Introduction
If you’ve been following the digestion series so far, we’ve been talking about several different places where there can be issues, or breaks in the chain of digestion. So far, we’ve covered what good digestion actually is, and then went on to talk about gut barrier dysfunction (leaky gut) and bacterial dysbiosis.
Today we’re going to be talking about acid, enzymes, and bile. Stomach acid can either be low or high, and many of the symptoms overlap considerably. Digestive enzymes are actually present all across the digestive system: In the mouth, in the stomach, in the small intestine secreted from the pancreas, and then the small intestine actually makes a few itself. Bile is created by the liver and stored in the gallbladder, and it helps to emulsify and digest fats, but it does a lot more than that. Bile is actually a critical signaling molecule as well.
We’re going to go through each of these pieces of digestion alone, and also discuss how they overlap, and how you might identify what issue is present.
The Stomach – Low or High Stomach Acid
Our stomach is a pretty impressive organ. Evolution has found a way to secrete a very powerful acid that would normally damage any other organ in the body, but the stomach has mechanisms in place to protect itself from it’s own acid. Having adequate stomach acid is incredibly important for several reasons:
- Stomach acid helps digest proteins and its presence is necessary for absorption of minerals like calcium, zinc, magnesium, iron, and other important micronutrients like folic acid and vitamin B12
- It sterilizes; meaning it kills parasites/bacteria/fungi that may be present on food. Low stomach acid is a primary risk factor for developing small intestinal bacterial overgrowth, or SIBO.
- It signals other parts of the digestive tract that food is on the way, thus priming them and ensuring good digestion all the way down the gut.
As you can see, if you have low stomach acid, you’re opening the door to development of chronic digestive issues, as well as many different micronutrient deficiencies.
Risks of low stomach acid include chronic stress, being over 60, being anemic, long term bulimia, having an autoimmune condition, chronic use of NSAIDs or other painkillers, and overconsumption of coffee and caffeine in those that are sensitive.
Let’s talk about the converse; high stomach acid. High stomach acid is going to be a little more rare than low stomach acid, but it can still happen. The main deleterious aspect of high stomach acid is that it can potentially cause ulcers and gastritis, which is inflammation of the stomach lining.
If severe gastritis is induced, then the situation will flip and the stomach will start producing significantly less acid, leading to low stomach acid. The main risk factors for high stomach acid include autoimmune conditions, food sensitivities, and H. Pylori overgrowth. H. Pylori more often causes low stomach acid, but depending on where it colonizes in the stomach and also the where in the time course of the infection we’re at, it can potentially cause high stomach acid.
In terms of food sensitivities, if you have a food sensitivity, histamine tends to be released. Histamine actually signals the stomach to produce more stomach acid; there are actually stomach acid-lowering medications that are histamine blockers. Zantac, for example, is an H2 blocker that reduces stomach acid.
Symptoms
As I mentioned earlier, the symptoms for low and high stomach acid overlap considerably – They both share these symptoms:
- Burping/belching
- Feeling excessively full after not eating much food/feeling like food is just sitting in your stomach
- Feeling bloated or stomach distension
- Heartburn/acid reflux/GERD
Yes, acid reflux can even happen with low stomach acid. It can actually occur with any level of stomach acid and isnt necessarily a problem of stomach acid levels, but more generally a problem of luminal esophageal dysbiosis, or dysbiosis of the microbiome at the bottom of the esophagus.
In any case, low stomach acid can also potentially contribute to GERD because the lower esophageal sphincter also needs a certain amount of stomach acid to signal it’s closing. If it doesn’t close, even the small amount of stomach acid that’s present can reflux into the esophagus.
Whatever issue is causing the low stomach acid can also potentially be contributing to the aforementioned esophageal dysbiosis as well.
Let’s talk about symptoms that distinguish low from high stomach acid. High stomach acid can have these additional symptoms that aren’t present with low stomach acid:
- A feeling of burning pain or discomfort in the upper abdomen below the chest, even on an empty stomach.
- Fatty food intolerance
- Nausea and occasional vomiting when/after eating
There are numerous other ways we can parse out low vs. high stomach acid, from clinical tests, which are the gold standard, to significantly rougher ways that aren’t necessarily diagnostic, but can help point you in the right direction.
As I stated earlier, the gold standard is going to be a Heidelberg Stomach Acid test. This is only done in clinics, and you’ll rarely get a western medicine doctor to run this, however. The patient generally swallows a capsule with a radio transmitter inside, and then drinks a baking soda solution to neutralize the stomach acid. The radio transmitter then measures how fast the stomach acid returns to normal, and based on the results, it can diagnose low stomach acid.
