Vitamins & Minerals: All Micronutrients

Bryan G. Miller

Every dog food has vitamins and minerals added to make it just right for proper dog nutrition. The technical term for most of the nutrients which the body requires in small amounts is “micronutrients.” These nutrients are required in the correct amounts and balance to maintain good health and vitality.

Because of the information which labels are required to show, many of us check out the amounts of protein, fat, fiber, and the macro-minerals calcium and phosphorus in the dog food we buy.

Many pet owners are well educated as to requirements and the best sources of these important nutrients. It is certainly a positive sign that many consumers are now carefully reading labels to compare these important nutrients when making buying decisions.

Unfortunately, most of us know much less when it comes to the sources and amounts of the micronutrients. Vitamins and minerals are also required for good health, and like protein and fat sources, there are better and worse sources of vitamins and minerals.

It’s nearly impossible to evaluate every vitamin and mineral in a dog food. However, it helps to know how to separate nutrition from “sales-hype.” The following are only some of the most commonly confused items.


Vitamins are small organic molecules that are required as “cofactors” in many metabolic reactions. They are generally characterized as either fat-soluble or water-soluble. The fat-soluble vitamins are A, D, and E; the water-soluble vitamins are the B vitamins. Vitamins are a relatively inexpensive part of the diet and most companies will provide a vitamin level in excess of AAFCO recommendations.

Fat-Soluble Vitamins

Today’s commercial sources of Vitamins A, D, and E are much more stable than forms from years past. That means your dog is more likely now to get all the vitamins he needs from his food.

Performance category dog foods, are high in fat to give high-performance dogs more energy. Likewise, these foods should contain greater amounts of the fat-soluble vitamins than similar foods of lower fat content. In addition, more Vitamin E may be used to compensate for the greater need of fat metabolism. This is especially true if the food contains fat which is high in polyunsaturates.

Vitamin A. Vitamin A is usually found as Retinyl Acetate. Most commercial sources are “packaged” in small gelatin beadlets which help extend shelf life by avoiding oxidation. Quite often, Vitamin A is combined with Vitamin D in these gelatin beadlets.When the food is made, the beadlets are mixed in.

Vitamin D. Vitamin D is added to food in the form of either Vitamin D3, Cholecalciferol, or Vitamin D2, Ergocalciferol. Both forms appear to be equally well-absorbed and active. Current Vitamin D products are quite stable.

Vitamin E. Alpha-tocopherol is the most biologically active form of Vitamin E. It’s available from natural sources or synthetic.

The all-natural sources have more activity per gram of Vitamin E; however, the synthetic forms may be more active. Vitamin E is a relatively expensive vitamin and it may be worth asking for activity levels when talking to manufacturers’ representatives. (New evidence points to a greater importance of Vitamin E in proper immune system function. Because of its high cost, most manufacturers don’t “overload” Vitamin E. Generally speaking, more E is better.)

More and more companies have been using tocopherols as additives to help prevent oxidation (rancidity) of fats in dog food. These tocopherols don’t add significantly to the Vitamin E content available for use by your dog’s body.

Water-Soluble Vitamins

Water-soluble B vitamins are generally susceptible to degradation, particularly in foods with high mineral and water content. This is one of the reasons you should select fresh bags of dog food as opposed to old inventory. Shop where the product has not been in storage for many months, and check the production code to determine when the food was made.

Although there are many B vitamins, you should consider the following three when selecting foods.

Thiamin. Thiamin is important for energy metabolism. Commercially, it is available as either Thiamin mononitrate or Thiamin hydrochloride. Both forms are active; however, thiamin mononitrate has a much greater shelf life.

Vitamin C. Vitamin C, ascorbic acid, has not been proven to be a necessary supplement for dogs. (Dogs make their own.) The addition of Vitamin C at this point may be more from a marketing point of view than a nutritional one. However, if you do want a food with Vitamin C, look for one containing ascorbyl polyphosphate.

