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Classification of Minerals

Mineral elements are required nutrients for all life. Higher animals require 21 minerals. Minerals are measured as ash and are grouped as major or macrominerals and minor or trace elements. The body needs trace elements in smaller amounts, in microgram quantities; it needs macrominerals in larger amounts, in gram quantities. The macrominerals can be separated into those that are abundant in body fluids and those that form bone minerals.

Macrominerals in Body Fluids

Body fluids consist of water and minerals known as electrolytes. Sodium is the primary macromineral electrolyte in extracellular body fluids. Sodium is primarily responsible for maintaining normal levels of extracellular fluid volume. Potassium, the primary intracellular mineral is at a low extracellular concentration. The difference in extracellular and intracellular concentrations is important for normal functioning of nerves, muscles, and secretory cells.

Total body water, sodium, and potassium must be regulated to maintain normal physiology. Mechanisms for monitoring blood pressure, body fluid volume, and concentrations of sodium and potassium regulate the amounts of water, sodium, and potassium in the body. The mechanisms release hormones such as angiotensin, aldosterone, and antidiuretic hormone to maintain the normal state. Most pet foods provide appropriate levels of sodium, potassium and chloride. Dogs or cats with heart or kidney disease may require diets with reduced amounts of sodium. Some medical problems require regulation of dietary potassium.

Macrominerals in Bone

Minerals are concentrated in bone as calcium and phosphorus. Bone minerals are from 12 to 24 percent of bone on a moist basis, or 55 to 75 percent of dry matter. The daily dietary requirement of calcium depends on its losses in urine and feces, the amount needed by bone, and the completeness of its absorption in the intestine. The latter, sometimes called bioavailability, is determined by many dietary factors, such as vitamin D, fat, protein, lactose, fiber, phytic acid, and acidity or alkalinity. The intestinal absorption of phosphorus depends on concurrent absorption of calcium and therefore indirectly, by all of the above factors. The body poorly absorbs phosphorus as phytic acid (inositol hexaphosphate) and that reduces the absorption of calcium, iron, and other bivalent cations such as zinc. These multiple interactions make it difficult to calculate optimal calcium and phosphorus contents for any diet. Pet owners must depend on manufacturers for making such decisions. If the content of bone minerals is adequate in a commercial pet food further supplementation with calcium, phosphorus, or vitamin D shifts these nutrients out of their optimal ranges. Chronic calcium deficiency induces rickets or osteoporosis. Excessive dietary calcium can cause pathologic changes that depend on other dietary nutrients. An excess can induce bone pathology if dietary copper is low or marginal, apparently by impairing copper absorption. It may also induce osteopetrosis if vitamin D is overabundant.

Trace Elements Or Minerals

Trace elements are nutrients needed in very small amounts. Trace elements are essential when they serve in a specific biochemical function. These functions usually arise from the association of the element with a particular protein. The element can be part of an enzyme (selenium in glutathione peroxidase), a co-enzyme (copper in cytochrome oxidase), a carrier (iron in hemoglobin), a hormone (iodine in thyroxine) or a vitamin (cobalt in vitamin B12). The list of trace elements essential in dogs and cats includes iodine, iron, copper, cobalt, zinc, manganese, molybdenum, fluorine, and chromium. Bioavailability of a trace element depends on many dietary factors. They include many interactions between dietary ingredients that reduce absorption, such as inhibition of copper and zinc absorption by calcium. Also, the body absorbs some forms of copper salts poorly while others it absorbs well. For these reasons, pet foods must be formulated to contain optimal ranges and types of essential trace elements. Further supplementation of commercial pet foods with trace elements is likely to change their concentrations to above optimal levels, perhaps into hazardous ranges.

Causes of Mineral Malnutrition

Deficiency of minerals and elements is possible with human beings preparing pet foods. In the wild carnivores such as dogs and cats rarely develop mineral deficiencies when they consume animal tissues, unless they consume meat containing little or no bone. Then they develop nutritional secondary hyperparathyroidism. These animals living in their natural state also do not develop mineral or trace element excesses. Many factors contribute to mineral malnutrition in animals eating pet foods. The factors are:

Dietary and gastrointestinal

A. Concentration of an essential mineral in the diet is too low to supply the body's needs.

B. Absorption of the mineral from the digestive tract is reduced.

1. Transit time for nutrients passing through the intestine is shortened as with diarrhea; contents pass through the intestine before adequate amounts can be absorbed.         

