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Trace Mineral Benefits

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There are seven trace minerals that have been shown to be needed in supplementing animal diets. They are iron, copper, zinc, manganese, cobalt, iodine and selenium. They are needed in very small amounts, or traces, in the diet. That is why they are called trace minerals.

ProVision can help with these traces and nutrients in your horses diet be more readily absorbed to ensure a healthier life for your horse in the future. Offer our Himalayan Salt too as your salt source, because it will offer your horse much more than any other salt can. It has 84 trace elements and minerals.

Modern U.S. agricultural practices, within the last 75 years, have nearly eradicated all of the naturally occurring organically complexed ionic trace minerals found in our soil. In doing so, we have eliminated these naturally occurring indispensable elements from the crops. Many diseases and sicknesses can be linked to mineral deficiencies. Organic Beauty's ProVision will not only offer your horse these essential missing traces of life, including Chromium which is being found to be very important to horses, but will also allow the proper absorption process to occur, which is also very critical. These supplement will also help make nutrients in your horse's diet more readily absorbed. By using ProVision and our Himalayan Salt you will be giving your horse back these extremely powerful missing links. These organic minerals, not synthesized, are greatly needed by the body in order for maximum health.

Subclinical trace mineral deficiencies occur more frequently than recognized by most livestock owners. Currently this is a bigger problem than clinical mineral deficiencies, because the livestock owner does not see specific symptoms that are characteristic of a subclinical trace mineral deficiency. Instead, the immune system can become depressed, insufficient bone development in foals, stillborns, central nervous system disorders in offspring, fertility complications with mares and stallions, etc can occur. In highly competitive animal enterprises, sufficient trace mineral absorption can be the difference between profit and loss.

There are several examples where an area of the country was not recognized to be trace mineral deficient in the past but now has been shown to require supplementation. For example, a selenium deficiency was not considered a problem in the United States until relatively recently. Now at least 44 states have been shown to contain low-selenium areas. In only a few states have the classical selenium deficiency symptoms been observed, but performance responses have demonstrated the need for selenium supplementation. When a cobalt deficiency was first found in Western Australia, the problem was believed to be confined to about 5,000 acres. Further studies showed that at least 25 million acres are cobalt-deficient in Western Australia.

Another factor to consider is the shipment of feeds from one region to others. This alone makes it almost impossible to isolate areas of specific trace mineral deficiencies. There is nothing to prevent feed grown in a trace mineral deficient area from being shipped to another area where the feed grown is supposedly adequate in that mineral. For example, corn and soybeans grown in Midwestern states with areas deficient in selenium, iodine and other trace minerals are shipped to and fed in many other areas of the United States and the world.

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Important Nutritional Information

Developmental orthopedic disease (D.O.D.) can be loosely defined as any musculoskeletal disorder that occurs in the young animal as a result of growth and maturation. Invariably, it is related to the process of endochondral ossification and the maturation of cartilage to bone in the developing skeletal system. In the horse there are four clinical manifestations; physitis, osteochondrosis, angular limb deformity, and flexural limb deformity. Etiological factors involved include trauma, excessive concussion, illness, conformation, genetic predisposition, and nutrition.

Nutritional factors related to D.O.D. in animals less than eight weeks of age include; unbalanced mineral intake of either major or trace minerals, excessive quantities of mare's milk or unbalanced minerals in the milk. D.O.D. in animals under 4 months of age is due to inadequate intake of a balanced ration, over production of milk by the mare, or the foal is experiencing a rapid growth rate. D.O.D. in weanlings and yearlings is usually due to a ration incorrectly balanced, or rapid growth rate and/or excess body weight.

Osteochondrosis is a local or generalized failure of endochondral ossification affecting epiphyseal and/or metaphyseal cartilage. In the horse there are two clinical syndromes: osteochondrosis dessicans (OCD) and subchondral cyst-like lesions (bone cysts). Normal endochondral ossification occurs in the bones of the extremities, vertebral column, pelvis, and base of the skull. The bone is formed from a hyaline cartilage matrix, which is replaced by bone. There are several steps in normal endochondral ossification. Chondrocytes mature and enlarge. The intracellular matrix thins and the mature chondrocyte produces alkaline phosphatase, which causes calcification of the intercellular matrix. Calcification of the matrix causes chondrocytes to die due to lack of adequate nutrition. Capillaries invade the region bringing osteoblasts and the osteoblasts produce bone, which matures to lamellar bone.

