What DGL licorice actually is
Licorice root (Glycyrrhiza glabra) has been used medicinally for thousands of years, including specifically for gastrointestinal complaints. The problem with standard licorice root taken in meaningful doses is glycyrrhizin, a naturally occurring compound that, when consumed regularly, can raise blood pressure, cause sodium retention, and deplete potassium. At therapeutic doses for gut conditions, these effects become a genuine clinical concern.
Deglycyrrhizinated licorice, or DGL, is licorice root that has had glycyrrhizin removed, typically more than 97 per cent of it, leaving behind the flavonoids and other bioactive compounds that drive its mucosal protective and anti-inflammatory effects. This process was developed specifically to make the therapeutic benefits of licorice accessible without the blood pressure risk, allowing it to be used at consistent supplemental doses.
The practical result is that DGL and standard licorice root are not the same supplement for gut health purposes. DGL is the form supported by the research on mucosal protection. Whole licorice root, unless used in very small amounts, carries side effect risks that DGL does not.
How DGL supports the gut lining
Unlike proton pump inhibitors or antacids, DGL does not work by reducing stomach acid. This is an important distinction, because acid suppression approaches address a symptom: the sensation of excess acid, rather than the condition of the mucosal barrier that is allowing acid to cause damage in the first place. DGL works upstream of that by acting on the lining itself.
The primary mechanism is mucus stimulation. DGL promotes the production and secretion of mucus by the goblet cells and mucus-secreting cells of the gastric and intestinal lining. This mucus layer is the physical buffer between acidic stomach contents and the epithelial cells beneath. When it is thin or compromised, acid, bile, and other irritants have direct access to the underlying tissue. When it is healthy and thick, it provides the protective coating that allows the lining to withstand normal gastric conditions.
Studies examining DGL's effect on gastric tissue have found that it increases the number of mucus-secreting cells in the stomach lining and promotes the thickness and quality of the mucus layer itself. One early but influential study found a significant increase in mucus-producing cells following DGL use. The mucus layer is the primary physical defence of the gut wall against both acid and microbial translocation. Thickening it is a direct structural contribution to mucosal protection rather than a symptomatic one.
DGL has demonstrated anti-inflammatory activity in gastric tissue. The flavonoid compounds retained after the deglycyrrhizination process, including liquiritin, isoliquiritin, and glabridin, inhibit pro-inflammatory pathways in the gastric mucosa. This matters because chronic mucosal inflammation is self-perpetuating: it damages the cells that produce protective mucus, which further reduces the barrier, which allows more irritants to inflame the tissue. Breaking that cycle is part of what DGL's anti-inflammatory activity achieves.
Research has identified that DGL promotes proliferation of the epithelial cells that make up the gastric and intestinal lining. The gut lining turns over rapidly. Intestinal epithelial cells renew approximately every three to five days under healthy conditions, and the quality of that renewal depends partly on the conditions in which cells are regenerating. DGL appears to create a more favourable environment for that regeneration by reducing the inflammatory signals that impair it.
DGL for acid reflux and heartburn
Acid reflux, the upward movement of stomach acid into the oesophagus, is one of the most common reasons people reach for DGL. Understanding why it can help requires separating it from the mainstream understanding of acid reflux as a problem of too much acid.
In reality, for a significant proportion of people with reflux symptoms, the issue is not excess acid production but a compromised lower oesophageal sphincter that allows normally-acidic stomach contents to travel upward, combined with an oesophageal lining that is not adequately protected when that happens. The oesophagus, unlike the stomach, does not produce the thick mucus layer that protects against acid. When acid repeatedly contacts the oesophageal lining, the tissue becomes inflamed, which produces the burning sensation of heartburn.
DGL's role in acid reflux is to support the mucosal lining of both the stomach and the oesophagus, and to reduce the local inflammatory response that makes the oesophageal tissue more sensitive. It does not prevent reflux events from occurring, but it can reduce the damage each reflux event causes to the tissue it contacts.
"DGL does not suppress acid. It builds the lining that acid has to get through first."
This is why DGL is often discussed alongside rather than instead of other approaches. For people managing reflux through dietary adjustment, eating patterns, and weight management, DGL provides direct mucosal support during the period when those changes are taking effect. For people who have been reliant on PPIs and are attempting to reduce or come off them, DGL is commonly used as part of the transition to manage the period of acid exposure during dose reduction.
For DGL to have the best effect on oesophageal tissue, it is typically recommended to chew the tablet rather than swallow it whole. Chewing allows the active compounds to mix with saliva and come into contact with the oesophageal lining during swallowing, rather than passing directly to the stomach in solid form.
