GERD & Acid Reflux: The Functional Approach

The Great Acid Lie

Here is one of the most persistent myths in modern medicine: heartburn means too much stomach acid. Millions of people swallow proton pump inhibitors every morning based on this assumption. And for a significant number of them, the assumption is dead wrong.

The burning sensation is real. The acid in the wrong place is real. But the reason acid is in the wrong place is almost never “too much acid.” It is a mechanical failure — a valve that does not close properly, a stomach that empties too slowly, or paradoxically, a stomach that produces too little acid.

Jonathan Wright, MD, and Lane Lenard, PhD, laid out this case meticulously in Why Stomach Acid Is Good for You. After testing thousands of patients presenting with heartburn, Wright found that the majority — particularly those over 40 — actually had low stomach acid, not high. The medical term is hypochlorhydria. And it mimics hyperacidity almost perfectly.

Think of it this way. A campfire burns clean when it has enough oxygen. Starve it of oxygen and you get smoke — incomplete combustion. Low stomach acid means incomplete digestion. Food sits in the stomach too long, ferments, produces gas, and that gas pressure pushes the lower esophageal sphincter (LES) open. Whatever acid is present then splashes upward. The problem is not too much fire. The problem is smoldering.

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The Low Stomach Acid Paradox

Why Hypochlorhydria Feels Like Hyperacidity

Adequate hydrochloric acid (HCl) serves multiple critical functions: it sterilizes incoming food, activates pepsin for protein digestion, triggers the release of pancreatic enzymes and bile, signals the LES to close tightly, and ensures proper mineral absorption (calcium, magnesium, iron, zinc).

When HCl is low, a cascade of dysfunction follows:

1. Delayed gastric emptying: Food sits and ferments, producing organic acids and gas
2. Intra-abdominal pressure rises: Gas pushes the LES open
3. Incomplete protein digestion: Large protein fragments trigger immune responses downstream
4. Poor mineral absorption: Setting up deficiency in calcium, magnesium, iron, and zinc
5. Bacterial overgrowth: Without the acid barrier, bacteria survive the stomach and colonize the small intestine (SIBO)
6. Reduced bile and enzyme release: The entire digestive cascade downstream depends on adequate acid signaling

The patient experiences burning, bloating, and reflux — and reaches for an antacid. This provides temporary relief by neutralizing what little acid remains, but deepens the underlying problem. The cycle escalates.

The HCl Challenge Test

This simple, inexpensive self-assessment helps identify low stomach acid:

1. Take one capsule of betaine HCl with pepsin (typically 500-650mg) at the beginning of a protein-containing meal
2. Monitor for warmth or burning in the stomach during or after the meal
3. If no warmth or burning is felt, increase by one capsule at the next protein meal
4. Continue increasing by one capsule per meal until a warm sensation is noticed
5. The dose that produces warmth is one capsule above your therapeutic dose — reduce by one capsule and use that amount with protein-containing meals

Some patients reach 5-7 capsules before feeling warmth — a clear sign of profound hypochlorhydria. A healthy stomach produces the equivalent of roughly 3,000-4,000mg of HCl per meal. If you feel burning at one capsule, your acid production is likely adequate and the reflux has another cause.

Important contraindications: do not perform this test if you are taking NSAIDs, corticosteroids, or other medications that increase ulcer risk. Do not use if you have a known gastric or duodenal ulcer.

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The PPI Problem

Proton pump inhibitors — omeprazole, esomeprazole, lansoprazole, pantoprazole — are among the most prescribed drugs in the world. Designed for short-term use (4-8 weeks) for severe GERD, erosive esophagitis, and H. pylori eradication, they have become lifelong medications for millions. The consequences accumulate.

Nutrient Depletion

PPIs reduce stomach acid by 90-95%. This profoundly impairs absorption of:

• Vitamin B12: Acid is required to cleave B12 from food proteins. Long-term PPI use increases B12 deficiency risk by 65% (Lam 2013). Consequences: neuropathy, cognitive decline, megaloblastic anemia.
• Magnesium: FDA issued a safety warning in 2011 for hypomagnesemia with long-term PPI use. Low magnesium causes muscle cramps, arrhythmia, seizures.
• Calcium: Reduced absorption increases fracture risk. A 2012 meta-analysis (Yu) found a 30% increased hip fracture risk with PPI use beyond one year.
• Iron: Acid converts ferric iron to the absorbable ferrous form. PPI users develop iron deficiency anemia at significantly higher rates.
• Zinc: Critical for immune function, wound healing, and gut barrier integrity — all further compromised by the deficiency PPIs create.

