ONE HUNDRED YEARS OF ALCOHOLISM: THE TWENTIETH CENTURY (2022)

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Volume 35 Issue 1

January 2000

Article Contents

  • Abstract

  • INTRODUCTION

  • THE HERITAGE OF THE 19TH CENTURY — A CONCEPT OF ADDICTION, TEMPERANCE AND DEGENERATION

  • TRYING TO ERADICATE ALCOHOLISM — DIFFERENT APPROACHES

  • AFTER PROHIBITION — THE CREATION OF A MODERN DISEASE CONCEPT

  • ONE OR MANY TYPES OF ALCOHOLISM — GENETIC FINDINGS AND POTENTIAL SUBTYPES

  • THE CORE OF ALCOHOL DEPENDENCE — TOLERANCE AND WITHDRAWAL OR SENSITIZATION AND REWARD CRAVING?

  • THE DISEASE CONCEPT REVISITED

  • NEW TREATMENT OPTIONS AND FUTURE DIRECTIONS

  • REFERENCES

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Journal Article

Karl Mann,

Karl Mann

Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, J 5, 68159 Mannheim, Germany

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Derik Hermann,

Derik Hermann

Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, J 5, 68159 Mannheim, Germany

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Andreas Heinz

Andreas Heinz

Department of Addictive Behaviour and Addiction Medicine, Central Institute of Mental Health, University of Heidelberg, J 5, 68159 Mannheim, Germany

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Alcohol and Alcoholism, Volume 35, Issue 1, January 2000, Pages 10–15, https://doi.org/10.1093/alcalc/35.1.10

Published:

01 January 2000

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Received:

02 October 1999

Published:

01 January 2000

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    Karl Mann, Derik Hermann, Andreas Heinz, ONE HUNDRED YEARS OF ALCOHOLISM: THE TWENTIETH CENTURY, Alcohol and Alcoholism, Volume 35, Issue 1, January 2000, Pages 10–15, https://doi.org/10.1093/alcalc/35.1.10

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Abstract

The past 100 years witnessed the formation of a disease concept of alcoholism and a rapid increase in the knowledge of its aetiopathology and treatment options. In the first half of the century, public sanctions aimed at the abolition of alcoholism. In the United States, alcohol prohibition was revoked in the economic turmoil of the Great Depression. In Germany, proposed medical procedures to reduce the fertility of alcoholics had catastrophic consequences during the fascist dictatorship. A revived focus on alcoholics as patients with a right to medical treatment came out of self-organized groups, such as Alcoholics Anonymous. The current disease concept includes the psychosocial and neurobiological foundations and consequences of alcoholism. Neurobiological research points to the dispositional factor of monoaminergic dysfunction and indicates that neuroadaptation and sensitization may play a role in the maintenance of addictive behaviour. New treatment options include pharmacological approaches and indicate that behaviour and motivational therapy and the attendance of patient groups may equally reduce the relapse risk. The task of the future will be to apply scientific discoveries in the best interest of the patients and to support their efforts to be respected like subjects suffering from other diseases.

INTRODUCTION

Alcoholism research and treatment underwent significant changes in the 20th century. Within the last 100 years, a disease concept was formed, which is now widely accepted, the psychosocial and neurobiological consequences of alcoholism have been characterized and treatment programmes have been established and continuously refined. First attempts were made to formulate models of the disposition and development of alcohol dependence that integrate both neurobiological and psychosocial findings. In this essay, we will highlight some of the cornerstones of our present understanding of alcoholism and reflect on some of the organizations and research traditions whose activities were crucial in the development of current concepts. Given the scope of the subject, this review will be both incomplete and subjective, and we will be unable to mention many subjects and institutions whose contributions to current alcoholism concepts were as important and fundamental as the ones we are able to discuss.

THE HERITAGE OF THE 19TH CENTURY — A CONCEPT OF ADDICTION, TEMPERANCE AND DEGENERATION

An uncontrollable, overwhelming and irresistible desire to consume alcohol was described by Benjamin Rush in 1784, and delirium tremens was independently described by both Pearson and Sutton in 1813 (Kielhorn, 1988). Alcohol craving and withdrawal symptoms were integral parts of the concept of addiction and of the destructive effects of alcohol consumption promoted by the temperance movement in the 19th century (Levine, 1984). In several European countries and in the United States, temperance movements were stimulated by the excessive consumption of liquor and other highly distilled alcoholic beverages, which was uninhibited by cultural traditions and appeared especially problematic among poor working class families during industrialization (Levine, 1984; Henkel, 1998). There was, however, a fundamental difference to current concepts of alcoholism: the temperance movement suggested that anyone who consumed excessive amounts of alcohol would suffer from alcohol-related problems and did not suggest that alcoholism could affect certain specifically vulnerable individuals primarily (Levine, 1984; Heather, 1992).

A focus on the individual was promoted by degenerationism, the theory that biological factors, toxic environmental influences or moral vices may trigger a cascade of social, moral and medical problems, which increase in each generation and will finally lead to the extinction of that family (Bynum, 1984). The theory of degeneration was based on the pre-Darwinian concept that acquired character traits were passed on to the offspring and assumed that an array of different symptoms and diseases, such as impulsivity, alcoholism, strokes, dementia, microcephaly and epilepsy, were all expressions of one underlying pathology — degeneration (Hermle, 1986).

Degenerationism thus offered a medical explanation for the social problems which were so visible at the end of the 19th century, and excessive alcohol consumption played a crucial role in the concept, as it was seen as a vice which also affects the next generation. In the early 20th century, the degeneration theory suffered from an increasing knowledge about modes of transmission of heritable traits, which pointed to the separate inheritance of different mental and physical diseases, and distinguished between heritable traits and toxic effects on the germ plasm or embryo, thus fundamentally questioning the postulate of the inheritance of acquired traits (Hermle, 1986). However, degenerationism substantially contributed to the concerns about the specific alcohol-related problems of certain individuals.

