The Basics of Equine Nutrition And Feeding Suggestions for Horses

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2 Contents S.No Chapter Page 01 Introduction Nutrients Feeding Guidelines and Rations Horse Diseases Related to Nutrition Feeding Cost Estimation Appendix 42 Page 2

3 Preface This monograph of The Basics of Equine Nutrition and Feeding Suggestions for Horses is compiled on the internet base study material and provided to guide the Horse owners about the Equine Nutrition to give the Balance Ration and to protect their specie from various diseases and health problems related to Nutrition. Ration and Health problems related to the nutrition are also presented in this document. It is hoped that it will provide service to the Horse owners. I am well aware that some errors and inaccuracies may have found into the text and hope that the users of this document will bring these to my attention so that to make corrections in the next editions. Thanks! Dr Atiq Ullah Khan Sa yem DVM (GCVS) RVMP (PVMC) Pakistan http// dratiqullahkhan@gmail.com Page 3

4 Dedication This Monograph is dedicated to my wonderful parents, who have raised me to be the person I am today. Hi Abba and Ammi! You have been with me every step of the way, through good times and bad. I thank you for all the unconditional love, guidance, and support that you have always given to me, helping me to succeed, and instilling in me the confidence that I am capable of doing anything I put my mind to. Thank you for everything. I love you! Page 4

5 Chapter # 01 A WELL-FED, HEALTHY HORSE will be content and alert, have a keen appetite, and will have a sleek, lustrous coat. About 75 percent of the cost of raising horses (aside from purchase of breeding stock) is feed. Overfeeding can be wasteful and expensive, and underfeeding or a nutritional deficiency will not permit optimum performance. Since horses depend so much on their wind, feeds should be clean and free of mold and excessive dust. In order for a horse to be in the best possible condition, observe the following feeding practices. Introduction Feed a balanced ration. The term "ration" denotes feed for a 24-hour period. Accustom horses to feed gradually. In general, they may be given as much hay as they will eat. It is safe to start horses on 1/2 pound of grain daily for each hundred pound's of the animal's weight. Thereafter, 1/2 pound of grain added to the total ration every third day is advisable. Of course, as the grain ration is increased, roughage consumption will decline. Feed horses regularly. In warm weather, early and late feeding during the cooler hours is preferred. Feed two or three times daily. Usually feed grain before roughage. Avoid sudden or abrupt changes in types of rations. Horses can go off feed. Keep troughs and water containers clean. Exercise horses every day. Be sure your horse's teeth are sound. Equine Digestive Tract Structure and Function A horse has the same requirements for energy, protein, vitamins and minerals as other animals but differs in the type and function of its digestive system, falling between a ruminant and non ruminant. Non ruminants (humans, pigs and dogs) digest carbohydrates, protein and fat by enzymatic action. Ruminants (cattle, sheep and deer) use bacteria in the fore stomachs to digest fiber by fermentation and use enzymatic digestion in the small intestines. In the horse, all true digestion is by enzymatic digestion and takes place in the fore gut ahead of the cecum. This accounts for 52-58% of the crude protein digestion and virtually all soluble carbohydrate digestion (fiber excluded). (1) In addition, bacterial or microbial digestion of fibre occurs in the cecum and colon where large quantities of volatile fatty acids are produced through fermentation and are subsequently absorbed. This dual system allows the horse to digest simple carbohydrate sources such as starch from grain in the fore gut. Fibrous sources such as oat hulls, soy hulls, beet pulp, hay and pasture are digested in the hind gut. For enzymatic and microbial action to digest feed efficiently, the horse needs healthy teeth to grind feed and allow enzymes and bacteria to attack the plant cell walls. Teeth should be examined during the annual health check to ensure that they are wearing normally and are effectively grinding the feed. The capacity of the stomach of the horse is only about 8-15 litres (eight quarts or two gallons), which makes it difficult to understand how a horse can consume large amounts of food or water. The emptying time of the stomach after filling can be about 12 minutes, and the rate of passage down the small intestine is about 1 ft/min. The net result is that food can go from the mouth to the cecum in about 1½ hours. The small volume of the stomach and rapid passage of food from the stomach is the reason horses eat almost continuously, thus the name "hay burners." The rate of passage of pelleted or wafered hay is faster than for loose hay. Various studies on total passage time, indicate two to three days is required from when food is ingested until it is passed in the manure. The mature horse's large intestine makes up more than half of the total volume of the digestive tract, is important for microbial digestion of food and is a major reservoir for water. The foal and growing horse have undeveloped cecal and colonic digestion as compared to the adult horse. There is very little microbial digestion before three months of age. Therefore, the foal requires a diet low in fibre and easily digested in the fore gut. Foals who are seen eating their mothers manure are thought to be obtaining a bacterial culture necessary for future microbial digestion. Feed Intake Horses normally consume 2 to 2.5% of their body weight in dry matter daily. However, it has been estimated that horses on pasture 24 hours a day, can consume up to 3.3% of their body weight in dry matter. As the dry matter and nutrient proportion derived from grain increases, horses will reduce their total dry matter intake. In addition, abrupt incorporation of grain into a horse's diet will increase the lactate concentration and lower the cecal and colonic ph from 6.7 to 6.3. This was evident when the grain content of the ration was greater than 30% of the dry matter intake. (2) Abrupt feeding changes, such as giving horses an extra proportion of grain prior to an event, can result in significant accumulation of feed related lactic acid. Page 5

6 Recommendations: Horses are herbivores and should receive a minimum of 50% of their dry matter intake from good quality forage (e.g. hay, pasture). Make changes in feed slowly over a period of 7-14 days and be careful about "topping the horses up" with grain prior to an event. Don't expect foals and growing horses to obtain all of their nutrient requirements from hay. Provide clean, fresh water at all times. Have your veterinarian examine your horses' teeth at the annual health visit. Basic Understanding of the Horse Digestive System & Equine Digestion Enhancement Strategies: Digestion is the process where feedstuffs that the horse consumes is broken down and converted to its simplest form so nutrients can be absorbed into the bloodstream. These nutrients provide fats, carbohydrates, vitamins, minerals, and amino acids (protein) required for growth and maintenance, or they can be stored until needed later. The digestive process in the horse primarily involved enzymatic action and fermentation. For you to feed your horse to its full potential, a basic knowledge of the digestive system is important. This information is based on a typical 1000-pound horse, but would be accurate for horses of any size and breed from miniature horses up to the draft breeds. Only the size and capacities of the various parts would differ. There are many different types of digestive systems used in animals. A horse is classified and a non-ruminate herbivore and differs substantially from both humans and ruminates, such as cattle. The digestive system uses both high levels of enzymatic action in the small intestine and high rates of microbial fermentation in the large intestine. A horse functions best by grazing, eating small amounts of roughage products over an extended period of time. In fact, research has shown that pastured horses will spend about 70% of their time eating. The other 30% will be spent sleeping and socializing. The digestive tract starts at the mouth and continues through the pharynx, esophagus, stomach, small intestine, cecum, large colon, small colon and ends at the rectum. Associated organs that aid in the total digestive process are the salivary glands, liver, and pancreas. The total digestive tract length is about 100 feet long that abruptly changes in diameter and is lined by mucous membranes along the way mostly excreting digestive fluids. The digestive tract also requires movement by the horse to help the various muscles mix and move digestive tract material. Research has shown that stall bound horses without much freedom of movement are more prone to impaction colic. The digestive process begins in the mouth where teeth reduce the particle size. The lips are extremely nimble and can select specific plants, small particles of feed, and sort stones and pebbles from what they graze and eat. The incisors sheer the plant stalk and the molars grind to the appropriate size. The chewing process stimulates the flow of saliva, which lubricates the feed prior to swallowing. Geriatric horses who have depressed saliva glands or horses who are aggressive eaters and often do not chew their food long enough are prone to choke. Steps such as wetting the feed or slowing down consumption need to be considered with these horses. If a horse does choke, the esophagus and trachea are two separate tubes down the throat, so suffocation is not an immediate threat. Do not allow the horse to eat or drink and a vet does need to be consulted to clear the choke to avoid any potential aspiration of other feed or liquid into the lungs. Once the horse swallows, the feed enters a simple stomach that is relatively small (8 to 19 quarts) and has an acidy ph. Stomach retention time is relatively small before passing into the small intestine. The small intestine is about 70 feet long, relatively small in diameter, and holds about 65 to 70 quarts. The ph in the small intestine and the rest of the digestive system is pretty neutral. The stomach and small intestine are primarily responsible for digesting and absorbing most of the starch, protein, fat, fat-soluble vitamins (A, D, and E), and most of the minerals. The starch (soluble carbohydrate) absorbed here is converted into glucose and used as energy or stored as glycogen to be used later. Material not digested in the stomach or small intestine pass into the cecum, large colon, and small colon know collectively as the large intestine or hindgut. The large intestine is very large and holds from 21 to 24 gallons of liquid and feed material. This is the primary site for fiber digestion. Since the horse does not have any natural enzymes for digesting plant fiber, the large intestine contains billions of bacteria responsible for fermenting the fiber into energy (volatile fatty acids) and micronutrients B vitamins and Vitamin K) the horse can use. One of the primary volatile fatty acids is proprionic acid, which is also commonly used as a preservative in feed to prevent mold. The large intestine is also the primary site for phosphorus absorption, important for skeletal growth, muscle contraction, and energy utilization. The large intestine is actually the main engine of the horse and is essential to the overall health of the animal. Without maintaining a healthy hindgut, significant problems such as colic and laminitis can easily occur. Also, since the large intestine is responsible for synthesizing and absorbing B vitamins, including biotin, the health of the Page 6

7 hindgut has a big influence on things you would not normally attribute to fiber digestion such as appetite stimulation and hoof and hair quality. Things you can do to help maintain hindgut integrity are: Do not overfeed grain. Excess grain that does not get digested in the small intestine passes into the large intestine and ferments extremely well. The excess fermentation causes changes in the ph and excess gas. Both can dramatically increase to potential for colic or laminitis (founder). A good rule of thumb is not to feed more than 0.5% of body weight of grain in a single feeding. Make sure clean, fresh water is available at all times at the right temperature. Dirty water or water that is too cold in the winter or too hot in the summer will inhibit consumption. The large intestine also serves as a large reservoir providing a reserve of electrolytes and excess water essential for cooling the body to sustain exercise. A lack of water will reduce the water required in the reservoir and will inhibit fermentation and material flow. Fiber quality and quantity are primary in any horse s diet. Poor hay quality will cause loss of weight and hay bellies. Lack of quantity will cause an imbalance between grain and fiber and increases the potential of colic or laminitis. Another good rule of thumb is to make sure that the fiber portion of the diet is always a minimum of 50% of the total or diet or a minimum of 1% of body weight. Reduce rapid fiber changes. Everyone knows not to change the type of grain overnight, but the same rule should also be followed with fiber. Ease into a new cutting or delivery of hay and gradually introduce the horse to new spring or different pastures. Early spring pastures can have as much soluble carbohydrates and grain. Allow adequate turnout time. The same research that has proven that rapid fiber changes are a leading cause of colic also indicates that lack of proper turnout is also a leading cause. Some indications that the hindgut is not functioning very well or that other feeding options need to be considered are: Hay belly indicates that poor quality forage is being provided. The large intestine will retain poor quality forages longer trying to get as much nutrition as possible. That will stretch the large intestine causing the hay belly appearance. Good quality forage will shrink the hindgut back to normal size. Cow flops rather than road apples. Manure that more resembles cow manure often indicates that the fermentation in the large intestine is not functioning optimally. This often occurs with rapid fiber changes, excess grain, or just poor intestinal health often associated with age. Do not overlook the potential for diseases or illnesses required the attention of a vet. Poor hair coat or hoof condition. Typically it would accompany one or both of the problems listed above. Research and practical experience has taught us that the healthiest horses are those that are allowed to be horses by feeding on quality fiber on a continual basis. However, outside influences such as pasture availability, energy and work requirements, owner life styles, and etc. have an influence on the digestive system of the horse that are not always positive. We know a lot more today about feeding horses in the 21 st century environment. Feeding for life styles, age and living conditions are now considered when designing feeds. Even forage alternatives and improved high fiber feeds are on the forefront of equine nutrition. Horses, like people, are individuals. Each has their own metabolic rate and some are easy keepers while others are a bit more of a challenge. By understanding how the internal process works, we can better understand how to feed them to their maximum potential and limit feeding related problems. - See more at: Digestive System Limitations Horses are non-ruminant herbivores (hind-gut fermentors). Their small stomach only has a capacity of 2 to 4 gallons for an average-sized 1000 lb. horse. This limits the amount of feed a horse can take in at one time. Equids have evolved as grazers that spend about 16 hours a day grazing pasture grasses. The stomach serves to secrete hydrochloric acid (HCl) and pepsin to begin the breakdown of food that enters the stomach. Horses are unable to regurgitate food, so if they overeat or eat something poisonous vomiting is not an option. Horses are also unique in that they do not have a gall bladder. This makes high fat diets hard to digest and utilize. Horses can digest up to 20 % fat in their diet, but it takes a span of 3 to 4 weeks for them to adjust. Normal horse rations contain only 3 to 4 % fat. The horse s small intestine is 50 to 70 feet long and holds 10 to 23 gallons. Most of the nutrients (protein, some carbohydrates and fat) are digested in the small intestine. Most of the vitamins and minerals are also absorbed here. Most liquids are passed to the cecum, which is 3 to 4 feet long and holds 7 to 8 gallons. Detoxification of toxic substances occurs in the cecum. It also contains bacteria and protozoa that pass the small intestine to digest fiber and any soluble carbohydrates. The large colon, small colon, and rectum make up the large intestine. The large colon is 10 to 12 feet long, and holds 14 to 16 gallons. It consists of four parts: right ventral colon, sternal flexure to left ventral colon, pelvic flexure to left dorsal colon, and diaphragmatic flexure to the Page 7

