Equine Carbohydrate Disorders Part 3: Metabolic Syndrome

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Written By Kris Hiney
Imagine a bright spring day. You excitedly turn your horse out to indulge in the fresh spring grass as a special treat. You return in a few hours to collect your companion, but instead are met by an unhappy painful horse, slowly limping its way back to the gate.
Sound familiar? Unfortunately for some owners, this is an all too real scenario. Many horses suffer from carbohydrate sensitivities, or metabolic syndrome, which make them extremely susceptible to changes in carbohydrates in the diet.  One may also hear these horses referred to as insulin resistant, almost like Type II diabetes in humans.  In recent years there has been an upsurge in the number of studies and articles written about metabolic syndrome in horses. While awareness in the general public has increased, many horsemen still wonder if their horse is, indeed, one of these individuals. Should they be paying strict attention to every type of carbohydrate their horse consumes? Should horses no longer consume grass? Does their horse need medication? How do you know if your horse truly has metabolic syndrome?
Classically, horses with metabolic syndrome are described by a certain appearance. They are typically obese horses which gain weight readily, and are considered “easy keepers”.   Breeds with a higher prevalence of metabolic syndrome include the traditional easy keepers such as ponies, Morgans, and Paso Finos. However, metabolic syndrome  can be seen in a wide spectrum of breeds including Quarter Horses, Arabians and Thoroughbreds.  Beyond just being obese, metabolic horses tend to have regional adiposity, or specific fat deposits on the crest of their neck, over their tailhead, the sides of their abdomen and also in the scrotal or mammary area.  The size of the crest of the neck is often the best physical predictor of metabolic syndrome. The thicker the crest, the more likely the horse truly fits into this category. However, it is important to note that it is possible for leaner horses to also suffer from metabolic syndrome. Despite being lean these horses still demonstrate regional adiposity, along with a susceptibility to pasture associated laminitis, as well as insulin resistance. Therefore, if your horse shows symptoms, it may be wise to have it tested, despite it not being overly obese.
Unfortunately the most common way horses are diagnosed with metabolic syndrome is the frequency of laminitic bouts. Usually this is seen following grazing on pasture, especially in the spring or fall.    These horses may be young or middle aged, which sets them apart from horses who suffer from Cushings disease. However, horses who suffer from metabolic syndrome early in life are certainly more likely to develop Cushings later on. Cushing horses are also distinct in the prevalence of hair coat which does not shed or long curly hair while the metabolic horse has a normal hair coat.
Physiologically, these horses demonstrate insulin resistance.   Essentially they must secrete larger amounts of insulin compared to a normal horse, in order to stabilize their blood glucose levels. Therefore, their insulin levels remain higher in their bloodstream, which can have a cascade of effects on their body. They also present with elevations in blood lipids, as well as an increase in leptin. Leptin is a hormone secreted by fat cells or adipocytes, that normally helps in the feeling of satiety (or fullness). However, increased concentrations of leptin may contribute to inflammation in the body. Metabolic horses also have a lower resting thyroxine levels (T4) then their normal counterparts. However, the low level of T4 does not cause insulin resistance and metabolic syndrome, but rather is merely a consequence of altered metabolic profiles.
So why are these horses so susceptible to laminitis? What could insulin resistance possibly have to do with painful feet? One of the commonalities between the myriad of disorders that can result in laminitis in horses is a disruption of the circulation to the hoof. Insulin is most commonly recognized for its role in glucose disposal, but it is a hormone with systemic effects. It is presumed that sustained hyperinsulinemia promotes vasoconstriction. It is already known that carbohydrate overload induces laminitis by creating vasoconstriction in the hoof, so the hyperinsulinemic horse may be even more susceptible to shifts in carbohydrate intake. This disruption of blood flow to the foot results in hypoxia and tissue damage to the sensitive laminae. Severe bouts may render the hoof wall unstable and allow the coffin bone to rotate downwards within the foot. This may lead to permanent alterations of the hoof structure.
Testing for metabolic syndrome frequently involves blood sampling after a short period of fasting (typically 6 hours). Blood is analyzed for glucose and insulin levels that are above normal. The presence of altered adrenocorticortropin releasing hormone can also be tested if Cushings is suspected in an older horse.   Further testing can be done if horse’s insulin levels are within the normal range, but metabolic syndrome is suspected. Horses are again removed from feed, and a standard blood sample is taken. Horses are then given a bolus of glucose and then insulin to determine how the body metabolizes these compounds. This provides a more dynamic picture of the horse’s metabolic response to carbohydrates.
If your horse has been diagnosed with metabolic syndrome, or has show signs of pasture associated laminitis, it is important to start them on a rigorous management protocol. First, as these horses have sensitivities to carbohydrates, concentrates should be removed from the diet. As these horses are typically obese anyhow, there is little need to supply concentrates to them anyhow. If the owner is concerned with mineral and vitamin intake, there are many products which are intended to complement forage only diets. Typically these are pelleted supplements which are fed at very low levels of intake. The obesity issue in the horse should also be addressed. Exercise should be increased to 5 days a week. Not only will this aid in reducing the body weight of the horse, but exercise also enhances glucose clearance from the blood in a non-insulin dependent manner. However, be sure that the horse is not recovering from any laminitic episodes. Pasture intake should also be limited in these horses. Horses should only have access to pasture for a short time or have access to a very small area. If more movement of the horse is desired, a grazing muzzle should be employed to prevent overconsumption of grass. The horse should receive an all forage diet, preferably of grass hay, with intake reduced in order to encourage weight loss. If weight loss is not able to be achieved at an intake of 2% of the body weight, then reduce feed intake to 1.5% of bwt. Unfortunately simple diet restriction may take a long time due to the efficiency of the horses prone to metabolic syndrome. If the horse has greater degrees of insulin resistance, it is advisable to monitor the non-structural carbohydrate composition of the hay, with it ideally below 10%.If horses have persistent issues with metabolic syndrome after calorie restriction, decrease in adiposity, alteration of diet, limitation of pasture intake and exercise have all been employed, then there are medical therapies which can be used. Levothyroxine is effective in improving insulin sensitivity. If all of these measures are followed faithfully, there is no reason that these horses cannot be returned to a metabolically normal state and enjoy a long healthy life.
Next month: We will discuss other strategies that have been employed to assist the metabolic horse.

