Dogs produce their own vitamin C in sufficient quantity that supplementing could actually be harmful.
Vitamin C
Innes (1931) demonstrated that the dog, unlike the guinea pig, was independent of an exogenous supply of vitamin C. Puppies fed a diet devoid of vitamin C for 147 to 154 days showed neither growth impairment nor lesions of bones or teeth, although the same diet killed guinea pigs within 25 days with severe signs of scurvy. Furthermore, the livers of dogs on the deficient diet contained the vitamin in sufficient amounts to prevent the onset of scurvy in guinea pigs, indicating that the dog can synthesize its own vitamin C. Naismith (1958) showed that this synthetic ability is present in puppies during the first weeks of postnatal life. Litters were divided: some puppies were left with the bitch; others were fed a synthetic diet minus vitamin C, or plus vitamin C. No significant differences in blood ascorbic acid concentration were evident, regardless of treatment. Naismith and Pellet (1960) reported that the concentration of ascorbic acid in the milk from bitches is approximately 4 times that of the blood. The comparative rates of hepatic synthesis of ascorbic acids in dogs and cats appear to be lower than that in ruminants, rodents, and lagomorphs (Chatterjee et al., 1975)
Despite the above evidence, a number of clinical case history reports (Garlick, 1946; Meier et al., 1957; Ditch-field and Phillipson, 1960; Holmes, 1962; Hunt, 1962; Sadek, 1962; Bendefy, 1965; Belfield, 1967, 1976; Vaananen and Wikman, 1979) have been published purporting to describe scurvy in the dog with or without concomitant hip displaysia or osteodystrophy. None of these reports included observations on control untreated animals. Also, the effect on the dog of pharmacological doses of ascorbic acid (e.g., 3,000 mg intravenously per day) may be quite distinct from its nutritional contribution. Teare et al. (1980) reported that 600 mg of ascorbic acid twice daily only aggravated the skeletal disease induced by overfeeding protein, energy, and calcium to Labrador Retriever puppies.
In addition, vitamin C has been proposed as a prophylactic agent against canine distemper (Belfield, 1967; Leveque, 1969), and some veterinary practitioners apparently advocate vitamin C for the treatment of kennel cough. Sheffy (1972) conducted some carefully controlled studies concerned with these issues and established that exogenous vitamin C was of no benefit in alleviating clinical signs of illness, mortality, or gross or microscopic pathology associated with experimentally produced canine herpes virus infection, kennel cough, or infectious canine hepatitis. In addition, as determined by measuring blood ascorbic acid levels, the latter disease did not affect vitamin C synthesis. Other data on blood and urine ascorbic acid values in the dog have been published by Majumdar et al. (1964), Kleit et al. (1965), Crilly et al. (1976), and Robinson et al. (1979). Csaba and Toth (1966), in controlled studies, established that ascorbic acid given before antigen challenge in dogs has no protective action against anaphylactic shock and does not influence histamine release. Weintraub and Griner (1974) found that high doses of ascorbic acid had no effect on biological half-life or kinetics of Warfarin-induced hypoprothrombinemia
It is concluded that there is no adequate evidence to justify recommendation of routine vitamin C additions to the diet of the normal dog. However, dogs with hepatic dysfunction may have lowered plasma concentrations of ascorbic acid (Strombeck et al., 1983). Whether lower plasma concentrations are of clinical significance remains to be demonstrated.
