Shortcuts to Recovery

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Shortcuts to Recovery

By Jeanene Swanson 12/01/14

A survey of four medical treatments to aid recovery.

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About eight million people in the US are alcohol dependent, but most will not receive treatment—even though anti-cravings medications like naltrexone have been clinically proven to be helpful. Why? “The community hasn’t accepted medications,” says Dr. Robert Swift of Brown University’s Center for Alcohol and Addiction Studies. “[Many people seeking treatment say] ‘It’s a crutch, I would never take that thing.’”  

However, while some might consider the use of medications to be a crutch, it is more accurate to call it an assist. No one considering moderation or abstinence should be faulted for trying. “There are no shortcuts to recovery,” Swift says.

Misunderstood

The use of medications to treat drug addiction has a long history. There are only four medications approved to treat alcohol use disorders (AUDs) in the US: disulfiram (Antabuse), oral naltrexone (Revia), acamprosate (Campral), and an intramuscular, once-a-month naltrexone injection (Vivitrol). The most widely prescribed AUD is naltrexone. While these drugs are not meant to be used alone—“they’re added on to counseling or psychosocial treatment,” Swift says. Many people still don’t want to touch them, including physicians. However, according to Dr. Larissa Mooney, Director of the UCLA Addiction Medicine Clinic, anti-craving medications should be tools in the arsenal. “I don’t view them as a cure,” she says. “It’s a tool that can increase the likelihood that someone will initiate [steps] toward abstinence [or] maintain sobriety.” Some consider harm reduction simply a copout—a free pass to keep drinking or using—but according to Kenneth Anderson, founder of the HAMS harm reduction network, “I think the word ‘shortcut’ is very strange to me, [and] we should talk about treatments that have evidence base and those that don’t.”

Another reason why many people misunderstand anti-craving medications is that they don’t get how the drugs work. Additionally—and probably most importantly—neither do their doctors. Subsequently, they are simply not offered to patients. According to a recent study published in the journal Psychological Services by the VA Center for Health Care Evaluation, the top four barriers to using drugs to treat AUDs are “perceived low patient demand, pharmacy procedures or formulary restrictions, lack of provider skills or knowledge regarding pharmacotherapy for alcohol dependence, and lack of confidence in treatment effectiveness.” Educating both doctors and patients will go a long way toward increasing prescription rates. According to NIDA, in 2010, doctors wrote 283,000 prescriptions for naltrexone and 16,000 prescriptions for Vivitrol—compare that with the aforementioned 8 million people in the US who are dependent on alcohol.

“The biggest issues are cultural and educational,” says Dr. Raymond Anton, Director of the Center for Drug and Alcohol Programs at Medical University of South Carolina (MUSC). “The overlying cultural effects, which permeate alcohol and substance abuse treatment, in many cases, preclude people from thinking about other approaches,” says Dr. Charles O’Brien, who has a treatment center named after him at the University of Pennsylvania and who was the first to show in clinical trial that naltrexone also worked for treating alcoholism. “I feel bad when I run into therapists who say, ‘No, I never use it.’ I think that’s unethical.”

Naltrexone

Dr. O’Brien has been using naltrexone since the 1980s. In fact, in the first double-blind clinical trial conducted between 1985 and 1988, he found that naltrexone helped reduce heavy drinking, cravings, and the pleasurable “high.” In studies since, naltrexone has helped patients either maintain abstinence or avoid full-blown relapses when used in conjunction with traditional psychosocial therapies.

Naltrexone is an opioid receptor antagonist, and it works indirectly in treating alcoholism by blocking opioid receptors in the brain and thereby, blocking or reducing the “high” from drinking. In this way, alcoholics experience less cravings and have less incentive to drink. “You still have free will when you’re on naltrexone,” O’Brien says. “A lot of people find they don’t have cravings, [and] if they do, it’s very much reduced.” Anton likens its use to that of a cast on a broken bone. “The brain has the ability to heal itself over time,” he says. “Once the brain recovers, you’re at much less risk than if you hadn’t recovered.” Naltrexone was FDA approved in 1994, a long-acting version (Vivitrol) in 2006, and the European EMA approved a drug similar in function to naltrexone, nalmefene, in 2013.

Studies have shown naltrexone to be only mildly effective—and, typically, it’s been trialed as an additional, not standalone, treatment for AUDs. The most recent Cochrane review found that naltrexone works, but to modest effect, and should be accompanied by counseling. Based on a total of 50 randomized, controlled trials evaluating almost 7800 patients, naltrexone reduced the risk of heavy drinking by only 15%, and decreased the number of drinking days by about 4%. 

In fact, says MUSC’s Anton, most clinical studies have aimed to show that naltrexone can make counseling work better. In the 2006 Combined Pharmacotherapies and Behavioral Interventions for Alcohol Dependence (COMBINE) study, Anton and team looked at how adding naltrexone or acamprosate to traditional behavioral therapies would affect treatment outcomes among nearly 1400 alcoholics. Surprisingly, he found that taking any pill was better than counseling alone—which goes to show how effective placebo can be. And, while there was a significant benefit to adding naltrexone to behavioral interventions, naltrexone was most effective in reducing heavy drinking when used alone, without behavioral interventions. Incidentally, acamprosate showed no significant effect, either by itself or with any combination of naltrexone, behavioral interventions, or both.

“The results were a little bit surprising in that it’s sort of like nobody won and nobody lost,” Anton says. “When we didn’t give any pills, [the psychosocial intervention] actually didn’t work as well.” One important implication of these results is that naltrexone can be offered by healthcare providers where traditional psychosocial treatment is not available.

A major drawback to naltrexone is that like most medications, they not only work moderately, but sometimes they don’t work at all. Not everyone responds to naltrexone, and this is partly based on genetics. Naltrexone binds to all three types of opioid receptors, each with different affinity. For some people with a mutation in one type of receptor, Anton found that naltrexone works well. For others—whites have this mutation less while blacks barely have this mutation leading naltrexone not to work as well for these groups. “People drink for many different reasons,” Anton says. “There may be different genetic susceptibility and different neurochemical systems, and it’s very possible that one drug may work for [only] one subset of people.”

It’s not a quick fix, and the idea, Anton says, is to use naltrexone to reduce the severity of slips, or at least keep them shorter. Patients sill have to develop cognitive-behavioral skills to fight cravings when they go off the medication, which is typically anywhere between six to 12 months—early sobriety presents the highest risk of relapse. “[After the medication is stopped,] the individual will still be exposed to places or situations that could be triggering, and he or she will have to use more cognitive skills to cope with the cravings,” UCLA’s Mooney says. “Part of relapse prevention is learning how to cope with the cravings. It will be an issue on or off [the medication].”

Anton simplifies things: “Get both [medication and CBT]  And if they can’t afford CBT, then naltrexone has a good chance of working on its own rather than doing nothing.”

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