• The ‘ascorbate-rich diet hypothesis’: This hypothesis tries to explain the inactivation of L-gulono-lactone through the presence of adequate vitamin C within the diet. In the habitat of our ancestors, abundant fruits containing ascorbate were available [4, 5]. Therefore, the GLO lacking species were adequately supplied with this micronutrient and antioxidant and did not need an endogenous synthesis.
• The ‘ascorbate and fertility hypothesis’: This hypothesis proposes that older individuals required more vitamin C than younger individuals did. It is argued that when this essential substance became rare, older and less reproductive, individuals died and the younger and fitter ones survived and reproduced more successfully [6].
• The ‘better electron ratio hypothesis’: During ascorbate biosynthesis, one ascorbate molecule is produced by consumption of glutathione (GSH) and by generation of one hydrogen peroxide molecule [7]. The net redox potential of this synthesis is electron neutral. Therefore, it was beneficial to pick up the required ascorbate by diet, which leads to an increase in the antioxidative capacity.
• The ‘free radical’ hypothesis was postulated by Challem and Taylor in 1998 [8] They hypothesized that not a mutation but a retrovirus inactivated the GLO. The decreased ascorbate concentrations led to generation and accumulation of more radical substances attacking the DNA. This should led to a higher rate of molecular evolution due to DNA oxidation, and consequently enabling faster adaptation to environmental changes.