Equine Carbohydrate Disorders Part 2: Understanding the Terminology

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Written By Dr. Kris Hiney
Last month we began a new series looking at carbohydrates commonly fed to horses, and the different forms they come in. We discussed the differences between simple sugars and polysaccharides and how the bonds which join these sugars have direct implications on how they are digested in the equine. We also discussed a few carbohydrates in particular in which many horse owners have particular interest, including fructans, which may carry health risks, and fructooligosaccharides, which can be used as digestive aids. In the following article I will attempt to define the wide array of terminology that one finds in equine nutrition, such as crude fiber, neutral detergent fibers, and non-structural carbohydrates, among others.
Horses’ diets primarily consist of plants which are largely made up of carbohydrates. Certainly plants also contain protein, lipids, vitamins and minerals, as well as water, but their primary composition is carbohydrates. If we use the carbohydrate definitions from last month, we know that the cell wall of plants is composed of cellulose, hemicellulose, lignin (which is indigestible by horses), beta glucans, gums and pectins. Inside the cell wall we find the more digestible cell contents which contain the simple sugars, starches, oligosaccharides and fructans. Often horse owners need to know what percentage of these compounds appear in a particular feedstuff. We use a variety of analytical methods to partition these carbohydrates into groups.
Crude Fiber
The most commonly used descriptor of carbohydrates on feed tags is usually crude fiber. Crude fiber content of a feed is determined using proximate analysis or the Weende system. Crude fiber is the residue remaining after subtracting water, lipids, proteins and the nitrogen-free extract from the feed. Nitrogen-free extract is said to represent mainly sugars and starches.   It uses a chemical method of solubilizing the feed using acids and bases. One of the problems in using crude fiber as a descriptor is that any lignin, cellulose or hemicellulose which is solubilized in the process is lost and appears in the nitrogen-free extract value for the feed. Thus, crude fiber values may actually underestimate the fiber value of the feed, and over estimate the nitrogen-free extract portion.
NDF and ADF
The Van Soest system of analysis improves on simple values of crude fiber, by separating out different fiber fractions into neutral detergent fiber and acid detergent fiber. These are the most common values which are reported if you have a forage analyzed. Unfortunately this method is most applicable to the value of feedstuffs for ruminants, rather than horses. Regardless, it still does offer the horse owner some important information. The neutral detergent fiber of a feed contains hemicelluloses, cellulose and lignin, although some soluble hemi-cellulose may escape into solution.    It does not provide information about fructans, pectins, gums, or beta glucans which are quite readily fermented by the equine digestive tract. Acid detergent fiber represents the lignin and cellulose content of the feed, as the hemicelluloses have been removed. The amount of hemi-cellulose in a feed, which is easily fermented by horses as well, is represented by the difference in value of the NDF and ADF value for the feed.
Total Dietary Fiber
Total dietary fiber is more frequently used in human nutrition, but may actually offer better information for species which are hind gut fermentors, as is the horse. Total dietary fiber combines many plant values together, and essentially represents the portion of the plant that resists enzymatic digestion which takes place in the small intestine. This includes the traditional fiber components of hemi-cellulose, cellulose and lignin, but also includes pectins, oligosaccharides, mucilages, gums, etc. which are often referred to as soluble fibers in human nutrition. Thus this method recovers more of the true fiber portion of the feed which is susceptible to fermentation in the horse and contributes to their energy supply. Unfortunately this method is not commonly used in commercial feed testing laboratories which serve the animal industry.
