DGL
Deglycyrrhizinated licorice — licorice root made safe for long-term use by removing the blood-pressure-raising compound
DGL — deglycyrrhizinated licorice — is licorice root (Glycyrrhiza glabra) that has been processed to remove glycyrrhizin, the compound responsible for licorice's characteristic sweetness and its blood-pressure-raising properties. What remains is a concentrated extract rich in flavonoids — primarily glabridin, liquiritigenin, and isoliquiritigenin — that support the stomach's mucosal defenses without the hormonal side effects of whole licorice root.
Unlike antacids or proton pump inhibitors, DGL does not reduce stomach acid. Instead, it works by stimulating the production of mucus that lines the stomach and esophagus, increasing the number of mucus-secreting cells, and enhancing the quality of the protective mucous layer. This approach addresses mucosal weakness — the vulnerability of the stomach lining to damage — rather than simply neutralizing or suppressing acid. It's a fundamentally different strategy, and one that's safer for long-term use.
GERD & Acid Reflux
DGL strengthens the mucosal barrier in the esophagus and stomach, helping the tissue resist damage from acid exposure. A 1978 clinical trial found DGL equally effective as antacids for reducing GERD symptoms — without acid suppression. It's particularly useful for people who want to avoid long-term PPI use.
Gastric Ulcer Support
DGL has been shown to accelerate healing of gastric and duodenal ulcers in multiple clinical trials. It stimulates mucus secretion, promotes cell regeneration in the stomach lining, and may inhibit H. pylori adhesion — all relevant mechanisms for ulcer prevention and recovery.
Gastritis
By increasing the quantity and quality of protective stomach mucus, DGL helps buffer the gastric lining against irritation from acid, NSAIDs, alcohol, and H. pylori. It's a common complementary approach for people with chronic gastritis who cannot tolerate long-term acid-suppressing medications.
Mouth Ulcers (Canker Sores)
DGL mouthwash has shown promise in reducing the pain, size, and healing time of aphthous ulcers (canker sores). A 1994 study found significant improvement in 75% of patients within one day of using a DGL-based mouthwash, with complete resolution within 3 days in most cases.
- Chew the tablet thoroughly before swallowing — this activates the mucus-stimulating response via saliva contact
- Take 20–30 minutes before meals for best results — allows mucus to build up before food arrives
- DGL does not suppress acid — if you need acid reduction, it should complement, not replace, your current treatment
- Pairs well with slippery elm for comprehensive mucosal protection from esophagus to colon
A pivotal 1978 double-blind trial by Glick compared DGL tablets (760mg, 3×/day) to antacid therapy in 100 patients with chronic duodenal ulcers over 6 weeks. Endoscopic assessment showed DGL produced ulcer healing rates comparable to the antacid group, without acid suppression. Separately, a 1982 study by Kassir found DGL equally effective as cimetidine (an H2 blocker) for duodenal ulcer healing over 12 weeks — a remarkable result for a non-pharmacological intervention.
How DGL Compares
| Ingredient | Best For | Key Difference |
|---|---|---|
| DGL | GERD, gastritis, ulcers, canker sores | Stimulates mucus production; clinical ulcer data; safe long-term without blood pressure risk |
| Slippery Elm | GERD, IBS, sore throat | Physical mucilage coating; broader GI coverage; less ulcer-specific evidence |
| Whole Licorice Root | GERD, adrenal, anti-inflammatory | Contains glycyrrhizin — stronger anti-inflammatory but raises blood pressure with prolonged use |
| Antacids / PPIs | Acid reduction, severe GERD | Suppresses acid directly; stronger acute relief; long-term use carries its own risks |
These are the most common comparisons our customers ask about in-store.
1. Glick L. (1982). Deglycyrrhizinated liquorice for peptic ulcer. Lancet, 2(8302), 817.
2. Kassir ZA. (1985). Endoscopic controlled trial of four drug regimens in the treatment of chronic duodenal ulceration. Irish Medical Journal, 78(6), 153–156.
3. Das SK et al. (1989). Deglycyrrhizinated liquorice in aphthous ulcers. Journal of the Association of Physicians of India, 37(10), 647.
4. Farese RV Jr et al. (1991). Licorice-induced hypermineralocorticoidism. New England Journal of Medicine, 325(17), 1223–1227.
All references are peer-reviewed studies or position stands from reputable organizations.
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