Crohn's disease and ulcerative colitis (IBD): dysbiosis, flares and diet

Chronic diarrhoea, abdominal pain, blood or mucus in the stool, a fatigue that weighs everything down: inflammatory bowel diseases (IBD) cover Crohn’s disease and ulcerative colitis (UC). Their incidence is rising in every country adopting the Western diet. This is the area where diet is most documented as a genuine therapeutic lever, not merely a matter of comfort.

Crohn’s and UC: two diseases, one spectrum

Both diseases share the same mechanism: chronic inflammation of the gut wall maintained by an immune response dysregulated towards the microbiome, on favourable genetic ground.

Ulcerative colitis remains confined to the colon and rectum, affects the mucosa continuously, and shows as bloody stools and urgency. Crohn’s disease can affect the whole digestive tract from mouth to anus (often the terminal ileum), penetrates the wall in discontinuous patches, and can be complicated by strictures and fistulas.

This anatomical difference has a major dietary consequence: small-bowel Crohn’s can compromise absorption (B12, iron, vitamin D, zinc), and strictures impose texture adaptations that UC does not require.

The dysbiosis of IBD: AIEC and the missing bacteria

The IBD microbiome is not ‘unbalanced’ in the vague sense: it has documented signatures.

AIEC (adherent-invasive E. coli): strains of Escherichia coli able to adhere to and penetrate the ileal mucosa are found more frequently in ileal Crohn’s. They stimulate local inflammation and thrive in the environment they create.

The loss of guardians: Faecalibacterium prausnitzii, a major producer of butyrate (the fuel of colonocytes and a local anti-inflammatory), is decreased in Crohn’s; its persistently low level after a flare predicts relapse. IBD dysbiosis is both a loss of guardians and an invasion of opportunists.

Hyperpermeability: the intestinal barrier is loosened, allowing contact between the microbiome and the mucosal immune system, which maintains the circle of inflammation. Leaky gut is a central mechanism here, not a theory.

Enteral nutrition: the treatment that feeds

The most counter-intuitive fact in IBD: in paediatric Crohn’s, exclusive enteral nutrition (a complete liquid feed replacing all meals for 6 to 8 weeks) induces remission as effectively as corticosteroids, without their effects on growth. It is the only dietary treatment that induces a documented remission in gastroenterology.

In adults, efficacy is real but adherence harder; partial versions (partial enteral nutrition plus targeted exclusions, the CDED protocol) are being validated. The message is broader than the protocol: in Crohn’s, what goes into the digestive tube has an effect comparable to a maintenance drug.

SCD, FODMAPs: the diets of remission

In remission, strategies change aim: no longer inducing, but maintaining and preventing deficiencies.

The SCD (Specific Carbohydrate Diet): exclusion of complex sugars (grains, starches, added sugars) to starve pro-inflammatory bacteria. Encouraging paediatric data exist; the method is demanding and must be supervised.

FODMAPs: the restriction-then-reintroduction protocol relieves the functional symptoms that often persist in remission (bloating, pain); the article on FODMAPs and Spleen Dampness details the method. Caution: FODMAPs treat the symptom, not the inflammation.

The background anti-inflammatory diet: reduce ultra-processed foods (emulsifiers such as carboxymethylcellulose and polysorbate 80 impair the mucosal barrier in animal models), favour the anti-inflammatory diet, adapt fibre to the calibre of the gut (soluble fibre tolerated, insoluble adjusted during flares).

Phase	State of the gut	Dietary strategy

The TCM reading: Damp-Heat and Spleen Deficiency

The Chinese classics knew this picture as li ji (痢疾), dysentery: bloody and mucous stools, urgency, pain. The reading is limpid: the flare is Damp-Heat burning the mucosa (the blood, the mucus, the urgency), and prolonged remission is a Spleen Deficiency that no longer transforms, letting Dampness reform.

Blood enters the reading: the bleeding of UC and the anaemia of Crohn’s belong to Blood Deficiency, and the chronic fatigue of the patient in remission is a classic Spleen and Blood deficiency. Dietetics follows the phase: clarify Damp-Heat during flares (warm, simple, without irritants), tonify the Spleen and nourish Blood in remission.

What requires medical advice

IBD belongs to the gastroenterologist: maintenance treatment (immunosuppressants, anti-TNF and anti-integrin biologics) prevents destructive complications (strictures, fistulas, colectomy). Any sudden worsening (abundant blood, intense pain, fever, obstruction) is an emergency. Diet is a powerful lever but integrates into the medical strategy; it does not replace it.

FAQ: IBD

Does stress cause flares?

It does not cause the disease but it can trigger or prolong flares via the gut-brain axis. Stress management is part of relapse prevention, on a par with treatment.

Should fibre be avoided?

Only during flares and in case of stricture. In remission, fibre (especially soluble) feeds the butyrate-producing bacteria that protect the mucosa. Lasting fibre restriction in remission is a common mistake.

Does enteral nutrition work in adults?

Yes, but adherence is harder and efficacy more modest than in children. Partial enteral protocols combined with targeted exclusions (the CDED diet) are being validated and show encouraging results.

Do probiotics help?

The data are modest: certain strains have shown a benefit in UC maintenance, almost none in Crohn’s. Feeding the microbiome (tolerated, diversified fibres) matters more than added strains.

IBD, the diseases where the plate is a medicine

Crohn’s and UC demonstrate that diet is not a comfort in inflammatory digestive disease: enteral nutrition induces remissions, ultra-processed foods maintain dysbiosis, and terrain work (Damp-Heat in flares, Spleen Deficiency in remission) stabilises the background. To situate your digestive terrain: the Yin Shi energy test traces the profile in a few minutes.