This month we will conclude our discussion of vitamins with the B vitamins. There are many vitamins that are traditionally referred to as the B vitamins, including thiamin, riboflavin, niacin, pyridoxal phosphate, panthothenic acid and cobalamin. You may even associate them with their “numbers” so to speak: B1, B2 etc. These are all water soluble vitamins which can be synthesized by the microbial population of the hindgut of the horse. In many circumstances this microbial synthesis of vitamins is adequate to support normal physiological functions in the horse. However, under some conditions, supplementation of these vitamins becomes necessary. Unfortunately relatively little is actually known about the true requirements of the horse for many of these vitamins. We will primarily focus on the vitamins which have the most information available; thiamin, niacin, riboflavin and biotin.
We will begin our discussion of the significant B vitamins with thiamin, one of the most commonly supplemented B vitamins. Thiamin is a vitamin which is required in many reactions which support energy metabolism, or the production of ATP. Deficiencies of thiamin in the horse can result in muscle fasciculation, ataxia and most frequently in appetence. However, true thiamin deficiencies in horses are very infrequent. Nevertheless, it is often supplemented when horses go off feed to restore their appetite. There is some evidence that the exercising horse may require more thiamin, which is presumably related to their higher rate of metabolism. Dietary sources of thiamin are typically found in the concentrate portion of a horse’s diet. Cereal grains, their by-products, and brewer’s yeast are especially high in thiamin. Overall, maintenance horses are currently recommend to consume 3 mg thiamin/kg of DM consumed while exercising horses should consume 5 mg of thiamin/kg of DM. If we use a standard 500 kg horse as an example, and assume it is consuming 2% of its body weight in dry matter (or 10 kg of feed), this horse should consume between 30-50 mg of thiamin per day.
Riboflavin, historically referred to a B2, is another vitamin which is required in energy producing pathways, especially in the electron transport chain. Riboflavin also functions in lipid metabolism and as an anti-oxidant. Riboflavin, like thiamin, is synthesized in the hindgut of the horse through microbial fermentation. Interestingly, no documented cases of riboflavin deficiencies have been reported in the equine. Legumes are relatively high in riboflavin, so horses consuming alfalfas or clovers should have little difficulty in meeting their riboflavin requirements. Even horses consuming grass sources of forages easily meet their riboflavin requirement. The current recommendation of horses is to consume 2 mg of riboflavin per kg of DM, but even grasses contain 7-10 mg of riboflavin/kg of DM. Therefore there appears to be little reason to supplement horses with riboflavin.
Niacin, traditionally referred to as B3, participates heavily in oxidation/reduction reactions in the body which are vital to energy metabolism. Niacin can not only be produced in the hindgut, but it can further be synthesized by the horse through the conversion of tryptophan to niacin within the liver. Like riboflavin, niacin deficiency has also not been described in the horse. Currently, there is not even a recommended dietary intake for horses for niacin.
Biotin is a water soluble vitamin which is a co-factor in many carboxylation reactions (addition of carbon to a compound). These are important reactions in gluconeogenesis (the synthesis of glucose by the body) and fatty acid synthesis. Of traditional horse feeds, alfalfa supplies the highest concentration. Once again, the microbial microflora are also quite capable of synthesizing biotin. While no distinct deficiencies of biotin have been reported, low quality hooves are often associated with low biotin. Supplementation of biotin in the range of 15-20 mg day has been reported to improve hoof wall integrity, structure and strength. However, when supplementing biotin, horse owners must realize that significant effects do take quite some time to be realized. The shortest time period of supplementation which achieved positive effects on hoof growth and hardness was 5 months, with some studies reporting a need to supplement for over a year.
Finally, there are certainly many other vitamins that may be of interest to the horse owner, such as folate, lipoic acid, cobalamin etc. We do know that synthesis of cobalamin, or B12 does require the mineral cobalt to be incorporated. However, horses appear to be quite capable of doing so and do not appear to need any supplementation. In fact, horses can graze cobalt deficient pastures with no ill effect where ruminants would die from deficiency diseases. Currently there is a paucity of information available to guide the horse owner in best practices concerning many of these other vitamins. Perhaps someday we will know more about these important vitamins and can make better recommendations for dietary values to enhance the health status of the horse. Until then, just be thankful your horse has its gut bugs, he couldn’t do it without them!
Previously, we have discussed two important fat soluble vitamins which serve an important anti-oxidant function in the horse, vitamin A and E. We will continue to discuss anti-oxidants as we transition to the water soluble vitamins essential to the health and well-being of the horse. As humans, we are probably very familiar with vitamin C or ascorbic acid/ascorbate, as it is a commonly supplemented vitamin. After all, who hasn’t reached for an orange in order to get their share of this important vitamin (Despite the fact there are many more nutrionally dense sources of vitamin C!)? People often turn to vitamin C during times of stress or illness, especially the common cold, to try and fight off pathogens. But what does vitamin C do in the horse, and should you be supplementing it?
Typically, most individuals are familiar with vitamin C’s role as an anti-oxidant, but it also serves as a co-factor for a host of enzymes. Specifically, vitamin C is necessary for the formation of collagen, which appears throughout the body in connective tissue of tendons, ligaments, blood vessels etc. Vitamin C also is necessary for the synthesis of carnitine (the molecule which allows fatty acids to be transferred into the mitochondria for oxidation) as well as tyrosine and other neurotransmitters. Vitamin C supplementation, along with other anti-oxidants, has actually been shown to improve cognitive disfunction in aging dogs.
Vitamin C is synthesized in horses, but not in man, guinea pigs or a variety of other species. Therefore in humans, vitamin C is a dietary necessity, but it is not required in the diet of the average horse. The horse is capable of converting glucose through a variety of enzymatic reactions into ascorbic acid. This synthesis is adequate in most scenarios. So when might vitamin C be beneficial to the horse? Presumably when there is a need for greater amounts of anti-oxidants in the body.
