Elsevier

Sleep Medicine Reviews

Volume 12, Issue 4, August 2008, Pages 307-317
Sleep Medicine Reviews

Clinical review
The relationship between insomnia and body temperatures

https://doi.org/10.1016/j.smrv.2008.02.003Get rights and content

Summary

Sleepiness and sleep propensity are strongly influenced by our circadian clock as indicated by many circadian rhythms, most commonly by that of core body temperature. Sleep is most conducive in the temperature minimum phase, but is inhibited in a “wake maintenance zone” before the minimum phase, and is disrupted in a zone following that phase. Different types of insomnia symptoms have been associated with abnormalities of the body temperature rhythm. Sleep onset insomnia is associated with a delayed temperature rhythm presumably, at least partly, because sleep is attempted during a delayed evening wake maintenance zone. Morning bright light has been used to phase advance circadian rhythms and successfully treat sleep onset insomnia. Conversely, early morning awakening insomnia has been associated with a phase advanced temperature rhythm and has been successfully treated with the phase delaying effects of evening bright light. Sleep maintenance insomnia has been associated not with a circadian rhythm timing abnormality, but with nocturnally elevated core body temperature. Combination of sleep onset and maintenance insomnia has been associated with a 24-h elevation of core body temperature supporting the chronic hyper-arousal model of insomnia. The possibility that these last two types of insomnia may be related to impaired thermoregulation, particularly a reduced ability to dissipate body heat from distal skin areas, has not been consistently supported in laboratory studies. Further studies of thermoregulation are needed in the typical home environment in which the insomnia is most evident.

Section snippets

Insomnia

Insomnia is a very generic term with the criteria including difficulty initiating sleep, maintaining sleep, and early morning awakening, accompanied by some form of daytime impairment (e.g., fatigue).1 This review will focus on these three areas of sleep difficulties and the relationship with body temperatures. The International Classification of Sleep Disorders (ICSD-2)1 elaborates several categories of insomnia primarily on the basis of its etiology and contributing causes such as

Body temperature and circadian rhythm timing

Periodic circadian (24-h) variations or rhythms are ubiquitous in the human body and include physiological and behavioral rhythms of core body temperature, melatonin secretion, sleep propensity and subjective alertness. The sleep–wake cycle and body temperature rhythms have a stable internal phase relationship in normally entrained conditions with the timing of sleep highly correlated with the timing or phase of the circadian body temperature rhythm.2 The temperature and melatonin circadian

Sleep onset insomnia and delayed sleep phase disorder

Sleep onset difficulties may occur when an individual's temperature rhythm is timed relatively late with respect to their attempted sleep period. In these cases the delayed temperature rhythm may result in a delay of the evening wake maintenance zone such that it coincides with the attempt to sleep. The evening wake maintenance zones of normal and sleep onset insomniacs are illustrated in Figure 2. Some studies have found that individuals experiencing sleep onset insomnia have a relatively

Early morning awakening insomnia and advanced sleep phase disorder

The ICSD-2 nosology describes advanced sleep phase disorder (ASPD), or earlier terminology ‘syndrome’, as a disorder in which the major sleep period is early (advanced) with respect to the desired sleep/wake period.1 Individuals with ASPD have overwhelming early evening sleepiness, an early sleep onset and early morning awakenings. For example, bedtimes could be as early as 19:00 and wake times at 03:00. If the person tries to obtain more sleep in the morning by staying in bed, frequent

The treatment of insomnia by phase shifting (re-timing) circadian rhythms

If treatments that appropriately shift the rhythms of sleep onset and early morning awakening insomnia are efficacious, it would support the prediction that temperature rhythm de-synchrony contributes to the etiology of these two insomnias. Initial studies have demonstrated that bright light can phase shift circadian rhythms,30, 31, 32 with bright light presented before the CBTmin delaying the circadian rhythm and bright light administered after the CBTmin advancing the rhythm.33, 34, 35, 36, 37

Insomnia from hyper-arousal

Independent of circadian factors, it is clear that insomnia can arise from a wide range of stimuli that promote arousal. These include environmental (e.g., noise, elevated ambient temperature), social (e.g., poor sleep habits, shiftwork), psychological (e.g., conditioned responses, anxiety) and physiological (respiratory impairment, restless legs, pain) stimuli. At a broad conceptual level it is generally held that such stimuli lead to a ‘hyper-aroused state’ that is the immediate cause of poor

Skin temperature's role in thermoregulation

We have already described the relationships between core body temperature and poor sleep. However, a review of insomnia and temperature would be incomplete without reference to the role of skin temperature in thermoregulation. The regulation of core body temperature occurs as a combination of heat production and heat loss.3 When heat production is greater than heat loss, core body temperature increases and, conversely, when heat loss exceeds heat production, as in the late evening, it

Skin temperature and the sympathetic nervous system

Heat loss from distal skin areas occurs most rapidly when AVAs are maximally dilated.4, 77 Conversely, when vasoconstriction occurs, the amount of blood flow is restricted causing distal skin temperature values to decrease towards ambient air temperature (e.g., 20–22 °C in a laboratory). Vasomotor activity of AVAs is directed primarily from sympathetic nervous system constrictor neurons. When these neurons are activated, smooth muscles around AVAs constrict causing vasoconstriction, sometimes to

Does insomnia limit the down regulation of core temperature as a result of impaired distal skin vasodilation?

Good sleepers are typically known to be relaxed when attempting sleep, and manage to fall asleep within a reasonable amount of time (e.g., within 10–15 min). In contrast, insomniacs take longer to fall asleep initially and following awakenings from sleep.15, 50, 56, 58 Unlike good sleepers, insomniacs are not relaxed, even to the point of being anxious when attempting sleep.58, 94 This view has been supported very recently with the finding that the normal reduction of cognitive arousal and

Supporting research

The first study to investigate the skin temperatures of insomniacs attempting sleep was conducted in 1979 by Brown97 who found that insomniacs did show increases in toe skin temperature when attempting sleep, but that sometimes there was no observable change. Yet, when toe temperature increases were observed, they were more variable, and took twice as long to reach the same amount of temperature change compared to good sleepers. Freedman and Sattler56 found that compared to good sleepers

Conclusion

Insomnia subtypes may be differentiated in terms of the aspect of sleep that is the predominant chronic difficulty (difficulty falling asleep, waking frequently for long periods during the night, early final awakening before sufficient sleep is obtained). There appear to be specific abnormalities of body temperature associated with some of these subtypes. Difficulty initiating sleep at a normal time (sleep onset insomnia) is associated with a circadian core body temperature rhythm that is

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