Alcohol and Sleep-Related Problems

Abstract

Alcohol is one of the most commonly used psychoactive substances in the community. Many individuals use alcohol for its sleep-promoting effects. Nonetheless, alcohol disrupts sleep through multiple mechanisms, such as disrupting electrophysiologic sleep architecture, triggering insomnia, and contributing to abnormalities of circadian rhythms and short sleep duration (SSD) in cross-sectional studies. Alcohol also increases breathing-related sleep events such as snoring and oxygen desaturation, especially in those with pre-existing problems. Emerging data demonstrate that insomnia may co-exist with SSD and circadian abnormalities. Future studies should unravel these tentative associations in individuals who misuse alcohol.

1. Introduction

Adults in the U.S. commonly drink alcohol. A recent survey demonstrated that more than half of the adult respondents consumed alcohol in the past month [1], many of whom drink in moderation, whereas some indulge in heavy drinking. Heavy drinking is defined as the consumption of ≥ 5 drinks per day for ≥ 5 days within the past 30 days [2]. This heavy drinking pattern is common among individuals with alcohol use disorder (AUD) and may be associated with an elevated risk for injuries or medical and psychiatric comorbid disorders [3]. A group of comorbidities at the interface of medical and psychiatric disorders are those that involve sleep. Prior studies have linked alcohol consumption and AUD with sleep-related disorders such as insomnia, circadian rhythm abnormalities, and breathing-related sleep disorders [4–6]. In this review, we highlight some of these findings and discuss how some of these disorders may be interlinked.

2.1. Common sleep-related problems

The homeostatic drive is responsible for the onset and maintenance of sleep in healthy individuals and it accumulates over the course of the day to reach a critical threshold before the onset of sleep in the evening. A commonly occurring disorder that is linked to a weakened homeostatic drive is insomnia disorder. Insomnia disorder involves problems with sleep continuity at night and daytime ramifications from the lack of sleep for about half the days of the week and for a duration of three or more months [7]. The complaints related to sleep continuity consist of one or more of the following: difficulty falling asleep, difficulty maintaining sleep, or waking up earlier than desired. The daytime dysfunction problems may include fatigue or malaise, concentration problems, impaired psychosocial functioning, mood disturbance or daytime sleepiness. Insomnia as a disorder may be perpetuated by behaviors such as lying in bed when not sleepy and by pairing the bed with non-sleep related behaviors such as watching television. Cognitive aspects of insomnia may include a preoccupation with the potential consequences of insomnia, such as an inability to fall asleep for an hour may lead to the individual to the conclusion that s/he will not be able to sleep through the entire night. These behaviors and cognitive distortions may lead to a conditioned arousal around bed time. Insomnia as a disorder (insomnia) is perpetuated when transient insomnia is coupled with such above-mentioned cognitive and behavioral abnormalities.

In addition to the homeostatic drive, the normal sleep-wake cycle is also linked to an underlying circadian rhythm. The suprachiasmatic nucleus within the hypothalamus in the brain is the master clock that synchronizes a host of internal rhythms with the sleep-wake cycle being one of them. Light is the primary stimulus involved in synchronizing an organism’s internal rhythm in the circadian clock with the external environment. In addition to light, other cues such as physical activity or feeding are considered as non-photic cues that can be used to reset the circadian clock. Non-photic phase-resetting is the process of shifting and/or synchronizing the circadian clock using non-photic stimulus. The circadian clock may modulate sleep-wake cycle with the help of melatonin.

Melatonin is a hormone produced by the pineal gland and is responsible for the onset of sleep during the circadian night. Dim Light Melatonin Onset (DLMO), a commonly used marker for the circadian pacemaker, measures the onset of melatonin secretion under dim light conditions [8]. DLMO usually occurs about 2–3 hours before sleep onset [9]. A mismatch between the individual’s internal (biological) rhythm and the required environmental schedule leads to circadian rhythm sleep disorders. These disorders are associated with complaints of an inability to fall asleep or stay asleep, with or without daytime sleepiness, and impaired daytime functioning. Two common types of circadian rhythm sleep disorders relevant to alcohol use include delayed sleep phase disorder (DSPD) and shift work disorder. DSPD is characterized by going to bed later at night and awakening later in the morning in order to function optimally through the day. In contrast, shift work disorder involves working against the individual’s normal sleep-wake rhythm by engaging in evening or night shifts.