Non-Fiber Carbohydrates (NFC)
Now the definitions are going to start getting a little trickier, and the horse owner may encounter many different acronyms. Non-fiber carbohydrates, or NFC, represent the carbohydrates which are not in the cell wall and are not recovered when doing an NDF feed analysis.    The NFC is what remains after subtracting the NDF, protein, fat and ash. It represents the sugars, starches, fructans, galactans, pectins, beta glucans and organic acids. NFC is determined via a mathematical procedure and not a chemical analysis. You may also see values reported as NSC, which stands for non-structural carbohydrates. These values are actually determined chemically and differ from NFC in that NFC values may also include pectins and gums which will not appear when analyzed for NSC.
WSC
Confused? Let’s add some more letters. Water soluble carbohydrates are also used in equine nutrition to determine the most easily digested carbohydrate portion. The monosaccharides, disaccharides, oligosaccharides and some polysaccharides appear in this portion of feed separation. Compared to the NSC value for feeds, it would equal the WSC portion added to the starch content of the feed. Starch content of feed can also be analyzed separately as well.
Finally, some equine specialists have suggested that carbohydrates need to be redefined in terms of horse nutrition. As they are hind gut fermentors, they handle carbohydrates much differently than do ruminants. Certainly, they also get much more use of cell wall components than do simple monogastrics. Many of the particular disorders found related to carbohydrate digestion in the horse may require us to look differently at feeds than is needed in other species. One of the suggested systems created by Rhonda Hoffman (currently of Middle Tennessee State University) is to separate equine carbohydrates into hydrolysable carbohydrates (CHO-H) subject to enzymatic digestion, and fermentable carbohydrates (CHO-F) which undergo fermentation in the hind gut. The fermentable carbohydrate fraction can further be defined as either rapidly fermentable carbohydrates (CHO-FR) or slowly fermentable (CHO-FS). Slowly fermentable carbohydrates would include those seen in NDF values, with the indigestible lignin portion removed from the value. The rapidly fermentable carbohydrates, whose presence can increase the energy content of a feed, include the oligosaccharides, fructans, beta glucans and pectins. Feeds higher in rapidly fermentable carbohydrates can offer more calories to the horse. Alternatively, some horse owners may need to be aware of the fructan content of feeds or forages in horses more prone to developing laminitis.
So what values do you need to know and why should you care?
In general, crude fiber values are listed on most feed tags. Typically the lower the crude fiber value, the higher the energy density of the feed. This is not true of feeds which are designed to have higher fat values, and may include fibers to provide a healthier type of feed for the horse. Owners who have horses with insulin resistance or metabolic syndrome, as well as PSSM horses, should try and choose feeds which are lower in the soluble carbohydrates such as sugars and starches. However, these values are not always provided on feed tags. Owners may also select away from forages which may be higher in sugars and starches as well for these particular types of horses with demonstrated metabolic disorders.
Next month, we delve more deeply into particular carbohydrate disorders seen in horses.

