Chapter 26. Common Nutrition Myths and Feeding Practices
FEEDING “HUMAN FOODS” TO DOGS AND CATS
Some owners enjoy feeding their dogs and cats “people foods” for the same reasons that they feed treats and snacks. Providing a special treat is a way of showing affection and love, and adding table scraps and other choice food items to a pet’s food allows owners to express their affection for their pet and to feel that they are enhancing their pet’s enjoyment of the meal. Although most of these foods become harmful only if they make up a high proportion of the pet’s diet, some human foods are unsuitable for companion animals and should not be fed at all (Box 26-1).
BOX 26-1
The addition of extra foods should be limited to no more than 5% to 10% of the pet’s daily caloric requirement.
Any meat, fish, or poultry that is fed should be well cooked, and all bones should be removed.
The use of milk and cheese should be strictly monitored. Some adult dogs and cats are lactose intolerant and cannot efficiently digest dairy products.
The exclusive use of any single food item should be avoided, even when adding it to the pet’s diet in small amounts.
Correction of the nutrient imbalances of a poor diet by adding table scraps should not be attempted.
Vitamin and/or mineral supplements are unnecessary for healthy pets when a complete and balanced pet food is fed, and they can be detrimental to health.
Pet owners should be aware of the development of undesirable behaviors, such as begging during mealtimes and stealing food.
The addition of all extra foods should be discontinued if weight gain, gastrointestinal tract upset, or signs of nutrient imbalance are seen.
Table Scraps
The table scraps that most owners select to feed to their dogs (and less frequently to cats) are the uneaten portions of meals that are highly palatable to dogs, such as fat trimmings and leftover meat. Vegetables and grains are less frequently fed. Therefore, while the leftovers that end up in the pet’s bowl may be very tasty (and much appreciated), they usually do not provide balanced nutrition for a dog or cat. If table scraps are fed to pets, the amount should be carefully monitored. A good rule of thumb is that table scraps should never make up more than 5% to 10% of a pet’s total daily caloric intake.
If table scraps are fed to dogs or cats, the amount should be carefully monitored, and the total amount should never make up more than 5% to 10% of a pet’s total daily caloric intake.
Meat and Poultry
Some owners believe that because cats and dogs are carnivorous in nature, they should be able to survive on an all-meat diet. However, the muscle tissue of meat and poultry alone cannot supply complete nutrition to companion animals. Although meat and poultry provide high-quality protein, as a single food source they are deficient in calcium, phosphorus, sodium, iron, copper, iodine, and several essential vitamins. It is true that, in the wild, the ancestors of dogs and cats survived on freshly killed meat. However, the fact that they consumed their entire prey, including bones, organs, and intestinal contents, is often overlooked. Just as with table scraps, the addition of meat and poultry to the diet should be strictly limited because of their potential to imbalance a pet’s diet (Table 26-1).
| ∗Imbalanced nutrients are expressed in bold print. Nutrient levels were compared to the Association of American Feed Control Officials’ Nutrient Profiles and corrected for differences in energy density. | ||||
| †Beef = fresh ground round. | ||||
| N utrient | D ry dog food | 75% D og food/25% B eef† | 50% D og food/50% B eef | 25% D og food/75% B eef |
|---|---|---|---|---|
| Protein | 34% | 39% | 46% | 55% |
| Fat | 23% | 24% | 25% | 26% |
| Carbohydrate | 35% | 30% | 23% | 14% |
| Crude fiber | 1.9% | 1.6% | 1.3% | 0.75% |
| Calcium | 1.3% | 1.1% | 0.87% | 0.53% |
| Phosphorus | 1.0% | 0.89% | 0.73% | 0.53% |
| Calcium:phosphorus ratio | 1.3:1 | 1.2:1 | 1.2:1 | 1:1 |
| Potassium | 0.87% | 0.89% | 0.92% | 0.96% |
| Sodium | 0.60% | 0.53% | 0.44% | 0.31% |
| Magnesium | 0.11% | 0.09% | 0.08% | 0.06% |
| Iron | 215 mg/kg | 183 mg/kg | 142 mg/kg | 85 mg/kg |
| Vitamin A | 21,700 IU/kg | 18,500 IU/kg | 14,400 IU/kg | 8600 IU/kg |
| Vitamin D | 1950 IU/kg | 1670 IU/kg | 1290 IU/kg | 770 IU/kg |
| Vitamin E | 153 IU/kg | 130 IU/kg | 100 IU/kg | 60 IU/kg |
| Thiamin | 19.5 mg/kg | 16.7 mg/kg | 13 mg/kg | 7.7 mg/kg |
| Riboflavin | 25 mg/kg | 21 mg/kg | 16.5 mg/kg | 10 mg/kg |
| Niacin | 64 mg/kg | 55 mg/kg | 42 mg/kg | 25 mg/kg |
| Metabolizable energy | 4700 kcal/kg | 4800 kcal/kg | 5000 kcal/kg | 5200 kcal/kg |
| Caloric distribution | ||||
| Protein | 27% | 31% | 35% | 41% |
| Fat | 45% | 45% | 47% | 48% |
