Licorice root has been used medicinally for over 4,000 years, appearing in ancient Egyptian, Chinese, and Ayurvedic medical traditions as a treatment for gastrointestinal complaints, cough, and inflammatory conditions. Modern pharmacological research has confirmed that licorice contains genuinely bioactive compounds â particularly glycyrrhizin and its metabolite glycyrrhizic acid â that have anti-inflammatory, antimicrobial, and gastroprotective properties. The problem: glycyrrhizin also causes sodium retention, potassium loss, and elevated blood pressure with chronic use, making therapeutic doses of standard licorice unsafe for long-term supplementation. Deglycyrrhizinated licorice (DGL) solves this by removing the problematic compound while preserving the gut-healing benefits. If you're recovering from SIBO, dealing with acid reflux, or healing an inflamed gut lining, DGL is one of the most useful and underrated tools in the supplement toolkit.
What Is DGL and Why Glycyrrhizin Is Removed
Standard licorice root (Glycyrrhiza glabra) extract contains 10-25% glycyrrhizin by weight. Glycyrrhizin is converted in the body to glycyrrhetinic acid, which inhibits an enzyme called 11-beta-hydroxysteroid dehydrogenase (11β-HSD). This enzyme normally inactivates cortisol in the kidneys. When 11β-HSD is blocked, cortisol acts on the mineralocorticoid receptors in the kidney, causing the same effect as the hormone aldosterone: sodium retention, potassium excretion, and increased blood pressure. With therapeutic doses over weeks, this pseudohyperaldosteronism can cause significant hypertension, hypokalemia, edema, and in severe cases, cardiac arrhythmias.
DGL (deglycyrrhizinated licorice) is produced by a specialized extraction process that removes more than 97% of the glycyrrhizin content. The resulting product retains the flavonoid compounds â primarily glabridin, liquiritin, isoliquiritin, and chalcones â that are responsible for licorice's gut-healing and anti-inflammatory effects. Glycyrrhizin itself is not entirely removed from the DGL formula but is reduced to levels below approximately 3 mg per serving, well below the threshold associated with blood pressure effects (which typically requires >100 mg/day glycyrrhizin chronically).
âšī¸DGL is considered safe for long-term use at standard doses (750-1500 mg daily) because the glycyrrhizin content is too low to cause meaningful pseudohyperaldosteronism. Standard licorice candy and licorice root extract supplements are not equivalent to DGL and should not be used interchangeably for therapeutic purposes.
How DGL Heals the Gut Lining: The Mechanisms
DGL supports gastric and intestinal mucosal integrity through several complementary mechanisms that together make it genuinely useful for gut healing â not just symptom masking.
Primary gastroprotective mechanisms of DGL:
- Mucus stimulation: DGL increases the production and secretion of mucus in the gastric and intestinal lining. This mucus layer is the physical barrier between the gut epithelium and luminal contents, including acid, bile, bacteria, and food antigens. Thicker, more robust mucus protects against the mucosal erosion that leads to gastritis and peptic ulcers.
- Prostaglandin synthesis: DGL stimulates the synthesis of cytoprotective prostaglandins (particularly PGE2) in the gastric mucosa. These prostaglandins increase mucosal blood flow, stimulate bicarbonate secretion, and promote mucosal cell turnover â all of which support healing. This is the same pathway targeted by misoprostol (a pharmaceutical PGE1 analog used to protect the stomach during NSAID therapy).
- Anti-inflammatory activity: Glabridin and other DGL flavonoids inhibit the NF-kB inflammatory pathway and reduce production of pro-inflammatory cytokines (TNF-alpha, IL-6, IL-1beta) in the gastric mucosa. This addresses the chronic low-grade inflammation that perpetuates gastritis and delays ulcer healing.
- Antimicrobial activity against H. pylori: Several DGL flavonoids have demonstrated activity against Helicobacter pylori in vitro, including strains that are resistant to standard antibiotic regimens. While DGL is not a primary H. pylori treatment, its antimicrobial properties complement the mucus-protective effects.
- Tight junction support: Emerging research suggests DGL flavonoids support the integrity of tight junctions between intestinal epithelial cells, helping to reduce intestinal permeability ('leaky gut') that commonly accompanies SIBO and chronic gut inflammation.
Clinical Evidence: Ulcers, Reflux, and H. pylori
DGL's evidence base, while not as extensive as pharmaceutical interventions, is meaningful. The most robust evidence comes from studies on peptic ulcer disease predating the H. pylori era, when licorice-based preparations (like carbenoxolone, derived from glycyrrhizic acid) were standard treatments. Multiple RCTs from the 1960s-1980s demonstrated that carbenoxolone was significantly superior to placebo for gastric and duodenal ulcer healing. DGL formulations showed comparable efficacy in several trials with fewer blood pressure side effects.
