What Causes Acidic Feces?
Fecal acidity is primarily caused by bacterial fermentation of unabsorbed carbohydrates and proteins in the colon, producing short-chain fatty acids (SCFAs) and other organic acids that lower stool pH. 1
Primary Mechanisms of Fecal Acidification
Carbohydrate Fermentation
- Bacterial fermentation of dietary carbohydrates is the dominant mechanism producing acetate, propionate, and butyrate, which directly lower colonic and fecal pH 1, 2
- Unabsorbed simple sugars and complex carbohydrates provide substrate for colonic bacteria, particularly Prevotella and Ruminococcus, which efficiently ferment fiber into SCFAs 1, 2
- Malabsorbed carbohydrates from conditions like pancreatic insufficiency or small intestinal bacterial overgrowth (SIBO) increase substrate availability, leading to excessive fermentation and more acidic stools 1
Protein and Fat Metabolism
- High protein diets, particularly from red and processed meats, increase bacterial fermentation of sulfur-containing amino acids, producing hydrogen sulfide and other acidic metabolites 1
- Fat malabsorption allows undigested fats to reach the colon, where bacterial metabolism produces additional organic acids 1, 3
- Bile acid malabsorption results in excess bile acids entering the colon, which can be metabolized by bacteria into acidic compounds 1, 3
Clinical Conditions Associated with Acidic Stools
Pancreatic Exocrine Insufficiency
- Fat, protein, and carbohydrate malabsorption occurs even in mild-to-moderate chronic pancreatitis, not just severe disease as traditionally taught 1, 4
- Reduced bicarbonate production by the damaged pancreas fails to neutralize gastric acid, leading to higher acidity throughout the GI tract 1
- SIBO complicates up to 92% of patients with pancreatic insufficiency, causing excessive fermentation and acid production 1, 4
Small Intestinal Bacterial Overgrowth
- SIBO increases bacterial fermentation in the small bowel, producing D-lactic acid and other organic acids that can cause systemic acidosis in severe cases 1, 5
- The Specific Carbohydrate Diet (SCD) theory postulates that bacterial overgrowth produces short-chain organic acids injurious to intestinal mucosa, though evidence for mucosal injury specifically is limited 1
Dietary Factors
- High carbohydrate intake, particularly FODMAPs (fermentable oligosaccharides, disaccharides, monosaccharides, and polyols), increases colonic fermentation and fecal acidity 1
- Low-fiber diets paradoxically may reduce SCFA production and raise fecal pH, while high-fiber diets (45-100g/day) increase fermentation and lower pH 1, 6
- High-fat diets alter bile acid composition and promote sulfate-reducing bacteria that produce acidic metabolites 1
Important Clinical Distinctions
D-Lactic Acidosis
- D-lactic acidosis is a rare but serious complication of short bowel syndrome where excessive bacterial production of D-lactate causes systemic acidosis and encephalopathy 1, 5
- This represents systemic absorption of bacterial acid production, not just local fecal acidity 1, 5
- Treatment includes carbohydrate restriction, antibiotics, and potentially fecal microbiota transplantation 5
Antibiotic-Associated Changes
- Antibiotics disrupt normal colonic bacterial carbohydrate metabolism, reducing SCFA production and potentially raising fecal pH 7
- Loss of normal flora can paradoxically lead to overgrowth of acid-producing organisms like Candida or C. perfringens 7
Diagnostic Approach
When evaluating patients with suspected abnormal fecal acidity:
- Consider pancreatic function testing (fecal elastase) if fat malabsorption is suspected, as this is often undertreated even in mild disease 1, 4
- Evaluate for SIBO with hydrogen breath testing in patients with bloating, distension, and diarrhea, particularly those with prior abdominal surgery or pancreatic disease 1, 4
- Assess bile acid malabsorption with SeHCAT scanning (where available), serum C4, or FGF19 levels in patients with chronic watery diarrhea 1, 3
- Consider dietary assessment focusing on carbohydrate, protein, and fat intake patterns 1, 2
Key Clinical Pitfalls
- Do not assume pancreatic insufficiency only occurs with >90% gland destruction—malabsorption occurs earlier and is commonly undertreated 1, 4
- SIBO should be considered even without prior surgery in patients with pancreatic disease, diabetes, or persistent symptoms despite treatment 1, 4
- Symptomatic improvement with dietary restriction (low FODMAP, low carbohydrate) may reflect functional symptoms rather than true inflammatory disease 1
- Bile acid malabsorption is found in 28% of IBS-D patients and is frequently overlooked 1, 3