Keys to Preventing Laminitis

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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.

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 1: Definitions and Relationship to Equine Diseases

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Written By Dr. Kris Hiney
Equine disorders related to carbohydrate consumption have received much attention by owners and researchers alike, as of late. This has resulted in almost a mistrust or fear of feeding horses carbohydrates.  But in reality, almost all of the horse’s calories come from carbohydrates – there is no way to avoid them in the horse’s diet. What one must do is understand all of the forms in which CHO (carbohydrates) are found, identify horses at risk for CHO disorders and select the appropriate feeds to keep them healthy.
To begin, carbodydrates are simply molecules composed of carbon, hydrogen and water. Monosaccharides are single units of sugars which vary slightly in their structure.  Common monosccahrides in the horse’s diet consist of glucose, galactose, fructose, mannose, arbinose and xylose. While these monosaccharides are not normally found in their single form in plants, they are joined together to make  longer polysaccharides. However, monosaccharides are produced through  enzymatic digestion by the horse.  Disaccahrides, then, are just two sugar units linked together. Common disaccharides include lactose (found in mare’s milk and is formed by glucose and galactose linked together) and maltose (two glucose units linked together).
Figure 1. Glucose and galactose. The two structures only differ by the location of the hydroxyl group on the left side of the structure.
Oligosaccharides are longer chains of a variety of monosaccharides linked together, typically between three and ten sugar units.  The primary oligosaccharides in the horse’s diet are stachyose, raffinose and fructo-oligosaccharides (FOS).  FOS have received attention in animal nutrition as a way to supply pre-biotics to the animal. Pre-biotics are often oligosaccharides which are resistant to digestion in the foregut of the horse but are digested by bacteria in the hindgut. These supply a source of nutrition which supports the growth of beneficial bacteria and perhaps reduces the population of disease causing – or “pathogenic” – bacteria. In fact they are looked at as an alternative to feeding antibiotics in livestock. FOS are believed to alter the pH of the colon to a more favorable environment for the most productive bacteria. Mannose specific oligosaccharides are also thought to reduce the adherence of pathogenic bacteria to the epithelium of the gut wall. In yearling horses, feeding FOS reduced fecal pH and increased the production of volatile fatty acids from the hind gut. FOS supplementation also decreased the incidence of diarrhea when fed to foals. It has also been shown to have a protective effect on the development of foal diarrhea when fed to their dams. However, it is not known if that was an indirect effect passed through the milk, or if the foals simply ingested some of their dams’ feed containing the supplement. While feeding oligosaccharides does not appear to have an immune boosting effect that has been suggested in other species, it does appear to have beneficial effects on gut health in the equine. Horses receiving FOS and challenged with a large barley meal had less lactobacilli in their colon compared to controls. Thus FOS may help prevent GI disturbances due to diet changes or CHO overload.
Fructooligosaccharides also belong to the category of carbohydrates labeled as fructans.  Fructans are polysaccharides which have multiple fructose units. Inulin is also classified  as a  fructan. Many horse owners have heard of fructans as a risk factor for pasture associated laminitis. A sudden increase in fructans in the diet can alter the microbial population in the hindgut which may then subsequently lead to the development of laminitis. Fructan concentrations in grasses vary with both season and time of day.  Fructans and other starch concentrations are highest in the spring, lowest in the summer and intermediate in the fall. During the day, the process of photosynthesis results in the highest concentrations of fructans in the afternoon with sometimes half or less in the morning or evening hours.
Other CHO include longer chains of sugar units and are known as polysaccharides. Most commonly we think of starches and fibers as the common polysaccharides in the equine diet. Starch occurs in either linear form known as amylose or branched form, amylopectin.  It is composed of only glucose linked by bonds that can be enzymatically digested by the horse. In contrast, cellulose is also a straight chain of glucose but is linked by a different type of bond , a beta bond, which must be broken by microbes. Fermentation of this fiber fraction results in formation of volatile fatty acids which are metabolized by the horse to produce energy. Pectin and hemicelluloses are also common polysaccharides found in the equine diet.
Figure 2. Amylose is a chain of glucose units linked by alpha bond.
Figure 3. Cellulose is a similar chain of glucose units, but linked by beta bonds instead, making it indigestible by mammals.
Those CHO linked with alpha bonds can be digested in the foregut, allowing the monosaccharides to be absorbed intact. In contrast, cellulose, hemicelluloses, pectin, raffinose and stachyose, which contain beta bonds, will all need to undergo microbial fermentation to provide energy to the horse.   Hemicellulose, compared to cellulose, is a mixture of arabinose, xylose, glucose , mannose and galactose. Pectin is made up of beta linked galacturonic acid, arabinose and galactose. Pectin and hemi-cellolose are more rapidly fermented than cellulose and increase the digestibility of the feed if present in a greater proportion.
Now that we know what different types of carbohydrates exist in the horse’s diet, let’s look more closely at some differences that occur in forages. Typically, forages should always make up the bulk of the horse’s diet. They are made up of structural CHO which make up the cell wall as well as some indigestible lignin.  The plant cell wall is made of cellulose, hemicelluloses and pectin. Forages also have non-structural CHO or NSC in the cell content, though certainly not as much as concentrates. The NSC is a mixture of monosaccharides (glucose, fructose, etc.) and disaccharides as well as starch and fructans.
If we compare common forages, cool season grasses are made up of primarily cellulose, then hemi-celluose and the fairly small amounts of pectin. Cool season grasses include Kentucky Bluegrass, orchard grass, fescues and ryegrass.  Legumes, which are typically high in digestible energy are relatively higher in pectin. Legumes would include alfalfa, clover, lespedeza and peanuts. Warm season grasses grow and mature more rapidly and have much more cell wall/kg DM and thus much more fiber. Warm season grasses include Bermuda grass, switchgrasses, and bluestem. Therefore warm season grasses at a later stage of maturity may be ideal for horses with carbohydrate sensitivities. In general, there is a higher proportion of cell content in a younger, or more immature plant. This makes grasses or hays harvested at an earlier stage more digestible.
Interestingly, the storage form of CHO in legumes and warm season grasses is primarily starch, while cool season grasses prefer to store energy in the form of fructans with much less starch. There is also a limit to how much starch the chloroplasts of warm season grasses and legumes can contain, yet there is no limit to fructan accumulation. Fructan also accumulates more to the base of the plant and more so in the stem than in the leaf. Cool temperatures and droughts (which typically don’t go together) may also increase the fructan production by the plant. Anything that promotes photosynthesis but retards growth ends up increasing NSC (lots of light with cool temperatures).   Therefore, be especially careful to observe growing conditions, especially if the horses are consuming cool season grasses and have carbohydrate sensitivities.