Vitamin C is extremely easily oxidized (which is its biological function, as well), and does not survive processing well. Within two months of processing, most of the “normal” Vitamin C will have naturally decayed away. The new polyphosphate forms are stable, and biologically active, but they are expensive.

Choline. Choline is required and important for the proper utilization of the sulfur-containing amino acids. Current recommendations are for 25 mg per kilogram of body weight in adults and 50 mg per kilogram of body weight for puppies. Choline should not be fed in great excess as it greatly increases the breakdown of the other vitamins.

Trace Minerals

Like vitamins, trace minerals are important cofactors in order for many enzymes to function. Trace minerals include copper, iron, zinc, manganese, iodine and selenium. Trace mineral nutrition is difficult to study due to the many interactions between trace minerals and other components of the diet and the many interactions between the trace minerals themselves.

Trace mineral nutrition is often blamed for poor coat appearance and color. Trace minerals can have an effect upon coat quality, as can a great many other nutrients in the diet.

Measuring trace mineral content of hair, blood, and plasma samples does not always provide an accurate appraisal of trace mineral nutrition. If you truly believe your dog has a mineral imbalance, have a liver biopsy done. It’s the best measure of current mineral status.

Trace minerals are available from inorganic sources such as oxides, carbonates and sulfates. Availability can vary with the source of the mineral. Generally speaking, sulfates are more available than carbonates, which are more available than oxides. Iron oxide has no biological activity but is sometimes added as a coloring agent. The major exception is zinc oxide, which is the most common form of supplemented zinc.

Be wary of any dog food that claims to have much greater concentrations of any one mineral. Because of the way in which trace minerals are absorbed and stored, an excess of one trace mineral may lead to either a deficiency or toxicity of other amino acids.

Some breeds have different mineral requirements, the most notable being Bedlington Terriers, which are susceptible to copper toxicity.

Many of the trace minerals are now also available attached to organic com-pounds in the form of chelates and proteinates. Trace minerals are often absorbed in connection with amino acid absorption. Most of the chelated products involve the attachment of the trace mineral to either an amino acid or a small protein molecule, although there are also polysaccharide complex products marketed as well.

Improved availability in the form of chelates and proteinates has not been conclusively proven. However, they probably help to reduce vitamin oxidation by preventing the interactions between vitamins and the trace minerals. Chelates (zinc-methionine, for example) are much more expensive than their inorganic counterparts.

If a manufacturer is using chelated minerals, be sure that they are supplied at a level of mineral (grams of mineral) equal to the requirement as established in research using inorganic forms. Improved bioavailability has not been conclusively proven to the extent that it should be considered when balancing a diet.

Bryan Miller has worked for companies which supply vitamins and minerals to pet food manufacturers. He has also developed formulations for several dog foods. 

Calcium and Phosphorus

Over 70% of the mineral content of the body is calcium and phosphorus. They play a vital role in everything from bones to the heart, from DNA to muscles.

These two minerals provide the body with the material necessary for making bones. While bones support the body, they also store calcium and phosphorus for use in times of need – when the supply of either mineral is too low to meet the dog’s requirement. This depositing and withdrawing occurs throughout the dog’s life. Puppies are an exception, as they have a limited amount of calcium at birth and do not have the same storage reserves as an older dog.

These two minerals are also critical to muscle tissue and body fluids. If the blood calcium level drops due to hormonal changes, the dog will have muscle spasms. Calcium can be mobilized from the bones, but not quickly enough to prevent the spasms.

Proper calcium levels are also essential for the clotting of blood and controlling the muscle and nerve impulses. If there is a severe decrease in the availability of calcium in the blood, clotting will not take place. High levels of calcium and iron can cause a decrease in muscle and nerve excitability.

