Peptic ulcers are open sores in the stomach or duodenal lining that go through the muscularis mucosae. Most are caused by H. pylori or NSAIDs131. Mastic gum, zinc carnosine5 and DGL (deglycyrrhizinated licorice) are studied as adjuncts alongside conventional H. pylori eradication; cabbage juice is of historical interest only6.
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Peptic Ulcer Disease (PUD) is the formation of open sores (ulcers) in the lining of the stomach (gastric ulcer) or the first part of the small intestine (duodenal ulcer). Unlike gastritis (surface inflammation), ulcers penetrate through the mucosa into the muscle layer below, making them deeper, more painful and more dangerous.
Most peptic ulcers are caused by H. pylori infection or NSAIDs13. Less common causes: Zollinger-Ellison syndrome (gastrin-secreting tumor), severe physiological stress (ICU patients), Crohn's disease, certain cancers. Lifestyle factors (smoking, alcohol, chronic stress) impair healing but rarely cause ulcers alone.
Untreated ulcers can bleed (sometimes massively), perforate the stomach or duodenum (medical emergency) or obstruct the gastric outlet. Most ulcers can be treated successfully with prescribed medicine, yet H. pylori-positive ulcers recur in a large proportion of patients within a year if H. pylori isn't eradicated3.
Located in the first part of the small intestine. Classic pain: 2 to 3 hours after meals, often relieved by eating. About 95% are associated with H. pylori11. Very rarely cancerous.
Severe stress ulcers in ICU patients (mechanical ventilation, burns, head injury). This group also includes chronic refractory ulcers that don't heal: investigate for Zollinger-Ellison, malignancy, hidden NSAID use or H. pylori resistance.
Classic textbook symptoms vary by ulcer location, but about two in three people found to have a peptic ulcer have no symptoms15, and some first learn of it from a complication such as bleeding13. Vague upper abdominal pain in NSAID users always warrants evaluation.
| Symptom | What happens |
|---|---|
| Pain Patterns | |
| Burning Epigastric Pain | Classic ulcer pain: gnawing, burning or aching in the upper central abdomen. Duodenal ulcer pain typically wakes patients at 1 to 3 AM (acid peak). Gastric ulcer pain often worsens with food. |
| Hunger Pains (Duodenal) | Duodenal ulcer pain occurs 2 to 3 hours after meals (when food has left the stomach) and is relieved by eating. Patients often wake at night with hunger-like pain. Antacids transiently help. |
| Food-Aggravated Pain (Gastric) | Gastric ulcer pain worsens shortly after eating. Leads to weight loss because patients avoid food. Distinguishes it from duodenal ulcers, which are relieved by food. |
| Nausea, Vomiting, Early Satiety | Particularly when ulcers are near the pyloric channel (causing functional obstruction). Vomiting that relieves pain is characteristic. |
| Red Flag & Complication Signs | |
| Hematemesis (Vomiting Blood) | Bright red OR "coffee ground" emesis. Indicates active bleeding ulcer. MEDICAL EMERGENCY. Call 911 or go to the ER immediately.4 |
| Melena (Black Tarry Stools) | Digested blood from upper GI source. Sticky, foul-smelling, jet-black. EMERGENCY. Distinguish from iron supplements (which darken stool but aren't tarry/foul-smelling). |
| Sudden Severe Abdominal Pain | Sudden, severe, "knife-like" pain with rigid abdomen = perforation. Surgical emergency. Mortality rises with delay. Call 911. |
| Unintentional Weight Loss | Especially with gastric ulcer pain. Patients avoid eating because of pain. Significant weight loss demands endoscopy to rule out malignancy. |
Two causes account for most peptic ulcers, H. pylori infection and NSAIDs, and a few others add to the risk or are rare13.