2. Bioavailability of a mineral in the diet is low. This may be because of its chemical form (e.g., iron present as iron phosphate that is poorly absorbed). Substances in the diet can interact with minerals to reduce bioavailability (e.g., phytic acid and phosphorus). Minerals can compete with others for absorption and reduce bioavailability. For example, zinc and copper compete for absorption and high concentrations of one reduce absorption of the other.

3. Dietary levels of factors that control mineral absorption may be inappropriate (e.g., vitamin D on calcium absorption).

4. Secretions into the digestive tract containing the mineral are not reabsorbed (e.g., vomiting resulting in chloride and potassium losses and diarrhea resulting in sodium and potassium losses.)


A. Urinary loss of a mineral often increases in an animal with kidney disease and can lead to a deficiency.

B. Kidney disease can reduce the excretion of minerals such as phosphorus; its retention results in renal hyperparathyroidism.

Metabolic Changes Reducing the Body's Mineral Concentration

A. Growth causes the pool size to expand for a mineral where its intake does not increase.

B  Loss to needs of fetus and fetal membranes and fluids can reduce concentration of minerals in the body pool.

C. Lactation results in mineral loss in the milk and concentrations can fall in the body pool.

Minerals and Bone Metabolism

Calcium, Phosphorus, Vitamin D and the Skeleton

Most of the body’s calcium and phosphorus is in bone which contains 99 percent of total body calcium and 85 percent of total body phosphorus. Dietary requirements for calcium and phosphorus are much greater than for any other minerals and are greatest during periods of skeletal growth and lowest at most other times. During skeletal growth, inappropriate calcium and phosphorus intake is more likely to cause clinical disease due to skeletal abnormalities. Inadequate intake in mature animals results in no or slow development of abnormalities because of the large calcium and phosphorus deposits in bone. Although calcium is essential for normal bone structure and function, its concentration in bone is not as critical as its concentration in extracellular fluids. Calcium concentration remains constant in body fluids (about 10 mg calcium/100 milliliters of blood plasma). Calcium deficiency results in its mobilization from bone to maintain blood levels. This constancy is necessary for maintaining important functions such as those of nerves, muscles, and blood clotting. These functions remain normal though there may be a deficiency of total calcium in the body.

All-Meat Diets Are Low-Calcium

 All-meat diets provide moderate amounts of phosphorus but very low amounts of calcium. Feeding an all-meat diet eventually results in nutritional secondary hyperparathyroidism. In the wild, carnivores consume not only visceral organs and skeletal muscle, but bones, particularly soft bones that provide adequate calcium. Frequently pet owners feed boneless meat products intended for human consumption. Because organ and skeletal tissue meats are low in calcium, feeding these foods without an adequate source of calcium causes bone to demineralize.

Calcium and phosphorus content of meats

  mg/ 100grams meat


   Organ/tissue      Calcium   Phosphorus 

    Liver (beef)             7        358      

    Heart                     9        203       

    Chuck                   11        117       

    Beef, ground          10        137

    Lamb, leg                9        177

    Chicken, breast       14        210

    Fish                      10        170

    Mackeral, canned    458       572

The calcium content of liver is 75 milligrams (mg) and its phosphorus content is 3800 mg per 1000 kcal of metabolizable energy. The NRC for dogs indicates a calcium requirement of 1600 mg and a phosphorus requirement of 1200 mg per 1000 kcal of metabolizable energy. Calculation shows the ratio of calcium to phosphorus in liver to be 1:50, whereas the NRC recommended ratio is 1.3:1. The very abnormal ratios of other meats are evident in this table. In the past some pet foods were marketed as all-meat diets to promote their sales to pet owners. The low calcium content of these diets resulted in animals developing nutritional secondary hyperparathyroidism. Since then all major commercial diets contain added minerals, making it possible for an all-meat diet to be complete.

