I understand that Re Via is an opiate. I have never been addicted to opiates. Why would that be prescribed, and will I become addicted?

Medications do two things: (1) They attach to a specific receptor, and (2) they alter the receptor in a specific way. Opiates are a class of medications that specifically target opiate receptors in the body. Normally one thinks of opiate receptors as pain receptors and opiates as pain medications. Hence, the term derives from Opium, the poppy and its analgesic properties. In fact, however, there is more than one opiate receptor, and each opiate receptor can be altered in more than one way. It is commonly known that some opiate receptors alter pain. It is not well known which other opiate receptors alter other physiological and psychological properties.

By thinking about the various physiological effects of opium, we can understand that better. Besides reducing pain, opiates can also cause sedation (neurological effects), can lead to respiratory depression (respiratory effects), can make us nauseous and constipated (gastrointestinal effects), and can produce euphoria (psychological effects). Each of these varying properties appears to be affected by its own set of opiate receptors. In addition to these specific receptors, various changes can occur in each receptor with a particular drug. For example, a drug can cause the receptor to respond positively or more strongly through agonism, a term used in pharmacology for stimulation, or a drug can cause the reverse effect or have the receptor respond in the opposite direction, known in pharmacology as reverse agonism. A drug can also block a receptor, rendering it completely inactive. This is known in pharmacology as antagonism. Finally, a drug can be created that acts as either an agonist or antagonist, depending on the local environment (i.e., the amount of endogenously available neurotransmitter). When the amount of neurotransmitter is low, the drug acts as an agonist. When the amount is great, the drug acts as an antagonist. Such a drug is known as a partial agonist.

Reverse agonism a chemical (drug) that has reverse activity on the receptor rather than just merely blocking the receptor.

Antagonism the mechanism that causes the blocking of the biological responses at a given receptor site, due to a drug or other chemical.

Agonist a drug capable of combining with a receptor on a cell and initiating a reaction or activity.

Endogenously functional causes occur from internal factors in the mind or the body.

Partial agonist a chemical (e.g., drug) that can both block and stimulate a receptor depending on the relative amount of neurotransmitter present in the synaptic cleft.

Naloxone generic for Narcan. It is an opioid antagonist and competes with opioids at the opiate receptor sites.

Narcan an opioid antagonist and antidote to opiate overdoses.

Thus, an entire array of effects can be produced on each particular receptor with varying chemicals, almost like fine-tuning a radio station to provide the best reception. As an example, when patients come to the emergency room because of a heroin overdose, they will receive a medication known as naloxone (Narcan), which is an antagonist that blocks the effect of heroin on all the opiate receptors. Thus, respiratory depression, the cause of death from heroin overdose, as well as all of the other effects, is reversed. The downside of this is that if the patient is heroin dependent, he or she will go into immediate withdrawal because, again, all of the effects of heroin are reversed.

Re Via is the trade name for a medication generically known as naltrexone (see Table 11). It is the second medication that the FDA approved and has been in use since 1994. Naltrexone is an opiate antagonist that blocks opiate receptors and thereby decreases the craving for alcohol, resulting in not only less interest in alcohol but also in less alcohol consumption. (See question 32 on p. 89 for additional information about the link between alcohol and opiates.) Consequently, there may be slips but fewer relapses. Studies in nonhuman animals clearly demonstrate that alcohol consumption causes an increase in endogenous opiates, and thus, it is postulated that naltrexone blocks the effects of this increase on the brain; thus, the "rush" associated with drinking alcohol is not felt. A recent brain imaging study showed that alcoholic persons have increased opiate receptors in a part of the brain associated with reward and pleasure and that the number of receptors correlates with the degree of craving. Additionally, naltrexone indirectly increases the amount of dopamine, the major neurotransmitter associated with reward (see Question 6). Unfortunately, the effect in reducing relapses is a modest 12% to 20%, depending on the study. Combining medications with other forms of therapy improves the outcomes by a third.

Table 11 Naltrexone: An Opiate Antagonist

Drug Name

Naltrexone (ReVia) — Patients must be abstinent for 5 — 7 days before beginning therapy. Monitor liver function during treatment. Expensive, approximately $4.50 per pill. Pure antagonist and is not addicting.

Adult Dose

50 mg PO qd

Some physicians give 25 mg for the first 2 days of therapy; some believe 100 mg works better than 50 mg, but no trials demonstrate this.

Pediatric Dose

Not established


Documented hypersensitivity, acute hepatitis, liver failure


Inhibits effects of opiates; patients currently taking opiates or who have been on long-term opiate therapy in previous 7 days can experience severe opiate withdrawal


C — Safety for use during pregnancy has not been established.


Nausea/vomiting, abdominal pain, daytime sleepiness, and nasal congestion were more common versus placebo in largest randomized trial to date; discontinuation due to adverse effects was uncommon in most clinical trials.

Naltrexone generic for ReVia. It is an opioid antagonist that competes with narcotics at opiate receptor sites, blocking the opioid analgesics.

Studies in nonhuman animals dearly demonstrate that alcohol consumption causes an increase in endogenous opiates, and thus, it is postulated that naltrexone blocks the effects of this increase on the brain; thus, the "rush" associated with drinking alcohol is not felt.

The main side effects of naltrexone are nausea and/or vomiting, abdominal pain, sleepiness, and nasal congestion.

Naltrexone use is controversial, which stems from the fact that it appears to moderate the amount of alcohol consumed rather then actually preventing one from consuming alcohol altogether. Thus, it paradoxically appears to be more effective for people who continue to drink alcohol and want to control their con sumption rather than those who are attempting to achieve complete abstinence. The idea of a medication to moderate one's alcohol consumption rather than to eliminate it altogether, however, is abhorrent to many and has led others to fear that it will not assist in attaining the ultimate goal of complete abstinence, which defeats the entire goal associated with alcoholism treatment. Remember that although there seems to be a continuum from problem drinker to alcohol abuser to alcohol dependence, when one looks at all alcoholics, it remains to be determined whether the continuum exists within individual alcoholics. Whether any individual with alcohol abuse will ultimately become alcohol dependent if left unchecked remains hotly debated. The abstinence-only model argues for this continuum, whereas the controlled-drinking models argue that at least some alcoholics can control their drinking and will never become alcohol dependent. Naltrexone may be most effective for the alcoholic who wants to continue to drink, through a process known as pharmacological extinction, where it acts on the opiate receptors to block the pleasurable effects that come from regular drinking thereby reducing the pleasure associated with the activity.

The main side effects of naltrexone are nausea and/or vomiting, abdominal pain, sleepiness, and nasal congestion. Pregnant women, individuals with severe liver or kidney damage, or those who cannot achieve abstinence for at least 5 days before starting should not use it. Also, people who are dependent on opiates such as heroin or morphine must stop their drug use at least 7 days before starting naltrexone or they risk precipitating withdrawal. Aside from side effects, which are usually short lived and mild, alcoholics report that they are largely unaware of being on this medication. Naltrexone usually has no psychological effects and patients don't feel either "high" or "down" while they are on naltrexone. It is not addictive. Naltrexone does not cause physical dependence, and it can be stopped at any time without withdrawal symptoms. In addition, available findings regarding cessation do not show a "rebound" effect to resume alcohol use when naltrexone is discontinued. If naltrexone is tolerated and the patient is successful in reducing or stopping drinking, the recommended initial course of treatment is 3 months. At that time, the individual and his or her physician should evaluate the need for further treatment on the basis of the degree of improvement, the degree of continued concerns about relapse, and the level of improvement in areas of functioning other than alcohol use.

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