TRYING TO ERADICATE ALCOHOLISM — DIFFERENT APPROACHES

In the first 30 years of the 20th century, degenerationism and the successors of the temperance movement sparked widespread political activities in the field of alcohol addiction. In the United States, the Anti-Saloon League followed the approach of the temperance movement and focused on the general problems of alcohol consumption. It succeeded in the implementation of alcohol prohibition, which was legally enforced from 1919 to 1933. Prohibition was initially successful in reducing alcohol intake; however, illegal alcohol consumption slowly increased in the late 1920s (Tyrrell, 1997). Prohibition was finally abolished not so much because it failed to abolish alcohol intake, but because of shifting priorities in the Great Depression, when it was argued that liquor production would create jobs and that alcohol taxes might help to reduce income taxes (Levine, 1984).

In Germany, the focus on the individual and their heritable vulnerability to alcohol addiction was imbued with alarmist concerns about the proliferation of the mentally ill, which was supposed to threaten the survival of the nation or ‘race.' Consequently, compulsory sterilization of ‘severe alcoholics' was already advocated by some medical doctors before it was legalized during the Nazi dictatorship. The number of alcohol-dependent patients murdered during the Nazi regime is unknown (Henkel, 1998).

AFTER PROHIBITION — THE CREATION OF A MODERN DISEASE CONCEPT

It was in the wake of the failure of prohibition that the current concept of alcoholism was formed, and the worldwide shock about the cruelty and inhumanity of Nazi politics may have promoted the modern disease concept with its focus on individual therapy and its emphasis that alcohol addiction is a disease just like any other physical or mental malady (Levine, 1984; Henkel, 1998). A decisive point was the foundation of Alcoholics Anonymous (AA) in the late 1930s. Similar to previous temperance movements, Alcoholics Anonymous displayed a sympathetic and supporting attitude towards the addicted person, but unlike previous groups, AA was only for alcoholics and was not concerned with the general level of alcohol consumption in the population. In fact, the view that all it would take to create an alcohol addict would be his excessive alcohol consumption was no longer persuasive after the end of prohibition (Levine, 1984). Likewise, the existence of alcohol tolerance and withdrawal was widely neglected in the 1930s and early 1940s, although delirium tremens due to alcohol withdrawal had clearly been described by Hare 1910 in the British Journal of Inebriety (Edwards, 1990). Jellinek (1942) and the Yale Summer School on Alcohol Studies agreed with AA that alcoholism would be a disease with a progressive character and not a moral failing. The 1954 report of the World Health Organization (WHO) reflected this new focus on the individual and stated that ‘the personal make-up is the determining factor, but the pharmacological action (of alcohol) plays a significant role’ (Edwards, 1990). However, it was not until the mid-1950s that convulsions and delirium tremens regained public attention as symptoms of alcohol withdrawal, largely due to the detailed reports of Victor and Adams (1953) and Isbell et al. (1955). In 1955, the WHO acknowledged that ‘very serious withdrawal symptoms’, such as convulsions or delirium, may follow the discontinuation of a prolonged period of very heavy alcohol intake (Edwards, 1990). In his famous book on the disease concept of alcoholism, Jellinek (1960) referred repeatedly to the WHO reports and placed the adaptation of cell metabolism, tolerance and the withdrawal symptoms at the heart of his alcoholism concept, because they would ‘bring about ‘craving’ and a loss of control or inability to abstain.’; In his review of the perception of alcohol withdrawal symptoms in the scientific literature, Edwards (1990) noted that Jellinek's new focus on withdrawal symptoms was ‘in very sharp contrast to the earlier stance of the Yale school.’ It is possible that it was easier to rediscover the physical complications of alcohol withdrawal, because the new disease concept allowed attribution of these complications to an individual disposition rather than to some general effect that prolonged alcohol intake would have on every consumer.

In Germany, the modern disease concept of alcoholism was promoted by Feuerlein (1967, 1996) and others who emphasized that alcohol-dependent patients should have the same entitlement to medical treatment as other patients. It was not until 1968 that a German federal court formally confirmed full insurance coverage of alcoholism-related medical treatment costs, although alcoholism had already been considered a disease since 1915 (Jellinek, 1960).

ONE OR MANY TYPES OF ALCOHOLISM — GENETIC FINDINGS AND POTENTIAL SUBTYPES

While it had long been observed that the familial risk for alcoholism is increased, it was only because of twin and adoption studies that a genetic contribution to alcoholism was confirmed (Kaji, 1960; Cadoret and Gath, 1978). The observation that family members who share half of their genes are not more likely to develop alcoholism compared with family members who share only a quarter of their genes was incompatible with the simple genetic mechanism of inheritance (Bleuler, 1955; Schuckit et al., 1972).

Based on adoption studies, Cloninger et al. (1981) suggested the existence of two types of alcoholism, a mostly environmentally triggered, late-onset type 1 and a male-limited type 2 with a high genetic loading, legal problems and moderate alcohol consumption. The attempt to distinguish between two subtypes of alcoholism stimulated considerable research efforts. Many authors, however, questioned the dichotomy and argued that once patients suffering from comorbid antisocial personality disorder were excluded, the distinction between type 1 and type 2 alcoholics no longer offered clinical subtypes with distinct severity (Irwin et al., 1990). Instead, subgrouping was suggested to be based on age of onset, the presence of childhood risk factors such as hyperactivity, and severity of alcoholism (Schuckit et al., 1995; Johnson et al., 1996). Alcoholism types may thus vary on a continuum of severity, rather than represent distinctly different disease entities (Bucholz et al., 1996). The genetic disposition to alcoholism may manifest in such unsuspicious forms as a low level of response to alcohol intake in subjects not yet accustomed to chronic alcohol intoxication (Schuckit and Smith, 1996). A low level of alcohol response has recently been associated with an increased availability of raphe serotonin transporters and a low central serotonin turnover rate (Heinz et al., 1998; Schuckit et al., 1999). A low serotonin turnover rate is a potential marker of early-onset alcoholism (Fils-Aime et al., 1996) and may be caused or aggravated by early social stress experiences (Higley et al., 1996a,b). These findings may help to link the clinical disposition to alcoholism with the growing literature on neurobiological alterations that precede and follow the manifestation of alcohol dependence.

