I recently found something in a drawer that stopped me in my tracks. A printed document — slightly yellowed, the kind of thing you print off at 11pm when you're deep in a research rabbit hole and the internet is still mostly text. I must have found it in the early 2000s. The title: Three Years of HCL Therapy. Published in The Medical World. Philadelphia, 1935. Republished by the Arthritis Trust of America, furnished for clinical education.
I sat down and read it again. The clinical observations in that document — hydrochloric acid as a critical component of immune defence, low stomach acid as a driver of pathogen vulnerability, nutritional malabsorption, and systemic dysfunction — are indistinguishable from what I see in clinical practice today. Ninety years ago, practitioners were documenting in detail what happens when the stomach fails to produce adequate acid. They were supplementing with HCl therapeutically and recording the results. The mechanism was understood.
And yet the default clinical response to stomach acid symptoms in 2026 remains the prescription of medication that reduces the already-insufficient acid further.
The biology hasn't changed. The evidence has been sitting in the literature for nearly a century. What's changed is that we now have a test — the GI-MAP — that measures the downstream consequences of low stomach acid directly: H. pylori load, pancreatic elastase output, pathogen burden, microbiome disruption. The 1935 practitioners were working from clinical observation and case evidence. We can now see it in the data. The picture they described is the same one.
The conventional medical concern about stomach acid runs almost entirely in one direction: too much. Antacids are one of the most widely sold over-the-counter medications on earth. Proton pump inhibitors — omeprazole, lansoprazole, esomeprazole — are among the most commonly prescribed drugs in the UK, taken by millions of people daily, many of whom have been on them for years without the original prescribing indication being revisited. The clinical obsession is with reducing stomach acid.
The functional medicine concern runs in precisely the opposite direction. In clinical practice, low stomach acid — hypochlorhydria — is one of the most common and most consequential findings in people with chronic gut problems, nutritional deficiencies, recurrent infections, and persistent food reactions. It is also almost never tested, because standard medicine has no routine test for it and no treatment interest in it beyond the prescription of acid-reducing medication for conditions where acid excess is assumed.
Understanding what stomach acid actually does — and what happens across every system downstream when it is insufficient — reframes the entire gut health conversation.
What Stomach Acid Actually Does
The stomach produces hydrochloric acid through specialised parietal cells in the gastric lining. At optimal function, gastric pH sits between 1.5 and 3.5 — highly acidic by any measure, and deliberately so. This extreme acidity is not incidental. It serves several specific and essential functions that cannot be replaced by anything further downstream.
Protein digestion. Pepsinogen — the inactive precursor of pepsin, the primary protein-digesting enzyme — is only activated by gastric acid. At pH above 4, pepsinogen remains largely inactive. Without adequate acid, protein digestion begins not in the stomach, where it should, but in the small intestine — inadequately, incompletely, and with consequences. Partially digested protein fragments arriving in the small intestine are antigenic — the immune system recognises them as foreign and mounts an IgG response. This is one of the primary mechanisms through which low stomach acid drives food sensitivity. The immune reaction is not to the food — it is to the incompletely digested proteins that low stomach acid failed to break down properly.
Mineral absorption. Iron, calcium, magnesium, zinc, and copper all require an acidic gastric environment for ionisation and absorption. As gastric pH rises, mineral absorption falls significantly. This is the clinical mechanism behind the iron deficiency anaemia and osteoporosis risk associated with long-term PPI use — findings that are well-documented in the literature but rarely discussed with patients at the point of prescription. Ferritin that does not respond to oral iron supplementation is a common presentation in people with hypochlorhydria. The iron is being supplemented. It is not being absorbed.
B12 absorption. Intrinsic factor — required for B12 absorption in the terminal ileum — is produced by the same parietal cells that produce hydrochloric acid. Low acid, low intrinsic factor, low B12 absorption. B12 deficiency presenting as fatigue, cognitive difficulty, and neuropathic symptoms in an older adult is frequently attributed to dietary insufficiency when the mechanism is often gastric insufficiency.
Microbial defence. The stomach is the body’s primary microbiological checkpoint. Food passing through the mouth carries enormous microbial loads — bacteria, yeasts, and pathogens that enter with every meal. At gastric pH 1.5–3.5, most of these organisms are killed before they reach the small intestine. As pH rises above 4, then above 5, pathogenic survival increases dramatically. The organisms that should be destroyed in the stomach survive into the small intestine, where they can establish and proliferate. This is the most important single upstream cause of SIBO — small intestinal bacterial overgrowth — in people with hypochlorhydria. SIBO treated without addressing low stomach acid will recur, because the mechanism that allowed it to establish remains in place.