In addition to disorders of the circadian rhythm, human beings also exhibit a trait-like preference for their timing of sleep and wakefulness that is called chronotype (also known as morningness-eveningness and circadian preference). Chronotype is a product of both the homeostatic sleep drive and the circadian timing [10]. Chronotype can be conceptualized as being categorical (“morning”, “evening”, and “indeterminate” or “neither” types) or dimensional (ranging from extreme morningness to extreme evenigness) in nature. The “evening” type (greater eveningness) individual prefers a later bedtime and a later rise time and has a greater need for sleep. This chronotype is commonly seen in adolescents and those with psychiatric disorders. Conversely, the “morning” type individual (greater morningness) prefers an earlier bedtime and an earlier rise time. Moreover, chronotype is a dynamic trait that changes across the lifespan. As children grow older and approach adolescence, many of them may experience a shift towards eveningness, a phenomenon seen commonly in boys [11]. Beyond the second decade of life, individuals tend to revert back towards morningness [12]. The clinical significance of eveningness is that emerging evidence has linked it with an increased risk for psychopathology such as alcohol misuse [5].

2.2. Alcohol’s association with sleep disorders

2.2.1. Alcohol & insomnia.

Alcohol use has been associated with sleep continuity disturbance in a bi-directional fashion. Studies using moderate doses of alcohol (<1g/Kg) have demonstrated decreased REM sleep duration as a consistent finding, especially in the second half of the night. However, in those drinking heavily (>1g/Kg), alcohol use (when compared to placebo), has been associated with a longer time to fall asleep, a lower percentage of time in bed spent sleeping, and an increased wake after sleep onset time; see review [4]. As the night progresses (and the blood alcohol level decreases), the first two stages of NREM sleep (N1 and N2) increase, REM sleep increases, multiple awakenings occur, and sleep efficiency (time spent in bed sleeping through the night) decreases. This disruption may continue even after the acute effects of alcohol have subsided[4].

In children and adolescents, difficulty falling asleep [13] and overtiredness have been linked to alcohol use [14]. Heavy alcohol use and AUD have been linked to subjective insomnia and objective sleep continuity disturbance**[15, 16]. Epidemiologic studies have shown that frequent alcohol consumption and heavy drinking episodes is associated with insomnia symptoms in different populations such as community adults [17], Veterans [18], and older adults [19]. Furthermore, Haario and colleagues demonstrated that this association between insomnia and heavy drinking is bi-directional. In other words, heavy drinking at baseline predicted future insomnia symptoms; conversely, insomnia symptoms at baseline increased the risk of future heavy drinking behavior [15]. In those with AUD, the prevalence of insomnia ranges from 36–91% (as compared to the 10% prevalence in the general population). Insomnia is prevalent in all stages of AUD, i.e., active during the active drinking phase, acute alcohol withdrawal, and during recovery [4, 20]. The prevalence of insomnia decreases when these individuals transition from active drinking to abstinence, with persistent insomnia being a risk factor for relapse for them [4]. Insomnia has been shown to remit with sobriety and an improvement in other lifestyle factors [21], whereas persistent drinking has been linked to continued complaints of disturbed sleep [22]. An underlying mechanism for this continued insomnia may be a blunted homeostatic drive after short-term partial sleep deprivation [23]. Furthermore, there may be some genetic overlap between insomnia and AUD, as demonstrated by data from adult twins from the Virginia twin registry *[24].

2.2.2. Alcohol and circadian rhythm abnormalities.

Alcohol consumption and AUD have been linked to abnormalities of the circadian rhythm. Animal studies indicate that alcohol disrupts circadian timing via effects on photic and non-photic phase-resetting [25]. In healthy adults, alcohol consumption has been shown to blunt their overall normal diurnal variation in core body temperature rhythm **[26] and decrease salivary melatonin levels [27]. A delayed onset of melatonin secretion has been linked to an increased severity of substance use and related problems in adolescents and young adults [5]. Furthermore, a growing body of knowledge has linked eveningness (later bedtime) with alcohol consumption. A twin study involving 1127 twin pairs has shown a genetic predisposition of eveningness with alcohol consumption. In this study, twins with greater eveningness, when compared to the twins with greater morningness, were more likely to consume higher amounts of alcohol and binge-drink*[28]. Other studies have also linked eveningness to alcohol consumption in a range of populations, such as adolescents **[29], college students [30, 31], and adults [32]. In contrast to these studies, one investigation failed to demonstrate such an association between chronotypes and alcohol consumption in high school students[33].

Increased alcohol use among those with eveningness may be a consequence of an effect called social jet lag (i.e., shifts between sleep timing on weekdays and weekends), that results in chronic circadian misalignment [5]. Indeed, multiple studies have reported that a variability weekday-weekend sleep timing is linked to alcohol use in cross-sectional and longitudinal studies [5]. Interestingly, one recent study in adolescents found that weekday-weekend shifts in sleep timing were associated with an altered neural response to reward [5]. This modified response to reward may increase the risk of developing substance abuse problems in adolescents.

