Metabolic Syndrome and Obesity in Horses

Equine nutritionists and wise horse owners have long known that obesity in horses is not a good thing. The obese horse often is incapable of performing even moderate tasks without becoming exhausted and, as a result, placing itself in danger of injury.

Now researchers are adding still another dimension to these concerns. That dimension involves laminitis as a result of the condition that has come to be known as equine metabolic syndrome. Researchers have learned that obesity can decrease a horse's ability to utilize glucose (sugar) in the bloodstream after eating grain. That condition occurs when the horse's cells don't respond appropriately to signals from insulin, a hormone, that instructs the cells to take in the glucose that is circulating in the bloodstream. The researchers believe--and are attempting to determine for certain--that often the end result of this process can be laminitis.

One of the leading researchers on equine metabolic syndrome is Philip J. Johnson, BVSc (Hons), MS, Dipl. ACVIM, MRCVS, professor of internal medicine at the University of Missouri's College of Veterinary Medicine. Working as a collaborator with Johnson at the University of Missouri have been Nat T. Messer IV, DVM, Dipl. ABVP, associate professor, and Seshu Ganjam, PhD, professor of endocrinology.

The three have taken issue with a position held by some horsemen and members of the research community that obesity problems in many horses can be traced directly to hypothyroidism (low levels of thyroid hormones) in horses. They maintain that horse owners have wasted millions of dollars by administering hormone therapy to horses suspected of hypothyroidism. In many cases, they say, the horse was suffering from metabolic syndrome and the drugs to combat hypothyroidism have no effect on that condition.

"There might be some value to thyroid supplementation in the short term (one to two months)," says Johnson, "but not likely the life of the horse (with metabolic syndrome). The client should not be told that there is a life-long need for thyroid supplementation or that the horse is affected with bona fide hypothyroidism."

In a paper on equine metabolic syndrome published in the International Journal of Pharmaceutical Compounding (Vol. 7, No. 1), Johnson addressed this matter thusly: "Traditional dogma has led to the misleading diagnosis of 'hypothyroidism' for these obese horses in which laminitis has developed. However, neither obesity nor laminitis develop in adult horses from which the thyroid gland has been removed (experimentally induced hypothyroidism). Moreover, appropriate diagnostic tests for disease of the thyroid axis (thyroid stimulation tests) in these horses (those horses with metabolic syndrome) invariably fails to identify hypothyroidism, and the histopathological appearance of thyroid glands from affected horses is normal. The syndrome has sometimes been erroneously attributed to disordered thyroid metabolism (hypothyroidism), but it is clear that this combination of laminitis and obesity are not manifestations of insufficient thyroid hormone production. Although lowered circulating thyroid hormones may sometimes be demonstrated in these horses, appropriate clinical testing--including a thyroid stimulation test--fails to support the diagnosis of hypothyroidism."

Diet Problems

If hypothyroidism isn't involved in the onset of obesity and, eventually, laminitis, what is? The answer in many cases, Johnson avers, is equine metabolic syndrome, and very often the culprit is the horse owner and the diet he or she designs for the horse. The problem diet frequently consists of a heavy intake of grain without a sufficient exercise regimen.

As the horse becomes obese because of its heavy grain diet, it sometimes also becomes glucose-intolerant and resistant to the action of insulin--referred to as an insulin refractory state.

Glucose intolerance means that there is an inappropriate insulin reaction after a horse consumes food. Normally, the intake of grain by a horse is followed by an increase of glucose or sugar in the bloodstream. The presence of sugar, in a normal horse, stimulates the release of insulin by the pancreas. As the amount of glucose in the blood increases, insulin signals the body's cells to take it in. Once in the cells, glucose is used for energy or converted to fat or glycogen for energy storage. When a horse is insulin-resistant, the normal release of insulin doesn't trigger the correct response from the cells.

What causes some horses to become insulin-resistant? Obesity, says Johnson, is a likely culprit, although there very likely are other mechanisms involved, and there are differences on a horse-by-horse basis.

"Different horses likely start life with different levels of insulin sensitivity," he says. "Those that are born with lower insulin sensitivity will likely have more problems should they be fed over time in such a way that they develop obesity."

Recent research, he says, has forced scientists to re-evaluate the role of fat cells known as adipocytes. In the past, it was thought that these fat cells were nothing more than that--fat cells that store energy--but research is indicating that they are important players in the game involving equine metabolic syndrome.

