Can we trust addiction medication?

Several drugs can dramatically increase recovery rates, but many patients remain resistent

Published October 4, 2012 10:09PM (EDT)

               (<a href='http://www.shutterstock.com/gallery-245650p1.html'>restyler</a> via <a href='http://www.shutterstock.com/'>Shutterstock</a>)
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This article originally appeared on The Fix.


No one should be paying $30,000 to go to what amounts to three 12-step meetings a day; a true treatment center should be providing something medically significant. So says Dr. Mark Willenbring, one of the nation’s staunchest advocates for a lot more medical intervention and a lot less spiritual journeying in the rehab and recovery industry. Otherwise, it’s like “going to an oncology center and getting prescribed a macrobiotic diet instead of chemotherapy,” says Willenbring, who is the founder and CEO of ALLTYR, which provides drug and alcohol addiction treatment based on cutting-edge science and research.

the fix Willenbring is by no means opposed to traditional 12-step programs in day-to-day life. He’s all for creating a robust arsenal for battling addiction; he’s interested in anything that yields results. But as you might expect from the former director of treatment and recovery research at the National Institute of Alcohol Abuse and Alcoholism, he is opposed to the prevailing resistance to, and ignorance about, the treatment of addiction with prescription drugs. The available medicines are admittedly limited and only partly effective. But no other approach—from the 12 Steps to psychotherapy to meditation to fire-walking and soul retrieval—has made a notable dent in this disease. Success rates remain low, and to exclude the tool of medical intervention from the treatment toolbox is, Willenberg says, "a crime."

Medicating addiction remains at best a tricky business. The more intricacies science reveals about the strange brew of compulsion and pleasure, endorphins and dopamine, neuro-this and neuro-that racing about in the human brain, the more elusive any single fix seems. (And no one is even talking cure.) Individually, each brain is unique—like snowflakes. Collectively, our brains are blizzards of synapses and information that make targeting addiction less hit than miss, less science than art.

Unfortunately, what works for one addicted brain—decimating both physical cravings and more slippery psychological urges—may not for another, and what works to mitigate one opiate may not for another. But for Willenbring, who is both a clinician and a researcher, this challenge is cause for tailoring the best treatment to the right patient and, most definitely, not for throwing out the prescriptions with the heroin. We have a few excellent tools at our disposal—some new drugs and some oldies-but-goodies (here’s looking at you, methadone!)—that make the task of at least managing the chronic, lifelong disease of addiction easier and, in the process, save lives.

Disulfiram, better known as antabuse, has about as much user-friendliness as that acrid polish nail-biters shellac their nails with to dissuade them from chomping down. But, instead of getting a bitter taste when indulging the bad habit, disulfiram will cause an alcoholic to have: “headache, nausea, vomiting, chest pain, weakness, blurred vision, mental confusion, sweating, choking, breathing difficulty, and anxiety.” Disulfiram is all about infusing the alcoholic with deep physical regret once they start drinking; it’s like the morning after a tequila binge when you say, “I’m never drinking again”—only the feeling starts ten minutes in and makes your worst hangover look like a mere cough and sniffle.

Tiparamate, or topmiax, is an anti-convulsant typically used for seizure-control in epileptics. But doctors prescribe it off-label for alcoholism because it can decrease the pleasurable effects from continued consumption of alcohol. This isn’t purely coincidence: Anticonvulsants reduce seizures in part by “decreasing abnormal excitement in the brain.” Where disulfiram punishes with a bang, tiparamate saps pleasure with a whimper.

Then there’s naltrexone, or nalmefene, an opiate antagonist that strives to block the pleasurable effects of alcohol and opioids like heroin and Oxycontin right at the neuroreceptors in the brain that register them, while simultaneously ebbing the cravings for drugs and alcohol altogether. There’s none of the sickness of disulfiram and the diminishing returns (This isn’t getting me high!) are offset by reduced cravings (Meh, who cares). This one-two punch is promising, but studies show only a little over 10% of patients are helped by naltrexone.

And that’s pretty standard when it comes to alcoholism, according to Willenbring. He likens disulfiram, tiparamate, and naltrexone to antidepressants, which have been shown to be much less effective over time than initially expected, requiring switching from one to another or adding on “booster” drugs and otherwise hoping for the best. Willenbring says that, in his experience, disulfiram, tiparamate, and naltrexone “reduce relapse in the neighborhood of 20%.” “Now, that’s not too bad,” he says. “It’s a tough disease, and I’ll take every arrow in my quiver—even if it’s just a leg up.” Magic bullets they ain’t.

If there’s any magic to be had, it may not be in the specific medication used itself but in how we think about their use. Best example? Long-term opiate-replacement therapy. For years, buprenorphine and, for decades, methadone have been prescribed to treat opiate addiction, for everything from heroin and morphine to Vicodin and Oxycontin. Buprenorphine and methadone are themselves opiates—though they are less-addictive, producing a less-intense high and none of the most dangerous side effects. They substitute for the addict’s drug of choice, replacing the effects and limiting the withdrawal.