We have discussed the role of anti-oxidants before. The body uses oxygen as the final electron acceptor in the electron transport chain during the capture of energy in the form of ATP. Normally this process produces a harmless, and even useful byproduct – water. However, a small proportion of these reactions does not go according to plan, but instead creates a harmful molecules known as reactive oxygen species or ROS. In actuality, the formation of free radicals is a normal part of metabolism and serves as cell signaling systems. In fact, the creation of free radicals stimulates the adaptive response seen with athletic training. Therefore, we should not aim to eliminate their presence entirely. However, in excess, these free radicals can do immense damage to the body as they damage DNA, cell membranes etc. Reactive oxygen species have been implicated in carcinogenesis, aging, cognitive function etc. Ascorbate aids in the anti-oxidant cascade by regenerating the reduced form of vitamin E and other anti-oxidants.
Horses which are intensely exercised will naturally produce a greater number of reactive oxygen species due to the increased rate of metabolism. It is not uncommon for those individuals involved in more strenuous equine sports (endurance rides, three day eventing etc.) to routinely supplement their horses with anti-oxidants. In studies which have examined the use of vitamin C in horses, there appears to be a difference in response relative to the intensity of the work being performed. In polo ponies, plasma ascorbic acid was higher in ponies which were considered to be more intensely working than the lighter worked ponies, despite both groups receiving supplemental vitamin C. Similarly, endurance horses supplemented with vitamin C had a higher plasma ascorbic acid level at the beginning of the race compared to the control horses, but the difference between plasma vitamin C levels between the two groups grew smaller throughout the race. The unsupplemented horses actually increased their plasma ascorbic acid levels throughout the race, presumably through the mobilization of body stores. This differed in previous studies which showed a decrease in plasma ascorbic acid in more intensely worked horses. This drop in ascorbic acid has also been reported in heavily raced sled dogs. Thus it may be the level of exercise which is important. Certainly this makes sense as the level of effort increases, the metabolic rate must increase and the greater percentage of ROS will be produced. Although lacking in concrete data, it appears that additional vitamin C may be beneficial for heavily exercised horses.
Exercise is not the only form of stress which horses may experience. Plasma vitamin C levels have been seen to be lower in horses following surgeries, traumatic wounds, strangles and episodes of exercised induced pulmonary hemorrhage. Horses with recurrent airway obstruction also have had lower plasma ascorbic acid levels, and supplementation appears to be helpful in creating better exercise tolerance and reduced airway inflammation. Supplementation of vitamin C also appears to help aged horses enhance their immune system and improves their response to vaccinations. Horses do appear to tolerate large doses of vitamin C quite well, horses received 20 g /d of ascorbic acid for 8 months with no measureable negative response. However, it has been shown that horses decrease their own natural synthesis of vitamin C when supplemented. Therefore, when the supplement is removed, horses will have a lower plasma concentration of vitamin C compared to normal. Therefore, prolonged supplementation may be ill advised. Overall, like all vitamins previously discussed, supplementation of vitamin C should not be done without careful consideration of whether or not the horse would truly benefit from supplementation.
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.
We have already discussed two of the fat soluble vitamins in a horse’s diet. This month we continue with a closer look at vitamin E, a vitamin which is commonly supplemented to horses for a variety of reasons. It is often used for aging horses, horses which have muscle disorders and horses which undergo strenuous exercise. But how do you know if your own horse needs more vitamin E in its diet?
First, let’s explore the role of vitamin E in your horse’s body. Vitamin E occurs in a variety of forms (both tocopherols and tocotrienols). Of these, there are then four subgroups, α, γ, β and δ. While γ is the most common in the natural diet, the alpha form is the most potent in activity, the most supplemented and the subject of most studies. In their natural diet, horses receive the most vitamin E as γ tocopherol from growing forages or harvested forage that was cut at an immature state. As the plant ages, vitamin E decreases in content. Vitamin E concentration also decays over time in harvested forages, as much as 50% over one month. Therefore, older hays which have been stored for some time will have little activity. If you also feed non-processed concentrates to your horse (such as oats, barley, corn etc.) they will also be low in vitamin E. However, most commercial equine feeds will be supplemented vitamin E, usually as α tocopherol acetate. It can be provided as either natural α tocopherol or synthetic, with natural forms having 36% more biological activity than synthetic. The natural form has been shown to increase plasma α tocopherol concenrations greater than its synthetic counterpart but both are effective supplements.
(This is the structure of alpha tocopherol.)
Despite its form, vitamin E’s function is most frequently thought of as an anti-oxidant. Vitamin E can work to eliminate free radicals which are formed through the incomplete oxidation of oxygen or other molecules. During normal metabolism some amount of free radicals are always formed. However, stress, work, aging, poor nutrition etc can increase the amount of free radicals in the body. These are essentially molecules which are missing an electron, making them highly reactive. This is an unstable condition and the free radical can remove electrons from other cell components, such as lipids, cell membranes etc. Vitamin E, along with other anti-oxidants donates an electron to the free radical, thus stabilizing it and preventing further damage. One oxidized, vitamin E itself must be reduced back to its active form. This is usually accomplished through the action of other anti-oxidants in the body such as ascorbic acid or glutathione peroxidase. As the cells of the immune system have a high amount of polyunsaturated fatty acids which are quite susceptible to damage by free radicals, vitamin E plays a vital role in the optimization of the immune system. Furthermore, vitamin E plays a role in reproduction, gene transcription and platelet aggregation.
(Traditional concentrates such as just corn and oats may be relatively low in vitamin E content.)
Currently, vitamin E is recommended to be fed to maintenance horses and breeding horses at 1 IU/kg of body weight (not sure if your horse is a maintenance horse, see Energy Requirements). Growing horses and lactating mares are suggested to need more vitamin E in their diet, at double the rate of maintenance horses or 2 IU/kg body weight. Vitamin E intake for the working horse may need to be a bit higher. While the current recommendation for working horses is 1.8 IU/kg body weight for moderate work and 2 IU per kg body weight for heavy work, many research studies have provided Vitamin E at higher levels. Supplementation rates from 150-250 IU/kg DM, 300 IU /kg DM or even as high as 11.1 IU kg/body weight (in a simulated endurance race) have been found to be necessary to maintain blood and muscle concentration of vitamin E in more rigorously exercised horses. To make these values seem more familiar, if we assume we are feeding a 500 kg horse 2% of its body weight, than the range of vitamin E would be between 1500 – 5500 IU of vitamin E per day in these studies.