Vitamin D and Bone Metabolism

Vitamin D is importantly involved in calcium metabolism and balance. The diet is the primary source of vitamin D which is absorbed with dietary fats.  Vitamin D in animal sources of food is cholecalciferol or vitamin D3. Its form in plant sources of food is ergosterol (vitamin D2 precursor) or ergocalciferol (vitamin D2). Vitamin D3 is also made in the skin where ultraviolet light converts a form of cholesterol to vitamin D3 (Insufficient amounts are produced in the skin of dogs so they need vitamin D3 or D2). Deficiencies of vitamin D can occur when dietary levels are inadequate or when small intestinal disease reduces absorption of dietary vitamin D. Vitamin D must be in the form of D3 or D2 to be effective in regulating calcium balance. Vitamin D, from the diet or epidermis, is transported to the liver where its forms are hydroxylated to cholecalciferol, 25-OH vitamin D3, and ergocalciferol, 25-OH vitamin D2. These compounds are hydroxylated again in renal tubular cells to either 1,25 OH2 vitamin D (calcitriol) or 1,25 OH2 vitamin D2, the final biologically active forms of vitamin D. Calcitriol is the most important form of vitamin D. Its synthesis is well regulated and is increased by parathyroid hormone, hypocalcemia, phosphorus deficiency, increased calcium needs, calcitonin and active growth. Calcitriol acts on the absorptive cells of the intestinal mucosa to stimulate the absorption of calcium and phosphorus. (Vitamin D can be toxic in that excessive amounts can promote excess calcium absorption and cause hypercalcemia.) Calcitriol also stimulates renal reabsorption of calcium and phosphorus and interacts with parathyroid hormone to promote decalcification of bone.

Parathyroid Hormone and Bone Metabolism

 Parathyroid hormone is released by reduced blood calcium levels. Such a reduction can result from feeding low calcium all-meat diets. Parathyroid hormone promotes calcitriol production which stimulates decalcification of bone. Parathyroid hormone also acts on bone to release calcium. The result of increased parathyroid hormone and calcitriol activities is maintenance of blood calcium levels but excess phosphorus release from bone increases its blood levels. Excess phosphorus is excreted renally. The loss of calcium and phosphorus from bones results in rickets and osteopenia.

Rickets and Osteopenia

 Rickets is a disease of young growing animals and and is manifested by defective calcification of growing bone. Its primary lesion is failure of calcification with persistence of hypertrophic cartilage and enlargement of the epiphyses. Poorly mineralized bone easily deforms under pressure, causing the classic signs of rickets. Rickets may be due to a deficiency of dietary calcium or phosphorus (rare in dogs and cats), or inadequate vitamin D, or a combined deficiency of these nutrients. In all cases the bone abnormalities are the same. Rickets causes stiffness of gait, lameness, and a reluctance to stand. Besides the bone enlargements, especially the increase in joint areas, enlargements are found in the ribs about half way down on the chest wall. Eruption of teeth is late and irregular, and teeth wear unevenly and are often maligned. Radiographs of long bones confirm rickets. Osteopenia is a disease of mature animals affecting bones in which growth and mineralization is complete. The characteristic sign of osteopenia is excessive noncalcified matrix. Demineralization allows bones to deform when bearing normal amounts of weight. Osteopenia occurs under the same conditions as rickets and is biochemically identical with rickets. The predisposing cause is not the increased requirement of calcium and phosphorus for growth, however. The cause is a deficiency that is sometimes added to increased mineral needs for pregnancy and lactation. Osteopenia causes animals to show similar signs as rickets, painful bones and joints, and when more severe, bone deformation and fracture. Rickets and osteopenia are treated with calcitriol injections and by feeding diets with adequate calcium, phosphorus and vitamin D. Phosphorus deficiency is unlikely in dogs or cats. Meat and cereals contain sufficient phosphorus. High levels of calcium added to a diet (such as by using calcium carbonate, ground limestone, calcium gluconate) reduce phosphorus availability, however. Aluminum antacids also lower phosphorus availability.


 Some causes of hypercalcemia are dietary. Diets high in active forms of vitamin D increase blood calcium. Other causes not related to feeding include hypercalcemia due to severe kidney disease, tumors such as lymphoma, and parathyroid gland tumors secreting excess parathyroid hormone.