Cephalic phase signalling. Adequate gastric acid stimulates the release of secretin from the duodenum, which triggers pancreatic enzyme and bicarbonate secretion. It stimulates cholecystokinin, which triggers bile release from the gallbladder. The entire downstream enzyme and bile cascade depends on the appropriate acidification of chyme leaving the stomach. Low gastric acid produces a cascade of downstream insufficiency: insufficient pancreatic enzymes, insufficient bile, and the fat malabsorption, carbohydrate fermentation, and protein antigenicity that follow.
The Symptoms of Low Stomach Acid
Common presentations of hypochlorhydria
Heartburn is the symptom most associated with excess stomach acid. In clinical practice, heartburn in people who have been eating a high-carbohydrate diet, who are under chronic stress, who have H. pylori, or who are over fifty is more commonly a sign of insufficient acid producing carbohydrate fermentation and gas pressure than of acid excess. The reflex is acid. The direction of the problem is often opposite to what treatment assumes.
The H. Pylori Connection
Helicobacter pylori — the pathogenic organism identified by Marshall and Warren in 1983 for which they received the Nobel Prize in 2005 — colonises the gastric mucosa and actively suppresses stomach acid production as a survival mechanism. H. pylori secretes urease, which converts urea to ammonia — raising the local pH around the organism to protect it from the acid that would otherwise destroy it. In doing so, it progressively reduces the acid output of the stomach it inhabits.
This creates a self-perpetuating cycle. H. pylori reduces acid. Reduced acid allows other organisms to survive the stomach. A less acidic environment is more permissive to H. pylori’s own spread and to other colonisers. The dysbiotic environment that follows is both a consequence of H. pylori and a condition that makes further dysbiosis more likely.
H. pylori is present in approximately fifty percent of the global population and forty percent of adults in developed countries. The majority are asymptomatic — at low load with low-virulence strains, the organism coexists with its host without causing overt pathology. But even at loads below the threshold for frank gastric ulceration, H. pylori’s acid-suppressing activity is clinically relevant in people with nutritional deficiencies, food sensitivities, and recurrent gut dysbiosis. The GI-MAP tests not just H. pylori presence but quantitative load and virulence factors — CagA and VacA — that determine how aggressively the organism is behaving.
The SIBO Cascade
The connection between low stomach acid and SIBO is mechanistic and direct. Remove the acid checkpoint, and organisms that enter with food survive to the small intestine. The small intestine — designed as an absorptive organ, not a fermentation chamber — has far fewer defence mechanisms than the stomach against microbial colonisation. Once established, small intestinal bacterial communities ferment dietary carbohydrates, consume B12 and B-vitamins, deconjugate bile acids, and damage the gut lining. The gas produced — hydrogen and methane — generates the bloating, distension, and altered motility characteristic of SIBO.
Treating SIBO with antimicrobials while leaving low stomach acid unaddressed is the most common reason SIBO recurs after treatment. The clearance protocol kills the established overgrowth. But the open door — the stomach that is no longer acidic enough to sterilise incoming food — allows the overgrowth to re-establish from each subsequent meal. This is the clinical reality behind the frustrating pattern of SIBO treated, SIBO returned.
What Causes Low Stomach Acid
Several factors consistently reduce gastric acid output. Chronic stress — sympathetic nervous system dominance suppresses the parasympathetic state required for the cephalic phase of digestion. The acid-producing reflex begins with the smell, sight, and anticipation of food — a purely parasympathetic process. Under chronic stress, this reflex is blunted before a meal begins. H. pylori infection, as described above. Age — gastric acid output declines progressively from around thirty onwards; by seventy, a significant proportion of adults produce markedly insufficient acid. Zinc deficiency — zinc is required for carbonic anhydrase, the enzyme involved in hydrochloric acid production. Proton pump inhibitors — obviously. And low protein intake, because protein ingestion is one of the primary stimuli for gastric acid secretion.
Betaine HCl — The Clinical Intervention
Betaine hydrochloride is a supplement form of hydrochloric acid — betaine (trimethylglycine) bonded to hydrochloric acid. Taken with protein-containing meals, it delivers additional acid to the stomach to supplement insufficient endogenous production. It is not a pharmaceutical. It is available without prescription. And used correctly, it is one of the most clinically significant gut interventions available — not because it treats a condition, but because it restores a physiological function that allows everything downstream to work correctly.
The starting dose is typically one capsule (usually 300–650mg of Betaine HCl with pepsin) with the first few bites of a protein-containing meal. Dosing is titrated upward by one capsule per meal every two to three days until a mild warmth is felt in the stomach — indicating that acid levels are now appropriate — at which point the dose is reduced by one capsule. The warmth sensation is the practical endpoint of titration.
