Carbohydrates (cats can't taste sugars!)

All animals have a metabolic requirement for glucose.  Carnivores, such as the cat, convert glucogenic amino acids and glycerol to glucose for the maintenance of blood glucose, and therefore, have no established dietary requirement for carbohydrates. 

Because cats have adapted to diets high in protein and low in carbohydrate, continuous activity of amino acid catabolic enzymes provides a continuous source of carbon skeletons for glucose or energy production and nitrogen for synthesis of dispensable amino acids and other nitrogenous compounds. This continuous metabolic state causes the cat to catabolize a substantial amount of protein after each meal, regardless of its protein content. The cat does not have the capability to conserve nitrogen from the body's general nitrogen pool leading to an obligate nitrogen loss and a higher dietary protein require merit than omnivores.

In general, an absence of dietary carbohydrate in the feline diet will not affect blood glucose levels or cause an energy deficiency; this is because the body can use protein and the glycerol portion of fat for glucose production, and fat and protein for energy.

It has been demonstrated that cats respond to salty, sour and bitter stimuli as well as to amino acids and nucleotides but do not show neural responses to sucrose and several other sugars.

Vitamins

Although the required levels of all the essential vitamins that should be included in cats' diets have not been firmly established, many important facts about vitamins in the cat's diet are known and should be heeded when selecting a diet for your pet. The  currently recommended amounts of vitamins should be fully available to a cat from his or her food. As with other nutrients, these levels will generally be lower than those actually present in commercial foods, since manufacturers must include higher levels when the food is formulated and first mixed to make up for nutrients that are not fully bioavailable from foods and losses caused by processing or storage.

Vitamin A

Cats cannot convert beta carotene (found in green vegetables) to vitamin A as can dogs and people, so you must be sure that other sources of fully formed vitamin A (found in animal tissues) are provided in the diet to prevent a deficiency that can result in skin, eye, and reproductive changes. On the other hand, hypervitaminosis A (too much vitamin A) is far more likely to be a problem. This condition is typically seen in cats whose diets have been oversupplemented with, for example, cod-liver oil, and those which have been fed excessive amounts of liver which is highly palatable to cats and may result in an apparent 'addiction'. Signs of toxicity, which usually develops from feeding the diet over a period of months or years, do not develop until the prolonged daily intake exceeds 17mg (57,000 IU)/kg BW.

Excesses of this fat-soluble vitamin are stored in the liver and a toxicity can lead to hepatic damage due to lipid infiltration. Clinically, the most recognizable, signs of hypervitaminosis A are those related to the skeletal changes that occur, particularly in the cervical vertebrae and the long bones of the forelimb. The periosteum appears to be particularly sensitive to high levels of vitamin A and subperiosteal hyperplasia occurs around the bony insertions of tendons and ligaments in response to physical forces exerted in these areas. Bony exostoses result and may invade joints, causing enlargement and ankylosis.

Initial signs may be of stiffness and pain, particularly of the neck and forelegs, and the owner may first observe the cat's reluctance to groom itself. This may be accompanied by anorexia, lethargy, weight loss and an unkempt appearance. The painful lesions may induce an affected cat to adopt a sitting 'kangaroo' posture in order to avoid weight bearing by the anterior regions.

Treatment consists primarily of dietary correction and the provision of a normal diet; supplementation with fish oils is strictly contraindicated. Non-steroidal anti-inflammatory drugs are useful in the initial stages for the control of pain, and food dishes may be elevated to facilitate eating and drinking. Early treatment may bring about a resolution of clinical signs and halt the progression of the disease, but established ankyloses are irreversible.
Feed an average-sized adult cat no more than 1 ounce (30 g) of beef liver twice weekly. If necessary, balanced vitamin-mineral preparations may also be used as dietary supplements, but avoid giving unbalanced supplements such as cod liver oil to cats, since 1 teaspoonful can contain more than 5000 IU vitamin A. Use only balanced vitamin-mineral supplements recommended by your veterinarian and follow directions for their use caref

B-group Vitamins

(Thiamine, Riboflavin, Pyridoxine, Pantothenic Acid, Niacin, B-12)

Cats have relatively high requirements for B vitamins in their diets. Foods for cats must contain at least twice the amounts of many B vitamins found in diets adequate for dogs-another good reason not to feed cats dog food. Several B vitamins are destroyed by heating, a process used in making commercial cat foods, so all good processed foods must be supplemented with B vitamins.

