The nutritional needs of the cat are quite specific and differ greatly from the nutritional requirements of other species, including the dog. The cat evolved from a strict carnivore and has not had the chance through evolution to change much from its carnivorous nature. Therefore cats require a much higher protein intake than an omnivore, such as the dog.
The cat’s need for dietary taurine, arginine, preformed vitamin A and high protein makes it characteristic and different from many other species. It is only in the recent decades that the nutritional peculiarities of the cat are beginning to be recognized and researched.
As occurs in other animal species, disease in cats may result from prolonged feeding of unbalanced diets. Diets composed of a single food item may result in deficiency disease or toxicity. It is not uncommon to see nutritional hyperparathyroidism in kittens who are fed homemade diets of high meat content.
Deficiencies of one or more nutrients may result in diseases such as pansteatitis, malnutrition and central retinal degeneration. Many of these conditions may be corrected with dietary alterations if the practitioner recognizes that the disease is nutritionally related. The use of nutrition as part of the medical management of certain disease conditions is also increasingly being used.
Management of feline urologic syndrome through alterations in diet is now accepted practice. Dietary alteration is used to prevent progression of renal destruction in kidney failure. So for veterinary practitioners and cat owners an understanding of feline nutrition is important in prevention of disease as well as treatment and management of disease.
Protein is necessary in the diet of any animal, to supply the essential amino acids, to supply the nitrogen necessary to synthesize those amino acids considered nonessential and to supply nitrogen for the formation of purines, pyrimidines, heme and creatinine.
The cat and fox are two species known to require a higher protein intake than most other mammalian species. In fact, one author suggests that adult cats require almost five times the amount of protein as adult dogs.
In the cat it seems that a fixed amount of dietary protein is always broken down for energy. After amino groups are removed from amino acids, the resulting keto acids can be used for energy or glucose production.
Unlike most other mammals the cat cannot adjust its catabolic enzymes to shifts in levels of dietary protein. These enzymes are always set to handle a medium to high level of dietary protein even though there may be too low a level of protein in the diet.
Insufficient intake of protein may result in a deficiency of the essential amino acids as well. Deficiency of the essential amino acids leads to decreased food intake and weight loss.
There are varied values given for the amount of protein necessary in the feline diet. One source recommends 25% – 30% protein in the diet on a dry weight basis, i.e., if the protein is of good biologic value (70 – 90 biologic value). This would mean 25% of the calories in the diet would be supplied as protein.
A much lower value of 12.5% is given by another source, saying that if a satisfactory amino acid level could be met, this diet could support body weight and nitrogen needs in adult cats. This value is still higher than that required by other mammals. The National Research Council (NRC) has recommended as a minimum 240 grams of protein / kg diet (on dry basis) for growing kittens, which is about 20% of a very palatable, high quality diet.
Protein, like fat, increases the palatability of the diet. It is best to avoid protein from a single protein source because this frequently leads to an imbalance of amino acids, as well as resulting in the cat becoming addicted to a single item diet.
The most critical period for ascertaining that the cat has sufficient protein in the diet is just after weaning. The NRC recommends about 20% protein (on a dry basis), whereas another source recommends 30% – 40% of the diet be protein during this critical period. The recommendation of the NRC is a minimum value and relates to a purified diet of high biologic value.
It is important to realize that all the amino acids ingested are not readily available to the body. The processing of foods may affect the digestibility of the food. For example, the digestibility of soy beans is increased during processing since the cooking inactivates trypsin inhibitors found in soybeans.
On the other hand, the drying of meats can decrease the nutritive value of the protein. When protein is heated in the presence of reducing sugars, the availability of amino acids is reduced. Also during storage, proteins in the presence of polyunsaturated lipids can be oxidized which reduces the levels of amino acids especially methionine, tryptophan, and histidine.
Therefore, if the diet is composed of a high quality protein, consider that about 80% – 90% is available. If it is made up of a low quality protein, consider 60% – 70% available.
Of the essential amino acids there are two that distinguish the cat as being quite different from other mammalian species. Arginine, which most animals can synthesize to some degree in the kidney, is necessary in the diet of cats. Taurine, another amino acid, has received much attention in the literature since studies have shown a taurine deficiency frequently leads to central retinal degeneration in cats.