Betaine HCl is contraindicated in active peptic ulcer disease, gastritis, or oesophagitis — conditions where the gastric lining is already inflamed and additional acid will worsen rather than help. It should not be taken alongside NSAIDs or aspirin. If H. pylori infection has been identified on GI-MAP, it should be addressed before Betaine HCl supplementation is introduced — adding acid to a stomach with active H. pylori gastritis may cause discomfort. Always introduce at low dose and titrate slowly. If in doubt, work with a practitioner.
Apple Cider Vinegar — The Less Concentrated Alternative
Apple cider vinegar — a tablespoon in a small amount of water, taken ten to fifteen minutes before a protein-containing meal — provides a modest acidifying effect through acetic acid. It is considerably less potent than Betaine HCl and in most cases of established hypochlorhydria is insufficient as a sole intervention. However, it serves a useful role in people who are not ready for Betaine HCl, as a gentle digestive bitter that also stimulates the cephalic phase reflex through taste, and in people whose acid insufficiency is mild rather than severe.
The bitter taste of ACV — and of bitter foods more broadly, bitters tinctures, and digestive aperitifs — stimulates gastric acid secretion through the vagal reflex before food arrives. This is the mechanism behind the pre-meal bitter aperitif that has existed in every traditional food culture, in various forms, for centuries. It was clinical knowledge before it was culinary tradition.
Sodium Bicarbonate — The Opposite Intervention
Sodium bicarbonate is alkaline — it neutralises stomach acid rather than supplementing it. In the context of confirmed gastric acid excess, acute heartburn, or as a post-meal alkalinising agent in specific circumstances, it has a role. In the context of hypochlorhydria, it is precisely the wrong intervention — it further reduces an already insufficient acid level. The widespread use of sodium bicarbonate and antacids for heartburn that is caused by low acid rather than high acid is one of the more ironic misapplications in common self-treatment.
The practical distinction: heartburn that occurs immediately with meals or within thirty minutes, that is associated with belching and bloating, and that is worse after high-carbohydrate meals is more likely to reflect low acid and fermentation gas pressure. Heartburn that occurs one to two hours after meals, that is relieved by food, and that is associated with a burning sensation rising toward the chest is more consistent with excess acid or reflux from mechanical causes. This clinical distinction guides whether acid support or acid suppression is the appropriate direction.
The Mucosal Barrier Connection
Adequate gastric acid maintains the integrity of the gastric mucosal barrier — the thick layer of bicarbonate-rich mucus that protects the stomach lining from its own acid. When acid output is chronically low, the signals that maintain mucosal thickness are diminished. Paradoxically, hypochlorhydria can produce a fragile gastric lining that is less well-protected than a normally acidic stomach with a robust mucosal layer. H. pylori exploits exactly this vulnerability — it damages the mucosa, reduces acid, and colonises the resulting less-protected environment.
Mucosal barrier support — distinct from gut barrier repair in the small intestine — is relevant alongside stomach acid support in people with established H. pylori history or chronic gastric symptoms. Zinc carnosine has the most robust evidence for gastric mucosal protection and healing. Deglycyrrhizinated liquorice (DGL) is the traditional botanical support for gastric mucosa. Both work upstream of the small intestine gut repair sequence that L-glutamine and collagen address.
Has H. pylori been tested and addressed? GI-MAP provides quantitative H. pylori assessment including virulence factors. If positive, address before introducing Betaine HCl.
Is ferritin not responding to oral iron? Suspect hypochlorhydria as the absorption barrier rather than insufficient dose. Address acid before increasing iron.
Is SIBO recurring after treatment? Assess stomach acid as the upstream cause. Betaine HCl post-treatment is standard practice in the TDG gut protocol.
Are multiple food sensitivities developing? Consider incompletely digested protein antigenicity from insufficient pepsin activation as a contributing mechanism.
Is the person on a PPI? Work with their prescribing practitioner to review whether the original indication is still current. Long-term PPI use without review is one of the most common modifiable causes of hypochlorhydria and its downstream consequences.
The stomach acid story is the story of where gut problems actually begin — not in the colon, not in the small intestine, but at the first chemical checkpoint of the digestive tract. A stomach producing insufficient acid sends incompletely digested protein into a small intestine that was not designed to finish the job, sends insufficiently sterilised food into an environment that can be colonised by what the stomach should have killed, and fails to trigger the downstream enzyme and bile cascade that fat absorption and nutrient delivery depend on. Addressing this upstream — before spending time and money on probiotics, gut repair nutrients, and antimicrobials that cannot fully succeed against an open upstream door — is what a logical gut protocol looks like.
Test, don’t guess. The GI-MAP identifies H. pylori, Candida, and the microbial consequences of hypochlorhydria. Low elastase on the GI-MAP reflects the downstream enzyme insufficiency. The Betaine HCl challenge — described above — is the practical functional assessment. Together they establish whether stomach acid is the upstream driver that needs addressing before anything else.