While reorganizing my collection of old veterinary books recently, I began to wonder: When did grass become dangerous for so many horses and ponies to eat?
Many of these books had been given to me by my clients over my 45 years of veterinary practice, and I had not revisited many of them since the discovery of the role of insulin as a cause of laminitis in horses with equine metabolic syndrome (EMS) or pituitary pars intermedia dysfunction (PPID, Cushing’s disease). I began re-reading sections regarding laminitis in each book, interested in seeing what was written years ago in light of the information we now have about the causes of the condition.
I started with G.H. Dadd’s The Modern Horse Doctor, published in 1854, and then moved on to books and journals from the early 20th century. I was particularly interested to see the laminitis risk factors listed by past authors. To my surprise I found no discussion of an association between the disease and eating grass in any of my old books. Nor did I find any mention of overweight animals with cresty necks being prone to laminitis.
I then expanded my search, exploring other older veterinary documents and texts at the University of Missouri’s historic Veterinary Medical Library with the assistance of Trenton Boyd, the library’s curator. What a revealing journey this proved to be!
In the 19th century literature, I found very detailed lists of laminitis causes, but eating grass is not one of them. The laminitis that our forefathers dealt with was often associated with concussion to the feet, the stress of exhaustion or a diet high in barley, corn or wheat. The horsemen of old knew that mares with retained placenta could develop laminitis and that the condition might occur after a high fever. Further, the texts warned that a horse with a severe leg injury could develop laminitis in the opposite limb if a sling was not used to support his weight.
In other words, the century-old veterinary literature describes two forms of laminitis that are well understood today. There are accounts of what we would call inflammatory laminitis—the intense pain and massive swelling of the laminae that occur in the wake of systemic illness, ingestion of toxic plants or excessive concussion to the feet. Likewise, horsemen of yore were aware of the condition that today is known as supporting-limb (or weight-bearing) laminitis, which results from mechanical stress—usually on the limb opposite one that has sustained a severe injury.
But there is no mention in the old literature of the endocrine form of laminitis, the type most commonly seen today. Linked to elevated levels of insulin in the blood, this type is usually seen in horses with EMS or PPID. It tends to develop slowly and causes soreness in the feet but not necessarily the severe pain associated with acute laminitis. (For more information, see “Pathways to Laminitis,” page 60.)
Did veterinarians of that era simply not recognize this kind of laminitis? Or was it so rare that it wasn’t mentioned?
The first reference to grass as a cause of laminitis I found in U.S. literature appears in Keeping Livestock Healthy: Yearbook of Agriculture 1942, which alludes to “the overeating and consumption of green foliage.” Until then, there are no references to this form of the condition. What changed?
Based on my review of historical texts, my four decades of experience as an equine veterinarian and clues found in more recent laminitis research, I believe three areas of change may account for the emergence of grass as a common cause of laminitis: the horse itself, the grass he eats and the soil the grass grows in.
Soils & Men: Yearbook of Agriculture 1938 presents a very complete description of the condition of the soil in the United States at that time. The authors write, “Within a comparatively short time, water and wind have flayed the skin off the unprotected earth, causing widespread destruction, and we have been forced to realize that this is the result of decades of neglect.”
The state of the soil had been compromised by farming practices of the era as well as the economic stresses on agriculture during the Great Depression. The authors advocated investing in the improvement of the soil in hopes that the resulting increase in productivity would enhance the general state of the rural farmers. “Most people will agree that the broad underlying purpose guiding the use of soil resources should be to maintain the highest possible standard of living for the people of the United States,” the authors wrote.
The Yearbook chronicles a revolution in agriculture. Previously, most farmers had used manure as fertilizer, but a byproduct of armaments production brought about a major change in the methods for improving the soil. Prior to World War I, the nitrogen needed to make explosives as well as fertilizer was mainly obtained through mining. But in the first decades of the 20th century, scientists developed a process that allowed for production of synthetic ammonia on an industrial scale. Then, after the war, plants that had manufactured explosives began producing fertilizer. “So far as the three chief fertilizer materials—nitrogen, phosphorus, and potassium—are concerned, the situation in the United States has changed remarkably since the World War [World War I],” noted the Yearbook’s authors.
Application of ammonium nitrate fertilizer increased annually from 5,000 tons in 1928 to 38,000 tons by 1936. Advances in the methods to treat superphosphate with ammonia produced ammoniated superphosphate, a nitrogen phosphate fertilizer which was now the cheapest form of nitrogen for farmers. Cheap and effective fertilizers led to dramatic increases in crop production—U.S. farmers could feed the world, they said!
But for all of these benefits, this change in the soil has not been so good for a certain genetic subset of horses and ponies. The metabolism of these horses is geared for living on sparse grass and walking a lot—expending energy—to find enough to eat. Today’s fertilized fields and pastures produce a much greater quantity of grass that provides far more nutrients than these horses need or in fact can cope with—putting them at risk of laminitis.
In veterinary literature from the United Kingdom, I found clues that a similar phenomenon occurred across the Atlantic even earlier. A 1900 British Veterinary Journal, in discussing chronic laminitis, contains this reference: “It is, however most commonly seen in fat horses and ponies that have little or nothing to do, and have been put in too good a grazing pasture.”
Did the phrase “too good a grazing pasture” mean that the British were improving their soils long before American farmers? Delving a little further, I had my answer: The use of fertilizer in the United Kingdom began with John Bennet Lawes, an English entrepreneur, who investigated the effects of various manures on plants growing in pots in 1837. A year or two later the experiments were extended to crops in the field. In 1842, Lawes patented an “artificial manure,” creating the first inorganic fertilizer by treating phosphates with sulfuric acid.
