Gastritis: A Comprehensive Reference in Nutrition and Natural-Health Context
1. Definition and Nature of the Condition
Gastritis is formally defined as any inflammation of the gastric mucosa confirmed on histology. The term is clinically broader than the histological definition suggests: gastritis encompasses a heterogeneous spectrum of inflammatory and structural alterations of the gastric mucosa arising from diverse etiologies, including Helicobacter pylori infection, autoimmune processes, and drug-induced mucosal injury.
Gastritis may occur suddenly (acute gastritis) or appear slowly over time (chronic gastritis). Acute gastritis is generally transient, either resolving or progressing to chronic gastritis; the major categories established in the literature are acute hemorrhagic/erosive gastritis (often related to chemical or irritant injury) and acute Helicobacter gastritis.
Erosive gastritis is most commonly caused by medications, excessive alcohol consumption, and radiation therapy; nonerosive gastritis is usually caused by infection, acute stress, or physical trauma. The inflammation may involve the entire stomach (pangastritis) or a region of the stomach (antral gastritis).
Gastritis is classified based on the acuity of the condition (acute versus chronic), the histological features of inflammation, or the etiology. In 1990, the "Sydney System" was established using both endoscopic and histologic findings to classify and grade chronic gastritis in a systematic manner. The Updated Sydney System integrates topography, morphology, and etiology to generate standardized diagnoses, recommending systematic biopsies from the antrum, corpus, and incisura, with grading of H. pylori density, neutrophilic activity, chronic inflammation, glandular atrophy, and intestinal metaplasia using a visual analogue scale.
2. Clinical Presentation and Symptoms
The majority of people with gastritis or gastropathy do not have any symptoms. No correlation exists between microscopic inflammation (histologic gastritis) and the presence of gastric symptoms such as abdominal pain, nausea, or vomiting; in fact, most patients with histological evidence of acute gastritis are asymptomatic.
When symptoms do occur, they span a range of upper-gastrointestinal complaints. In both acute and chronic cases, symptoms range from abdominal pain, nausea, and vomiting, with the caveat that chronic gastritis may be asymptomatic in some individuals. The typical signs of gastritis are stomach pain, feeling full, and bloating. The most common symptom of acute gastritis is sudden nondescript epigastric discomfort.
Persistence of H. pylori causes H. pylori chronic gastritis, which is usually asymptomatic but may manifest as epigastric pain, nausea, vomiting, anorexia, early satiety, or weight loss. Symptoms may occur with the development of complications of chronic H. pylori gastritis, which include peptic ulcers, gastric adenocarcinoma, and mucosa-associated lymphoid tissue (MALT) lymphoma.
In the specific subtype of autoimmune gastritis, the clinical manifestations are primarily related to a deficiency in cobalamin, which is not adequately absorbed because of intrinsic factor deficiency resulting from severe gastric parietal cell atrophy. Cobalamin deficiency affects the hematologic, gastrointestinal, and neurologic systems; the most significant hematologic manifestation is megaloblastic anemia.
If gastritis progresses, erosions or ulcers may develop, causing the stomach lining to bleed. Alarm features warranting urgent investigation include: new-onset symptoms at an advanced age, weight loss, evidence of bleeding, dysphagia, the presence of an abdominal mass, fever, persistent vomiting, or a family history of esophageal or gastric cancer.
3. Body Systems Involved
The Gastric Mucosa and Digestive System
Gastritis is an inflammatory disorder that affects the mucosal membranes of the stomach. The contributing factors negatively impact the protective barrier lining the stomach by affecting cellular regeneration, mucus production, and bicarbonate secretion, in addition to abolishing the antioxidant capacity of gastric tissues.
H. pylori-induced inflammation occurs through an increase in interleukin (IL)-8 production by gastric epithelial cells. IL-8 subsequently triggers the activation of neutrophils and the recruitment of other inflammatory cells into the mucosa. Persistent inflammation ultimately leads to the depletion of gastrin-producing (G) cells and acid-producing parietal cells. Over time, atrophy and intestinal metaplasia develop.
The Hematological System
H. pylori gastritis can cause problems absorbing iron from food, and autoimmune gastritis can cause problems absorbing iron and vitamin B12 from food. The known consequence of autoimmune gastritis is vitamin B12 deficiency and pernicious anemia. Loss of parietal cells reduces secretion of gastric acid, which is also required for absorption of inorganic iron; thus, iron deficiency is commonly found in patients with autoimmune gastritis, usually preceding vitamin B12 deficiency and found mainly in young women.