Arginine is necessary for the conversion of ammonia to urea. If arginine is lacking or deficient in the diet ammonia accumulates in the blood. Cats on arginine restricted diets have shown signs of hyperammonemia soon after a meal. The cats display any of the following signs: hyperactivity, hyperesthesia, ataxia, emesis, ptyalism, apnea, cyanosis and sometimes death.
Since arginine is involved in the metabolism of the waste products of protein metabolism, some say that the arginine requirement increases when a high protein diet is fed as compared to a diet where protein is near the minimum requirement level. Arginine deficient diets occur rarely under natural circumstances.
Cats are very sensitive to a dietary deficiency of taurine. Other species are able to make taurine from methionine, whereas cats have a very limited ability to use methionine to synthesize taurine.
Additionally, there is a constant loss of taurine in the conjugation of bile salts. Cats predominantly use taurine in conjugating bile salts, whereas other mammals are able to use either taurine or glycine in bile salt conjugation.
The demand for taurine is increased even more during growth as muscle mass increases. Most taurine in the body is found in three main tissues: bile, the retina and the olfactory bulb.
In one experiment, cats fed a taurine-free diet for eleven months showed rapid decrease in their plasma taurine levels and about half showed central retinal degeneration. Visual acuity in the cats did not appear to be affected. The lesions are in the central area of the retina and the normally bright yellow tapetum becomes dark and granular and later a hyper-reflective focal lesion develops as photoreceptor cells are lost.
With chronic deficiency the entire fundus appears atrophied. Vision does not seem to be affected until retinal degeneration is advanced, therefore routine ophthalmoscopic exam on cats may be a good practice. Changing the diet to one with adequate taurine will not reverse the damage, but it will help prevent further progression of the disease.
Taurine is high in meat, seafood and milk. It is low in vegetables and most dog foods. Cases of central retinal degeneration have occurred when cats were fed dog foods or when a diet had casein as the only source of protein. Reasons given for feeding cats dog food were the lower cost, some cats preferring dog food over cat food and the instructions of veterinarians who felt that dog food reduced the incidence of feline urolithiasis.
As taurine is also found in the olfactory bulb in rather high levels, it is suggested that smell or taste may also be affected but this is uncertain.
Fat in the diet provides a concentrated source of energy. It is also essential for absorption of fat soluble vitamins, for providing the essential fatty acids and increasing the palatability of the diet. Cats can tolerate and digest high levels of fat in the diet quite well.
Cats are influenced by the amount and source of dietary fat. Commercial canned cat foods tend to have a higher percentage of crude fat on a dry matter basis than dry commercial cat foods. Usually, there is from 10% – 40% crude fat in canned diets, as compared to 10% – 12% in dry diets. Many cats seem to prefer about 20% – 30% crude fat, rather than a much lower or higher percentage.
The type of fat is also important in palatability. Cats tend to prefer animal fats over vegetable fats. Diets high in levels of hydrogenated coconut oil were refused by many cats. The cats preferred hydrogenated beef tallow diets over high levels of hydrogenated coconut oil.
Chicken and turkey fats are known to increase palatability. Commercial cat food manufacturers also learned that cats could be stimulated to eat diets with fat content at 4% on a dry basis, if the fat was sprayed on the surface of pelleted foods.
As fat provides about 2.25 times the metabolizable energy as protein or carbohydrate, adding fat to the diet greatly alters the energy concentration of the diet. The concern is over the fact that cats will take in sufficient energy, but not sufficient protein, vitamins or minerals when a diet is supplemented with fat. If adjustments are not made in these other nutrients, the result may be a cat that is malnourished due to a deficiency in one or more of these nutrients.
Fat is necessary in that it provides linoleic and arachidonic acids, the two fatty acids considered essential in cats. Most other mammals can convert linoleate to arachidonate by desaturation and elongation which occurs in the liver. The ability of the cat to convert linoleate to arachidonate is very minimal, so both fatty acids are considered essential in the cat diet.
Linoleate is not simply a precursor to arachidonate, but is in itself essential for certain body functions. If linoleate was deficient in the diet, scaly skin, enlarged fatty livers and loss of water transepidermally occurred. It is known that linoleate has a function in the structuring of membranes for proper growth, lipid transport and normal skin and coat condition.
Arachidonate also has a structural function and is a precursor to prostaglandin, PGE2. It is necessary for normal reproduction and blood platelet aggregation.
