Low Stomach Acid: Everything You Need To Know

What Is Stomach Acid?

The stomach produces secretions to help facilitate digestion. 

Stomach secretions contain hydrochloric acid, digestive enzymes (e.g. pepsinogens, lipase), mucus, and water.1 

Hydrochloric acid (HCL) is the primary acid produced by our stomach which helps to acidify stomach contents.2 

The main purpose of stomach acid is thought to be the inactivation of harmful ingested microbes and pathogens, which works to reduce the risks of intestinal infections.3 

Acidification also helps to break down the structure of ingested foods to promote better digestion and absorption of certain micronutrients and proteins, while limiting excessive bacterial growth in the small intestine.3,4  

The production of stomach acid is an energy-consuming, and sometimes even hazardous task (e.g. acid-related diseases) that is found in all vertebrates.3 
The conservation of stomach acid in multiple species over time reflects the biological significance of stomach acid for survival and general fitness.3 

What Is Normal Stomach Acidity?  

The pH scale ranges from 0-14, with a lower pH being more acidic, and a higher pH being less acidic. A pH of 7 is considered to be neutral. 

The pH of our stomach is most acidic while we’re fasting.

During the fasted state, the volume of stomach secretions is low; just under an ounce, with a fluid secretion rate of only 1 ml per minute, and a total fasted volume around 25 mLs. After eating a meal, the secretion rate drastically increases up to 10–50 mLs per minute, with total stomach juice volume reaching as much as 2–3 liters per day. 1 

Fasting stomach pH can vary from person to person, with a typical fasting stomach pH having been shown to range from 0.3 to 2.5.1,5 

A fasting stomach pH of less than 3.0 is considered normal.6 

Fasting values above a pH of 3.0 are deemed to be gradually more hypochlorhydric6  

While stomach acid production begins to ramp up after meals, it’s important to note that it’s normal for stomach acidity to be reduced temporarily after meals due in part to the pH buffering effect of food.1  

Physiologically, the stomach pH immediately rises up to a 4.5 to 5.8 range after meals, but it falls to less than 3.1 within 1 hour after the meal.1  

Even more, the contents of our stomach are not uniformly acidic after ingesting meals. 

At the top of the stomach lies a 1.0-3.0 cm undiluted acid pocket that sits on top of our ingested meal.7 

Parts of the meal may remain in the upper portion of the stomach for up to 2-3 hours undiluted by stomach secretions, followed by a gradual diffusion of stomach acid into the meal.7  

The rate at which stomach acid infiltrates the food in our stomach can vary from person to person and may partly be related to the composition of the foods we eat (e.g. certain macronutrients, solids, liquids, or blenderized foods) our emotional state, individual rates of stomach emptying into the small intestines, and stomach contraction patterns. 

Certain digestive enzymes that break down carbohydrates or fats (some of which are remnants from early digestion in the mouth) become inactive with a more acidic pH. For instance, salivary amylase begins digestion in the mouth but is deactivated when it enters the acidic enviroment of the stomach. Other digestive enzymes, which breakdown protein, work more efficiently in the stomach when it is highly acidic.7 

The lack of a uniform acidity of our stomach contents along with the rate of stomach acid diffusion into meal contents may allow for partial digestion of carbohydrates and fats during a pH plateau, followed by diffusion of stomach acid which assists with protein digestion, vitamin and mineral absorption, and destruction of potentially harmful pathogens.7 

When Does Reduced Stomach Acid Become A Problem? 

Low stomach acidity is problematic when it’s not simply a transient response to a meal but a chronic occurrence, with a low fasting pH within the normal range not being achieved on a routine basis. 

A stomach pH that routinely remains at 4.0 or greater is called hypochlorhydria.8 A diagnosis of hypochlorhydria means levels of hydrochloric acid in the stomach are low.

A true lack of stomach acidity, or achlorhydria, has been defined in the following three ways:

1. An intragastric pH greater than 5.09 in men and greater than 6.81 in women.
2. A maximal acid output of less than 6.9 m/mole/h in men and less than 5.0 m/mole/h in women.
3. A ratio of serum pepsinogen I/pepsinogen II of less than 2.9.9 

Achlorhydria is characterized by very limited acid production even when medically stimulated by acid-promoting histamine or the acid-stimulating hormone, gastrin.6 

Low stomach acidity can also present at meal time, with some individuals showing an excessively prolonged amount of time to re-acidify the contents of the stomach after ingesting a meal, even in the setting of a normal acidic fasted stomach pH.6 

Two decades ago, the University of Michigan performed studies on younger and older participants to measure stomach re-acidification after a meal. The time it took to re-acidify the stomach to a pH of 3.0 happened within 42 minutes on average for younger participants, but was 89 minutes in the older subjects, averaging nearly an hour longer to reach a pH of 2.0.6 

16.4% of the elderly subjects did not return to a pH of 2.0 within four hours.6 

These data suggest that a decline of gastric acid secretion may gradually worsen with aging, which cannot be readily detected in the fasted state6

What Causes Low Stomach Acidity? 

