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Vitamins divide into two groups, the fat-soluble vitamins A, D, E, and K and the water soluble vitamins. As a group the metabolic functions of fat-soluble vitamins have little in common. Their common property is being fat soluble, and their intestinal absorption improves with moderate dietary fat and lessens with reduced dietary fat absorption. Causes of reduced absorption include pancreatic enzyme deficiency and small intestine mucosal diseases.

Fat Soluble Vitamins-Vitamin A

Vitamin A Metabolism   

Vitamin A (or its precursor, carotene) is a dietary essential for all animals. Intestinal mucosa converts the precursors to vitamin A. Conversion of carotene to vitamin A is a limiting step and prevents absorption of excess vitamin A. Vitamin A absorption is not regulated and excess dietary vitamin A can result in absorption of toxic amounts. After absorption vitamin A is stored in the liver. The liver's large storage capacity protects against vitamin A deficiency when little is consumed. It also allows for storage of excess and toxic amounts of vitamin A. Carnivores consuming fish, containing rich sources of vitamin A, store large amounts of vitamin A in their liver. Such a carnivore is the polar bear. Dogs consuming liver from this animal develop vitamin A toxicity. The kidneys also store vitamin A, but not as much as the liver.

Vitamin A Deficiency

Vitamin A deficiency is rare in dogs and cats. When seen vitamin A deficiency affects growing animals due to the vitamin's role in cell differentiation. Vitamin A is important for many functions that control cell growth and differentiation. Without vitamin A abnormal cells develop. Deficiency of this vitamin results in defects in vision, bone growth, nervous system functions, reproduction, skin growth, and overall growth. Vision defects result from loss of retinal pigment that leads to night blindness and ultimately total blindness. Early pigment loss is in retinal rods, structures sensitive to dim light. Vitamin A deficiency in young, growing animals leads to bone overgrowth, resulting in secondary nerve damage. Inappropriate deposition of bone causes the bony changes. Bone development in and around ear structures destroys auditory nerves, leading to deafness. Bony changes also include failures in bone remodeling. Previously formed bone is not reabsorbed and subsequent bone thickening reduces spaces around bones. The loss of space causes nerve constriction for the senses of smell and vision and for face and neck muscles.  Similar changes in vertebrae can compress spinal nerves and can increase cerebrospinal fluid pressure because its circulation is restricted. Vitamin A deficiency affects reproduction in both sexes. Deficiency in males causes testicular atrophy and failed sperm production. Deficiency in females causes heat cycle irregularities, conception and embryo implantation failures, and inability to maintain pregnancy and lactation. Death of the unborn and spontaneous abortion are common. Newborns can have many different congenital malformations. Vitamin A deficiency changes growth and differentiation of epithelial cells. Skin becomes highly cornified. Respiratory tract epithelium changes so that an often fatal pneumonia develops. Digestive tract epithelium also changes and its functions are affected. Similar changes develop in epithelium of the urinary tract and reproductive system of females, and in the eye.

Vitamin A Toxicity

Vitamin A toxicity develops when dietary levels exceed the body’s storage capacity, primarily the liver’s. Vitamin A toxicity occurs in cats fed large amounts of beef liver from cattle raised on pasture (where carotene intake results in high liver concentrations of vitamin A). Toxicity produces bone and joint pathology. Abnormalities develop more quickly in growing cats. During pregnancy vitamin A excess damages the fetus.

Vitamin toxicity is more commonly subtle. Small excess of vitamin A can act synergistically with other substances to damage the liver. For example, moderate levels of copper, iron, and many drugs are not toxic to the liver. With a background of high, but seemingly safe levels of vitamin A, the addition of one of these other substances can damage the liver. Also, endotoxin absorbed from the intestine normally has little effect to damage the liver. The addition of vitamin A, however, can act synergistically with the endotoxin to damage the liver. Therefore, supplementation to give excess vitamin A is not innocuous and can contribute to liver damage due to other causes.