Several B vitamins are synthesized by bacteria in the intestines of healthy cats. Intestinal problems, e.g., diarrhea, can eliminate this source, and antibiotics may also interfere with it. Vitamin supplementation is often necessary during prolonged illnesses involving the intestine or during prolonged antibiotic treatment.

Niacin

The cat is unable to to convert the essential amino acid tryptophan to niacin.  The regular consumption of a carnivorous diet throughout the cat's evolutionary history has not resulted in selective pressure for the cat to synthesize niacin from precursor substances.. However the inability of the cat to convert tryptophan to niacin is of little practical significance to the feeding management of pet cats provided a carnivorous diet is fed because animal tissues are well supplied with nicotinamide.

Thiamin

Thiamin (vitamin B,) is a water-soluble vitamin, with limited storage in the body, which plays an essential part in energy metabolism and neural impulse transmission. It can be destroyed during prolonged storage; interaction with high levels of glutamate, such as those present in vegetable protein, can lead to a thiamin deficiency; and it is progressively, but not immediately, destroyed by high temperatures and under certain conditions of processing. Most cat food manufacturers supplement their products to compensate for possible losses, but some home prepared diets may require additional thiamin. A deficiency of thiamin can also occur when cats are fed large amounts of certain types of raw fish which contain the enzyme thiaminase, although this is destroyed by cooking.   Death may develop in cats fed inadequately cooked fish or soy-based food and/or cooked products inadequately supplemented with thiamin.

Initial signs of thiamin deficiency appear within 1-2 weeks of the introduction of a deficient diet and include salivation and a failure to eat despite being interested in food. Weight loss, vomiting and mild ataxia may also be apparent. This progresses to a critical stage in which there are severe neurological disturbances with impaired righting reflexes and short tonic convulsions with ventroflexion of the-neck. Mydriasis, circling, dysmetria and spinal hypersensitivity may also be observed. Eventually, there is a spasticity of all the limbs such that the cat appears to be 'walking on its toes' and there may be cardiac irregularities. The terminal stage of the disease is characterized by semi-coma, continuous crying, opisthotonos and, ultimately, death.
 

Vitamin C (Ascorbic acid)

Ascorbic acid, commonly known as vitamin C, has a chemical structure that is closely related to the monosaccharide sugars. It is synthesized by plants and most animal species, including dogs and cats. Ascorbic acid is produced in the liver from either glucose or galactose through the glucuronate pathway. With the exception of humans and a few other animal species, all animals, including cats,  are capable of producing adequate levels of endogenous vitamin C and therefore do not have a dietary requirement for this vitamin.  Therefore, unless there is a high metabolic need or inadequate amounts are being synthesized by the body, a dietary source of ascorbic acid is unnecessary in cats. In addition to being unwarranted, ascorbic acid supplementation in cats may be detrimental. Excess ascorbic acid is excreted in the urine as oxalate, and high concentrations of oxalate have the potential to contribute to the formation of calcium oxalate uroliths in the urinary tract.
 

Vitamin E

Vitamin E functions as a biological, chain-breaking antioxidant that neutralizes free radicals and prevents the peroxidation of lipids within cellular membranes. In the diet, it limits the peroxidation of dietary lipids and the development of rancidity; greater amounts of this vitamin are thus required when the diet contains high levels of polyunsaturated fatty acids, which are easily oxidized. The vitamin is preferentially oxidized before the unsaturated fatty acids, thus protecting them from rancidity. However, in this process, vitamin E is destroyed.  A cat's requirement for vitamin E depends on dietary levels of polyunsaturated fatty acids (PUFAs) and selenium, a trace mineral. Vitamin E and selenium function synergistically. Therefore, as the level of unsaturated fatty acids in pet foods increases, the amount of vitamin E should increase.  There is individual variation between cats in their dietary requirements for vitamin E, which can also be affected by dietary levels of selenium, sulphur amino acids, other anti-oxidants and pro-oxidants in prepared foods, and by individual susceptibility to peroxidation.

