Digestive Disorders: A Comprehensive Functional Approach

Overview

The gastrointestinal system is far more than a food-processing tube. It is the body’s largest immune organ (housing 70-80% of immune cells), the site of the enteric nervous system (containing 500 million neurons — more than the spinal cord), the primary interface between the body and the external environment (with a surface area of approximately 32 square meters), and the habitat of the gut microbiome (38 trillion microorganisms encoding 150 times more genes than the human genome). When this system malfunctions, the consequences extend far beyond digestive symptoms to include immune dysregulation, neuropsychiatric disorders, hormonal imbalances, and systemic inflammation.

Digestive disorders affect a staggering proportion of the population. Irritable bowel syndrome (IBS) affects 10-15% of the global population. Small intestinal bacterial overgrowth (SIBO) is present in up to 78% of IBS patients. Inflammatory bowel disease (IBD) — Crohn’s disease and ulcerative colitis — affects over 6.8 million people worldwide, with incidence rising sharply in developing nations adopting Western diets. Functional dyspepsia, GERD, bile acid malabsorption, and exocrine pancreatic insufficiency add millions more to the burden of GI suffering.

Conventional gastroenterology excels at ruling out structural pathology (through endoscopy, colonoscopy, and imaging) and managing acute disease (IBD flares, GI bleeding, obstruction). However, for the vast majority of patients with chronic digestive complaints — particularly functional GI disorders — conventional approaches offer primarily symptom suppression through acid blockers, antispasmodics, and dietary restriction, without addressing the underlying drivers. This article explores the functional medicine approach to digestive disorders, integrating cutting-edge understanding of the microbiome, SIBO, bile acid physiology, and the enteric nervous system.

Small Intestinal Bacterial Overgrowth (SIBO)

Understanding SIBO

SIBO is defined as an abnormal increase in bacterial population in the small intestine — an area that should normally contain relatively few bacteria compared to the colon. The small intestine is kept relatively sterile by several protective mechanisms: gastric acid (which kills most ingested bacteria), bile (which has antimicrobial properties), the migrating motor complex (MMC — the “housekeeper wave” of peristalsis that sweeps bacteria distally between meals), the ileocecal valve (which prevents backflow from the colon), and secretory IgA (which neutralizes bacteria in the intestinal lumen).

When any of these protective mechanisms fail, bacteria proliferate in the small intestine, where they ferment carbohydrates that should be absorbed upstream, producing hydrogen, methane, or hydrogen sulfide gas. This bacterial fermentation causes the hallmark symptoms of SIBO: bloating (often described as looking “six months pregnant” by evening), abdominal distension, gas, diarrhea and/or constipation, abdominal pain, and nausea. Beyond GI symptoms, SIBO drives intestinal permeability (bacterial endotoxins damage tight junctions), nutrient malabsorption (bacteria consume B12 and iron; bile acid deconjugation impairs fat absorption), and systemic inflammation.

SIBO Subtypes

Recent research has identified three distinct SIBO subtypes based on the predominant gas produced:

Hydrogen-predominant SIBO: Caused by hydrogen-producing bacteria (E. coli, Klebsiella, Streptococcus). Associated with diarrhea-predominant symptoms.

Methane-predominant (now called IMO — Intestinal Methanogen Overgrowth): Caused by archaea (primarily Methanobrevibacter smithii) rather than bacteria. Methane directly slows intestinal transit by acting on the enteric nervous system, causing constipation. IMO can occur in both the small and large intestine.

Hydrogen sulfide-predominant: Caused by sulfate-reducing bacteria (Desulfovibrio, Bilophila). Associated with diarrhea, sulfurous flatulence, and potential systemic toxicity. The trio-smart breath test now measures all three gases, but hydrogen sulfide testing is not yet widely available.

SIBO Diagnosis and Treatment

Diagnosis: Lactulose or glucose breath test measuring hydrogen and methane at 15-minute intervals over 2-3 hours. Glucose testing has higher specificity but lower sensitivity (it is absorbed before reaching the distal small intestine). Lactulose has better sensitivity for distal SIBO but can produce false positives from colonic fermentation. A positive test shows a rise of 20+ ppm hydrogen or 10+ ppm methane above baseline within 90 minutes.

Treatment: SIBO treatment follows a three-phase approach:

Phase 1 — Reduce: Kill the overgrown bacteria.

