Insulin Resistance: How to diagnose and deal with this common disorder
This article first appeared in EQUUS magazine.
How a common but little-known condition similar to Type II diabetes triggered a painful and frustrating episode of laminitis.
Some years ago, when my then 7-Year-old Morgan gelding foundered for no apparent reason, I was determined to find out what had caused the painful and frightening episode that left him unrideable for nearly a year. In the course of my research, I was surprised to discover that a common but at the time little-known condition called insulin resistance (IR), which is similar to Type II diabetes, had triggered his laminitis. I also learned that my horse had been exhibiting the classic signs of IR for some time, and had I recognized those signs, the whole devastating experience could likely have been avoided.
Thinking back, it was clear that Gryphon, although never truly obese, was an easy keeper who could put on weigh very quickly, even on a diet consisting of nothing but pasture, grass hay and a token handful of pelleted grain when the other horses got their rations. When Gryphon did bulk up on the lush spring grass each year, the weight was most noticeable in the crest of his neck and in pads of fat that formed behind his shoulders and around the tail head. However, with his sturdy Morgan build and naturally strong, arched neck, his annual weight gain of about 100 pounds didn't seem like anything drastic, especially as I knew he would lose it again over the winter.
Even so, I had heard that overweight, cresty necked horses were more prone to founder, so I made an effort to pull him off the pasture early each day, especially as my own bad back prevented me from giving him as much exercise as I would have liked. He seemed healthy and happy but was always ravenous, never pausing for a breather when he was on pasture and cleaning up every last wisp of hay he could get.
How a common but little-known condition similar to Type II diabetes triggered a painful and frustrating episode of laminitis.
Some years ago, when my then 7-Year-old Morgan gelding foundered for no apparent reason, I was determined to find out what had caused the painful and frightening episode that left him unrideable for nearly a year. In the course of my research, I was surprised to discover that a common but at the time little-known condition called insulin resistance (IR), which is similar to Type II diabetes, had triggered his laminitis. I also learned that my horse had been exhibiting the classic signs of IR for some time, and had I recognized those signs, the whole devastating experience could likely have been avoided.
This horse is obviously obese, with a cresty neck and fat pads around the tail head that indicate insulin resistance. This horse should NOT be on grass. |
Even so, I had heard that overweight, cresty necked horses were more prone to founder, so I made an effort to pull him off the pasture early each day, especially as my own bad back prevented me from giving him as much exercise as I would have liked. He seemed healthy and happy but was always ravenous, never pausing for a breather when he was on pasture and cleaning up every last wisp of hay he could get.
The winter before Gryphon foundered, a veterinarian suggested that I put my horse on injectable glucosamine sulfate as a prophylactic measure to prevent arthritis, which she felt he would be prone to due to the overly straight conformation of his hocks. I began giving him a monthly 10cc injection, never suspecting that his body was unable to properly process glucosamine and that this inability would contribute to an episode of acute laminitis. The day after his June shot, Gryphon was dead lame. X rays confirmed that he had foundered, with rotation in both front feet, though thankfully the rotation was not severe.
I was baffled because I had managed to keep him slimmer than he had been the previous two springs. He had not gotten into any grain and he was out on the same pasture that he had been on every single day for the past several years. If the veterinarian was right and the spring grass was the cause, why hadn't Gryphon foundered before? If the veterinarian was correct in thinking that my horse's weight was a factor, why didn't the episode occur when he was much heavier the year before?
Thus began my search to find answers. Like many people these days, I turned to the Internet and was fortunate to find Kathryn Watts, a forage researcher, and Eleanor Kellon, VMD, an expert on insulin resistance and related disorders, whom I credit with putting my horse on the road to recovery. Through them, I was greatly relieved to learn that insulin resistance is quite manageable in most cases and that making certain changes, primarily in Gryphon's diet and exercise regimen, would help him to avoid another episode. Gaining insight into the nature and prevalence of the condition also helped me to better deal with how it was affecting my horse. Here is what I learned.
