By Wayne Persky |
We're all well aware of the fact that using certain medications, including nonsteroidal anti-inflammatory drugs, (NSAIDs), especially when used for long-term treatment, is associated with the development of microscopic colitis (MC). And after the disease develops, their use tends to trigger a flare. In a study of 155 adult subjects, researchers compared the respective drug use of those subjects for the prior 30 days, with a stool specimen that each of them submitted (Rogers, and Aronoff, 2016).1 Interestingly, it was clear that certain drugs had established unique microbiome populations.
Compared with those who were using no medications,
for example, those who were using aspirin, showed gut bacteria populations that consisted primarily of Prevotella spp. (spp. is an abbreviation standing for the plural of species), Bacteroides spp., Family Reminococaceae, and Bamesiella spp.. Those using celecoxib or ibuprofen, showed higher population levels of Acidaminococcaceae and Enterobacteriaceae. Distinctive gut bacteria population patterns could be distinguished by the combination of medications that the subjects were using. So it's quite clear that using any drugs in this class alters our gut bacteria population to attain a specific profile, unique to that combination of medications.
While that's interesting, it tells us nothing about the actual mechanism by which medications can lead to intestinal inflammation.
What we would really like to know is, “Why do certain medications lead to gut inflammation?” An important clue can be found in the process that the body's immune system uses to protect the gut against inflammation. A recent study led by researchers at Harvard Medical School suggests that any attempts to use medications to block pain may actually lead to increased intestinal damage (Yang, Jacobson, Meerschaert, Sifakis, Wu, Chen, and Chiu, 2022).2
The pain is there for a reason,
and attempting to block it, or ignore it, rather than treating the cause of that pain, is likely to be counterproductive. The reason for that, as pointed out in a Medscape article that discusses the research, is that the pain may be a key part of the process that the body uses to protect the intestines from further damage (Shiffer, 2022, November 21).3
As the Medscape article points out, the researchers looked at pain neurons in the intestinal linings of mice, and how those neurons help to regulate the release of protective mucus as a response to inflammation. The process is defined in detail by the research article (anyone who wishes to review the actual details of the process should click on the links to the references), but to cut to the chase, their research findings suggest that interfering with the mucus production process can lead to dysbiosis, and raise the risk of an adverse event, such as the development of IBD.
As the Medscape article points out, the researchers looked at pain neurons in the intestinal linings of mice, and how those neurons help to regulate the release of protective mucus as a response to inflammation. The process is defined in detail by the research article (anyone who wishes to review the actual details of the process should click on the links to the references), but to cut to the chase, their research findings suggest that interfering with the mucus production process can lead to dysbiosis, and raise the risk of an adverse event, such as the development of IBD.
Many newly diagnosed MC patients complain of excess mucus production.
But the mucus is simply a sign of intense intestinal inflammation. It's the body's last-ditch protective efforts to prevent additional intestinal damage. And in view of this research evidence, we have to conclude that the presence of copious amounts of mucus in our stool is a good thing. Although it clearly implies that our digestive system is highly inflamed, it also reveals that our immune system is doing everything within it's power to attempt to prevent additional intestinal damage. And as always, the proper treatment involves doing everything we can to prevent the inflammation from recurring, rather than to treat the symptoms.
That means carefully following a safe diet at all times.
And rather than looking for medications to block the pain, it's much more effective to prevent the pain from occurring in the first place, by preventing the inflammation. As the research cited above shows, using medications to block the pain caused by an MC reaction will probably lead to an increase in intestinal damage, which will eventually lead to increased pain. That's counterproductive, and it's a good example of jumping from the frying pan into the fire.
References
1. Rogers, M. A. M., and Aronoff, D. M. (2016). The Influence of Nonsteroidal Anti-Inflammatory Drugs on the Gut Microbiome. Clinical Microbiology and Infection, 22(2), 178. e1-178.e9. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4754147/
2. Yang, D., Jacobson, A., Meerschaert, K. A., Sifakis, J. J., Wu, M., Chen, X., and Chiu, I. M. (2022). Nociceptor neurons direct goblet cells via a CGRP-RAMP1 axis to drive mucus production and gut barrier protection. Cell, 185(22), P4190-4205.e25. Retrieved from https://www.cell.com/cell/fulltext/S0092-8674(22)01196-5?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS0092867422011965%3Fshowall%3Dtrue
3. Shiffer, E. (2022, November 21). Are Pain Meds Bad for Your Gut? Retrieved from https://www.medscape.com/viewarticle/984416?src=mkm_ret_230121_mscpmrk_neuro_brain-diet&uac=95382HN&impID=5102249