Researchers at UT Southwestern report that mice engineered to be unable to make vitamin C developed much milder schistosome infections because female worms failed to form normal reproductive tissue and produced few eggs. The PNAS study shows vitamin C is critical for the worm’s vitellarium and egg production. While the findings offer a plausible evolutionary reason for humans losing vitamin C synthesis, authors warn this does not prove causation and note deliberately inducing deficiency would be unsafe. The work suggests new therapies might target parasites’ vitamin C uptake.
Why Losing Vitamin C Might Have Helped Ancestors Fight Parasites — New Mouse Study
Millions of years ago, humans lost the ability to produce vitamin C, a mystery that has puzzled scientists for decades. Now, new research suggests this evolutionary change may have protected our ancestors. Katharina Frenzel/dpa
Millions of years ago our ancestors lost the ability to synthesise vitamin C. A new study from UT Southwestern offers a provocative explanation: vitamin C deficiency in the host may hamper parasitic worms and reduce the disease they cause.
Researchers at the Children’s Medical Center Research Institute at UT Southwestern infected genetically engineered mice that cannot make vitamin C with schistosomes, the parasitic worms that cause schistosomiasis. In those vitamin C–deficient mice the female worms failed to develop normal reproductive tissue, produced malformed or few eggs, and the animals showed far less organ damage than normal mice — although they did develop scurvy if completely deprived of the vitamin.
How Vitamin C Affects the Parasite
The team found that vitamin C is essential for the development of the female schistosome’s vitellarium, a reproductive organ that works alongside the ovary to produce eggs. Without adequate vitamin C the vitellarium does not mature properly, egg formation is abnormal, and infected hosts shed few or no eggs in their feces — a key route for transmission and the primary driver of disease pathology.
Key Experiments and Findings
Because ordinary mice can make vitamin C, investigators used engineered mice lacking the enzyme for vitamin C synthesis. After schistosome infection, normal mice developed classic signs of disease — enlarged livers and spleens and granulomas around lodged eggs. Vitamin C–deficient mice showed much less organ damage. Importantly, administering small, intermittent doses of vitamin C to engineered mice before and shortly after infection prevented scurvy while preserving protection against most organ damage.
Publication and context: The results appear in Proceedings of the National Academy of Sciences (PNAS). Experts caution the study suggests a plausible evolutionary benefit for loss of vitamin C synthesis but does not prove the gene was lost specifically to defend against schistosomes; that genetic change occurred millions of years ago.
Implications and Cautions
These findings point to new therapeutic possibilities, such as drugs that block the parasite’s uptake or use of host-derived vitamin C. Researchers emphasise that deliberately restricting vitamin C in people would be unsafe and is not a treatment strategy. The standard drug for schistosomiasis remains praziquantel, but not all patients tolerate it, so alternative approaches would be valuable.
The study also raises broader questions: do other parasites rely on host vitamin C in similar ways? Follow-up research will test whether this dependency is unique to schistosomes or shared by multiple parasites.
Disease burden: Schistosomiasis infects more than 200 million people worldwide and places nearly 800 million at risk, making research into new interventions a public health priority.
Help us improve.
