protein (CRP) [66, 67]. Population-level studies have also shown short sleep to be associated with elevated TNF-α [68], IL-6 [69, 70], and CRP [15, 71].

The role of the sympathetic nervous system in the development of cardiovascular disease is well described [72, 73]. One of the primary mechanisms is through the hypothalamic–pituitary–adrenal (HPA) axis, which represents the regulatory/secretory system that induces the release of corticosteroids such as cortisol and catecholamines such as epinephrine (EPI) and norepinephrine (NE). For example, this is key in regulation of blood pressure [74, 75]. Several studies have shown that short sleep is associated with increased blood pressure [76, 77], and this may be reflected in 24-h blood pressure variability [78], which may represent downstream effects of HPA axis activation. A recent study showed that one of the mechanisms by which sleep deprivation disrupts insulin signaling is via alterations in protein kinase B phosphorylation in adipocytes [58]; it should be noted that the primary upstream signal for this process is sympathetic nervous system. In addition, several studies have shown that insufficient sleep is associated with increased HPA axis activity [79–84].

For example, Robertson and colleagues showed that even minor reductions in sleep duration lead to changes in insulin sensitivity, body weight, and other metabolic parameters which vary during the exposure period [85]. Further, short sleep duration is a significant independent risk factor for hypertension [86] and diabetes [87], perhaps because short sleepers demonstrate elevated ghrelin, and reduced leptin, which are likely to increase appetite, thus possibly explaining weight gain associated with short sleep duration [41].

Other systems have been implicated as well. For example, Specker and colleagues investigated the effect of chronic sleep deprivation on bones in 1146 individuals by performing bone measurements on distal radius, spine, and hip [88]. The study then compared bone measurements between sleep-deprived and sleep adequate individuals after controlling covariates. The study found that sleep-deprived women had lower bone mineral density than sleep adequate women and sleep-deprived men had lower levels of torsional bending strength, relative to than sleep adequate men.

Effects Across Age Groups

Sleep deprivation has implications across the age spectrum. For example, sleep-deprived adults manifest symptoms including daytime sleepiness, psychomotor slowing to impaired cognition, and memory. In contrast, children are more likely to present with emotional and behavioral symptoms, including aggressive and delinquent behaviors, attention and social problems, anxiety/depression, and hyperactivity. A number of studies have tried to elucidate the impact of sleep deprivation on children. Fallone and colleagues studied children aged 6–12 years and found a direct effect on academic performance and attention problems associated with reduced in sleep opportunity, even among students that had no prior history of behavioral or academic problems [89]. Touchettte and colleagues found that patterns of persistent short sleep duration or tendency for short sleep duration in childhood (2.5–6 years) predict high hyperactivity and impulsivity scores and poor performance on neurodevelopmental tasks at time of school entry (ages 5–6 years) [90]. A subsequent study aimed at investigating risk factors associated with short nighttime sleep duration and hyperactivity between ages 1.5 and 5 years using a large database of 2057 children found that children with high hyperactivity scores had a higher risk of short nocturnal sleep time (OR 5.1, 95 % CI [3.2–7.9]) than risk of finding high hyperactivity scores in short sleepers (OR 4.2, 95 % CI [2.7–6.6]). This, it may be the case that it is more plausible that hyperactivity may interfere with nighttime sleep duration rather than short sleep resulting in higher hyperactivity scores. Risk factors for having short sleep duration and high hyperactivity scores included male sex, low household income, lower maternal education and a pattern of receiving comfort outside the bed during nocturnal wakings at 1.5 years of age.

The trajectories of sleep problems between ages 4 and 16 years of age also correlate with general executive function at age 16 years [91]. Individuals whose sleep problems decrease more across time show better general executive control in late adolescence [91]. These findings suggest a probable critical period during childhood when disruptions to the stabilization and consolidation of sleep could very well result in the development of hyperactivity.

