Though it’s unclear whether Candida plays a causal role, researchers have found low or altered fungal diversity in patients with inflammatory bowel disease (IBD),[1] and emerging evidence indicates that Candida species tend to predominate in the mycobiomes of patients with IBD.[2]
Some species of Candida can colonize and delay the healing of gastric and intestinal ulcers. One small observational study found that certain species were detectable in inflamed regions of the intestines in Crohn’s disease but absent from the non-inflamed areas.[3] One nonrandomized, uncontrolled study reported that two weeks of antifungal treatment in patients with ulcerative colitis and significant fungal colonization reduced disease activity and mucosal inflammation.[4]
Without diagnostic criteria or the quantification of Candida colonization in these studies, however, it’s impossible to determine whether these cases would be characterized as IC or some form of fungal imbalance. Patients with IBD often use certain medications that increase the risk for fungal disease, which could also explain these findings.[5]
Candida abundance is also associated with visceral hypersensitivity (a heightened sense of pain in response to normal gut functions) in a subgroup of IBS that responds well to antifungal treatment.[6] Exploratory studies have noted that higher Candida abundance is associated with more severe bloating.[7] Though Candida species are present in people with and without IBS, other emerging evidence suggests that C. albicans in people with IBS is genetically distinct from the same species in healthy people. The correlations between Candida and certain bacteria also differ between people with IBS-D and healthy controls.[8] There is still no conclusive link between IBS and Candida, though. Despite some unique variations in IBS versus healthy controls, the mycobiome isn’t a useful biomarker for IBS due to high levels of individual variability and lack of any causal relationships.