| Cause | How It Contributes to Peptic Ulcer Disease | What Helps |
|---|---|---|
| H. pylori infection | Associated with 95% of duodenal and 70% of gastric ulcers11; it spreads through contact with an infected person's vomit, stool or saliva, or food and water contaminated by them13. | Prescribed eradication therapy and a test to confirm it has cleared, which sharply cuts the chance of the ulcer coming back (conventional care); no food or supplement on this page clears it |
| NSAIDs and aspirin | They act throughout the body to weaken the stomach lining's protection, so enteric coating does not remove the risk1. The risk is higher with long-term or high-dose use, more than one NSAID or H. pylori infection at the same time13. | Stopping NSAIDs where possible; if one must continue, acid-reducing medicine alongside it, decided with your prescriber (conventional care) |
| Other medicines taken with NSAIDs | Corticosteroids, medicines for low bone mass and some antidepressants raise ulcer risk, especially when combined with NSAIDs13. | A medication review with your prescriber; do not stop a prescribed medicine on your own (conventional care) |
| Smoking and older age | Ulcers are more common in people who smoke, and the risk rises with age14. | Stopping smoking (Nutritional Strategy) |
| Serious illness | Life-threatening conditions that need critical care, and some severe long-term diseases, can cause ulcers13. | Treatment of the underlying illness by the hospital or specialist team (conventional care) |
| Rare causes | Zollinger-Ellison syndrome, in which gastrin-making tumors drive excess acid, and diseases such as cancer or Crohn's disease that affect the stomach13. | Testing when ulcers are multiple, recurrent or unusual, including a gastrin level, and biopsy of stomach ulcers (Diagnosis; conventional care) |
| Test | What it shows |
|---|---|
| Direct Visualization | |
| Upper Endoscopy (EGD) | Gold standard. Directly visualizes ulcer location, size, presence of bleeding. Biopsies confirm H. pylori, rule out cancer (especially gastric ulcers), check for premalignant changes. Allows therapeutic intervention if bleeding. |
| Upper GI Series (Barium Swallow) | X-ray after drinking barium contrast. Less accurate than endoscopy, so it can miss ulcers. Used when endoscopy unavailable or contraindicated. No biopsy capability; endoscopy is still required for confirmation. |
| H. pylori Testing & Workup | |
| Urea Breath Test or Stool Antigen | Non-invasive H. pylori detection. Ask your prescriber about stopping your proton pump inhibitor (PPI) 2 weeks before the test, for accuracy. Used to confirm eradication 4+ weeks after treatment.2 |
| Biopsy + Rapid Urease Test (CLO) | During endoscopy, gastric tissue biopsy is tested for urease activity. Highly specific for H. pylori. Histology also identifies inflammation severity, atrophy, intestinal metaplasia. |
| CBC, Iron Studies, Fecal Occult Blood | Check for iron-deficiency anemia from chronic blood loss. Positive fecal occult blood in someone with epigastric pain raises suspicion for bleeding ulcer. |
| Serum Gastrin (for Refractory Cases) | Elevated in Zollinger-Ellison syndrome (gastrinoma). Consider in multiple ulcers, refractory ulcers, ulcers in unusual locations or ulcers with severe symptoms. |
Mastic gum, zinc carnosine, DGL, glutamine and other supportive nutrients
No food treats an ulcer; prescribed medicine does that. The aim of diet is to avoid irritating the ulcer and to cut out what slows recovery, such as smoking, alcohol and NSAIDs.
Foods that are easier on an ulcer, and what to limit
| What to eat or do | Details |
|---|---|
| โ Prioritize These: | |
| Broccoli Sprouts | In a small trial, sulforaphane-rich sprouts lowered markers of H. pylori and stomach inflammation while they were eaten, but the markers returned after stopping and the infection was not cleared16. The trial used 2.5 oz (70 g) of sprouts a day. |
| Manuka Honey (high grade) | It inhibits H. pylori in laboratory culture only17; eating it is not a treatment for the infection. 1 tsp 2 to 3x/day soothes. Standard honey doesn't have the same effect. |
| Bone Broth & Soothing Soups | Claims that they repair the stomach lining are unproven. Easy to digest during acute phase. Add ginger and turmeric for anti-inflammatory benefit. |
| โ Limit or Eliminate: | |
| NSAIDs (Avoid Where Possible) | NSAIDs such as ibuprofen, aspirin and naproxen are, with H. pylori, the most common causes of ulcers13. Ask your prescriber about alternatives such as acetaminophen, and if you take a prescribed low-dose aspirin, keep taking it unless you are advised to stop18. |
| Smoking | Raises ulcer risk and slows healing. Stopping is one of the most important changes once H. pylori and NSAIDs are dealt with. |
| Alcohol | Direct mucosal irritant. Impairs ulcer healing and increases bleeding risk. Complete avoidance during healing phase; minimal/none long-term. |
| Coffee & Acidic Drinks | Stimulate acid secretion and directly irritate. Avoid during acute phase; gradually reintroduce as ulcer heals. Decaf is still problematic; both forms stimulate acid. |
These supplements are used alongside prescribed treatment, for symptom relief and for the nutrient shortfalls long-term PPI use can cause; none of them clears H. pylori.
