Minerals generally are divided into two categories: macrominerals, which are needed in larger quantities (relatively speaking) in the daily diet; and microminerals, or trace minerals, which are needed only in infinitesimal amounts (usually expressed as parts per million, or ppm--or sometimes as mg/kg). Macrominerals, which include calcium, phosphorus, magnesium, sodium, potassium, sulfur, and chlorine (as chloride), are described in parts per hundred, or percentages; to provide some perspective, the micromineral "unit" ppm is 10,000 times smaller. Iodine, manganese, iron, cobalt, zinc, copper, and selenium all are considered trace minerals necessary to the horse--although sometimes the optimum amounts required are debated.
The roles of various minerals are not always clear-cut. There are some trace minerals that seem to play a role in metabolism, but have not yet been proven to produce any symptoms of deficiency when they are not present. These "mystery minerals" include vanadium, tin, silicon, nickel, chromium, molybdenum, fluorine, and arsenic. It’s interesting to note that some of these also are minerals that can be categorized as "heavy metals." They are capable of doing significant damage if ingested in large enough amounts. Potentially toxic are lead, arsenic, nickel, aluminum, and cadmium, all heavy metals that might have a tiny role to play in nutrition. On-going research likely will reveal more about these ingredients as time goes on.
All minerals can have an adverse effect if present in the diet in large enough amounts, but there often is a broad safety zone. Within that safe range, feeding the minimum amount of a mineral can be just as effective as feeding the maximum amount--and often, considerably less expensive. Of course, some of the companies that market feed supplements would prefer that you believe otherwise.
Making matters even more complicated is the fact that some minerals are "linked"--the amount of one mineral present can affect the absorption and utilization of another. Calcium and phosphorus are the most famous partners; both are essential to the growth and repair of healthy bone, but must be present in a certain proportion (with at least as much calcium as phosphorus, never the reverse) in order to do their job. Copper, zinc, and iron (with the possible addition of magnesium and manganese) form another linkage, which has received a good deal of scrutiny by researchers exploring developmental bone abnormalities in young horses. There might be many more connections we don’t yet fully understand.
Finally, the absorption of minerals in the horse’s gut varies widely. Most of these elements can bind in a number of different molecules (remember your high school chemistry?), some of which are easier for the horse’s digestive system to break down than others. (Zinc, for example, can be found in the diet as zinc carbonate, zinc sulfate, or zinc oxide, to name only three.) The result is that, of the amount of a mineral listed on a product’s feed tag, only a very small percentage might actually be used by the horse. For example, the average absorption of calcium varies between 10-40%, while phosphorus is somewhat better utilized, at about 70%. Iron absorption ranges from 2-20%, with about 4% being the average; zinc’s range is from 5% all the way up to 90%, and between 25-75% of ingested magnesium is absorbed, with an average of 43%.
Feed company chemists have tried to address the absorption problem in a number of innovative ways, some more successful than others. Organic (plant) sources of minerals often are better absorbed than are the inorganic (artificial) sources feed companies can use to supplement a feed--but even this is not a hard-and-fast rule. For some minerals, absorption can be significantly improved by "chelating" them--a process that bonds minerals to two or more amino acids to form stable biochemical ring compounds, which can be metabolized as much as 300-500% more efficiently than their inorganic counterparts. Alas, there is no one magic formula for improving absorption, as what works for one mineral might be a dismal failure with another. This is true even with chelation, which produces very good results with some minerals (including most of the macrominerals), but not with all.
Mineral absorption (which can be roughly determined by measuring the amount of the mineral remaining in the manure, compared with the amount contained in the ingested feed) also can be affected by a whole host of other factors. The amount of other nutrients in the diet, such as fats, indigestible fiber, and vitamins, can have an influence on mineral utilization; so can the pH balance of the gut (which affects the solubility of the minerals).