Lipid Nutrition: Part 2, Performance Benefits of Fat

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Written By Dr. Kris Hiney
 
Last month we discussed the usefulness of fat in the equine diet, as well as some examples of typical feeds which contain fats. Fats are an easily digestible source of calories which can readily supply the extra energy that performance horses may need. Fat may lower the heat load on the horse compared to traditional diets, which may aid in performance in hot climates. Finally, fat may even help calm the horse compared to when they are fed high starch diets. But is there any other reason to feed fats that may help you get to the winner’s circle?
Fat Metabolism
Lipid2_skeet.bmp When horses are fed fat in the diet, their body responds by increasing the number of enzymes that are involved with lipid metabolism. These include the enzymes needed to remove fat from the bloodstream and enter muscle or adipose tissue, and those that ultimately oxidize the fatty acids. Feeding fat to horses results in a lowering of plasma triglycerides which is believed to be caused by a decrease in synthesis of triglycerides in the liver. The horse becomes more efficient at utilizing dietary fats for energy, rather than needing to use carbohydrate or protein.  This adaptation has repeatedly been shown to take at least three weeks after the change in diet.  Complete adaptation may take as long as 2-3 months.  Therefore, if switching your feeding regimen, don’t expect to see instantaneous results.
Exercise and Fuel Sources
rice branWhen fatty acids are oxidized in the body for fuel, their final metabolic pathway involves the Tricarboxylic cycle (TCA)* or Kreb’s cycle. This cycle is dependent on oxygen (through its connection to the electron transport chain) in order for it to work.   The TCA cycle supplies the bulk of Adenosine Triphosphate (ATP)** for horses when they are working aerobically, or at lower intensities. Technically, aerobic work is at a low enough intensity that the requirement of ATP can be met by the slower metabolic pathway of the TCA cycle.   At low intensities of exercise, fat typically supplies up to 50-60% of the calories needed.  All dietary energy sources – fats, carbohydrates and protein – can be utilized in aerobic metabolism, provided there is sufficient intake of oxygen.   That means that the horse’s heart and lungs can keep up in the race to deliver oxygen to the tissues. However, when the horse’s muscles are contracting faster or harder than the ability of the cardiovascular system to keep pace, they then enter into anaerobic metabolism. The horse must then switch to a different supply of fuel, primarily carbohydrate metabolism. They are simply working too hard for the aerobic system to keep up with the demands of the muscles for ATP. Therefore, horses undergoing intense exercise, or sprinting type of activities, must rely on their carbohydrate stores for energy. These include blood glucose, liver and muscle glycogen, and the body’s ability to perform gluconeogenesis (make glucose from other sources).
Can Fat Save Glucose?
It is presumed that due to the adaptation of the horse to become more efficient at fat metabolism, they are less reliant on their carbohydrate stores (blood glucose, muscle and liver glycogen) to supply their energy needs.    This should allow the horse to work longer before turning to carbohydrate metabolism. This may be advantageous for two reasons. One is that carbohydrate stores in the body are much more limited in comparison to lipid stores, and two, usage of carbohydrate through anaerobic metabolism can result in the production of lactic acid.  This may contribute to the onset of fatigue, due to depletion of energy sources or the accumulation of lactic acid. Therefore, fat fed horses may have some advantage in their resistance to fatigue.
Most studies of horses fed high fat diets have reported an increase in resting muscle glycogen stores. However, there have been a few reports which have shown an opposite effect of lowered muscle glycogen. In these studies, the horses were either untrained or receiving low intensity exercise. In studies which exhibit an increase in resting muscle glycogen, the horses received more intensive training, including sprinting exercise. This may be the key in seeing a response to the fat added diet. In addition, the amount of fiber and starch in the rest of the diets differed between studies, which also clouds interpretation. If horses do have higher glycogen stores at rest, it is unclear if this results in an increase in glycogen utilization during exercise. Some researchers found an increase in glycogen utilization while, again, others have found no change in glycogen metabolism during race simulations or long term sub-maximal exercise.   But would an increase in glycogen utilization improve performance? Again results are mixed. Horses fed 12% fat for four weeks improved their run time to fatigue in a high intensity exercise bout on a treadmill. Others have found increased performance in sprinting exercise and in a simulated cutting event, while some have found no clear advantage to feeding fat in improved performance.
Is Anything Consistent?
Lipid2_SkeetsSugarNSpice.jpgIn studies looking at blood metabolites in exercising horses fed a fat added diet, some consistent results have been seen. Feeding fat does decrease the exercise related drop in blood glucose. This is seen simultaneously with an increase in serum triglycerides and free fatty acids. Presumably these horses have indeed shifted toward a more efficient utilization of fatty acids during exercise, sparing their glucose stores. This seems to be supported by data which shows that horses on fat supplemented diets have a higher blood pH during exercise versus non-supplemented controls. The above effects are seen at lower intensities of exercise.  When the horse increases its ATP demand, they will need to draw more from anaerobic metabolism and must shift to carbohydrate usage.
So with all of these conflicting results, what should you believe? It is clear that feeding performance horses fat rather than carbohydrates is a much healthier alternative. High carbohydrate diets carry with them the risk of laminitis, colic, ulcers and insulin resistance. As of now, no negative effects of feeding fats to horses have been found. The potential benefits are many, including a potentially calmer horse, a decrease in reliance on blood glucose (at least at lower intensities), and a possibility of increased performance in anaerobic activities. With little to lose, and benefits to gain, it is no wonder fat added diets are so popular in the equine industry.
 
Next month – The usage of fat added diets in metabolic diseases.
* TCA – Tricarboxylic cycle, also known as Citric acid Cycle, has been described as the “central metabolic hub of the cell”. A sequence of reactions taking place in mitochondria where acetyl units attached to CoA are degraded to carbon dioxide and the electrons produced transferred to the coenzymes NAD⁺ and FAD.
**ATP – adenosine triphosphate, an adenine nucleotide used as the energy currency in metabolism. The free energy released when ATP is hydrolyzed is used to drive reactions in cells.