Iron deficiency is the most frequent hematological manifestation of autoimmune gastritis, and the prevalence of iron and B12 deficiency in autoimmune gastritis patients is estimated to be 50% and 37–60%, respectively.
The Immune System
The pathophysiology of H. pylori–induced gastritis involves a complex interaction between bacterial virulence factors and the host's immune responses. This interplay disrupts the gastric mucosal barrier and leads to chronic inflammation. H. pylori possesses virulence factors that facilitate cell adhesion, cause cell damage, disrupt tight junctions, and evade the host immune response. Notably, the cytotoxin-associated gene A (CagA) is a potent inducer of inflammation and is associated with the development of gastric cancer.
Autoimmune gastritis exhibits a chronic mononuclear inflammation accompanied by severe atrophic gastritis, which usually affects the corpus, along with the presence of autoantibodies against parietal cells or the intrinsic factor.
The Neurological System
Patients who develop vitamin B12 deficiency from chronic atrophic gastritis will suffer from gastrointestinal and neurological complaints such as malabsorption, diarrhea, weight loss, glossitis, peripheral numbness, and paresthesias.
4. Contributing and Associated Factors
Helicobacter pylori Infection
Helicobacter pylori is the leading cause of chronic gastritis, peptic ulcer disease, gastric adenocarcinoma, and primary gastric lymphoma. The infection affects around half of the population in the world, but prevalence varies according to location and sanitation standards. H. pylori infection most often begins during childhood; it is present in about 10–15% of U.S. children younger than age 12 and in about 50–60% of U.S. adults older than age 60.
H. pylori gastritis typically starts as an acute gastritis in the antrum, causing intense inflammation, and over time it may extend to involve the entire gastric mucosa, resulting in chronic gastritis.
NSAIDs and Medications
Overuse of NSAIDs (nonsteroidal anti-inflammatory drugs), such as aspirin and ibuprofen, is one of the most common causes of acute gastritis. NSAIDs are the most common noninfectious cause of peptic ulcers and can cause life-threatening bleeding, obstruction, or perforation of the stomach or small intestine.
Alcohol
Reactive gastropathy is caused by long-term contact with substances that irritate the stomach lining, most often nonsteroidal anti-inflammatory drugs, alcohol, and bile reflux — the backward flow of bile from the small intestine to the stomach. It is generally advised to avoid alcohol consumption for the prevention and mitigation of gastrointestinal injury; some sources describe alcohol as a potential cause of gastritis, while others describe it as a potential contributor to the erosion of the stomach's mucosal lining when ingested in large doses.
Autoimmune Mechanisms
Autoimmune gastritis occurs when the immune system attacks healthy cells in the stomach lining. Autoimmune gastritis is an immune-mediated disease characterized by the destruction of parietal cells and atrophy of the oxyntic mucosa due to anti-parietal cell antibodies. It may lead to serious conditions including iron/vitamin B12 and micronutrient deficiencies, neurological disorders, and gastric malignancies. The exact mechanism is not fully understood; however, dysregulated immunological mechanisms appear to be major contributors.
Stress, Severe Illness, and Other Factors
Acute erosive gastropathy may occur after contact with irritating substances such as NSAIDs, alcohol, or cocaine. A form of acute erosive gastropathy called stress gastritis develops when serious health problems — such as severe injuries or burns, critical illness, or sepsis — are present.
Other causes include smoking, cocaine, severe illness, autoimmune problems, radiation therapy, and Crohn's disease. Bile reflux gastritis is caused by a retrograde flow of bile from the small intestine to the stomach; because bile is an alkaline digestive fluid, it can damage the gastric mucosa. It is frequently associated with an incompetent pyloric valve or procedures that involve manipulation of the biliary tree and pyloric sphincter.
5. Nutrients, Herbs, and Natural Ingredients
5.1 Probiotics
Traditional Use: Fermented foods containing live bacterial cultures — including yogurt, kefir, kimchi, and sauerkraut — have been used across many food cultures as part of traditional diets to support digestive health. These were not specifically directed at gastritis in early traditional medicine but formed part of broadly recognized dietary patterns for gastrointestinal well-being.
Scientific Evidence: Probiotics are among the most extensively studied natural interventions in the context of H. pylori-associated gastritis. A meta-analysis including data on 6,997 participants from 45 randomized controlled trials found overall eradication rates of 82.31% in the probiotic group versus 72.08% in the control group. A more recent systematic review and meta-analysis, searching PubMed, EMBASE, the Cochrane Library through January 2024 and including 12 eligible RCTs with 2,144 participants, found that the overall eradication rate of H. pylori was higher in the probiotics pretreatment group compared to controls (80.34% vs. 70.49%, RR 1.14, 95% CI: 1.08–1.19) and side effects were substantially lower (16.0% vs. 28.3%, RR 0.59, 95% CI: 0.41–0.84).
