Introduction

Recent studies have established the relationship between insomnia and alcohol use to be bi-directional,[1–3] illustrating the predictive nature of one morbidity on the other. Alcohol use causes around 88,000 deaths annually in the U.S. and these mortalities are largely attributed to high rates of alcohol use disorder (AUD).[4] AUD is a chronic disease characterized by heavy and uncontrolled drinking.[2,3] Almost two-thirds of individuals who have AUD have been found to suffer from comorbid insomnia.[5,6] Insomnia is a disorder of sleep continuity with symptoms including difficulty falling asleep or staying asleep.[3,7] About 55% of individuals who suffer from comorbid alcohol use disorder (AUD) and insomnia use alcohol, a common psychoactive substance, as a sleep aid.[5] Despite the perceived sleep benefits of alcohol,[1,2,8] difficulty falling asleep and overtiredness have been linked to alcohol use.[1–3,8,9]

Due to its sedative properties, alcohol is commonly used to self-medicate sleep abnormalities.[5,1,2,7] Within recent years, however, the concern over whether the use of alcohol for sleep can foster substance abuse disorders has become more relevant as one in four 18 to 30-year-olds reported binge drinking in 2021.[1] According to the scientific literature, heavy drinking is defined as the consumption of  ≥ 5 drinks per day for ≥ 5 days within the past month.[3,7] Researchers have more recently explored the bi-directional relationship between alcohol consumption and insomnia under an allostatic framework.[2] Through a feed-forward mechanism, the pathologies of insomnia and AUD affect one another; heavy drinking can serve as a predictor of insomnia and insomnia can serve as a predictor of heavy alcohol use.[2]

Although the mutual effects of insomnia and alcohol use have been investigated,[1,8,3,7] the literature on treatment interventions for individuals with comorbid AUD and insomnia is scarce. Similar reviews have explored the bi-directional relationship between alcohol use and insomnia, along with the extent to which each can serve as a potential risk factor for the other.[7-10] Current treatment interventions for insomnia and AUD, however, have remained virtually exclusive. No review to the best of the author’s knowledge has investigated the integration of this relationship into existing or novel treatment methods. Due to the frequent co-existence of both alcohol use and insomnia,[5,6] there is a specific need to utilize the bi-directional relationship between the two comorbidities in order to treat patients presenting with symptoms of both insomnia and AUD. Further investigation on this relationship can be used to develop novel intervention methods, specifically those that can simultaneously target comorbid insomnia and AUD.

This review provides an up-to-date summary of the bi-directional relationship between insomnia and alcohol use in order to frame the perspective in which possible treatment interventions for individuals with comorbid AUD and insomnia will be investigated. The misconceptions around the sleep benefits of alcohol will be analyzed through a feed-forward mechanism and then used to explore psycho-behavioral consequences such as hyperarousal, memory impairment, and anxiety. The feasibility of potential pharmacological and non-pharmacological treatments for patients with comorbid AUD and insomnia will also be evaluated.

Bi-directional Relationship of Comorbid Alcohol Use and Insomnia

Recent findings in the literature have demonstrated a discrepancy between the perceived sleep benefits of alcohol use and the objective measures of varying sleep parameters.[1,8,3] Alcohol consumption is said to have a hypnotic effect,[3,6] with its ingredients carrying sedative properties that result in feelings of relaxation, drowsiness, and reduced anxiety.[8,2,11] Many alcohol-dependent individuals with insomnia use alcohol as a way to self-medicate their sleep issues.[8-3] The subjective perception of improved sleep, therefore, propagates the use of alcohol, ultimately creating a feed-forward cycle in which insomnia and alcohol use promote one another.[2]

Alcohol use and sleep disturbances are associated in a bi-directional fashion.[1,2,7] This relationship has been understood through a feed-forward cycle, where alcohol-related disorders cause sleep dysregulation which further exacerbates alcohol use.[8,2] The allostatic framework in which this cycle is understood indicates that the physiological pathways that regulate the sleep-wake cycle are impacted by alcohol use.[2] As the body’s metabolism adjusts in response to heavy consumption, the homeostatic state is reset to an abnormal point that further drives alcohol use.[2] The adjustment in homeostasis is evident through the significant association between AUD patients and altered expression of circadian rhythm proteins.[12] As a result, general conclusions from recent studies have been drawn on the acute effects of alcohol on sleep. These effects include an increase in time spent awake after sleep onset, a reduction of the Rapid Eye Movement (REM) sleep stage, and a decrease in sleep efficiency.[8,2,7]

Inconsistencies exist between the available objective and subjective data on sleep efficiency among heavy-drinking individuals.[1,8,3] Previous literature has highlighted the impact of the interrelationship between alcohol use and insomnia, indicating that false beliefs have been formed about the effectiveness of alcohol as a sleep aid.[2] Self-reports by heavy-drinking young adults have indicated improved sleep efficiency on heavier-drinking days and on nights in which alcohol was consumed closer to bedtime.[1] Improvements in sleep quality is not supported, however, by objective data using wrist actigraphy or polysomnography.[1,8] Despite this contradiction, subjective sleep parameters such as sleep onset latency and sleep efficiency have been found to have a stronger association with future drinking behaviors than objective sleep measures such as time spent in REM sleep.[1] A novel interrelationship found in a 2022 study indicated an increase in the N2 light sleep stage in response to an increase in alcohol consumption.[8] As a result of this increase, the perceived sleep benefits of alcohol can be attributed to a faster sleep onset,[1-2] despite an objectively higher rate of sleep disturbances, poorer sleep quality, and higher nocturnal heartrate.[1-3]

