Monday, March 30, 2009

Pet Nutrition: Requirements and related diseases Part 3 Vitamins & Minerals

While American Feed Control Officials (AAFCO) and the National Research Council (NRC) cooperate to publish dog and cat nutrient profiles for growth, maintenance, and reproduction, this series goes beyond the percentages suggested by these organizations and explores in more detail why nutrients are required and what happens if they are not supplied in sufficient quantities. In part 1 we discussed water and energy, in part 2 we talked about protein, fats, carbohydrates and fiber. Today we are going to address the nutritional requirement for vitamins and minerals.

Most commercial dog and cat foods are fortified with vitamins to levels that exceed minimal requirements. There is no AAFCO dietary requirement for vitamins C or K for dogs. Cats have no documented dietary requirement for vitamin C. Deficiencies of fat-soluble vitamins (A, D, and E in dogs; A, D, E, and K in cats) and some of the 11 water-soluble B-complex vitamins have been produced experimentally. Water-soluble vitamins are usually readily excreted if excess amounts are consumed and are thought to be far less likely to cause toxicity or side effects when ingested in mega doses. Vitamin B12 is the only water-soluble vitamin stored in the liver, and dogs may have a 2- to 5-yr depot. Fat-soluble vitamins (except for vitamin K in cats) are stored to an appreciable extent in the body, and when vitamins A and D are ingested in large amounts (10-100 times daily requirement) over a period of months, toxic reactions may be seen. Only clinically relevant vitamin-related imbalances are described below.

Vitamin A: Excessive consumption of liver can lead to hypervitaminosis A and may produce skeletal lesions, including deforming cervical spondylosis, osseocartilaginous hyperplasia, osteoporosis, inhibited collagen synthesis, and decreased chrondrogenesis in growth plates of growing dogs.
Unlike most other mammals, cats cannot convert β-carotene to vitamin A because they lack intestinal carotenase. Therefore, cats require a preformed source in their diet, such as that supplied by liver, fish liver oils, or synthetic vitamin A. Signs of a vitamin A deficiency in cats are similar to those in other species, except that classic xerophthalmia, follicular hyperkeratosis, and retinal degeneration are rarely seen and usually are associated with concomitant protein deficiency. Nonetheless, cats fed diets deficient in vitamin A exhibited conjunctivitis, xerosis with keratitis and corneal vascularization, retinal degeneration, photophobia, and slowed pupillary response to light. Certain of these alterations also result from the retinal degeneration that is seen in taurine deprivation. Hypovitaminosis A in cats may exhaust vitamin A reserves of the kidneys and liver; affect reproduction causing stillbirths, congenital anomalies (hydrocephaly, blindness, hairlessness, deafness, ataxia, cerebellar dysplasia, intestinal hernia), and resorption of fetuses; and cause the same changes in epithelial cells noted in other animals. Squamous metaplasia of the respiratory tract, conjunctiva, endometrium, and salivary glands has been noted. Changes such as subpleural cysts lined by keratinizing squamous epithelium and extensive infectious sequelae are frequent in the lungs and are occasionally noted in the conjunctiva and salivary glands. Focal dysplasia of pancreatic acinar tissue and marked hypoplasia of seminiferous tubules, depletion of adrenal lipid, and focal atrophy of the skin have been reported. Borderline deficiency is more common, especially in chronic ill health. Retinol at 9,000 IU/kg of diet should meet dietary needs for vitamin A during gestation and lactation and exceed the needs of the growing kitten. Excessive consumption of liver can lead to hypervitaminosis A, which is characterized by new bone formation without osteolysis. Vitamin A toxicosis produces skeletal lesions of deforming cervical spondylosis, ankylosis of vertebrae and large joints, osseocartilagenous hyperplasia, osteoporosis, epiphyseal plate damage, and a narrowing of the intervertebral foramina.

Vitamin D deficiency results in rickets in young animals and osteomalacia in adult animals. Classic signs of rickets are rare in puppies and kittens and most often are seen when homemade diets are fed without supplementation. Rickets has been reported in kittens fed diets deficient in vitamin D, even though dietary amounts of calcium and phosphorus were normal. In rickets, serum calcium and phosphorus are decreased or low normal with a corresponding high parathyroid hormone level; bone mineralization is decreased, and the metaphyseal areas are enlarged. Osteomalacia rarely causes clinical signs in dogs or cats. Hypervitaminosis D causes hypercalcemia and hyperphosphatemia with irreversible soft-tissue calcification of the kidney tubules, heart valves, and large-vessel walls. Death in dogs is either related to chronic renal failure or acutely due to a massive aortic rupture. Death in cats is related to chronic renal failure.

Vitamin E: In cats, steatitis results from a diet high in polyunsaturated fatty acids, particularly from marine fish oils when these are not protected with added antioxidants. Kittens or adult cats develop anorexia and muscular degeneration; depot fat becomes discolored by brown or orange ceroid pigments. Lesions are seen in cardiac and skeletal muscles and are similar to those described for other species.