Vitamin A Requirements

Most commercial cat and dog foods provide large amounts of vitamin A. Vitamin A is quite stable during storage if the diet is adequately protected with vitamin E and lipid antioxidants such as ethoxyquin. Oxidation especially in the presence of metals destroys vitamin A. Cats require dietary vitamin A; they cannot convert carotene to vitamin A. The dog can convert one milligram of dietary carotene to about 800 IU of vitamin A. The maximum safe level for vitamin A is unknown for the dog and cat. The recommended level for dogs is approximately double the minimum level needed. The recommendation for a growing puppy is about 200 IU and for an adult dog about 75 IU per kilogram of body weight daily. The requirements for cats are similar. Many canned feline diets have vitamin A levels greater than 300,000 IU per kilogram of diet dry matter and some as high as 500,000 IU per kilogram diet dry matter. These diets contain large amounts of liver. 

Fat Soluble Vitamins-Vitamin E

 Vitamin E Metabolism  

Vitamin E constitutes a group of tocopherols that are antioxidants of cellular polyunsaturated fatty acids. Without vitamin E these fatty acids are oxidized, producing lipid peroxides which damage cell membranes. Vitamin E requirements depend on dietary polyunsaturated fatty acid levels; high fatty acid levels require increased vitamin E to protect against lipid peroxidation. Selenium acts with vitamin E to prevent peroxide formation. The two also remove peroxides once they form. Selenium requirements are less with high dietary levels of vitamin E and low levels of polyunsaturated fatty acids.

Vitamin E Deficiency

Vitamin E deficiency appears in cats consuming large amounts of polyunsaturated fatty acids and inadequate amounts of vitamin E. Steatitis results and shows signs of inappetance, weight loss, fever and pain. Inadequate vitamin E absorption or high dietary levels of polyunsaturated fatty acids with low levels of vitamin E causes brown bowel syndrome in dogs. Deficiency of vitamin E with or without deficiency of selenium causes many additional problems in other animals. They do not appear in dogs or cats, except vitamin E deficiency can cause male sterility in dogs. Although its causes are mostly unknown, aging is associated with accumulation of pigments produced by oxidation. Protection against lipid oxidation by vitamin E may slow aging processes such as osteoarthritis.

Vitamin E Toxicity

Vitamin E is the safest fat soluble vitamins. There are no reports of vitamin E toxicity. Excess vitamin E antagonizes the effects of vitamin K, however, and in vitamin K deficient or anticoagulant poisoned animals, excess vitamin E prolongs clotting times.

Vitamin E and Selenium Requirements

Vitamin E requirements depend on dietary polyunsaturated fatty acids levels. Fish products are rich in unsaturated fatty acids and must contain high levels of vitamin E to protect against steatitis.  The NRC vitamin E recommendation for dogs is to provide 22 IU per kilogram of food and for cats to provide 30 IU per kilogram of food. These recommendations are for diets low in polyunsaturated fatty acids. Diets high in these fatty acids require more vitamin E to protect cats against steatitis. A diet containing five times this level (150 IU vitamin E per kilogram of food) does not protect cats fed a red tuna fish diet. Cats require greater than 800 IU per week to prevent clinical signs of steatitis when eating this diet.

Selenium requirements are unknown for cats and dogs. However, 0.05 parts per million is probably adequate and 0.10 parts per million should be sufficient. Selenium toxicity is unknown in dogs and cats but it can appear from excess supplementation of the diet with vitamins and minerals. Vegetable and seed oils are generally the major source of vitamin E (tocopherols) in the diet. Animal products are poor sources of vitamin E.

Fat Soluble Vitamins-Vitamin K

Vitamin K Metabolism

Vitamin K prevents bleeding and has a unique naphthoquinone structure. Vitamin K is need for production of blood clotting factors.

Vitamin K Deficiency

Vitamin K deficiency is uncommon. It occurs most commonly after ingesting a vitamin K antagonist such as warfarin. Deficiency can also develop when digestive tract disease reduces fat absorption. For an unknown reason vitamin K deficiency sometimes develops in cats fed fish diets (salmon and tuna).    

