Butyric acid, a short-chain fatty acid (SCFA), is produced naturally in the colon through bacterial fermentation of dietary fibers. Its use in supporting or treating colitis—especially ulcerative colitis—has a scientific basis. Butyric acid serves as the primary energy source for colonocytes (cells lining the colon) and plays a critical role in maintaining intestinal barrier integrity, regulating inflammation, and modulating immune responses.

Several preclinical studies and small-scale clinical trials have evaluated the effects of butyric acid (administered as oral or rectal butyrate) in patients with colitis. Results suggest that butyrate supplementation can reduce inflammation, promote mucosal healing, and alleviate symptoms. For example, randomized controlled trials have shown that rectal butyrate enemas improved clinical and endoscopic indices in patients with distal ulcerative colitis who were refractory to standard therapies. The proposed mechanisms include inhibition of nuclear factor-kappa B (NF-κB) signaling, suppression of pro-inflammatory cytokine production, and enhancement of mucin synthesis.

However, larger, high-quality studies are limited, and the therapeutic effect appears to be modest and variable among individuals. Current clinical guidelines do not universally endorse butyrate as standard therapy, but it is recognized as a potentially valuable adjunct, particularly for patients with mild-to-moderate distal colitis. In summary, there is scientific validation for the use of butyric acid in colitis, but the evidence is moderate and further research is warranted to clarify its clinical utility.