Like any farrier, Matthew Frederick has dealt with his share of laminitic horses.

What sets him apart is that Frederick has done more than just battle individual cases of the disease. Frederick and his wife, Susan Tierney Frederick, have developed a theory on the root cause of refractory laminitis. They have also developed a suggested course of treatment that could offer new hope for horses suffering from refractory laminitis that once had to be put down.

What’s more, while Frederick notes that his study was done on laminitis cases that were refractory — laminitis cases that do not respond to conventional or medical treatment of any kind — he believes the theory actually applies to most laminitic horses. His research caused a stir when it was presented at the Bluegrass Laminitis Symposium last year and continues to attract attention today.

Diabetes In Horses

The Fredericks hypothesize that — in effect — horses with refractory laminitis are diabetic. They believe that laminitic syndrome can be compared to the development of DM2-type diabetes in humans. Insulin resistance is a defining characteristic of DM2 diabetes, and they believe insulin resistance can be found in virtually all of the conditions usually believed to have caused laminitis.

SIGN OF LAMINITIS. This hoof shows sole bruising as well as stretched laminae. Frederick noticed that these signs were often present in horses he found had had “laminitic episodes” after senior supplements were added to their diets.

The Fredericks believe most laminitic horses share this common trait of insulin resistance. They believe that it is most commonly found in conjunction with “Cushing’slike” or “Cushingoid syndrome” — often undiagnosed — in horses.

Successes And Failures

Frederick, an American Farrier’s Association (AFA) Certified Farrier from Napa, Calif., had his share of successes over the years battling laminitis using mechanical approaches such as the Equine Digital Support System (EDSS) designed by Gene Ovnicek. He expanded his own knowledge of the disease by attending the Bluegrass Laminitis Symposium in Lexington, Ky.

But Frederick also had his share of setbacks. Despite what he thought was “proper shoeing,” some horses would refounder. He typically kept severe cases on Styrofoam pads, waiting for them to recover enough to be shod. Sometimes that took a matter of days, sometimes a matter of weeks. Sometimes, the horses never did seem to recover.

Frederick began to ask himself what caused the differences in the recovery times for laminitic horses.

SIGN OF LAMINITIS. These hooves show the hoof wall bruising that is often a sign of laminitis. The hooves are those of a horse included in the Frederick study.

Pieces Of A Puzzle

The first pieces of the puzzle began to fall into place when Frederick noted some common traits in the refractory laminitis cases he saw over the years.

He found that sole bruising and lightly stretched laminae that are indicative of a laminitic episode often followed a change in the particular horse’s diet that involved the addition of a senior supplement to its feed. He also came to realize that when this condition occurred, it invariably involved horses with cresty necks and lumps of fat on the rump and/or neck and withers. Some had a history of foundering on grass and a high percentage of those animals were ponies, Morgans, Arabs or gaited breeds, which Frederick believes had a genetic disposition toward the development of Cushing’s syndrome and laminitis.

The Fredericks began to look for a “common pathway” to laminitis. They began their search with an informal field study of 43 laminitic horses, of which 22 were refractory (meaning they had been displaying continuing acute laminitic symptoms for 3 to 7 months).

SIGH OF LAMINITIS. This hoof is from another horse in the Frederick study. It shows sole bruising, stretched laminae and a seedy toe. All three are tell-tale signs for laminitis. Frederick, a farrier from California, believes that most cases of laminitis can be traced to insulin resistance.

Ellie’s Case

One of the subjects of that study was Ellie, a 12-year-old Morgan mare. Ellie had been suffering from refractory laminitis for 6 months when Frederick first saw her in September, 1998. The horse had a pronounced genetic tendency toward Cushing’s syndrome (her sire, dam and a number of siblings and half-siblings had been destroyed after developing refractory laminitis, secondary to Cushing’s syndrome). But a negative serum glucose test had caused a veterinarian to say she did not have Cushing’s herself.

When Frederick began to work on Ellie’s case, a new vet, Tom Casselberry, decided to retest for Cushing’s based on the mare’s family history. Frederick kept Ellie’s feet on Styrofoam while awaiting lab results and eventually shod her with EDSS shoes. Ellie seemed to make good progress for about a week, then her laminitis worsened.

When the lab results returned, Ellie’s serum glucose was 215 (normal is 75-115) and her ACTH level was 37.5 (normal is 10 to 32.7). Both readings suggested Cushing’s and Casselberry put the horse on Permax (pergolide mesylate), a drug that has been used successfully in controlling symptoms of Cushing’s syndrome, including laminitis, in ponies and horses.

Ellie quickly showed improvement and went home sound and was back pulling a cart by June of 1999.

HORSE IN TROUBLE. Farrier Matt Frederick with Rosie, a 5-year-old paint mare. Rosie was suffering from severe refractory laminitis in 1997 when this photo was taken. She was a “sinker” and was unable to stand for more than a few minutes a day for 3 1/2 months.

What Does It Mean?

The Fredericks and Casselberry reasoned that if they had not retested for Cushing’s, they never would have treated Ellie with Permax. The next step was to wonder if other cases of refractory laminitis were due to undiagnosed cases of Cushing’s. If such was the case, other horses might benefit as dramatically as Ellie had from the drug.

They began a process of “looking for Cushing’s” in other horses by testing for glucose and ACTH levels. Many of the horses did test positive. In those cases, if the laminitis was refractory, the horses were started on Permax.