THE CORE OF ALCOHOL DEPENDENCE — TOLERANCE AND WITHDRAWAL OR SENSITIZATION AND REWARD CRAVING?

The last three decades of the twentieth century witnessed a rapidly increasing knowledge of the neurobiological correlates of alcohol dependence. Edwards focused on the development of alcohol tolerance and the manifestation of withdrawal when chronic alcohol intake is terminated (Edwards et al., 1977). His groundbreaking work was used by the WHO in the International Classification of Diseases (ICD-9) and operationalized in the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R) as criteria of dependence (Jurd, 1992).

Neurobiological research pointed to alcohol-induced stimulation of inhibitory GABAergic, and the inhibition of excitatory glutamatergic, neurotransmission (Koob, 1992; Tsai et al., 1995). To ensure homeostatic regulation, GABAA receptors may be down-regulated and, indeed, brain imaging studies observed reduced cortical GABAA receptors among alcoholics (Abi-Dargham et al., 1998). When the sedative effects of alcohol are suddenly withdrawn during early abstinence, reduced GABAergic inhibition and increased glutamatergic excitatory neurotransmission may manifest as anxiety, seizures and autonomic dysregulation (Tsai et al., 1995). Alcohol consumption may then be reinstated to reduce withdrawal, thus acting as a negative reinforcer (Edwards, 1990). Associative learning may transform neutral emotional or environmental stimuli into alcohol-associated cues that induce a conditioned compensatory response to alcohol, ‘conditioned withdrawal’, and craving (Ludwig et al., 1974; McCusker and Brown, 1990). Acamprosate, a drug used to reduce craving in abstinent alcoholics, blocks glutamatergic N-methyl-d-aspartate receptors and may exert its therapeutic effects by decreasing conditioned withdrawal (Verheul et al., 1999).

However, cue-induced craving is only moderately associated with the severity of physical reactions such as changes in heart rate and skin conductance to cue presentation (Niaura et al., 1988). A secondary, potentially independent pathway has been suggested that may induce alcohol craving due to the mood-enhancing, positive-reinforcing effects of alcohol consumption (Wise, 1988; Koob and Le Moal, 1997). This pathway seems to involve the so-called dopaminergic reward system and its opioidergic stimulation via μ-opiate receptors (Spanagel et al., 1992; Di Chiara, 1995). The role of the dopaminergic system may lie in the direction of attention towards reward-indicating stimuli, rather than in the induction of euphoria or positive mood states (Schultz et al., 1995; Berridge and Robinson, 1998), which are associated with alcohol consumption and may be mediated by opioidergic neurotransmission (Volpicelli et al., 1995). Stimulus-dependent dopamine release may be specifically vulnerable to sensitization, thus mediating a stronger behavioural response upon re-exposure to the drug-associated cue (Robinson and Berridge, 1993). These observations may have important implications for our understanding of the ‘addiction memory’ and for therapeutic strategies: systematic cue exposure and response prevention might help to extinguish conditioned craving, although therapeutic study results so far are ambiguous (O'Brien et al., 1998), and naltrexone medication may prevent cue-induced reinstatement of alcohol craving (Katner, 1999).

THE DISEASE CONCEPT REVISITED

The focus on cue-induced craving and the underlying learning mechanisms (Glautier et al., 1994; Carter and Tiffany, 1999) has revived the discussion on whether the disease concept of alcoholism should be replaced by a social learning perspective (Heather, 1992). What was not being denied are the organic consequences of chronic alcohol intake, such as brain atrophy (Mann et al., 1995) or neuroadaptive processes such as a reduction of central dopamine D2 receptors (Volkow et al., 1996). Rather, it is argued that cigarette smoking similarly causes physical dependence or neuroadaptation without therefore being considered a disease. The disease concept may label patients and promote apathy associated with the ‘sick role’ (Heather, 1992).

A response to these concerns rests on several arguments. Firstly, it is argued that the sick role per se does not stigmatize patients and that the stigma associated with specific diseases such as ‘consumption’ never promoted similar attempts to deny its disease status, and instead promoted relabelling as tuberculosis (Keller, 1976). Secondly, it is argued that a state may be called a disease even in the absence of abnormalities of anatomic structure. A case in point may be essential hypertension, which is commonly understood as a disease, although the aetiology and pathogenesis are currently unknown. Keller (1976) suggested calling alcoholism a disease, because its behavioural manifestations represent a disablement. This argument resembles the concept of a mental disorder given by the American Psychiatric Association (1987), which argued that a mental disorder is characterized by present distress, disability, or a significantly increased risk of suffering death, pain, disability, or an important loss of freedom. Culver and Gert (1982) added that the state must exist ‘in the absence of a distinct (external) sustaining cause’, so that distress due to political oppression may be distinguished from a mental malady. Applying this definition to cigarette smoking indicates that smoking should be considered a mental disorder, as it is associated with the increased risk of suffering death, and it would thus be considered a malady or disease by Culver and Gert (1982). This brings up the question of whether fast driving then must be called a disease, as it increases the risk of dying in a traffic accident. It could be answered that the association between fast driving and traffic accidents is rather low and that the habit of driving fast might be terminated without experiencing the distress associated with drug withdrawal symptoms.

