Vitamin B1 Reveals Promising Approach to Combat Sepsis by Reducing Lactate Accumulation

Researchers in Ghent have made significant advances in sepsis treatment through a groundbreaking study. In experiments conducted on mice, they discovered that vitamin B1 (thiamine pyrophosphate, TPP) plays a crucial role in restoring mitochondrial energy metabolism, markedly decreasing lactate production, and improving survival rates in sepsis conditions. The findings, published in Cell Reports, suggest a new avenue for targeted therapies.

Sepsis, often called blood poisoning, is a severe and often fatal condition where the body's immune response to infection spirals out of control, leading to widespread organ damage. One of the key features of sepsis is an excess buildup of lactic acid in the blood, which results from mitochondrial energy failure. Annually, sepsis affects nearly 50 million people worldwide, claiming approximately 11 million lives, yet effective targeted treatments remain elusive.

The Ghent team, led by Professor Claude Libert, uncovered that a deficiency of vitamin B1 within the mitochondria causes a biochemical disruption. Normally, vitamin B1 is essential for efficient energy production in cells. Its shortage hampers the conversion of pyruvate into energy, causing excess pyruvate to be transformed into lactate, which in turn leads to dangerous acidosis and organ dysfunction.

This research builds on earlier work by the same group in 2021, which identified impaired clearance of lactate in sepsis patients. Now, they have elucidated why lactate levels rise so dramatically—fundamentally linked to vitamin B1 deficiency—and have identified a simple intervention.

Treatment experiments with mice demonstrated that administering vitamin B1 could significantly restore energy metabolism. When combined with glucose, this therapy became even more effective, redirecting glucose metabolism away from lactate production toward safe energy generation. Remarkably, nearly all mice treated with both vitamin B1 and glucose survived severe sepsis models, indicating a powerful metabolic intervention that could be rapidly translated into critical care settings.

This approach is promising because it tackles the root biochemical defect rather than just addressing symptoms. By reprogramming cellular metabolism, the therapy aims to prevent the cascade of organ failure characteristic of sepsis. This research also offers hope for treatments in humans, although further studies in larger animals are necessary before clinical application.

The societal impact is notable, given the public awareness generated by recent media coverage like the Flemish documentary "Bad Blood," which highlighted the urgent need for effective therapies. If future clinical trials confirm these findings, vitamin B1 supplementation combined with glucose could become a simple, accessible treatment for sepsis, transforming patient outcomes worldwide.

While these findings are promising, it is essential to proceed with caution: human trials are required to validate safety and efficacy. Nevertheless, this research marks a significant step forward in understanding and potentially managing one of the most challenging critical illnesses.

For more details, read the full study by Louise Nuyttens et al., available in Cell Reports (2025): [DOI: 10.1016/j.celrep.2025.116032].