IBD: Crohn’s & Ulcerative Colitis — The Functional Approach

When the Immune System Attacks Its Own Territory

Inflammatory Bowel Disease is not IBS with a worse attitude. It is a fundamentally different process — an autoimmune assault on the intestinal wall that causes tissue destruction, ulceration, and in severe cases, fistulae, strictures, and the slow erosion of the gut’s capacity to function. The distinction matters clinically, prognostically, and therapeutically.

Crohn’s disease can strike anywhere from mouth to anus, though it favors the terminal ileum and colon. It is transmural — inflammation cuts through the entire intestinal wall, from mucosa to serosa, like a fire burning from one side of a building clear through to the other. It creates skip lesions (inflamed segments alternating with healthy ones), granulomas, fistulae (abnormal tunnels between organs), and strictures (scarred narrowing). Immunologically, Crohn’s is driven primarily by Th1 and Th17 pathways — a cell-mediated immune response gone haywire, with TNF-alpha, IL-12, IL-23, and IL-17 as central inflammatory mediators.

Ulcerative colitis is confined to the colon and rectum. It is mucosal — the inflammation stays in the inner lining, extending continuously from the rectum proximally without skip areas. It produces a different immune signature: Th2-dominant, with IL-5, IL-13, and NKT cells driving mucosal damage. The hallmark is continuous superficial ulceration, bloody diarrhea, and urgency.

Both conditions involve a fundamental failure of mucosal immune tolerance. The immune system, which is supposed to coexist peacefully with the trillions of commensal bacteria in the gut, begins attacking them — and the intestinal tissue itself becomes collateral damage.

The Microbiome Connection

The gut microbiome in IBD is not merely altered — it is impoverished. Patients consistently show:

Reduced diversity: Fewer species, less resilience
Loss of Faecalibacterium prausnitzii: This keystone bacterium produces butyrate, the primary fuel for colonocytes and a potent anti-inflammatory molecule. Its absence correlates with disease activity and relapse risk. Sokol 2008 demonstrated that F. prausnitzii abundance at the time of surgical resection predicted post-operative recurrence in Crohn’s disease.
Loss of Roseburia and other butyrate producers: Further depleting the anti-inflammatory short-chain fatty acid pool
Increased adherent-invasive E. coli (AIEC): Darfeuille-Michaud’s research identified AIEC strains that adhere to and invade intestinal epithelial cells, replicate within macrophages, and trigger TNF-alpha production. AIEC is found in ileal mucosa of 36-38% of Crohn’s patients versus 6% of controls.
Increased sulfate-reducing bacteria: Producing hydrogen sulfide, which is directly toxic to colonocytes
Reduced Bacteroidetes-to-Firmicutes ratio: Shifted toward a pro-inflammatory configuration

Whether dysbiosis is cause or consequence remains debated. The functional view: it does not matter. Both are true. The dysbiosis perpetuates inflammation, and the inflammation perpetuates dysbiosis. Breaking the cycle requires addressing both simultaneously.

Testing and Monitoring

Inflammatory Markers

Fecal calprotectin: The single most useful non-invasive marker. A protein released by neutrophils infiltrating the intestinal wall. Levels correlate tightly with mucosal inflammation. Below 50 mcg/g is normal. 50-250 suggests mild inflammation. Above 250 indicates significant active disease. Use for monitoring treatment response and detecting subclinical relapse before symptoms flare.
Fecal lactoferrin: Another neutrophil-derived marker of intestinal inflammation. Complementary to calprotectin.
CRP (C-reactive protein): Systemic inflammatory marker. More often elevated in Crohn’s than UC. Useful for tracking disease activity but less gut-specific.
ESR (erythrocyte sedimentation rate): Non-specific systemic inflammation marker. Trends are more useful than single values.

