Many people reach for acid-reducing drugs when heartburn or reflux appears, assuming the problem is too much stomach acid. In reality, excess acid is rarely the root cause. Most reflux and gastritis symptoms begin when the protective mucosal lining of the stomach or esophagus becomes thin, inflamed, or slow to repair.

Acid itself is essential for digestion and defense—it breaks down proteins, absorbs nutrients, and prevents infection. The real issue is often a weakened barrier that allows normal acid levels to irritate exposed tissue.

Deglycyrrhizinated licorice (DGL) supports this barrier. Instead of suppressing acid, it strengthens the mucous layer and promotes healing of the digestive lining. For many people, this makes it a logical alternative or companion approach to acid-blocking medications.

Two Ways to Calm Acid

Proton-pump inhibitors (PPIs) and H₂ blockers reduce stomach-acid production to ease reflux. Deglycyrrhizinated licorice (DGL) takes a different path: it reinforces the protective mucous barrier that lines the digestive tract.

Rather than neutralizing acid, DGL works to protect tissue integrity. This distinction matters because stomach acid itself plays essential roles in digestion and defense.

The Acid-Suppression Model

Conventional acid-blocking drugs reduce symptoms by lowering acid levels, yet they do not address why the stomach or esophagus became sensitive to acid in the first place.

Why the Body Produces Acid

Stomach acid supports:

• Protein digestion and activation of digestive enzymes.
• Nutrient absorption, especially vitamin B₁₂, iron, calcium, and magnesium.
• Pathogen control, killing microorganisms in food.

What Happens When Acid Is Suppressed Long-Term

• Nutrient absorption suffers. A low-acid environment limits nutrient extraction, causing deficiencies.
• Rebound hypersecretion develops. The stomach compensates for chronic suppression by increasing acid-producing cells. When PPIs are stopped, these extra cells can overproduce acid, intensifying symptoms.
• Underlying vulnerabilities persist. Weak mucosal barriers, slow gastric emptying, or lower-esophageal-sphincter dysfunction remain uncorrected.
• Physiologic dependency forms. Because of rebound effects, many users cannot discontinue PPIs without severe discomfort, even if the initial reflux was mild.

Acid blockers can relieve pain effectively, but they suppress a normal digestive function instead of restoring healthy protection. For people seeking root-cause solutions or hoping to avoid nutrient depletion, therapies that strengthen the tissue barrier become relevant.

What DGL Is

DGL comes from Glycyrrhiza glabra (licorice root) after removing glycyrrhizin—the compound that can raise blood pressure and cause fluid retention. The deglycyrrhizinated form retains therapeutic flavonoids and saponins while avoiding those side effects.

How DGL Protects the Digestive Lining

DGL focuses on mucosal defense rather than acid suppression. It stimulates production of protective mucus in the stomach and esophagus, enhances local blood flow, promotes glandular-cell differentiation, and increases the lifespan of intestinal cells.

How the Mucus Barrier Works

The stomach’s mucus layer prevents acid from directly contacting tissue. When this layer is thin or damaged, acid irritates the surface, causing the burning of heartburn or gastritis.

Mechanisms of Action

DGL strengthens this system through:

• Mucus stimulation. Increases thickness of the protective barrier between acid and tissue.
• Improved microcirculation. Better blood flow delivers oxygen and nutrients to promote repair.
• Glandular-cell support. Encourages healthy replacement of mucus-producing cells.
• Longer-lived epithelial cells. Extends cell lifespan for a more stable, intact lining.

Reflux can occur even with normal acid levels if the mucosal barrier is weak. By fortifying that barrier, DGL can reduce irritation without interfering with stomach acid’s digestive role.

DGL vs Acid Blockers

Function	DGL	PPIs / H₂ Blockers
Mechanism	Strengthens mucosal barrier	Reduces or neutralizes acid
Acid production	Unchanged (normal digestion preserved)	Suppressed
Nutrient absorption	Maintained	Often impaired
Rebound effect	None observed	Common after withdrawal
Onset of action	Gradual (protective buildup)	Rapid (symptom suppression)

DGL requires consistent use to rebuild the mucus layer, while acid blockers give faster relief but can create dependency.

Clinical Evidence and Research

Although research historically focused on peptic ulcers, recent trials extend to reflux and functional dyspepsia.

Peptic-Ulcer Trials

• Controlled trial (33 gastric-ulcer patients): DGL 760 mg three times daily vs placebo for one month → ulcer size reduced 78 % vs 34 %, complete healing 44 % vs 6 %.
• Large cohort (874 patients): DGL vs antacids or cimetidine for chronic duodenal ulcers → 91 % healed within 12 weeks; relapse rates DGL 8.2 %, cimetidine 12.9 %, antacid 16.4 %.
• Licorice vs bismuth: 95 % ulcer-healing vs 70 % for bismuth; H. pylori eradication 70 % vs 45 %.

