Is Your Horse An Easy Keeper or Good Doer?
By D. Graig Barnett, DVM, Intervet, Inc.
Is your horse one of those “easy keepers” or “good doers” who puts on weight very easily or who stays overweight even when diet is restricted? Does he/she have abnormal bady fat distribution (e.g. a thick, “cresty” neck; pads of fat that have formed behind the shoulders and around the tail head)? Does he/she have a ravenous appetite? Has he/she ever experienced an episode of founder/laminitis? If so, your horse may have equine metabolic syndrome.
Definition:
Equine Metabolic syndrome is a common endocrine disorder of mature horses characterized by obesity, insulin resistance, and risk of laminitis/founder. Horses affected with metabolic syndrome are refractory to the action of insulin (insulin resistant) and subsequently glucose intolerant (unable to properly uptake and utilize blood glucose. In the healthy state, insulin is secreted by the pancreas in response to elevated glucose in the horse’s bloodstream following a meal. The insulin released into the bloodstream stimulates uptake and utilization of the glucose by muscle, adipose tissue (fat), and liver cells with a subsequent decrease in the blood glucose level. Insulin therefore functions to clear glucose from the bloodstream and deliver it into cells that utilize it for fuel.
Insulin resistance indicates that certain cells in the horse’s body have a reduced sensitivity and don’t respond properly to the action of insulin. When this happens, the body tried to compensate by stimulating the pancreas to secrete more insulin, which leads to elevated insulin levels in the blood(hyperinsulinemia). In addition, because there is insulin resistance and the blood glucose is not being taken up and utilized properly by the cell, the horse may have elevated blood glucose levels ( hyperglycemia).
Cause:
The specific mechanism responsible for the development of metabolic syndrome/insulin resistance is not completely understood but is most likely related to a genetic susceptibility in combination with excessive caloric intake and physical inactivity. Susceptible individuals who are prone to metabolic syndrome seem to have inherited “thrifty gene” that permit highly efficient use of their dietary intake. For horses in the wild or for horses faced with periods of environmental harshness this efficient use of dietary intake is obviously an advantage. However, for the domesticated horse who has inherited these “thrifty gene”, it may actually be a disadvantage in that the susceptible horse may become obese, especially when excess food is coupled with restricted physical activity. This is especially evident when wild Spanish Mustangs who have evolved to be
Able to sustain in harsh terrain, are captured and domesticated. These horses tend to quickly become overweight and develop signs of equine metabolic syndrome when fed diets that far exceed, in both quantity and quality, the diet on which the species evolved in nature and especially when coupled with limited physical activity. Although virtually any breed can develop metabolic syndrome, the breeds that tend to predisposed include domesticated Spanish Mustangs, Pony breeds, Morgans, European Warmbloods, Peruvian Pasos, Paso Finos, American Saddlebreds, Arabians, miniature breeds, donkeys and mules seem to be predisposed to this condition. Many of these breeds developed in areas where environmental conditions favored those who could get by on little food.
When susceptible horses become obese, there is an over abundance of fat cells (adipocytes) in the abdominal cavity, These abdominal fat cells (omental adipocytes) produce a host of hormaones (adipokines) and enzymes that interfere with the action of insulin and contribute to insulin resistance. One of these enzymes converts circulating inactive cortisone into physiologically active cortisol (corticosteroid), which is a recognized factor not only in the development of insulin resistance but also laminitis. In humans, as in horses, insulin resistance leads to the development of increased blood glucose levels (hyperglycemia). The hyperglycemia stimulates the production of more insulin to stimulate uptake of glucose by the cells. In approximately 20% of humans with insulin resistance the pancreas eventually becomes “exhausted” and can not produce any more insulin. The inability of the pancreas to produce more insulin leads to a decrease in blood insulin levels and type 2 diabetes (hyperglycemia). In horses however, “pancreatic exhaustion” is relatively uncommon and most horses with insulin resistance maintain elevated insulin levels (hyperinsulinemia). Diabetes-associated vascular complications as a result of hyperglycemia are well recognized in humans. In the horse with metabolic syndrome, the elevated glucose levels in the blood also causes vascular complications with the most evident being compromise of blood flow to the feet and subsequent laminitis. In addition to the vascular manifestations of the elevated blood glucose levels, the laminitis also develops as a consequence of elevated cortisol levels as indicated above.
Recognition:
Horses affected with metabolic syndrome are typically between the ages of 8 and 18 years. These horses are generally presented to the veterinarian for the treatment of laminitis. The degree of pain associated with the laminitis is often, but not always, mild. Further evaluation of the feet may reveal that the horse has experienced previous episodes of laminitis that may also have been mild or even subclinical. These horses are often overweight even when not being fed in excess (“easy keepers”). They generally have abnormal fat distribution (thick, “cresty” neck; fat accretions “pads” at the tail head and behind the shoulders, and fatty thickening of the prepuce in geldings). These horses often have ravenous appetites. If they are severely hyperglycemic they may also have excessive thirst (polydypsia) and excessive urination (Polyuria). Affected broodmares often have fertility problems and abnormal heat cycles.
Diagnosis:
Metabolic syndrome/insulin resistance is best determined through a series of tests involving administration of glucose followed by drawing of multiple blood samples to measure glucose and insulin levels. However, for practical purposes, a one time blood sample demonstrating hyperinsulinemia in the presence of normal or moderately elevated blood glucose levels is clinically practical and strongly suggest that insulin resistance is present. It should be recognized that in addition to metabolic syndrome, there are other conditions that may cause insulin resistance and that may need to be ruled out.
Laminitis from other causes will result in pain which results in an increase in cortisol levels and subsequent insulin resistance. Therefore, in some situations it is difficult to determine if the laminitis produced the insulin resistance or if the insulin resistance produced the laminitis.
