Lifestyle and Behavioral Enhancements of Sleep: A Review

Abstract

Background: Sleep is a foundational pillar of health, influenced by numerous genetic, behavioral, lifestyle, and environmental factors. As non-pharmacologic strategies gain prominence, evidence-based approaches are needed to guide clinical practice. Methods: This expert narrative review synthesizes findings from observational studies, randomized trials, meta-analyses, and clinical guidelines, emphasizing the importance of lifestyle and behavioral interventions for sleep enhancement. Topics include sleep hygiene, circadian rhythm regulation, cognitive behavioral therapy for insomnia (CBT-I), exercise, nutrition, substance use, menopause, and consumer sleep technology. Results: Key findings support the importance of circadian alignment through light exposure, sufficient sleep quantity and timing, and behavior modification in sleep health. Exercise and weight management benefit general sleep quality and specific conditions like obstructive sleep apnea. While nutrition shows mixed direct effects on sleep, Mediterranean and low-glycemic diets are associated with fewer insomnia symptoms. CBT-I is a first-line treatment for chronic insomnia. Substances such as alcohol, cannabis, and caffeine exert varied and potentially deleterious effects on sleep regulation. Conclusion: Sleep is critical in health. Multidimensional behavioral interventions offer significant potential for improving both sleep quality and quantity. Clinicians should integrate these low-risk strategies into patient care to address the growing burden of sleep disorders and to promote overall well-being.

“Obesity is linked to impaired sleep quality, short sleep duration, nocturnal GERD, and increased RLS and OSA risk.”

Introduction

This expert narrative review synthesizes the current evidence around non-pharmacological and behavioral strategies to improve sleep, with emphasis on mechanisms, population-level impacts, and clinical applications. This builds on the expanding understanding of the foundational nature of sleep and sleep health in enhancing well-being, health span, and life span.^1,2 Extensive literature has emerged around the relationship of sleep upon both general and neurocognitive health. Impaired sleep quality has been associated with the development of hypertension, ³ obesity and type 2 diabetes mellitus, ⁴ and cognitive decline.^5,6 Alterations in circadian health have demonstrated adverse outcomes affecting alertness, cardiovascular health, metabolic health, mental health, academic and cognitive performance, and health and safety. ⁷ Sleep disordered breathing, and the Apnea-Hypopnea Index (AHI) specifically, have emerged as significantly related to all-cause mortality, composite cardiac events, stroke, diabetes, and depression. ⁸ Insomnia and poor sleep have been implicated in a bidirectional relationship with mood disorders. ⁹ Further, the roles of alcohol, sedative-hypnotic class medications, and other psychoactive drugs including marijuana have fallen under scrutiny for their negative impacts on both sleep quantity and quality.^10,11

These sleep-health associations have naturally led to broader discussions of sleep optimization in the context of health enhancement. Indeed, expanded interest in lifestyle and behavioral interventions around sleep, sleep health, and insomnia have simultaneously both mirrored and been propelled by expanded public interest in the beneficial impacts of nutrition, exercise, and psychosocial enhancements towards overall well-being.

Normal Sleep

Sleep is essential to every process in the body. Sleep, or sleep-like states, are observed in nearly every animal, and are vital for our survival and overall health. They are critical for cardiovascular health, metabolic processes, and the immune system, and they facilitate memory consolidation and learning. Disruption in sleep can impair these vital functions.^12,13

Normal sleep is divided into two distinct stages: non-rapid eye movement (NREM) sleep and rapid eye movement (REM) sleep. These stages alternate in cycles throughout the night, with each cycle lasting approximately 90-110 minutes and repeating four to six times per night. NREM sleep dominates in the early part of the night and is primarily involved in restorative processes, such as muscle repair, immune system strengthening, and energy conservation. REM sleep becomes more prevalent towards the morning and is primarily associated with learning, memory consolidation, and emotional regulation.^14,15

The regulation of sleep is governed by two key processes: the circadian rhythm (Process C) and the internal or homeostatic sleep drive (Process S). Process C, the internal biological clock, regulates the timing of sleep and wakefulness in alignment with the 24-hour light-dark cycle. Process S, the homeostatic sleep drive, increases “in pressure” during wakefulness and decreases during sleep. Together, these two processes interact in a “push-pull” fashion to regulate sleep timing, duration, and quality. ¹⁶

The duration of normal sleep varies by age and individual factors. For adults, the National Sleep Foundation recommends at least 7-9 hours of sleep each night for optimal health and well-being. Children and adolescents require longer sleep durations, with children ages 6 to 13 needing 9-11 hours and teenagers ages 14 to 17 needing 8-10 hours of sleep per night. ¹⁷