Vitamin K Sources and Requirements

Vitamin K is found widely in plant and animal sources of food. All leafy green plant sources are rich in vitamin K. Liver, egg and some fish meals are good sources. Other meat and dairy product are moderate sources. Fruits and grains are poor sources. Bacteria living in the intestinal tract produce vitamin K and under normal circumstances this provides an animal's needs. Drugs that reduce these bacteria or their production of vitamin K make the dietary source more important. There is no substantial evidence that vitamin K should be added to a pet's diet. Both commercial foods and ones prepared by owners appear to contain adequate amounts for dogs and cats. Since the NRC has not advised on any requirements for dogs and cats most pet food manufacturers do not list Vitamin K levels on the label (and apparently do not add it). There are exceptions. When added, synthetic vitamin K (menadione) is the form used. The NRC suggests adding vitamin K to provide 100 micrograms per kilogram of food. Diets can contain one of three forms of the menadiones with menadione sodium bisulfite most commonly used. Massive amounts of vitamin K do not adversely affect dogs or cats. Very large amounts of menadione also have no harmful effects.

Fat Soluble Vitamins-Vitamin D

Vitamin D Metabolism

Vitamin D absorption is normal when dietary fat digestion and absorption are normal. Precursors of vitamin D in animal and plant food sources are cholesterol and ergosterol, respectively. Both require ultraviolet irradiation for conversion to D3 or cholecalciferol and D2, respectively). Both require biochemical conversion by the liver and kidney to their metabolically active forms. Calcitriol is the most active form of vitamin D3. Calcitrol stimulates intestinal absorption of calcium and phosphorus and assists in mobilizing calcium from bone for maintaining normal blood calcium levels. Blood calcium and phosphorus levels regulate calcitriol production.

Vitamin D Deficiency

Vitamin D is most important during growth. It is essential for normal bone development; its deficiency causes rickets. Fortunately, rickets is rare. Cats need less dietary vitamin D because ultraviolet irradiation of precursors in skin produces vitamin D. Dogs need dietary vitamin D because ultraviolet light does not make that conversion in skin. Puppies raised in sunlight and receiving no dietary vitamin D develop rickets. Despite these species differences sunlight is unimportant in producing vitamin D in the cat as well as the dog; the dietary amount is important.

Vitamin D Toxicity

Fat-soluble vitamins should not be given to greatly exceed requirements. Because of their prolonged storage and lipid solubility, they are not readily cleared from the body as water-soluble vitamins. Excess fat-soluble vitamin supplementation causes a pet to receive toxic amounts of vitamin D. Dietary vitamin D is readily absorbed, such as the other fat-soluble vitamins; there are no controls regulating its absorption. After its absorption there is little regulation of the biochemical activity that converts vitamin D in the kidneys and liver to its most active form that controls the absorption of calcium. Thus, excess dietary vitamin D levels promote calcium absorption and cause hypercalcemia. Soft tissues such as kidneys, blood vessels and heart tissue calcify. Calcification of renal arteries severely reduces blood flow. The potency of vitamin D for producing hypercalcemia is so great that compounds with its properties are very effective rodent poisons. The poison's vitamin D is readily available so rodents ingesting excess amounts develop hypercalcemia and death quickly follows.

Vitamin D Requirements

Most pet foods contain more vitamin D than is required. Vitamin D is quite resistant to inactivation by heat and oxidation so its potency in the finished product remains high. (In contrast, vitamin A is much more sensitive to oxidative destruction.) Vitamin D3 (its biochemically active derivative) is 10 to 20 times more toxic than the provitamin from which it comes. For most species of animals, the presumed safe level of vitamin D3 for long-term feeding (greater than 60 days) is 4 to 10 times the recognized nutritional requirement. The NRC recommends giving puppies 22 IU per kilogram of body weight daily and adults 8 IU per kilogram. Growing or adult cats require 20 IU vitamin D per kilogram of body weight per day. These requirements are based on feeding a diet with an optimum ratio of calcium to phosphorus (1.2 calcium to 1.0 phosphorus). With a poorer ratio or with low dietary levels of calcium and phosphorus, animals require more vitamin D. Studies in dogs show that hypercalcemia occurs only with very high levels of vitamin D, over 1000 IU given per kilogram of body weight. This leads to the belief that vitamin D addition to pet foods need not be precise. Some commercial pet foods caused an unusually high incidence of kidney disease in cats because the level of vitamin D was higher than it should have been. The result was absorption of large amounts of calcium that were not enough to cause hypercalcemia but were high enough to calcify kidney tissue and cause kidney failure. How much vitamin D should an animal receive? The requirement may be so low that any reasonable diet is bound to supply adequate quantities.