While there are multiple reasons why chronic low stomach acidity might occur, most causes are related to one of the three following root problems:  

1. Destruction of our acid-secreting parietal cells
2. Altered parietal cell functioning 
3. Neutralization of stomach secretions

Let's run through these 3 now.

• 1. Destruction of our acid-secreting parietal cells

• Chronic Atrophic Gastritis Type A  

  • Autoimmune disorder which stimulates production of parietal cell antibodies.10 
  • Destroys parietal cells and gastric glands10 
  • May result in failure to secrete hydrochloric acid and intrinsic factor (protein produced by the parietal cells which aids B12 absorption).10 When severe can lead to B12 deficiency (if not treated)  pernicious anemia (enlarged red blood cells) and nerve destruction10 
  • Pernicious anemia results from chronic achlorhydria10 
  • Iron deficiency is also common occurring in 50% of individuals with autoimmune atrophic gastritis.11  
  • Autoimmune atrophic gastritis is a rare disorder that’s often associated with other autoimmune conditions, such as Hashimoto thyroiditis, type 1 diabetes mellitus, and Addison disease.11 

  Chronic Atrophic Gastritis Type B (Helicobactor pylori infection) 

  • Inflammatory disease of the stomach caused by pathogen H. pylori10 
  • Cause of more than 90% of gastritis cases12 
  • Inflammatory response to infection damages the parietal cell mass and releases acid-inhibiting compounds (interleukin 1beta)10 
  • Of note, H. pylori infection is capable of causing both high and low levels of stomach acid.
  • If the infection is localized to the antrum of the stomach (the lower grinding portion), it may cause excessive release of the acid-stimulating hormone gastrin OR inhibit acid-regulating somatostatin from being released.10 If there is a healthy amount of parietal cells that have not yet atrophied due to inflammation, this can result in high levels of stomach acidity.10 
  • Can cause gastric atrophy 10
  • Can also result in stomach cancers (gastric adenocarcinoma and MALT lymphoma)10 
  • Treatment and eradication of H. pylori with antibiotics can reverse inflammatory changes, but cannot reverse atrophy that has already occurred to the acid and intrinsic factor secreting parietal cells.10
  • Medical treatment is imperative, but if lasting damage exists, special attention may need to be paid to avoid nutrient deficiencies (e.g. B12, Iron)

• 2. Altered parietal cell functioning

• A)  Use of antisecretory medications:9  

• i)  Proton Pump Inhibitors
• PPIs are the most effective drugs for treating acid-related diseases, blocking stimulation of stomach acidity by three primary stimulators of stomach acid production: gastrin, histamine, and acetylcholine.10 
• (see supplementary materials at the end for more information about acid production and regulation)
• Works by blocking the proton pump found on parietal cells.10 
• Commonly used to treat acid-related conditions such as gastroesophageal reflux disease (GERD), peptic ulcers, or excessive and damaging acid production found in Zollinger-Ellison disease.10 
• However, overuse of PPIs to treat non-acid related diseases is a widespread problem13 
• PPIs raise stomach pH > 4 for 12-20 hours per day.10 
• Common PPIs include: Omeprazole (Prilosec, Prilosec OTC), Yosprala, lansoprazole (Prevacid), dexlansoprazole (Dexilent), rabeprazole (Aciphex), Pantoprazole (Protonix), esomeprazole (Nexium), esomeprazole magnesium/naproxen (Vimovo), omeprazole/sodium bicarbonate (Zegerid) 

ii)  Histamine-2 Receptor Antagonists (H2RAs)

• H2RAs decrease stomach acid secretion by binding to histamine receptors on parietal cells.14 
• The onset of action for H2RAs starts 60 minutes after taking the medication, with the duration of action lasting 4-10 hours.14 
• Names of H2RAs include: cimetidine (Tagamet, Tagamet HB), ranitidine (Zantac), nizatidine (Axid), or famotidine (Pepcid, Pepcid AC) 

B) Vagotomy

• Surgical therapy that was more common in the 1980’s to reduce stomach acidity resulting in peptic ulcer disease.10 
• Very rarely used now due to the success of acid lowering medications such as PPIs and H2RAs. 
• The surgery severs the vagal innervation to stomach parietal cells.10 Works by inhibiting secretion of acetylcholine which inhibits secretion of gastric acid.10 Causes higher stomach pH

C) Gastric bypass: 

• Gastric bypass is a gastric exclusion operation sometimes performed in patients with severe obesity to reduce food intake. 
• Studies show that the acid secretion unbuffered by food in the surgically excluded stomach results in lowered gastrin; a hormone which acts to stimulate the parietal cells to secrete acid. This can lead to achlorhydria in individuals who have previously undergone gastric bypass.15 