 

Lipid Nutrition: Part 1, Feeding Fat to Horses

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Written By Dr. Kris Hiney

This month we begin a series looking at the value of incorporating fat into the diets of our horses. We will discuss how fat is digested and handled in the equine, the types of fats fed to horses, and the many beneficial effects that can be realized through the addition of fat to the diet of our horses.
 
Fat digestion
Feeding fat to horses became more popular in the 1980’s and has continued to see an increase in the share of the feed market. Most feed stores now offer a selection of fat added feeds, or specific fat supplements. While one may not think of horses as a species that routinely consumes fats, horses can handle fats quite well in their digestive system. Lipid digestion occurs primarily in the small intestine, via the production and release of digestive enzymes and bile salts. As the horse does not possess a gall bladder, bile salts are continually released into the intestine. Fats that are added to the diet in the form of oils or fat are very well digested, typically up to 90%. Comparatively, naturally occurring fats in the diet (muchsmaller percentages of fat are actually present in forages and cereal grains) are less well digested, between 40-50% for forages and 50-75% for grains. Addition of fat to the diet does not alter digestibility of other components of the diet, unless the amount of lipid exceeds 22% of the total diet. However, typically this is not a concern, as acceptability and practicality of such diets make them improbable. There are some published studies which do report a lowered fiber digestibility in horses fed soy oil, however, these horses were also rapidly introduced to the fat in the diet. Ideally horses should be gradually transitioned onto a higher fat diet in order to adapt and increase the necessary fat digesting enzymes in their system. This should take place over one to two weeks, depending on how much fat is being added to the diet.
 
Acceptability
Palatability of fat added feeds is quite good, especially if supplied by vegetable oils. Typical vegetable oils include corn oil, soybean oil, canola oil and linseed oil. Horses will consume animal fats and fish oil, but typically not as readily as vegetable sources. The acceptability of fats in the diet is good up to about 15% of the diet. After that consumption rates do drop off.   There are commercially available feeds which have a higher percentage of fat, but these are typically extruded feeds which are more acceptable. Again, these are fed at a smaller percentage of the diet, such that 15% of the total diet is never exceeded. When feeding fat added feeds, it is important to realize that they do have a shorter shelf life than non-fat added feeds. This is due to the peroxidation that takes place, especially in polyunsaturated fats. These feeds then develop an off taste and flavor. If your feed smells rancid, it is best to avoid feeding it. Storing feeds in a cool, dry area will help to preserve their shelf life as well. These feeds often have anti-oxidants added to them to aid in protection against oxidation. Some products, such as Omega Horseshine, specialize in stabilized fats with a prolonged shelf life, up to 12 months.
 
Benefits to feeding fat
The most readily realized benefit to adding fat to the diet is in order to help meet the animals’ caloric needs. Fat is very readily digestible as already stated, and is much more energy dense than other components of the horse’s diet. Compared to proteins and non-structural carbohydrates which contain 4 Mcal/kg, fat is 2.25 times more energy dense at 9 Mcal/kg. Thus inclusion of fat allows a horse to gain weight much more readily or conversely, need to consume less feed to obtain the same amount of calories. Lowering the total amount of feed may be advantageous to horses working in hotter climates as it lowers the total heat production associated with digestion. Furthermore, fat itself is a relatively cool feed, as there is no fermentation and thus heat production associated with its digestion. Replacing high energy cereal grains with fats is an additional benefit, as less digestive risk is associated with feeding fats. Horses fed large amounts of cereal grains over time are at greater risk for ulcer formation, potential development of  stereotypies such as cribbing, laminitis and insulin resistance. This does not mean that starch needs to be eliminated from normal equine diet (the exception are horses with metabolic disorders which render them more sensitive to starch in the diet), but fat can make a very useful substitution. Another benefit to replacing starch in the diet with fats appears to be a calming effect on the horse. Horses fed fat added diets compared to typical sweet feeds have been found to be  less reactive to novel stimuli. Therefore, there is a second reason that fat is a cool feed, not only does it produce less heat during digestion, but it appears to “cool” the hot minded horses. Now obviously it is not a substitute for proper training and exercise!
 
Essential fat and fatty acids
 Horses must also consume some amount of fat for normal body function. Lipids are used in the synthesis of steroid hormones, and  all of the fat soluble vitamins (ADEK) are contained within the fat portion of the feed.  However, the exact amount of fat necessary in the diet of the equine has not been determined. Additionally, the horse, like all other animals, must consume its essential fatty acids, linoleic (18:2 omega 6) and linolenic acid, (18:3, omega 3) from the diet. They lack the enzymes necessary to produce these particular fatty acids within the body. Important sources of these fatty acids include pasture grasses, canola oil and linseed oil or flax seed.
 
