MONOAMINE OXIDASE-B ACTIVITY IN ALCOHOL WITHDRAWAL OF SMOKERS: IS THERE ANY RELATIONSHIP WITH AGGRESSIVENESS?{dagger}

Ertugrul Esel,*, Kader Kose1, M. Tayfun Turan, Mustafa Basturk, Seher Sofuoglu, Suat Sabri Aslan, Ihsan Yabanoglu, Ali Saffet Gonul and Cevat Yazici1

Erciyes University School of Medicine, Departments of Psychiatry and
1 Biochemistry, Talas Road, 38039-Kayseri, Turkey

Received 19 July 2001; in revised form 9 November 2001; accepted 21 November 2001


    ABSTRACT
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
— There is a considerable inconsistency in terms of the association between alcoholism and alterations in monoamine oxidase (MAO) activity. The main objectives of this study were to investigate the changes in platelet MAO-B activity throughout the alcohol withdrawal period and whether or not MAO-B activity differed between patients with high- and low-aggression tendency. We assayed platelet MAO-B levels spectrophotometrically in 22 male inpatients with alcohol dependence in their first and fourth weeks of withdrawal and in 20 healthy controls. Patients were divided into two high- and low-aggression subgroups according to scores obtained in a Brown–Goodwin Assessment for Life History of Aggression. Our data revealed that the significantly lower platelet MAO-B activity observed during the first week of alcohol withdrawal in patients, compared to controls, did not continue in the fourth week, and that there was no relationship between aggressiveness and MAO activity. These results suggest that low platelet MAO activity may be a state marker of alcohol withdrawal period or a result of high alcohol consumption rather than a trait marker of alcoholism.


    INTRODUCTION
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Monoamine oxidase (MAO) is a mitochondrial enzyme that catalyses the oxidative deamination of biogenic amines, including catecolamines, indolylamines and synthetic amines. MAO exists in two catalytically active forms, MAO-A and MAO-B. MAO-B is a subtype of MAO found in neurons of serotonergic pathways and also in circulating platelets (Donnelly and Murphy, 1977Go). Brain and platelet MAO-B activity have been shown to be highly correlated (Oreland and Shaskan, 1983Go).

Although platelet MAO-B activity has been extensively investigated in alcoholism, there is a considerable inconsistency in terms of the association between alcoholism and alterations in MAO activity. A significant number of studies reported a decrease in MAO-B activity in platelets during the alcohol consumption period (Alexopoulos et al., 1983Go; Faraj et al., 1987Go; Lykouras et al., 1987Go, 1989Go; Rommelspacher et al., 1994Go), during an active withdrawal syndrome (Pandey et al., 1988Go; Rommelspacher et al., 1994Go) or after an abstinence period (Major and Murphy, 1978Go; Alexopoulos et al., 1983Go; Faraj et al., 1987Go, 1994Go; Pandey et al., 1988Go; Sullivan et al., 1990Go; Rommelspacher et al., 1994Go). Therefore, it has been suggested by some authors that low platelet MAO-B activity represents a biochemical marker for alcohol dependence (Sullivan et al., 1990Go; Faraj et al., 1994Go; Rommelspacher et al., 1994Go). However, the finding of low platelet MAO activity in alcohol-dependent patients has not been consistently replicated (Giller and Hall, 1983Go; Sherif et al., 1992Go; Farren et al., 1998Go). Furthermore, some recent papers have suggested that decreased MAO activity is not a marker for alcoholism, but rather, is due to cigarette smoking, which is claimed to inhibit MAO activity and is seen far more prevalently in alcoholic patients than in the normal population (Anthenelli et al., 1995Go, 1998Go; Whitfield et al., 2000Go). Nevertheless, in Farren et al.'s study (1998), no correlation was found between platelet MAO activity and smoking status.