Calcium in the bloodstream also regulates the heart rate. More calcium causes a faster heartbeat and vice versa. If there is a severe decrease in blood calcium immediately after a female has given birth, she may develop “milk fever.” The heart rate slows, the female loses control of her legs and has muscle spasms. If unchecked, the dog could go into a coma and die. A bowl of milk will usually get her back on her feet, but check with your veterinarian.

Growing dogs need calcium and phosphorus – and so do lactating females. A female dog can’t produce a normal supply of milk if she doesn’t have enough calcium. If the supply is extremely low, she will stop producing milk altogether.

As for phosphorus, one of its critical roles is as a phospholipid, a component of cell membranes. Phosphorus is also an important constituent of all nucleotides – the molecules which participate in nearly all biochemical processes. They are precursors of DNA and RNA – the substances in which genetic information is contained and transferred. In the form of phosphate, phosphorus is also an important component of several enzymes.

Calcium and phosphorus are major minerals – animals have relatively large requirements for them. Other major minerals are salt (sodium and chlorine), magnesium, potassium and sulfur.

Calcium and phosphorus are dis-cussed together because they work together in the body. They are also closely associated with each other in metabolism, and an in-adequate supply of either in the diet limits the nutritive value of both.

How The Body Uses Calcium

Calcium is primarily absorbed in the small intestine. The dog’s ability to use it efficiently depends on the form of calcium ingested – insoluble salts such as calcium oxalate decrease the ability to absorb it.

The presence of other minerals also affect the dog’s ability to absorb and utilize calcium. Excessive amounts of iron, manganese and zinc will depress the dog’s ability to use calcium. Even the level of calcium in the diet can influence the dog’s ability to absorb calcium. High levels can decrease the efficiency of absorption.

High levels of fatty acids and fats in the diet will cause insoluble forms of calcium – which the dog will have a difficult time assimilating. On the other hand, a certain amount of fat is necessary for the proper absorption of calcium.

Sufficient levels of vitamin D are also important for proper absorption of calcium. Too little vitamin D decreases the amount of calcium-binding protein, which is critical for the absorption of calcium.

The correct ratio of calcium to phosphorus is also extremely important. An imbalance can alter the entire absorptive mechanism of both minerals.

The dog’s ability to absorb and utilize calcium and phosphorus thus depends upon three main factors: both elements in sufficient supply, a correct ratio of each element and the presence of vitamin D. The bottom line is this: an excess of either calcium or phosphorus interferes with the absorption of the other, which is why they must be present in the dog’s food in the correct ratio.

The addition of calcium to the dog’s diet without considering the interrelation-ship between other minerals is detrimental to the dog and decreases the dog’s ability to absorb and utilize all the minerals.

Too Much? Too Little?

A deficiency of calcium and phosphorus often shows up in the development of the bones – called rickets in young animals and osteomalacia in older animals. Bones will continue to grow even if the two minerals are insufficiently provided, but the bones will be soft and will bend out of shape by the weight of the animal. Rickets can also be caused by a Vitamin D deficiency.

Osteomalacia is the weakening of the bones of an older animal. The calcium in the bone has been used to meet the dietary needs of the animal. The bones, lacking proper calcium, become porous and weak.

Too much calcium or phosphorus is bad, too. The body tries to rid itself of the excess by depositing it in the bone and in the soft tissue. Typically, this occurs in the tendons which connect the muscles to the bones. In more severe cases of calcium overdose – toxicity – calcium may end up in the heart muscle, or cause the formation of urinary calculi.

A phosphorus deficiency in mature animals may lead animals to eat dirt, bones, wood or other foreign material. It can also cause reproductive problems. Another symptom, called nutritional redwater, is caused by the excretion of blood in the urine.

Excessive intake of calcium or phosphorus also decreases the absorption of zinc and magnesium, and vice versa.

Is your dog getting too much calcium and phosphorus because you’re supplementing an
already balanced diet with cottage cheese, milk, eggs or calcium? You better reconsider. Commercial dog foods provide just the right amounts of everything, in just the right ratios. Don’t do anything to mess up the balance.