Practical guidelines for feeding fat to horses.
As stated previously, most fats in horse feed actually come from vegetable oils. The oils can either be extracted and purified, or the actual oil seed can be fed. Examples of common oilseeds include cottonseeds, soybeans, canola and flaxseeds. If these seeds are referred to as meal, such as cottonseed meal, the fat has already been extracted and then they are being fed typically for their high protein content, not for additional fat. Thus, feeding linseed meal provides a much different percentage of fat compared to feeding flax, despite it being the product of the same plant! Pure vegetable oils can also be fed to horses as a top dressing to their feed. One cup of vegetable oil provides as many calories as 1.5 lbs of oats or 1 lb of corn, allowing you to decrease the amount of cereal grains fed.   If feeding a fat added feed, typically these feeds will allow you to feed less concentrate for a similar work class of horse, due to the increased caloric density of the feed. The benefit of feeding a fat added feed, rather than top dressing, may be in its simplicity, as well as the fact that these rations are rebalanced with the knowledge that the horse may consume total less feed. However, if you are just top dressing fat to existing feeds, and thereby decreasing the total amount of feed, be sure that the total diet still meets the horse’s other nutritional requirements.
 
In the next part, we will discuss the potential for performance enhancing effects of feeding fat beyond merely an easy way to supply calories.

Developmental Orthopedic Diseases: Part 2, Can They be Prevented?

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Written By Dr. Kris Hiney

Now that we are aware of the potential problems of the skeletal system of the foal, we will address some management techniques that may aid in preventing their occurrence. These include dietary management of the mare and foal, exercise needs, controlling growth rate and even selection of appropriate breeding stock.

Size and growth rate

One of the commonalties amongst all developmental orthopedic diseases (DOD) includes the size and growth rate of the foal. Obviously the larger the foal, the more stress which will be placed on the limbs simply due to weight. Bigger and more rapidly growing foals have been repeatedly shown to be at more risk for DODs. Body size is inherently a genetic issue, while growth rate can be modulated by the owner. If you are breeding for larger foals, more caution should be taken with their diet to ensure a more moderate rate of growth. This includes avoiding sudden changes in rate of growth. One way to limit changes in growth rate is to avoid ad libitum feeding or to avoid stress placed on the foal. Stresses may include environmental (weather dependent) or social stress, such as weaning. One method to manage stress of weaning in foals is to creep feed foals prior to weaning to accustom them to consuming concentrates. Also, the manner in which the foal is weaned can reduce their stress. Babies weaned in isolation exhibit more stress behaviors than foals weaned with a pasture-mate. Try to keep their environment as close as possible to what they experienced prior to weaning.

Exercise

The amount of exercise the foal receives can also influence the development of DOD. Excessive trauma to the joint through overwork can influence development of osteochondrosis (OC) as well as restriction of exercise. So what exercise program is correct for a foal? Foals in adequate pasture size typically spend their time sleeping, nursing, following their dam, and playing in short bursts of activity with other foals. Foals without peers may spend less time playing. Similarly if they are confined to too small of a space they exhibit less play behavior. In addition, if their environment is too small with no novel objects or activities, foals tend to be less active. At the furthest extreme would be foals and young horses confined to stalls without access to voluntary exercise. The best advice for proper bone development in the young foal is to provide adequate pasture space to allow them to run and play on their own. How do you know your pasture is big enough? Simple observation will tell you if your foals are playing. If the foals just stand around, or if you have a single foal with no playmates, they may not have the stimulus to run and play.

Diet

Many nutritional causes of DOD have been proposed with very few providing direct causative relationships in a research setting. However, that may be due to a lack of combining the correct causative factors in this multifactorial disease. Perhaps the foals used in the studies need to have a genetic predisposition for DOD, and then must be exposed to the right management conditions to initiate the disease process. However, the most commonly proposed theories include excess energy, mineral imbalances, and inadequate protein. One of the proposed theories in the development of DOD is feeding of excessive non-structural carbohydrates to growing horses. These feedstuffs (think traditional cereal grains like corn) cause a more rapid increase in blood glucose post feeding versus feeds containing more fiber. Higher levels of blood glucose increase insulin levels in the young horse, which may have a cascade of metabolic consequences down to the level of cartilage maturation. While it has been shown repeatedly that feeding high concentrate diets alters the glucose/insulin response and reduces insulin sensitivity, the direct causative relationship to DODs has not been established. The most important guideline appears to be to avoid unregulated feeding of concentrates. High protein diets have also fallen under the radar of causing DOD, but this has not been able to be shown in a research setting.