Therefore, Vitamin E is often part of the suggested management protocols for horses which are heavily exercising or may have muscle disorders. In fact, in a study looking at endurance horses and supplementation of Vitamin E, the authors were unable to create a control group as no riders were willing to not supplement their horses! However,i t has been difficult to prove the effectiveness of supplementation for the enhancement of the horse’s health. In exercised horses receiving 300 IU/kg DM of vitamin E compared to 80 IU/kg DM, or no supplementation of vitamin E, the higher rate of supplementation did increase the muscle concentration of vitamin E. However, it did not affect the indicators of oxidative stress in the muscle following a submaximal exercise test. Perhaps a difference would have been observed with a more aggressive exercise regimen. More recently, horses supplemented at a rate of 3000 IU per day of vitamin E compared to 80 IU/kg DM, underwent a training protocol. The anti-oxidant capacity of all the horses increased following training, which is a natural adaptation to exercise. There were no differences in reduced or oxidized glutathione peroxidase at rest, or total glutathione peroxidase. However after a standard exercise test, the horses receiving 3000 IU vitamin E did have more reduced gluthathione peroxidase, suggesting a greater anti-oxidant capacity. Horses exercised to fatigue following 8 weeks of supplementation of 3000 IU of vitamin E had less muscle oxidation as measured by myofibril carbonylation( a measure of protein oxidation).
(Heavily exercised horses may need more vitamin E in their diet than maintenance horses or lightly worked horses.)
Determining if your horse has a vitamin E deficiency may not be as straight forward as taking a blood sample. It has been shown that the concentration of vitamin E in the horse’s blood varies irrespective of diet. In one study, the variation within an individual horse in a 72 hr period would have shown the same horse as more than adequate in vitamin E, to marginal as well as deficient. Therefore, it may be more important to look at your feeding regimen and the feedstuffs your horse consumes to determine whether or not they may have a deficiency. The diet your horse is on may also affect his vitamin E needs. Vitamin E is protective against the peroxidation of lipids in the body, especially the polyunsaturated fatty acids. Horses which consume diets higher in PUFAs, which is certainly recommended in many cases, may increase the need for anti-oxidants in the body to prevent lipid perodixation. Thankfully, many sources of PUFAs may be higher in vitamin E content.
If your horse is older, they may also be a candidate for vitamin E supplementation. As horses’ age, their body systems may not function at the same level seen in their younger years. As in people, the immune system of our aged horses may begin to fail. When horses over 20 years of age were vaccinated for influenza, they were unable to mount the same immune response as their younger counterparts. Therefore, older horses may be prime candidates for supplements which are known to complement the immune system. In older horses fed vitamin E at 15 IU/kg of body weight, the bacterial killing ability of specific immune cells was increased, along with an increase in some, but not all, of the specific types of immunoglobins (or antibody). However, in this study, the horses were previously on a marginally deficient amount of vitamin E. Therefore, it is not known whether it was the correction of the deficiency or the over supplementation that yielded positive effects.
Horses are fairly tolerant of relatively high amounts of vitamin E in the diet. The upper range of vitamin E intake has been set at 1,000 IU/kg of DM. To think of this in more common terms, we will do a brief example using an 1100 lb horse that consumes 2% of its body weight. Thus this horse would typically consume 22 lbs of feed per day. We will convert this to kg to look at our total amount of vitamin E the horse should ever safely consume. 22 lbs of feed is equivalent to 10 kg of feed. Thus, the upper range of safe intake of vitamin E is 10,000 IU per day for a 500 kg horse.
However, vitamin E should not be used without caution. In human medicine supplementation of vitamin E has not always yielded positive results, and if fact can actually enhance the disease state. In humans undergoing heavy exercise, vitamin E supplementation actually decreased some of the positive adaptations to exercise. In addition, heavy supplementation has been actually linked to mortality. As always, supplementation is never the answer for a properly balanced diet. Overzealous supplementation may actually work against your horse’s health! But if your horse is older, more heavily worked or has added poly-unsaturated fatty acids in its diet, you might want to examine your diet for its Vitamin E content.
Next month we will finish our discussion of the fat soluble vitamins with vitamin K.
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.
This month we will begin a series examining the function of vitamins in the health and well-being of horses. We will also discuss natural sources of vitamins which occur in the horse’s normal feed, as well as different forms which are offered in supplements. Finally, we will look at the latest research on vitamins in equine nutrition. Unfortunately, there is a paucity of information regarding vitamin requirements in the equine. While recommended intakes have been established for vitamins A, D, E, thiamin and riboflavin, all others essentially fall into the category of educated guesses. Often equine nutritionists must rely on published information in other species, and extrapolate that to the equine. These suppositions may or may not be valid, but often allow the only approach available.
(If we were feeding these two hays, you would most likely need to supplement your horse with vitamin A if you were feeding the discolored hay.)
We will begin with a discussion of the fat soluble vitamins in a horse’s diet, in particular vitamin A. The fat soluble vitamins will be absorbed out of the gut of the horse along with the lipid component of the diet. While that may seem odd considering that horses naturally consume a very low amount of lipid in an all forage diet, remember that plant cells do contain waxes, sterols and other compounds that are soluble in ether. Even hay will typically contain around 2-3% crude fat on a DM basis.
