International Society For Biomedical Research On Alcoholism Research Articles

30th Anniversary of Alcohol and Alcoholism

The first author, ADT, was the Founding Editor when Alcohol and Alcoholism was launched 30 years ago with the help of my able colleagues, Deputy Editor Dr Spencer Madden and Assistant Editor Dr Abdulla Badaway. It has been a great pleasure to watch the journal develop through a succession of very dedicated editors, and especially our present editors Professors Jonathan Chick and Philippe de Witte, into one of the leading alcohol journals in the world. Alcohol and Alcoholism is the journal of The Medical Council on Alcohol (MCA) and the official journal of the European Society for Biomedical Research on Alcoholism (ESBRA). The MCA was founded in London, in 1967, by a group of doctors from a range of different specialties, at a time when services for alcohol problems were poorly developed in the UK (Walton et al ., 1966). In an effort to highlight the health problems caused by alcohol, the MCA originally produced a journal called The British Journal on Alcohol and Alcoholism (the ‘blue’ journal) and this was distributed free of charge, quarterly, to General Practitioners throughout the UK. The primary objective of the journal was to provide reliable information and to raise awareness of the growing problem of alcoholism, especially to medical and paramedical practitioners and it was extremely successful in achieving this (Evans, 1990). The next logical step was to develop the journal as a multi-disciplinary, international research journal and it was re-launched in 1983 as Alcohol and Alcoholism (the ‘red’ journal) . The red journal was distinct and different from the outset and was aimed at the international community and focused on advancing alcohol research and integrating new knowledge into clinical practice. The International Society for Biomedical Research on Alcoholism (ISBRA) had its inaugural meeting in Cardiff in 1980 and the ESBRA was …

Laboratory models available to study alcohol-induced organ damage and immune variations: choosing the appropriate model.

The morbidity and mortality resulting from alcohol-related diseases globally impose a substantive cost to society. To minimize the financial burden on society and improve the quality of life for individuals suffering from the ill effects of alcohol abuse, substantial research in the alcohol field is focused on understanding the mechanisms by which alcohol-related diseases develop and progress. Since ethical concerns and inherent difficulties limit the amount of alcohol abuse research that can be performed in humans, most studies are performed in laboratory animals. This article summarizes the various laboratory models of alcohol abuse that are currently available and are used to study the mechanisms by which alcohol abuse induces organ damage and immune defects. The strengths and weaknesses of each of the models are discussed. Integrated into the review are the presentations that were made in the symposium "Methods of Ethanol Application in Alcohol Model-How Long is Long Enough" at the joint 2008 Research Society on Alcoholism (RSA) and International Society for Biomedical Research on Alcoholism (ISBRA) meeting, Washington, DC, emphasizing the importance not only of selecting the most appropriate laboratory alcohol model to address the specific goals of a project but also of ensuring that the findings can be extrapolated to alcohol-induced diseases in humans.

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Risk factors for suicide attempts in patients with alcohol dependence or abuse and a history of depressive symptoms: A subgroup analysis from the WHO/ISBRA study

Alcoholism, depression and suicide attempts (SA) are strongly interrelated. The aims were to determine risk factors and develop a prognostic predictor model for SA in a subgroup of patients with a history of alcohol dependence or abuse and depressive symptoms. A subgroup analysis from the data of the World Health Organisation (WHO)/the International Society for Biomedical Research on Alcoholism (ISBRA)-collaborative study on biological state and trait marker of alcohol use and dependence, an international multi-centre study with a cross-sectional design, based on a standardised questionnaire. We analysed from 1314 variables 43 factors-including demographic characteristics, dependence variables, comorbid disorders, personality trait markers and family history-that were supposed to be most predictive for SA according to the literature. Correlation analyses by the chi(2)-test and Mann-Whitney U-test were performed to obtain statistical meaningful parameters for logistic regression analysis. Of the 1863 persons included in the WHO/ISBRA study, 292 had both a history of depressive symptoms and alcohol dependence or abuse and were included in the subgroup analysis. In the logistic regression analysis, drinking status, depressive symptoms, adverse drinking experiences during alcohol consumption, bad experiences from drug abuse and antidepressant therapy were found to be independent risk factors for SA. Positive family history of alcoholism was a model-improving co-factor. This predictive model explains approximately 60% of the variance (Nagelkerkes' square). This prognostic model derived from data of the WHO/ISBRA collaborative study shows important risk factors for SA in patients with history of alcohol abuse or dependence and depressive symptoms.

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IS THERE A FUTURE FOR QUANTIFYING DRINKING IN THE DIAGNOSIS, TREATMENT, AND PREVENTION OF ALCOHOL USE DISORDERS?

