Vitamin C

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Written By Dr. Kris Hiney

Previously, we have discussed two important fat soluble vitamins which serve an important anti-oxidant function in the horse, vitamin A and E.  We will continue to discuss anti-oxidants as we transition to the water soluble vitamins essential to the health and well-being of the horse.  As humans, we are probably very familiar with vitamin C or ascorbic acid/ascorbate, as it is a commonly supplemented vitamin.  After all, who hasn’t reached for an orange in order to get their share of this important vitamin (Despite the fact there are many more nutrionally dense sources of vitamin C!)?  People often turn to vitamin C during times of stress or illness, especially the common cold, to try and fight off pathogens.  But what does vitamin C do in the horse, and should you be supplementing it?

Typically, most individuals are familiar with vitamin C’s role as an anti-oxidant, but it also serves as a co-factor for a host of enzymes.  Specifically, vitamin C is necessary for the formation of collagen, which appears throughout the body in connective tissue of tendons, ligaments, blood vessels etc.  Vitamin C also is necessary for the synthesis of carnitine (the molecule which allows fatty acids to be transferred into the mitochondria for oxidation) as well as tyrosine and other neurotransmitters.  Vitamin C supplementation, along with other anti-oxidants, has actually been shown to improve cognitive disfunction in aging dogs.

Vitamin C is synthesized in horses, but not in man, guinea pigs or a variety of other species.  Therefore in humans, vitamin C is a dietary necessity, but it is not required  in the diet of the average horse.  The horse is capable of converting glucose through a variety of enzymatic reactions into ascorbic acid. This synthesis is adequate in most scenarios.  So when might vitamin C be beneficial to the horse?   Presumably when there is a need for greater amounts of anti-oxidants in the body.
We have discussed the role of anti-oxidants before.  The body uses oxygen as the final electron acceptor in the electron transport chain during the capture of energy in the form of ATP.  Normally this process produces a harmless, and even useful byproduct – water.  However, a small proportion of these reactions does not go according to plan, but instead creates a harmful molecules known as reactive oxygen species or ROS.  In actuality, the formation of free radicals is a normal part of metabolism and serves as cell signaling systems.  In fact, the creation of free radicals stimulates the adaptive response seen with athletic training.  Therefore, we should not aim to eliminate their presence entirely.  However, in excess, these free radicals can do immense damage to the body as they damage DNA, cell membranes etc.  Reactive oxygen species have been implicated in carcinogenesis, aging, cognitive function etc.  Ascorbate aids in the anti-oxidant cascade by regenerating the reduced form of vitamin E and other anti-oxidants.

Horses which are intensely exercised will naturally produce a greater number of reactive oxygen species due to the increased rate of metabolism.  It is not uncommon for those individuals involved in more strenuous equine sports (endurance rides, three day eventing etc.) to routinely supplement their horses with anti-oxidants.  In studies which have examined the use of vitamin C in horses, there appears to be a difference in response relative to the intensity of the work being performed.  In polo ponies, plasma ascorbic acid was higher in ponies which were considered to be more intensely working than the lighter worked ponies, despite both groups receiving supplemental vitamin C.  Similarly, endurance horses supplemented with vitamin C had a higher plasma ascorbic acid level at the beginning of the race compared to the control horses, but the difference between plasma vitamin C levels  between the two groups grew smaller throughout the race.   The unsupplemented horses actually increased their plasma ascorbic acid levels throughout the race, presumably through the mobilization of body stores.  This differed in previous studies which showed a decrease in plasma ascorbic acid in more intensely worked horses.  This drop in ascorbic acid has also been reported in heavily raced sled dogs. Thus it may be the level of exercise which is important. Certainly this makes sense as the level of effort increases, the metabolic rate must increase and the greater percentage of ROS will be produced.   Although lacking in concrete data, it appears that additional vitamin C may be beneficial for heavily exercised horses.

Exercise is not the only form of stress which horses may experience.  Plasma vitamin C levels have been seen to be lower in horses following surgeries, traumatic wounds, strangles and episodes of exercised induced pulmonary hemorrhage.  Horses with recurrent airway obstruction also have had lower plasma ascorbic acid levels, and supplementation appears to be helpful in creating better exercise tolerance and reduced airway inflammation.  Supplementation of vitamin C also appears to help aged horses enhance their immune system and improves their response to vaccinations.  Horses do appear to tolerate large doses of vitamin C quite well, horses received 20 g /d of ascorbic acid for 8 months with no measureable negative response.  However, it has been shown that horses decrease their own natural synthesis of vitamin C when supplemented.  Therefore, when the supplement is removed, horses will have a lower plasma concentration of vitamin C compared to normal.  Therefore, prolonged supplementation may be ill advised.  Overall, like all vitamins previously discussed, supplementation of vitamin C should not be done without careful consideration of whether or not the horse would truly benefit from supplementation.

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.