May 22, 2024 | Jerry Bergman

Why Don’t Humans Make Their Own Vitamin C?

Problems with the Vitamin C
Alleged Evidence for
It’s More Complex
Than it First Appears.



by Jerry Bergman, PhD

Much has been written about the loss of the ability to produce vitamin C (L-ascorbic acid) in primates and its implications for evolution. What are the facts?

One common evolutionary theory is that some ancient prehuman ancestor lost the ability to synthesize vitamin C. The evolutionary relatives of this alleged ancestor, including the higher primates (primarily chimpanzees and orangutans) and humans, inherited this mutated gene. Thus, evolutionists postulate that this fact proves humans and the higher primates have a common ancestor. They use this as evidence for human evolution from some higher ape. As will be reviewed, this explanation suffers from numerous problems. What is not disputed is vitamin C is a very important molecule. In an open-access paper in Nature Communications on May 16, Boverio et al. state that it

plays a pivotal role in nature. It is a highly soluble, carbohydrate-like compound that acts as a powerful antioxidant and co-substrate for many redox enzymes involved in a range of processes from biosynthesis of collagen, carnitine, and neurotransmitters to chromatin modification.[1]

The genetic story of the loss of the ability to synthesize vitamin C was repeated in this paper. Going back to 2011, the common argument for evolution was also elucidated by evolutionary biochemists Hornung and Biesalski in Evolutionary Medicine and Public Health back in 2011:

During evolution, some species including humans, monkeys and fruit bats lost the ability for ascorbic acid (AA) biosynthesis due to inactivation of the enzyme l-gulono-lactone oxidase (GULO) and subsequently became dependent on dietary vitamin C.[2]

Humans require ascorbic acid to survive but, in contrast to the vast majority of vertebrate and invertebrate species and even plants and yeasts, humans are unable to manufacture it. But they are not the only ones. Animals unable to synthesize it include teleost fishes, anthropoid primates, guinea pigs, and some bat and passerine bird species.[3] The evolutionary explanation is that these animals lost the capacity to synthesize vitamin C as a result of mutations.[4] Note that the list includes not only some primates, but also some fish, bats, and birds. This creates problems for the evolution explanation.

Anecdote: Lack of vitamin C causes scurvy, a condition discovered by sailors who lived on a diet lacking fruits and vegetables when on ocean voyages. A cure was demonstrated when ships began routinely carrying fruit, such as lemons, on ships as part of the required sailor diet. As a result, British sailors were called “limeys” by the Americans.

Problems with the evolutionary explanation

A major weakness of the evolutionary claim is that living animals’ genes are compared. In living animals, for the synthesis of aldonolactone oxidoreductases, flavoenzymes are required to manufacture vitamin C. Evolutionists then extract backward from extant genes to make inferences about common ancestors. Here’s a simple illustration of the logical error in  backward extrapolation:

Animal A and B produce the same oxidoreductase. Plants A and B produce a very different oxidoreductase. Thus, it is reasonable to assume that animals A and B have a very different phylogeny than plants A and B. But what if animal A (an ape) and plant A (an oak tree) have the same oxidoreductase? Could we then assume that animal A and plant A have the same phylogeny dating far back in history? Obviously, we cannot assume this because, according to Darwinism, animals and plants had very different phylogenies for most of their recent evolutionary history.

The error results from making up a phylogeny based on one gene or one trait, such as the ability, or the loss of the ability, to produce ascorbic acid. The expected biochemical similarity in various plants, and a different biochemistry in animals, results from a very different phylogeny.

From a creation view, however (see below), it may also be the result of a design difference, or from a mutation in a genetic hotspot. The evidence supports the latter in the case of vitamin C:

In all cases so far studied, the inability to synthesize vitamin C is due to mutations in the L-gulono-γ-lactone oxidase (GULO) gene which codes for the enzyme responsible for catalyzing the last step of vitamin C biosynthesis.[5]

Because the mutation in this particular gene only affects vitamin C production, it is not lethal if the animals are able to obtain enough vitamin C in their diet, as is typically true of most humans in the developed world.

Figure 1. Illustration from Drouin, G., et al. “The genetics of vitamin C loss in vertebrates.” Current Genomics 12(5):371–378, August 2011.

More Complications with the Evolutionary Explanation

Let’s examine the evolutionary assumption further.

Phylogeny: If we assume that the inability to produce vitamin C is caused by a mutation early in evolutionary history, we would expect certain outcomes. One is that all, or most, of the animals unable to synthesize ascorbic acid have descended from the ancestor that first lost the ability. If our alleged common ancestor with primates lost the ability, all of the primates that descended from this postulated common ancestor would have the mutation. Judging by the phylogenetic charts reproduced below, it appears that inactivation of the gene which prevents synthesis of vitamin C is often random and does not always follow a phylogenetic prediction.

