Trace Minerals Important for Horses During Recuperation from InjuryBy Kentucky Equine Research Staff · April 13, 2011
The most important trace minerals in the equine diet are iron, manganese, selenium, iodine, chromium, copper, and zinc. Although regular intake of these minerals is necessary for optimal health, their importance during recuperation from an injury should not be overlooked.
While anemia can impair healing, this will only occur if it is related directly to blood loss. In this situation, low oxygen tension inhibits fibroblastic function and reduced blood supply deprives the injured tissue of materials required for the healing process. In the case of injury leading to significant blood loss, correction of the low blood volume is as important as supplying the nutrients needed for the production of new red cells. These include iron, copper, cobalt, vitamin B12, folic acid, and other B vitamins.
Iron is efficiently absorbed at low levels of intake. Iron absorption decreases as iron intake increases and in the presence of high concentrations of copper, zinc, manganese, cadmium, and cobalt. Additionally, due to the effective iron conservation mechanism, net iron excretion is low, and iron appearing in the feces appears to result primarily from unabsorbed dietary iron rather than from net endogenous fecal losses.
Practical dietary constituents contain 40-50 ppm (mg/kg) iron for cereal grains, 100-150 ppm iron for oilseed meals, and 200-1000 ppm iron for many of the forages. In Nutrient Requirements of Horses, the NRC (2007) lists the iron requirement of performance horses as 400–500 mg per day so natural feeds will easily meet the iron requirement. It is possible that in attempts to stimulate the "blood picture," some horsemen are unwittingly causing interactive deficiencies of other minerals (e.g., copper). More times than not, low hematocrits are an indicator of infection, copper deficiency, low-grade systemic disease, inflammation, or even marginal B-vitamin status brought about by stressed large colon or cecal microbial populations, and not a deficient dietary intake of iron.
The best-known function of manganese is its role in bone formation. Manganese is needed in the formation of chondroitin sulfate and in the synthesis of the organic matrix of bone. Manganese deficiency is expressed as a disorganization of the cells making up the epiphyseal plate, a narrowing of the epiphyseal plate, and a reduction of blood vessel migration into the growth plate. Additionally, the cartilage of the growth plate in manganese-deficient animals contains lower levels of chondroitin sulfate than do the growth plates of normal animals. With respect to this function of manganese, two- and three-year-old horses in which skeletal maturation is not complete may have a slightly higher requirement for manganese than do older animals. Manganese is also an effective chelating agent allowing for more efficient and rapid transfer of amino acids.
Manganese deficiency does not appear to be a concern for horses grazing fresh forage. Manganese concentrations in forage range from 50-300 ppm, and these levels should meet the requirements of most horses. However, cereal grains contain less manganese and may range in concentration from 5 ppm (corn) to 15 ppm (barley). For athletic horses on high-grain diets and consuming grass hay of variable quality, it is probable that some supplemental manganese may be required. High concentrations of calcium and phosphorus in feeds or forages may inhibit manganese absorption, and this should be taken into account in the formulation of feeds for all classes of horses.
Selenium is best known as an essential component of the selenium-dependent enzyme glutathione peroxidase and functions as part of the cellular antioxidant defense system. Like vitamin E, selenium is a biological antioxidant, and there are a number of deficiency symptoms of selenium that may be partially corrected by vitamin E.
The antioxidant defense system allows for the trapping of free radicals and superoxides, which cause oxidative damage to lipid membranes of cells. Because exercise results in increased oxygen delivery to the tissues and oxidation of energy substrate, ending in the generation of reactive oxygen by-products called peroxides, the selenium requirement for athletic horses should be increased. A similar principle would apply to horses recovering from athletic injuries, especially muscle injury.
Researchers have suggested that the appropriate concentration of selenium in the total diets of horses is 0.3 ppm or 2.5-3 mg per day, rather than the 0.1-ppm listed by the NRC (2007). This would mean that if a concentrate mix was 50% of the diet and the forage component of the diet was 0.1 ppm selenium, the grain mix would need to be roughly 0.5 ppm (mg/kg). Alternatively, use a supplement that supplies 2 mg in a daily dose. Some supplements now contain organic selenium, which has a greater availability than inorganic forms and is retained more efficiently by the exercising horse.
The only known function of iodine is as part of the thyroid hormones thyroxine and triiodothyronine. The classic deficiency symptom for iodine is a hypoiodine goiter, and the classic toxicity symptom is a hyperiodine goiter. As such, the only real way to assess the adequacy of the diet is to evaluate the ration.