A misalignment in the circadian rhythm may also result from shift work where the work schedule may push the sleep-wake cycle out of synchrony with the circadian clock and its preferred sleep-wake cycle. A link between shift work and alcohol use has recently started to emerge. Those working on the evening shifts may have a higher risk of circadian phase delay with alcohol use, i.e., later sleep-wake times. In one study of healthy adults (N=22), night-shift workers who consumed 0.5 g/kg of alcohol for seven days demonstrated a circadian phase delay [34]. In contrast, no such phase delay was demonstrated in those working the daytime shift. In another study involving multiple industries, workers in long rotating shifts were demonstrated to consume a greater number of drinks within a 24-hour period. Furthermore, workers who complained of more frequent sleep problems were seen to have higher alcohol consumption *[35].

2.2.3. Alcohol and Short Sleep Duration (SSD).

Alcohol consumption and AUD have been linked to SSD, i.e., sleep duration <6 hours at night [4]. Furthermore, community-based studies have demonstrated that insomnia comorbid with SSD is associated with an increased risk of morbidity and mortality **[36] although its prevalence in the alcohol-consuming population is unknown. These combined disorders may have an impact on treatment response and recidivism, Figure 1.

Figure 1.

The Association between Alcohol and Sleep-Related Disorders

2.2.4. Alcohol and Breathing Related Sleep Disorder.

Drinking has been linked to snoring and obstructive sleep apnea syndrome (OSA). In a recently-published meta-analytic review of 14 studies, alcohol consumption was shown to worsen breathing-related events in sleep, especially in those with a history of snoring and OSA*[6]. Moreover, alcohol prolonged the duration of respiratory events and lowered the minimum oxygen saturation levels, but it did not seem to influence the therapeutic positive airway pressure needed to control these disordered-breathing events during sleep. In summary, patients with breathing-related sleep disorders should avoid consuming alcohol, especially before bedtime.

2.3. Do complex phenotypes involving insomnia and circadian rhythm abnormalities co-exist?

Borbely’s two-process model explains that sleep commences at the intersection of the peak homeostatic (sleep-promoting) and nadir of the circadian (alertness-promoting) drives [37]. Given the above evidence that alcohol disrupts both the homeostatic and circadian drives, it is possible that insomnia and circadian abnormalities may coexist in some individuals who are using or recovering from alcohol misuse. Evidence for such an association comes from multiple areas of research. Recent genetic epidemiologic studies have linked insomnia (associated with alcohol use) to polymorphisms on PER2 and PER3 genes involved in the regulation of the circadian clock [38, 39]. Clinical evidence from recovering individuals with AUD (but without habitual circadian phase delay or advance) has demonstrated the presence of circadian abnormalities. In one study, increased sleep latency was associated with a delayed onset of the plateau of nocturnal serum melatonin level [40]. Another study showed an 18-minute delay in DLMO, when compared to healthy controls [41]. Thus, individuals with AUD may have a delay in nocturnal melatonin parameters that may be coupled with difficulty falling asleep, a feature of insomnia disorder. Therapeutic evidence for such a phenomenon comes from a recent open-label study that evaluated cognitive behavioral therapy for insomnia (CBT-I) in Veterans with comorbid depression and insomnia. This study showed that CBT-I not only improved insomnia and depression scores but also shifted individuals towards a morning chronotype*[42].

2. Conclusion.

In summary, alcohol misuse (heavy alcohol use and AUD) appears to be linked in a bi-directional fashion to sleep-related problems such as insomnia and circadian rhythm abnormalities. Furthermore, an evening chronotype and greater shifts in weekday-weekend sleep-wake schedules have been linked to alterations in the brain sensitivity to reward and possibly a change towards greater substance use behavior. The recommended treatment for insomnia disorder in the community, as well as those with AUD, is CBT-I. Given that some individuals with insomnia have intertwined circadian abnormalities, it may be useful to consider chronotherapeutic interventions such as bright light in addition to CBT-I in these individuals, as it has been shown to be efficacious for sleep onset insomnia [43].

Many questions arise as new data elaborates on sleep problems associated with alcohol use. Alcohol consumption decreases with increasing age. Individuals shift from an evening to a morning chronotype as they grow older. Is it possible that this shift in the sleep-wake cycle towards morningness with aging is associated with a decrease in alcohol consumption? Are individuals with insomnia and coexisting chronobiologic abnormalities at a higher risk of relapse to insomnia and/or alcohol use after being treated for insomnia? In other words, is CBT-I sufficient as monotherapy in these individuals, or should additional interventions targeting circadian disorders be considered, such as melatonin, bright light therapy or circadian phase delay (Figure 1)? We hope that future studies in this field will answer these emerging questions.

Highlights.

• Alcohol use is linked to disruption of architecture of electrophysiologic sleep

• It has been affiliated with insomnia, short sleep and circadian abnormalities

• Alcohol can aggravate breathing-related sleep problems during sleep

• A link between alcohol use and complex insomnia phenotypes is also emerging