What Actually Causes GERD and Acid Reflux? Why Long-Term PPI Use Often Makes It Worse — Why "too much stomach acid" is rarely the actual mechanism

The lay understanding of GERD is that the stomach produces too much acid, the acid backs up into the esophagus, and the acid burns the esophageal lining. Suppressing the acid solves the problem. This narrative is intuitive but mechanistically incorrect for most patients. The amount of acid the stomach produces is not the primary determinant of whether reflux occurs. Patients with GERD frequently have normal or even reduced gastric acid output (hypochlorhydria) on careful testing. The actual mechanism of reflux involves the lower esophageal sphincter, the muscular valve at the junction between the esophagus and the stomach. When the LES is functioning properly, it remains closed between swallows, allowing the stomach to retain its contents under positive pressure. When the LES fails to close properly, stomach contents (which include acid in normal amounts, but also bile, pepsin, and partially digested food) flow upward into the esophagus, where the mucosa is not designed to handle them. The LES can fail in several ways. Transient LES relaxations occur when the LES briefly opens at inappropriate times, allowing reflux. These transient relaxations are the most common mechanism of GERD and are triggered by gastric distension, by certain foods (alcohol, caffeine, fat, mint), by certain medications, and by mechanical pressure on the stomach. Persistent LES hypotonia (a chronically we