Fructan Possible Key to Laminitis

Common "grass founder," the bane of fat ponies and aged broodmares, might be the key to understanding the bigger picture of systemic laminitis according to a recent study completed by Christopher C. Pollitt, BVSc, PhD, of the Australian Equine Laminitis Research Unit at the University of Queensland. Pollitt presented 10 seminars on the role of fructan in laminitis across Europe in early March of 2002.

Karen Hinckley, PhD, of the University of Sheffield, proposed in 1997 that fluctuating fructan (a water-soluble carbohydrate) levels in pasture grass was a factor in developing grass founder. Pollitt took note of this and the subsequent work of Longland & Cairns of the Institute of Grassland & Environmental Research, Aberyswth, UK, and spent two years confirming that fructan does directly cause laminitis by disrupting the balance of microflora in the equine hindgut. At sufficient doses, the fructan induces digestive upset and will cause an uncontrolled activation of MMPs (matrix metalloproteinases; these enzymes are thought to be a factor in laminar degradation), triggering laminitis.

"In preliminary trials, we have induced mild laminitis by administering commercially available fructan," Pollitt reported. "A dose of 7.5g/kg (of body weight) results in laminitis 48 hours later; (this is) one-half the amount of starch (such as found in sweet feed) required to induce laminitis.

"The animals developed a fever and diarrhea, just as they do with the starch induction model (veterinary science's usual method of inducing laminitis for research), but without colic. By 36 hours, the animals' normal appetites, metabolism, and feces returned, but they had laminitis, confirmed by histopathology.

"This is a new, more humane model for laminitis induction unique to our laboratory," Pollitt said. "At 24 hours," he continued, "the feces contained no Gram-negative organisms, only Gram-positive rods and diplococci, a fact which supports our contention that Gram-positive organisms, rapidly proliferating on excess substrate, are responsible for laminitis. Thus, we have discovered a pathway that links the metabolism of pasture grass, via fructan production, to fermentative activity in the equine large bowel that leads to laminitis.

"Domestic horses encounter fertilized, irrigated, monoculture pastures (planted with a single crop) across all the seasons and have little choice in what they consume," Pollitt stressed. "Agricultural scientists strive to breed high fructan pastures to increase production in cattle and sheep with no thought to the consequences for horses. Horses seek out grass varieties rich in fructan, greedily consuming the sweet stems, sometimes unwittingly to their own detriment."

Pollitt's laboratory has embarked on a three-year study, "Pasture Fructan Concentration as a Cause of Equine Laminitis," funded by the Rural Industries Research and Development Council in Australia, where an estimated 50% of laminitis cases are attributed to grass. Some aspects of Pollitt's clinical procedures are funded by the U.S.-based Animal Health Foundation.

The task ahead is to devise ways to manage horse pastures to reduce fructan production, managing horses to reduce pasture fructan consumption, and managing fructan-fermenting hindgut bacteria to prevent formation of laminitis trigger factors. "Difficult, but not impossible," Pollitt concluded.

For more information on fructans and grass-induced laminitis, see Article #278 at

About the Author

Fran Jurga

Fran Jurga is the publisher of Hoofcare & Lameness, The Journal of Equine Foot Science, based in Gloucester, Mass., and Hoofcare Online, an electronic newsletter accessible at Her work also includes promoting lameness-related research and information for practical use by farriers, veterinarians, and horse owners. Jurga authored Understanding The Equine Foot, published by Eclipse Press and available at or by calling 800/582-5604.

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