In mouse models of inflammatory bowel disease, taking inositol hexakisphosphate by mouth is associated with decreased intestinal permeability, which occurs through increased HDAC3 activity and...

We analyzed the available evidence on oral inositol hexakisphosphate and intestinal permeability in mouse models of inflammatory bowel disease. What we’ve found so far is that eight studies or assertions support the idea that taking inositol hexakisphosphate by mouth is linked to reduced intestinal permeability in these mice. None of the evidence we reviewed contradicts this. The mechanism described in the supporting evidence suggests that inositol hexakisphosphate may work by increasing HDAC3 activity, a protein involved in regulating gene expression, and by lowering the activity of MMP genes, which are linked to tissue breakdown in the gut lining. These changes appear to help strengthen the barrier between the inside of the intestine and the rest of the body. It’s important to note that all of this evidence comes from mouse models — not humans — and the studies focus only on inflammatory bowel disease conditions in these animals. We don’t have data on how this might apply to people, or whether the same biological pathways work the same way outside of mice. We also don’t know how much inositol hexakisphosphate was used, how often, or for how long in these studies. The evidence doesn’t clarify whether the effect is strong, temporary, or dependent on the type of bowel disease being studied. So far, the evidence we’ve reviewed leans toward a connection between oral inositol hexakisphosphate and reduced intestinal permeability in mice with inflammatory bowel disease, but we can’t say if this would work the same way in other animals or humans. If you’re considering inositol hexakisphosphate for gut health, keep in mind that mouse results don’t always translate to people — and this is still early, limited evidence.