Lactic acidosis — a dangerous accumulation of lactate in the blood — was the original clinical application that drove DCA research beginning in the 1970s. Understanding this history gives important context for how DCA’s mechanism was characterised.

Lactic acidosis occurs when lactate production exceeds the body’s capacity to clear it. This happens in septic shock, liver failure, certain inherited metabolic disorders, and with some medications. The resulting acidosis can be life-threatening.

DCA’s mechanism — activating PDH and reducing pyruvate-to-lactate conversion — directly addresses the metabolic cause of lactic acidosis. Clinical trials throughout the 1980s and 1990s demonstrated DCA’s ability to lower blood lactate levels. The most significant trial, published in the New England Journal of Medicine in 1992, showed DCA effectively reduced lactate and improved acidosis — though without a survival benefit in the critically ill population studied.

This research established DCA’s pharmacokinetics, safety profile, and effective doses in humans — providing the foundation for all subsequent research. Both sodium and potassium DCA forms have been used in lactic acidosis research, though sodium is far more common.

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