Sleep Maintenance (Staying Asleep)

Sleep Maintenance (Staying Asleep): A Nutritional and Natural-Health Reference

1. Definition and Clinical Presentation

Sleep maintenance refers to the ability to sustain continuous, consolidated sleep once it has been initiated. The DSM-IV defines insomnia as difficulties in sleep onset (or initiation), difficulties in sleep maintenance, or sleep that is non-restorative. Sleep maintenance insomnia is thus the subtype characterised by nocturnal disruption rather than difficulty falling asleep in the first place.

Sleep maintenance problems may take several forms, including frequent awakenings, an increase in time spent awake after initially falling asleep (wake time after sleep onset, or WASO, which is a robust measure of sleep maintenance), sleep fragmentation (transient microarousals appearing on an EEG but not necessarily involving full wakefulness), and unrefreshing sleep.

Insomnia is defined as difficulties of initiating and maintaining sleep, early awakening, and poor subjective sleep quality despite adequate opportunity and circumstances for sleep, with impairment of daytime performance. From an epidemiological perspective, insomnia is a highly prevalent condition associated with significant morbidity, reduction in quality of life, and increase in healthcare costs, and is a risk factor for multiple physical and mental disorders.

2. Body Systems Involved

2.1 The Two-Process Model of Sleep Regulation

Sustained sleep depends on the interaction of two complementary biological systems. The urge to sleep is guided by two factors: sleep drive and the circadian rhythm. Sleep drive refers to a homeostatic system in the brain which makes one feel sleepy; with every hour of wakefulness, sleep drive grows stronger. The homeostatic sleep drive (Process S) accumulates during wakefulness and promotes the initiation of sleep. After the first half of the sleep episode, this sleep drive rapidly diminishes. This diminishment in the second half of the night is why sleep maintenance difficulties frequently manifest as early-morning awakening or fragmented sleep in the latter portion of the night.

A properly aligned circadian system maintains low alertness during the night, particularly in the latter half of the night, helping to promote sleep consolidation until morning wake-up time. Sleep continuity or sleep consolidation is an important determinant of sleep quality. The circadian process has a strong impact on this characteristic of sleep, such that the duration of awakenings is much shorter during the biological night than during the biological day.

2.2 The Central Nervous System: Key Structures

From a neurobiological perspective, sleep is a highly regulated physiologic state with multiple neural substrates for sleep and wakefulness that are extensively distributed throughout the brain. Studies of how VLPO (ventrolateral preoptic area)-mediated sleep maintenance can be disrupted via input from various pathways may yield insights into basic mechanisms of arousal during NREM and REM sleep. Evidence that the galaninergic cell group in the VLPO shrinks with age in humans raises the possibility that this cell group may be the basis for insomnia that develops in the elderly.

Comorbid insomnia originates from neurodegenerative, inflammatory, traumatic, or ischaemic changes in sleep-regulating brainstem and hypothalamic nuclei with consecutive changes of neurotransmitters. Gamma amino butyric acid (GABA) is a sleep-promoting neurotransmitter in the central nervous system. Benzodiazepines exert their effect by increasing GABA binding to the GABA-A receptor, resulting in increased intracellular chloride, membrane hyperpolarisation, and signal inhibition — a mechanism that illustrates the central importance of GABAergic tone in sustaining sleep.

2.3 The Circadian and Neuroendocrine Systems

The intrinsic circadian timekeeping system modulates many physiological processes, including daily rhythms in core body temperature, melatonin secretion, cortisol, endocrine and immune function, and metabolism. Circadian rhythms play a vital role in a person's ability to sleep in one consolidated block of time at night. As the sun sets in the evening, the brain begins producing melatonin, a hormone that induces sleepiness.

Insomnia with the prominent and persistent symptoms of difficulties in initiating and maintaining sleep is in general not considered a circadian sleep disorder. Yet an excessive strength of the evening wake maintenance zone or reduced circadian promotion of sleep during the night may contribute to these symptoms. It has been reported that in 10–22% of insomnia patients, the timing of sleep relative to the melatonin rhythm is abnormal, such that sleep is attempted to be initiated at an early "melatonin time."