Osteochondrosis occurs when cartilage cells proliferate normally but maturation and differentiation is abnormal. Failure of cartilage matrix to calcify or failure of vascular penetration and osseous replacement results in thickened cartilage. Cartilage necrosis develops in deeper layer fissures due to lack of nutrition and a cartilage flap (OCD) formation occurs. Another scenario is the thickened cartilage persists without fissuring and becomes surrounded by subchondral bone as adjacent cartilage continues endochondral ossification; the retained cartilage dies resulting in a subchondral cyst-like lesion.

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Iron has been recognized as an essential nutrient for hundreds of years. Even though, iron deficiency is still a major problem in several areas of the livestock industry.

Iron is a part of hemoglobin, the compound in blood that transports oxygen. It is also important in the enzyme systems that produce adenosine triphosphate. ATP is the body's energy currency that drives muscle contraction during exercise.

Approximately two-thirds of body iron is present in hemoglobin in red blood cells and myoglobin in muscle, 20% is in labile forms in liver, spleen and other tissues with the remainder in unavailable forms in tissues such as myosin and actomysin and in metalloenzymes. In hemoglobin, which contains 0.34% iron, an atom of ferrous iron in the center of a porphyrin ring connects heme, the prosthetic group, with globin, the protein. The iron in hemoglobin is essential for the proper function of every organ and tissue of the body. Iron also plays a role in other enzymes involved in oxygen transport and the oxidative process.

Iron is mainly absorbed in the duodenum. However, only 5% to 10% of what is consumed is absorbed. Once absorbed, the body tenaciously holds on to the iron for reuse. For example, most of the iron released from red blood cell breakdown is used to synthesize new hemoglobin. However, if the red blood cells are not replaced as rapidly as they are destroyed, anemia occurs. Anemia may occur at any stage of life. To help prevent anemia from occuring we recommend giving ProVision and offering the Himalayan Salt to your horse.

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Copper is required for the activity of enzymes associated with iron metabolism, elastin and collagen formation, melanin production, and the integrity of the central nervous system. It is required for normal red blood cell formation by allowing iron absorption from the small intestine and release of iron in the tissue into the blood plasma. Ceruloplasmin is the copper-containing transport protein. Copper is required for bone formation by promoting structural integrity of bone collagen and for normal elastin formation in the cardiovascular system. Copper is required for normal myelination of brain cells and spinal cord as a component of the enzyme cytochrome oxidase which is essential for myelin formation. Maximum immune response is also dependent on copper.

Copper plays a very important role in the synthesis of cartilage during bone development in growing horses. Low intakes of copper have been linked to increased incidence of developmental orthopedic disease, osteochondrosis, wobbler syndrome and many other manifestations in growing horses.

There is a chance that copper deficient mothers can produce offspring with permanent central nervous system disorders, that may not be reversed even with adequate supplies of copper after birth. This is why it is very important for pregnant mares to have these important trace minerals in their diet.

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Zinc is used for bone metabolism, reproduction, and immunity; Zinc is required for normal protein synthesis, and it is also a component of insulin so that it functions in carbohydrate metabolism. Because zinc plays so many important roles in the body, it is required by all livestock.

Absorption of zinc occurs throughout the small intestine and usually ranges from 5% to 40% of the intake. Transfer of zinc out of the intestinal mucosal cells to the plasma is regulated by metallothionine.

Increased levels of protein intake can decrease zinc absorption and increase zinc excretion.Zinc absorption can be reduced whenever diets are high in calcium and copper.This means that the kind of hay being fed can have a major impact on the amount of zinc required by a horse.Plant protein supplements ,like soybean meal and others, can sometimes create losses of zinc by phytate phosphorus.

Zinc deficiency in horses can have results such as parakeratosis, retention of nuclei in the cells of the stratum corneum of the epidermis, observed in many scaling dermatoses such as psoriasis and subacute or chronic dermatitis, reduced insulin levels and reduced glucose tolerance as well as increased insulin resistance, especially showing up in the peripheral tissues. A decrease in glucose utilization has also been seen with an increase in fat catabolism. Zinc deficiency directly inhibits in bone metabolism the growth of cartilage. A zinc deficiency in a foal can result in reduced appetite and growth rate, parakeratosis with considerable lesions in the feet, legs and head and loss of hair. Horses will also show reduced tissue and blood zinc levels and reduced blood alkaline phosphatase.

Research suggests that zinc along with copper and calcium play key roles in the prevention of Developmental Orthopedic Disease (DOD).

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Manganese was first recognized as a necessary nutrient for animals in the early 1930s. Bone, kidney, liver, pancreas, and pituitary gland are the sites of highest manganese concentration. awardRelative concentration is quite low compared to the other trace minerals. For example, in humans, total body manganese is approximately 1% of the zinc and 20% of the copper. Although concentrations are low, it is a critical nutrient for several functions.