• Pharmaceutical: Rifaximin 550mg three times daily for 14 days (hydrogen-predominant); rifaximin plus neomycin or metronidazole (methane/IMO); bismuth subsalicylate may address hydrogen sulfide.
• Herbal: Allicin (garlic extract, 450mg 2-3x daily), oregano oil (200mg emulsified, 2-3x daily), berberine (500mg 2-3x daily), and neem (300mg 2-3x daily). The Johns Hopkins SIBO study by Chedid et al. (2014) demonstrated that herbal antimicrobials were as effective as rifaximin for SIBO eradication.

Phase 2 — Restore: Optimize the protective mechanisms that prevent recurrence.

• Prokinetics to restore the MMC: low-dose erythromycin (50mg at bedtime), prucalopride, or herbal prokinetics (ginger, artichoke extract, 5-HTP). The MMC only fires during fasting, so meal spacing (4-5 hours between meals, no snacking) is essential.
• Address root causes: low stomach acid (betaine HCl with meals), bile insufficiency (ox bile supplements), ileocecal valve dysfunction (manual therapy), adhesions (visceral manipulation).

Phase 3 — Reinoculate: Gradually reintroduce beneficial bacteria and prebiotic fibers as tolerated. Spore-based probiotics (Bacillus coagulans, B. subtilis, B. clausii) may be better tolerated in SIBO patients than Lactobacillus/Bifidobacterium species, as they do not colonize the small intestine.

IBS: The Functional Gut-Brain Disorder

Beyond “It’s Just Stress”

IBS is the most common functional GI disorder, diagnosed by the Rome IV criteria: recurrent abdominal pain at least one day per week for the past three months, associated with defecation, change in stool frequency, or change in stool form, with onset at least six months before diagnosis. IBS is subtyped as IBS-D (diarrhea predominant), IBS-C (constipation predominant), IBS-M (mixed), and IBS-U (unsubtyped).

While IBS is often dismissed as a stress-related or psychological condition, research has identified multiple biological mechanisms:

Visceral hypersensitivity: IBS patients have a lower threshold for pain and discomfort from balloon distension of the colon, indicating sensitization of visceral afferent nerves — analogous to central sensitization in chronic pain.

Post-infectious IBS: 10-15% of people who develop acute gastroenteritis will go on to develop IBS, with risk persisting for up to 8 years. Post-infectious inflammation, altered microbiome composition, and increased intestinal permeability are proposed mechanisms.

Microbiome alterations: IBS patients consistently show reduced microbial diversity, increased Firmicutes:Bacteroidetes ratio, reduced Bifidobacterium and Faecalibacterium prausnitzii, and altered bile acid metabolism.

SIBO: Present in 30-78% of IBS patients depending on the study, SIBO may be the underlying mechanism in a large subset of IBS diagnoses. A 2020 meta-analysis confirmed a significant association between SIBO and IBS.

The Low-FODMAP Diet

The low-FODMAP diet, developed by Monash University, is the most evidence-based dietary intervention for IBS. FODMAPs (Fermentable Oligosaccharides, Disaccharides, Monosaccharides, And Polyols) are short-chain carbohydrates that are poorly absorbed in the small intestine and rapidly fermented by colonic bacteria. A 2016 meta-analysis found that a low-FODMAP diet improves overall symptoms in 50-86% of IBS patients.

The diet follows three phases: strict elimination (2-6 weeks), systematic reintroduction (testing one FODMAP group at a time), and personalization (long-term diet incorporating tolerated FODMAPs while avoiding triggers). Important: the low-FODMAP diet is an elimination and testing protocol, not a permanent diet. Long-term FODMAP restriction reduces Bifidobacterium populations and may compromise gut health.

Inflammatory Bowel Disease: Functional Approaches

Crohn’s and Ulcerative Colitis

IBD — comprising Crohn’s disease (which can affect any part of the GI tract, typically in a transmural, skip-lesion pattern) and ulcerative colitis (which affects only the colon, in a continuous, superficial pattern) — involves chronic, relapsing intestinal inflammation driven by an overactive immune response to the gut microbiome in genetically susceptible individuals.

While biological medications (infliximab, adalimumab, vedolizumab, ustekinumab) have transformed IBD management, they are expensive, carry infection risks, and lose efficacy over time in many patients. Functional approaches aim to complement conventional treatment by addressing the upstream drivers of intestinal inflammation.