Water-Soluble Vitamins

There are important differences between the fat-soluble and water-soluble vitamins. Body reserves of fat-soluble vitamins are more extensive than for water-soluble vitamins because of fat-soluble vitamins’ solubility in adipose tissue and specific storage mechanisms in the body. Deficiencies of fat-soluble vitamins take longer to appear than those for water-soluble vitamins. Excess water-soluble vitamins are relatively nontoxic compared to greater than required amounts of vitamins A and D. Natural deficiencies of B complex vitamins often occur as multiple deficiencies compared to deficiencies developing for a single vitamin with fat-soluble vitamins. This is due to the distribution of B vitamins in foods; foods high in one B vitamin are often high in other members of the group. Water-soluble vitamins function in many enzyme systems involved with numerous biochemical reactions. Consequently their role is more diffuse than the fat-soluble vitamins. Clinical signs of B vitamin deficiencies frequently involve multiple systems whereas those of the fat-soluble vitamins cause specific abnormalities confined to one system or chemical reaction.

Thiamin - Vitamin B1

Thiamin Metabolism

Thiamin participates as a coenzyme in several key chemical conversions in carbohydrate metabolism. Thiamin requirements are dependent on a diet's carbohydrate content. A high fat and low carbohydrate diet requires less thiamin than a high carbohydrate diet.

Thiamin Deficiency

Thiamin deficiency can occur because of dietary insufficieny, resulting in beri-beri in humans on a diet of white polished rice. The clinical signs appear because of impaired carbohydrate metabolism. Signs of thiamin deficiency in people are a loss of appetite, weakness, neurological signs and heart failure.  Dietary deficiency is also possible when cooking destroys thiamin. Food processing can destroy thiamin especially under alkaline-high temperature-high moisture conditions. In some commercial canning processes only 15 percent of added thiamin is available in the finished product. Some food additives accelerate thiamin destruction. They include sodium tripolyphosphate or calcium metabisulfite used in gel formation processes and sodium metabisulfite that produces sulfur dioxide and acts as a food preservative and flavor enhancer. Because commercial processing of pet foods destroys thiamin, deficiency of the vitamin is a risk to dogs and cats. Thiamin deficiency is also possible where naturally occurring thiamin-destroying enzymes destroy thiamin in foods. Such enzymes are found in some fish and they remain until cooking destroys them. Thiamin deficiency causes inappetance and weight loss followed by neurologic signs (including seizures, ataxia, vestibular abnormalities, pupillary dilation, and ventroflexion of the head).

Thiamin Availability and Requirements

Normal dietary levels of thiamin are readily absorbed from the intestinal tract. Commercial pet foods may have inadequate amounts of thiamin to supply a dog's or cat's requirements, however. Thiamin deficiency occurred in a colony of cats fed a very-well formulated specialty diet for cats (one purportedly to be complete for cats). The deficiency appeared with thiamin levels that were 100 times the NRC recommendation. After feeding the food for seven months the cats developed signs of thiamin deficiency. Apparently, thiamin destruction by processing and during storage resulted in a thiamin-deficient diet. Currently the manufacturer adds ten times more thiamin than previously added. Thiamin levels will be questionable in processed and stored foods.

Thiamin is found in many natural foods such as whole cereal grains, brewer's yeast, lean pork, liver, kidney, and egg yolk. Cooking can reduce thiamin levels to between 50 and 75 percent of pre-cooked levels; the amount remaining still exceeds an animal's requirement. For example, the owner-prepared cottage cheese and cooked rice diets described in this website gives a dog four to five times the thiamin it needs. This is in contrast to commercial pet foods that have to add great excesses of the vitamin before cooking. Even then the food may be deficient in thiamin after cooking. Thiamin requirements for the growing and adult dog are 54 and 20 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the requirements are 200 and 100 micrograms per kilogram body weight per day, respectively. Meeting these requirements depends largely on how much dietary thiamin remains during a food's processing or preparation.