Mineral nutrition has probably seen the greatest attention related to DODs. To begin with the simplest, imbalances of deficiencies of calcium (Ca) and phosphorus (P) can clearly lead to abnormalities of bone development. (Please see the articles about calcium and phosphorous in my series, Minerals for Horses, for more details.) However, just because foals are fed adequate amounts of Ca and P in the correct ratios does not guarantee they will be free from abnormalities.

Another mineral which has received much attention is copper. One of the original studies which pointed to deficiencies of Cu causing OC in foals unfortunately also allowed deficient levels of Ca and P to be fed to the foals, thus making it difficult to point to only one cause. Later studies found highly contradictive results and have not offered any protective benefits to feeding supplemental copper. Taken all together, the most promising results of supplementing copper have been seen when providing copper to the dam in late gestation, or in supplementing copper to promote the repair of OC lesions.

Trauma

Included in the list of “just bad luck”, trauma may also result in a DOD. Young horses have a great propensity to get themselves into trouble. They can get kicked by a pasture mate, run into a stationary object (believe me I’ve seen it), or even tumble head over heels for no great reason other than they are still learning their balance. While not much prevention can occur here, at least try to ensure that no overly aggressive horses are housed with young stock, and that dangerous obstacles are not in the pasture. For example, I’ve seen weanlings during a running fit run headlong into an automatic waterer, somersault over the top, and, luckily, continue on their way. If you raise foals, always expect some sort of trauma to arise. Just try to ensure their environment is as safe as possible.

Genetics

Unfortunately, the genetics of your foal may be the single largest contributing factor to DOD. Many recent studies have found numerous markers across a number of chromosomes that have been linked to OC. While this sheds some interesting new light on the problem, it is also difficult to select against. Compared to a single point mutation like HYPP, horses cannot be identified as simple carriers of the gene for the disease. Screening for potential carriers of OC would be costly and ineffective. However, that does not mean the breeder has little recourse. If your mare has consistently produced foals with OC, one of two things may be true: one, your management program may be inadequate or, two, she may have a genetic likelihood to produce these types of foals. You can often hear rumblings in the horse community about certain stallions which also tend to throw a lot of foals with OC. Perhaps these are individuals we should select against. However, the amount of research currently being conducted on the genetic link to OC does provide some promise that we may be able to limit this disorder in the future.

Taken all together, the best plan for avoiding DOD may be, first, to select genetically healthy individuals to breed, and, second, foals should be managed with attention to diet and exercise until they are two years of age. Many causes of DOD may be unavoidable, but hopefully with proper care and management, one can produce a healthy normal adult.

Next month we begin talking about the usage of fat in the equine diet, and how it may be able to improve the health or performance of your horse.

 

Developmental Orthopedic Diseases: Part 1, What are they and why do they occur?

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Written By Dr. Kris Hiney

Developmental orthopedic diseases are a serious concern for the equine breeder.  All of the hard work and preparation of selecting the right match between mare and stallion, the hours put into proper mare care, culminates hopefully in the arrival of a sound, healthy foal.  All of this excitement and hope can be ruined if your foal ends up having skeletal abnormalities which may jeopardize his future success.  With this article we will explore some of the many causative factors of this spectrum of disorders and what you may be able to do to prevent or reduce the likelihood of their occurrence.

First of all, developmental orthopedic diseases, or DOD, is actually a generic term for a host of disorders.  Simply put, anything which is an abnormality of the horses’ skeletal system during its formative years can be classified as a DOD. The most commonly occurring maladies are angular limb deformities, flexural limb deformities, osteochondrosis and physitis.

Angular limb deformities

Angular limb deformities are very common in all breeds of foals. These can include either an inward deviation of the joints (varus) or outward deviation of the joints (valgus).  Most commonly these deviations are seen in the knee, hock and fetlock joints. The foal can have one or more joints affected, and can also vary quite widely in the severity of the condition.  The causes of this condition vary; with some the manager can address, while others are due to random chance.   Both premature and dismature foals very commonly have angular limb deformities due to the lack of strength in supporting structures, or the failure of complete ossification of the cuboidal bones (small bones of the knee and hock).  The causative factors of these conditions may be an infection or inflammation of the placenta or uterus, twinning, and severe stress in the mare.  Development of angular limb deformities post foaling is due to a difference in the growth rate across the inside and outside of the growth plate.  In essence, the difference in speed in bone development causes the bone to veer to one side or the other.  This can be due to a variety of factors including dietary imbalances or environmental factors, as well as genetics.

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Premature foals are those born before 320 days of age, while dismature foals may be of a normal gestational age but are weak, small and appear unready to have been born.  These foals are typically thin, are slow to stand, have poor suckle reflex, can chill rapidly and are marked by fine silky hair coats and soft ears and lips.  These foals will require a high level of assistance in their care, but with proper supportive care and a lot of time and effort, can continue on to lead normal lives.