While many of us know these fat soluble vitamins as their familiar names of vitamin A, D, E and K, we may not be as familiar with their scientific nomenclature. Vitamin A falls into the sub group of trans-retinols. Vitamin A, or retinol, serves a host of functions in the body, far beyond the traditional role of assisting in night vision. Vitamin A is also involved in gene expression, reproduction, embryological development and immune function. Metabolically, retinol can be converted to either retinal or irreversibly to retinoic acid. While retinal plays a role in vision, retinoic acid is more active in epithelial cells health, anti-oxidant function and gene expression. As retinol cannot be stored by itself in the body, it is stored in animal tissues as retinyl palmitate, or retinol linked by an ester bond to palmitic acid. In supplements, vitamin A typically is provided as retinyl-acetate or retinyl palmitate. In the intestine, retinyl palmitate is cleaved to just retinol. In the natural equine diet, horses primarily receive vitamin A as carotenoids, which are precursors to vitamin A synthesis in the body. The functional carotenoids include alpha, beta and gamma carotene, as well as beta cryptoxanthin. Of these beta carotene provides the highest vitamin A activity. Beta carotene is cleaved into two, to form retinal. The rate of conversion of beta carotene to vitamin A is actually dependent on vitamin A status, and will decrease if vitamin A intake is sufficient. Thus, no direct conversion ratio is actually appropriate, as the individual animal’s vitamin status alters its conversion rate. Additionally, as beta carotene intake increases, the rate of conversion to vitamin A may decrease, at least has been proved to do so in other species. Beta carotene is thus considered a very safe form of supplementation, as no toxicities have been linked to beta carotene consumption. Animals will decrease the conversion to vitamin A, thus avoiding toxicities.
With that said, we can attempt to generalize the biological activity of the different forms of vitamin A. For instance, .3 micrograms of all trans-retinol is equivalent to 1 IU, or international unit, of vitamin A. In the conversion of beta carotene to vitamin A, differing values are used for equine diets. Original estimates were 400 IU of vitamin A are created for every mg of beta carotene consumed. However, beta-carotene may have a different conversion rate between life stages of the equine. In brood mares, an estimate of 555 IU for every mg of beta carotene is used, while it is presumed to be only 333 IU of vitamin A per mg of beta carotene in growing horses. While this conversion data is actually extrapolated from studies in rats, it does appear to be reflected in horses. Mares kept on the same pastures as yearlings had higher serum retinol concentrations than the yearlings, while the yearlings had higher serum beta carotene concentrations. This does indicate that the mares were more efficient in converting beta carotene to retinol.
Natural sources of vitamin A are higher in fresh, growing forages, and are associated with the bright green color in hay. Many horse owners associate the bright color of corn with a substantial amount of vitamin A, but it actuality it contains only about 6 mg/kg of DM of beta carotene. Concentrations of beta carotene in hay can range as much as only 30 mg/kg of DM to as much as 380 mg/kg of beta carotene. Thus, corn, is typically much lower in beta carotene activity than hay. Typically, the content of beta carotene is reflected in the quality of the hay. What we typically call low quality hay, that of excessive maturity, lengthy storage, rain damaged, sun exposure etc. will be potentially deficient in vitamin A. The type of the hay also influences vitamin A content. Legume hays not only have higher concentrations of vitamin A, but it may be more available as well. We can do a quick calculation using an intermediate conversion number of 400 IU of Vitamin A/mg of beta carotene and the range of beta carotene seen in hays. Per kg, forage can vary from 1200 IU of vitamin A per kg, to as much as 152,000 IU per kg of hay. The requirement for vitamin A for a maintenance horse is recommended to be 30 IU/kg of bwt. Thus our 500 kg horse is would need 15,000 IU per day. Assuming he was eating 2% of his body weight in a low vitamin A forage (typically mature ), he would be receiving only 12,000 IU per day, which would be short of his requirement. Horses which were fed a low quality forage with no grain supplementation were depleted of their vitamin A stores within two months. Comparatively, horses which had access to pasture at the same time experienced no change in vitamin A. Therefore, horses on fresh pasture, or more brightly colored forage would easily meet his vitamin A requirement and should need little supplementation. A horse eating a high quality forage may actually be receiving the equivalent of 1,520,000 IU of vitamin A! While this may seem excessive, remember, the horse will essentially decrease the rate of vitamin A synthesis from the beta carotene in the diet.
(Despite its bright appearance, corn offers relatively little beta carotene compared to forages)
Many horse owners are also interested in the synthetic vitamin A which may be found in feeds, and how that compares with the natural carotenoids. A water soluble, synthetic beta carotene was not able to support vitamin A status to the similar extent seen in naturally occurring beta carotenoids, or in comparison to retinyl palmitate. This may be similar to trials even in humans, where water soluble supplements were not as beneficial as fat soluble. However, an alternative synthetic beta carotene source was able to increase blood concentrations in of beta carotene in the horse. Thus subtle differences in chemical composition may be key. Retinyl esters, or retinol attached by an ester bond to either short chain or long chain fatty acids, are also used in equine diets. Again, these represent the similar form to how retinol is found in the actual animals body. Due to their increased stability both retinyl acetate and retinyl palmitate have been used in feeds which allow for longer storage. If we look at these two sourced, retinyl acetate offers .344 micrograms for each IU while .550 micrograms of retinyl palmitate is needed for 1 IU of vitamin A.
(Retinyl palmitate. The storage form of retinol in animal tissues, as well as a common supplement in animal feeds.)
So how much vitamin A should a horse consume? The original information provided concerning vitamin A requirements was obtained as the concentration needed to prevent the classical deficiency diseases. Deficiencies of vitamin A are actually quite hard to produce, at least as the classical symptoms of vitamin A deficiency diseases are known. These include night blindness, hair loss, and ataxia. Certainly as has been stated before, as the content of beta carotene decreases in the diet, the animal may adapt to becoming more sensitive to absorption and assimilation into the body. Furthermore, as vitamin A is a fat soluble vitamin, it can be stored in the liver and in adipose tissue, and mobilized to support peripheral tissues when the diet is insufficient. Growing and exercising horses are recommended to receive 45 IU /kg bwt, while pregnant and lactating mares require 60 IU/kg bwt. However, there may be a difference between the amount of vitamins in the diet to prevent deficiency diseases, compared to what is optimal for overall health and well-being. It has been suggested that broodmares can benefit by receiving 400-500 mg per day of beta carotene in late gestation and early lactation. This is truly the area of future research, establishing how much should be fed to offer health benefits without exceeding either the safety margin, or simply wasting money as no additional response can be seen. Certainly fat soluble vitamins should be considered more carefully as they are also more likely to cause toxicities, as they can be stored in association with lipid, while water soluble vitamins fed in excess are typically excreted more rapidly. Many horse owners may reach for supplements too often, with little regard to actual dietary concentrations. Over-supplementation of vitamin A has actually been linked to developmental disorders in young horses. However, no direct information is available to state at which exact level vitamin A can interfere with proper bone development.
