Tag Archives: laminitis

  • Strategies to Modulate Insulin Concentrations

    Written By Dr. Kris Hiney

    Much recent research in the horse industry has centered on fluctuations in insulin concentrations under a variety of conditions and the effects on the health of the horse.  Many horse owners are aware that traditional feeding practices which rely on a larger proportion of concentrate feeding may result in prolonged insulin secretion by the pancreas.  In young horses, it is thought that prolonged elevations in insulin may lead to cartilage abnormalities, promoting epiphysitis and osteochondrosis.  High starch diets are linked to behavioral issues such as more excitable or reactive horses;  and certain typing up disorders such as polysaccharide storage myopathy and recurrent exertional rhabdomylosis. Finally, high concentrate diets can certainly contribute to the development of insulin resistance and laminitis. As a result of this information, many  current horse feeds are now designed to minimize insulin fluctuations in the horse.  These feeds are typically low in traditional cereal grains such as corn and oats, may be higher in fat and fiber, or may be processed differently.   All of these techniques are designed to either minimize or slow the absorption of glucose out of the small intestine, and thus lower the need of the pancreas to secrete insulin to regulate blood glucose.  But what if switching feeds or eliminating concentrate is simply is not enough?  Are there other options available to the horse owner which can potentially help regulate insulin and glucose in their horses?
    One of the concerns for owners of insulin resistant horses is the frequent bouts of laminitis which occur if the horse is allowed access to pasture high in fructans.   Owners of these horses need to monitor their horses grazing carefully.  In order to avoid plants with high fructan content owners are advised against allowing access to pasture during the afternoon (when photosynthesis is at its peak rate), the spring, late fall or when grasses are stressed.  Further, warm season grasses offer a lower fructan concentration than cool season species of grasses and make better grazing choices for insulin resistant horses.

    But why are fructans such a concern?

    One of the theories addressing the laminitis inducing effect of high fructan content in plants is that fructans when consumed by the horse ,create changes in the bacterial population of the hindgut.  They undergo rapid fermentation, can alter pH of the gut and may result in bacterial endotoxin release.  However, this explanation does little to explain why insulin resistant horses in particular are so sensitive to fructans.  It may be that fructans trigger an increase in insulin itself that creates alterations to the vasculature of the hoof and the accompanying painful syndrome.   Insulin, while typically thought of as having a primary role in glucose disposal, has tremendous effects on the vasculature.  Insulin can act as both a vasodilator, or a vasoconstrictor.   Insulin resistance has been repeatedly been shown to cause cardiovascular dysfunction in many other species.  However, this role has not been fully explored in the equine.

    In attempt to explore this issue, researchers conducted a trial examining changes in insulin and glucose in horses allowed access to pasture during two different eight hour periods.  Horses were allowed to graze between 7 am and 3 pm or between 12:30 pm and 10:30 pm.   In this experiment, nonstructural carbohydrate content of the grass varied from 13.5% to 19.1% from 8 am to 10 pm.  The study did find a detectable, though not large, increase in insulin, in the horses fed during the afternoon grazing period when NSC values were there highest.   While the number of horses used in the study was small, and the grazing period did overlap, this study does indicate that the concentration of insulin in the horse may be sensitive to fructan content of grasses. The horses used in this study were also not insulin resistant horses.   Insulin resistant horses  may have differed in their insulinemic response to the feeding schedules.  However, this study may offer information as to why bouts of laminitis are triggered in the insulin resistant horse exposed to the wrong type of grasses.

    While we know that insulin resistant horses need to be stringently maintained on low soluble carbohydrate diets, other horses may benefit by paying attention to how we feed them.    While simply avoiding feeding grain may be an easy solution to avoiding insulin and glucose fluctuations, some horses  may require a diet higher in concentrates to meet their energy needs.  A common sense approach is to divide the horse’s meals into several smaller meals.  This is certainly an effective strategy in lowering glucose and insulin response.  However, one approach rather than running out to the barn multiple times per day to split up your horse’s meals, is to use a feeding system designed to slow down the horse’s consumption rate.  Researchers interested in this technique attempted to slow feed intake by adding grids to feed buckets, small hard balls or soaking the feed completely in water.   Using physical obstructions to feeding did prove to be successful  in increasing total feeding time, while adding water did little to alter consumption rate.  The best technique to lower insulin response was to add bocci balls to the bucket so that the horses had to move the balls around to gain access to the feed.  This idea has been elaborated to produce commercial feeding balls, which trickle out small amounts of concentrate as the horse rolls it about.  This also provides the added benefit of increasing the mental stimulation of the horse simultaneously!