Manganese is essential for chondroitin sulfate synthesis, which is critical to the organic matrix of bone. Many enzymes required for the synthesis of polysaccharides and glycoproteins require manganese to be active. Manganese is a key component of the metalloenzyme, pyruvate carboxylase, a critical enzyme in carbohydrate metabolism. Lipid metabolism is also dependent on manganese to allow the liver to convert mevalonic acid to squalene. Deficiencies of Manganese are expressed as disorganized cells that make up the epiphyseal plate, which causes a narrowing of the epiphyseal plate and a reduction of blood vessels going to the growth plate of the horse. Manganese is a very, very essential trace mineral in the role of bone formation and cartilage formation.

High dietary intake of calcium, phosphorus, and iron reduce manganese absorption. The body has only a limited storage of mobilizable manganese reserves. The absorption of manganese in all domestic livestock is poor. This is where ProVision and a salt lick can be of benefit.

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Cobalt is important for the synthesis of vitamin B12, which is produced by microbes in the horse's large intestine, and once absorbed is used for red blood cell formation. Cobalt deficiencies have not been observed in horses. In a few instances where cobalt has created some response, it is assumed that the diet lacked vitamin B12.

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Iodine is a major component of thyroid hormone, which is an important regulator of metabolic processes. Although iodine is essential, too much can be toxic. Supplements containing kelp might be very high in iodine and should be used cautiously, particularly if other iodine supplements are included in the diet.

Iodine deficiency might affect thyroid hormone concentrations. Pregnant mares may not show external signs of iodine deficiency but may produce a stillborn foal or one showing extreme weakness at birth, resulting in an inability to stand and suckle the mare. Foals born alive with a well developed goiter will usually die or will remain weaklings the rest of their life if they live. Deficient mares may exhibit abnormal estrus cycles in the absence of goiter. Navel ill in foals may be lessened by making sure broodmares have adequate balances. Insufficient levels of iodine may decrease sex drive and may effect semen quality in breeding stallions.

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Selenium is very important in the body's immune response in trapping free radicals and superoxides. It is a very important part of the enzyme glutathione peroxidase. This enzyme is the one that destroys peroxides and turns them into harmless alcohols before they can damage body tissues. This conversion prevents loss of membrane integrity. This further shows that exercise creates increased oxygen delivery to the tissues and can produce reactive oxygen by-products, peroxides, meaning that selenium is a very important trace mineral to performance horses also. Vitamin E is also effective as an antioxidant. Therefore, both selenium and vitamin E help to prevent peroxide damage to body cells. This aids the body's defense mechanisms against stress. Most feeds contain compounds that can form peroxides. Unsaturated fatty acids are a good example. Rancidity in feeds causes formation of peroxides that destroy nutrients. Vitamin E for example, can be easily destroyed by rancidity. Selenium spares vitamin E by its antioxidant effect as a constituent of glutathione peroxidase.

Selenium and vitamin E are interrelated. Both are needed by animals and both have metabolic roles in the body in addition to an antioxidant effect. Sometimes vitamin E will substitute in varying degrees for selenium, or vice versa. However, in some cases there are deficiency symptoms that respond only to selenium or vitamin E. Selenium cannot replace vitamin E in nutrition, but it can reduce the amount of vitamin E required and delays the onset of vitamin E deficiency symptoms.

Selenium deficiency can cause weak foals. When mares are consuming selenium-deficient diets, foals can be born with white muscle disease, which affects their hearts and skeletal muscles, often resulting in death


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Chromium is a component of the glucose tolerance factor (GTF). In Chromium deficient tissue, GTF can multiply the action of insulin.

Insulin has anabolic characteristics as it helps the cell take glucose and stimulates the synthesis of amino acids and restrains tissue lipase, or fatty acid. It plays a large role in protein metabolism along with carbohydrate and lipid metabolism and in the clearance process of blood glucose. This makes chromium very important to the athletic horse especially. Chromium may help horses that routinely tie-up by it's role in GTF and assisting in clearing glucose and making glycogen utilization and storage more efficient. The excretion of chromium can be greater during athletic activity, thus making the requirement of chromium increased by physical activity. Chromium has an important role, just as all of the other trace minerals do, in a healthy immune system.

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Disclaimer: All information contained on this website is based on research and testing to date and is for informational and educational purposes and is not intended to make any unsupported medical claim or the claim that any product is intended to cure, treat or prevent any disease. These statements have not been evaluated by the Food & Drug Administration (FDA). Any serious health concern should be treated by a qualified veterinarian or physician.

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