8 right dorsal colon. The sternal and diaphragmatic flexures are a common place for impaction. The small colon leads to the rectum. It is 10 feet long and holds only 5 gallons of material. Page 8

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10 Colic In the mature horse, the exit and entrance to the cecum (blind gut with a capacity of about litres or approximately 7-9 gallons) are separated by only about 2 inches. This creates a certain amount of difficulty due to the two-way movement of feed in this region. As a result, the cecum can be a site of colic, which may develop when a horse is shifted from a poor quality ration to one which is rapidly digested. Bacteria which are best at digesting high fibre type diets will be replaced with a population of bacteria which are more suited to convert high quality and easily digested fibre to soluble products. As easily digested hay enters the cecum, microbial populations flourish and there is an increase in fermentation rate. The coarse roughage will cause a relative occlusion at the exit of the cecum and will result in gas accumulation and the pain associated with colic. This is the principle behind the recommendation that "a horse should be shifted from one type of feed to another over a period of one to two weeks." Impaction of the cecum and colon is common and results from the ingestion of poorly digestible material. This, coupled with inadequate water intake or exercise, will predispose horses to impaction. To prevent impactions, a similar one to two weeks should be allowed for conversion from a high quality, easily digested, ration to one of low digestibility. This allows time for the gastrointestinal micro flora to adjust to new substrates. Very low quality roughages should not be fed since they predispose to impactions. Laminitis Young lush fast-growing plants are low in fibre, can contain 22-25% protein and equally large amounts of highly digestible carbohydrates. Sudden switches between different feed qualities result in rapid changes to the bacterial flora and the sudden death of the less favoured bacteria. Death of large numbers of bacteria will, in turn, lead to the release of large amounts of endotoxin from the bacteria. Horses placed directly on pasture after being fed hay all winter may develop laminitis due to the sudden shift to a highly digestible feed. Grass founder or laminitis is the sequella. Climatic conditions, such as high rain fall and hot weather, can also result in the rapid growth of plants such as white clover which are high in digestible protein and energy and low in fibre. Page 10

11 Chapter # 02 Nutrients Nutrients Horses require six main classes of nutrients to survive; they include water, fats, carbohydrates, protein, vitamins, and minerals Water: Water is the MOST IMPORTANT nutrient; horses can t live long without it! Always make sure there is an adequate, clean supply of water. The average mature light horse may drink about 10 to 12 gallons of water daily varying with the amount of work, the type of feed, and the weather. Horses should be watered regularly and frequently. After heavy exertion, very warm or very thirsty horses should be watered lightly until they are properly cooled. In very cold weather, water should be heated to 40 or 500 F. Horses generally drink about 2 quarts of water for every pound of hay they consume. In high temperature, hard work, or for the lactating mare the water requirement may be 3 to 4 times the normal consumption. Signs that your horse may be water deficient include decreased feed intake and physical activity, and signs of dehydration like dry mucous membranes in the mouth, dry feces, and decreased capillary refill time. Possible causes of water deficiencies include no water source, low water palatability, or accessibility (frozen or receiving or contaminated), or illness. Energy Energy isn t one of the six nutrients because the horse cannot physically consume energy, however, it is a requirement for sustaining life. The most dense source of energy is fat (almost three times more than carbohydrates or proteins); however, carbohydrates in the forms of fermentable fiber or starch are the most common source. Horses exercising, growing, pregnant in late gestation or early lactation need increased energy in their diet. Signs of energy deficiency include weight loss, decreased physical activity, milk production, and growth rate. However, feeding a diet too high in energy can cause obesity increasing the risk of colic, laminitis, and contribute to increased sweat loss and exercise intolerance. The basic ration for a horse is hay plus grain. The amount of grain a horse needs depends on the growth or performance expected. The amount of total ration is based on a consumption of 2-1/4 pounds of airdry fed per cwt. Thus a 1,000-pound horse would receive a total daily ration of 22-1/2 pounds. The energy need is often expressed as total digestible nutrients (T.D.N.). Generally grains provide more energy than hays because they analyze higher in T.D.N. and lower in crude fiber (C.F.). Table 2 gives grain requirements for several types of horses. Table 2. - Amount of Grain To Be Included in a Horse's Ration Per Cwt. of the Horse's Weight Grain per cwt., lb. Work expected from the horse Grain or growth Breeding stock None Idle mature horse Maintenance Light (0 to 3 hours per day) Light Moderate (3 to 6 hours per day) Average Mere in drylot nursing foal 1.25 Heavy (More than 6 hours per day) Faster growth or fattening Stallion in heavy service The table suggests that an idle mature horse weighing 1,000 pounds should receive 22-1/2 pounds of hay with no grain while a similar horse doing heavy work or a stallion in heavy service should receive about 10 pounds of hay and 12.5 pounds of grain daily. It is usually sound economically to feed and grow weanlings well the first and second years because young horses are more efficient and generally need less feed per pound of weight increase. Some horses can be safely fed more than 1-1/4 pounds of grain per hundredweight. However, when fed heavily, care should be taken to see that horses get plenty of exercise and do not become swollen or puffy in their legs. Fat can be added to a feed to increase the energy density of the diet. Fat has 9 Mcal/kg of energy, which is three-times that of any grain or carbohydrate source. Fat is normally found at 2 to 6% in most premixed feeds; however, some higher fat feeds will contain 10 to 12% fat. See Fat Supplements section for more. Page 11

12 Carbohydrates are the main energy source used in most feeds. The main building block of carbohydrates is glucose. Soluble carbohydrates such as starches and sugars are readily broken down to glucose in the small intestine and absorbed. Insoluble carbohydrates such as fiber (cellulose) bypass enzymatic digestion and must be fermented by microbes in the large intestine to release their energy sources, the volatile fatty acids. Soluble carbohydrates are found in nearly every feed source; corn has the highest amount, then barley and oats. Forages normally have only 6 to 8% starch but under certain conditions can have up to 30%. Sudden ingestion of large amounts of starch or high sugar feeds can cause colic or laminitis. Protein Protein is used in muscle development during growth or exercise. The main building blocks of protein are amino acids. Soybean meal and alfalfa are good sources of protein that can be easily added to the diet. Second and third cutting alfalfa can be 25 to 30% protein and can greatly impact the total dietary protein. Most adult horses only require 8 to 10% protein in the ration; however, higher protein is important for lactating mares and young growing foals. Signs of protein deficiency include a rough or coarse hair coat, weight loss, and reduced growth, milk production, and performance. Excess protein can result in increased water intake and urination, and increased sweat losses during exercise, which in turn lead to dehydration and electrolyte imbalances. Horses need protein for muscle growth, for lactation, and for reproduction. Protein needs are expressed as percent crude protein (C.P.) or more precisely as percent digestible protein (D.P.) of the ration. Horsemen usually add supplemental protein such as linseed meal, soybean meal, or other purchased protein to grass hay and grain rations. Legume hays such as alfalfa and red clover are also good protein sources. The average ration should contain approximately 12 percent crude protein. Two good common oilmeal protein supplements that can be added to grass hay and grains are linseed meal (36 percent C.P.), and soybean meal (44 percent C.P. with hulls; 50 percent C.P. without hulls). Soybean meal is more palatable and of higher quality for foals and young horses. Other purchased protein supplements without urea can be used. In some cases peanut meal, cottonseed meal, and safflower meal are good substitutes if they are economical. Protein needs of various types of horses are summarized in Table 1. Type of Horse Table 1. - Summary of Protien Needs for Horses Percent Percent crude protein Digestable Protein (C.P.) (D.P.) Lb. oilmeal or protein equivalent to add to grass hay or grain rations daily a Mature idle Dry mare in early pregnancy Yearling or 2-year old Mare in last quarter of gestation Lactating mare 14 b Stallion in heavy service 14 c Foal under 6 months 14+ d a Four pounds of quality legume hays (alfalfa or clover) furnish approximately the same amount of digestible protein as 1 pound of soybean, linseed, or cottonseed meal. b The highest amount of protein is needed during early lactation. Later the amount can be reduced. c The amount of protein needed depends on how heavy is the breeding service. The minimum is 14 percent. d A very young foal may need up to 20 percent protein. At 6 months, 14 percent is sufficient Vitamins Vitamins are fat-soluble (vitamin A, D, E, and K), or water-soluble (vitamin C, and B-complex). Horses at maintenance usually have more than adequate amounts of vitamins in their diet if they are receiving fresh green forage and/or premixed rations. Some cases where a horse would need a vitamin supplement include when feeding a high-grain diet, or low-quality hay, if a horse is under stress (traveling, showing, racing, etc.), prolonged strenuous activity, or not eating well (sick, after surgery, etc.). Most of the vitamins are found in green, leafy forages. Vitamin D is obtained from sunlight, so only horses that are stalled for 24 hours a day need a supplement with vitamin D. Vitamin E is found in fresh green forages, however, the amount decreases with plant maturity and is destroyed during long term storage. Horses that are under Page 12

13 heavy exercise or under increased levels of stress also may benefit from vitamin E supplementation. Vitamin K and B-complex are produced by the gut microbes. Vitamin C is found in fresh vegetables and fruits, and produced naturally by the liver. None of these are usually required in a horse s diet. Severely stressed horses, however, may benefit from B-complex and vitamin C supplements during the period of stress. Special attention should be given to a horse's needs for vitamins. Generally, green grasses and hays furnish carotene that the horse converts to vitamin A. Vitamin A is important in maintaining the skin and epithelial linings of the digestive, respiratory, urinary, and reproductive tracts. Vitamin D is often called the sunshine vitamin because the sun's rays convert substances in the animal's skin and substances in sun-cured forages into vitamin D. Vitamin D is especially important in the absorption and metabolism of calcium and phosphorus for normal bone growth and maintenance. An average pleasure horse needs about 20,000 to 30,000 International Units (I.U.) of vitamin A and about 3,000 I.U. of vitamin D daily. Vitamin E is often associated with improved reproduction and muscle maintenance. Green feeds, wheat bran, and wheat germ oil are usually rich in vitamin E. Under conditions of barn confinement, drouthy pastures, or feeding poor-quality forage, horses may not receive adequate amounts of vitamins A, D, and E. In such cases, economical supplements of these vitamins can be mixed in the feed, injected intramuscularly, or furnished in stabilized mineral blocks. Vitamin K, necessary for blood clotting, is synthesized sufficiently in the body. The necessary 13 vitamins are synthesized in the horse's cecum. Small supplemental amounts may be beneficial under stress conditions of fast growth, intense training, heavy racing, or breeding. Spent brewers' yeast may be an economical supplemental source of B vita mins. An economical premix of vitamins, as listed below, can be added to grain mixtures if desired at the rate of 0.5 percent (10 pounds) per ton of the grain mixture. Some horsemen prefer to add a small amount daily over the grain. Vitamin A B 1 (Thiamine) B 2 (Riboflavin) B 6 (Pyridoxine) B 12 C D E Choline Chloride Folic Acid Niacin Pantothenic Acid Ammount per lb of premix 1,000,000 I.U. 1,000 mg. 1,000 mg. 300 mg. 1,500 mg. 10,000 I.U. 100,000 I.U. 10,000 I.U. 25,000 mg. 300 mg. 2,000 mg. 1,500 mg. Minerals : Minerals are required for maintenance of body structure, fluid balance in cells (electrolytes), nerve conduction, and muscle contraction. Only small amounts of the macro-minerals such as calcium, phosphorus, sodium, potassium, chloride, magnesium, and sulfur are needed daily. Calcium and phosphorus are needed in a specific ratio ideally 2:1, but never less than 1:1. Alfalfa alone can exceed a Ca:P ratio of 6:1. Sweating depletes sodium, potassium, and chloride from the horse s system, therefore, supplementation with electrolytes may be helpful for horses that sweat a lot. Normally, if adult horses are consuming fresh green pasture and/or a premixed ration, they will receive proper amounts of minerals in their diet, with the exception of sodium chloride (salt), which should always be available. Young horses may need added calcium, phosphorus, copper, and zinc during the first year or two of life. Common farm feeds provide minerals, but most horses need extra calcium, phosphorus, salt, and possibly some trace minerals such as iron, copper, zinc, manganese, iodine, and selenium. The daily salt requirement is about 2 to 3 ounces. Routinely providing free-choice salt that is trace-mineralized for horses will satisfy Page 13

