GERD

Gastro-oesophageal reflux disease occurs when the lower oesophageal sphincter and diaphragmatic crura fail to contain gastric contents, allowing acid, pepsin and sometimes bile to reach the oesophagus. It is defined clinically by troublesome symptoms occurring twice weekly or more, or by evidence of erosive oesophagitis on endoscopy. Reflux is not simply excess acid. Transient lower oesophageal sphincter relaxations, hiatus hernia, delayed gastric emptying, increased intra-abdominal pressure from central adiposity and visceral hypersensitivity all contribute. This explains why a subset of patients have normal acid exposure yet severe symptoms, and why acid suppression alone fails around a third of the time. Proton pump inhibitors remain the most effective medical therapy for erosive disease and healing, and the widely publicised observational harms — dementia, kidney disease, fracture — have not been reproduced in randomised data such as the COMPASS three-year safety analysis. That said, long-term use without a clear indication is worth reviewing, and rebound hypersecretion makes abrupt cessation unpleasant, so tapering matters. Alginate preparations deserve more attention than they get: they form a physical raft on the gastric pool and reduce postprandial acid pocket exposure, with head-to-head data showing benefit added to or comparable with acid suppression for postprandial symptoms. Melatonin, deglycyrrhizinated liquorice and slippery elm have thin evidence, and apple cider vinegar has none worth citing.

• •Burning retrosternal pain, typically after meals or lying down
• •Regurgitation of acid or food into the throat
• •Chronic cough, particularly at night
• •Hoarseness and throat clearing
• •Sensation of a lump in the throat
• •Difficulty or pain on swallowing
• •Disturbed sleep from nocturnal reflux
• •Dental erosion from chronic acid exposure

• •Hiatus hernia
• •Central obesity raising intra-abdominal pressure
• •Large or late evening meals
• •Pregnancy
• •Smoking and alcohol
• •Delayed gastric emptying
• •Medications relaxing the lower oesophageal sphincter
• •Connective tissue disease such as scleroderma

Mechanical and physiological failure of the antireflux barrier: transient lower oesophageal sphincter relaxations, hiatus hernia, raised intra-abdominal pressure from obesity or pregnancy, delayed gastric emptying, impaired oesophageal clearance, and reduced salivary bicarbonate. Contributing factors include smoking, alcohol, large late meals, and medications that relax the sphincter such as calcium channel blockers, nitrates, anticholinergics and some benzodiazepines.