Medizinische Hochschule Hannover
1 Georg-August Universität, Göttingen,
2 Johann-Wolfgang-Goethe Universität, Frankfurt,
3 Medizinische Universität, Lübeck,
4 Klinikum der Hansestadt Stralsund,
5 Zentrum für Soziale Psychiatrie, Bad Emstal,
6 Klinik für Psychiatrie und Psychotherapie der Universität Rostock,
7 Psychiatrische Klinik der Heinrich Heine Universität, Düsseldorf,
8 Zentrum für Drogenkranke, Hannover,
9 Universitätskrankenhaus, Hamburg,
10 Gilead, Psychiatrische Klinik, Bielefeld,
11 Reinhard-Nieter Krankenhaus, Wilhelmshaven,
12 Klinikum Nord, Hamburg,
13 Nds. Landeskrankenhaus, Göttingen,
14 Klinik für Psychiatrie und Psychotherapie III des Zentralkrankenhauses Bremen Ost/Universität Oldenburg,
15 Christian-Albrechts Universität, Kiel,
16 Tagesklinik Königstraße, Hannover,
17 Nds. Landeskrankenhaus, Hildesheim,
18 Klinik für Psychiatrie und Psychotherapie, Langenhagen,
19 Nds. Landeskrankenhaus, Osnabrück,
20 Paracelsus-Wiehengebirgsklink, Bad Essen,
21 Charite, Berlin,
22 Fachklinik Holstein, Lübeck,
23 Paracelsus Berghof-klinik, Bad Essen,
24 Nds. Landeskrankenhaus Wehnen, Bad Zwischenahn, Germany
Received 10 July 2000; in revised form 10 November 2000; accepted 10 December 2000
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ABSTRACT |
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INTRODUCTION |
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Although the impact of co-occurring disorders remains controversial (Schuckit, 1985; Bean-Bayog, 1988
) it is reasonably clear that alcohol-dependent individuals who meet diagnostic criteria for one or more comorbid psychiatric disorders differ from those without comorbidity in many clinically relevant ways. Among alcohol-abusing and alcohol-dependent patients, prevalence rates for psychiatric comorbidity of between 57% and 84% have been reported (Powell et al., 1987
; Regier et al., 1990
; Wittchen et al., 1992
). Depressive disorders as well as anxiety disorders were found very frequently (Arolt and Driessen, 1996
; Schuckit et al., 1997
; Berglund and Ojehagen, 1998
; Swendsen et al., 1998
; Tondo et al., 1999
).
The amount of pure alcohol consumed is higher in Germany than in most other European countries. However, there is a paucity of data concerning psychiatric comorbidity in alcohol-dependent patients (Driessen et al., 1998). This multicentre study, which is the largest in sample size yet undertaken in Germany, aimed to close that gap. The CART (Classification and Regression Trees) procedure was used for data analysis. Two main issues were addressed by the study: (1) to investigate the current (6 months) prevalence of psychiatric comorbidity in alcohol-dependent patients in 25 treatment centres; (2) to analyse the relation of comorbid disorders and gender on alcohol-related variables.
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SUBJECTS AND METHODS |
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The patients were interviewed face to face after a minimum of 10 days and a maximum of 28 days of sobriety and when withdrawal symptoms could no longer be observed by clinical means. The patients were selected consecutively. The Mini-DIPS (Markgraf, 1994) and a standardized psychosocial interview were applied. The DIPS represents the German version of the Anxiety Disorders Interview Schedule (Di Nardo and Barlow, 1988). The Mini-DIPS is the short form of this structured interview according to DSM-IV and ICD-10 criteria for current (6 months) comorbidity and covers the following disorders: anxiety, affective, somatization, obsessivecompulsive, post-traumatic stress, acute stress, dissociative, and eating disorders (F30F50). Furthermore, it allows the exclusion of patients with schizophrenic psychoses. The Mini-DIPS distinguishes between primary and additional diagnoses. Primary diagnoses are those that are clinically most significant and severe in each patient; additional diagnoses are defined when other disorders with a lower degree of severity are present. However, the Mini-DIPS does not cover personality disorders (Axis II diagnoses). The additional interview systematically obtained information about sociodemographic characteristics and alcohol-related history. Twenty-three interviewers from the participating centres were trained in the use of the Mini-DIPS, but testretest reliability and inter-rater reliability were not determined in this study.
Data analysis
The following statistical analyses were performed: main group comparisons used 2-test or Fisher's exact test for categorical variables, and the t-test for continuous variables. For these analyses, SPSS 8.0 for Windows was used.
