Sleep, Stress, and Burnout

Sleep, Stress, and Burnout

Torbjörn Åkerstedt, Aleksander Perski, and Göran Kecklund Abstract Long-term exposure to stress is usually seen as a major cause of insomnia. Cross-sectional studies consistently support this view and demonstrate close relations between reported stress and impaired sleep. Prospective studies are rare, however, but the few that are available indicate that new cases of insomnia follow increases in prior stress at work. With respect to polysomnography, minor effects, such as a slightly increased sleep latency or sleep efficiency, follow periods of increased stress. The level of stress in these studies is usually rather modest, however. One key factor seems to be worries at bedtime, often related to upcoming difficulties during the subsequent day: anticipatory stress seems to be important and often involves bedtime rumination. One interesting link between sleep loss and stress is their similarity of endocrine/metabolic effects. Both involve increased levels of cortisol, lipids, and insulin resistance, for example. Furthermore, typical “stress diseases” such as cardiovascular disease or type 2 diabetes are linked also to prior sleep disturbance. Burnout, a characteristic outcome of long-time exposure to stress involves extreme fatigue, cognitive impairment, and lowered mood. Patients with burnout also show pronounced sleep fragmentation,

From a general perspective, psychosocial stress refers to the “the rate of wear and tear in the organism,” and the biological definition of stress refers to the nonspecific response to any demand5 to increase the chances of successful handling of a threatening situation. Contemporary physiologic stress models derive from the pioneering work of Cannon6 and of Selye.5 Cannon6 developed the concept of the “fight–flight” response, which linked the emotional perception of a “threat” to physiologic changes in the periphery. Selye7 proposed a model of stress, the general adaptation syndrome, which was composed of three stages—alarm, resistance, and exhaustion—and reflected the physiologic nonspecific response to a challenge. The resistance stage of the general adaptation syndrome has extreme energy requirements, which, if persistent over time, deplete the person’s capacity and leads to exhaustion. Markers of the fight–flight response are the catecholamines epinephrine and norepinephrine and other physiologic indicators associated with the autonomic nervous system.8,9 The hypothalamic-pituitary-adreno­cortical (HPA) axis is also fundamental in the stress reaction. When the sympathetic-adrenal-medullary system is activated and neuropeptides such as corticotropin-releasing hormone (CRH) and vasopressin are released, they, in turn, stimulate release of adrenocorticotropic hormone (ACTH) into the general blood circulation within the pituitary.9,10 Long-term effects of stress are described by the term allostasis, which refers to the ability of the body to increase or decrease the activation level of vital functions to new steady states dependent on the characteristics of the chal814

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increased sleep latency, reduced sleep efficiency, and reduced slow-wave sleep. Sleep impairment seems to be a prerequisite for developing burnout. It is concluded that there is supporting evidence that stress affects sleep negatively but that we know too little about the details of the effects. The details include the critical levels and durations of stress necessary to cause insomnia and the process of the development of stress-related insomnia across time. Stress research often refers to the observation that repeated stress with insufficient restitution in between episodes of stress will lead to a gradual increase in physiologic activation and eventually an allostatic upregulation of wear and tear.1 Although the duration or type of rest in-between bouts of stress may be important factors, it is obvious that sleep is one of the major physiologic means of restitution.2 This involves the elimination of subjective or behavioral fatigue, the physiologic substrates of this elimination, and the peripheral physiologic changes that maintain proper metabolic balance and a well-functioning immune system. The amount of available data on stress and sleep is relatively modest, however.3,4 Some of the findings are summarized here.

lenge and the person’s emotions and appraisal of the event.1 The resulting allostatic load represents the cumulative cost to the body when the systems start to malfunction after a stressful event. It is suggested that serious pathophysiology can occur if overload is not relieved in some way.1 One of the outcomes may be insomnia. With respect to working life there are systematic theories, however. One of the leading ones in work stress research is the so-called demand/control model.11,12 According to this model, high demand and low decision latitude have been found predictive of cardiovascular and other types of stress diseases.13-15 Another approach is that of the “effort/reward model,” which focuses on the contrast between demands and resources.16 Resources include salary, career opportunity, and other rewards. In this model, “immersion” has an important role, representing major commitment of effort. Immersion (or commitment) involves experiences of “not being able to stop thinking of work in the evening” or “starting to think of work immediately on awakening,” for example. Another important work-related factor may be the amount of social support received at work. Several studies have indicated the impact of lack of such support on cardiovascular disease, depression, and other outcomes.12,17