14 both salt and trace mineral requirements with the possible exception of those for selenium. Not all trace mineral salt formulations contain selenium; check the feed label when in doubt. The calcium requirement varies from as little as 0.3 percent dietary calcium for fully mature horses to as much as 0.85 percent in,vealiling foals. The phosphorus requirement may range from 0.2 percent dietary phosphorus for fully mature horses to 0.6 percent in weanling foals. The calcium and phosphorus needs of mares in early lactation are approximately double those of mature horses that are not providing milk for foals. A calcium-to-phosphorus ratio of 1:1:1 should be provided for young horses. Older horses can usually tolerate a higher ratio, possibly one as high as 6:1. There should not be more phosphorus than calcium in a horse's diet. A good way to furnish supplemental minerals is to offer a freechoice mixture of equal parts of dicalcium phosphate and trace-mineralized salt in a box protected from the weather. In formulating complete mixed hay and grain rations, about I percent dicalcium phosphate and 0.5 percent trace-mineralized salt should be added. A. Forages Forages are classified as legumes or grasses. The nutrients in the forage vary greatly with maturity of the grasses, fertilization, management, and environmental conditions. In order to determine the nutrient content in forage it is best to take samples and get them analyzed by a forage testing lab (contact your local County Extension Office for testing information or see the fact sheet, FS714, Analysis of Feeds and Forages for Horses). Legumes are usually higher in protein, calcium, and energy than grasses. They have more leaves than grasses and require optimal growth conditions (warm weather and good soil) to produce the best nutrients. Some legumes include clover and alfalfa. Some commonly used grasses include orchard grass, timothy, bluegrass, and fescue. Hay is forage that has been harvested, dried, and baled before feeding to horses. Legume hay can contain 2 to 3 times more protein and calcium than grass hay. However, it is usually more costly. Common grass hays include timothy, brome and orchard grass. They have fine stems, seed heads and longer leaves than legumes. They are most nutritious when cut earlier in their growth stage. Maturity at harvest is key to quality. Second cut grass hays average 16 to 20% protein. Appearance can be a good indicator of the amount of nutrients in the hay, however, color should not be used as sole indicator. Moldy or dusty hay should not be fed to horses. For more information see Table 1. Table 1. Evaluating Hay Quality Characteristics of Good-Quality Hay Low moisture content (12 to 18%). Green in color. Sweet smelling, like newly cut grass. Free of mold and dust. Cut before maturity. Grass hays before seed heads mature and alfalfa cut early in bloom. Free from weeds, poisonous plants, trash, or foreign objects. Characteristics of Poor-Quality Hay Damp. Too much moisture causes mold. Brown, yellow or weathered in color. Gray or black indicates mold. Musty, moldy or fermented odor. Dusty and moldy hay is unacceptable. Cut late in maturity. Mature seed heads with grass hay or alfalfa cut late in bloom. High weed content, poisonous plants, or animal carcasses in hay bales. Roughage Hay is used in the ration for bulk and energy, and can be fed loose, pelleted or chopped. While growth, work, and reproduction require that some of the ration consists of grain, nonlactating broodmares and idle mature horses can get along satisfactorily on hay alone. On the other hand, working horses can easily be fed too much roughage, resulting in labored breathing and lack of stamina. Grass hays usually contain about 5 to 10 percent crude protein. However, this figure can be higher if grass hays are harvested in early bloom. Bromegrass is a perennial, palatable forage. Orchard grass is a perennial, palatable forage often seeded with bromegrass. Timothy is highly regarded but, in Illinois, it is a less-productive hay. Page 14

15 Prairie hay is a mixture of grasses of western or south-western origin. Legume hays usually contain about 15 percent crude protein or more when they are cut at the one-third bloom stage. Very green legume hays may be a little laxative and may cause more frequent urination, however no real harm will ensue. Alfalfa, a perennial, is hardy and productive. Red clover, a biennial, will need reseeding after two years. Occasionally, second-cutting red clover may cause slobbering. Lespedeza is commonly grown in southern Illinois. Mixed hays include grass and legumes. They offer variety and more protein than straight grass hay. Straws are used primarily for bedding but clean oat and wheat straw can be used as a filler roughage. Oat straw is more palatable. Pastures Good pastures are an excellent source of nutrients. Pastures can supply the complete ration, but usually working horses and lactating mares are fed additional grain. Foals on pasture are often creep-fed as well. The pasture season in central Illinois begins about the first week in May and lasts until about the middle of October. It begins about a week earlier for each 100 miles south of central Illinois and a week later for each 100 miles north of central Illinois. Both temporary (one-season) and permanent pastures are used to provide feed for horses. An example of a temporary pasture schedule is given below. Season Forage Seeding time Grazing time Spring Oats and barley Late March and April May and June Summer Pearl millet Late April and May June until frost Fall Wheat and rye Late August and September October and November; April Some horsemen use sudangrass during the summer, but an occasional case of urinary cystitis infection has been recorded from sudangrass grazing. Sudangrass is not safe for grazing immediately after frost or when severely stunted by drouth. Cured sudangrass can be used as hay. Mixtures of legume and grasses in permanent pasture provide variety and more forage. Bromegrass or orchardgrass with alfalfa are suitable in most of Illinois. Fescue with lespedeza is often used in southern Illinois, however deficient milk production and foaling problems have been reported in some mares grazing in fescue pastures. Establishment of a permanent pasture involves a considerable investment in money and labor. Good management is also required. The following suggestions will help you establish and maintain a good permanent pasture. Test the soil fertility and add necessary limestone, phosphorus, potassium, and nitrogen. Prepare a good seedbed. Use recommended and adapted seeds and inoculate legumes. Use a grass-legume mixture. Seed at the proper time, preferably in early spring or fall. Seed with a nurse crop. Oats are good. Remove the nurse crop early when oats are in the dough stage. Cover the seed with 1/4 to 1/2 inch of soil. Firm the seedbed by rolling. Clip weeds, setting the sickle bar high. Do not pasture the first season because horses will trample the seedlings. To improve forage growth, topdress pastures with nitrogen in early spring (where legumes are less than 25 percent) with 50 to 70 pounds of actual N per acre. Permanent and rotation pasture mixtures per acre for central and northern Illinois: Alfalfa 8 lb. Alfalfa 8 lb. Bromegrass 12 lb. Bromegrass 6 lb. = 20 lb. Orchardgrass 6 lb. = 20 lb. These mixtures are very productive for both pasture and hay. The inclusion of orchardgrass with bromegrass will furnish more grazing in midsummer when bromegrass may be semidormant. Seed mixtures in late March or early April or in early fall, preferably before August 25. Permanent pasture mixture per acre for southern Illinois where bromegrass and orchardgrass may not be as productive: Page 15

16 B. Concentrates Kentucky fescue (low endophyte) Alfalfa or lespedeza 14 lb. 8 lb. =22 lb. Grains Oats have been the preferred grain for horses because they contain 12 percent crude protein and are more safely fed than other grains because of their fiber or bulk. However, the price of oats often becomes prohibitive. Sometimes they are crimped or crushed for cleaning and palatibility. Horses like variety, so mixed grains are often fed. Other grains can be substituted for oats, but shelled corn, milo, wheat, and rye are low in fiber or bulk and much denser than oat in volumeto-volume comparison. Occasionally these grains can cause impaction or colic if they are fed alone or if they are eaten too fast by greedy horses. It may be safer to mix shelled corn, milo, wheat, or rye with oats or place some baseballsized stones in the grain box to slow ravenous eating. Whenever one of these more dense grains is substituted for oats, it should be substituted on a weight basis rather than a volume basis. Barley also has hard hulls that should be processed to allow easier digestibility. It has moderate fiber and energy content, and can be a nutritious and palatable feed for horses.barley also has hard hulls that should be processed to allow easier digestibility. It has moderate fiber and energy content, and can be a nutritious and palatable feed for horses. Shelled corn is high in energy and contains little fiber. It is better utilized by the horse when it is coarsecracked before feeding. Corn is generally more economical than oats and is nearly twice as high in energy on a volume basis. Corn is the second most palatable grain for horses. It provides twice as much digestible energy as an equal volume of oats and is low in fiber. Because it is so energy dense it is easy to over feed corn, causing obesity. Moldy corn should never be fed it is lethal to horses. Ear corn or ground ear corn can be fed and it will minimize gulping the grain. Milo needs to be crushed or cracked; otherwise it may be voided as whole grain in the manure. Wheat is often expensive and needs cracking or crushing. Wheat and rye have a tendency to gum when chewed and should not make up over 50 percent of the grain mix. Wheat is generally not used as a feedstuff because of its high cost. Its small hard kernels should be processed for horses to digest. Wheat is higher in energy than corn and best used in a grain mix because of its low palatability. Rye is not very palatable and, like wheat, needs cracking or crushing. Wheat bran is good as bulk. One pound a day is enough for a mature horse. A warm, soaked mash of 3 to 4 pounds of wheat bran alone or mixed with oats is an excellent idle-day feed. High levels of bran should not be fed routinely to young, growing horses because wheat bran is relatively low in calcium but very high in phosphorus. Sorghum (Milo) is a small hard kernel that needs to be processed (steam flaked, crushed, etc.) for efficient digestion and utilization by the horse. It is not palatable when used as a grain on its own, however, it can be used in grain mixes. Like corn, sorghum is high in digestible energy and low in fiber. Protein Supplements Soybean meal is the most common protein supplement, which averages around 44% crude protein. The protein in soybean meal is usually a high-quality protein with the proper ratio of dietary essential amino acids. Cottonseed meal (48% crude protein) and peanut meal (53% crude protein) are not as common for horses as soybean meal. Brewer s grains (the mash removed from the malt when making beer) are a byproduct of the brewing industry. It is nutritious and palatable with about 25% crude protein and is also high in fat (13%) and B vitamins. Fat Supplements Vegetable oil is the most commonly used fat source in horse feeds. If adding the oil supplement as a top dress to feed start with ¼ cup/feeding and increase to no more than 2 cups/day over the course of 2 weeks for the average size horse (1000 lbs.). Rice bran is a newer fat supplement on the market. It is distributed by some commercial feed dealers. It consists of about 20% crude fat, giving it an energy content of 2.9 Mcal/kg. Page 16

17 Chapter # 03 Feeding Guidelines and Rations A. Feeding Guidelines 1. Forage is the base! Always try to feed the most forage possible then add concentrate. 2. Feed at a rate of 1.5 to 2% of the horse s body weight (1000 lb. horse = 20 lbs.). 3. Feed by weight not volume! ** A 1 lb. scoop of Oats does not equal 1 lb. of Corn** 4. Stomachs are small so concentrates, if used, should be fed twice a day if not more with no more than 0.5% body weight per feeding. 5. To maintain body weight, most horses need only good forage, water, and a mineral block. 6. Store feed properly: it should be kept free of mold, rodents, or contamination. 7. Keep Ca:P ratios around 2 parts Ca to 1 part P. 8. Feed on a set schedule (horses are creatures of habit and are easily upset by changes in routine). 9. Change feeds gradually (horses stomachs cannot cope with drastic changes in feed; could cause colic). 10. When work or exercise decreases, decrease the grain. 11. Be aware of the pecking order in your horse s pen are they getting their feed? 12. Examine teeth at least once a year to make sure they are able to chew feed. B. Consumption and Weight Horses can eat about 2 to 2-1/2 pounds of air-dry feeds (as grain in the bin and hay in the bale) daily per 100 pounds (cwt.) of their body weight. In average condition, a light-legged mature mare over 14.2 hands (58 inches) will weigh approximately 1,100 pounds while mature geldings and stallions will weigh about 1,200 pounds. Mature ponies under 46 inches will weigh from 400 to 600 pounds. Taller ponies up to 56 inches will average 700 to 900 pounds. Weanling horse foals will weigh from 400 to 600 pounds when 7 months old. Pony foals will weigh from 200 to 300 pounds when 7 months old. Well-fed foals will reach about 50 to 60 percent of their mature weight during the first year and about 75 percent at the end of the second year. Horses reach maturity between four and five years of age. C. Formulating Horse Rations Water, protein, minerals, vitamins, and energy are essential nutrients in a horse ration. Observe the following points when formulating the ration. Is the total quantity of the ration adequate? Is the energy produced by the ration suitable for the work or the performance required? Is the amount of crude protein (digestible protein) adequate? Is the proper amount of minerals and of vitamins A and D included in the ration? Is the ration economical but still nutritionally adequate? D. Examples of Daily Rations Some examples of daily rations for several types of horses are given below. Modifications can be made in these rations depending on the availability and cost of feeds. Example A: Idle mature horse or pony Nutrient requirements. Weight, lb Daily Ration, lb. Daily T.D.N., lb Daily D.P., lb Horse 1, to Pony to Ration 1: Horse: 20 to 24 pounds mixed hay (1/3 alfalfa and 2/3 grass). Pony: 16 pounds mixed hay. Ration 2: Horse: 20 to 24 pounds grass hay and 1/2 pound linseed meal or soybean meal. Pony: 14 to 16 pounds grass hay and 1/4 pound oilmeal. Page 17