Current clinical research on antagonism of H. pylori primarily focuses on certain strains of Lactobacillus, Bifidobacterium, and Saccharomyces. These probiotics have been shown to reduce H. pylori infection rates and attenuate gastrointestinal symptoms, while also enhancing the efficacy of antibiotic treatments.
Limitations: There is no standardized protocol regarding the species of probiotic, the dose, or the duration of supplementation in these studies, which will inevitably affect the results. It also seems that not all probiotics contribute equal beneficial effects. There have been no trials involving patients from North America or Black individuals. More studies with rigorous designs, large sample sizes, and multiregional cooperation are required.
5.2 Vitamin C (Ascorbic Acid)
Traditional Use: Ascorbic acid is an essential dietary nutrient found abundantly in fruits and vegetables. Its use in supporting gastric health was not codified in ancient herbal traditions per se, but diets rich in fresh produce have long been empirically associated with protection against upper gastrointestinal disease in epidemiological observation.
Scientific Evidence: Vitamin C levels both in gastric acid and serum have consistently been found to be low in subjects with H. pylori-infected gastritis and peptic ulcers. H. pylori causes chronic gastritis that is associated with the generation of reactive oxygen species and nitric oxide metabolites and a reduction in antioxidant vitamin C levels.
Ascorbic acid may be protective against gastric cancer by its antioxidant effect in gastric cytoprotection, regenerating active vitamin E and glutathione, inhibiting endogenous N-nitrosation, reducing toxic effects of ingested nitrosodimethylamines, and potentially preventing H. pylori infection. Eradication of H. pylori may lead to recovery of vitamin C secretion by gastric epithelium and enable regression of premalignant gastric lesions, thereby interrupting the Correa cascade of gastric carcinogenesis.
Several clinical studies have shown that higher prevalence of H. pylori infection is associated with low vitamin C levels in serum and gastric juice; however, there is no consensus regarding the usefulness of vitamin C supplementation in the management of H. pylori infection. The role of vitamin C as an anti-H. pylori agent in peptic ulcer disease appears to be preventive rather than curative.
Limitations: Most evidence on vitamin C and gastritis is observational or derived from studies of gastric cancer risk. Robust interventional data specifically for gastritis endpoints remain limited. Findings on mucosal ascorbic acid levels in H. pylori infection are not uniform across all studies.
5.3 Zinc-L-Carnosine (Polaprezinc)
Traditional Use: No classical traditional medicine tradition specifically used zinc-L-carnosine, as it is a synthetic chelated compound. It was developed in Japan as a pharmaceutical agent.
Scientific Evidence: Zinc-L-carnosine (ZnC), also called polaprezinc (PepZin GI™), is a chelated compound containing L-carnosine and zinc. It is a relatively new molecule that has been associated with multiple health benefits. Zinc carnosine was initially developed in Japan in the 1990s to support stomach health. Studies have shown that adding zinc carnosine (dosed 75 mg twice daily) to triple antibiotic therapy may enhance the management of H. pylori infection.
Clinical investigations include a prospective, multicenter, randomized clinical trial of polaprezinc combined with clarithromycin-based triple therapy for H. pylori-associated gastritis (Tan et al., PLoS ONE, 2017), which evaluated the compound's effect on eradication rate and mucosal healing. There are several studies that support ZnC's benefits in restoring the gastric lining.
Limitations: Most rigorously controlled clinical data are from Japanese populations. It is approved as a pharmaceutical in Japan but is sold as a supplement in some other markets. More large-scale multinational RCTs are warranted.
5.4 Sulforaphane (from Broccoli Sprouts)
Traditional Use: Brassica vegetables, including cabbages and related plants, were used in various traditional folk medicine systems across Europe and Asia for stomach complaints. Cabbage juice, in particular, was described in older folk medicine contexts as a remedy for stomach ailments, though this predated any identification of active phytochemicals such as sulforaphane.
Scientific Evidence: Isothiocyanate sulforaphane, an abundant compound in broccoli sprouts, has been reported as a potent bacteriostatic agent against H. pylori in vitro, tested against 48 strains.
In a landmark randomized controlled trial, 48 H. pylori-infected patients were randomly assigned to 70 g/day of broccoli sprouts (containing 420 μmol of sulforaphane precursor) for 8 weeks or to alfalfa sprouts as placebo. Intervention with broccoli sprouts decreased levels of urease measured by urea breath test and H. pylori stool antigen (biomarkers of colonization) and serum pepsinogens I and II (biomarkers of gastric inflammation). Values recovered to their original levels 2 months after treatment was discontinued.