    An interesting new theory is that perhaps the stress we expose our horses to may contribute to elevated insulin levels.  Chronic stress does increase cortisol concentrations which may have inhibitory effects on insulin, thus creating a greater need for insulin secretion, or in essence an insulin resistant horse.  In humans, stress and high cortisol can result in insulin resistance and a shift in the deposition of fat in the body. Perhaps stress in horses may also be contributing to insulin resistance and why we see regional adiposity in these animals.  In an initial foray into stress evaluation in horses, researchers examined whether different feeding schedules resulted in an elevation in cortisol.  However, in this study feeding schedules were not a sufficient stressor to elicit any dramatic increase in cortisol.   It is interesting that equine researchers are starting to look in new directions to solve the puzzle of insulin resistance in the horse.  While at this time, the effect of stress on cortisol and thus insulin in the horse is just a theory, maybe it wouldn’t hurt us to avoid stressing our horses unnecessarily!

    Much about insulin resistance and developing best practices still remains unknown.

    For example, in a study in which pregnant mares were fed high concentrate diets and gained rapidly in body condition in the last trimester of pregnancy, foals from the grain fed mares were actually more sensitive to insulin and had lower resting blood glucose. This does indicate that fetal programming, or the in utero environment can have long lasting effects on the offspring, but not what management protocols may be best are unknown.  While we have learned much about insulin resistance in horses, so much remains unknown. We often have to look at studies in other species and try to extrapolate this information to our management practices.  So over all, the willingness to try new methods and incorporate new information may be our best option.  Continue to monitor grazing tightly in insulin resistant horses, get creative when feeding grain, and don’t stress your horse!

  • Keys to Preventing Laminitis

    Written By Dr. Kris Hiney

    In previous articles we have discussed some of the key strategies in preventing laminitis in the equine.  Many of these have centered on grazing strategies which limit the horse’s access to pastures high in fructan content.  Remember that fructans are carbohydrates which are enzymatically unable to be digested in the small intestine of the horse.  These fructans pass into the hindgut of the horse where they are fermented by the microbial population, specifically gram positive bacteria. The production of certain organic acids and amines enhance the permeability of the gut wall allowing these and other endotoxins to enter the bloodstream of the horse and ultimately effect  the circulation to the digit.  However, it is not practical to simply right off all horses’ ability to graze.  Rather, we should try and identify those individuals which may have a susceptibility to fructan content in the grass.  With this month’s article, we will try to identify which individuals may be at risk, and other strategies that may be employed to reduce your horse’s risk.

    While the outward appearance of your horse may give you an indication to whether they are susceptible to laminitis (See Carbohydrates III: Metabolic Syndrome), there may be more to it than just which horses are overweight.  There certainly appears to be a genetic link to laminitis, with pony breeds leading the list of susceptible horses.  Their comparatively thrifty genotype may make their utilization of carbohydrates and insulin sensitivity differ from breeds which typically do not possess these characteristics. For example, thoroughbreds, which typically have the reputation for being “harder keepers” do not experience the same rate of laminitis.  However, the lifestyle and management of thoroughbreds may differ significantly enough to partially explain the decreased incidence of laminitis.  Even within ponies, there does appear to be a decided link to genetics.  In a study examining the pedigrees of an inbred herd of ponies, 37% of these ponies had experienced laminitic episodes.  Of those, half had at least one parent which had also experienced laminitis.  Even in controlled research trials which attempt to examine the effects of various carbohydrate loads on horses, wide variability exists between individuals. This leads to the supposition that individual variation, thus genetics, is at play.  Thus, if you aware of your horse’s pedigree and know of relatives which have experienced laminitis, you might want to manage your own horse more carefully.  Perhaps some day the genes which make a horse more susceptible to laminitis will be identified, and we can use genetic tests in developing management protocols.