18 Example B. Mature horse or pony doing moderate work Nutrient requirements Weight, lb Daily Ration, lb. Daily T.D.N., lb Daily D.P., lb Horse 1, to Pony to Ration 1: Horse: 15 pounds mixed hay (1/3 alfalfa and 2/3 grass) and 9 pounds oats. Pony: 10 pounds mixed hay and 6 pounds oats. Ration 2: Horse: 15 pounds mixed bay (1/3 red clover and 2/3 grass), 6 pounds oats, and 3 pounds cracked corn. Pony: 10 pounds mixed hay, 4 pounds oats, and 2 pounds cracked corn. Ration 3: Horse: 15 pounds grass hay, 6 pounds oats, 3 pounds cracked corn, and 1/2 pound linseed meal or soybean meal. Pony: 10 pounds grass hay, 4 pounds oats, 2 pounds cracked corn, and 1/4 pound linseed meal or soybean meal. Example C: Mare nursing foal Nutrient requirements. Weight, lb. Daily ration, lb Daily T.D.N., lb. Daily D.P., lb. Mare 1, to Ration 1: Pasture and 6 pounds grain. The grain might consist of 4 pounds oats, 1 pound cracked corn, and 1 pound bran. Ration 2: 11 pounds mixed hay (1/3 alfalfa and 2/3 grass), 7 pounds oats, 3 pounds cracked corn, and 1 pound linseed meal or soybean meal. Ration 3: 11 pounds grass hay, 7 pounds oats, 3 pounds cracked corn, and I -1/2 pounds linseed meal or soybean meal. Foals can be offered grain in a creep feeder. Example D: Weaning 6 months to 1 year old Nutrient reauirements: Weight, lb. Daily ration, lb Daily T.D.N., lb. Daily D.P., lb. Weanling to to Ration 1: 8 pounds mixed hay (1/3 alfalfa and 2/3 grass), 6 pounds oats, and 1/2 pound linseed meal. Ration 2: 8 pounds grass hay, 3 pounds oats, 3 pounds cracked corn, and 1 pound soybean meal or linseed meal. Example E: Yearling to 2-year-old horses Nutrient requirements: Weight, lb. Daily ration, lb Daily T.D.N., lb. Daily D.P., lb. Yearling to 2-year-old to Ration 1: 11 pounds mixed hay (1/3 red clover and 2/3 grass), 6 pounds oats, 3 pounds cracked corn, and 1/2 pound linseed meal or soybean meal. Ration 2: 11 pounds grass hay, 6 pounds oats, 3 pounds cracked corn, and I pound linseed meal or soybean meal. Example F: Breeding stallion in moderate service Nutrient requirements: Weight, lb. Daily ration, lb Daily T.D.N., lb. Daily D.P., lb. Stallion 1, to Page 18

19 Ration 1: 12 pounds mixed hay (1/3 alfalfa and 2/3 grass), 8 pounds oats, 4 pounds cracked corn, 1 pound wheat bran, and 1 pound linseed meal. Ration 2: 12 pounds grass hay, 8 pounds oats, 4 pounds cracked corn, 1 pound wheat bran, and 1-1/2 pounds linseed meal or soybean meal. Example G: Creep rations for a nursing foal A creep ration is commonly fed free choice where only foals can eat it. Ration 1: 5 parts crimped oats, 3 parts cracked corn, and 1 part linseed pellets. Ration 2: 8 parts crimped oats and 1 part linseed pellets. Ration 3: This is a formula for a highly palatable creep ration. It analyzes approximately 18 percent C.P. (13.5 percent D.P.), 70 percent T.D.N., and 8 percent C.F. Ingredient Percent Crimped oats 40 Cracked Corn 30 Soybean meal (50-percent) 20 Dehydrated alfalfa 4 Dried Molasses 4 Dicalcium phosphate 1 Trace-mineralized salt.5 Vitamin mix a.5 Aurofac b + a To furnish 5,000 I.U. of vitamin A per pound of ration plus B vitamins b To furnish 40 mg. of antibiotic per pound of ration. Example H: Complete pelleted ration This formula analyzes approximately 14 percent C.P. (9.8 percent D.P.), 58 percent T.D.N., and 24 percent C.F. Ingredient Percent Alfalfa hay (chopped) 62 Oats 15 Cracked Corn 15 Dried Molasses 4 Soybean meal (50 percent C.P.) 2 Dicalcium phosphate 1 Trace-mineralozed salt.5 Vitamin premix a.5 a To furnish 2,000 I.U. of vitamin A per pound of ration. Ration Calculations A knowledge of the composition of a ration along with feed analyses (Table 3) makes it possible to calculate the percent protein and percent energy of a ration. Research shows that the maintenance requirement of a horse is about 0.8 pound of T.D.N. per cwt. and that a pound of gain above maintenance requires about 3.63 pounds of T.D.N. per cwt. The percent of crude protein (C.P.) and digestible protein (D.P.) in a typical ration for an 800-pound yearling can be calculated as in the following example. The C. P. figures are taken from Table 3. Daily Ration of: lb. X C.P. = lb.c.p. Oats Corn Page 19

20 Alfalfa Bromegrass Soybean meal Totals Dividing the total C.P. in pounds by the total amount of the ration (2.255/18.75) gives a C.P. content of 12 percent. The average digestion coefficient for crude protein of grain is about 75 percent and about 65 percent for the crude protein of roughages. Taking an average of 70 percent and multiplying the C.P. figure by this amount (12 X.70), a result of 8.4 percent for the digestible protein (D.P.) in the ration is obtained. The percent T.D.N. in the ration can be calculated in a similar manner. The figures for percent T.D.N. in various feeds in the following example are taken from Table 3. Daily Ration of: lb. X T.D.N. = lb.t.d.n. Oats Corn Alfalfa Bromegrass Soybean meal Totals Dividing the total T.D.N. in pounds by the total amount of the ration (11.52/18.75) gives a T.D.N. content of 61.4 percent. Table 3. - Average Analyses of Some Horese Feeds on an Air-Dry Basis Feed Total Digestable Nutriants (T.D.N.) Crude Protein (C.P.) Digestible Protein (D.P.) Crude Fiber (C.F.) percent percent percent percent Grains Oats Shelled Corn 80 8 to Brly Milo Ground Ear Corn Wheat Wheat Bran Prorein oil meals Linseed meal Soybean meal with hulls Soybean meal without hulls Cottenseed meal Peanut meal Grass hays Bromegrass 45 to 50 5 to 6 3 to Orchard grass 45 to 50 5 to 6 3 to Timothy 45 to 50 5 to 6 3 to Prairie hay (western) 45 to 50 5 to 6 3 to Legume hays Alfalfa 50 to Red clover 50 to to Mixed hays 1/3 alfalfa and 2/3 grass 50 8 to Straw Oats Wheat 40 3 to 4.5 to The 800-pound yearling used in the examples requires 6.4 pounds T.D.N. for maintenance (800 lb. X 0.8 lb. per cwt.). Subtracting 6.4 pounds from (the T.D.N. in the ration) leaves 5.12 pounds T.D.N. available after Page 20

21 maintenance. Dividing 5.12 pounds by 3.63 pounds (the amount of T.D.N. required for I pound of gain) gives a daily gain of 1.4 pounds for an 800-pound yearling fed the ration used in the above examples. Chapter # 04 Horse Diseases Related to Nutrition Horse Diseases Related to Nutrition Nutritional Diseases of Horses: Descriptions of uncomplicated nutrient deficiencies in horses are rare. The nutrients most likely to be deficient are caloric sources, protein, calcium, phosphorus, copper, sodium chloride, and selenium, depending on age and type of horse and geographic area. Signs of deficiency are frequently nonspecific, and diagnosis may be complicated by deficiencies of several nutrients simultaneously. The consequences of increased susceptibility to parasitism and bacterial infections may be superimposed over still other clinical signs. Simple excesses are more common. Nutrients most commonly given in excess of needs, leading to toxicity or induced deficits of other nutrients, are energy, phosphorus, iron, copper, selenium, and vitamin A. Energy Deficiency Many nonspecific changes found in horses with nutritional deficiencies are related to caloric deficiency and can result from inadequate intake, maldigestion, or malabsorption. In partial or complete starvation, most internal organs exhibit some atrophy. The brain is least affected, but the size of the gonads may be strikingly decreased, and estrus may be delayed. The immune system is adversely affected, resulting in increased risk of viral diseases. The young skeleton is extremely sensitive, and growth slows or may completely stop. A decrease in adipose tissue is an early and conspicuous sign and is seen not only in the subcutis but also in the mesentery; around the kidneys, uterus, and testes; and in the retroperitoneum. Low-fat content of the marrow in the long bones is a good indicator of prolonged inanition. The ability to perform work is impaired, and endogenous nitrogen losses increase as muscle proteins are metabolized for energy. Energy Excess Overfeeding of high-calorie feeds results in obesity in horses and may contribute to developmental orthopedic disease in growing horses. Obesity increases the risk of laminitis and colic due to strangulation of the small intestine by pedunculated mesenteric lipomas. Obese horses and ponies have decreased insulin sensitivity and reduced heat and exercise tolerance. Protein Deficiency A deficiency of dietary protein may represent either an inadequate intake of high-quality protein or the lack of a specific essential amino acid. The effects of deficiency are generally nonspecific, and many of the signs do not differ from the effects of partial or total caloric restriction. In general, the horse will have poor quality hair and hoof growth, weight loss, and inappetence. In addition, there may be decreased formation of Hgb, RBC, and plasma proteins. Milk production is decreased in lactating mares. The following liver enzymes have shown decreased activity: pyruvic oxidase, succinoxidase, succinic acid dehydrogenase, D-amino acid oxidase, DPN-cytochrome C reductase, and uricase. Corneal vascularization and lens degeneration have been noted. Antibody formation is also impaired. Mineral Deficiencies and Excesses Nutritional Secondary Hyperparathyroidism (Bighead, Bran disease) Horses of all ages fed grass hay or pasture and supplemented with large amounts of grain-based concentrates or wheat bran are most likely to develop relative or absolute calcium deficiencies leading to nutritional secondary hyperparathyroidism. Excess phosphorus intake (Ca:P ratio <1.0) causes the same clinical signs. Blood concentrations of calcium do not reflect intake due to homeostatic mechanisms, though blood inorganic phosphorus may be elevated due to mobilization of bone mineral content. Serum alkaline phosphatase activity is usually increased, and clotting time may be prolonged slightly. Young, growing bone is frequently rachitic and brittle. Fractures may be common and heal poorly. Swelling and softening of the facial bones and alternating limb lameness are frequently reported. (Also see Dystrophies Associated with Calcium, Phosphorus, and Vitamin D:Osteomalacia.) Phosphorus Deficiency This is most likely in horses being fed poor-quality grass hay or pasture without grain. Serum inorganic phosphorus concentrations may be decreased and serum alkaline phosphatase activity increased. Occasionally, serum calcium levels may be increased. An insidious shifting lameness may be seen. Bone changes resemble those described for calcium deficiency. Affected horses may start to consume large quantities of soil or exhibit other manifestations of pica before other clinical signs are apparent. Page 21

