Treatment of alcohol dependence: the alcoholic patient.
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BACKGROUND: There is very little work that has investigated the self-reported sleep status of alcohol misusers. This study addressed that imbalance. METHODS: The study consisted of two parts: 1) the outpatient study, a sample of DSM-IV alcohol-dependent subjects who were referred to an outpatient clinic and were given a series of questionnaires, including the Pittsburgh Sleep Quality Index (PSQI); and 2) the inpatient study, a group of DSM-IV alcohol-dependent subjects whose sleep was assessed by the Nottingham Health Profile (NHP) sleep subscore at the start of the study and again at the 12-week follow-up. Both the PSQI and NHP are self-report indices whereby higher scores indicate a poor sleep quality. RESULTS: In the outpatient study, the PSQI scores were significantly higher in the alcoholics (n = 31) compared with the controls (n = 49). There were no differences in the PSQI scores among mildly (n = 11), moderately (n = 10), and severely (n = 11) dependent drinkers. The PSQI total scores correlated with the Beck Depression Index but not with severity of dependence or alcohol problem scores. Sleep latency emerged as the most significant predictor of relapse, and sleeping badly was associated with poor outcome at the 12-week follow-up in the inpatient study. CONCLUSION: Self-reported sleep disturbance can provide clinicians with information to plan better treatment for alcohol misusers.
BACKGROUND: Alcohol dependence is a major risk factor for suicidal behavior. Although a number of risk factors have been suggested there is still no well-defined risk profile for attempted suicide in alcoholic patients. Alterations of serum lipids have been associated with completed as well as attempted suicide and with suicidal ideation. This study investigated potential demographic and clinical risk factors for attempted suicide in alcohol-dependent patients taking serum lipids additionally into consideration. METHODS: One-hundred ten alcohol-dependent patients who were admitted to a psychiatric university hospital department for inpatient treatment were grouped according to whether or not they had a lifetime history of attempted suicide. Attempters versus nonattempters as well as attempters who used a violent versus a nonviolent suicide method were compared. RESULTS: Patients who had attempted suicide at least once in their life differed significantly from those who had no history of suicide attempts. Univariate analyses showed that they were younger (41.7 years vs 46.8 years; p = 0.003), were more often smokers (97% vs 77%; p = 0.011), had more frequently coabused benzodiazepines (54% vs 17%; p = 0.002), and scored currently higher on the Montgomery and Asberg Depression Rating Scale (MADRS) global scale (26.3 vs 20.2; p = 0.005) as well as the "suicidal thoughts" item (1.8 vs 0.6; p = 0.001). Additionally, they had higher serum triglyceride levels (178.9 vs 127.5; p = 0.039). A logistic regression analysis left coabuse of benzodiazepines [odds ratio (OR), 5.26; p = 0.001], younger age (OR per year increase of age, 0.91; p = 0.006), and current MADRS item 10 ("suicidal thoughts") score (OR per point increase in MADRS item 10 score, 1.43; p = 0.019) as significant factors. Suicide attempters who had used a violent method were significantly more often male (82% vs 44%; p = 0.035), were younger (38.2% vs 45.1 years; p = 0.008), and had less frequently coabused tranquilizers (35% vs 78%; p = 0.018) than nonviolent attempters. CONCLUSIONS: These findings contribute to the development of a more specific profile of alcohol-dependent individuals at risk for suicidal behavior. Further research is required to determine the role of serum triglycerides for suicidal behavior in patients with alcohol dependence.
Alcohol dependence is a complex disorder with a substantial genetic contribution to susceptibility. The Collaborative Study on the Genetics of Alcoholism is a multi-site study whose purpose is to detect, localize, and characterize genes contributing to this susceptibility. Previous linkage analyses of the trait of alcohol dependence in Collaborative Study on the Genetics of Alcoholism have used affected sib-pair methods with a dichotomous phenotype definition. In contrast, the analysis in this paper uses a sex-adjusted and age-adjusted multiple threshold liability model. The use of such a model, in that it includes unaffected as well as as affected subjects and in that it utilizes the differential severity of a diagnosis scale, should heuristically be more powerful than a straight affected sib-pair analysis. Three regions of interest are found on chromosome 1 (lod 5.17), chromosome 4 (lod 3.46), and chromosome 8 (lod 4.31). The region on chromosome 1 near the marker D1S532 is in the region previously reported as linked to alcohol dependence and correlated phenotypes in this dataset. The region on chromosome 4 near the alcohol dehydrogenase gene cluster has been reported to be linked to alcohol dependence in other studies, as well as to the alcohol consumption phenotype 'Maximum Number of Drinks in a 24-Hour Period' in this dataset. The region on chromosome 8 near the marker D8S1988 is homologous to a section of rat chromosome 5 to which an alcohol consumption phenotype has been linked.
