Insomnia, Self-Medication, and Relapse to Alcoholism

Department of Psychiatry, the Alcohol Research Center, University of Michigan Medical School, Ann Arbor, MI 48108, USA.
American Journal of Psychiatry (Impact Factor: 13.56). 04/2001; 158(3):399-404. DOI: 10.1176/appi.ajp.158.3.399
Source: PubMed

ABSTRACT This study was an investigation of the frequencies of insomnia and its self-medication with alcohol in a group of alcoholic patients, as well as the relationship of these variables to alcoholic relapse.
The subjects were 172 men and women receiving treatment for alcohol dependence. They completed a sleep questionnaire, measures of alcohol problem severity and depression severity, and polysomnography after at least 2 weeks of abstinence.
On the basis of eight items from the Sleep Disorders Questionnaire, 61% of the subjects were classified as having symptomatic insomnia during the 6 months before treatment entry. Compared to patients without insomnia, patients with insomnia were more likely to report frequent alcohol use for sleep (55% versus 28%), had significantly worse polysomnographic measures of sleep continuity, and had more severe alcohol dependence and depression. Among 74 alcoholics who were followed a mean of 5 months after treatment, 60% with baseline insomnia versus 30% without baseline insomnia relapsed to any use of alcohol, a significant difference. Insomnia remained a robust predictor of relapse after application of logistic regression analysis to control for other variables. A history of self-medicating insomnia with alcohol did not significantly predict subsequent relapse.
The majority of alcoholic patients entering treatment reported insomnia symptoms. Given the potential link between insomnia and relapse, routine questions about sleep in clinical and research settings are warranted.