| Carbohydrate | 28% | 24% | 18% | 10% |
Fish
Most cats and some dogs love the taste of fish. Interestingly, the cat food advertising campaigns used by some pet food companies have convinced people that cats prefer the taste of fish over many other food items. In reality, cats enjoy fish to about the same degree that they enjoy many other animal-source proteins. Although fish is a good source of protein for dogs and cats, similar to meat and poultry, it does not supply complete nutrition. In general, most types of deboned fish are deficient in calcium, sodium, iron, copper, and several vitamins. Some types of fish also contain small bones that are difficult to remove before cooking. Care should be taken if feeding fish because these bones may lodge in a pet’s throat or gastrointestinal tract and cause perforation or obstruction.
FISH (TUNA) AND PANSTEATITIS
Tuna is commonly fed to cats because it is readily available and inexpensive, and because most cats love the taste. Although less available than tuna packed in water, canned tuna packed in oil is preferred by many cats, because of the enhanced flavor and texture provided by the oil. However, tuna (and several other types of fish, such as sardines) that is packed in oil also contains high levels of polyunsaturated fatty acids (PUFAs). If tuna is fed regularly, the excessive intake of PUFAs can result in a vitamin E deficiency. This risk occurs because an animal’s vitamin E requirement is directly affected by the level of unsaturated fatty acids present in the diet. As the level of PUFAs increases, an animal’s vitamin E requirement also increases. When cats are fed high amounts of PUFAs with no concomitant increase in vitamin E, their body fat is not sufficiently protected from oxidative degradation, resulting in oxidative stress and the formation of peroxides and hydroperoxides. 1 Over time, the accumulation of reactive peroxides in adipose tissue leads to a pathological condition called pansteatitis, which is characterized by chronic inflammation and yellow-brown discoloration of body fat.
Clinical signs of pansteatitis in cats include anorexia, depression, pyrexia, and hyperesthesia of the thorax and abdomen. The cat may demonstrate changes in behavior and agility and develop a poor or roughened hair coat. 2. and 3. Owners typically report that their cat has become intolerant of being picked up or held. Palpation of subcutaneous and intraabdominal fat deposits is painful to the cat and reveals the presence of granular or nodular fat deposits. Information concerning the cat’s dietary history is needed for diagnosis, and confirmation is provided by histological examination of a fat biopsy sample. The fat of cats with pansteatitis is very firm and deep yellow to orange, with a diffuse inflammatory response. 3. and 4. The orange pigment (commonly referred to as ceroid) is believed to be an intermediate polymerization product of unsaturated fatty acids that have undergone peroxidation as a result of insufficient intracellular vitamin E (Box 26-2).
BOX 26-2
Depression and anorexia
Hyperesthesia (sensitivity to touch) of the chest and abdomen
Reluctance to move and decreased agility
Presence of abnormal fat deposits under the skin and in the abdomen
Dietary history that includes items that are high in unsaturated fats and low in vitamin E
Some of the earliest published cases of pansteatitis occurred in cats that were fed canned, fish-based commercial cat foods comprised wholly or predominantly of red tuna and that were deficient in vitamin E. 4.5. and 6. Pansteatitis has also been described in cats that were fed unconventional or homemade diets consisting largely of tuna, sardines, or other oily fish. 7.8. and 9. Although reported infrequently, there is evidence that cats fed all-meat diets may be at increased risk of developing pansteatitis. 9
Treatment of pansteatitis involves changing the cat’s diet from one that is comprised primarily of fish and replacing it with a well-balanced cat food. Dietary changes may be difficult in cats that have become accustomed to eating only a single food item. This problem has been most commonly reported in cats receiving only red tuna as the principal component of their diet for an extended period of time. Along with correction of the diet, vitamin E (alpha-tocopherol) should be administered orally at a dose of 10 to 25 international units (IU) twice daily for several weeks, until all clinical signs have resolved and the cat is reliably consuming a balanced food. 9 Corticosteroid therapy may be used in severe cases to decrease inflammation and reduce pain. Prognosis for recovery from pansteatitis is usually very good, but may take several months in advanced cases.