D) Hypothyroidism: 

• Thyroid hormone plays a role in hydrochloric acid secretion. 
• Hypothyroidism if untreated may lead to achlorhydria.15  

• Animal model studies suggest that thyroid hormones exert their effects on stomach acid production through parietal cells, with high levels of thyroid hormone (hyperthyroidism) increasing the number or size of parietal cells, while the reverse may be true of low thyroid hormone levels (hypothyroidism).16,17

 

3. Neutralization of Stomach Acid

 

• Antacids work rapidly to offer relief of mild or sporadic acid-related symptoms. The effect of antacids on the stomach is through partial neutralization of stomach acid. The effective time for antacids to reduce stomach acidity is relatively short on an empty stomach, but can be prolonged to 1–3 h if taken with food.18 
• Commonly used antacids contain sodium bicarbonate, calcium carbonate, magnesium hydroxide and aluminum hydroxide.18 
• Routine use of antacids might result in frequent episodes of hypochlorhydria

How Common Is Low Stomach Acid?

Reports of the prevalence of hypochlorhydria are not consistent in the literature. 
Aging is regularly associated with decreased gastric acid production, while fasting hypochlorhydria is reported to be less common (10% or less) in elderly American subjects.6 

Fasting hypochlorhydria is reported to be more common (>60%) in elderly Japanese subjects, and as high as 80% in a small cohort of Norwegian subjects in their eighth and ninth decades of life (average age: 84 years, range: 80-91).6 

Some variance could be related to the prevalence of underlying disease states and infections which might lead to low stomach acidity. 

For example, the prevalence of Helicobacter pylori infection is approximately 50% worldwide, 30% in the United States, and as high as 90% in developing countries.11 

It’s also known that the incidence of H. pylori infection and atrophic gastritis increases with age.19  

Likewise, the rate of use of acid inhibiting medications would need to be taken into account as well. For instance, in the United States in 2012 alone, 14.9 million patients received 157 million prescriptions for proton pump inhibitors.20 

While precise prevalence data on the occurrence of hypochlorhydria may be missing, it’s evident that the most common causes of hypochlorhydria (antisecretory medications and H. pylori) are widely prevalent, suggesting a significant portion of the population may be experiencing hypochlorhydria or are at risk of developing hypochlorhydria. 

Why Stomach Acid Is Important

Or said differently...the potential health consequences for low stomach acid levels.

Inadequate levels of stomach acid can result in a number of health consequences including:

1. Increased risks of infection from food borne pathogens
2. Small Intestinal Bacterial Overgrowth (SIBO)
3. Digestion and nutrition consequences
4. Increased allergenic potential of foods
5. Altered medication absorption

1.  Increased risks of infection from food borne pathogens

• Stomach acid plays a role in suppressing the density of ingested microorganisms and assists in preventing infection by pathogens. A pH of 1–2 is the primary restrictive component of the stomach, and severely limits bacterial colonization and survival.8 
• Reduction of stomach acid secretion, from loss of hydrochloric acid producing cells (parietal cells), or from medications which reduce stomach acidity, can lead to hypochlorhydria or even achlorhydria, and increases the risk of bacterial overgrowth and possible damaging infections throughout the GI tract.8 
• A Dutch study in 2004 looked at 364,683 patients and showed a 4.5 times higher risk of community acquired pneumonia in patients on acid suppressing medications such as PPIs or histamine-2 (H2) receptor antagonists. In a meta-analysis of 12 papers in 2007, there was an increased risk of Clostridium difficile; as well as Campylobacter, Salmonella, and other enteric infections in patients on acid-suppressive medications.21 
• Low acid output states can also predispose to infections from E. coli and V. cholerae, amongst other pathogens.22 
• Localized Candida infections of the esophagus have repeatedly been linked to use of antisecretory drugs.3 
• Growth of Candida albicans in the stomach has been noted following vagotomy, partial gastrectomy, H2RA therapy, and during treatment with PPIs. Moreover, localized Candida infections of the duodenum and the small intestine have been reported in association with the use of antisecretagogues.3 

2. Small Intestinal Bacterial Overgrowth (SIBO)

Intestinal bacteria concentrations are elevated in 50-100% of subjects with little to no stomach acidity, since most bacteria swallowed or ingested in foods are normally destroyed by a stomach acid pH < 3.0.4 

Bacteria that grow in the upper small bowel as a result of low stomach acidity may affect the absorption of certain nutrients by binding to or using nutrients and/or reducing the nutrients’ ability to be absorbed by the body. 4 

Some bacteria which might not typically reside in the small intestine can be toxin producing, resulting in intestinal injury.23 

