The endometriosis research case for DCA applies equally to both salt forms. Endometriotic lesions exhibit the Warburg effect — using aerobic glycolysis to drive their survival and proliferation. DCA’s PDK inhibition mechanism targets this metabolic phenotype directly.

The Oxford EPiC trial used sodium DCA. However, the active mechanism is the dichloroacetate anion, and potassium DCA delivers the same anion at molar-equivalent doses. Researchers or individuals following low-sodium protocols for other health reasons might consider KDCA as an alternative, applying the 1.147 molar conversion factor.

Preclinical endometriosis studies — including mouse model work showing lesion size reduction, reduced inflammatory markers, and increased apoptosis in lesion cells — used sodium DCA. The mechanism is directly translatable to potassium DCA.

The EPiC trial results — 79% pain reduction — remain the strongest human evidence for DCA in endometriosis. Larger trials are ongoing. DCA is not an approved treatment for endometriosis.

This article is for informational and educational purposes only. AuraDCA products are intended for research use only.