A commonly cited study compared DGL (760 mg three times daily before meals) to antacids and cimetidine (an H2 blocker) for maintenance of remission in duodenal ulcer patients, finding that DGL was equivalent to these pharmaceutical options for preventing ulcer recurrence. More recent research has focused on DGL's anti-H. pylori activity: a 2019 study in the Journal of Ethnopharmacology demonstrated that specific licorice flavonoids significantly reduced H. pylori adherence to gastric cells and impaired its virulence factors.
For acid reflux and GERD, DGL evidence is more modest â there are no large RCTs, but several smaller trials and observational studies report improved reflux symptoms and reduced esophageal irritation with DGL use. The mechanism is plausible: enhanced esophageal and gastric mucus production and reduced inflammation in the lower esophageal mucosa would logically reduce the burning sensation from refluxate.
DGL for Post-SIBO Gut Lining Repair
After SIBO treatment, the gut lining is often damaged. Bacterial toxins (lipopolysaccharides, bacterial proteases), the inflammatory response to chronic overgrowth, and in some cases the antimicrobial treatment itself can compromise the intestinal mucosa, contributing to increased intestinal permeability ('leaky gut'), food sensitivities, and ongoing digestive symptoms even after bacterial overgrowth has been cleared.
DGL is a logical component of a post-SIBO gut healing protocol for several reasons: it directly stimulates mucus production to restore the protective barrier, reduces ongoing mucosal inflammation, and supports prostaglandin-mediated tissue repair. It's typically used as part of a broader gut-healing stack that might include L-glutamine (epithelial cell fuel), zinc carnosine (mucosal regeneration), colostrum (growth factor support), and marshmallow root or slippery elm (additional demulcent support).
đĄFor gut healing applications, DGL is most effective when taken before meals â 20-30 minutes before eating. This timing allows DGL to coat and protect the gastric mucosa before acidic digestive secretions are triggered by food. For reflux or nighttime symptoms specifically, an additional dose at bedtime can be helpful. The chewable tablet form may be more effective than capsules for upper GI conditions, as chewing starts the mucosal contact earlier in the GI tract.
Chewable vs. Capsule DGL: Does It Matter?
DGL is available in two primary forms: chewable tablets and capsules. For upper GI conditions â gastritis, reflux, esophageal irritation, peptic ulcers â the chewable form is generally preferred. Chewing increases mucosal contact time with the oral, esophageal, and gastric tissues, which is relevant for conditions involving these upper structures. Saliva mixed with DGL may also allow some absorption through the oral mucosa, providing earlier systemic availability of the flavonoids.
For lower GI applications â intestinal permeability, post-SIBO gut repair, distal intestinal inflammation â capsules are equivalent or preferable, as they deliver the active compounds to the small intestine and colon rather than releasing them in the upper GI tract. If using DGL for SIBO-related gut healing, capsule form reaching the small intestine is the primary target.
Dosing and Safety
DGL dosing by application:
- Acid reflux and GERD: 380-760 mg (chewable tablet) 20 minutes before meals and at bedtime. Start with a lower dose and increase if tolerated.
- Peptic ulcer support: 760 mg three times daily before meals, continuing for 8-16 weeks or until symptoms resolve. This was the dose used in clinical trials.
- H. pylori support (adjunct to antibiotic therapy): 400-500 mg twice daily alongside prescribed eradication therapy.
- Post-SIBO gut healing: 400-500 mg in capsule form before meals, for 4-12 weeks.
- General gut maintenance: 250-380 mg once daily, taken 20 minutes before the largest meal.
DGL is well-tolerated at standard doses. Because the glycyrrhizin is removed, blood pressure effects are not a concern at therapeutic DGL doses. Rare adverse effects include mild GI upset or loose stools. DGL should be used with caution during pregnancy â licorice compounds have been associated with adverse pregnancy outcomes at high doses in epidemiological studies, and while DGL's lower glycyrrhizin content makes it much safer, caution is warranted. There are no significant drug interactions at standard DGL doses. People with any history of hormone-sensitive conditions (estrogen-receptor-positive cancers, etc.) should discuss DGL with their oncologist before use, as some licorice flavonoids have weak estrogenic activity.
**Disclaimer:** This article is for informational purposes only and does not constitute medical advice. Always consult with a qualified healthcare provider before starting any new treatment or making changes to your existing treatment plan.