About this Video

• Video Title: Surprising Reason Why Humans Can't Produce Vitamin C Anymore
• Channel: Anton Petrov
• Speakers: Anton Petrov
• Duration: 00:15:24

Introduction

This video explores the surprising reason why humans and certain other animals cannot produce vitamin C. It begins with the story of James Lind's discovery of a cure for scurvy and then delves into the recent research suggesting that the inability to produce vitamin C might be an evolutionary advantage in fighting parasitic infections.

Key Takeaways

• James Lind's Experiment: James Lind conducted the world's first controlled medical experiment in 1753, discovering that oranges and lemons cured scurvy in sailors.
• Vitamin C's Role: Ascorbic acid (vitamin C) is a crucial co-factor in many enzymatic processes, essential for collagen synthesis, neurotransmitter production, and acting as an antioxidant.
• Inability to Produce Vitamin C: Humans and some other animals lack the ability to produce vitamin C internally, unlike most other animals.
• Parasitic Infection Hypothesis: Recent research suggests that the inability to produce vitamin C offers protection against certain parasitic infections, specifically schistosomes, by hindering their reproduction.
• Evolutionary Trade-off: The loss of vitamin C production may be an evolutionary trade-off, where the risk of scurvy was outweighed by protection against parasitic diseases. This is supported by experiments on mice genetically modified to lack the ability to produce vitamin C.

The video proposes that the inability of humans and some other animals to produce vitamin C is not a random evolutionary event but a significant adaptation to combat certain parasitic infections. The research centers on Schistosoma mansoni, a parasitic flatworm causing schistosomiasis, which affects millions worldwide. These worms live in the host's circulatory system, laying thousands of eggs daily. These eggs lodge in organs like the liver, causing severe damage.

To test the hypothesis that the lack of vitamin C production offers protection against this parasite, researchers used two groups of mice: normal mice that could produce their own vitamin C and genetically modified mice that couldn't. Both groups were infected with S. mansoni. The normal mice experienced the typical severe symptoms: enlarged livers and spleens, extensive granulomas, and high parasitic egg counts, leading to many deaths. However, the vitamin C-deficient mice were remarkably protected. The worms could survive but couldn't produce viable eggs, resulting in minimal liver damage and no eggs in their feces, preventing disease transmission. Experiments mimicking natural vitamin C fluctuation showed that intermittent vitamin C depletion still offered a significant survival advantage.

The mechanism seems to be that host-derived vitamin C is crucial for the development of specific egg-producing cells in female worms. Without sufficient vitamin C, these cells fail to mature, effectively disabling the parasite's reproduction and its ability to cause disease. This suggests that the inability to produce vitamin C wasn't a neutral evolutionary change but a trade-off: the risk of scurvy was less significant than the benefit of protection against widespread parasitic diseases. The video speculates that similar mechanisms may exist for other parasites as well.

1. James Lind story (00:00:00)
2. Ascorbic acid and what it does (00:02:10)
3. Why can't we make vitamin C? (00:02:50)
4. How most animals make it (00:03:40)
5. Animals without vitamin C production - but why? (00:05:10)
6. Is it because of parasites? (00:06:50)
7. Experiment testing this hypothesis (00:07:50)
8. Major discoveries (00:09:00)
9. How does this work? (00:10:00)
10. What does this mean and what are the implications? (00:11:00)

The eighth chapter, "Major Discoveries," summarizes the key findings of the experiment comparing normal mice and genetically modified vitamin C deficient mice infected with Schistosoma mansoni. The major discovery was that the vitamin C deficient mice showed significant protection against the parasite, with greatly reduced parasitic egg production and resulting organ damage compared to the control group. The lack of viable eggs also prevented the disease's spread. This suggested that the parasite relies on the host's vitamin C for reproduction, offering an evolutionary advantage to animals that lost the ability to produce their own vitamin C.