Antabuse Disulfiram And Other Antialcoholism Drugs

Alcohol Free Forever

Ways To Quit Drinking

Get Instant Access

Antabuse (disulfiram), a drug used as a supplementary therapy for alcoholism, was originally used in the manufacture of rubber. When the chemical got into the air in one factory and settled on the workers' skin, many developed dermatitis (Schwartz & Tulipan, 1933). If they inhaled the disulfiram, they discovered that they could no longer tolerate alcohol. Beginning in the 1940s, therapists tried using the drug as a therapy for alcoholism, on the theory that alcoholics would learn to avoid alcohol because of its now unpleasant aftereffects.

Antabuse alters the metabolism of alcohol. Ethanol (ethyl alcohol) is metabolized in the liver by the enzyme alcohol dehydrogenase into acetaldehyde, a toxic chemical. Acetaldehyde is then metabolized by the enzyme aldehyde dehydrogenase (also known as aldehyde NAD-oxidoreductase) into acetate (acetic acid), which is a source of energy. Antabuse and a similar drug, Temposil (calcium carbimide), bind to the copper ion of acetaldehyde dehydrogenase and thereby inactivate it. Consequently, after someone drinks ethanol, it is converted as usual to aldehyde, but the aldehyde then accumulates instead of being converted to acetate. Symptoms of acetaldehyde accumulation include flushing of the face, increased heart rate, nausea and vomiting, headache, abdominal pain, and labored breathing. People using Antabuse are advised to take a 200 to 500 mg pill daily and warned that drinking alcohol within a day or two after taking a pill can cause severe illness. They need to avoid even using shampoos containing alcohol, because of the danger of skin rashes. Giving someone Antabuse without his or her knowledge would be unethical and hazardous because of the likelihood that the person would unknowingly drink enough alcohol to become severely ill.

For genetic reasons, some people produce lower than average amounts of the enzyme aldehyde dehydrogenase. Drinking alcohol produces for them symptoms similar to, although generally milder than, those associated with Antabuse. About half of Chinese and Japanese people have low amounts of this enzyme, and partly because of this lack alcohol abuse has historically been less common in China and Japan than in most other countries (Tu & Israel, 1995).

Many sources state that Antabuse is not significantly more effective than a placebo, citing a study by Fuller and Roth (1979). That criticism is misleading, however. The study included one group who were correctly told that they were taking a placebo and one who were given placebos but intentionally misinformed that they were taking Antabuse. The group taking Antabuse and the placebo group who believed they were taking Antabuse fared similarly: In both cases about one fourth of the individuals abstained completely throughout the year, whereas the others quit taking the drug and resumed drinking. Both of these groups did far better than the group who knew they were taking a placebo, who unsurprisingly continued drinking heavily. In other words, taking Antabuse, or believing one is taking Antabuse, is an effective deterrent to drinking and a useful adjunct to a decision not to drink. The pharmacological properties of Antabuse were irrelevant in this study, simply because those alcoholics who wished to resume drinking stopped taking the pill.

One review of 24 studies concluded that Antabuse on the average decreases the number of drinking days and the total consumption of alcohol but does not significantly increase the probability of remaining abstinent over the long term (Hughes & Cook, 1997). The problem in evaluating the effectiveness of Antabuse is the high frequency of non-compliance among participants in most of the research. Many alcoholics, even if they begin with good intentions, quit taking the pills or take them only sporadically. When therapists have taken measures to increase compliance, such as having someone's friend or relative supervise the daily pill-taking, the results have been more encouraging (Azrin, Sisson, Meyers, & Godley, 1982). A review of just those studies that maintained enough supervision to assure compliance concluded that supervised Antabuse is statistically and clinically effective in preventing relapse of al coholism (Brewer, Meyers, & Johnsen, 2000). One possible way to improve compliance is to develop an implant that would provide sustained release in controlled quantities. However, effective and reliable implants have not yet been developed (Hughes & Cook, 1997).

The other drug approved in the United States for use against alcoholism is naltrexone, which blocks opioid receptors in the brain. Naltrexone is an antidote for excessive heroin use and helps decrease heroin cravings. Alcohol indirectly activates opioid pathways, and naltrexone decreases cravings for alcohol (Swift, 1999). The drug acam-prosate (Campral) is sometimes used against alcohol in Europe, but as of 2002 it was not available in the United States. Acamprosate increases activity at glutamate type NMDA receptors in the nucleus accumbens, in contrast to alcohol, which decreases glutamate transmission (Berton, Francesconi, Madamba, Zieglgansberger, & Siggins, 1998). Acamprosate has shown promise in helping abstaining alcoholics to avoid relapse, with an effectiveness approximately equal to that of naltrexone (Kranzier & Van Kirk, 2001). Another drug used in Europe is tiapride, which blocks dopamine receptors (Swift, 1999). Dopamine activity is critical for nearly all types of reinforcement, so although blocking it may have potential for decreasing alcoholism, it runs the risk of decreasing other motivations as well.

For all of these drugs used against alcoholism, the problem is compliance. Many alcoholics have mixed feelings about quitting alcohol and decreasing their own cravings and at various times many of them quit taking the drugs. In short, any of these drugs can be a useful supplement to other forms of treatment, but only under conditions of adequate supervision to assure compliance.


Azrin, N. H., Sisson, R. W., Meyers, R., & Godley, M. (1982). Alcohol treatment by disulfiram and community reinforcement therapy. Journal of Behavior Therapy and Experimental Psychiatry, 13, 105-112. Berton, F., Francesconi, W. G., Madamba, S. G., Zieglgansberger, W., & Siggins, G. R. (1998). Acamprosate enhances N-methyl-D-aspartate receptor-mediated neurotransmission but inhibits presynaptic GABA(B) receptors in nucleus accumbens neurons. Alcoholism: Clinical and Experimental Research, 22, 183-191. Brewer, C., Meyers, R. J., & Johnsen, J. (2000). Does disulfiram help to prevent relapse in alcohol abuse? CNS Drugs, 14, 329341.

Fuller, R. K., & Roth, H. P. (1979). Disulfiram for the treatment of alcoholism: An evaluation in 128 men. Annals of Internal Medicine, 90, 901-904. Hughes, J. C., & Cook, C. C. H. (1997). The efficacy of disulfiram:

Areview of outcome studies. Addiction, 92, 381-395. Kranzier, H. R., & Van Kirk, J. (2001). Efficacy of naltrexone and acamprosate for alcoholism treatment: A meta-analysis. Alcoholism: Clinical and Experimental Research, 25, 1335-1341. Schwartz, L., & Tulipan, L. (1933). An outbreak of dermatitis among workers in a rubber manufacturing plant. Public Health Reports, 48, 808-814.

Swift, R. M. (1999). Medications and alcohol craving. Alcohol Research & Health, 23, 207-213.

Tu, G. C., & Israel, Y. (1995). Alcohol consumption by Orientals in North America is predicted largely by a single gene. Behavior Genetics, 25, 59-65.

James W. Kalat

North Carolina State University

Was this article helpful?

0 0
Beat The Battle With The Bottle

Beat The Battle With The Bottle

Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.

Get My Free Ebook

Post a comment