Nor is the mineral content of feeds etched in stone. It can vary with soil mineral concentrations, plant species, stage of maturity, and conditions at harvesting. All of these factors keep feed industry chemists on their toes as they formulate feeds and supplements for the horse’s maximum benefit.
Still, there is much we do understand about the macrominerals, and at least some of the trace minerals. Here, then, is a rundown of the most important minerals in your horse’s diet.
Calcium And Phosphorous
First on the feed tag, and in most discussions of minerals, is calcium, a versatile player best known for its role in bone structure and repair. Calcium makes up about 35% of the horse’s bone structure, but it also is involved in a host of other functions, including cardiac muscle contraction, cell membrane integrity, glandular secretion, temperature regulation, and blood clotting mechanisms. The absorption efficiency of calcium seems to decline with age, and to range from as high as 70% in young horses, to 50% or less in older ones.
It is difficult to discuss calcium without considering its partner, phosphorus, which also is essential to the growth and maintenance of healthy bones and teeth, as well as to energy metabolism and numerous cellular functions. It also plays an important role in late pregnancy and lactation, during which times a mare’s phosphorus requirements increase. The ratio of calcium to phosphorus in the equine diet is crucial; symptoms of deficiency will result if the horse does not receive at least as much calcium as phosphorus. That 1:1 ratio serves as a baseline, although interestingly, horses can tolerate quite a lot of calcium (more than five times the recommended level), provided the base level of phosphorus is adequate. Most researchers feel that the ideal balance is about 1.2 parts calcium to 1 part phosphorus, up to about 1.6:1. Excess dietary phosphorus, in any form, binds calcium and prevents its absorption, but the same is not true in reverse. Excess calcium has almost no effect on the absorption of phosphorus.
Symptoms of calcium deficiency (or excess phosphorus) can include developmental bone abnormalities in foals, "big head disease" (also called bran disease) in adult horses, decreased bone density, stiffness and possible lameness, weight loss, loose teeth, and fragile bones that fracture easily. Most of the same symptoms will occur if a phosphorus deficiency exists. Deficiencies of either mineral result in mobilization of these minerals from the bone--that is, they are drawn from the bone matrix and re-introduced to the blood plasma. In this way, while the bone is weakened, the other body functions to which calcium and phosphorus are pivotal are maintained.
Under most circumstances, horses eating forage have a hard time developing a calcium deficiency, as hay (especially legume hay) is calcium-rich; however, a diet very low in forage and high in grains (which are naturally high in phosphorus) can produce these symptoms. Historically, horses fed diets rich in wheat bran often developed this imbalance; today, it’s rare. One of the few other causes of calcium deficiency in horses is the ingestion of plants containing high amounts of oxalate compounds, which inhibit calcium absorption. Plants like sorrel, dock, rhubarb, purslane, kikuyu grass, and lambsquarter can contain potentially harmful amounts of oxalates. They are primarily a problem for young horses, and also can cause diarrhea and gastroenteritis.
Sodium And Chloride
Even those for whom chemistry was never a strong subject know that sodium and chloride together make table salt. And the vast majority of horse owners know that salt is a crucial part of the equine diet. The two elements (Na+ and Cl-) are responsible for the regulation of all the horse’s body fluids, as well as the conduction of electrical impulses in nerves and muscles, and they are the most important of the minerals known as electrolytes (minerals which are lost in the sweat and urine during exercise stress). Chloride also is an essential ingredient of bile, and it is important in the formation of hydrochloric acid, a component of the gastric secretions necessary for digestion.
For maintenance, the horse’s diet (as dry matter) should contain at least 0.25% salt (a level which will supply a maintenance level of 0.1% sodium), and if the horse is exercising hard enough to sweat on a regular basis, he should receive 0.75% salt per day. Exact chloride requirements for horses have not been established, but they are thought to be satisfied when the horse ingests enough salt to take care of his sodium requirements. (Salt is not a 50/50 proposition, by the way--chemistry being the complicated thing it is, it works out to be about 39% sodium and 61% chloride.)