What IR is, who it affects
Insulin resistance, sometimes referred to as equine metabolic syndrome, occurs when certain cells in the body have reduced sensitivity to the action of the hormone insulin. A major function of insulin is to clear glucose from the bloodstream and deliver it into cells that need it for fuel. When this function is hampered, the body compensates by having the pancreas secrete more insulin, which leads to elevated levels in the blood (hyperinsulinemia). Glucose levels may be slightly to moderately elevated (hyperglycemia) as well.
Insulin resistance is most commonly seen in horses age 6 and older, but it can appear at virtually any age, in either sex. The consequences of the condition are varied and complex, but the most dangerous and most common is laminitis. The mechanisms by which IR triggers the condition are not completely understood; because little research has been done, veterinarians often turn to the scientific data that exist for other species. In addition to laminitis, horses with IR can manifest many of the same signs reported in people, including:
- exercise intolerance
- poor muscular development
- ravenous appetite
- fertility problems in females
- excessive thirst
- excessive urination
- easy weight gain.
This last factor is particularly important because fat tissue plays a key role in insulin resistance. Recent research has shown that fat cells (adipocytes) produce a host of hormones (adipokines) that have significant effects. Some adipocytes convert the inactive metabolite cortisone into active cortisol--a recognized factor in the development of IR and laminitis. Many adipokines hamper the action of insulin and thus contribute to the condition. It's fair to wonder, therefore, whether excessive fat causes IR, or if IR causes horses to get fat. "It's probably both," says Kellon. "Data from many species, including horses, show that obesity leads to insulin resistance or at least a decrease in insulin sensitivity, and that even small weight losses can reduce insulin resistance. However, ponies are more often insulin resistant than full-size horses, and there appears to be a significant difference among horses by breed, which indicates a genetic predisposition. All of this needs further study, but most IR equines have a tendency for easy weight gain once mature."
According to Kellon, although horses of virtually any breed can become insulin resistant, breeds that appear to show a higher tendency include Morgans, European warmbloods, American Saddlebreds, Arabians, domesticated Spanish Mustangs, Peruvian Pasos, miniature breeds, donkeys, mules and various types of ponies. Many of these breeds developed in areas where environmental conditions favored the survival of those that could get by on very little sustenance. This has led some to theorize that IR is not so much an illness as an adaptation that becomes a problem only when such horses are fed too much or the wrong things. Philip J. Johnson, BVSc, MS, MRCVS, is a researcher at the University of Missouri-Columbia who specializes in laminitis and endocrinology. He believes that current horse keeping practices are increasing the incidence of IR. "Under the constraints and luxuries afforded by contemporary management practices, domesticated horses tend to be fed rations that are broadly excessive with respect to the metabolic requirements for the level of physical activity to which they are subjected," he says. Ironically, he also points out that starvation can induce IR, as can stress, inflammation, an excess of the hormone cortisol and drugs such as dexamethasone, which
mimic the action of cortisol.
Physical clues of insulin resistance
Horses with IR may be obese and their body fat often is abnormally distributed. This is usually seen in the crest of the neck, which becomes thickened and hard, and in spongy "pads" on the body, most commonly behind the shoulders, around the tail head and at times in the sheath of males. Some horses may exhibit "fullness" above the eyes from fat accumulation there. Visible changes in the hoof, indicative of laminitis that has existed for some time, also are common with insulin resistance. These include prominent growth lines, growth lines that are further apart at the heels, and a flat or convex sole, all of which often go unnoticed until a horse becomes severely lame with a flare-up of acute laminitis. X rays usually confirm that the condition, though appearing to be sudden in its onset, has existed for months or even years.
In addition, horses with Cushing's disease (formally known as pituitary adenoma) frequently are insulin resistant. The most characteristic sign of Cushing's is an unusually long, shaggy, sometimes wavy coat that often fails to shed properly. Other signs include lethargy, laminitis, excessive drinking and urination, a loss of muscle mass (especially along the topline and rump) and a potbellied appearance. Though not all horses with
Cushing's are insulin resistant, a current theory suggests that chronic and severe IR may cause the disease in horses with a certain genetic makeup.