Selenium is a potentially toxic element that is also an essential mineral.

Franke and Potter in 1935 identified a toxic factor in forage which causes a peculiar disease in livestock, commonly Studies by K. Schwarz around 1950 found that the toxic factor, which he called “factor 3,” was different from Vitamin E. It prevented dietary liver necrosis in rats and a hemorrhagic disease in chickens –  exudative diathesis. The factor was later found to be selenium.

Schwarz also discovered that only minute “trace” amounts of the mineral, 0.1 ppm, is required to prevent exudative diathesis in chickens. From this time onward, selenium became recognized as a useful and necessary dietary ingredient, as well as a potentially harmful one.

In 1958 researchers from Oregon and Cornell reported that white muscle disease (red muscle is white upon autopsy), lameness and difficulty in locomotion in lambs could be prevented with the addition of selenium. Researchers from New Zealand reported similar findings with cattle. The New Zealand investigators also found that periodically feeding small amounts of selenium to cattle decreased the mortality rate and improved growth rates.

Because the diseases, liver and pancreas degeneration, white muscle disease and exudative diathesis could be prevented by Vitamin E, many nutritionists were reluctant to list selenium as an essential mineral.

Investigators from Cornell formulated a diet with only 0 .005 ppm selenium and with high levels of Vitamin E. The animals fed this selenium deficient diet showed signs of pancreas degeneration and slow growth. The researchers then added selenium to the diet and, within 14 days, the pancreas returned to normal and the animals showed signs of normal growth.

Selenium supplementation in selenium-deficient diets has improved reproductive efficiency and reduced the incidence of retained placentas, as well as pancreas and liver degeneration. Dietary deficiencies of selenium in dogs are rare when commercial diets are fed. Both meats and cereal grains are good sources of selenium.

Wisconsin investigators reported that selenium is an essential component of glutathione peroxidase. This is an enzyme that protects cells by removing damaging peroxides from the tissue. Likewise, Vitamin E also offers protection from peroxides. Removing peroxides from the cells and tissues is the antioxidant role of both selenium and Vitamin E and the cause of nutritionists’ confusion about the need for selenium.

Most dietary selenium is absorbed in the large intestine. Selenium’s metabolic end product is excreted in the urine and sometimes in the feces.

Selenium Deficiency

Selenium deficiencies are numerous. Each species of animal manifests different symptoms. For example, in dogs, cattle, sheep and goats the skeletal and cardiac muscles degenerate. The condition is called white muscle disease because normally red muscle tissue is white when autopsied.

Selenium deficiency in chickens is called exudative diathesis. This causes capillaries to become more permeable, resulting in hemorrhage. In other animals, liver and pancreas degeneration is seen.


Selenium toxicities produce a condition called “blind staggers” or alkali disease. In dogs, an excess of selenium kills the heart muscle. It also causes toxic hepatitis and nephritis (kidney diseases). Symptoms of selenium toxicity in all animals may include loss of hair, slough-ing hooves or toenails, lameness, anemia, excessive salivation, grinding of the teeth, blindness, paralysis, embryonic deformities (including missing eyes, legs or feet) and death. Young animals are especially susceptible to selenium toxicity.

Selenium Toxicity – An Area Problem

In the U.S., there are certain areas where grains and forage material grown are low in selenium in terms of animal needs – Pacific Northwest, Northeast and Southeastern Seaboard. Crops and forage material grown in the Midwestern part of the United States contain high levels of selenium. In some areas the soil may contain as much as 40 ppm.

Any soil content above 5 ppm contains potentially toxic levels of selenium because the concentration in the plant is generally greater than that of the soil. For example, if the soil contains 9 ppm of selenium, certain crops have been found to contain as much as l200 ppm. Selenium content decreases as the plant matures. A chronic toxicity can be caused by rations containing as littIe as 8.5 ppm of selenium.