22 Salt Deficiency Horses are most likely to develop signs of salt (NaCl) deficiency when worked hard in hot weather. Sweat and urinary losses are appreciable. Horses deprived of salt tire easily, stop sweating, and exhibit muscle spasms if exercised strenuously. Hemoconcentration and acidosis may be expected. Anorexia and pica may be evident in chronic deprivation, although these are not specific signs of salt deficiency. In lactating mares, milk production seriously declines. Polyuria and polydipsia secondary to renal medullary washout may be seen in prolonged deficits. Potassium Chronic dietary deficiency of potassium results in a decreased rate of growth, anorexia, and perhaps hypokalemia. However, most forages contain more than sufficient potassium for the average horse. Acute deficits due to sweat losses are more likely and may cause muscle tremors, cardiac arrhythmias, and weakness. Excess potassium intake, especially if given as a bolus PO or IV, also will induce cardiac arrhythmias such as atrial fibrillation. Magnesium Foals fed a purified diet containing magnesium at 8 mg/kg (3.6 mg/lb) exhibited hypomagnesemia, nervousness, muscular tremors, and ataxia followed by collapse, with increased respiratory rates, sweating, convulsive paddling, and death after a few weeks. However, most commonly used feeds contain magnesium well in excess of the mg/kg dry ration currently recommended. Oversupplementation of this mineral is more likely. Though the effects of excessive magnesium intake in horses have not been determined, based on data from other species it may cause clinical signs of calcium deficiency. Iron Iron deficiency may be secondary to parasitism or chronic blood loss and results in microcytic, hypochromic anemia. However, it is highly unlikely that even anemic horses are iron deficient. Iron excess interferes with copper metabolism and also causes microcytic, hypochromic anemia. Blood transferrin concentrations are the most reliable method to determine the iron status of a horse. Zinc Zinc deficiency in foals causes reduced growth rate, anorexia, cutaneous lesions on the lower extremities, alopecia, decreased blood levels of zinc, and decreased serum alkaline phosphatase activity. Excesses (>1,000 ppm) were associated with developmental orthopedic disease in young horses. The effects of excesses or deficits of zinc have not been documented in adult horses. Copper An apparent relationship between low blood copper concentrations and uterine artery rupture in aged parturient mares suggests reduced copper absorption with age or reduced ability to mobilize copper stores. Dietary deficiency may cause aortic aneurysm, contracted tendons, and improper cartilage formation in growing foals. Excessive copper intake may interfere with selenium and/or iron metabolism. Selenium Selenium deficiency results in reduced serum selenium, increased AST activity, white muscle disease, and perhaps rhabdomyolysis in working horses. Selenium excesses of as little as 5 ppm in the ration cause loss of mane and tail hairs and sloughing of the distal portion of the hoof. Vitamins A Vitamin A deficiency may develop if dried, poor-quality roughage is fed for a prolonged period. If body stores of vitamin A are high, signs may not appear for several months. The deficiency is characterized by nyctalopia, lacrimation, keratinization of the cornea, susceptibility to pneumonia, abscesses of the sublingual gland, incoordination, impaired reproduction, capricious appetite, and progressive weakness. Hooves are frequently deformed, with the horny layer unevenly laid down and unusually brittle. Metaplasia of the intestinal mucosa and achlorhydria have been reported. Genitourinary mucosal metaplasia may be expected. Bone remodeling is defective. The foramina do not enlarge properly during early growth, and skeletal deformities are evident. The latter may be seen in foals of vitamin A-deficient mares. If sun-cured hay is consumed or the horse is exposed to sunlight, it is doubtful that a vitamin D deficiency will develop. Prolonged confinement of young horses offered only limited amounts of sun-cured hay may result in reduced bone calcification, stiff and swollen joints, stiffness of gait, irritability, and reduced serum calcium and phosphorus. Signs of experimental thiamine deficiency include anorexia, weight loss, incoordination, decreased blood thiamine, and increased blood pyruvate. At necropsy, the heart is dilated. Similar signs have been seen in bracken fern poisoning. Under normal circumstances, the natural diet plus synthesis by microorganisms in the gut probably meet the need for thiamine. However, needs may be increased by stress. Although natural feeds plus synthesis within the gut normally provide adequate riboflavin, limited evidence indicates an occasional deficiency when the diet is of poor quality. The first sign of acute deficiency is catarrhal conjunctivitis in one or both eyes, accompanied by photophobia and lacrimation. The retina, lens, and ocular fluids may deteriorate gradually and result in impaired vision or blindness. Equine recurrent uveitis has been linked to riboflavin deficiency but may be a sequela of leptospirosis or onchocerciasis. The normal feedstuffs of horses generally contain very little vitamin B12. However, the horse Page 22

23 can synthesize this vitamin in the gut, from which it is absorbed. Last full review/revision July 2011 by Sarah L. Ralston, VMD, PhD, DACVN There are many horse diseases that are affected by horse nutrition in some manner. Diseases related to horse nutrition are split into two categories: those that are directly related to nutrition and those that are indirectly related to nutrition. Diseases that are directly related to nutrition are good news and bad news. They are usually pretty serious, but at the same time, with proper management, they are also completely preventable. Some examples of problems that are directly related to nutrition are: Developmental Orthopedic Disease Obesity Nutritional Secondary Hyperparathyroidism (NSH) Mycotoxicosis (Mycotoxin poisoning) Diseases that are indirectly related to nutrition are a bit more complex, as modifying the horse s diet alone usually cannot treat or prevent these. In fact, some of these diseases are not preventable at all. However, proper nutritional management often plays an important role in managing the problem. Some diseases that are indirectly related to nutrition include: HYPP Polysaccharide Storage Myopathy (PSSM or EPSM) Enterolithiasis (intestinal calculi) Insulin Resistance Then there are those horse diseases that fall into both categories...diseases that can be brought on by nutrition conditions or completely unrelated conditions. These diseases can usually be managed to some extent by nutritional management. Included in this category is: Laminitis Equine Colic Equine Gastric Ulcer Syndrome (Equine Ulcers) These diseases listed above are all diseases that most owners recognize as related to nutrition in one way or another. However... Did you know that many other diseases are also related to nutrition? Things like: Rain Rot Thrush Allergies can all be related to nutrition too! These diseases are usually caused by a compromised immune system. Often, simply improving your horse's nutrition level can improve his immune function and as a result prevent diseases such as these. I've come across many horses that were diagnosed as having chronic cases of rain rot. When they were provided with a high quality vitamin and mineral supplement they no longer dealt with the disease at all! No owner wants to deal with horse disease, but it is part of living with horses. Learning all you can about horse nutrition will enable you to manage or prevent a number of diseases, making you and your horse s lives that much easier. Developmental Orthopedic Disease Developmental Orthopedic Disease, or DOD, refers to a number of different ailments which afflict growing horses. The conditions include: Angular Limb Deformities (ALD) Physitis Subchondral bone cysts Osteochondrosis (OC) Flexural Limb Deformities Horse Diseases Related to Nutrition Page 23

24 Don't worry if you don't know what a single one of those diseases are...chances are you actually do know of them -- but you probably know their common names instead. So, let's quickly discuss them: Angular Limb Deformities ALD is more often known as crooked-legged foals. Foals born with this disease have legs that deviate outward or inward from straight down. Usually the knee joint is the area where the leg is affected, though it can be in the fetlock or hock joint as well. The cause of ALD is very complex, but is associated with unequal growth of long bones...one side of the bone grows faster than the other, resulting in the limb being deviated from normal. This abnormal growth occurs next to the joint in the growth plate. Causes of ALD include lameness (which causes abnormal weight-bearing), physitis, excessive body growth in relation to bone/joint growth, and growth plate injury. Treatment of ALD depends on how old the foal is, how severe the ALD is, and how soon the ALD is diagnosed. In general, the earlier it is diagnosed, the easier it is to treat. Strict stall rest and diet modification, as well as correct hoof trimming, is a part of the treatment for all cases of ALD. Depending on the severity and limbs affected, other means of treatment may include casts, splints, or surgery. Physitis Physitis is nothing more than swelling around the growth plate of a bone. It usually occurs in the bones of the legs, and usually in bones that are closer to the ground. There are a few theories about why physitis occurs, including malnutrition, faulty hoof growth, and compression of the growth plate. Compression of the growth plate seems to be the most likely cause, as physitis is most often seen in foals that are large for their age, grow quickly, and are top-heavy. It is most often seen in the summer when the ground is hard and dry. It is also seen a lot when the calcium:phosphorus ratio is unbalanced. Treatment includes reducing feed intake to reduce weight and/or growth rate. The diet also needs to be evaluated to ensure that the calcium:phosphorus ratio is correct (for treatment purposes it should be around 1.6:1) and the amount of protein is not excessive. Confining exercise to small areas where the footing is soft is also part of treatment, as is ensuring that the feet are trimmed correctly and often. Subchondral Bone Cysts Subchondral bone cysts are small holes in the bone. They usually occur when the cartilage has excessive pressure or stress placed on it (such as happens during quick growth). These cysts most often occur in the stifle. Some horses respond to a conservative treatment of 4-6 months of rest and treatment with bute. If the horse doesn't respond to this treatment, the only other option is surgery. However, since surgery has very favorable results, sometimes it is done before the conservative treatment is attempted. Osteochondrosis Osteochondrosis (OC) occurs when cartilage fails to harden into bone. The more severe form of this disease is osteochondrosis dissicans, or OCD. When the cartilage fails to harden into bone, a flap of cartilage remains on the articular cartilage or growth plate. OC is a fairly wide-spread disease, affecting up to 30% of some breeds. There is a "window of susceptibility" for each joint, during which the cartilage is forming into bone and can be affected. Once this window has passed, it is almost impossible for the problem to be corrected without surgery. However, before this window passes, it is possible for many mild cases of OC to resolve themselves over time. Because of this, it is essential that growing foals have a balanced diet, so that a diet problem doesn't prevent the lesions from resolving themselves. Flexural Limb Deformities Flexural Limb Deformities (FLD) are often more well-known as "contracted tendons." In FLD, the heel is pulled up off the ground causing the foal to stand more on the toe instead of a flat surface of the hoof. FLD can occur because of bad positioning in the uterus, limited exercise, overfeeding, and dietary imbalances. Page 24

25 Excess Energy So, what do all of these diseases have in common? They all appear to be linked to (and possibly caused by) excess energy intake in growing horses. Young horses that are fed to achieve quick and excessive growth appear to be the most susceptible. It does not appear to make a large difference what the diet is composed of...if they are fed in excess of energy requirements, foals appear to be at a larger risk for developmental orthopedic disease. It is thought that high levels of starches and sugars may contribute to hormonal imbalances in foals. These hormonal imbalances then affect the insulin response, and higher levels of insulin are often found in the blood of foals suffering from OCD. It is known that high starch/sugar diets affect the insulin response, but at this time it is unknown (due to much conflicting data) whether or not this promotes occurrences of developmental orthopedic disease. So, until more research is done, it is best to conclude that diets excess in energy might promote developmental orthopedic disease. As a result, growing horses will benefit from being fed a diet that promotes moderate growth rates instead of fast growth rates. Mineral Imbalances Unlike the studies about excess energy's relation to OCD, there is clear evidence that unbalanced mineral intakes cause OCD. OCD can be caused by feeding a diet with an unbalanced calcium:phosphorus ratio, even if the foals have normal weight gain. Copper is another important mineral related to OC and physitis. Because copper is an important part of collagen (which is an important part of the bone matrix), inadequate intakes can cause both OC and physitis. Exercise Exercise is a very important part of a foal's life. Exercise causes greater bone turnover and remodeling, which is a good thing, and helps make the young horse's bones stronger. Both voluntary and enforced exercise both prevent developmental orthopedic disease compared to foals that are kept in confinement with little or no exercise. However, on the flip side, intensive exercise can cause developmental orthopedic disease. Therefore, it is ideal to provide the growing foal with as much voluntary exercise as possible, and only supplement with enforced exercise if voluntary exercise is not possible. Page 25

