This article on EMS was written for the Natural Horse Magazine (Vol 16 Issue 1 Jan/Feb/Mar 2014 pp20-23)(Some aspects of EMS were covered in greater depth elsewhere in this magazine. (A Horse Guardian’s Guide to Feeding a Metabolically Challenged Horse. – Stephanie Krahl) + (A Lesson in Blood Chemistry Analysis and Interpretation for EMS/IR Horses – Joseph Thomas PhD)
It has been known for a long time that horses with Cushing’s Disease (now often referred to as Pars Pituitary Intermedia Disease – PPID) commonly developed laminitis. In studies of PPID in horses, it was found that some of the symptoms that were associated with the disease were not directly related to the condition and were found in horses that had a normal pituitary gland and the name ‘Peripheral Cushing’s’ was adopted to refer to these cases. These other symptoms were found to be due to insulin resistance, which led to the adoption of the term ‘Equine Metabolic Syndrome’ (EMS) to describe this condition in horses, because of its similarities to the human ‘Metabolic Syndrome’.
The changes occurring in Metabolic Syndrome in humans are also due to insulin resistance, and this typically occurs in overweight people with a large waist size due to abdominal fat stores, and they have raised triglyceride levels in the blood, raised blood glucose (this is not the case in horses), and have high blood pressure (hypertension), similar to those seen with EMS. These individuals are more susceptible to developing Type 2 Diabetes as well as a range of cardio-vascular disorders, whereas 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, personally, 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?
Keeping things as simple as possible, 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. The role of insulin is to try to maintain constant levels of blood glucose and it does so by increasing uptake of glucose by cells by activating receptors on cell walls (GLUT4 receptors), but also by initiating the storage of excess glucose as glycogen. Glucose is used as a source of energy by cells, and whereas 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. Because of this, with insulin resistance, higher levels of insulin will commonly be found in blood samples from affected horses. The horse’s pancreas is able to maintain these high levels of production of insulin, whereas in humans the pancreas can become ‘exhausted’ which then leads on to Type 2 Diabetes.
What cause’s IR?
The mechanisms for how IR develops are still not fully understood, but the three prime suspects for causing these changes are adipokines, corticosteroids and insulin itself. Body fat (adipose tissue) that was once just considered a store for fat, is now found to be metabolically active, releasing hormones and other active proteins (‘adipokines’) that appear to contribute to the problem and, in man, it has been demonstrated that abdominal fat is the most hormonally active. Corticosteroids have opposite actions to insulin on the metabolism of carbohydrates, proteins and fats and they cause an increase in blood glucose levels, with a compensatory increase in insulin levels, as well as exerting 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. The significance of these is that the fatter the horse, the greater likelihood of IR developing, anything that stresses the horse, thus increasing corticosteroid release, will worsen IR and diets that contain high levels of sugars and starch will cause higher levels of insulin release.
Insulin resistance might be considered a metabolic ‘disease’, since its effects in humans and horses can be devastating, however, IR really should be considered as a ‘natural’ adaption that becomes uncontrolled due to the changes in management of the domesticated horse, and the modern lifestyle of people. It is a condition that occurs in many animal species, 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 the times of year 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 have been able to survive this change in food availability better than others. Unfortunately, those races and breeds that have the ability to become insulin resistant more readily are the ones who now are more likely to suffer the consequences of a high calorie diet (and alcohol) and a lack of exercise, which has contributed to the great increase in obesity and insulin resistance particularly in these races and breeds. It is a particular problem in ‘native breeds’ of horses and ponies, and also affects certain races of people. For instance, the ‘hunter-gathering’ Australian aborigines are particularly prone to insulin resistance and for developing type 2 Diabetes and cardiovascular disease when they change to a ‘westernized’ life-style.
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 an energy-rich diet that provides starch in grain and grass or hay that is fairly consistently much higher in sugars than the grasses and plants that wild horses generally feed on, and this diet is maintained the whole year. Another equally important factor is the relative amount of movement that wild horses have, as they search for food, compared to the large percentage of horses that have limited exercise and often limited space for them to move around in.
- Although not all fat horses are insulin resistant and some thin horses develop IR, it occurs most commonly in the fat or obese horse, pony and donkey.
- IR horses exhibit ‘regional adiposity’, but as well as an accumulation of abdominal fat, as occurs in people, fat is laid down in more superficial areas of the body. A prominent and firm crest on the neck is the most obvious symptom associated with IR. If IR is not under control, this crest is hard and immovable and should set off alarm bells that something urgently needs to be done to control it. A neck crest that is soft and movable is a reasonable indicator that insulin 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.
Changes in the feet
It seems that IR causes weakening of the laminae of the feet. Laminitis can be caused experimentally 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 cases of IR we see ‘in the field’, but it seems the lower levels will cause some weakening of the laminae to cause low-grade laminitis, and with uncontrolled IR there can be sufficient weakening to cause clinical laminitis.
Diagnosis of IR
Diagnosis of IR by blood samples is discussed in another article in this magazine, but a diagnosis of IR can reasonably be made if there is evidence of ‘regional adiposity’, whether it is 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.
Although there are some factors that cause a horse to become insulin resistant that have not been fully identified, the majority of cases of IR are in fat horses that are under-exercised. We are unable to change a horse’s genetic predisposition for developing IR, but there are three aspects of management that can be addressed when managing a horse with IR, and these also apply to how to prevent them from developing it. Two of these relate to diet, the quantity and the ‘sugar’ content of it, and the third aspect is exercise. Nutrition and feeding the IR horse is dealt with in greater depth elsewhere in this magazine, but it may be of benefit to explain these management practices here. 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 potentially cause IR, or worsen IR when it is present. 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. Quantities of food over the requirements of the individual horse will cause the horse to put on weight. The larger the fat stores in the body the greater amounts of adipokines released, and these contribute to the development of IR, therefore keeping the horse’s weight right and not letting it get overweight will help to prevent IR. Another effect of these adipokines is to disrupt the horse’s control over appetite, giving it a greater appetite. The IR horse, if fed ad lib on hay or pasture, will consume more than normal, and this will tend to further increase an affected horse’s weight, thus compounding the problem.
Increasing exercise has been shown to be of benefit in the management of IR in both humans and horses. The reason for this is that exercise increases glucose uptake in muscle independent of insulin, so that those that 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 there.Unfortunately, for many owners, the first time that they are forced to confront the problem of IR is when their horse or pony has already developed laminitis. In these cases, exercise may well cause further separation of the laminae and therefore cannot be effectively used as a management tool for IR so that, in these cases, IR must be managed by dietary means alone. (See article in this magazine,)
Do not let your horse become overweight. Feed it to its 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 discussed further in my article on Laminitis in Vol 16, Issue 2 (April, May/June).