Read my article published in the Aiken Horse

What Could Your Horse’s Cresty Neck Be Telling You?

Holly Bedford, DVM, MS



Do you have a horse with a cresty neck? When you stand to the side of your horse do you see uneven fatty deposits along the hindquarters (especially above the tail head), behind the shoulders, or slightly bulging above the eyes? Do you describe your horse an “easy keeper”? Has your horse had repeated episodes of mild laminitis (founder)? If you answered yes to any of these questions your horse could be at risk for Equine Metabolic Syndrome.

The term Equine Metabolic Syndrome (EMS) was first coined in 2002 to recognize a clinical syndrome in horses that exhibited obesity, tissue insulin resistance, and repeated episodes of mild laminitis. The typical clinical picture in horses with EMS are obesity which may be generalized or regional, appearing as fat pads along the tail head, behind the shoulder, or above the eye sockets. The mammary gland in mares or prepuce (sheath) in geldings are also common sites of abnormal fat deposition. The hallmark sign and the anatomic region where the most clinically significant and metabolically active fat deposition occurs is along the nuchal ligament (neck) giving the classic cresty neck. While obesity is common in horses with EMS, not all overweight horses or horses with cresty necks have EMS and some horses with EMS may appear normal or lean with noticeable fatty deposits in the previously described areas. In addition to obesity, horses with EMS historically have had repeated episodes of mild laminitis that may have been previously attributed to other causes of lameness such as arthritis, sole bruising, or recent foot trimming. Obese horses with a history of repeated episodes of mild laminitis, especially if associated with feeding changes or pasture access that cannot be attributed to any other causes should be evaluated for EMS.

Historically, horses with EMS have been described by their owners as “easy keepers” and it is because of this that for years past horses with EMS were suspected of and treated for hypothyroid (low thyroid hormone). Why horses with EMS have a greater tendency towards obesity remains undetermined. Some researchers suspect that obesity may be related to genetics with EMS horses being more metabolically efficient than non-EMS horses, although level of activity, feeding, and management practices also likely play a role in the development of obesity.

The clinical significance of obesity lays in fat tissue’s function as an endocrine organ. Previously, adipose tissue (fat) was looked upon as an inert storage depot for excess energy. Today, we now know that fat behaves more like an endocrine organ versus simply a storage depot and is responsible for secreting many hormones including adipokines and adipocytokines. These hormones play an integral role in initiating the inflammatory cascade suggesting that obese horses may be in a chronic state of low-grade systemic inflammation.

As mentioned previously, tissue insulin resistance is a key feature in horses with EMS and demonstration of hyperinsulinemia (elevated insulin levels in the blood) supports the diagnosis. The presence of reduced tissue sensitivity to circulating insulin and subsequent high blood glucose liken this condition to type II diabetes in humans. Under normal conditions, insulin is secreted by the pancreas in response to elevated glucose levels in the blood that occurs following ingestion of a meal. Insulin then binds to insulin-specific receptors in body tissues which then facilitates uptake of glucose from the blood into the tissues for energy production. In obese horses, body tissues are not as sensitive to insulin, meaning that they do not respond to insulin’s binding to the receptor, resulting in less uptake of glucose from the blood and subsequently elevated blood glucose levels in blood samples. It has been proposed that the adipokines and adipocytokines secreted by adipose tissue and the state of chronic inflammation may be contributing factors to the reduced tissue sensitivity to insulin in obese horses. Alteration to the normal composition of the insulin tissue receptor negatively affecting insulin’s binding capability may also play a role in decreased tissue insulin sensitivity. The body’s response to combat reduced tissue sensitivity to insulin and high blood glucose levels is to secrete more insulin from the pancreas which produces the hyperinsulinemia (elevated insulin levels in the blood) observed in some horses with EMS.

The link between the presence of excess adipose tissue (fat) and laminitis is not completely understood and continues to be the center of ongoing research on EMS. A key piece to the puzzle may be hyperinsulinemia. Experimentally, laminitis has been induced by intravenous administration of supraphysiological amounts of insulin over 2-3 days in ponies. It has been recognized that insulin has vaso-regulatory effects on blood vessels meaning that the presence of insulin can cause constriction or dilation of blood vessels, including the blood vessels in the horse’s foot which may be the connection between laminitis and insulin resistance in horses with EMS. Activation of the insulin receptor in tissues that occurs following binding of insulin to the receptor leads to activation of two possible pathways resulting in either dilation or constriction of blood vessels. In humans with insulin resistance, studies have shown that the pathway leading to constriction of blood vessels is stimulated, resulting in enhanced blood vessel constriction. The significance of blood vessel constriction in the horse’s foot is an overall reduced blood supply which may deprive laminar tissue in the foot of glucose needed for normal metabolism and cause increased production of free radicals causing oxidant damage and inflammation in the foot leading to laminitis.