Many feeds contain less than 0.1% sodium, which is less than is needed even by horses which are idle. This is why horses always should have access to free-choice salt, in the form of a lick or in loose form. Alternatively, you can put additional salt in your horse’s feed, although this is a less-perfect solution--horses have a certain amount of "nutritional wisdom" when it comes to salt, and are best left to ingest the amount their bodies tell them they need. (Contrary to popular belief, this nutritional wisdom does not extend to other minerals--horses don’t wake up with a craving for cobalt or manganese any more than we do.)
The absorption levels of sodium and chloride are quite high--from 75-95%, by most researchers’ estimations. Excesses are readily excreted in the urine, provided the horse has access to fresh, clean water. The only time high salt intake (from adding too much salt to the feed, from drinking brine or sea-water out of desperation, or from a salt block-munching habit) is likely to become a problem is when fresh water is restricted. Clinical signs of salt toxicity include colic, diarrhea, frequent urination, paralysis of the hind limbs, staggering and weakness, and eventually, death. It is treated by offering water in small amounts at frequent intervals; too much, too soon can produce cellular swelling and intracranial pressure problems, which can be very dangerous.
Because horses usually will consume salt in excess of their nutritional needs if it is available, salt deficiencies are almost as rare as real toxicities. However, such losses can occur in stressful situations, such as 100-mile (or more) endurance races in very hot, humid conditions. If a sodium chloride deficiency occurs rapidly, muscle contraction and chewing might become uncoordinated, sweating will decrease (with a corresponding decrease in performance), the gait might become unsteady, and plasma concentrations of both sodium and chloride will decrease while potassium will increase. Generally, however, a salt deficiency occurs more slowly and might only be noticeable because the horse begins to lick objects and surfaces that might have salt on them. If salt is not provided, he might become dehydrated and constipated, lose his appetite, and become weakened.
When you provide salt to your horse, you can choose between salt blocks that are iodized, those with added trace minerals, and those which are just plain salt. While the trace mineral blocks are a good idea, they still contain mostly salt (about 95% on average), so should not be depended on to supply all of your horse’s other mineral needs. Furthermore, some horses object to the taste of a trace-mineral block and thus will not ingest all the salt they require. The best solution might be to provide both plain or iodized salt, and a trace-mineral-plus-salt block, in your horse’s pasture or stall, and give him the choice.
Potassium, designated by the chemical symbol K, is a crucial element of cellular osmotic pressure and the maintenance of the body’s acid/base balance. It also is considered an electrolyte, and is usually the other major mineral horse owners are concerned about replacing when a horse is working hard. Without sufficient potassium, horses are prone to fatigue, muscle weakness, exercise intolerance, and decreased water and feed intake. Increased restlessness and spookiness, especially in response to loud noises, also have been reported. Because sweating increases potassium loss, both in the sweat itself and in the urine, deficiencies are a particular concern for high-level three-day event and endurance horses, particularly when they are training or competing in hot, humid conditions. Potential potassium losses also can be aggravated by the administration of diuretics such as Lasix (often used to treat racehorses with pulmonary hemorrhages, sometimes called "bleeders"), and are a risk in horses with diarrheal diseases such as Potomac horse fever.
Outside of these conditions, however, potassium deficiencies are rare, because most forages contain between 1-4% potassium, plenty to satisfy the horse’s daily requirement of about 0.4%--or even the hard-working horse’s requirement of 0.6%. (Even most cereal grains, containing between 0.3% and 0.5% potassium, usually can fulfill the daily requirement without difficulty.) Fortunately, excess potassium intake is not harmful, as it is readily excreted in the urine. The exception is horses which suffer from the genetic abnormality HYPP (hyperkalemic periodic paralysis), in which excess potassium tends to build up in the system. The disease, limited to Quarter Horses, Paints, and Appaloosas descended from the Impressive line, is treated nutritionally by keeping the dietary intake of potassium under 1% (usually by feeding a high-grain, low-forage diet and avoiding particularly young forage and molasses, which also contain high amounts of the mineral). There now are grain rations with low potassium levels marketed specifically for HYPP horses.