Human cases of selenium toxicity have also been reported in white flour milled from wheat grown in areas of high selenium content soil. Selenium occurs in the milk and eggs from cows and hens fed rations containing high amounts of selenium.


J.T. Rotruck et al., Biochemical role of selenium as a component of glutathione peroxidase, Science l79:588-590, 1973

W.E. Julien et al., Selenium and Vitamin E and incidence of retained placenta in parturient dairy cows, J. Dairy Sci., 59:1954-1959, 1976

J. Kubora and Associates, Selenium in crops in the United States in relation to selenium-responsive diseases in animals, J. Agr. Food Chem., 15:448-453, 1967

O. E. Olson, Selenium as a toxic factor in animal nutrition, Proc. Georgia Nutrition Conference, 1969 pp 68-72

K. Schwarz, D. B. Milne, and E. Vinyard, Growth effects of tin compounds in rats maintained in a trace element-controlled environment, Biochem. Biophys. 40: 22-29, 1970

K.Schwarz and W. Mertz, Chromium (III) and the glucose tolerance factor, Arch. Biochem. Biophys., 85:292-294, 1959

Ammerman, C. B. and S.M. Miller: Selenium in ruminant nutrition: A review, J. Dairy Sci. 58:1561-1577, 1975

Zinc Deficiency It’s usually misdiagnosed!

Zinc is found throughout the body. The highest concentration of zinc is found in the epidermal tissues such as skin and hair. It is also found in lesser quantities in bones, muscles, blood and milk. Zinc is an essential element in many body functions from digestion to reproduction.

Usually, food provides enough zinc to prevent deficiencies, despite the fact that less than 10% of the available zinc is absorbed due to relationships with other minerals such as calcium, and organic com-pounds such as phytic acid. Excess calcium in a dog’s diet can decrease the absorption of zinc, which is primarily absorbed and excreted via the pancreatic duct and in bile.

Zinc’s major role is with enzymes. It is a part of many enzyme molecules, and also activates many enzyme systems.

Some of the enzymes zinc is involved with are the ones necessary for metabolizing proteins and carbohydrates. For example, it is part of the enzyme system for the secretion of hydrochloric acid – stomach acid used for digestion.

Another extremely important role of zinc is in the action of FSH (Follicle Stimulating Hormone) and LH (Luteiniz-ing Hormone) – two of the sex hormones which function to stimulate the ovaries and the production of estrogen in bitches. In males, the two hormones function to stimulate spermatogenesis and secretion of testosterone. The zinc concentration of the canine prostate’s secretions is higher than in most species.

Zinc is also an important component of the respiratory enzyme carbonic anhydrase, which is necessary for the transport of carbon dioxide in the blood. There is also evidence that zinc plays a role in calcification of bones and teeth, as well as in the keratinization of tissues such as foot pads, toenails, and skin.

In 1953 two researchers, Kerncamp and Ferrin, described a diseased condition found in swine called parakeratosis. Two years later, Tucker and Salmon reported that this disease was related to a zinc deficiency. In the beginning, this disease was characterized by skin lesions, retarded growth, and poor feed utilization. It was also found that zinc deficiency is aggravated by excess calcium intake.

Within the next decade, scientists all over the country were describing zinc deficiencies in many animal and avian species. To confirm their finding, experimental diets completely absent of zinc were fed to many forms of livestock. More scientists became interested in zinc deficiency, and more symptoms were noted. Most noted that excess calcium is an aggravating factor in all species.

Some of the primary symptoms of a zinc deficiency in animals are: slow growth, embryonic anomalies, inflamed skin around the nose and mouth, stiffness of joints, loss of hair, rough scaly skin, and low survivability of the young. In chickens, additional symptoms include poor feathering and a thickening of the leg bones. It was also found that the blood and tissue values for zinc in the blood as carbonic anhydrase was also decreased.

Recent studies suggest that border-line zinc deficiencies usually go undetected. They are usually misdiagnosed and blamed on other causes. Borderline deficiencies are much more common than most people realize.