    As mentioned previously, development of obesity and insulin resistance certainly predisposes the horse to laminitis.  One theory behind the development of laminitis in the insulin resistant horse is the glucose deprivation model.  When a horse becomes insulin resistant, more and more insulin release is needed to elicit a normal tissue response.  In essence, the tissues become “desensitized” to insulin.  One of the key roles of insulin in the body is to allow cellular uptake of glucose.  Due to the polarity of glucose, it cannot freely enter the cell without the presence of specialized protein transporters. Glut 4 is a protein transporter which is located internally in the cell until insulin binds to the cell membrane.  Binding of insulin to the receptor causes a cascade of intracellular reactions to occur and initiates the translocation of Glut-4 to the cell membrane.  The insulin insensitivity may result in Glut 4 no longer moving to the cellular membrane, and the inability of glucose to enter into the lamellar tissue of the foot, thereby starving it of glucose.  A recent study looked at the presence of different glucose transporters  found in skeletal muscle, the coronary band and lamellar tissue.  Glut-4 is the insulin dependent transporter found primarily within muscle, while Glut 1 is found in other tissues which have non-insulin dependent uptake of glucose, such as the brain.  While Glut 4 was heavily expressed in skeletal muscle, only Glut 1 was found within hoof tissues of both normal and insulin resistant ponies.    Therefore, glucose uptake in the hoof is thought to be insulin independent  and glucose deprivation within the hoof is unlikely to be the cause behind laminitis.  However, in a subsequent study, laminitis was induced in normal healthy ponies using a hyperinsulinemia-euglycemia clamp technique.   In this model, insulin is infused into the ponies at a constant rate, while glucose is infused at a sufficient rate to maintain euglycemia, or normal blood glucose levels.   Therefore, it is not an absence of glucose which causes laminitis, but perhaps the sustained levels of insulin or other hormones which causes this disorder.  This would certainly support the observation of the increased laminitis risk to the insulin resistant horse which suffers from hyperinsulinemia.

    If owners wish to try and avoid the development of insulin resistance, the diet the horse receives may be critical.  Diets which avoid high amounts of sugars and starches, and have a low glycemic response, result in less insulin release.  For horses which still need a significant amount of calories, diets which are fat and fiber based and properly formulated, rather than those which provide a higher glucose or insulinemic response, may prevent the development of insulin resistance.   Certainly just monitoring body condition in the horse may be the easiest way to avoid insulin resistance.  Although if you ask any horse owner if that is easy you may get a different response!  In addition, horses which receive regular exercise seem to be fairly protective against laminitis.  However, it is difficult to know whether the exercise regimen aids in increasing insulin sensitivity, or is simply protective against obesity.

    Many horse owners wonder if there is a magic pill or supplement that they can provide their horse in order to prevent laminitis.   One approach is to reduce the gram positive, lactate producing bacteria which prefer to ferment sugars and fructans.  Antibiotics are commonly used in the livestock industry in order to promote growth by shifting the microbial population within the gut. Some antibiotics select against gram positive bacteria, thus have been studied in the horse as a way to prevent laminitis.  While this may work, the use of anti-biotics in livestock for growth promotion has been banned in the Europe Union over concerns of anti-biotic resistance.  Similarly many in the United States have followed suit, searching for other ways to influence growth and increase immune status.  The use of probiotics and prebiotics may influence the gut microflora in favor of less potentially problem causing bacteria.  Ironically enough, short chain fructo-oligosaccharides have been demonstrated to improve insulin sensitivity, if not glucose levels, in obese horses.   However, none of these methods have been proven to prevent laminitis.  I would caution individuals to monitor diet, grazing patterns, and body condition first, before relying on supplements to prevent laminitis.

  • Laminitis In The Equine

    Written By Dr. Kris Hiney

    Earlier we posted an article on the typical causes of laminitis and some feeding strategies that may help in preventing laminitis (Feeding Horses for the Prevention and Management of Laminitis).  We also discussed how we might approach feeding a horse which has already experienced  laminitis.  This month we will begin to delve deeper into the causative factors of laminitis and how to prevent its development.

    Remember that laminitis is actually a systemic disease, with just the symptoms being visualized within the hoof.  Some insult to the horse’s system creates an alteration in circulation, ultimately leading to tissue damage of the sensitive laminae.   This period of time, referred to as the development phase or prodromal phase, includes the actual insult prior to the development of symptoms.    It is thought to be due to some change within the vasculature, that leads to ischemia, or lack of blood flow to the digit.  Whether it is a lack of nutrients or oxygen due to the decreased blood flow, tissue damage or death results.  This initial insult is then followed by the acute phase of laminitis.

    In the acute phase, blood flow returns to the foot, typically at an increased rate, as this is the body’s normal response to tissue injury.  Even this reperfusion response can cause tissue damage.  This is when the owner now recognizes the development of symptoms. The horse will appear very stiff and reluctant to move, and may even lie down.  A particular stance may be assumed by the horse as he appears to rock back on the hindquarters and place the forefeet forwards in order to limit weight bearing.  Due to the pain and anxiety the horse is experiencing, his heart rate and respiration rate may both be elevated.  Finally, the owner may even be able to detect an increase in temperature of the hoof wall and a bounding or throbbing digital pulse. 