Functional Dyspepsia

• Randomized double-blind trial (50 adults): Glycyrrhiza glabra extract (GutGard®) 75 mg twice daily × 30 days → significant improvement in upper-abdominal pain, heartburn, and regurgitation.
  
  
  Note : GutGard® is a standardized high-flavonoid extract; typical retail DGL products are less concentrated, though many users report similar benefit.
  

Gastroesophageal Reflux (2024 Phase III)

• Trial (200 participants): GutGard® 150 mg daily × 28 days → heartburn resolution superior to placebo (days 14 & 28) and regurgitation improved (days 7 – 28); quality-of-life scores rose significantly.

Helicobacter pylori Eradication

• Double-blind study (107 subjects): GutGard® 150 mg daily × 60 days → H. pylori cleared in 56 % vs 4 % for placebo.

Combination Formulations

• 8-week trial: Pantoprazole + alginate vs pantoprazole + alginate + glycyrrhetinic acid (25 mg twice daily) + bilberry anthocyanosides → significant symptom reduction by week 2 (chest pain, heartburn, bloating); side effects 6.9 % vs 27.6 %, no BP increase or weight gain.

NSAID-Induced Gastric Damage

• DGL 350 mg chewed with each aspirin dose reduced gastric bleeding in human studies.

Canker Sores (Aphthous Stomatitis)

• DGL mouthwash (200 mg powder in 200 mL warm water × 4 daily) → 75 % experienced 50–75 % improvement in 1 day; complete healing by day 3.

Evidence Summary

Across small-to-moderate studies, DGL demonstrates comparable ulcer-healing to standard drugs, lower relapse rates, and added protection against NSAID damage. The most consistent benefits appear in mucosal repair and symptom reduction across ulcer, reflux, and H. pylori–related conditions.

However, the research base remains limited, and most trials used standardized extracts like GutGard® with >10 % flavonoid content, while typical commercial DGL products contain only 0.75 – 1 %.

Interpreting the Evidence

While ulcer data are robust, GERD-specific studies are still emerging. Functional dyspepsia overlaps symptomatically with reflux, suggesting that DGL’s protective mechanisms apply broadly even if direct GERD trials are few.

User reports and smaller clinical data together suggest that the mucosal-strengthening model is viable, especially for individuals wishing to reduce PPI dependence.

Practical Use and Common Protocols

DGL is most often used in chewable tablet form, as chewing activates the compound through contact with saliva. Most clinical studies have used 75–380 mg doses taken two to three times daily, with 760 mg three times daily employed in ulcer treatment.

Typical Usage Patterns

• Timing: 20 minutes before meals to allow mucus formation before food and acid increase.
• Dosage: 200–300 mg chewable tablets three times daily before meals and at bedtime.
• Consistency: Protective effects develop gradually with regular use, not instantly like antacids.

DGL provides mucosal protection, not instant neutralization. Regular dosing builds a durable barrier over time.

Limitations of Effect

DGL cannot correct mechanical causes of reflux such as hiatal hernia or lower esophageal sphincter weakness. It protects tissue from acid damage but does not alter structural factors that cause backflow.

Who Might Consider DGL — and Why

Long-term PPI use can create physiological and nutritional complications. The literature documents three major concerns:

Nutrient Absorption

PPIs interfere with absorption of vitamin B₁₂, vitamin C, calcium, iron, and magnesium. For those with pernicious anemia, iron deficiency, or autoimmune nutrient malabsorption, suppression compounds existing problems. The mechanism is pH-related: reduced acidity impairs nutrient release from food and subsequent uptake in the intestine.

Rebound Acid Hypersecretion

Stopping PPIs abruptly triggers temporary acid overproduction.

• 40–50 % of patients experience gastrointestinal symptoms after discontinuation, including some who never had reflux before therapy.
• Symptoms usually appear 5–14 days after stopping and persist ~4–5 days, but after >1 year of PPI use, rebound may last 8–26 weeks.

Root-Cause Considerations

PPIs control symptoms by suppressing acid, not by correcting:

• Lower esophageal sphincter dysfunction
• Delayed gastric emptying
• Hiatal hernia
• Dietary and inflammatory triggers

For individuals seeking to heal tissue while addressing these root mechanisms, DGL can provide supportive protection during evaluation or tapering.

User Experiences

Clinical data are limited, but user reports are numerous and consistent. Selected accounts include:

“I used to suffer from recurrent ulcers and gastritis for almost a decade and had tried every treatment under the sun (antibiotics, PPIs, temporary H₂s) with only temporary relief. I was recommended DGL by a pharmacist at my local independent pharmacy and was skeptical at first but noticed symptom relief quickly & eventually had complete resolution of my stomach issues… Before trying DGL I was at the point where the ulcer pain was so severe I was feeling it in my back. Should also add I rarely need to use them now unless I have a flare-up.”
— Short-Taro-5156, Reddit (2025)

“I’ve been using chewable DGL for my acid reflux, and it’s the only thing that’s kept my symptoms under control without meds.” — Reddit user, r/gerd

“DGL licorice literally saved my stomach. After months of gastritis, nothing helped until I started chewing the tablets 20 mins before meals.” — Reddit user, r/SIBO

“I was skeptical, but DGL has made a huge difference with my IBS and heartburn. Just make sure you chew it thoroughly!” — Reddit user, r/Probiotics

These consistent anecdotes align with clinical findings that symptom improvement occurs progressively with sustained use.