Testing and treatment
Insulin resistance in horses can be determined through a series of tests involving either injectable insulin and glucose or the oral administration of glucose followed by the drawing of multiple blood samples. However, for practical purposes a veterinarian can test a single blood sample for insulin and glucose levels. Ideally, the horse will not have eaten for eight to twelve hours or at least not have eaten anything that could elevate blood glucose (such as grain) for at least five hours prior to testing.
The most effective way to treat and prevent insulin resistance is through diet and exercise. Because the condition most often is discovered as a result of acute laminitis, exercise may not be possible initially, but significant improvements can be achieved with appropriate dietary management. The primary goal is to reduce the levels of sugar and starch by eliminating all grain products, including oats, corn, barley and wheat bran in any significant amount. Check the ingredients label of pelleted feeds and supplements to determine whether they are made of grain or grain products. Feedstuffs that contain sugar or molasses are out, too, unless the sweet coating can be rinsed off. It's also necessary to stop feeding apples and carrots. Even in small amounts, these seemingly healthy treats contain enough sugar to trigger problems in some IR horses.
In most cases, it's also best to keep insulin-resistant horses from eating grass. This may seem like heresy, considering that horses evolved to graze grass, but the lives of modern-day domesticated horses bear little resemblance to those of their ancestors. In addition, many pasture grasses have been designed to have high sugar content so they are better able to withstand heavy grazing, as well as to promote weight gain and increase milk production in beef and dairy cattle. Such grasses and the hays made from them are bad news for IR horses.
Starches that accumulate in plants also pose a threat, so it is important to look at the overall level of nonstructural carbohydrates (NSC), which is the total percentage of sugars and starch. According to Watts, NSC can be extremely high at times when you least expect it. "I have some recent data that show that even dead winter grass can have dangerous levels of NSC if there wasn't enough rain or snow to leach out the sugars," she says. Watts emphasizes that grasses stressed from drought, overgrazing or low fertility often contain the highest NSC, and that sugar levels in grass can fluctuate from morning to afternoon and in response to nighttime temperatures.
Eliminate sugar, supplement with care
The cornerstone of a good IR diet is a low-sugar hay, ideally with NSC at 10 percent or less. Unfortunately, it is impossible to estimate the NSC or overall nutritional value of hay by its type or appearance, so it must be analyzed. Current hay testing protocols will allow you to look at the ESC (sugar) and starch: add those two together and you want a figure of less than 10% in the "as fed" column. There are, however, some general guidelines that may help until you can get your hay tested. According to Watts, "Hays made from grain crops tend to be very high in NSC. Wheat, rye, barley and oat hay are high in sugar, especially when cut just before the heads form. Any kind of grass can have high sugars under certain conditions, but perennial rye, fescue and brome generally show the highest numbers in experiments done to purposely increase NSC. These may have acceptable NSC if managed for optimum growth. The lowest-sugar hays tend to be Bermuda and other warm-season grasses grown in cloudy, humid climates. Native prairie hay is often low, unless it is cut under drought stress." If you can't find low-sugar hay, it's possible to reduce the sugar content by soaking it. Watts' research has demonstrated that soaking hay in room-temperature water for an hour removes an average 30 percent of the sugar, with a similar reduction in hay soaked in hot water for 30 minutes. The percentage decreases in colder water but can still be significant. If you do soak your hay, feed it soon enough to prevent mold growth, which can happen quickly during warm weather. And if you choose a high-sugar hay, it's wise to dry a sample after soaking and retest the sugar, because some hays do not show a decrease after soaking.
Another staple of an IR diet is beet pulp, preferably a brand with no molasses added. If your beet pulp contains molasses rinsing, soaking and straining it will remove the substance. Beet pulp is low in soluble carbohydrates, giving it a low glycemic index (GI). The GI is a ranking of carbohydrates based on their immediate effect on blood glucose levels. A low GI food causes little if any rise in blood glucose, while a high GI food, such as corn, causes blood glucose to spike. Studies have shown the GI of beet pulp to be essentially zero, making it an excellent choice to replace as much as 40 percent of a horse's daily hay intake, at a rate of approximately one pound (dry weight) of beet pulp per 1.5-2 pounds of hay. However beet pulp is high in calcium, so Kellon recommends adding either two ounces of no-calcium-added rice bran per pound of beet pulp, or a teaspoon of monosodium phosphate to keep the calcium-phosphorus ratio balanced. For horses whose IR is not well controlled, omit the rice bran or feed no more than two ounces per day.