Diet: If the animal is able to obtain a sufficient amount of vitamin C in their diet, survival will not be greatly affected, and natural selection will be blunted.

Hotspot Mutations: As the charts show, the loss appears to be a genetic mutation in a specific area of the genome that is prone to mutate because it is in a mutational hotspot (Figure 1, see part showing primates). A mutational hotspot is a genetic location more prone to mutations than others.

Selective Evidence: The phylogenetic diagram appears to show evidence for evolution except that this set of comparisons does not show all of the primates. When more primates are included in the comparison, the evidence for the evolutionary argument is largely lost because the mutation is not in many cell lines in many animals.

Anomalies: The figure shows seven primates are unable to synthesize vitamin C, specifically owl monkey, marmoset, macaque, gibbon, orangutan, gorilla, and humans. It looks like evidence for inheritance of a mutation from a common ancestor, but the bat and guinea pig violate the pattern. Furthermore, the pattern in the primates listed could show that, for some reason, the primate genetic design is more prone to get the GULO mutation at the mutational hotspot.

The more complete chart shows even more anomalies. The table below from Drouin 2011 shows only two primates unable to synthesize vitamin C, in contrast to the remaining fifteen. Furthermore, for some reason, neither the diagram nor the chart show another surprise. Evolutionists claim our supposed closest relatives are the chimpanzees, but chimps can synthesize vitamin C. Other authorities claim that the chimpanzees have the GULO mutation.[6]

Table from Drouin, G., et al. “The genetics of vitamin C loss in vertebrates.” Current Genomics 12(5):371–378, doi: 10.2174/138920211796429736, August 2011.

Reactivation: Another problem is that GULO mutations in fish, anthropoid primates, and guinea pigs are irreversible. In contrast, some of the GULO genes in bats and some passerine bird species can be reactivated by a backward mutation in the hotspot which “repairs” the gene by reverting to the previous genetic sequence. For these reasons, vitamin C presence or absence as phylogenetic evidence for common ancestry is problematic in attempting to show that humans evolved from some ape-like ancestor.

Vitamin C Differences in a Creation Context

Loss of the ability to produce vitamin C appears to be due to a hotspot mutation. This implies that Adam and Eve, and possibly Noah, had operational vitamin C synthesis, but it was lost by mutations possibly more than once in human history (or once at the genetic bottleneck during the Flood). If we assume Adam was perfectly free of mutations at the start, the loss in humans could have occurred as early as the Fall described in Genesis 3, or sometime before the Flood described in Genesis 6-9. If so, someone in Noah’s family could have inherited it shortly before or after the Flood, but before the Tower of Babel dispersion.

To help answer the question of whether vitamin C loss in humans is universal, it would be instructive to test for the mutation in small, isolated populations, such as the Australian Aborigines. If some isolated population of humans does not have the mutation, or has a very different mutation, it would indicate that the mutation occurred after the Flood and, depending on how rapid the dispersion was, sometime before the dispersion was complete.

The Charts Showing the Mutation Pattern

All of the following illustrations (and those in the text above) are from Drouin, G., et al.,[7] Note the loss of the ability to synthesize vitamin C (gray bars) appears to be random and not due to inheritance from an evolutionary ancestor.



This paper raises some questions that need to be explored further. The claim that loss of the ability to manufacture vitamin C provides limited evidence for human evolution can be answered in several ways that largely negate its support for human evolution. The loss of the ability to manufacture vitamin C can also be effectively explained within a creation model.


[1] Boverio, A., et al. “Structure, mechanism, and evolution of the last step in vitamin C biosynthesis.” Nature Communications 15: 4158., 2024.

[2] Hornung, T.C., and H.-K, Biesalski. “Glut-1 explains the evolutionary advantage of the loss of endogenous vitamin C-synthesis.” Evolutionary Medicine and Public Health  2019(1):221–231, 2019..

[3] Boverio, et al., 2024.

[4] Drouin, G., et al. “The genetics of vitamin C loss in vertebrates.” Current Genomics 12(5):371–378, doi: 10.2174/138920211796429736, August 2011.

[5] Drouin, et al., 2011.

[6] Zhang, Q., “Using pseudogene database to identify lineage- specific genes and pseudogenes in humans and chimpanzees”, Journal of Heredity, 105(3). 436-443. 2014.

[7] The genetics of vitamin C loss in vertebrates Current Genomics 12(5):371–378, August 2011. doi: 10.2174/138920211796429736.

Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,900 publications in 14 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,800 college libraries in 27 countries. So far over 80,000 copies of the 60 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.

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