Those who do wish to increase their horse’s potassium intake (usually in anticipation of, or response to, high-stress competition) can do so with a commercial electrolyte product, or by adding 50-100 grams of "lite" or "low sodium" salt (half sodium chloride, and half potassium chloride--containing about 26% potassium) to the feed. Lite salt is available in most major supermarkets.
About 60% of the body’s store of magnesium is tied up in the skeletal structure, but it also is an important activator of many enzymes. Fortunately for the horse, his magnesium needs of about 0.1% per day are easily met by a normal diet (the magnesium content of most horse feeds is between 0.1% and 0.3%). Magnesium absorption tends to be in the 40% range, with utilization of added dietary sources, such as magnesium oxide or magnesium sulfate, sometimes somewhat better (up to about 70%).
Neither magnesium deficiencies nor toxicities have been reported in horses being fed normal diets, except in the rare case of lactating mares which have demonstrated tetany (intermittent muscle spasms, similar to those produced by the disease tetanus) as a possible result of a high-potassium, low-magnesium diet and high levels of magnesium being excreted in the milk. The condition is far more common in milking cattle, which do not absorb magnesium as efficiently as horses. Experimentally induced magnesium deficiencies in foals have produced muscle tremors, nervousness, uncoordinated movement, and eventually, collapse, convulsive paddling, and death. There also was, on autopsy, some mineralization (deposits of calcium and phosphorus) in the aorta. There have been no studies on the effects of high-magnesium diets, although horses apparently have a high tolerance for this mineral.
We don’t tend to think of sulfur as an important mineral, but it is an essential constituent of several amino acids (methionine, cystine, and cysteine) as well as the B vitamins biotin and thiamin, and a number of other important molecules such as insulin, taurine, and chondroitin sulfate (a component of cartilage, bone, tendons, and blood vessels). The concentration of sulfur in the body is highest in hooves and hair, which both contain the protein keratin (4% sulfur). Overall, it makes up about 0.15% of the horse’s total body weight.
Despite its importance, the exact sulfur requirements of the horse have not yet been determined. Most horse feeds contain about 0.15% organic sulfur, which seems to be enough to meet daily requirements. Inorganic sulfur is not readily absorbed by the horse, but organic (bound into amino acids) is.
Sulfur deficiencies have not been reported in horses, although in other species a deficiency produces decreased appetite, growth, and milk production. In pigs and ruminants, excess dietary sulfur interferes with copper absorption, but so far there is no evidence that this occurs in horses; in fact, no side-effects have been noted from high sulfur intake in equines, as the mineral is easily excreted in the urine and feces.
Trace Minerals: Selenium
Although it is needed in infinitesimal amounts, selenium is a mineral that has received a lot of press in recent years. Selenium and vitamin E function in a partnership that helps protect body tissues from free-radical damage that occurs during oxidation (the conversion of feedstuffs into energy). In particular, they act as a defense mechanism against damage to cell membranes and enzymes. While vitamin E blocks free radical attacks on lipids, selenium is a component of the enzyme glutathione peroxidase, which helps prevent the formation of free radicals and destroys lipid peroxidases that are released into the cells. This dynamic duo works best when both are present in the correct amounts.
Selenium is a tricky mineral for several reasons. First, unlike most minerals that have a broad safety range, selenium has a very low threshold of toxicity for horses--only a few parts per million beyond the recommended levels. (Most other livestock species have a much higher tolerance, partly because their absorption rates are lower than horses’.) Thus the assumption that "if some is good, more is better" can be a dangerous one for this mineral--and the effects of selenium toxicity can be worse than the effects of a deficiency. They can include patchy sweating, blind staggers, colic, diarrhea, and increased heart and respiration rates if acute (as in, for example, when a horse is given selenium injections), or when chronic, loss of hair, especially in the mane and tail, the cracking of hooves around the coronary band, and occasionally hooves that slough off completely.
