We thank Dr Szilagyi for his very interesting comments in his letter regarding dysbiosis in inflammatory bowel disease (IBD).¹

The main question remains as to why beneficial bacteria such as bifidobacteria might be lacking in IBD (Gut 2004;53:1–4). Dr Szilagyi describes an interesting hypothesis of colonic prebiotic deficiency as a possible mechanism for dysbiosis. A suggestion is made that this deficiency could be linked to increased proximal small intestinal permeability with enhanced absorption of prebiotic substrate, causing a relative deficit of prebiotics distally. Certainly, the phenomenon of increased small bowel permeability has been documented in Crohn’s disease; its importance in ulcerative colitis is less clear however. As lactulose is not a major component of the normal human diet, long term epidemiological dietary trends should also have to be consistent with a significantly decreased intake of common prebiotic substrates, if this hypothesis is correct. Unfortunately, there is currently little clinical evidence to support or refute this theory, as dietary studies in IBD have been subject to many biases inherent in their study design.

Bifidobacteria are strongly glucidolytic and show nearly no growth in the absence of fermentable sugars or polysaccharides. One group of good substrates are mucins, which are often increased in Crohn’s disease. Perhaps differences in ease of glycosylation between some substrates affect the ability of the flora to metabolise them. This has not been well studied in IBD. There are also likely to be other influences on the host’s dominant flora, including genetic factors. Observations among some of our healthy cohorts with low levels of bifidobacteria have revealed highly variable responses of bifidobacterial counts to prebiotic treatments. Whether a poor response might represent a risk factor for IBD is also an interesting question.