Thiamine: Deficiency generally does not develop in cats fed properly prepared commercial diets. Thiaminase, which tends to be high in uncooked freshwater fish, can produce a deficiency by rapid destruction of dietary thiamine. Although canned commercial cat foods may contain fish, the heat associated with canning is sufficient to destroy thiaminase. Destruction of thiamine has also resulted from treatment of food with sulfur dioxide or overheating during drying or canning, but deficiencies are now rare. Thiamine-deficient cats develop anorexia, an unkempt coat, a hunched position, and with time, convulsions that become more severe, leading later to prostration and death. At necropsy, small petechiae may be found in the cerebrum and midbrain. Diagnosis can be confirmed in the early stages by giving 100-250 mg thiamine, PO or IM, bid for several days. Recovery occurs in minutes to hours but, if the diet is not supplemented after this treatment, relapse can be expected. Thiamine deficiency may cause a number of other neurologic disorders, including impairment of labyrinthine righting reactions, seen as head ventroflexion and loss of the ability to maintain equilibrium when moving or jumping; impairment of the pupillary light reflex; and dysfunction of the cerebellum, suggested by asynergia, ataxia, and dysmetria.

Minerals can be classified into 3 major categories: macrominerals (sodium, potassium, calcium, phosphorus, magnesium) required in gram amounts/day, trace minerals of known importance (iron, zinc, copper, iodine, fluorine, selenium, chromium) required in mg or µg amounts/day, and other trace minerals important in laboratory animals but that have an unclear role in companion animal nutrition (cobalt, molybdenum, cadmium, arsenic, silicon, vanadium, nickel, lead, tin). A balanced amount of the necessary dietary minerals in relation to the energy density of the diet is important. As intake of a mineral exceeds the requirement, an excessive amount may be absorbed, or a large amount of the unabsorbed mineral may prevent intestinal absorption of other minerals in adequate amounts. Indiscriminate mineral supplementation should be avoided due to the likelihood of causing a mineral imbalance. Mineral deficiency is rare in well-balanced diets. Manipulation of dietary intake of calcium, phosphorus, sodium, magnesium (dogs and cats), and copper (dogs) for therapeutic effect is common. Limited evidence exists for the recommendations of dietary mineral requirements for cats made in
Table: AAFCO Nutrient Requirements for Cats; many are based on the mineral content of successfully fed diets.

Macrominerals: Calcium and phosphorus deficiency is uncommon in well-balanced growth diets. Exceptions may include high-meat diets that are high in phosphorus and low in calcium and diets high in phytates, which inhibit absorption of trace minerals. In both dogs and cats, the requirements for dietary calcium and phosphorus are increased over maintenance during growth, pregnancy, and lactation. In dogs, the calcium:phosphorus ratio should be ~1.2-1.5:1; a range of 1:1 to 2.5:1 is sufficient. Less phosphorus is absorbed at the higher ratios, so an appropriate balance of these 2 minerals is necessary. Also, insufficient supplies of calcium or excess phosphorus decrease calcium absorption and result in irritability, hyperesthesia, and loss of muscle tone with temporary or permanent paralysis associated with nutritional secondary hyperparathyroidism. Skeletal demineralization, particularly of the pelvis and vertebral bodies, develops with calcium deficiency. By the time there is a pathologic fracture and the condition can be confirmed radiographically, bone demineralization is severe. Often, there is a history of feeding a diet composed almost entirely of meat, liver, fish, or poultry. Excess intakes of calcium are more problematic for growing (weaning to 1 yr) large- and giant-breed dogs. Excessive supplementation (>3% calcium [dry-matter basis]) causes more severe signs of osteochondrosis and decreased skeletal remodeling in young, rapidly growing large-breed dogs than in dogs fed diets with lower dietary calcium (1-3% [dry-matter basis]). The clinical signs of lameness, pain, and decreased mobility have not been reported in small-breed dogs or more slowly growing breeds fed the higher calcium amounts.
Magnesium is an essential cofactor of many intercellular metabolic enzyme pathways and is rarely deficient in complete and balanced diets. However, when calcium or phosphorus supplementation is excessive, insoluble and indigestible mineral complexes form within the intestine and may decrease magnesium absorption. Clinical signs of magnesium deficiency in puppies are depression, lethargy, and muscle weakness. Excessive magnesium is excreted in the urine. In cats, there is evidence that magnesium concentrations >0.3% (dry-matter basis) may be detrimental if the diet is too alkaline.

Trace Minerals:
Iodine deficiency is rare when complete and balanced diets are fed but may be seen when high-meat diets are used (dogs and cats) or when diets contain saltwater fish (cats). Deficient kittens show signs of hyperthyroidism in the early stages, with increased excitability, followed later by hypothyroidism and lethargy. Abnormal calcium metabolism, alopecia, and fetal resorption have been reported. The condition can be confirmed by thyroid size (>12 mg/100 g body wt) and histopathology at necropsy. The etiology of hyperthyroidism that develops in older cats with increased blood thyroxine and triiodothyronine is unknown.

Iron and copper found in most meats are utilized efficiently, and nutritional deficiencies are rare except in animals fed a diet composed almost entirely of milk or vegetables. Deficiency of iron or copper is marked by a microcytic, hypochromic anemia and, often, by a reddish tinge to the hair in a white-haired animal. Deficiency of zinc results in emesis, keratitis, achromotrichia, retarded growth, and emaciation. Decreased zinc availability has been noted in canine diets containing excessive levels of phytate, which emphasizes the value of feeding trial tests over laboratory nutrient analyses of pet foods. Manganese toxicity has been reported to produce albinism in some Siamese cats; a deficiency of manganese in other species results in bone dyscrasia.
Stay tuned for part 4 with a discussion of Pet food labels and Food product types.
Notes: Contribution
Merck Veterinarian Manual

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