As aloof as these discussions sometimes appear, they have important implications for the treatment of alcoholism. In 1956, a Board of the American Medical Association (AMA) passed a resolution that urged hospitals to admit patients with alcoholism equally with patients treated for other diseases. This act is usually seen as the moment when alcoholism was formally recognized as a disease in the United States; however, alcoholism was already listed as a disease in 1933 in the Standard Classified Nomenclature of Diseases, which was approved by the AMA and the American Psychiatric Association (Keller, 1976). Yet the 1956 resolution highlights the important legal issues that are associated with the disease status of alcoholism, not least being the question of whether treatment costs should be covered by health insurances (Jurd, 1992). Research in the field of costs and benefits of alcoholism therapy supported the demand to treat alcoholism within the medical system (Holder, 1998).

NEW TREATMENT OPTIONS AND FUTURE DIRECTIONS

The last decade of the 20th century witnessed substantial progress in treatment options and strategies. Of special importance is the general practitioner, who sees the vast majority of patients with alcohol problems, while fewer than 10% actually enter specialized treatment programmes (Wienberg, 1992). Brief interventions in primary health care institutions are very often effective in reducing alcohol consumption (Bien et al., 1993). For those patients who need more extensive treatment, primary health care services have a gatekeeper function. Motivational enhancement in primary health care (Miller and Rollnick, 1991) can effectively increase the participation in treatment programmes and was associated with reduced subsequent relapse rates (Bien et al., 1993). Specialized treatment programmes were evaluated in project MATCH. Project MATCH examined three treatment options, cognitive behaviour therapy, twelve-step facilitation according to the AA programme and motivational enhancement therapy, and found them similarly effective (Project Match Research Group, 1998). As disappointing as this result may be for the discovery of prospective indicators of treatment response, it shows that the major treatment options available to alcoholics worldwide work successfully and that the eclectic combination of behaviour therapy and the attendance of self-help groups may indeed combine two powerful treatment strategies. With naltrexone and acamprosate, two pharmaceuticals are available that successfully reduce the relapse risk during early abstinence (O'Malley et al., 1996; Sass et al., 1996). However, even with an accompanying medical treatment, most alcoholics relapse. The goal of the future will therefore be to describe subgroups of patients that may respond positively to specific medications. As acamprosate and naltrexone affect different neurotransmitter systems, neurobiological screening of alcoholics may help to discover predictors of treatment response. Preliminary results indicate that sleep disorders, EEG activity and delayed recovery of dopamine receptor sensitivity during early abstinence are associated with the relapse risk and may help to identify patients who require specific treatment strategies (Bauer, 1994; Heinz et al., 1996; Brower et al., 1998; Winterer et al., 1998).

Basic research has profoundly helped to understand alcohol effects at the level of signal transduction. We now know that drugs affect neurotransmitter release, receptor sensitivity, post-synaptic second-messenger mechanisms and, perhaps most importantly, gene expression (Koob, 1992; Nestler, 1994). These observations indicate that human fate is not passively determined by the genetic constitution, but rather that biological and ultimately environmental stimuli regulate gene expression. Increasing knowledge of the molecular mechanisms of dependence may enable us to target these pathological conditions more specifically than we are able today.

Finally, the history of the last 100 years warns us that ‘ethics are not an option,’ as Edwards stated in a 1999 conference at the Central Institute of Mental Health, Mannheim. That alcoholism had been considered a disease in Germany since 1915 (Jellinek, 1960) did not prevent the dehumanizing treatment of patients with alcohol dependence during the Nazi era. It is an integral part of the professional mission to assist patients in their effort to be treated equally inside and outside of medical therapy. Our increasing knowledge about the disposition towards alcohol dependence and a high relapse risk can help to identify patients with demands for special therapeutic efforts, it should never be used to stigmatize these subjects. To monitor the consequences of our research is part of the professional duty.

REFERENCES

Abi-Dargham, A., Krystal, J. H., Anjivel, S., Scanley, B. E., Zoghbi, S., Baldwin, R. M., Rajeevan, N., Ellis, S., Petrakis, I. L., Seibyl, J. P., Charney, D. S., Laruelle, M. and Innis, R. B. (

1998

) Alterations of benzodiazepine receptors in type II alcoholic subjects measured with SPECT and [123]Iomezanil.

American Journal of Psychiatry

155

,

1550

–1555.

American Psychiatric Association (1987) Diagnostic and Statistical Manual of Mental Disorders, 3rd edn, revised. American Psychiatric Association, Washington, DC.

Bauer, L. O. (

1994

) Electroencephalographic and autonomic predictors of relapse in alcohol-dependent patients.

Alcoholism: Clinical and Experimental Research

18

,

755

–760.

Berridge, K. C. and Robinson, T. E. (

1988

) What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience?

Brain Research Reviews

28

(Video) Learn American English★Learn to Listen to English★ Advanced English Listening Lessons 11✔

,

309

–369.

Bien, T. H., Miller, W. R. and Tonigan, S. J. (

1993

) Brief interventions for alcohol problems: a review.

Addiction

88

,

315

–336.

Bleuler, M. (1955) Familial and personal background of chronic alcoholics. In Etiology of Chronic Alcoholism, Dietholm, O. ed., pp. 110–166. Charles C. Thomas, Springfield, IL.

Brower, K. J., Aldrich, M. S. and Hall, J. M. (

1998

) Polysomnographic and subjective sleep predictors of alcoholic relapse.

Alcoholism: Clinical and Experimental Research

22

,

1864

–1871.

Bucholz, K. K., Heath, A. C., Reich, T., Hesselbrock, V. M., Kramer, J. R., Nurnberger, J. I., Jr. and Schuckit, M. A. (

1996

) Can we subtype alcoholism? A latent class analysis of data from relatives of alcoholics in a multicenter family study of alcoholism.

Alcoholism: Clinical and Experimental Research

20

,

1462

–1471.

Bynum, W. F. (

1984

) Alcoholism and degeneration in 19th century European medicine and psychiatry.

British Journal of Addiction

79

,

59

–70.