Dietary Sources of Calcium and Phosphorus

Plant Sources

 All cereal grains are poor dietary sources of calcium but moderate to good sources of phosphorus (Table below).  Phosphorus in plant sources is less available than in animal sources. Much of the phosphorus in plants is chemically bound in forms such as phytate phosphorus, which dogs and cats do not digest well.

Calcium and Phosphorus Content of Cereals


Calcium %


   Ratio: Ca to P  













Animal Sources

Commercial pet foods provide most calcium and phosphorus as bone meal. Mineral matter in bone is largely calcium phosphate with the remainder being 13 percent calcium carbonate and 2 percent magnesium phosphate. Bone should contain the ideal ratio of calcium to phosphorus for any diet. As a dietary source the composition of bone is about 10 percent deficient in calcium, however. As stated earlier, the dietary ratio of calcium to phosphorus should be about 1.3:1. Instead of using a ratio, it is more important to consider the amount of calcium or phosphorus an animal requires. If animals receive this requirement, the ratio of calcium to phosphorus is less important. When the ratio is the problem, there usually has been inadequate amounts of calcium or phosphorus in the diet. Acceptable ratios range from 2:1 to 1:2 when animals receive adequate amounts of both minerals. As the diet approaches the least value for either mineral the ratio becomes more important. This is because large amounts of the mineral in excess suppress absorption of the mineral present at a minimum level.

 Minerals Associated with Body Fluid Balance

Sodium, Potassium and Chloride


Sodium is the primary mineral determining the body's water content. Excess body sodium is the cause of water retention with ascites or edema due to circulatory diseases. Sodium deficiency leads to signs of dehydration and hypovolemia. Deficiencies appear with diarrhea or vomiting where the lost fluids are not replaced. Plants require very little sodium, therefore, feeds derived from plants are very low in sodium. Carnivores consuming animal tissues are unlikely to develop sodium deficiency because of the high level of sodium in all animal products. Animals can develop a sodium deficiency because of 1) inadequate levels in the diet, 2) excess loss of sodium-containing secretions from the body such as with vomiting and diarrhea, and 3) increased loss in urine. A deficiency of sodium intake is possible if a pet eats a strictly vegetarian diet. Some diets for management of congestive heart failure are low sodium. Such diets are formulated with high levels of cereal and low-sodium protein foods. The minimum sodium requirement for dogs and cats is not very precise. The NRC minimum for dogs is 150mg for each 1000 kcal of food consumed. Thus, a 35 to 36 pound dog consuming 1000 kcal per day should receive at least 150mg sodium. Commercial pet foods contain 1 percent sodium so this 35‑pound dog will receive 1500mg sodium or ten times the minimum requirement. Excess sodium does not adversely affect a dog unless it has a medical problem causing fluid retention. The minimum recommendation is unknown for cats. The NRC recommends a minimum intake of 100mg for each 1000 kcal of food consumed.

Sodium Content of Foods

mg/100 grams food

Foods from plants

mg sodium

Foods from animals

mg sodium

Barley (pearled)


Beef hamburger


Rice (white)


Beef chuck




Chicken lt meat




Chicken dk meat




Cottage cheese


Baked breads


Egg yolk


Potatoes (sweet)




Corn flakes


Beef kidney




Beef liver




Beef heart




Bacon and ham


Soybean (tofu)




Corn meal


Cheese (proc)


Potatoes (White)


Canned beef stew


It is evident that processed foods are generally very high in sodium, especially snack type foods.


Potassium is the most abundant intracellular electrolyte. Those levels are thirty times higher than extracellular concentrations. Loss of intracellular potassium affects all physiologic functions. Loss of extracellular potassium is often identified on measuring plasma electrolytes. With that loss it is predictable that there is also loss of intracellular potassium. The body cannot conserve potassium as well as sodium. With vomiting or diarrhea potassium is lost at an excessive rate, more so than for sodium. Considerable potassium can also be lost with some kidney problems. Depletion of body potassium is unlikely in normal animals because the diet usually contains excess amounts of potassium. Plants have a high nutritional requirement for potassium so most foods made from plant products contain abundant amounts of potassium. By feeding plant products, deficiency of potassium is unlikely to occur. Grains contain less potassium compared to the vegetative parts of plants. The potassium requirement of animals depends on acid-base balance of the diet. High-protein diets promoting an acid state appear to increase the potassium requirement. The kidneys excrete more potassium with a high-protein diet, making it necessary to increase potassium intake.    The potassium requirement for dogs is about 0.5 percent in the diet; this is about 1200mg for each 1000 kcal of food consumed, a need that is 12 times that for sodium. The minimum requirement for cats is 800mg for each 1000 kcal of food consumed. The growing dog and cat need more; the requirement for growth is about three times the requirement for adult maintenance.