This commentary is based on a Plenary Address at th 2006 Meetingof the International Society for Biomedical Research on Alcoholism (ISBRA) held in Sydney, Australia, which posed the simple question: Is There a Future for Quantifying Drinking in the Diagnosis, Treatment, and Prevention of Alcohol Use Disorders? The intention is to stimulate dialogue among the many disciplines represented in the alcohol field about where we should be going with respect to diagnostic criteria for alcohol use disorders (AUDs), now that the American Psychiatric Association (APA) and the World Health Organization (WHO) have launched initiatives for the construction of the fifth revision of the APA Diagnostic and Statistical Manual (DSM-V) and the l1th edition of the WHO International Classification of Diseases (ICD-11). Our position is that quantifying drinking is very relevant to the diagnosis, treatment, and prevention of AUDs. Good examples are the diagnostic criteria developed over time for other complex diseases (e.g. hypertension and diabetes), in which diagnoses are a combination of quantifiable measures (e.g. blood pressure and blood glucose level) and risk factors for disease (e.g. age, weight, lifestyle, and co-morbid conditions). For each of these disorders, diagnostic criteria have developed from simple cutpoints (e.g. diastolic and systolic blood pressure cutpoints for diagnosing hypertension in relation to heart attack and stroke), but have been continually refined as data on other dimensions of risk became available. The data to develop multidimensional, scalable diagnostic criteria for AUDs similar to those for hypertension (National Heart, Lung, and Blood Institute, 2001a), diabetes (American Diabetes Association, 2006), and high blood cholesterol (National Heart, Lung, and Blood Institute, 2001b) are not yet sufficiently refined owing to the absence of quantifiable biomarkers. However, as described below, we do have enough data to begin developing diagnostic criteria for AUDs based on symptom severity and the quantification of …

Alcoholic Neurobiology: Changes In Dependence and Recovery

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October, 2004. Chronic alcoholism follows a fluctuating course, which provides a naturalistic experiment in vulnerability, resilience, and recovery of human neural systems in response to presence, absence, and history of the neurotoxic effects of alcoholism. Alcohol dependence is a progressive chronic disease that is associated with changes in neuroanatomy, neurophysiology, neural gene expression, psychology, and behavior. Specifically, alcohol dependence is characterized by a neuropsychological profile of mild to moderate impairment in executive functions, visuospatial abilities, and postural stability, together with relative sparing of declarative memory, language skills, and primary motor and perceptual abilities. Recovery from alcoholism is associated with a partial reversal of CNS deficits that occur in alcoholism. The reversal of deficits during recovery from alcoholism indicates that brain structure is capable of repair and restructuring in response to insult in adulthood. Indirect support of this repair model derives from studies of selective neuropsychological processes, structural and functional neuroimaging studies, and preclinical studies on degeneration and regeneration during the development of alcohol dependence and recovery form dependence. Genetics and brain regional specificity contribute to unique changes in neuropsychology and neuroanatomy in alcoholism and recovery. This symposium includes state-of-the-art presentations on changes that occur during active alcoholism as well as those that may occur during recovery-abstinence from alcohol dependence. Included are human neuroimaging and neuropsychological assessments, changes in human brain gene expression, allelic combinations of genes associated with alcohol dependence and preclinical studies investigating mechanisms of alcohol induced neurotoxicity, and neuroprogenetor cell expansion during recovery from alcohol dependence.

Health Risks of Chronic Moderate and Heavy Alcohol Consumption: How Much Is Too Much?

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October 2004. Most of what we know about the deleterious effects of alcohol in vivo has been gleaned from studies in sober alcoholics recruited from substance abuse treatment programs. Little is known about effects of chronic drinking in the moderate or heavy range encountered in a much larger fraction of modern society. Extrapolation of information on the adverse effects of chronic drinking on organ function from clinical samples to social drinkers in the general population has to be met with great skepticism, as it may lead to wrong conclusions about the chronic effects of alcohol in social drinkers. Several recent studies suggest that moderate alcohol consumption has certain beneficial health effects, whereas heavy social alcohol consumption has recently been associated with organ abnormalities and cognitive deficits. These social drinking effects have attracted great public interest; reports of benefits of moderate drinking have also inspired inappropriate publications by the media, including misleading advertisements by the alcohol producing and distributing industry. Although adverse effects of moderate to heavy drinking on heart, liver, and cancer development have attracted attention by clinicians and researchers for some time, its compromising effects on brain and cognition have only recently been studied. This symposium brought together researchers from different disciplines, who reviewed and presented new data on consequences of social drinking in the areas of clinical neuropsychology and behavior (Drs. Nixon and Meyerhoff), neurophysiology (Dr. Nixon, Ms. De Bruin), neuroimaging (Ms. de Bruin, Dr. Meyerhoff), hepatic disease (Dr. Bode), and cancer (Dr. Seitz). The symposium aimed to clarify both the potential health benefits of moderate alcohol consumption and risks of moderate and heavy drinking on proper organ function and to provide insights and new data to practicing physicians and public health authorities for education on problem drinking.