Cadoret, R. J. and Gath, A. (

1978

) Inheritance of alcoholism in adoptees.

British Journal of Psychiatry

132

,

252

–258.

Carter, B. L. and Tiffany, S. T. (

1999

) Meta-analysis of cue-reactivity in addiction research.

Addiction

94

,

327

–340.

Cloninger, C. R., Bohman, M. and Sigvardsson, S. (

1981

) Inheritance of alcohol abuse. Cross-fostering analysis of adopted men.

Archives of General Psychiatry

38

,

861

–868.

Culver, C. and Gert, B. (1982) Philosophy in Medicine. Oxford University Press, Oxford.

Di Chiara, G. (

1995

) The role of dopamine in drug abuse viewed from the perspective of its role in motivation.

Drug and Alcohol Dependence

38

,

95

–137.

Edwards, G. (

1990

) Withdrawal symptoms and alcohol dependence: fruitful mysteries.

British Journal of Addiction

85

,

447

–461.

Edwards, G., Gross, M. M., Keller, M. et al. (1977) Alcohol-related Disabilities. WHO Offset Publication No. 32. World Health Organization, Geneva.

Feuerlein, W. (

1967

) Der Alkoholismus in sozialpsychiatrischer Sicht.

Medizinische Klinik

62

,

922

–926.

Feuerlein, W. (

1996

) Alkoholismus als Krankheit.

Herz

21

,

213

–216.

Fils-Aime, M. L., Eckhardt, M. J., George, D. T., Brown, G. L., Mefford, I. and Linnoila, M. (

1996

) Early-onset alcoholics have lower cerebrospinal fluid 5-hydroxyindolacetic acid levels than late-onset alcoholics.

Archives of General Psychiatry

53

,

211

–216.

Glautier, S., Drummond, C. and Remington, B. (

1994

) Alcohol as an unconditioned stimulus in human classical conditioning.

Psychopharmacology (Berlin)

116

,

360

–368.

Heather, N. (

1992

) Why alcoholism is not a disease.

The Medical Journal of Australia

156

,

212

–215.

Heinz, A., Dufeu, P., Kuhn, S., Dettling, M., Gräf, K. J., Kürten, I., Rommelspacher, H. and Schmidt, L. G. (

1996

) Psychopathological and behavioral correlates of dopaminergic sensitivity in alcohol-dependent patients.

(Video) English Listening Practice Level 3

Archives of General Psychiatry

53

,

1123

–1128.

Heinz, A., Higley, J. D., Gorey, J. G., Saunders, R. C., Jones, D. W., Hommer, D., Zajicek, K., Suomi, S. J., Lesch, K. P., Weinberger, D. R. and Linnoila, M. (

1998

) In vivo association between alcohol intoxication, aggression and serotonin transporter availability in non-human primates.

American Journal of Psychiatry

155

,

1023

–1028.

Henkel, D. (1998) ‘Die Trunksucht ist die Mutter der Armut.’ In Sucht und Armut, Henkel, D. and Vogt, L. eds, pp. 13–79. Leske and Budrich, Opladen.

Hermle, L. (

1986

) Die Degenerationslehre in der Psychiatrie.

Fortschritte der Neurologie und Psychiatrie

54

,

69

–79.

Higley, J. D., Suomi, S. J. and Linnoila, M. (

1996

) A non-human primate model of type II excessive alcohol consumption? Part 1. Low cerebrospinal fluid 5-hydroxyindoleacetic acid concentrations and diminished social competence correlate with excessive alcohol consumption.

Alcoholism: Clinical and Experimental Research

20

,

629

–642.

Higley, J. D., Suomi, S. J. and Linnoila, M. (

1996

) A non-human primate model of type II alcoholism? Part 2. Diminished social competence and excessive aggression correlates with low cerebrospinal fluid 5-hydroxyindoleacetic acid concentrations.

Alcoholism: Clinical and Experimental Research

20

,

643

–650.

Holder, H. D. (

1998

) The cost offsets of alcoholism treatment.

Recent Developments in Alcoholism

14

,

361

–374.

Irwin, M., Schuckit, M. and Smith, T. L. (

1990

) Clinical importance of age of onset in type 1 and type 2 primary alcoholics.

Archives of General Psychiatry

47

,

320

–324.

Isbell, H., Fraser, H. F., Wikler, A., Belleville, R. E. and Eiserman, A. J. (

1955

) An experimental study of the etiology of ‘rum fits' and delirium tremens.

Quarterly Journal of Studies on Alcohol

16

,

1

–33.

Jellinek, E. M. (1942) Alcohol Addiction and Chronic Alcoholism. Yale University Press, New Haven.

Jellinek, E. M. (1960) The Disease Concept of Alcoholism. Hillhouse, New Brunswick.

Johnson, E. O., van den Bree, M. B. M. and Pickens, R. W. (

1996

) Subtypes of alcohol-dependent men: a typology based on relative genetic and environmental loading.

Alcoholism: Clinical and Experimental Research

20

,

1472

–1480.

Jurd, S. M. (

1992

) Why alcoholism is a disease.

The Medical Journal of Australia

156

,

215

–217.

Kaji, L. (1960) Alcoholism in Twins: Studies on the Etiology and Sequels of Abuse of Alcohol. Almqvist and Wiksell, Stockholm.

Katner, S. N., Magalong, J. G. and Weiss, F. (

1999

) Reinstatement of alcohol-seeking behavior by drug-associated discriminative stimuli after prolonged extinction in the rat.

Neuropsychopharmacology

20

,

471

–479.

Keller, M. (

1976

) The disease concept of alcoholism revisited.

Journal of Studies on Alcohol

37

,

1694

–1717.

Kielhorn, F. W. (

1988

) Zur Geschichte des Alkoholismus: Pearson, Sutton und das Delirium tremens.

Suchtgefahren

34

,

111

–114.