    If permanent changes to the architecture of the foot occur, whether in PIII displacement, permanent changes to the normal lamellar architecture of hyperkeritization of the hoof wall, the horse has entered into the chronic phase. These horses are typically more susceptible to recurrent episodes of laminitis.  Diet restrictions and specialized hoof care are typically required to allow the horse to lead a comfortable life (Feeding Horses for the Prevention and Management of Laminitis).

    Obviously laminitis can be a devastating disease for the owner, and most would strive to prevent the disease, rather than address a symptomatic horse.  If we look more closely at the causative factors in these alterations to circulation of the horse’s digit, we may be able to do a better job at identifying horses at risk.

    We will begin with a review of pasture associated laminitis, which has been addressed in previous articles (Feeding Horses for the Prevention and Management of Laminitis and Carbohydrates III: Metabolic Syndrome).  Remember that pastures grow more rapidly at certain times of the year, and may store their energy as different types of polysaccharides depending on the species of the plant.  Frequently fructans are noted as the culprit in causing laminitis. Fructans are found in greater quantities in cool season grasses, as well as during periods where photosynthesis is favored over plant growth. As fructans contain beta bonds, which are not digested enzymatically by the equine small intestine, they pass through the tract and arrive at the large intestine where they then undergo bacterial fermentation.   Other types of carbohydrates may act similarly, including sugars and starches which escape the small intestine undigested (the classic carbohydrate overload model of the horse in the grain bin), as well as other types of carbohydrates that may be rapidly fermented (pectins, resistant starches etc). (For more information on carbohydrates, please revisit Carbohydrates: Definitions and Relationship to Equine Diseases.)


    In this first model of carbohydrate/rapidly fermentable fiber overload, too much of this rapidly fermentable material reaches the hindgut of the horse. These feedstuffs favor the proliferation of a particular bacterial population.  These bacteria produce more lactate as their excretory waste.  Excess lactate production lowers the pH of the hindgut which allows the mucosal cell wall to become permeable. In addition, too low of a pH stresses the bacteria causing them to either die or release endotoxins. Furthermore, altering the bacteria’s environment also changes their metabolism, releasing vasoactive amines into the hindgut.  As the gut wall becomes more permeable, these toxins and amines are able to cross the mucosal wall and enter the bloodstream of the horse, where they then can exert their effects at the level of the hoof.


    Horses which need to be restricted from pasture typically include ponies, as they are highly susceptible to laminitis.  In addition, any horse that has a history of laminitis, or has been diagnosed with PPID (pituitary pars intermedia disfunction)(Carbohydrates III: Metabolic Syndrome) should be grazed with care.  Horses with elevated insulin levels, or insulin resistant horses, also have a greater sensitivity to pasture associated laminitis, due to the influence of insulin on the vasculature of the horse.  Hyperinslulinemia increases the production of endothelin-1, and down regulates the production of nitric oxide.  A decrease in nitric oxide production has been linked to an elevation of homocysteine.  Incidentally, elevations in blood homocysteine are also linked to heart disease in humans. There has even been a suggestion, although with no scientific data to support this theory, that excessive supplementation of sulfur amino acids to horses with insulin resistance is unwarranted.  Typically sulfur amino acids (ie methionine) are included in hoof supplements, and homocysteine originates from methionine metabolism.   To further confuse the issue, it does appear that individuals are more susceptible to this disease, even if they are the same age, sex, breed and are managed the same as non-effected individuals.

    Obviously preventative measures aimed at reducing carbohydrate related laminitis issues center on diet management.  Certainly it is not practical or even advisable to state that all horses must be kept away from pastures.  However, knowledge of which horses are susceptible to pasture associated laminitis is key.  Once these individuals are identified, they should be placed on a principally harvested forage diet.  The forage chosen should have very little rapidly fermentable material.  However, horse’s which do not have these susceptibilities can continue to be managed with relative ease.

    Next month we will continue to discuss laminitis at a more detailed tissue level, and address further strategies to limit your horse’s chances of acquiring this disease.