However, most participants were positive for H. pylori after 6 months of intervention, indicating that broccoli sprout treatment reduced H. pylori colonization but did not completely eradicate it.
Mechanistic work in mouse models showed that oral treatment with sulforaphane-rich broccoli sprouts in mice infected with H. pylori and maintained on a high-salt diet reduced gastric bacterial colonization, attenuated mucosal expression of tumor necrosis factor-α and interleukin-1β, mitigated corpus inflammation, and prevented expression of high salt-induced gastric corpus atrophy.
Limitations: The primary clinical RCT had a small sample size (48 patients) and effects were transient after cessation. A separate RCT by Chang and colleagues did not show improvement in H. pylori density with broccoli sprout extract but found it inhibited lipid peroxidation in the gastric mucosa, suggesting a cytoprotective rather than bactericidal role in that study context. Overall, clinical evidence remains preliminary.
5.5 Deglycyrrhizinated Licorice (DGL)
Traditional Use: Licorice root (Glycyrrhiza glabra) has been used for millennia across Ayurvedic, traditional Chinese, and Mediterranean herbal medicine for gastrointestinal complaints including stomach ulcers, gastritis, and dyspepsia. It was prepared as decoctions, teas, and chewed as root pieces. Licorice has been used for many years in the treatment of gastric disorders. The serious side effects of whole licorice, related to its constituent glycyrrhizinic acid (which can cause pseudohyperaldosteronism), led to the development of a deglycyrrhizinated form (DGL) in the mid-20th century.
Scientific Evidence: Clinical data on DGL specifically in gastritis are limited; most published evidence addresses peptic ulcer disease rather than gastritis per se. Mechanistically, DGL is proposed to support the gastric mucosal lining by stimulating mucus-producing cells and increasing blood flow to the affected area. No large, high-quality RCTs in gastritis specifically are available as of the current literature review. Evidence remains largely based on older ulcer-disease studies and mechanistic rationale.
5.6 Mastic Gum (Pistacia lentiscus)
Traditional Use: Mastic gum is a resin harvested from trees on the Greek island of Chios (Pistacia lentiscus var. Chia) and has been used since antiquity in Greek and Mediterranean folk traditions as a stomach remedy for dyspepsia, gastric pain, and peptic complaints. It was chewed directly or dissolved in preparations.
Scientific Evidence: Mastic gum has a long folk reputation as a stomach remedy. A randomized controlled trial of 148 people found that 350 mg of mastic gum taken three times daily significantly improved symptoms of functional dyspepsia (chronic indigestion) after three weeks — a meaningful outcome for discomfort, bloating, or pain. However, the evidence for mastic gum actually clearing H. pylori from the stomach is much weaker. Earlier small studies that suggested eradication have not been consistently replicated.
Limitations: Among published clinical trials in relevant databases, there is only one registered trial analyzing the activity of mastic gum against H. pylori. Evidence remains preliminary and specific to symptom relief in functional dyspepsia.
5.7 Garlic (Allium sativum)
Traditional Use: Garlic has been employed in traditional medicine across Asian, Mediterranean, and Middle Eastern traditions for millennia, historically attributed with antimicrobial and gastrointestinal-protective properties. Raw garlic consumption as a stomach remedy is well documented in traditional Chinese and Ayurvedic medicine.
Scientific Evidence: Garlic oil significantly suppressed H. pylori viability in vitro, and garlic extracts suppressed early stages of H. pylori-induced gastritis in Mongolian gerbils when administered at 1, 2, and 4% concentrations. A systematic review on food-based therapies for gastritis — finding 28 clinical studies evaluating garlic, turmeric, red peppers, broccoli sprouts, cranberry juice, honey, oils, and probiotics contained in various food matrices — confirmed garlic among the most investigated food-based agents in clinical studies. However, overall clinical evidence for garlic as a standalone anti-gastritis intervention is limited and largely derived from preclinical work or studies with other confounders.
Limitations: Research on alternative therapeutics using food or food-based products is extensive, mostly in preclinical research. Clinical evidence for garlic in human gastritis is preliminary.
5.8 Flavonoids and Polyphenols
Traditional Use: Flavonoid-rich plants — including green tea, chamomile, berries, and spices — have been used in traditional medicine traditions across Asia and Europe to soothe gastrointestinal inflammation. Traditional Chinese and Ayurvedic medicine both incorporate flavonoid-rich botanicals for stomach conditions.
