Abstract It has been previously theorized that free-radical reactions led to the first life on Earth, and their ability to randomly cause mutations may have subsequently led to the evolution of life. One of the most efficient free-radical quenchers is ascorbate, which most animals manufacture endogenously. It is generally believed that, approximately 25 million years ago, an ancestor of the Anthropoidea primate suborder, which includes Homo sapiens, lost the ability to produce its own ascorbate, and all descending species inherited this genetic defect. The first of three hypotheses presented here proposes that a genetic defect, caused by either free radicals or a virus, deleted the gene needed by Anthropoidea to manufacture endogenous ascorbate. The second hypothesis proposes that this evolutionary accident permitted large numbers of free radicals to remain metabolically unquenched. The third hypothesis proposes that the presence of these excessive free radicals increased the likelihood of free-radical-induced genetic mutations, and these mutations propelled the evolution of Anthropoidea, leading to Homo sapiens.