In one study, male cats fed a diet deficient in the essential fatty acids for about two years showed extensive testicular degeneration. They found that if linoleate was included in the diet, degeneration of the testes did not occur.
When linoleate was supplied in the diet, levels of arachidonate in the testes increased, which was thought to be due to the conversion of some linoleate to arachidonate by the testes. The levels of arachidonate in the plasma did not increase, even though it seemed apparent that the testes converted some linoleate to arachidonate. So it seems that linoleate can help prevent testicular degeneration in a cat consuming a diet deficient in arachidonate.
In the female cat on an arachidonate free diet, adding linoleate to the diet did not help her reproductive function. She could not bear kittens unless a certain level of arachidonate was present.
Sources of these essential fatty acids differ. The richest source of arachidonate is the lipid portion of organ meats. Warm water fish and shellfish are other good sources. Tuna oil contains arachidonate, but it also contains a 22 carbon chain fatty acid, which seems to interfere with arachidonate.
The possibility of developing an arachidonate deficiency is greatest in cats fed dry cat foods, as they have a lower fat content then commercial canned cat foods. Vegetable oils lack arachidonate and most rendered animal fats, if limited to 10% fat in the diet, would not provide the necessary arachidonate.
A good source of linoleic acid is safflower oil. In one study, cats on a diet deficient in these essential fatty acids developed severe fatty liver, fat in the kidneys, dystrophic mineralization of the adrenal glands, testicular degeneration and hyperkeratosis of the skin.
These deficiency signs disappeared when safflower oil (as a means of supplying linoleate) was added to the diet. In this same study, some cats were fed diets containing hydrogenated coconut oil, safflower oil and chicken fat and fatty livers developed despite the presence of high levels oflinoleate. The fatty livers were thought to have resulted from the effects of the medium-chain triglycerides in hydrogenated coconut oil.
The researcher suggests that hydrogenated coconut oil may have accentuated an essential fatty acid deficiency, which has also been shown to occur in rats eating high levels of hydrogenated coconut oil. The level of fat in the diet beyond what is necessary to supply these two essential fatty acids has not been demonstrated.
Certain vitamins are fat soluble and require the presence of some fat in the diet for absorption. These fat soluble vitamins are A, D, E and K.
The vitamin requirements of the cat are quite specific. Cats in general have a higher need for the B-complex vitamins than other animals. The values of minimum requirements of some B-vitamins are 2 – 8 times greater for cats than dogs.
For example, vitamin B6, pyridoxine, provides the prosthetic group of transaminases and since cats have a high transaminase level, their requirement for B6 may be four times that of the dog.
Thiamine is a B-vitamin which has received attention due to its easy destruction during cooking and storage. High losses can occur when canned foods are processed. Up to 80% of thiamine can be lost in processing so manufacturers should supplement the food with several times the thiamine requirement to insure adequate levels after processing. Thiamine deficiency can also result from prolonged ingestion of uncooked fish which contains thiaminase.
Thiamine deficiency is characterized by ataxia, cerebellar tremors, loss of righting in the air and seizures. Cats with thiamine deficiency will tend to keep their head ventroflexed on the sternum when they are suspended by the hind limbs. Normally a cat put in this position will dorsoflex its head. Diagnosis can be confirmed by giving thiamine orally or intramuscularly and observing for improvement which usually occurs within a few hours.
Cats are also characterized by their inability to convert Beta-carotene to vitamin A. Cats must have preformed vitamin A in the diet, unlike many other mammals who have the ability to convert Beta-carotene to the needed vitamin. This need for preformed vitamin A is part of the strict carnivorous nature of the cat.
Considering that liver is one of the highest sources of the preformed vitamin, the cat as a carnivore had no need to retain an ability to convert Beta-carotene to vitamin A, as the diet in most cases provided an abundance of preformed vitamin A. Beta-carotene is found in many vegetables and is not toxic if consumed in large amounts.
On the other hand, vitamin A consumed in large amounts in the diet is very toxic. Cats fed a diet consisting mainly of liver may be receiving toxic doses of vitamin A, which frequently presents as skeletal demineralization. There may be extreme tenderness of joints, especially of the cervical skeleton, due to bony exostoses that develop along muscular insertions of the cervical vertebrae, ribs and long bones.
To avoid the possibility of hypervitaminosis, no more than one ounce of liver a day should be fed to an adult cat. Since vitamin A is a fat soluble vitamin, excesses are not excreted but stored in the body, especially in the liver. Therefore, deficiency is rare.