The alcohol withdrawal syndrome is the result of a complex ‘mal adaptation’ of the main neurotransmitter systems. It generally reflects altered neurotransmitter function of the brain involved in the development of tolerance to alcohol. Withdrawal is a combination of reduced central inhibition (e.g. by {gamma}-aminobutyric acid) and increased excitation (e.g. by N-methyl-d-aspartate, dopamine, noradrenaline) (Nutt, 1999Go). As in alcoholism in general, previous studies have yielded equivocal results with regard to MAO-B activity changes during the withdrawal period. Thus, whereas some authors reported a transitory increase in platelet MAO activity during withdrawal (Alexopoulos et al., 1981Go; Alling et al., 1982Go), others showed a decrease (Major and Murphy, 1978Go; Pandey et al., 1988Go; Rommelspacher et al., 1994Go; Berggren et al., 2000Go).

Besides alcoholism, low MAO-B activity has been suggested to be linked to some personality traits, such as aggressiveness, impulsiveness and sensation-seeking behaviour (Fowler et al., 1980Go; Zuckerman, 1984Go; Schalling et al., 1987Go; Stalenheim et al., 1997Go) and type II alcoholism, a proposed subgroup associated with early onset alcoholism, male predominance, and a history of sociopathic activity (Cloninger et al., 1981Go; von Knorring et al., 1985Go; Sullivan et al., 1990Go).

The objectives of the present study were to test the hypothesis that MAO-B activity, even if it is abnormal, may not be stable during the period of alcohol withdrawal, and to investigate whether MAO-B activity changes during the withdrawal period are related to the level of aggressiveness of alcoholic patients.


    SUBJECTS AND METHODS
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Subjects
Twenty-two hospitalized male patients (mean age ± SD: 43.45 ± 9.22, range 30–60 years) who had been diagnosed using DSM-IV criteria (American Psychiatric Association, 1994Go) as alcohol dependent or in alcohol withdrawal, participated in the study (Table 1Go). Diagnoses were made independently by two psychiatrists (E.E. and S.S.) using the DSM-IV criteria for alcohol dependence and alcohol withdrawal. Patients were in the state of withdrawal on admission to hospital, and none presented with delirium. All patients had been alcohol-dependent for >5 years (mean ± SD: 19.7 ± 8.3) with an alcohol intake of >175 g/day (mean ± SD: 422 ± 117). Only subjects with normal levels of transaminases were included in the study. All patients were cigarette smokers. Thirteen of the patients had a positive family history of alcoholism. Patients who were suspected to be affected by major psychiatric, neurological or medical illnesses or substance other than from alcohol and smoking, on the basis of medical history, physical and psychiatric examinations or laboratory tests, were excluded from the study. Twenty age-matched healthy men with no history of alcohol dependence, drug dependence, or psychiatric or neurological illnesses, even among first-degree relatives, served as control subjects (mean age ± SD: 38.35 ± 7.63 years, range 30–55). The controls were also smokers.


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Table 1. Some clinical variables of the patients with alcohol dependence
 
During the first 2 weeks of withdrawal, the patients were given diazepam (mean dose ± SD: 33.4 ± 12.9 mg/day) and multivitamins, and were drug-free from 2 weeks after admission onwards.

Demographic and clinical procedures
Demographic and clinical data were collected after the patients had returned to sobriety. Severity of anxiety and depressive symptoms were assessed with the Clinical Anxiety Scale (CAS) (Snaith et al., 1982Go) and the 21-item Hamilton Rating Scale for Depression (HRSD) (Hamilton, 1960Go), respectively. Patients obtaining a HRSD depression score of >=10 in evaluations performed at either the first or fourth week were excluded from the study. All patients also completed the Brown–Goodwin Assessment for Life History of Aggression (BGARS), which assesses several elements of lifetime aggression history (Brown et al., 1981Go). The patient group was divided into two subgroups: a low-aggression group and a high-aggression group, according to their BGARS scores. Those who had scores of <=8 on this scale were considered the ‘low-aggression group’ (n = 13, mean age ± SD: 43.8 ± 8.6 years, mean BGARS score ± SD: 2.0 ± 1.41), and those with scores >=8 formed the ‘high-aggression group’ (n = 9, mean age ± SD: 43.0 ± 10.1, mean BGARS score ± SD: 9.0 ± 1.2).

