If you've ever had heartburn, your doctor probably told you that you have "too much stomach acid" and prescribed something to suppress it — a proton pump inhibitor (Prilosec, Nexium, Prevacid) or an H2 blocker (Pepcid, Zantac). The medications work in the short term because they reduce acid, and acid is what's burning when reflux occurs. Problem solved, right?
Except that for a substantial portion of GERD patients, the underlying cause is actually low stomach acid, not high. The "too much acid" framing made intuitive sense in the 1980s when PPIs were first marketed — but research has consistently shown that stomach acid production tends to decrease with age, not increase. By the time most patients develop chronic reflux, they're often producing too little acid, not too much.
"The medication makes the symptom go away, but it's also driving the underlying problem deeper. Patients end up on PPIs for years — and the longer they're on them, the worse the underlying gut function gets."
Here's the mechanism. Your stomach is supposed to be highly acidic — that's how it sterilizes incoming food, activates digestive enzymes, and signals the lower esophageal sphincter to close tightly. When acid is low, the sphincter doesn't close properly, food sits in the stomach undigested, fermentation produces gas, gas pushes stomach contents — including whatever acid is present — upward into the esophagus. The result feels like "too much acid" because acid is what's coming up. But the upstream problem was too little acid to begin with.
Suppressing acid further with PPIs makes the immediate burning sensation go away, but it deepens the underlying dysfunction. Over time, patients develop SIBO (because acid no longer sterilizes incoming bacteria), nutrient deficiencies (B12, magnesium, iron — all dependent on stomach acid for absorption), increased fracture risk, increased infection risk, and rebound hyperacidity when trying to discontinue the medication.
PPIs were originally approved for short-term use — typically 8 weeks. Most patients today have been on them for years or decades. The research on long-term use is concerning enough that the FDA has issued multiple safety communications.
Stomach acid is required to absorb B12, magnesium, iron, calcium, and zinc. Long-term acid suppression produces measurable deficiencies in all of these. B12 deficiency in particular can cause neurological symptoms that often get attributed to "aging" but are actually iatrogenic.
Stomach acid is your first defense against incoming bacteria. Suppressing it for years allows bacterial overgrowth in the small intestine and shifts the broader microbiome. PPIs are one of the most common drivers of SIBO that we see clinically.
FDA-documented increased risk of hip, wrist, and spine fractures with long-term PPI use, particularly in patients over 50. Driven by reduced calcium absorption and effects on bone metabolism.
Trying to discontinue PPIs often produces severe rebound reflux symptoms — sometimes worse than the original problem. The body up-regulates acid-producing cells while on suppression, then they all fire when the medication stops. This is why patients can feel "stuck" on PPIs.
Dr. Dubroff's approach to GERD is built around addressing the underlying drivers — not just suppressing the symptom. The protocol varies based on testing and what's actually happening for you, but the components typically include:
Book a free consultation. Dr. Dubroff will tell you what's likely driving your reflux — and what a real resolution protocol could look like.