 Most plant materials provide adequate amounts of chloride. Most animal sources of food contain chlorides that reflect sodium levels. Chloride deficiency is rare in normal animals. Disease can cause excessive chloride loss, however. Vomiting results in chloride loss and alkalosis can develop. Diarrhea and some kidney diseases also result in excessive chloride loss.


Magnesium is the body's fourth most abundant cation, with the vast majority stored in bone. Bone magnesium is not available for short term maintenance of plasma magnesium concentration. This balance is maintained by limiting intestinal absorption of magnesium and by increasing renal excretion of any excess. Magnesium is necessary for normal activity of 300 enzyme reactions. Magnesium deficiency is rare in dogs and cats. Magnesium is adequate in most pet foods formulated primarily with muscle, bone and organ tissues. Bone supplements are useful sources of calcium and phosphorus but feeding high levels of bone provides too much magnesium. Some special diets marketed for management of urinary tract stone disease contain low levels of magnesium. Low levels are inadequate for satisfactory reproduction in a female cat, however. Magnesium from plant material is less available than that from animal tissue. A low magnesium diet based on most of its magnesium coming from plant sources can be deficient.

Magnesium and Disease

Magnesium may be important for urinary tract stone development in cats. Magnesium is a component of struvite stones. To reduce the risk of stones developing, cat foods are formulated to contain less than 0.2 percent magnesium. The role of magnesium in causing stone formation is unimportant compared to the role of acid urine pH in preventing stone formation, however. Reducing magnesium levels without correcting the diet's ability to produce acid urine will have little effect on reducing struvite stone formation. Magnesium importantly increases calcium excretion so calcium stone formation is less likely. Feeding low-magnesium diets may reduce struvite stone formation but increases the incidence of calcium stones.

Magnesium Requirements

The minimal magnesium requirement for growth of kittens is 0.04 percent of the diet (400 mg/kg dry diet, about 80 mg per 1000 kcal consumed). At intakes of 50 and 100 mg magnesium/kg diet, growth rate of kittens decreases and at the lower level kittens show muscular weakness, hyperirritability, convulsions and loss of appetite. Adult cats appear to do well on 160 to 200 mg per kilogram of diet. The magnesium requirement of growing dogs is about 400 mg magnesium/kg diet dry matter (about 125 mg per 1000 kcal consumed or about 10 mg per pound of body weight per day). In Dogs the aorta can calcify with diets containing much less magnesium, 30 and 100 mg magnesium/kg diet. Inadequate magnesium is available to promote renal excretion of calcium. The requirement for adult dogs is about one-third of that for growing dogs. Increased dietary calcium and phosphorus increase the requirement for magnesium.

Trace Minerals


Physiological Functions

Copper is a component of many enzymes and cell structures. Most copper is stored in the liver. Copper is necessary for normal immune defenses, skeletal development, skin pigmentation, structure and function of the central nervous system, and iron metabolism. Because most copper is stored in the liver copper deficiency is rare in cats and dogs, even animals eating foods that are not commercially prepared. There is no easy method for assessing the status of copper in a pet.

