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After detoxification from alcohol, the hard part starts.  Detox is easy; most people have experienced enough negative occurrences in their lives that they are motivated to tolerate withdrawal and stop drinking.  However, the guilt, regret and fears that made them get sober soon begin to become more distant and may be forgotten.  If they have not progressed into recovery by this time, relapse can occur.  At first, it may only be a single drink.  However, the pleasure and subsequent cravings they derive from that drink usually results in a pattern of escalating alcohol abuse until they find themselves exactly where they had been or worse.  AA and counseling are  important resources.  However, there are also medicines that reduce craving.  

Remember, to the alcoholic, the alcohol feels good in a way no non-addicted person can understand.  Because of some problem with the underlying neuro-physiology, the alcohol fits as a round peg into a round hole and the desire and cravings for the alcohol can be likened to a desire for food.  When was the last time you went on a diet for years without cheating once?  If we can somehow change this physiology, perhaps we can prevent the first drink or at least stop it from leading to a full relapse.


The first drug to come out with this indication was Antabuse (disulfiram).  Alcohol gets metabolized to acetaldehyde which gets broken down further.  Antabuse prevents the breakdown of acetaldehyde so that the acetaldehyde builds up.  This leads to nausea, flushing and a sense of being ill.  There has been concern that any exposure to alcohol will lead to sickness; however, many people can get about half of a standard drink into their bodies before they get sick.  In fact, I have had several patients drink regularly while taking the recommended dose of 250 mgs.  They have done better with twice the recommended dose.  

The drug is infrequently used because of several reasons.  The main problem is that it is unclear how well the medicine works.  When the studies examining effectiveness were done, it was found that just as many people had relapsed by six months regardless of whether they took the drug.   

It seems that those who were eventually going to relapse managed to avoid taking the medication for a few days, and than, they began to drink.  It is thought that only those patients who would do well anyway remain on the antabuse.  The result is that the use of Antabuse minimally prolongs alcohol free time in those drinkers who eventually relapse.  This seems like only a small benefit with a drug that had some potentially severe side effects.  However, it is still valuable to use early in recovery as there was evidence that relapse is delayed.

I have seen patients successfully use this medication long term. Perhaps they were would have done well anyway;  yet, they felt the use of the medication gave them the control that they needed.


There have been many attempts to use anti-depressants to reduce cravings.  Early studies seemed to indicate that they benefit only that portion of the alcoholic population with coexistent psychiatric problems. However, more recent studies have examined the use of anti-depressants in groups consisting of only type one or ty
pe two alcoholics.  (see Alcohol Subtypes) Type one alcoholics did better with certain anti-depressants(Zoloft) .  Type two alcoholics did worse. 

I have been partial to the use of Wellbutrin for various drugs because of anti-craving effects.  It had not been found to be effective for alcohol in the past; but, it has not been examined in populations separated by alcohlism subtype.  I have found it useful at times and I use it in type two alcoholism.  

NALTREXONE (you may also want to read Naltrexone in opiate dependency)       

There is a medication called naltrexone that has been used successfully.  This medication is actually an opiate blocker.  It was designed to prevent someone addicted to heroin or pain medication from getting high.  The medication will sit in the nerve’s opiate receptor without stimulating it.  This creates a chemical wall between the bloodstream and the brain.   It would prevent abused heroin and/or pain medication from interacting with the receptor.   The addicts would not feel anything if they used their drugs so their drug use went down. 

It was noted that people drank less alcohol while using this medication.  Now many studies have demonstrated the value of this medication in alcoholism.  A person given this medication clearly has a better chance of staying sober than someone who received placebo especially during the first few months of sobriety.  

How does this work? 

Alcohol causes the release of B-endorphins in the brain; this chemical stimulates the opiate receptors in the body.  When we block this pathway, we block the pleasure of drinking.  Since drinking is no longer pleasurable, why drink? 

