Blocker for Heroin Addiction? A Cautionary Tale About Press Hype and Truth

If you were paying attention to news about successful treatments for opioid addiction you probably fell out of your chair when you saw a stream of headlines one mid-month morning proclaiming that a way to “block” addiction to heroin had been found. All of the articles were based on one of two press releases, both of which were issued by the institutions where the lead authors of an animal study work (University of Colorado and University of Adelaide). The study was published in the August 15 issue of the Journal of Neuroscience.

In fact, the study was about how a promising new immune system component can contribute to pain relief with lower amounts of opioids. It was not about addiction.

Thanks to SciCurious, a Scientific American blogger, the truth got out pretty fast. But it was too late for the hundreds of articles that have already been published—with no retractions or corrections that we can find.

This is a cautionary tale about journalists who, instead of going to the easily-findable study itself, rely on the press release.

What the headline of the actual article says: “Opioid Activation of Toll-Like Receptor 4 Contributes to Drug Reinforcement.”

What the press release headline from the University of Colorado says: “New study involving CU-Boulder shows heroin, morphine addiction can be blocked.”

What the press release headline from the University of Adelaide says: “Scientists can now block heroin, morphine addiction; clinical trials possible within 18 months.”

This major disconnect between press release and study—and the authors appear to have willingly participated in it because they are quoted in the press releases as saying their study shows addiction can be blocked—was dutifully perpetuated by the press.

What Fox News said: “Researchers find way to block heroin, morphine addiction.”

From BusinessWeek: “Heroin Immune Cell Seen as Hope for 21 Million Abusers.”

And don’t blame it only on the lay media. The internet is full of websites like “Medical News Daily” which ran its write-up of the press release under this headline: “Morphine and Heroin Addiction Can be Bed by Targeting Immune System.”

For those who are interested, here’s how the abstract begins: “Opioid action was thought to exert reinforcing effects solely via the initial agonism of opioid receptors. Here, we present evidence for an additional novel contributor to opioid reward: the innate immune pattern-recognition receptor, toll-like receptor 4 (TLR4), and its MyD88-dependent signaling. Blockade of TLR4/MD2 by administration of the nonopioid, unnatural isomer of naloxone, (+)-naloxone (rats), or two independent genetic knock-outs of MyD88-TLR4-dependent signaling (mice), suppressed opioid-induced conditioned place preference. (+)-Naloxone also reduced opioid (remifentanil) self-administration (rats), another commonly used behavioral measure of drug reward. Moreover, pharmacological blockade of morphine-TLR4/MD2 activity potently reduced morphine-induced elevations of extracellular dopamine in rat nucleus accumbens, a region critical for opioid reinforcement. Importantly, opioid-TLR4 actions are not a unidirectional influence on opioid pharmacodynamics, since TLR4−/− mice had reduced oxycodone-induced p38 and JNK phosphorylation, while displaying potentiated analgesia.” (For the entire abstract, go to http://www.jneurosci.org/content/32/33/11187.abstract.)

Maybe this is too difficult for your average journalist to understand. But the average journalist should at least know to call an addiction treatment expert to find out if such a thing is possible, and there must be health care journalists who have heard of methadone and buprenorphine.

What SciCurious said:

“1. Is this paper good? Oh yes! Really neat! Cool new mechanism!
2. Does it “block” heroin addiction? No.”

The study was funded by the National Institute on Drug Abuse and the Australian Research Council. The NIDA press office didn’t respond to a request for an explanation about whether this study actually shows a way to block addiction.

SciCurious explains (and we paraphrase): For the study, rats self-administered remifentanil – a form of fentanyl, highly reinforcing – very quickly because it made them feel good. Then they were given (+)-naloxone, a mirror isomer of naloxone, immediately prior to self-administration of remifentanil. They did not self-administer it at all. So it did block the rewarding effects of the drugs. But, as SciCurious wrote, “these rats were not addicts, and they did not look at things like reinstatement for drug-seeking behavior or other measures.” She added, “there’s a big difference between blocking the effects in a rat that’s only had a few days experience, and blocking them in a years-long addict.”

Should (+)-naloxone be tested? Yes, said SciCurious. But she noted that there have been many drugs that block self-administration for morphine, but these drugs haven’t worked in patients.

What (+)-naloxone does do—and what the study shows it does—is potentiate the effects of pain relief. This was tested by measuring the length of time it takes for a mouse to remove its tail from a hot plate. When the mouse is on remifentanil, it takes longer to remove its tail because it can’t feel the pain. When it’s on (+)-naloxone and remifentanil, it takes even longer.  “(+)-naloxone has not cured addiction,” writes SciCurious. “But it could do great things with pain.”

For the Scientific American blog, go to http://blogs.scientificamerican.com/scicurious-brain/2012/08/15/stop-the-presses-we-cured-heroin-addiction/

Alison Knopf for AT Forum

Comments

  1. On September 20th Robert Newman responded to AT Forum:

    Absolutely shameful on the part of the researchers and – even more, because of its pretty unique responsibility to the public whose dollars helped pay for the study – NIDA. Kudos to Alison Knopf and ATForum for calling attention to this gross, inexcusable and seemingly knowing and intentional distortion of findings For my part, I confess I was far too superficial in my own initial readings of the news media reports (embarrassingly, I did not bother to read the original publication of the study) to pick up on all that is revealed here – a reflection of my cynicism regarding a purported new breakthrough in “preventing addiction” based on a study of rats.

    Having now confessed my tendency to give inadequate thought to what I read, if anyone thinks I am too harsh on the colleagues from Adelaide and from Colorado, please tell me – with criticism as harsh as you feel I deserve – and I promise to share that criticism with the bcc list that is receiving this email. Really – I‘d be delighted to learn that my conclusions are unwarranted. But for now . . . . Bob Newman

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