SIBO is a condition that can result from low stomach acidity, where an abnormally increased bacterial load in the small intestines results in excessive microbial fermentation and inflammation, leading to a variety of complaints including bloating, diarrhea, and even weight loss.23 

3. Digestion and nutrition consequences

Protein digestion

• We produce inactive digestive enzymes in the stomach and pancreas called zymogens. One type of zymogen created in the stomach is called pepsinogen.
• Pepsinogen is the precursor to an active protein digestive enzyme called pepsin. 
• HCL, hydrochloric acid, secreted by the parietal cells in our stomach activates pepsinogen, turning it into pepsin.24 
• Therefore, pepsin depends on an acidic environment for protein digestion.25 The enzyme is most effective at a pH of approximately 1.5 to 2.25 It is this low pH that allows pepsinogen to be converted into its active form, pepsin; however, when it reaches the duodenum, it assumes its inactive form as the pH rises above 6.25
• Pepsin activity is maximized at pH 2, drops to less than 50% by pH 3, and is inactive at pH > 5.7 
• Because of this, low stomach acidity is accompanied by lower levels of the active protein digestive enzyme, pepsin.26 
• When we have enough stomach acidity, roughly 10-15% of protein can be partially digested in the stomach, with the rest being digested and absorbed in the small intestine.24  
• The acidic environment of the stomach also helps to denature proteins, (sort of how acidic lime juice denatures fish or shrimp proteins in ceviche) allowing protein digestive enzymes to work even more efficiently.24  
• While not ideal, the body can compensate for low stomach acidity and still digest protein in other ways. In fact, people can and do live with their stomachs entirely removed for medical reasons.24  
• With or without stomach acid, protein continues to be broken down by digestive enzymes in the non-acidic small intestine.24 
• At the time of this writing, I was unable to identify any studies which assessed parameters of protein insufficiency in the setting of hypochlorhydria or achlorhydria (e.g. nitrogen balance tests, serologic markers such as albumin,or acute phase markers such as transthyretin) 
• While protein may not be digested quite as efficiently without a more acidic stomach pH, eating excess protein due to low stomach acid is likely not necessary as protein is mostly digested in the small intestine. If you personally have concerns regarding protein sufficiency it’s best to work with your physician to assess your protein status with medical tests before making adjustments to your diet. 
• Because protein needs can vary due to age, body composition, disease states, and activity level, working with a registered dietitian to assure appropriate protein intake for your individual needs may be helpful.
  

Delayed Stomach Emptying 

• Stomach acid entering into the small intestine from the stomach can trigger feedback mechanisms that lessen stomach contractions and slow the rate of stomach emptying.1  
• Additionally, solid components of meals may take longer to break down with less stomach acidity, likely due to a loss of the activity of the digestive enzyme pepsin.1 
• Studies are mixed on the rate of stomach emptying with a higher, less acidic stomach pH (as is the case in PPI use).1 
• Generally, PPIs have been shown to slow stomach emptying of solid components of meals, but no clear effect has been demonstrated on the rate of emptying of liquids.1 
• However, the slowing of stomach emptying related to a higher, less acidic, stomach pH is minor. The use of acid suppressing medications like PPIs might only pose an additional challenge to stomach emptying in cases where underlying disease states have already caused a slower rate of stomach emptying (e.g. Diabetes or Parkinson’s disease).1

Facilitates the absorption of a variety of important nutrients

In particular, folate, B12, B6, vitamin C, iron, calcium, magnesium, and zinc 2,6  

4. Increased allergenic potential of foods

In sensitive individuals, certain proteins in foods may elicit an allergic response

The ability of a food protein to stay structurally intact may increase the allergenic potential of that food for some individuals. 

Impaired protein digestion in the stomach due to low levels of stomach acid may result in more structurally intact proteins, potentially lowering the threshold dose of an allergen to induce food allergy symptoms in sensitive individuals.53

5. Altered medication absorption

The absorption efficiency of drugs depends on the structural and functional integrity of the gastrointestinal tract and gastric acid seems to play a substantial role in this process.54  

Several drugs, including ketoconazole and itraconazole (antifungals) atazanavir (HIV antiviral), cefpodoxime and enoxacin (antibiotics), and dipyridamole (blood thinner) have been shown to exhibit low absorption under high pH conditions, thought to be due to their low solubility and incomplete dissolution in the stomach at higher pH.7 

Likewise, associations have been reported between poor bioavailability of l-thyroxine (thyroid medication)  and l-dopa (Parkinson’s disease medication) and H. pylori infection.55 

What Are Common Symptoms Of Low Stomach Acid?