The mineral content of a horse's ration is another important aspect of the IR diet. According to Kellon, there is considerable evidence linking insulin resistance with certain dietary imbalances and deficiencies of key nutrients including magnesium, zinc, vitamin E, chromium, calcium, vitamin C, vitamin D and essential fatty acids. Kellon explains that supplements alone are not enough to reverse the effects of IR, but they can help when used in conjunction with an appropriate overall diet. To ensure that an IR horse's ration is supplying the nutrients he needs, first have his hay analyzed for mineral content. Then consult with a reputable equine nutritionist to get appropriate recommendations on mineral supplementation. Determining the amounts of these vital ingredients is complex: The total amount of each mineral is significant; equally important is the ratio of each one to the others because of the way they interact. To know which minerals need supplementation, and in what amounts, it's necessary to know how much is present in the diet .
The benefits of exercise
If an IR horse is sound enough to exercise, it's wise to make every effort to get him moving on a daily basis, as even moderate exercise has been shown to decrease insulin resistance. Barry Fitzgerald, BSc, PhD, a researcher at the University of Kentucky, explains that proteins produced during exercise may help. "Although controversial, there is growing support that proteins secreted by muscle cells sensitize peripheral tissues, primarily muscle and adipose, to the action of insulin. If a similar relationship can be demonstrated in the horse, it may explain why exercise without weight loss is sufficient to increase insulin sensitivity." Regardless of the mechanism, it has been known for some time that exercise stimulates the uptake of glucose by muscle cells using mechanisms that do not require insulin.
I n contrast, forced exercise is never a good idea for horses with acute laminitis. In these cases excessive movement places increased stress on already compromised feet, increasing the potential for serious damage.
I am glad to relate that Gryphon is doing well, thanks to the information I accessed on the Internet, and to my veterinarian, who had the grace to admit what he didn’t know, and the willingness to consult with an expert regarding diagnosis and treatment options. It now appears that my horse’s laminitis was likely triggered by eating drought-stressed grass, as well as the glucosamine injection – both of which could push an IR horse over the edge.
I am glad to relate that Gryphon is doing well, thanks to the information I accessed on the Internet, and to my veterinarian, who had the grace to admit what he didn’t know, and the willingness to consult with an expert regarding diagnosis and treatment options. It now appears that my horse’s laminitis was likely triggered by eating drought-stressed grass, as well as the glucosamine injection – both of which could push an IR horse over the edge.
Gryphon is now on a strict IR diet of low-sugar hay, beet pulp, and minerals custom blended to supplement our hay, which was analyzed and found to be deficient or excessive in a number of key minerals (a very common finding). It is frustrating for me to have to keep him out of the pastures where all his friends play and graze, but it's much better than watching him suffer the agony of laminitis again.
SUPPORT
The Cushing’s List
Started by Robin Siskel in 1999 and now co-owned and managed by Eleanor Kellon, VMD, the website known as the Cushing’s List
(http://groups.yahoo.com/EquineCushings) is a source of information and support for those whose horses have been diagnosed with Cushing’s disease, insulin resistance or laminitis. Siskel formed the list as a way of exchanging research and medical information with other owners of horses with metabolic disorders. In 1994, her beloved mare, Tina, was diagnosed with Cushing’s disease. "I never dreamed our little group would turn into such a wonderful resource,” Siskel says, “but we now have thousands of members from around the world. Many are owners with ailing horses, but we also have researchers, veterinarians, and other equine health professionals who have joined to learn and contribute.” After signing onto the list, which is free, members can ask questions of each other and of experts. Among the sites most popular features are the extensive “files” section, with articles ranging from the lay-friendly to the extremely technical, as well as numerous member success stories.
Thanks for reading! If you would like to be notified when new articles are added to this blog, just click the "follow" button on the upper left part of any page.
Thanks for reading! If you would like to be notified when new articles are added to this blog, just click the "follow" button on the upper left part of any page.