Vitamin K

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Written By Dr. Kris Hiney

This month we will wrap up our discussion of the fat soluble vitamins with a vitamin that is not discussed all that often in regards to horses, vitamin K.  Vitamin K is actually a family of fat soluble vitamins from both plant and animal origins. Vitamin K in the diet occurs in the form of phylloquinone,  which is found in plants.  Phylloquinone can be converted to menaquinone via intestinal bacteria, or by other tissues within the animal.  Menaquinone is the active form of the vitamin for animals.  Most people recognize vitamin K’s role in blood clotting, but it is also a part of bone metabolism, vascular health, and even brain metabolism.

Vitamin K acts to cause the carboxylation of glutamate (an amino acid) in proteins.  This carboxylation reaction allows proteins to bind to Ca.  This is a key part of the cascade of events which occur during blood clotting.  Vitamin K deficiency is typically seen as a decreased ability to clot blood, or internal hemorrhaging.  Vitamin K is also important for the action of osteocalcin, which is a hormone needed for bone metabolism.  It is thought that supplementing vitamin K may help with osteoporosis in the elderly. Luckily in horses, deficiencies of vitamin K from consuming a nutritionally inadequate diet have not been reported.  The amount of phylloquinones present in green forages combined with the menaquinone production in the body leave little reason for supplementation.  If supplementation is desired, both phylloquinones and menaquinones have wide safety margins.  However, menadione has been linked with toxicity issues when given at manufacturer’s recommendations.  Typically vitamin K would only need to be administered to horse’s if they are on a therapeutic regimen of warfarin, an anti-clotting drug.

However, it is possible for horses to become vitamin K deficient by consuming substances which interfere with vitamin K.  Dicoumarol is a substance which is an antagonist of vitamin K, and blocks the blood clotting cascade.   Coumarin is the original chemical which is converted to dicoumarol by fungi. Clovers naturally contain a high content of coumarin, which in and of itself has no ability to affect coagulation. It is only through the action of fungi which transforms coumarin to dicourmarol.  Thus, moldy sweet clover hays are to be avoided.  Unfortunately the mold may not always be visually detectable.  Luckily, this syndrome, often referred to as sweet clover poisoning, rarely occurs on pasture.  It is important when creating clover hay that adequate drying time is achieved, which decreases the likelihood of molding.  However, this is often difficult when drying clovers due to their coarser stem.  Crimping may help decrease drying time and help to avoid molding.  Large round bales, especially the outer layer of hay, tend to be much higher in mold content.  Overall, sweet clover poisoning is seen much more commonly in cattle than it is in horses, but is not unheard of.  Unfortunately, as dicoumarol poisoning results in internal bleeding, it is often hard to detect in animal which has been exposed.  Stiffness of gait may be an indicator due to bleeding within the muscle.  Unfortunately it is often death that results in diagnosis.  As it is almost impossible to determine visually if sweet clover hay contains dicoumarol it is often recommended to be avoided.  If not, sweet clover hay can be fed intermittently with a high quality alfalfa which is high in vitamin K.   Feeding sweet clover hay for a period of no more than 7-10 days is recommended. No animals which may soon undergo surgery or parturition should be given sweet clover hay for the period of four weeks prior.  Overall, it may just be easier to forego sweet clover hay altogether.

Next month we will begin discussion of the many water soluble vitamins, their functions, and requirements by the horse.

Vitamin D

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Written By Dr. Kris Hiney

Last month we began a discussion of what we currently know about the vitamin requirements in horses.  Unfortunately, the actual vitamin requirements for a particular horse are often hard to define.  Most vitamin requirements represent the amount needed in the horse’s diet to prevent the classic deficiency symptoms.  However, as stated previously, that may not be the same as the amount required for optimum health, well-being, or even performance.  It is certainly possible that the vitamin requirements for the horse might also alter with their stage of life, work load and management.  With this in mind, we will continue our vitamin discussion with the fat soluble vitamin D and what we currently know.