Generally, with very low stomach acid levels, the following symptoms may be experienced in order of their prevalence:15

• Upper abdominal pain below the ribs
• Weight loss
• Heartburn
• Nausea
• Bloating
• Diarrhea
• Acid regurgitation
• Early satiety
• Vomiting
• Indigestion 
• Constipation
• Difficulty swallowing 
• Inflamed tongue

How To Test For Low Stomach Acid

Professional Tests

1. Conventional Aspiration Tests

The gold-standard method for assessing stomach acidity is performed by aspiration; which basically means suctioning acid from the stomach using a nasogastric tube, or during endoscopy or intubation. This test can be used to measure baseline fasting levels of stomach acid as well as stomach acid produced after stimulation (e.g. from a meal or by using histamine and gastrin hormone analogs). 

These tests are regarded as the most accurate quantitative tests for measuring stomach acid secretion; however, they require an experienced provider to perform the test. Moreover, the test is invasive and may be uncomfortable.22 Due to its invasive nature and patient discomfort; the aspiration test has decreased in favor of endoscopic options.58 

2. Endoscopic Gastric Analysis

An endoscopic gastric analysis monitors acid production through pH-dependent color changes in dye. Congo red dye is introduced in the stomach after stimulation with a gastrin analogue to promote acid secretion.

The dye changes colors from red to black or blue at a pH of less than 3. This approach helps diagnose patients with gastric atrophy and early stomach cancers.58 

3. The Heidelberg Capsule

Heidelberg pH capsules are a less invasive method of measurement used to determine the ability of the stomach to secrete acid with stimulation. The test is performed after a fast of at least 8 hours. During the test, a tethered Heidelberg capsule is swallowed, followed by ingestion of a sodium bicarbonate solution.

The ingested sodium bicarbonate increases the pH of the stomach, making it less acidic. This results in the parietal cells working to compensate by excreting more hydrochloric acid to reestablish acidity.22,26,59  

4. SmartPill

The smart pill is a validated wireless device for monitoring meal-stimulated stomach acid output. Compared to the Heidelberg capsule, the SmartPill is larger, does not leave the stomach as quickly, and is not tethered.60 x 

At-Home Tests

1.  The Betaine HCL Test

• Betaine HCL is a supplement which has been used in clinical trials to help acidify the stomach.61  The protocol and test procedures are stated below.
• Betaine is a naturally occurring substance found in foods such as spinach or beets. The HCL stands for hydrochloric acid, which is the same acid secreted by parietal cells in our stomach. 
• It’s been proposed that Betaine HCL can be used to test for hypochlorhydria. 
• Commonly, members of the integrative medicine community recommend a test for low stomach acid by supplying increasing doses of betaine HCl over sequential meals. Betaine HCL is supplemented until a dose threshold is met that results in discomfort after eating., Thehe acidity is then  neutralized to restore comfort using a set dose of baking soda as an antacid.6 
• Improvements of hypochlorhydria associated symptoms and the lack of side effects at a tolerable betaine HCL dose is thought to serve as confirmation of low stomach acid levels.6  

At this time, this popular protocol hasn’t been rigorously tested in a research setting, though thousands of clinicians follow such recommendations with positive anecdotal outcomes. It’s important to note that the following protocol is not only used to test for low stomach acid levels but also to establish tolerable doses of betaine HCL.6  

The Betaine HCL Test Protocol:.6

Like with everything on our site, this is for information purposes only.  Please consult with your healthcare professional before trying this or any other gut health protocols.

1. Begin by taking one capsule of betaine HCL containing 350-750 mg (5-12 grains) with a protein-containing meal.

• Capsules containing both pepsin and betaine HCl can also be used and may be superior for overall benefit.
• If no discomfort or burning sensation is experienced, you can begin taking two capsules with each subsequent protein-containing meal.
• If discomfort or a burning sensation occurs after taking this (or any) dose, you can  neutralize the acid with 1 tsp of baking soda in water or milk and reduce the dose of betaine HCl to the last tolerated dose at a prior meal, or discontinue the protocol.
• If you experience no noticeable reactions to the betaine HCl after two days, increase the number of capsules to three capsules per meal.
• Continue increasing the number of capsules every two days up to a maximum dose of 3,000 mg of betaine HCl with each protein containing meal if necessary, until a dose results in tingling, burning, or any other form of discomfort. Once discomfort is experienced, decrease the dose by one capsule per meal. If the discomfort continues, then discontinue the betaine HCl supplementation and consult with a qualified healthcare professional.
• Once a tolerable dose is established, continue this dose at subsequent meals.
• Less betaine HCl may be needed for smaller meals, so a reduced dose may be adequate. 
• Reportedly, individuals with very moderate HCl deficiency generally show rapid improvement in symptoms and have early signs of intolerance to the acid. This is thought to indicate a return to normal acid levels in the stomach.

Precautions: Ingesting HCl/pepsin is not appropriate for people with peptic ulcer disease as HCl can irritate sensitive tissue. HCL can also be corrosive to teeth; therefore, capsules should NOT be emptied into food or dissolved in beverages. The betaine HCL test should only be taken along with a sufficiently sized meal of 500 calories or more containing adequate protein. Do not take Betaine HCL on an empty stomach unless you plan to immediately consume a meal after taking the supplement. 

