A study published this week in Science suggests that the active ingredient in marijuana, cannabinoids—which include THC and other chemicals—may limit the body’s ability to tamp down pain responses, and, as a result, turn short term acute pain into more long term discomfort. While there has been a growing amount of research analyzing the pain reduction effects of cannabis, an international group of researchers led by Hanns Ulrich Zeilhofer from the University of Zurich’s Institute of Pharmacology and Toxology and collaborators from the University of Texas Medical Branch at Galveston think they may have uncovered evidence that marijuana can achieve just the opposite effect.
By applying a mimic of endocannibanoids, the body’s homegrown version of cannibanoids, to the spinal columns of mice, researchers saw that instead of amplifying the capacity of pain inhibitor neurons, the chemical managed to shut them down. That is, the electrical signals that indicate pain inhibition is underway effectively went dark. In a second trial, they attempted the same technique on mice that had been genetically engineered to lack the specific receptors necessary for endocannibanoids. In this group, pain inhibition neurons functioned normally.
Yet, does the apparent neuronal on/off switch flicked by cannabis chemicals actually signify an increased sensation of pain? To test that out, researchers put rats who had endocannabinoids in their systems under anesthesia, and then injected small amounts of capsaicin—the chemical that makes chillies spicy—into their hindpaws. The result was a quick uptick in pain response. And for these rats, even stimuli that wouldn’t have caused discomfort earlier now produced a pain response, a phenomenon known as allodynia. When the researchers administered an endocannabinoid blocker, however, “this increase was reversed,” they write.
Finally, to see if this trend persisted in humans, they subjected volunteers to mild electrical shocks on the forearm to induce hyperalgesia—heightened pain sensitivity—in that specific region. They then gave half of the volunteers a placebo, and half the endocannabinoid receptor blocker rimonabant to take for a month, after which time they came back to get tested again. There was little change in the placebo group, but, consistent with their findings in mice and rats, the researchers say, there was a marked decline in hyperalgesia and allodynia in the previously tested regions of those who had taken the blocker. There was not, however, any reduction in acute pain—the discomfort caused at the site of the new round of shocks.
Their conclusion? While the researchers began their project with the idea that cannabis should help dull pain, in fact they found that endocannabinoids play an “unexpected role” in governing pain-inhibitor neurons in the spine, and may even possibly increase the risk for turning short term, sharp pain, into more long term pain. And, since the active ingredient in pot is so chemically similar to endocannabinoids, marijuana could potentially cause the same problems. Yet, while these results certainly open the door for further research—and might provide a word of caution for recreational pot smokers—many more studies still have to be done before these findings can upend the existing evidence for the predominately pain-reducing qualities of cannabis.