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PubMed1993

Cocaine dependence: alcohol and other drug dependence and withdrawal characteristics.

In this study, a cocaine abstinence syndrome is confirmed. Moreover, the cocaine withdrawal syndrome was found to be medically and psychiatrically benign and required no medication for detoxification in this inpatient setting. The 150 patients who underwent cocaine withdrawal did not show the three distinct phases of the abstinence symptomatology previously described. No patients required pharmacological intervention for cocaine withdrawal, and the dropout rate was 8% of the 150 cocaine dependents. The common symptoms of acute cessation of cocaine were transient craving, hyperactivity, slight tremor, insomnia and apprehension. The diagnosis of cocaine dependence alone without an additional drug or alcohol diagnosis was unusual in this study at 5%, as is the solitary use of cocaine also uncommon according to other studies. Studies clearly document that the concurrent and simultaneous use and dependence on multiple drugs and alcohol is present in the majority of treatment populations and common in the general population. As many as 54% of cocaine dependents qualified for alcohol dependence in this study, and many were dependent on alcohol prior to their cocaine dependence. Cocaine dependence appears to be yet another diagnosis in the spectrum of the multiple drug and alcohol dependent.

Adolescent↗
PubMed2004

A randomized trial of concurrent versus delayed smoking intervention for patients in alcohol dependence treatment.

OBJECTIVE: Fear of jeopardizing drinking outcomes has resulted in a reluctance to treat tobacco dependence concurrently with alcohol dependence, in spite of the high prevalence of smoking among patients with alcohol dependence. The objective of this study was to compare the effects of smoking treatment and intensive treatment for alcohol dependence, delivered concurrently, with delayed smoking treatment on smoking and alcohol use. METHOD: For the study, 1,943 patients in intensive treatment for alcohol dependence or abuse were screened for participation. Of these, 499 smokers were enrolled and randomized to concurrent (during alcohol treatment) or delayed (6 months later) smoking intervention. The smoking intervention included individual behavioral counseling and nicotine replacement. The main smoking outcome measure was 7-day point prevalent tobacco abstinence, and the main drinking outcome was 6-month prolonged abstinence from alcohol; both measured 18 months after study enrollment. RESULTS: Participants in the concurrent group were more likely to participate in smoking treatment than those in the delayed group (78.5% vs 64.5%, p = .005), but there was no significant difference in cessation rates at 18 months (12.4% vs 13.7%). Prolonged, 6-month abstinence from alcohol was worse in the concurrent group than in the delayed group at 6, 12 and 18 months (41% vs 56%, p =.001; 33% vs 42%,p = .06; 41% vs 48%, p = .14, respectively), and 30-day prolonged alcohol abstinence was also worse in the concurrent treatment group (51% vs 64%, p = .004; 46% vs 53%, p = .11; 48% vs 60%, p = .01, respectively). CONCLUSIONS: These data show that patients in alcohol treatment are interested in smoking cessation, participate in treatment and demonstrate success; but there was no benefit of concurrent treatment. Drinking outcomes were worse with concurrent tobacco treatment. These findings suggest that smoking cessation intervention should be provided to patients after intensive alcohol treatment; however, the data require confirmation because they are not consistent with the existing literature.

Adult↗
PubMed2004

Pharmacodynamic effects of acamprosate on markers of cerebral function in alcohol-dependent subjects administered as pretreatment and during alcohol abstinence.

Animal studies suggested that acamprosate modulates neuronal hyperexcitability of acute alcohol withdrawal, acting through the glutamatergic neurotransmission. In the present study, we further investigated whether treatment with acamprosate could attenuate the post-alcohol withdrawal hyperexcitability or hyperarousal in humans using brain magnetoencephalography mapping of spontaneous fields. A double-blind, randomised, placebo-controlled study with a parallel group design comparing 2,000 mg/day of acamprosate versus placebo was conducted in alcohol-dependent subjects meeting DSM-IV criteria for alcohol dependence. Treatments were initiated 8 days before alcohol withdrawal and prolonged during the 15 following (abstinence) days. The study demonstrated that during alcohol withdrawal, acamprosate decreased the arousal level as reflected by alpha slow-wave index (ASI) measurement. This effect was mostly evidenced in left parietotemporal regions and, to a lesser extent, in the contiguous anterior, posterior and right-sided regions. In the placebo group, on the contrary, ASI measures increased between day 2 (acute withdrawal) and day 14 (prolonged withdrawal). The present results suggest a sustained effect of acamprosate on the hyperexcitability state due to alcohol withdrawal in alcohol-dependent patients and that acamprosate may have a protective effect when administered 8 days before alcohol withdrawal.

