Insomnia

Insomnia disorder is defined by complaints about sleep at night together with impairment during the day. The night-time complaints are a long time taken to fall asleep, difficulty staying asleep and waking too early; the daytime impairments include fatigue, reduced attention, poorer thinking, irritability, anxiety and low mood [1]. A diagnosis requires that the problem occurs despite adequate opportunity and circumstances for sleep, which separates insomnia from sleep deprivation caused by a lack of time in bed.

Insomnia can be short-term, usually following a stressful event, or chronic. It may be the main complaint, but more often it occurs alongside other medical or psychiatric conditions such as pain and depression [11]. Earlier classifications separated primary insomnia from insomnia secondary to another condition; current systems treat insomnia as a disorder in its own right even when other conditions are present [11].

Diagnosis rests mainly on self-report, through a clinical interview, sleep diaries and questionnaires such as the Insomnia Severity Index [12]. Objective measures such as actigraphy (a wrist-worn movement sensor) or polysomnography are used in research but are not part of routine diagnosis [1]. A sleep study is used when another sleep disorder, such as obstructive sleep apnea, is suspected.

Estimates of how common insomnia is depend on the definition. A review of more than 50 population surveys found that about one-third of the general population reports at least one insomnia symptom; 9 to 15% report symptoms with daytime consequences; 8 to 18% are dissatisfied with their sleep; and about 6% meet the criteria for an insomnia diagnosis under the DSM-IV [2].

Under current definitions, chronic insomnia disorder affects up to 10% of the adult population [1]. All definitions show higher rates in women than in men. Insomnia symptoms become more common with age, while rates of sleep dissatisfaction and of formal diagnoses change little with age [2].

Insomnia is closely linked with depression. People with insomnia are more likely to have major depression, and in long-term studies persistent insomnia is associated with the later appearance of a new depressive episode [2].

The most widely supported explanation for chronic insomnia is the hyperarousal model. Studies of the autonomic nervous system, stress hormones, the immune system, brain electrical activity and brain imaging show raised levels of arousal in people with insomnia during both night and day. On this model, insomnia is a final common pathway from a genetic tendency toward an imbalance between arousing and sleep-promoting brain activity, combined with stressors and with habits and thought patterns that keep the problem going [3].

The 3P model, set out by Spielman and colleagues in 1987, describes how short-term insomnia becomes chronic through predisposing, precipitating and perpetuating factors. Predisposing factors are traits such as a tendency to worry. A precipitating factor is the trigger, often a stressful life event. Perpetuating factors are the responses that maintain the problem after the trigger has passed, such as spending extra time in bed, napping and worrying about sleep [13].

Conditioned arousal is one of these perpetuating mechanisms. After repeated nights of lying awake, the bed and bedroom can become learned cues for wakefulness and frustration instead of sleep. The stimulus control model, proposed by Bootzin in 1972, describes this learned association and forms the basis of a treatment that limits the bed to sleep and has the person leave the bed when unable to sleep [14].

Circadian misalignment produces symptoms that resemble insomnia. When the internal clock runs later than the schedule a person must keep, as in shift work, jet lag or delayed sleep phase (a clock that runs markedly late, common in adolescents), the problem is the timing of sleep rather than the ability to sleep. Evening light shifts the clock later [15], and exposure to natural daylight shifts it earlier [16]. The regulation of the clock is described in sleep physiology.

Caffeine blocks the adenosine receptors that register sleep pressure. In a controlled study, 400 mg of caffeine taken 6 hours before bedtime still reduced total sleep by more than 1 hour [17]. A 2023 meta-analysis of 24 studies found that caffeine reduced total sleep time by 45 minutes and sleep efficiency by 7%, lengthened the time taken to fall asleep by 9 minutes and increased time awake after falling asleep by 12 minutes. Deep sleep fell by 11.4 minutes. The authors estimated that a typical cup of coffee (107 mg per 250 mL) needs to be drunk at least 8.8 hours before bedtime to avoid reducing total sleep time [8].

Light in the evening delays the circadian clock and suppresses melatonin. In a randomized crossover study, reading a light-emitting e-reader before bed rather than a printed book suppressed evening melatonin by 55%, delayed the clock by 1.5 hours and lengthened the time taken to fall asleep by nearly 10 minutes [15].

Temperature affects the fall in core body temperature that accompanies sleep. In older adults, sleep was most efficient at bedroom temperatures of 20 to 25 °C, and efficiency fell by 5 to 10% as temperatures rose from 25 to 30 °C [18]. A warm shower or bath of 40 to 42.5 °C taken 1 to 2 hours before bed shortened the time taken to fall asleep [19].

Alcohol shortens the time taken to fall asleep and deepens sleep in the first half of the night, but increases sleep disruption in the second half; it also delays the first REM period and, at moderate and high doses, reduces total REM sleep [20]. Falling asleep quickly and sleeping well are separate measures: sleep latency (time taken to fall asleep) can improve while sleep architecture (the amount of deep and REM sleep and how often sleep is broken) worsens.