So what is the bottom line for vitamin A? If your horse is grazing fresh growing pastures or consuming high quality, bright green hay, it is probably more than adequate in vitamin A. However, if your hay is of lower quality, or your horse does not have access to pasture, you should consider a supplement or a grain that is fortified with vitamin A. If you are concerned with toxicities, remember that beta carotene is by far a safer choice. Perhaps some time in the future we will have better information as to what values are optimal for growth, reproduction or performance.
In previous articles we have discussed some of the key strategies in preventing laminitis in the equine. Many of these have centered on grazing strategies which limit the horse’s access to pastures high in fructan content. Remember that fructans are carbohydrates which are enzymatically unable to be digested in the small intestine of the horse. These fructans pass into the hindgut of the horse where they are fermented by the microbial population, specifically gram positive bacteria. The production of certain organic acids and amines enhance the permeability of the gut wall allowing these and other endotoxins to enter the bloodstream of the horse and ultimately effect the circulation to the digit. However, it is not practical to simply right off all horses’ ability to graze. Rather, we should try and identify those individuals which may have a susceptibility to fructan content in the grass. With this month’s article, we will try to identify which individuals may be at risk, and other strategies that may be employed to reduce your horse’s risk.
While the outward appearance of your horse may give you an indication to whether they are susceptible to laminitis (See Carbohydrates III: Metabolic Syndrome), there may be more to it than just which horses are overweight. There certainly appears to be a genetic link to laminitis, with pony breeds leading the list of susceptible horses. Their comparatively thrifty genotype may make their utilization of carbohydrates and insulin sensitivity differ from breeds which typically do not possess these characteristics. For example, thoroughbreds, which typically have the reputation for being “harder keepers” do not experience the same rate of laminitis. However, the lifestyle and management of thoroughbreds may differ significantly enough to partially explain the decreased incidence of laminitis. Even within ponies, there does appear to be a decided link to genetics. In a study examining the pedigrees of an inbred herd of ponies, 37% of these ponies had experienced laminitic episodes. Of those, half had at least one parent which had also experienced laminitis. Even in controlled research trials which attempt to examine the effects of various carbohydrate loads on horses, wide variability exists between individuals. This leads to the supposition that individual variation, thus genetics, is at play. Thus, if you aware of your horse’s pedigree and know of relatives which have experienced laminitis, you might want to manage your own horse more carefully. Perhaps some day the genes which make a horse more susceptible to laminitis will be identified, and we can use genetic tests in developing management protocols.
As mentioned previously, development of obesity and insulin resistance certainly predisposes the horse to laminitis. One theory behind the development of laminitis in the insulin resistant horse is the glucose deprivation model. When a horse becomes insulin resistant, more and more insulin release is needed to elicit a normal tissue response. In essence, the tissues become “desensitized” to insulin. One of the key roles of insulin in the body is to allow cellular uptake of glucose. Due to the polarity of glucose, it cannot freely enter the cell without the presence of specialized protein transporters. Glut 4 is a protein transporter which is located internally in the cell until insulin binds to the cell membrane. Binding of insulin to the receptor causes a cascade of intracellular reactions to occur and initiates the translocation of Glut-4 to the cell membrane. The insulin insensitivity may result in Glut 4 no longer moving to the cellular membrane, and the inability of glucose to enter into the lamellar tissue of the foot, thereby starving it of glucose. A recent study looked at the presence of different glucose transporters found in skeletal muscle, the coronary band and lamellar tissue. Glut-4 is the insulin dependent transporter found primarily within muscle, while Glut 1 is found in other tissues which have non-insulin dependent uptake of glucose, such as the brain. While Glut 4 was heavily expressed in skeletal muscle, only Glut 1 was found within hoof tissues of both normal and insulin resistant ponies. Therefore, glucose uptake in the hoof is thought to be insulin independent and glucose deprivation within the hoof is unlikely to be the cause behind laminitis. However, in a subsequent study, laminitis was induced in normal healthy ponies using a hyperinsulinemia-euglycemia clamp technique. In this model, insulin is infused into the ponies at a constant rate, while glucose is infused at a sufficient rate to maintain euglycemia, or normal blood glucose levels. Therefore, it is not an absence of glucose which causes laminitis, but perhaps the sustained levels of insulin or other hormones which causes this disorder. This would certainly support the observation of the increased laminitis risk to the insulin resistant horse which suffers from hyperinsulinemia.
If owners wish to try and avoid the development of insulin resistance, the diet the horse receives may be critical. Diets which avoid high amounts of sugars and starches, and have a low glycemic response, result in less insulin release. For horses which still need a significant amount of calories, diets which are fat and fiber based and properly formulated, rather than those which provide a higher glucose or insulinemic response, may prevent the development of insulin resistance. Certainly just monitoring body condition in the horse may be the easiest way to avoid insulin resistance. Although if you ask any horse owner if that is easy you may get a different response! In addition, horses which receive regular exercise seem to be fairly protective against laminitis. However, it is difficult to know whether the exercise regimen aids in increasing insulin sensitivity, or is simply protective against obesity.