Acamprosate↗
PubMedDate not supplied

A study of the temporal course of phenomenology of alcohol dependence.

The natural history of alcoholism was first charted out in 1946 by Jellinek, whose original results have been replicated by multiple research groups. They have verified a general progression of alcohol dependence through a series of identifiable phases. The study investigated the sequence of events in the course of alcohol dependence and its deviations from randomness. The study consisted of 36 patients with alcohol dependence, subjected to a structured questionnaire containing 34 items describing the phenomenology of alcohol dependence, based on the lines of SCID. The items experienced by each patient were identified and then plotted on a timeline graph according to an important life event, the items being represented on cards given to the patients randomly. The subjects were re-interviewed after one week and asked to rank their symptoms again to analyze test-retest reliability. The analysis of the item ordering was determined by null hypothesis of randomness. The ordering showed three phases. The early phase was characterized by features of increased tolerance loss of flexibility, and salience. The middle phase consisted mainly of the need for alcohol, and the late phase was predominated by features of physiological withdrawal, tremors, nausea, panics, and hallucinations. There is a characteristic ordering of new events and symptoms, which suggests a developmental process of alcoholism, but this is apparent only if attention is confined to a limited part of the broad spectrum. This process is obscured by consideration of the social concomitants of alcohol dependence. The study of the natural history of alcohol dependence is essential in recognizing and treating the problem and determining whether an intervention appears to be working.

Adult↗
PubMed2006

ADH1C*2 allele is associated with alcohol dependence and elevated liver enzymes in Trinidad and Tobago.

Variants in alcohol dehydrogenase (ADH) genes differ between ethnic groups and have, in some studies, been found to be associated with alcohol dependence and alcoholic liver disease. This study sought to determine whether an association exists between ADH (ADH1C previously ADH3, ADH1B*2 previously ADH2*2) genotypes, alcohol dependence, drinking history, and liver function tests in the two major ethnic groups of Trinidad and Tobago (TT). One hundred and forty-five alcohol-dependent individuals of both East Indian (Indo-TT) and African (Afro-TT) ancestry, and 108 controls matched by age, sex, and education participated in the study. Serum levels of alanine and aspartate aminotransferase (ALT, AST), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), and gamma-glutamyltransferase (GGT) as well as presence of HIV, hepatitis B surface antigen, and anti-hepatitis C virus antibody were determined. There was a significant difference in the distribution of ADH1C allele polymorphisms between the ethnic groups (P<.0001). Forty-three percent of the Indo-TT were found to have one ADH1C*2 allele and 5% were homozygous, whereas, only 23% of Afro-TT had one allele and one was homozygous. Only three individuals had an ADH1B*2 allele (one Indo-TT alcohol dependent, two Indo-TT controls). The ADH1C*2 allele was significantly associated with alcohol dependence overall and within Indo-TT ancestry, however, it was not associated with current or heaviest alcohol consumption levels. Individuals with at least one ADH1C*2 allele also had significantly elevated levels of ALP (P<.02) and GGT (P<.02) as compared to individuals homozygous for ADH1C*. Additionally, GGT levels were also found to be elevated (P<.02) within Indo-TT alcohol dependents with at least one ADH1C*2 allele but not within the Afro-TT alcohol dependents with that allele. A linear regression that included alcohol dependence and levels of alcohol consumption confirmed that levels of serum GGT were significantly associated with the ADH1C*2 genotype. These results suggest that ADH1C polymorphisms are associated with alcohol dependence and alcohol associated elevations of liver enzymes in a population with a low frequency of ADH1B2 alleles.

Adult↗
PubMed2005

New achievements and pharmacotherapeutic approaches in the treatment of alcohol dependence.