But while they thought they had found the key to part of the laminitis puzzle, some of the tests done on horses that were laminitic came back without the elevated readings that are indicative of Cushing’s.

The Fredericks persuaded veterinarians to try Permax experimentally on a group of 10 horses with refractory laminitis that had not tested positively for Cushing’s. The vets agreed, as there was virtually no other hope for any of the horses. All 10 horses exhibited the same kind of dramatic improvement that Ellie had.

LAMINITIS COMPLICATIONS. Frederick kept Rosie on Styrofoam when he first began treating her. The horse was severely underweight and was suffering from pressure sores from 5 to 6 months of refractory laminitis.

A Unification Theory

The Fredericks believe that most cases of refractory laminitis are in fact Cushingoid or undiagnosed Cushingoid cases, and will respond to treatment with Permax and strict diet control.

They begin by drawing on research by Australian equine veterinarian, Dr. Christopher Pollitt. Pollitt’s research suggests that all of the apparently disparate causes of laminitis might be attributed to altered glucose metabolism. In Pollitt’s invitro studies, hoof samples which were not deprived of glucose remained intact, while those deprived of glucose separated.

This suggests that the lack of glucose, or its improper matabolization, might cause matrix metalloproteinases to be activated, causing the dissolution of the basement membrane of the hoof and the separation of the dermal laminae from the epidermal laminae.

Frederick reasoned that lack of glucose to the peripheral tissues can be caused by insulin resistance (a lack of normal response to insulin by insulin-sensitive cells). Insulin must be produced in adequate levels and function properly for the cells to utilize glucose.

COFFIN BONE PENETRATION. Laminitis had reached the stage where Rosie’s coffin bone had penetrated the sole.

How It Works

The Fredericks believe that a model for laminitis would be insulin resistance secondary to hypercortisolemia. Hypercortisolemia is an abnormal excess of cortisol caused by a reaction to other increased hormone levels due to a benign tumor on the pituitary gland in Cushingoid horses.

High levels of cortisol disable insulin, with the result that the cells cannot utilize glucose. Permax is effective, because it works by lowering the increased hormone production from the pituitary gland, thus lowering cortisol levels, in turn allowing insulin to regain its function and the cells to correctly utilize glucose.

The model would be different for Peripheral Cushing’s, recently proposed by University of Missouri researchers Dr. Philip Johnson and Dr. Nat Messer. In Peripheral Cushing’s, excess amounts of cortisol are produced in the peripheral tissues rather than in the blood. This is not caused by a tumor on the pituitary gland but by an excess of the enzyme which converts inactive cortisone to active cortisol.

BACK ON HER FEET. Rosie being ridden in August, 1998. The horse made a remarkable recovery from refractory laminitis. Farrier Matt Frederick believes that the same course of treatment that helped Rosie can help many other laminitic horses.

Other Causes

While the Fredericks believe many refractory laminitis cases are, in fact, undiagnosed cases of Cushing’s, they know there are other conditions that researchers have associated with laminitis. But they believe that research also indicates insulin resistance is a common factor present in many of these conditions, including:

DUAL-APPROACH TREATMENT. Farrier Matthew Frederick believes a treatment based on shoeing a laminitic horse with a system such as the Equine Digital Support System shoe show here and putting the horse on Permax (pergolide mesylate) and strict diet control offers new hopes for horses suffering from refractory laminitis.

• Carbohydrate overload
• Retained placenta
• Endotoxemia/exotoxemia
• Foal founder
• Severe systemic illness or infection
• Exogenous steroids
• Laminitis as a complication of surgery

The Role of Genetics

The Fredericks believe most horses in the study responded to Permax because their laminitis is due to insulin resistance. They believe “susceptible” horses (predominantly Arabs, mustangs, ponies, Morgans and related gaited breeds, such as Paso Finos, Saddlebreds, Tennessee Walkers, Foxtrotters, Icelandics, etc.), have an inherent degree of insulin resistance; a “thrifty gene.”

This gene (which could achieve its goals by altered secretion or metabolism of cortisol) insured that, in times of plenty, excess consumed glucose would be stored as fat to be drawn upon during leaner times (harsh climatic conditions, famine, etc.).

This predisposition would be an advantage in the wild, but becomes a problem in captivity. Well-meaning owners give the animals virtually unlimited access to rich pasture, concentrated carbohydrates in the form of grain and “complete feeds” and various supplements.

SIGN OF CUSHING’S SYNDROME. This horse displays the cresty neck associated with Cushing’s Syndrome and the subsequent development of laminitis. Farrier Matthew Frederick believes that most horses who develop refractory laminitis are in fact “Cushingoid,” even though the condition may be undiagnosed. He believes that insulin resistance is the underlying cause of most laminitis cases.

Spring Grass And Founder

The Fredericks also believe this inherent insulin resistance could explain grass founder. They believe that only horses and ponies that are Cushingoid, whether diagnosed or undiagnosed, would be at risk for grass founder.

They theorize that this insulin resistance could be exacerbated by any feed that could cause a glycemic response. They believe that this response could be caused by a diet of spring grass because its high levels of carbohydrates with high levels of protein and fructose react with already high cortisol levels.

Another possible explanation for the glycemic response to spring grass draws on research by Annette Longland and Andrew Carins in Wales.

The Welsh research indicates spring grass is high in fructan, a complex carbohydrate made up of linked molecules of fructose. They believe that resident flora in a horse’s hindgut may be capable of fermenting the fructan, setting off the chain of events that leads to laminitis.