Since nearly nobody will have access to this unless there’s a very serious issue, here are a few easy, but slightly less reliable at-home tests:
- Baking soda test: Dissolve ¼ tsp of baking soda in 4 oz of water and drink, then time how long it takes you to burp. If you dont burp after 3-5 minutes, chances are you have low stomach acid.
- Note the possibility of swallowing air with the solution; if you have one small burp immediately and then nothing for 3 minutes, there’s a good chance that it was just swallowed air.
- Betaine HCl challenge
- Considered slightly more accurate than the baking soda test. When you eat a meal, take betaine HCl pills in the middle. Start with 1 and wait a few minutes, then take another. Repeat this until you feel a burning sensation in your stomach. The next time you eat, your dose is going to be 1-2 pills less than that. If you feel a burning sensation after 1-2 pills, then your stomach acid levels are most likely fine.
Digestive Enzymes
As I mentioned before, digestive enzymes are all along the digestive tract.
In the mouth, by chewing longer, you allow your salivary amylases and lipases (carb and fat digesting enzymes) to act on the food for a longer period of time, taking a load off the rest of the gut. The importance of slower eating and chewing your food well cannot be understated!
In the stomach, gastric proteases (protein digesting) and lipases (fat digesting) further act on the food in the stomach. Gastric proteases specifically also need adequate levels of stomach acid to become active.
Then the majority of enzymatic digestion comes from secretions from the pancreas. The pancreas secretes proteases, lipases, and amylases into the first part of the small intestine for continued digestion.
Finally, there are enzymes along the small intestinal wall that break down any small particles remaining into their foundational constituents (sucrose into glucose and fructose, for instance).
Since there are many organs along the digestive tract that secrete enzymes, all it takes is one of those links in the chain to start secreting less to have digestive issues.
If you’re not chewing enough, you’ll have less salivary enzyme action, which puts more of a load on the stomach and other organs to ensure good digestion. This is why its especially prudent to chew your food well if you think you’re already suffering from low stomach acid.
If you have stomach inflammation for any reason, you’re most likely going to have less active proteases and perhaps lipases.
As far as the pancreas, if you have type 1 diabetes or advanced type 2 diabetes, you’re going to have less pancreatic enzyme secretion. There’s also evidence that some cases of IBS involve a component of lower pancreatic enzyme secretion. One study found that 6.1% of people with IBS had pancreatic enzyme insufficiency, so it’s not necessarily too common. If you have digestive issues, its more likely an issue elsewhere.
Finally, if you’ve got gut barrier dysfunction, the enzymes along the intestinal wall are going to be depleted as well.
Now that you know this information, it might be intimidating to try and figure out where a potential issue might lie. The good news is that I wouldn’t try to worry over where the source of a possible enzyme deficiency is or even if you have enzyme deficiency vs. other issues like leaky gut/dysbiosis.
The solution is the same; working on the basics of digestion, and if that doesn’t work, initiating a gut protocol involving elimination of offending foods along with targeted supplementation.
Part of that targeted supplementation is going to be digestive enzymes, which can be used alone as well. We’re looking for a supplement with at least a good amount of proteases, lipases, amylases, peptidases, and other things like bromelain/etc would be a bonus. If you have gut issues, a digestive enzyme supplement is safe to add and studies show great efficacy as part of a treatment protocol for IBS.
Bile
Bile is a substance that is created in the liver from cholesterol and is stored in the gallbladder for easy release into the small intestine. It’s actually one of the main disposal routes of cholesterol in the body.
Bile emulsifies fats at the beginning of the small intestine; you can think of it as a hammer that smashes large lipid droplets into tiny ones in order to increase their surface area so that lipases can act on them to finish fat digestion. There’s several aspects of bile that can be off; we can have too much bile release, we can have too little bile release, or we can lack reabsorption.
Nearly 100% of bile that’s released into the small intestine is reabsorbed at the end of the small intestine. One of the reasons fiber and fiber supplements can help lower cholesterol is because they trap bile in the intestines and prevent it from being reabsorbed, which causes the liver to use cholesterol to make more.
In any case, it’s been known that approximately 25-33% of those with IBS-D or diarrhea dominant IBS suffer from bile acid malabsorption, so having unregulated bile acid release and bile acid reabsorption issues is most likely more common than not having enough bile.
A current hypothesis about how this may occur involves SIBO and other forms of dysbiosis disrupting bile signaling, which causes bile not to be reabsorbed. If certain bacterial populations in SIBO are present, they create beta-glucuronidases, which modify bile acids and prevent them from binding to the correct receptor, which ultimately prevents them from being reabsorbed.
Not only is this going to cause malabsorption diarrhea, but I also mentioned earlier that bile acids are also a critical signaling molecule. If the bile acids can’t bind to their receptors which cause reabsorption, they also can’t bind to the receptors that regulate metabolism. Bile acids play a strong role in both lipid and glucose homeostasis, altering insulin sensitivity negatively if they cant do their job, and they also play a role in immune system homeostasis as well.
