Sleep

Actigraphy uses a wrist-worn accelerometer to infer sleep-wake states from movement patterns over days to weeks, providing an ambulatory and low-burden alternative to polysomnography for longitudinal sleep assessment. Validated algorithms translate raw activity counts into estimates of total sleep time, sleep efficiency, sleep-onset latency, and waking after sleep onset. It is recommended by the American Academy of Sleep Medicine for evaluating insomnia, circadian rhythm disorders, and treatment response in naturalistic settings. Actigraphy systematically overestimates total sleep time and sleep efficiency relative to PSG, particularly in patients with insomnia, and cannot reliably stage sleep.

Adenosine is a purine nucleoside that accumulates in the brain during wakefulness as a byproduct of neuronal energy metabolism and acts on A1 and A2A receptors to promote sleepiness and suppress arousal, serving as the primary molecular mediator of homeostatic sleep pressure. Its levels are highest after prolonged waking and decline during sleep. Caffeine exerts its alerting effects principally by competitively blocking adenosine receptors without depleting adenosine itself, which is why the sleepiness rebound after caffeine clearance is pronounced. Beyond sleep regulation, adenosine is involved in cerebrovascular autoregulation and has been implicated in the glymphatic clearance process that intensifies during slow-wave sleep.

Chronotype is the individual disposition toward earlier or later sleep-wake timing, commonly described as morning, intermediate, or evening type. It is shaped by genetics, age, light exposure, and social schedules. Chronotype influences cognitive peak times, athletic performance, and cardiometabolic risk, and a mismatch with imposed work or school hours, known as social jetlag, has been linked to obesity, mood disorders, and impaired metabolic health.

The circadian rhythm is the body's roughly 24-hour internal cycle that coordinates sleep-wake timing, hormone release, body temperature, and metabolism. It is governed by the suprachiasmatic nucleus in the hypothalamus and entrained primarily by light exposure. Stable circadian alignment supports cardiometabolic health, immune function, and cognitive performance, while chronic disruption is linked to obesity, type 2 diabetes, and accelerated biological aging.

The cortisol awakening response (CAR) is a sharp rise in salivary cortisol of roughly 50 percent on average (commonly reported in the range of about 38 to 75 percent) from the awakening sample to a peak about 30 to 45 minutes after waking. It reflects healthy hypothalamic-pituitary-adrenal axis activation, mobilising energy and focus for the day. A blunted or exaggerated CAR is associated with chronic stress, burnout, depression, sleep disorders, and adverse cardiometabolic outcomes, making it a useful marker in longevity and stress research.

Deep sleep, or slow-wave sleep (N3), is the stage characterised by high-amplitude delta waves on EEG and the highest arousal threshold. It dominates the first third of the night and drives growth hormone release, cardiovascular recovery, immune regulation, and glymphatic clearance of metabolic waste. Deep sleep declines with age, and lower amounts are associated with poorer memory and increased risk of neurodegenerative disease.

The glymphatic system, described by Iliff, Nedergaard and colleagues in 2012, is the brain's waste-clearance pathway, in which cerebrospinal fluid flows along perivascular spaces, exchanges with interstitial fluid, and removes metabolic byproducts such as beta-amyloid and tau. Activity increases substantially during sleep (and under anaesthesia in animal models), when the interstitial space expands by roughly 60 percent (Xie et al., 2013). Impaired glymphatic clearance is implicated in Alzheimer's disease and other neurodegenerative conditions, making sleep a key intervention point for brain longevity.

Melatonin is a hormone secreted by the pineal gland in response to darkness, signalling biological night and helping align the circadian system. It facilitates sleep onset, modulates core body temperature, and exerts antioxidant effects. Endogenous melatonin declines with age, and bright evening light suppresses its release. Low-dose exogenous melatonin is used to address jet lag, shift work, and delayed sleep-phase patterns.

Polysomnography (PSG) is the gold-standard multi-channel sleep study conducted in a laboratory setting, simultaneously recording electroencephalography (EEG), electrooculography (EOG), electromyography (EMG), electrocardiography (ECG), respiratory airflow, effort, and oxygen saturation. Sleep stages—N1, N2, N3 (slow-wave), and REM—are scored in 30-second epochs according to the AASM manual using EEG, EOG, and EMG channels. PSG is the reference standard for diagnosing obstructive and central sleep apnea (via apnea-hypopnea index), narcolepsy, REM sleep behavior disorder, and periodic limb movement disorder. Consumer wearables and actigraphy are validated against PSG but typically underestimate N3 and N1 and overestimate sleep efficiency.

REM (rapid eye movement) sleep is a sleep stage marked by fast eye movements, vivid dreaming, near-waking brain activity, and skeletal muscle atonia. It increases toward the second half of the night and supports memory consolidation, emotional processing, and synaptic plasticity. Reduced REM duration has been associated in epidemiological studies with higher all-cause mortality, cognitive decline, and impaired mood regulation.

Sleep apnea is a disorder of repeated breathing pauses or shallow breathing events (apneas and hypopneas) during sleep, most commonly obstructive sleep apnea from upper-airway collapse, less often central sleep apnea from disrupted respiratory drive. The AASM diagnoses it at an apnea-hypopnea index of at least 5 per hour with symptoms, or at least 15 without. Untreated, it raises the risk of hypertension, atrial fibrillation, stroke, type 2 diabetes, cognitive decline, and all-cause mortality.

Sleep architecture refers to the cyclical organisation of sleep stages across the night, typically comprising four to six 90-minute ultradian cycles each progressing through N1, N2, N3 (slow-wave sleep), and REM, with N3 dominating early cycles and REM expanding in later ones. Healthy young- to middle-aged adult sleep contains roughly 13–23% N3 and 20–25% REM (with N3 declining to <10% by age 70), though normative ranges vary with age, sex, and assessment method. Disruptions to architecture—including suppression of N3 by alcohol, fragmentation of REM by sleep apnea, or the age-related decline of slow-wave sleep—have functional consequences for memory consolidation, hormonal secretion, immune regulation, and cardiovascular recovery, making architectural metrics a key target in longevity-oriented sleep assessment.

Sleep efficiency is the percentage of time spent asleep relative to the total time in bed, calculated as total sleep time divided by time in bed. Values of 85 percent or higher are generally regarded as healthy in adults. Low sleep efficiency reflects fragmented or inefficient sleep and is associated with daytime fatigue, impaired glucose metabolism, elevated cardiovascular risk, and poorer subjective quality of life.

Sleep latency is the time from lights-out to the first epoch of sleep, typically measured in minutes during polysomnography. A latency of about 10 to 20 minutes is considered healthy; very short latencies (under roughly 5 to 8 minutes) can indicate sleep deprivation or excessive daytime sleepiness, while persistently longer values suggest insomnia or circadian misalignment. It is a core metric in polysomnography and consumer sleep trackers used in longevity contexts.

The two-process model, proposed by Alexander Borbély in 1982, describes sleep-wake regulation as the interaction of two independent processes: Process S (homeostatic sleep pressure), which accumulates as adenosine and other somnogens build up during waking and dissipates during sleep, and Process C (the circadian signal), generated by the suprachiasmatic nucleus and imposing a roughly 24-hour oscillation in alerting drive that opposes increasing sleep pressure toward evening to maintain sustained wakefulness. Sleep occurs when Process S exceeds the circadian alerting threshold. The model successfully explains phenomena such as the post-lunch dip, rebound deep sleep after sleep deprivation, and the sharp morning wake boundary, and remains the dominant framework for circadian and sleep medicine research.