To investigate the relationship between comorbid disorders and alcohol-related variables, the method using the CART software (Breiman et al., 1984; see also Steinberg and Colla, 1997) was applied. Since in this study the target variables are continuous, regression tree analyses were performed. The goal in a regression tree is to partition the data into relatively homogeneous (low standard deviation) terminal nodes; e.g. the study patients are partitioned into relatively homogeneous subgroups with the different target variables such as amount of consumed alcohol through the predictor variables comorbid disorders. The results are presented in the form of decision trees; a 10-fold cross-validation was used to assess the tree accuracy. To compare the resulting subgroups respective to the alcohol-related variables, one-way analysis of variance was performed. The differences in the nodes were all statistically significant at P < 0.05.
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RESULTS |
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All the patients (n = 538) consumed an average (± SD) of 345 ± 218 g of pure alcohol/day. There was a sex difference: males (n = 451) with 357 ± 220 and females (n = 87) with 285 ± 198) g of pure alcohol/day (P = 0.0001). Those patients with a PTSD drank more alcohol (n = 34; 447 ± 230 g/day) than those without (n = 503; 338 ± 215 g/day) (P = 0.0037). Of those without a PTSD disorder, male patients consumed more alcohol (n = 424; 351 ± 216 g/day) than female patients (n = 79; 273 ± 197 g/day) (P = 0.0029). Among the female patients, those with an anxiety disorder (n = 28; 318 ± 230 g/day) drank more than those without (n = 41; 232 ± 148 g/day) (n = 0.062).
The age of onset of first alcohol consumption was 15.4 ± 4.7 years. Males started with 15.2 ± 4.8 years, females with 16.5 ± 4.1 years (P = 0.0172). Males with an obsessive compulsive disorder started earlier to consume alcohol than those without (12.2 ± 2.8 vs 15.3 ± 4.8 years; P = 0.0336). Females with anxiety disorders started drinking earlier than those without anxiety disorders (15.5 ± 4.1 vs 17.6 ± 3.8; P = 0.014).
On average, males started a regular drinking style at the age of 22.2 ± 7.9 years, females some years later (28.3 ± 9.6 years; P = 0.0001). Those females with an anxiety disorder started earlier than those without (24.7 ± 6.9 vs 31.9 ± 10.5 years) (P = 0.0003).
Withdrawal symptoms first occurred at a mean age of 34.2 ± 9.8 years for all patients. Those patients with a PTSD disorder usually suffered earlier from withdrawal symptoms (29.3 ± 8.1 vs 34.5 ± 9.9 years; P = 0.0036) and underwent more detoxifications than those without (4.0 ± 6.7 vs 7.8 ± 9.1; P = 0.0016). Of patients with no PTSD, females had a higher age of onset of withdrawal symptoms than males (37.5 ± 9.9 vs 24.7 ± 6.9 years; P = 0.0001). A higher age of onset of withdrawal symptoms was also observed in females without PTSD but with anxiety disorders, compared with those without anxiety disorders (46.9 ± 10.3 vs 34.0 ± 7.9 years; P = 0.0022).
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DISCUSSION |
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One shortcoming of this study is that the minimum delay between starting sobriety and assessment was short (10 days). In Germany, acute inpatient detoxification of alcoholics is carried out by health insurance funds, but, in most cases, it is limited to 10 days. In a very few cases the health insurance funds agreed to pay for further in-patient treatment programmes (duration about 3 weeks) that have been established in some psychiatric hospitals. Since many hospitals participating in this study are limited to a treatment programme of 10 days each, patients were included after a minimum of 10 days of sobriety. Knowing that prolonged withdrawal symptoms could bias the evaluation of psychiatric comorbidity, patients with continuing withdrawal symptoms were excluded.
Withdrawal symptoms were measured by clinical means. Patients with prolonged symptoms, such as sweating, tremor, agitation, nausea, headache, clouding of sensorium, auditory, visual or tactile disturbances, hypertension, tachycardia, etc. were excluded. Assuming that many patients with prolonged withdrawal symptoms have been included as comorbid, a higher rate of comorbidity than in other studies might be inferred; in this study, the comorbidity rates were not higher than in other studies. However, there are no strong reasons to suspect that prolonged withdrawal symptoms considerably biased the results of this study.
Another, more general shortcoming of the present study is that the prevalence of comorbid disorders was evaluated retrospectively. A longitudinal study and a greater delay between starting sobriety and assessment would reduce the bias of prolonged withdrawal symptoms. Therefore the results of this study should be interpreted cautiously.