RAW FISH AND THIAMINASE
Certain types of fish, such as carp and herring, contain a compound that destroys thiamin and may cause a thiamin deficiency. 10. and 11. Consumption of these types of fish has been shown to cause thiamin deficiency in a variety of species. For example, experimental studies with cats have produced signs of thiamin deficiency within 23 to 40 days of consuming diets composed solely of raw carp or raw salt-water herring. 10 The subcutaneous administration of thiamin resulted in recovery in all cases. Although both carp and herring can cause thiamin deficiency, perch, catfish, and butterfish do not show thiaminase activity. Other common types of fish that contain thiaminase include whitefish, pike, cod, goldfish, mullet, shark, and flounder. However, it is not known whether the thiaminase levels present in these fish are sufficient to produce deficiency in animals. 11 Thiaminase is a heat-labile enzyme and is denatured by normal cooking temperatures. As a result, the potential for thiamin deficiency exists only when uncooked fish is fed to pets.
Although naturally occurring thiamin deficiency is uncommon in dogs and cats, clinical cases have been reported. Cats appear to be more susceptible because of their high dietary requirement for thiamin and because of the tendency of owners to feed cats diets containing fish products. 12 Most clinical cases have involved cats fed diets that contained a large proportion of raw fish. 10. and 13. Similarly, a group of sled dogs that was fed a diet consisting of frozen, uncooked carp developed clinical signs of thiamin deficiency during a 6-month period. 14 The addition of oatmeal, a dry dog food, and 100 milligrams (mg) of thiamin per day to the diets of the affected dogs resulted in complete recovery within 2 months.
Because thiamin is essential for normal carbohydrate metabolism, the central nervous system is severely affected by a deficiency of this vitamin. Initial clinical signs of deficiency include anorexia, weight loss, and depression. 13. and 15. As the deficiency progresses, neurological signs of ataxia, paresis, and, eventually, convulsive seizures develop. The terminal stage is characterized by severe weakness and prostration and eventually leads to death. A diagnosis of thiamin deficiency in dogs and cats is made based on clinical signs and the dietary history of the animal. Elevated plasma pyruvate and lactate concentrations are also useful in confirming a diagnosis.
Treatment includes dietary correction that includes elimination of raw fish from the diet and its replacement with a well-balanced pet food and thiamin therapy. Thiamin should be administered intravenously or subcutaneously at a dose of 75 to 100 mg twice daily until neurological signs subside. 12 Oral thiamin supplementation should also be administered for several months following the initial clinical episode. 14 In most affected pets, these clinical signs will decrease within several days. However, if severe neurological damage has occurred, the pet may never make a full recovery. A permanent intolerance of physical exercise and some degree of persistent ataxia occasionally occurs in animals that have recovered from thiamin deficiency.
Because of the risk of inducing thiamin deficiency, raw fish should never be fed to dogs and cats. There is also the potential for parasite transmission when raw fish is fed. Therefore, if any type of fish is added to a pet’s diet, it should always be well cooked, and only very small amounts should be fed.
Liver
Liver is an excellent source of iron, protein, copper, vitamin D, and several B vitamins. However, like other single food items, it is not a nutritionally complete food. Liver is severely deficient in calcium and excessively high in vitamin A (see below). Both of these nutritional imbalances can cause bone disorders. Vitamin A toxicosis has been shown to develop slowly over a period of years in cats that were regularly fed fresh liver as their primary dietary protein source (see below). 16. and 17. Although small amounts of liver added to a cat’s diet are not harmful, liver as a primary component of the diet should be avoided.
