EMS is increasingly being seen and may be referred to as Peripheral Cushing’s or Syndrome X, but the preferred name is Equine Metabolic Syndrome.
Signs include obesity; either the horse is fat at the time of diagnosis or it has been fat at sometime in the past.
The condition can also be instigated or exacerbated by gross overweight in the mature horse.
The typical sufferer is the horse who is a good doer that seems to thrive on next to no feed and restricting the diet does not seem to result in a corresponding loss of weight.
The neck is cresty i.e. the neck appears over developed or stallion-like and there is fat immediately beneath the mane that is hard. The hindquarters too are fat.
The gelding may have a heavy fat sheath with some fluid accumulation and the overweight brood mare fail to hold or cycles abnormally.
The horse is lethargic and there is a gradual onset of low grade chronic laminitis that may be difficult to detect and that is difficult to control or improve.1
In the past the condition was considered to be associated with abnormal thyroid function. The thyroid gland is found either side of the larynx (voice box) in the trachea (throat) that produces thyroid hormone (TH). At the cellular level the hormone increases the absorption and utilisation of glucose. Reduced function of this gland is characterised by lethargy and fat deposition, but this theory has been largely discredited.3
EMS is considered to be caused by evolutionary mechanisms 4 that are now no longer necessary; diet, breeding and human selection has combined to produce horses that are inherently fat. Typically it’s the overweight horse or pony that is highly placed by judges in the show ring, and breeders, trainers and owners are encouraged to produce large and well grown youngsters.3
The modern domesticated horse tends to receive concentrated meals of high protein and energy value that together with limited exercise seems to have triggered a failure of insulin function.
When the horse receives a concentrate feed there is a rise in blood glucose levels as the feed is digested and glucose is released into the blood. This is followed by a rise in insulin that controls the amount of glucose uptake by cells and its storage as glycogen (source of energy and stored in muscle and liver) and fat. If there is too much glucose production, then insulin production is unable to keep up.
The basis of the EMS seems to be a failure of cells to respond to even high levels of insulin.
Affected horses can have elevated levels of insulin as the body increases insulin production in the effort to move glucose into cells. Glucose levels too may be elevated. Another culprit driving the condition seems to be the steroids cortisone and cortisol. These hormones have anti-inflammatory effects and also affect carbohydrate metabolism. Significantly, fat is preferentially laid down in the abdomen, where it is known as omental fat. Until recently, it was thought that these fat cells (adipocytes) were just benign stores of energy. However research has shown that adipocytes are in fact active and it appears that the omental adipocytes generate an increase in the level of cortisol. This steroid is instrumental in inhibiting the action of insulin and results in insulin resistance and a degree of hyperglycaemia.1
Equine metabolic syndrome can be compared to Syndrome X or Type 2 late onset diabetes that occurs in middle aged humans and that is increasingly prevalent in children and young people.
Grains or commercial feeds that have a high glyceamic index e.g. maize, barley, wheat, rice, oats, soybean meal, sorghums high protein grass meal and molasses. This causes peaks and troughs of glucose and insulin production. Meals of 5lbs/ 2.5kg incur an increasing risk of insulin resistance,2 and when combined with inadequate exercise or work, pose a problem for certain breeds e.g. ponies, native breeds, warm-bloods and cold bloods. Thoroughbreds are less risk at as they have greater glucose tolerance and greater insulin sensitivity.
To prevent and manage EMS, the diets of young stock are of particular importance. Professor Derek C. Knottenbelt OBE, BVM&S, DVMS, DipECEIM, Philip Leverhulme Equine Hospital, University of Liverpool, says that a healthy young horse (2-4 years) should be slightly thin. The ribs should be clearly visible when breathing in. Any degree of fatness beyond the above may lead to a degree of insulin resistance developing. He states “Young horses should be kept lean and kept active- a young horse left on the hill and fed hay will probably not develop it. The horse that is carefully nurtured, fed an excessive volume of a high glyceamic index ration and given little exercise is probably a high risk horse. Fat horses are welfare issues at least as serious as starved ones…it is cruelty by kindness”.3
If you suspect or your horse is diagnosed with the condition, the recommendations are to feed adlib (if stabled) double soaked hay/chaff i.e. a forage/fibre diet of low nutritional value, and a little vegetable oil,3 ( the metabolic process for the production of energy from oil follows a different pathway to that of glucose), together with a quality mineral and vitamin supplement such as Equilibrate COMPLETE. We also make Specifically Formulated supplements that include Garcinia and magnesium that are helpful. Please use Enquiries.
And ensure your horse receives regular and appropriate exercise!
- Hamilton-Fletcher R (2005) Equine Metabolic Syndrome Horse and Hound 12 May
- Johnson PJ Messer NT and Ganjan VK (2004) Cushing’s Syndromes, insulin resistance and endocrinopathic laminitis. Equine Veterinary Journal 36; 194-198
- Knottenbelt DC (2009) Equine Metabolic Syndrome: What it means to you and your horse? In: Know your horse SAEVA; 75-80
- Treiber KH, Kronfeld DS, Hess TM, Byrd BM, Evaluation of genetic and metabolic predispositions and nutritional risk factors for pasture-associated laminitis in ponies. Journal of the American
‘, ”, ‘full_html’);