A recent study by researcher Michaelis Agatokleos of the University of Texas Southwestern Medical Center offers a preliminary new perspective, suggesting that the loss of the GULO enzyme may be a defense mechanism against parasites.
Agatokleos explained that "one reason for the loss of this metabolic gene, which produces an important molecule, is that the body has adapted to fight infections, including parasites." According to him, a vitamin C deficiency may have a positive effect on animals infected with parasites.
Researchers have observed that many parasites also lose the ability to synthesize ascorbate (vitamin C) during their development. Since parasites depend on their host for nutrients, a vitamin C deficiency in the host may limit their reproductive cycle. In laboratory experiments, adding vitamin C to schistosoma parasites enabled the worms to lay eggs, confirming their dependence on this nutrient.
To test the hypothesis, the team developed mice lacking the GULO enzyme, mimicking vitamin C deficiency in humans. These mice, along with normal laboratory mice, were then infected with the schistosomiasis parasite Schistosoma mansoni, and the vitamin C-deficient mice were fed a diet containing minimal ascorbate.
The researchers observed that normal mice developed enlarged livers and spleens, along with severe inflammation caused by parasite eggs. Mice deficient in vitamin C, however, developed the parasites, but the females did not lay mature eggs, thus limiting transmission and reducing mortality.
Agatocleus explained: "If the animal produces vitamin C itself, its levels will always remain high, and the schistosomiasis parasites will continue to lay eggs continuously. In the case of vitamin C deficiency, the protection is strong enough."
This raises the question: Doesn't this deficiency lead to scurvy, a fatal disease linked to a lack of vitamin C? Agatocleos pointed out that scurvy symptoms develop several months after the vitamin deficiency, while parasites act much more rapidly.
He said, "The parasite works faster than the host's response to the vitamin C deficiency, and this fact creates a significant advantage," meaning that the parasites stop reproducing before the host develops scurvy symptoms. Therefore, a vitamin C deficiency may protect the host without causing rapid disease damage.
The study suggests that the loss of the ability to synthesize vitamin C may have been a strategic evolutionary step to reduce parasite proliferation, rather than a random loss. According to the scientists, this data expands our understanding of vitamin C's role in immune defense and offers a new explanation for the mysteries of human evolution.
The study was published in the journal PNAS.