Severe zinc deficiencies can result in dwarfism and the absence of sexual maturation. Zinc deficiency is also a problem afflicting humans; poor growth, poor appetite, and impaired taste discrimination of children are reported to be caused by a less than severe deficiency.
The zinc requirement varies greatly depending upon the level of calcium, and sources and levels of protein. Other factors such as the presence of phosphorus in the form of phytic acid may depress zinc absorption from the intestinal tract.

To give you an example of how greatly the zinc requirement can vary, let us look at swine, where much of the initial research into zinc needs was conducted. If the diet’s primary ingredient is isolated soybean proteins and contains the recommended calcium level for swine, the zinc requirement is 50 mg per kilogram of diet. If the primary ingredient of the feed is corn, and the calcium content is high, 100 mg of zinc per kilogram of diet would not necessarily prevent slow growth or a poor use of feed.

Zinc toxicities are unusual, but can show themselves as anemia. This appears to be due to an interference with iron and copper utilization.

To summarize, animals can become deficient in zinc for two reasons: the diet is deficient in zinc, or too rich in calcium. If you supplement your dog’s balanced diet with calcium – milk, cheese, calcium tablets, calcium diphosphate or cottage cheese, watch out! Calcium decreases the ability of the dog to utilize zinc, and zinc deficiency can show up as retarded or slow growth, bone problems, severe delays in wound healing, an impairment of glucose tolerance, loss of hair, scaly skin, fetal anomalies, and other symptoms.

The good news about zinc deficiency is that when excess calcium is removed from the diet or the zinc level is brought up to the requirement, the symptoms disappear – almost as fast as they appeared.

Determining the proper amounts of minerals for dogs is complex and best left to professionals who understand the interrelationships among minerals and other nutrients.
If you feel your dog is suffering from any of these symptoms, reevaluate your feeding program and have your veterinarian test for a mineral deficiency.


Apgar, J.,  Effects of zinc deficiency and zinc repletion during pregnancy on parturition in two strains of rats, J. Nutrition 107:1399-1403 (1977)

Miller, W.J., Newer candidates for essential trace elements, Fed. Proc. 33:1747 (1974

Tucker, H.F. and Salmon, W.D., Parakeratosis or zinc deficiency disease in the pig, Proc. Soc. Expt. Biol. Med. 88:613-616 (1955)

Miller, J.K. and W.J., Development of zinc deficiency in Holstein calves fed a purified diet, J. Dairy Sci. 43:1854-1856 (1960

Mayland, H.F., Zinc increases range cattle weight gain, J. Animal Sci. 41:337 (Abstr. 1975

Flagstad, T., Lethal trait A46 in cattle. Intestinal zinc absorption, Nord. Vet-Med. 28:160-169 (1977

Reis, B.L. and Evans, G.W., Genetic influence on zinc metabolism in mice, J. Nutrition, 107:1683-1686 (1977)

Flaten, T.P., An investigation of the chemical composition of Norwegian drinking water and its possible relationships with the epidemiology of several diseases. PhD. thesis. U. of Trondheim (Norway, 1986)

Erway, L. Hurley, L.S., and Frazer, A. Neurological defects: manganese in phenocopy and prevention of a genetic abnormality of inner ear, Science 152:1766-1768 (1966)

Hurley, L.S., Amelioration by copper supplementation of mutant gene effect in the crinkled mouse, Proc. Soc. Expt. Biol. Med., 149:830-834 (1975

Hurley, L.S., Amelioration by copper supplementation of mutant gene effect in the crinkled mouse, Proc. Soc. Expt. Biol. Med., 149:830-834 (1975)

Trace Minerals

Dogs, like all animals, need minerals in their diet. Minerals serve the body as important components of bones and teeth, giving rigidity and strength. They are also constituents of proteins and lipids, which make up the body’s tissues (muscles, organs and blood cells).