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Available from: Robert A Zucker, Sep 03, 2015
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    • "Among abstinent alcohol-dependent (AD) patients, sleep disorders are a wide-spread and persistent problem entailing the risk of relapsing into drinking (Brower 2003). The polysomnographic characteristics of AD patients include prolonged sleep-latency and decreased sleep-efficiency (Brower et al. 2001). Furthermore, abstinent alcohol-dependent patients show abnormal evening melatonin-profiles (Kuhlwein et al. 2003). "
    Psychiatria Danubina 12/2013; 25(4):416-8. DOI:10.5167/uzh-89440 · 0.65 Impact Factor
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    • "One difficulty in devising integrated treatment for comorbid disorders is the limited research identifying reciprocal relationships between the disorders and the processes that may underlie these relationships. A number of processes have been proposed to underlie comorbidity between anxiety, depression, and alcohol dependence including 1) “self-medicating” a mood or anxiety disorder with alcohol [21,22], 2) the arousing and depressant properties of alcohol causing symptoms similar to anxiety and depression, and 3) trait-like factors such as anxiety sensitivity leading to poorly tolerated withdrawal [23,24]. Targeting specific mechanisms that may underlie comorbidity during treatment is likely to be a productive strategy. "
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    ABSTRACT: A major barrier to successful treatment in alcohol dependence is psychiatric comorbidity. During treatment, the time to relapse is shorter, the drop-out rate is increased, and long-term alcohol consumption is greater for those with comorbid major depression or anxiety disorder than those with an alcohol use disorder with no comorbid mental disorder. The treatment of alcohol dependence and psychological disorders is often the responsibility of different services, and this can hinder the treatment process. Accordingly, there is a need for an effective integrated treatment for alcohol dependence and comorbid anxiety and/or depression. We aim to assess the effectiveness of a specialized, integrated intervention for alcohol dependence with comorbid anxiety and/or mood disorder using a randomized design in an outpatient hospital setting. Following a three-week stabilization period (abstinence or significantly reduced consumption), participants will undergo complete formal assessment for anxiety and depression. Those patients with a diagnosis of an anxiety and/or depressive disorder will be randomized to either 1) integrated intervention (cognitive behavioral therapy) for alcohol, anxiety, and/or depression; or 2) usual counseling care for alcohol problems. Patients will then be followed up at weeks 12, 16, and 24. The primary outcome measure is alcohol consumption (total abstinence, time to lapse, and time to relapse). Secondary outcome measures include changes in alcohol dependence severity, depression, or anxiety symptoms and changes in clinician-rated severity of anxiety and depression. The study findings will have potential implications for clinical practice by evaluating the implementation of specialized integrated treatment for comorbid anxiety and/or depression in an alcohol outpatient service.Trial registration: Identifier: NCT01941693.
    Addiction science & clinical practice 11/2013; 8(1):19. DOI:10.1186/1940-0640-8-19
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    • "Verminderte Schlafqualität, Tagesbefindlichkeit und Performancedefizite kçnnten durchaus als negative Verstärker einen konsumaufrechterhaltenden Faktor darstellen. Einige Studien zeigten, dass Patienten mit Abhängigkeitserkrankungen verschiedene Substanzen gezielt zur Verbesserung des Schlafs einsetzen (Bolla et al., 2008; Burke et al., 2008; Brower, Aldrich, Robinson, Zucker & Greden, 2001) und zumindest bei alkoholabhängigen Patienten waren entzugsassoziierte Schlafstçrungen mit einer erhçhten Rückfallwahrscheinlichkeit assoziiert (Foster & Peters, 1999; Conroy et al., 2006; Drummond, Gillin, Smith & Demodena , 1998; Brower et al., 2001). Ebenso relevant ist die Fragestellung, in wie weit sich durch Einflussnahme auf insomnische Beschwerden Rückfälle verhindern lassen. "
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    ABSTRACT: Aim: To address how illicit drugs as either stimulating or tranquilizing substances induce effects on the general brain alertness and affect sleep regulation. Results: Whereas stimulating substances like cocaine and Ecstasy (MDMA) induced insomnia-like sleep changes, cannabis and benzodiazepines had sleep enhancing effects. Although benzodiazepines are no typical illicit drugs they have a high and frequent risk for abuse and addiction, therefore their remarkable effects upon sleep are reported here. Opioids showed significant sleep inhibiting effects as well as increased sleep associated breathing abnormalities. In most substances, REM-suppression was found during acute intake. During withdrawal, most often insomnia-like sleep changes were detected (cannabis, benzodiazepines, opioids), whereas in cocaine and less intensive in MDMA and cannabis users a REM-rebound was found, too. LSD had less intense effects on sleep efficiency but REM-sleep was altered, too. Next day hangover effects were often found in MDMA-, opioid- and benzodiazepine-users, intensifying day time drowsiness, deficits in concentration and performance and increased risk for falls and motor accidents. Conclusions: Clinical and therapeutic implications of these substance induced sleep changes remain unclear and methodologically well designed studies investigating the relationship between insomnia, psychiatric and general comorbidity, drug seeking behavior and relapses, are needed. Fragestellung: Ziel ist die Darstellung des Einflusses von Drogen als stimulierende oder sedierende psychotrope Substanzen auf Änderungen im allgemeinen Wachheitszustand des Gehirns und auf die Schlaf-Wachregulation. Ergebnisse: Stimulanzien wie Kokain und Ecstasy (MDMA) führten zu einem gestörten Schlaf, während Cannabis und Benzodiazepine eher schlaffördernde Effekte hatten aber bereits bei mittelfristiger Gabe zu qualitativen Schlafveränderungen von funktioneller Relevanz führten. Obwohl keine illegalen Drogen im klassischen Sinne, weisen auch Benzodiazepine ein hohes Abhängigkeitspotenial auf, werden häufig missbräuchlich konsumiert, weshalb deren Effeke auf den Schlaf an dieser Stelle berichtet werden. Opioide wiederum hatten deutliche Schlafstörungen und eine Zunahme schlafbezogener Atmungsstörungen zur Folge. Einen gemeinsamen Effekt stellt die Suppression des REM-Schlafs dar. Als Entzugsphänomene traten häufig insomnische Beschwerden (Kokain, Cannabis, Benzodiazepine, Opioide), teilweise begleitet von einem REM-Rebound (Kokain, zumindest teilweise bei MDMA und Cannabis) auf. LSD beeinflusste die Schlafeffizienz wenig, führte aber auch zu Veränderungen des REM-Schlafs. MDMA-Opioid- und Benzodiazepin-Konsumenten zeigten oft Hangover-Effekte am nächsten Tag mit Tagesmüdigkeit, Konzentrations- und Leistungsdefiziten, vermehrten Stürzen und Verkehrsunfällen. Schlussfolgerungen: Die klinischen und therapeutischen Implikationen der beschriebenen Schlafveränderungen bleiben noch ungeklärt. Insbesondere mit dem Zusammenhang zwischen Insomnie, psychiatrischer und somatischer Komorbidität, Drogenkonsum und Rückfälligkeit werden methodisch belastbare Untersuchungen benötigt.
    Sucht 04/2013; 59(2):69-80. DOI:10.1024/0939-5911.a000234
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