Imaging and Endoscopy

Colonoscopy with biopsies: Gold standard for diagnosis, disease extent, and surveillance for dysplasia/cancer
Capsule endoscopy: For small bowel Crohn’s disease that colonoscopy cannot reach
MR enterography: Non-invasive imaging for small bowel Crohn’s — detects strictures, fistulae, and active inflammation without radiation

Nutritional Assessment

IBD patients are chronically malnourished. Screen and monitor:

Iron: Deficiency anemia (blood loss + impaired absorption) — check ferritin, iron, TIBC, transferrin saturation
Vitamin B12: Ileal Crohn’s disease damages the absorption site. Check serum B12 and methylmalonic acid
Folate: Depleted by sulfasalazine and methotrexate, and by malabsorption
Zinc: Depleted by diarrhea and inflammation. Critical for immune function and wound healing
Vitamin D: Deficient in 60-70% of IBD patients. Required for immune regulation, mucosal barrier integrity
Vitamin K: Malabsorbed due to bile salt disruption. Needed for bone health and coagulation

Dietary Approaches

Diet is not adjunctive in IBD. Diet is foundational. The explosion of research since 2010 has made this undeniable.

Specific Carbohydrate Diet (SCD)

Developed by Elaine Gottschall based on the work of Dr. Sidney Haas. The premise: complex carbohydrates (disaccharides and polysaccharides) feed pathogenic bacteria, while monosaccharides are absorbed before they can be fermented. SCD eliminates all grains, most dairy (except 24-hour fermented yogurt and aged cheeses), sugar, starch, and processed foods. Multiple case series and small trials show remission induction and maintenance in both Crohn’s and UC.

Crohn’s Disease Exclusion Diet (CDED)

Levine 2019 published a landmark RCT in The Lancet Gastroenterology & Hepatology: the CDED — a whole-food diet that excludes specific components hypothesized to promote dysbiosis and barrier dysfunction (emulsifiers, maltodextrin, gluten, dairy, animal fat) — achieved 75% remission in pediatric Crohn’s at 12 weeks, compared to 59% with exclusive enteral nutrition. The CDED was better tolerated and sustained remission after diet liberalization.

This is remarkable. A food-based intervention outperformed liquid nutrition in inducing remission in an autoimmune disease.

IBD Anti-Inflammatory Diet (IBD-AID)

Developed at UMass Medical School by Barbara Olendzki. Olendzki 2014 published a case series of 11 IBD patients following the IBD-AID — which modifies SCD by adding prebiotic and probiotic foods — and all 11 achieved clinical response, with a significant reduction in disease activity scores. The diet is phased: restriction during flares, gradual reintroduction during remission.

Mediterranean Diet

Anti-inflammatory by nature: high in omega-3, polyphenols, fiber, and fermented foods. Lewis 2021 (the DINE-CD study) compared Mediterranean diet to SCD in mild-to-moderate Crohn’s and found similar outcomes at 12 weeks, suggesting that a less restrictive anti-inflammatory diet may be sufficient for some patients.

Supplement Protocol

Anti-Inflammatory Core

Curcumin: Hanai 2006 published a randomized, double-blind, placebo-controlled trial in Clinical Gastroenterology and Hepatology: UC patients in remission on mesalamine who added curcumin 2g/day had a relapse rate of 4.7% over 6 months, compared to 20.5% with placebo. The NNT was 6 — meaning for every 6 patients treated with curcumin, one additional patient maintained remission. Use a bioavailable formulation (phytosomal, liposomal, or with piperine). Dose: 2-4g/day in divided doses.

Omega-3 fatty acids: EPA and DHA from fish oil reduce TNF-alpha, IL-1beta, and leukotriene B4 production. Dose: 2-4g combined EPA/DHA daily. Some studies show stronger benefit in UC than Crohn’s. Use a high-quality, third-party tested product to avoid oxidized oils.

Boswellia serrata (H15 extract): Gerhardt 2001 published a controlled trial comparing boswellia H15 extract to mesalamine in active Crohn’s disease. Boswellia was non-inferior to mesalamine in inducing remission, with an CDAI response rate of 70% versus 75% for mesalamine. Boswellia inhibits 5-lipoxygenase, reducing leukotriene synthesis. Dose: 400mg three times daily of standardized extract.

Immune Modulation

Vitamin D: Target serum 25(OH)D of 50-80 ng/mL. Start with 5,000-10,000 IU daily, adjusted by lab monitoring. Vitamin D modulates T-cell function, supports Treg cells (which suppress autoimmune responses), maintains tight junction integrity, and produces antimicrobial peptides (cathelicidin, defensins) in the gut epithelium. Jorgensen 2010 demonstrated reduced relapse rates in Crohn’s patients supplementing 1,200 IU/day — and many functional practitioners use far higher doses with monitoring.