Many horse owners wonder if there is a magic pill or supplement that they can provide their horse in order to prevent laminitis. One approach is to reduce the gram positive, lactate producing bacteria which prefer to ferment sugars and fructans. Antibiotics are commonly used in the livestock industry in order to promote growth by shifting the microbial population within the gut. Some antibiotics select against gram positive bacteria, thus have been studied in the horse as a way to prevent laminitis. While this may work, the use of anti-biotics in livestock for growth promotion has been banned in the Europe Union over concerns of anti-biotic resistance. Similarly many in the United States have followed suit, searching for other ways to influence growth and increase immune status. The use of probiotics and prebiotics may influence the gut microflora in favor of less potentially problem causing bacteria. Ironically enough, short chain fructo-oligosaccharides have been demonstrated to improve insulin sensitivity, if not glucose levels, in obese horses. However, none of these methods have been proven to prevent laminitis. I would caution individuals to monitor diet, grazing patterns, and body condition first, before relying on supplements to prevent laminitis.
Earlier we posted an article on the typical causes of laminitis and some feeding strategies that may help in preventing laminitis (Feeding Horses for the Prevention and Management of Laminitis). We also discussed how we might approach feeding a horse which has already experienced laminitis. This month we will begin to delve deeper into the causative factors of laminitis and how to prevent its development.
Remember that laminitis is actually a systemic disease, with just the symptoms being visualized within the hoof. Some insult to the horse’s system creates an alteration in circulation, ultimately leading to tissue damage of the sensitive laminae. This period of time, referred to as the development phase or prodromal phase, includes the actual insult prior to the development of symptoms. It is thought to be due to some change within the vasculature, that leads to ischemia, or lack of blood flow to the digit. Whether it is a lack of nutrients or oxygen due to the decreased blood flow, tissue damage or death results. This initial insult is then followed by the acute phase of laminitis.
In the acute phase, blood flow returns to the foot, typically at an increased rate, as this is the body’s normal response to tissue injury. Even this reperfusion response can cause tissue damage. This is when the owner now recognizes the development of symptoms. The horse will appear very stiff and reluctant to move, and may even lie down. A particular stance may be assumed by the horse as he appears to rock back on the hindquarters and place the forefeet forwards in order to limit weight bearing. Due to the pain and anxiety the horse is experiencing, his heart rate and respiration rate may both be elevated. Finally, the owner may even be able to detect an increase in temperature of the hoof wall and a bounding or throbbing digital pulse.
If permanent changes to the architecture of the foot occur, whether in PIII displacement, permanent changes to the normal lamellar architecture of hyperkeritization of the hoof wall, the horse has entered into the chronic phase. These horses are typically more susceptible to recurrent episodes of laminitis. Diet restrictions and specialized hoof care are typically required to allow the horse to lead a comfortable life (Feeding Horses for the Prevention and Management of Laminitis).
Obviously laminitis can be a devastating disease for the owner, and most would strive to prevent the disease, rather than address a symptomatic horse. If we look more closely at the causative factors in these alterations to circulation of the horse’s digit, we may be able to do a better job at identifying horses at risk.
We will begin with a review of pasture associated laminitis, which has been addressed in previous articles (Feeding Horses for the Prevention and Management of Laminitis and Carbohydrates III: Metabolic Syndrome). Remember that pastures grow more rapidly at certain times of the year, and may store their energy as different types of polysaccharides depending on the species of the plant. Frequently fructans are noted as the culprit in causing laminitis. Fructans are found in greater quantities in cool season grasses, as well as during periods where photosynthesis is favored over plant growth. As fructans contain beta bonds, which are not digested enzymatically by the equine small intestine, they pass through the tract and arrive at the large intestine where they then undergo bacterial fermentation. Other types of carbohydrates may act similarly, including sugars and starches which escape the small intestine undigested (the classic carbohydrate overload model of the horse in the grain bin), as well as other types of carbohydrates that may be rapidly fermented (pectins, resistant starches etc). (For more information on carbohydrates, please revisit Carbohydrates: Definitions and Relationship to Equine Diseases.)
In this first model of carbohydrate/rapidly fermentable fiber overload, too much of this rapidly fermentable material reaches the hindgut of the horse. These feedstuffs favor the proliferation of a particular bacterial population. These bacteria produce more lactate as their excretory waste. Excess lactate production lowers the pH of the hindgut which allows the mucosal cell wall to become permeable. In addition, too low of a pH stresses the bacteria causing them to either die or release endotoxins. Furthermore, altering the bacteria’s environment also changes their metabolism, releasing vasoactive amines into the hindgut. As the gut wall becomes more permeable, these toxins and amines are able to cross the mucosal wall and enter the bloodstream of the horse, where they then can exert their effects at the level of the hoof.
Horses which need to be restricted from pasture typically include ponies, as they are highly susceptible to laminitis. In addition, any horse that has a history of laminitis, or has been diagnosed with PPID (pituitary pars intermedia disfunction)(Carbohydrates III: Metabolic Syndrome) should be grazed with care. Horses with elevated insulin levels, or insulin resistant horses, also have a greater sensitivity to pasture associated laminitis, due to the influence of insulin on the vasculature of the horse. Hyperinslulinemia increases the production of endothelin-1, and down regulates the production of nitric oxide. A decrease in nitric oxide production has been linked to an elevation of homocysteine. Incidentally, elevations in blood homocysteine are also linked to heart disease in humans. There has even been a suggestion, although with no scientific data to support this theory, that excessive supplementation of sulfur amino acids to horses with insulin resistance is unwarranted. Typically sulfur amino acids (ie methionine) are included in hoof supplements, and homocysteine originates from methionine metabolism. To further confuse the issue, it does appear that individuals are more susceptible to this disease, even if they are the same age, sex, breed and are managed the same as non-effected individuals.
Obviously preventative measures aimed at reducing carbohydrate related laminitis issues center on diet management. Certainly it is not practical or even advisable to state that all horses must be kept away from pastures. However, knowledge of which horses are susceptible to pasture associated laminitis is key. Once these individuals are identified, they should be placed on a principally harvested forage diet. The forage chosen should have very little rapidly fermentable material. However, horse’s which do not have these susceptibilities can continue to be managed with relative ease.
Next month we will continue to discuss laminitis at a more detailed tissue level, and address further strategies to limit your horse’s chances of acquiring this disease.