Sleep quality and duration are influenced by genetic, physiological, psychological, lifestyle, and environmental factors. Inconsistent sleep schedules, caffeine or alcohol consumption, and lack of physical activity can disrupt sleep patterns. ¹⁸ Environmental factors like noise, light, and room temperature affect the sleep environment, while medical conditions such as sleep apnea can impair sleep continuity. ¹⁹ Psychological factors such as stress, anxiety, and depression are also linked to poor sleep and insomnia. Addressing these factors is essential for improving sleep and overall health. ²⁰

Sleep Hygiene

Sleep hygiene broadly describes behaviors and modifiable lifestyle and environmental factors that promote sleep quality. Sleep hygiene encompasses both behaviors before bed (e.g., diet, exercise, substance use) and environmental conditions during the sleep period (e.g., light, noise, and temperature). Nor is sleep hygiene limited only to the 1 or 2 hours immediately prior to the sleep period—outdoor time, daily sunlight exposure, exercise, and other daytime behaviors also may exert strong influences. Importantly, sleep hygiene principles are applicable both in the presence (e.g., insomnia) and absence of sleep disorders and are universally relevant to all persons.^21,22

Sleep hygiene is frequently employed in clinical sleep research as a treatment for insomnia, yet there is little consensus on what actually constitutes optimal sleep hygiene. ²² Based on the sleep hygiene review by De Pasquale, observational and interventional studies most commonly include sleep hygiene components such as caffeine, alcohol, exercise, sleep timing/regularity, light, napping, smoking, noise, and temperature. ²¹

The American Academy of Sleep Medicine guidelines for behavioral and psychological treatments for chronic insomnia disorder advise against the use of sleep hygiene as a single-component treatment for insomnia. ²³ Three randomized clinical trials examined the effect of sleep hygiene vs control therapy on patients with chronic insomnia.^24-26 The delivery and education of sleep hygiene varied widely and, when used alone, did not produce clinically significant improvements in insomnia symptoms. ²³ When sleep hygiene was used as a control group in studies evaluating other interventions, it was found to be less effective than the active treatments. ²⁷ Sleep hygiene education is often considered inexpensive; however, it can be resource intensive. While no formal cost analyses have been performed, this minimally effective treatment may redirect resources from more effective alternatives. ²³

Although sleep hygiene is not recommended as a standalone treatment for insomnia due to limited evidence supporting its effectiveness, certain basic principles (e.g., avoiding excessive caffeine or alcohol) can still be beneficial as part of a broader treatment plan. Additionally, addressing sleep hygiene factors is a key component of Cognitive Behavioral Therapy for Insomnia (CBT-I) (discussed below), the gold standard treatment for insomnia.

Sleep Quantity

Improving sleep health starts with sleep quantity, as inadequate sleep is the most prevalent sleep disorder in the world. According the 2009 Morbidity and Mortality Weekly Report, ²⁸ 35% of respondents reported sleeping less than 7 hours nightly on average and nearly 5% reported nodding off at the wheel within the preceding month. Underscoring the public health urgency of this topic, the 2013 review by de Mello et al ²⁹ estimated that in the United States alone 56,000 accidents annually are related to inadequate sleep and, in the United Kingdom, driver fatigue is implicated in 20% of highway accidents and up to 1 quarter of fatal and serious collisions.

As reported in the systematic review by Cappuccio et al, ³⁰ habitual short or long duration sleep, commonly defined as either less than 5-7 hours per night (12% greater risk) or greater than 8-9 hours per night (30% greater risk) are both longitudinally associated with increased all-cause mortality. The heightened mortality for long duration sleep was primarily attributable to an increase in non-cardiovascular deaths, whereas the heightened mortality associated with short sleep duration were predominantly linked to cardiovascular causes. Importantly, the study authors point out that the mechanisms underlying these associations are not fully understood, with hypothesized putative mechanisms including increased calorie intake, reduced energy expenditure, impaired glycemic control, cortisol secretion derangements, and low-grade inflammation, whereas long duration sleep factors include confounding medical comorbidities, mood disorders, low socioeconomic status, unemployment, lack of physical activity, poor general health, and cancer-related fatigue.

Circadian Health, Light, and Wellness

Whereas behavioral influences such as sleep quantity and “time awake” affect “Process S” [of the two-process sleep model], light inputs and circadian consistency affect “Process C,” our internal biological clock. Light is the key zeitgeber—“timekeeper”—in the circadian rhythm. The body’s “master clock” is governed by neurons in the suprachiasmatic nucleus (SCN) of the hypothalamus. There, the circadian system receives input—primarily light—through the retina to align the internal clock with the external light-dark cycle.^31,32 The SCN also synchronizes peripheral clocks in organs such as the liver, adipose tissues, gastrointestinal tract, thyroid gland, and adrenal gland, regulating metabolism and energy homeostasis through neuronal and humoral signals.^33-35