BACKGROUND: Reduced metabolism, blood flow, and tissue volume have been detected in the dorsolateral prefrontal cortex (dlPFC) of neurologically intact alcoholic subjects and these deficits are accompanied by lower density of neurons and glial cells. Another prefrontal region, the orbitofrontal cortex (ORB), functionally and structurally differentiated from the dlPFC, and heavily involved in decision-making processes, also shows functional alterations in alcoholic subjects. However, it is unknown whether changes in the packing density of neurons or glial cells also occur in the ORB and whether that density may be related to the increased suicide probability of alcoholic subjects or to the duration of alcohol dependence. METHODS: The present study used a 3-dimensional cell-counting method in postmortem brain tissue to determine the packing density of neurons and glial cells in the ORB (area 47) of 15 subjects with alcohol dependence (8 suicides, 7 nonsuicides) and 8 normal controls and to determine whether cell density is correlated with suicide and duration of alcohol dependence. RESULTS: There was a significantly lower density of both neurons (by 27%) and glial cells (by 25%) in the ORB of alcoholic subjects compared with controls. Packing density of either neurons or glial cells was not significantly different in alcoholic suicides compared with alcoholic nonsuicides. Age was not correlated with neuronal or glial density in either group. However, the duration of alcohol dependence and the ratio of that duration to the length of life span were significantly and negatively correlated to the overall density of neurons. CONCLUSION: The present results indicate that alcohol dependence is associated with a decrease in the packing density of neurons and glia in the ORB and that the reduction in neuronal but not glial density progresses with the duration of alcohol dependence.
Chronic alcohol abuse is often co-morbid with depression symptoms and in many cases it appears to induce major depressive disorder. Structural and functional neuroimaging has provided evidence supporting some degree of neuropathological convergence of alcoholism and mood disorders. In order to understand the cellular neuropathology of alcohol dependence and mood disorders, postmortem morphometric studies have tested the possibility of alterations in the number and size of cells in the prefrontal cortex and other brain regions. The present review compares the cell pathology in the prefrontal cortex between alcohol dependence and depression, and reveals both similarities and differences. One of the most striking similarities is that, although pathology affects both neuronal and glial cells, effects on glia are more dramatic than on neurons in both alcohol dependence comorbid with depression and idiopathic depression. Moreover, prefrontal cortical regions are commonly affected in both depression and alcoholism. However, the cellular changes are more prominent and spread across cortical layers in alcohol dependent subjects than in subjects with mood disorders, and changes in glial nucleus size are opposite in alcoholism and depression. It could be argued that one defining factor in the manifestation of the depressive pathology is a reduction in the glial distribution in the dlPFC that is reflected in a reduced glial density. In alcoholism reduced glial nuclear size might be related to the cytotoxic effects of prolonged alcohol exposure, while in MDD, in the absence of alcohol abuse, other processes might be responsible for the increase in average size of glial nuclei. In either case abnormal function related to glial reduction would be associated with depression due to insufficient glial support to the surrounding neurons.
