What Actually Causes GERD and Acid Reflux? Why Long-Term PPI Use Often Makes It Worse — What actually drives the LES dysfunction

Five mechanisms contribute to LES dysfunction in GERD. Most patients have features of several. Mechanism 1: Pressure from below The LES is positioned at the junction between two pressure systems. The thoracic cavity above is at negative pressure relative to atmospheric. The abdominal cavity below is at positive pressure. The LES holds the gastric contents in the higher-pressure stomach against the lower-pressure esophagus. When pressure in the abdominal cavity rises, the LES has more work to do. Several conditions raise intra-abdominal pressure substantially. Obesity, particularly central adiposity, increases baseline abdominal pressure throughout the day. Pregnancy raises pressure mechanically and through progesterone-mediated LES relaxation. Chronic constipation produces colonic distension that displaces other organs and raises pressure. Gastroparesis produces gastric distension that directly pushes against the LES. Most relevantly for the framework: SIBO produces substantial fermentation gas that distends the small intestine and stomach, pushing upward against the LES from below. This is the connection between SIBO and GERD that the standard treatment paradigm misses. The PPI suppresses the acid that produces the burning symptom, but the SIBO continues to produce gas, the gas continues to distend the upper GI tract, and the pressure continues to push reflux through the LES.