2.4 The Hyperarousal Model and the HPA Axis

Hyperarousal is a 24-hour state of elevated cognitive and physiological activation and is a core feature of insomnia. The extent to which sleep quality is affected by stressful events — so-called sleep reactivity — is a vulnerability factor for developing insomnia. Insomnia is a highly prevalent disorder and a state of 24-hour hyperarousal is considered a key factor of this condition. Various physiological markers of hyperarousal have been investigated, including the activity of the HPA axis.

Results suggest that patients with insomnia show moderately increased cortisol levels (SMD = 0.50, 95% CI: 0.21–0.80). This elevation in cortisol, the primary end product of HPA axis activity, is thought to promote arousal and interfere with the normal suppression of wakefulness that is required for sustained sleep.

It appears that (1) central nervous system hyperarousal, either as pre-existing and/or induced by psychiatric pathology and deteriorated by stressful events, (2) specific personality traits and inadequate coping mechanisms, and (3) aging- and menopause-related physiological decline of sleep mechanisms, are at the core of this common sleep disorder.

3. Contributing and Associated Factors

3.1 The Three-P Model

The most commonly accepted model of insomnia aetiology is the 3P model, which characterises aetiology based on predisposing, precipitating, and perpetuating factors. When a patient with particular predisposing factors experiences a trigger or precipitant, they develop a maladaptive pattern of coping which leads to the perpetuation of insomnia.

3.2 Age-Related Changes

Evidence that the galaninergic cell group in the VLPO shrinks with age in humans raises the possibility that this cell group may be the basis for insomnia that develops in the elderly. The lack of sleep or poor sleep patterns can have significant impacts on a variety of essential day-to-day functions. The various chronic health conditions linked to irregular rhythms include diabetes, obesity, depression, bipolar disorder, seasonal affective disorder, and other sleep disorders.

3.3 Menopause and Hormonal Transitions

Hot flashes, hormones, and psychosocial factors contribute to insomnia risk in the context of the menopausal transition. The incidence of sleep disturbance increases from 16–42% to 39–47% at peri-menopause and 35–60% at postmenopause. Spectral EEG analyses from large cohort studies demonstrate elevated beta power during NREM sleep, suggesting a state of physiological hyperarousal that persists across menopausal stages. Collectively, these findings indicate that menopause is associated with a shift toward lighter, more fragmented, and less stable sleep architecture, which contributes to poor subjective sleep quality and increased vulnerability to insomnia and daytime impairment.

Postmenopausal women frequently exhibit reduced circadian robustness and increased rhythm fragmentation. In a controlled study evaluating rest–activity cycles, wrist temperature, cortisol profiles, and polysomnography, postmenopausal women demonstrated phase advances of approximately one hour, lower rhythm amplitude, and greater circadian instability compared with premenopausal women. Melatonin secretion also declines with ovarian hormone deprivation.

3.4 Stress and Psychological Factors

Given the precipitation and apparent maintenance of insomnia by emotional distress, the relationship between the neurobiology of emotion and the neurobiology of sleep regulation is a potentially fruitful avenue for discovery. Several psychological and physiological factors contribute to the onset and perpetuation of insomnia, such as anxious-ruminative personality traits, stressful events, age-related sleep homeostasis weakening mechanisms, menopause, and biological–genetic diathesis of CNS hyperarousal.

3.5 Comorbid Medical and Neurological Conditions

Symptoms of neurological disorders (e.g., motor deficits), comorbidities (e.g., pain, depression, anxiety), and some disease-specific pharmaceuticals may cause insomnia and/or other sleep problems. Insomnia is highly prevalent in clinical practice and can present independently or alongside other medical and mental health disorders. Insomnia is a risk factor for the development and exacerbation of medical and mental health conditions.

3.6 Circadian Disruption

Disruptions from factors like irregular schedules, travel, shift work, screen time, or underlying health issues can throw off the internal clock and negatively impact sleep and overall well-being. Desynchrony between the internal circadian timing system and desired or required sleep-wake times, or alterations in the timing system itself, can result in one of six circadian rhythm sleep-wake disorders.