Protocol adapted from this source:.6  

Validity of the betaine HCL test

In order to state with assurance that the betaine HCL challenge is a sufficient test to identify hypochlorhydria, clinical trials would need to be conducted on this protocol along with the use of a validated conventional method of  measuring stomach acid content. No such studies exist at this time, which only allows for speculation and anecdotes regarding the validity and usefulness of the betaine HCL test. With this in mind, there are a few important parameters that the betaine HCL test measures that can be discussed further:

1. The absence of symptoms and pain upon ingestion of betaine HCL followed by subsequent discomfort once an excessive dose is achieved
2. The rapid resolution of symptoms related to hypochlorhydria after supplementation

2.  The Baking Soda Test

• The baking soda test is another proposed method of checking for adequate stomach acid production at home. 
• The rationale? Stomach acid when mixed with a small dose of orally ingested baking soda will release carbon dioxide (CO2) resulting in belching if you have normal levels of stomach acid. 
• How the test is done: 
• Combine ¼ teaspoon of baking soda in 4-6 ounces of cold water first thing in the morning while still fasted. 
• Drink the baking soda solution
• Time how long it takes before you belch, timing up to five minutes. 
• Proponents of this method claim that a belch should happen within 2-3 minutes if you’re producing adequate stomach acid, whereas early and repeated belching is thought to indicate an excess of stomach acid. 
• A belch that takes longer than 3 minutes to happen is thought to indicate  a low stomach acid level.64 

Validity of the Baking Soda Test

• No clinical trials have been performed on the baking soda test using time parameters around belching as determining factors to assess the acidity of the stomach. 
• In this way, there is currently no verifiable means to indicate that the baking soda test can measure what it claims to measure. 
• However, studies and case reports are available regarding the ingestion of baking soda for other purposes, and these studies may offer some insight.
• Researchers have investigated the ability of baking soda, when used as an antacid, to produce CO2 in the stomach.65 
• Multiple factors, some of which have nothing to do with the pH of the stomach, can impact the level of gas produced upon ingestion of baking soda. Things like the total volume of stomach juices and stomach mixing.65  
• Higher stomach juice volume offers more substrate for gas production,65 though the volume of stomach juices are often at their lowest in the fasted state -- the time in which this test is recommended to be carried out.1 
• Likewise, more vigorous mixing releases higher volumes of gas by allowing for greater surface reactions between hydrochloric acid and baking soda.65
• It’s important to note that normal physiological stomach mixing is generally not a ‘vigorous’ process.65  
• The study authors reported that, while gas production was instantaneous once the baking soda mixed with hydrochloric acid, overall, gas was still produced at a ‘slow’ pace.65  
• Likewise, belching reportedly does not always occur upon ingesting baking soda.65  
• The study concluded that: “Based on our results, we believe that ingestion of the recommended dose of sodium bicarbonate (one-half teaspoon in this study) would result in only small amounts of sudden gas release…” 65 
• Given the variables at play including total volume of acidic gastric juices in the fasting state, and differences in stomach mixing between individuals, the baking soda test is likely not a reliable means of assessing stomach acidity.

3.  The Beet Test

• Some have proposed that a simple means of determining if you have low stomach acid is by eating beets. 
• This may sound like an odd test, but the rationale goes like this: The red pigments found in beets (called betacyanins) are readily decolorized by light, heat, and the extremes of pH; losing their color in alkaline conditions and undergoing irreversible decomposition from the color red to yellow in acidic conditions.66  
• Eating beetroot can result in red urine and feces in approximately 14% of the general population, and is particularly prevalent in individuals with iron-deficiency anemia (80% where no previous iron therapy had been given, decreasing down to 49% after iron therapy) and in 48% of individuals with pernicious anemia or malabsorption.66 
• Beetroot pigment is most stable around a pH of 4 to 5; which would be a hypochlorhydria level in the human stomach.66 
• Experiments in animals have suggested that the stomach is the main site in the body responsible for decolorizing beetroot due to acidity. 66 
• This hypothesis has recently been supported by a report of an elderly man who had never produced red urine following beetroot ingestion, but suddenly developed beeturia after taking acid suppressing medications (H2RAs) for reflux esophagitis.66 

