20 • NATURAL HORSE Magazine – VOLUME 16 ISSUE 1 www.naturalhorse.com

FEaTuRE aRTIc LE

S tudies have proven that horses with Cushing’s disease (now often referred to as pars pituitary intermedia disease

– PPID) are predisposed to develop laminitis. Studies of equine PPID have revealed that some of the symptoms associated with the disease are not directly related to the condition and are found in horses with a ‘normal’ pituitary gland. The name ‘peripheral Cushing’s’ was adopted to refer to these cases, however these other symptoms are now attributed to insulin resistance, which has led to the adoption of the term ‘equine metabolic syndrome’ (EMS) to describe this condition in horses.

The changes occurring in metabolic syndrome in humans are also due to insulin resistance. This typically occurs in people with large stores of abdominal fat, raised triglyceride levels in the blood, raised blood glucose (this is not the case in horses), and high blood pressure (hypertension) similar to horses with EMS. These humans are more susceptible to developing type 2 diabetes as well as a range of cardio- vascular disorders. For horses with EMS the end result is laminitis. While laminitis is

included as a symptom of EMS, it would appear that the other symptoms associated with it are due to insulin resistance, either associated with the development of the condition or its resulting effects. For this reason, I have stopped using the term EMS and use ‘insulin resistance’ (IR) since this appears to be the basis of the problem and by controlling the IR, the risk of laminitis is greatly reduced.

What is Insulin Resistance?The hormone insulin is released into the blood stream from the pancreas mainly in response to increased levels of glucose in the blood (e.g. following eating). Ideally, insulin maintains constant levels of blood glucose by increasing uptake of glucose by cells by activating receptors on cell walls (GLUT4 receptors) and also by initiating the storage of excess glucose as glycogen. Glucose is used as a source of energy by cells, and although many cells of the body are able to take up glucose from the blood via receptors that do not require insulin, important ones that do are muscle, fat, and liver cells. In certain circumstances, these cell wall receptors (GLUT4) become

less sensitive to the effect of insulin (decreased insulin sensitivity = increased insulin resistance), so that the pancreas has to increase its output of insulin in order to maintain the constant level of glucose in the blood. Therefore, higher levels of insulin will commonly be found in blood samples from affected horses.

What Causes IR?The causative agents of IR are not fully under-stood, but the three prime suspects are adipo-kines, corticosteroids, and insulin itself. Body fat (adipose tissue) that was once just considered a store for fat, has been found to be metabolically active, releasing hormones and other active proteins (adipokines) that appear to contribute to the problem. Corticosteroids have opposite actions to insulin on the metabolism of carbohydrates, proteins, and fats. They cause an increase in blood glucose levels and a compensatory increase in insulin levels, and also exert a direct effect on the tissues. IR also seems to be a response to high levels of insulin circulating in the blood, thus perpetuating the problem. Simply stated, the more over-weight the horse, the greater the likelihood of IR

EMSThe Ins & Outs of (EquInE METabOlIC SyndROME)

by John Stewart, MA Vet, MB, MRCVS

A fat pony that was not exercised and lived out in a grass field. This pony was insulin resistant and had developed low-grade laminitis.

www.naturalhorse.com NATURAL HORSE Magazine – VOLUME 16 ISSUE 1 • 21

developing. Anything that stresses the horse, thus increasing corticosteroid release, will worsen IR as will a diet high in sugar and/ or starch.

Insulin resistance might be considered a meta-bolic ‘disease’ since its effects in humans and horses can be devastating. However, IR really should be considered a ‘natural’ adaption that becomes uncontrolled due to the changes in management of the domesticated horse and the modern human lifestyle. It is a condition that occurs in many types of animals, not just in people and horses, but it has come to prominence in these two species because of the severity of the problems it causes. It appears to be a change in metabolic state that enables an animal to make best use of food in seasons when it is plentiful in order to be able to survive when food is scarce. There appears to be an underlying genetic basis to IR, which has enabled some races of people and some breeds of horse to survive this change in food avail-ability better than others. Unfortunately, races and breeds that have the ability to become insulin resistant more readily are the ones who are now more likely to suffer the conse-quences of a high-calorie diet and a lack of

exercise – both contributing factors to obesity and insulin resistance. It is a particular problem in ‘native breeds’ of horses and ponies, and in certain races of people.

Although horses in the wild develop IR, they do not develop the problems that are encountered when kept under the domesticated environment that we subject them to. The domesticated horse is fed a year-round, energy-rich diet. They receive starch in grain and forage that is often much higher in sugar than the vegetation that wild horses generally consume. Another equally important factor is the relatively high mobility that wild horses have compared to the largely sedentary domestic horse.

Physical Signs•Although not all overweight horses are insulin resistant – and some thin horses develop IR – the condition occurs most commonly in obese equines.•A prominent and firm crest on the neck is the most obvious indication of IR. In cases of uncontrolled IR, the crest is hard

The pancreas is a glandular organ that lies close to the stomach and upper small intestine. It releases digestive enzymes into the small intestines to help break down proteins, carbohydrates, and fats into smaller units so that they can be absorbed from the gut. The pancreas also releases hormones into the bloodstream (insulin and glucagon) that control the usage and storage of these absorbed dietary units by the body.