Other problems in children have been well documented. For example, the association between autism spectrum disorders (ASDs), attention deficit hyperactivity disorders (ADHDs), and disordered sleep has been commonly reported. Corkum and colleagues reported sleep problems in 25–50 % of children with ADHD [92]. Sleep problems are endemic to children with ASDs with a prevalence ranging from 40 to 86 % [93–96]. The prevalence of sleep disorders among children with ASD is higher than children with other development delays [97, 98] and is unrelated to intellectual quotient [99] or age [100]. In addition to these behavioral issues, several studies have documented poor health outcomes in sleep-deprived children, including metabolic syndrome [101] and visceral adiposity [102].

Questions regarding healthy adolescent sleep date back to 1975, when Webb and Agnew [103, 104] showed that on average, young people between the ages of 8 and 17 were getting 1.5 h less sleep per night than their counterparts did in 1910 and 1911. Since then, various studies and surveys have reported some degree of disrupted or deficient sleep in adolescents. According to the National Sleep Foundation, teens need between 8.5 and 9.25 h of sleep per night, with some laboratory data indicating that 9.2 h is optimal; thus, sleep deprivation can be defined as anything under about nine hours per night. Yet experts generally agree that most adolescents achieve less sleep. After analyzing data from a 2007 Youth Risk Behavior Survey data of US high school students, McKnight-Eily and colleagues found that nearly 70 % reported getting less than eight hours of sleep on school nights [105]. Emphasizing the value of awareness of the impact of sleep insufficiency, the authors agreed with other experts that chronic sleep deprivation in adolescents stems from “social, employment, recreational, and academic pressures as well as biologic changes” in the sleep–wake cycle.

Sleep needs do not markedly decline after puberty, perhaps because of the increased metabolic expenditures associated with growth during adolescence [106]. Yet Wolfson and colleagues, in a study of 3120 American high school students, reported a reduction in total sleep time of 40–50 min and a decline in the average amount of sleep on school nights from about 7.7 h for younger students to about seven hours for older ones [107]. The same study found that 26 % reported that they “usually” sleep less than 6.5 h per night [107]. The sleep loss was due to increasingly later bedtimes, while rise times were reported to be more consistent across ages (likely due to standard school start times). Not surprisingly, in surveys, 13–24 % of adolescents have reported falling asleep in class at least once [107]. Although one recent study concluded that US children and adolescents do get between nine and 10 h per night, as recommended, [108], an accompanying editorial cautioned, “We are still far from understanding what a ‘normal,’ ‘ideal,’ or ‘adequate’ sleep duration is for an individual child to promote optimal health and functioning.” [109]

Sleep time restores the neurocognitive functioning of brain [110, 111]. Curcio et al. [112] asserted that insufficient sleep in adolescence impairs behavioral, physiological, and neurocognitive processes vital for learning capacity and academic performance. Several studies involving actual manipulation of sleep in teenagers and college students have documented the effects of lack of sleep on cognitive functioning, showing impairment of psychomotor abilities, increase in sleepiness, poor memory and computational speed, reduced cognitive achievement, reduced awareness of cognitive impairments, and impaired performance on verbal creativity and abstract thinking [112]. Although the relationship between compromised neurobehavioral functioning and insufficient or disrupted sleep has been well studied in adults, relevant literature on children and adolescents is limited. That said, sleep disruptions in adolescents have also been associated with memory and attention deficits and declines in academic performance [107, 113]. McKnight-Eily and colleagues found that insufficient sleep was associated with many high-risk behaviors; for example, sleep-deprived teens were more likely to engage in physical fighting; seriously consider suicide; and use cigarettes, alcohol, and marijuana [105].

The response to a life stressor may be different among sleep-deprived adolescents. Talbot et al. investigated the impact of sleep deprivation in adolescents and adults on affective functioning and found that participants reported a greater increase in anxiety during a catastrophizing task when sleep deprived than when rested [114]. Further, chronic sleep restriction among adolescents may increase suicidal risk. Lee et al. [115] recruited 8530 students to investigate the association between behaviorally induced insufficient sleep and suicidality. They reported that adolescents with behaviorally induced insufficient sleep syndrome (BISS) had higher SSI score than those who slept 7 h or more on weekdays. They also found that weekend oversleep was associated with suicidality independently of depression, daytime sleepiness, snoring, and insomnia.

