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Circadian and Sleep Disruption in Chronic Stress

Educational exploration of how stress disrupts sleep and circadian rhythms, with metabolic consequences.

Sleep Architecture and Normal Sleep

Sleep is a complex state characterised by distinct stages with specific physiological signatures and functions. Non-REM (non-rapid eye movement) sleep comprises three progressively deeper stages (N1, N2, N3 or "deep sleep"), characterised by progressive slowing of brain electrical activity, reduced muscle tone, and decreased responsiveness to external stimuli. REM (rapid eye movement) sleep, also called paradoxical sleep, is characterised by rapid eye movements, brain electrical activity resembling waking, paralysis of voluntary muscles, and vivid dreaming. A typical night's sleep cycles through these stages approximately every 90 minutes, with earlier cycles dominated by deep sleep and later cycles emphasising REM sleep. This structured architecture is essential for restorative functions, including memory consolidation, synaptic remodelling, glymphatic clearance, and metabolic recovery.

Stress and Sleep Initiation

Chronic stress impairs sleep initiation and quality through multiple mechanisms. Elevated cortisol suppresses melatonin production—melatonin is the hormone produced by the pineal gland in response to darkness that promotes sleep onset and maintenance. Activation of the sympathetic nervous system during stress—the "fight or flight" response—increases arousal and vigilance, making sleep onset more difficult. Additionally, stress activates the hypothalamic-pituitary-adrenal axis, which maintains elevated cortisol throughout the day and night, further antagonising sleep. The result is difficulty falling asleep, increased sleep latency (time to fall asleep), and overall reduced sleep duration.

Sleep Fragmentation and Reduced Sleep Continuity

Beyond difficulties with sleep initiation, chronic stress fragments sleep—increasing the number of awakenings and transitions between sleep stages. Stressed individuals often experience frequent brief awakenings throughout the night, sometimes without conscious awareness but registered in objective sleep measurements. This sleep fragmentation prevents the consolidation of deep sleep and REM sleep, disrupting sleep restorative processes. Physiologically, stress-induced elevation of the sympathetic nervous system and maintenance of elevated arousal thresholds makes sleep more easily disrupted by minor disturbances that would not awaken well-rested individuals.

Circadian Rhythm Desynchronisation

The body's master circadian clock, the suprachiasmatic nucleus in the hypothalamus, normally maintains a nearly 24-hour rhythm of cortisol, body temperature, and other physiological functions. This rhythm is entrained to external time by light exposure and other cues. Chronic stress disrupts circadian timing, often flattening the normal robust cortisol rhythm and desynchronising multiple circadian-regulated processes. When circadian rhythms become desynchronised from external time-of-day, the biological timing of hormone secretion, metabolism, and physiological function becomes misaligned with behaviour and environmental demands. For example, elevated cortisol at night (normally a low-cortisol period) can severely disrupt sleep when combined with sleep fragmentation and reduced melatonin.

Metabolic Consequences of Sleep Loss

Sleep loss independently impairs metabolic regulation through multiple mechanisms. Sleep deprivation reduces glucose tolerance, impairing the ability to regulate blood glucose levels after carbohydrate consumption. This effect appears mediated through reduced insulin sensitivity. Additionally, sleep loss increases ghrelin (appetite-stimulating hormone) secretion and decreases leptin (appetite-suppressing hormone), creating a state of increased hunger drive. Sleep loss also increases sympathetic nervous system activation and systemic inflammation, further impairing metabolic health. Finally, sleep loss reduces energy expenditure, likely through reduced physical activity and metabolic adaptation to energy deficit. These multiple metabolic effects of sleep loss contribute substantially to altered energy balance during periods of stress-induced sleep disruption.

Circadian Misalignment and Metabolic Disruption

Beyond simple sleep loss, circadian rhythm desynchronisation impairs metabolism through disruption of the normal circadian timing of metabolic processes. Metabolic rate, insulin sensitivity, and substrate utilisation all show circadian variation—they function optimally at certain times of day and poorly at others. When circadian rhythms become desynchronised from behavioural patterns (eating when the body's circadian clock indicates "night," being active when it indicates "sleep time"), metabolic dysregulation results. Chronotype misalignment (living on a schedule misaligned with one's natural circadian preference) shows associations with impaired glucose regulation, increased visceral adiposity, and metabolic syndrome—partly through disruption of circadian-regulated metabolic processes.

Stress, Sleep, and Appetite Hormones

Sleep loss and circadian misalignment both increase ghrelin and decrease leptin, creating a state hormonally consistent with energy deficit despite adequate or excessive caloric intake. This hormonal state drives increased appetite and food intake, particularly preference for energy-dense foods. When combined with the NPY/POMC changes induced by chronic cortisol elevation and the reward-system alterations induced by stress, sleep loss creates a powerful combined effect favouring increased energy intake. The sleep-loss-induced shift toward increased appetite drive and decreased satiety signals synergises with stress-induced appetite stimulation.

Metabolic Substrate Shifts

Sleep loss alters metabolic substrate utilisation, shifting metabolism away from fat oxidation and toward carbohydrate utilisation. During sleep loss, the body becomes less efficient at fat metabolism and preferentially oxidises carbohydrates, which are depleted during sleep loss-induced increased wakefulness. This shift away from fat oxidation, combined with increased energy intake, favours net fat storage. The specific shift toward decreased visceral fat oxidation may be particularly important, potentially contributing to preferential visceral fat accumulation during periods of chronic stress-induced sleep disruption.

Research Evidence

Polysomnographic studies document sleep fragmentation, reduced deep sleep and REM sleep, and circadian rhythm alterations in chronically stressed individuals. Hormonal studies show altered cortisol rhythm, suppressed melatonin, elevated ghrelin, and suppressed leptin in sleep-deprived individuals. Metabolic studies demonstrate impaired glucose tolerance, reduced insulin sensitivity, and increased systemic inflammation following sleep loss. Longitudinal epidemiological studies show associations between short sleep duration and weight gain, particularly visceral weight gain. This convergent evidence supports the concept that stress-induced sleep disruption significantly contributes to metabolic dysregulation and weight changes.