A deficiency of vitamin E (ά-tocopherol) in cats results in pansteatitis (yellow fat disease) which is a painful inflammatory condition of the subcutaneous fat.  The condition is usually associated with diets of oily fish (especially red tuna) which are rich in polyunsaturated fatty acids or with feeding rancid, oxidized fat (commonly found in dry foods). The clinical signs of vitamin E deficiency are related to the deposition of ceroid, the end product of lipid peroxidation, in adipose tissue. This provokes a foreign body reaction and results in inflammation, with massive neutrophilic infiltration, and fat cell necrosis. Fat thus affected is firm, painful and nodular on palpation; in the latter stages of the disease it assumes a dirty orange or mustard yellow color attributable to the ceroid pigment. Subcutaneous fat is most notably affected, but fat within the body cavities may have a similar appearance.

Initially, the affected cat will be inappetant and show pain and hypersensitivity to touch. A fever develops, which is related to the inflammatory and necrotic lesions, and is unresponsive to antimicrobial therapy. Abdominal pain is apparent and vomiting may occur. Subsequently, the nodular character of the subcutaneous fat may be detected on palpation but this procedure may be vigorously resented by the cat.

Dietary correction is required and additional supplementation with 75-100 mg a-tocopherol acetate per day PO may be given initially to replace body stores. Short-term therapy with prednisolone is valuable in controlling the inflammatory reaction. Parenteral nutritional support may be necessary, but this should be administered intravenously as subcutaneous fluid therapy is likely to be painful and absorption reduced. Recovery is slow and may demand several weeks or even months of continued therapy. Occasionally, severely affected cases do not respond to treatment and they continue to deteriorate until they either die or are euthanized. Rarely, sudden death occurs.  Therefore, foods with high levels of polyunsaturated fatty acids (PUFAs) should be avoided unless expressly ordered by a veterinarian.
 

Vitamin D

Cats cannot manufacture vitamin D or its precursor 7-dehydrocholesterol.  Cats appear to have an extremely low dietary requirement for vitamin D provided that they have exposure to some sunlight and are otherwise well nourished. However, vitamin D toxicity can be produced relatively easily and is usually the result of overzealous dietary supplementation with, for example, cod-liver oil. As with all fat-soluble vitamins, excesses are stored in the body and their effects are cumulative. The resulting hypercalcaemia and hyperphosphataemia lead to soft tissue calcification, which may be demonstrated radiologically, and to multiple organ dysfunction. There may be neuromuscular abnormalities, typified by general weakness and poor motor reflexes, and resorption of bone resulting in pathological fractures. Cases are normally presented because of the most. obvious signs of renal failure, and the prognosis is always guarded. Treatment is symptomatic and the cat should be encouraged to eat a balanced diet without additional supplementation.

Vitamin K

The synthesis of vitamin K by bacteria in the large intestine of dogs and cats can contribute at least a portion, if not all, of the daily requirement in these species. Therefore a dietary supply of this vitamin only becomes significant when bacterial populations in the large intestine are reduced, such as during medical treatment with certain types of antibiotics, or when there is interference with the absorption or use of vitamin K from bacterial sources.

Minerals

There is a paucity of data available on the mineral requirements of the cat. Nevertheless calcium, phosphorus, sodium, potassium, magnesium, iron, copper, zinc and iodine are all indispensable in this species; their presence is essential for the maintenance of acid-base balance and tissue structure and as enzyme cofactors. The overall balance of the diet is affected not only by the finite levels of these minerals but also by the interactions between them. For example, the ratio of calcium: phosphorus is important in the maintenance of bone and cellular integrity; in cats, this should be within the acceptable range of 0.5:1 to 2:1. A mineral excess may therefore be as harmful as a deficiency. Home prepared, meat-rich diets may well require mineral supplementation as meat is a poor source of calcium but a relatively rich source of phosphorus.

