Considerations for the IR Horse

By Eleanor Kellon, VMD, Staff Veterinary Specialist for Uckele Health & Nutrition

 Equine insulin resistance (IR) has been so well publicized everyone has heard of it. However, few really understand what it is, what causes it and what to do about it.

 

 Parallels have been drawn between equine insulin resistance/metabolic syndrome and human type 2 diabetes. While some of them are indeed valid, others are not.

 

 

There is nothing new about equine IR. What's new is that we recognize it. The stereotype of an overweight pony as high risk for pasture laminitis is timeless. The existence of laminitis prone lines in horse breeds such as Arabians and Morgans had been more of a secret, with caretakers knowing to avoid grain and limit high risk pasture exposure.

 

Between 1975 and 2002, when Dr. Phillip Johnson published his first paper using the term equine metabolic syndrome, there were three papers published linking insulin resistance and laminitis. These did not make mainstream veterinary medicine, let alone veterinary school curricula.

 

Dr. Johnson's 2002 paper brought equine insulin resistance to the forefront, but there was considerable resistance to the idea that insulin resistance not related to Cushing's disease (high cortisol in Cushing's disease causes insulin resistance) even existed. One of the most vocal early critics was Dr. David Kronfeld from the Virginia Polytechnic Institute, but a 2006 study by his group did a complete reversal.  Review of pedigrees also strongly pointed to a genetic component.  From that point forward 6 years ago, recognition of the significance of insulin resistance among practicing veterinarians and in veterinary schools has sky rocketed.

 As is often the case with high profile newly defined disorders, IR is now being overdiagnosed without proper testing. One outgrowth of the rush to blame IR for everything is that every overweight horse is being labeled as insulin resistant. However, a large field study done by the Maryland Virginia Regional College of Veterinary Medicine found that only 35% of even very obese horses are actually insulin resistant. The prevalence of IR across all weights and breeds is about 10 to 15%. With an estimated equine population in this country of about 10 million horses, that's still a large number.

 

Diagnosis by symptoms is simply not reliable. Fortunately, blood work usually clearly differentiates between normal and insulin resistant horses. You need a serum insulin and glucose taken after 12+ hours of nothing to eat except hay or pasture. No fasting. Hay or pasture available all the time. This protocol comes from the Virginia Polytechnic pony field study. Results can then be uploaded to the IR calculator for interpretation:

 http://www.freil.com/%7Emlf/IR/ir.html

 

The most recently available test is serum leptin, available from Cornell University's diagnostic laboratory:

 http://ahdc.vet.cornell.edu/test/list.aspx?Species=&Test_Name=leptin&TstTyp=&WebDisc=

 

Leptin is a hormone released by fat cells which in normal horses turns off appetite. However, IR horses are leptin resistant and have elevated levels of this hormone.

 

Insulin's job is to trigger the uptake of glucose from the blood into tissues that are dependent on insulin for this function - fat, skeletal muscle and liver. The involvement of liver in horses may be different from other species though.

 

Experiments using infusions of either insulin or glucose in normal horses and ponies have established that the laminitis associated with IR is caused by high insulin, not high glucose.

 

 In humans, insulin resistance in the liver results in high blood glucose from glucose production in the liver. This is why, even with fasting, a human with IR/type II diabetes will have elevated blood glucose (and insulin). On the other hand, fasting a horse with insulin resistance can lead to a false negative test, with insulin and glucose normal.

 

The most successful therapy for insulin resistance in both humans and horses is exercise and diet control. Exercise primes the muscle to take up glucose by pathways that are independent of insulin, resulting in less work for insulin to do and improved insulin resistance.  The effect lasts for about 24 hours.

 

Feral horses are often insulin resistance but their high level of exercise protects them from problems. Very few domesticated horses cover the 20 miles a day a feral horse does. Without the protective exercise, susceptible horses are primed to develop problems with IR if their diet is not carefully restricted. Most IR horses need a hay based diet with combined simple sugars (ESC on hay analysis) and starch of 10% or lower.

 

So, what does work for insulin resistant horses?

 Ø  Diet of hay or hay and beet pulp, with ethanol soluble carbohydrates (ESC = simple sugars) plus starch no higher than 10%

Ø  Added flax seed to supply essential fatty acids in a ratio that approximates the naturally found level in grasses

Ø  Balanced minerals, preferably based on a hay analysis, with generous magnesium (calcium:magnesium ratio no higher than 2:1) and careful balancing of trace minerals, with supplemental salt and vitamin E

Ø  When possible/not laminitic, exercise, exercise, exercise!

 

On the drug front, there are multiple options for people but the only one that actually improves insulin sensitivity is metformin. Metformin has also been studied in horses and while results are somewhat contradictory is does appear to be a good choice for getting rapid control of IR, at least for a few weeks.

 

Most herbals used for human type II diabetes are not appropriate for horses because they raise insulin without really addressing insulin resistance.

 

Acetyl-L-carnitine is a naturally occuring metabolite that influences a "master switch" enzyme in the cells causing increased glucose utilization and improved glycogen levels. Glycogen is a storage form of glucose that is typically low in insulin resistance. This metabolite is also helpful for neurogenic pain; pain resulting from alterations in nerves in situations of chronic laminitis. As a side bonus, abnormal fatty deposits typical of IR, like fatty neck crests, improve slowly with acetyl-L-carnitine supplementation.

 

IR in horses is not so much a "disease" as it is a metabolic type. Insulin resistance allows horses to gain weight easily and hold their weight better under conditions of sparse food supply. It's roots are almost certainly genetic. However, what worked for ancestors struggling to find food does not work under domestication.

 

There are no magic bullets and no short cuts with insulin resistance. Exercise is the missing element with domestic horses. This necessitates tighter control of sugar and starch in the diet of horses prone to IR. While this may seem like more trouble on the surface, it's really not and the IR prone horse is much less expensive to keep on the bottom line.

 

Eleanor Kellon, VMD, currently serves as the Staff Veterinary Specialist for Uckele Health & Nutrition.  An established authority in the field of equine nutrition for over 30 years, Dr. Kellon is a valuable resource in the field of applications and nutraceuticals in horses. She formerly served as Veterinary Editor for 'Horse Journal' and John Lyons 'Perfect Horse' and is owner of Equine Nutritional Solutions, a thriving private practice.  A prolific writer, Dr. Kellon is the author of many best-selling books on a variety of medical and nutritional topics and has contributed to both lay and professional publications.