Suppression of the HPA axis stress-response: implications for relapse.

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October 2004. This symposium explored the potential role of hypothalamic-pituitary-adrenal (HPA) axis dysregulation upon relapse. HPA axis stimulation induces the release of the glucocorticoid cortisol, a compound with profound effects upon behavior and emotion. Altered stress-responses of the HPA axis in abstinent alcohol-dependent subjects, therefore, may influence their affective and behavioral regulation, thus impacting their potential for relapse. Bryon Adinoff began the symposium with a review of HPA axis dysfunction in alcohol-dependent subjects, including recent studies from his lab demonstrating an attenuated glucocorticoid response to both endogenous and exogenous stimulation in one-month abstinent men. Klaus Junghanns presented his work demonstrating that a blunted ACTH or cortisol response to subjective stressors (social stressor or alcohol exposure) is predictive of a return to early drinking. The final two presenters examined the interaction between naltrexone and HPA responsiveness in alcohol-dependent or at-risk subjects, as naltrexone induces an increase in ACTH and cortisol. Falk Kiefer discussed the relationship between basal HPA axis responsivity and clinical outcome following treatment with naltrexone or acamprosate. Plasma ACTH significantly decreased over the course of the study in the placebo group, but not the medication groups [corrected] Lower basal concentrations of ACTH and cortisol were associated with quicker relapse in the placebo group only. Suchitra Krishnan-Sarin described her preliminary work, in which family-history positive (FH+) and family history negative (FH-) subjects were administered naltrexone, followed by an assessment of alcohol-induced craving. The cortisol response to alcohol was significantly and inversely related to craving in the FH+, but not the FH-, subjects. Alterations in HPA axis responsivity may therefore have a negative impact upon clinical outcome in alcohol-dependent subjects, and disinhibition of the axis with medication may have therapeutic potential.

Health Economics of Addiction

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October 2004. The symposium covered some crucial of the manifold aspects in the field of health economic research of alcoholism, for example, results of cost of treatment studies, evolution of health economic research in past years, methodological problems of cost‐effectiveness studies, and the effects of tax or price policies for alcohol consumption and the increase of alcohol‐related problems. Studies from the United States, the United Kingdom, Switzerland, and Germany were presented, underlining that even in these highly industrialized countries, health economic research is far from providing the essential evidence needed for adequate service planning or effective cost containment strategies in the field of alcoholism or addiction in general.

New Developments in Alcoholism Treatment Research in Europe

This article presents the proceedings of a symposium held at the meeting of the International Society for Biomedical Research on Alcoholism (ISBRA) in Mannheim, Germany, in October 2004. The organizers and chairs were Karl F. Mann, Fred Rist and Carrie L. Randall. The presentations were (1) Searching for the acamprosate and naltrexone responders, by Karl Mann on behalf of the Project Predict Research team (K. Mann, R. Bruck, H. Gann, U. Zimmermann, A. Heinz, M. Smolka et al.), (2) Treatment outcomes from the United Kingdom Alcohol Treatment Trial (UKATT), by Nick Heather on behalf of the UKATT research team (N. Heather, A. Copello, Ch. Godfrey, R. Hodgson, J. Orford, D. Raistrick, I. Russell, G. Tober), and (3) Conjoint screening and Brief intervention for Alcohol and Nicotine misuse in primary health care (BrIAN), by Fred Rist on behalf of the BrIAN research team (Ralf Demmel, Ines Aulhorn, Jutta Hagen, Barbara Scheuren, Fred Rist).

ESBRA: passport for the development of biological research on alcoholism in Europe.

When founded in 1980, the International Society for Biomedical Research on Alcoholism (ISBRA) co-existed with the American Research Society on Alcoholism (RSA) and the Japanese Medical Society of Alcohol Studies (JMSAS). To strengthen European alcohol research and cooperation between European scientists involved in alcohol research, it appeared desirable to build up a counterpart to the North American and Japanese societies which would cover all of Europe. On the initiative of J.-P. von Wartburg, at that time President of ISBRA, a Steering Committee for the foundation of a European Alcohol Research Society was set up during the 1982 ISBRA Congress in Munich, Germany. R. Nordmann was asked to, and accepted the chair of this Committee, which, among other activities, sent all European ISBRA members as well as other European scientists involved in alcohol research a questionnaire, Organizational Survey for the Foundation of a European Alcohol Research Society. A large majority of those to whom this questionnaire was addressed expressed their strong interest in the foundation of such a society. The Steering Committee therefore established tentative by-laws, which were sent to their European colleagues and approved by a vote which took place during the ISBRA Congress in Helsinki in 1986. The name chosen for the new Society was the European Society for Biomedical Research on Alcoholism (ESBRA) and its by-laws were deposited in Brussels and the Society was registered on 12 March 1987 as a scientific non-profit-making association by the Belgian Ministry of Justice under the authority of King Baudouin. ### General assembly The Annual General Assembly, during which the activities and budget of ESBRA are discussed and submitted to the membership for approval, meets alternately during the ESBRA Congresses (organized during uneven years) and the ISBRA Congresses (organized during even years). ### Officers of ESBRA The Society is managed by a Board of Directors elected by the membership …