Both the paradoxical effects of alcohol and misconceptions around the sleep benefits of alcohol foster a learned behavior of using alcohol to self-medicate insomnia symptoms.[2,3] This learned behavior can perpetuate alcohol dependency and, consequently, sleep-related disorders.[1] The long-term effects of alcohol dependence for mitigating sleep issues can develop into a tolerance towards its hypnotic effects,[3] ultimately promoting an increased level of alcohol consumption. The feed-forward cycle between insomnia and heavy alcohol use, therefore, directly impacts alcohol-related factors such as withdrawal and relapse.[2,3,10] Abstinent AUD individuals experience an increase in sleep onset latency and time spent awake after sleep onset.[2] This relationship is due to the experience of higher alcohol cravings, which have been associated with difficulty falling asleep.[2,3,7]

Psycho-behavioral Consequences of Alcohol Use and Insomnia

Recent literature has investigated the extent to which insomnia is a moderator of alcohol-related consequences and vice-versa.[11,10] Mutual outcomes resulting from alcohol-related and insomnia-related effects reinforce the bi-directional relationship between the two comorbidities. Additionally, psychological and behavioral factors associated with comorbid insomnia and alcohol highlight potential areas for targeted interventions. The psycho-behavioral consequences of comorbid alcohol use and insomnia can be explored through the mutual symptoms of hyperarousal,[8,10] memory impairment,[5,8,11] and anxiety.[2,4,10,13] 

Hyperarousal[8,10] and memory impairment[5,8,11] have been commonly found in both AUD and insomnia patients. Poor sleep has been associated with heightened cognitive arousal and poor cognitive performance,[8,11] with many insomnia patients using alcohol to cope with pre-sleep cognitive arousal.[8] Insomnia resulting from alcohol-induced hyperarousal has not been significantly associated with negative morning-after effects such as dysphoria or impaired psychomotor performance.[8] Additionally, a 2022 study that investigated the extent to which insomnia is a moderator of alcohol-related consequences did not demonstrate a significant association between insomnia and blackouts, or alcohol-induced amnesia.[11] It should be noted that despite the lack of association between insomnia and alcohol-related consequences, another finding in the literature has suggested a heightened sensitivity to alcohol-related effects in insomnia patients.[11] This finding suggests that less alcohol is needed to experience the physiological effects of alcohol use in individuals with insomnia.

Anxiety is often a comorbidity shared by individuals with AUD or insomnia.[2,4,10,13] Feelings of anxiety in alcohol-dependent individuals are commonly associated with alcohol withdrawal syndrome.[2,4,10] Patients presenting with comorbid addictive disorders and mental health disorders have been found to experience symptoms at a higher severity.[4] AUD individuals with co-occurring anxiety, therefore, present an increased risk for developing insomnia.[10] Excessive worrying, perfectionism, and neuroticism are all anxiety-related traits that can cause sleep disturbances among individuals with insomnia.[13] As a result, the diagnosis of an insomnia disorder can foster anxiety in AUD individuals.[10] The mediating effects of anxiety provides a mechanism by which emotional dysregulation and insomnia are linked in AUD individuals.[10] This interrelated association between AUD, insomnia, and anxiety suggests that targeting anxiety symptoms in AUD patients can potentially prevent the development of insomnia.

Current Treatments for AUD and Insomnia

Well-known pharmacological and non-pharmacological treatments currently exist for individuals presenting with either insomnia or AUD.[4,13,14] Clinical guidelines currently address alcohol use or insomnia as a precipitating factor for the other,[4,13] suggesting the treatment of one disorder can have downstream effects on the other.[5] The bi-directional relationship established between alcohol use and insomnia, however, proposes the use of treatment interventions that can target both comorbidities.

Recent literature has explored gabapentin as a potential drug treatment for both AUD and insomnia patients.[2,13-15] The observed effectiveness of gabapentin on alcohol withdrawal symptoms and short-term relapse prevention have been attributed to its ability to regulate sleep.[16] For people with insomnia, gabapentin has demonstrated an improvement in wakefulness after sleep onset, sleep efficiency, and total sleep time.[13,14] Additionally, in alcohol-dependent patients with comorbid insomnia, gabapentin has proven to have significantly reduced the risk of relapse to heavy drinking.[14] Quetiapine is another drug that has demonstrated improvements in both sleep continuity and alcohol cravings among individuals with comorbid insomnia and AUD.[3,15] In one study, however, quetiapine was found to exclusively improve sleep and not heavy drinking.[2] While the novel use of gabapentin and quetiapine for the treatment of comorbid insomnia and AUD is promising, other preliminary evidence on the efficacy of these drugs has been moderate or inconsistent[2,6,17,15]; therefore, the current literature on the use of gabapentin and quetiapine as pharmacological treatments for comorbid insomnia and AUD is limited.

