Most mammals produce their own vitamin C (L-ascorbic acid) in the liver using the enzyme L-gulonolactone oxidase, encoded by the GULO gene. However, roughly 63 million years ago, an ancestor of haplorhine primates—a suborder that includes tarsiers, monkeys, apes, and humans—suffered a deleterious mutation in this crucial gene. The loss of functional GULO turned it into a pseudogene, an inactive genomic sequence that no longer codes for a functional enzyme.
Because these early primates consumed a fruit-rich diet packed with natural ascorbic acid, the inability to synthesize vitamin C internally did not result in an immediate evolutionary penalty. Without selective pressure to maintain a working GULO gene, additional mutations accumulated over generations, permanently sealing the pseudogene's fate. This evolutionary trade-off left haplorhines dependent on dietary sources to prevent scurvy, a physiological constraint shared by only a few other mammals, such as guinea pigs, teleost fish, and certain bats.
The study of the GULO pseudogene serves as a classic example of neutral evolution, where functional gene loss persists simply because environmental abundance renders the loss harmless at the time.