Koob, G. F. (

1992

) Drugs of abuse: anatomy, pharmacology and function of reward pathways.

Trends in Pharmacological Sciences

13

,

177

–184.

Koob, G. F. and Le Moal, M. (

1997

) Drug abuse: hedonic homeostatic dysregulation.

Science

278

,

52

–58.

Levine, H. G. (

1984

) The alcohol problem in America: from temperance to alcoholism.

British Journal of Addiction

79

,

109

–119.

(Video) From the Drunkard to the Alcoholic, via the Monomaniac, Inebriate and Degenerate

Ludwig, A. M., Wikler, A. and Stark, L. H. (

1974

) The first drink: psychobiological aspects of craving.

Archives of General Psychiatry

30

,

539

–547.

Mann, K., Mundle, G., Strayle, M. and Wakat, P. (

1995

) Neuroimaging in alcoholism: CT and MRI results and clinical correlates.

Journal of Neural Transmission

99

,

145

–155.

McCusker, C. G. and Brown, K. (

1990

) Alcohol-predictive cues enhance tolerance and precipitate ‘craving’ for alcohol in social drinkers.

Journal of Studies on Alcoholism

51

,

494

–499.

Miller, W. R. and Rollnick, S. (1991) Motivational Interviewing: Preparing People to Change Addictive Behavior. Guilford Press, New York.

Nestler, E. J. (

1994

) Molecular neurobiology of drug addiction.

Neuropsychopharmacology

11

,

77

–87.

Niaura, R. S., Rohsenow, D. J., Binkoff, J. A., Monti, P. M., Pedrazza, M. and Abrams, D. B. (

1988

) Relevance of cue reactivity to understanding alcohol and smoking relapse.

Journal of Abnormal Psychology

97

,

133

–152.

O'Brien, C., Childress, A. R., Ehrman, R. and Robbins, S. J. (

1998

) Conditioning factors in drug abuse: can they explain compulsion?

Journal of Psychopharmacology

12

,

15

–22.

O'Malley, S. S., Jaffe, A. J., Chang, G., Rode, S., Schottenfeld, R., Meyer, R. E. and Rounsaville, B. (

1996

) Six-month follow-up of naltrexone and psychotherapy for alcohol dependence.

Archives of General Psychiatry

53

,

217

–224.

Project MATCH Research Group (

1998

) Matching alcoholism treatment to client heterogeneity: project MATCH three-year drinking outcomes.

Alcoholism: Clinical and Experimental Research

22

,

1300

–1311.

Robinson, T. E. and Berridge, K. C. (

1993

) The neural basis of drug craving: an incentive-sensitization theory of addiction.

Brain Research Reviews

18

,

247

–291.

Sass, H., Soyka, M., Mann, K. and Zieglgänsberger, W. (

1996

) Relapse prevention by acamprosate: results from a placebo-controlled study on alcohol dependence.

Archives of General Psychiatry

53

,

673

–680.

Schuckit, M. A. and Smith, T. L. (

1996

) An 8-year follow-up of 450 sons of alcoholics and control subjects.

Archives of General Psychiatry

45

,

211

–216.

Schuckit, M. A., Goodwin, D. A. and Winokur, G. (

1972

) A study of alcoholism in half-siblings.

American Journal of Psychiatry

129

,

1132

–1136.

Schuckit, M. A., Tipp, J. E., Smith, T. L., Shapiro, E., Hesselbrock, V. M., Buchholz, K. K., Reich, T. and Nurnberger, J. I. (

1995

) An evaluation of type A and B alcoholics.

Addiction

90

,

1189

–1203.

Schuckit, M. A., Mazzanti, C., Smith, T. L., Ahmed, U., Radel, M., Iwata, N. and Goldman, D. (

1999

) Selective genotyping for the role of 5-HT2A, 5-HT2C, and GABAα6 receptors and the serotonin transporter in the level of response to alcohol: a pilot study.

Biological Psychiatry

45

,

647

–651.

Schultz, W., Dayan, P. and Montague, P. R. (

1995

) A neural substrate of prediction and reward.

(Video) Paul Laurence Dunbar: Traveling and Abroad

Science

275

,

1593

–1599.

Spanagel, R., Herz, A. and Shippenberg, T. S. (

1992

) Opposing tonically active endogeneous opioid systems modulate the mesolimbic dopaminergic pathway.

Proceedings of the National Academy of Sciences of the USA

89

,

2046

–2050.

Tsai, G., Gastfriend, D. R. and Coyle, J. T. (

1995

) The glutamatergic basis of human alcoholism.

American Journal of Psychiatry

152

,

332

–340.

Tyrrell, I. (

1997

) The US prohibition experiment: myths, history and implications.

Addiction

92

,

1405

–1409.

Verheul, R., Van den Brink, W. and Geerlings, P. (

1999

) A three-pathway psychobiological model of craving for alcohol.

Alcohol and Alcoholism

34

,

197

–222.

Victor, M. and Adams, R. E. (

1953

) The effect of alcohol on the nervous system.

Research Publications of the Association for Research on Nervous and Mental Disease

32

,

526

–573.

Volkow, N. D., Wang, G. J., Fowler, J. S., Logan, J., Hitzemann, R., Ding, Y. S., Pappas, N., Shea, C. and Piscani, K. (

1996

) Decreases in dopamine receptors but not in dopamine transporters in alcoholics.

Alcoholism: Clinical and Experimental Research

20

,

1594

–1598.

Volpicelli, J. R., Watson, N. T., King, A. C., Sherman, C. E. and O'Brien, C. P. (

1995

) Effect of naltrexone on alcohol ‘high’ in alcoholics.

American Journal of Psychiatry

152

,

613

–615.

Wienberg, G. (1992) Die vergessene Mehrheit. Zur Realität der Versorgung alkohol- und medikamentenabhängiger Patienten. Psychiatrie Verlag, Berlin.