If tons of bile acids are reaching the large intestine, as in bile acid malabsorption, this is going to induce a serious dysbiosis there, as bile acids are heavily antimicrobial. Bile acids are one of the main reasons the small intestines have a lower level of bacteria normally, and it’s seen in literature that if we experimentally stop bile flow in animals, they develop SIBO almost instantaneously. This has implications for bile acid deficiency and SIBO.
How to Test?
A rough test (not diagnostic) to see whether we’re dealing with bile acid malabsorption vs. bile acid deficiency specifically in IBS-D is testing with a few supplements. Since gel forming fibers trap bile and prevent them from causing diarrhea, if you supplement a psyllium husk fiber supplement with every meal and this alleviates your diarrhea, there is most likely bile acid malabsorption happening.
On the other side of things, if you take an ox bile supplement with meals and this takes care of your diarrhea, then it was most likely a bile acid deficiency.
The gold standard is 75SeHCAT test, which isn’t available in the US. The US gold standard is the 48 hour fecal bile acid collection done in clinic. It’s still rather rare that a gastroenterologist will run this. A blood test called 7αC4 can also be used, although this is another one thats quite hard to get as well.
Bile acid malabsorption can eventually turn into bile acid deficiency, however. Since malabsorption causes the liver to continue to make more bile, whereas this doesn’t happen in normal physiology, the liver can begin to produce less when stressed to produce more.
Fortunately, bile acid supplements are relatively cheap and widely available, and are also safe to supplement even if you’re not 100% sure you have bile acid malabsorption or insufficiency. Ideally you want to look for a supplement that lists out each bile acid and the amounts.
Conclusion
That wraps up the final part in our four part series on digestion. If you have a client with bad gut issues, diagnosed IBS or SIBO, etc, digestive enzymes and bile acid supplements are a safe bet to add. I’d make enzymes of first priority since it’s more likely they’re needed.
Check to see if your clients are suffering from a stomach acid issue. I’ve noticed in my personal experience one of the most prominent give-aways for a stomach acid issue is that feeling of food just sitting in the stomach like a rock, and/or having very early satiety from meals. If you notice that, try one of the tests above to see which issue it might be.
If you want to become a master of dealing with gut issues and truly be able to hash all this out for yourself; this is exactly what we do within our Metabolism School program, FNMS. If you’d like to learn more to see if you’re a fit, check it out here.
References
Talley NJ, Holtmann G, Nguyen QN, Gibson P, Bampton P, Veysey M, Wong J, Philcox S, Koloski N, Bunby L, Jones M. Undiagnosed pancreatic exocrine insufficiency and chronic pancreatitis in functional GI disorder patients with diarrhea or abdominal pain. J Gastroenterol Hepatol. 2017 Nov;32(11):1813-1817. doi: 10.1111/jgh.13791. PMID: 28332731.
Majeed M, Majeed S, Nagabhushanam K, Arumugam S, Pande A, Paschapur M, Ali F. Evaluation of the Safety and Efficacy of a Multienzyme Complex in Patients with Functional Dyspepsia: A Randomized, Double-Blind, Placebo-Controlled Study. J Med Food. 2018 Nov;21(11):1120-1128. doi: 10.1089/jmf.2017.4172. Epub 2018 Aug 29. PMID: 30156436; PMCID: PMC6249666.
Money ME, Walkowiak J, Virgilio C, Talley NJ. Pilot study: a randomised, double blind, placebo controlled trial of pancrealipase for the treatment of postprandial irritable bowel syndrome-diarrhoea. Frontline Gastroenterol. 2011 Jan;2(1):48-56. doi: 10.1136/fg.2010.002253. Epub 2010 Nov 3. PMID: 22095308; PMCID: PMC3009417.
Leeds JS, Hopper AD, Sidhu R, Simmonette A, Azadbakht N, Hoggard N, Morley S, Sanders DS. Some patients with irritable bowel syndrome may have exocrine pancreatic insufficiency. Clin Gastroenterol Hepatol. 2010 May;8(5):433-8. doi: 10.1016/j.cgh.2009.09.032. Epub 2009 Oct 14. PMID: 19835990.
Vijayvargiya P, Busciglio I, Burton D, Donato L, Lueke A, Camilleri M. Bile Acid Deficiency in a Subgroup of Patients With Irritable Bowel Syndrome With Constipation Based on Biomarkers in Serum and Fecal Samples. Clin Gastroenterol Hepatol. 2018 Apr;16(4):522-527. doi: 10.1016/j.cgh.2017.06.039. Epub 2017 Jun 27. PMID: 28666948; PMCID: PMC5745308.