26 Nutritional Secondary Hyperparathyroidism Nutritional Secondary Hyperparathyroidism is a bone diseasae in horses. Anyone who owns horses and knows the tiniest bit about horse nutrition knows that the calcium:phosphorus ratio is important to growing horses. The main reason is that an imbalanced Ca:P ratio can cause bone diseases in growing horses......one of which is Nutritional Secondary Hyperparathyroidism, commonly abbreviated NSH. NSH is caused by diets that contain too much phosphorus or not enough calcium. This can be caused simply by a calcium deficiency, or it can be caused by excess phosphorus in the diet. Not only does excess phosphorus in the diet change the Ca:P ratio, but an excess in phosphorus can actually create a calcium deficiency by hindering calcium absorption. Symptoms of NSH Nutritional Secondary Hyperparathyroidism can easily go unnoticed in the early stages, due to its general symptoms. The two earliest signs of this disease are a shifting lameness and tender joints. However, since this disease often affects horses anywhere from weaning to 7 years of age, these first two symptoms can easily be attributed to the horse's training or exercise regimen. Because of this, it is sometimes hard to catch this disease in its early stages. However, the next two symptoms, reluctance to move and a stiff gait are usually serious enough symptoms to warrant a call to the vet in the eyes of most owners. Therefore, when these symptoms appear, the horse is more likely to get early treatment. All the symptoms of NSH are caused by the bone losing its mineral content, and as a result, tiny fractures occurring in the bone. This eventually leads to a loss of bone integrity, and a cartilage disruption, which eventually leads to tearing and/or detachment of tendons and ligaments. As the minerals in the bone are replaced with fibrous tissue, the bones thicken, and a physical distortion occurs. Because the facial bones are most often affected with this disease, it has been termed "big head" in the past. In the early 1900's when it was most prevalent, Nutritional Secondary Hyperparathyroidism was often called "bran disease" or "miller's disease" because horses that consumed large amounts of bran by-products, particularly that of wheat bran, were most often afflicted. When the facial bones are affected, the horse often has trouble breathing, which is what usually warrants the veterinary call that leads to eventual diagnosis. As NSH progresses in the facial bones, the horse will eventually have trouble chewing as well as dental pain. This will lead to a decreased intake of food, which will eventually result in weight loss and a poor body condition. What kind of diet causes it? The most common equine diet that results in Nutritional Secondary Hyperparathyroidism is the diet that consists of mature grass forage (hay or pasture) and large amounts of cereal grain-based supplements. These diets are often borderline or low in calcium and borderline or high in phosphorus. This is because most grasses, though they vary in calcium content, often have a Ca:P ratio around 2:1, compared to 4:1 for legume forages. Compounding the problem in these diets are the cereal grains, which are extremely low in calcium, while being very high in phosphorus. Most cereal grains have a Ca:P ratio of 1:6 or higher! Unfortunately for most horses, this diet is still very common in today's horse population. Many horses receive grass hay as their forage and then corn or oats, or some combination of both as their grain. Fortified commercial products usually do not have this issue, as they contain added calcium for the most part, but it is still something to keep in mind if you are feeding large amounts of cereal grains (more than 4-5 pounds/day). Diets that are heavily supplemented with wheat bran or rice bran can also cause NSH. However, there are fortified rice brans available on the market today that contain added calcium to keep the ratio where it should be. How is it treated and prevented? The good news about NSH is that it is easy to treat. The diet must simply be altered to provide more calcium while reducing the phosphorus so that a correct Ca:P ratio is reached. For early treatment of the disease, a diet with Ca:P ratios ranging from 3:1 to 6:1 has been advocated. Page 26

27 In older horses that contract the disease, the prognosis is very good. The bony changes will take a few months to reverse, and some slight facial distortion may be permanent, but they will usually not have lifelong problems resulting from the disease. However, in younger horses, this disease is much more serious, because their bones are still growing. This disease can cause serious problems to the long bones, and how serious the problems are depends on if the horse will suffer lifelong problems as a result of the disease. The easiest and most effective way to prevent this disease is to ensure that your horses receive a diet that has a balanced Ca:P ratio, particularly if there are growing horses in your herd. Just as essential is to ensure that the horses have enough calcium, as that can cause problems even if the Ca:P ratio is correct. Mycotoxicosis and Mycotoxins: How do they affect YOUR horse? Mycotoxicosis is the disease caused by ingestion of mycotoxins, which are toxins produced by fungi living on or in a plant at harvest time. This disease is very serious because of the possible severe reactions (including death in some cases) in horses. Thankfully, it is also a fairly rare disease. Some of these toxins are fatal within hours of ingestion, such as ergotamine, produced from ergots from the fungi Claviceps spp. This fungi has been found contaminating fresh pasture in Europe. Other mycotoxins, however, do not have such serious consequences of ingestion. These include slaframine, produced by Rhizoctonia leguminicola which is found in red clover and alfalfa. This mycotoxin causes excessive salivation and increased water intake. However, it breaks down in stored forages over time, so its less likely to cause problems. The biggest problem, from a management standpoint, is the fact that there are no reliable predictors of mycotoxin infestation. A number of plant variables, such as plant health, growth status, and plant maturity all affect whether or not mycotoxicosis is a potential problem. Conditions at harvest, including weather and how quickly the feed is stabilized also play a major role. Temperature and moisture content at harvest time, as well as during storage, are two of the biggest indicators of whether or not mycotoxicosis might be a problem. However, the various temperature and moisture combinations at which the different fungi produce harmful levels of mycotoxins is largely unknown. Complicating the matter even further is the fact that there are so many various fungi that produce mycotoxins, creating a wider range of conditions under which problems may occur. Mycotoxins can be found in fresh pasture, stored forage, or grains. The fungi need heat and moisture to thrive and produce the toxins, so mycotoxins will usually not be found in feeds that have been properly harvested and stored. This is one reason it is so important to only feed your horse feeds that you know have been properly harvested and stored. When in doubt, don't feed! Below is a table that summarizes some of the various fungi and their toxins. Don't be alarmed by the size of the table...like I mentioned above, mycotoxicosis is a pretty rare disease, despite the various organisms and plants involved. Fungus Family Specific Source Specific Plant Toxin Toxin Symptoms Fungus Claviceps spp. Pasture Ryegrass; Canarygrass; Dallisgrass; Native European species Toxic alkaloids Page 27

28 Rhizoctonia spp. Fusarium spp. Asperigillus spp. Penicillium spp. Pasture Hay R. leguminicola Pasture Hay F. roseum; F. graminearum Pasture Hay Silage Hay Silage Hay Silage Red Clover; Alfalfa slaframine tricothicenes fumonisins zearalenone vomitoxin aflatoxins dicoumerol patulin Excessive salivation; Increased water consumption Kidney damage; Nervous system problems Blind staggers; Death Reproduction problems Carcinogenic; Liver problems Nasal bleeding; Joint Swelling; Lameness; Respiratory problems Carcinogenic Like most diseases that face our horses today, mycotoxicosis is much more easily prevented than treated. Use common sense when buying feed products for your horse, especially hays. Ask the producer how it was stored and what the weather and drying conditions were when it came out of the field. Store feeds properly yourself...keep them off the ground and in a place where they won't get rained on or other moisture drawn into them. I personally also salt my hay bales for extra protection, giving me one less thing to worry about. Hyperkalemic Periodic Paralysis (HYPP) Hyperkalemic periodic paralysis, better known in the horse world as HYPP, can be a devastating disease. There are horses that have it that never show a symptom a day in their life, and horses that have repeated severe episodes, to the point that their owners choose to humanely euthanize them instead of watching them suffer. A large part of the management of hyperkalemic periodic paralysis is based around the diet, so we are going to discuss today what aspects of the HYPP horse's diet are most important. However, to understand how this diet helps the HYPP-positive horse, its essential to understand how this disease works, and what it does to the horse. HYPP: The Genes Behind It In big words, hyperkalemic periodic paralysis is a codominant single autosomal gene disorder. In easier-tounderstand language, this means that: It's genetic It is located on one single autosomal gene It is co-dominant (more on these last two in a minute!) Now for a very basic genetic lesson: Page 28

29 Genes are made up of parts called "alleles"...each horse has one from its sire and one from its dam for each gene. So, in respect to hyperkalemic periodic paralysis, a horse could be N/N, which is two normal alleles on the gene...this horse would not have HYPP, and could not possibly pass it on to its foals. These horses are HYPP negative. Or, the horse could be N/H...this is where the co-dominance comes in. In a gene that is not co-dominant, either the animal has the disease, or he doesn't. However, with co-dominance, there is an "intermediate" which is different from the positive and negative. Horses that are N/H have one affected allele, and one normal allele. They can show symptoms of the disease, but they are less likely to show symptoms than horses that have two affected alleles. However, it can still happen, and they CAN still pass it on to their foals. For all intents and purposes, these horses should be treated and managed as if they have hyperkalemic periodic paralysis. These horses are often referred to as HYPP "carriers" because they carry the disease in their genes, but they don't always exhibit symptoms. And lastly, horses can be H/H. These horses have two copies of the problematic allele, and are considered HYPP positive. These horses are most prone to HYPP attacks, and need to be managed very carefully. H/H horses will ALWAYS pass on an affected gene to their foals. This means that if they are bred to a N/N horse, all of their foals will be N/H (carriers). If they are bred to a N/H horse, their foals will all be N/H (carriers) or H/H (positive). HYPP: Abnormal Muscle Cells In a normal muscle cell, there is an electrical gradient across the cell membrane when sodium is pumped out of the cell and potassium is pumped in. This gradient is usually around 85 millivolts (mv) This gradient is able to be maintained because the only way sodium can get into a cell is through the sodium channels. However, these channels are not always open. In fact, most of the time they are closed -- they are only opened when a nerve impulse is received by the cell. When the sodium channel is closed, sodium collects outside the cell while potassium collects inside the cell. As long as the electrical gradient remains close to 85 mv, the cell will stay at rest and the muscle will not contract. When a nerve impulse is received by the cell, the sodium channel changes shape and allows sodium to rush into the cell. At the same time, potassium rushes out, because both ions are positive, so potassium moves to the more negatively charged area, which is outside the cell. As the sodium rushes in and potassium rushes out, the electrical gradient gets close to 0 mv. This is called an action potential and causes calcium to be released from storage sites in the cell. The calcium then binds with areas on the muscle fibers called myosin. Once the calcium is bound, the muscle contracts and stays contracted until the calcium pump in the cell gets all the calcium put back into the storage site. Then the entire process starts over again with another nerve impulse. That is how it is supposed to work. However, in horses that have hyperkalemic periodic paralysis, the sodium channels are "leaky". They are not able to completely close, thus sodium is constantly leaking into the cell. All this leaking of sodium causes the electrical gradient to be repeatedly brought close to 0mV, which causes the muscles to release the calcium and it to bind. This happens over and over, causing the muscles to repetitively contract. Large muscles All of the repetitive contractions of the muscles works the muscles even when the HYPP horse is at rest. Because a muscle grows the more it is worked, any muscles that are being affected will grow larger than normal. However, not every HYPP positive horse has visibly large muscles. Likewise, not every horse will abnormally large muscle groups will have HYPP. There is absolutely NO way to tell if a horse has HYPP just by looking at it. The only way to tell for sure is to have the horse tested. UC Davis is the most well known place to have a horse tested for HYPP...you simply send a hair sample in and they send you the results after it has been tested. You can also tell if a horse is definitely negative if he has two parents that have been tested and are both N/N. The Impressive Disease Hyperkalemic Periodic Paralysis is often known as the "Impressive" disease because it is thought that the gene mutation that causes it started with the famous Quarter Horse stallion named Impressive. However, there are some people in the horse world that believe it may go back further than Impressive. I've heard accounts of at least 2 horses that tested positive for Hyperkalemic Periodic Paralysis at UC Davis without having Impressive in their pedigree. However, both mares that did test positive (UC Davis tested 3 different samples from each mare and all came back positive) did have Impressive's dam, Glamour Bars, in their pedigree. These mares just happened to be tested because they were part of a good-sized breeding operation that tests all of their horses regardless of bloodlines, before sale. There is speculation that the gene mutation goes back further in Glamour Bars' pedigree, probably carried through the dams. This is rational, as mares usually average foals throughout their lifetime at most, so the chances of them having large amounts of offspring affected would be minimal. Even if half the foals from one mare carried the Page 29

30 disease or were afflicted by it, news about it would not spread much further than the foal's immediate locale, thus a problem like this carried through the dam's line would probably not be caught. Regardless of how far the HYPP mutation does go back, research has proven that it goes back to Impressive for sure. Thus every horse that has Impressive in his pedigree has a chance of carrying the disease (unless his parents have been tested negative) and should be tested. Nutritional Management of HYPP The overall goal of treatment and management of Hyperkalemic Periodic Paralysis is to limit increases in serum potassium levels. This is done by a combination of: Limiting dietary potassium intake Promoting entry of potassium into cells Eliminating excess potassium from the body through urine The single most important aspect of treatment is limiting dietary potassium intake. If a Hyperkalemic Periodic Paralysis-positive horse consumes a diet that is more than 1% potassium, clinical signs, or "attacks" are more common. However, if the diet is maintained below 1% potassium, the disease can often be managed without any other preventative measures. The largest source of potassium in a horse's diet is his hay. In general, grass hays tend to have less potassium than legumes such as alfalfa. However, the potassium content of hay depends on where it was grown, when it was cut, and conditions during growth and harvest, as well as the grass fertility and moisture content. Due to this great variation, it is imperative that if you are managing a HYPP horse, you have your hay tested at a laboratory for potassium content. It is usually a good idea to maintain an HYPP horse on grass hays such as timothy, Bermudagrass, or prairie hay. If legumes such as alfalfa must be included in the diet, it may be necessary to use other measures to control the disease. Inclusion of larger amounts of cereal grains in the HYPP horse's diet is also a way to decrease the potassium level, as cereal grains are fairly low in potassium. Not only will the intake of cereal grains decrease the potassium content of the diet, but it may also increase the uptake of potassium into cells by promoting insulin release, which promotes uptake of potassium into cells. However, intake of commercial mixes that contain molasses, soybean meal, or dehydrated alfalfa should be monitored, as these feeds can contain large amounts of potassium. Management beyond nutrition In cases where nutritional management is not enough to control Hyperkalemic Periodic Paralysis, a few other options are available. Mild exercise, insulin release, and administration of other cations have all been shown to increase potassium uptake. Insulin release can be achieved by feeding cereal grains high in starch, or administering glucose either IV or orally. Sodium or calcium administered through IV will increase potassium uptake as they are both cations. Another prevention method that can be used under the supervision of a veterinarian is the administration of acetazolimide, which is a diuretic that increases the excretion of potassium in the urine. Hyperkalemic Periodic Paralysis is a scary disease to have to deal with. Thankfully it can usually be managed through dietary changes. If dieatary changes are not sufficient to manage the disease, there are other options available. Knowledge of what the disease does, how it is passed on, and what causes it all help you be prepared should you end up with a HYPP positive horse in the future. Page 30