This study was carried out in accordance with the Helsinki Declaration of the World Medical Association and was approved by the local Ethics Committee. All subjects gave their written informed consent after full understanding of the study.

Biochemical procedures
A single blood specimen was obtained after fasting from all subjects, at 07.00–08.00. The blood sampling procedure was carried out during the first week (7 days after alcohol cessation) and fourth week (28 days after alcohol cessation) of alcohol withdrawal for patients, but only once for controls. The patients remained in hospital throughout the study. Venous blood was divided into three portions. One part was placed into the EDTA-containing tube for platelet counts, whilst the second was allowed to clot at room temperature and serum was collected for total protein measurement. Platelet number was measured by a Coulter® Max M autoanalyser (USA), and total serum protein level was assayed using a Konelab 60i analyser (Thermoclinical lab systems OY, Ruukintie 18, FIN-02330 Espoo, Finland).

The third portion of the blood sample was drawn into an ice-cold heparinized tube and centrifuged at 4°C. Platelet-rich plasma (PRP) (2.0 ml aliquots) was removed from the top of the plasma samples. The separated PRP sample was kept at –70°C until analysis. MAO-B activity in PRP was measured by the method described by McEwen (1971), a spectrophotometric assay based on the measurement of the conversion of benzylamine into benzaldehyde by the catalytic activity of MAO-B. One unit of MAO activity was defined as the amount of enzyme catalysing the production of 1 nmol of benzaldehyde per hour at 37°C. The protein content of PRP was also measured by the biuret reaction using bovine albumin as the standard. MAO-B activity in PRP was expressed in units per mg of protein as specific activity (nmol/mg protein/h).

Statistical analysis
The numbers of cigarettes consumed per day by both patients and controls in the first and fourth weeks were compared using independent samples and paired t-tests, respectively. Statistical comparison of the MAO values obtained in the first and fourth weeks was performed by using paired t-test. Two-tailed independent samples t-test was used to compare the MAO-B values of both patients and controls. Comparison of MAO-B values obtained in the low- and high-aggression groups and in patients with and without family history of alcoholism, during both the first and fourth weeks of the withdrawal period were carried out by using the Mann–Whitney U-test due to the small sizes of the groups. Platelet numbers and total serum protein levels of the patients in the first and fourth weeks and those of controls were compared using one-way analysis of variance (ANOVA). Statistical correlations between MAO values and clinical variables were tested by means of Pearson's correlation test.


    RESULTS
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
The number of cigarettes smoked per day by patients was counted throughout the first and fourth weeks of withdrawal; no statistically significant difference was found between the number of cigarettes consumed daily in the first and fourth weeks (the mean number of cigarettes/day ± SD: 22.2 ± 8.3 in the first week, and 21.0 ± 7.1 in the fourth week (P > 0.05 by paired t-test). There was also no statistically significant difference between the number of daily cigarettes in the patient and control groups (mean number of cigarettes/day ± SD: 21.1 ± 7.8 in the control group; P > 0.05 by independent samples t-test).

MAO-B values obtained for patients during the first week of withdrawal were significantly reduced, compared with both those of controls and those obtained during the fourth week (P < 0.001 in both cases) (Table 2Go). However, no difference was observed between the MAO-B values obtained from patients during the fourth week of the withdrawal and controls (P > 0.05).


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Table 2. Monoamine oxidase-B (MAO-B) activities in platelet-rich plasma (PRP), platelet numbers and total serum protein levels of controls and patients during the first and fourth weeks of alcohol withdrawal
 
We found no significant difference in MAO-B activity between the low- and high-aggression subgroups in both the first and fourth weeks of withdrawal (U = 33.5, P > 0.05; U = 52.0, P > 0.05, respectively) (Table 3Go). Furthermore, no significant difference was observed in MAO-B values between patients who had a family history of alcoholism and those who did not, in both the first and fourth weeks (U = 45.0, P > 0.05; U = 53.5, P > 0.05, respectively) (data not shown).