Rebound Hypersecretion

When you suppress acid production for weeks or months and then stop, the acid-producing parietal cells — which have been upregulated in response to the suppression — roar back. The result is rebound hypersecretion: acid levels temporarily exceed what they were before you started the medication. This creates the illusion that you “need” the PPI, trapping patients in a dependency cycle.

Reetz 2009 demonstrated this effect in healthy volunteers: after just 8 weeks of PPI use, discontinuation produced dyspepsia symptoms in 44% of subjects who had never had reflux before.

Increased Infection Risk

Stomach acid is your first-line immune defense against ingested pathogens. PPIs increase risk of:

• C. difficile infection: 65% increased risk (Janarthanan 2012)
• SIBO: The acid barrier normally prevents bacterial migration into the small intestine
• Pneumonia: Aspiration of bacteria that would normally be killed by gastric acid
• Foodborne illness: Salmonella, Campylobacter, and other enteric pathogens

Kidney Disease

A 2016 study in JAMA Internal Medicine (Lazarus) found a 20-50% increased risk of chronic kidney disease with PPI use, likely related to acute interstitial nephritis and magnesium depletion.

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PPI Deprescribing Protocol

Stopping PPIs requires a gradual taper to avoid rebound. This process takes 4-12 weeks depending on duration of use.

Week-by-Week Taper (Example for omeprazole 20mg daily)

• Weeks 1-2: Continue current dose while adding supportive supplements (below)
• Weeks 3-4: Reduce to every other day
• Weeks 5-6: Reduce to every third day
• Weeks 7-8: Switch to H2 blocker (famotidine 20mg) if needed as bridge
• Weeks 9-12: Taper H2 blocker, rely on natural support

Support During Taper

• DGL (Deglycyrrhizinated Licorice): 400mg chewable, 20 minutes before meals. Stimulates mucus production and protects the esophageal and gastric lining without affecting blood pressure (the glycyrrhizin has been removed).
• Zinc carnosine: 75mg twice daily. Mahmood 2007 demonstrated that zinc carnosine heals gastric mucosal damage and reduces H. pylori colonization. It stabilizes the mucosa and accelerates repair.
• Melatonin: 3-6mg at bedtime. Kandil 2010 published a striking study showing that melatonin at 6mg/day was comparable to omeprazole 20mg for GERD symptom relief. The mechanism: melatonin inhibits gastric acid secretion, increases LES pressure, improves esophageal blood flow, and reduces nitric oxide-mediated LES relaxation. It also has antioxidant and anti-inflammatory effects on the esophageal mucosa.
• Calcium/magnesium supplement: To replete what PPIs depleted.

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Root Causes of GERD

H. pylori

The relationship between H. pylori and reflux is complex. H. pylori can cause both increased and decreased acid production depending on where in the stomach it colonizes. Antral-predominant infection increases acid output; corpus-predominant infection decreases it. Eradication of H. pylori sometimes worsens reflux and sometimes improves it. Test and treat — but do not assume eradication alone will resolve GERD.

Food Sensitivities

Gluten and dairy are the two most common triggers. Gluten increases zonulin and intestinal permeability, driving systemic inflammation. Dairy — particularly the A1 beta-casein in conventional cow’s milk — triggers inflammatory cascades in susceptible individuals. A strict 30-day elimination of gluten and dairy resolves or significantly improves GERD in a remarkable number of patients.

Other common triggers: chocolate (relaxes LES), coffee (increases acid and relaxes LES in some individuals), alcohol, peppermint (relaxes LES), carbonated beverages, spicy foods, and tomato-based foods.

Hiatal Hernia

When the upper portion of the stomach slides upward through the diaphragmatic hiatus, the LES loses its anatomical reinforcement from the crural diaphragm. This mechanical failure allows reflux regardless of acid levels.