Light exposure is fundamental in regulating both sleep patterns and overall wellness, and how and when we experience light has broad neurocognitive impacts.^36,37 Exposure to natural light during the day, especially in the morning, helps synchronize our rhythm with the external environment. ³⁷ Natural daylight at high intensities has been shown to advance the timing of sleep to earlier hours, lengthen the sleep duration, and improve sleep quality.^38,39 Daytime light exposure can also enhance mood, memory, and cognitive performance.^40,41 Additionally, sunlight exposure facilitates vitamin D synthesis, which is crucial for bone health and immune system function. ⁴² Circadian rhythms play a crucial role in cardiovascular health by modulating blood pressure, heart rate, catecholamine levels, blood coagulation markers, and vascular endothelial function, each of which have 24-hour rhythms. ⁴³ A well-regulated circadian system supports mood stability and reduces the risks of depression, anxiety, and cognitive decline by maintaining neurochemical balance and emotional resilience.^32,44

Circadian misalignments—such as delayed or advanced sleep-wake phase disorders, and shift-work disorder—occur when the body’s internal clock is out of synchrony with external cues like light and darkness. ³⁵ These disruptions, often caused by irregular sleep schedules or excessive nighttime light exposure, can lead to serious health effects. They are linked to altered lipid metabolism, endocrine effects including reduced insulin sensitivity, increased nocturnal cortisol, impaired thyroid-stimulating hormone secretion, and increased risk of metabolic syndrome, inflammation, cardiovascular disease, and cancer.^34,36,39,40 Chronic circadian disruptions are also linked to mood disorders including depression and anxiety and risks of neurodegenerative disease progression.^45,46

While exposure to natural light during the day is beneficial, excessive or mistimed exposure to artificial light, particularly blue light emitted by electronic devices, can be harmful. Studies have shown that evening blue light specifically suppresses melatonin production, delays sleep onset, and reduces sleep quality by reducing the amount and timing of REM sleep. ⁴⁷ This is physiologic, as naturally occurring blue wavelength light is most prevalent mid-day, roughly 10 a.m. to 2 p.m. Mistimed (evening) artificial blue wavelength light, such as that emanating from ubiquitous smart phones, televisions, and computers, has been found to shift circadian rhythms, impair next-morning alertness, increase cognitive fatigue, and lead to insomnia and other sleep disorders. ⁴⁸ Bedtime and in-bed use of portable screen-based devices is associated with an increased likelihood of inadequate sleep quantity, poor sleep quantity, and excessive daytime sleepiness. Mechanisms of adverse impact are hypothesized to include direct displacement, delay, and interruption of sleep time, psychological stimulation, and a direct light-circadian effect. ⁴⁹ These sleep disruptions are particularly relevant in adolescents, who are at increased risk of poor mental health, including depression. ⁵⁰ Long-term, these sleep pattern disruptions are associated with an increased risk of obesity, diabetes, and cardiovascular diseases. ⁵¹

In addition to the harmful effects of mistimed artificial light, insufficient exposure to natural light, often caused by modern indoor lifestyles or a reduced amount of sunlight during the winter, can lead to mood disorders, such as seasonal affective disorder (SAD). ³⁷

It is also notable that the varied dimensions of circadian health and sleep quantity (e.g., duration, efficiency, regularity, and timing) are not equally distributed across the population. Racial and ethnic minorities are, on average, more likely to suffer from insufficient sleep (e.g., <7 hours), lower sleep efficiency, greater variability in sleep timing, circadian misalignment, and excessive daytime sleepiness. ⁵²

Several interventions can help mitigate the adverse effects of artificial light exposure. ⁵³ Dimming lights in the evening and increasing exposure to natural light during the day can result in appropriate light exposure that aligns with the circadian, neuroendocrine, and neurobehavioral functions. ⁵³ Reducing evening exposure to blue light by using blue-light-blocking glasses is a potentially effective strategy, although the evidence is mixed.^54,55

Structured light exposure therapy, such as bright light therapy, has been shown to improve circadian alignment and alleviate symptoms of mood disorders like SAD. ⁵⁶ Physicians should advise limiting the use of electronic devices before bedtime, including the implementation of targeted educational programs emphasized healthy sleep hygiene practices and the risks associated with nighttime digital media use.^50,57

Given the significant health consequences of circadian misalignment and insufficient sleep, healthcare providers play a crucial role in identifying and addressing these issues. Behavioral approaches such as cognitive behavioral therapy for insomnia (CBT-I), light therapy, and chronotherapy (gradual adjustment of sleep-wake times) help realign sleep schedules with natural circadian rhythms. ⁵⁸ For example, bright light exposure in the morning can help patients with delayed sleep-wake phase sleep disorder advance their sleep-wake schedule, while appropriately timed melatonin supplementation has proven effective in resetting the circadian clock for individuals with jet lag or shift-work disorder. ⁵⁹ Physicians may also consider screening for sleep disorders such as sleep apnea or restless leg syndrome, which can further exacerbate circadian disruptions and worsen sleep deprivation.^60,61