Riboflavin - Vitamin B2

Riboflavin Metabolism

Riboflavin is essential for dogs and cats. Deficiencies occur mainly in animals fed grain because grain is a poor source of riboflavin. Enzyme systems require riboflavin for energy production and use.

Riboflavin Deficiency

Deficiency of riboflavin causes many nonspecific clinical signs that do not correlate with the vitamin’s known biochemical roles. In dogs, conjunctivitis accompanied by a purulent or watery discharge can develop and progress to severe abnormalities of the cornea. Skin changes and muscular weakness can also appear. In cats, weight loss and loss of hair around the eyes is possible.

Riboflavin Availability and Requirements

Animal products such as milk, eggs, liver, kidney, heart and muscle meat are good sources of riboflavin. Riboflavin binds to tissue proteins that require digestion before intestinal absorption of the vitamin. Commercial pet foods are mostly based on cereals as the source of protein and energy, making them deficient in riboflavin. Most, but not all, commercial diets for dogs and cats contain added riboflavin which is inexpensive. The NRC recommendations for riboflavin in a dog's diet (1985) are marginal. Because riboflavin in natural foods is not completely available, a marginal level of riboflavin could result in deficiency. Riboflavin requirements for the growing and adult dog are 100 and 50 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the requirements are 160 and 100 micrograms per kilogram body weight per day, respectively. Meeting these requirements depends largely on how much dietary riboflavin remains after a food's processing or preparation.

Niacin - Nicotinic acid, Nicotinamide

Niacin - Nicotinic acid, Nicotinamide Metabolism

Niacin is a component of two very important enzymes needed for the metabolism of all major nutrients. Niacin is found in many foods and is readily absorbed from the intestinal tract. Dogs but not cats can also produce niacin from the amino acid tryptophan.

Niacin Deficiency

Deficiency of niacin played a historical role in the understanding of vitamin deficiency in both people and dogs. The basis of the deficiency was a diet of corn and salt pork for both. People developed the condition called pellagra and dogs black tongue. The requirements for niacin depend on either dietary niacin or tryptophan metabolism. Deficiencies of vitamin B2 and B6 reduce niacin conversion from tryptophan. Corn is deficient in niacin and much of it is in a bound form. Corn is also low in tryptophan, so when adequate calories are available from a corn diet there will be inadequate amounts of the vitamin or tryptophan, its precursor. Mexican Indians lived on a corn-based diet and did not develop niacin deficiencies because they pretreated corn with alkaline powders that converted the bound niacin to a free form. Niacin deficiency is unlikely in dogs and cats today.

Niacin Availability and Requirements

Manufacturers fortify many diets for dogs with synthetic niacin although they contain more than 20 percent crude protein on a dry matter basis. This level of protein would supply enough tryptophan to meet the niacin requirements if the protein was largely meat. The niacin is added because corn is the major ingredient and source of protein in most commercial dog foods. The cat in contrast to dogs is unable to convert tryptophan to niacin so it is necessary to add niacin in diets for cats. Meat, especially liver, is a good source of niacin. Half the vitamins in liver are available in their free form. Milk is not a good source of niacin but it is a good source of its precursor tryptophan. Grains are poor sources of niacin, much of which may be bound and unavailable. For usual diets with small quantities of tryptophan, 225 micrograms of niacin per kilogram of body weight satisfies the daily requirement for adult dogs and for the growing dog the amount is 450 micrograms. For dogs, 132 milligrams of tryptophan can produce one milligram of niacin. To satisfy the daily requirement, adult cats need 900 micrograms of niacin per kilogram of body weight and growing cats need 1600 micrograms per kilogram of body weight. Large amounts of niacin orally do not harm dogs.