Alcoholism is a relatively common, chronic, disabling and often treatment-resistant disorder. Evidence from twin and adoption studies indicates a substantial genetic influence, with heritability estimates of 50-60%. We conducted a genome scan in the Irish Affected Sib Pair Study of Alcohol Dependence (IASPSAD). Most probands were ascertained through alcoholism treatment settings and were severely affected. Probands, affected siblings and parents were evaluated by structured interview. A 4 cM genome scan was conducted using 474 families of which most (96%) were comprised by affected sib pairs. Nonparametric and quantitative linkage analyses were conducted using DSM-IV alcohol dependence (AD) and number of DSM-IV AD symptoms (ADSX). Quantitative results indicate strong linkage for number of AD criteria to a broad region of chromosome 4, ranging from 4q22 to 4q32 (peak multipoint LOD=4.59, P=2.1 x 10(-6), at D4S1611). Follow-up analyses suggest that the linkage may be due to variation in the symptoms of tolerance and out of control drinking. There was evidence of weak linkage (LODs of 1.0-2.0) to several other regions, including 1q44, 13q31, and 22q11 for AD along with 2q37, 9q21, 9q34 and 18p11 for ADSX. The location of the chromosome 4 peak is consistent with results from prior linkage studies and includes the alcohol dehydrogenase gene cluster. The results of this study suggest the importance of genetic variation in chromosome 4 in the etiology and severity of alcoholism in Caucasian populations.
BACKGROUND: Patients with a double diagnosis of alcohol dependence and phobic disorders are a common phenomenon in both alcohol and anxiety disorder clinics. If we are to provide optimum treatment we need to know more about the clinical characteristics of this group of comorbid patients. OBJECTIVE: To answer the following questions. (1). What are the clinical characteristics of treatment-seeking alcohol-dependent patients with a comorbid phobic disorder? (2). Are alcohol dependence and other clinical characteristics of comorbid patients different from those of 'pure' alcohol-dependent patients? (3). Are the anxiety symptoms and other clinical characteristics of comorbid patients different from those of 'pure' phobic patients? METHOD: Three groups of treatment-seeking patients were compared on demographic and clinical characteristics: alcohol dependent patients with a comorbid phobic disorder (n = 110), alcohol-dependent patients (n = 148) and patients with social phobia or agoraphobia (n = 106). In order to diagnose the comorbid disorders validly, the assessment took place at least 6 weeks after detoxification. RESULTS: Comorbid patients have high scores on depressive symptoms and general psychopathology: 25% of patients have a current and 52% a lifetime depressive disorder. The majority have no partner and are unemployed, they have a high incidence of other substance use (benzodiazepine, cocaine, cannabis) and a substantial proportion of comorbid patients have been emotionally, physically and sexually abused. They do not have a more severe, or different type of alcohol dependence or anxiety disorder than 'pure' alcohol-dependent patients and phobic patients respectively. CONCLUSION: Comorbid patients constitute a complex part of the treatment-seeking population in alcohol clinics and psychiatric hospitals. These findings should be taken into account when diagnosing and treating alcohol-dependent patients with a comorbid phobic disorder.
Optimal cut-off points on the Severity of Dependence Scale (SDS) indicative of clinically significant dependence have been determined for a range of substance types. This study aims to determine a cut-off point on SDS that discriminates between the presence and absence of a DSM-IV diagnosis of alcohol dependence. A structured interview was administered to 90 alcohol users in Sydney, Australia. Receiver Operating Characteristic curve analysis confirmed the utility of the SDS-alcohol for characterising and diagnosing persons with respect to their alcohol-dependent status to an accuracy of 85%. A SDS score of 3 or above was determined as optimal for characterising alcohol dependence. Evidence is also provided confirming that the SDS-alcohol is a valid, reliable uni-dimensional scale for measuring alcohol dependence. It has been demonstrated that the SDS-alcohol can be used to characterise an individual's alcohol-dependent status. A cut-off value for SDS-alcohol provides additional meaning and value to the scale for clients and clinicians and will enable researchers to characterise the prevalence of alcohol dependence in their target populations.
In an attempt to clarify the genetic factors in alcoholism among the Japanese, polymorphism of alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes has been investigated. Genetic polymorphism of ADH2/ALDH2 in 66 cases of normal subjects, 90 cases of alcohol dependent, and 31 patients with alcoholic liver disease among Japanese has been analyzed using a polymerase chain reaction assay followed by a direct sequencing method, because ethanol is mainly catabolized by ADH and ALDH and less by cytochrome P450IIE1 and catalase. The incidence of both ADH2*1/*1 and ALDH2*1/*1 was significantly higher in patients with alcohol dependence and in patients with alcoholic liver disease when compared with that in control subjects. In addition, the incidence of ALDH2*1/*2 and ALDH2*2/*2 was significantly reduced in alcoholics compared with control subjects. Genetic polymorphism of ADH2/ALDH2 in patients with alcoholic liver disease was not different from that of alcohol dependents. According to these results, not only ALDH2 gene, often claimed to be responsible for alcohol dependence among Japanese, but also ADH2 gene polymorphism, which modulates the metabolism of ethanol, play important roles in habitual alcohol intake behavior in Japanese patients and in some patients leads to alcoholic liver diseases.
