Low Stomach Acid: What’s Real, What Isn’t, and How to Check

Some years ago I found a printed document in a drawer, the kind of thing you print at 11pm when the internet is still mostly text. The title was Three Years of HCL Therapy, from The Medical World, Philadelphia, 1935, republished by the Arthritis Trust of America. Its authors were giving hydrochloric acid to patients and writing down what they saw.

I used to read that as proof that the old practitioners knew something modern medicine had forgotten. It's history, not evidence. Case reports from 1935 can't tell you whether people improved because of the acid, and the idea behind them, that stomach acid runs low in most people as they age, was later tested and didn't hold up. This page sets out what did hold up, what didn't, and how low stomach acid is actually checked.

What’s real

Low stomach acid (hypochlorhydria) is a real condition with known causes:

• Atrophic gastritis: long-term inflammation that destroys the acid-making glands of the stomach lining. It is mostly caused by H. pylori infection, and sometimes by autoimmunity (Shah 2021, AGA clinical practice update).
• Stomach surgery, including some weight-loss operations.
• Acid-suppressing medicines: PPIs such as omeprazole and lansoprazole, and H2 blockers.

It matters for three reasons:

• Vitamin B12. Intrinsic factor, which you need to absorb B12, is made by the same cells that make acid.
• Iron. The AGA update advises checking for atrophic gastritis in people with iron or B12 deficiency that has no other explanation (Shah 2021).
• Some medicines need an acid stomach to be absorbed.

Atrophic gastritis also raises the risk of stomach cancer, which is why it’s confirmed by biopsy and some people are offered surveillance (Shah 2021). Grade: well established.

That last point is why this page exists. If you genuinely have low stomach acid, that is a diagnosis that needs working up, not a supplement decision.

Doesn’t stomach acid fall with age?

That was mainstream medicine’s view for about sixty years. It came from a large Mayo Clinic series of gastric acid measurements published in 1932 (Vanzant and colleagues, Archives of Internal Medicine; pre-dates PubMed, so I haven’t been able to check it against the original). Functional medicine inherited the idea honestly.

Later studies separated age from what the 1932 data were really picking up:

• In healthy adults, the older group (44 to 71) secreted more acid than the younger group, not less. Age had an independent positive effect on acid output; H. pylori infection had a negative one (Goldschmiedt 1991).
• In healthy older men without atrophy, acid output was the same as in young men. Atrophic gastritis was the only factor that independently lowered it (Katelaris 1993).
• In 248 independently living adults aged 65 and over, 84% had acidic stomach contents at rest. Most of the consistent low-acid group had blood markers of atrophic gastritis (Hurwitz 1997).

Grade: strong for the correction. Acid falls with atrophic gastritis, which becomes more common with age, not with age itself. One small study disagrees: 12 of 15 healthy people aged 80 to 91 had low acid, without checking for atrophy (Husebye 1992). It doesn’t overturn the larger studies, but it is there. The 1932 cohort lived before H. pylori was discovered in 1983, so nobody could have separated the two.

Is heartburn a sign of low acid?

This is the claim I used to make on this page, and I was wrong to make it as a general rule.

• People with reflux disease had higher meal-stimulated acid secretion and stomach acidity than healthy controls (Gardner 2003).
• In reflux oesophagitis, peak acid output was one of three independent factors, alongside poor acid clearance from the oesophagus and a weak lower sphincter (Cadiot 1997).
• H. pylori lowers acid output. If low acid caused reflux, infection would make reflux more common. In practice it is associated with less reflux, not more.

Grade: the “usually low acid” claim is contradicted. Reflux isn’t always a high-acid problem either; it is mostly about the valve between the stomach and the oesophagus, and anything that distends the stomach (large meals, a hiatus hernia) can trigger it. There is no reliable way to tell from the timing of your heartburn whether acid is high or low, so I’ve removed the rule of thumb this page used to give.

