Traditional Treatments Focus on the Acid

Traditional Treatments Focus on the Acid

Written by Paula Owen

Expert Review By KBS Research Team

Antacids (e.g., Tums®, Rolaids®):

Neutralize stomach acid temporarily, like putting water on a fire. Like drying off with a towel, but you’re still standing in the rain.

  • Problem: They wear off quickly, so symptoms return soon after. Overuse can cause imbalances in minerals such as magnesium and calcium, leading to constipation, kidney issues, or other health problems (Tytgat 2013).

H₂ Blockers (e.g., famotidine, cimetidine, nizatidine):

Reduce acid production moderately by blocking histamine receptors in the stomach.

  • Problem: They take longer to work than antacids and, with chronic use, can interfere with nutrient absorption (especially vitamin B₁₂, iron, and calcium) (Ito and Jensen 2010).

Proton Pump Inhibitors (PPIs, e.g., omeprazole, esomeprazole, lansoprazole):

Shut down stomach acid production almost completely.

  • Problem: Long-term use has been linked to nutrient deficiencies, increased risk of Clostridioides difficile infection, pneumonia, chronic kidney disease, and even bone fractures (Freedberg et al. 2017). Over time, PPIs may lose effectiveness, and discontinuation often triggers acid rebound hypersecretion, where symptoms return stronger than before (Scarpignato et al. 2016).

  • Problem: Chronic use of PPIs can cause physiologic changes in the stomach such as an increase in parietal cell count, which are the cells that make acid. (Morris et al. 2023). This change conditions the user to involuntary dependency upon the PPI, otherwise a very large and disproportionate amount of acid is secreted with meals, making reflux more severe if a dose is missed. Morris, N., Nighot, M. Understanding the health risks and emerging concerns associated with the use of long-term proton pump inhibitors. Bull Natl Res Cent 47, 134 (2023). https://doi.org/10.1186/s42269-023-01107-9

Alginate Formulations (e.g., Gaviscon®):

Form a floating “raft” or gel-like barrier on top of stomach contents, preventing reflux into the esophagus.

  • Benefit: Provides fast, physical protection without altering acid production (Kwiatek et al. 2011).

  • Limitation: Works mainly as a mechanical shield; it does not repair the lower esophageal sphincter (LES) or improve motility.

Prokinetics (e.g., metoclopramide, domperidone, itopride):

Enhance gastric emptying and improve esophageal motility.

  • Problem: Not widely available OTC in the U.S. and often limited by significant side effects, including neurological complications (Camilleri et al. 2018). Contraindicated for people with Parkinson’s, seizure disorders, history of bowel obstructions.

Natural Demulcents & Herbal OTC Remedies (e.g., deglycyrrhizinated licorice [DGL], slippery elm, aloe vera, marshmallow root):

Create a soothing coating along the esophagus and stomach lining, reducing irritation.

  • Problem: Evidence is largely anecdotal or from small clinical trials. Quality and potency vary, and they do not directly address LES dysfunction or delayed gastric emptying (Zalewski et al. 2021).

The Real Problem: Acid in the Wrong Place

All of these treatments reduce or buffer acid, but none address why acid escapes:

  • A weak or relaxed lower esophageal sphincter (LES) that fails to close properly

  • Delayed gastric emptying, leaving food in the stomach too long

  • Poor esophageal clearance, allowing acid to linger and cause damage

By lowering acid too much, conventional therapies can weaken digestion over time — since stomach acid is vital for nutrient absorption, protein breakdown, and defending against harmful bacteria.

And this is our new one…..Albeit I changed the title to: Most reflux products fight the wrong enemy. That’s why they don’t fix reflux.

Most reflux products are fighting the wrong enemy

Walk down the heartburn aisle and almost everything falls into one of three categories.

1. Raft builders & barriers

Alginate-based products are formulated to float on top of gastric contents and create a low-density “raft” that acts as a physical barrier between the stomach and esophagus.¹⁻³

While these formulations can reduce post-prandial acid reflux by displacing the acid pocket, they do not improve gastric emptying, motility, or lower esophageal sphincter (LES) competence.²

2. Acid neutralizers

Antacids provide fast, short-term relief by chemically neutralizing existing gastric acid.⁴

They do not modify acid production, gastric motility, LES tone, or the physiological drivers that cause reflux in the first place.⁴⁻⁵

3. Acid suppressors (H₂ blockers & PPIs)

H₂-receptor antagonists reduce acid output for several hours, while proton pump inhibitors (PPIs) provide profound and prolonged suppression of gastric acid secretion.⁶⁻⁸

However, multiple clinical studies demonstrate that acid suppression does not improve gastric emptying or motility, meaning the mechanical causes of reflux persist despite reduced acidity.⁹⁻¹⁰

Long-term suppression can also impair nutrient absorption and alter normal digestive physiology.¹¹

All three share the same assumption

Acid is the problem.