THE CROSS-SECTIONAL CONNECTION BETWEEN STRESS AND SLEEP Considering the physiologic activation involved in the stress response it seems logical to expect a connection



with sleep disturbances. In fact, stress is considered the primary cause of persistent psychophysiologic (primary) insomnia.18 The evidence is, however, surprisingly modest, at least in terms of systematic studies of causal relations in a longitudinal perspective. Cross-sectional epidemiologic studies are readily available, however. They indicate a strong link between questionnaires on stress and sleep.19-26 There are far fewer studies on stress and sleep using polysomnography (PSG). However, Shaver and associates27 studied women with insomnia and did not find that stress ratings differed from those of good sleepers. Differences were found, however, in neuroendocrine activation and similar measures, suggesting increased stress. With respect to the particular character of the stress involved, Ribet and colleagues21 studied more than 21,000 subjects in France, using a sleep disturbance index and logistic regression analysis. It was found that shift work, a long work week, exposure to vibration, and “having to hurry” appeared to be the main risk factors for reports of impaired sleep, when controlled for age and gender. The demand component of the demand/control model of stressful work conditions has also been shown to have a link to reported sleep impairment.19-23 In Åkerstedt and associates,22 it was found that the strongest item of the demand index was “having to exert a lot of effort at work,” not simply “having too much to do,” for example. The distinction may be interpreted as a lot of work per se may not be the key factor but that the response to the work situation is more important. It was also found that when the item “not being able to stop thinking about work in the evening” was added to the regression this variable became the most important predictor of disturbed sleep. Again, it is the response to the work load that predicts sleep impairment. The effort-reward imbalance has also been related to disturbed sleep.28 With regard to socioeconomic group, sleep complaints are more frequently found in blue-collar workers. Thus, Partinen and coworkers29 investigated several occupational groups and found disturbed sleep to be most common among manual workers and much less so among physicians or managing directors. Geroldi and associates30 found in a retrospective study of older individuals (older than 75 years) that former white-collar workers reported better sleep than blue-collar workers. Kupperman and colleagues31 reported fewer sleep problems in subjects who were satisfied with their work. On the whole, bluecollar workers exhibit higher levels of stress than whitecollar workers but the origins seem more related to living conditions in general (e.g., economy, social situation, neighborhood) than work stress. Social support is usually seen as a countervailing force in demand/control models and seems to counteract the effects of high demands.17 Lack of social support may thus function as a risk factor for disturbed sleep.32 Nordin and associates33 demonstrated an interactive effect on sleep between social support, high demands at work, and lack of control. In a second study the same group showed that disturbed sleep may be a mediator between poor social support and coronary heart disease.33 Poor social support

CHAPTER 74  •  Sleep, Stress, and Burnout  815

has been associated for instance with sleep complaints in Vietnam War veterans.34

