Have you ever wondered why we humans need to have vitamin C in our diet, but dogs and cats don’t?
American schoolchildren often begin their study of U.S. history by learning about the 14th and 15th century European explorers. I distinctly remember a story we were told about how sailors eventually learned to carry potatoes or limes on their long voyages in order to prevent the disease called scurvy. We now know that scurvy is caused by a deficiency in ascorbic acid, also known as vitamin C.
Thus, vitamin C is considered an “essential” vitamin because we simply must have it in our diet. Without it, we cannot make collagen and our tissues lose integrity, bones become brittle, we bleed out of various orifices, and our bodies basically fall apart. That’s scurvy.
However, have you noticed that neither dog food nor cat food contains any citrus fruit? Both dogs and cats can get by on meat and rice, with no vitamin C whatsoever, and they never develop scurvy. How do they do it? They make their own vitamin C.
In fact, the cells of nearly all animals on the planet make plenty of their own vitamin C and thus have no need for it in their diets. Humans and other primates are pretty unique in our need to have vitamin C in our diet. This is an example where our ancestors clearly had more functionality than we have now. Somewhere in our lineage, we actually lost the ability to make vitamin C.
[Update: the popularity of this post helped inspire me to write my new book, “Human Errors,” a tour through many design flaws in humans. Check it out!]
How did we lose it? It turns out that we do have all of the genes that are necessary, but one of them is “broken.” The broken gene, nicknamed GULO, codes for an enzyme called L-gulonolactone oxidase, which is responsible for a key step in vitamin C synthesis. We have the gene, but it has been mutated to the point of being nonfunctional, making it a so-called pseudogene.
Somewhere in the ancestor of primates, the gene suffered a mutation, rendering it inoperable, and then random mutation continued, littering the gene with tiny errors. We can still easily recognize the gene. It’s there and the vast majority of the code is the same, but there are a few key parts that have been mutated. It’s like if I were to remove the spark plug from a car. It’s still a car. You can easily see that it is still a car. In fact, you would have to look very carefully to see that anything was wrong at all. But yet, it cannot function as a car, even slightly. It’s totally inoperable, even though most of it is still together.
That’s what happened to our GULO gene, way back in our history. The spark plug was removed by a random mutation. Random mutations happen all the time. Often, they are of no consequence, but sometimes they occur right smack in a gene. When that happens, it is almost always bad because the mutation disrupts the functioning of the gene. The individuals suffering this mutation are then a little worse off (or a lot worse off) and harmful mutations are eventually eliminated from the population.
This begs the question: why wasn’t the GULO gene mutation eliminated? Scurvy is fatal. The consequences of this mutation ought to have been quick and harsh.
Well, maybe not. What if this disrupting mutation happened to a population of mammals that already had lots of vitamin C in their diet anyway? There would be no consequence of losing the ability to make vitamin C, if they were already eating foods that contain it. What foods contain a lot of vitamin C? Citrus fruits. And where do citrus fruits mostly grow? Tropical rain forests. And where do most primates live? Bingo.
The reason that the ancestors of primates could tolerate a mutation in the GULO gene was because, with plenty of vitamin C in their diet anyway, scurvy wasn’t an issue. Since that time, primates have pretty much stuck to the rainforests and their inability to make vitamin C might be part of why that is. After all, while it’s easy to break a gene by mutation, it’s much more difficult to fix it. It’s like slamming your hand on your computer when it’s not working right. You might fix it, but more likely, you’ll do more harm.
Primates aren’t totally unique for having a screwed up GULO gene. A few other animals have this also. Not surprisingly, the ones that tolerate having a broken GULO genes are ones that get plenty of vitamin C in their diet. Take fruit bats, for example. They eat, um, fruit.
Interestingly, our bodies, like those of other animals that have lost the ability to make vitamin C, have attempted to compensate by increasing our dietary absorption of it. Animals that make their own vitamin C are typically very poor at absorbing it from their food; they don’t need it anyway. So yes, we have attempted to correct this malfunction, but if we were to “design” a human from scratch, it would be far better to just give us a functioning GULO gene, like most of the rest of the animals. Our inability to make vitamin C puts strict constraints on our diet, upon pain of disease and death.
Our broken GULO gene is an example of how the human body, though intricate, efficient, and beautiful, is definitely not perfect. There are a few design flaws under the hood.