How low stomach acid is actually checked

What doesn’t check it:

• Symptom checklists.
• The “take capsules until you feel warmth” test.
• Stool tests. The GI-MAP can pick up H. pylori and shows how well you digest fat and protein, but it doesn’t measure stomach acid.

Research studies measure stomach pH directly with a swallowed capsule, but that isn’t a routine test.

Betaine HCl: what the evidence actually says

Betaine hydrochloride is sold as a stomach acid supplement. Here is everything I can find on it in people:

• It does acidify the stomach, briefly. In six volunteers whose acid had been switched off with a PPI, a single dose brought stomach pH down within minutes, for a little over an hour (Yago 2013).
• Food gets in the way. After a meal, the lower doses tested didn’t re-acidify the stomach at all. Only a dose several times larger than a typical capsule did (Surofchy 2019).
• Every human study was in drug-induced low acid, and all of them were about helping medicines absorb. I can’t find a single trial of betaine HCl for indigestion, reflux, bloating or any other symptom.
• The US regulator ruled on it in 1988. The FDA found that betaine hydrochloride is not generally recognised as safe and effective as an over-the-counter stomach acidifier (21 CFR 310.540). That is a finding about the evidence submitted, not proof it doesn’t work. But it is why it moved from the pharmacy shelf to the supplement shelf.

Grade: no trial evidence for any symptom.

The warmth test has no validation. Raising the number of capsules until you feel warmth or burning, then dropping back one, has never been checked against a pH measurement. It asks someone whose complaint may be burning to produce more burning and treat it as a dosing signal, with no way to tell that from harm. I don’t recommend it, and I’ve removed it from this page.

Acid supplements are also not for anyone with an ulcer or gastritis, or anyone taking NSAIDs (ibuprofen, aspirin and similar) or steroid tablets. If you are already taking betaine HCl and feel better, that’s worth discussing at a consultation rather than stopping in a panic, but it’s a reason to check for the conditions above, not to keep going without knowing.

Apple cider vinegar

A PubMed search on 5 October 2026 found no randomised trial of vinegar for heartburn or indigestion. Grade: none. What is known is that vinegar is an acid and regular use can erode tooth enamel, which matters more if your teeth already meet refluxed acid.

Antacids and sodium bicarbonate

Antacids, including sodium bicarbonate, neutralise acid that’s already there. They give short relief and are fine occasionally. Sodium bicarbonate carries a lot of sodium, which matters if you’ve been told to limit salt. Grade: standard pharmacology. If you need them most days, that’s a reason to see your GP rather than a sign of low acid.

The PPI question, treated the same way

The functional critique of PPIs isn’t empty, but the parts that hold up aren’t always the ones usually quoted.

• Rebound is real. In a randomised trial, 44% of healthy volunteers given a PPI for 8 weeks developed acid symptoms after stopping, against 15% on placebo (Reimer 2009). So stopping is a conversation with your prescriber, with a taper, not a self-experiment. A failed attempt to stop doesn’t prove you needed the drug. Grade: strong.
• Iron: taking acid-suppressing medicines for 2 years or more was associated with a higher risk of iron deficiency in a large case-control study (Lam 2017). Grade: observational.
• Bone, kidney and dementia: associations have been reported in observational studies. The large randomised trial (17,598 people, about 3 years) found no difference in fractures, kidney disease, dementia, pneumonia or deaths, and only a small rise in gut infections (Moayyedi 2019). Grade: not supported by the trial; three years isn’t a lifetime.
• SIBO: the link with PPIs depends on the test. It showed up when SIBO was diagnosed by culturing fluid from the small intestine, but not with the glucose breath test (Lo 2013). A large breath-test study found no link at all (Ratuapli 2012). Grade: mixed. The wider claim that low stomach acid is “the most common cause of SIBO” is mechanistic and untested, and I’ve removed it.