Visceral manipulation — a manual therapy technique practiced by osteopathic physicians and specially trained physical therapists — can reduce hiatal hernia by gently pulling the stomach inferiorly while the patient exhales. Barral and Mercier’s work on visceral manipulation has shown significant clinical improvement in patients with hiatal hernia-associated reflux who did not respond to medication.

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The Functional GERD Protocol

Mucosal Protection and Healing

Supplement	Dose	Timing	Mechanism
DGL (chewable)	400mg	20 min before meals	Mucus production, mucosal coating
Zinc carnosine	75mg	Twice daily	Mucosal repair, anti-H. pylori
Slippery elm	400-800mg	Before meals or at bedtime	Demulcent — coats and soothes
Aloe vera juice (inner leaf)	2-4 oz	Before meals	Anti-inflammatory, mucosal healing
Marshmallow root	500mg	Before meals	Demulcent, mucilage coating

Acid Support and Digestive Optimization

Supplement	Dose	Timing	Mechanism
Betaine HCl + pepsin	Titrated (see above)	With protein meals	Restore adequate acid
Digestive bitters	1-2 mL	15 min before meals	Stimulate HCl, bile, enzymes
D-limonene	1000mg	Every other day for 20 days	Coats esophagus, promotes peristalsis
Apple cider vinegar	1 tbsp in water	Before meals	Gentle acid support

Additional Support

• Melatonin: 3-6mg at bedtime (Kandil 2010)
• Probiotics: Lactobacillus and Bifidobacterium strains to restore gastric and esophageal microbiome
• Chamomile tea: Anti-inflammatory, calming to the gastric mucosa

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Dietary and Lifestyle Foundations

These are non-negotiable:

1. Smaller, more frequent meals: A distended stomach increases LES opening pressure
2. No eating within 3 hours of bedtime: Gravity is your ally against reflux
3. Elevate the head of the bed 6-8 inches: Wedge pillow or bed risers — not just extra pillows, which kink the neck without changing the angle
4. Chew thoroughly: Digestion begins in the mouth. Thirty chews per bite is not obsessive — it is functional
5. Do not drink large amounts of fluid with meals: Dilutes digestive secretions
6. Identify and eliminate individual triggers: Keep a food-symptom diary for 2-4 weeks
7. Address abdominal adiposity: Visceral fat increases intra-abdominal pressure and mechanically pushes the LES open
8. Stress management: The vagus nerve controls LES tone. Chronic sympathetic activation (stress) reduces vagal tone and loosens the valve

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LPR: The Silent Reflux

Laryngopharyngeal reflux (LPR) is GERD’s stealth cousin. Acid and — critically — pepsin reach the throat, larynx, and airways without causing classical heartburn. Symptoms include chronic cough, throat clearing, hoarseness, globus sensation (feeling of a lump in the throat), post-nasal drip, and even asthma-like symptoms.

Dr. Jamie Koufman, a pioneer in LPR research, demonstrated that pepsin can become embedded in the tissues of the larynx and pharynx and be reactivated by dietary acid (anything below pH 4). This is why LPR patients improve on an alkaline diet even when their reflux episodes are minimal.

Koufman’s key recommendations for LPR:

• Alkaline water at pH 8.8 irreversibly denatures pepsin in vitro and reduces its tissue damage
• Strict avoidance of acidic foods and beverages: citrus, tomato, vinegar, carbonated drinks, wine
• No eating 3-4 hours before bed
• Pepsin-binding agents: alginate-based products (Gaviscon Advance — the UK formulation, which uses sodium alginate rather than the aluminum-based US version) create a physical raft on top of stomach contents, preventing reflux

LPR often requires a longer treatment course than classical GERD — 3-6 months of strict dietary and lifestyle modification before mucosal healing is complete. Patience is part of the protocol.

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The Bigger Picture

GERD is not an omeprazole deficiency. It is a signal — from a digestive system that needs its mechanical, chemical, and microbial foundations restored. The functional approach asks: is the acid adequate? Is the valve intact? Is the stomach emptying properly? Are food triggers being addressed? Is the microbiome supporting or undermining digestive function?

When you treat the terrain rather than suppress the symptom, the fire finds its proper hearth.

What would change in your patient’s life if you addressed the root cause of their reflux rather than reflexively suppressing their acid for another decade?