By addressing these factors and promoting healthy sufficient sleep, healthcare providers can help mitigate the negative effects of poor sleep and improve patient outcomes. Healthcare providers can and should encourage patients to adopt healthy sleep habits, such as maintaining a consistent sleep schedule, limiting artificial light exposure before bedtime, and creating a sleep-friendly environment. ⁶²

Insomnia

Insomnia is defined as difficulty initiating or maintaining sleep, or poor sleep quality, that occurs despite adequate opportunity for sleep, and which results in significant daytime dysfunction. ⁶³ This condition is highly prevalent and affects about one third of the general population. Risk factors for insomnia include increasing age; female gender; comorbid medical, psychiatric, sleep, and substance use disorders; and shift work. ⁶⁴ Chronic insomnia, as opposed to short-term insomnia disorder, exceeds 3 months. ⁶⁵ Chronic insomnia has important adverse public health and societal impacts, impairing individual health, mood, and quality of life; decreasing academic performance and work productivity; increasing risk of motor vehicle accidents; and increasing health care utilization. ⁶³

Cognitive behavioral therapy for insomnia (CBT-I) is a mainstay of treatment. ⁶⁴ Sessions are typically delivered over six to 8 weeks, focus on each individual’s specific sleep patterns, and address underlying perceptions about sleep based on a “3P model” that targets predisposing, precipitating, and perpetuating factors of insomnia. ⁶⁶

CBT-I is typically comprised of two core components: sleep restriction and stimulus control, as well as two adjunctive components: sleep hygiene and cognitive therapy. ⁶⁷ Sleep restriction (SR) aims to match an individual’s total sleep time to their time spent in bed. In this way, SR increases the homeostatic sleep drive thus reducing the sleep onset latency, or the time it takes to fall asleep. Stimulus control (SC) aims to strengthen a learned association of the bed with sleep by avoiding engaging in screen-time and other activities in bed aside from sleep or sex. ⁶⁷ Finally, cognitive therapy involves reframing any maladaptive perceptions about sleep that can perpetuate insomnia.

Based on large-scale meta-analyses, there is compelling evidence that sleep restriction reduces insomnia severity and improves self-reported perception of sleep continuity and sleep quality.^68,69 Additionally, stimulus control effectively improves total sleep time. ⁶⁸ Importantly, studies have shown that CBT-I is at least as effective as pharmacologic therapy at treating insomnia, ⁷⁰ and CBT-I has an advantage over pharmacologic therapy in both its permanence and that it carries neither the side effect profiles of the various sedative-hypnotics nor the inherent concerns related to the neurocognitive impacts of long-term use. Studies examining sedative-hypnotics use and dementia risk have shown significant associations, particularly in the elderly population.^71,72 By empowering patients, CBT-I may also have more durable longer lasting effects as compared to pharmacologic therapy.^66,70

Nutrition, Sleep, and Fasting

Patterns of eating, including food choice, timing of eating, and the presence or absence of caloric excess, all have significant sleep influences. Obesity is at epidemic levels and has increased in prevalence worldwide over recent decades. Per the Centers for Disease Control February 2020 report on obesity, the age-adjusted prevalence of obesity among U.S. adults was 42.4% in 2017-2018. ⁷³ Medical implications and associations of obesity are widespread and include obstructive sleep apnea (OSA), cardiovascular disease, type 2 diabetes mellitus (T2DM), non-alcoholic steatohepatitis, osteoarthritis, and several cancers, among others. ⁷⁴ Obesity contributes to obstructive sleep apnea via increased upper airway fat deposition and anatomic obstruction, increases in abdominal girth leading to decreases in lung volumes and resultant increased risk of nocturnal hypoxemia, and neuronal dysfunction of pharyngeal dilator muscles. ⁷⁵

Obstructive sleep apnea exists in a bidirectional relationship with T2DM, with each serving as a risk factor for the other. ⁷⁶ The Apnea-Hypopnea Index (AHI), the primary measure of sleep apnea severity, has been identified as an independent risk factor for insulin resistance, with increases in the AHI associated with increases in insulin resistance independent of the presence of absence of obesity. ⁷⁷  Weight loss, however, has been demonstrated to result in clinically significant AHI reductions in obese patients with T2DM and obstructive sleep apnea, with 3 times as many study participants in the active weight loss intervention group achieving total remission of their OSA as compared to the non-intervention group. ⁷⁸

In addition to the direct deleterious effects of sleep apnea upon sleep quality and excessive daytime sleepiness, both increasing body mass index (BMI) and OSA are positively correlated with the occurrence of gastroesophageal reflux disease (GERD),^79,80 which is itself associated with a risk of insomnia, short sleep duration, and sleep disturbance. ⁸¹ Treatment of OSA highly significantly decreases the frequency of nocturnal GERD symptoms. ⁸²

Short sleep duration, as well as other dimensions of poor sleep, are associated with obesity, obesity risk, and longitudinal rate of weight gain. This relationship between poor sleep and obesity may also exist bidirectionally, with poor sleep affecting poor dietary choice. ⁸³ Mechanistically, this short sleep and obesity association may be in part related to sleep duration impacts on appetite regulating hormones. In a 2020 systematic review and meta-analysis, Lin and colleagues ⁸⁴ noted significantly elevated ghrelin levels in short sleepers, as well as rises in both leptin and ghrelin in sleep deprivation groups. And also in 2020, Spaeth and colleagues ⁸⁵ demonstrated that sleep restriction is associated with daily caloric excess (+527 kcal).