In agreement with previous studies (Regier et al., 1990; Kessler et al., 1997
) anxiety and affective disorders were most frequent among Axis I comorbidity. Phobias were the most frequent comorbid diagnoses among alcoholic patients with anxiety disorders. Although there were only a few patients in the sample with a PTSD disorder the daily alcohol consumption in this group was the highest. Additionally, this group of patients underwent detoxifications very often, and suffered from withdrawal symptoms at an earlier age. In a study of civilians, Helzer et al. (1987) used Epidemiologic Catchment Area survey data to estimate the lifetime prevalence of PSTD among adults, which was found to be 1% for both sexes combined (0.5% for males and 1.3% for females). In a study by Deykin and Stephen (1997) the current prevalence of PTSD was found to be 19.2%. In our study, it was 6.1% of the study population (PTSD = 34). These discrepancies among the studies are unlikely to be due only to methodological differences (both Helzer and Deykin used the DIS); the sample population was also different. Deykin and Stephen (1997) investigated chemically dependent adolescents, whereas Helzer et al. (1987) studied a community sample.
Several causal pathways may explain the co-occurrence of PTSD and alcoholism (Pihl and Stewart, 1991). Alcohol misuse might increase anxiety and arousal levels through psychological processes, such as stressful life events, causing heavy drinking (Kushner et al., 1990
). These effects could serve to induce a hyper-arousal state in which the individual may be more vulnerable to develop stress disorder following a traumatic event. Some patients might begin or continue abusing alcohol in order to reduce or control their stress symptoms. This notion of self-medication of drug misuse suggests that individuals who are susceptible to certain aversive states are at a high risk of abusing drugs in order to reduce these aversive states (Khantzian, 1985
). The consistent finding of an association between trauma exposure and alcoholism suggests that clinicians working with individuals who abuse alcohol should look carefully for a history of traumatic life events. In patients with comorbid diagnoses of PTSD disorder and alcoholism, treatment needs to address both disorders. Unfortunately, many physicians who are specialized in the treatment of people exposed to trauma regard alcoholism as secondary to the PTSD disorder and thus assume that drinking will normalize following alleviation of PTSD symptoms (Hurley, 1991
). There are several problems inherent to this point of view. Independent of aetiological factors, once abusive drinking has begun, the alcohol disorder may follow its own course (Pihl and Stewart, 1991
). On the one hand, it seems difficult for individuals to discontinue drinking after PTSD symptom management. On the other hand, if the PTSD symptoms are not treated, the patient may experience a re-emergence or intensification of the PTSD symptoms following sobriety and may again turn to alcohol for a temporary symptom relief. Therefore, both problems should be treated simultaneously.
Among the group of female patients, alcohol consumption was highest in the group of patients with comorbid anxiety disorders. Our study also suggests that female patients with an anxiety disorder experienced onset of drinking, regular drinking, and first occurrence of withdrawal symptoms earlier than females without anxiety disorders. Hesselbrock et al. (1985) reported more panic disorders and phobia among hospitalized female, than male, alcoholics. Possibilities include: having an anxiety disorder may promote the development of an alcohol disorder (alcohol as self-medication); having an alcohol disorder may promote the development of an anxiety disorder; a third variable (e.g. genetic factor) may promote the development of both an alcohol use disorder and an anxiety disorder (Nunes et al., 1988; Pohorecky, 1991
). The extent to which one disorder promotes the other or whether the influence of other variables actually accounts for some or all of these associations remains speculative (Schuckit and Hesselbrock, 1996
; Kushner et al., 1999
). Schuckit and Hesselbrock (1994) argued that the interaction is very complex and the available data do not prove a close relationship. These authors hypothesized that the high rate of comorbidity reflects a mixture of true anxiety disorders among alcoholics at a rate equal to or slightly higher than that of the general population, along with temporary, but at times, severe substance-induced anxiety syndromes. Kushner et al. (1999) concluded that both alcohol and anxiety disorders demonstrate a reciprocal causal relationship over time, with anxiety disorders leading to alcohol dependence and vice versa. The debate over the impact of anxiety and stress disorders in the pathogenesis of alcoholism continues. Our data are not qualified to contribute to this debate with regard to pathogenesis, but indicate that PTSD in alcoholic patients and anxiety disorder in female alcoholic patients are substantially associated with the course and severity of alcoholism.
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FOOTNOTES |
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