Microbiome Restoration in IBD

IBD patients show profoundly disturbed microbiome composition: reduced diversity, reduced Firmicutes (particularly Faecalibacterium prausnitzii — a major butyrate producer with anti-inflammatory properties), increased adherent-invasive E. coli, and reduced Roseburia and Bifidobacterium species. Strategies for microbiome restoration include:

Dietary interventions: The Specific Carbohydrate Diet (SCD), the Autoimmune Protocol (AIP), and the Mediterranean diet have all shown clinical benefit in IBD trials. The DINE-CD trial demonstrated that the SCD and Mediterranean diets both improved symptoms in Crohn’s disease patients, with the Mediterranean diet showing better adherence and comparable efficacy.

Targeted probiotics: VSL#3 (a high-potency multi-strain probiotic) has shown efficacy for inducing and maintaining remission in pouchitis and ulcerative colitis. Saccharomyces boulardii reduces Crohn’s disease relapse when combined with standard therapy. E. coli Nissle 1917 is as effective as mesalamine for maintaining UC remission.

Fecal microbiota transplantation (FMT): Multiple RCTs have demonstrated that FMT induces remission in 24-32% of ulcerative colitis patients (compared to 5-9% with placebo). Donor selection, preparation method, and delivery route all influence outcomes. FMT for Crohn’s disease shows less consistent results.

Butyrate and short-chain fatty acids: Butyrate is the primary energy source for colonocytes and has potent anti-inflammatory effects (inhibits NF-kB, promotes Treg differentiation). Butyrate-producing bacteria are consistently depleted in IBD. Butyrate enemas have shown benefit in distal UC. Oral tributyrin (a butyrate prodrug) at 2-4g daily may support colonic health.

Bile Acid Dysfunction

The Forgotten Digestive Factor

Bile acids, synthesized in the liver from cholesterol and stored in the gallbladder, are essential for fat digestion and absorption, fat-soluble vitamin absorption (A, D, E, K), cholesterol homeostasis, antimicrobial defense in the small intestine, and metabolic signaling through the farnesoid X receptor (FXR) and TGR5 receptor. Bile acid malabsorption (BAM) is an underdiagnosed cause of chronic diarrhea, present in up to 30% of IBS-D patients and commonly occurring after cholecystectomy (gallbladder removal), ileal resection, or radiation.

Diagnosis can be made through the SeHCAT test (not available in the US), serum C4 levels (7-alpha-hydroxy-4-cholesten-3-one — a marker of bile acid synthesis), or empirical trial of bile acid sequestrants (cholestyramine, colesevelam). Treatment includes bile acid sequestrants, ox bile supplementation (for those with bile insufficiency rather than excess), and addressing the microbiome (gut bacteria are essential for bile acid metabolism, converting primary bile acids to secondary bile acids through the enzyme bile salt hydrolase).

Post-Cholecystectomy Syndrome

Approximately 40% of patients who undergo cholecystectomy continue to experience GI symptoms afterward — a phenomenon called post-cholecystectomy syndrome. Without the gallbladder’s concentrating and regulated-release function, bile continuously drips into the duodenum, leading to: bile acid diarrhea (excess bile acids reaching the colon cause secretory diarrhea), fat maldigestion (inadequate bile concentration for large fatty meals), SIBO risk (reduced bile’s antimicrobial effect), and altered gut microbiome (changed bile acid profile shifts bacterial composition). Management includes ox bile supplementation with larger meals (150-500mg), bile acid sequestrants if diarrhea predominates, digestive enzymes with lipase, and gradual dietary fat titration.

The Enteric Nervous System

The Second Brain

The enteric nervous system (ENS) — embedded in the walls of the GI tract from esophagus to rectum — contains approximately 500 million neurons organized into two main plexuses: the myenteric (Auerbach’s) plexus controlling motility and the submucosal (Meissner’s) plexus controlling secretion, absorption, and blood flow. The ENS can function autonomously from the brain (as demonstrated in denervated intestinal preparations) and communicates bidirectionally with the CNS primarily through the vagus nerve.

The gut-brain axis — the bidirectional communication highway between the ENS and the CNS — operates through multiple channels: vagal afferents (conveying 80-90% of information from gut to brain), spinal afferents (visceral pain signals), immune mediators (gut-derived cytokines influencing brain function), microbial metabolites (short-chain fatty acids, tryptophan metabolites), and endocrine signals (gut hormones like GLP-1, CCK, PYY, and ghrelin influencing brain centers for appetite, mood, and stress response).