Within 60 years, the use of inorganic fertilizer was common in the United Kingdom. In short, British farmers started using fertilizer long before the practice was adopted in the United States, and subsequently “grass laminitis” was recognized in the United Kingdom that much earlier than in this country—some 40 years before it was reported in the 1942 USDA Yearbook.
I would also note that when feral horses in the United States grazing on unimproved grassland in the West are examined, no evidence of “grass laminitis” is found. But my personal observations—and that of many of my colleagues—of mustangs or BLM (Bureau of Land Management) horses adopted and moved to Missouri showed a high tendency to develop grass laminitis after arriving. Is this from eating the improved domestic pasture? No study has been done to measure any potential hormonal changes, but these horses develop the characteristic cresty neck and rings on their feet that are associated with elevated insulin levels prior to showing lameness from laminitis. Are soil changes responsible for the increased incidence seen on “improved” pasture? Animals derive nourishment from the soil, and the soil affects the composition of all the food grown on it.
In addition to the composition of grass grown on “improved” (fertilized) soils, the grass plant itself has been transformed through selective breeding and genetic modification. The result is a grass with higher sugar content. Sugar increases palatability for increased consumption for rapid weight gain in cattle. Most USDA grass research is focused on livestock—cattle, sheep, hogs and goats. But little horse-related research is done on grass. Therefore, the hay we feed our horses has not been designed for them.
Much attention has recently been given to the nonstructural carbohydrate (NSC) (starch and sugar) content of hay. Higher levels of NSC are associated with increased levels of insulin and the development of laminitis. Native grasses are lower in NSC and would seem a better choice for horse owners because they are considered safer for horses to eat. But native grass is difficult to grow because it cannot compete with the newer grasses like fescue. In many instances, attempts by horse owners to grow a native pasture have been met with frustration and failure.
In the last 100 years, the lifestyle of the average horse has gone from one of hard work to one of pampering and relative inactivity. Many modern horses are overfed and overweight. Under natural conditions, a horse would normally lose a little weight in the winter as his body uses the fat stored during the summer for energy. But owners often feed more during the winter, while providing blankets and shelter. In fact, many domestic horses actually gain weight in the winter and come into the spring overweight. This is the opposite of what nature intended.
Most horses—even if they are overweight—have normal insulin levels and can eat the lush spring grass without peril. However, if your horse is in a particular genetic subset, signaled by a cresty neck and a tendency to gain weight, he will have abnormally high insulin levels and will be at risk of developing laminitis on spring grass.
The latest research shows horses in this genetic subset are likely to have elevated resting insulin levels. Compared to their normal peers, these horses respond to a small dose of oral sugar with higher insulin levels that remain elevated for a longer period. And when they receive a diet high in nonstructural carbohydrates they often develop laminitis, but not always—it’s as if a piece of the puzzle is still missing.
A new area of study is hormones called incretins that are produced in the GI tract. When they enter the bloodstream, incretins act as messengers, traveling to the pancreas to trigger the release of insulin and to the liver to delay the destruction of cir-culating insulin. Interest in incretins intensified when reduced insulin levels were observed in people who underwent gastric bypass surgery, often within days of the procedure. The surgery is thought to limit the production of these incretins in people.
In addition, a paper recently published by Melody de Laat, BVSc, PhD, and Martin Sillence, PhD, of Queensland University of Technology in Australia showed a significant elevation in an incretin hormone in ponies with EMS, compared with normal ponies, after they were fed a diet high in carbohydrates. Blocking this pathway using an incretin inhibitor may provide a new treatment for EMS by reducing insulin levels.
This observation has also sparked investigations into the bacteria living in the GI tract, also called the microbiome. Changes in the human microbiome are associated with fluctuations in blood levels of insulin and glucose. A recent study showed the drug Metformin, which is used in people to lower blood sugar, caused a dramatic increase in one type of the bacteria in the GI tract. This drug is also used in horses but is known to be poorly absorbed by the horse’s circulatory system, raising questions about its effectiveness. But many clinicians feel Metformin helps reduce insulin levels. Perhaps its effect in the horse occurs inside of the intestine and does not require absorption into the circulation to be effective.
Research is just beginning to look at the horse’s microbiome—and most interestingly at its relation to insulin and glucose metabolism and laminitis. Questions regarding the effect of changes in the soil and the grass on the bacterial population inside the horse’s GI tract may shed light on the cause of this form of laminitis. New methods of studying the DNA of the bacteria in the GI tract have recently become more affordable, making this research possible, but funding is still needed.
So the answer to the question “When did grass become so dangerous for your horse?” is perhaps when man started significantly changing the soil and grass in the 1930s. If we have created this disease, “endocrine laminitis,” we should be able to fix the problem and return these horses to normal health. Understanding just how this occurs will be crucial to finding the solution.
About the author: Donald M. Walsh, DVM, is the founder of the Animal Health Foundation (www.ahf-laminitis.org), a nonprofit organization dedicated to funding research into causes, treatments and prevention of laminitis in horses. Now retired, he is the director of clinical research at Homestead Veterinary Hospital, a large- and small-animal practice he founded in Villa Ridge, Missouri. He received his veterinary degree from the University of Missouri–Columbia.
This article first appeared in EQUUS issue #463, April 2016.