Another benefit of the drug is that some persons taking it state they do not crave the alcohol at all.  This may be related to its' ability to act as an INVERSE AGONIST at the mu opioid receptor.  These receptors have a baseline activity and have a certain level of activity even in the absence of a drug or a naturally occurring neuro-transmitter.  As an inverse agonist, naltrexone reduces this activity.  It leads to a resensitizing of a cell to the natural endorphins, reduced cravings and an improved sense of well being. 

Another possible mechanism is that naltrexone reduces appetite in general.

Naltrexone is safer to use than Antabuse.  It can potentially cause liver problems but usually only at doses higher than typically prescribed.  At prescribed doses, it affects the liver in three out of every 1000 persons and only to a mild degree.  It may also cause stomach upset in a minority of persons on the drug. 

People have drank on the medication.  Since there is no euphoria, it changes the experience of drinking.  Now, one only feels the side effects of alcohol and they are not pleasant.

Of course, there is still the problem of getting the drinker to take the medication.  Network therapy is a technique that helps with this.  Dr. Galanter of NYU has described it.  It involves the person’s significant other, parents or any one else with whom the person is close.  The drinker makes a contract with their counselor to take the medication in the presence of this person.  It is the drinker’s responsibility to do this.  If this is not done, there is to be no fighting, no criticism and no anger.  The person doing the monitoring simply calls the drinker’s therapist and than it becomes a clinical issue between the drinker and his therapist.  It improves compliance with the medication and the overall success of treatment.  This technique also can be used for improving compliance with Antabuse use as well.


In 2006, an injectible form of naltrexone emerged called Vivitrol.  It is once monthly injectible medication.  Compliance is less of an issue.  
The injections have worked surprisingly well.  Patients who could not stop drinking did so with Vivitrol and their cravings were far less.  It was unexpected considering how effective the naltrexone pills were.  My belief is that the high blood levels seen in the first 7-10 days (much higher than that obtained with the pills) had an outsized effect on the brain and significantly changed endorphin biology.  It is almost a different drug.  It has become my treatment of choice.

Side effects are minimal except for injection site discomfort.  Some patients develop lumps at the injection site.  It occurrs in about 10% of the woman a a smaller percentage in men.  The lumps take 2-3 months to resolve.

The main problem is the price.  It is 700-800 dollars per treatment.  The company does have discounts if you check.


Over the last several years, we have learned about a “hyper-excitable” brain that causes irritability, sleep disturbances and cravings.  One aspect of this is too much stimulation of the NMDA-type glutamate receptors.  Campral is able to reduce this activity, which results in a reduction in cravings.

Studies show reduce cravings and less relapse.  They even show fewer drinks used in those patients who continue to drink.   It is particularly helpful for cue-associated cravings, as well as optimizing a sense of well being.  

I must admit that my initial enthusiasm for this drug has dampened.  Some patients do quite well, but others have minimal benefit.  I mainly use this medication in combination with other agents.


Over the past few years, I have also used anti-epileptic drugs to treat many patients.  I found that the symptoms of irritability and cravings were lessened.  More recently, topiramate (Topamax) has emerged as an effective drug.  The mechanism of action is complex as topiramate has several effects.  Two effects, the augmentation of GABA inhibition and the reduction of glutamate hyperactivity are likely the reasons the medicine is effective.  

Topamax can cause sedation, tingling and stomach upset.  I increase the dosage quite slowly.  Even with slow titration, some mental slowness is seen 10% of the time.


As stated elsewhere in this website, triggered cravings are dependent on the association of the alcohol with release of dopamine.  The release of dopamine maes the thought stic in our head and we cant get rid of the craving.
Zofran is small dosages is able to blunt the release of dopamine.  It does this by blocing a certain type of seratonin receptor- the 5HT3 receptor.  It has been shown to be effective especially in the type two alcoholics.  This enhanced response by type two alcoholics is one reason that abnormalties in the seratonin receptors are one type of abnormality that causes addiction to begin with.

Unfortunately, blocing the 5HT3 receptors has other effects as well.  In higher concentrations, it can stimulate appetite and the anti-craving effect is lost.  The dosages presently available to treat nausea are to high and will not help.  I have a local pharmacy compound the medication for me.  It has clearly been helpful.

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