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Companion Animals: Vitamin A

Vitamin Safety

In general, the possibility of vitamin A toxicity for dogs and cats is remote. However, of all vitamins, vitamin A is most likely to be provided in toxic concentrations to dogs and cats. Excess vitamin A has been demonstrated to have toxic effects in most species studied. Presumed upper safe levels are four to 10 times the nutritional requirements for nonruminant animals, including dogs and cats (NRC, 1987). Most of the harmful effects have been obtained by feeding over 100 times the daily requirements for an extended period of time. Thus, small excesses of vitamin A for short periods of time should not exert any harmful effects. Recommended upper safe levels of vitamin A for dogs are 33,330 IU per kg (15,150 IU per lb) of diet and 10,000 IU per kg (4,545 IU per lb) of diet for cats.

Excessive consumption of foods or supplements high in vitamin A can lead to hypervitaminosis A. This metabolic disorder in cats is most frequently associated with diets having a high liver or fish liver oil content (Lucke et al., 1968; Goldman, 1992; Goldston and Hoskins, 1995). Special care should be taken to avoid long-term feeding of such diets when trying to stimulate appetite in anorexic cats. When a cat is found to be sick and its diet consists wholly or partly of raw liver, vitamin A toxicity should be suspected. The feeding of raw liver should be stopped and a balanced feline diet instituted (Goldman, 1992).

Vitamin A toxicosis in cats results in a disorder called deforming cervical spondylosis (Illus. 1) (Case et al., 1995). The clinical signs are pain, difficult movement, lameness, and crippling in severe cases. In a crippling bone disease there is tenderness of the extremities associated with gingivitis and tooth loss that has been described in cats given prolonged excessive doses of this vitamin either as vitamin A itself or by feeding large quantities of raw liver (Seawright et al., 1965; Seawright and Hrdlicka, 1974). Cats consuming raw beef liver containing 20,000 to 40,000 µg per kg (9,091 to 18,182 µg per lb) for two to five years produced the main clinical findings of cutaneous hyperesthesia of neck and forelegs, forelimb lameness, pain and skeletal immobility due to bony exostoses of the cervical vertebrae and tendinous tuberosities of long bones (Illus. 2) (Seawright et al., 1965). Feeding liver to kittens for five to 12 months with dietary intakes of vitamin A exceeding 150,000 µg per kg (68,182 µg per lb) body weight per day caused weight loss, cachexia, inanition, exophthalmos, hindleg weakness with abnormal gait and death. Bone changes reflected the level of toxicity, with the proliferative effect of vitamin A stimulation manifested by bony exostoses at moderately high doses followed by thinning or lysis of bone in more advanced stages of toxicity (Seawright et al., 1967).

Feeding kittens high vitamin A for four to five weeks depressed appetite and resulted in damage to the epiphyseal plate, altering growth and development of long bones. Peeling of the footpad epithelium and frequent blinking were also observed. A gait abnormality was evidenced by restricted movement of the stifle joint (Clark, 1973).

Historically, it has been known for centuries among Eskimos and Arctic travelers that the ingestion of polar bear liver by men and dogs causes severe illness (Rodahl, 1949). There are stories of polar bear liver having been given to dogs, who later became sick and eventually suffered from loss of hair. It is also said that the Eskimos used to throw the livers of polar bears into the sea so the dogs would not get them. On the other hand, it is known that dogs are reluctant to eat the liver of polar bear, as is generally experienced by the European trappers in North East Greenland with their sled dogs. On one occasion a liver was given to a dog; because the dog was very hungry, he ate a small portion of the liver and subsequently suffered from diarrhea (Rodahl, 1949).

Dosed with 100,000 µg per kg (45,455 µg per lb) body weight per day, greyhound pups had poor appetite after 30 days and lost weight with rapid deterioration in condition after seven weeks (Maddock et al., 1949). After 53 days, a variety of clinical signs rapidly appeared, including continuous shivering. Hyperesthesia of the skin and extreme tenderness of the extremities were evident. The puppies were unwilling to stand, although no fractures were noted. The long bone epiphyseal cartilage was markedly narrower; cortices of the femur, tibia, radius, and ulna were less dense and thinner. Remodeling processes were greatly accelerated, and hemorrhage was common in these areas.

Ralston Purina (1987) recorded an incident in which a dog breeder initiated routine supplementation of a concentrated "vitamin mix" for all dogs in the kennel. Within two years, fertility was severely depressed and numerous stillbirths, neonatal deaths of puppies and the deaths of two bitches were associated with extraordinary high liver vitamin A concentrations, suggesting that vitamin A toxicity was the principal cause of the problems.

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