To our knowledge, the occurrence of symptomatic insomnia and drinking to self-medicate insomnia have not been simultaneously studied in alcoholic patients. Using a measure derived from the SDQ, over 60% of our sample reported high levels of insomnia symptoms during the 6 months prior to treatment. Also, nearly 45% of alcoholic patients reported using alcohol often
in order to get to sleep during the 6 months prior to treatment. Patients with insomnia were about twice as likely to report using alcohol to sleep as patients without insomnia were (55% vs. 28%). Similar rates of insomnia (4
) and its self-medication with alcohol (8
) have been reported in other studies of alcoholic patients in treatment, even though frequency rates across studies will vary according to sample characteristics, time frame, and measures of insomnia. A similar rate of self-medicating insomnia with alcohol among patients with schizophrenia (56%) (28
) suggests that some of our findings may generalize to other patient populations as well.
That alcohol-dependent patients use alcohol to self-medicate insomnia is both understandable and maladaptive. On the one hand, if insomnia is a withdrawal symptom, either acute or protracted (6
), then relief drinking is a likely strategy, especially given that alcohol has a reinforcing effect in individuals with insomnia (30
). On the other hand, there is general scientific consensus that both acute and chronic alcohol use disrupt sleep patterns (1
). Therefore, self-medication of insomnia with alcohol, even if reinforcing, may paradoxically worsen insomnia. Consequently, a vicious cycle may develop in which alcohol initially makes it easier to fall asleep; but as tolerance to this sedative effect develops, the sleep-disruptive effects of alcohol become more apparent if not more severe (31
). Some patients may persist with self-medication despite worsening insomnia, because their drinking behavior is ingrained and reinforcing, and they feel desperate for sleep.
Severity of both alcohol dependence and depression was significantly associated with insomnia. Because we excluded patients with current major depression, depressive symptoms in this study were most likely related to alcohol, dysthymia, or social stressors. We did not find higher rates of insomnia in women than in men, or as a function of increasing age, contrary to some studies of the general population (33
) and primary care practices (35
). Age and gender differences for insomnia may disappear among patients seeking treatment for alcohol dependence. Although alcohol severity and depression severity were significantly associated with insomnia, we did not measure anxiety symptoms despite recent studies that support a significant relationship between anxiety and sleep disturbance in alcoholic patients (36
). Therefore, further studies are needed before making more than tentative conclusions about the correlates of insomnia among alcoholic patients.
Consistent with other studies (8
), baseline insomnia predicted relapse to alcohol. Baseline insomnia remained a predictor of relapse even after controlling for severity of alcohol dependence and depressive symptoms. Contrary to our hypothesis, patients with a history of self-medicating insomnia with alcohol were not significantly more likely to relapse than non-medicating patients.
Of the eight insomnia items, “I feel that I have insomnia” and “I have been unable to sleep at all for several days” were least sensitive, with only 6% and 4% of the sample endorsing these respective items (). Other insomnia items were endorsed by 18% to 32% of the sample. This suggests that patients who report symptoms of insomnia do not necessarily think of themselves as having insomnia. Asking patients if they have insomnia may be analogous to asking them if they are alcoholic; patients may avoid these labels because of denial, stigma, their own definitions of these terms which exclude themselves, and/or fear of treatment implications. Not being able to sleep at all for several days is uncharacteristic of alcohol dependence except for extreme cases of alcohol withdrawal, such as delirium tremens that occur in only about 5% of alcohol-dependent patients (38
). This may explain the insensitivity of that question. Future studies should address the optimal screening questions for insomnia among alcoholic patients.
Several methodological issues may limit the interpretation of results. First, we studied alcoholic patients who underwent PSG for research purposes. It is possible that alcoholics in treatment who have sleep complaints are very likely to volunteer for sleep studies, thus skewing our frequency rates for insomnia and its self-medication with alcohol. However, our rates of insomnia were comparable in range to other studies (4
), and provide further evidence of the frequency of these phenomena. Nevertheless, many patients may have entered the study because of their sleep problems, which could limit the generalizability of these results.
Second, our eight-item measure of insomnia was derived from a standardized and validated sleep questionnaire (20
), but full psychometric testing of the abbreviated questionnaire was beyond the scope of this article. For example, we did not calculate the sensitivity and specificity of the eight-item insomnia measure, because we did not conduct standardized clinical interviews for insomnia, and PSG by itself is not a gold standard for the evaluation of insomnia (39
). Nevertheless, in addition to face validity, the insomnia measure was associated with drinking and depression severity, with polysomnographic measures of sleep fragmentation, and with relapse, providing evidence of concurrent, external, and predictive validity, respectively.
Third, only 43% of patients were followed over time. The low follow-up rate reflects the fact that longitudinal outcomes were added as a secondary area of interest after starting our primary investigations on the effects of alcoholism and aging on sleep abnormalities (17
). It is true that followed and not followed patients did not differ on any baseline variables except depression and WASO; and when these two variables were entered into the logistic regression analysis, insomnia remained a robust predictor of relapse. Nevertheless, the low follow-up rate remains a limitation, because patients lost to follow-up have potentially higher relapse rates than followed patients. Fourth, only one night of sleep was recorded, which did not allow subjects to adjust to the “first night effect” of sleeping under novel conditions. Fifth, relapse status was determined solely by self-report without biochemical or other corroboration, such as by a friend or family member. Still, whatever self-report bias occurred was expected to be similar across comparison groups.
In summary, symptoms of chronic insomnia and the use of alcohol to aid sleep were prevalent in alcoholic patients. Insomnia was significantly associated with severity of alcohol dependence, depressive symptoms, and polysomnographic measures of poor sleep continuity; and it was predictive of drinking during the follow-up period. These results suggest that alcoholic patients at risk for relapse are easily identifiable by routine questions about sleep. The potential for improved drinking outcomes by treating insomnia in alcoholic patients is now being investigated (41