Treatment of alcohol dependence among older alcoholic patients should be multidimensional to address as many potential relapse factors as possible. As the literature suggests, alcohol-related disorders often are under diagnosed and under treated. More efforts are needed to identify and improve diagnosis of these disorders in older alcoholic patients. For better outcomes, age-specific programs should be implemented. Furthermore, when treating elderly patients, basic therapeutic principles like respect for privacy and a respectful attitude should be adopted. Adequate medical, pharmacologic, and psychiatric treatment should be provided when appropriate. Medication to reduce cravings should be considered in patients without contraindications to its use. Participation in individual, group, and family therapy and attendance at self-help group meetings such as AA should be encouraged (Table 8). Despite the lack of empiric testing to validate these recommendations in an elderly population, clinical experience suggests that adherence to these recommendations will benefit elderly patients just as it has the general adult population. Research is necessary to explore the benefits of alcohol treatments in elderly patients. Until then, adherence to these recommendations should be the best available approach.
A total of 86 women, attending three different agencies, were interviewed on their help-seeking behaviours for problem drinking. Each agency represented a different type of help available in the community. Self-help was represented by Alcoholics Anonymous; the non-statutory sector by a regional council on alcoholism's offices; and the statutory sector by an alcohol treatment unit's out-patient department. Differences between the groups in terms of demography and drinking history are explored in this paper. It was found that the regional council group resembled the female problem drinkers in other alcohol treatment agencies in terms of alcohol dependency, pattern of alcohol consumption and drinking styles, but differed in age and abstinence behaviour.
Alcohol-dependent populations have a high lifetime suicide rate (between 7 and 15%, relative risk = 7), and alcoholism is one of the two psychiatric disorders most frequently found in suicidal cases (between 15 and 25%). Biological factors that would detect patients at risk could thus be of value. Carbohydrate-deficient transferrin, monoamine oxidase B, soluble interleukin-2 receptor and cholesterol have been proposed as markers of suicidal risk in alcohol-dependent patients, although nonspecific and with low predictive value. On the other hand, there is large and convergent data stressing the importance of serotonin dysregulation as increasing the risk for aggressive behaviour toward the self, although it is not clear whether serotonin is involved through the altered behavior inhibition system, enhancement of anxiety and depression, or association with specific subtypes of alcohol-dependence, such as early-onset type II alcoholism. Considering the complex but significant impact of alcohol on serotonin metabolism and turnover, it is likely that serotonin mediates a large part of the proneness of ethanol to commit impulsive-aggressive behavior.
Alcohol abuse is a very common problem all over the world. Identification of alcoholism is crucial in preventing some adverse health effects, economical and social consequences of excessive alcohol consumption. The aim of this study was to determine sialic acid (SA) and gamma-glutamyltransferase (GGT) levels in serum samples of alcoholics and to compare the diagnostic accuracy of SA with the conventional marker, GGT. The results have shown that serum SA (p<0.01) and GGT levels (p<0.001) were significantly increased in alcohol-dependent individuals as compared with healthy controls. No significant relationship was observed between SA and GGT levels in alcohol-dependent subjects and control group. Interestingly, a positive correlation was found between amount of alcohol consumption and serum SA level (r = 0.381, p<0.05). In order to evaluate the ability of SA and GGT determinations to discriminate between alcohol-dependent subjects and healthy controls, an analysis of receiver operating characteristic (ROC) curve was performed. Data suggest that GGT and SA levels in serum may be used as valuable biological markers for detecting and monitoring alcohol abuse. In view of the findings, introducing serum SA determination can be recommended as a part of diagnostic tests for identifying alcohol abuse.