Vagal Tone and Digestive Function

The vagus nerve is the primary parasympathetic innervation of the GI tract, promoting digestive function through: increased gastric acid and enzyme secretion, enhanced intestinal motility, gallbladder contraction, pancreatic enzyme release, and anti-inflammatory signaling (the cholinergic anti-inflammatory pathway). Low vagal tone — measured through heart rate variability (HRV) — is associated with reduced digestive capacity, IBS, IBD flares, and visceral hypersensitivity.

Vagal tone enhancement strategies include: slow, deep breathing at 6 breaths per minute (the resonant frequency that maximally stimulates the baroreflex-vagal loop), cold water face immersion (triggers the dive reflex), gargling (activates vagal motor fibers to the pharynx), singing and chanting (prolonged exhalation and pharyngeal muscle activation), and HRV biofeedback training.

Clinical Applications

A Comprehensive Digestive Assessment

History: Detailed symptom timeline, dietary patterns, medication history (PPIs, antibiotics, NSAIDs), surgical history (cholecystectomy, appendectomy), travel history, stress and trauma history.

Testing:

• Comprehensive stool analysis (GI-MAP or similar): parasites, pathogenic bacteria, beneficial bacteria diversity, digestive markers (elastase, steatocrit), inflammatory markers (calprotectin, lactoferrin, secretory IgA)
• SIBO breath test (lactulose or glucose)
• Food sensitivity testing (mediator release testing or elimination diet — noting that IgG food panels have limited clinical validity)
• Intestinal permeability markers (zonulin, I-FABP, anti-LPS antibodies)
• Organic acids test (includes markers of bacterial and yeast overgrowth, mitochondrial function, nutrient status)
• Bile acid markers if diarrhea-predominant (serum C4 or empirical cholestyramine trial)
• Celiac panel (tTG IgA, DGP IgA/IgG, total IgA) — celiac disease must be ruled out before gluten-free diet

Foundational Digestive Support Protocol

1. Optimize stomach acid: Betaine HCl with pepsin (starting at 650mg with protein-rich meals, titrating up until warmth sensation, then reducing by one capsule) for patients with hypochlorhydria. Contraindicated with active ulcers or NSAID use.
2. Support bile and pancreatic function: Ox bile (150-500mg) and pancreatic enzymes with meals, particularly after cholecystectomy or in the elderly.
3. Address dysbiosis: Targeted antimicrobials for SIBO, parasites, or fungal overgrowth, followed by strategic probiotic supplementation.
4. Repair the gut lining: L-glutamine (5-10g daily), zinc carnosine (75mg twice daily), colostrum (1-2g daily), butyrate (300-600mg daily or via resistant starch).
5. Restore motility: Meal spacing (4-5 hours between meals), prokinetics if SIBO history, vagal tone exercises.
6. Manage stress: Diaphragmatic breathing before meals (“rest and digest”), HRV training, mindful eating.

Four Directions Integration

• Serpent (Physical/Body): The digestive system is where the outside world becomes the inside world — where food is deconstructed into molecules and reassembled into human tissue. Physical digestive health requires attention to every step of this alchemical process: thorough chewing (initiating salivary enzyme digestion), adequate stomach acid (sterilizing food and activating pepsin), bile and enzyme secretion (emulsifying fats and breaking down proteins), intestinal motility (moving contents at the right pace), microbial fermentation (extracting additional nutrients and producing beneficial metabolites), and barrier integrity (allowing nutrients in while keeping pathogens out). The serpent teaches that digestion is not passive — it is an active, intelligent process that requires the body’s full metabolic attention.

• Jaguar (Emotional/Heart): The gut is an emotional organ. “Butterflies in the stomach,” “gut feeling,” “I can’t stomach this” — these expressions reflect the ENS’s sensitivity to emotional states. Anxiety increases intestinal permeability, fear inhibits gastric acid secretion, anger accelerates motility, and grief slows it. The emotional roots of digestive disorders are not imaginary — they are mediated by the vagus nerve, the HPA axis, and the gut-brain axis. The jaguar’s emotional healing directly serves digestive healing: processing the emotions that are “stuck in the gut,” releasing the chronic tension held in the abdominal wall, and creating the emotional safety that allows the parasympathetic nervous system to support full digestive function.