Winterer, G., Klöppel, B., Heinz, A., Schmidt, L. G., Frick, K. and Herrmann, W. M. (

1998

) Quantitative EEG (QEEG) analysed with artificial neural networks predicts relapse in patients with chronic alcoholism and points to a frontally pronounced disturbance.

Psychiatry Research

78

,

101

–113.

Wise, R. A. (

1988

) The neurobiology of craving: implications for the understanding and treatment of addiction.

Journal of Abnormal Psychology

97

,

118

–132.

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© 2000 Medical Council on Alcoholism

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FAQs

What do alcoholics suffer from? ›

Long-term effects. Alcohol contributes to over 200 diseases and injury-related health conditions including dependence and addiction, liver cirrhosis, cancers, and unintentional injuries such as motor vehicle accidents, falls, burns, assaults, and drowning.

What percentage of the world is alcoholic? ›

It's estimated that globally around 1.4 percent of the population have an alcohol use disorder. At the country level, as shown in the chart, this ranges from around 0.5 to 5 percent of the population.

When was alcoholism invented? ›

The term alcoholism was first used in 1849 by the Swedish physician Magnus Huss to describe the systemic adverse effects of alcohol.

What is the main purpose of the book Alcoholics Anonymous? ›

Alcoholics Anonymous, also known as the “Big Book,” presents the A.A. program for recovery from alcoholism. First published in 1939, its purpose was to show other alcoholics how the first 100 people of A.A. got sober. Now translated into over 70 languages, it is still considered A.A.'s basic text.

Which person would be most likely to develop alcoholism? ›

Age Factors

Individuals in their early to mid-twenties are the most likely to abuse alcohol and suffer from alcohol use disorders. The younger that an individual starts consuming alcohol, the more likely they are to develop alcoholism later in life. This is especially true of individuals who start drinking before 15.

What happens daily when you stop drinking? ›

Symptoms/outcomes you may see

Onset of withdrawal symptoms which may include hand tremors, retching, excessive sweating, restlessness and anxiety. Withdrawal symptoms continue. Alcohol cravings, reduced energy and feeling low or depressed are common. Sleep is likely to be disturbed.

What is the drunkest country? ›

Australians have been named the heaviest drinkers in the world in a survey after spending more time drunk in 2020 than any other nation.

What is the average age of death for an alcoholic? ›

Conclusion. People hospitalized with alcohol use disorder have an average life expectancy of 47–53 years (men) and 50–58 years (women) and die 24–28 years earlier than people in the general population.

What country has the highest Alcoholism rates? ›

Belarus had the world's highest level of alcohol consumption, with 17.5 liters of alcohol consumed per capita. The country's high level of consumption has had serious health consequences on its residents.

What are the 3 types of alcoholic? ›

Alcohols bind with other atoms to create secondary alcohols. These secondary alcohols are the three types of alcohol that humans use every day: methanol, isopropanol, and ethanol.

What is the oldest alcoholic drink? ›

Chemical analyses recently confirmed that the earliest alcoholic beverage in the world was a mixed fermented drink of rice, honey, and hawthorn fruit and/or grape. The residues of the beverage, dated ca. 7000–6600 BCE, were recovered from early pottery from Jiahu, a Neolithic village in the Yellow River Valley.

Why do humans drink alcohol? ›

A number of different motives for drinking alcohol have been examined, including drinking to enhance sociability, to increase power, to escape problems, to get drunk, for enjoyment, or for ritualistic reasons. Despite this diversity, most research has focused on two broad categories of motivation.

What word is used the most in the Big Book of Alcoholics Anonymous? ›

While the program is considered a suggested method for dealing with the disease of Alcoholism, there are places within the Big Book where the authors used the word 'MUST.

What are the four horsemen in AA? ›

Some of us sought out sordid places, hoping to find understanding com- panionship and approval. Momentarily we did—then would come oblivion and the awful awakening to face the hideous Four Horsemen—Terror, Bewilderment, Frustration, Despair.

What does the Big Book say about recovery? ›

At the very beginning of the big book Alcoholics Anonymous it reads: “How many thousands of men and women have recovered from alcoholism.” Later it reads: “to show other alcoholics precisely how we have recovered is the main purpose of this book.” There are other mentions to the word recovered.

Does your memory improve if you stop drinking? ›

Over time, people with alcoholism commonly experience significant disruptions in their higher-level mental functions. One of the chief higher-level disruptions caused by chronic alcohol exposure is a reduction in the ability to make, store and organize memories.

Are you born an alcoholic? ›

Because of the interaction of genetics and environment, a person cannot be born with an alcohol use disorder. Although people can have genes that predispose them to developing an alcohol use disorder, genetics only accounts for approximately half of a person's overall risk.

Which organ breaks down alcohol in your bloodstream? ›

After alcohol is swallowed, it is absorbed primarily from the small intestine into the veins that collect blood from the stomach and bowels and from the portal vein, which leads to the liver. From there it is carried to the liver, where it is exposed to enzymes and metabolized.

What alcohol does to your face? ›

Alcohol causes your body and skin to lose fluid (dehydrate). Dry skin wrinkles more quickly and can look dull and grey. Alcohol's diuretic (water-loss) effect also causes you to lose vitamins and nutrients.

What are the first signs of liver damage from alcohol? ›

What are the early signs of liver damage from alcohol?
  • swelling of your liver, which may lead to discomfort in the upper right side of your abdomen.
  • fatigue.
  • unexplained weight loss.
  • loss of appetite.
  • nausea and vomiting.
Aug 28, 2020

What are the 4 types of drinker? ›

There are four types of drinker – which one are you?
  • Social drinking. To date, nearly all the research on drinking motives has been done on teens and young adults. ...
  • Drinking to conform. ...
  • Drinking for enhancement. ...
  • Drinking to cope.

