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One of the most frustrating scenarios in chronic illness is "Refractory GERD"—severe heartburn or reflux that does not improve, even when taking high doses of Proton Pump Inhibitors (PPIs) like Omeprazole or Pantoprazole.
For many in the Lyme and chronic illness community, the issue isn't just "too much acid." The issue is Mast Cell Activation Syndrome (MCAS).
If you are taking acid reducers but still feel like your chest or throat is on fire, you may be treating the wrong mechanism. Today, we are breaking down the biology of "Histamine-Induced Reflux" and why H2 blockers might be the missing piece of your puzzle.
🔬 The Biology: How Histamine "Hacks" the Stomach
To understand why PPIs fail, we have to look at how stomach acid is produced.
Your stomach lining contains Parietal Cells, which are responsible for pumping acid. These cells have three main "on switches" (receptors) that tell them to produce acid:
Gastrin (Hormone)
Acetylcholine (Vagus Nerve)
Histamine (via the H2 Receptor)
The MCAS Problem:
The Gastrointestinal (GI) tract is home to a massive density of Mast Cells. When you have MCAS, these cells are unstable. When triggered (by food, stress, or Lyme bacteria), they degranulate and dump massive amounts of histamine directly into the gut tissue.
The Chain Reaction:
Mast cells release histamine in the stomach lining.
This histamine attaches to the H2 receptors on the Parietal Cells.
The cells receive a constant, aggressive signal to "MAKE ACID NOW."
💊 The Medication Gap: PPIs vs. H2 Blockers
This is why your current medication might be failing.
1. Proton Pump Inhibitors (PPIs)
Examples: Omeprazole (Prilosec), Esomeprazole (Nexium).
Mechanism: These drugs shut down the final "pump" that releases acid.
The Failure: In MCAS, the histamine signal is so loud and constant that it can overwhelm the PPI's ability to block the pump. Furthermore, PPIs do nothing to stop the inflammation caused by the mast cell chemicals. You might have less acid, but your esophagus is still swollen and reactive from the chemical mediators (Prostaglandins and Cytokines).
2. H2 Blockers (The Missing Link)
Examples: Famotidine (Pepcid), Cimetidine (Tagamet).
Mechanism: These drugs specifically sit on the H2 Receptor. They act like a shield, blocking histamine from docking onto the stomach cells.
The Result: They stop the acid signal at the source (the histamine trigger) rather than just trying to plug the drain.
🚩 Signs Your Reflux is MCAS-Driven
How do you differentiate between standard GERD and Histamine-Driven Reflux? Look for these clues:
Non-Acid "Burn": You feel burning or pain, but an endoscopy shows normal tissue or "mild" irritation that doesn't match your pain level (Hypersensitivity).
Trigger Timing: You flare immediately (within minutes) of eating high-histamine foods (spinach, fermented foods, leftovers, alcohol) rather than just "spicy" or "fatty" foods.
Systemic Symptoms: Your heartburn comes with other symptoms like flushing, heart palpitations, itching, or sudden diarrhea (the "GI Dump").
Throat Issues: You have "Silent Reflux" (LPR)—chronic throat clearing, lump in the throat (globus), or hoarseness, which is often caused by aerosolized pepsin and inflammatory mediators, not just liquid acid.
🛡️ The Therapeutic Pivot: Treating the Mast Cells
If this science resonates with you, simple acid suppression is likely not enough. A comprehensive approach involves targeting the mast cells themselves.
1. The H2 Blocker Protocol
Many MCAS specialists prescribe high-dose H2 blockers (often twice daily, morning and night) to keep the histamine signal blocked 24/7.
Note: Famotidine is often preferred over Cimetidine as it has fewer drug interactions, but individual responses vary.
2. Oral Mast Cell Stabilisers
H2 blockers stop the acid, but they don't stop the mast cell from exploding.
Cromolyn Sodium (Oral): This liquid medication coats the GI tract and prevents mast cells from degranulating. It is specifically effective for GI symptoms (pain, nausea, diarrhea).
Ketotifen: A systemic mast cell stabilizer that also has H1-blocking properties.
3. The Low Histamine Diet
Reducing the incoming load of histamine allows the gut lining to calm down, reducing the burden on your H2 receptors.
📝 Doctor Discussion Guide
If you are suffering from refractory heartburn, bring this up with your doctor:
"I've been on PPIs for X months without relief. Given my other symptoms, could this be Histamine-mediated?"
"Can we trial adding an H2 Blocker (like Famotidine) at night to see if blocking the histamine receptor helps?"
"Should we consider Cromolyn Sodium to stabilise the gut mucosa?"
These are all questions I really welcome, and need to know when seeing patients, to help best decide how to make you better.
Remember: Do not stop PPIs cold turkey, as this can cause a severe "Acid Rebound." Tapering should always be done under medical supervision, often while bridging with H2 blockers.
Stay Well
Disclaimer: This newsletter is for educational purposes only. It does not constitute medical advice. GERD can lead to serious complications; always consult a medical professional for diagnosis and treatment.