• The caveat? The pigment in beets can be stabilized, remaining red, by other compounds such as oxalic acids which are found in beets themselves,66 as well as in other commonly eaten foods such as spinach, rhubarb, or oysters.67 
• Even individuals who typically don’t experience beeturia may experience this phenomenon if they happen to eat beets along with other high oxalate foods.67  
• This means that people with normal stomach acidity under certain circumstances might have this experience. 
• Beeturia has also been associated with iron deficiency anemia, with certain forms of iron potentially reacting with and decolorizing beet pigment through a redox reaction.66 
• The absence of appropriate iron levels may result in a lost opportunity to decolorize beet pigment, though this theory has been called into question.66 
• It’s important to bear in mind that iron deficiency anemia is often associated with hypochlorhydria, too. 
• Genetic alterations have also been proposed to explain the occurrence of beeturia, but so far, no such genetic trait has been identified to explain this phenomenon.68 
• Current Evidence points primarily to stomach acidity, the rate of stomach emptying, and potential enzymatic and microbial reactions in the colon for the eradication of beet pigment.66,69 
• Because there is the possibility that microbial actions in the colon might also eradicate beet pigment for some, the beet test is not fail-proof in identifying hypochlorhydria; meaning that the absence of beeturia or red stools after eating beets may not preclude you from having low stomach acid levels.  
• It’s also important to know that the rate in which the stomach empties into the small intestine could also impact the level of acid exposure beets undergo in the stomach, potentially preserving some of the beet pigment. It is possible that those with rapid stomach emptying  may have the ability to produce stomach acid and still have beeturia or red stools after beet consumption. 
• Key takeaways? 
• The presence of red stools or beeturia may genuinely be a sign of low stomach acid levels. Be mindful that your individual rate of stomach emptying, eating beets along with other high oxalate foods, and enzymatic actions in the colon can impact the validity of the beet test. 
• The beet test should not be used for diagnosis of hypochlorhydria, but may indicate the need for conventional testing of stomach acid levels and/or assessment for nutritional adequacy, particularly in the case of iron deficiency anemia. 

If you want to try the beet test, here are a few pointers: 

• Avoid pickled beets as the pickling solution helps to stabilize the beet pigment. 
• We suggest trying the beet test by eating beets in a fasted state away from other foods to avoid interference from additional compounds such as oxalates. 
• Choose purple beets; golden beets will not work for this challenge
• We suggest a dose of 100 grams of fresh beets for the beet test; roughly ⅔ of a cup of chopped beets.

Potential Treatments For Low Stomach Acid

1. Bitters

• Bitter-tasting plants or plant extracts (bitters), have been commonly used in many herbal medicinal traditions to promote digestion and to relieve digestive complaints. 
• Bitters such as gentian root and wormwood help to stimulate blood flow to the stomach after meals, which improves the production of digestive secretions, the absorption of nutrients, and the removal of metabolic wastes.70 
• Some have also hypothesized that bitters such as caffeine may induce defense mechanisms in the stomach, which lead to increases in stomach acid secretion as a means for the body to mitigate potential toxins.59 
• A common naturally occurring bitter that many people consume is coffee. Coffee is known to stimulate the production of the hormone gastrin,71  which stimulates the parietal cells to secrete acid. Coffee may also slightly increase acidity by suppressing the secretion of the acid-regulating hormone, somatostatin.37 
• A minimum dose of bitters is essential to produce cephalic responses. For supplemental bitters, we suggest single doses of gentian or wormwood of 1000 mg.70  
• Keep in mind that for bitters to be effective in stimulating stomach acid production, an adequate amount of functioning parietal cells have to be in place. If stomach acid production is blocked by medications or through parietal cell loss, then bitters will not be able to facilitate stomach secretions.
  

2. Acidic Foods: 

While it’s intuitive that eating or drinking acidic foods and beverages might help increase stomach acidity , studies looking at this issue in particular are lacking. 

• However, there are several studies which suggest that acidic foods likely help to lower the pH, increase acidity, of the stomach contents. 
• Commonly ingested foods and beverages  having a pH < 4 include coffee, tea, ketchup, apple juice, carbonated beverages, wine, lemonade, orange juice, and vinegar.72 

• The acidity of Coca-Cola (pH 2.5) has been successfully used in certain circumstances to help acidify the gut to increase medication absorption. (e.g. ketoconazole; itraconazole)73,74  
• Evidence also suggests that vinegar (pH of 2-3.5) when eaten in normal culinary doses (e.g. on a salad, or in olive oil and dipped with bread) might also lower the pH of the stomach.72 
• The evidence for this lies in the fact that vinegar has been shown to slow the rate that the stomach empties its contents into the small intestine.75 
• A reduced rate of stomach emptying as a result of more stomach acidity is a normal physiological response.76 
• This slowed rate of emptying is governed by acid-sensing neurons which trigger a cascade of events to ensure acidic stomach contents enter the small intestine at an appropriate pace.76 
• Likewise, just as low stomach acidity has been found to enhance the potential for food allergies, vinegar has been shown to decrease the allergenic response to certain foods (e.g.  lentils and eggs)77 

• The evidence suggests that acidic foods are helpful in lowering the pH of the stomach; however, ingesting a large volume of acidic foods to properly acidify the gut can come with consequences to oral and dental health, and may also be inappropriate for individuals with GERD.61