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Table 3. Monoamine oxidase-B (MAO-B) activities in platelet-rich plasma (PRP) of the low- and high-aggression groups in the first and fourth weeks of alcohol withdrawal
 
Since platelet number and protein level might have affected the measurements of MAO activity in PRP, we compared platelet numbers and serum total protein levels in the patient and control groups, and during the first and fourth weeks of withdrawal in the former group. There was no statistically significant difference between the groups and across time for these two variables (F = 0.11, P > 0.05; F = 0.98, P > 0.05, respectively, by one-way ANOVA) (Table 2Go).

No significant correlations were found between MAO-B values and other clinical variables (age, age at onset of alcohol dependence, duration of alcohol dependence, amount of alcohol consumed daily, number of cigarettes smoked daily, benzodiazepine doses, CAS and HRSD scores) (data not shown).


    DISCUSSION
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Our data demonstrate that MAO-B activity in PRP is significantly lower in alcoholic patients than in controls at the end of the first week, but not during the fourth week, of alcohol withdrawal. There is no agreement in the literature as to whether platelet MAO-B activity increases or decreases after withdrawal in alcohol-dependent patients. The finding of the present study of significantly lower platelet MAO-B activity in alcoholics during the first week of withdrawal is in line with some previous studies (Major and Murphy, 1978Go; Pandey et al., 1988Go; Rommelspacher et al., 1994Go; Berggren et al., 2000Go), but not with others which reported a transitory increase in MAO-B activity during the early withdrawal period (Alexopoulos et al., 1981Go; Alling et al., 1982Go). The fact that only patients in the early withdrawal period have low MAO-B activity may reflect the abnormal physiological states of withdrawal affecting MAO-B activity. However, since we did not measure MAO activity during active alcohol consumption, it is not possible to determine whether platelet MAO activity is low during drinking and slowly returns to control values over about 4 weeks, or whether it falls abruptly when drinking ceases and then returns to a higher value. Taking into account previous studies reporting a decrease in platelet MAO activity during active drinking in alcoholic patients (Alexopoulos et al., 1983Go; Lykouras et al., 1987Go, 1989Go; Rommelspacher et al., 1994Go), and Berggren et al.'s study (2000) reporting a significant reduction of this activity solely during the first and eighth weeks of alcohol withdrawal, but not during intervening weeks, the explanation that low platelet MAO activity is a biochemical marker of alcoholism, and that decreased MAO activity during active alcohol consumption in patients may be concealed by a transitory increase during a certain period of withdrawal (2–8 weeks) seems to be more logical. It has been suggested that low platelet MAO activity may be a result of chronic alcohol intake and may originate from a secondary effect of alcohol on certain enzymatic co-factors, such as iron and riboflavin (Pandey et al., 1988Go). Altogether, we cannot definitely infer from our results whether decreased platelet MAO activity is a trait marker of alcoholism or a state marker of high alcohol consumption or of recent withdrawal.

Since smoking status has recently been reported to be an important factor that can alter MAO activity (Anthenelli et al., 1995Go, 1998Go; Whitfield et al., 2000Go), and seems to be the biggest confounding factor in the results of MAO studies (Farren and Tipton, 1999Go), we selected all patients and control subjects from among cigarette smokers and thus equated this variable. In contrast to these studies reporting that there is no link between alcoholism and MAO activity, and that decreased platelet MAO activity is associated with cigarette smoking, we found a relation between alcohol dependence and reduced MAO activity, but only during the first week of withdrawal.