4. Melatonin

Traditional Use

Melatonin is an endogenous hormone secreted by the pineal gland in response to darkness. Its exogenous use as a supplement emerged primarily in Western countries beginning in the 1990s, drawing on the understanding that endogenous melatonin signals the onset of the biological night. It has been used across many populations specifically to realign the sleep-wake cycle after jet lag, shift work, or age-related decline in melatonin secretion rather than as a direct hypnotic in the traditional herbal medicine sense.

Scientific Evidence

Multiple databases were searched yielding 35 randomised controlled trials (RCTs) meeting the inclusion criteria of one systematic review. Overall, according to GRADE methodology, weak recommendations were made for preventing phase shifts from jet lag, for improving insomnia in both healthy volunteers and individuals with a history of insomnia, and for initiating sleep and/or improving sleep efficacy.

With respect to sleep maintenance specifically, the evidence is more limited and mixed. In patients with long-term insomnia, one systematic review reported no difference in sleep maintenance in patients who received melatonin (2 mg) compared to placebo, as measured using sleep diaries. In non-comorbid insomnia in adults, melatonin was not significantly effective in improving sleep onset latency, total sleep time, and sleep efficiency according to a meta-analysis of 24 RCTs published in 2022.

Findings from a network meta-analysis support the effectiveness of melatonin in improving sleep-onset difficulties, and of meditative movement therapies for self-reported sleep efficiency and severity of the insomnia disorder. As melatonin was not effective considering the sleep-efficiency index and severity of the disorder, it is likely that the use of melatonin should be combined with CBT-I to obtain significant clinical benefits.

Dose-response meta-analysis showed that melatonin gradually reduces sleep onset latency and increases total sleep time, peaking at 4 mg/day. Although the absolute benefit of melatonin compared to placebo is smaller than other pharmacological treatments for insomnia, melatonin may have a role in the treatment of insomnia given its relatively benign side-effect profile. Overall, the evidence for melatonin primarily supports effects on sleep onset and circadian realignment rather than sleep maintenance per se, and should be characterised as preliminary to moderate in strength for maintenance outcomes.

5. Magnesium

Traditional Use

Magnesium is an essential dietary mineral found in nuts, seeds, legumes, and leafy greens. Its use as a sleep-promoting remedy has roots in broader traditional practices associating magnesium-rich foods with nervous system calm, and it has been administered for muscle relaxation and anxiety in various European naturopathic traditions. It was not historically used as a targeted sleep botanical in the way that herbal medicines were, but modern nutritional medicine has applied it widely in this context.

Scientific Evidence

Observational research associates greater magnesium consumption with better sleep quality, including shorter sleep onset latency, longer sleep duration, and reduced daytime sleepiness. Clinical trials further suggest that magnesium supplementation enhances sleep efficiency and reduces insomnia severity, potentially through mechanisms such as increased melatonin production and reduced cortisol levels. A recent systematic review found an association between magnesium status and sleep quality in observational studies, but highlighted inconsistencies in interventional trials: two RCTs showed improvements in sleep efficiency, time, or latency, while three found no significant effects.

Magnesium deficiency in rats could disrupt the normal sleep-wake cycle by increasing wakefulness and reducing slow-wave sleep (SWS), and this effect was reversed upon the reintroduction of magnesium into their diet. This animal evidence provides a plausible mechanistic rationale, though its direct translation to human supplementation remains subject to the mixed clinical trial record described above.

Results from one study suggest that 6 weeks of magnesium L-threonate (Magtein®) improves overall cognition, cognitive age, working memory, reaction time, and some subjective, but not objective, measures of sleep in healthy adults with self-reported dissatisfied sleep. Importantly, this study received funding from Threotech Inc., which also provided the investigational product and was involved in the conceptualisation of the study design — a conflict of interest that limits interpretation.

Preclinical studies support associations between magnesium status, sleep quality, and symptoms of anxiety. The extent to which these claims are evidence-based is unclear. Overall, the evidence for magnesium supplementation on sleep maintenance in humans is preliminary and inconsistent; the mechanistic rationale is stronger than the current clinical trial data.