The treatment of alcohol dependence mainly consists of psychological, social, and pharmacotherapeutic interventions aiming to reduce physical withdrawal, craving, and alcohol relapse. During the last years, it has become increasingly clear that adjuvant pharmacotherapy is efficacious especially in rehabilitation programs for alcohol dependent patients. The development of alcohol dependence seems to involve adaptive changes in amino acid neurotransmitter systems, stimulation of dopamine and opioid peptide systems, and changes in serotonergic activity. Disulfiram, naltrexone and acamprosate are approved treatments for the management of abstinence maintenance treatment. New compounds are under investigation. This review discusses the neurobiological basis of alcohol addiction, pharmacological targets for relapse prevention treatment and pre-clinical and clinical results with the most promising drugs.

Alcohol Deterrents↗
PubMed1993

Self-regulation of slow cortical potentials in psychiatric patients: alcohol dependency.

Ten unmediated alcohol-dependent male inpatients participated in a Slow Cortical Potential (SCP) self-regulation task utilizing biofeedback and instrumental conditioning. These patients were hospitalized for treatment of alcohol dependency after chronic abuse of alcoholic beverages. Somatic withdrawal symptomatology had occurred recently and the patients were free of any withdrawal symptoms of the autonomic nervous system. Immediately after hospitalization patients were unable to control their SCPs without the reinforcement of immediate feedback across 4 sessions. Seven patients participated in a fifth session an average of 4 months later. Six out of these 7 patients had not had a relapse at the follow-up. In the fifth session these patients were immediately able to differentiate between the required negativity and negativity suppression, whereas the seventh patient, who had relapsed, was unable to control his brain potentials successfully. Results are further evidence that some of the frontocortical dysfunctions in alcohol-dependent patients are reversible. This could covary with a morphological restitution of the cortex.

Adult↗
PubMed2004

Genomic screen for loci associated with alcohol dependence in Mission Indians.

Alcohol dependence is a leading cause of morbidity and mortality in Native Americans, yet biological factors underlying the disorder in this ethnic group remain elusive. This study's aims were to map susceptibility loci for DSM-III-R alcohol dependence and two narrower alcohol-related phenotypes in Mission Indian families. Each participant gave a blood sample and completed an interview using the Semi-Structured Assessment for the Genetics of Alcoholism (SSAGA) that was used to make alcohol dependence diagnoses and the narrower phenotypes of withdrawal, and drinking severity. Genotypes were determined for a panel 791 microsatellite polymorphisms. Analyses of multipoint variance component LOD scores for the dichotomous DSM-III-R phenotype revealed no peak LOD scores that exceeded 2.0 at any chromosome location. Two chromosomes, 4 and 12, had peak LOD scores that exceeded 2 for the alcohol use severity phenotype and three chromosomes 6, 15, 16 were found to have peaks with LOD scores that exceeded 2 for the withdrawal phenotype. Evidence for linkage to chromosomes 4 and 15, and 16 have been reported previously for alcohol related phenotypes whereas no evidence has as yet been reported for chromosomes 6 and 12. Combined linkage and association analysis suggest that alcohol dehydrogenase 1B gene polymorphisms are partially responsible for the linkage result on chromosome 4 in this population. These results corroborate the importance of several chromosomal regions highlighted in prior segregation studies in alcoholism and further identify new regions of the genome that may be unique to either the restricted phenotypes evaluated or this population of Mission Indians.

Adolescent↗
PubMed2001

Stress hormone dysregulation at rest and after serotonergic stimulation among alcohol-dependent men with extended abstinence and controls.