Research Limitations and Open Questions

The strongest clinical evidence concerns ulcer treatment, not reflux specifically. Trials on GERD and dyspepsia remain fewer and smaller in scale.

Key constraints include:

• Formulation variation: Most trials used GutGard®, a high-flavonoid standardized extract (> 10 % total flavonoids). Common retail DGL products contain only 0.75–1 % flavonoids, meaning dosage equivalence is uncertain.
• Limited comparative data: Few head-to-head studies versus PPIs or H₂ blockers for reflux.
• Variable quality control: Many supplements differ in purity and may retain traces of glycyrrhizin, causing side effects such as elevated blood pressure or anxiety.

Still, even standard DGL products show consistent user-reported benefit, indicating a broadly effective mucosal-support mechanism.

Preparing to Discuss DGL with a Healthcare Provider

When integrating DGL into a treatment plan—especially when tapering PPIs—collect relevant information in advance to support clinical review:

• Current PPI dose and duration of use
• Documented nutrient deficiencies (B₁₂, iron, magnesium, calcium)
• Timeline: whether symptoms began before or after acid suppression
• Endoscopy findings or imaging showing structural issues
• Other medications that may interact with licorice compounds
• Specific product details: standard DGL vs high-flavonoid extract

The rebound hypersecretion phase following PPI withdrawal presents a separate physiological challenge. Some patients start DGL before and during this transition to buffer the mucosa as acid production normalizes.

Product Forms and Quality Differences

DGL is widely available as chewable tablets, capsules, powders, and wafers.

13.1 · The “Chewable Activation” Debate

Traditional guidance favors chewable tablets under the belief that saliva activation is necessary. However, no clinical data confirm this superiority. Current understanding suggests the intestinal mucus layer, not oral activation, is the critical factor for DGL’s effectiveness.

The popularity of chewable forms likely stems from their use in early studies rather than proven mechanistic need.

Quality and Regulation

• Glycyrrhizin content should be below 3 % to avoid hypertension and water retention.
• Flavonoid content varies; higher concentrations correlate with stronger clinical outcomes.
• Because the FDA does not regulate supplements, ingredient accuracy and purity differ widely. Selecting products with third-party testing or pharmaceutical-grade certification helps ensure safety.

Integrating DGL into Broader Care

DGL can be considered part of an integrative approach that includes:

• Identifying mechanical or dietary causes of reflux.
• Restoring gut microbial balance.
• Monitoring for nutrient deficiencies caused by long-term acid suppression.
• Coordinating with a physician to taper PPIs safely.

The key distinction: DGL strengthens the body’s innate mucosal defense rather than suppressing an essential digestive function.

Key Takeaways

• DGL is derived from licorice root with glycyrrhizin removed to avoid blood-pressure effects.
• It works by stimulating and repairing the mucus barrier, not by reducing stomach acid.
• Studies show comparable ulcer healing to conventional drugs, lower relapse rates, and benefits for H. pylori and NSAID-related injury.
• No rebound acid effect has been observed when discontinuing DGL.
• Quality and formulation matter: high-flavonoid extracts (e.g., GutGard®) show the strongest results.
• DGL supports root-cause healing for those seeking to transition away from chronic acid suppression.

References and Further Reading

• Medical News Today (2024). “DGL for acid reflux: Benefits, risks, and other options.”
• National Institutes of Health (2012). “An Extract of Glycyrrhiza glabra (GutGard) Alleviates Symptoms of Functional Dyspepsia.”
• National Institutes of Health (2013). “Outcomes in patients with nonerosive reflux disease treated with a proton pump inhibitor and alginic acid ± glycyrrhetinic acid and anthocyanosides.”
• National Institutes of Health (2016). “Integrative Treatment of Reflux and Functional Dyspepsia in Children.”
• National Institutes of Health (2020). “Glycyrrhiza glabra (Licorice).”
• National Institutes of Health (2025). “Efficacy and Safety of GutGard® in Managing Gastroesophageal Reflux-Related Symptoms.”
• Natural Medicine Journal (2022). “Deglycyrrhizinated Licorice for Gastrointestinal Ulcers.”
• ScienceDirect Topics (2022). “Glycyrrhiza glabra Root — Nutrition and Functional Foods in Boosting Digestion.”
• Healthline (2023). “PPI Withdrawal: Symptoms, Timeline, and Treatment.”
• Healthline (2024). “Can You Use Deglycyrrhizinated Licorice (DGL) to Treat Acid Reflux?”
• PubMed Central (2011). “Rebound acid hypersecretion after PPI therapy.”
• PubMed Central (2013). “Effect of GutGard in the Management of Helicobacter pylori.”