THE PROSPECTIVE CONNECTION BETWEEN STRESS AND SLEEP The question if stress actually causes impaired sleep can only be resolved in longitudinal studies. One such study is that of Dahlgren and colleagues,35 who followed whitecollar workers before and during a period of intense work stress. Reported sleep duration and sleep quality (by sleep diary) was reduced, as was evening alertness. The latter was probably due to the intense work pressure. Finally, the cortisol pattern was flattened. In another study, Sadeh and associates36 found reduced sleep (by actigraphy and diary ratings) during a period of examination stress. Still, with both studies it is not clear if some of the reduced sleep could be partly due to simply trading sleep time for more study time rather than stress affecting the ability to sleep. Linton and coworkers37 studied employees with no reported initial sleeping problems and found that 14.3% developed a sleeping problem during the ensuing year. Even when controlling for possible confounders, stress in the form of a “poor” psychosocial work environment doubled the risk of developing a sleep problem. In a similar vein, Jansson and associates38 showed the effects of present stress on later complaints of disturbed sleep. The results showed that among individuals with no insomnia at baseline, high work demands increased the risk of developing insomnia 1 year later. Among participants with insomnia at baseline, high leader support decreased the risk of still reporting insomnia at follow-up. Finally, low influence over decisions and high work demands were related to the maintenance of insomnia. In another longitudinal study, Vahtera and colleagues showed that the effect of a self-rated tendency to respond strongly to stress predicted later sleep disturbances as a response to negative life events.39 This points to a consistent pattern of disturbed sleep in response to stress. Similarly, Drake and coworkers showed that those who reported a higher habitual sleep vulnerability to stress also showed longer sleep latency and lower sleep efficiency on the first night in the sleep laboratory.40 This suggests that sleep vulnerability to stress is somewhat of a trait. The scale Ford Insomnia Response to Stress (FIRST, from the Ford hospital) has also been shown to predict long sleep latency in response to caffeine.40 In the earlier mentioned study by Sadeh and associates,36 it was demonstrated that a stronger sleep duration response to examination stress was seen in those individuals who showed a high emotion-focused coping. Åkerstedt and colleagues41 recorded sleep in the home of 50 participants on four occasions across several weeks and showed that nighttime ratings of stress/worries at bedtime were related to reduced sleep efficiency, increased wake time after sleep onset and increased latency to slowwave sleep. Every-3-hour ratings of “stress” in the sleep diary were also increased both on the day before and the day after this sleep. Also in this study, differential vulnerability was seen. Those individuals who showed an increase in stress ratings showed a significantly higher level of

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depression on the Hospital Depression and Anxiety Scale.42 In other PSG studies, sleep on the night before an important examination43 and also before a day of skydiving44 was investigated. The results indicate a slightly negative effect on sleep efficiency and the amount of deep sleep. In addition, a number of early laboratory studies of stress and sleep have been performed but the stressors have been rather artificial (e.g., an unpleasant movie) and the results are unclear.45 It is probably the case that the stressor needs to be of some significance to the individual to have any effect on PSG measures of sleep. There are also studies of the effects of major life events, including stressors at the national/societal level. Cernovsky and coworkers46 demonstrated a clear increase in population-wide negative life events preceding an outbreak of insomnia. Haynes has shown similar results.47 The economic recession in Finland in 1993 was apparently related to reported reductions in sleep quality.48 It has also been shown that sleep is disturbed in response to threats to national security, for example, after the nuclear accident at the facility at Three Mile Island and during the scud missile attacks on Israel during the Gulf War.49,50 The effect of losing a life partner has in one study been shown to have surprisingly modest effects, and then mainly an increase in rapid-eye-movement (REM) intensity.51

RUMINATION AND ANTICIPATION Indirectly, many of the studies just described suggest that it is not the stress experience itself that impairs sleep but rather the anticipation of untoward events and worries about the immediate future. Examinations, high work demands, and external threats are likely to cause this type of worried anticipation. Cropley and colleagues52 coupled the relation between strain and poor sleep in teachers to rumination. The previous cross-sectional study by Åkerstedt and associates22 found that not being able to turn off thoughts of work in the evening was strongly related to subjectively disturbed sleep. This may manifest itself as a form of rumination, and rumination is seen as a major cause of disturbed sleep.53 Hall and coworkers26 have demonstrated in a cross-sectional study that intrusive thoughts at bedtime are related to increased alpha and beta power in the subsequent sleep EEG. Similarly, increased cognitive arousal at bedtime is related to increased sleep latency.47,54 Closely related to rumination is the worrying and the tension before sleep owing to a very early (and unpleasant) time of awakening before an unusually early morning shift.55,56 The resulting sleep contained less slow-wave sleep, which supports the notion that it is the anticipation of difficulties that is important in the stress reaction. A similar study was carried out with machine officers on container ships.57 Sleep recorded during a night on call (but without any call occurring) showed a reduction of slow-wave sleep and a corresponding increase in stage 2 sleep. Also, heart rate was increased. This was interpreted as an activation in the face of a possibility that the alarm would sound, which happened on average every second night on call. In the previously mentioned study on stress/