Minerals are important in the activation of many enzyme systems in the body. They also serve to keep the body in an osmotic equilibrium – where salts in the bloodstream and other body fluids remain in their proper places. For example, the balance between calcium, sodium, and potassium in the fluid which bathes the heart muscle is essential for normal relaxation and contraction.

Each mineral also has a specific role to play in the body. Some minerals are needed in large amounts. They are called major minerals. Those needed in small amounts are called trace minerals. Trace and major do not refer to the importance of the minerals – both kinds are equally important. Rather, the terms refer to the amount required by the dog.

Determining the proper trace mineral amounts for dogs can be a quite complex problem due to the physiological roles, and interrelationships with other minerals. Complicating matters is the fact that there is a very fine line between providing the right amount of a trace mineral for optimum health, and providing too much of a good thing, resulting in illness.

Trace minerals have a surprisingly narrow margin of safety between optimum and toxic amounts. You must take extra care when adding supplements to an already balanced dog food because of this slim margin of safety.

Eighteen mineral elements are known to be required by the dog. The major minerals are sodium, chlorine, calcium, phosphorus, magnesium, potassium and sulfur. The trace minerals are chromium, cobalt, copper, fluorine, iodine, iron, manganese, molybdenum, selenium, silicon and zinc.

Several factors influence the utilization of minerals. For example, many minerals interrelate with each other, such as calcium, which interferes with the utilization of zinc. This sort of relationship between minerals and other elements in the dog’s food increases or decreases the utilization of the minerals.

Other factors include the actual amount of a specific mineral in the dog’s food, and the present mineral status of the dog. For example, if a diet contains more calcium than the required amount, the percentage absorbed will be smaller. This same diet, containing more calcium than necessary, will have an effect on the utilization of other minerals, such as zinc. In the article on the next page you will see how the feeding of excess calcium can cause a zinc deficiency, and the impact.

The mineral status of a dog also plays a role in current mineral requirements. A dog who is deficient in iron will absorb more iron from the food than a dog who has adequate stores of iron already.

The form the mineral is in can also make a difference in how much is taken from the food. Iron in the form of iron oxide, commonly called rust, can’t be used by the dog, but ferrous sulfate will easily supply needed iron. The Association of American Feed Control Officials lists the minerals that may be added to animal feeds, and determines how they should be labeled when added.

Genetics and Nutrition

Nutritional needs  are sometimes a direct  result of genetics. Researchers Hurley and
Erway showed that one strain of mice requires a high dietary level of copper, while another strain requires a high level of manganese. One line of cattle which has a genetic defect in zinc metabolism was identified by the work of T. Flagstad et al. Reis and Evans showed the genetic influence on zinc metabolism in mice. They created a strain of mice resistant to zinc depletion.

What’s the point? Simply that mineral deficiencies could be unknowingly bred into your dog’s line. Here’s one way: sup-pose you feed your dogs something other than a balanced, commercially prepared dog food, or you supplement your dogs’ already balanced diet. If you constantly feed a diet with a mineral imbalance, generation after generation after generation, you will have genetically selected a strain of dogs which will survive on your imbalanced “witch’s brew.” What happens when you place a puppy selected and raised on this type of feeding practice onto a commercially prepared diet? It wouldn’t be strange to think it wouldn’t do as well. It’s been selected, bred and raised on the mineral imbalance.

Other mineral deficiencies may be due to local conditions. There’s the case of  cattle which grazed on grass in Maracay, Venezuela. These cattle would come across an old carcass and chew on the bones in a decidedly un-cattlelike move. The grass was tested, and grass and soil were found to be deficient in phosphorus. The cattle needed the phosphorus, and got it by chewing on the bones.

In dogs, mineral imbalances might be seen where acidic water sits in copper pipes. A study in Norway found that water with a pH of 4.5 is not uncommon, and may result in higher levels of copper in the water after it stagnates in copper pipes.