• Hummingbird (Soul/Mind): The soul’s relationship with food is profoundly personal and culturally shaped. What we eat, how we eat, with whom we eat, and the meaning we assign to food all influence digestive function. Mindful eating — bringing full attention to the sensory experience of food — activates the cephalic phase of digestion (vagally mediated gastric acid and enzyme release triggered by sight, smell, and anticipation of food). Eating while distracted, stressed, or emotionally dysregulated impairs this cephalic phase. The hummingbird invites us to rediscover food as sacred nourishment rather than fuel, convenience, or emotional coping.

• Eagle (Spirit): From the eagle’s perspective, the epidemic of digestive disorders reflects a profound disruption of the human relationship with food, earth, and the cycle of nourishment. Industrial agriculture, processed food, pesticides, and the loss of food culture have severed the connection between humans and the living systems that feed them. Spiritual digestive healing involves reconnecting with the source of food — knowing where food comes from, preparing it with intention, eating with gratitude, and understanding that every meal is an exchange with the living earth. In many indigenous traditions, food preparation and consumption are sacred acts — and this sacred orientation toward nourishment may be the most powerful digestive intervention of all.

Cross-Disciplinary Connections

Digestive health connects to virtually every medical discipline. Immunology recognizes the gut as the largest immune organ, with gut-associated lymphoid tissue (GALT) producing 80% of the body’s immunoglobulins. Neurology is increasingly studying the gut-brain axis as a driver of neuropsychiatric conditions (depression, anxiety, autism, Parkinson’s disease). Endocrinology recognizes that the gut produces more hormones than any other organ, influencing appetite, metabolism, and mood. Dermatology observes the gut-skin axis: rosacea, eczema, psoriasis, and acne all correlate with GI dysbiosis and permeability. Traditional Chinese Medicine places the Spleen-Stomach system at the center of health, with treatment focusing on transforming and transporting food essence (gu qi), resolving dampness (analogous to SIBO and fungal overgrowth), and harmonizing the middle jiao. Ayurveda considers agni (digestive fire) the foundation of health, with all disease ultimately originating from impaired digestion and the resulting accumulation of ama (toxic metabolic waste).

Key Takeaways

• SIBO is present in up to 78% of IBS patients and has three distinct subtypes (hydrogen, methane/IMO, hydrogen sulfide) requiring different treatment approaches.
• Herbal antimicrobials are as effective as rifaximin for SIBO eradication (Johns Hopkins study).
• The low-FODMAP diet is the most evidence-based dietary intervention for IBS but should be used as an elimination protocol, not a permanent diet.
• IBD management can be enhanced through microbiome restoration, targeted probiotics, dietary intervention, and butyrate support.
• Bile acid malabsorption is an underdiagnosed cause of chronic diarrhea, particularly after cholecystectomy.
• The enteric nervous system contains 500 million neurons and communicates bidirectionally with the brain through the vagus nerve.
• Vagal tone enhancement (breathing, HRV training, cold exposure) directly supports digestive function.
• Comprehensive digestive healing addresses stomach acid, bile, enzymes, motility, microbiome, barrier integrity, and the nervous system.

References and Further Reading

• Pimentel, M., et al. (2020). “ACG Clinical Guideline: Small Intestinal Bacterial Overgrowth.” American Journal of Gastroenterology, 115(2), 165-178.
• Chedid, V., et al. (2014). “Herbal therapy is equivalent to rifaximin for the treatment of small intestinal bacterial overgrowth.” Global Advances in Health and Medicine, 3(3), 16-24.
• Halmos, E.P., et al. (2014). “A diet low in FODMAPs reduces symptoms of irritable bowel syndrome.” Gastroenterology, 146(1), 67-75.
• Moayyedi, P., et al. (2015). “Fecal Microbiota Transplantation Induces Remission in Patients With Active Ulcerative Colitis.” Gastroenterology, 149(1), 102-109.
• Fasano, A. (2020). Gut Feelings: The Microbiome and Our Health. MIT Press.
• Siebecker, A. (2018). SIBO: The Definitive Guide. siboinfo.com.
• Mayer, E. (2016). The Mind-Gut Connection. Harper Wave.
• Mullin, G.E. (2019). The Gut Balance Revolution. Rodale Books.