Vitamin C beings. According to this theory, the loss of ascorbic acid's anti-oxidizing properties would have led to an increase in free radicals in the body. Free radicals are known to increase the frequency of genetic mutations, which would subsequently increase the speed of evolution. It has also been noted that the loss of the ability to synthesize ascorbate strikingly parallels the inability to break down uric acid, also a characteristic of primates. Uric acid and ascorbate are both strong reducing agents. This has led to the suggestion that, in higher primates, uric acid has taken over some of the functions of
Vitamin B6 4-pyridoxic acid. Several studies have shown that 4-pyridoxic acid is undetectable in the urine of vitamin B-deficient subjects, making it a useful clinical marker to assess the vitamin B status of an individual. Other products of vitamin B metabolism excreted in the urine when high doses of the vitamin have been given include pyridoxal, pyridoxamine, and pyridoxine and their phosphates. A small amount of vitamin B is also excreted in the feces. The classic clinical syndrome for vitamin B deficiency is a seborrhoeic dermatitis-like eruption, atrophic glossitis with ulceration, angular cheilitis, conjunctivitis, intertrigo, and neurologic symptoms of somnolence, confusion, and