What age do French children drink? ›

"The age of first drink is about 12 years old in France," he says. That first drink is usually at home with the family, which has made it difficult, says Nalpas, to get out the message that alcohol can be dangerous. If kids see their parents and grandparents drinking, he says, they think, "I can drink also."

Which nationality drinks the most? ›

Here's the top ten countries ranked by the number of times respondents from each country said they got drunk per year:
  • Finland: 23.8.
  • United States: 23.1.
  • United Kingdom: 22.5.
  • Canada: 22.
  • Ireland: 20.
  • France: 17.5.
  • Sweden: 16.
  • Netherlands: 15.7.
Dec 3, 2021

Why do some heavy drinkers live so long? ›

Even though heavy drinking is associated with higher risk for cirrhosis and several types of cancer (particularly cancers in the mouth and esophagus), heavy drinkers are less likely to die than people who don't drink, even if they never had a problem with alcohol.

How long will you live if you drink alcohol everyday? ›

The study of 600,000 drinkers estimated that having 10 to 15 alcoholic drinks every week could shorten a person's life by between one and two years. And they warned that people who drink more than 18 drinks a week could lose four to five years of their lives.

Do teetotalers live longer? ›

Previous studies have consistently found that light to moderate drinkers live longer than lifetime teetotallers. The evidence from cancer research gives a different impression: even light to moderate alcohol consumption is linked with an increased risk of cancer.

What country drinks the least alcohol? ›

Top 10 Countries with the Lowest Alcohol Consumption in 2019 (in liters of pure alcohol per capita):
  • Somalia, Bangladesh, Kuwait, Mauritania, Saudi Arabia (5-way tie) - 0.00.
  • Afghanistan - 0.013.
  • Libya - 0.027.
  • Yemen - 0.034.
  • Egypt - 0.14.
  • Syrian Arab Republic - 0.19.
  • Bhutan - 0.21.
  • Indonesia - 0.22.

Who drinks the most alcohol in the US? ›

Per capita alcohol consumption of all beverages in the U.S. by state 2020. New Hampshire is currently the state with the highest per capita alcohol consumption in the United States. Per capita alcohol consumption has increased since the mid-1990s with beer as the most commonly consumed alcoholic beverage.

What is the drinking age in Russia? ›

Drinking age in Russia is. 18.

What is the strongest alcohol? ›

Spirytus Stawski (96% Alcohol) This is the world's most strongest and potent liquor, that has a gentle smell and a mild taste. It is made using premium ethyl alcohol with a grain base.

What is the least harmful alcohol to drink? ›

Take a look at this list of the least-damaging alcoholic drinks from Legends at White Oak to help you drink consciously.
  • Red Wine. ...
  • Light Beer. ...
  • Tequila. ...
  • Gin & Rum & Vodka & Whiskey.
Mar 7, 2021

What does alcoholism do to your heart? ›

Long-term alcohol abuse weakens and thins the heart muscle, affecting its ability to pump blood. When your heart can't pump blood efficiently, the lack of blood flow disrupts all your body's major functions. This can lead to heart failure and other life-threatening health problems.

What does alcohol do the brain? ›

Alcohol interferes with the brain's communication pathways and can affect the way the brain looks and works. Alcohol makes it harder for the brain areas controlling balance, memory, speech, and judgment to do their jobs, resulting in a higher likelihood of injuries and other negative outcomes.

Did cowboys drink alcohol? ›

Cowboys never had a reputation for being very sophisticated connoisseurs. The whiskey they drank was simply fuel for the saloons' many other pastimes, whatever those happened to be. Quality and flavor among whiskies in the late 1800s varied widely.

Which is older wine or beer? ›

Beer is believed to be older than wine, but the most expensive bottle of wine ever sold brought in much more than the priciest brew.

Do humans need alcohol? ›

The truth is that no one needs alcohol to live, so regardless of what you've heard or want to believe, alcohol is not essential in our diets. We consume alcohol to relax, socialize, and/or celebrate.

Why does being drunk feel so good? ›

When the concentration of alcohol begins to increase in your bloodstream, you'll start to feel good. You might feel happy, more social and confident, and less inhibited. This is because alcohol stimulates the release of dopamine and serotonin, which are rightfully referred to as your “feel good” hormones.

Why do I enjoy alcohol so much? ›

The key to this is that alcohol triggers the brain's endorphin system. Endorphins are opioid neurotransmitters that form part of the brain's pain management system. Indeed, weight for weight, endorphins are 30 times more effective as analgesics than morphine.

What is AA slang? ›

A slang term for the book Alcoholics Anonymous. It is a jokey reference that goes back to AA's humble beginnings.

What does the Big Book say about emotional sobriety? ›

By looking at yourself instead of others, you are well on your way to living the 3 words that they big book describes as the key to emotional sobriety – sober, considerate, and helpful, no matter what anyone else says or does.

What does the Big Book say about the first drink? ›

We are without defense against the first drink. Only to have that thought supplanted by "Well, I'll stop with the sixth drink."

What are the 4 types of drinker? ›

There are four types of drinker – which one are you?
  • Social drinking. To date, nearly all the research on drinking motives has been done on teens and young adults. ...
  • Drinking to conform. ...
  • Drinking for enhancement. ...
  • Drinking to cope.

What are the 3 types of drinkers? ›

There are three main categories that users of alcohol fall into; social drinker, alcohol abuser or alcoholic. Most people who drink alcohol will not have any problems with their consumption; however, for those who do have a problem handling it, oftentimes, their problem will gradually worsen.

What are the four stages of drinking? ›

If you or your loved ones need help to identify the signs of problem drinking, four stages of alcoholism have been identified: pre-alcoholic, early alcoholic, chronic alcoholic, and end-stage alcoholism.

What are the 3 types of alcoholic? ›

Alcohols bind with other atoms to create secondary alcohols. These secondary alcohols are the three types of alcohol that humans use every day: methanol, isopropanol, and ethanol.

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