Gastritis,
an inflammation of the gastric mucosa, is a prevalent and clinically
significant condition that affects millions globally, often resulting from
multifactorial etiologies such as poor dietary habits, psychosocial stress,
alcohol consumption, prolonged use of nonsteroidal anti-inflammatory drugs
(NSAIDs), and infection by Helicobacter pylori. The inflammatory process
involves damage to the gastric epithelial lining and the infiltration of
inflammatory cells, leading to a disruption in the protective mucosal barrier
and increased vulnerability to gastric acid injury. The disease may manifest as
either acute or chronic gastritis, characterized by symptoms including
epigastric pain, nausea, bloating, early satiety, and heartburn. These symptoms
contribute to substantial discomfort, decreased nutritional intake, and a
reduction in overall quality of life. Chronic gastritis, in particular, has
been associated with more severe and long-term complications such as peptic
ulcer disease, gastrointestinal bleeding, mucosal atrophy, intestinal
metaplasia, and an increased risk of gastric carcinoma [1]. The management of
gastritis typically includes pharmacological interventions designed to suppress
gastric acid secretion and alleviate mucosal irritation. Standard treatments
involve proton pump inhibitors (PPIs), H2-receptor antagonists, and antacids,
which are effective in controlling symptoms and promoting mucosal repair.
However, these medications often provide temporary relief and are associated
with adverse effects such as rebound acid hypersecretion, nutrient
malabsorption, and potential dysbiosis of the gut microbiota. Furthermore,
pharmacotherapy does not always address underlying etiological factors,
particularly H. pylori infection, which remains a major contributor to the
onset and persistence of both acute and chronic gastritis [2]. The persistence
of H. pylori may lead to recurrent mucosal inflammation despite adequate acid
suppression therapy, indicating a need for complementary or alternative strategies
that target both physiological and behavioral aspects of the disease.In this
context, non-pharmacological interventions, including dietary modifications,
stress management, and holistic lifestyle adjustments, have gained prominence
as adjunctive approaches in gastritis management. Such interventions aim to
modulate the physiological balance between gastric acid secretion and mucosal
defense mechanisms while promoting overall digestive health. Evidence suggests
that incorporating dietary discipline, reducing irritant foods, and maintaining
regular meal patterns can significantly reduce symptom recurrence and improve
gastric mucosal resilience. Within this framework, fasting practices particularly
those observed during the Islamic month of Ramadan have emerged as a promising
complementary modality for gastrointestinal health. During Ramadan, Muslims
observe a unique fasting pattern from dawn to dusk, abstaining from food,
drink, and other physical indulgences. This structured fasting regimen induces
metabolic adaptations that have been linked to a variety of physiological
benefits, including improved insulin sensitivity, lipid profile regulation,
enhanced autophagy, and reduction of oxidative stress. Despite the extended
fasting hours, Ramadan fasting has been associated with improved metabolic
homeostasis, better weight management, and enhanced gastrointestinal function
[3,4]. From a gastrointestinal perspective, studies indicate that intermittent
fasting during Ramadan may decrease gastric acid secretion, allowing the mucosa
to recover from acid-induced inflammation and promoting epithelial regeneration
[5,6]. Furthermore, fasting induces hormonal and neuroendocrine adjustments,
such as reductions in gastrin secretion and modulation of the vagal tone, which
collectively help stabilize gastric acid production. This may explain the
observed clinical improvement in dyspeptic symptoms among fasting individuals.
Recent research has also highlighted the role of fasting in promoting a healthy
gut microbiota composition, which exerts anti-inflammatory and immunomodulatory
effects that may contribute to mucosal healing and improved gastrointestinal
function [7].