-NHL (@nathanlents)
The Human Evolution Blog 
i dont think its a flaw. like a broken miror in a car isnt a flaw of the original design. we find a motor called flagellum in bacteria. we know that a motor is the product of design and not natural process(even if it have a self replicating system).
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If you mention the bacterial flagellum as an example of intelligent design, I think we won’t be seeing eye to eye on just about anything on this blog.
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Nathan,
I was reading your spot on vitamin C and saw your response to the bacterial flagellum argument. I find this interesting because the community thinks this problem was solved by Judge Jones ruling in Dover, PA. Somehow Ken Miller and others gave the impression that the evidence must have been presented that showed a detailed evolutionary account of this organelle. But in a flagellum review article published by Academic Press in 2009 (four years after the Dover Trial), S. I. Aswawa has this quote:
“Since the flagellum is so well designed and beautifully constructed by an ordered assembly pathway, even I, who am not a creationist, get an awe-inspiring feeling from its ‘divine beauty’. If the flagellum has evolved from a primitive form, where are the remnants of its ancestors? Why don’t we see any simpler forms of flagella that what they are today? How was it possible that the flagella have evolved without leaving traces in history?”
S.I. Aizawa (2009) in Flagella and Pili; Current Research and Future Trends, Academic Press; 91-98.
So one of the preeminent scientist working on this structure contradicts the consensus.
So one of the world’s leading authorities on flagellum genetics and biophysics has this view in contrast to others who have not worked on this system. To be fair, both Aizawa and Kelly Hughes have made Salmonella flagellar gene knockouts and found compensatory mutations that restored motility in one or two genes in attempts to refute irreducible complexity but this is a far cry from demonstrating an evolutionary pathway.
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Since flagella don’t fossilize and the evolution of it was more or less completed to its present form before all know extant bacterial clades diversified, I’m not sure what traces to look for except the genetic ones that you’re underwhelmed by. But I agree it is a beautiful molecular design. I don’t find it at all difficult to imagine incremental evolution but it’s obviously speculation. If we discover a long lost prokaryotic clade, that may help clarify how it evolved.
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Why would you think it’s not a flaw? Being that so many suffered or died of scurvy, it’s pretty obvious it is. There’s also things like wisdom teeth, retinal detachment, the unusual development of male gonads having to pass through the abdominal wall thus creating a permanent weak spot along with other issues, etc.
Also, comparing the flagellum is a false equivalent; it’s not like a man-made motor. Actually, we have a pretty good idea of how the flagellum evolved. Google for it, since apparently I can’t post links. Just because something looks complicated doesn’t mean it was designed. Snowflakes, for example, have intricate patterns, but that doesn’t mean an elf was sitting on a cloud designing each one.
The flagellum aside, there’s still mountains of evidence for evolution. Even if scientists don’t know something at first, they are always filling in gaps as new evidence comes to light.
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Givin that citrus will erode the enamel on one’s teeth……it is a bit of a mystery why we need it….potatoes (or starch) gets quickly converted to sugar too; and will rot the teeth
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Reblogged this on pankeahomtfy.
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Fascinating! A few comments:
Could ancestral primates also have gotten sufficient vitamin C from diets high in leaves, which I understand contain some vitamin C as well?
As early humans left Africa in waves, how did they get enough vitamin C when they got to higher latitudes? Vegetables or other fruits must have been vital to their diets, or could they have gotten vitamin C from a high-meat diet?
Make spark plug plural.
Thanks for the interesting post!
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Reblogged this on Site Title.
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This article is the perfect example of why scientists need to go put their lab coats on and collect their data and stop right there. However, they don’t. They go on to then interpret their data and they are totally untrained in the metaphysical disciplines to do this. Classic case of going beyond the bounds of your field. Seems scientists fancy themselves logicians and philosophers as well. Yet they usually have ZERO training in these areas. Go collect your data, which is actual science btw, then hand over your data to the Logicians, Philosophers, Theologians, and Ethicists to interpret your data. That is their specialty not yours, as your insistence that this sort of thing constitutes a “design flaw” evidences.
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In reality, our ancestors had a good motive to get rid of this gene, the syntesis of vitamin C, produces subproducts that are nocive to the cell as hydrogen peroxide.
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