The influence of specific nutritional constituents upon sleep quality however is less clear. In their 2023 review of influences of nutrition and food on sleep, Netzer and colleagues ⁸⁶ concluded that there was no evidence that certain food types have a measurable impact on sleep, either subjectively or via polysomnography. Arab and colleagues ⁸⁷ however, in their 2024 systematic review and meta-analysis, concluded that higher adherence to the Mediterranean diet, a high-quality diet, and diets with low-glycemic loads and indices were associated with a lower prevalence of insomnia symptoms.

Finally, in their 2021 review of intermittent fasting impacts upon sleep, McStay and colleagues noted that neither time restricted eating nor alternate day fasting appeared to have significant impacts on sleep quality, duration, or insomnia symptoms, though, as the authors point out, study participants had healthy sleep at baseline, and thus the studies were likely underpowered to detect significant changes. ⁸⁸

Restless Legs Syndrome

Restless legs syndrome is a sleep disorder characterized by primarily lower extremity unpleasant sensations, typically with an evening or bedtime onset, associated with an irresistible urge to move the legs. Both age and family history are important determinants of primary RLS, whereas secondary RLS is associated with various conditions including iron deficiency, diabetes, renal failure, Parkinson’s disease, and pregnancy. In a 2016 prospective cohort study assessing lifestyle factors and risk of restless legs syndrome, a dose response relationship between healthy lifestyle factors defined as normal weight, physical activity, non-smoker, and some (as opposed to none) alcohol activity had a lower risk of developing RLS. Obesity in particular was associated with RLS symptoms, with each increase of BMI by 5 kg/m² increasing the odds of having RLS. ⁸⁹

Substances (Alcohol, Cannabis, Caffeine)

Alcohol

Psychoactive substances exert profound influences upon sleep, with alcohol being amongst the most used. According to a 2023 National Survey on Drug Use and Health, 67% of US adults aged 18+ consumed alcohol in the past year. ⁹⁰ Alcohol profoundly impacts both normal and pathologic sleep. It acts as an indirect y-aminobutyric acid (GABA) agonist, increases the sensitivity of serotonin receptors, enhances dopaminergic activity, and antagonizes N-methyl-D-aspartic acid (NMDA) receptors, all of which are involved in the regulation of sleep.^45,46

Although some individuals may use alcohol as a sleep aid due to its hypnotic properties, it is ineffective in treating insomnia. Alcohol’s effects include reduced sleep onset latency and increased slow-wave sleep the first half of the night; however, this is typically followed by fragmented and disturbed sleep the second half. The effect on REM sleep appears to be dose dependent with reduced REM density in the first half of the night, followed by increased stage 1 sleep in the second half of the night.^47,48

There is a high correlation between insomnia and alcohol use disorder. Studies have demonstrated insomnia rates of 36-91% either while drinking or within several weeks of abstinence. Chronic alcohol use has also been associated with lower slow-wave sleep and increased REM sleep, which may persist despite abstinence from alcohol. Individuals in early sobriety from chronic alcohol use experience decreased sleep efficiency and increased self-reported sleep disturbances, which should be taken into clinical account when treating patients for alcohol use disorder. ⁵⁰

Alcohol also weakens pharyngeal dilator muscle tone, thus increasing upper airway resistance and exacerbating obstructive sleep apnea. ⁴⁶ A meta-analysis of 21 studies estimated that individuals who consume alcohol have a 25% higher relative risk of obstructive sleep apnea compared to non-drinkers, with the risk of OSA increasing proportionally with the amount of alcohol intake. ⁵¹ Moreover, a study with 11,800 participants found that STOP-BANG scores correlated with the frequency of alcohol consumption, quantity of alcohol consumed, and frequency of binge drinking. ⁵²

Cannabis

The increasingly frequent use of cannabis in disordered sleep outpaces the evidence supporting its benefit.^53,54

The two most widely studied compounds in marijuana are cannabidiol (CBD) and Δ⁹-tetrahydrocannabinol (THC). ⁵⁵ Other compounds found in cannabis include cannabinol (CBN), cannabigerol (CBG), and cannabichromene (CBC).^54,56 CBD has been proposed to have anxiolytic effects.^55,57