6. Tryptophan and Serotonin Precursors

Traditional Use

L-Tryptophan, an essential amino acid, has been used as a sleep-promoting supplement since at least the 1970s in Western naturopathic and nutritional medicine. Its use is grounded in its role as the dietary precursor to serotonin and subsequently melatonin, with the assumption that increasing substrate availability could support endogenous melatonin synthesis and promote sleep. Foods rich in tryptophan, such as warm milk, turkey, and seeds, have a deep folkloric association with sleepiness across multiple Western cultures.

Scientific Evidence

One study found that a novel nutritional blend consisting of tryptophan, glycine, magnesium, tart cherry powder, and L-theanine shortened sleep onset latency (P=0.002), increased total sleep time (P=0.01), improved sleep efficiency (P=0.03), and reduced morning drowsiness (P=0.02). However, because this was a multicomponent intervention, the independent contribution of tryptophan cannot be isolated from these results.

The tryptophan→5-HTP→serotonin→melatonin pathway is well-established biochemically. The melatonin and tryptophan content of tart cherries may contribute to their sleep-enhancing properties. Evidence for isolated tryptophan supplementation on sleep maintenance in robust human RCTs remains limited, and the multi-ingredient nature of most positive studies prevents attribution of effects to tryptophan alone.

7. Glycine

Traditional Use

Glycine is a non-essential amino acid and inhibitory neurotransmitter. It has no specific traditional use as a sleep remedy in classical herbal systems; its investigation as a sleep-promoting agent is a product of modern nutritional neuroscience research, beginning largely in Japanese academic laboratories in the 2000s and 2010s.

Scientific Evidence

The use of glycine as a therapeutic option for improving sleep quality is described as a novel and safe approach. However, despite clinical evidence of its efficacy, the details of its mechanism remain poorly understood. In animal studies with acute sleep disturbance, oral administration of glycine induced non-rapid eye movement (NREM) sleep and shortened NREM sleep latency with a simultaneous decrease in core temperature. Oral and intracerebroventricular injection of glycine elevated cutaneous blood flow at the plantar surface in a dose-dependent manner, resulting in heat loss. This thermoregulatory mechanism — promoting peripheral vasodilation and core cooling — is thought to be relevant to sleep maintenance because the maintenance of a lower core body temperature is important for sustaining consolidated sleep.

Glycine has been explored for its sleep-promoting properties due to its ability to interact with key neurotransmitter systems, including NMDA receptors. While evidence remains inconclusive, some studies suggest that glycine supplementation at a dose of 3 g can enhance sleep quality and reduce daytime fatigue, highlighting its potential as a supportive agent in sleep management. L-theanine and glycine seem to present promising sleep-promoting properties but the evidence base is currently classified as preliminary, with most human studies being small and short-term.

8. L-Theanine

Traditional Use

L-Theanine is a non-protein amino acid found almost exclusively in the leaves of Camellia sinensis (tea). It has been consumed as a constituent of green and black tea in East Asian cultures — particularly China and Japan — for centuries, with the relaxing yet non-sedating quality of tea being well recognised in those traditions. Its targeted use as a concentrated sleep supplement is a modern development.

Scientific Evidence

L-theanine and glycine seem to present promising sleep-promoting properties, while ashwagandha, myoinositol, Rhodiola rosea, and phosphatidylserine may be considered as subsidiary sleep aids by working in synergy with other soporific nutrients. A combination of GABA and L-theanine has been studied in one investigation showing that a GABA and L-theanine mixture decreases sleep latency and improves NREM sleep, published in the journal Pharmaceutical Biology. A magnesium-L-theanine complex has also been explored: a novel theanine complex, Mg-L-theanine, was reported to improve sleep quality via regulating brain electrochemical activity, published in Frontiers in Nutrition (2022). The overall evidence base for L-theanine as a standalone sleep-maintenance agent is preliminary, with many positive findings coming from combination-product trials that cannot attribute effects specifically to L-theanine.

9. Valerian (Valeriana officinalis)

Traditional Use

Valerian's medical use dates back to ancient Greece and Rome. Throughout history, people have treated migraine, tiredness, stomach cramps, and insomnia with valerian. In European herbal medicine traditions, the dried root was prepared as a tea or tincture for sedative and anxiolytic effects. It was widely listed in European pharmacopoeias during the 19th and 20th centuries as a mild nervous system sedative.