Most individuals with some nutritional knowledge are familiar with vitamin D’s role in calcium absorption, and that it is synthesized  by the skin when exposed to sunlight.   However, the various precursors of vitamin D, and its active and inactive forms may be less familiar.  To provide some background, vitamin D is actually a steroid hormone.   Horses consume  vitamin D naturally from plants in the form of ergocalciferol, or vitamin D2.   In manufactured diets, vitamin D is typically supplemented in the form of vitamin D3, or cholecalciferol. Horses also synthesize D3  from skin exposure to ultraviolet light, through the conversion of  7-dehydrocholesterol into cholecalciferol.  Dietary  ergocalciferol and cholecalciferol are absorbed out of the small intestine and where it is converted to 25, hydroxycholcalciferol in the liver, or calcidiol.  Calcidiol is the compound that is typically used as an indicator of vitamin D status, as it closely reflects both dietary intake and skin synthesis.  However, horses do differ in the concentration of calcidiol in the blood in comparison to other animals, as it is much lower. All of the forms listed above represent inactive forms of the vitamin. One more reaction must take place in the kidney  before vitamin D is in its active form of the vitamin: 1,25- dihydroxycholecalciferol, or calcitriol. This final reaction is actually tightly regulated according to body needs.  More calcidiol will be converted to this active form, calcitriol, when needed.

Activated vitamin D directly acts to regulate the amount of calcium and phosphorous circulating in the blood.  It can act to increase the amount of calcium in the body by increasing its rate of absorption out of the small intestine, and increasing reabsorption by the kidney.    Vitamin D promotes mineralization of the skeleton through its regulation of calcium, and deficiencies of vitamin D result in osteomalacia.   In young animals and humans, this is referred to as rickets.  While the function of calcium regulation is commonly known,  vitamin D is actually involved in the normal function of a variety of tissues.  Beyond bone health, vitamin D also has a role in in cell growth and tissue differentiation.  Vitamin D receptors have been found in all cell types in the body, emphasizing its much wider role in the physiology of the body.

In human nutrition, vitamin D and its role in other body functions, particularly immune function, has been more fully explored than in any of our animal species.   Macrophages, large immune cells capable of engulfing pathogens, produce calcitriol locally.  Here vitamin D is used as a cytokine , or a substance released in response to the presence of an antigen, which acts as a cellular mediator and enhances the immune response.  In humans, low vitamin D status has been linked to cardiovascular disease, auto immune disorders, neoplasias, infectious disease and even psychiatric disease.  Of the autoimmune diseases linked to vitamin D deficiency, these include type I diabetes mellitus, Crohn’s disease, rheumatoid arthritis and multiple sclerosis.  Indeed many cancers have also been linked to hypo-vitamin D status.   However, with this said, large scale studies have been inconclusive, yielding conflicting results.    Recently,  supplementation of vitamin D in controlled studies was found to be ineffective in preventing the common cold or upper respiratory infections.  However, the possibility exists that some of the diseases listed above may actually result in the destruction of vitamin D rather than being caused by its deficiency.   It is interesting that here in the US, the only legal claim which can be made in regards to vitamin D supplementation is that it can reduce the risk of osteoporosis, yet in the European Union, products can also state that vitamin D helps with normal function of the immune system, and normal inflammatory response.

Most work in animals has really only centered on bone metabolism and calcium homeostasis, which is not surprising as the link to overall health and human nutrition is somewhat new.  Human nutritionists have now recognized that the amount of vitamin D needed to prevent rickets is inadequate to maintain other vital functions.  However, remember that random supplementation is never advised, and results in humans can never be directly extrapolated to animals in general, let alone horses specifically.   In addition, over-supplementation is never recommended.  While vitamin D toxicity is unlikely, it has occurred experimentally.  Vitamin D toxicity is marked by calcification of the soft tissues, and can be fatal.  Interestingly, it is actually used in lethal doses in baits as a rodenticide, when combined with calcium.

So what does all of this mean for your horse?   It has been shown repeatedly that vitamin D in the blood is higher in the summer than the winter, which would certainly make sense as the sun is the principle source of vitamin D for most horses. Most management systems where the horse is regularly pastured or turned out  where it is exposed to sunlight will be sufficient to provide enough vitamin D.  However, many performance horses are stalled almost continuously, even more so in the winter.  For these horses, it is important that they do receive a feed which contains vitamin D. In the past, the vitamin D requirements of the horse have been stated to be 300 IU of vitamin D per 100 lbs.  Currently, the requirement is 6.6 IU/kg bwt for horses not exposed to sunlight, with the exception of growing horses.  Growing horses requirements are stated to be much higher, 22.2, 17.4, 15.9 and 13.7 IU/kg bwt for horses from 0-6, 7-12, 13-18 and 19-24 months respectively.  This is due to the need to form bone properly as the animal grows.  To provide a quick example, a 650 lb horse who is 15 months old would require:

650 lbs converted to kg-  295 kg * 15.9 IU/kg bwt = 4698 IU of vitamin D per day.

Next month will discuss the role of vitamin E and its  various effects on the health of your horse.