This month we will discuss other aspects of horse management that directly affect the nutritional status of your horse. While most horse owners are familiar with deworming their horses regularly, current recommendations from many equine practitioners are to be much more strategic with our deworming. There is a growing concern that parasite populations are developing resistance to almost all types of anthelmentics (drugs used to eliminate internal parasites). As no new anthelmentics will soon be offered to the public, this could represent a real risk to the health of our horses. In order to understand these issues, we will begin with a review of the major parasite classes in horses.
While there are many types of worms which infest horses, we will address the major classes that represent the most health risk to your horse; ascarids, strongyles, tapeworms, bots and pinworms. Ascarids, or Parascaris equorum, are a type of round worm which grow to a substantial size of 8-15 inches within the intestine. They are yellowish in color and may be occasionally seen in the feces. Despite their robust size, much of the damage created by these parasites involves their life cycle and migratory journey through the horse. Adult females pass eggs into the horse’s feces, where they spend 1-2 weeks in the environment before they are capable of infecting a new host. Horses ingest the infective eggs by grazing or eating in contaminated areas. Once inside, the larvae burrow through the intestinal lining and enter the bloodstream, where they travel to the liver. They then travel to the heart and then the lungs. Ultimately they enter the alveoli of the lungs where the horse coughs them into the oral cavity and then are swallowed back down into the stomach and intestines. The entire life cycle of the ascarid takes about three months and the journey these parasites take can cause significant damage and scarring of the tissues. A heavy parasite load of adult worms can even lead to blockage of intestines. Young horses are the most susceptible group of horses to acquire ascarids, as well as weak, or malnourished horses. Coughing and nasal discharge in young horses may actually be a sign of ascarid infection. Older horses eventually develop an immunity to these parasites, so ascarids are primarily an issue with horses under two years of age.
Strongyles exist as both large and small strongyles, with many sub-species. The three main species of the large strongyles are Strongylus vulgaris, Strongylus edentus, and Strongylus equinus. Small strongyles actually have about 50 different species. Strongyles are also the most damaging of the parasites that horses will encounter. Similar to the ascarid, the females lay eggs which are shed in the feces. Unlike ascarids, they hatch into infective larvae that the horse ingests. The larvae molts three times before it is ready to infect the horse. The larvae actually crawl up the blades of grass in the dew. The larvae can crawl up or down multiple times waiting for a host, or even burrow into the ground when the weather isn’t favorable. Unfortunately for the horse owner, these parasites are extremely hardy and can persist through the winter.
The characteristics of the large and small strogyles life cycle make them particularly damaging. Large stronglye’s life cycle involves two stages where they migrate through the arterioles and arteries which supply blood to the intestine. Unfortunately, wherever these larvae burrow through the intestinal wall to migrate, all of them will return to one single location, the cranial mesenteric artery. Here they congregate and can cause immense damage. They can cause hemorrhaging, blood clots, or even rupture. The blood clots themselves can break free and travel further down through the blood supply to where they block blood flow and create a thromboembolic colic and even death. Oddly, enough lameness can also result from blood clots traveling to the legs as well.
Small strongyles have an additional strategy to help them survive. As they pass through the horse’s intestinal wall, the horse’s immune system is also trying to wage war against the larvae. However, the larvae are too big and travel too fast to be eliminated. The final migration of the larvae and complete maturation is actually held in check by the presence of adult strongyles in the lumen of the intestine. Essentially the adults provide feedback to the larvae that there is no room at the inn. When the larvae get that message and slow their migration, they become encysted within the intestinal wall by the immune cells. Here they can lie in wait for several years to take their turn at being the adult worms in the intestine. The horrifying reality is that when the adults die of either natural causes or by our purge deworming of the horse, the encysted larvae “wake up” and emerge to replace the newly vacated intestine. Within 6-8 weeks they will have matured and begin laying their own eggs to begin the cycle anew. Again, it is the pattern of traveling through the tissue that can cause a great deal of damage to the horse.
Relative to those bad boys, the rest of the worms which typically invade horses are mild in nature. The other major parasite classes which trouble horse owners are pinworms, stomach bots and tapeworms. Pinworms have a very simple life style compared to ascarids and strongyles. Adult females have a rather interesting feature, however. Not content to just shed her eggs into the feces, she actually deposits the eggs on the horse’s anus. This causes irritation to the horse who then scratches on anything available in the environment, effectively dispersing them. The horse then incidentally ingests the eggs, which hatch in the intestine where the larvae mature. Thankfully, these worms do little damage to the horse because their life cycle does not involve migrating through sensitive tissues. However, they can cause great irritation to the horse and robust itching of the tail head.
Tapeworms in horses can also cause reduced nutrition and potential blockages due to the preferred location in the horse’s gastrointestinal tract. The main species of tapeworm which inhabits the horse fixes at the ileocecal junction, or where the terminus of the small intestine joins into the cecum. A heavy parasite load can result in blockages, thickening of the ileocecal valve or even intusussecption, when the intestine rolls over itself due to regular peristaltic action. The tapeworm also has a separate host for part of its life cycle. While the adult parasite resides in the horse, the eggs of the tapeworm are actually ingested by a type of mite, which the horse then later ingests while grazing. There does not appear to be any age related immunity to tapeworms, as they are found in all ages of horses.