Absorption and Storage of Copper

The form of dietary copper determines its absorption or availability. Copper in cupric oxide is poorly absorbed but in cuprous oxide is nearly completely absorbed. Commercial pet foods usually contain poorly absorbed forms. Copper deficiency is rare, however. Normal dogs weighing 35 pounds ingest and absorb one milligram copper per day. Normal adult humans also ingest and absorb about one milligram per day. Why does the much smaller dog ingest so much more copper than larger people? It is probable that commercial dog foods contain excess copper, amounts that greatly exceed needs. The NRC states dogs’ minimum requirement for copper to be 0.8 mg copper per 1000 kcal consumed. Commercial dog foods contain levels that range from 5 to 10 mg per kilogram of food (1 to 2 mg per 1000 kcal food consumed; or 0.03 mg per pound body weight for adults and 0.08 mg per pound body weight for growing dogs). Normally excess for any trace element hedges against deficiency developing. Here, excess copper could cause problems. As stated above, the body efficiently absorbs readily available forms of copper. After its absorption copper moves to the liver for storage. To prevent an excess and its toxic consequences, the liver excretes copper from the body, but only effectively through bile (80 percent appears in bile). The body conserves copper when it is deficient but the body does not have an efficient means for disposing of excess copper. Liver has the highest concentration of copper in the body. Copper is ten times higher in dog liver than in human liver. That is not necessarily a species difference. More than likely the difference reflects the amount of copper consumed, being much greater in the dog. Before dogs ate commercial pet food, the content of copper in their liver was much lower than it is today. The liver concentration of copper increased during the last 60 years from less than 10 micrograms copper per gram dry weight of liver to over 200 today. That twenty fold increase results from a dietary level of copper in commercial pet foods that is much higher than needed. When a dog consumes commercial pet food it can become copper loaded.

Copper Toxicosis (Poisoning)

Copper levels in pet food are important because copper can be toxic and cause both acute and chronic liver disease. Chronic toxicity is frequent in dogs. Liver disease causes reduced excretion of copper in bile, and liver copper levels increase. Greater copper levels damage the liver further and worsen its ability to excrete copper. Not too many years ago veterinarians believed liver disease was uncommon or rare in dogs. The low incidence of liver disease was at a time that owner-prepared foods, not commercial pet foods, were most commonly fed. It is likely that the increasing liver copper concentrations act with other insults to damage the liver and cause liver disease to be more common today. Pet foods continue to contain too much copper. In addition copper is added in forms where the amount absorbed is difficult to predict. Manufacturers may be adding excess copper to avoid any risk of deficiency, a rare problem in pets.


Zinc is necessary for nucleic acid and protein metabolism. Deficiencies are rare and excess zinc seldom causes problems. The absorption of zinc interacts with that of dietary copper and calcium. Increased dietary copper and calcium reduce the absorption and availability of zinc. Sometimes zinc is given to reduce abnormally high liver levels of copper.


Manganese is necessary for normal function of many enzymes. Deficiencies of manganese are unknown for the dog and cat.


Iodine is essential because of its incorporation into thyroid hormone. Dogs and cats develop conditions of thyroid hormone excess and deficiency but none involve abnormalities in dietary intake of iodine. Feline hyperthyroidism causes thyrotoxicosis and is usually seen in cats over six years of age. This is a new disease in that it was unknown before 1975. There is evidence to suggest that the problem relates to cats being fed commercial canned cat foods more frequently now than in the past. A number of iodine-containing compounds such as the dye erythrocin is added to color cat foods. The iodine in this dye is not available, however.


Physiological Functions

Iron is essential for normal erythrocyte production. These cells contain two-thirds of the body's iron. Almost all of the remainder is stored or in tissue proteins. Total body iron amounts to no more than two grams. All iron is in metalloproteins which include hemoglobin, myoglobin, and cytochromes that are all concerned with oxygen transport and energy functions.

Storage to Prevent Iron Toxicity

The body efficiently salvages and reuses iron. Small losses occur in the shedding of intestinal mucosal and epidermal cells, and in trace amounts of blood lost from the digestive tract. With saturation of  body iron stores, adult animals are resistant to iron deficiency causing anemia for long periods of time, whatever the amount of iron in the diet. Iron is the only metabolite for which there is no mechanism for regulating its excretion from the body. So iron can accumulate in the body. Excess iron is toxic and the body prevents toxicity by having many iron-proteins to protect tissues against toxicity of free iron. Primary protective iron storage proteins are ferritin and hemosiderin. Ferritin is the major storage protein under normal conditions. It is produced by reticuloendothelial cells in liver, spleen, and bone marrow. These tissues store most of the iron in the body. When the body accumulates toxic levels of iron and have used all the protective proteins, excess iron can be reduced only by bleeding.