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If your foal does have angular limb deformities, there are actually many therapeutic management techniques used to help straighten the limb.  They range from quite simple to the complex and expensive, usually depending on the severity of the deviation.  Conservative techniques involve stall rest in order to prevent uneven loading of the foal’s developing legs.  The foal may be bandaged or splinted, or the hoof can be trimmed or glue-on extensions can be used to help straighten the limb.  For example if the foal has a valgus deformity in in its knee (the lower leg will sweep outwards), the outside hoof wall is lowered, or a glue on extension is placed on the inside of the hoof.  Often dramatic improvements are seen with these simple techniques.  If the limb deviation is more severe, and budgets allow, corrective surgery may be required.  These include periosteal stripping, or placing screws, staples or wires across the growth plate.  The goal of periosteal stripping (removing a section of the periosteum, or membrane covering the bone) is to accelerate growth of the side of the bone growing too slowly. Typically this procedure is done in young foals.  Alternatively, transphyseal bridging is used to slow down the rate of growth on the side of the bone with too fast a growth rate.  However, before deciding on which management technique is the correct one for your foal, be sure to consult with your veterinarian.  Mismanagement can acerbate the problem, and it is also possible to overcorrect the foal, and end up with a deviation in the opposite direction!

Flexural limb deformities

Flexural limb deformities are more commonly referred to as contracted Glue on shoe extension can correct contracted tendonstendons.  Foals can either be born with flexural limb deformities, or they may develop later in life.  Foals born with flexural limb deformities may be due to poor positioning in the uterus, toxicities, genetics or infections in utero.  If the condition is mild, foals can recover typically with just restricted exercise.  Foals should be allowed some exercise either in a paddock or by hand walking for short periods of time.  Additionally, the veterinarian may choose to use oxytetracycline to help relax tendons in more severely affected foals.  Some foals may require splints or casts to help in straightening the limb.  However, this should only be done with a veterinarian’s  supervision as  it is quite easy for the foal to develop pressure sores and may be painful.  Acquired flexural limb deformities can be due to traumatic injuries which cause the foal to protect the limb and not bear full weight on it.  The reduced stretching of the tendons with normal loading results in tendon contracture.  They can also be due to a discrepancy in the growth rate between the flexural tendons and the long bones.  It can also be completely normal to see young horses having temporary periods of being over at the knees.  If the foal is showing signs of being over at the knees, the rate of growth should be modulated and caloric intake should be reduced.

Physistis

Physitis or inflammation of the growth plate is usually seen at the distal end of the radius or tibia, or within the distal end of the cannon bone.  It is seen as puffiness in the affected joint and may be associated with heat and swelling.  Physitis is typically seen in foals on too high of a plane of nutrition, or in foals being fed for rapid growth.  If the foal is still nursing, the mare may actually be contributing to the development of physitis.  Some mares are simply better milkers than others.  Suggested management techniques may be to discontinue any creep feeding of the foal, or do not allow them access to the mare’s feed.  In addition, the foal may be muzzled periodically to decrease his milk intake, or the foal may be weaned and put on a less calorie-rich diet.

Osteochondrosis

Osteochondrosis or OC is caused by a failure of the endochondral bone (the bone underlying the cartilage) to properly ossify.  Bone growth occurs first with the growth of cartilage which is then replaced by bone. If this fails to happen, essentially the bone has a weakened area underlying the cartilage.   It can cause further development of bone cysts or osteochondrosis dissecans (OCD). While these terms are often used interchangeably, OCD refers to a flap of cartilage displacing away from the joint surface.  Causes of OC in young horses are quite diverse and include dietary mismanagement, traumatic injuries, inadequate or excessive exercise, genetics, toxicities, body size, and growth rate.

Osteochondrosis: Is it the end of the world?

One of the interesting things about this disorder is how frequently it may actually appear in the equine population.  Many figures are given, with some stating that 20-25% of European foals will develop an OC (Barnevald and van Weeren), while others have found an incidence of 32% in Hanoverian Warmbloods.  However, in the latter study, there was no correlation between radiographic findings of OC and lameness. Indeed, in a recent study of Dutch Warmblood horses presented for a pre-purchase exam, 44.3% of clinically sound horses were found to have OC lesions  (Voss).  Therefore, even if your foal has radiographic evidence of lesions, unless accompanied by joint effusion or lameness or presenting as fragmentation within the joint, it may never represent a soundness issue.

Next month we will look at what we can do to try and prevent our foals from acquiring any of these development orthopedic diseases.

Voss, N.J. 2008. Incidence of osteochondrosis (dissecans) in Dutch Warmblood horses presented for pre-purchase exams.  Irish Veterinary Journal. 61:1)

 

 

What is the difference between premature and dismature?