worries at bedtime,41 sleep recordings preceded by moderately increased subjective “stress/worries” at bedtime showed a moderate impairment, which may be interpreted as due to rumination. Interestingly, Meerlo and colleagues58 have shown that intense stress increases deep sleep in rats. Presumably this is due to the increase in the metabolic rate of the central nervous system due to the stress, without any anticipatory component. Whether stress has a similar effect on humans is unknown, but several studies in humans have shown that brain use (increased mental activity) leads to more intense sleep59 and that nonuse leads to reduced sleep intensity.60 The observations on the effects of brain use could mean that acute stress will improve subsequent sleep as long as there is no remaining negative anticipation. This question has not been addressed, however.

POSTTRAUMATIC STRESS Posttraumatic stress disorder (PTSD) is another wellestablished cause of disturbed sleep, even if many of the more common indicators of sleep quality (e.g., sleep latency, efficiency of sleep, total length of sleep, and amount of slow-wave sleep) are only moderately affected61-64 and sometimes not affected at all.65 Instead, these studies suggest that the major effect of PTSD is to disturb REM sleep by either increasing or decreasing its duration and by increasing its intensity. It also increases the number of awakenings. The unpleasant dreams associated with traumatic memories also tend to produce conditioned avoidance responses in affected individuals, resulting in postponements on a daily basis of retiring or of even entering the sleeping area. The effects on sleep seem to mediate long-term health effects.66 SLEEP PHYSIOLOGY THAT SEEMS TO LINK SLEEP WITH STRESS Insights into the connection between sleep and stress may also be obtained through comparing the physiologic changes during sleep or after sleep loss with those of stress. Among the basic observations on sleep physiology is the reduction of rectal temperature, rate of breathing, heart rate, blood pressure, and so on that occur during non– REM (NREM) sleep.67 In adults, the first part of sleep is characterized by increased growth hormone (GH) release (together with increased slow-wave sleep and low levels of REM sleep) and suppressed secretion of the hormones of the HPA system.68,69 This means that CRH, ACTH, and cortisol are suppressed. These changes directly oppose the effects of stress. GH promotes protein synthesis, which means that it is essential for growing and for repairing tissue. When sleep is prevented, cortisol secretion will increase70 and the rate of sleep fragmentation (microarousals) is related to increased levels of cortisol.71 Thus, sleep reduction has effects similar to those of stress. The secretion of GH, on the other hand, is strongly reduced if no sleep occurs.72 Sleep not only regulates stress hormone secretion but also is affected by it. Thus GH-releasing hormone (GHRH) causes increased slow-wave sleep and GH secretion, as well



as reduced cortisol levels in men but not in women.68 CRH exerts the opposite effects. It appears that the quality of sleep partly depends on an interaction of GHRH and CRH. The reduced glucose clearance after sleep loss70,73 also possibly reflects similar changes as a result of stress.2 The immune system is strongly suppressed by stress, via, for example, increased activation of the HPA axis.2 On the other hand, reduced or fragmented sleep causes increased levels of proinflammatory cytokines such as interleukin1β, interleukin-6, and tumor necrosis factor-alpha.74,75 Hall and associates have suggested that disturbed sleep may serve as a mediator in the link between stress and the immune system.76 Essentially, lack of sleep seems as linked with the metabolic syndrome as does stress.77,78