Vitamin E is another fat soluble vitamin that deserves special attention since occasionally deficiencies occur. Diets high in polyunsaturated fatty acids, as contained in fish oil may increase the vitamin E requirement three or four times.
Vitamin E stabilizes the unsaturated lipids. When large amounts of unsaturated fatty acids are taken in without sufficient antioxidant (vitamin E), peroxidation of depot fat may occur and later fat necrosis. The adipose tissue becomes yellow to orange-brown in color and firm. This condition is called pansteatitis or yellow fat disease.
Most commercial cat foods have vitamin E added but these additional quantities become insufficient if the owner is supplementing the commercial foods with high proportions of red tuna or some other fish. Some fish oils, such as cod liver oil, are very high in unsaturated fatty acids and low in antioxidants, such as vitamin E.
Clinical signs of pansteatitis are anorexia, pyrexia, tenderness of palpation of the abdomen and thorax. Small nodules may be present in the subcutaneous tissues. Biopsy of the subcutaneous fat may show fat cell necrosis and infiltration by neutrophils.
One case study alerts practitioners to the fact that pansteatitis can resemble feline infectious peritonitis in its clinical appearance. An eight-month-old male Persian cat presented with ascites, anorexia, weight loss, low grade fever and diarrhea. The conditon progressed to a chronic debilitating disease resembling FIP in clinical appearance.
The author stresses the importance of considering pansteatitis as a differential diagnosis when a cat presents with effusive abdominal disease and fever which is antibiotic resistant.
Other diseases on the differential list for these clinical signs should include toxoplasmosis and lymphosarcoma. Laboratory data should allow differentiation of these diseases. Pansteatitis can usually be treated successfully with alpha-tocopherol.
Minerals are needed by the body to maintain acid-base balance, tissue structure and osmotic pressure. They are also essential in the function of many enzyme systems.
Even though minerals in a food may meet the minimum requirements, the bioavailability must also be considered. Phytic acid and chitin can greatly reduce the availability of minerals in a feed.
If the phosphorus in a diet is largely plant-derived, it should only be considered about 30% bioavailable, as it is likely to be bound to phytate to a great degree.
Zinc, a mineral component of many body enzymes, may need to be tripled in amount in a diet containing large amounts of phytate and fiber. In phytatecontaining diets, which contain excess calcium, zinc is bound in the gut in an insoluble zinc-calciumphytate complex and therefore not available for absorption.
Adding supplements of several different minerals to the diet may result in problems due to the interaction of different minerals. An excess of one mineral in the diet may decrease the absorption of another. For example, an excess of phosphorus in the diet lowers the bioavailability of iron.
The NRC suggests that values of iron, copper and iodine be mutiplied by a factor of 1.3 to help correct for decreased bioavailability. Zinc and manganese should be multiplied by a factor of 1.5.
Secondary hyperparathyroidism is a condition which results when the levels of calcium and phosphorus are altered in the body. Diets low in calcium or very high in phosphorus may lead to this disease.
It is essential that these minerals be maintained in a specific ratio in the diet. A calcium to phosphorus ratio of 1:1 to 2:1 is thought to be acceptable. Diets composed primarily of cardiac and skeletal muscle can upset this ratio greatly. Beef heart has a calcium to phosphorus ratio of 1:40. Horse meat has a ratio of 1:10.
The great excess of phosphorus in these foods can lead to inadequate absorption of calcium which results in a hypocalcemia. Hypocalcemia stimulates the parathyroids to release parathormone in an attempt to restore the serum calcium to normal levels. Parathormone acts on bone, kidneys and the intestine in its attempt to increase the calcium and decrease the phosphorus levels.
The adult cat has 18 – 40 grams of calcium in its skeleton and these stores can be used to restore serum calcium to a normal level. The increased serum parathormone causes more bone resorption, which results in a loss of bony mass.
In the wild, cats would eat a predominantly meat diet, but calcium would be provided when the bones of small rodents were also consumed.
Clinical signs of nutritional hyperparathyroidism are lameness, limping or reluctance to move. There may also be signs of posterior paresis, bone and joint pain and constipation.
Radiographic findings show loss of bone density, possibly pelvic deformities and pathologic fractures especially of the vertebrae. Serum calcium and phosphorus levels are usually within the normal range. Occasionally blood clotting times may be extended.
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