Cannabis can have varied effects, including relaxation, sedation, and appetite stimulation, whereas observed adverse effects have been noted to include impaired concentration and psychomotor coordination, paranoia, psychosis, conjunctival injection, dry eyes, dry mouth, inhalation burns, and cannabinoid hyperemesis syndrome.^55,58,59 Cannabinoids can be smoked, taken orally (via sublingual absorption, edibles or THC-infused beverages), or inhaled through an experimental dry powder inhaler.^60-62 At higher doses, liver function test abnormalities have been observed in cannabis users, and cannabinoid receptor upregulation has been noted in liver disease.^63-65

Cannabis can also affect sleep, although the evidence of its effects on specific stages of sleep is mixed and warrants further investigation. Cannabis use within 3 hours prior to sleep has been associated with increased proportion of stage 1 sleep, ⁹¹ as well as correlated with an increase in stage 3 non-REM sleep. ⁹² THC in particular has been shown in several studies to reduce percentage of REM sleep ⁹³ and also to decrease sleep latency and increase sleep duration. ⁹⁴ Acute THC ingestion has been associated with increased slow-wave sleep, whereas chronic use has been associated with decreased slow-wave sleep, which may suggest tolerance with long-term use. ⁹⁵ Total sleep time is decreased in chronic THC use. ⁹⁵ There is mixed evidence as to the effect of cannabis on wake after sleep onset (WASO), with some studies suggesting an increase in WASO(93) and others suggesting a decrease. ⁹⁵

Cessation of cannabis can precipitate withdrawal symptoms, including difficulty with sleep initiation and maintenance as well as depressed mood, anxiety, and restlessness. ⁹⁴ Prior studies have noted sleep disturbance in approximately 76% of daily marijuana users who stop using marijuana. ⁹⁶ Acute abstinence has been associated with reduced total sleep time, sleep efficiency, percentage of total sleep time spent in REM, and increased wake after sleep onset and periodic limb movements. Marijuana users who experience sleep disturbances in the setting of acute cessation have reported a relapse in cannabis use as well as other substances such as alcohol.^96,97

Cannabinoids in Insomnia

In recent years, trials have shifted away from THC monotherapy for insomnia, focusing more on combination therapies or other cannabinoids, such as CBD and CBN. ⁵⁴

Despite the known sedative effect of CBD, the evidence for use of CBD in sleep is limited. In a study of 28 healthy participants randomized to 50 mg of CBD vs placebo, there was no significant difference in sleep quantity. However, the CBD group reported improved sleep quality based on a self-reported questionnaire. ⁶⁷ Other studies suggested that this may be due to a psychological effect rather than a direct sleep-related change. ⁶⁸ Subjective accounts of improved sleep can conflict with diagnostic data from more objective measures of sleep.^98,99 When measured against objective polysomnography in a crossover, double-blind trial of 27 healthy volunteers receiving 300 mg CBD vs placebo, there were no significant differences in wake after sleep onset, sleep onset latency, or sleep efficiency. ⁶⁹

A separate study of combination therapy with THC:CBN:CBD, in an experimental 20:2:1 mg/mL formulation, noted subjective improvement in sleep. There was also an objective increase in total sleep time and decrease in wake after sleep onset when measured by home actigraphy over two weeks, although this effect was not found on a single-night polysomnogram.^93,100

The generalizability of the above trials is limited but these findings warrant further investigation.

Cannabinoids in Obstructive Sleep Apnea

The use of cannabinoids in obstructive sleep apnea (OSA) has been explored and is subject to an ongoing debate within the literature.

The Pharmacotherapy of Apnea by Cannabimimetic Enhancement (PACE) Trial was a Phase II, fully blinded, parallel group, placebo-controlled randomized clinical trial of dronabinol in patients with moderate to severe OSA. Dronabinol at 2.5 and 10 mg per day dosed over 6 weeks was found to reduce the apnea-hypopnea index (AHI) compared to placebo in adults with moderate or severe OSA. ⁷⁰

Nevertheless, the American Academy of Sleep Medicine (AASM) published a position statement cautioning that the long-term safety and tolerability of dronabinol remained unknown, and, as such, did not recommend cannabinoids for treatment of OSA. ⁷¹

Cannabis in Restless Leg Syndrome

There is limited evidence supporting the use of cannabinoids for restless leg syndrome (RLS). Cannabinoids may provide relief of RLS through nociceptive pathways. ⁷² A small observational study of six patients who had already failed other therapies, including dopamine agonists such as ropinirole and pramipexole, suggested complete relief of RLS symptoms following cannabinoid ingestion via smoked marijuana or sublingual CBD. ⁷³ However, the mechanism of relief remains unclear, as this may be related to cannabis’ anxiolytic and sedative-hypnotic properties. ⁷² A post hoc exploratory analysis of patients with Parkinson’s disease and REM sleep behavior disorder in a parallel, double-blind, placebo-controlled phase II/III trial evaluated the effects of CBD (75 to 300 mg) on RLS symptoms. After 14 weeks, there was no significant difference between the CBD and placebo groups based on responses to the Restless Legs Syndrome Rating Scale. ⁷⁴ Reviews have concluded that there is insufficient evidence for the routine use of cannabinoids for the treatment of sleep disorders due to the lack of large-scale randomized clinical trials, potential bias, and reliance of subjective assessments, although existing findings suggest future direction for research.^54,75

