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.