The newest serious opiate-fighting drug is Suboxone, a mixture of buprenorphine and naloxone, which binds to opiate receptors to mimic the effects of, say, heroin, but then resists abuse by making the addict sick if they try to shoot up the Suboxone. This two-pronged approach has been shown to provide substantially better outcomes in young adult users than in those patients who just received the standard short-term detox and counseling. What’s more, addicts taking Suboxone were “less likely to use opioids, cocaine and marijuana, to inject drugs, or drop out of treatment.”

“These findings should reassure and encourage providers who have been hesitant to offer extended Suboxone treatment,” said National Institute on Drug Abuse Director Dr. Nora Volkow.

Unfortunately, as of 2008, just 8% of all treatment facilities nationally were even certified opioid treatment programs—that is, allowed to administer these medications. That means, of course, that a whopping 92% of treatment facilities offered no opiate analgesics to their heroin patients at all. “So now we have this crime where thousands of addicts are going to abstinence-only-based treatment for opiates,” Willenbring says. “But not one study validates this approach—while there are hundreds of studies demonstrating the effectiveness for Suboxone and methadone.”

Offering severe opiate addicts medication is important because the startlingly acute concentration of opiates found in heroin or Oxycontin create profound neuroadaptations, sometimes permanently impairing the brain’s ability to control use. So for many severe opiate addicts, Willenbring says, simply taking away the addictive substance results in an internal chemical deficiency. And no higher power can fill that hole.

What’s more, when used consistently and for the long term, opiate replacement therapy is in fact very successful. Despite the prevalence of abstinence-only models, patients taking buprenorphine can integrate this drug into their daily routines and live otherwise-drug-free healthy lives; but, according to one study, once off the drug—even after tapering and counseling—close to 100% of patients relapsed. Opiate replacements can literally be the difference between using and not using, between high-quality and low-quality mental health, and finally between life and death. “It’s highly effective, clearly save lives, and stabilizes people,” says Willenbring, adding that contrary to popular myth, these patients are not “high” on their new medications, just normal.Willenbring is a proponent of the long-term use of opiates to treat addiction—possibly even lifelong (if no serious side effects get in the way or if science delivers a new breakthrough). For many people, Willenbring says, it’s a matter of “once you develop dependence, it’s there for life.” That means Suboxone, buprenorphine, and methadone may be the only chemical shield between an addict and relapse. Without the presence of opiate replacements, death rates shoot up to about 50% in severe addicts—mostly from overdoses. Not giving a severe opiate addict meds is “like telling a diabetic to go to a support group,” Willenbring says. When you have an insulin deficiency, a thyroid deficiency, what do you do? You replace it. Sometimes for life. And today that’s the answer so far for managing a chronic lifelong opiate deficiency.

Which isn’t to say, it’s a perfect answer. Maintaining opiate replacement therapy in the long run usually means taking a daily dose in pill form. And that means entirely likely events—like a missed pill, a forgotten prescription refill, or a lost vial—can be the thin line between a patient and a deadly relapse. And for some addicts, the sheer plausibility of forgetting to take a pill would be excuse enough to use again. (Desire for a new way of life? Meet the cunning and baffling addicted brain.) Imagine staying on top of that for the rest of your days.

One new drug, Vivitrol, an injection of naltrexone that lasts 30 days, both eases the daily pressure to take one’s meds and ups the ante on the necessity to remember to do so in awkward 30-day increments. It’s a variation on a theme; not a new story.

As for real, new exciting scientific breakthroughs, don’t hold your breath. The science has slowed down—both in the private sector and in government. This is at least in part due to high hopes for watersheds in brain-imaging science and the human genome—innovations that would explode the science of addiction!—that never quite panned out. According to Willenbring, unraveling the genome—let alone divining helpful solutions to mental diseases like addiction—proved to be spectacularly more complex than scientists first appreciated. (Remember when we were going to decode the human genome in a decade?) Conversely, brain imaging, says Willenbring has been “grossly oversold.” All of those “very seductive pictures” of brains reveal something a bit more ho-hum: When “thinking changes, the brain changes.” Willenbring calls brain imaging the new phrenology.

So, all of the excitement many of us have heard about vaccines for addiction has tapered off. “Industry has pulled back from investing in these medicines because new science isn’t there,” says Willenbring. That’s why there are a lot of useful tweaks of existing drugs—such as Vivitrol or Suboxone—but nothing like a game-changer. “We need more investments,” says Willenbring. “Otherwise we’ll continue to see a bunch of these ‘me too’ drugs.” We can only hope that this dry drug pipeline does not persist as long as it has for the treatment of depression and related mental health problems, which has seen only variations in the Prozac-type class of antidepressants for three decades. Willenbring says that, in his view, the most promising place to look for an addiction advance is in drugs that affect stress-response systems.

Until then—or until some other “next big thing"—three things are certain. One is that, as Willenbring says, “The more we learn, the more complicated it gets.” Another is that the potential market for a cure—tens of millions of people—is only growing. And the third? The deep resistance of many in the recovery community to the medical treatment of addiction will do nothing to bring new and better drugs out of the lab and into the brains of the people who need them.

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