Caffeine

Caffeine is the most widely consumed stimulant in the world. In the United States, up to 89% of adults consume caffeine. ⁷⁶ Caffeine, also known as 1,3,7-trimethyxanthine, reaches peak circulation within approximately 1 hour. ⁷⁷ The half-life of caffeine is estimated to be 4-5 hours in healthy adults, although this range can vary widely depending on concurrent use of substances such as tobacco, as well as environmental and genetic factors. ¹⁰¹ The amount of caffeine per serving of coffee varies based on preparation method, coffee blend, and even between the same blend of coffee purchased on serial days.^77,78 In addition to coffee and tea, caffeine is found in cocoa beans and kola nuts, and is added to energy drinks and other food products. ⁷⁶

Caffeine modulates sleep as an adenosine receptor antagonist.^77,79 Adenosine, a byproduct of ATP degradation in the brain, is thought to increase in concentration during both wakefulness and sleep deprivation, and is likely involved in the adaptive homeostatic sleep drive. ¹⁰² Specific agonists of adenosine A₁ and A_2A receptors have been shown to increase slow-wave sleep and EEG slow-wave activity. Studies in animal models in the 1980s and 1990s showed an increase in extracellular adenosine levels during wakefulness and a decrease during sleep. Caffeine enhances the perception of alertness or wakefulness.^80,81 Caffeine intoxication, however, can lead to restlessness, insomnia, muscle twitching, and psychomotor agitation, among other symptoms. ⁸² Withdrawal symptoms may include sleepiness, attentional lapses, headaches, mood disturbances, low motivation, flu-like symptoms, and impaired cognitive performance.^82-85

The timing of caffeine consumption influences sleep. A 200 mg dose in the early evening was found to delay endogenous circadian melatonin rhythm by approximately 40 minutes. ¹⁰² In a randomized controlled study of 12 healthy subjects, 400 mg of caffeine 6 hours before bedtime reduced total sleep time by more than 1 hour. ⁹⁰ Consumption even earlier in the day, at approximately 7 am, was still found to lower sleep propensity and total sleep time. ¹⁰³ Finally, in a double-blind crossover study of caffeine and total sleep deprivation, caffeine consumption during continuous wakefulness was associated with decreased recovery total sleep time and N3 sleep,^87,91 and in sleep deprived individuals with routine daily caffeine intake, recovery sleep was more fragmented with an increased frequency of long awakenings, decreased sleep stability, and greater wake after sleep onset duration. ⁸⁷

Patients should be counseled on appropriate caffeine use and its potential exacerbating effects on insomnia. Caffeine-induced sleep disruption can lead to a cycle that perpetuates insufficient sleep followed by more caffeine intake. Patients with persistent insomnia are advised to abstain entirely from caffeine.

Menopause and Hormonal Changes Affecting Sleep

Menopause brings significant hormonal changes that directly impact sleep quality and patterns. As estrogen and progesterone levels decline, many women experience increased sleep disturbances. Estrogen plays a role in regulating body temperature and modulating key neurotransmitters. Its decline can lead to hot flashes and night sweats that disrupt sleep continuity. ¹⁰⁴ Progesterone has natural sedative properties through its action on GABA receptors. ¹⁰⁵ Progesterone levels also decrease during menopause, contributing to fragmented sleep. Progesterone helps maintain upper airway muscle tone and respiratory drive, and its loss may make postmenopausal women more vulnerable to airway collapse during sleep, increasing the risk of obstructive sleep apnea. ¹⁰⁶

Sleep disruption is extremely common during the perimenopausal period, with 40-70% of peri- and postmenopausal women reporting sleep-related issues (Moline 2003). However, these disturbances are frequently underdiagnosed, as they are often misattributed to normal aging or comorbid conditions such as anxiety and depression. ¹⁰⁷ As a result, sleep disorders in menopausal women often go untreated, despite their significant impact on overall health and quality of life.

There are several treatment options for managing menopause-related sleep disruption. Hormone replacement therapy can be effective in reducing hot flashes and improved sleep quality, though it must be used with medical guidance due to potential risks of coronary heart disease, stroke, venous thromboembolism, and dementia. ¹⁰⁸ Cognitive behavioral therapy for insomnia (CBT-I) can be an effective treatment for menopausal insomnia. ¹⁰⁹ For women with suspected sleep apnea, evaluation and possible treatment with CPAP may be necessary. In some cases, short-term use of sleep aids may be considered under a clinician’s supervision. An individualized approach, addressing both hormonal and behavioral factors, is typically the most effective strategy.