3. Betaine HCL 

• Betaine HCL is a supplement which has been used in clinical trials to help acidify the stomach.61 
• Betaine is a naturally occurring substance found in foods such as spinach or beets. The HCL stands for hydrochloric acid, which is the same acid secreted by parietal cells in our stomach. 
• Betaine HCL has benefits more advantageous than the use of acidic foods when it comes to lowering the pH of the stomach, as it is encapsulated, which helps to prevent damage to tooth enamel and acid related damage to the esophagus. Likewise, tailored dosing is more easily achieved with betaine HCL as opposed to acidic foods.61 
• A study was performed on healthy volunteers who were given medications to purposefully cause hypochlorhydria. In the fasted state, Betaine HCL was found to rapidly help acidify the gut using a dose of 1500 mg provided with 90 mL of water. Betaine HCl was well tolerated by all subjects and was successful in lowering the average pH of the stomach from a pH of 5.2 down to a 0.6 within 30 minutes.61  
• A separate small study was performed on healthy adults aged 18-64. No participants were found to have low stomach acidity, with all individuals having a stomach pH no greater than 2 at a fasting baseline.78 
• The study participants were broken down into 4 groups: a control group that received a standard meal, and three treatment groups receiving a standard meal and the following doses of betaine HCL: 1500 mg, 3000 mg, and 4500 mg.78 
• Individuals who only received the test meal but no betaine HCL were found to achieve their baseline level of acidity within 49.7 minutes. Individuals receiving 1500, 3000, and 4500 mg of betaine HCL were able to achieve baseline acidity within 27.8, 29.6, and 17.5 minutes, respectively.78 
• The purpose of this study was to determine how rapidly the stomach could be acidified in the setting of food consumption for the sake of improving absorption of medication. The study authors determined that a dose of 4,500 mg was appropriate for rapid acidification for this purpose, but noted that this dose has several practical limitations and might not be clinically useful given those current limitations.78 
• We suggest not exceeding a dose of 3,000 mg without medical supervision. 
• Because this study was done on individuals without hypochlorhydria, it doesn’t provide enough insight into how people with hypochlorhydria might respond to varying doses of betaine HCL. Likewise, the goal of supplementation was to achieve better medication absorption more so than to achieve normal physiological levels of stomach acidity for proper digestion. 
• Future studies will need to explore the use of betaine HCL along with meals in the setting of hypochlorhydria to determine the doses and lengths of time needed to achieve normal physiological levels of stomach acidity.
• Case reports indicating improvement of hypochlorhydria linked symptoms with betaine HCL supplementation suggest that betaine HCL may very well be able to achieve normal physiological levels of stomach acidity.63 
• To identify a tolerable dose on an individual basis, following the betaine HCL test may be the best way to do so.

When it’s Inappropriate to Treat Low Stomach Acid

• While ideally it may be best to treat low stomach acid through the use of bitters, acidic foods, and betaine HCL, doing so isn’t an option for everyone. 
• If you’ve been prescribed an acid regulating medication such as H2RAs or PPIs by a physician, your healthcare provider has determined that suppressing the acidity in your stomach is of clinical benefit to you. 
• In such cases, it is not recommended to treat low stomach acid, as treatment with acidifying agents runs counter to the therapeutic goals of your prescribed medications.
• All questions and concerns about acid-suppressing medications should be discussed with your physician. 
• If you have GERD or any active ulcerations, ingesting acidifying agents is not appropriate and could cause further damage and injury. 
• Likewise, avoid treatment if you have an active H. pylori infection in need of treatment, or any other active stomach infections. 

Who Should Treat Low Stomach Acid?

When It’s Appropriate to Treat Low Stomach Acid

• If you have consulted with your physician prior to doing so
• If you’re not on prescribed acid lowering medications 
• If you have no active stomach infections or acid-related disease states (e.g. GERD, peptic ulcers, zollinger-ellison disease, etc.) 
• If you have clinically verified hypochlorhydria.

When it’s Inappropriate to Treat Low Stomach Acid

• While ideally it may be best to treat low stomach acid through the use of bitters, acidic foods, and betaine HCL, doing so isn’t an option for everyone. 
• If you’ve been prescribed an acid regulating medication such as H2RAs or PPIs by a physician, your healthcare provider has determined that suppressing the acidity in your stomach is of clinical benefit to you. 
• In such cases, it is not recommended to treat low stomach acid, as treatment with acidifying agents runs counter to the therapeutic goals of your prescribed medications.
• All questions and concerns about acid-suppressing medications should be discussed with your physician. 
• If you have GERD or any active ulcerations, ingesting acidifying agents is not appropriate and could cause further damage and injury. 
• Likewise, avoid treatment if you have an active H. pylori infection in need of treatment, or any other active stomach infections.