Therefore the only strategies are to block it, buffer it, or build a wall against it.

But reflux is rarely just an “acid issue.” Many symptomatic episodes are weakly acidic or non-acidic, especially in people already taking PPIs, and are driven by motility issues, LES dysfunction, or esophageal hypersensitivity rather than excess acid.¹²⁻¹³

 

Where Re:Flux is different

Re:Flux isn’t here to wage war on acid.

It’s here to help your system work the way it’s designed to.

Re:Flux is formulated to support the four core mechanisms that determine whether reflux occurs:

  1. Stomach motility – promoting effective gastric emptying rather than allowing food to sit, ferment, and push upward.

  2. LES tone – supporting the strength and responsiveness of the gastroesophageal valve.

  3. Inflammatory balance – reducing the hypersensitivity and irritation that amplify symptoms.

  4. Acid balance—not suppression – maintaining physiologic acidity essential for digestion while reducing the conditions that allow reflux to occur.

The Re:Flux Difference

Most reflux products:

  • Create a raft/barrier on gastric contents¹⁻³

  • Neutralize existing acid⁴⁻⁵

  • Suppress acid production for hours or days⁶⁻⁸

Re:Flux:

  • Supports gastric motility

  • Supports LES function

  • Helps promote a healthier inflammatory environment

  • Helps balance, not suppress, stomach acid

References (Vancouver Style)

  1. Dettmar PW, Sykes J. A comparative study on the raft-forming properties of various alginate formulations. Int J Pharm. 2011;405(1-2):76-82.

  2. McGlashan J, Johnstone LM, Sykes J, et al. Post-prandial reflux: displacement of the acid pocket by alginate-antacid formulations reduces acid reflux episodes. Aliment Pharmacol Ther. 2009;29(7):703-11.

  3. Kwiatek MA, Pandolfino JE, Kahrilas PJ. The acid pocket: a target for treatment in reflux disease? Am J Gastroenterol. 2011;106(1):195-203.

  4. Schubert ML, Peura DA. Antacids revisited: a review of their mechanisms and clinical uses. J Clin Gastroenterol. 2008;42(5):558-64.

  5. IFFGD (International Foundation for Gastrointestinal Disorders). Antacids and their role in symptom relief. IFFGD Clinical Resource. 2020.

  6. Fackler WK, Ours TM, Vaezi MF, Richter JE. Long-term effect of H₂-receptor antagonists on gastric acid secretion. Clin Gastroenterol Hepatol. 2004;2(4):307-14.

  7. Sachs G, Shin JM, Howden CW. The pharmacology of proton pump inhibitors. Aliment Pharmacol Ther. 2006;23 Suppl 2:2-8.

  8. Robinson M. Review article: current therapeutic options for GERD—proton pump inhibitors and beyond. Aliment Pharmacol Ther. 2006;23 Suppl 1:10-7.

  9. Xu X, Zhang X, Zhang Q, et al. Effects of proton pump inhibitors on gastric emptying: a systematic review. Dig Dis Sci. 2018;63(9):2181-8.

  10. Kahrilas PJ, Shaheen NJ, Vaezi MF. American Gastroenterological Association technical review: management of gastroesophageal reflux disease. Gastroenterology. 2008;135(4):1392-413.

  11. Ito T, Jensen RT. Association of long-term proton pump inhibitor therapy with bone fractures and effects on absorption of calcium, vitamin B12, iron, and magnesium. Curr Gastroenterol Rep. 2010;12(6):448-57.

  12. Bredenoord AJ, Weusten BL, Timmer R, Smout AJ. Characteristics of acid, weakly acidic, and non-acid gastroesophageal reflux in patients with persistent symptoms despite proton pump inhibitor therapy. Gut. 2004;53(12):1656-61.

  13. Zerbib F, Roman S, Bruley des Varannes S, et al. Normal values and day-to-day variability of 24-hour ambulatory impedance–pH monitoring in GERD. Gastroenterology. 2005;129(2):487-96.