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Obstructive sleep apnea is a separate disorder that also causes poor and unrefreshing sleep. The upper airway repeatedly narrows or closes during sleep, causing pauses in breathing (apneas) and shallow breathing (hypopneas) followed by brief awakenings that fragment sleep, often without the sleeper noticing. Severity is measured by the apnea-hypopnea index, the number of such events per hour of sleep; 5 or more is classed as mild, 15 or more as moderate and 30 or more as severe [21].

The condition is common. In the United States, moderate to severe sleep apnea was estimated to affect 10% of men aged 30 to 49, 17% of men aged 50 to 70, 3% of women aged 30 to 49 and 9% of women aged 50 to 70 [22]. Worldwide, an estimated 936 million adults aged 30 to 69 have mild to severe sleep apnea and 425 million have moderate to severe sleep apnea [10].

Untreated sleep apnea is associated with higher mortality. In the Wisconsin Sleep Cohort, 1,522 adults followed for 18 years, severe sleep apnea was associated with three times the all-cause mortality of no sleep apnea (hazard ratio 3.0, 95% CI 1.4 to 6.3) [21]. A meta-analysis of 12 cohort studies with 25,760 participants found that severe sleep apnea was associated with 92% higher all-cause mortality (relative risk 1.92, 1.38 to 2.69) and more than double the risk of stroke (2.15, 1.42 to 3.24) [23].

Sleep apnea is diagnosed with a sleep study and treated mainly with physical or mechanical approaches, most commonly continuous positive airway pressure (CPAP), rather than with the behavioral treatments used for insomnia.

Cognitive behavioral therapy for insomnia (CBT-I) is a structured treatment that usually combines several components: stimulus control, sleep restriction (limiting time in bed to the time actually spent asleep), cognitive therapy for worry about sleep, relaxation and sleep hygiene education. The American College of Physicians recommends CBT-I as the initial treatment for all adults with chronic insomnia disorder (strong recommendation, moderate-quality evidence) [4].

A 2015 meta-analysis of 20 randomized trials with 1,162 participants found that CBT-I shortened the time taken to fall asleep by 19.03 minutes (95% CI 14.12 to 23.93), reduced time awake during the night by 26.00 minutes (15.48 to 36.52) and increased sleep efficiency by 9.91 percentage points (8.09 to 11.73). Total sleep time increased by 7.61 minutes, which was not statistically significant, and the improvements appeared to last at later follow-up [5]. A larger 2018 meta-analysis of 87 randomized trials found the largest effect on insomnia severity and the smallest on total sleep time, and found that face-to-face treatment of at least four sessions was more effective than self-help or shorter treatment [24].

For adults in whom CBT-I alone has not worked, the American College of Physicians gives a weak recommendation, based on low-quality evidence, for short-term medication decided jointly by patient and clinician [4]. In observational studies, users of hypnotic and anti-anxiety drugs had 43% higher mortality than non-users (hazard ratio 1.43, 1.12 to 1.84) and benzodiazepine users 60% higher mortality (1.60, 1.03 to 2.49); these studies cannot separate the effect of the drugs from the health of the people prescribed them [9].

Melatonin has modest effects in primary sleep disorders. A meta-analysis of 19 randomized trials with 1,683 participants found that it shortened the time taken to fall asleep by 7.06 minutes and increased total sleep time by 8.25 minutes [25]. Other supplements studied for sleep are described in magnesium, glycine, L-theanine, valerian and ashwagandha.

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Chronic insomnia disorder is regarded as an important and independent risk factor for physical and especially mental health problems [1]. It is associated with depression [2] and with higher levels of the inflammatory markers C-reactive protein and interleukin-6 [26].

The link with mortality depends on the symptom. A 2019 meta-analysis of 29 cohorts with 1,598,628 people followed for a median of 10.5 years found that difficulty falling asleep was associated with 13% higher all-cause mortality (hazard ratio 1.13, 95% CI 1.03 to 1.23) and non-restorative (unrefreshing) sleep with 23% higher mortality (1.23, 1.07 to 1.42). Insomnia disorder as a whole, difficulty staying asleep and early morning waking were not associated with all-cause or cardiovascular mortality, and no insomnia symptom was associated with cancer mortality [6].

Another 2019 meta-analysis of 17 studies with 36,938,981 people followed for a mean of 11.6 years examined frequent insomnia (3 or more nights a week for at least a month) and found no significant association with mortality after full adjustment (hazard ratio 1.07, 0.96 to 1.19). It noted a tendency toward higher mortality with sleeping-pill use [7]. In 1,969 Australians aged 65 or older followed for a median of 9.2 years, the most severe insomnia symptoms were associated with 26% higher mortality, an association driven by daytime symptoms (hazard ratio 1.66, 1.39 to 2.00); night-time symptoms alone were not associated with higher mortality [27].