SIMILARITY OF MORBIDITY DUE TO STRESS AND SLEEP LOSS Poor sleep is associated with an increased prospective risk of diseases that are classic “stress diseases.” This association holds true for myocardial infarction, particularly when poor sleep is combined with increased resting heart rate—a marker of sympathetic overactivity.79 Also, hypertension is increased in both short and long sleepers.80 In women undergoing rehabilitation from a myocardial infarction, the risk of recurrent myocardial events is increased in selfreported poor sleepers.81 In addition, the frequent occurrence of waking and feeling exhausted in the morning is a predictor of subsequent myocardial infarction.82 The exhausted state is also associated with reduced amounts of sleep stages 3 and 4.83 Also, diabetes, another classic “stress disease,” has a relationship with sleep. For example, patients with type 2 diabetes report more sleep problems than nondiabetic subjects.84 This finding could be partly confounded by obesity or by obstructive sleep apnea. However, in a prospective follow-up study of healthy middle-aged men from Malmö, Sweden, it was shown that the 12-year risk of developing type 2 diabetes was independently predicted by selfreported difficulties in falling asleep and by elevated resting heart rate, after full adjustment for obesity, lifestyle factors, and other risk factors.85 One possible explanation is obstructive sleep apnea, which was not measured in the Malmö study, but another possibility would be chronic low-grade inflammation, both linked to insomnia and risk of type 2 diabetes. Short sleep duration is also involved in the metabolic syndrome.77 BURNOUT AND SLEEP Recently, there has been considerable interest in the problem of “burnout” in western countries. This has been particularly so in Sweden because of burnout’s contribution to the large increase in long-term sickness absence from work that occurred over the past 15 years.86,87 The concept of burnout describes a state of “chronic depletion of an individual’s energetic resources”88 and is usually conceived of as an outcome of prolonged occupational stress.89,90 Originally, the symptoms were seen as occurring only in people-oriented (e.g., nursing, social services, edu-

CHAPTER 74  •  Sleep, Stress, and Burnout  817

cation) occupations90 but have since been found in virtually all types of work.91,92 The characteristic symptoms of burnout are persistent and excessive fatigue, emotional exhaustion, and cognitive dysfunction.93,94 Frequently, the condition also includes components of depersonalization or cynicism toward clients/patients and reduced personal efficacy, with a tendency to evaluate oneself negatively.90 However, no single conceptualization is accepted as standard, and in the 10th revision of the International Classification of Diseases (ICD10)95 burnout is broadly defined as “a state of vital exhaustion” (category # Z73.0). Recently, exhaustion syndrome has been established as a diagnosis in the Swedish version of the ICD-10 classification system (KSH97, category #F43.8A).96 Burnout is not a diagnostic entity in the ICD-9, which is used in the United States. Perhaps the closest diagnosis is “ICD 309 Adjustment reaction: includes reaction to chronic stress.” The physiologic mechanism behind the fatigue in burnout has not been identified, but the role of long-term stress suggests that the HPA axis is involved.97,98 Several studies seem to find a blunted cortisol response in the dexamethasone suppression test.99,100 In the former study a reduction of hippocampal size was also observed. This is interesting in relation to the links between circulating cortisol levels and impaired cognitive function,101,102 because the latter is a characteristic symptom in burnout. The other persistent finding is the exaggerated cortisol release at awakening, suggesting increased anticipation of stress. This response has been mainly observed among female patients with exhaustion syndrome.103 Also, increased activity of proinflammatory hormones has been suggested.103 Even if some endocrine and links between chronic stress exposure and burnout have been established, the results do not seem robust in the sense that they might “explain” the symptoms. An alternative or complementary factor could be disturbed sleep. It has recently been demonstrated that burnout scores are closely related to reports of disturbed sleep.103,104 There are, as yet, only a couple of studies of sleep in burnout using PSG. In one investigation of young individuals in the Internet technology industry with high burnout scores105 an increased level of sleep fragmentation was found. Also, sleepiness ratings (taken every 3 hours during waking) were increased during the working week compared with normal individuals but sleepiness during the days off fell only marginally, whereas in normal individuals there were dramatic decreases in sleepiness on days off. In a study of individuals on long-term sick leave with a diagnosis of burnout, a similar increase in sleep fragmentation was seen, but also lower sleep efficiency, more wake time after sleep onset, a doubled sleep latency, and reduced amounts of stages 3 and 4 sleep.106 The fragmentation of sleep was highly correlated with morning levels of cortisol, lipids, and other stress-related variables.71 A qualitative approach to a subsample of the patients just discussed showed that they described long periods of stress before becoming burnt out, that self-imposed sleep reduction was used to obtain more time to carry out work