Low Dose Naltrexone (LDN): Smith 2007 published a pilot study of LDN (4.5mg at bedtime) in Crohn’s disease: 89% responded, 67% achieved remission. Smith 2011 followed with a randomized controlled trial: 88% response rate with LDN versus 40% with placebo. The mechanism: brief opioid receptor blockade upregulates endogenous endorphin and enkephalin production, which modulates immune function and reduces inflammation. LDN requires a prescription (compounding pharmacy) and is off-label. Side effects are minimal — vivid dreams initially, which typically resolve.

Gut Barrier and Microbiome

Probiotics: Not all strains are equal in IBD.

VSL#3/Visbiome: The most studied probiotic in IBD. 450 billion CFU of 8 strains. Sood 2009 demonstrated that VSL#3 induced remission in 42.9% of active UC patients versus 15.7% with placebo. Also effective for maintaining remission and preventing pouchitis.
E. coli Nissle 1917 (Mutaflor): Rembacken 1999 published a landmark study showing E. coli Nissle was equivalent to mesalamine for maintaining remission in UC. This non-pathogenic E. coli strain colonizes the colon, competes with pathogens, produces antimicrobial substances, and modulates immune responses.
Saccharomyces boulardii: 500mg twice daily. Reduces Crohn’s disease relapse rates (Guslandi 2000).

Butyrate: The colonocyte’s primary fuel source. Butyrate enemas (100mM sodium butyrate) deliver this directly to inflamed colonic mucosa in UC. Oral sodium butyrate 300-600mg three times daily for systemic effect.

L-glutamine: 10-15g daily in divided doses. Fuel for enterocytes, maintains tight junction integrity.

Aloe vera gel: Langmead 2004 published a randomized, double-blind, placebo-controlled trial of oral aloe vera gel in active UC: clinical response occurred in 47% of the aloe vera group versus 14% with placebo at 4 weeks. Dose: 100mL of aloe vera gel twice daily.

Fecal Microbiota Transplantation (FMT)

FMT — transferring stool from a healthy donor to a patient’s colon — is the most direct microbiome intervention available. Multiple randomized controlled trials (Moayyedi 2015, Paramsothy 2017, Costello 2019) demonstrate FMT’s ability to induce remission in UC, though response rates vary by donor (“super donors” with specific microbiome compositions produce better outcomes). FMT for Crohn’s is less studied but shows promise. Access remains limited outside of clinical trials and C. difficile treatment.

Medication Integration

Functional medicine does not exist in opposition to conventional IBD medication. It exists alongside it.

5-ASA (mesalamine): First-line for mild-to-moderate UC. Works locally in the colon. Compatible with all functional approaches.
Steroids (prednisone, budesonide): For flare induction, not maintenance. While a patient tapers steroids, functional support can reduce the likelihood of relapse.
Immunomodulators (azathioprine, methotrexate): For steroid-dependent disease. Monitor for nutrient depletion (folate with methotrexate).
Biologics (infliximab, adalimumab, vedolizumab, ustekinumab): For moderate-to-severe disease. These medications have transformed IBD outcomes. Curcumin, omega-3, vitamin D, and LDN can be used as adjuncts. Some patients achieve sufficient remission with functional approaches to taper biologics under gastroenterology supervision — but this must be individualized and monitored with calprotectin and endoscopy.

The Stress-IBD Connection

IBD flares do not follow a random pattern. Ask any patient and they will tell you: stress precedes relapse. This is not psychological weakness. This is psychoneuroimmunology.

The vagus nerve — the primary parasympathetic highway between brain and gut — directly regulates intestinal inflammation through the cholinergic anti-inflammatory pathway. Vagal tone, measured by heart rate variability (HRV), is reduced in IBD patients. Lower vagal tone means less braking on inflammation.

Bonaz 2016 demonstrated that vagus nerve stimulation reduced intestinal inflammation in a Crohn’s disease pilot study. Non-invasive vagal toning — deep diaphragmatic breathing, meditation, cold water face immersion, gargling, singing — represents a zero-risk adjunct to IBD management.

Chronic stress also increases intestinal permeability, shifts the microbiome toward dysbiosis, activates mast cells in the intestinal wall, and suppresses secretory IgA (the gut’s mucosal immune defense). Stress management is not optional in IBD. It is therapeutic.

What if remission depended not only on what enters the gut — but on the state of the nervous system that governs it?

IBD: Crohn's & Ulcerative Colitis — The Functional Approach