addiction and relapseIn my last post I mentioned that one of my patients on buprenorphine had relapsed. Relapse on buprenorphine reminds me of the philosophical cliché, ‘if a tree falls in a forest and nobody hears it, did it make a sound?’ For those not familiar with the cliché, the question and the answers–from standpoints of science, art, and metaphysics—are discussed in great depth, I just discovered, on Wikipedia. I now know more about the question than I will ever need to know!

When a person on buprenorphine maintenance uses opioids, what happens? The answer, depending on perspective, ranges from ‘nothing’ to ‘everything.’ For example, we could focus solely on the effects experienced by the addict. Because of the blocking effects of buprenorphine, an addict may take significant doses of heroin without having any subjective response. One might argue that since the addict experienced no ‘high’ from the use of heroin, he/she didn’t really relapse. Someone else may focus on the intake of chemicals, and consider such use to be a ‘relapse’ whether or not the heroin had a noticeable effect.

From my perspective, the issue with addiction is not whether a chemical was ingested, or even whether a ‘high’ was experienced. I consider the hallmark of addiction to be ‘obsession’—with relapse being a return to the cycle of obsession, using, and shame—regardless of the subjective effects of the addict’s drug of choice. From this perspective, a person given an opioid agonist without his/her knowledge would not be considered to have relapsed—even if the agonist caused significant subjective effects. But I would diagnose relapse in a person who engaged in addictive behavior in order to obtain and take an agonist, even if the drug yielded no effect at all.

So when we ask ‘what happens when a person on buprenorphine maintenance uses agonists?’ we have to distinguish between the actual subjective effects of the abused agonist, vs. the consequences of returning to addictive behavior. Today we will focus on the first of those two issues.

As savvy patients know, all significant opioid-blocking effects from Suboxone are from buprenorphine, not from naloxone. A person taking the usual dose of 8-16 mg will experience little effect from 80 mg of oxycodone—so little that patients who have relapsed on such a dose are divided when I ask if they ‘felt’ anything. And even those who claim effects from agonists qualify their answer with ‘but maybe I imagined it.’

In my last post I wrote that my patient had used a very large amount of oxycodone, on the order of 500 mg. Agonist doses of that magnitude will certainly yield significant opioid effects, along with significant risk of overdose. Molecules of buprenorphine, like other receptor-binding chemicals (molecules that bind to receptors are called ‘ligands’), do not simply attach to their binding sites. Receptor ligands are constantly binding and unbinding from their receptors, their movements described by association and dissociation constants. The ratio of dissociation to association constants is the ‘affinity’ of the molecule for a given receptor. Buprenorphine has a very high affinity for the mu opioid receptor.

Opioid agonists such as oxycodone, fentanyl, or heroin have varying affinities for the mu receptor. When multiple agonists, antagonists, or partial agonists are present in the body, the molecules compete for the receptor like swarms of butterflies around a single flower, each landing momentarily before flitting away, replaced by another visitor in random order. If the swarm contains a hundred white cabbage butterflies and one monarch, the most likely visitor, at any one time, will be a cabbage butterfly. But the monarch will land every now and then, and its larger wings, for a moment, will keep others from landing. Opioid agonists and buprenorphine compete for receptors in a similar way, but at quantum speed.

The chance that an agonist will result in a subjective ‘high’ depends on the amount of agonist, the amount of buprenorphine, and the tolerance level of the individual. Subtle differences between one person and the next, such as expectation and mood, seem to play into the equation as well.

Physicians can make use of the competition between agonists and buprenorphine when people on buprenorphine maintenance need medication for pain. People on buprenorphine require surgery from time to time, just as people without opioid dependence. Post-operative pain can be treated using high doses of opioid agonists. Interestingly, patients on buprenorphine maintenance report pain relief if high-enough doses of an agonist are used, but will often say—disappointedly– that the medication ‘feels different’ from what they remember from their using days. They tell me that the agonists do not have the warm feeling of contentment that they got from their drug of choice—that while on buprenorphine, agonists ‘only’ provide pain relief, without the euphoria.

What happens when a person on buprenorphine takes an agonist? Usually, the person feels little in the way of a ‘high’ or any other subjective effects. Instead, the person feels something else—an unpleasant sense of disappointment and shame for letting himself/herself down.

My job is to help the person maintain enough self-criticism in order to motivate an honest look into what changes are necessary—while at the same time helping the person recognize that sobriety is a long-term challenge. A person in such a position can learn to tolerate feelings of shame instead medicating them away. Such a person can feel positive about the positive steps taken so far, and realize that nobody is perfect.

Photo by Nickton, available under a Creative Commons attribution license.

 


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    Last reviewed: 11 Apr 2011

APA Reference
Junig, J. (2011). If A Tree Falls…. Psych Central. Retrieved on October 1, 2014, from http://blogs.psychcentral.com/epidemic-addiction/2011/04/if-a-tree-falls/

 

 

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