Finally, stomach bots are frequently seen in horses as well. The stomach bot, or Gasterophilus, also has subspecies, which include the horse bot fly, the throat latch bot, and the nose bot fly. The adult fly form can actually fly for several miles in search of a suitable subject on which to lay its eggs. The female hovers near the horse and deposits single eggs on one hair at a time. The eggs actually hatch into larvae within 7-10 days of being deposited. They then wait to emerge until the horse licks or scratches at the eggs. The larvae then enter the mouth and bury themselves in the gums, tongue or lining of the mouth where they hang out for a month. As they mature to later stages of larvae, they move into the stomach where they attach to the non-glandular or upper part of the stomach. The larvae live in the horse’s stomach for 9-12 months, before they and pass out into the feces. This typically occurs in late winter to early spring. There the larvae pupate and remain in the feces for several months. The flies then emerge in late summer or early fall, find mates and renew their life cycle. The damage the bots cause to the horse can occur in the mouth where they cause great irritation and even form pus pockets or cause the teeth to loosen. Large numbers of larvae in the stomach can cause blockages and erosion of the stomach lining. They, like all internal parasites, can result in reduced nutrition being delivered to the horse. An important heads up to horsemen: when handling horses with bot fly eggs on their hair, use caution. While rare, the larvae are capable of burrowing into human skin, and if one rubs their eye after handling bot eggs, they larvae can actually invade the eye. I’m quite sure the last thing anyone wants is a bot larvae living in your eye!
Next month we will use what we know about these parasites to develop management strategies to reduce their ability to infect our horses. After that, we will discuss strategic methods in using anthelmentics in order to reduce our reliance on medications and reduce the spread of resistance in parasites which invade our horses.
In Part I of this series, we talked not only about the difficulty in removing extra pounds from our equine companions, but also the health benefits that our horse will gain from doing so. Our strategies included seeking a more mature grass hay with a lower caloric density and reducing the amount of forage offered to the horse. The horse will probably need to be confined to a dry lot, but fed in a way to minimize boredom related to reduced feeding time. This month’s article will look more closely at the diet of our horse, to ensure that we are reducing the calories the horse receives, but are still feeding a balanced diet that provides sufficient amounts of our other nutrients.
We will continue to use the example of our 1300 lb horse who was at a body condition score of 8 and a goal weight of 1165 lbs. The maintenance requirement for the 1165 lb horse was 17.7 Mcal per day. We decided to feed the horse at a rate of 1.5% of its target weight in order to achieve the desired weight loss. That would mean our horse would consume 17.5 lbs of feed per day. Now, because we specifically chose a lower calorie hay which is more mature, it probably is lower in other nutrients as well. In order to ensure that your horse’s amino acids, vitamin and mineral needs are met, one should look for a low calorie supplement. Fortunately many reputable feed companies produce feeds that are designed for the easy keeper. Typically these feeds will be much higher in crude protein, minerals and vitamins and are designed so that you only need to feed one to two pounds per day. This ensures that your horse will not suffer from deficiencies while we achieve the desired weight loss.
Additionally, we can accelerate the horse’s weight loss by instituting a regular exercise program. Now, assuming our horse was at a body condition score of 8, it probably wasn’t on a consistent exercise program earlier. The key in implementing an appropriate exercise program is to realize that the horse is relatively unfit and we should begin exercise carefully. Ideally the horse should be ridden or worked five to six days per week. If this is not possible, try to institute an exercise program at least every other day. Begin with intermittent periods of walking and trotting, and slowly increase the duration of the trotting periods. You should notice that the horse is able to recover its heart rate and respiration rate more quickly during the walking recovery periods as it becomes more fit. Then you can increase the intensity of its exercise program.
Now let’s take a look at how much exercise your horse needs for increased energy expenditure. For every 45 minutes the horse spends walking per day, it will expend an additional one Mcal/d of net energy. But what exactly is net energy? To this point in time, we have always discussed the energy needs of the horse in terms of dietary energy or DE. Dietary energy refers to the energy available in the feed once the digestibility of the feed is taken into account. When we determine how much to feed our horse, it is always based on the DE concentration of the diet compared to the horse’s DE requirements. Net energy is more specific about the flow of energy through the horse’s body. Net energy refers to the amount of energy needed to support exercise, growth, lactation, etc. after other energy losses to the horse have been accounted for. These other energy losses include the energy lost from gas production, urine, the work of digestion and the heat lost from the digestion and fermentation of the feed. The energy that is left over after all of these losses is what is available for the animal to use for other purposes.
The efficiency of conversion of dietary energy to net energy of a horse in light-to-moderate exercise is only about 40%. Therefore, if the horse expends 1 Mcal of net energy, he actually used 2.5 Mcal of DE. Even regular trail riding will greatly help the horse with our weight loss goals, but increasing the exercise intensity will increase the calorie expenditure even more. If we use the horse’s heart rate as a guide, we can determine how much exercise they need to perform to represent significant calorie expenditure. Let’s say we would like to increase our horse’s energy expenditure to 20% over his maintenance energy requirements. Our goal for our original horse, then, is to use an additional 3.5 Mcal every day. Our horse’s typical heart rate when he is walking is usually around 60 bpm while trotting will elevate the horse’s heart rate to around 90 bpm. This relates to 24 kcal/min and 56 kcal/min of net energy respectively for walking and trotting. If we convert that to Mcal of DE, our horse is consuming .06 Mcal /min or .14 Mcal of DE/min. To achieve an energy expenditure of 3.5 Mcal, that would mean we would walk our horse for almost an hour a day, or about a half hour of trotting. However, these are heart rates of horses which already are fit. For the obese horses we are discussing, the heart rates are usually higher, thus less time will need to be devoted initially to exercising these guys. Good news for them! Heart rates for an unfit horse trotting have been recorded at 120 to 140 bpm! This would correspond to about 0.25 Mcal of DE per minute. Thus only about 15 minutes per day would achieve our increase in energy expenditure of 20%. Remember, this would be 15 minutes total of trotting with intervals of walking. As the horse begins to become more fit and its heart rate lowers, he will tolerate more exercise and will need to increase the amount of time he works to continue using the same amount of calories.
Alternatively, once our horse is fit, we can also add bouts of cantering or loping to his exercise program. A horse which is cantering typically has a heart rate between 110 and 130 beats per minute and utilizes about .25 Mcal of DE/min. If we add 10-20 minutes of cantering to our exercise program, the duration the horse needs to be ridden to achieve our target energy expenditure would be about 45 minutes per day, which is probably more realistic for most horse owners. This would include a mix of walking, trotting and loping. Combining this regular exercise program with our restricted diet will help your horse add years to his life.
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