Most commercial dog foods are fortified with vitamins to levels that exceed minimal requirements. There is no AAFCO dietary requirement for vitamin C for dogs because they are able to synthesize it in the liver. Although dogs can synthesize vitamin C in levels sufficient to prevent signs of deficiency, supplementation may provide additional health benefits because vitamin C functions as a free radical scavenger and an antioxidant in the body.
There is also no AAFCO dietary requirement for vitamin K for dogs because intestinal bacteria are able to synthesize it. However, any condition that alters the intestinal microflora, such as antibiotic therapy, may result in vitamin K deficiency. As a result, NRC recommends vitamin K at 0.33 mg/1,000 kcal ME in puppies, at 0.45 mg/1,000 kcal ME in adult dogs.
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 adverse effects when ingested in megadoses. 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 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) throughout 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, ankylosis of vertebrae and large joints, osseocartilagenous hyperplasia, osteoporosis, inhibited collagen synthesis, decreased chrondrogenesis in growth plates of growing dogs, and narrowed intervertebral foramina.
Vitamin D:
Vitamin D deficiency results in rickets in young animals and osteomalacia in adult animals. Classic signs of rickets are rare in puppies and most often are seen when homemade diets are fed without supplementation. 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. 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.
Minerals:
Minerals can be classified into three 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 mcg 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 because of 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 copper (dogs) for therapeutic effect is common.
Macrominerals:
Calcium and phosphorus deficiencies are uncommon in well-balanced growth diets. Exceptions may include high-meat diets high in phosphorus and low in calcium and diets high in phytates, which inhibit absorption of trace minerals. In dogs, the requirements for dietary calcium and phosphorus are increased over maintenance during growth, pregnancy, and lactation. In dogs, the optimal calcium:phosphorus ratio should be ~1.2–1.4:1; however, minimum and maximum ratios by AAFCO are 1:1 to 2.1:1. Less phosphorus is absorbed at the higher ratios, so an appropriate balance of these two 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.
Trace Minerals:
Iodine deficiency is rare when complete and balanced diets are fed but may be seen when high-meat diets are used (dogs).
Iron and copper found in most meats are used 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.
A deficiency of manganese in other species results in bone dyscrasia.
Source: https://www.merckvetmanual.com/management-and-nutrition/nutrition-small-animals/nutritional-requirements-and-related-diseases-of-small-animals