The honest summary: PPIs work, are over-prescribed and under-reviewed, and are hard to stop because of rebound. Asking your GP whether you still need one is reasonable. The alternative usually offered, acid supplements, has no trial evidence at all, which is a weaker position than the drug it’s meant to replace.

The stomach lining

Zinc carnosine and DGL (deglycyrrhizinated liquorice) are often suggested to support the stomach lining. Grade: traditional use; trial evidence for using them on your own is thin. Neither is a substitute for finding out why the lining is irritated.

Sources

1. Goldschmiedt M et al. Effect of age on gastric acid secretion and serum gastrin concentrations in healthy men and women. Gastroenterology 1991;101(4):977–90. PMID 1889722. doi
2. Katelaris PH et al. Effect of age, Helicobacter pylori infection, and gastritis with atrophy on serum gastrin and gastric acid secretion in healthy men. Gut 1993;34(8):1032–7. PMID 8174948. doi
3. Hurwitz A et al. Gastric acidity in older adults. JAMA 1997;278(8):659–62. PMID 9272898.
4. Husebye E et al. Fasting hypochlorhydria with gram positive gastric flora is highly prevalent in healthy old people. Gut 1992;33(10):1331–7. PMID 1446855. doi
5. Gardner JD et al. Meal-stimulated gastric acid secretion and integrated gastric acidity in gastro-oesophageal reflux disease. Aliment Pharmacol Ther 2003;17(7):945–53. PMID 12656697. doi
6. Cadiot G et al. Multivariate analysis of pathophysiological factors in reflux oesophagitis. Gut 1997;40(2):167–74. PMID 9071926. doi
7. Zagari RM et al. Diagnostic performance of the combination of pepsinogen, gastrin-17 and anti-H. pylori antibodies serum assays for the diagnosis of atrophic gastritis. Aliment Pharmacol Ther 2017;46(7):657–67. PMID 28782119. doi
8. Shah SC et al. AGA clinical practice update on the diagnosis and management of atrophic gastritis. Gastroenterology 2021;161(4):1325–32. PMID 34454714. doi
9. Yago MR et al. Gastric reacidification with betaine HCl in healthy volunteers with rabeprazole-induced hypochlorhydria. Mol Pharm 2013;10(11):4032–7. PMID 23980906. doi
10. Surofchy DD et al. Food, acid supplementation and drug absorption — a complicated gastric mix: a randomized control trial. Pharm Res 2019;36(11):155. PMID 31485804. doi
11. US Code of Federal Regulations, 21 CFR 310.540: drug products containing active ingredients offered over-the-counter for use as stomach acidifiers (Federal Register 53 FR 31271, 1988).
12. Reimer C et al. Proton-pump inhibitor therapy induces acid-related symptoms in healthy volunteers after withdrawal of therapy. Gastroenterology 2009;137(1):80–7. PMID 19362552. doi
13. Lam JR et al. Proton pump inhibitor and histamine-2 receptor antagonist use and iron deficiency. Gastroenterology 2017;152(4):821–9. PMID 27890768. doi
14. Moayyedi P et al. Safety of proton pump inhibitors based on a large, multi-year, randomized trial of patients receiving rivaroxaban or aspirin. Gastroenterology 2019;157(3):682–91. PMID 31152740. doi
15. Lo WK, Chan WW. Proton pump inhibitor use and the risk of small intestinal bacterial overgrowth: a meta-analysis. Clin Gastroenterol Hepatol 2013;11(5):483–90. PMID 23270866. doi
16. Ratuapli SK et al. Proton pump inhibitor therapy use does not predispose to small intestinal bacterial overgrowth. Am J Gastroenterol 2012;107(5):730–5. PMID 22334250. doi
17. NICE. Suspected cancer: recognition and referral (NG12).

Updated 5 October 2026. This page used to recommend betaine HCl and apple cider vinegar with doses, a warmth-based titration, and a rule for telling low-acid from high-acid heartburn. None of those survived checking, and they’ve been removed. The record of changes is on the corrections page.