Vitamin B6  Pyridoxine

Pyridoxine or vitamin B6 is essential for enzyme systems involved in amino acid metabolism. Deficiency results in a loss of appetite, growth retardation and anemia in dogs. In cats, deficiency causes growth retardation, anemia, skin disease, convulsions, and the urinary excretion of excess oxalate crystals. Most foods contain adequate pyridoxine. Good sources include yeast, cereals, wheat, corn and liver. Manufacturers add pyridoxine to many commercial dog and cat foods. The vitamin is stable to heat but is destroyed by sunlight. Excess amounts are not toxic. Pyridoxine requirements for the growing and adult dog are 60 and 22 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the requirements are 160 and 80 micrograms per kilogram body weight per day, respectively.

Pantothenic Acid

Pantothenic acid is found in many foods so naturally occurring deficiencies are unlikely. Signs of deficiency include loss of appetite, skin disease, diarrhea and some neurologic problems. Natural sources for the vitamin are yeast, egg yolk, kidney, beef, milk and whole grains. Manufacturers fortify many commercial dog and cat foods with calcium pantothenate even though deficiency is not likely. Excess pantothenate is not toxic. Pantothenic acid requirements for the growing and adult dog are 400 and 200 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the requirement is 200 micrograms per kilogram body weight per day.


Biotin is essential for biochemical reactions involving carbon dioxide and energy production. Deficiencies are rare but can appear after feeding large amounts of egg whites, which bind biotin and prevent its absorption from the intestine. Intestinal bacteria also produce biotin in amounts that are probably sufficient if the diet contains no biotin. Good dietary sources include yeast, egg yolk, kidney, liver, peanuts, and whole grain. The availability of biotin in wheat is poor but in corn it is readily available. Manufacturers fortify many cat and dog foods with biotin. Excess biotin causes no signs of toxicity. Biotin requirements for growing and adult dogs are unknown. For the growing and adult cat the requirements are 2.8 and 1.0 micrograms per kilogram body weight per day.

Ascorbic Acid (Vitamin C)

Vitamin C is important for many biochemical processes. Cats and dogs produce vitamin C in the liver and they produce enough so none is necessary in the diet. Cats and dogs have no general dietary requirement for vitamin C. It is possible that if these animals have liver disease to the extent that they do not produce enough vitamin C, a deficiency could develop. Commercial pet foods usually contain added vitamin C but their amounts may be insufficient if liver disease reduces vitamin C production. People take vitamin C supplements with the idea that they help many health problems. There is no evidence that excess vitamin C is helpful in managing any known disease. Vitamin C does have antioxidant properties, however, and it may be beneficial when given to animals with tissue damage from lipid oxidation. Very large doses are sometimes given without evidence of any harm.

Folic Acid

Folic acid and vitamin B12 together are essential for normal erythrocyte production. Folic acid is available in foods such as green leafy vegetables, lima beans, citrus fruits, and meats. Poor sources are yeast, milk, eggs, and many fruits. Folic acid content is unknown for most pet food ingredients. Diets do not need folic acid, however. Intestinal tract bacteria produce folic acid and provide adequate amounts. Folate in commercial pet foods can be destroyed by prolonged cooking, especially if the food is acid. Folic acid requirements for the growing and adult dog are 8 and 4 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the requirements are 32 and 20 micrograms per kilogram body weight per day, respectively.