The most effective, first-line non-pharmacological treatment for insomnia is Cognitive Behavioral Therapy for Insomnia (CBT-I).[5,9,6,10,15] Recent studies evaluating the effectiveness of CBT-I in the treatment of alcohol-related disorders have recommended CBT-I for individuals with co-occurring insomnia and AUD.[5,7,10,15] Binge-drinking individuals who underwent CBT-I to treat their alcohol disorder have demonstrated a decrease in alcohol-related consequences without any alcohol-related interventions.[5] By improving insomnia symptoms during the early stages of AUD treatment, CBT-I has been found to reduce cravings and relapse.[10,15] A contradicting study, however, demonstrated that CBT-I was not significantly effective in improving long-term abstinence.[6] A weakness identified in CBT-I intervention for AUD treatment is participant drop-out with the in-person time commitment being cited as a major reason.[5] Alternative online CBT-I interventions such as SHUTi have demonstrated efficacy in reducing insomnia severity and improving sleep efficiency[5,9]; however, research is currently not available on the efficacy of online CBT-I for treating insomnia patients with AUD. A study protocol proposed in 2018 has sought to address this gap in the literature but no follow-up has been provided.[9]

Conclusion

Under the mechanism of a feed-forward cycle,[2] the bi-directional relationship between heavy alcohol use and insomnia can be used to explain the mutual effects of one on the other.[1,2,7] Through the allostatic framing of comorbid AUD and insomnia,[2] alcohol has been found to have paradoxical effects on the mind and body.[8,2] This is best illustrated in the discrepancies found between objective and subjective data regarding the effects of alcohol on sleep.[1,8,3] Measures of perceived improvement in sleep onset latency and sleep efficiency have demonstrated to be more important to the subjective experience than contradicting objective measures.[1] Misconceptions of alcohol as an effective sleep aid, therefore, perpetuates both heavy drinking and sleep disturbances, ultimately fostering the development of AUD and insomnia disorders. Future research should aim to reconcile the discrepancies found between objective and subjective data on individuals with comorbid AUD and insomnia, specifically with a focus on preventing relapse in AUD individuals experiencing cravings during withdrawal. Furthermore, these findings suggest that clinical treatments should target the aforementioned subjective measures in order to mitigate the consequences of false misconceptions regarding the effects of alcohol and sleep.

Hyperarousal,[8,10] memory impairment,[5,8,11] and anxiety[2,4,10,13]  represent mutual symptoms of AUD and insomnia. Insomnia has not been found to be a significant moderator of alcohol-related consequences such as alcohol-induced blackouts[11] or morning-after effects.[8] Contrasting studies, however, suggest insomnia results in an increased sensitivity to effects of alcohol in patients presenting with insomnia.[11] On the other hand, anxiety plays a significant mediating role in individuals with AUD or insomnia.[10] The interrelationship between anxiety, AUD, and insomnia signifies anxiety’s role as a risk factor of comorbid AUD and insomnia. As a result, there is a need for further investigation on the psycho-behavioral mechanisms by which insomnia and AUD operates. The available research on the extent to which insomnia or AUD is a moderator of the other is inconsistent and limited. Future studies should investigate insomnia as a moderator of other alcohol-related consequences, such as alcohol-related harm, in order to extend the literature on the severity levels of comorbid insomnia and AUD outcomes. Additionally, the clinical treatment of anxiety as a risk factor can potentially provide a mediating effect to patients with comorbid AUD and insomnia.

The bi-directional relationship between insomnia and alcohol use suggests the use of multi-target pharmacological and non-pharmacological treatment options for addressing the related pathologies of each.[1,2,7] Pharmacological treatments, such as gabapentin and quetiapine, propose potential interventions for targeting mutual symptoms of insomnia and AUD.[3,13,14,15] The efficacy of these novel treatments for the simultaneous treatment of comorbid AUD and insomnia remains uncertain, however, due to inconsistent findings.[2,6,17,15] CBT-I, a non-pharmacological therapy, has demonstrated significant effectiveness in the treatment of comorbid AUD and insomnia patients, specifically in the improvement of alcohol-related factors such as cravings and relapse.[10,15] Due to reported concerns over the time commitment for CBT-I,[5] however, alternative options such as online CBT-I should be further explored in order to better cater to young adults, the major demographic of heavy-drinking and AUD individuals. Additionally, future research should work to develop novel behavioral therapies or modify existing CBT-I interventions in order to more effectively improve alcohol-related factors such as abstinence.

Klea Gjoka is a recent alumnus of the University of Florida where she earned her BS in Biology on the pre-professional track. Through her minor in Health Disparities in Society, she developed a passion for addressing the social determinants of health. She has been able to explore these ideas further through her involvement in a nonprofit student organization that serves Gainesville's homeless population as well as through her work at several free medical clinics in her hometown Jacksonville, FL.  

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