DGL for gastritis and mucosal damage
Gastritis, inflammation of the stomach lining, is one of the conditions where DGL has the most directly relevant mechanism. The two most common causes of gastritis in the UK are H. pylori infection and regular NSAID use, both of which damage the gastric mucosa through different but converging pathways.
H. pylori damages the gastric lining through the direct action of its virulence factors and through the chronic inflammation it sustains. NSAIDs, including ibuprofen, aspirin, and naproxen, work by inhibiting COX enzymes, which reduces prostaglandin synthesis. Prostaglandins are not only involved in inflammation; they also stimulate mucus secretion and bicarbonate production in the stomach lining. Suppressing them with regular NSAID use progressively reduces the stomach's own protective layer.
In both cases, DGL's mechanism is directly relevant. By stimulating mucus production, reducing mucosal inflammation, and supporting epithelial cell regeneration, it addresses the core consequences of gastric mucosal damage regardless of whether the original cause was bacterial or pharmacological. It is not a treatment for H. pylori infection and cannot eradicate the bacteria, but it provides meaningful support for the lining that H. pylori has damaged, both during and after eradication treatment.
DGL and broader gut lining repair
The research on DGL has historically been focused on the stomach and upper gastrointestinal tract: gastric ulcers, duodenal ulcers, gastritis, and oesophageal symptoms. But the mechanisms through which DGL works, covering mucus stimulation, anti-inflammatory activity, and epithelial support, are not exclusive to the stomach. The intestinal lining faces many of the same structural challenges.
In the context of intestinal permeability, often referred to as leaky gut, the tight junction proteins that hold intestinal epithelial cells together are compromised by chronic inflammation, microbial dysbiosis, and various dietary and pharmacological insults. DGL's anti-inflammatory activity, and its promotion of epithelial cell health, creates conditions that are supportive of tight junction integrity alongside more targeted interventions.
DGL is rarely used as a standalone intervention for intestinal permeability. It is more commonly paired with nutrients that have direct tight junction mechanisms, specifically L-Glutamine, zinc, and butyrate, as part of a broader gut lining support protocol. Its contribution in that context is largely mucosal coating and anti-inflammatory support of the upper GI tract, which reduces the burden on the intestinal barrier further downstream.
Who is DGL most relevant for
DGL is a well-tolerated botanical with a clear mucosal mechanism and a good safety profile in the deglycyrrhizinated form. The people for whom it is most relevant tend to share a common thread: the mucosal lining of their upper GI tract is under stress and needs direct structural support.
How to use DGL effectively
The standard supplemental dose of DGL used in research and clinical practice is 380 to 760 mg taken before meals. The timing matters: taking DGL before eating means the active compounds are present in the stomach lining before food and acid production peak. Taking it after eating significantly reduces its mucosal coating effect.
For oesophageal symptoms specifically, including heartburn, reflux, or oesophagitis, chewing the tablet before swallowing is recommended rather than swallowing it whole. Chewing releases the active flavonoids and allows them to coat the oesophageal lining as they pass through, which is where the protective effect is most relevant for upper-tract symptoms.
DGL is generally used in courses of four to twelve weeks in clinical studies, though longer use is common in supplemental contexts. Because glycyrrhizin, the compound associated with blood pressure effects, has been removed, DGL can be taken at consistent supplemental doses without the concerns that apply to whole licorice root. However, some residual glycyrrhizin remains in most preparations (typically below three per cent), so people with hypertension should note this and discuss with their GP if they intend long-term use.
- Take DGL before meals rather than after: the mucosal coating effect is most relevant pre-acid peak
- For oesophageal symptoms, chew the tablet rather than swallowing whole
- Standard dose in research is 380 to 760 mg; most supplements provide one to two tablets in this range
- DGL can be stacked with L-Glutamine, zinc, and marshmallow root for a more comprehensive gut lining protocol. read about marshmallow root and how it complements DGL
- People with hypertension should confirm with their GP before long-term use, even in the deglycyrrhizinated form
- DGL is not a treatment for H. pylori infection and should not replace prescribed eradication therapy
In terms of combinations, DGL works well alongside other mucosa-supportive botanicals and nutrients. Marshmallow root (also a mucilaginous coating botanical), L-Glutamine (primary fuel for enterocytes), and zinc (essential for tight junction integrity and epithelial repair) are commonly paired with DGL in gut lining protocols, with each contributing a distinct but complementary mechanism.
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