Consumer Sleep Trackers/Wearables

Consumer wearable sleep trackers (CWSTs)—such as smartwatches, rings, and wristbands—have seen rapid growth since their introduction in the late 2000s, driven by affordability and user-friendly technology. ¹⁰⁹ Patients increasingly bring CWST data to clinicians seeking insights into their sleep, yet no standardized guidelines exist for interpreting this information. ¹¹⁰ As these devices gain popularity, clinicians must understand their benefits and limitations to use them effectively in practice.

CWSTs use multisensory modalities including accelerometry to assess motion, photoplethysmography to assess heart rate variability, and other sensors that collect data such as respiratory rate, oxygen saturation, and skin temperature. These data are processed via proprietary algorithms to estimate sleep stages and physiologic assessments.^110,111 While newer CWSTs demonstrate improved performance, limitations remain. Most validation studies compare CWSTs to polysomnography in healthy individuals, limiting their applicability in those with sleep or cardiopulmonary disorders. Additionally, some biosensors, such as pulse oximeters, have not been validated for all skin pigmentation types, potentially under-detecting hypoxemia in individuals with darker skin.^112,113 CWSTs often overestimate sleep and underestimate wakefulness due to difficulty detecting motionless wake periods. As lifestyle or entertainment devices, CWSTs are not regulated by the Food and Drug Administration ¹¹⁴ and there is a lack of transparency regarding the proprietary algorithms that each device uses, which raises concern regarding the accuracy and reliability of data. ¹¹¹

While some studies suggest that CWSTs can improve patient perception of sleep quality and function as an adjunctive treatment to CBT-I,^115-117 further data validation is needed across diverse patient populations before they can be reliably incorporated into clinical care.

Exercise

Exercise is essential for the maintenance of overall sleep health. Moderate aerobic exercise increases sleep duration and slow-wave sleep, which is important for memory consolidation, growth, and immune function. ¹¹⁸ By reducing stress levels, physical activity can improve overall sleep quality in terms of both sleep onset and sleep maintenance.^62,119 Exercise has also been found to increase production of melatonin, which may help to regulate the circadian sleep-wake cycle. ¹²⁰

In patients with obstructive sleep apnea (OSA), weight loss has been associated with improved OSA severity and sleep architecture, and decreased excessive daytime sleepiness.^121,122 Even in the absence of significant weight loss, the implementation of regular physical activity through an exercise program of 150 minutes/week of moderate-intensity aerobic activity led to improvement in the severity of OSA, reduced fatigue, and decreased excessive daytime sleepiness, and to an overall significant improvement in daytime functioning and quality of life.^123,124 In patients with chronic insomnia, exercise has led to improved sleep quality, reduced sleep onset latency, and an increase in total sleep time.^125,126

Conclusion

Sleep and sleep health have innumerable lifestyle and behavioral correlates. Importantly, many of these relationships can be described only as associations, with undefined or unproven biochemical and molecular pathways. That said, there exists a clear picture of complex but readily apparent bidirectional relationships between “healthful” habits, both directly sleep-related and not, which benefit both sleep and overall health.

Sufficient sleep quantity is the bedrock of sleep health, with a recommended adult duration of 7 to 9 hours. Adolescents, teenagers, and younger children require even more. Circadian consistency is equally important, using the light and dark queues of the Sun to anchor our sleep schedule. To maintain that consistency, patients should avoid behavioral and social disruptors of sleep timing, including keeping artificial light—and, in particular, the ubiquitous smartphone—out of the darkened nighttime bedroom.

Exercise, nutrition, and avoidance of excess adiposity are not just pillars of general health and well-being—they support, enhance, and nourish healthy restorative sleep. Exercise increases both sleep duration and slow-wave sleep. Nutrition, specifically the Mediterranean diet and diets prioritizing low-glycemic loads, have been associated with a lower prevalence of insomnia symptoms. Obesity is linked to impaired sleep quality, short sleep duration, nocturnal GERD, and increased RLS and OSA risk.

These lifestyle and behavioral targets—and numerous others—are examples of “no harm” interventions that clearly have broad health benefits extending well beyond the silo of sleep and sleep health. They are neither groundbreaking nor revolutionary and are in line with longstanding doctor-to-patient recommendations. Unfortunately, the barrier to progress is also a familiar one—resistance to change. Multidisciplinary strategies to overcome behavioral inertia include clinician time investment in the educational process, goal setting and action planning, behavioral counseling with allied health professionals including dieticians and therapists, and follow-up with accountability.

ORCID iD

Artal Roy https://orcid.org/0009-0006-9083-8924