Does low stomach acid reduce absorption of non-heme iron from plant foods?

Gastric acidity is a vital driver of dietary non-heme iron bioavailability, which is the primary iron form found in plant-derived foods.

Mechanistic pathways of iron absorption

• Acid-Dependent Solubilization: Normal gastric acid (pH 1–2) is required to release ferric iron ($\text{Fe}^{3+}$) from plant food matrices. When gastric pH rises above 3.6, iron rapidly precipitates into insoluble hydroxides and phosphates, rendering it unabsorbable.
• Valence Reduction: Acidic conditions favor the chemical reduction of $\text{Fe}^{3+}$ to its divalent ferrous state ($\text{Fe}^{2+}$), which is the essential substrate for transport via Divalent Metal Transporter 1 (DMT1) on the duodenal brush border membrane.
• Secondary Hepcidin Upregulation: Beyond raising gastric pH, proton pump inhibitors (PPIs) can upregulate the systemic hormone hepcidin through an aryl hydrocarbon receptor-mediated pathway. Elevated hepcidin degrades the basolateral exporter ferroportin, further restricting systemic iron export.

Clinical implications

• Vulnerability in Plant-Based Diets: Unlike animal-derived heme iron, plant-derived non-heme iron absorption is highly pH-dependent. This makes individuals relying on vegetarian or vegan diets particularly susceptible to iron deficiency when stomach acid is compromised.
• Impact of Acid Suppression: Pathological states (such as atrophic gastritis) or pharmacological interventions (PPIs and $\text{H}_2$ receptor antagonists) shift the gastric environment toward neutrality, severely restricting the bioavailable iron pool arriving at the duodenum.

Bottom line

• Low stomach acid directly impairs the solubilization and reduction of non-heme ferric iron to its absorbable ferrous state, an effect compounded by drug-induced hepcidin upregulation, which significantly reduces overall iron absorption from plant foods.