31 Polysaccharide Storage Myopathy Polysaccharide Storage Myopathy is a disease that occurs when excess glycogen (storage form of glucose) or glucose-6-phosphate (form of glucose taken into cells) is present in muscles. Often referred to as PSSM, this disease is called equine polysaccharide storage myopathy, or EPSM, when it occurs in draft horses. A clinical diagnosis of PSSM can be made when a horse that suffers from chronic exertional rhabdomyolys (ER) is found to have amylase-resistant polysaccharide in his muscles. Amylase is the enzyme that breaks starches down to sugars. ER is a syndrome of muscle pain and cramping that is associated with exercise. However, the build-up of amylase-resistant polysaccharide may take quite some time to build up before it can be detected. In one study, Quarter Horse foals that showed symptoms of chronic ER did not have the amylase-resistant polysaccharide apparent in their muscles until they were two years old! The good news about PSSM is that its symptoms can be controlled by diet to an extent. Signs and Symptoms Most of the signs and symptoms of PSSM have to do with the muscles, which makes sense, as the disease affects the muscles. Common signs and symptoms include: Exertional Rhabdomyolysis Exercise Intolerance Muscle Stiffness Shifting Lamenss Back Pain Camped-out stance - standing with legs behind or in front of body instead of directly under Muscle atrophy Colic-like symptoms In draft horses and other related breeds such as Warmbloods, the symptoms of EPSM appear as muscle soreness in the back and hindquarters, stiffness, and sometimes ER. In Belgains, EPSM may occur in conjunction with a disease known as "shivers", which shows up as muscle tremors and over-extension of the back legs. Controlling Symptoms with Diet To control the symptoms of PSSM with diet, horses must be fed a diet that is low in starch and sugar and high in fat. This type of diet has been shown to reduce the frequency and severity of symptoms. To be helpful, the total diet must contain less than 8% of the digestible energy from starch and sugar. In addition, it must contain more than 10% of digestible energy from fat. Horses with PSSM must also be exercised regularly, as lack of exercise increases the frequency and severity of symptoms. In fact, even if the diet is changed, there will usually not be a reduction in symptoms unless the horse also receives regular exercise and turnout. The exact recommendations for a PSSM diet are: Feed a minimum of 1.5% body weight of forage per day Remove all concentrates containing grain or molasses from diet Use alternative energy sources if digestible energy needs are more what is provided by forage alone. It is suggested that the forage provided be grass or oat hay, as these hays are lower in starch and sugar than legume hays. Alternative energy sources include vegetable oil, rice bran, non-molassesed beet pulp, and black oil sunflower seeds. Some horses may need a fat content higher than 10% of the diet, so you may have to do some experimentation with your individual horse to find the correct balance of starch and sugar content, fat content, and exercise. Page 31

32 Polysaccharide Storage Myopathy can be a scary disease until it is properly managed. Knowledge of the disease allows you to manage it through diet and exercise. By following the recommendations of: Adequate forage intake No grains or molasses Use of alternative energy sources as well as ensuring adequate daily exercise you will be able to successfully manage almost every case of PSSM or EPSM. Once PSSM is managed through diet and exercise, it becomes much less of a problem for both the horse and his owner. Enterolithiasis Enterolithiasis is the presence of intestinal calculi, called enteroliths. These calculi are deposits, or build-up, in the large intestine. This is a problem, because they can cause blockages of varying degrees, usually resulting in colic to varying degrees. In fact, during one study, more than 15% of horses admitted to the large animal clinic at UC Davis for colic complaints can blame enterolithiasis for the colic episode. So what exactly are enteroliths? They are a build-up of struvite crystals, which are composed of magnesium ammonium phosphate. The crystals are laid down in concentric rings, and the larger the ring, the bigger the blockage. The rings usually start around a foreign body in the intestine, such as a small piece of cloth or hair that has been ingested. These rings can form into one large enterolith, or they can form into numerous small enteroliths in groups. If one large enterolith is formed, usually the horse will experience colic to varying degrees as the calculi gets lodged in areas of the large intestine, causing bloating and digesta back-up to varying degrees. However, if small enterolith groups are formed, usually the horse will just display symptoms of mild abdominal pain, as the small crystals usually don't cause blockages. Instead, they irritate the tract lining as they move. Which horses are at risk? Like I mentioned before, in one study more than 15% of horses admitted to UC Davis for colic were suffering from enterolithiasis. Yet, at the same time period, less than 2% of horses admitted to a clinic in Texas for colic had enterolithiasis. This is due to the fact that it appears horses in certain geographical regions are more prone to the disease. California and the southeastern US appear to be the areas with the highest number of cases. Page 32

33 However, horses in every geographical region can have enterolithiasis. Breeds that tend to be over-represented include Arabians (and Arabian crosses), Morgans, American Saddlebreds, donkeys, and miniature breeds. There also appears that there might be a genetic component to the disease, as the reported occurrence in siblings is high. It used to be thought that young horses would not suffer from intestinal calculi due to the length of time it usually takes the crystals to form. However, there have been reported confirmed cases in horses less than one year of age. This suggests that in the right conditions, it is possible for the crystals to form to a problematic size in a short amount of time. What causes enterolithiasis? A number of studies have pointed to increased large intestine ph as a cause of this disease. Normal ph in the horse large intestine is usually somewhere around 6.9, while horses with substantial enteroliths usually have a ph somewhere around 7.3. Affected horses also have a lower content of dry matter in their colon, as well as higher concentrations of magnesium, phosphorus, calcium, and potassium, as well as other nutrients in the digesta. Also, horses that are fed large amounts of alfalfa (more than 70% of forage intake) appear to be at higher risk. This is because alfalfa has very high buffering capacities, and buffers are used to promote a higher ph. It also has more protein and magnesium than grass hays, both of which are thought to contribute to the formation of the crystals. However, due to the large number of horses that consume large amounts of alfalfa and do not have enteroliths, alfalfa is obviously not the only factor in causing the formation of struvites. One of the last risk factors for enterolithiasis is lack of daily access to pasture. It is not clear whether pastured horses are at less risk because of increased grass intake or increased exercise, but for one reason or the other, or maybe a combination of both, horses that have daily access to pasture are at less risk than those that are stalled for more than 50% of the day. Nutritional Management A diet low in magnesium, phosphorus, and protein has been shown to reduce the occurrence and size of enteroliths in dogs in cats. Likewise, in horses it appears that dietary modifications can also be used as prevention of enteroliths. Dietary recommendations that increase the acidity of the colon that have been suggested include: exclusion of alfalfa from the diet exclusion of wheat bran from the diet increased grain:hay ratio supplementation with apple cider vinegar Page 33

34 Though these methods have all been suggested in one study or another, there is no solid evidence of how well they increase the acidity of the colon or prevent struvite formation. However, in lab studies, when the colon ph was below 6.6, the size and weight of enteroliths present decreased. In another study, ponies that were supplemented with 1/2 cup apple cider vinegar daily saw a reduction in the size of their enteroliths. So, for horses that have experienced problems with enterolithiasis, it is recommended that grass hay (instead of alfalfa) is fed, along with some form of grain (approximately 5 pounds/day for a 1000 pound horse) and 2 cups of apple cider vinegar (1 cup twice a day) to help prevent future occurrences. This is, of course, assuming the horse has no other issues that would be negatively affected this diet. It is also recommended that horses at risk receive daily turnout, preferably in a good pasture if possible. Equine Laminitis Equine laminitis may be one of the scariest diseases in horse nutrition...at least until you learn how to successfully manage it. The good news is that it can be successfully managed and prevented through nutrition. According to the 2000 National Animal Health Monitoring System, 50% of the laminitis cases seen every year could be prevented through correct nutritional management! Considering that almost 5% of horses that undergo surgery for laminitis end up dead management affects it. Nobody ever wants to hear that their horse has laminitis, but it happens way too often in the horse world. In fact, this very serious disease is the second-leading killer of horses...only colic takes more equine lives each year. What is laminitis in horses? Equine laminitis is caused when the laminae become inflamed. In normal conditions, these soft tissues connect the hoof wall to the coffin bone and other structures within the hoof...much like Velcro is used to fasten two things together. However, when the laminae become inflamed, the connections start to break, which causes catastrophic damage to the bones and other structures within the hoof. The inflammation also causes a constriction of blood vessels to the area, leading to ischemia, or lack of blood, to the cells. When the cells cannot get the nutrients they need, they start to die, compounding the problems. The Four Stages of Equine Laminitis Developmental Laminitis This stage is the time period between the triggering event and the first appearance of lameness. This period will usually last approximately 40 hours, and the horse will usually not show any symptoms during this period. Common triggering events of equine laminitis include: Over-consumption of grain or lush pasture Prolonged high fever Pneumonia Potomac horse fever Excessive stress Unrelated lameness in another limb Road founder or excessive prolonged concussion Stall shavings that contain black walnut Mastitis founder affecting lactating mares Page 34

35 Placenta retention beyond 12 hours Colic, especially after surgery It has been proposed (and substantiated by human medicine and limited studies in horses) that cold hosing and/or applying ice water to affected limbs during this period may prevent the progression of the disease. In one study 1, 6 Standardbreds were dosed with oligofructose (given in amounts known from previous studies to induce laminitis in 100% of cases). After treatment, one front foot of each horse was placed in a rubber boot with 50% ice cubes and 50% water while the other three feet were left untreated. For the entire 48-hours of the study, the ice was replenished to keep the level just below the carpus. At the end of the study period, the untreated feet on all 6 horses had clinical laminitis, ranging from mild to severe. However, the treated feet on all 6 horses showed no signs of laminitis at all. The horses all tolerated the boots well, and showed no ill effects from wearing them. Because the horses were humanely euthanized at the end of the study, it is still unclear whether or not the treated feet would eventually develop laminitis after the cold therapy was stopped. However, the cold therapy during the developmental period of the disease clearly prevented the progression of laminitis. Due to these results it is thought that a horse that is a suspected laminitis case will benefit from cold therapy. Once the horse has started to show signs of pain, it is too late for the cold therapy to do any good, as the disease has moved on to the acute phase. Acute Laminitis The acute stage has one of two outcomes: either the horse makes it through the next 72 hours with no physical or radiological collapse, or the horse suffers a digital collapse (rotation or sinking of the coffin bone) and the disease moves into the chronic stage. Subacute Laminitis If the horse does not suffer digital collapse during the acute stage, he moves inot the subacute stage which lasts for 8-12 weeks. During this stage, the horse is considered to be recovering from the damage done during the developmental and acute stages. Chronic Laminitis If the horse does suffer a digital collapse during the acute stage, he is considered to have chronic laminitis. Thus, any horse that has suffered from rotation or sinking of the coffin bone is considered to have chronic laminitis, regardless of how long he displayed signs of pain during the initial onset of the disease. Nutritional Management of Equine Laminitis One of the easiest ways to prevent laminitis brought on by over-consumption of grains is to properly store your feed to ensure that the horses have no access to it. If you have smart horses in your barn, this may mean measures as drastic as padlocking the feed room door and/or feed bins. To prevent most cases of equine laminitis caused by over-consumption of lush pasture, ensure that horses are slowly introduced to pasture whenever they have not had constant access to it for some time. Most generally this will be in the spring, but can also be in the fall, if they have been removed from the pasture during a late summer drought period. To prevent laminitis from being triggered by an upset to the ph and digestive process in the lower digestive tract, it has been suggested that any meal given to horses contain no more than 2-4 grams of starch per kilogram of body weight. For a 1000 pound horse, this means no more than 1-2 kg ( pounds) of starch each meal. Therefore, if a horse is being fed a grain product that is 30% starch (which many on the market are that or higher) that means the safe upper limit for each meal in this respect is anywhere from 7-14 pounds. In general, the concentrations are going to be high in spring, intermediate in autumn, and lowest in mid-summer. However, the levels also fluctuate daily, based upon when the plant is creating and storing energy. The levels tend to rise during the morning hours, reaching a maximum in the afternoon, before falling during the evening and overnight hours. Therefore, the levels during the afternoon may be 2-4 times greater than the levels in the same pasture during the morning hours and overnight hours. Removing laminitic horses from pasture during the day and turning them out for grazing overnight will help minimize their intake of these water-soluble carbohyrdates. For the horse with chronic laminitis, it is prudent to keep his body weight within a desirable range. Overweight horses bear more weight on each limb than those at an ideal weight, so keeping these horses at an ideal weight will minimize the impact and trauma on the affected limb from daily activities. It is also essential that these horses receive a high nutrition level so that they have adequate nutrients necessary to repair and maintain hoof quality. For many of these horses, like Babs, a ration balancer can be an ideal solution, providing minimal calories and high levels of nutrition. Lush pasture is often a problem because of the water-soluble carbohydrates such as glucose, fructose, and fructan. Page 35