Johnson explained it this way: "Recent discoveries have forced us to re-evaluate our thinking about the adipocyte. It can no longer be regarded as a simple passive fat storage depot, but as an active and integrated player in the regulation of energy balance in the body that is both sensitive to hormonal and neuroendocrinological signals and is involved in the genesis of important hormonal factors. In this regard, the accumulation of intra-abdominal and omental (the omentum is a fold of peritoneum extending from the stomach to adjacent organs in the abdominal cavity) adipocytes is much more significant than adipocyte accumulations at other locations in the body. Much investigative effort has been expended in search of an explanation as to why and how the development of intra-abdominal obesity tends to cause an insulin refractory state. Many explanations have been proposed, and it is highly likely that more than one mechanism is involved.

"The fact that insulin resistance is directly correlated with weight gain and weight loss suggest a cause-and-effect relationship, rather than a simple association," he continued. "Metabolically active substances are released from adipose tissue and interfere with the action of insulin. Numerous candidate 'factors' have been incriminated for the role of adipose-derived mediators of insulin resistance. There is substantial evidence that free fatty acids represent an important link between the development of obesity and the development of insulin resistance--and type-2 diabetes--in human patients. Excessive fat accumulation (obesity) leads to elevated circulating levels of free fatty acids that cause insulin resistance in skeletal muscle and the liver."

Most discussions about laminitis, says Johnson, have centered on the development of the condition as a consequence of alimentary tract disease and endotoxemia (the presence of endotoxins in the blood). He believes, however, there are a number of laminitis cases that definitely can be traced to metabolic syndrome.

"We have hypothesized," he reported, "that laminitis occurring insidiously in mature, obese horses has a different explanation and may involve different pathways. However, in both scenarios there exists an underlying commonality in that laminitis arises from aberrations in the regulation of blood flow through the lamellae (also called laminae, the leaf-like projections that anchor the hoof to the coffin bone). In obese horses, altered blood flow results from endothelial dysfunction arising from insulin insensitivity and increased vasospasticity (spasming of blood vessels). Obese horses with impaired glucose tolerance are insulin-resistant and hyperinsulinemic (they have too much insulin) and are at increased risk for the development of laminitis."

So the discussion comes full circle. Obesity can lead to equine metabolic syndrome, which involves glucose intolerance and insulin resistance, and those conditions can bring on a bout of laminitis. Is there a pattern in types or ages of horses afflicted with equine metabolic syndrome?

Age Influence

Horses affected are typically between eight and 18 years of age, says Johnson. Pony breeds, Morgans, and domesticated Spanish Mustangs appear to be predisposed to this condition. Also listed in the at-risk category are European warmbloods, Peruvian Pasos, and Paso Finos.

The physical condition of affected horses, according to Johnson, is often characterized as being overweight or obese. In most cases, he adds, the owner denies feeding an excessive amount of grain and declares simply that the horse is an "easy keeper."

Johnson reports that, "Accumulations of subcutaneous (beneath the skin) fat may be particularly evident in the neck, near the shoulders, and in front of the tail head. In geldings, the appearance of the prepuce is abnormal due to the accumulation of subcutaneous fat. The physical condition is typically assigned a 'body score' in the order of 7 to 9."

In most cases, Johnson says, horses found to be suffering from equine metabolic syndrome often are first presented to a veterinarian for treatment a bout of laminitis.

Prevention and Treatment

Prevention is the preferred approach, Johnson indicates. That means feeding a sensible, balanced diet and providing the horse with sufficient exercise to keep it from becoming obese.

Once the horse is afflicted with equine metabolic syndrome, Johnson says, the first step in a treatment approach should be a weight-loss program. This can mean decreased food intake and increased exercise. However, if the horse already has developed laminitis, increased exercise might not be an option in the early going.

"The most important aspect of feeding a horse with metabolic syndrome--especially one suffering from laminitis--is limitation of soluble carbohydrates in the diet," stresses Johnson. "Simply eliminating grain products and the use of a hay-only diet may result in dramatic improvements in laminitis pain within the space of a few days."

Unfortunately, there are no drugs that deliver a quick fix for metabolic syndrome. Two drugs that are utilized in the treatment of Cushing's, says Johnson, are not appropriate for metabolic syndrome.

The two drugs are pergolide and cyproheptadine, both of which tend to suppress the secretion of pancreatic insulin as well as acting on the pituitary gland. Lack of proper function on the part of pancreatic insulin is part of the problem when metabolic syndrome is involved.

Johnson is the first to say that there still is much to learn about metabolic syndrome, but progress by researchers has done much to clear away some of the mysteries about this rather complicated malady.

About the Author

Les Sellnow

Les Sellnow is a free-lance writer based near Riverton, Wyo. He specializes in articles on equine research, and operates a ranch where he raises horses and livestock. He has authored several fiction and non-fiction books, including Understanding Equine Lameness and Understanding The Young Horse, published by Eclipse Press and available at or by calling 800/582-5604.

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