818  PART II / Section 9  •  Occupational Sleep Medicine

tasks, and that suddenly they “stopped sleeping.”107 The latter was followed by extreme fatigue, which brought them to medical attention, resulting in a diagnosis of burnout. The fragmentation and reductions in sleep efficiency suggest a link to the fatigue and performance impairment in burnout. Such links are well established in experimental sleep research.108-110 If there is a causal link between burnout and sleep one should see at least the latter predict the former in longitudinal studies. This has been demonstrated in one study.111 The persons who benefited poorly from sleep at baseline had higher exhaustion levels at follow-up than those who benefited from sleep. Trouble falling asleep and less refreshing sleep at baseline hampered eventual full work resumption. Armon and colleagues112 complicated interpretations by finding that burnout and insomnia recursively predict each other’s development and intensification over time, thus suggesting that either might be a risk factor for the other across time. But this study has been conducted with previously healthy workers and burnout patients. Finally, recovery from burnout was found to be linked to improvements in sleep fragmentation, sleep efficiency, and sleep latency. The degree of reduction in sleep fragmentation correlated with the reduction in fatigue, and the latter correlated with return to work after being on long-term sick leave.113

MEASURING STRESS From the previous discussion it may be obvious that “stress” has had many meanings. It was previously defined as an activating response to demands. In many of the previously mentioned studies this may mean high levels on the demand/control questionnaire and/or common sense notions that the anticipation of an examination or of sky diving should be stressful. Very seldom has the concept of stress per se been used. The reason may be that there is no generally accepted operational scale for measuring stress. There have been several such attempts, but they have taken very broad approaches and frequently include many nonspecific consequences of stress. For example, the Perceived Stress Questionnaire (PSQ)114 contains 20 items such as “tension,” “worries,” and “joy” in addition to items on pressure and demands. The Perceived Stress Scale (PSS)114 contains 14 items such as “upset,” “on top of things,” and “nervous” in addition to items on demands and stress. The Stress Response Inventory (SRI) contains 39 items, including scales on depression, frustration, anger, and others.115 The Calgary Symptoms of Stress Inventory116 is a similar scale. Because these types of scales combine the cause (e.g., stress, demands, pressure) with the effects (e.g., anger, anxiety) they are not well suited for use in cause-and-effect studies of, for example, stress and sleep. Understanding the role of stress in sleep disorders probably requires the development of unambiguous instruments for measuring stress. CONCLUSION Although there seems to be clear evidence of stress causing impaired sleep we still know very little about the effects on

sleep architecture, at what level or type of stress sleep is impaired, and after what duration semichronic levels occur, causing insomnia. We also lack information on what contributes to vulnerability. Apparently, there is a need for long-duration longitudinal studies. When meeting a patient who suffers from insomnia that may be stress related, the clinician may find it useful to conduct a structured stress interview around the patient’s life situation. In our experience, much information may be gained from questions that focus on preoccupation with work and presence of ruminations and worries about the immediate future. It may be phrased: “Are you often unable to stop thinking about work in the evening?” Another area to explore with patients is work pressure. This may be phrased: “Do you have to exert a lot of effort at work,” “do you get enough time for sleep, or “do you reduce sleep duration to make room for work?” For treatment of sleep problems due to stress, the reader is referred to the chapter on psychological treatment for sleep disturbances (see Chapter 79). However, it might also be useful to refer the patient to a short stress management course (based on cognitive therapy), which is often efficient in reducing sleep problems and may well be combined with cognitive behavior therapy for sleep disorders. The stress management courses usually involve stress reduction techniques, teaching basic life hygiene, as well as relaxation techniques to improve bedtime practices. Two groups of patients with extreme stress problems will demand special attention: patients with PTSD117 and patients with work-related burnout. In those patients a sleep treatment based on cognitive techniques (see Chapter 79) may greatly contribute to their chances to be free of their primary disease.

❖  Clinical Pearl Insomnia is often a result of long-term exposure to stress. Even modest amounts of day-to-day variations in stress may significantly affect sleep architecture. Patients with complaints of incapacitating fatigue (e.g., burnout) should be investigated for disturbed sleep and long-term exposure to stress. From the point of view of prevention, as well as treatment, it is important to realize that impaired sleep results from anticipatory stress. Stress that has been dealt with, and is out of the system, may even improve sleep.

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