BACKGROUND: Alcohol dependence has been associated with long-lasting alterations in limbic-hypothalamic-pituitary-adrenal (LHPA) axis and serotonin (5-hydroxytryptamine [5-HT]) function. Other conditions that are associated with alcoholism (cigarette smoking and antisocial personality disorder [ASPD]) have been linked with disturbances in these interrelated systems. We evaluated the stress hormone response to 5-HTergic stimulation in alcohol-dependent men with extended abstinence (average abstinence duration, 4.3 months) and controls to determine the relative contributions of alcoholism, cigarette smoking, and ASPD on baseline and provoked plasma cortisol and adrenocorticotropin hormone (ACTH) concentrations. METHODS: One hundred nine alcohol-abstinent men with alcohol dependence (62%), habitual smoking (70%), and ASPD (43%) received D,L-fenfluramine (100 mg po) in a randomized, double-blind, placebo-controlled, crossover trial. The group of recovering alcohol-dependent individuals included abstinent primary alcohol-dependent men and alcohol-dependent men with ASPD, whereas the group of non-alcohol-dependent men comprised healthy controls and non-alcohol-dependent men with ASPD. Plasma cortisol and ACTH levels were obtained at AM baseline and at half-hour intervals after drug administration. Subjective ratings of drug response and physiological measures were also obtained at baseline and every 30 min. RESULTS: Abstinent alcohol-dependent men had significantly lower (approximately 20%) AM baseline plasma cortisol concentrations than non-alcohol-dependent men on both challenge days; however, no differences between the groups were observed with regard to resting AM plasma ACTH levels. After adjusting for these baseline differences, recovering alcohol-dependent men (area under curve = 35.6 +/- 37.4 [microg/dl] x min) had a twofold greater cortisol response to fenfluramine than non-alcohol-dependent men (area under curve = 17.5 +/- 32.5 [microg/dl] x min) (F = 5.1; df = 1,105; p < 0.03). The elevated cortisol response, which occurred primarily along the descending limb of the response curve, was paralleled by a nonsignificant statistical trend for alcohol-dependent men to also exhibit a greater ACTH response to fenfluramine at the 210-min (p < 0.07) and 240-min (P < 0.09) time points as compared with non-alcohol-dependent men. Cigarette smoking and ASPD did not affect hormonal responses, nor could the groups' subjective ratings and physiological measures be distinguished. CONCLUSIONS: Alcohol-dependent men with extended abstinence differed from age- and race-matched non-alcohol-dependent men in resting AM and fenfluramine-induced plasma cortisol levels. This dysfunction in glucocorticoid homeostatic mechanisms was associated with alcoholism and not with smoking or ASPD. We also observed a nonsignificant statistical trend for plasma ACTH levels to be elevated among alcohol-dependent men along the descending limb of the response curve. Alcohol-dependent men seemed to have inherited or acquired damage to 5-HT-regulated LHPA axis function, the precise mechanisms and sites of which remain to be determined.

Adrenocorticotropic Hormone↗
PubMed1999

Quality of life in alcohol-dependent subjects--a review.

Although alcohol misuse is a major cause of morbidity and mortality and an important health care burden, the Quality of Life (QoL) of alcohol misusing subjects has been little studied to date. For example, only 5 out of 442 accepted abstracts at a recent international QoL conference concerned alcohol-dependent subjects. This paper reviews the ongoing and published work in the area focusing upon QoL characteristics of alcohol-dependent subjects, the link between QoL comorbidity and alcoholism, QoL alcohol dependency and social environment, changes in QoL status as a result of abstinence, minimal or controlled drinking, QoL as a predictor of relapse to heavy drinking and the importance of using a QoL measure when assessing treatment outcomes together with some of the present difficulties with existing measures. The main conclusions from the review were that the QoL of alcohol-dependent subjects is very poor but improved as a result of abstinence, controlled or minimal drinking. The important factors in the QoL of alcohol-dependent subjects are psychiatric comorbidity, social environment and disturbed sleep.

Alcoholism↗
PubMed2004

The psychosocial work environment and alcohol dependence: a prospective study.

AIMS: To examine whether a stressful psychosocial work environment predicts alcohol dependence. METHODS: Alcohol dependence of participants in the Whitehall II occupational cohort of London based civil servants (1985-88) was measured in 1991-93 using the CAGE questionnaire. The psychosocial work environment was measured by self report questions on the job demand-support-control model and on the model of effort-reward imbalance. Potential mediators including physical illness and poor mental health (GHQ) were measured at follow up in 1989. RESULTS: Effort-reward imbalance at work was associated with alcohol dependence in men after adjustment for employment grade and other baseline factors related to alcohol dependence. Although effort-reward imbalance predicted future longstanding illness, poor mental health and negative aspects of close relationships, the association between effort-reward imbalance and alcohol dependence in men was only partially mediated through these health and social support measures. In women, low decision latitude was related to alcohol dependence to some extent, but alcohol dependence among women was more prevalent in higher occupational grades. Men with high job demands or with low work social supports had a slightly reduced risk of alcohol dependence. No association was found between objectively assessed demands, job control, and alcohol dependence in either men or women. CONCLUSION: A stressful psychosocial work environment in terms of effort-reward imbalance was found to be a risk factor for alcohol dependence in men. In view of the public health importance of alcohol dependence in working populations these findings call for more emphasis on psychosocial factors in occupational health research and prevention.

Adult↗