Scientific Evidence

The evidence on whether valerian is helpful for sleep problems is inconsistent. In its 2017 clinical practice guidelines, the American Academy of Sleep Medicine recommended against using valerian for chronic insomnia in adults.

Valerian (Valeriana officinalis L.) is a popular herbal medicine used as a sleep aid; however, the outcomes of previous clinical studies are inconsistent. Studies were conducted to update and re-evaluate the available data in order to understand the reason behind the inconsistent outcomes. PubMed, ScienceDirect, and Cochrane Library were searched; a total of 60 studies (n=6,894) were included in this review, and meta-analyses were performed to evaluate the effectiveness to improve subjective sleep quality (10 studies, n=1,065) and to reduce anxiety (8 studies, n=535).

By contrast, popular herbal remedies with a long-standing history of traditional medicinal use, namely valerian root extracts, lack adequate support to justify their use in individuals experiencing sleep disorders, according to a 2025 narrative review in Nutrition Reviews. One combination trial found that among 91 adults with insomnia treated with a fixed combination of valerian (300 mg), passionflower (80 mg), and hops (30 mg) or zolpidem at bedtime for 2 weeks, sleep time and insomnia index improved similarly in both groups. The overall evidence for valerian as a standalone sleep-maintenance agent is weak and inconsistent, and the herb's proposed mechanism via GABA modulation requires further elucidation in human trials.

10. Passionflower (Passiflora incarnata)

Traditional Use

Passiflora incarnata (maypop) is indigenous to the United States and Central and South America and was used by Native Americans to treat insomnia, hysteria, epilepsy, and as a mild analgesic. Passionflower is a flowering plant, extracts of which have been used as a mild sedative and sleeping aid. The genus Passiflora includes more than 500 species, which typically have complex and unique structures and flowers, and are found throughout much of the world. It was also incorporated into European herbal traditions as a calmative and was included in some national pharmacopoeias.

Scientific Evidence

Passionflower contains several flavonoids (apigenin, benzoflavone, and others), harmala alkaloids (hamaline, harmalol, harmine, and harmol), coumarins, maltol, phytosterols, and glycosides. A review of psychopharmacology and clinical evidence ranks passionflower as having evidence level "C" for efficacy in insomnia in humans. The evidence for passionflower specifically on sleep maintenance is very limited; most positive clinical signals come from small single trials or combination products, and the evidence is characterised as preliminary.

11. Ashwagandha (Withania somnifera)

Traditional Use

Ashwagandha, an adaptogen, is an important herb of Ayurveda used as a Rasayana for its various health benefits. In Ayurvedic practice, the root has been used for centuries as a tonic to support vitality, reduce stress, and promote restorative sleep. The name somnifera itself (Latin: "sleep-inducing") reflects this longstanding traditional association. It was traditionally prepared as a powder or decoction in warm milk.

Scientific Evidence

A total of five randomised controlled trials containing 400 participants were analysed in a 2021 systematic review and meta-analysis. Ashwagandha extract exhibited a small but significant effect on overall sleep (SMD –0.59; 95% CI –0.75 to –0.42; I² = 62%). The effects on sleep were more prominent in the subgroup of adults diagnosed with insomnia, and with treatment dosage ≥600 mg/day and treatment duration ≥8 weeks.

With specific reference to sleep maintenance, participants who took ashwagandha extract showed improvements in sleep efficiency (time in bed spent in sleep), total sleep time, sleep latency, and awakening after sleep onset as assessed by actigraphy. They also reported improvements in quality of life, according to the NIH Office of Dietary Supplements fact sheet on ashwagandha. Ashwagandha extract with a dosage ≥600 mg/day and treatment duration ≥8 weeks seems more effective. However, data on the serious adverse effects of ashwagandha extract are limited, and more safety data would be needed to assess whether it would be safe for long-term use. The evidence is preliminary to moderate in strength; most trials are small and many use proprietary extracts (KSM-66 or Shoden), and the high I² (62%) indicates substantial heterogeneity between studies.

12. Tart Cherry (Prunus cerasus)

Traditional Use

Sour or tart cherries have been cultivated across Europe and Asia for millennia and consumed as a food. Their specific use as a sleep aid is not part of a well-documented traditional medical system; interest in their sleep-related properties is an outgrowth of modern research into their phytochemical composition, particularly their naturally occurring melatonin and anthocyanin content.