36 These substances are thought to cause problems in hind-gut fermentation similar to the problems caused by excessive starch. These digestive problems then trigger equine laminitis. Therefore, it is prudent to limit pasture access to horses with chronic laminitis, or at risk for laminitis, during periods when these substances are at high concentrations. Knowledge of equine laminitis and how to prevent it can assist you in preventing this disease in your horses. Because it is such a devastating disease, and treatment success rates plummet so rapidly, it is essential that horse owners treat any suspected case of equine laminitis as if it is an actual case, until it has been determined that the hoof pain was caused by something else. I hope that you are lucky enough to never have to deal with equine laminitis personally, but now you have more knowledge of the disease in the event you need it. Equine Ulcers: Are They Causing Your Horse Problems? Don't think you have to worry about equine ulcers? Does your horse suffer from any of the following?? Chronic colic Poor body condition Loss of or poor appetite, especially when grain is involved Poor performance Bad attitude while being handled and/or ridden Generally ill tempered Continually fluctuating body weight If so, your horse could be suffering from Equine Gastric Ulcer Syndrome, the official term for equine ulcers. This is a very common problem in horses, much more prevalent than many owners realize. Some reports show as many as 85% of pleasure horses suffer from this problem. Rates for horses with stressful lives, such as show horses or race horses have been reported to have rates higher than 95%. Ages of Horses Affected Equine ulcers can affect any age of horse, from newborn foal to geriatric animals. Thankfully, they can be treated by various methods, and management practices can be altered to help prevent them. Young Foals The condition in very young foals is known as neonatal gastric ulceration. It is usually accompanied by another severe illness, such as generalized sepsis. Suckling Foals In suckling foals, the condition is known as gastroduodenal ulcer disease. This form of ulcers is characterized by ulcer in the upper digestive tract -- usually the lower esophagus, stomach, or upper part of the small intestine. The cause is unknown, but researchers suspect the problem starts with inflammation in the small intestine. This inflammation causes a back-up of acidic digesta, which then causes ulcers in the stomach and lower esophagus. It is suspected that a viral or bacterial disease causes the initial problems that lead to equine ulcers in these foals. Mature Horses The main form of equine ulcers to affect mature horses is erosion or ulceration of the squamous mucosa. This means the protective mucous layer of the stomach and digestive tract breaks down and can no longer protect the underlying tissue from the acidic environment. When the underlying tissue is exposed to the acid, the acid eats away at it, much like happens to our skin when we spill acid on it. Risk Factors A number of risk factors can predispose a horse to equine ulcers. The most obvious is a stressful lifestyle such as that of a show or race horse. Other factors include housing situations, feeding situations, and temperament of the animal. Intense Exercise Intense exercise has been shown to play a major role in the formation of ulcers. One study of Thoroughbred racehorses showed an ulcer prevalence of 100% in horses actively racing. Horses in race training weren't much better off, as the prevalence in that group was 91%. A study of endurance horses showed that they had an ulcer prevalence of 67% after races. The current speculation is that tightened abdominal muscles caused by intense exercise cause acidic digesta to back up into the upper digestive tract and remain there longer than usual. Page 36

37 Electrolyte administration Surprisingly, it has been found that routine administration of electrolytes, such as is done for endurance horses during races, can cause the formation of equine ulcers. In a study of 14 horses, those that received 8 hourly doses of commercial electrolytes showed a higher number of ulcers compared to the control group. The horses that received electrolytes also had more severe ulcers than the control group. Confinement Housing Confinement housing, particularly in a stall, is another risk factor for developing ulcers. Horses with no prior ulcer history who were moved from a pasture situation to stall confinement showed ulcers after only 7 days! It has been suggested that these types of housing situations cause ulcers due to: Lack of socialization with other horses Changes in diet composition Decreased meal frequency Decreased grazing time Temperament of Animal Temperament is also thought to play some role in ulcer formation, though it is not clear exactly how big of a role it may play. Nervous horses have been proven to have a higher prevalence of ulcers than their more calm counterparts. Though we are not sure of the exact reason nervous horses are more prone to ulcers, it is currently suspected that this higher frequency might be caused by the body being under continual stress. Meal Composition Meal composition is thought to play a role in equine ulcer formation because of how it affects saliva production. When a hay meal is fed to a horse, more chewing is required, and therefore more saliva (which is an important buffer for the digestive tract) is produced. If an equal weight of grain replaced the hay meal, only half the amount of saliva would be produced. Saliva is also more continually passed into the digestive tract with a hay meal, since it takes the horse longer to eat the hay meal than the grain meal. This makes a more stable lower digestive tract, because the acidity of the tract is not able to drop dramatically. Meal Size Meal size also plays a role in ulcer formation. Large grain meals produce more acid than an equal weight of hay (and less saliva as mentioned above!). The large grain meal will also empty from the stomach more slowly than small grain meals or hay. So not only have we created more acid, we've also created a situation where it sits in the stomach for a longer period of time. This is practically screaming to ulcers to make themselves at home... Meal Frequency Related to both of the above risk factors, meal frequency also plays a role in ulcer formation. Horses are one of the few animals that constantly produce gastric acid whether or not there is feed in their stomach. This should not be surprising, since they evolved as animals that continually grazed. Since there is always acid being produced, if there is not a buffer (like saliva!) from eating many times a day, the acidity in the tract will increase. The longer a horse goes without any food in front of him, the more acidic his digestive tract becomes. Like we've mentioned before, this is practically screaming at ulcers to make themselves at home... The all too common practice of feeding horses twice daily has been shown to be a contributing factor to ulcers. The best way to prevent this problem is to provide enough forage in those two feedings that the horse goes very little time without forage between meals. Prevention and Treatment of Equine Ulcers Eliminating as many risk factors as possible from your horse's life is the best way to prevent ulcers. Obviously, some factors, such as frequent showing or racing cannot be changed. However, other factors such as meal composition and frequency can be changed with small changes to management practices. If you suspect that your horse has ulcers, there are a few things that can be done. Some owners choose to have their vet scope the animal to check for ulcers before treatment. However, others choose to just assume the horse has ulcers because of the cost of scoping, as well as the fact that the procedure often misses ulcers lower in the tract, where most ulcers are actually located. Horses will usually show a great improvement within a few weeks of treatment being started, except in the most severe cases. Change of Management Practices Changing management practices is often the easiest and most cost-effective way to not only prevent ulcers, but to treat them as well. Page 37

38 Reducing the acid level in the digestive tract by providing continual forage often goes a long way towards treatment of mild cases of ulcers. Removal of high starch meals (or decreased size and increased frequency) also helps to reduce the acidity. Commercial Products Changing management practices may not be enough to take care of more severe cases of ulcers. In these cases, commercial ulcer products are often very helpful in protecting the digestive tract long enough for it to heal. However, its important to note that management changes will need to be made to minimize the risk of the ulcers returning. Commercial Prevention Products For horses with chronic ulcers who are not helped even after treatment with commercial products and all feasible management changes have been made, there are commercial prevention products available. These products are usually added to the feed on a daily basis to help maintain the ph of the digestive tract. However, these preventatives can be very costly, so are often a last resort for most horse owners. Equine ulcers can be a very painful problem for many horses. However, with proper management and treatment they can be eliminated from most horses. Equine Thrush Equine thrush is a disease that affects the horse's hoof. It is a bacterial infection which usually settles in the frog of the foot, but can spread throughout the hoof if not treated properly. The good news is that the bacteria that causes thrush is anaerobic. This means that it cannot survive in the presence of oxygen......so all you need to do to keep your horse's hooves free from thrush is to keep them exposed to air......which is WAY easier said than done, I know! Signs of Equine Thrush Horse thrush can be recognized by two distinctive signs: 1. A black gooey like substance that leaves a dark stain 2. An odor so offensive that it'll almost knock you off your feet Now, we all know our horse's feet go through some pretty nasty things on a daily basis...so their feet can smell pretty bad anyways, even when there is not thrush. But if the stench is accompanied by the goo, or gets excessively worse fairly sudden, there is a pretty good chance that it is probably thrush. The picture below shows what equine thrush looks like: Page 38

39 Equine Thrush Remedies There are a number of remedies on the market for equine thrush, all which work pretty well. Make sure when you apply these remedies that you coat all areas of the hoof well, working it into the cracks and crevices. Products such as Hoof Magic Thrush Antiseptic Treatment (left) are available in most tack stores, as well as horse product catalogs. You can click on the bottle to the left to purchase Hoof Magic from Shop.com, or both Stateline Tack and Jeffers Equine have a good selection of thrush remedies if you prefer a different brand. Click on the name of either of these companies to be taken to their website where you can view and purchase their thrush products. Do be aware, if you are not already, that many of these treatments are dyed, allowing you to see clearly where they have been applied. However, they also dye everything else they touch, including you, the barn floor, the too-curious-for-hisown-good barn dog's nose......and the list goes on. After having treated numerous cases of thrush and having green hoof-prints marching up and down my concrete driveway, I stumbled (literally!) upon a great solution to the staining problem......i put the medicine to be applied in a cheap spray bottle and spray it on the hoof. One or two squirts effectively covers the entire bottom of the hoof, and gets into the cracks and crevices pretty good. Because the spray bottle only applies a thin layer (instead of the thick layer you usually get if you try to apply from the bottle) it also shortens the drying time from unbearable minutes (which seem like hours when your horse is tired of this and tries to turn it into a tug-o-war game!) to under a minute. I do still wear gloves when using the squirt bottle though... I learned that lesson the hard way when the sprayer malfunctioned and I ended up with green hands for a week! (Try explaining that one to your school teachers!) So, what does thrush have to do with nutrition? I'm glad you asked! Thrush is one of those opportunistic infections. The bacteria that cause thrush are always living in your horse's environment. Most of the time they don't cause a problem. However, if something compromises the hoof, they are more than happy to move in! In the case of equine thrush, many times the hoof is simply compromised by not having access to dry areas to stand. However, if your horse often gets thrush, even when he has dry places to stand, his nutrition could be playing a role. If he is not getting adequate nutrition, not only is his immune system compromised, but his hoof will not be as strong as it could be...which leads to him suffering from medical problems that otherwise would probably not occur. Improved nutrition will increase the strength and durability of his hoof, and allow him to fight off the thrush-causing bacteria on his own more easily before it ever becomes a problem. Confused by Horse Nutrition? (and don't know where to start?!?) Are you hopelessly confused by horse nutrition? Or are you confused about one or two smaller aspects of it? You are not alone! Just like the little guy below, you want help and reassurance that you are doing things right (or you wouldn't be searching the internet), but you also want to understand this stuff for yourself. I understand, because I've been there. You want the best for your horse, but understanding horse nutrition can be confusing...this website will help give you the knowledge you need and start you on your path. You ve probably been asking yourself some of these questions: Where do I start? What does my horse need? Page 39

40 How do I know if my feed is the best for my horse? What does all that information on the feed bag mean? What are all those ingredients? How do they affect my horse? At one point I was asking myself the same questions. When I started researching to find answers, I was hopelessly lost. The more I researched, the more I realized how little I knew, and the more questions I had. The biggest problem was that no one knew MY horse and his situation...i didn t want someone -- like that annoying feed salesman we've all met -- to tell me what THEY thought MY horse needed, I wanted someone to tell me how to figure out what my horse needed, and in words I could understand! Understanding the items on the list below helps you understand horse nutrition, so you can relax and know that you are feeding your horse to his highest potential! Things that every horse owner should understand include: How the horse digestive system works Roughages and why they are essential Other feedstuffs and if your horse needs them The roles of major nutrients, vitamins, and minerals How to read and understand the information on a feed tag It sounds pretty simple, but as you probably know already, it can be daunting when you start trying to figure it out. The good news is that it IS easy to understand, once you get over the initial hump! Page 40