Thyroxin and the tissue-active form of the hormone, triiodothyronine (T3), serve a multitude of metabolic and regulatory roles. The thyroid hormones affect all of the organ systems as well as muscle metabolism. Thyroxine also controls growth rate, metabolic rate, and oxidative metabolism. Unfortunately, no one has determined whether this apparent lack of thyroactive hormones is due to a lack of iodine in the diet, a lack of selenium for the conversion of T4 to T3, or dysfunction of the thyroid gland.
Current NRC (2007) recommendations for iodine are 0.1 ppm, though Kentucky Equine Research (KER) proposes that the 1,100-lb (500-kg) horse at light work requires 1.75 mg of iodine, at moderate work 2.5 mg, and in intense training 2.75-3 mg/day of iodine. There is still a great deal of work to be done in understanding the relationship between dietary iodine and thyroid function.
Because the iodine content of individual feed ingredients is difficult to measure, it seems logical to choose a supplement that supplies at least 2 mg or a premixed feed that contains at least 0.5 mg/kg. Seaweed meal products are a popular supplement that contains lots of iodine and precious little of anything else. If you feed seaweed meal your horse will not be iodine deficient, but unfortunately some products have a narrow safety margin as they contain 50% of the toxic dose in the recommended daily intake. Never feed seaweed meal as a free-choice supplement.
The recognized function of chromium is as a component of glucose tolerance factor (GTF). GTF is thought to potentiate the action of insulin in chromium-deficient tissue. Insulin has anabolic characteristics as it promotes glucose uptake by the cell, stimulates amino acid synthesis, and inhibits tissue lipase.
Because of its role in carbohydrate, lipid, and protein metabolism and in the clearance of blood glucose, it is interesting to consider the requirements of the athletic horse for chromium. Chromium excretion is greater in athletic than in sedentary humans, and the chromium requirement is increased by physical activity. Chromium supplementation has increased lean body mass in humans and pigs and has resulted in a partitioning effect on nutrients that favors tissue anabolism and muscle protein accretion. In calves, chromium excretion is greater during stress and chromium supplementation has resulted in stimulation of the immune system and less mortality and morbidity in shipped feedlot cattle.
The role of copper in the copper-dependent enzyme lysyl oxidase and that enzyme's role in the formation and maturation of cartilage are important in recovery from joint injuries. It is interesting to note that in addition to its role in cartilage and bone metabolism, copper is also involved in hemoglobin formation, nerve conductivity, and coordination. Ceruloplasmin, the principal copper-carrying protein in blood, increases rapidly following injury and inflammation. This protein is essential for collagen formation, collagen cross-linking, and collagen maturation so connective tissue is strong and elastic. Copper protects the healing tissues from the effects of superoxide radicals produced by phagocytes during the debridement stage of healing. Ascorbate and cysteine, two important cofactors in healing, are activated by ceruloplasmin.
Currently, KER recommends that an 1100-lb (500- kg) performance horse receive 130-190 mg/day of copper depending on workload. With protein and calcium intakes often elevated due to the use of alfalfa (lucerne) hay and with typical premixed feeds ranging from 0.6-1% calcium, there is justification for higher copper inclusion rates than previous recommendations. Low copper levels are common in pastures, hay, and grains relative to these requirements. Look for a supplement that supplies at least 120 mg per day or a feed that contains at least 35 mg/kg.
Zinc is involved as a cofactor in a multitude of enzyme systems. In addition to the role of zinc as enzyme activator/cofactor, there are more than 200 zinc-containing proteins. About 55% of the zinc in the body is stored in the muscle. In terms of bone metabolism, zinc deficiency directly inhibits the effectiveness of somatomedin in stimulating cartilage growth. The classic symptom of zinc deficiency is disrupted keratogenesis.
High levels of calcium and copper can reduce zinc absorption, so the kind of hay being fed may have an impact on the amount of zinc required by the horse. Increased levels of protein have been shown to reduce zinc absorption and increase zinc excretion. KER currently recommends the zinc intake of the performance horse in moderate and heavy work should be 500 mg/day, with 400 mg/day considered adequate for the horse in light work. When the efficacy of hoof supplements is considered, the inclusion of organic (chelated) zinc-methionine along with 15 mg biotin and 3 g of methionine appears to result in greater growth of the tubular horn of the hoof wall than does the feeding of biotin alone.