Second, the selenium content of feeds varies depending on where the plants were grown--and across North America, the soil content of selenium fluctuates significantly. Some areas are so selenium-deficient that crops grown there are considered to contain no selenium at all, necessitating supplementation. Some locations have adequate selenium in the soil, and others actually have toxic concentrations of selenium, making any supplementation positively reckless. Pockets where toxic levels exist are located in California, Colorado, Idaho, Montana, Oregon, South Dakota, Utah, and Wyoming; however, all of these states except Wyoming also report areas that are deficient. The Great Lakes region, and almost all of Canada except for southern Manitoba, Saskatchewan, and Alberta, tend to be severely selenium deficient.
This extreme variation from region to region is the reason that regulations exist, in Canada and in most of the United States, to make sure feed companies print a warning to consumers if there is selenium added to a feed. What might be appropriate to feed in one region would be a very poor choice in another.
Because the toxicity threshold of selenium is so low (between 2 and 5 ppm), you should be aware of the selenium content of your local soils (and thus, your pasture and your hay) before you choose a vitamin E and selenium supplement, or a selenium-added feed, for your horse. Even some trace-mineral salt blocks contain added selenium, so be sure to check the label before you place them in the pasture. Information on the selenium content of your local soils can be obtained from your local agriculture extension specialist, or even your local feed store or co-op.
The level of selenium currently recommended for horses is between 0.1 ppm and 0.3 ppm (dry matter), although some researchers feel that this is a little conservative. In mild deficiencies, the only symptom might be an increased susceptibility to disease, due to a depressed immune system, and/or decreased fertility in breeding stock. Far less common are severe selenium deficiencies, which are characterized by weakness, impaired movement, difficulty in swallowing, impaired cardiac function, and respiratory distress. They also have been implicated in certain types of "tying up" in performance horses.
Young foals, from birth to about four weeks of age, are most likely to demonstrate clinical symptoms (which occur as a result of inadequate selenium intake by the dam during pregnancy). They can develop muscle pain, an inability to nurse, and a stilted, hopping gait in the rear legs, or be stillborn or die within a few days of birth. In areas where selenium deficiency is a documented problem in foals, the dam should receive supplementation throughout her pregnancy, and the foal given a vitamin-E-and-selenium injection just after birth.
Iodine is a specialist. It is essential for the synthesis of thyroid hormones thyroxin (T4) and tri-iodothyronine (T3), which help regulate basal metabolism--and unlike some other minerals, which fulfill numerous functions, this is iodine’s only known role in the diet.
The horse’s estimated daily requirement of iodine is 0.1 ppm (or 1-2 mg per 500 kg horse per day), and like selenium (and unlike practically every other mineral), iodine’s toxicity threshold is quite low, about 5 ppm (40 mg/horse/day). Most horse feeds contain between 0.05 and 0.2 ppm (dry matter) of iodine, but some can contain as much as 2 ppm, depending on the soils in which the feed was grown. Thus, it is possible for horses to become iodine-deficient on a normal diet, although feeding an iodized or trace-mineral salt (at a level of as little as half an ounce a day) easily can prevent deficiencies. It also is possible for horses to ingest toxic amounts of iodine, either as a result of over-supplementing with iodized salt (if it is more than 4% of the total diet), or by feeding seaweed (kelp) or supplements containing it, on top of a feed already enriched with iodine. Seaweed can contain as much as 1,850 ppm of iodine--and at that level, as little as 0.7 ounces a day can be harmful.