Scientific Evidence: Preliminary studies suggest that various bioflavonoids can inhibit H. pylori growth. Studies evaluating whether bioflavonoids from fruits and vegetables have anti-H. pylori activity have yielded encouraging preliminary findings. However, large RCTs in human gastritis populations are lacking. Evidence for flavonoids in this context remains primarily preclinical or at early clinical stage.
5.9 Vitamin B12 in the Context of Atrophic Gastritis
Scientific Evidence: Malabsorption of vitamin B12 is a direct consequence of oxyntic mucosal atrophy, since gastric parietal cells are responsible for the production of intrinsic factor, which is crucial to the absorption of vitamin B12 in the terminal ileum. The management of patients with autoimmune atrophic gastritis aims to correct iron and vitamin deficiencies; vitamin B12 deficiency can be successfully treated with intramuscular or sublingual vitamin B12 supplementation.
Vitamin B12 deficiency in autoimmune gastritis is not only caused by loss of intrinsic factor but also by loss of gastric acid, which is needed for release of the vitamin from food sources. Pernicious anemia is a rather late finding in autoimmune gastritis and is diagnosed mainly in elderly patients.
5.10 Iron in the Context of Gastritis
Scientific Evidence: Decreased uptake of inorganic iron due to missing reduction of ferric iron, missing degradation of iron–protein complexes as a result of lack of gastric acid, and reduced levels of ascorbic acid are the likely causes of iron deficiency in autoimmune gastritis. Iron deficiency anemia is typically found in autoimmune atrophic gastritis patients and may precede the development of pernicious anemia. It is related to the hypochlorhydria present in such patients, which is associated with failure to reduce iron from Fe³⁺ to its absorbable form Fe²⁺.
6. Dietary and Lifestyle Factors
Overall Role of Diet
Researchers have not found that eating, diet, and nutrition play an important role in causing the majority of cases of gastritis or gastropathy. However, diet is recognized as relevant to symptom management, mucosal protection, and nutritional status in established disease.
Dietary Salt
Positive risk factors for gastric cancer in the context of chronic gastritis, as incorporated into the Correa carcinogenesis pathway in 1992, include H. pylori infection, dietary salt, and N-nitroso compounds; negative risk factors include vitamin C and β-carotene. High-salt diets have been shown in animal models to potentiate H. pylori-induced mucosal injury.
Dietary Patterns and Food Choices
Meals should be consumed in small, frequent portions with long chewing time. In the course of chronic gastritis, vitamin B12 and vitamin C deficiency and absorption problems occur quite often; to address these deficiencies, it is important to consume antioxidant-rich fruits and vegetables.
For autoimmune gastritis specifically, dietary guidance includes eating a diet rich in vegetables, grains, and fruits, while avoiding trigger foods such as spicy and fatty foods, citrus fruits, caffeine, alcohol, and carbonated beverages.
Smoking
Healthcare professionals believe sensitivity to H. pylori could be inherited, but sensitivity may also be caused by lifestyle choices, such as smoking and diet. Lifestyle changes for gastritis often focus on weight management, stress reduction, and smoking cessation.
Stress
Psychological and physiological stress is a recognized contributing factor in stress-induced (or stress-ulcer) forms of gastric mucosal injury. Stress gastritis can develop due to various factors, including uremia, ischemia, shock, corrosive agents, medications, radiation, trauma, severe burns, and sepsis.
Eating Patterns
A 2022 cohort study found that people with gastritis symptoms tended to eat at irregular times. For some people, food sensitivities or allergies can trigger gastritis; in these cases, identifying and avoiding these foods may help ease symptoms or prevent gastritis.
Alcohol Avoidance
Prevention involves avoidance of things which irritate the gut and which trigger symptoms, including alcohol, NSAIDs, tobacco, and certain foods.
7. Nutritional Consequences and Monitoring Considerations
Decreased or absent levels of hydrochloric acid and intrinsic factor have a marked effect on gastrointestinal function, including deficiency of iron, vitamin B12, and other micronutrients. Autoimmune gastritis may lead to serious conditions including iron/vitamin B12 and micronutrient deficiencies, neurological disorders, and gastric malignancies.
In the course of chronic gastritis, vitamin B12 and vitamin C deficiency and absorption problems can be seen quite often. In order to meet the deficiency of these vitamins, it is important to consume antioxidant-rich fruits and vegetables. In cases where nutritional deficiency cannot be met through food, supplementation is warranted.
The most common conditions prompting investigation in patients who were subsequently diagnosed with autoimmune gastritis were abdominal bloating-related symptoms (47%) and iron/vitamin B12 deficiency anemia (33%).
References
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