| Supplement | What it is for | Typical range | Timing | Notes & cautions |
|---|---|---|---|---|
| Mastic Gum | Inhibits H. pylori in the laboratory, but it has not been shown to clear the infection and is not a substitute for eradication therapy. | 500 to 1,000 mg 2x/day | Empty stomach | 4 to 8 week courses; can repeat. |
| Zinc Carnosine | Approved ulcer drug in Japan. Small trials suggest a benefit to the stomach lining; it does not clear H. pylori. | 75 mg 2x/day, roughly 17 mg elemental zinc per 75 mg dose | Empty stomach | Take separately from antibiotics & iron. |
| DGL Licorice | Stimulates mucus secretion and prostaglandin synthesis. Soothes inflammation. No BP effect (vs regular licorice). | 380 to 760 mg chewable, 2 to 3x/day | 20 min before meals | Chewable form is used for action in the stomach. |
| L-Glutamine | A fuel for gut lining cells; evidence in peptic ulcer is limited. | 5 g 2x/day | Between meals, in water | Tasteless. Ask your oncology team before taking it if you have cancer; avoid it with severe liver disease. |
| S. boulardii + L. reuteri | Added to prescribed antibiotics, S. boulardii modestly raised eradication and reduced side effects such as diarrhea in pooled trials19; it does not treat the infection on its own. | S. boulardii 250 mg (about 5 billion CFU) to 500 mg (about 10 billion CFU) + L. reuteri per label | Throughout the antibiotic course + 2 weeks after | S. boulardii is safe with antibiotics (yeast, not bacteria). Use caution with immunosuppression or a central line, as yeast bloodstream infections have been reported; discuss with your team. |
| Vitamin C | Concentrates in gastric mucosa; evidence that it helps ulcers is limited. Low gastric vitamin C is associated with H. pylori and gastric cancer. | 500 to 1,000 mg/day | With meals (buffered forms if sensitive) | Don't take large doses on empty stomach during active ulcer. |
| Vitamin E + Selenium | Antioxidant duo concentrates in gastric tissue. Evidence that it helps ulcers is limited. | 200 to 400 IU E + 100 to 200 mcg selenium daily | With fat meal | Selenium dose should not exceed 200 mcg/day chronically. Vitamin E can raise bleeding risk with blood thinners or aspirin; do not take it with an active or recent bleeding ulcer unless your clinician agrees. |
| Vitamin B12 (post-PPI/eradication) | PPIs & H. pylori both impair B12 absorption. Test serum B12, methylmalonic acid; supplement if deficient. | 1,000 mcg/day sublingual | Any time | High-dose B12 by mouth or under the tongue works even when stomach acid is low, because a small share is absorbed passively. |
Most ulcers are treated with prescribed medicine: H. pylori is an infection cleared with antibiotics, and diet supports recovery around that treatment.
Acid-reducing medicine is usually taken for 4 weeks for a duodenal ulcer (4 more for some) and for 4 to 8 weeks for a benign gastric ulcer8. If H. pylori is present, a prescribed 14-day course of several medicines is the preferred first treatment9. Take every dose, even once the pain eases, because stopping early can let some bacteria survive and become resistant to antibiotics20. NSAIDs are stopped where possible.
Once H. pylori is cleared, relapse is much less common: duodenal ulcers came back in 12.9% after eradication, against 64.4% with no treatment11. Acid-reducing medicine is not continued past the planned course unless your clinician advises it.
If an NSAID must continue, acid-reducing medicine is taken alongside it. Stopping smoking lowers the risk of another ulcer. If symptoms return, see your doctor14.
Call 911 or go to the emergency department now, without waiting or trying diet first, if you vomit blood or material like coffee grounds, pass black, sticky or bloody stools, have sudden severe abdominal pain or a belly that is painful to touch, or feel faint with a racing pulse1413. Bleeding and perforation can be fatal, and delay raises the risk12.
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Modern medicine has made peptic ulcers highly treatable. Treating the cause (clearing H. pylori and stopping NSAIDs where possible) is what prevents recurrence; diet supports recovery around that treatment.
Each numbered entry below is either a source you can follow or a note setting out what the evidence does and does not support. Both are numbered together so the markers in the text line up.
Last reviewed October 20, 2026. Supplement entries are cross-checked against the NIH National Center for Complementary and Integrative Health and the Linus Pauling Institute Micronutrient Information Center.7 The single most useful thing here: most peptic ulcers are caused by Helicobacter pylori infection or by NSAIDs, and both causes are addressable. If you have an ulcer, get tested for H. pylori, and if it is present, take the eradication course and have the cure confirmed with a test afterward. Untreated infection is why ulcers come back. Nothing on this page eradicates H. pylori; the supplements here support mucosal healing alongside treatment. Some symptoms are emergencies rather than nutrition problems: vomiting blood or coffee-ground material, black tarry stools, sudden severe abdominal pain with a rigid abdomen, fainting or a rapid pulse with breathlessness. Those mean bleeding or perforation and need an emergency department immediately.