Pregnant and lactating mares seem to be less tolerant of high levels of iodine than other horses. Overall, in recent years, reports of iodine toxicosis have been more frequent than reports of deficiencies. Some researchers have chalked this up to overzealous supplementing by well-meaning owners.
Complicating matters is the fact that both iodine deficiencies and excesses produce very similar symptoms--they both can result in a goiter, a swelling of the thyroid gland on the underside of the horse’s throat, just under the jaw. This can make it rather difficult to discern, at first glance, whether you are dealing with too much iodine or too little. The best way to determine which is the problem is to evaluate the iodine levels in the diet, as blood plasma levels of thyroid hormones can fluctuate quite a lot. If no seaweed or supplemental sources of iodine are being fed, then chances are you are dealing with a deficiency.
Other symptoms of an iodine imbalance are a dry, lusterless haircoat, hair loss, decreased growth and decreased bone calcification in young horses, lethargy and drowsiness, and cold intolerance and possible hypothermia (low body temperature). Sometimes an iodine deficiency (but not an excess) will produce a thickened skin due to the accumulation of mucinous material under the skin of the limbs. This is called myxedema. As is the case with many mineral imbalances, detrimental effects of too much or too little iodine are most obvious in foals. Severely affected foals (usually born to mares with iodine imbalances) are weak, have difficulty standing, suffer persistent hypothermia (with an abnormally low rectal temperature of less than 100¡ Fahrenheit), and have a weak sucking response. They might suffer respiratory distress, as well, and have noticeably enlarged thyroids; most die within a few days of birth. Those who survive can suffer from various bone and joint abnormalities. Iodine toxicosis, but not deficiency, also can increase a horse’s susceptibility to infectious diseases.
This mineral is a component of several enzymes involved in the synthesis and maintenance of elastic connective tissue, the mobilization of iron stores (more on iron in a moment), and synthesis of the body pigment melanin, as well as being involved in bone collagen stabilization. Copper deficiencies can play a role in developmental orthopedic diseases of young horses (although some researchers now believe its participation might have been over-rated), and it also has been implicated in ruptures of the aorta or uterine arteries in aged foaling mares.
The liver regulates copper metabolism by storing it or excreting it in the bile. Its absorption in the gut might be influenced by the levels of other minerals, such as zinc, iron, and molybdenum, making it somewhat difficult to estimate how much dietary copper is utilized. But because copper toxicity only occurs at relatively high levels in horses (in contrast to some other species--sheep in particular are very sensitive to it), most feed companies err on the side of generosity when it comes to copper, in the hopes that enough will be absorbed to meet the horse’s needs. The exact optimum levels of copper in the equine diet have not yet been established. The National Research Council recommends a level of 10 ppm, which many researchers feel is low. (Some have suggested a level of 50 ppm for creep-feeding foals, and at least 25 ppm for weanlings up to 12 months of age.)
Real copper deficiencies rarely have been noted in horses; a foal taking in inadequate amounts of copper might have abnormal bone or cartilage development, but will not suffer slowed growth. Because copper absorption decreases with increased copper intake, symptoms of copper excess have only been noted in horses in experimental situations when very high levels have been fed.
Most of us are familiar with iron’s role in hemoglobin, the molecule in red blood cells that enables them to transport oxygen throughout the cells of the body. Approximately 60% of the body’s iron is involved in this task, with another 40% incorporated in muscle myoglobin, storage forms, and various enzymes. The horse’s estimated iron needs are about 50 ppm per day for pregnancy and lactation, and for growth, and 40 ppm for other mature equines. Most forages contain between 50 and 250 ppm (occasionally, up to 400 ppm) of iron, so under most conditions horses receive plenty of iron in their normal diets, and clinically recognized iron deficiencies rarely occur in either foals or mature horses at any performance level. Only under conditions of severe or chronic blood loss is an iron deficiency likely; sometimes this blood loss is not obvious (it might be the result of a severe intestinal parasite problem, or even a serious case of lice).