VITAMIN A TOXICOSIS IN CATS: DEFORMING CERVICAL SPONDYLOSIS
Cats that are fed diets composed exclusively of liver or other organ meats are at risk of developing vitamin A toxicosis. This practice is usually the result of well-meaning but poorly informed owners who believe that cats, being carnivores, will thrive on an all-meat or all-liver diet. The bone deformities of vitamin A toxicity develop very gradually and may go undetected for several years. However, over time severe and irreversible crippling occurs, and diagnosis is often too late to be of any help. 18. and 19.
The pathological result of vitamin A excess in cats is the development of a syndrome called deforming cervical spondylosis. The effects of excess vitamin A on bone growth and remodeling lead to the development of bony exostoses (outgrowths) along the muscular insertions of cervical vertebrae and the long bones of the forelimbs. Over time, these bony processes cause pain and impaired mobility. 20 Vitamin A–induced skeletal disease is not a practical problem in dogs, but it has been produced experimentally. Although uncommon in dogs, studies have shown that extremely high intakes of vitamin A during growth will result in decreased length and thickness of long bones, premature closure of epiphyseal growth plates, and the development of osteophytes. 21 However, dogs appear to be relatively resistant to vitamin A toxicosis because subsequent studies found that feeding up to 400,000 IU/kilogram (kg) of dry matter (DM) to puppies or 787,000 IU/kg of DM to adult dogs for periods of 6 months or 1 year caused no signs of toxicity and did not adversely affect bone density measurements. 22. and 23.
Initial clinical signs of deforming cervical spondylosis in cats include anorexia, weight loss, lethargy, and an increasing reluctance to move. Cats become unkempt in appearance, presumably because of an inability to self-groom. As the disease progresses, a very characteristic postural change is observed; cats adopt a marsupial-like sitting position, holding the front legs elevated off the ground. They also often walk with their hind limbs flexed, and ventriflexion of the head is decreased or altogether absent. A fixed-stare expression is often observed, probably as a result of reduced ability to move the neck and turn the head. Lameness in one or both of the front limbs is seen in the later stages. 24 Development of exostoses occurs primarily in the first three joints of the cervical vertebrae and joints of the forelegs. It has been theorized that the normal movements involved in a cat’s regular licking and grooming practices result in these predilection sites. It appears that chronic intoxication with vitamin A increases the sensitivity of the periosteum to the effects of low levels of trauma and repetitive movements that would normally be insufficient to cause an inflammatory response (Box 26-3). 25
BOX 26-3
Anorexia and weight loss
Increased lethargy and reluctance to move
Persistent lameness in one or both front legs
Decreased ability to self-groom
Decreased ventriflexion of the head
Posture changes by adopting a marsupial-like sitting position
Dietary history that includes items that contain a high concentration of vitamin A
Experimental studies show that the level of vitamin A required to produce skeletal lesions within only a few months’ time in growing kittens is between 17 and 35 micrograms (μg)/gram (g) of body weight. 25 A 1-kg (2.2-pound [lb]) kitten would have to consume a minimum of 17,000 μg (~56,000 IU) of vitamin A per day to attain this level. According to the National Research Council’s (NRC’s) current Nutrient Requirements, a 1-kg kitten requires approximately 50 μg of vitamin A per day (1000 μg/kg of dry diet). 26 The safe upper limit for a kitten of this size is approximately 4000 μg per day. Using the previous study’s data, the dose of vitamin A necessary to produce acute toxicity is therefore more than 300 times the recommended allowance. An adult cat weighing 5 kg (11 lb) would have to consume at least 85,000 μg of vitamin A daily to reach this toxic level. The daily vitamin A requirement for an active 5-kg adult cat is approximately 80 μg/day. Therefore an adult cat would have to consume 1000 times its daily requirement of vitamin A to achieve toxic levels. It is indisputable that a cat will never consume this level when being fed a nutritionally balanced pet food.
