The core issue is retrograde flow of gastric contents (acid, pepsin, bile) into the esophagus, leading to mucosal erosion. Key mechanisms include:

• Reduced lower-esophageal-sphincter (LES) pressure or frequent transient LES relaxations (TLESRs) that disable the anti-reflux barrier
• Hiatus hernia, which weakens the diaphragmatic crus and creates an acid pocket
• Impaired esophageal clearance (weak peristalsis, reduced saliva) that prolongs acid exposure
• A damaged mucosal barrier (widened intercellular spaces, thinner mucus layer) lowering resistance to aggressive factors

Obesity, pregnancy, late-night meals, high-fat diet, smoking, alcohol and drugs such as aspirin raise intra-abdominal pressure or directly relax the sphincter, aggravating reflux. Chronic reflux activates inflammatory mediators, inducing erosions and ulcers that may progress to circumferential disease or columnar metaplasia (Barrett esophagus).

Key step	Main change	Precipitating factors
Anti-reflux barrier ↓	Low LES pressure, TLESRs, hiatus hernia	High-fat meals, smoking, alcohol, obesity
Clearance function ↓	Weak peristalsis, low saliva, long acid dwell	Dehydration, supine position, ageing
Mucosal barrier ↓	Widened intercellular spaces, less mucus	Bile acids, NSAIDs, prolonged acid
Aggressive factors ↑	Acid, pepsin, bile reflux	Large meals, coffee, aspirin