Effects Across Racial/Ethnic Groups

Several studies have attempted to understand whether habitual sleep patterns differ according to race/ethnicity group. Ruiter and colleagues [116] conducted a meta-analysis that found that Blacks/African-Americans obtained approximately 28 min less polysomnographic sleep than Whites; they also obtained less slow-wave sleep. These findings are consistent with those of other studies, who found that Blacks/African-Americans obtained less slow-wave sleep [117–121] and had a poorer sleep efficiency [119, 121] than non-Hispanic Whites. This suggests that, on average, for Blacks/African-Americans, sleep is less deep and less restful. Similarly, this meta-analysis evaluated 6 studies of subjective sleep duration [116] that found a similar pattern, with Blacks/African-Americans reporting less sleep on average than Whites (15.1 min less, p < 0.05) [116]. A few studies compared sleep among racial/ethnic groups using wrist actigraphy. Several studies reported significantly shorter mean sleep duration and poorer sleep quality for minorities compared to Whites [122–124]. Many of these effects persist after adjustments for socioeconomic factors.

Another approach that has been taken is to evaluate whether people of various groups are more or less likely to report sleep duration by category (usually short or long, relative to normative [7–8 h]). Hale and Do [125] found that, relative to non-Hispanic White Americans, Blacks/African-Americans, non-Mexican Hispanics, and those in the “Other” category were more likely to be short sleepers. Regarding long sleep duration, the only group that was more likely than non-Hispanic Whites to be long sleepers (9 or more hours) was Blacks/African-Americans. Similarly, Nunes and colleagues found that Blacks/African-Americans were less likely to report sleep of 7–8 h, versus non-Hispanic Whites, with increased likelihood of both short and long sleep [126] and Stamatakis and colleagues [127] found that African-Americans were about twice as likely to be short sleepers, and those in the “Other” category were approximately 50 % more likely.

In a more recent study, Whinnery and colleagues examined nationally representative data from the 2007–2008 National Health and Nutrition Examination Survey [128]. The sleep duration categories examined were very short sleep (less than 5 h), short sleep (5–6 h), and long sleep (9 or more hours), compared to normal sleep duration (7–8 h). Those who identified as Black/African-American were approximately 3 and a half times as likely to be a very short sleeper; similarly, non-Mexican Hispanics/Latinos were approximately 3.5 times as likely and Asians/Others were approximately 5 times as likely to be a very short sleeper. Regarding short sleep, those who identified as Black/African-American were about twice as likely to be short sleepers, and those who identified as Asian/Other were approximately 2 and a half times as likely. Mexican–Americans were 60 % less likely to be long sleepers.

This study also examined the degree to which these relationships are attenuated by other factors, including age, sex, relationship status, primary language spoken at home, immigration status, education, income, access to health insurance, home ownership, and food security. Self-identified Blacks/African-Americans were approximately 2.5 times as likely to be very short sleepers and approximately twice as likely to be short sleepers. Mexican–Americans were approximately 60 % less likely to be long sleepers. Non-Mexican Hispanics/Latinos were approximately 2.7 times as likely to be very short sleepers, and Asians/Others were approximately 4 times as likely to be very short sleepers and twice as likely to be short sleepers [128].

It is possible that sleep plays an important role in health disparities. Knutson and colleagues [129] found that racial differences in 5-year change in blood pressure were mediated by differences in sleep duration. In another study, Grandner and colleagues [15] found that the relationship between sleep duration and C-reactive protein (a cardiovascular risk marker) differed by race. Grandner and colleagues also examined whether the relationship between sleep duration and cardiometabolic disease risk depended on race/ethnicity [61]. For all outcomes (self-reported and objectively determined hypertension, hyperlipidemia, diabetes, and obesity), race/ethnicity by sleep duration interactions was significant (all p < 0.0001). When the sample was stratified by self-identified race/ethnicity, different patterns emerged.