Stress/excitement may also result in insulin resistance in much the same manner (stress induced increase in blood cortisol).
Administration of exogenous glucocorticoids/steroids.
Cushing’s syndrome (pituitary pars intermedia dysfunction; PPID) which is an abnormality of the pituitary gland at the base of the brain and results in increased blood cortisol levels and subsequent insulin resistance.
Prevention & Treatment:
The most effective way to treat and prevent metabolic syndrome/Insulin resistance is through diet and exercise. The fact that insulin resistance is directly correlated with weight gain and that even small weight losses can reduce insulin resistance suggest a cause-and-effect relationship. Therefore, when animals are obese, weight reduction through diet and exercise represents the key therapeutic objective. Exercise not only enhances weight reduction, but has also been shown to increase the cells sensitivity to insulin thereby increasing glucose uptake and utilization by skeletal muscle. This exercise induced glucose uptake and utilization persist for up to 24 hours and is of obvious benefit to the horse y helping reduce weight and decrease blood glucose levels. Unfortunately, in certain situations, exercise may be limited due to laminitis or other physical restrictions (i.e. arthritis).
The most important part of feeding a horse with metabolic syndrome/insulin resistance is limitation of the soluble carbohydrate content of the diet. Reduction in levels of sugar and starch by eliminating or significantly reducing grain products is very important. Feedstuffs or treats that contain sugar or molasses should be avoided as should feeding apples and carrots. In most situations, hay with a low total nonstructural carbohydrate (NSCs; sugar, starch) content should be the cornerstone of the diet. Ideally, hays for insulin resistant horses should contain no more that 10% sugar and starch combined. The lowest sugar hays tend to be Bermuda grass. Native prairie hay is also often low in soluble carbohydrate content and may be a good choice as well. In general, perennial rye, fescue and brome show the highest levels of nonstructural carbohydrates. However, it should be recognized that with any hay the carbohydrate content may vary greatly depending upon growing conditions, stage of growth when cur, and drying conditions. Unfortunately, it is impossible to determine the carbohydrate composition of hay by visual inspection. Therefore, when evaluating hay to be fed to horses with metabolic syndrome, it is a good idea to have the hay analyzed for total nonstructural carbohydrates (NSC). If you can’t find low NSC hay or if you hay has been determined to have a high NSC content, it’s possible to reduce the soluble carbohydrate content of the hay by soaking in room temperature water for an hour on in hot water for 30 minutes. Soaking hay in water removes an average of 30% of the sugar. For grass hays with an average digestible energy content of 0.65 to 0.75 kcal/lb, feeding 1.5% to 2.0% of the estimated target ideal body weight works well in most cases. Therefore, a horse with a target body weight of 1,000 lb would be fed 15 to 20 lbs of hay/day. Grass hays containing 7.5% protein and consumed at 2% of body weight meet crude protein requirements. At feeding rates of 1.5% of body weight/day, 10% protein is needed. If one feels the need to feed the horse something other than hay, you should chose a feedstuff with a low glycemic index (GI). Glycemic indexes are used to rank foods according to how they affect blood glucose levels. Foods with a high glycemic index quickly release glucose into the blood when digested. Low glycemic index foods break down slowly, releasing glucose gradually into the bloodstream. Studies have shown that one of the safest feedstuff in terms of maintaining blood glucose levels was beet pulp with a GI of 1. Other feedstuffs with low GI values are alfalfa, rice bran, and soy hulls. Bermuda hay and alfalfa hay also generally have low GI values. On the contrary, sweet feeds, oats and corn generally have high GI values, especially if missed with molasses.
In most cases, free choice access to grass should be avoided for horses with insulin resistance/metabolic syndrome. Plant stresses (overgrazing, cold temperatures, drought, etc.) increase the concentration of sugar in the grass. In addition, sugar concentrations tend to be highest in the lower part of the plant. This is why laminitis may develop in horses that have been grazing very short, overgrazed, or mowed pastures. Because the sugar content of grasses can change dramatically in a very short period of time (i.e.hours), allowing horses with metabolic syndrome to graze is always risky and is probably best avoided. If horses are turned out, they must be monitored closely for any signs of laminitis or weight gain. Another option is to turn the horse out with a graing muzzle that can be completely or partially taped.
Designing a low sugar/starch (low glycemic index) ration that contains good quality forage and is balanced with respect to minerals and vitamins is beyond the scope of this article. Therefore, it is highly recommended that you consult with you veterinarian or equine nutritionist when designing a diet for your horse with metabolic syndrome/insulin resistance. There is some evidence linking insulin resistance with certain dietary imbalances and deficiencies. Therefore, supplementation of certain nutrients including vitamin E, vitamin C, vitamin D, chromium, magnesium, zinc, calcium and fatty acids in conjunctions with an appropriate overall diet may be justified. However, further investigation to demonstrate any therapeutic value of supplementation for insulin resistant horses is warranted.
In summary, certain genetic predispositions and management practices tend to promote the development of equine metabolic syndrome and insulin resistance. Inappropriate feeding in conjunction with physical inactivity in susceptible individuals leads to excessive abdominal fat cells (omental adopocytes), the production of hormonal mediators including cortisol, the development of insulin resistance and glucose intolerance, and the development of laminitis as a result of the elevated cortisol levels and vascular changes that occur with elevated blood glucose levels. Strict control of dietary intake along with exercise is the most effective way to treat and to prevent equine metabolic syndrome. Be cognizant of you horse during periods of inactivity and adjust the diet accordingly, especially if your horse is an “easy keeper” with a potential genetic predisposition towards this condition.