Scientific Evidence

Tart cherries contain active compounds such as melatonin and anthocyanins that may be effective in improving sleep quality. In a systematic review incorporating seven interventional studies, three studies reported significant improvements in sleep indicators such as sleep duration, sleep efficiency, or sleep onset time. Three studies also reported an increase in melatonin levels after tart cherry consumption. Two studies also reported a decrease in inflammatory markers such as CRP and MDA.

The capacity of tart cherry juice to reduce oxidative stress and regulate healthy sleep–wake patterns has mostly been investigated in athletic populations. Converging evidence from these studies points to tart cherry juice supplementation as a potential strategy to improve recovery and exercise performance, and improving subjective sleep quality. One study reported significant improvements in the time spent in bed, total sleep time, and total sleep efficiency in the tart cherry group compared with the placebo group, as measured by actigraphy, in a 7-day crossover design. Tart cherry juice and its supplements appear to be well-tolerated, with no significant adverse effects reported in clinical trials. The overall evidence is preliminary but positive; trials are small and often short in duration, and the relative contributions of melatonin, tryptophan, and anthocyanins remain incompletely characterised.

The current body of literature converges to suggest that melatonin, magnesium, omega-3 fatty acids, tart cherry juice, kiwifruit, and apigenin-containing chamomile subjectively and objectively improve several sleep-related parameters and outcomes in young, older, and clinical cohorts.

13. Chamomile (Matricaria chamomilla / Chamaemelum nobile)

Traditional Use

Chamomile tea has been used as a calming bedtime beverage in European folk medicine for centuries, appearing in botanical texts since at least the Middle Ages. Its use as a mild sedative and anxiolytic was documented in German, British, and Southern European herbal traditions. The German Commission E has recognised Matricaria chamomilla flower preparations for use as a mild sedative and to relieve nervous restlessness.

Scientific Evidence

Apigenin-containing chamomile is among the ingredients supported by current literature as subjectively and objectively improving several sleep-related parameters. Apigenin, a flavonoid found in high concentrations in chamomile flowers, binds to benzodiazepine receptors on GABA-A receptors, providing a plausible mechanism for mild sedation. Evidence from human clinical trials on chamomile for sleep maintenance specifically remains limited in number and scale, and should be characterised as preliminary.

14. Dietary and Lifestyle Factors

14.1 Alcohol

Alcohol, a widely used psychoactive substance, produces a paradoxical sleep profile: it may facilitate sleep initiation immediately after ingestion but tends to fragment sleep later in the night, alter normal architecture (particularly decreasing REM sleep during the latter part of the night), and increase awakenings and non-restorative sleep. Consumption of alcohol decreases sleep latency and may disrupt sleep later due to its ability to influence levels of serotonin and norepinephrine. This rebound effect — with initial sedation followed by increased arousal and fragmentation in the second half of the night — makes alcohol a particularly salient contributing factor to sleep maintenance problems specifically, as distinct from sleep-onset problems.

Abstinence from alcohol (withdrawal) in alcoholics results in severe and protracted sleep disruptions. While acute withdrawal accompanies severe insomnia (difficulty in falling and staying asleep), insomnia, sleep fragmentation, and alteration in sleep architecture are observed for several years during sustained withdrawal from alcohol.

14.2 Caffeine

The observed increase in wake after sleep onset indicates that the consumption of caffeine disrupts sleep maintenance. Caffeine may cause brief episodes of wake across the sleep bout by reducing homeostatic sleep propensity and heightening arousal state. Consequently, sleep appears to be fragmented by recurrent awakenings following caffeine. Caffeine also affects sleep continuity/fragmentation — specifically increasing the number of long awakenings per hour of actual sleep time and increased frequency of awakenings from N1 sleep — as well as sleep stability and organisation.

Research indicates that the effects of caffeine on sleep depend on both dose and timing of administration, with a 100 mg dose having no significant impact on sleep up to 4 hours before bedtime, while a 400 mg dose negatively affects sleep when consumed anytime within 12 hours of bedtime.