Introduction to personality-biological interactions in alcoholism: 'The Markku Linnoila Memorial Symposium'.

Although a number of specific personality disorders, including anti-social personality, passive-dependent personality, and explosive personality, have been associated with the diagnosis of alcoholism, studies of the relationship of underlying personality and/or temperament to the nature, phenomenology, psychobiology, prognosis, and treatment of alcoholism have occurred much less frequently. However, there is a growing body of evidence that core or underlying personality and temperament are important determinants of vulnerability to becoming an alcoholic and of the nature of alcoholic subtypes. Furthermore, these personality and temperament variables appear linked to biological and/or genetic mechanisms. In parallel to human studies, experiments using rodents and primates have demonstrated animal behavioural characteristics, such as impulsivity, excessive or deficient behavioural inhibition, and a tendency to explore, which appear to parallel human personality characteristics, and these characteristics may predict genetically determined excessive alcohol consumption in animals. This special section is devoted to the memory of our esteemed colleague, Dr Markku Linnoila, honouring his many contributions to the field of alcoholism research and specifically to the theme of this special section. It is derived from a symposium presented at the Ninth Congress of the International Society for Biomedical Research on Alcoholism (ISBRA), held during the period 27 June‐2 July 1998 in Copenhagen, Denmark. As a world renowned expert on serotonin, Dr Linnoila led a team that was widely recognized as the world’s leading research group investigating serotonin and behaviour. His work was particularly focused on the relationship between serotonin and personality and he published numerous papers showing a relationship between the two. His 1983 landmark research paper investigating serotonin, fire-setting, and violence, bridged three disparate research fields: suicide, alcoholism, and aggression, and showed that the common link between these serotonin-mediated psychopathologies was impulsivity. While pursuing cutting-edge research with scientists in his homeland of Finland, where he was able to investigate the biological correlates of personality in violent offenders and alcoholics, he forged a relationship with those who were investigating non-human primate personality, leading to the first comprehensive non-human primate model linking serotonin and psychopathology. This model has been instrumental in understanding the biological and psychosocial correlates of Type 2-like excessive alcohol consumption. In this special section, we explore the interface

International Society for Biomedical Research on Alcoholism: relationship of cell necrosis and proliferation, free radicals and other agents to alcohol-related cancers.

Alcohol, tobacco and diet are the three major human cancer risk factors. A community-based study carried out by the American Psychiatry Association showed that approximately 13% of the adult population in the United States has had alcohol abuse and dependence sometime in their life. The proportion of the population that is alcohol-dependent is even larger in some other countries. The problems associated with alcohol abuse are highlighted in presentations and discussions of the International Society for Biomedical Research on Alcoholism (ISBRA) and its regional affiliates including its European counterpart, ESBRA and the US Research Society on Alcoholism (RSA). Regional affiliates normally meet each year while ISBRA holds a conference in a different country every other year. This year the ISBRA conference was held at Bristol (England) with two satellite meetings at Bordeaux (France) and Lund (Sweden) from 18 June to 1 July 1992. This report deals with areas relating to alcohol and cancer that were discussed in the conferences at Bordeaux and Bristol. Since epidemiological studies have indicated a strong association between chronic alcohol consumption and cancer risk, animal models are developed to determine the mechanisms that underlie this risk. A mechanism proposed suggests that ethanol could modulate carcinogenesis by its ability to induce enzymes of the cytochrome P-450 system that convert pro-carcinogens to their reactive intermediates, which are DNA-reactive and mutagenic. Another mechanism involves the effect of ethanol on cell injury and cell proliferation. Ethanol is cytotoxic and its presence causes cell atrophy that is followed by a proliferative cell response. H.K. Seitz (Heidelberg, FRG) at the meeting in Bordeaux presented data indicating that chronic ethanol consumption led to an atrophy and lipomatic metamorphosis of the parenchyma of the salivary glands, a condition that is associated with a striking reduction in saliva secretion. He also found