Alcoholism is a condition in which a person’s intention to control their alcohol consumption cannot rely on an adequate ability to exercise that control. Once control has been lost, it tends not to be regained; rather, the situation worsens over time, in a succession of periods of abstinence and periods of uncontrolled drinking, with the associated consequences. The person’s will is continually, or recurrently and forcefully, “magnetized” toward the behavior of seeking and consuming alcohol, even without a specific connection to an effect desired from alcohol. An alcoholic does not drink for a purpose, but because of their alcoholism. An alcoholic does not choose how to drink; alcoholism imposes a pattern of drinking that goes beyond their own intentions and therefore interferes with mental functioning, produces various forms of collateral harm, and obstructs and destroys social relationships and productive abilities.
All treatments for alcoholism aim to restore control over drinking according to the person’s own intentions. The intention to control drinking (or not to drink at all) is present in the alcoholic and should not be confused with the ability to do so, which is precisely what is lacking. There are no “relapsed alcoholics,” because relapse is the rule: it is precisely what is expected when this diagnosis is made, regardless of whether the person happens to be in a period of sobriety.
One of the available treatments is disulfiram. The drug acts when alcohol enters the bloodstream and alters its metabolism in such a way as to produce a sort of “poisoning” reaction due to the accumulation of acetaldehyde. The most common symptoms of this reaction are flushing, generalized malaise, nausea and vomiting, palpitations, and headache. Depending on the amount of alcohol consumed and the dose of disulfiram taken, the reaction may range from mild to severe and may potentially be dangerous from a cardiovascular standpoint.
An alcoholic who takes disulfiram therefore learns that drinking makes them feel ill. Consistent with their alcoholism, the person seeks a way out that would allow them to drink without becoming ill; but if it is not possible to stop taking the medication, they are eventually forced to avoid drinking.
The more severe the alcoholism, the more episodes of intoxication may occur before the person stops drinking while taking disulfiram. In the most severe cases, the person may be unable to abstain, resulting in severe acetaldehyde intoxication. In such cases, the balance between risks and potential benefits should be carefully evaluated because, as already mentioned, the effects of acetaldehyde can be severe and potentially fatal.
Disulfiram therapy should be administered by another person, or at least under the supervision of another person who verifies that the medication has actually been swallowed and that the person does not immediately vomit it. Disulfiram prescribed to be taken “on one’s own” is ineffective, simply because in that case it merely mirrors the situation: if the person takes it, this means that the desire to drink is low or absent. But if the person is alcoholic, there will eventually be a day when the desire increases; at that point, they will simply stop taking the disulfiram, wait a day or more, and begin drinking.
Disulfiram has no “deterrent” effect if the person has never experienced the “poisoning” reaction. And if they have experienced it, it is obvious that continued administration must be supervised by another person. No alcoholic is capable of putting their own “handcuffs” on to prevent themselves from drinking freely; if they were, they would not be alcoholic.
The package leaflet explicitly indicates that, after several days of treatment, the person should consume a modest amount of alcohol in order to provoke and experience the toxic reaction. Obviously, this should be done in a medical setting and under supervision. This also prevents the person from first experiencing the effect—whose severity they may not believe in—during a subsequent, potentially heavy relapse, without being able to predict the consequences of the intoxication.
Conditioning is therefore not a “negative” side effect or an incidental possibility; it is the central part of the mechanism by which this treatment works. If the person has never become ill after drinking while taking disulfiram, it is impossible to establish whether the treatment is actually effective.
Studies consistently indicate that when people are free to self-administer disulfiram, they probably do not take it, or take it only when they are not drinking.
For example, the results obtained by a group of people taking a standard dose (250 mg) are the same as those obtained by a group unknowingly taking a dose of 1 mg (which is ineffective). This probably indicates that the 250-mg group was not actually taking the medication, just as the 1-mg group was not. In a series of people who were known with certainty to have taken the medication, it was the “real” drug (250 mg) that was associated with positive outcomes.
When administration is supervised, people with alcoholism become able to follow rehabilitation or psychotherapy programs. By contrast, when they are required to demonstrate continued sobriety in exchange for financial or housing benefits, they are unable to do so when the medication is self-administered and may therefore lose those benefits.
One way to make disulfiram treatment feasible is to link its daily administration to the maintenance of benefits or to the avoidance of negative consequences.
Disulfiram therapy is often referred to as “aversive” or “revulsive” therapy, in the sense that it induces an association between alcohol and feeling ill rather than between alcohol and pleasure. The simplest mechanism that can be hypothesized is that the desire to drink, under conditions in which drinking is immediately associated with an effect that is frightening as well as intrinsically negative—and that makes it impossible to experience pleasure—leads to a conditioned reduction in craving, keeping it “suppressed.”
The person is therefore not necessarily “disgusted” by the idea of drinking, but rather prevented from accessing alcohol and its pleasurable effects, and consequently “retreats” mentally into a position of being forced to give up the behavior.
More recently, it has been demonstrated that disulfiram also acts on the brain’s dopamine system as a “selective inhibitor of monoamine oxidase type B.” This action may account for symptoms of anxiety and agitation, and potentially even hallucinations in severe cases, during an alcohol–disulfiram reaction.
Furthermore, on this basis, disulfiram has been studied in cocaine abusers, because interference with dopamine metabolism alters the brain’s response to cocaine. It appears that in people taking disulfiram, the pleasurable effect is immediately accompanied by anxiety and agitation, with a consequent “deterrent” effect in those who have experienced this reaction.
Disulfiram has been found to be effective in cocaine abuse associated with alcohol use, as well as in cocaine abuse itself.