14.3 Evening Diet Composition and Meal Timing

Research has explored the direct and indirect pathways from an evening diet high in ultra-processed foods, caffeine, and/or alcohol to sleep quality, including the roles of evening latency and individual factors, in a population-based study of 2,050 adults aged 18–65 years. Sleep quality was assessed using a composite score incorporating sleep duration, nocturnal awakenings, sleep latency, insomnia, and self-reported sleep quality. An increase in the sleep quality score (indicating poorer sleep) was observed for an evening sleep-disturbing diet.

There is evidence that particular whole foods affect sleep. The interval between the last eating event and sleep onset (evening latency) has been identified as a relevant mediating variable in dietary–sleep research, though optimal timing intervals have not been definitively established in large, controlled trials.

14.4 Physical Activity

Physical activity is identified consistently as a modifier of sleep quality in the nutritional and lifestyle literature. Structural equation modelling has been used to test the direct and indirect effects of an evening sleep-disturbing diet, evening latency (time between the last eating event and sleep onset), screen time before bedtime, age, physical activity, marital status, and BMI on sleep quality score. Physical activity was identified as a relevant factor in this model, and consistent with the broader literature, regular exercise appears to support sleep consolidation, though the relationship with sleep maintenance specifically is less well characterised than the effect on total sleep time and sleep onset.

14.5 Light Exposure and Screen Time

Maintaining a dark bedroom at night and getting sunlight as soon as one wakes can help keep melatonin levels in sync with the circadian rhythm. The circadian rhythm is the 24-hour internal clock in the brain that regulates cycles of alertness and sleepiness by responding to light changes in the environment. Exposure to artificial light — particularly short-wavelength blue light from screens — in the evening hours delays melatonin secretion onset and can reduce both sleep duration and consolidation; however, the specific effect on mid-night awakening requires further investigation distinct from its effects on sleep onset.

14.6 Sleep Hygiene and Behavioural Factors

Maintaining a consistent sleep schedule and daily routine, along with strategies like timed light exposure and melatonin supplementation when needed, are described as among the most effective ways to support a healthy circadian rhythm. Irregular sleep-wake schedules are associated with circadian desynchrony, which in turn impairs sleep consolidation in the latter half of the night when circadian sleep-promoting signals are critical for sustaining sleep.

15. Summary of Evidence Strength

• Melatonin: Moderate evidence for sleep-onset effects; weak-to-mixed evidence for sleep maintenance/WASO specifically. Primarily useful in circadian-related disruption and older adults with documented melatonin decline.
• Magnesium: Preliminary evidence; mechanistically plausible via GABA modulation and cortisol reduction. Inconsistent results across human RCTs. Animal data stronger than clinical data.
• Tryptophan: Most evidence from combination trials. Biochemical pathway well established. Insufficient isolated human clinical evidence for sleep maintenance.
• Glycine: Promising preliminary evidence, predominantly from small Japanese trials. Proposed thermoregulatory mechanism is plausible and novel. Needs larger independent replication.
• L-Theanine: Preliminary evidence; most positive findings from combination products. Standalone sleep-maintenance evidence very limited.
• Valerian: Inconsistent clinical evidence; recommended against by the American Academy of Sleep Medicine (2017). Long traditional use, but evidence does not adequately support efficacy for sleep maintenance insomnia.
• Passionflower: Very limited clinical evidence; evidence level rated "C" in systematic reviews of herbal psychopharmacology. Traditional use well documented.
• Ashwagandha: Preliminary-to-moderate evidence (5 RCTs, n=400). Small but significant effect on sleep including WASO in one NIH ODS-cited trial. Effect more prominent at ≥600 mg/day and ≥8 weeks.
• Tart Cherry: Preliminary positive evidence from small trials; plausible mechanism via melatonin and anthocyanin content. Most evidence from athletic populations and short interventions.
• Chamomile: Preliminary evidence; apigenin-GABA-A receptor mechanism plausible. Included among a broader list of convergently supported ingredients in recent reviews.
• Dietary factors (alcohol, caffeine, ultra-processed foods): Moderate-to-strong evidence that these disrupt sleep maintenance. Alcohol's rebound arousal effect in the second half of the night is among the better-established dietary contributors to nocturnal awakening.

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