However, it would also be difficult for a cat to consume this high a level of vitamin A while being fed an all-liver diet. Beef liver contains approximately 160 μg (530 IU)/g. 27 An adult cat consuming 6 ounces (oz) of liver per day would be ingesting only 27,200 μg of vitamin A per day, quite a bit less than the levels described previously needed to create acute toxicity. However, all of the case studies reported in the literature found that deforming cervical spondylosis developed in cats that were fed liver diets. There are two possible explanations for this discrepancy. First, it is known that the livers of production animals vary greatly in vitamin A content. 27 The level of 160 μg of vitamin A per gram of beef liver is an average, not an absolute value. Second, and more importantly, all of the reported case studies occurred in adult cats that had been fed liver diets for a very long time. 28. and 29. The experimental work that has been conducted involved much higher levels of vitamin A and produced signs of toxicity in very short periods of time (i.e., months, rather than years). At lower doses of vitamin A, cervical spondylosis appears to develop slowly over the lifetime of the cat, and clinical signs of the disease do not become evident until much later in adult life. This conclusion is supported by the fact that the average age for the diagnosis of cervical spondylosis in pet cats is 4.25 years. 20 Therefore the reported level of vitamin A required to produce toxicity in the cat (17 to 35 μg/g of body weight) may reflect the experimental production of acute toxicity, but the level that can produce deforming cervical spondylosis, if excess vitamin A is consumed by pet cats for a long time, is probably significantly lower.
Regular supplementation of a cat’s diet with liver, even if added to a balanced diet, has the potential to cause skeletal problems if the practice is continued for several years. When liver is fed exclusively, vitamin A toxicosis may occur concurrently with nutritional secondary hyperparathyroidism because of the low-calcium, high-phosphorus content of organ meats. 28 Cod liver oil fed as a supplement also has the potential to induce vitamin A toxicity. Adding 1 tablespoon (tbsp) of cod liver oil to a cat’s food twice daily will result in an intake of approximately 10,000 μg of additional vitamin A per day. Fish liver oils are also excessively high in vitamin D, and excessive supplementation may result in the combined effects of vitamin A and vitamin D toxicosis.
The treatment of vitamin A toxicosis in cats includes removing the source of excessive vitamin A from the diet, replacing the source with a complete and balanced pet food, and providing supportive therapy. The prognosis is guarded because resolution of skeletal lesions may never be complete. In addition, if the cat has been fed a liver diet for a long time, the change to a balanced pet food may be difficult, if the cat has developed a fixed food preference.
Milk and Dairy Products
Almost all cats and dogs love the taste of milk. Although milk and dairy products are excellent sources of calcium, protein, phosphorus, and several vitamins, excessive intake may cause diarrhea in young and adult pets. Milk contains the simple sugar lactose. Lactose requires breakdown in the intestinal tract by the enzyme lactase. Intestinal lactase activity declines as puppies and kittens reach adulthood. As a result, many adult cats and dogs do not produce sufficient amounts of lactase to handle the large quantity of lactose present in milk. Lack of sufficient lactase results in an inability to completely digest milk and subsequently causes digestive upsets and diarrhea. Dairy products such as cheese, buttermilk, and yogurt contain slightly lower levels of lactose. Even though these products may be better tolerated by some dogs and cats, they still have the potential for causing diarrhea and dietary imbalances if large quantities are fed. Most pets can tolerate and enjoy an occasional bowl of milk, but like all supplementation, the practice of feeding milk should be carefully limited.
Dairy products should not be used as a supplemental source of calcium or protein. Excess dietary calcium can contribute to the development of skeletal disorders in growing dogs and is not helpful in preventing eclampsia in lactating females (see Section 4, pp. 205-206 and Section 5, pp. 497-500). Although dairy products supply high-quality protein, they contain deficiencies and excesses of other nutrients and may contribute to a dietary imbalance if large amounts are added to an otherwise adequate diet.
Oils and Fats
Cod liver oil, vegetable oils, and animal fats are occasionally added to a pet’s food to improve taste or to supply fat and additional vitamins. It is true that fish oils are excellent sources of vitamin A, vitamin D, and the omega-3 (n-3) fatty acids. However, both of these vitamins are toxic when consumed in excess. Because vitamins A and D are stored in the liver, the effects of excess intake are cumulative and develop over long periods. The daily addition of 1 or 2 tbsp of cod liver oil (or another vitamin A supplement) to a small pet’s diet has the potential of eventually developing into a toxicity problem. In addition, oversupplementation with fat may result in either obesity or an eventual decrease in the quantity of food that is consumed. Food intake may decrease because energy needs will be met with a lower quantity of food. Deficiencies of other nutrients may then develop. Excessive intake of dietary fat may also cause digestive problems in some pets.
