What makes a good pain reliever? I remember taking diclofenac for months after a herniated disc. It helped me manage the recurring pain, but I couldn’t get rid of it.
Current research now shows us that pain relievers that work by inhibiting the COX enzyme (such as diclofenac, ibuprofen, acetaminophen, and aspirin) can actually prevent resolving the inflammation.
Here’s how it works: COX produces prostaglandin E2, which causes inflammation and pain. If COX is inhibited, the pain is reduced.
However, we also need COX to resolve inflammation. If we inhibit it over the long term, we also prevent the inflammation from resolving.
There are actually specific signaling molecules responsible for resolving inflammation: resolvins and maresins. These are based on a specific omega-3 fatty acid called 18-HEPE.
The omega-3 pathway produces EPA and DHA, which are the well-known fish and algae oils. With the help of COX, these are converted into 18-HEPE. This is then converted into resolvin, which resolves the inflammation. This is how inflammation is naturally inhibited, and this is how supplemental omega-3 helps combat inflammation. NSAIDs, on the other hand, prevent this process.
This is a new finding.
Every doctor will tell you that you shouldn’t take diclofenac and similar drugs long-term. There’s a serious reason for this. Now we know more precisely why.
Diclofenac, acetaminophen, and ibuprofen are excellent pain relievers and are generally not dangerous. It’s no problem to take them for pain—as long as you take them for only one day or perhaps up to three days. We’re just learning, however, that they can actually prolong the inflammation itself as they inhibit our own production of 18-HEPE.
By the way, you can also buy and take 18-HEPE directly, just like the popular fish oils. We’re proud to offer a fish oil with a particularly high concentration of it—that’s our Resolvix.
Finally, a special case: ASA (“Aspirin”). It’s also a COX inhibitor, so it belongs in the same category. And it’s even often taken long-term to thin the blood. However, ASA works by converting COX into a form that should actually be beneficial for 18-HEPE—and thus effective against inflammation even in the long term.
Unfortunately, this has not been confirmed in human studies.