  • Feeding Horses for the Prevention and Management of Laminitis

    Written By Dr. Kris Hiney

    Nothing is more devastating to the horse owner than to have a treasured partner be afflicted by the painful, crippling disease of laminitis. Laminitis can be a debilitating disease that may ultimately result in the death of the horse or humane euthanization. Unfortunately there are so many factors that can manifest in development of this syndrome that it can be difficult to sort through.
    To understand the development of laminitis one should really understand the physiology of the equine foot. Essentially the hard keratinized tissue which forms the hoof wall is held to the soft tissue by the interdigitation between the sensitive and insensitive laminae. The insensitive laminae (seen here in Figure 1) is formed in vertical sheets on the inside of the hoof wall. 
    Figure 1. An interior view of a horse’s hoof with the soft tissues removed. 1b. A schematic of the vertical lines of insensitive laminae lining the interior of the horse’s foot.
    Connecting to the insensitive laminae is the sensitive laminae, which is living tissue requiring an adequate blood supply of oxygen and nutrients to survive. When an alteration of blood flow or a vascular insult occurs inflammation or even death of the sensitive laminae can occur. The sensitive laminae ultimately stabilize the internal structures of the horse’s hoof, including the third phalanx (or coffin bone). When this stable connection is lost, the pull of the deep digital flexor tendon on the base of PIII rotates it out of place. This condition is referred to as chronic laminitis or founder.
    Figure 2. The sensitive laminae which connect the hoof wall to the horse’s foot.

    Figure 3. A foundered hoof where PIII has rotated out of place due to the pull of the deep digital flexor tendon.
     
    There are many reasons why blood flow can be disrupted to the equine digit. Laminits is often a systemic disease which is only visualized in the foot. While digestive issues lead the list of causes of laminitis there are other physical insults which can occur as well. When procuring wood shavings from a reputable dealer, care should be taken never to include those of the black walnut tree. These shavings contain the chemical juglone, actually a toxin which can kill other plants in the black walnut environment. Other physical causes are concussive trauma, from being ridden on hard surfaces resulting in decreased blood flow to the foot, and excessive loading (i.e., one limb is severely lame resulting in extra loading to the sound limb). Endotoxemia, such as what might be seen in a mare with a retained placenta, may also result in the development of laminitis.
     Nutritionally, a whole series of gastric insults can alter blood flow to the foot.  These include a carbohydrate overload (the classic example of the horse breaking into the feed bin) which leads to an alteration of fermentation in the hindgut.  In order to prevent starch from escaping enzymatic digestion in the small intestine and escaping to the hind gut, it is recommended to avoid a starch intake of more than 2-4 g/kg of body weight per meal. Therefore, a 500 kg horse should receive no more than 1-2 kg of starch per meal.  Pasture grasses have also long been known to precipitate bouts of founder, but typically only in susceptible populations. Ponies, and horses with thrifty genotypes are the most likely to suffer from pasture-associated laminitis. It is believed to be caused by a high level of fructans, although the quantity of fructans required to cause laminitis is unknown. Fructan content is known to vary with the time of year, with a higher content seen in the spring, when most pasture-associated laminitis occurs. Horses which are susceptible to pasture-associated laminitis should also limit their intake of pasture grass in the afternoon, when photosynthesis throughout the day has resulted in a higher level of fructans in the plant. The levels of water soluble carbohydrate gradually decline through the night, making grazing in the morning relatively safer. As the majority of horses which develop laminitis due so on pasture, rather than through the owner feeding excessive concentrates, at least some thought or caution should be used when grazing horses. Ideally horses should be introduced gradually to consuming fresh grass, and susceptible horses' grazing should be limited to when fructan concentrations are at their minimum.
    If a horse does develop chronic laminitis, unfortunately there is little the owner may do nutritionally to manage the horse. Obviously exposure to pasture grasses at peak times of fructan concentration should be avoided. Also, the horse should be managed to lower body weight to decrease the mechanical load on the laminae. Low energy forage should be the primary feed for the foundered horse. However, because low energy forages will typically be deficient in protein, minerals and vitamins, it is important to ensure that the horse is supplemented with a low energy concentrate to make up for dietary insufficiencies. As these horses are often in a great deal of pain, NSAID administration may often be needed, but can also contribute to gastrointestinal upsets. Alternatives to NSAIDS, such as Omega-3 fatty acid supplementation, may help to alleviate some discomfort, without the negative side effects.
    Overall, close attention to the diet of the horse, avoiding GI disturbances or causing fluctuations within the hind gut, and limiting grass intake during periods of time where fructan concentrations can be high, will hopefully prevent the horse from ever experiencing this deadly disease.

  • Equine Carbohydrate Disorders Part 3: Metabolic Syndrome

    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.

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