The predisposition for laminitis in horses with EMS and the tendency for laminitis to reoccur is why early clinical recognition, accurate diagnosis, and proper dietary management are imperative to preserving long term soundness. Diagnosis is based on abnormal fat deposition present on physical exam, evidence of laminitis on radiographs of the feet, and results of laboratory screening tests. At present, the recommended laboratory screening tests consists of measurement of fasting insulin and glucose which can be obtained from a simple blood draw. Horses with EMS typically have elevated insulin levels; however, normal insulin concentrations have been observed and do not necessarily rule out EMS. Glucose levels are rarely above the normal reference range due to compensatory responses to hyper secretion of insulin, but are typically in the higher end of the normal reference range. In cases where screening tests are inconclusive, dynamic testing is recommended to properly assess tissue insulin sensitivity. Dynamic testing is accomplished by performing a combined glucose insulin tolerance test where a dextrose (sugar) solution and insulin are administered simultaneously and the body’s response is observed over time by serial blood glucose measurements. This is a relatively simple test and following intravenous catheter placement can be completed in an hour at the farm.

Following diagnosis, dietary management and weight loss play an important role in treatment of horses with EMS. Goals of dietary management are to facilitate weight loss in obese horses by reducing the amount of energy provided in the diet and lowering the carbohydrate content of the diet to reduce glycemic and insulinemic responses to meals. Current recommendations are to feed obese horses 1.5% of their “ideal” body weight in hay per day (1.5 lb hay per 100 lb body weight) to facilitate weight loss. If weight loss does not occur within a 30 day feeding period hay amounts can be reduced to 1% of body weight. Ideally, hay with a lower structural carbohydrate level should be selected; however, carbohydrate concentrations in hay can be reduced by soaking hay in water for minimum of 30 minutes prior to feeding. In obese horses concentrates should be replaced with a low-calorie commercial protein-vitamin-mineral supplement (ration balancer) fed in small amounts (0.5–1.0 kg total per day) to balance the low vitamin E, vitamin A, copper, zinc, selenium, and other minerals typically found in mature grass hays . In non-obese horses or horses that cannot be managed on forage alone, feeding low-carbohydrate feeds supplemented with fat such as vegetable or corn oil may be an acceptable alternative to higher carbohydrate feeds.

            Since many horses with EMS have seasonal episodes of laminitis associated with the non-structural carbohydrate content (fructans and starches) of grass, the question of whether it is safe to turn out a horse with a history of laminitis and EMS on grass pastures is a gray area. Initially, restricting pasture access may be necessary to control caloric intake or in cases with active laminitis that require stall rest. A conservative approach to pasture management is to avoid grass pasture until insulin sensitivity has improved (weight loss) because carbohydrates consumed on pasture can trigger gastrointestinal events that lead to laminitis in susceptible horses. Once weight loss has occurred and insulin sensitivity and clinical signs of laminitis have improved turn out on grass pasture may be possible in some horses with EMS, but care must be taken to restrict pasture access when the grass is going through dynamic phases, such as rapid growth in the spring or preparation for cold weather in the fall. The use of grazing muzzles or restricting pasture size or limiting turnout time may be reasonable options. The safest grazing time, in regards to carbohydrate content of grass, is early morning except after a hard frost. Conditions that increase carbohydrate (fructan) content in grass include regular cutting, cool, and bright conditions and predominance of certain grass species such as ryegrass. Unfortunately, despite the best of efforts, some horses with EMS suffer repeated episodes of laminitis when returned to grass pasture and must be confined to dirt paddocks indefinitely.

In addition to dietary control, regular physical exercise is also key to facilitating weight loss, maintaining a healthy weight, and improving insulin sensitivity. Exercise should be included as part of the immediate treatment plan provided that the horse does not have active laminitis. Initially, 2–3 exercise sessions per week (riding and/or lunging) for 20–30 minutes per session is recommended. Over time, the frequency, duration, and intensity of exercise can be increased with the end target of 5 sessions per week.

Most horses and ponies with EMS can be effectively managed by controlling diet, providing regular exercise, and limiting access to grass pasture. In cases where dietary management alone is not enough or exercise is contraindicated weight loss and insulin sensitivity may be improved by use of certain medications, such as metformin and levothyroxine sodium (Thyro-L). Chromium, magnesium, cinnamon, and chasteberry (Vitex agnus-castus) are common ingredients found in over the counter supplements recommended for the management of EMS; however, at this time there is insufficient scientific evidence to support their efficacy in the treatment of EMS.

If you are concerned that your horse may be at risk for EMS, please consult your regular veterinarian for further evaluation, diagnostic testing, and treatment recommendations as the treatment options mentioned here may not be suitable for all horses with EMS.



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