Regulation of Dietary Iron Absorption

Diets contain two forms of iron, a ferrous form and a ferric form. The ferrous form is absorbed very well; but not the ferric form. Iron in heme is also easily absorbed. Iron absorption is complicated. Acidity of digestive tract contents, the form iron is available, and interactions of iron with other substances in the digestive tract determine its absorption. Acid conditions increase the availability of iron for absorption. Anything that reduces the acidity of the stomach contents can reduce iron absorption. Nutrients such as amino acids, sugars and vitamin C promote iron absorption. Iron bound to phytate or phosphate and iron in some foods are mostly unavailable. Dietary sources with a readily available high iron content include red meats, fish, and soy. Dietary sources with a high iron content that is mostly unavailable are leafy vegetables, eggs, and liver. Egg protein depresses heme iron absorption and heme iron from red meat enhances absorption for other forms of dietary iron. The body regulates iron absorption very well; without such regulation the body would soon accumulate toxic levels of iron. The amount of iron in the body controls how much iron it absorbs. When iron stores are full, iron absorption from the intestine is minimal. Normally the intestine does not absorb more than 15 percent of the iron in the diet.

Requirements for Iron

 Growing animals have the greatest need for iron. This is more acute during the nursing stage since milk has little iron. Moreover, body reserves of iron at birth are also low. Some manufacturers produce orally administered iron supplements for newborn animals. Unfortunately, some of these result in the absorption of toxic amounts of iron. Iron deficiency anemia is seldom a problem in very young dogs and cats unless there has been blood loss. An example of this occurs in young animals infested with hookworms which cause intestinal blood loss. Microcytic hypochromic anemia is caused by the resulting iron deficiency. This anemia is uncommon in dogs and cats and when seen is usually the result of chronic blood loss causing iron depletion. Manufacturers fortify pet foods with different forms of iron. The availability of iron is greatest for ferrous salts and iron from the ferric salts are either unavailable (ferric oxide) or poorly available. Thus, it is not possible to evaluate iron availability for diets supplemented with ferric salts.

Miscellaneous Trace Minerals

Nutritionists recently discovered that many other minerals are essential. They include chromium, fluorine, tin, silicon, nickel, and vanadium. Currently, they have no known importance in being involved in diseases caused by deficiency or excess in the dog and cat.

 Mineral Requirements

Mineral recommendations for cats and dogs are based on the number of calories consumed. Each 1000 kilocalories of pet food should contain a certain level of each mineral. The recommendations are more precise for growing animals than for adults. All of the diets in this website contain minerals at levels based on the caloric content. None of these diets need to be supplemented with minerals unless the recipe states that a supplement is required. It is also possible to make mineral recommendations based on an animal's body weight. Table 4 gives mineral recommendations on an animal's weight. It is apparent that a growing animal has greater requirements than an adult. The mineral content based on amounts per 1000 kilocalories is almost the same for growing and adult animals. The growing animal gets more minerals because it eats more per pound body weight.

Mineral Requirements For Growing and Adult Cats and Dogs

(minimum amounts per kilogram body weight per day)


Growing Cat    

Adult Cat 

Growing Dog

Adult Dog


   400 mg  

    128 mg

    320 mg 

    119 mg


   300 mg  

     96 mg

    240 mg 

     89 mg


    25 mg  

      8 mg

     30 mg 

     11 mg


   200 mg  

     64 mg

    240 mg 

     89 mg


    95 mg  

     30 mg

     46 mg 

     17 mg


    20 mg  

    6.4 mg

     22 mg 

      8 mg


     4 mg  

   1.28 mg

   1.74 mg 

   0.65 mg


  0.25 mg  

   0.08 mg

   0.16 mg 

   0.06 mg


  0.25 mg  

   0.08 mg

   0.28 mg 

   0.10 mg


   2.5 mg  

    0.8 mg

   1.94 mg 

   0.72 mg


  .017 mg  

   .006 mg

  0.032 mg 

  0.012 mg


5 ug  

1.6 ug

6 ug 

2.2 ug


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.

Hazewinkel HAW: Dietary Influences on Calcium Homeostasis and the Skeleton. in Proc. Purina International Nutrition Symposium at Eastern States Veterinary Conference, 1991, pp51-59.

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.