If adequate amounts of calcium and phosphorus in the proper ratio are provided but without sufficient vitamin D, abnormalities of bone result again. Insufficient levels of vitamin D interfere with calcium absorption in the intestine. Excessive amounts of vitamin, D in the presence of adequate levels of calcium and phosphorus may result in excessive mineralization of bone, abnormal teeth, and calcification of the soft tissues of the body. The delicacy of these relationships is remarkable.

Unthinking or uninformed owners most often distort the calcium-phosphorus balance of their cat's diet by feeding a diet consisting almost exclusively of muscle meat or organ meats such as liver, heart, or kidney. All of these meats contain phosphorus but are devoid of calcium, which results in a calcium--phosphorus ratio of 1 to 15 or greater. Prolonged feeding of such a diet results in severe demineralization of bones, pain, and sometimes fractures or paralysis, a condition called nutritional secondary hyperparathyroidism. An adult cat may exist on such a diet for years without showing signs of disease, but the body changes are occurring nevertheless.  Remember that the wild ancestors and living relatives of the domestic cat relied on a variety of foods found in the entire body of their prey.

Magnesium

Magnesium is probably the mineral of the most concern in cat nutrition for owners, and especially to owners of male cats because of its role in the formation of struvite uroliths (magnesium ammonium phosphate). However, magnesium is not a "bad guy".  Magnesium is a macromineral, its amount in the body is much lower than that of calcium and phosphorus. Approximately 60% to 70% of the magnesium found in the body exists in the form of phosphates and carbonates in bone. Most of the remaining magnesium is found within cells, and a very small portion is present in the extracellular fluid. In addition to its role in providing structure to the skeleton, magnesium functions in a number of metabolic reactions; a magnesium ATP complex is often the form of ATP that is used as a substrate in many of these processes. As a cation in the intracellular fluid, magnesium is essential for the cellular metabolism of  protein. Protein synthesis also requires the presence of ionized magnesium. Balanced in the extracellular fluids with calcium, sodium, and potassium, magnesium allows muscle contraction and proper transmission of nerve impulses.

A commercial cat food should not be selected only on the basis of its magnesium content. The quantity of magnesium required to saturate urine with struvite at alkaline pH is very small.  As pH decreases below 6.4, the amount of magnesium required to saturate the urine with struvite increases exponentially.  Conversely, as urine pH increases above 6.9, the amount of struvite that forms in the urine increases markedly.  When urine pH is alkaline, the amount of struvite formed in urine is proportional to the dietary magnesium concentration. At urine pH values less than 6.1, struvite does not form regardless of the magnesium concentration of the diet.  Thus, the tendency of struvite to form is a function of urine pH. The magnesium content of the diet only becomes important when urine pH is greater than 6.1.

The food's caloric density, digestibility, and urine-acidifying properties should all be considered when selecting a commercial cat food for the prevention of struvite urolithiasis.  Constituents of foodstuffs exert major effects on urine pH. Sulphur-containing amino acids, phospholipids, and phosphoproteins naturally found in a carnivorous diet naturally acidify the urine, whereas salts of organic acids alkalinize it.  Salts of dietary organic acids, which come primarily from plant material and found in high quantities in dry food, have an alkalinizing effect.

The percentage of magnesium in the diet is not as important as the total amount of magnesium that a cat consumes. Diets that are moderate in caloric density and are highly digestible will be consumed in smaller amounts, thus lowering both DM and magnesium intake.  High-quality canned food is typically >90% digestible whereas equal quality dry food is ~80% digestible.  The lower DM intake results in decreased fecal matter and fecal water and increased urine volume. Feeding a canned diet with these characteristics further contributes to increased urine volume and decreased urine specific gravity reducing the risks of urolithiasis while supplying the cat's dietary magnesium requirements.  Although many  brands of dry cat food may contain relatively low concentrations of magnesium, they are often lower in digestibility than canned and contain high levels of cereal grains. Because the cat's requirement for dietary magnesium is substantially lower than the amount usually found in cat food, a general rule of thumb is to select a high-quality, highly digestible, canned food that contains 0.12 % magnesium or less.