Effects for Men and Women

Though the response to altered sleep homeostasis is uniform in general, variation based on gender has been studied across different age groups. In a study aimed at examining gender differences in sleep habits in 11–13 year olds, Natal et al. [130] studied a cohort of 200 students based on a questionnaire. The authors found that girls displayed longer sleep duration over the weekend in comparison with boys.

Arber et al. [131] studied gender and socioeconomic patterning of self-reported sleep problems in Britain using the British Psychiatric Morbidity Survey 2000. The authors report that women reported significantly more sleep problems than men, as did the divorced and widowed compared with married respondents. After adjusting for socioeconomic characteristics, the sleep problems were halved, suggesting a major role for socioeconomic status in these gender differences.

Rodriguez-Munoz et al. [132] studied 240 physicians in Madrid with the aim to assess insomnia and sleep quality in primary care physicians. The study reported a higher frequency of insomnia among women (23 %) compared to men (9.6 %). This relationship between gender and insomnia remained significant even after controlling sociodemographic variables. In terms of sleep quality, as defined by Pittsburgh Sleep Quality Index (PSQI) score of 5 or more than 5, the study reported women scored significantly higher than men on global sleep quality. Sleep problems were more prevalent among women than men (40 vs. 25.3 %).

Goel et al. [133] studied gender differences in polysomnographic sleep in 31 young men and women over a three consecutive overnight sessions in a sleep laboratory. They concluded that women have better sleep quality (shorter sleep onset latency, higher sleep efficiency) compared with men. Yet women of all adult age groups have been found to report more sleep problems, such as inadequate sleep duration and insomnia [134, 135].

Similarly, the susceptibility to various sleep disorders and their consequences differ among men and women. Morrish et al. [136] compared the mortality risk of men and women who were diagnosed with obstructive sleep apnea and were receiving treatment with CPAP between 1995 and 1998 by reviewing hospital records of 292 men and 47 women. Eighty percent of men died compared to 23 % of women (p = 0.003). There was a 3.44 greater mortality risk of women diagnosed with OSA and treated with CPAP, mostly due to greater comorbidity. Also, Johnson et al. [137] studied 1014 adolescents from a random sample of an urban health maintenance organization population and found no difference in risk of insomnia in prepubertal girls compared with boys—but the onset of menses in girls conferred a 2.75-fold increased risk of insomnia.

Effects According to Relationship Status

Sleep and spousal relationship/cohabitational status have been a topic of much recent interest. Various studies have tried to decipher the exact nature of such relationship. Troxel et al. [138] conducted an observational longitudinal study aimed at finding associations between marital status and cohabitation history and sleep in midlife women. The authors reported that at the time of the study, partnered women had better sleep quality than unpartnered women; however, with covariate adjustment, most of these associations become nonexistent. Additionally, the prior history showed advantages in sleep for women who were consistently partnered versus women who weren’t consistently partnered. This association persisted even after covariate adjustment.

Research suggests that divorced individuals, particularly women, have higher rates of sleep disturbances as compared to married individuals [139]. However, all marriages and marital relations are not equal. So does marital quality translate into better sleep? This was explained by Troxel et al. [140] in a multi-site, multiethnic, community-based study that examined the association between marital happiness and self-reported sleep disturbances in a sample of 2148 midlife women drawn from the Study of Women’s Health Across the Nation (SWAN). The Dyadic Adjustment Scale was used to assess marital happiness, and sleep disturbance was assessed using 4 items from the Women’s Health Initiative Insomnia Rating Scale (WHIIRS). After controlling for relevant covariates, maritally happy women reported fewer sleep disturbances, with the association evident among Caucasian women and to a lesser extent among African-American women. In an earlier study, Troxel et al. in 2007 [141] had found that women with bed partners display better sleep efficiency and that married women have shorter sleep latencies as compared with never-married women.

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