It is generally reported that low platelet MAO activity may be principally associated with type II alcoholism (Cloninger et al., 1981Go; von Knorring et al., 1985Go; Sullivan et al., 1990Go; Anthenelli et al., 1995Go). According to a suggested classification, type I alcoholism is characterized by late onset alcohol dependence in both men and women as a consequence of adverse psychosocial factors and low heritability. Type I alcoholics have been reported to have normal MAO levels (von Knorring et al., 1985Go; Sullivan et al., 1990Go). Type II alcoholism seems to be highly heritable, and limited to males. Type II alcoholics have an early onset of dependence, some social complications, more impulsive, more sensation-seeking, disinhibited characteristics, and significantly lower levels of platelet MAO-B than type I alcoholics (Cloninger et al., 1981Go; von Knorring et al., 1985Go; Sullivan et al., 1990Go). However, some studies found no difference between Type I and II alcoholic patients with regard to MAO activity (Anthenelli et al., 1998Go; Farren et al., 1998Go). In accordance with this division of alcoholics, an association has been reported between low platelet MAO-B activity, which represents an index of brain serotonergic function (Oreland and Shaskan, 1983Go; Diaz-Marsa et al., 2000Go), and some personality traits such as aggressiveness, sensation-seeking behaviour and impulsiveness (Fowler et al., 1980Go; Zuckerman, 1984Go; Schalling et al., 1987Go; Rommelspacher et al., 1994Go; Stalenheim et al., 1997Go). In contrast to these studies, we did not find any correlation between MAO-B values and lifetime aggression scores, although we observed a non-significant tendency for a decrease in MAO-B levels in the high-aggression group, compared to the low-aggression group, during the first week. In other words, our results did not confirm the association of low platelet MAO-B activity and type II alcoholism, or lifetime aggression history. Instead, we found that low MAO-B activity was limited to the first week of the withdrawal period in both the low- and high-aggression groups. However, it must be kept in mind that this discrepancy may have been caused by the facts that these two samples were quite small and that even patients in the high-aggression group were not actually aggressive (at least during the study), being represented by inpatients who were eager to stop drinking and who did not fully meet the criteria of antisocial or borderline personality disorder. If we had been able to compare the low-aggression alcoholic group with, for example, imprisoned violent alcoholics, the results might have been different.

It has been reported in some recent animal studies that there is a higher degree of correlation between aggressiveness and MAO-A activity rather than MAO-B activity (Shih and Chen, 1999Go; Shih et al., 1999Go). MAO-A gene knock-out mice showed elevated brain levels of serotonin, norepinephrine and dopamine, and manifested aggressive behaviour. However, since only the B-form of MAO is present in blood platelets (Donnelly and Murphy, 1977Go), it was impossible to measure MAO-A activity in the periphery with our method.

In conclusion, our data showed that platelet MAO activity was lower during the first week of withdrawal in alcohol-dependent patients, compared with that in controls, and approached control values by the fourth week of withdrawal as symptoms were subsiding. The findings of the present study also indicated no difference between patients with high- and low-aggression history in terms of platelet MAO activity during withdrawal. If we had found a difference in MAO activity between these two subgroups, it might have suggested that this trait is related to the serotonergic system. Our results suggest that low platelet MAO activity may be a state marker of alcohol withdrawal or a result of high alcohol consumption, rather than a trait marker of alcoholism. Nevertheless, since we did not measure platelet MAO activity during active alcohol consumption or later than 1 month after alcohol cessation, we cannot readily exclude the hypothesis that low platelet MAO activity may be a trait marker of alcoholism. The fact that only smoking subjects were included in the study allows us to eliminate the smoking effect on platelet MAO activity and thus strengthens our results. Although a 4-week duration is usually adequate for relieving withdrawal symptoms, one cannot be sure that enzyme activity will remain stable after the fourth week of withdrawal. Therefore, longer-term longitudinal studies in larger samples are needed to clarify this issue.


    FOOTNOTES
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
* Author to whom correspondence should be addressed. Back

{dagger} Report presented at the 13th European College of Neuropsychopharmacology Congress, 9 September 2000, Munich, Germany. Back


    REFERENCES
 TOP
 FOOTNOTES
 ABSTRACT
 INTRODUCTION
 SUBJECTS AND METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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