If a deficiency does occur, the horse will exhibit impaired performance, followed by anemia (low red blood cell count). Treatment consists of first determining and correcting the cause of the anemia, then administering injectable iron to help the horse begin to manufacture more hemoglobin. Because iron levels are tied to fitness, iron supplements have a reputation for enhancing athletic performance, but they should never be administered unless a blood test has demonstrated actual anemia. Iron toxicosis is far more common in horses than is iron deficiency.
Foals are particularly susceptible to iron excesses in the first few days of their lives. Excess iron is stored in various tissues, especially the liver, and severely affected foals (who have usually received inappropriate doses of iron) can suffer depression, dehydration, diarrhea, liver failure, and death. It’s important to note that the body has no way to excrete excess iron. Its only means of protection is decreased absorption, which works with oral supplements, but not with injectables.
High levels of iron in the horse’s system also can make him more vulnerable to bacterial infections. All living organisms need iron--and bacteria will multiply more efficiently when it is readily available. Corticosteroids are a source of iron, which is one reason why these drugs can increase a horse’s susceptibility to bacterial infections.
The metabolism of proteins and carbohydrates is assisted by a number of enzymes containing zinc. The absorption of this mineral can vary widely, and it is affected by the level of many other minerals, including copper and iron. Forty ppm of zinc per day has been recommended for adult horses, and a higher level might be beneficial for foals. Zinc is considered as playing a role in growth and the prevention of developmental orthopedic disorders, but to what extent, no one is sure.
Horses are quite tolerant of high levels of zinc. Zinc toxicosis, resulting from horses grazing in pastures contaminated by nearby zinc smelters or mines, brass foundries, or other industrial plants, has been noted (with symptoms including bony limb deformities, growth plate enlargements, and in severely affected foals, lameness and a strange low-headed, arched-back stance), but it does not occur under normal conditions. Clinical symptoms of zinc deficiency have not been reported either, although the average level of dietary zinc in most feeds--about 15 ppm--would appear to be inadequate (and is often supplemented by feed companies).
Lipid and carbohydrate metabolism depend on manganese, and this mineral also is essential for the synthesis of the chondroitin sulfate needed for cartilage formation. These are functions involved mostly in reproduction and growth. The exact amount of manganese needed by horses has not yet been determined, although based on other species, 40 ppm per day is generally considered ample. Although manganese deficiencies sometimes are a problem in ruminants, they have not been described in horses. If such a deficiency did occur, it would likely result in fertility problems in adult breeding stock and in limb deformities in foals. More good news--no harmful level of manganese has been established for horses, who seem to be able to tolerate large quantities of this mineral with no ill effects.
Cobalt’s only known function is as a component of vitamin B12--so a cobalt deficiency results in a B12 deficiency. Based on levels recommended for cattle, a minimum of 0.1 ppm of cobalt, and a maximum of 10 ppm, is suggested for horses, but neither deficiencies nor excesses of this mineral (nor of vitamin B12) have been described in horses as yet. Most researchers suspect that neither is likely to occur.
A complete and comprehensive rundown of every mineral in the equine diet isn’t possible at this time, because there is still much we have yet to understand, particularly about trace minerals such as vanadium, molybdenum, and heavy metals like lead and arsenic. New research is uncovering surprising things almost on a daily basis, and feed companies are doing their best to incorporate the new findings to provide optimal nutrition. We’ll try to keep you posted as the picture changes.
About the Author
Karen Briggs is the author of six books, including the recently updated Understanding Equine Nutrition as well as Understanding The Pony, both published by Eclipse Press. She's written a few thousand articles on subjects ranging from guttural pouch infections to how to compost your manure. She is also a Canadian certified riding coach, an equine nutritionist, and works in media relations for the harness racing industry. She lives with her band of off-the-track Thoroughbreds on a farm near Guelph, Ontario, and dabbles in eventing.
POLL: University Equine Hospitals