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Pain-killers less effective when we don’t know what they are

PainSci » bibliography » Amanzio et al 2001
Tags: chronic pain, treatment, medications, mind, pain problems, self-treatment

One article on PainSci cites Amanzio 2001: Placebo Power Hype

PainSci notes on Amanzio 2001:

This study tested the effects of pain-killing drugs with and without the patients knowing they were being medicated. They also blocked neurotransmitters to stop the brain from doing any of its own pain-killing, which we know can happen when people believe they are being medicated (placebo effect). The results showed that the effects of drugs are strongly affected by awareness. “We found that the hidden injections [of pain killer] were significantly less effective and less variable compared with open injections.”

On the one hand, this seems profound and seems to show the “power” of placebo and the mind. On the other, it’s merely a good demonstration of what we already know: that meaning and expectation are an important factors in every therapeutic equation.

original abstract Abstracts here may not perfectly match originals, for a variety of technical and practical reasons. Some abstacts are truncated for my purposes here, if they are particularly long-winded and unhelpful. I occasionally add clarifying notes. And I make some minor corrections.

Individual differences in pharmacokinetics and pharmacodynamics, the type of pain and the method of drug administration can account for the response variability to analgesics. By integrating a clinical and an experimental approach, we report here that another important source of variability is represented by individual differences in non-specific (placebo) activation of endogenous opioid systems. In the first part of this study, we analyzed the effectiveness of buprenorphine, tramadol, ketorolac and metamizol in the clinical setting, where the placebo effect was completely eliminated by means of hidden infusions. We found that the hidden injections were significantly less effective and less variable compared with open injections (in full view of the subject), suggesting that part of the response variability was due to non-specific factors (placebo). Since we could not administer the opioid antagonist, naloxone, to these patients, in the second part of this study, we induced experimental ischemic arm pain in healthy volunteers and found that, as occurred in clinical pain, the analgesic response to a hidden injection of the non-opioid ketorolac was less effective and less variable than an open injection. Most importantly, we obtained the same effects by adding naloxone to an open injection of ketorolac, thus blocking the opioid-mediated placebo component of analgesia. These findings indicate that both the psychological (hidden injection) and pharmacological (naloxone) blockade of the placebo response reduce the effectiveness of, and the response variability to, analgesic drugs. Therefore, an important source of response variability to analgesics appears to be due to differences in non-specific activation of endogenous opioid systems.

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