Most mammals synthesize their own vitamin C in the liver or kidneys without needing dietary sources. However, ancestors of haplorhine primates—which include humans, apes, monkeys, and tarsiers—lost this ability due to a dramatic genetic mutation. The final step in ascorbic acid synthesis requires the enzyme L-gulonolactone oxidase, encoded by the GULO gene.
Roughly 61 million years ago, deleterious mutations accumulated in the GULO gene of a shared haplorhine ancestor, rendering it an inactive pseudogene. Because these ancestral primates consumed diets naturally rich in fresh fruit, losing internal synthesis was not fatal; dietary intake compensated for the missing enzyme. Without selection pressure to repair the broken gene, the GULO pseudogene spread across the entire haplorhine lineage.
Today, humans still carry this inactivated gene remnant on chromosome 8, requiring us to consume vitamin C to prevent fatal collagen breakdown. Similar independent pseudogenization events occurred in guinea pigs, fruit bats, and certain birds.