Some owners add fat to their pets’ diets with the intention of improving coat quality. Dogs have a requirement for the essential fatty acid linoleic acid and possibly for alpha-linolenic acid, and cats require these fatty acids plus dietary arachidonic acid (see Section 2, pp. 81-86). Animals that are deficient in essential fatty acids will develop poor coat quality and skin problems. Poor quality or improperly stored pet foods may contain inadequate levels of these fatty acids. However, if a high-quality food is being fed, adding fat or oil should not be necessary. In most cases, diet is not the principal cause of skin problems or poor coat quality in companion animals. More probable causes of skin disorders include internal and external parasitic infections, allergies, and various hormonal imbalances. If a coat or skin problem persists in a dog or cat, even when a high-quality food is fed, a veterinarian should be consulted.
Eggs
Many dog owners are in the habit of regularly supplementing their dog’s diet with eggs. The reasons for this practice are varied. Some owners believe that feeding eggs improves hair quality and adds luster and shine to their dog’s coat. Others wish to increase or improve the protein in their dog’s diet by adding egg protein. Eggs can also increase a food’s palatability and acceptability for some dogs and cats.
It is true that egg protein has one of the highest biological values of common protein sources. Cooked egg protein is highly digestible and provides all of the necessary essential amino acids required by dogs for adequate growth and maintenance. Eggs are also a good source of iron, vitamin A, vitamin D, and several B vitamins. Eggs are also a source of essential fatty acids; approximately 4% of the fat in egg yolk is in the form of linoleic acid.
Although egg is a high-quality food ingredient, the white of the egg (albumen) contains several inhibitory substances that alter the metabolism of specific nutrients. The two most important are avidin, an inhibitor of biotin absorption, and a compound that interferes with the action of the pancreatic protease, trypsin (trypsin inhibitor). The antitryptic activity of egg white is a characteristic that is much less well documented in current literature than avidin, yet one that has the potential for causing severe nutritional imbalances.
AVIDIN AND BIOTIN
A syndrome termed “egg white injury” was first described in the 1920s. Animals fed raw egg whites as a component of their food developed a scaly skin rash, elevated blood cholesterol levels, and defects in nerve transmission. Eventually, the underlying cause was identified as a deficiency of biotin, brought about by an inhibitory substance in egg white that decreased availability of biotin. This factor was named “avid-albumin” or avidin. Avidin is a protein that is a secretory product of the hen’s oviduct and is subsequently deposited in the albuminous portion of the egg. When consumed, avidin combines with dietary biotin in the intestine and prevents its absorption. The avidin in egg white is so effective in this capacity that raw egg white has been used to experimentally induce biotin deficiency in laboratory animals. Regardless, the danger of a pet owner inducing a biotin deficiency in a dog or cat by feeding supplemental eggs is slight because the yolk of the egg contains large quantities of biotin. In addition, cooking eggs denatures avidin and destroys its biotin binding ability. Practically speaking, potential risk for biotin deficiency will only occur if an owner supplements the pet’s food with only the white of the raw egg. As in other species, signs of biotin deficiency in dogs and cats include dermatitis, loss of hair and poor growth rate.
EGG WHITE TRYPSIN INHIBITOR
The white of the egg also contains another potentially damaging inhibitory substance. This substance is actually a group of proteins that have antitryptic activity. The antitryptic effect of feeding raw egg white has received less attention than avidin, yet its capacity for causing nutritional problems in pets is potentially much greater. Early studies reported that dogs fed as little as two raw egg whites per day in their food exhibited loose stools, and when the amount was increased further, chronic diarrhea and weight loss developed. 30 Dried (uncooked) egg white was found to be just as active in causing diarrhea and weight loss as was fresh, raw egg white. The utilization of raw egg white protein (as determined by apparent digestibility) was reported to be only 58.6%. Subsequent feeding studies and in vitro tests of protein digestibility confirmed that the factor responsible for these effects was a group of trypsin inhibitor proteins found in the white of the egg. 31 Egg white trypsin inhibitor reduced a food’s protein digestibility when included at just 7% of the diet, and a linear relationship was reported between the amount of egg white trypsin inhibitor and loss of protein digestibility. 32
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