Vitamin B12

Vitamin B12 deficiency produces the same type of anemia as folic acid deficiency. Deficiencies are rare, however. Diets containing milk and other animal products are good sources of vitamin B12. Plant sources contain little or no vitamin B12. Neither animals nor plants manufacture the vitamin, however. Bacteria produce all the vitamin B12 in the world. Animals with bacteria producing the vitamin in their intestinal tract, absorb and store the vitamin in their tissues. Thus meat in pet foods becomes a source of the vitamin. Enough vitamin B12 is stored in the body to supply an animal's needs for three years. Intestinal absorption of vitamin B12 is totally dependent on a protein, intrinsic factor. Gastric mucosa and the pancreas (in dogs) produce intrinsic factor. Intrinsic factor binds to vitamin B12 and is necessary for its absorption in the small intestine. Deficiency of intrinsic factor results in vitamin B12 deficiency and anemia develops. Such deficiencies are rare in dogs and cats. Deficiency of the vitamin is also possible with a large increase in small intestinal bacteria; bacteria consume the diet’s vitamin B12 and little is left to absorb. Disease of the ileum, where absorption of the vitamin takes place, also can cause a deficiency. Low dietary concentration of vitamin B12 sometimes causes deficiency. Vitamin B12 requirements for dogs and cats are unknown. Suggested requirements for the growing and adult dog are 1 and 0.5 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the suggested requirements are 0.8 and 0.4 micrograms per kilogram body weight per day, respectively. There is no confirmed toxicity associated with large amounts of the vitamin. Dogs and cats sometime receive injections of the vitamin to stimulate appetite and improve general well-being; such treatment has no proven efficacy.


Choline is a component of structural lipids in cell walls and choline is necessary for synthesis of acetylcholine. Choline can also be a precursor for the synthesis of methionine. All animals can produce choline from methionine in the liver. With limited dietary methionine, the liver is limited in the choline it produces. With excess methionine the diet needs to supply little choline. Choline deficiency causes the liver to store large amounts of fat. Fat accumulations cannot leave because choline is necessary for its transport from the liver. Choline is generally added to the diet because it is more efficient to add choline than excess methionine. Methionine is more expensive than choline and it is also more toxic. Excess choline can be toxic to dogs. Consumption of 5 grams of soybean lecithin (source of choline) per kilogram body weight per day causes anemia within two to three weeks. Choline requirements for the growing and adult dog are 50 and 25 micrograms per kilogram body weight per day, respectively. For the growing and adult cat the requirements are 96 and 40 micrograms per kilogram body weight per day, respectively.

Vitamin Requirements

 Vitamin recommendations for cats and dogs are based on caloric consumption. Each 1000 kilocalories of food should contain a certain level of each vitamin. The recommendations are more precise for growing animals than for adults. All of the diets in this website contain vitamins at levels based on the caloric content. It is not necessary to supplement any diet with vitamins unless the recipe states that a supplement is required. It is also possible to make vitamin recommendations based on an animal's body weight. Table 1 gives vitamin recommendations based on an animal's weight. Although a growing animal has greater requirements than an adult, the vitamin content based on amounts per 1000 kilocalories is almost the same for growing and adult animals. The growing animal receives more vitamins because it eats more per pound body weight.

Vitamin Requirements For Growing and Adult Cats and Dogs

(amounts per kilogram body weight per day)


 Growing Cat 

Adult Cat 

Growing Dog    

 Adult Dog


200 IU        

75 IU      

202 IU       

75 IU


20 IU         

8 IU       

22 IU        

8 IU


1.2 IU        

.5 IU      

1.2 IU        

.5 IU      


2 ug         

2 ug         

2 ug         

2 ug         


200 ug       

200 ug       

54 ug       

20 ug


160 ug       

160 ug       

100 ug       

50 ug


200 ug       

200 ug       

400 ug      

200 ug       


1600 ug      

1600 ug      

450 ug      

225 ug


160 ug       

160 ug       

60 ug       

22 ug

Folic acid    

32 ug        

32 ug        

8 ug        

4 ug


2.8 ug       

2.8 ug       




.8 ug        

.8 ug        

1 ug       

.5 ug


96 mg        

96 mg        

50 mg       

25 mg


Burger IH. A Basic Guide to Nutrient Requirements. in The Waltham Book of Companion Animal Nutrition. Ed. By I.H. Burger Oxford: Pergamon Press, 1993, pp5-24.

Earle KE, Smith PM: A balanced Diet for Dogs and The Waltham Book of Companion Animal Nutrition. Ed. By I.H. Burger Oxford: Pergamon Press, 1993, pp45-55.

Kienzle E, Hall DK: Inappropriate Feeding: The Importance of a Balanced Diet. in The Waltham Book of Clinical Nutrition of the Dog and Cat. Ed. J.M. Wills and K.W. Simpson. Oxford: Pergamon Press, 1994, pp1-14.