Sodium butyrate, a short-chain fatty acid salt, has gained interest in recent years for its potential role in modulating immune responses, including in autoimmune disorders. The scientific rationale centers on its function as a histone deacetylase (HDAC) inhibitor, which allows it to influence gene expression, inflammation, and immune cell differentiation. Preclinical research, especially in animal models of autoimmune diseases such as multiple sclerosis (experimental autoimmune encephalomyelitis) and inflammatory bowel disease, has demonstrated that sodium butyrate can reduce inflammation and disease severity by promoting regulatory T cells and inhibiting pro-inflammatory cytokines.

However, robust clinical evidence in humans is still lacking. Most data come from cell-based or animal studies. A few small pilot studies in humans with inflammatory bowel disease have shown some improvement in symptoms when using butyrate enemas or supplements, but these studies are limited by small sample sizes and lack of control groups. There is currently insufficient evidence from large, well-conducted clinical trials to firmly recommend sodium butyrate as a treatment for autoimmune disorders in humans. As such, its use is supported by a scientific rationale and preclinical studies, but clinical validation remains limited, justifying a moderate evidence score.