Insulin resistant horses may have a less obvious cresty neck than pony breeds, but still have abnormal deposits of fat. Condition score 7 or 8 out of 9.

InCREaSEd aPPETITE

Body fat

adipokinES

pancrEaS

inSulin

Converts corticosteroids from inactive to active form

InaCTIvE FORM aCTIvE FORM

corticoStEroidS

decrease

blOOd gluCOSE

Increase

ir cHanGES in tiSSuES

PIllS OR InjECTIOn

adrEnal GlandSTRESS

PPId

22 • NATURAL HORSE Magazine – VOLUME 16 ISSUE 1 www.naturalhorse.comwww.naturalhorse.com

and immovable – a sign that immediate action is necessary to rectify the situation.A soft, movable neck crest indicates thatinsulin resistance is relatively under control, but while there is still an obvious crest,IR-control measures need to be maintained.

Other sites where abnormal fat deposits may be seen are over the tail-head, in front of mammary glands or prepuce, over the loins, and behind the shoulders. Additionally, fat deposits in the supra-orbital fossa can cause a bulge above the eyes (where normally there is a hollow).•An increase in appetite •Infertility•Laminitis

Changes in the HoovesChanges, such as obvious growth rings or a widened ‘white line,” are sometimes present in the hooves, yet do not cause lameness. The term ‘low-grade laminitis’ is often used to describe these changes.

IR appears to cause weakening of the laminae within the hoof. Laminitis can be induced by giving extremely high doses of insulin by intravenous drip. The dose given in these experiments is much higher than the levels found in the majority of IR cases we see ‘in the field,’ but it seems the lower levels will cause some weakening of the laminae, causing low-grade laminitis. With uncontrolled IR there can be sufficient weakening to cause clinical laminitis.

diagnosis of IRDiagnosis of IR by blood samples is discussed in A Lesson in Blood Chemistry Analysis and Interpretation for EMS/IR Horses on page 8, but a diagnosis of IR can reasonably be made if there is evidence of ‘regional adiposity,’ whether present in an obese or thin horse.

Since many cases of PPID are also insulin resistant, it is important to ascertain which of these conditions (or both) are present, since the treatment for them is different.

ManagementAlthough not all IR triggers have been identi-fied, the majority of cases occur in overweight, under-exercised horses. While we are unable to change a horse’s genetic predisposition for developing IR, there are three simple, yet effec-tive, approaches to managing an IR or IR-prone horse. Two of these relate to diet – the quantity and ‘sugar’ content of it. The third aspect is exer-cise. Feeding the IR horse is addressed in greater detail in the article A Horse Guardian’s Guide to Feeding a Metabolically Challenged Horse on page 16 but it may be of benefit to explain these management practices here.

Above: Acute laminitis in a Welsh Pony. He was reported to have never had laminitis before but the widening of the white line and the presence of splits indicate that this horse has had low-grade laminitis occurring prior to this.

A fat, insulin resistant Welsh pony with large neck

crest and bulging of the supra-orbital fossa.

www.naturalhorse.com NATURAL HORSE Magazine – VOLUME 16 ISSUE 1 • 23

Diets that contain high amounts of simple sugars and starch (which is broken down to produce simple sugars) cause an increased insulin response. High blood levels of insulin can cause IR, or worsen existing IR. For this reason, a low-sugar, high-fiber diet will help to reduce this insulin response and the levels in the blood. The second aspect of dietary management is the amount of food. Excess feed will cause a horse to gain weight. The larger the fat stores in the body, the greater the amount of adipokines released and the greater the likelihood of IR developing. Simply stated, maintaining a healthy weight will help prevent IR. Some adipokines also increase the horse’s appetite and the IR horse, if he has free access to hay or pasture, will consume more than normal. This will increase his weight, thus compounding the problem.

Increased exercise has been shown to benefit both IR horses and humans. Exercise increases glucose uptake in muscles independent of insulin, and so, those who exercise more are able to maintain their blood glucose levels with lower levels of insulin release. Keeping insulin levels lower reduces its effects on the horse’s feet, thus reducing any damage to the laminae that might be occurring. Unfortunately for many owners, the first time they are forced to confront the problem of IR is when their horse or pony has already developed laminitis. In these cases, exercise may cause further separation of the laminae, and so IR must be managed by dietary means alone. See page 16.

Prevention•Do not let your horse become overweight – feed according to work requirements.•Feed a diet low in simple sugars and starch. A forage diet (grass/ hay) is often sufficient for the work load of many horses and ponies. Addition of a vitamin and mineral ‘balancer’ supplement is recommended.•Exercise your horse regularly.

The effects of IR will be further discussed in my upcoming laminitis article in Volume 16, Issue 2 (April/May/June, 2014).

About the author:John Stewart obtained his veterinary degree from Cambridge University, then worked in mixed practice for fifteen years before setting up his own predominately equine practice. He became interested in laminitis due to his own frustration in dealing with the condition; this led to in-depth study of the horses’ feet. His book, Understanding the Horse’s Feet, has just been released. See the book review in Book Bits, page 81 in this issue. John now works as a barefoot trimmer in southern California. John_the_vet@hotmail.com