When you think Pseudomonas, think “food sensitivities”. 

These guys like to hang out in the upper small intestine, and they THRIVE on partially digested proteins. If you know anything about food sensitivities and how they develop, you know that undigested proteins are at the heart of the matter, working to trigger an immune response from the body. 

Usually, this happens in foods with large proteins, such as gluten or casein, though it could technically happen with any protein that fails to get broken down by the stomach acid. Food sensitivities = low stomach acid.

In one recent paper about celiac patients, the Pseudomonas aeruginosa species were found to be directly altering gluten metabolism, and were making metabolites from undigested gluten more immuno-stimulating to the body. In fact, if this marker is elevated with the presence of an increased anti-gliadin IgA marker, the two may be linked. It’s possible that normalizing the Pseudomonas aeruginosa levels could help to normalize the anti-gliadin marker in non-celiac cases. 

An interesting tidbit about these Pseudomonas meat-lovers: because they are all about them proteins, they secrete protein digesting enzymes called proteases to aid them in digesting this food. Now, usually we look at the Elastase-1 marker to determine whether or not innate pancreatic enzyme production is sufficient, aiming for a reading around 500. However, if this Elastase marker is elevated along with an overgrowth of Pseudomonas, it may be the strain’s Protease output driving the marker upward, and thus should be read with a grain of salt. 

This is especially true if the inflammation marker Calprotectin is elevated as well. Only after the strain and inflammation is under control can we get an accurate read on the Elastase marker. 

The takeaway? If you have elevated Pseudomonas, especially if you’re dealing with some food sensitivities, you’ve got to focus on your stomach acid first to remove the incoming undigested protein-fuel for this strain.

Streptococcus & Enterococcus

Both of these guys are gram-positive aerobic species, and both occur normally in our environment, upper respiratory, and oral tissue. 

Enterococcus is associated with sterile environments such as hospitals and dental offices, and is unfortunately often resistant to common antibiotic interventions for this reason. 

Enterococcus faecalis, in fact, is found in 30-90% of re-infected root canals, demonstrating its intimate relationship with the oral cavity. It’s no wonder then, that an impaired stomach acid barrier that fails to kill or neutralize the organisms as they travel down through the digestive tract, is highly associated with its overgrowth in the intestines.

Likewise, Streptococcus commonly occupies the respiratory organs, being the culprit behind scarlet fever, strep throat, and other ailments associated with that system. It’s important that when the microbe occupies our respiratory tract that stomach acid levels are sufficient to neutralize any accidental exposure that gets swallowed in the mouth.

Elevated presences of both of these strains are also associated with being risk factors in infection from another bad guy on this list: C. Diff. More evidence to throw in the pile for fixing your dang stomach acid should these markers arise.

Clostridium difficile

C Diff. – named for how difficult the species is to eradicate in those infected – may have a promising new intervention to embrace via resurrecting the stomach acid.

It’s important to mention that the GI-MAP only tests for the genes of the toxins produced by the organism: toxin A, and toxin B. It does not test for the organism itself. Regardless, if these toxins are present along with any negative symptoms such as digestive distress, it almost always warrants intervention.

Most medical professionals treat this problem with heavy antibiotics, and most functional practitioners go a similar route with potent natural antimicrobials. However, emerging research shows this infection is highly associated with insufficient stomach acid production via increased protein fermentation in the colon and the advantage this gives C. Diff to proliferate. This points to normalizing acid levels potentially diminishing this protein-fuel, and easing eradication.  

Maybe, reacidifying the tummy will prove eradicating the microbe to not be so difficult after all?

Klebsiella

Klebsiella is a common oral strain. However, its intestinal colonization has been associated with several negative health outcomes, such as inflammatory bowel disease, ulcerative colitis, and Crohn’s disease. 

In many instances, Klebsiella is resistant to common antibiotic interventions. 

The strange part? Klebsiella hangs out in our saliva, we’re literally constantly swallowing it. So when we find overgrowths of this guy, we know there’s a) a lot of dysbiotic activity happening in the intestines to allow such a common dude the opportunity to overgrow, and 2) the tummy acid is incredibly impaired when this normally present pal makes it through the furnace of the stomach. 

Helicobacter pylori

H. Pylori is a resident of the stomach – not the intestines. And let me tell you, in the functional medicine community it is con.tro.ver.sial. Discussing it with colleagues feels akin to bringing up politics at Thanksgiving. But, to be honest, in my opinion it doesn’t feel that complicated.

Some argue that because H. Pylori was found in the tummies of many ancestral populations that it can be considered a healthy symbiote whose presence is normal. I’m not sure I take issue with this, really it’s just the overgrowth of the species and resulting symptoms that is problematic, or the presence of virulent strains associated with things like cancer and ulcer. 

The thing about the GI-MAP, though, is that is it a stool test. Not a tummy test. So whatever H. Pylori numbers are showing up in the stool can be inferred to be microbes that have died and are being carried out into the stool. If there is a ton of dead H. Pylori in your stool, it likely indicates you have too much of it. 

But, also, if you just have a little in your stool - within the lab range maybe - but you have horrible symptoms of low stomach acid… girl, address that sucker!

H. pylori makes the stomach inhabitable for itself by damaging the stomach’s acid producing cells, potentially impairing the body’s long-term ability to produce acid if it goes unaddressed for long enough. 

A recent paper also describes cases where the pathology of H. Pylori actually mimicked the pathology of Celiac Disease via an inflamed mucosa. Further, when the H. Pylori was eradicated, so too were the Celiac-like symptoms. Celiacs would do well to remember this, and to be sure to test for H. Pylori if they have never done so. 

What to do about it 

If you have any of these elevated markers on your GI-MAP, I would highly suggest engaging with the process of resurrecting your stomach acid before you proceed with any intensive rebalancing protocol. The only exception to that would be if you have a pathogen presence, in which case I would suggest doing both at the same time. 

Want to get started on that tummy acid? Learn about our 4-step S.E.E.D. process here.

Did you know there are certain signs and symptoms that present with low stomach acid as well? Click here to take our free quiz to find out whether to not you have low stomach acid.